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Geriatric medicine

Diseases associated with aging are diseases that are often seen accompanying an increase in the rate of physiological aging. In general, we can say that diseases associated with aging are complications resulting from aging. Physiological aging. We must distinguish between diseases associated with aging and aging itself. All humans and animals age, but there are only exceptional cases of them who suffer from diseases associated with aging. Not every elderly person suffers from diseases associated with aging, while everyone who suffers from diseases associated with aging is elderly. Diseases associated with aging is a term that means “diseases of the elderly.” Diseases associated with aging must be distinguished from diseases of accelerated aging, although they are all caused by a genetic disorder. Examples of diseases associated with aging include the fact that the incidence of these diseases increases with age, and in the case of cancer, the rate increases many times over. Approximately 150,000 people die every day in the world, 100,000 of whom die from diseases related to age, and in industrialized countries the rate reaches 90%. Different patterns: 30% of mice develop cancer by the time they are three years old, while 30% of humans develop cancer by the time they are 85. People, dogs and rabbits get Alzheimer's disease, but rodents do not. Older rodents often die from cancer or kidney disease, not cardiovascular disease. Cancer rates in humans increase dramatically with age but may decline or stop by age 60-75. People with progeria or senility are at risk for many diseases. People with Werner syndrome have but are not at risk for Alzheimer's disease or neurodegeneration. People with Down syndrome have type 2 diabetes and Alzheimer's disease but are not at risk for high blood pressure, osteoporosis or cataracts. People with Bloom syndrome often die from cancer. Research: Age increases the risk of diseases associated with aging, while genes reveal who is susceptible and who is resistant among species and individuals within a species. For example, there are some changes that are often seen with age, such as the common saying that it has nothing to do with the death rate, but there are some specialists in the science of aging and everything related to the elderly, biogerontologists, who believe that there are changes that are not yet known or invisible behind the appearance of white hair, and this invisible factor increases the rate of malfunction of the rest of the body's organs, which accelerates the death of the organism. They claim that understanding and accepting the concept of diseases associated with aging will enhance and advance the biology of the elderly, just as knowledge of childhood diseases advanced knowledge of human evolution. Strategies for Engineered Negligible Senescence SENS is a systematic research institution that aims to correct some of the root causes of diseases and malfunction of vital functions associated with aging and to develop medical procedures and follow-up periodically to correct all the imbalances that affect the human body, and thus maintain eternal youth in the literal sense. SENS has developed a program that includes 7 factors that cause vital malfunction related to aging and has identified solutions for them. However, critics say that SENS has greatly exaggerated, to say the least, and that aging is a complex process and the knowledge that SENS has does not qualify it to be scientific or applicable in the near future.

Geriatric medicine

Elder abuse is the neglect or mistreatment of older adults by someone responsible for their care. The abuse can be physical, psychological, or financial. Elder abuse can occur at home, in residential care, or in the community. Elder abuse is a serious social and health issue that affects more older adults in Canadian society. It is estimated that between 4% and 10% of older adults in Ontario experience some form of abuse. Harm to older adults includes harm to people they know or have a relationship with, such as a spouse, partner, family member, friend, or neighbour, or people the older person relies on for services. Many forms of elder abuse are considered types of domestic violence or family violence because they are perpetrated by family members. Some paid caregivers have also been known to abuse their elderly patients. There are a variety of situations that constitute elder abuse, but they do not include general criminal activity toward older people, such as home invasion, street “robbery,” or “distraction burglary,” where a stranger distracts an older person on the doorstep while someone else enters to steal their belongings. Elder abuse by caregivers is a global problem. In 2002, the World Health Organization brought international attention to the issue of elder abuse. Over the years, government agencies and professional community groups around the world have identified elder abuse as a social problem. In 2006, the International Network for the Prevention of Elder Abuse designated June 15 as World Elder Abuse Awareness Day. A growing number of events are held around the world on this day to raise awareness of elder abuse and highlight ways to challenge such abuse. Although some older people with dementia or mental illness make false accusations of theft and other forms of abuse against caregivers or family members, all reports of abuse should be investigated. Although there are common themes of elder abuse across countries, there are unique manifestations that depend on the history, culture, economic power, and societal perceptions of older people within countries. The primary common denominator is the use of power and control by an individual to influence their peers and the status of an older person. There are several types of elder abuse that are generally recognized as elder abuse, including: Physical: such as hitting, punching, slapping, burning, pushing, kicking, restraining, unjustified imprisonment/confinement, giving excessive or inappropriate medication, withholding treatment and medications. Psychological/emotional: such as humiliating a person. A common feature is that the perpetrator identifies something that is important to an older person and then uses it to coerce them into doing something. It may take verbal forms such as yelling, name-calling, ridicule, constant criticism, accusation, or blaming, or it may take nonverbal forms such as ignoring, silence, ostracism, or withdrawal of affection. Elder financial abuse: Also known as financial exploitation, it involves the misappropriation of financial resources by a family member, caregiver, or stranger, or the use of financial means to control a person or facilitate other types of abuse, and sometimes the failure to provide financial support to poor older adults in jurisdictions with caregiving responsibility laws, such as France, Germany, and most of the United States. Sexual abuse: For example, forcing a person to engage in any sexual activity without their consent, including forcing them to engage in sexual conversations against their will, which may also include situations in which the person is no longer able to give consent. Neglect: For example, depriving a person of appropriate medical treatment, food, heat, clothing, rest, or essential medications, or depriving a person of services necessary to enforce certain types of actions, financial or otherwise. Neglect can include leaving a vulnerable older person unattended. The deprivation may be intentional or occur due to a lack of knowledge or resources. In addition, some state laws also recognize the following as elder abuse: Abandonment: Abandoning a dependent person with the intent to abandon or leave them unattended in a place for a period of time that may endanger their health or care. Abuse of rights: Denying an elder’s civil and constitutional rights, or failing to inform a court that they are mentally incapacitated. This is an aspect of elder abuse that is increasingly recognized and embraced in various states. Self-neglect: Anyone who neglects themselves by not caring for their own health or safety. Self-neglect is treated as conceptually different from abuse. Elderly self-neglect can lead to illness, injury, or even death. Common needs that older adults may deny or ignore include: sustenance, hygiene, adequate clothing for climate protection, adequate shelter, adequate safety, clean and healthy surroundings, medical care for serious illnesses, and essential medications. Self-neglect is often due to a person’s reduced awareness or mental capacity. Some older adults may choose to deny themselves certain health or safety benefits, which may not be self-neglect. This may simply be their personal choice. Caregivers and other responsible individuals should respect these choices if the older person is mentally sound. In other cases, older adults may lack the necessary resources, due to poverty, or another social condition. This is also not considered “self-neglect.” Institutional abuse refers to physical or psychological harm, as well as violations of rights, in settings where care and assistance are provided to dependent or other older adults, such as nursing homes. Recent studies of nearly 2,000 residents of nursing home facilities in the United States reported a 44 percent increased rate of abuse and a 95 percent increased rate of neglect, making elder abuse in nursing homes an increasing risk. Accurate statistics are scarce because elder abuse in general and especially nursing homes are often a silent phenomenon. The key to preventing abuse and intervening to stop elder abuse is to be able to recognize the warning signs. Signs of elder abuse vary depending on the type of abuse the victim is experiencing. Each type of abuse has distinct signs associated with it. In addition to noticing signs in the elderly individual, abuse can also be detected by observing changes in the caregiver’s behavior. For example, the caregiver may not allow them to talk to or greet visitors, show indifference or lack of affection toward the elderly, or refer to the elderly person as a burden. Caregivers who have a history of substance abuse or mental illness are more likely to commit elder abuse than other individuals. Abuse can sometimes be subtle and therefore difficult to detect. Regardless, awareness and research organizations advise taking any suspicion seriously and addressing it adequately and promptly.

Geriatric medicine

Elderly trauma refers to an accidental injury to an older person. The top three accidental deaths in older adults are falls, collisions, and burns. Severe declines in central nervous system function lead to loss of proprioception or sensory coordination, balance, and gross motor coordination, as well as reduced hand-eye coordination, reaction time, and unsteadiness in walking. These destructive changes are often accompanied by joint stiffness, which results in reduced range of motion of the head, neck, and extremities. Older adults also often take multiple medications to control multiple diseases and conditions. Side effects of some of these medications can lead to injury or worsen a previous injury; for example, someone taking blood-thinning medications may experience a cerebral hemorrhage if they sustain a minor head injury. These activities combined put older adults at greater risk for injuries and accidents. Both the incidence of accidents and falls and the severity of their complications increase with age. Virtually all organs in the body experience declines in function as they age. One example is the decline in circulatory function due to enlarged heart muscles. This can lead to pulmonary edema or heart failure. Brain atrophy accelerates around age 70, leading to a dramatic decrease in brain volume. Since the skull does not decrease in volume, there is a large space between the two, exposing older adults to a higher risk of brain hematomas after head injuries. Decreased brain volume can lead to decreased vision, hearing, and mental status. The elderly are the fastest growing demographic in developed countries. Although they are less likely to sustain injuries and accidents than children and young adults, the death rate from accidents and injuries is higher in older adults than in children and young adults. In the United States, this age group accounts for approximately 14% of all accidental injuries, the majority of which are due to falls.

Geriatric medicine

Eating for older people should take into account how people’s experiences and lives change as they age. That is, including conditions such as taste, diet and food choice. This primarily occurs when most people approach age 70 or older. Influencing variables can include: social and cultural environment; gender; personal habits; as well as physical and mental health. Scientific studies explain why people like or dislike certain foods. There is a lot of work and scientific research that goes into studying the variables that cause older people to change their diets. An example of such studies would be an experiment conducted by the Senior Nutrition Programme. To improve the quality of meal programmes, the European Neighbourhood Policy explored how food preferences differed by biological sex and ethnic group. A total of 2,024 ENP participants aged 60 or older were interviewed. The majority of participants were female, or served through group meal programmes, or meals served in community settings such as senior centres, churches or senior living communities. The overall impression of the meals was assessed for the top 13 food groups. After adjusting for other variables, older men had a greater preference for deli meats, meats, legumes, canned fruits, and ethnic foods than did women. Additionally, compared to African Americans, “Caucasians showed a higher preference for 9 of 13 food groups including pasta, meat, and fresh fruit. To improve the quality of the ENP and to increase older adults’ adherence to nutritional programs, food services require a strategic meal plan that seeks out and integrates the best foods for older adults.” There are multiple parts of an older person’s life that can influence their food preferences. Aspects such as environment, mental and physical health, and lifestyle choices all contribute to how a person decides what foods they like or dislike. An article on the effects of cognitive function in older adults states that “the nutritional status of older adults is related to their quality of life, ability to live independently, and risk of developing costly chronic diseases.” Well-being can be influenced by multiple socio-environmental factors, including access to healthy and affordable foods, food outlet locations, and nutritious restaurant choices. The Academy of Nutrition and Dietetics, the American Dietetic Association, and the Society for Nutrition Education have identified older adults’ access to a balanced diet as critical to preventing disease and promoting nutritional wellness so that quality of life and independence can be maintained throughout the aging process and excessive health care costs can be reduced. An individual’s environment and health can influence the foods they choose and prefer to eat. As people age, their bodies change. This includes their taste buds, their needs for certain vitamins and nutrients, and their desire for a variety of foods. In a study by the Monell Chemical Senses Center, five hundred young men and forty older adults participated. The young adults ranged in age from eighteen to thirty-five, and the older adults were sixty-five or older. There were more females than males in the study, but there were roughly equal proportions of males and females in both age groups. The study noted that younger women had stronger cravings for sweets than older women. They linked this difference in preference to the younger female test subjects’ shorter menstrual cycles and the fact that older women are no longer going through menopause. The study also determined that “ninety-one percent of cravings associated with a cycle occur in the second half of the cycle.” These physical changes could explain why someone who is older may not be getting the nutrition they need. As taste buds change with age, some foods may not be perceived as appetizing. For example, one study by Phyllis B. Grzegorszyk, Ph.D., suggests that as we age, our sense of taste for salty foods slowly disappears. When older adults in nursing homes eat frozen meals that are high in salt, they don’t enjoy them. This can lead to depression, anxiety, or suicidal thoughts. Not only are there differences in food preferences between ages, but also in biological sex. In a study conducted by the Nutrition Program in the Elderly, researchers explored male and female subjects’ preferences for 13 individual food groups. From this study, it was clear that older men “were more likely to prefer deli meats, meats, legumes, canned fruits, and ethnic foods than were females.” Another study conducted by the Monell Chemical Sensitivity Center concluded that females had a greater desire for sweets and chocolate than males. The results of the study confirmed that males had greater cravings or preferences for appetizers than for sweets. As people age, some people tend to avoid food and are unwilling to modify their diet due to oral health problems. Oral health problems, such as ill-fitting dentures or gum disease, are associated with significant differences in dietary quality, a measure of diet quality using a total of eight recommendations for food and nutrient consumption. From the National Academy of Sciences. Approaches to reducing food avoidance and encouraging dietary changes are urgently needed for people with eating difficulties due to oral health conditions, such as their inability to chew or eat food properly, as their health is greatly improved and their food preferences are greatly limited. A decline in physical health can lead to a deterioration in diet due to difficulties in preparing and eating food as a result of conditions such as arthritis. At the 2010 Healthy and Safe Eating in Aging conference sponsored by the Institute of Medicine, Dr. Catherine Tucker noted that older adults are less active and have a lower metabolism with a reduced need to eat. They also tend to have existing diseases and/or take medications that interfere with nutrient absorption. With changing nutritional requirements, one study developed a modified food pyramid for adults over the age of 70. The impact of certain diseases can also affect the quality of food in older adults, especially those in nursing homes. Often, when some suffer from Alzheimer’s disease, they do not receive the necessary care, and a decline in mental health is seen. It is a proven fact that those who have relationships with others live longer. When a person falls victim to such a mentally limiting disease, they can die earlier than they would have if they had not had the disease. This can be changed with proper care and a general sense of well-being, but when a person does not have the right nutrition and food choices, they will fall victim to this. As a result of certain mental health conditions and/or diseases - such as Alzheimer's - a person's food preferences may be affected. With some diseases, people tend to develop specific preferences or aversions to different types of food. For example, people with Alzheimer's experience many large and small changes as a result of their symptoms. One change identified by Suszynski in "How Dementia Tampers With Taste Buds" is the taste of the dementia patient's brain, which contains taste receptors. Since they do not experience flavor as they once did, people with dementia often change their eating habits and take on entirely new food preferences. In this study, the researchers found that these dementia patients had problems identifying flavors and appeared to lose the ability to remember tastes. Thus, leading to the theory that dementia caused patients to lose their knowledge of flavors. This in turn could lead to changes in eating behaviors. Psychological conditions can affect eating habits in older adults. For example, prolonged widowhood can affect nutrition. Depression in older adults is also associated with a risk of poor nutrition. Older adults can make different lifestyle choices about healthy eating. Food choices are often the result of personal beliefs and preferences. Other research has found that adults, regardless of age, tend to increase their fruit and vegetable consumption after being diagnosed with breast, prostate, or colorectal cancer. The environment can greatly influence food preferences in older adults. Those 75 and older tend to have limited mobility due to health conditions and rely on others to shop for and prepare food. Homebound older adults tend to receive one meal a day from communities that provide group meals, or meals served in community settings such as senior centers, churches, or senior living communities. These meal programs are encouraged to provide this meal to seniors at least five times a week. Access to transportation may also be less important, especially in rural areas where public transportation is scarce. However, the Iowa study failed to find problems with food shopping among seniors in open rural towns and cities, as those who do not rely on their own transportation rely on family, friends, and senior services. A separate study found little difference in urban areas with seniors who do not own a car. Aside from transportation, the type and quality of food available can also shape food choices if a person lives in a so-called “food desert.” The type of social network can also influence individuals’ choices in older individuals as well. For example, someone with a larger social network and lower economic status is more likely to be well-nourished than someone with a smaller social network and higher economic status. This means that it is important for our younger aging population to maintain social networks so that they can live longer and have more active lifestyles, especially when it comes to food.

Geriatric medicine

Normal-pressure hydrocephalus, also called symptomatic hydrocephalus, is a brain disorder caused by decreased absorption of cerebrospinal fluid. Typical symptoms include gait disturbances, urinary incontinence, and dementia or mental decline. It is difficult to diagnose because these symptoms are common to many other diseases. The usual treatment is to place a shunt to drain excess CSF to another part of the body. This treatment may reverse symptoms and restore normal function, may do so partially, or may not. The term normotensive comes from a paper published in 1965 before the development of intracranial pressure measurement techniques, and it is now recognized that the term normotensive in the name of this disease is a misnomer. There are two types of normotensive hydrocephalus: idiopathic and secondary. Secondary hydrocephalus can be the result of subarachnoid hemorrhage, head trauma, tumor, infection of the central nervous system, or complications of skull surgery. Normal pressure hydrocephalus is an increase in intracranial pressure due to the accumulation of cerebrospinal fluid in larger than normal quantities in the ventricles of the brain, causing ventricles to enlarge. The intracranial pressure gradually decreases but remains slightly elevated, with the CSF pressure reaching the upper limits of the normal range of 150 to 200 mm H2O. These patients do not usually have elevated intracranial pressure numbers, so they do not experience the classic symptoms of increased intracranial pressure such as headache, nausea, vomiting, or altered consciousness, although some studies have shown that they do have intermittent pressure increases. However, the enlarged ventricles compress the adjacent cortical tissue, causing myriad effects on the patient. The classic symptomatic triad was first described by Hakim and Adams in 1965. Normative hydrocephalus is often misdiagnosed as Parkinson's, Alzheimer's, or dementia, due to its chronic nature and nonspecific symptoms. Normotonic hydrocephalus presents with the classic triad of clinical findings of urinary incontinence, unsteady gait, and cognitive impairment. Gait disturbance is usually the initial and most prominent symptom of the triad and may be progressive, due to dilatation of the ventricular system, especially at the level of the lateral ventricles. This compresses the motor fibers that descend through the corticospinal tract to the lumbosacral spinal cord, causing them to be pulled upward. Unsteady gait can be classified as mild, characterized by ataxia, or severe in the early stages. This gait disturbance often presents as ataxia and loss of balance, especially when climbing stairs and sidewalks. Muscle weakness and fatigue in the legs may be part of the complaint, although examination shows no paralysis or ataxia. The patient usually uses something to help him walk steadily without ataxia as he moves from mild to marked. A wheeled crutch or quadrupedal crutch is an aid to this. The patient's gait in the marked stage shows a lack of foot clearance when walking or the patient drags the foot on the ground while walking, in addition to a decrease in walking speed. This pattern is commonly referred to as a magnetic gait, where the foot appears to be stuck to the surface on which it is walking, and the gait disturbance is the characteristic symptom of normotonic hydrocephalus. The gait may begin to mimic a parkinsonian gait, with short, shuffling steps, a hunched, forward-bending posture, but no stiffness or tremor. An increased tendency to fall backwards is also seen, and the patient may also use a wide-based gait to increase their base of support and thus their stability. In the very late stages, the patient may deteriorate from the inability to walk to the inability to stand, sit, rise from a chair, or roll over in bed. This advanced stage is referred to as "ataxia of standing and walking due to hydrocephalus." Cognitive dementia: Cognitive dementia usually predominates in the frontal lobe and is a subcortical type of dementia. It manifests as apathy, forgetfulness, rigidity, inattention, and a decrease in the speed of processing complex information. Disorders of processing acquired knowledge, reflecting loss of frontal lobe integrity. Memory disturbances are often a component of the overall problems and are the most prevalent in some cases, which may lead to misdiagnosis as Alzheimer's. However, in normotonic hydrocephalus there may be a marked contrast between memory impairment and intact or less affected cognition. Dementia Dementia is thought to result from traction of the frontal and myelinated fibers that run in the periventricular area. Urinary incontinence: This appears late in the disease and is found to be caused by spastic hyperreflexia, increased urgency associated with decreased inhibition of bladder contractions and detrusor muscle instability. In the most severe cases, bladder hyperreflexia is associated with loss of interest in urination due to severe cognitive damage to the frontal lobe. This is also known as frontal incontinence, where the patient is indifferent to his frequent urinary symptoms. Diagnosis of normotonic hydrocephalus is usually made initially by brain imaging, either CT or MRI, to detect any mass brain injury. This is followed by lumbar puncture and evaluation of the clinical response to removal of CSF. This may be followed by continuous lumbar drainage of CSF over 3-4 days. CT may show dilated ventricles without atrophy of the cerebral convolutions. MRI may show minimal degrees of migration of CSF surrounding the ventricles into the ependymium in the second/Flier time sequence. Radiography may not differentiate between clinically similar pathologies such as Alzheimer's dementia, vascular dementia, or Parkinson's dementia. After radiography, lumbar puncture is the first step in the diagnosis and the CSF opening pressure is carefully measured. In most cases, the pressure is usually above 155 mm H2O. Clinical improvement after removal of CSF has a high predictive value for the success of subsequent shunt placement. This is called a lumbar puncture or Miller Fisher test. Conversely, a negative test has very little diagnostic value, and many patients improve after shunt placement despite no improvement after CSF removal. A leak test is a test that may have higher sensitivity and specificity than a lumbar puncture but is not performed in most centers. Some centers consider the velocity of CSF egress to be a significant predictor of the success of hydrocephalus surgery. The velocity of egress can be determined by a leak test. This is not a test usually performed before shunt placement but may be useful in determining the likelihood of a patient improving after shunt placement. In some centers, an external lumbar puncture has been shown to have high sensitivity and specificity for the expected success of surgery. Patients with dementia who are dependent on home nursing care and whose only diagnosis of hydrocephalus is stress are likely to become independent once treated. To date, only one study has been able to assess the prevalence of normotonic hydrocephalus in both diagnosed and undiagnosed populations and has shown a prevalence of 9-14%. Patients with normotonic hydrocephalus may recover surgically by implanting a ventriculoperitoneal shunt to drain excess CSF into the abdomen where it is absorbed. Once the shunt is in place, the ventricles usually shrink within 3-4 days, regardless of the duration of hydrocephalus. Despite the reduction in ventricular swelling, only 21% of patients show significant improvement in symptoms. Patients most likely to show improvement are those with only mild or no gait disturbance, mild cognitive impairment, or mild cognitive impairment. A more recent study in 2004 found better results, concluding that if patients with normotonic hydrocephalus are correctly identified, shunt implantation will result in beneficial outcomes in 86% of patients, with 81% of patients experiencing gait disturbance, 70% of patients experiencing improvement in grip strength, or both. Note also that measurements in the diagnostic triad, cortical sulcus size, and periventricular flare are all related to outcome. However, other factors such as patient age, duration of symptoms, ventricular dilatation, and degree of dementia before surgery are also related to outcome. Recent population studies have estimated the prevalence of normotonic hydrocephalus to be about 0.5% in people over 65 years of age with an incidence of about 5.5 patients per 100,000 population per year. This is consistent with similar findings that although normotonic hydrocephalus can occur in both men and women of any age, it has been found to occur predominantly in the elderly and peak incidence in the sixth or seventh decade of life.

Geriatric medicine

It should not be confused with Lewy body dementia, an umbrella term that includes Parkinson's disease and dementia with Lewy bodies. Dementia with Lewy bodies (DLB) is a type of dementia characterized by changes in sleep, behavior, cognition, movement, and autonomic functions. Memory loss is not always an early symptom. The disease worsens over time and is usually diagnosed when cognitive decline interferes with normal daily functioning. Along with Parkinson's disease, dementia with Lewy bodies is one of two conditions that fall within the category of Lewy body dementia. It is a common form of dementia, but its prevalence is not precisely known and many cases go undiagnosed. The disease was first described by Kenji Kosaka in 1976. REM sleep behavior disorder—in which people lose the muscle paralysis that normally occurs during REM sleep and act out their dreams—is a key feature. REM sleep behavior disorder may appear years or decades before other symptoms. Other key features are visual hallucinations, marked fluctuations in attention or alertness, and tremors. Not all features must be present for a diagnosis. A definitive diagnosis usually requires an autopsy, but a presumptive diagnosis is made based on symptoms and tests that may include blood tests, neuropsychological tests, imaging, and sleep studies. Most people with dementia with Lewy bodies do not have affected family members, although dementia with Lewy bodies sometimes runs in families. The exact cause is unknown, but it involves widespread deposits of abnormal protein clumps that form in the nerve cells of the affected brain. Known as Lewy bodies — discovered by Friedrich Lewy in 1912 — and Lewy bands, these clumps affect the central nervous system and the autonomic nervous system. Heart function and some gastrointestinal functions, from chewing to defecation, may be affected. Constipation is the most common symptom. Low blood pressure upon standing may also be a symptom. Dementia with Lewy bodies also affects behavior; mood changes such as depression and apathy are common. Dementia with Lewy bodies usually begins after age 50, and people with the disease have an average life expectancy of about 8 years after diagnosis. There is no treatment or medication to stop the disease from progressing, and people in the later stages of dementia with Lewy bodies may not be able to care for themselves. Treatments aim to relieve some of the symptoms and reduce the burden on caregivers. Medications such as donepezil and rivastigmine are effective in improving cognition and overall functioning, and melatonin can be used for sleep-related symptoms. Antipsychotics are usually avoided, even for hallucinations. Because severe reactions occur in about half of people with dementia with Lewy bodies, their use can be fatal. Dealing with the many different symptoms is difficult, as it involves multiple disciplines and caregiver education. Dementia with Lewy bodies is a type of progressive, neurodegenerative dementia. That is, it is characterized by deterioration of the central nervous system that gets worse over time. Dementia with Lewy bodies is sometimes classified in other ways. It is one of two types of Lewy body dementia, along with Parkinson's disease. Atypical Parkinson's syndromes include dementia with Lewy bodies, along with other conditions. Finally, dementia with Lewy bodies is an encapsulated neuropathy, meaning it is characterized by abnormal deposits of the protein alpha-synuclein in the brain. Other neuropathies include Parkinson’s disease, multiple system atrophy, and other rare conditions. This type of dementia is characterized by cognitive impairment, recurrent visual hallucinations, REM sleep disturbances, and parkinsonism immediately after or after the dementia is diagnosed, according to Melissa Armstrong. People with dementia with Lewy bodies have a wide range of symptoms, and it is generally more complex than most other types of dementia. The disease affects different areas of the nervous system; the accumulation of alpha-synuclein deposits damages these areas, causing the diverse neurological manifestations of the disease. Dementia with Lewy bodies begins with a specific set of early signs and symptoms called the prodromal phase of the disease or pre-dementia. These signs and symptoms may appear 15 or more years before the onset of dementia. These symptoms include constipation and dizziness due to autonomic nervous system dysfunction, decreased sense of smell, visual hallucinations, and rapid eye movement (REM) sleep disorder. REM sleep disorder may appear years or decades before other symptoms. Early symptoms do not always include memory loss. The manifestations of dementia with Lewy bodies can be divided into core, essential, and supporting features. Dementia is the core feature and must be present for diagnosis, while essential and supporting features are additional evidence to support the diagnosis. Dementia is diagnosed after cognitive decline has progressed to a point where it interferes with normal daily activities or social or occupational functioning. Dementia is a core feature of dementia with Lewy bodies, but it does not always appear early on and tends to appear as the condition progresses. Core symptoms vary but typically include: disturbance of cognition, alertness, or attention, disturbance of REM sleep, one or more parkinsonian features, and recurrent visual hallucinations. These features are classified as core features based on the 2017 Fourth Consensus Report of the Dementia with Lewy Body Consortium. The report relied on high-quality evidence to support the quality of these disease manifestations. Cognitive dysfunction is the most common and characteristic feature of Lewy body dementia. Cognitive dysfunction associated with this type of dementia is distinguished from other types of dementia by the associated disturbance in attention and alertness. It is also characterized by its spontaneous onset and by a clear distinction between the worst and best cases, according to McKeith. These fluctuations vary in severity, frequency, and duration. Each episode lasts from seconds to weeks and is separated by normal intervals. Cognitive tests will not accurately reflect the severity of the disease when relatively normal intervals coincide with monthly medical appointments. The disease affects three areas of cognition: executive function, visuospatial function, and attentional control. Episodic cognitive dysfunction appears early in the course of the disease. People with dementia with Lewy bodies are easily distracted, have difficulty concentrating on tasks, or are described as absent-minded, and may experience periods of blurred consciousness, confusion, agitation, and incoherent speech. People with dementia with Lewy bodies have trouble coherent speech and may have changes in their ability to organize their thoughts throughout the day. Executive functions describe attention, behavior, memory, and the cognitive flexibility that helps with problem solving and planning. Executive function problems occur in activities that require planning and organization. Deficits may include poor performance, inability to follow a conversation, difficulty multitasking, and problems with driving—such as misjudging distances or getting lost. A person with dementia with Lewy bodies may have problems with wakefulness and sleep in addition to REM sleep disorder, and these problems can be severe. Sleep and wakefulness disorders include daytime sleepiness, drowsiness or naps lasting more than two hours a day, insomnia, periodic limb movement disorder, restless legs syndrome, and sleep apnea. REM sleep disorder is a sleep disorder. People with dementia with Lewy bodies lose the normal muscle paralysis during REM, which can cause them to act out movements they do in their dreams or make other unusual movements or sounds. About 80% of people with dementia with Lewy bodies have REM sleep disorder. Abnormal sleep behaviors may begin before cognitive decline is noticed, may appear decades before any other symptoms, and are often the first clinical sign of dementia with Lewy bodies and an early sign of synucleinopathy. Autopsy evidence of synucleinopathy in individuals with REM sleep disorder confirmed by electroencephalography shows 94–98% of individuals with REM sleep disorder, with dementia with Lewy bodies and Parkinson's disease being the most common, with approximately equal rates. People with REM sleep disorder are diagnosed with a neurodegenerative disorder within 10 years, and neurodegenerative manifestations may be delayed for up to 50 years after the diagnosis of the sleep disorder. REM sleep disorder may lessen over time. Some people with REM sleep disorder are unaware that they are acting out their dreams. REM sleep disorder behaviors may include screaming, laughing, crying, slurred speech, nonviolent hitting, violent punching, kicking, choking, and scratching. Reported behaviors are violent and often in the context of a chase or attack. People with REM sleep disorder may fall out of bed or injure themselves or their bed partner, which can cause bruising, fractures, or subdural hematomas. People often remember violent dreams and behaviors and report them or seek medical attention when an injury occurs. Therefore, selection and recall bias may explain the high frequency of violent behaviors reported in the context of REM sleep disorder. Parkinsonism is a clinical syndrome characterized by slowness of movement, rigidity, balance disturbance, and tremor. Parkinsonism is seen in dementia with Lewy bodies and several other conditions, including Parkinson's disease, Parkinsonian dementia, and others. Parkinsonism is diagnosed in more than 85% of people with dementia with Lewy bodies; these patients usually have one or more of the core features of the syndrome, but tremors at rest are less common. Motor symptoms may include parkinsonian gait, balance disturbance, falls, rigid facial expressions, and soft speech. Motor symptoms vary in their presentation, but are usually symmetrical. Patients with dementia with Lewy bodies may have only one of the parkinsonian features, and the severity may be less than in Parkinson's disease.

Geriatric medicine

Reminiscence therapy is a technique used to provide counseling and support to older adults, and is used in patients with brain damage who have symptoms of “Alzheimer’s disease and other forms of cognitive impairment.” A 2018 article from the American Association of Retired Persons focused on a separate project called Gleaner Town Square that looked at individuals who had symptoms of Alzheimer’s disease or other forms of dementia. The goal of the Gleaner project was to “photograph the years 1953 to 1961,” with participants going back in time and reminiscing about their lives between the ages of 10 and 30, the period when “our strongest memories are formed.” The American Psychiatric Association defines reminiscence therapy as “the use of life histories, written, oral, or both, to improve psychological well-being. It is often used in older adults.” This type of therapeutic intervention respects the individual’s life and experiences and helps the patient maintain mental health. Most research on reminiscence therapy has been conducted in older adults, particularly those suffering from depression, though some studies have looked at other older populations. Reminiscence therapy has been researched and implemented in many areas across cultures, in Japan, the United Kingdom, and the United States. Reminiscence is described as “the process of voluntarily or involuntarily bringing to mind one’s past memories.” It involves reliving and reliving events in one’s life. This requires that “autobiographical memory” be intact in order to be able to recall specific life events. Reminiscence is meaningful to the extent that the memories retrieved are meaningful. There are different ways to make memories meaningful, including asking questions that suggest the significance of the event as well as using old memories from the past. Reminiscence has different psychological functions. Webster’s classification offers eight reasons why people reminisce: to relieve boredom, to revive emotional pain, to prepare for death, to have conversations and identity, to maintain intimate relationships, to solve problems, to teach, and to inform. Psychologists believe that the therapeutic use of reminiscence has positive results in improving coping skills and emotions, although its effectiveness is controversial. Recent data suggest that there are positive and lasting effects of reminiscence therapy among older people. There are different types of reminiscence. The two main types are interpersonal reminiscence and interpersonal reminiscence. Interpersonal reminiscence is cognitive in nature and is conducted individually. Interpersonal reminiscence is more conversational and is a group therapy. Reminiscence can be divided into three types: informative, evaluative, and urgent. Informative reminiscence is for the pleasure of retelling past stories. This type can be used to help people who have lost interest in life and relationships. Recalling good memories helps them focus on what they were happy about. Evaluative reminiscence is the main type used in reminiscence therapy because it is based on the “life review” introduced by Dr. Robert Butler. This process involves retrieving memories from across one’s life and sharing stories with other people. This is often done in group therapy. Urgent reminiscence is when an individual needs to let go of persistent emotional distress or guilt. By working through these issues, individuals can find peace with themselves. Reminiscence is used to help people cope with the death of a loved one by sharing stories about their life, remembering fond memories, and coming to terms with death. Reminiscence therapy is often used in nursing homes. The structure of reminiscence therapy can vary widely. In one documented session, the therapist played different songs from the 1920s to the 1960s and asked patients which songs held special meaning for them. In another session conducted by the same therapist, participants shared photos and talked about why they were important to them. Psychological research identifies two types of reminiscence therapy as particularly effective: integrative and procedural. Prior to the late 1950s, remembering the past was viewed as a negative symptom that often led to a decline in mental functioning. Erik Erikson introduced his concept of eight stages of psychological development from birth to death. The final stage is known as “late adulthood,” and it introduces the idea of “integration versus despair.” It is important at this stage to look back on one’s life with satisfaction and contentment before one dies. In 1963, Dr. Robert Butler published a paper on the critical points regarding the importance of life review and reminiscence. Butler is credited with starting the reminiscence therapy movement. Charles Lewis took the next step in the field in 1971. He conducted the first experimental study of reminiscence. Lewis wanted to investigate the cognitive changes that the process of remembering the past might cause, and how individuals viewed themselves. This experiment proved to be important, and in the years that followed it became a popular area of research. Subsequent research focused on the functions and benefits of remembering the past. In 1978, the U.S. Department of Health and Social Security began a project called the “Reminiscence Assistance Project.” The goal of the project was to begin using reminiscence as a therapeutic method. In the 1980s, reminiscence therapy was recognized by health care institutions and began to be used as a group therapy. During this time, the number of professionals trained to provide this therapy increased. Reminiscence therapy remains a research area to this day. Although much research has been done in this area, Butler and Erickson remain the researchers most closely associated with it.

Geriatric medicine

Home care or in-home care is supportive care provided in the home. Care may be provided by health care professionals who provide health care or by caregivers who provide day-to-day care and ensure that daily activities are maintained. Home care is often called "home health care" or primary care. The term home health care is often used to distinguish non-medical care from foster care and special care provided by people other than nurses, doctors, or licensed medical professionals. Home care services help adults, seniors, and children recover from hospitalization or need extra help to ensure their safety at home and avoid unnecessary hospitalizations. Home care is mostly made up of licensed and unlicensed non-medical staff who assist the patient with caregiving tasks. There are also unlicensed staff who help individuals with daily tasks such as eating, bathing, cleaning the house, and preparing meals. Caregivers work to meet the needs of individuals in need and this care helps them stay in their own homes rather than in a health care facility. Non-medical home care is paid for by the individual in need or a relative. The term “private duty” refers to the out-of-pocket nature of these services, as opposed to government- or insurance-sponsored health care. These traditional differences in home care are changing as the world’s population ages, so individuals are increasingly choosing to be independent and using these services to maintain their lifestyles. Government agencies and insurance companies are increasingly subsidizing these services instead of health care facilities because they are less expensive in the long run. Specialties associated with home care include licensed nurses, registered nurses, home health aides, physical therapists, occupational therapists, and social workers. Rehabilitation services are provided by physical therapists, occupational therapists, speech and hearing pathologists, and dietitians. Professionals may work as independent practitioners, as part of a larger organization, or as part of a branch. Licensed nurse aides and caregivers are trained to provide non-medical or non-custodial care, such as helping patients get dressed, get up, go to bed, and use the bathroom. They may also prepare meals, accompany patients to medical visits, go to the grocery store, and perform a variety of errands. The terms "home care" and "in-home care" are used interchangeably in the United States to mean any type of care provided to a person in their home. These terms have historically been used interchangeably to refer to caregivers who do not have the necessary skills to do so. However, there has recently been a movement to differentiate between in-home care providers, which are licensed nurses, and home care providers, meaning non-medical care. Home care aims to make it possible for people to stay at home rather than in long-term housing or health care institutions. Caregivers provide services to patients in their own homes. These services can be a combination of professional health care services and assisted living services. Professional home health services can include medical or psychological assessment, wound care, medication education, pain management, disease education and management, physical therapy, speech therapy, or occupational therapy. Assisted living services include assistance with daily tasks such as meal preparation, medication reminders, laundry, light housekeeping, errands, shopping, transportation, and companionship. Home care is often an integral part of the recovery period after treatment, especially in the first few weeks when the patient needs the most daily assistance. Although there are differences in the terminology used to describe home care or home medical care in the United States and around the world, the description is similar for most parts. In the United States, it is estimated that most home care is informal, with family and friends providing the substantial amount of care. Health care professionals are most often associated with nurses, physical therapists, and home health aides in formal care. Other care providers include respiratory therapists, occupational therapists, and mental health therapists. Home health care is usually paid for through Medicaid, Medicare, long-term insurance, or the patient's own resources. Home health care applications or home care applications fall under the umbrella category of health care information technology. Home health information technology is "information processing applications including mechanical, electronic, and computer system software that store, retrieve, and share input information and use health care information and knowledge for communication and decision-making." Requirements are determined by each state's health department. Candidates for care are tested to become legally eligible for the title of "nursing aide." Other requirements in the United States include general background checks, drug and alcohol safety checks, and a background check. California does not provide licensing for non-health care services, so there are no requirements for admission. Full-service agencies conduct background checks of applicants, including criminal background checks. In addition, mediation agencies are trained to monitor and supervise home care providers. California licenses home care businesses under the California Home Health Administration. Florida licenses at several levels that relate to the services provided. Home aide agencies provide assistance to home care providers, although nursing and daily activities services are provided by home health agencies or nursing homes. Compensation varies by discipline, but Department of Labor statistics estimate that in 2012, home care providers were paid an hourly wage of $10.01 with an average annual wage of $20,820. A rule published by the Department of Labor titled “Application of Fair Labor Standards for Special Services” went into effect on January 1, 2015, and was written to revise “the definition of ‘attendant services’ to clarify and limit the duties that fall under the term; and third-party workers such as home care agencies will not be able to claim both exemptions.” The most significant effect of the recent law will be that more private-sector workers are protected from low wages, overtime, and record-keeping provisions for fair labor standards.” However, the Home Care Organization of America and a local home care organization sued the Department of Labor over the law being enforced in federal court. The Labor Department was subsequently appealed. The law was upheld in August 2015 by the U.S. District Court for the District of Columbia Circuit. $710,000 was paid by Medicare, if that is the primary carrier between the two types of insurance. Also, if a patient has Medicare and needs a skilled nurse practitioner, the patient’s case is often billed by Medicare. $235,000 is paid by private insurance or his/her own family. Private insurance includes the Veterans Administration and some health plans or private insurance for iron and steel workers. There are specialists and organized companies that provide home health care services. Lotus Shiu and Lee found that home nursing is better suited for patients with serious illnesses than for patients with non-critical conditions. Modin and Verhoeff stated that the role of physicians is more important than that of nurses and care workers. From an epidemiological point of view, the risk of infectious diseases acquired by home nursing is higher than that of inpatient and home care nurses. In terms of financial expenditure, home nursing is more effective than inpatient and home care nurses. The quality angles of home nursing are reviewed by Riccio. Christensen and Grönvall examine the challenges and opportunities presented by technical communication. Although health workers provide care to mature people and family members, health workers advocate appreciation for the mutual effort.

Geriatric medicine

Fall prevention is a set of actions that help reduce the number of falls suffered by older adults. Fall-related injuries are one of the most serious health problems in older adults. About one-third of older adults suffer from falls at least once a year. Half of them suffer from more than one fall a year. Due to osteoporosis, decreased mobility, and slowed reflexes, falls cause fractures of the pelvis and head, and sometimes cause death in these older adults. Fractures resulting from accidents are the fifth leading cause of death in older adults. In about 75% of fracture cases, patients suffer from incomplete recovery and general deterioration in health. Indicators of risk of falling include a history of a fall in the past, and problems with walking and balance. Some studies consider the following conditions to be associated with an increased risk of falling: impaired vision, certain medications, and deterioration in daily living activities and cognition. The role of orthostatic hypotension in increasing the risk of falling is unclear. Research indicates that intervention programs that reduce the risk factors for falls in adults reduce falls by 27 percent in the general population and by 14 percent in patients with a history of falls or other risk factors. This information is based on scientific studies conducted in this area. Although more research is needed, preventive measures that have shown the greatest impact in preventing falls include: balance, reducing household hazards, drug withdrawal effects resulting from stopping psychotropic medications, pacemakers, patients with carotid artery hypersensitivity, and Tai Chi. Tai Chi has shown a 47 percent reduction in falls in some studies, but it is not an aid to stability when standing. Tai Chi may help increase self-confidence rather than directly affecting balance when standing. Assistive technology can be implemented, although it may lead to reactions in cases of falls. Preventive improvements include handles that help with balance in the home and outside. It is advisable to have such bars next to the stairs and on the floors and when the floors have dangerous patterns such as slippery and unclear ones. There are special handles that can be placed in the bathrooms. In addition to crutches and supports that will facilitate movement and reduce falls. The lighting factor is important in human engineering in order to reduce the risks resulting from falling due to obstacles and dangerous places. The lamps must be available with high power and efficiency in places where there is danger in order to avoid it. These lamps must be fast in working and not the type that works late. This emphasis on the importance of adequate lighting comes because patients with macular degeneration and cataracts find it difficult to see. The stability factor while standing is also very important and for this reason it is recommended that the floors be as rough as possible to avoid slipping. In addition to wearing suitable shoes for this purpose, for example, shoes made of rubber and synthetic rubber. Padded floors such as carpets padded with foam and rubber may help to mitigate the damage caused by falls. Rubber tiles and covering and smoothing furniture with sharp corners can help. The risk of slipping increases when there are slippery rugs, banana peels, or spilled liquids on the floor. Floors should be free of obstructions. Bifocal and trifocal glasses used for reading only are not safe for walking and moving around while wearing them. It is recommended to wear separate glasses for reading and walking. The goal of health care is to identify the causes of falls and fractures, such as osteoporosis, multiple medications, balance and mobility problems, vision loss, and a history of falling. There are medications that are not recommended for use in older adults, which Pierre listed in his name. The evaluation of each patient's fall is aimed at identifying the causes and how to avoid them in the future. Some clinical tests are performed when the fall is not due to loss of consciousness in order to identify the causative factors. Studies have shown that strengthening flexibility, balance, and stability in patients improves movement and also prevents falls. The majority of older adults do not exercise regularly, and 35% of those over the age of 65 do not participate in recreational activities. Many people who have fallen stop exercising for fear of falling. The home can be a source of danger, especially the bathroom, shower and stairs. Home improvements can be made to reduce the risks surrounding the elderly patient, such as reducing clutter and increasing handles in necessary places such as the shower and next to the toilet. Installing anti-slip mats on the floor, providing iron bars next to the stairs, and adequate lighting can also help. Currently, there is no scientific evidence that these home improvements are effective in reducing risks. We have shown that these improvements. Falls are common in the age group of 65 years and older. The risk of falling is doubled when the person is hospitalized. The differences between falls in patients have not been determined in studies. The study says that 60% of elderly people with cognitive and memory problems suffer from falls each year. Most falls are due to patients with chronic health problems and are over the age of 65. Internal and external factors have been discovered to cause falls. In order to prevent falls, we must find solutions to the causes that lead to falls and try to find the necessary alternatives.

Geriatric medicine

Osteolysis is the active breakdown of the bone matrix by osteoclasts during the normal formation of healthy bone. Osteolysis can be thought of as a reversible process of bone formation. This breakdown usually occurs in the proximal portion of the prosthesis due to either an immune response or changes in the structural load of the bone. Diseases such as bone tumors, cysts, and chronic inflammation can cause osteolysis. Although osteolysis is often associated with a variety of diseases or joint problems, the term "osteolysis" generally refers to a common problem in artificial joint replacements such as total hip replacements, total knee replacements, and total shoulder replacements. Osteolysis can also be associated with radiographic changes seen in a person with biphosphate-related osteonecrosis of the jaw. There are several biological mechanisms that may lead to osteolysis. In total hip replacements, the generally accepted explanation for osteolysis involves wear particles. As the body attempts to clean these particles, it causes an autoimmune reaction that in turn leads to soft tissue damage. Osteolysis can occur as early as 12 months after implantation and is often progressive. This may require revision surgery. Although clinically asymptomatic, osteolysis can result in implant loss or bone fractures, which can lead to serious medical problems. Distal clavicle dissection is often associated with weightlifters' problems with the acromioclavicular joints resulting from the high stresses placed on the clavicle at its junction with the acromion. This condition is often referred to as "weightlifter's shoulder." Ultrasonography readily depicts resorption of the distal clavicle as irregular cortical erosions, whereas the acromion remains intact. Associated findings include a swollen joint capsule, soft tissue swelling, and joint instability. On physical examination, the joint is tender and the adduction maneuver toward the horizontal axis is painful. The acromioclavicular joint is usually stable but may have a crackling sound. The range of motion of the glenohumeral joint should be complete. The differential diagnosis may include metabolic, 1. autoimmune, and 2. malignant causes. Since distal clavicle degeneration usually involves a single joint, the presence of inflammation suggests that both joints are involved. Patients who fail conservative treatment are first restricted in their activities and may be considered for surgical treatment. Surgery is generally avoided in cases where surgery is contraindicated. Most operations are performed under general anesthesia, so nonsurgical treatment is continued for those patients who may be at risk from anesthesia. A common surgical procedure for distal clavicle degeneration involves resection of the distal portion of the clavicle and then removal of a few millimeters of bone from the distal end. Medications may be given to relieve pain and inflammation, and medications may be used to help the body form new bone cells more quickly. Follow-up with your doctor should be done if you feel that the medication is not working or if you experience side effects. He should also be informed in case of any allergy to any medication and keep a list of all medications, vitamins and herbs that are taken with the doses, and keep it with the patient at all times for emergencies. Exercise with caution and know the types of sports that can be practiced, as sports that require physical contact increase the chance of bone fractures. You should contact your doctor in case of: 8 Feeling pain in the chest, back, hip, groin, knee or foot with sudden movement or during rest. You should go to the emergency room in case of:

Geriatric medicine

Parkinsonism is a chronic neurological disorder characterized primarily by muscle stiffness. Parkinsonism is sometimes referred to as Parkinson's disease. Parkinsonism includes rigidity, tremor, slowness of movement, and impaired balance in posture. The name comes from Parkinson's disease, which is characterized by these symptoms. Parkinsonism can also be found in conditions other than Parkinson's disease, such as Lewy body dementia and Parkinson's disease dementia. Parkinsonism is a clinical syndrome characterized in Parkinson's disease by four motor symptoms: tremor, slowness of movement, contracture, and postural instability. Parkinsonian gait problems can lead to falls, and serious physical injuries are other common symptoms:

Geriatric medicine

The All-Inclusive Senior Care Program is a program that provides comprehensive health services to individuals age 55 and older who are frail enough to be classified as “home-care eligible” by their state’s Medicaid program. Services include primary and special health care, nursing, social services, therapies, pharmaceuticals, day health center services, home care, health-related transportation, minor home modifications to accommodate the disabled, and anything else the program determines is medically necessary to improve the health of the member. PACE programs are designed to provide health care and directly employ a comprehensive group of health care workers to care for frail seniors—they are paid a fixed monthly fee per member and, in exchange, are responsible for providing all health services, sometimes including transportation. Because only the most severely frail and incapacitated are enrolled in PACE programs, they are precisely the patient population for whom prevention and health care will make a real difference. Most PACE patients receive multiple diagnoses, with an average of more than seven diagnoses per member. Among the most common diagnoses are heart problems, diabetes, hypertension, and vascular disease. PACE programs have strong incentives to help keep their members as healthy as possible—patients enrolled in these programs, if left unattended, are likely to require extensive nursing home care, which is very expensive. PACE programs therefore tend to provide high levels of preventive services, such as very frequent checkups, exercise programs, nutritional monitoring, strength and balance programs, etc. PACE programs also organize their services into “PACE Centers.” These centers tend to have a day health center, doctors’ offices, nursing, social services, rehabilitation services, and administrative staff, all in one location. Members’ visits to these centers are determined by their care plans. Care is planned with the member, his or her care team, and appropriate family members; most members attend two days a week. PACE was developed by OnLook Premium Health Services, a nonprofit organization that originated in the early 1970s in San Francisco’s North Beach Chinatown neighborhood. With research and administrative funding from the federal Administration on Aging, OnLock opened a day health center in 1972, modeled after the British Day Hospital Program. In 1978, they expanded this model to include full health care and social support for the frail elderly, and in 1979 they obtained federal waivers that allowed reimbursement for all outpatient and health-related services. In 1980, inpatient services were added, including skilled nursing care and hospitalization for acute illness. Amendments to the Social Security Act in 1983 gave OnLock authority to test a risk-based financing system that would include Medicare, Medicaid, and private pay. Major grants from the Robert Wood Johnson Foundation, the John Augustine Hartford Foundation, and the Retirement Research Foundation ensured that research and development activities could be established to support this model program. Congress extended OnLock’s waivers indefinitely, and provided waivers for similar programs at 10 sites. This support enabled OnLook to provide technical assistance to help new sites create and develop a cross-site database to track performance. In 1990, the first such sites received Medicaid and waivers as model programs, and this model became known as the All-Inclusive Senior Care Program, or PACE. The Balanced Budget Act of 1997 made PACE programs a permanent part of the Medicare program and an option under state Medicaid programs. The current PACE model programs became PACE providers by 2003. The Deficit Reduction Act of 2005 authorized the Rural PACE Initiative, and in 2006 the Centers for Medicare and Medicaid Services announced 15 rural PACE grantees. As of August 2010, 76 PACE programs and 5 pre-PACE programs operated in 30 states. The largest of these programs had more than 2,500 frail seniors enrolled, but most served a few hundred on average.

Geriatric medicine

Geriatric care management is the process of planning and coordinating care for the elderly and others with physical and/or mental disabilities to meet their long-term care needs, improve their quality of life, and maintain their independence for as long as possible. It involves working with older people and their families to manage, deliver, and refer a variety of health and social care services. Geriatric care managers accomplish this by combining a working knowledge of health, psychology, human development, family dynamics, public and private resources, and funding sources with advocacy for their clients throughout the continuum of care. For example, they may assist families of older adults and others with chronic needs such as those with Alzheimer’s disease or other types of dementia. Geriatric care management integrates health and psychological care with other needed services such as housing, home care services, nutrition services, assistance with activities of daily living, and socialization programs, as well as financial and legal planning. A care plan tailored to the specific circumstances is developed after a comprehensive assessment, and is continually monitored and modified as needed. A comprehensive geriatric assessment is an in-depth, comprehensive/complete evaluation that can take anywhere from 2 to 5 hours, and is divided into two or three assessment visits with the patient and family members. The comprehensive assessment is actually a series of smaller individual assessments, beginning with an initial assessment that includes demographic data as well as health history, social history, and legal/financial history. It then assesses the medication profile, as well as assessing ADLs and IADLs. Other assessments may include a fall risk assessment, home safety assessment, nutritional assessment, depression assessment, pain assessment, mini-mental status examination, mini-clock drawing test, balance assessment, and gait assessment. If the comprehensive geriatric assessment is performed by a registered nurse, a physical assessment may be included, such as vital signs such as temperature, pulse, respiration, blood pressure, oxygen saturation, and sometimes diabetes tests such as FBS or RBS. Physical assessments are also performed in areas such as cardiopulmonary, gastrointestinal, musculoskeletal, genitourinary, eye, ear, nose and throat, lower extremity examination, modified neurological assessment and medication compliance assessment. Geriatric care managers typically have prior training in nursing, social work, geriatrics or other health services fields. They are expected to have extensive knowledge of the costs, quality and availability of services in their communities. In some countries and jurisdictions, they may be certified by various professional associations, such as the National Association of Professional Geriatric Care Managers in the United States. Professional care managers help individuals, families and other caregivers adapt to and meet the challenges of aging or disability by:

Geriatric medicine

Lumbar spinal stenosis is a medical condition in which the spinal canal narrows, compressing nerves and blood vessels at the level of the lumbar vertebrae. Spinal canal stenosis can also affect the cervical or thoracic vertebrae, and these conditions are known as cervical spinal stenosis or thoracic spinal stenosis. Lumbar spinal stenosis can cause pain or abnormal sensations in the lower back or buttocks, loss of sensation in the legs, thighs, feet, or buttocks, or loss of bladder and bowel control. The exact cause of lumbar spinal stenosis is not clear. Narrowing of spinal structures such as the spinal canal, lateral cavities, or intervertebral foramen is present, but is not sufficient to cause lumbar spinal stenosis alone. Many people who have an MRI have these changes but do not have symptoms. These changes are usually seen in people with degenerative spinal disease that occurs with aging. Lumbar spinal stenosis may also be caused by osteoporosis, osteophytes, tumors, trauma, or skeletal dysplasia such as dysplasia malformans and chondrodysplasia. Specialists diagnose lumbar spinal stenosis using a clinical history, physical examination, and CT or MRI. Electromyography may be helpful if the diagnosis is unclear. Age and widespread pain that worsens with prolonged standing or walking and is relieved by sitting, lying down, bending forward at the waist, and walking with long strides are helpful signs that may include: focal weakness or decreased sensation in the legs, decreased reflexes in the lower extremities, and difficulty with balance. All of the above signs are strongly associated with lumbar spinal stenosis. Most people with lumbar spinal stenosis are candidates for initial conservative, nonsurgical treatment. Nonsurgical treatments include medications, physical therapy, and injections. Surgery may slightly improve outcomes but carries more risks than conservative treatment. Overall, there is limited evidence to support the choice of surgical or nonsurgical treatment for people with symptoms of lumbar spinal stenosis. Similarly, evidence to support the use of acupuncture is also limited. Lumbar spinal stenosis is a common condition that causes significant morbidity and disability. It is the most common reason for spinal surgery in people older than 65 years. The condition affects more than 200,000 people in the United States. Understanding the meaning of the signs and symptoms of lumbar stenosis requires understanding what the syndrome is and how common it is. A recent review of lumbar spinal stenosis in the Journal of the American Medical Association Clinical Review Series confirmed that the syndrome can be considered when lower extremity pain occurs with back pain. The syndrome occurs in 12% of community-dwelling elderly men and up to 21% of retired men. The symptoms of lumbar spinal stenosis are similar to those of vascular claudication, which is why the term pseudoclaudication is used to describe the symptoms of lumbar spinal stenosis. These symptoms include pain, weakness, and tingling in the legs, which may radiate to the feet. Additional symptoms in the legs may include fatigue, heaviness, weakness, tingling, numbness, or cramping, in addition to bladder symptoms. Symptoms are most often symmetrical and bilateral, but may be unilateral. Leg pain is usually more bothersome than back pain. Pseudoclaudication, now referred to as neurogenic claudication, worsens with standing or walking, improves with sitting, and is often associated with postures that stretch the lumbar cord. Lying on the side is more comfortable than lying on the back, as it allows for greater lumbar flexion. Vascular claudication may mimic those of neurogenic claudication, with some individuals experiencing unilateral or bilateral symptoms that radiate to the legs, rather than the classic symptoms of true claudication. The first symptoms of stenosis include episodes of low back pain. After a few months or years, this may progress to claudication. The pain may be radiating, following classic neural pathways. This occurs as the spinal nerves or spinal cord become increasingly trapped in a smaller space within the canal. It is difficult to tell whether pain in older adults is caused by reduced blood flow or narrowing, but tests can distinguish between the two. However, some patients may have both conditions. In people with lower extremity pain and back pain, lumbar stenosis is twice as likely to be the cause in those over 70 years of age, and less than half as likely in those under 60 years of age. Characteristics of the pain are also helpful in diagnosis. When discomfort does not occur while sitting, lumbar spinal stenosis is significantly more likely, about 7.4 times more likely. Other features that increase the likelihood of lumbar spinal stenosis include: symptoms improve when bending forward, pain that occurs in either the buttocks or legs, and the presence of neurogenic claudication. On the other hand, the absence of neurogenic claudication makes lumbar stenosis less likely to explain the pain. Nonsurgical treatments and laminectomy are the standard treatment for lumbar spinal stenosis, and conservative treatment is usually recommended. Individuals are generally advised to avoid stress on the lower back, especially during spinal extension. Physical therapy programs that strengthen the core and provide aerobic exercise may be recommended. There is no conclusive scientific evidence on whether conservative or surgical treatment is better for lumbar spinal stenosis. Evidence for the use of pharmacologic interventions in the treatment of lumbar spinal stenosis is weak. Injectable calcitonin, rather than intranasally, may be helpful for short-term pain relief. Epidural injections may also provide temporary pain relief, but there is no evidence of long-term benefit. Adding corticosteroids to these injections does not improve outcomes, and the use of epidural steroid injections is controversial and the evidence for their effectiveness is conflicting. Nonsteroidal anti-inflammatory drugs, muscle relaxants, and opioid analgesics are used to treat low back pain, but evidence of their effectiveness is limited. Surgery appears to be better if symptoms persist after 3–6 months of conservative treatment. Laminectomy is the most effective surgical treatment. Surgery improves 60–70% of cases where symptoms worsen despite conservative treatment. Another procedure used an interbody abduction device called X-Stop was less effective and more expensive when repairing multiple levels of the spine. Both surgeries are more expensive than medical treatment.

Geriatric medicine

Gerontology is the scientific study of the aging process. It is a multidisciplinary field that draws from the biological and psychological sciences. Geriatric medicine is the practice that focuses on the physiology, pathophysiology, diagnosis, and management of disorders and diseases of the elderly. Because aging is a natural process, the care of the elderly cannot be limited to a single specialty but rather through a collaborative effort. Geriatric nursing is a multidisciplinary approach to providing care that combines expertise and resources to provide comprehensive geriatric assessment and nursing interventions. Nurses collaborate with a medical team to provide appropriate services to patients and provide comprehensive care.

Geriatric medicine

Dementia with Lewy bodies, also known as Lewy body dementia or diffuse Lewy body disease, is a type of dementia that usually accompanies Parkinson's disease. Anatomically, it is characterized by the presence of Lewy bodies and alpha-synuclein and ubiquitin protein deposits in the nerves. These substances can be detected during a postmortem brain autopsy. Lewy body dementia is a progressive memory loss that primarily affects older adults. The characteristic feature of this disease is a gradual decline in cognitive ability, which leads to hallucinations and poor comprehension and attention to what is in the patient's surrounding environment compared to a healthy person. People with Lewy body disease show an inability to plan and think and varying changes in perception. The alertness of these patients varies from day to day, and their attention and short-term memory vary. Persistent or intermittent visual hallucinations accompanied by clear images and visions are early signs of this disease. The patient's sleep pattern can be disturbed, accompanied by vivid visions, recurring dreams, violent deliberate movements, and then falling out of bed. Lewy body disease overlaps medically with Alzheimer's and Parkinson's diseases, but it accompanies Parkinson's disease more. For this reason, when this disease was discovered in its early years, it was not diagnosed correctly. In Lewy disease, it was believed that the loss of acetylcholine-producing neurons was the cause of the decline in cognitive function - which is somewhat similar to Alzheimer's - while the loss of dopamine-producing neurons was responsible for the gradual loss of control over voluntary functions - which is similar to Parkinson's disease - so this disease resembles both of the previous diseases. Therefore, the overlap between these three diseases makes the diagnosis of Lewy body disease more difficult, so that it can sometimes be confused with the early symptoms of Alzheimer's disease and vascular dementia. However, it is possible to distinguish between Alzheimer's, which develops slowly, and Lewy body disease, which develops and begins suddenly and rapidly, especially in the first months of the disease. Although it is difficult to identify and identify this disease, an accurate diagnosis is necessary to avoid the greatest number of side effects of antipsychotic drugs and thus provide treatment that can improve the life of the person with Lewy body disease and the people around him. The use of medications containing benzodiazepines, antidepressants, anticholinergics, and over-the-counter cold medications may lead to psychosis and hallucinations for a short period. The known dementia associated with Parkinson's disease and that associated with Lewy bodies can be distinguished by the time they appear with Parkinson's disease. In the first, dementia associated with Parkinson's disease is diagnosed when the dementia appears more than a year after Parkinson's disease has started. While dementia associated with Lewy bodies is diagnosed when the time of the patient's mental decline is known at the same time as the onset of Parkinson's disease symptoms or during the first year of its onset. Symptoms vary from person to person, but the core symptoms of the disease include changes in the level of cognition with large differences in the level of attention and comprehension from day to day and from hour to hour, varying episodes of hallucinations, and motor symptoms associated with Parkinson's disease. Other symptoms such as sleep disturbances and other signs can be detected by CT scan. Parkinson's disease symptoms associated with Lewy body dementia include a shuffling gait, decreased ability to control facial muscles, stiffness or rigidity when moving, a low voice level when speaking, thick saliva and difficulty swallowing. Involuntary body tremors in people with Lewy body disease are less common than in Parkinson's disease. People with this disease also have problems with postural hypotension, falls and frequent loss of consciousness. Sleep-disordered breathing can be a symptom of multiple system atrophy. A well-known and important medical sign of this disease is severe sensitivity to antipsychotic and antiemetic drugs that affect the nerves that produce acetylcholine and dopamine. This sensitivity can lead to complete paralysis, complete loss of consciousness or can expose him to a dangerous state of muscle rigidity. Therefore, these drugs should not be used or used with caution. Hallucinations that people with Lewy body disease often see people or animals that are not there, which may indicate the presence of Lewy bodies in the temporal lobe. Symptoms of psychosis include the feeling of being in two or more different places at once, etc. Hallucinations and psychoses can be disturbing, but not all of them are experienced as being pleasant or knowing that they are not real. Patients also suffer from visual disturbances, including double vision and misinterpreting what they are looking at, such as thinking that what they are looking at is a group of snakes when it is actually a pile of socks. The exact cause of Lewy body disease is not yet understood, but a link has been described to the gene PARK11. Like Alzheimer's and Parkinson's, Lewy body disease tends to run in generations, so its genetic link is not strong. However, like Alzheimer's, the risk of developing the disease increases when a person inherits the ε4 allele of apolipoprotein E. Pathophysiologically, Lewy body disease is characterized by deposits of Lewy body proteins in various parts of the brain. These deposits are known as Lewy bodies. These bodies are somewhat similar to the protein deposits under the cerebral cortex in Parkinson's disease. In addition, the neurons that produce both dopamine and acetylcholine are lost or destroyed, just as occurs in Parkinson's and Alzheimer's diseases, respectively. Also, the brain shrinks or shrinks in size as the cerebral cortex deteriorates. Postmortem examination of the brain showed epidemiological signs similar to Alzheimer's disease. The deposits of Lewy bodies that appeared in the cortex also appeared in Alzheimer's disease, but they were found deposited in the hippocampus, in addition to granular deposits in the space around the hippocampus. It is not yet known whether Lewy body disease is a type of Alzheimer's disease or a separate disease. Unlike Alzheimer's, Lewy body disease does not show any visible atrophy when the brain is examined. There is no cure for Lewy body disease. However, there is a medication that works to relieve the symptoms of this disease but does not help in its disappearance and is used as a pain reliever. We can divide the current treatment methods into drug therapy and care. Drug therapy is treated by balancing the treatment of the motor, emotional, and cognitive symptoms of this disease. Motor symptoms respond to the drug used to treat Parkinson's disease, and cognitive problems may improve with Alzheimer's medication. An estimated 60 to 75% of people diagnosed with dementia have either Alzheimer's disease or a combination of the two. 10 to 15% of dementia cases are due to Lewy body disease, with other types of dementia accounting for the last 15-20%, such as frontotemporal lobe atrophy known as Pick's disease, alcoholic dementia, and others. Lewy body disease affects men more than women. This disease affects about one million people in the United States alone. The protein deposits that cause this disease were first discovered by the scientist (Frederick Lewy) in the early eighteenth century. But the first person to describe the disease was the Japanese neuropsychologist in 1976. The diagnosis of Lewy body disease began in the mid-nineties after the discovery of the alpha-synuclein stain, which revealed Lewy bodies in the cerebral cortex during autopsies of patients who had dementia. The disease was not included in the Diagnostic and Statistical Manual of Mental Disorders, which was published in 1994, but it was briefly described in the 2000 edition of the manual under the name . In 1996, some scientists called for an amendment and then a revision of the diagnostic guidelines for this disease.

Geriatric medicine

The Lothian Birth Cohort studies comprise three cohort studies, combining research in psychology, epidemiology, and gerontology. The Lothian Birth Cohort of 1921 investigated childhood intelligence, at age 11, and health outcomes in old age. The study included a group of 551 adults born in the Lothian area of Scotland in 1921. The publications that resulted from this study contributed to the emerging field of cognitive epidemiology. One of the most important findings of this study was that children with higher IQs at age 11 were not better protected against cognitive decline in later life. Instead, they had better cognitive ability in old age, attributable to greater stability in intelligence across their lives. The 1936 Lothian Birth Cohort Study is a similar cohort to the 1921 study, but includes 1091 participants born in 1936. The sample size was larger than the 1921 cohort, and more detailed information was collected on those born in 1936. Additional intelligence tests were administered to 1208 people born on the first day of the intercalary months of 1936, and detailed information on the home environment was provided. These additional data were collected annually for the following 16 years, and included home visits by the researcher. The Lothian Birth Cohort studies can provide information on the determinants of cognitive decline, because they have a measure of premorbid intelligence measured at age 11. They can also be used to provide information on health differences in old age, taking childhood factors into account. The 1921 Lothian Birth Cohort Study was funded by several UK research funding councils and other agencies. The 1936 Lothian Birth Cohort Study was funded by the charity Older People UK and the charity Help Older People, which has recently become part of the Unplugged Mind Project. The Lothian Birth Cohort Study is supervised by Professor Ian Derry in the Department of Psychology at the University of Edinburgh.

https://ar.wikipedia.org/wiki/%D8%AF%D9%86%D9%81

Geriatric medicine

Cachexia is weight loss, muscle atrophy, fatigue, weakness, and significant loss of appetite in a person who is not actively trying to lose weight. The official definition of cachexia is a loss of body mass, with minimal accumulation of adipose tissue, that cannot be reversed nutritionally: even if the person eats more calories, some of the body mass is lost, reflecting the presence of an underlying disease. Cachexia is seen in patients with cancer, AIDS, celiac disease, chronic obstructive pulmonary disease, multiple sclerosis, rheumatoid arthritis, congestive heart failure, tuberculosis, familial amyloid polyneuropathy, mercury poisoning, and hormonal imbalances. Cachexia is a well-established risk factor, meaning that if a patient has cachexia, the chance of dying from the underlying disease is greatly increased. Cachexia can be a clinical sign of various underlying disorders. When a patient with cachexia is seen by a doctor, he or she will generally consider the possibility of adverse drug interactions, cancer, metabolic acidosis, certain infectious diseases, chronic pancreatitis, and some autoimmune diseases. Cachexia weakens patients Physically to a state of immobility caused by loss of appetite, weakness, and anemia, and the response to standard therapy is usually poor. Cachexia includes sarcopenia as part of its disease course. Cachexia is usually seen in the final stages of cancer and is called cancer cachexia. Patients with congestive heart failure may suffer from wasting syndrome. Cachexia is also seen in patients with any of the group of diseases classified as chronic obstructive pulmonary disease. Cachexia is also associated with advanced stages of chronic kidney disease, cystic fibrosis, multiple sclerosis, motor neuron disease, Parkinson's disease, dementia, HIV, and progressive diseases. About 50% of all cancer patients suffer from cachexia. Those with pancreatic and upper gastrointestinal cancers have a higher incidence of developing cachexia symptoms. This figure rises to 80% in patients with terminal cancer. In addition to increased morbidity and mortality, worsening side effects of chemotherapy, and decreased quality of life, cachexia is a direct cause of death for a large proportion of cancer patients, ranging from 22% to 40% of patients. Symptoms of cachexia include progressive weight loss and depletion of host stores of adipose tissue and skeletal muscle. Cachexia should be suspected if 5% of precachexia weight is lost involuntarily within 6 months. Conventional treatment approaches, such as appetite stimulants, 5-HT3 antagonists, nutritional supplements, and COX-2 inhibitors, have not been shown to reverse the metabolic abnormalities in cachexia. The exact mechanism by which these diseases cause cachexia is not understood, but there may be a role for inflammatory cytokines, such as tumor necrosis factor-alpha, interferon-gamma, and interleukin-6, as well as tumor-secreted proteolytic factor. Syndromes associated with cachexia include kwashiorkor and marasmus, although these syndromes have no underlying cause and are often symptoms of severe malnutrition. Those with eating disorders such as anorexia nervosa have elevated levels of ghrelin in Plasma. Ghrelin levels are also elevated in patients with cancer-induced cachexia. Much research is currently focused on determining the mechanism of cachexia. The two main theories for the pathogenesis of cancer cachexia are: Although the mechanism by which cancer cachexia occurs is not understood, the involvement of biological pathways can be discerned, including pro-inflammatory cytokines such as tumor necrosis factor-alpha, neuroendocrine hormones, insulin-like factor 1, and tumor-specific factors such as protein degradation-inducing factor. Inflammatory cytokines involved in wasting diseases are interleukin-6, tumor necrosis factor-alpha, interleukin-1β, and interferon-gamma. Although many different tissues and cell types may be responsible for the increased cytokines in circulation in some cancers, evidence points to tumors as an important source. Cytokines are capable of weight loss. TNF-alpha has been shown to have a direct catabolic effect on skeletal muscle and adipose tissue and to cause muscle atrophy through a pathway Ubiquitin – a proteolytic proteasome. The mechanism involves the formation of reactive oxygen species that leads to increased expression of the transcription factor nuclear factor kappa light chain enhancer in activated B cells. NF-κB is a known regulator of genes encoding cytokine synthesis and cytokine receptors. Excess cytokine secretion stimulates proteolysis and breakdown of myofibrillar proteins. How cachexia is treated depends on the underlying cause, overall prognosis, and related factors related to the individual. Reversible causes, underlying diseases, and contributing factors are treated if feasible and acceptable. A growing body of evidence supports the efficacy of β-hydroxy β-methylbutyrate as a treatment to reduce, or even reverse, the loss of muscle mass, muscle function, and muscle strength that occurs in hypercatabolic conditions such as cachexia. Consequently, as of June 2016, it is recommended that prevention and treatment of cachexia include HMB supplementation, regular strength training, and high-protein diets. Progestins such as megestrol acetate are used as an option Treatment for intractable cachexia with anorexia as the main symptom. Cachexia now occurs less frequently in HIV/AIDS than in the past due to the advent of HAART. Combination therapy for cancer cachexia is recommended in Europe, as a combination of nutrition, medication, and non-drug therapy may be more effective than monotherapy. Non-drug therapies that have been shown to be effective in cancers caused by cachexia include nutritional counseling, psychotherapeutic interventions, and physical training. Anabolic androgenic steroids such as oxandrolone may be helpful in cancer cachexia but are recommended for use for a maximum of two weeks; Longer treatment times increase the burden of side effects. Other medications that have been used or are being investigated for the treatment of cachexia, but conclusive evidence of efficacy or safety is lacking, and are generally not recommended: Medical marijuana is legal for the treatment of cachexia in some states, including Illinois, Maryland, Delaware, Nevada, Michigan, Washington, Oregon, California, Colorado, New Mexico, Arizona, Vermont, New Jersey, Rhode Island, Maine, New York, Hawaii, and Connecticut. There is insufficient evidence to support the use of oral fish oil for the treatment of cachexia associated with advanced cancer. There are limited options for treating cancer cachexia patients. The current strategy is to improve appetite using aphrodisiacs to ensure adequate nutrient intake. Pharmacological interventions using appetite stimulants, nutritional supplements, 5-HT3 antagonists, and COX-2 inhibitors have been used to treat cancer cachexia, but with limited effect. Studies have suggested that increasing calorie-dense calories and increasing protein intake can at least stabilize weight, although lean body mass did not improve in these studies. Treatment strategies are based on Inhibition of cytokine synthesis or action. Thalidomide has been shown to inhibit the production of TNF-α in mononuclear cells in vitro and to normalize TNF-α levels in vivo. A randomized, placebo-controlled trial in patients with cachexia cancer showed that it was well tolerated and effective in reducing weight loss and lean body mass in patients with advanced pancreatic cancer. Improvement in lean body mass and quality of life was also observed in a randomized, double-blind trial of a protein- and calorie-dense, omega-3 fatty acid supplement, provided that its consumption was equal to or greater than 2.2 g eicosapentaenoic acid (EPA) per day. It also works by reducing TNF-α production. However, data from a large, double-blind, placebo-controlled, multicenter trial suggest that EPA alone is not successful in treating weight loss in patients with advanced gastrointestinal or lung cancer. Peripheral muscle protein degradation, as occurs in cancer Cachexia, mobilizes amino acids required for liver and tumor protein synthesis. Therefore, the administration of amino acids from an exogenous source theoretically acts as a metabolic fuel for protein conservation by providing substrates for muscle metabolism and gluconeogenesis. Studies have shown that dietary supplementation using a specific combination of high-protein, leucine and fish oil improves muscle function, daily activity and immune response in cachexia-bearing mice. In addition, the use of beta-hydroxy beta-methylbutyrate derived from leucine catabolism as a nutritional supplement in tumor-bearing mice prevents cachexia by modulating NF-κB gene expression. A phase II study involving the use of antioxidants, nutritional-pharmacologic support, progestins (megestrol acetate and medroxyprogesterone acetate), and cyclooxygenase-2 inhibitors, demonstrated efficacy and safety in the treatment of advanced cancer patients with cachexia in different locations. These data support the use of multi-step therapies in the treatment of cachexia cancer. New studies It is suggested that nonsteroidal anti-inflammatory drugs, such as sulindac, significantly reduced cachexia. Studies have also shown that branched-chain amino acids can revert the metabolism of cachexia patients from catabolic weight loss to anabolic muscle gain, in 55% of patients. Branched-chain amino acids are composed primarily of leucine and valine. A paper published in the Indian Journal of Palliative Care concluded that branched-chain amino acids interfere with the activity of serotonin in the brain and prevent the stimulation of critical muscle protein degradation pathways. The potential role of branched-chain amino acids as appetite suppressants and anti-wasting agents was suggested many years ago, but since then experimental studies and clinical trials have tested their ability to stimulate food intake and counteract muscle loss in anorexic and overweight patients. In experimental models of cancer cachexia, BCAAs were able to induce significant suppression of body weight loss, produce significant increases in skeletal muscle wet weight, and improve muscle performance and daily activities. The essential amino acid glutamine has been used as a component of oral supplements to reverse cachexia in patients with advanced cancer or HIV/AIDS. According to the 2007 AHRQ National Inpatient Sample, in 129,164 hospitals surveyed in the United States, cachexia was listed as at least one of 14 recorded diagnosis codes for 26,325 unweighted cases. A sample of 32,778 unweighted outpatients in the United States collected in the CDC National Ambulatory Care Survey did not list any cases in which cachexia was one of up to three recorded diagnoses during visits.

Geriatric medicine

Elderly care or hospice care is the provision of special needs and requirements for senior citizens. The term includes services such as assisted living, adult day care, long-term care, nursing homes, nursing home care, and home care. Because elder care is so widespread internationally, as well as culturally diverse views on senior citizens, it cannot be limited to a single practice. For example, many countries in Asia use government-sponsored elder care as a very rare practice, preferring traditional methods of caring for younger family members. Elderly care emphasizes the social and personal needs of senior citizens, who require some assistance with daily activities and health care, but who wish to age with dignity. It is an important distinction, in that the design of housing, services, activities, and staff training should be truly customer-focused. It is also worth noting that many elder care services around the world are voluntary and unpaid. The form of care provided to the elderly varies greatly between countries and is constantly changing. Even within a single country, religious differences are taken into account in elder care. However, it has been noted that The elderly around the world consume the most health expenditures of any age group, and the observation that comprehensive care for the elderly is perhaps very similar. One must also explain the large increase in the proportion of elderly people in the world, especially in developing countries; As the pressures of continued fertility are limiting and family size is decreasing. Traditionally, care for the elderly has been the responsibility of family members and has been provided through the extended family home. As modern societies have grown, care for the elderly has become more and more often provided by the state or charitable organizations. Reasons for this change include shrinking family size, increasing life expectancy for older people, geographic dispersion of families, and women entering education and working outside the home. Although these changes initially affected Europe and North America, they are now increasingly affecting countries in Asia as well. In most Western countries, elderly care facilities are residential family homes, self-contained assisted living facilities, nursing homes, and continuing care for retirees. A family home is a residential home with support staff and supervision by an agency, organization, or individual who provides room, board, personal care, and rehabilitation services in a family environment of at least two and no more than six people. According to the Family Care Alliance, most caregivers are women. “Many studies look at the role of women and families as caregivers. Although not Issues that address gender and caregiving specifically, the results are still generalizable” to be: - Estimates of the age of household or informal caregivers who are women range from 59% to 75%. - The average caregiver is 46 years old, female, married and working outside the home for an annual income of $35,000. - Although men also provide care, female caregivers may spend more than 50 percent of the time that male caregivers do. According to the U.S. Department of Health and Human Services, the senior population—those 65 years of age or older—numbered 39.6 million in 2009. They represented 12.9 percent of the U.S. population, about one in eight Americans. By 2030, they will number 72.1 million, double the number in 2000. People 65 and older represented 12.4 percent of the population in 2000, but that percentage is expected to increase to 19 percent by 2030. This means that the demand for senior living facilities will increase in the coming period. There were more than 36,000 assisted living facilities in the United States in 2009, according to the Assisted Living Federation of America in 2009. More than One million seniors were served by these assisted living facilities. Last year's spending in the United States represented 22 percent of total medical spending, 26 percent of total Medicare spending, 18 percent of total non-Medicare spending, and 25 percent of total Medicaid spending. In the United States, most large multi-facility providers are publicly owned and operated by for-profit businesses. There are exceptions. The largest in the United States is the Lutheran Good Samaritan Society, a nonprofit organization that operates 6,531 beds in 22 states, according to a 1995 study by the American Health Care Association. If given the opportunity; Most seniors would prefer to continue living in their homes. Many seniors gradually lose their ability to function and require either additional assistance at home or a transition to a nursing home. Adult children of seniors often face difficult challenges in helping their parents make the right decision. Assisted living is one option for seniors who want help with daily tasks. It costs less than nursing home care, but is still considered expensive for many people. Home care services may allow seniors to live longer in their homes. One relatively new service in the United States that can help seniors stay in their homes longer is respite care. This type of care gives caregivers the opportunity to go on a vacation or business trip and know that their elderly loved ones are receiving high-quality temporary care, since without such assistance the elderly would probably have to move permanently to an outside facility. Another unique type of care in American hospitals, called acute hospice care, provides a “family placement” within a medical center designed for seniors. For information about long-term care options in the United States, see: You can contact your local area agency on aging, or senior referral agencies such as Place for Mom. Additionally, the U.S. government rates health care facilities through websites that use aggregated data from sources such as Medicare. In Canada, there are also such facilities that are privately run and not for profit. Due to cost factors; Some provinces operate public facilities that are funded by the government and managed by the health department of each province or territory, or the government may subsidize the costs of these facilities. In these care homes, senior Canadians may pay for their care on a sliding scale, proportional to their annual income. Their payment range depends on whether the care is “long-term” or “assisted living.” For example, starting in January 2010, seniors living in government-subsidized “long-term care” in British Columbia will pay 80% of their after-tax income, unless their after-tax income is less than $16,500. The price of “assisted living” is simply 70% of their after-tax income. As we saw in Ontario, there were waiting lists for long-term care homes, however, families may need to resort to home health care, or pay for accommodation in a private retirement home. Aged care in Australia is designed to ensure that each Australian citizen contributes as much as possible to the cost of care, based on their individual income and assets. This means that residents only pay what they can afford. They can afford it, and the Commonwealth Government is paying what they can't. An Australian statutory body, the Productivity Commission, conducted a review of aged care that began in 2010 and reported in 2011. This review concluded that almost 80% of care for Australians aged was provided informally, by family, friends and neighbours. About a million people received government-subsidised aged care, most of whom received low-subsidised community care, with 160,000 people in permanent residential care. Aged care spending by all governments in 2009–10 was almost $11 billion. The need to increase the amount of care, and the recognition of weaknesses in the care system, led several reviews in the 2000s to conclude that Australia's aged care system was in need of reform. This culminated in the Productivity Commission's 2011 report and subsequent reform proposals. According to the Living Longer and Living Better amendments of 2009–10, 2013, Assistance was provided according to established care needs, with additional supplements for people experiencing homelessness, dementia, and veterans. Aged care for Australians is often complex due to different state and federal funding. Furthermore, there are many shortcuts that clients need to be aware of. Aged care in England is increasingly rationed according to a joint report by the King’s Fund and the Nuffield Trust. People are left to struggle on their own without support. Large numbers of older people need assistance as a result of ageing housing but are paid for less. Millions of people who need care find neither formal nor informal assistance. Due to health and economic benefits; life expectancy in Nepal has increased from 27 years in 1951 to 65 years in 2008. Most older Nepalis, around 85%, live in rural areas. Because of this; There is a significant lack of government-sponsored programs or nursing homes. Traditionally, parents live with their children, and today, it is assumed that 90% of the elderly live in their family homes. This number is changing as more and more children leave their homes for work or study, leading to loneliness and mental problems for the elderly Nepalis. The Ninth Five-Year Plan included policies to try to take care of the elderly left without their children as guardians. A health facility fund for the elderly has been established in each province. The implementation guide for the health facility program for the elderly, “2061BS” provides medical facilities for the elderly, and those suffering from poverty, with medical and health care in all provinces. The government has planned to fund free health care for all heart and kidney patients above 75 years of age. Unfortunately, many of these plans are difficult to achieve, as the Nepalese government has learned. Nepal is a developing country and cannot afford all these programs after developing the Old Age Allowance, or OAA. The OAA provides a monthly stipend to all citizens over 70, and widows over 60. There is a small amount of day care for the elderly, but it is limited to the capital. Day care services are expensive, and the general public cannot afford them. Thailand has observed global patterns of an expanding elderly population: fertility control has been encouraged, medical advances have made life difficult, and the birth rate has declined. The Thai government has noticed and been alerted to this trend, but has left care to family members, rather than creating outsourced policies for them. As of 2011, only 25 countries had guaranteed nursing homes, with no more than a few thousand elderly people in each home. Such programs are largely run by volunteers, and the quality of care is questionable, given that care is not always guaranteed. Private care is difficult to follow, and is often based on assumptions. Because children are less likely to be cared for, Their parents; private care is provided. Voluntary NGOs are available but in very limited quantities. While there are certainly elderly care programs in Thailand, equity contributions have increased since their introduction. Richer elderly people in Thailand are more likely to have access to care resources, while poorer elderly people are more likely to use already acquired health care, as noted in a study by Phumisuk Khananurak. However, more than 96% of the country has health insurance, with varying degrees of care available. India’s view of elderly care is similar to Nepal’s. Parents are usually cared for by their children in old age, and it is common for their children to do so. In this country, older citizens, especially men, are held in high esteem. Traditional values demand honor and respect for the elderly, and the wiser. India faces the same problems as its developing counterparts in that its elderly population is growing rapidly, with approximately 90 million people aged over 60. Using data on health and living conditions from the 60th National Survey In India, the study found that nearly a quarter of the elderly suffer from poor health. Reports of poor health clustered around the poor, isolated, less educated, and economically disadvantaged groups. In its 11th Five-Year Plan, the Indian government took many steps similar to those taken by Nepal. The 41st clause of the Indian Constitution states that social security for the health and social welfare of elderly citizens will be ensured. Part of the Criminal Procedure Code, 1973, refers to its traditional background, that sons take care of their parents if they are no longer able to do so. However, NGOs are widespread in India to care for the elderly, providing them with homes and voluntary care, but government policies and organizations are available. Population aging is a challenge worldwide; China is no exception. Due to the “one-child” policy, rural/urban migration, and other social changes; Traditional long-term care for the elderly, which was provided by direct family care, is no longer sufficient. It barely exists now, and both institutional and community services need to expand to meet the growing need. China is still at an early stage of economic development and will face a challenge in meeting these services and training staff. A distinction is generally made between medical and non-medical care, with non-medical care being provided by people who are not medical professionals. Non-medical care is less likely to be insured or covered by public funds. In the United States, 67 percent of the million or so residents of assisted living facilities pay for their care out of pocket. The rest are cared for by family, friends, or state systems. Medicare pays for medical care only if skilled nursing is needed and is provided by certified skilled nursing facilities or by a skilled nursing home agency. Assisted living facilities typically do not meet Medicare requirements. However, Medicare does pay for some skilled care if it is approved. The elderly person that the care met the specifications of the Home Health Grant for the programme. There are 32 states in America that pay for care in assisted living facilities through their Medicaid waiver programmes. Similarly, in the UK, the National Health Service provides medical care for the elderly, and it is free for everyone to use, but social care is the only one paid for by the state in Scotland, but England, Wales and Northern Ireland have not yet introduced legislation on this, so social care is currently only funded by the public authorities when a person exhausts their own resources, for example if they sell their home. The money paid for elderly care in Britain fell by 12% per person in the ten years between 2005 and 2015, and in real terms the fall has been even greater. Experts claim that vulnerable people in Britain are not getting what they need. However, elderly care focuses on satisfying the expectations of two levels of customers: the resident customer and the purchasing customer, who are often different people, because it is parents, relatives or the public authorities who pay for the care rather than the Population. In cases where the elderly are confused or have difficulty communicating; It can be very difficult for relatives or other interested parties to know what level of care is being provided to their loved ones, and they may be constantly concerned that their elderly loved ones are being mistreated there. The Adult Protective Services Agency, a component of the Human Services Agency in most states, is usually responsible for investigating reports of elder abuse in the home and providing families with assistance and guidance. Other professionals such as doctors, nurses, police officers, lawyers, and social workers can also help. Encouraging independence in self-care allows older adults to maintain their independence longer and provides a positive feeling when they accomplish a task without assistance. Older adults who need help with daily activities are at high risk of losing their independence in self-care tasks, as personal behaviors are reinforced by caregivers. It is important for caregivers to make sure that they are putting in place measures to maintain their function, rather than to worsen the condition of older adults with physical limitations. Caregivers need to be aware of the events and behaviors that cause older adults to become dependent. And dependent on others, and also need to allow the elderly patients to maintain their independence as much as possible. Providing information to the elderly about the importance of independence in caring for themselves; allows them to see the benefit of performing self-care independently without needing anyone. If the elderly can do their care activities themselves, or even if they need supervision; Encouraging their efforts to maintain their independence provides them with a sense of accomplishment and the ability to continue to rely on themselves for longer. Deteriorating mobility is a major concern for older adults, affecting 50 percent of people over the age of 85, and at least a quarter of those over the age of 75. Older adults lose the ability to walk, climb stairs, and get out of a chair, becoming completely disabled. The problem cannot be ignored because people over the age of 65 represent the fastest growing segment of the U.S. population. Treatment aimed at improving mobility in older adults usually centers on diagnosing and treating specific problems, such as decreased strength and poor balance. It is appropriate to compare older adults seeking to improve their mobility to runners seeking to improve their time to a certain distance. People in both groups perform better when they link their progress and the work they have done to specific goals related to strength, respiratory capacity, and other physical attributes. The person trying to improve the mobility of an older adult must identify the deficit he or she wants to focus on, and in many cases, there are Little scientific evidence exists to explain any choice. Today, many caregivers focus on leg strength and balance. New research suggests that limb speed and core strength may be important factors in mobility. Family is one of the most important caregivers for an elderly person. In fact, most caregivers for an elderly person are family members, often their daughter or granddaughter. Family and friends can provide a home, provide money, visit to meet their social needs, take them on trips, and so on. One of the biggest causes of deterioration in the elderly is hyponatremia, an electrolyte imbalance that occurs when the sodium level in a person's blood falls below 135 meq/l. Hyponatremia is the most common electrolyte imbalance in the elderly. Studies have shown that elderly patients are more susceptible to this disease due to several factors, including physiological changes associated with aging, such as decreased glomerular filtration rate, the tendency to conserve sodium, and increased vasopressin activity. Mild hyponatremia increases the risk of fracture in elderly patients, because hyponatremia causes severe neurological impairment, which affects walking and attention, similar to moderate alcohol consumption. Incapacity law is a common and sometimes difficult legal process. It requires a person to file a petition in local courts, stating that the elderly person lacks the ability to perform activities that include making medical decisions, voting, making gifts, seeking public benefits, marrying, managing property and finances, and choosing where to live and with whom to socialize. Most state regulations require that at least two doctors or health professionals submit reports as evidence of the person's incapacity, and each person must have a representative. Only then can the individual's legal rights and duties be removed and attributed to his or her agent or guardian. A legal guardian or guardian is a person who is authorized by the court to act on behalf of the incapacitated person and must report regularly to the court on his or her activities. A less restrictive alternative to incapacity law is the use of "advance directives," powers of attorney, living wills, and health care directives. The person who has these documents should prepare them with his or her attorney when he or she is able to do so. Therefore, if the time comes and the person lacks the capacity to carry out the tasks set forth in the documents, the person they have appointed as their "agent" can step in and make these decisions on their behalf. This person has a duty to do this to the best of his or her ability and with the utmost care.

Geriatric medicine

Futile care is the continuation of health care and treatment for a patient despite the lack of reasonable benefit or hope of cure. It may take the form of surgery for advanced cancer despite the fact that it does not help or cure the disease or continuing to put a brain-stem-dead patient on a ventilator. Futile care is a sensitive issue that must be approached with caution and professionalism. It is often debated between health care providers and each other and between the elderly's families and each other. This is due to the lack of clarity about all the facts of the care or the patient's current situation or the suffering of loss. Health care is one of the means of maintaining and restoring health to improve the quality of life of the elderly. The decision to accept or refuse health care is an important, vital and complex one. This decision is governed by many variables such as the ethics and regulations of the profession, traditions and beliefs, the availability of eligibility, the educational level of the elderly and their family, the availability of communication skills, and the time, information and health education experience of the health care provider.

Geriatric medicine

Falls are a major cause of illness and even death for the elderly, and are among the preventable causes of injury. The causes of falls for the elderly depend on several factors and may require several precautionary measures to treat any injury that caused a previous fall and prevent future falls. Falls include collapsing from a standing position or from places where a person is exposed to falling, such as stairs. The severity of the fall depends largely on the height from which the person fell, but the nature of the ground on which the person fell also plays a role in the severity of the fall; falling on a hard floor causes more damage than falling on a soft floor. Falls can be avoided by taking several measures, such as ensuring that the carpet is attached to the ground and not raised above it, keeping electrical wires away from walking areas, wearing shoes with low heels and rubber bottoms, ensuring that the person's hearing and visual abilities are working efficiently and at their best, and avoiding walking if the person is dizzy or has consumed a large amount of alcohol. The European Food Safety Authority has conducted several studies which have shown that it is preferable for the elderly, especially those over 60, to include vitamin D as a nutritional supplement to reduce the risk of falls and osteoporosis, and falls are an aspect of great importance in the field of geriatrics. Other definitions are more comprehensive and do not exclude “major events” as falls. Falls are of great importance, especially in medical treatment facilities, and fall prevention measures are a priority in health care services. In 2006, a publication was presented urging the development of a definition for naming falls due to the clear differences in its definition that appeared in several other studies. The European Association for Fall Prevention has developed a definition of falls and recorded cases resulting from falls in an attempt to alleviate this problem. ProFane states that a fall is an unexpected event in which a person falls from a high place to the ground or to a lower place. This definition developed by ProFane is now used as a framework for evaluating research and studies related to the subject of falls. Falls have many causes. A person can live with many factors that may one day lead to a fall, but the problem begins to appear with the emergence of a new, unprecedented factor. Therefore, treatment is often specific to the cause of the fall and not to treat all the factors that may lead to the accident. These factors can be divided into two groups: a group that includes the presence of a disease or a specific condition that caused the fall, and another group that includes external factors such as the surrounding environment and how it affects the fall, such as the lighting of the place. When evaluating a person who has fallen to the ground, it is important to obtain the statements of anyone else who witnessed the incident, as the person who fell may have suffered from loss of consciousness, which leads to an inaccurate description of the incident, but these witnesses are often not available. It should also be taken into account that about 30% of mentally and cognitively healthy older adults cannot remember a previous fall that occurred more than 3 months ago. Important points to examine: Fall prevention is primarily done after identifying the causes that lead to such an accident. A lot of evidence indicates that when making an effort that includes doing some exercise, the risk of future falls is reduced. There are several things that can be done to reduce the occurrence of such an incident, such as: Interventions to reduce the consequences of falls: People admitted to hospital are at risk of falling, and a randomized trial showed that the use of a set of special tools led to a decrease in the rate of falls in hospitals. Nurses prepare a complete scale of risks and factors that cause falls, through which a complete system is created aimed at addressing the main reasons that cause people to be exposed to this incident. These tools also include posters that are placed on patients’ beds with a brief text about how to prevent this incident from happening again in the future. Both the American Society and the British Society of Geriatric Medicine recommend that all older people undergo regular screening to see if they have had any type of fall in the past year; as having had this incident in the past is a major factor in its recurrence in the future. Older people who have had at least one fall in the past six months or who think they may have one in the coming months should be screened to reduce the risk of recurrent falls. Several health organizations in the United States have developed screening questionnaires. These questionnaires include questions about difficulty walking or balance, use of medications to help sleep or regulate mood, loss of sensation in the feet, vision problems, fear of falling, and use of walking aids. Older adults who report falling should be asked about their circumstances and frequency of falls to assess the risk to walking and balance that may be causing the fall. A fall risk assessment is performed by a physician and includes a history of any past falls, a physical examination, a functional assessment, and an environmental assessment. Falls increase gradually with age. According to current research, approximately one-third of older adults experience one or more falls each year, while 10% experience multiple falls each year. However, the risk is much higher for people over age 80, where the annual fall rate can reach 50%. Researchers have been working together to define falls since the 1980s and have finally come to define a fall as “an event that results in the unintentional impact of a person on the floor or other lower level and is not necessarily the result of a significant event or imminent hazard.” The impact on health care and costs of falls in older adults is increasing dramatically worldwide and the cost of falls is categorized into two types: direct costs and indirect costs. Direct costs are what patients and insurance companies pay to treat injuries caused by falls. This includes fees for hospitals, nursing homes, doctors and other professional services, rehabilitation, community services, the use of medical equipment, prescription drugs, and changes to the home to ensure that the event does not occur again. Indirect costs include the loss of productive capacity of the family and the long-term effects of falls such as physical disability, dependency, and reduced quality of life. In the United States alone, the total cost of fall-related injuries for people over age 65 was $31 billion in 2015. The costs included millions of emergency room visits, nonfatal injuries, and more than 800,000 hospitalizations, and it is estimated that by 2030 the annual number of fall injuries will reach 74 million seniors.

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Geriatric medicine

Sarcopenia is actually a degenerative loss of skeletal muscle mass, efficiency and strength due to aging or lack of movement, and it is a disease that may be defined as any pathological or abnormal condition that affects muscle tissue, especially skeletal muscle, in which muscle weakness is the primary complaint, as a result of the inability of the affected muscles to perform their functions to the fullest extent. Therefore, muscle weakness or sarcopenia is a disease that affects muscle fibers, which leads to their inability to perform their function for several reasons, resulting in weakness in the muscle in general. Sarcopenia expresses a defect in the muscle itself, despite the efficiency of the nerve or nerves connected to it, and differs from problems that arise from a defect in the nerves or higher brain centers. Accordingly, muscle diseases can be classified according to their nature into two main categories: the first is neuromuscular disorders, which includes several types, and the second is what is known as the musculoskeletal motor type, while what is known as polymyositis can be considered a mixture of the two previous types. There was no specific and unified general medical definition for sarcopenia until 2009. A group of European doctors identified sarcopenia in the elderly and developed a general medical and diagnostic definition for age-related sarcopenia. Sarcopenia is diagnosed when there is a decrease in muscle mass and a decrease in motor ability. Sarcopenia or muscle weakness can be divided into several groups, some of which are hereditary, and some are acquired as a result of contracting another disease. The most famous of these are those that occur as a result of taking certain substances or medications, and some of which occur with some diseases, such as polio, and some of which occur with skin infections, as we will list as follows: As for doctors, the modern classification of sarcopenia is through the modern international classification, approved by the World Health Organization and known as the ICN - Codes, which we mean the international statistical classification of diseases and health problems, which includes more than 14,400 codes, which leads to many modern diagnoses of diseases, which then reach more than 16,000 codes. As for the symptoms of the disease, they can be summarized as a weakness in the person's or child's ability to use the affected muscles, and the matter may develop into repeated contractions, or muscle stiffness, and muscle spasms may occur. As for the treatment, because its causes are numerous and vary in the ways they occur, there is no comprehensive treatment method for all types, but it differs from one type to another. There are some types that benefit from some drug treatments, and some of them require physical therapy, and some of them require treatment with acupuncture, and recent research has begun to benefit from the system and science of stem cells to treat some types of this disease. However, periodic follow-up with the attending physician remains the most important thing in the subject, for several reasons, including knowing the development of the condition, and the extent of the effect of drug or physical therapy on not developing complications of the disease, as well as following up on all new modern treatment methods that may develop, which may benefit these patients. An accurate diagnosis of the type of atrophy or weakness of the meat is very important, because it is the first step in determining the type of treatment program appropriate for the case. It is known that a careful clinical examination by the examining physician of the patient is the first thread of diagnosis, through an accurate medical history and an accurate clinical examination. Then there is an initial laboratory examination of a specific enzyme. If its levels are high, we begin examining the affected muscles through electromyography. We may often need to perform a puncture operation on part of the affected muscles, to know the histopathological analysis of these tissues in the muscles, which allows for estimating the ideal treatment program for each case individually.

Geriatric medicine

Geriatric dentistry is the provision of dental care to older adults, including the diagnosis, prevention, and treatment of age-related problems and age-related diseases as part of a specialized team with other health care professionals. The past century has seen a number of striking statistical changes in the health, disease, longevity, and mortality of populations around the world. Currently, one-third of the world's elderly population lives in developing countries, and one in twelve people in these developing countries is over the age of sixty-five. The twentieth century witnessed a significant aging of the global population in terms of life expectancy, and the twenty-first century is set to see significant gains in longevity worldwide, both in developed and developing countries. This increase in life expectancy is primarily due to the significant reduction in mortality rates throughout the lifespan that has occurred with the development of health care facilities, sanitation, environmental and public health improvements coupled with better hygiene and living conditions. As a result of increasing life expectancy, the proportion of elderly people in the total population is expected to be around 25% in India and 32% in developed countries by 2050. Taking this increase in life expectancy into account, the retirement age in many sectors in India is increasing, in some of them it may even reach 70 years. In some states, the retirement age has not been increased due to concerns about the eventual loss of jobs to the younger generation. According to the Government of India’s classification, elderly people are those aged 60 years or above; these citizens become eligible for various exemptions and concessions granted by the government and other agencies. In developing countries, elderly people are those above 65 years. The mouth is considered a mirror of overall health, and hence oral health is an integral part of overall health. Poor oral health in an elderly population is a risk factor for overall health problems. On the other hand, elderly people are more susceptible to oral conditions and diseases due to the increase in chronic conditions and physical and mental disabilities. Thus, the elderly constitute a prominent group with regard to precautionary care. The dental diseases that the elderly are most susceptible to are root caries, erosion, periodontal disease, tooth loss due to early neglect, edentulism, poor quality of the alveolar margin, poorly fitting dentures, mucosal lacerations, oral ulcers, dry mouth, oral cancers, and extensive caries. Many of these are consequences of neglect in the early years of life, e.g. consumption of carious foods, lack of awareness regarding preventive aspects, and habits such as smoking and/or tobacco, frying, and chewing betel nut. All of these problems can be significantly aggravated by the decline in immunity with age and by coexisting health problems. As a result of poor systemic health, elderly patients do not pay enough attention to their oral health. In addition, medications such as antihypertensives, antipsychotics, antianxiety drugs, etc., lead to dry mouth, and the loss of the protective effect of saliva in the oral cavity increases the susceptibility to oral diseases. Financial constraints, lack of family support or transportation are major barriers to accessing dental services in later life. Untreated oral cavity has detrimental effects on comfort, aesthetics, speech, chewing and, consequently, quality of life in old age. The extent of root caries in the elderly can be as high as 1.6 root surfaces for every root surface at risk. The nature of root caries in men is more severe and is more pronounced in the molar area. Several major factors are associated with the development of root caries including decreased salivary flow, poor manual dexterity and systemic infections requiring the use of drugs that cause decreased salivation. In addition, more serious risk factors include erosion of the cementum enamel margin, clinical preparation for a fixed bridge, removable dentures and a restricted diet that includes refined sugars and viscous and fermentable carbohydrates. Prevention and treatment of root caries include topical fluoride application and nutritional counselling on diet planning, prevention of plaque formation and prevention of gum recession. Conservative dental treatment for the elderly must take into account dental, functional and medical considerations to ensure a level of care equivalent to that of younger patients, as well as taking into account the structural changes that have occurred in the tooth and the health status when preparing conservative treatment for the elderly patient. Dental implants have become a strategic measure to replace missing teeth and as a dental component of the treatment plan for elderly patients, dentists should generally consider this type of treatment during their training. The elderly often resort to replacing missing teeth, but they face medical, social and economic complications that must be taken into account when preparing the treatment plan. Dentists should pay full attention to the assessment of the patient's ability, diagnostic criteria and diagnostic procedures to help the patient and his/her family understand the risks and challenges of each type of dental prosthetic treatment. It is important to compare implants with fixed and removable prosthetics. For a large number of dentists, dental implants are becoming a more popular option for replacing missing teeth. With the increasing proportion of the elderly population around the world, dentists will encounter many medically and socially complex cases whose owners desire dental prosthetic treatment. Therefore, it is necessary to increase attention to this branch of dentistry during the period of training of doctors.

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Geriatric medicine

Geriatrics or geriatric medicine is the branch of medical science that deals with the health of the elderly and the elderly. It aims to study the health of the elderly and treat common diseases of old age and treat the effects and disabilities resulting from them. Gerontology was initially affiliated with internal medicine, then it became a science in its own right, like pediatrics. It is known to devote its attention to the care of the elderly, diseases characteristic of the elderly, and problems that affect people with advancing age. To improve the quality of life and stimulate increased safety and preserve dignity, comfort and independence for the elderly. It arose due to the special nature of the elderly and their differences from other age groups. It is also known as geriatrics, geriatric medicine, and dentistry. It is concerned with treating diseases of the elderly and preserving their health by conducting a comprehensive assessment of the elderly and providing medical education to patients, their families, and the caregiver team on the difference between natural aging and pathological aging in the elderly and achieving healthy aging through preventive measures such as elderly vaccinations and others and the benefits of medical screening for some diseases; consultations on sports and nutrition in the elderly. The elderly are distinguished by their special nature from other age groups due to the difference in the performance of the body's organs of their functions. It is necessary to differentiate between changes that occur in the functions of each organ of the body and diseases that occur in each organ. For example, a decrease in functional reserve in the kidneys is considered a natural change with old age, but renal insufficiency or renal failure is considered a disease in any age group. Cases of confusion/delirium, senile dementia and Alzheimer's disease, depression or anxiety, drug overuse disorders and drug interactions, movement and balance disorders and falls, urinary incontinence, dehydration and malnutrition, chronic pain, problems of bedridden patients, osteoporosis, dealing with various ulcers, rehabilitation and physical medicine for the elderly, sensory impairment, palliative care and terminal care. Such as femoral neck fracture, pressure ulcers, deep vein thrombosis, acute arterial insufficiency, prostate diseases and preoperative medical evaluation. The geriatric medical care team consists of geriatricians, rehabilitation physicians, nurses, psychologists, dietitians, cognitive and speech rehabilitation specialists, occupational therapists, and social workers. There are some sub-branches within the geriatric specialty such as geriatric psychiatry and cardiology of the elderly. Some modern care methods that are already provided or can be provided to the elderly. It is a sub-system of social policy and is the mechanism used by governments to allocate limited resources and as such deals with multiple variables such as limited resources, unmet needs, and poorly defined goals.

Geriatric medicine

Geriatric psychiatry, also known as geriatric medicine or gerontological psychiatry, is a branch of medicine and a subspecialty of psychiatry that deals with the study, prevention, and treatment of neurodegeneration, cognitive impairment, and mental disorders in older adults. Geriatric psychiatry as a subspecialty has significant overlap with the specialties of geriatrics, behavioral neurology, neuropsychiatry, neurology, and general psychiatry. Geriatric psychiatry has become a formal subspecialty of psychiatry with a defined curriculum and core competencies. The origins of geriatric psychiatry began with Alois Alzheimer, a German psychiatrist and neuropathologist who first identified amyloid plaques and neurofibrillary tangles in a fifty-year-old woman he named Auguste Dieter. These plaques and tangles were later identified as responsible for her behavioral symptoms, short-term memory loss, and psychiatric symptoms. These brain abnormalities would become the determinants of what later became known as Alzheimer's disease. The subspecialty of geriatric psychiatry originated in the United Kingdom in the 1950s. The geriatric unit, the term for a hospital-based geriatric psychiatry program, was first introduced in 1984 by Norman White, when he opened New England's first specialty program at a community hospital in Rochester, New Hampshire. White is a pioneer in geriatric psychiatry, being among the first psychiatrists in the nation to be board certified in the field. The prefix psychiatry was suggested for the geriatric program, but White, who knew the New Englanders' aversion to anything psychological, successfully pressed for the name geriatrics rather than psychiatry. Diseases and disorders diagnosed or managed by geriatric psychiatrists include: A geriatric psychiatrist is a physician who specializes in the medical subspecialty called geriatric psychiatry. A geriatric psychiatrist is board-certified after specialized training following a medical degree, residency, and additional geriatric psychiatry fellowship. Requirements may vary by state. Geriatric psychiatrists are also psychiatrists qualified in the general diagnosis and treatment of mental disorders. Some geriatric psychiatrists also conduct research to determine the cause and best treatment for neurodegenerative disorders and mental health disorders in later life. Geriatric psychiatrists may perform neurological examinations, mental status examinations, laboratory tests, neuroimaging, and cognitive assessments to investigate the causes of psychiatric or neurological symptoms in old age. The International Geriatric Psychiatry Association is an international community of scientists and geriatric care professionals working in the field of geriatric mental health. International Geriatric Psychiatry is the official journal of the International Psychiatric Association. The Royal College of Physicians and Surgeons of Canada is responsible for the training and certification of geriatric psychiatrists in Canada. Geriatric psychiatry requires an additional year of subspecialty fellowship training in addition to general psychiatric training. The Royal College of Psychiatrists is responsible for the training and certification of psychiatrists in the United Kingdom. Within the Royal College of Psychiatrists, the Faculty of Geriatric Psychiatry is responsible for training in geriatric psychiatry. Physicians who are members of the Royal College of Psychiatrists can undertake a three- or four-year training program to become a geriatric psychiatrist. There is currently a shortage of geriatric psychiatrists in the United Kingdom. The American Geriatric Psychiatry Association is a national organization representing health care providers who specialize in late-life mental disorders. The American Journal of Geriatric Psychiatry is the official journal of the association. Both the American Board of Psychiatry and Neurology and the American Osteopathic Board of Neurology and Psychiatry issue board certification in geriatric psychiatry. After a 4-year residency in psychiatry, a psychiatrist can complete a 1-year fellowship in geriatric psychiatry. There are several geriatric psychiatry fellowships.

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Geriatric medicine

The word “longevity” is sometimes used synonymously with “life expectancy” in demography—especially when it concerns someone or something that lives longer than expected—however, the two words have slightly different definitions. In a similar vein to “discipline” and “precision,” “longevity” refers to the average number of years a human being lives, while “life expectancy” refers to the number of years the average population lives. This is illustrated by the fact that a large increase in life expectancy can be accompanied by a small increase in the overall longevity of the population. Speculations about longevity have gone beyond the recognition of the shortness of human lifespans, and have included consideration of ways to prolong life. The topic of longevity has been raised not only in the scientific community but also among travelers, science fiction writers, and utopian novelists. There are many difficulties in ascertaining the absolute longest human lifespan by contemporary standards, due to inaccurate or incomplete birth statistics. Novels, myths, and folklore have claimed past or future lifespans that are much longer than those proven by modern standards, and unconfirmed claims of longevity continue to abound, with talk of cases of longevity in the present.

Geriatric medicine

The geriatric medical care team consists of geriatricians, rehabilitation doctors, nursing staff, psychologists, nutritionists, cognitive and verbal rehabilitation specialists, occupational therapists, and social workers. He has postgraduate studies and clinical training in geriatric medicine: His role in the care team: The problem is defined as a disability or something that is functionally and structurally harmful and stands in the way of satisfying human needs, or a condition that is believed to threaten social value, but can be changed through constructive social actions. It is also defined as the difficulties that a person is exposed to and that affect his behavior, actions, performance, and relationships with others, and their presence may result in undesirable consequences that affect social life as a whole. Thus, the problems of the elderly can be defined as individual or collective non-consensual situations that hinder their social adaptation to their social environments, and hinder their investment of available resources. The health status of the elderly depends on a set of social factors such as the standard of living, the level of education, the extent of his interest in periodic medical examinations and his ability to bear the costs of treatment or not, in addition to the extent of the elderly and his family's awareness of the diseases of old age and the elderly's neglect of himself and not asking for help until his condition worsens. The health of the elderly is also affected by the type and quantity of food, the nature of the profession in which he worked, and the environment to which he belongs, whether natural or social, because the frequent use of any part of the body delays aging. The most important diseases that the elderly are exposed to: If the physical disease imposes some precautions and restrictions on the patient in his way of life, then psychological problems affect the patient and hinder his compatibility, and it is possible that it has physical symptoms including weight loss and constipation. Among the most important problems that the elderly suffer from: Mental problems of the elderly are represented in senile psychosis, which includes memory loss and forgetfulness, and paranoia disorders. Have postgraduate studies and clinical training in geriatric nursing: Role in care: • Organizing the transfer and admission of patients to the department. • Providing medical education to the patient, his family and caregivers. • Coordinating patient care by the rest of the geriatric care team during the team meeting. • Evaluating the patient. • Setting treatment goals and developing. • Reviewing the treatment plan. The social worker uses the system analysis model in social work by the two scientists "Allen Banks and Ann Minahan" to enhance the effectiveness of professional intervention to address problems and situations with the elderly. The general practitioner helps in addressing multiple problems of systems of dealing in the field of geriatric care by using different methods as well as when assuming many roles. The role is a behavior and activity that is united in performing some specific tasks and responsibilities. The most important roles of the general practitioner in the field of geriatric care: Physical medicine doctor and rehabilitation specialist: Selecting the appropriate patient for treatment by the geriatric doctor and the geriatric care team: Studies have shown that medical geriatric care programs achieve success with certain cases of elderly patients. Studies have not proven the relationship between chronological age and benefit from medical geriatric care programs. Although as age increases, problems of multiple morbidities, frailty, and common geriatric syndromes increase. Characteristics of elderly patients who will likely benefit from geriatric care programs: § Chronological age 60 years or older § Multiple medical problems, functional performance problems, and some psychological and social problems. § Age who suffers from one or more common geriatric syndromes such as: dementia, delirium, functional decline, urinary incontinence, polypharmacy, elderly abuse, unsteady gait/falls, malnutrition, or depression. Characteristics of elderly patients who will likely not benefit from geriatric care programs:

Geriatric medicine

Risk dignity is the idea that self-determination and the right to take responsible risks are essential to dignity and self-esteem and should not be denied by overly cautious caregivers concerned with their duty of care. The concept applies to adults in care, such as elderly caregivers, people with disabilities, and people with mental health problems. It also applies to children, including children with disabilities. Allowing people in care to take risks is often seen as a counter to the duty of caregivers to care. It can be difficult to balance these conflicting considerations when developing policies and guidelines for caregiving. Overprotection of people with disabilities results in low self-esteem and lower achievement because of the low expectations that accompany overprotection. Internalization of low expectations causes a person with a disability to believe that they are less capable than others in similar situations. In older people, overprotection can lead to learned dependency and reduced ability to care for themselves. Physical care can have positive outcomes and enable the individual to function at their full potential. However, if they are not included in the caregiving process, allowed to make decisions, and respectfully assisted in their daily activities, it is likely to lead to psychological harm by weakening and undermining the dignity of that individual.

Geriatric medicine

Tea and toast syndrome is a common form of malnutrition in older adults who are unable to prepare meals for themselves, and so their diet is limited to tea and toast, resulting in vitamin and other nutrient deficiencies. This syndrome often manifests as hyponatremia due to a lack of salt in the diet. This syndrome often occurs when children move out of the home or when a spouse dies or is near death. An older adult who is left alone with no one to prepare food for him or her and lacks the skills to prepare food for himself will resort to a diet of simple foods such as bread, cheese, crackers, and canned foods. According to the New York Times, up to 60 percent of older adults living at home are malnourished or at risk of malnutrition. In addition to the problems caused by nutritional deficiencies, this condition means that complications from other illnesses, even the common cold, can be extremely dangerous. Factors that lead to this syndrome include social isolation, psychological problems such as depression, illnesses, and physical limitations. The increasing number of medications that older adults take can affect eating habits, although this is a less serious factor than psychological problems. However, these medications can reduce appetite, change the taste of food, or affect the way nutrients are absorbed, making it difficult for older adults to get the nutrients they need. Typical laboratory findings for tea-and-toast syndrome include low serum osmolality with normal urine osmolality, because antidiuretic hormone levels are normal.

Geriatric medicine

Parkinson's disease, also known as shaking palsy, is a degenerative disorder of the central nervous system that mainly affects the motor system. Symptoms start slowly at the onset of the disease, the most noticeable being tremors, contractions, decreased movement and gait abnormalities. Problems with thinking and behavior may also occur. Dementia becomes common in the later stages of the disease. Depression and anxiety are also common symptoms, occurring in more than a third of people with Parkinson's disease. Sensory symptoms include sleep disturbances and emotional problems. The main motor symptoms are collectively called "parkinsonism", or "parkinsonian syndrome". The cause of Parkinson's disease is generally unknown, but is thought to involve genetic and environmental factors. There is also an increased risk in people exposed to certain pesticides and among those who have had head injuries, while there is a lower risk in tobacco smokers and those who drink coffee or tea. The motor symptoms of the disease result from cell death in the substantia nigra, an area of the midbrain. This leads to insufficient dopamine in these areas. The cause of cell death is not understood, but it involves the accumulation of proteins in the bodies of the brain. Lewy in neurons. Diagnosis of typical cases is based mainly on symptoms, with tests such as neuroimaging used to rule out other diseases. There is no cure for Parkinson's disease. Initial treatment is usually the antiparkinsonian drug levodopa with a dopamine agonist. As the disease progresses, neurons continue to be lost, so these drugs become less effective. Diet and some forms of rehabilitation have shown some effectiveness in improving symptoms. Neurosurgery to place microelectrodes to stimulate the brain has been used to reduce motor symptoms in severe cases when drugs are ineffective. In 2015, Parkinson's disease affected 6.2 million people and resulted in about 117,400 deaths worldwide. Parkinson's disease usually occurs in people over the age of 60. Males are more affected than females. When the disease affects people under the age of 50, it is called juvenile Parkinson's disease. The average life expectancy after diagnosis of Parkinson's disease is between 7 and 14 years. The disease was discovered by the English physician James Parkinson, who published the first detailed description in a paper on shaking palsy, in 1817. Public awareness campaigns include World Parkinson's Day and the use of a red tulip as a symbol for the disease. People who have suffered from Parkinson's disease and have helped raise public awareness of the condition include actor Michael J. Fox, Olympic cyclist Davis Finney, and the late boxer Muhammad Ali. The movement difficulties found in Parkinson's disease are called "parkinsonism." The motor symptoms of "parkinsonism" are bradykinesia (slowness in initiating voluntary movements, with a gradual decrease in speed), plus one of three other physical signs: muscle rigidity, tremor, and postural instability. Parkinson's disease is sometimes called "idiopathic Parkinsonism," because no specific cause is known. Identifiable causes of Parkinson's disease include toxins, infections, drug side effects, metabolic deterioration, and brain lesions such as strokes. Several neurological disorders can also occur with Parkinsonism, sometimes referred to as "atypical Parkinsonism" or "Parkinsonism plus." They include multiple system atrophy, progressive supracentral palsy, Cortical degeneration, dementia and Lewy body disease. Scientists sometimes refer to Parkinson's disease as a synucleinopathy to distinguish it from other neurodegenerative diseases, such as Alzheimer's disease, in which the protein tau accumulates in the brain. There is considerable clinical and pathological overlap between tonopathies and synucleinopathies. In contrast to Parkinson's disease, Alzheimer's disease is most commonly associated with memory loss, and the cardinal signs of Parkinson's disease are not typical features of Alzheimer's disease. Dementia and Lewy body disease are closely related to Parkinson's disease. The relationship between Parkinson's disease and Lewy body disease is quite complex. They may represent parts of a continuum with distinct clinical and pathological features or may prove to be separate diseases. The most characteristic symptom of Parkinson's disease is difficulty with movement. Non-motor symptoms, which include autonomic dysfunction, neuropsychiatric problems, sensory and sleep difficulties, are also common. Some of these non-motor symptoms may be present at the time of diagnosis. The four cardinal motor symptoms in Parkinson's disease are tremor, decreased The most common motor symptom in Parkinson's disease is a slow tremor of the hand that disappears during voluntary movement of the affected arm and in the stages of deep sleep. This tremor usually occurs in one hand, but the other hand eventually becomes affected as the disease progresses. The tremor frequency in Parkinson's disease is between 4 and 6 hertz per second. A characteristic of the hand tremor is the tendency of the index finger and thumb to touch each other and make a circular motion. Hypokinesia is present in all cases of Parkinson's disease, and is due to disturbances in the motor planning of movement initiation, and is associated with difficulties along the movement process, from planning to initiation to execution of a movement. Motor performance is impaired. Bradykinesia is the most disabling symptom of Parkinson's disease, leading to difficulties in daily tasks such as dressing, feeding, and bathing. It leads to particular difficulty in performing two independent motor activities at the same time, and can be worsened by psychological stress or concurrent illnesses. Ironically, patients with Parkinson's disease can often ride a bicycle or climb a mountain. Stairs are easier to climb than walking. While most doctors may easily notice slowness of movement, a formal evaluation requires the patient to make repetitive movements of the fingers and toes. Rigidity is a symptom of Parkinson's disease and is a stiffness and resistance to movement of the limbs caused by increased muscle tone and excessive and persistent muscle contraction. Rigidity is a combination of tremor and increased muscle tone at the same time. Rigidity may be associated with joint pain. This pain is a frequent initial manifestation of the disease. In the early stages of Parkinson's disease, rigidity is often asymmetrical and tends to affect the neck and shoulder muscles before the face and limbs. As the disease progresses, rigidity usually affects the entire body and reduces the ability to move. Postural instability is common in the later stages of Parkinson's disease, leading to poor balance and frequent falls that can lead to bone fractures, loss of confidence, and decreased mobility. Instability is often absent in the early stages, especially in young people, especially before the onset of bilateral symptoms. Up to 40% of people diagnosed with Parkinson's disease fall to the ground frequently. Other recognized signs and symptoms include The symptoms that affect the patient's motor system are: , and also signs: quiet voice, a face that does not move, and the patient's handwriting becomes noticeably smaller over time. Parkinson's disease can cause neuropsychiatric disorders, which can range from mild to severe disorders. These include disorders of perception, mood, behavior, and thought. Cognitive disorders can occur in the early stages of the disease and sometimes before diagnosis, and these disorders increase with increasing age of the patient and the progression of the disease stages. The most common cognitive deficit in Parkinson's disease is impaired execution and planning, which can include problems with planning, cognitive flexibility, abstract thinking, inhibiting inappropriate actions, initiating appropriate actions, and working memory. Other cognitive difficulties include slow cognitive processing speed, decreased neurotransmission, poor perception, and time estimation. Vision problems are also part of the disease, for example, when an individual is asked to perform facial recognition tests and perceive the direction of drawn lines, they cannot easily determine this. A person with Parkinson's disease has two to six times the risk of dementia compared to the general population. The prevalence of dementia increases with age and the length of the disease. Dementia is associated with With a reduced quality of life for people with Parkinson's disease and their caregivers, the patient is more likely to require home nursing care. Behavior and mood changes are more common in Parkinson's patients without cognitive impairment than in healthy people, and behavioral and mood changes are often associated with dementia. The most common mood problems are depression, apathy, and anxiety. Diagnosing depression is complicated by the fact that the body language of depression can masquerade as Parkinson's disease, such as a sad, expressionless face, slow movements, and a quiet, broken voice - all of which could be Parkinson's disease or just depression, and thus distinguishing between them using these symptoms alone is very difficult. Up to 30% of people with Parkinson's disease may have symptoms of anxiety, ranging from generalized anxiety disorder to social anxiety disorder, panic disorder, and obsessive-compulsive disorder. Dissociative identity disorder, in which repetitive, purposeless, stereotyped behaviors occur only for a few hours, is another disorder caused by anti-Parkinson's medication. Hallucinations or delusions occur in about 50% of people with Parkinson's disease over the course of the disease, and can be a sign of Dementia. These range from minor hallucinations—“feeling like you’re passing by” or “feeling like you’re there”—to visual hallucinations and paranoid thoughts. Auditory hallucinations are uncommon in Parkinson’s disease, and are rarely described as voices. Psychosis is now thought to be an integral part of the disease. Psychosis with associated delusions and delirium is a recognized complication of anti-Parkinson’s therapy and can also be caused by urinary tract infections, but drugs and infections are not the only factors behind the pathology or changes in neurotransmitters or their receptors are thought to play a role in psychosis in Parkinson’s disease. In addition to neuropsychiatric and motor symptoms, Parkinson’s disease can be compounded by problems with other systems. Sleep problems are a feature of the disease and can be exacerbated by medications. Symptoms can include daytime sleepiness, sleep disturbances, or insomnia. Rapid eye movement (REM) sleep, where the patient acts as if they are dreaming, and sometimes injures themselves or their bed partner, may begin many years before the motor system or cognitive features of Parkinson’s disease develop. Changes in the autonomic nervous system can lead to orthostatic hypotension, seborrheic dermatitis, excessive sweating, urinary incontinence, and altered sexual function. Constipation and stomach weakness can be severe enough to cause discomfort and even endanger health. Changes in cognition may include a poor sense of smell, blurred vision, and pain. All of these symptoms can occur years before the disease is diagnosed. Exposure to pesticides and head injury have been linked to Parkinson's disease, but the risk is relatively low. People who have never smoked cigarettes have an increased risk of Parkinson's disease and moderate consumption of caffeinated beverages increases the risk of the disease. Low serum concentrations of urate may increase the risk of Parkinson's disease. Parkinson's disease is presumed to be a non-inherited disorder, but it appears to be the product of a complex interaction of genetic and environmental factors. About 15% of individuals who have a close relative with the disease also have the disease, and 5-10% of people with Parkinson's disease may be caused by a mutation in one of several specific genes. These gene mutations lead to the disease, and they put an individual at increased risk, often in combination with other risk factors, but in most cases, people with these mutations will develop Parkinson's disease. The genes involved in the development of Parkinson's disease are: alpha-synuclein, LRRK2, GBA, PRKN, PINK1, PARK7, VPS35, EIF4G1, DNAJC13 and CCHHD2. SNCA gene mutations are important in Parkinson's disease because the protein the gene encodes, alpha-synuclein, is a major component of Lewy bodies that accumulate in people's brains. Mutations in certain genes, including SNCA, LRRK2, and GBA, have been found to be risk factors. Mutations in the LRRK2 gene are the most common cause of Parkinson's disease, accounting for about 5% of individuals with a family history of the disease and 3% of sporadic cases. A mutation in GBA greatly predisposes a person to the development of Parkinson's disease. Several genes associated with the disease are involved. Parkinson's disease in lysosomal function. It has been suggested that some cases of Parkinson's disease may be caused by lysosomal dysfunctions that reduce the cells' ability to break down alpha-synuclein. The main pathology of Parkinson's disease is cell death in the basal ganglia of the brain as well as in many of the remaining neurons. This is accompanied by neuronal loss, astrocyte death, and a significant increase in the number of microglia in the substantia nigra. There are five major pathways in the brain that connect other brain regions to the basal ganglia. These are known as the motor cortex, oculo-motor cortex, temporal cortex, limbic system, and orbitofrontal cortex. All of them are affected in Parkinson's disease, and disruption of these brain regions explains many of the symptoms of the disease, because these circuits are involved in a wide range of functions, including movement, attention, and learning. There is a particular conceptual model of the motor system and its alteration in Parkinson's disease that has been influential since the 1980s, although some limitations have led to some modifications. In this model, the basal ganglia typically exert a persistent inhibitory influence on a wide range of systems. Motor, preventing them from becoming active at inappropriate times. When a decision is made to perform a certain action, the inhibition of the required motor system is reduced, thus releasing it for activation. Dopamine acts to facilitate this release from the motor system, so high levels of dopamine tend to promote motor activity, which is what happens in Parkinson's disease where the patient requires more effort for any given movement. Thus, the net effect of dopamine depletion is to produce hypokinesia, a general decrease in motor output. Drugs used to treat Parkinson's disease may work by increasing dopamine, allowing motor systems to be activated. There are several mechanisms by which brain cells can be lost. One mechanism consists of an abnormal accumulation of the ubiquitin-bound protein alpha-synuclein in damaged cells. This insoluble protein accumulates within neurons forming derivatives called Lewy bodies. According to Braak, the disease is classified on the basis of pathological findings. Lewy bodies first appear in the olfactory bulb, medulla oblongata and pontine tegmentum. Individuals at this stage may be asymmetrical or may have They have early non-motor symptoms. As the disease progresses, Lewy bodies develop in the substantia nigra, areas of the midbrain and basal forebrain, and finally, the neocortex. These sites in the brain are the main sites of neuronal degeneration in Parkinson's disease. However, Lewy bodies may not cause cell death and may be protective. Other forms of alpha-synuclein that do not aggregate into Lewy bodies while Lewy neurites are toxic forms of the protein. In people with dementia, Lewy bodies are common in cortical areas. Neurofibrillary tangles and senile plaques, which are characteristic of Alzheimer's disease, are not common unless the person is demented. Other mechanisms of cell death include dysfunction of the proteasomal and lysosomal systems and reduced mitochondrial activity. Iron accumulation in the substantia nigra is often seen in conjunction with protein inclusions. It may be related to oxidative stress, protein aggregation, and neuronal death, but the mechanisms are not fully understood. The physician initially evaluates Parkinson's disease with a history Careful medical and neurological examination. The patient may be given levodopa, and any resulting improvement in motor system dysfunction helps to confirm the diagnosis of Parkinson's disease. The finding of Lewy bodies in the midbrain on autopsy is usually considered definitive evidence that the person has had Parkinson's disease. The clinical course of the disease over time may reveal it is not Parkinson's disease, requiring periodic review of the clinical presentation to confirm the diagnosis. Other causes that can secondarily resemble Parkinson's disease are stroke and drugs. Progressive suprarenal palsy and multiple system atrophy should be excluded. Antiparkinsonian drugs are usually less effective in controlling symptoms in Parkinson's plus syndromes. Rates of progression, early cognitive impairment, or postural instability may initially indicate Parkinson's disease. Genetic forms with an autosomal or recessive pattern of inheritance are sometimes referred to as familial Parkinson's disease. Medical organizations have developed diagnostic criteria to ease and standardize the diagnostic process, especially in the early stages of the disease. The most widely recognized criteria come from the British Neurological Disorders Bank and the National Institute of American Neurological Association and Stroke. The Kingdom criteria require bradykinesia plus either rigidity, tremor, or postural instability. Other possible causes of these symptoms need to be ruled out. Finally, three or more of the following supporting features are required during the onset or progression of the disease: disease on only one side of the body, tremor at rest, asymmetry of motor symptoms, and response to levodopa therapy for at least five years. When diagnoses of Parkinson's disease are examined by autopsy, movement disorders are found to be an average of 79.6% accurate at initial assessment and 83.9% accurate after their diagnosis has been refined at follow-up examination. When clinical diagnoses performed primarily by nonpsychologists are examined by autopsy, average accuracy is 73.8% and 82.7% of diagnoses using brain bank criteria. A task force of the International Parkinson's and Movement Disorders Society has proposed diagnostic criteria for Parkinson's disease, as well as research criteria for the diagnosis of prodromal disease, but they require validation of the more established criteria. Computed tomography is usually It appears normal in people with Parkinson's disease, and MRI has become more accurate in diagnosing the disease over time, specifically iron-sensitive T2* and magnetization-weighted MRI at at least 3T, both of which can show the absence of the characteristic "swallow tail" imaging pattern in the dorsolateral substantia nigra. In a meta-analysis, the absence of this pattern was 98% and 95% specific for this disease. Diffusion MR imaging shows the potential to differentiate between Parkinsonism and Parkinson's plus syndrome, although its diagnostic value is still under investigation. CT and MRI are also used to rule out other diseases that can be secondary causes of parkinsonism, most commonly encephalitis and chronic brain insults, as well as less common entities such as basal ganglia tumors and hydrocephalus. Dopamine-related activity in the basal ganglia can be measured directly with PET and SPECT scans. The detection of decreased dopamine-related activity in the basal ganglia can rule out drug-induced parkinsonism, but decreased dopamine-related activity Basal ganglia dopamine in both Parkinson's and Parkinson's Plus disorders is not reliable in distinguishing Parkinson's disease from other disorders. Exercising in middle age may reduce the risk of Parkinson's disease later in life. Caffeine also appears to be protective against Parkinson's disease and shows a greater reduction in risk than occurs with a higher intake of caffeinated beverages such as coffee. People who smoke cigarettes or use smokeless tobacco are less likely than nonsmokers to develop Parkinson's disease, and the more tobacco they use, the less likely they are to develop it. It is not known what underlies this effect. Tobacco use may actually protect against Parkinson's disease. Antioxidants, such as vitamin C and vitamin E, have been suggested to protect against the disease, but study results have been inconsistent and no positive effect has been demonstrated. Results regarding fatty acids have been inconsistent, with studies reporting different protective effects and increased risk effects. There have been preliminary indications that the use of anti-inflammatory drugs and calcium channel blockers may be protective. A 2010 analysis found that nonsteroidal anti-inflammatory drugs, NSAIDs, were associated with a 15 percent At least reduce the incidence of Parkinson's disease progression. There is no cure for Parkinson's disease, but medications, surgery and physical therapy can provide relief to patients and are much more effective than treatments available for other neurological disorders such as Alzheimer's disease, motor neuron disease, Parkinson's syndrome and multiple sclerosis. The main families of medications useful for treating motor symptoms are levodopa, dopamine agonists and MAO-B inhibitors. The stage of the disease and age at onset of the disease determine which group is most useful. Three stages can be distinguished: an initial stage where the individual with the disease has developed some disability requiring drug therapy, a second stage associated with the development of complications related to the use of levodopa, and a third stage with symptoms unrelated to dopamine or levodopa deficiency. Treatment in the first stage aims at an optimal trade-off between symptom control and treatment of side effects. Levodopa can be delayed initially by using other medications such as MAO-B inhibitors and dopamine agonists instead of levodopa itself, in the hope of delaying the onset of complications due to the use of levodopa. However, levodopa remains the most effective treatment for motor symptoms and should not be delayed in patients whose quality of life is impaired by those symptoms. Dysfunction is associated with Levodopa is more potent with the duration and severity of the disease, so delaying this treatment is not the best solution in this case. In the second stage, the goal is to reduce the symptoms of Parkinson's disease while controlling fluctuations in the drug's effect. Abrupt withdrawals from the drug or overuse must be managed. Oral medications are not sufficient to control symptoms and therefore surgery, deep brain stimulation, subcutaneous injections of apomorphine and intestinal dopa pumps can be of benefit. The third stage presents many difficult problems requiring a variety of treatments for psychological symptoms, orthostatic hypotension, bladder dysfunction, etc. In the final stages of the disease, care is provided to improve the quality of life. Levodopa has been the most widely used treatment for more than 30 years. L-DOPA is converted to dopamine in neurons by dopa-decarboxylase. Since motor symptoms result from a lack of dopamine in the substantia nigra, the use of L-DOPA temporarily reduces motor symptoms. Only 5-10% of L-DOPA crosses the blood-brain barrier. The rest is often converted to Dopamine elsewhere, causing a wide range of side effects including nausea, dyskinesia. Carbidopa and benserazide are dopa decarboxylase inhibitors that inhibit the formation of dopamine elsewhere, thereby minimizing the side effects of treatment as much as possible. They inhibit the metabolism of L-DOPA elsewhere, thereby increasing the delivery of levodopa to the central nervous system. Current inhibitors are carbidopa/levodopa and benserazide/levodopa. Tolcapone inhibits the enzyme catechol-O-methyltransferase, which degrades dopamine and levodopa, thereby prolonging the therapeutic effects of levodopa. Tolcapone is used, in combination with peripheral dopa decarboxylase inhibitors, to increase the therapeutic potency of L-DOPA. However, this treatment is limited, due to its potential side effects such as liver failure. A similar drug, entacapone, has not been shown to cause significant changes in liver function and maintains adequate COMT inhibition over time. Entacapone can be used as a treatment or in combination Along with carbidopa and levodopa, the results of using levodopa work to reduce the body's own formation of L-DOPA, in the long term treatment can cause the development of motor complications characterized by involuntary movements, motor dysfunction, and fluctuations in response to medications. When this happens, a Parkinson's patient goes from a patient who responds very well to treatment and has a noticeable improvement in the disappearance of symptoms of the disease to a patient who does not respond at all to treatment and the appearance of the disease symptoms in a bad way. For this reason, Parkinson's patients are given as low doses of levodopa as possible to reduce this problem. Delaying the initiation of drug treatment, rather than using alternatives for some time, is also common to avoid this problem. The previous strategy to reduce motor complications was to withdraw L-DOPA from patients for some time. But it was a bad thing because it could bring serious side effects such as the syndrome. Most patients eventually need levodopa and later on motor complications will appear. The phenomenon of pathological complications due to the use of treatment is called in English and is an almost constant result of sustained levodopa treatment in patients with Parkinson's disease. Stages Immobility and disability associated with depression. All of these symptoms are responsible for the treatment, and despite all the problems caused by pharmacological agents in Parkinson's patients, evidence is presented to indicate the importance of treating with levodopa. Redistributing the doses of levodopa to smaller and more frequent doses may be useful in controlling oscillations in some patients. Restricting dietary protein and using selegiline hydrochloride and bromocriptine may also temporarily improve motor fluctuations. A new approach to treatment involves the use of apomorphine subcutaneously, and the release of small amounts of levodopa with a peripheral dopa decarboxylase inhibitor. This helps reduce complications resulting from the use of L-DOPA. The dopamine agonist has a similar effect to levodopa because it binds to dopamine receptors in the brain. Dopamine agonists were initially used for patients with L-DOPA treatment problems and dyskinesia as an adjunct to levodopa, but are now used mainly on their own as a first-line treatment for motor symptoms with the aim of delaying motor complications. Dopamine agonists include: bromocriptine, Pergolide, pramipexole, ropinirole, piribedil, cabergoline, apomorphine, lisuride. Dopamine agonists have many side effects, albeit mild, such as drowsiness, hallucinations, insomnia, nausea, constipation. Sometimes, side effects occur even at the lowest clinically effective dose, leading the physician to look for a different agonist. Compared to levodopa, dopamine agonists delay motor complications, and control symptoms worse than levodopa. However, they are usually effective enough to manage symptoms in the early years. Dopamine agonists are also more expensive. Dopamine agonists at high doses cause impulse control disorders. Dyskinesias with dopamine agonists are rare in younger patients, and more common in older patients. All of this illustrates the importance of dopamine agonists as a first-line treatment for Parkinson's disease over levodopa. Apomorphine, a dopamine agonist that is not taken orally, can be used to reduce motor loss in the later stages of the disease. Since secondary effects such as confusion Hallucinations are not uncommon with apomorphine treatment, and patients should be closely monitored. Apomorphine can be administered by subcutaneous injection using a small pump carried by the patient. A low dose is administered automatically throughout the day, thus limiting fluctuations in motor symptoms by providing consistent doses of dopamine agonists. When using an apomorphine pump, the injection site should be changed daily to avoid nodules forming. Apomorphine is also available in large doses as an autoinjector pen used for emergency dosing such as falls or first thing in the morning. Nausea and vomiting are common with apomorphine, and may require domperidone. In a study evaluating the efficacy of dopamine agonists compared to levodopa, the results showed that patients who took dopamine agonists were less likely to develop dyskinesia, dystonia, and movement fluctuations, although they were more likely to discontinue treatment due to negative side effects such as nausea, constipation, etc. MAOIs work by increasing the level of dopamine in the basal ganglia. They inhibit monoamine oxidase-B, which By breaking down dopamine released from neurons. Therefore, reducing MAO-B leads to higher amounts of L-DOPA. Like dopamine agonists, MAO-B inhibitors improve motor symptoms and delay the need to take levodopa as a monotherapy in the early stages of the disease, but these inhibitors produce more negative effects and are less effective than levodopa. Their effectiveness in the advanced stage of the disease is also poor. The metabolites of selegiline include: L-amphetamine and L-methamphetamine. This may lead to side effects such as insomnia. Another side effect can be inflammation of the mouth. Unlike other monoamine oxidase inhibitors, foods containing tyramine do not cause hypertensive crisis. Some evidence suggests that other drugs such as amantadine and anticholinergics may be useful as treatments for motor symptoms in early and late Parkinson's disease, but these drugs are not considered the first-line treatment for the disease. In addition to motor symptoms, Parkinson's disease is accompanied by a range of different symptoms and different compounds are used to improve some of these problems. An example of this is the use of clozapine For psychosis, cholinesterase inhibitors for dementia, and modafinil for drowsiness. A preliminary study suggests that taking donepezil may help prevent falls in Parkinson's patients. Donepezil boosts levels of the neurotransmitter acetylcholine, and is currently the approved treatment for the cognitive symptoms of Alzheimer's disease. The introduction of clozapine represents a major breakthrough in the treatment of psychotic symptoms of Parkinson's disease. Before the introduction of clozapine, treatment of psychotic symptoms relied on dopamine reduction therapy or treatment with first-generation antipsychotics, all of which were detrimental to motor function in patients. Atypical antipsychotics useful in treatment include quetiapine, ziprasidone, aripiprazole, and paliperidone. Clozapine is thought to have the highest efficacy and fewest side effects. Parkinson's disease used to be treated with surgery, but after the discovery of levodopa, surgery was limited to only a small number of cases. Studies in the past few decades have led to significant improvements in surgical techniques, and surgery is being used again in people with advanced Parkinson's symptoms who are no longer treated. Medication is sufficient for them. Less than 10% of Parkinson's patients qualify as suitable candidates for surgical response. Three different mechanisms of surgical response for Parkinson's disease are: , deep brain stimulation, or restorative surgery. Target areas for deep brain stimulation include the thalamus, globus pallidus, or subthalamic nucleus. The neuronal lesion is destroyed by heat, and parts of the brain associated with producing parkinsonian neurological symptoms are destroyed. Procedures generally involve thalamotomy and/or globus pallidus. For the thalamus, a portion of it is destroyed, particularly the ventromedial thalamic nucleus (nucleus pallidus), to suppress tremor in 80-90% of patients. If akinesia is evident, the site of ablation is the subthalamic nucleus. In patients with akinesia or

Geriatric medicine

Assisted living or assisted living facilities are residential facilities for individuals with disabilities. These facilities provide supervision or assistance with activities of daily living, coordination of services by outside health care providers, and monitoring of residents' activities to protect their health, safety, and well-being. Assistance may include medication administration or supervision, or personal care services provided by a trained staff member. Assisted living emerged in the 1990s as an alternative to hospice care to continue the care of individuals who are not suitable for independent care, do not require 24-hour nursing care, and are less advanced in age than nursing home care. Assisted living is a philosophy of providing care and services in a manner that promotes independence and dignity. Within the United States, there is no national definition of assisted living. Assisted living facilities are regulated and licensed at the state level in each state. More than two-thirds of states use the term “assisted living.” Some of the licensed terms used to describe this philosophy include nursing home, assisted living facility, and personal care home. Each state licensing agency has its own definition of the term it uses to describe assisted living. Because the term assisted living is not defined in some states, it is a marketing term used by a variety of licensed and unlicensed senior living associations. Assisted living facilities in the United States had a national average monthly rate of $3,261.00 in 2011, an increase of 2.39% over 2010 and 5.99% over the six-year period from 2005 to 2011. Physical models of buildings offering assisted living services vary widely, as do state licensing and definitions. Assisted living facilities range in size from small single-resident homes to very large assisted living facilities serving hundreds of residents. Assisted living facilities fall somewhere between independent care associations and highly specialized nursing facilities in terms of the level of care provided. Assisted living facilities combine independent care, assisted living, and nursing care in a single facility. Individuals living in a new assisted living facility are provided with private housing. There is usually no special medical monitoring facility available at a nursing home, and nursing staff may not be available all the time. However, trained staff are usually on site 24 hours a day to provide other necessary services. Housekeeping is performed: changing sheets, washing items, and preparing and serving food is part of the basic rent and included utilities. Depending on the services advertised, assisted living services may include medical treatment, assistance with bathing and dressing, companionship to meals and activities, toileting and transportation, and insulin injections by a registered nurse. Some nursing homes have a beauty salon on site. Grocery services are also available. Where available, private apartments are generally self-contained; that is, they have private bedrooms and bathrooms, and may include a separate living area or kitchenette. Registered nurses and qualified nurse practitioners are available by phone or email 24 hours a day, to ensure appropriate education and/or guidance for the staff on hand. Alternatively, individual care areas can resemble a dormitory or hotel room with a private or semi-private sleeping area and a shared bathroom. There are usually several common areas for sharing social activities with others, such as a central kitchen or lunchroom for preparing and eating meals. Professionals have defined a person living in an assisted living facility as someone who requires assistance with at least one activity of daily living. The typical resident of an assisted living facility is usually an adult who does not require the level of care provided by a nursing home but would prefer more companionship and needs assistance with daily living. Age groups vary at each facility. There is a shift in long-term care today, with assisted living communities accepting higher levels of care, and nursing homes becoming a place for those undergoing rehabilitation after a hospital stay or individuals who need intensive assistance. Many assisted living communities now accept individuals who need assistance with all activities of daily living. The American Association for Assisted Living reports that the average age of an assisted living facility resident is 86.9 years. Female residents outnumber male residents by 3 to 1. The majority of residents in assisted living facilities are still married or have a partner. The average stay in assisted living facilities is 28.3 months. The residence can help arrange appropriate medical, dental or health care services for each resident. The resident generally chooses his or her own medical or dental care provider. Residents who are temporarily disabled due to illness, injury or convalescence from surgery are often allowed to remain in the residence or return to a rehabilitation center, specialized nursing facility or hospital if the assisted living facility can provide appropriate services. It is important to remember that assisted living facilities are a bridge between living at home and living in a nursing home. However, assisted living facilities do not typically provide the same level of skilled, ongoing nursing care as nursing homes or hospitals. Some newly built facilities have been designed to ensure that services are easily accessible to people with disabilities. Bathrooms and kitchens are designed with wheelchairs and walkers in mind. The entrances and doors are wide enough to accommodate wheelchairs. These facilities are necessarily fully compliant with the Americans with Disabilities Act of 1990 or similar legislation elsewhere. The socialization features of assisted living facilities are very beneficial to residents. The facility usually has a variety of scheduled activities to accommodate residents with varying disabilities and needs. In addition, many assisted living facilities cater to the mentally ill population, primarily individuals with dementia, including Alzheimer's, but also others who do not pose a significant risk to themselves or others. In the United States, state legislation not only specifies the level of care, but also often the conditions that prevent home care in such cases.

Geriatric medicine

The Beers Criteria for Potential Risks of Medications in Older Adults, commonly known as the Beers List, is a guide for healthcare professionals to help improve the safety of medications prescribed to older patients. The criteria encourage the avoidance of unnecessary medications, reducing risk-benefit ratios, polypharmacy, drug interactions, and adverse drug interactions. The Beers Criteria are used in geriatric clinics to monitor and improve the quality of healthcare services. They are also used in clinical practice, training, research, and healthcare policy as a tool for performance evaluation and recording outcomes. The Beers Criteria lists medications that are likely to have risks that outweigh their benefits for patients over the age of 65. By taking these criteria into account, healthcare professionals can reduce the risk of serious or fatal side effects from medications. As the number of people entering older age increases, the importance of providing safe and effective healthcare services is becoming increasingly important. The Beers Criteria are intended as a general guide for healthcare professionals and are not intended to replace expert opinion when prescribing medications to individual patients. The Bednitz and STOPP/START criteria have been shown to be useful as a complement to the Beers criteria to guide healthcare practitioners in safely dispensing medications to older adults. Mark Beers, MD, developed the Beers criteria in 1991 through a consensus-based expert group using the Delphi method. The criteria were published in the Archives of Internal Medicine in 1991 and were updated in 1997, 2003, and 2012. In 2011, the American Society for Aging brought together eleven experts from a variety of health care disciplines, including physicians, nurses, and pharmacists, to develop and update the Beers criteria. The updated Beers criteria from the American Society for Aging in 2012 differ from previous versions in several areas. In addition to using the updated Delphi method, the expert group used the same evidence-based approach that the group used to develop the initial Guide to Continuous Pain in 1998. In its 2011 report, the Medical Foundation advised all guideline developers to complete a systematic review of the evidence they use. At the recommendation of the Medical Foundation, the American Society for Aging added a general comment section that was updated in parallel with the general review. In a significant departure from previous versions of the Beers criteria, each recommendation was evaluated on the quality of the evidence supporting the expert panel’s recommendations and the strength of their recommendations. It is also important to note that the clinical evidence for this patient population is limited, making the evidence specific to this patient population scarce. In another departure from previous versions of the Beers criteria, the updated version of the guidelines has been divided into three categories instead of two. Category 1 includes medications with significant side effects or limited efficacy; Category 2 includes medications that are inappropriate for patients with a specific disease and that may exacerbate it; and Category 3 includes medications that should be used with caution, which may cause greater harm than good in general, but in certain cases are indispensable if used with caution. The importance of the added category is to focus on tailoring treatment to the needs of the patient. The updated Beers Criteria by the American Society for Aging were published in February 2012 in the online version of the American Society for Aging, are updated periodically, and can be found here: http://www.americangeriatrics.org Medications on the Beers List are categorized by their potential risks into: Use with caution, Avoid, Avoid with certain conditions, and Restricted for use in the elderly. Examples of medications include diphenylhydramine, an antihistamine that causes sedation, confusion, and falls.

Geriatric medicine

Maxim Healthcare Services is a privately held medical staffing company headquartered in Columbia, Maryland. Maxim Healthcare Services was founded in 1988 as Medical Staffing Corporation. President Brian Wynne opened the company's first office in Towson, Maryland, and the following year, Maxim began expanding, opening offices in Orlando, Florida; Springfield, New Jersey; and Silver Spring, Maryland. Maxim Healthcare's subsidiaries include Maxim Healthcare Services, Maxim Staffing Solutions, Maxim Medical Resources, Timeline Staffing, TravelMax, and Centras Home Care. Under the Medical Cal name, Maxim initially served almost exclusively the nursing home industry, but soon began providing staffing services to hospitals, clinics, schools, and assisted living facilities. In 1992, Medical Cal acquired NSI, a California-based home care and staffing company. As Medi-Cal continued to expand across the country, several trademark lawsuits forced the company to change its name, and in the spring of 1993, the company became known as Maxim Healthcare Services. Maxim Healthcare Services has three core service lines: Maxim Home Care, Maxim Health Systems and Maxim Staffing Solutions, which oversee 18 divisions. Maxim provides the following core services: home care, non-medical care, staffing in medical facilities, influenza treatment and recovery services, autism and applied behavior analysis. In 2008, Maxim Healthcare Services received accreditation from the Commission on Accreditation of Healthcare Organizations. Beginning in 2009, Maxim and some of its employees came under government scrutiny for submitting fraudulent billings and false statements to health officials, which was “a common practice at Maxim from 2003 through 2009,” according to the U.S. Attorney’s Office in New Jersey. Between 2009 and 2011, nine current and former Maxim employees, including three senior managers, were convicted of criminal charges. In 2011, Maxim entered into agreements with the U.S. Department of Justice and affected states, paying $150 million to dismiss the criminal and civil charges. However, the company has filed claims for millions of dollars for work that was not performed and offices that were not properly licensed. The company entered into a deferred prosecution agreement with the U.S. Attorney’s Office in New Jersey, a corporate integrity agreement with the Office of the Inspector General and the U.S. Department of Health and Human Services, and civil settlement agreements with the United States and 43 other countries.

Geriatric medicine

A primary caregiver is a person who has primary responsibility for someone who cannot fully care for themselves. This can be a family member, a trained professional, or other people. Depending on the culture, there can be multiple family members involved in Care. This concept can be important in relation to attachment theory as well as family law, for example in guardianship and child custody. Some states in the United States, such as California, have defined the responsibilities of the primary caregiver.

Geriatric medicine

In biology and physiology, senescence is a series of dysfunctional processes that follow a period of growth in an organism. The science of geriatrics is particularly concerned with this process of senescence and includes what is called life extension. Cellular senescence is a phenomenon in which cells lose their ability to divide and thus regenerate. As a result of DNA damage in cells, either senescence occurs or self-destructs if the error cannot be corrected. The term aging or longevity is frequently used here as a companion term and similar to senescence. The terms senescence and senescence are now used interchangeably in most articles. Aging is characterized by a diminished ability to cope with stress, an increase in homeostasis, and an increased risk of diseases of old age, including cancer and heart disease. Aging has been defined as "a progressive weakening of bodily functions and an intrinsic age-related process involving loss of vitality and increased susceptibility to illness." As a result, death is the inevitable consequence of aging. Senescence, or biological aging, is the gradual deterioration of the functional properties of an organism. The word senescence may refer to cellular senescence, or to the senescence of the organism as a whole. Organic senescence involves an increase in mortality rates and/or a decrease in fertility rates with age, at least during the latter part of an organism's life cycle. Senescence is the inevitable fate of all multicellular organisms in which both sex and somatic cells divide, but it can be delayed. In 1934, it was discovered that caloric restriction could extend the lifespan of mice by 50%. There are species in which senescence is almost nonexistent, such as Hydra, and the possibility of their immortality has inspired researchers to investigate the field of delaying senescence, and thus delaying age-related diseases. We know that some mutations in humans can cause accelerated diseases of senescence. Environmental factors can also affect aging. For example, excessive exposure to ultraviolet radiation accelerates skin aging. Different parts of the body may age at different rates, and two organisms of the same species may age at different rates, making biological aging and chronological aging two different concepts. There are a number of hypotheses about how aging occurs. Organic aging is the aging of all organisms. Actuarial aging can be defined as the increase in mortality and/or decline in fertility with age. According to the Gompertz-Mackeham Mortality Law, the effect of the age-dependent factor increases steadily with age. In 2013, a group of scientists identified nine common aging markers in organisms, focusing primarily on mammals: Aging is characterized by a decreased ability to respond to stress, increased homeostatic imbalance, and increased risk of age-related diseases including cancer and heart disease. Aging is defined as a gradual decline in physiological function, an intrinsic age-related process in which there is a loss of viability and an increase in vulnerability. Environmental damage occurs at several levels, such as damage to DNA or damage to tissues and cells caused by exposure to oxygen radicals, some of which is irreversible and accumulates over time. Cloning from somatic cells rather than sex cells makes an individual’s life more vulnerable to damage; Dolly the sheep died young from a lung disease, but more data on cloned organisms is needed to measure mortality rates. George Williams writes: “It is remarkable that after this miracle seemed possible, the cyclic complex could not perform the simpler task of preserving what had already been formed.” The rate of aging varies among species; mice, for example, live on average three years, whereas humans currently live 80 years. Almost all organisms age, including bacteria, which have no particular symmetry that allows us to know the resulting bacteria and the bacteria that divide after division. There is a slight aging in some groups, such as the genus Hydra. The flatworm Planaria has the ability to renew its telomeres indefinitely, because it contains a population of highly reproductive stem cells. These planaria are not biologically immortal, but their death rate increases slowly with age. Some species show negative aging, in which the ability to reproduce increases or remains stable, and their death rate decreases with age. Natural selection may favor lethal or deleterious alleles if their effects appear after reproduction. The geneticist J. B. S. Haldane wondered why the dominant mutation that causes Huntington's disease in humans persists and why natural selection has not eliminated it. Huntington's disease onset is on average around age 45, and always ends in death within 10 to 20 years. Haldane hypothesized that in prehistoric times few people survived to age 45, and since only a few of them were found alive, their impact on their cohorts was minimal. Peter Medrow formalized this observation in his mutational accumulation theory of aging. Another theory of aging proposed by George C. Williams is the pleiotropy of opposite phenotypes. A single gene may affect several traits, some of which are important for health early in life but may have negative effects later on. However, since many individuals survive early and fewer later, the identification of these negative effects is poor. Williams suggests the following example: "A gene that encodes proteins that promote bone calcium deposition, which promotes survival in adolescence, may be favored by natural selection, but the same gene promotes calcium deposition in arteries, causing atherosclerosis in the elderly and thus increasing mortality. Thus, the deleterious biological changes of aging result from the selection of pleiotropic genes that are beneficial early in life but become harmful later on in life." The reproductive cell cycle theory proposes that aging is regulated by changes in hormonal signals during an individual's lifetime. Cell damage accumulates over time, but this is balanced by natural selection that removes damaged cells, primarily their DNA. Somatic cells in most multicellular species will eventually encounter what is known as senescence, and will not be able to divide, which may prevent the cell from becoming cancerous. For example, a fibroblast cell can give rise to a maximum of 50 dividing cells, and this limit is known as the Heilich limit. Replication senescence occurs as a result of short telomeres that will eventually lead to a response to DNA damage. Cell senescence may be triggered by elevated reactive oxygen species and activation of oncogenes regardless of telomere length. Many organisms have asymmetric cell division, for example, a stem cell divides to give rise to a stem cell and a non-stem cell, so that cellular debris is not divided equally among the new cells. Cancer cells avoid replication senescence and become immortal. In 85% of tumors, the reason for the absence of senescence is the activation of telomere genes. Senescent cells in multicellular organisms can be eliminated through cell competition, but this increases the risk of cancer, leading to an inevitable dilemma, which presents us with two possibilities: the first is the accumulation of senescent cells that are of no physiological use, and the second is the development of cancer, both of which will lead to increased mortality rates with age. One of the first theories to attempt to explain aging was the heartbeat hypothesis described by Raymond Pearl in 1928, which states that a fast basal metabolic rate corresponds to a small upper age limit.

Geriatric medicine

The 2019–20 coronavirus pandemic has affected long-term care facilities and nursing homes around the world. Thousands of residents of these facilities, who are in high-risk groups, have died from the disease. As of mid-April 2020, nearly half of Canada’s COVID-19 deaths were residents of long-term care facilities. Facilities are regulated at the provincial level, which means that standards are inconsistent regarding staff-to-resident ratios, as is minimal training. In British Columbia, the number of cases in long-term care facilities jumped from 9 to 235, including 143 residents and 92 staff. In Ontario, an outbreak began on March 18 at Pinecrest Nursing Home in Bobcaygeon, and as of April 6, 29 of its 65 residents had died from COVID-19. On April 6, the City of Toronto discovered that a large shipment of Chinese-made masks delivered to long-term care facilities were defective. In Quebec, a team of health care professionals inspecting the Residence Herron after a resident died of COVID-19 found the facility largely deserted by staff. Living conditions inside were akin to a “concentration camp,” officials said. About a third of reported COVID-19 deaths have been among residents — more than 3,000 — leaving the facilities short on body bags. More than 2,300 homes have reported at least one case. Nursing home residents are being isolated in their rooms to slow the spread of the disease, while hospitals are reluctant to admit patients with little chance of recovery. On March 18, the first case was identified at the Hans-Lege retirement home in Wolfsburg. As of March 31, at least 17 people had died from COVID-19 at the facility. On April 2, Robert Koch of the institute in Germany confirmed that out of 1,000 Germans who have died, 87% were older than 70. Of these, more than 50 were residents of nursing homes in Bavaria, Cologne and Wolfsburg. By April 9, 29 were residents of a nursing home in Wolfsburg. As of April 9, 3,859 people had died in nursing homes run by the RSA since February 1, 133 of whom had tested positive and 1,310 had symptoms consistent with coronavirus. Prosecutors are investigating a nursing home in Milan where 27 people died of suspected coronavirus in the first week of April. Many nursing homes in Spain are understaffed because they are for-profit businesses and elderly Spaniards cannot necessarily afford adequate care. In some nursing homes, elderly victims were found abandoned in their beds by Spanish soldiers, prompting an emergency response. Defense Minister Margarita Robles said anyone found guilty of neglecting them would be prosecuted. By March 23, five nursing homes in the Madrid region had reported cases of the virus. More than 65% of deaths were in those aged 80 or over, compared with 50% in Italy and just 15% in China. By 3 April, at least 3,500 Spaniards had died in nursing homes, with another 6,500 infected there. Thousands of nursing home workers are also infected. Sky News correspondent Alex Crawford wrote an editorial about nursing homes in general. In relation to Covid, she suggested that the situation was a “scandal” that future generations would question. She also pointed to the working conditions of care assistants, including zero-hour contracts and homes that urged sick staff to attend anyway. To prevent Covid-19 spreading to Liverpool’s Beachside home, the assistants moved there from April 2020. Nearby Oak Spring had 14 deaths in a fortnight, up to mid-April. Only two of the dead had been tested, both positive for Covid-19. As of early April, the facility was operating with a quarter of its normal staff, after staff or their families developed symptoms and were self-isolating. Two-thirds of the remaining residents had symptoms. Liverpool MP Paula Parker has criticized the lack of personal protective equipment in long-term care facilities, compared with NHS workers. According to an Associated Press tally, more than 2,755 confirmed deaths have been reported in long-term care facilities, though the actual number of deaths is likely much higher because many victims were never tested for the virus. In addition to the steps taken by individual facilities, the federal government has banned visitors, ended group activities and instituted mandatory testing for workers. However, that is not necessarily effective in preventing infection. In California, Gov. Gavin Newsom announced on April 10 that some healthy residents in nursing homes would be transferred to a U.S. Navy hospital ship called the USNS Mercy. The ship had previously been expected to take patients from Southern California hospitals, freeing up space there for COVID-19 patients. Six hundred nurses trained in infectious disease control will be sent to nursing homes and senior care facilities to contain the outbreak. Some facilities have reorganized residents into safe buildings for those with and without the virus. Minnesota held a legislative hearing on April 7 on the senior care industry, after weeks of closures. The CEO of one facility noted that her residents were showing signs of depression and anxiety from confinement. On April 11, 2020, The New York Times reported that there had been nearly 2,000 deaths of nursing home residents in New York, New Jersey, and Connecticut. As of April 10, there were 4,630 positive cases in New York’s 613 licensed nursing homes. On April 15, 2020, it was reported that a nursing home in Andover, New Jersey, was storing the bodies of 17 residents in a small morgue. By mid-April 2020, Florida Governor Ron DeSantis was considering a request to grant nursing homes “sovereign immunity” from negligence lawsuits during the pandemic. The petition was filed by a trade group representing nearly 700 nursing homes in the state. The Life Care Center facility in Kirkland, Washington, was the site of a major COVID-19 outbreak in 2020. On February 19, 2020, there were 120 residents and 180 staff members there. By March 18, 2020, 101 residents had been diagnosed with COVID-19, and 34 had died. On April 2, 2020, Life Care Center was fined $611,000 for deficiencies in its response to the outbreak, and has until September 16, 2020, to correct the deficiencies or face termination of its Medicare/Medicaid participation.

Geriatric medicine

The Saudi Society for the Support of the Elderly is a non-profit charitable association established in 1437 AH and headquartered in Riyadh. It seeks to support the elderly, support their rights, assist in their care and raise the level of interest in their status. The association aims to achieve integration between the sectors that serve the elderly in Saudi Arabia, and to create programs and initiatives that suit them, in addition to contributing to improving the type of services provided to them, as well as enhancing the status of the elderly in society and highlighting their role, and raising awareness of their issues. It also aims to employ the energies of volunteers to support and serve them, and work to support knowledge enrichment efforts in the fields of the elderly.

Geriatric medicine

An adult day care center is a non-residential facility that supports the health, nutritional, social, and daily needs of adults in a professionally staffed setting. These facilities provide transitional care and short-term rehabilitation for adults after discharge from the hospital. Most centers provide meals, purposeful activities, and general supervision. The care provided is often a social or medical model that is provided in order to improve the health of participants and guide their progress. Adult day care centers primarily focus on providing care for people with a specific chronic condition, including: Alzheimer's disease; In addition, these services may be available to any adult with a disability as well as the elderly population. Many centers maintain an on-site nurse and set aside a room for participants who need to have their vital signs checked and evaluated regularly; or who need other health services from a nurse during their visit. Facilities may also provide transportation and personal care provided by a support group or support groups for caregivers. The presence of an adult day care center prevents re-hospitalization and may delay admission to long-term care. For participants who would otherwise remain at home alone, social stimulation and recreational activities have been known to improve or maintain physical and cognitive function. The more severe the illness, the greater the burden on the caregiver. Therefore, 19.1% of caregivers with clients could benefit from these services. Adult day care centres may be able to provide respite care, allowing caregivers to work or take a break from their caregiving responsibilities. These facilities are beneficial for many, as the activities encourage interaction with others which has been known to improve the participant’s health and emotional well-being. All accredited adult day care centres are monitored and staffed to protect participants, as well as being a helping hand for newcomers who have difficulty communicating with others or who do not feel comfortable in certain environments. This programme aims to build confidence and the ability to maintain an independent lifestyle along with improving physical and mental health. Another important aspect of an adult day care centre includes information about healthy eating plans and exercise regimens that are appropriate for some people. These centres can help improve health as some people lose the ability to keep up with and maintain good sedentary lifestyles. Especially after participants come from rehabilitation or dementia departments, who may forget what they have. These centers introduce participants to new activities and may stimulate or arouse a new interest or hobby that they may want to pursue and explore further. Adult day care centers have grown over the past few decades because health services are available and currently exceed those of any other time, both in service and care required. As adult day care centers have become more in demand, more locations are participating, primarily in the United States, where more than fifty cities participate in this program to some degree. This is largely due to variations in the name in different countries. Thus, under the name “adult day care” specifically, the United States retains the majority of research because other countries call these facilities by many different names, for example: Australia and some European countries use the term “respite” or “care community” most commonly, while others may use terms such as community outreach, nursing home, or support group. The primary goal of an adult day care center is to provide quality care and enrich interactions with other participants in the center. This will enhance participants’ skills and knowledge levels when they are involved in fun, active programs that suit them and their abilities. Aged day care centers also include activities such as: arts and crafts, music, games, exercise regimes, discussion of interest through, general socialization and conversations aimed at forming friendly friendships. Adult day care centers in Australia aim to promote independence and free thinking for people with disabilities, older people or people from diverse language backgrounds. The purpose is to integrate them back into normal social settings, which are observed by staff so that they can have a new experience by providing a forum for making friends and new skills. There are many facilities in Australia that offer this program, but Australia refers to these centers as “respite” or “community care” which is most common. In Western Australia alone there are 23 facilities from Joondalup to Mandurah, 13 of which are for older people, focusing on people with Huntington’s disease, and the remaining eight are for younger people with disabilities and rehabilitation patients. In Australia, the cost of a day at an adult day care centre is currently between $25 and $70 depending on the person’s needs and requirements. In addition, there are facilities that charge an hourly rate to non-resident participants who may come to participate in activities or social interaction, and these rates generally range from $5 to $15. In 2013, there were more than 5,000 adult day centres operating in the United States, caring for more than 260,000 older people in America each day. 72% of centres were operated by non-profit organisations, and 16% were public sector. Daily fees can be less than a home health visit and half the cost of a nursing home facility, but vary depending on the services provided. Funding comes from participant fees, insurance, public and philanthropic sources. According to the 2010 MetLife National Study of Adult Day Services, adult day care centers in the United States have one direct care worker for every six participants. About 80% of adult day centers have a nurse on staff, about 50% have a social worker on staff, and about 60% provide case management services. Research suggests that centers with increased staffing so that each patient has a caregiver provide more individualized, person-centered care. Adult day care is a facility that is becoming increasingly in demand, as more and more people need help and guidance to re-enter the real world after injury, illness, addiction, or simply aging. With these programs, people have a much better chance of achieving their goals and returning to their former lives.

Geriatric medicine

Long-term care insurance is an insurance product sold in the United States, United Kingdom, and Canada that helps cover the costs of long-term care. This type of insurance covers care that is not covered by Medicare, Medicaid, or Medicaid. In general, people who need long-term care are not sick in the traditional sense, but are unable to perform two of the six activities of daily living—dressing, bathing, eating, toileting, controlling urination, transferring, and walking. Age is not a determining factor in the need for long-term care. About 70 percent of people over the age of 65 will need at least one type of long-term care service during their lifetime. Currently, about 40 percent of those receiving long-term care are between the ages of 18 and 64. Long-term care insurance may not be available once there is a change in health. Early-onset Alzheimer’s and Parkinson’s disease—before age 65—are rare. Long-term care is an issue because people are living longer. As people age, they often need help with activities of daily living or require supervision due to severe cognitive impairment. This affects women more than men because they often live longer than men and automatically become caregivers for others. Long-term care insurance can cover home care, assisted living, adult day care, respite care, hospice care, nursing homes, Alzheimer’s facilities, and home modifications to accommodate disabilities. If home care coverage is purchased, long-term care insurance can pay for home care, often from the first day it is needed. It will pay a caregiver, whether a visitor or resident, a companion, a housekeeper, a caregiver, or a private nursing home up to seven days a week, 24 hours a day, up to the maximum insurance benefit. Many experts suggest shopping between ages 45 and 55 as part of a comprehensive retirement plan, to protect assets from the high costs and burdens of extended health care. Other Benefits of Long-Term Care Insurance: In the United States, Medicaid provides long-term care services to the poor or those who are spending their assets and depleting them due to care. In most states, you must spend up to $2,000. If there is a surviving spouse or partner, they can keep an additional amount. Medicare: Medicaid provides for people with limited means who “need nursing care with the possibility of remaining at home and special community care services.” However, Medicaid generally does not cover long-term care provided at home or in assisted living facilities. People who need long-term care often prefer care at home or in a private room in an assisted living facility. Private long-term care insurance is growing in popularity in the United States. However, premiums have risen dramatically in recent years, even for current policyholders. Coverage costs can be prohibitive if consumers wait until retirement to purchase long-term care coverage. As it relates to insurance policies in the United States, there are two types of long-term care insurance policies offered: As it relates to U.S. income taxes, there are two types of long-term care insurance policies offered: Non-tax-qualified policies are sold less frequently. One reason is that consumers want to be eligible for the tax deductions available when purchasing a tax-qualified policy. Tax issues can be more complicated than the deductions alone, and it is advisable to seek good advice on all the pros and cons of a tax-qualified policy versus a non-tax-qualified policy, because the benefits that result from a good non-tax-qualified policy are better. By law, tax-qualified policies impose restrictions on the time that the holder can receive benefits. One survey found that sixty-five percent of purchasers did not know whether the policy they purchased was tax-qualified or not. Once a person purchases a policy, the insurance company cannot change the language, and the policy is usually guaranteed to renew for life. The insurance company cannot cancel it for health reasons, but it can be canceled for nonpayment. Most benefits are paid on a per diem basis, and a few companies offer benefits on a per diem basis at a higher rate. Most policies cover care only in the continental United States. Policies that cover care in select foreign countries typically cover only nursing care, and do so in the event of a classified benefit. Group policies may include provisions for unrestricted or open enrollment periods and a bond guarantee may be required. Group plans may or may not be guaranteed renewable or tax-eligible. Some group plans include language that allows the insurer to replace the policy with a similar policy and change the premiums at that time. The insurer can cancel some group plans. To compensate for the higher insurance risk, group plans may have higher deductibles and lower benefits than individual plans. Some group plans may require the inability to perform three daily activities for nursing care. The Consolidated Omnibus Budget Reconciliation Act gives some former employees, retirees, spouses, former spouses, and dependent children the right to temporarily continue health coverage at group rates. Retirement systems such as CalPERS may offer long-term care insurance similar to a group plan. These organizations are not regulated by state insurance departments. They can raise rates and make changes to policies without state review and approval. Long-term care insurance rates are determined by six main factors: the person's age, daily benefits, the length of the benefit payment, the liquidation period, inflation protection, and health rating. Most companies offer discounts for couples and multiple-lifetime discounts on individual policies. Some companies define "couples" as not just married couples, but also two people who meet the criteria for living together in a committed relationship and sharing basic living expenses. The average age of buyers has declined from 68 in 1990 to 61 in 2005, and the number of buyers under 65 has increased significantly. Most companies offer multiple ways to pay premiums: annually, semiannually, quarterly, and monthly. Companies may add a percentage to the annual payment for more frequent payments. Most plans have options such as continuation of marriage, automatic renewal, reinstatement of benefits, and premium refund. The Disability Reduction Act of 2005 makes partnership plans available to all states. The partnership provides “lifetime asset protection” from Medicaid spending requirements. As of March 2014, 41 states had active partnership programs for long-term care insurance. Most policies pay benefits when the policyholder needs assistance with two or more of the six activities of daily living or has a cognitive impairment. According to the U.S. Department of Health and Human Services, all tax-qualified long-term care insurance plans have the same payer. Most policies have an exclusion period or waiting period similar to the deductible. This is the period of time you pay for care before you receive your benefits. Exclusion days can be 30 to 120 days after a long-term care event, such as a fall or illness. Some policies require intended claimants to provide proof of 30 to 120 days of paid care service before any benefits are paid. In some cases, there may be the option to set zero exclusion days when covered services are provided in the home under the care plan. The policyholder can choose a maximum daily or monthly benefit. This is the maximum that the insurance company will pay for care on a daily or monthly basis. Long-term care insurance supplements that are generally available in Canadian policies include: In Germany there are two different types of long-term care insurance: compulsory long-term care insurance and voluntary private insurance. German law requires people to have basic long-term care insurance. It is one of five compulsory insurances, the others being health insurance, accident insurance, unemployment insurance and pension insurance. As is customary in the German statutory insurance system, the costs are divided equally between employers and employees. There are three types of private long-term care insurance: About 7 million people have some form of long-term care insurance. The vast majority have what is known as conventional, or long-term care health insurance. The opposite is true for new policy sales. About 350,000 new policies are sold each year, 84% of which are benefit or life insurance policies that include long-term care benefits. In the United States, long-term care insurers paid a record $11 billion in 2019 to about 310,000 policyholders.

Geriatric medicine

The role of family caregivers is becoming more common, and care in the familiar home environment can delay the onset of some symptoms and postpone or prevent the need for more expensive, professional levels of care. Home care can also be costly economically and psychologically, as family caregivers often give up work hours and wages to spend an average of 47 hours a week with a loved one who is ill and cannot be left alone on a frequent basis. In a 2006 survey of long-term care insureds, the direct and indirect costs of providing care for Alzheimer’s patients averaged $77,500 in the United States. Caregivers themselves are at increased risk for depression, anxiety, and, in some cases, health problems. Schulz and colleagues conclude that the transition to institutional care is most difficult for spouses, about half of whom visit their sick spouses daily and continue to provide care in addition to professional care during their visits. Clinical interventions that better prepare caregivers for the patient’s transition and address their depression and anxiety could be of great benefit to them. In a Norwegian study, Thomsen and colleagues found that the most commonly reported causes of anxiety were “disruption of household routines, difficulties leaving during holidays and festivals, restrictions on social life, and sleep disturbances…” and that these symptoms were common among caregivers of people with dementia, stroke, and Parkinson’s disease. A Japanese study by Hirono and colleagues estimated that “patients’ functional and neuropsychological impairments were the main factors that increased caregiver burden.” An Italian study by Marvardi and colleagues found that “patients’ behavioral disturbances and disability were the main indicators of time-related burden, and that psychological burden was mainly manifested in caregiver anxiety and depression.” Caregivers can experience anticipatory grief and ambiguous loss.

Geriatric medicine

Long-term care is a diverse group of services that help meet the medical and non-medical needs of people with a chronic illness or disability, or who are unable to care for themselves for extended periods. Long-term care focuses on individualized, coordinated services that promote independence, improve patients’ quality of life, and meet patients’ needs over a significant period of time. Long-term care commonly provides custodial, unskilled care, such as assistance with normal daily activities such as dressing, feeding, and toileting. Increasingly, long-term care requires a level of medical care that requires the expertise of skilled practitioners to address the multiple chronic conditions associated with older populations. Long-term care can be provided at home, in the community, in assisted living facilities, or in nursing homes. People of any age may need long-term care, although it is most common among older adults. Long-term care can be provided formally or informally. Facilities that provide formal long-term care services provide housing for people who need supervised care around the clock, including professional health services, personal care, and services such as meals, laundry, and housekeeping. These facilities may have different names, such as nursing home, personal care facility, continuing care residential facility, etc., and are operated by different providers. While long-term care organizations have asked the U.S. government not to combine health and personal care services in large facilities, the government instead continues to consider this service as the primary use of taxpayer dollars. Greater success has been seen in areas such as subsidized housing, which may continue to use older apartment complexes or buildings, or may have been part of new federal initiatives in the 2000s. Long-term care provided in the home, also known as home health care, can include a wide range of clinical services ( ). These services are usually ordered by a physician or other professional. Some of the costs of these services may be covered by health insurance or long-term care insurance depending on the country and the nature of the health and social care system. Modern forms of government-reimbursed long-term services and supports include user-directed personal services, family-directed options, independent living services, benefits counseling, mental health facility services, family education, and even self-advocacy and employment, among many others. Home services can be provided by individuals other than nurses and therapists, who do not install elevators, and who belong to long-term support and services systems in the United States. Informal long-term home care is care and support provided by family members, friends, and other volunteers on a voluntary, unpaid basis. It is estimated that 90% of all home care is provided informally by a loved one without compensation. In 2015, some families sought reimbursement from their government for care. “Long-term services and supports” is the modern term for community-based services, which may or may not be funded by Medicare and fall under the traditional hospital-based medical system. The Citizens with Disabilities Alliance, which works with the United States Congress, notes that many non-acute long-term services are provided to help individuals live and participate in the community at the same time that hospitals provide acute care. Examples of this include the group’s international motto, Community Living and Deinstitutionalization, and the variety of supportive services. The term is also commonly used by aging groups, such as the American Association of Retired Persons, which annually provides many services to the elderly in the United States. Long-term services and supports are discussed in depth in the U.S. Department of Community Services' new support force includes direct technical support, largely nonprofit or for-profit, and government, often unionized, in communities across the United States. The core competencies of the Federal-State Interface for "institutional and community-based" helpers in age and physical disabilities, intellectual and developmental disabilities, and behavioral health were identified in 2013. President Barack Obama, Speaker of the U.S. House of Representatives John Boehner, Minority Leader Nancy Pelosi, Majority Leader Harry Reid, and Minority Leader Mitch McConnell received copies of the U.S. Senate Committee on Long-Term Care on "service delivery, workforce, and financing issues that have challenged policymakers for decades." The new commission envisions “a comprehensive financing model that balances private and public funding to underwrite catastrophic expenses, encourage savings and insurance for immediate LTSS costs, and provide a safety net for those without resources.” The direct care workforce envisioned by MDs in America in 2013 was described as: care aides, home health aides, nursing assistants, and independent providers. The United States has diverse and competing health care systems, and hospitals have adopted a model of “community money to the hospital.” In addition, “hospital studies” refer to M-LTSS as billable services. In addition, allied health workers have been largely trained in specialized science and disability centers that theoretically and practically support modern personal assistance services across populations and “manage” behavioral health care as a “subset” of mental health services. Legislation and long-term support services, as well as community-based services and personnel, have been developed to meet the needs of “individuals with disabilities” who have been litigated against state governments and, in many cases, have had to report regularly on the development of a community-based system. These services originally included basic services such as rehabilitation or vocational and residential rehabilitation, family care or foster care, small intermediate care facilities, "group homes," and later employment support, clinics, family support, supportive living, and day services. The original state departments had intellectual and developmental disabilities, mental health offices, major classifications in health departments in brain injury for communities, and later, alcoholism and substance abuse were dedicated state agencies.

Geriatric medicine

Geriatric medicine

Auguste Dieter, born in Kassel, Germany, was the first person to be diagnosed with Alzheimer's disease. She married Karl Dieter in 1880 and had only one daughter. Auguste lived a normal life until the late 1890s, but later began to show symptoms of dementia, such as memory loss, delusions, sleep problems, and screaming late at night. Her husband Karl was a railway worker, so he had to admit her to a mental institution in Frankfurt for the mentally ill and epileptic so that he could continue his work. On November 25, 1901, she was examined by Dr. Alois Alzheimer, who asked her several questions and repeated the same questions later to make sure she remembered her answers the first time. He also asked her to write her name, she tried to write it but couldn't and kept repeating the phrase "I am lost". After that, he put her in an isolation room for a period of time, and when he returned to her to take her out, she ran away and screamed, saying: "I did not hurt myself and I will not hurt myself." Her words guided them in the sanatorium to an important work, which is the condition she was suffering from and was called "Alzheimer's Stories". Several years later, she completely lost her mind and died on April 8, 1906. The dialogue below is the one that took place between Auguste Dieter and Dr. Alois Alzheimer as documented in the medical records and translated from the German language: "What is your husband's name?" She hesitated a long time before finally answering, saying: “I think it’s… Auguste.” “Ah… you visited us.” “Ah… I feel lost.” “Here and everywhere, here and now, you mustn’t think badly of me.” “We still live here.” After Mrs. Auguste had eaten her lunch, which was pork and spinach, although she was chewing on the pork, “What did you have for lunch now?” “First I had potatoes and radishes.” “Auguste,” she wrote, and as she wrote she kept repeating, “I think I’ve lost myself.” Thus, Dr. Alois Alzheimer concluded that she was unaware of time and place, could barely remember any details of her life, and gave answers that had nothing to do with the questions. Her mood also changed rapidly from anxiety to fear and mistrust. They did not allow her to walk around the sanatorium for fear that one of the residents would harm her. This was not the first time that Alzheimer's disease had destroyed the patient's psyche, but it had occurred in patients over the age of seventy. The curiosity to discover the disease was because the patient was young, only in her fifties. In the following weeks, he continued to interrogate her and record her answers. Most of the time, she would repeat, "Oh God, I think I've lost myself." It seems that she was aware that she was suffering from this disability. Dr. Alois Alzheimer named this disease "forgetfulness." In 1902, Dr. Alois Alzheimer left the sanatorium, but he kept in regular contact to check on her health. In 1906, he received a phone call informing him that Auguste Dieter had died. He asked them to send him all of her medical records and brain scans from the last years of her life. He noticed that her health had deteriorated significantly, and her death was the result of sepsis caused by the peeling of the infected skin. In a study of her brain scans, she was found to have neurofibrillary tangles, a sign of dementia.

https://ar.wikipedia.org/wiki/%D8%A3%D8%AF%D9%83%D8%A7%D9%86%D9%8A%D9%85%D8%A7%D8%A8

Geriatric medicine

Adcanemab is a human monoclonal antibody being studied as a treatment for Alzheimer's disease. It was developed by Biogen Idec, which licensed the drug from its discoverer, Neuroimmun. The antibody targets beta-amyloid receptors in the brains of people with Alzheimer's, hoping to reduce their buildup. Biogen halted development of the drug in March 2019 after preliminary data from two Phase 3 clinical trials suggested it would not achieve its primary goal. On October 22, 2019, Biogen announced that it would restart the FDA-approved process after new analyses of larger data sets showed that the drug reduced clinical decline in patients with early-onset Alzheimer's when given at higher doses. A reanalysis of data from the halted trials found that patients receiving the higher doses had a 23% reduction in decline. Interim results from the second phase 1 study were reported in March 2015. Phase 1b results were published in August 2016, based on one year of “monthly intravenous administration” of adecanemab, with brain imaging to monitor amyloid plaques. A phase 3 clinical trial had been underway since September 2016, but was cancelled in March 2019 after an independent group analysis showed the trial was unlikely to meet its primary goal. However, in October 2019 the company announced its intention to seek regulatory approval, following a reanalysis of the data.

Geriatric medicine

Aloysius "Alois" Alzheimer - German psychiatrist and neuropathologist and a colleague of Emil Kraepelin. Alzheimer studied at the universities of Aschaffenburg, Tübingen, Berlin, and Würzburg, and received his medical degree from the University of Würzburg in 1887. He is best known for discovering and documenting the first case of "presenile dementia", which Kraepelin later called Alzheimer's disease. Alois Alzheimer died in Breslau at the age of 51 from heart failure, and it is believed that Alzheimer had contracted a streptococcal infection, which had caused him to suffer from rheumatic fever and kidney failure. The following year, Alzheimer spent five months helping mentally ill women before taking up an office at the mental asylum in Frankfurt. Emil Scioli, a well-known psychiatrist, was the dean of the asylum. Another neurologist, Franz Nissl, began working at the same asylum as Alzheimer. Together they conducted research on diseases of the nervous system, specifically the normal and pathological anatomy of the cerebral cortex. Alzheimer was the co-founder and co-publisher of the journal, although he never wrote a book that can be fully attributed to him. While at the Frankfurt asylum, Alzheimer also met Emil Kraepelin, one of the most prominent German psychiatrists of the day. Kraepelin became a mentor to Alzheimer, and the two worked closely together over the next several years. When Kraepelin moved to Munich to work at the Royal Psychiatric Hospital in 1903, he invited Alzheimer to join him. At the time, Kraepelin was conducting clinical research on psychosis in geriatric patients; Alzheimer, on the other hand, was more interested in laboratory work on diseases of the geriatric population. The two faced many challenges involving the politics of the psychiatric community. For example, formal and informal arrangements were made between psychiatrists at the asylums and universities for the reception of cadavers. In 1904, Alzheimer completed his habilitation at the Ludwig Maximilian University of Munich, where he was appointed professor in 1908. He then left Munich for the Silesian Friedrich Wilhelm University in Breslau in 1912, where he accepted a position as professor of psychiatry and director of the Institute of Neurology and Psychiatry. His health deteriorated shortly after his arrival at the hospital. Alzheimer died three years later. In 1901, Alzheimer noticed a patient at the Frankfurt center named Auguste Dieter. The 51-year-old patient was suffering from strange behavioral symptoms, including short-term memory loss; these became his obsession for the next few years. Auguste Dieter was a victim of the politics of the time in the psychiatric community; the Frankfurt asylum was too expensive for her husband. Herr Dieter made several requests to have his wife transferred to a less expensive facility, but Alzheimer interfered with these requests. August Dieter, as she was known, remained in the Frankfurt asylum after Alzheimer struck a deal to keep her records and brain after her death. On April 8, 1906, August Dieter died and her medical records and brain were brought to Munich, where Alzheimer was working in Kraepelin's laboratory. In collaboration with two Italian doctors, Alzheimer used Pilschowski's techniques to identify amyloid plaques and neurofibrillary tangles. These brain abnormalities became clear definitions of what later became known as Alzheimer's disease. Another hypothesis advanced by Claire O'Brien was that August Dieter was actually suffering from vascular dementia.

Geriatric medicine

Depression is one of the most common psychiatric symptoms in Alzheimer’s disease and occurs at all stages of the disease, but it manifests in ways that are different from other depressive disorders. In 2000, a task force at the National Institute of Mental Health created a set of provisional criteria for diagnosing depression in Alzheimer’s disease, as a separate diagnostic entity in its own right. In 2005, a group of psychologists at Johns Hopkins University created a set of working criteria to help diagnose depression in Alzheimer’s disease in clinical practice. Although caregivers often feel that a diagnosis of Alzheimer’s disease must generate depression in a person with the disease, there is little or no evidence to support this. In fact, it is unclear how many individuals come to terms with their diagnosis of Alzheimer’s disease at the time of its occurrence. Symptoms of depression in Alzheimer’s disease can arise at any point in the course of the disease, and are most evident in the later stages of cognitive decline. Several neurological studies have found a relationship between abnormalities in the brain and depression in dementia. Specifically for Alzheimer's disease depression, PET studies have found metabolic changes in the superior frontal gyrus. The diagnostic criteria for Alzheimer's disease depression require three of the possible symptoms of major depressive disorder rather than the five required for major depressive disorder itself, and the symptoms can be variable. Thus, Alzheimer's disease depression is often not recognized in the spectrum of Alzheimer's disease symptoms. In general, individuals with Alzheimer's disease depression tend to be anxious, agitated, delusional, or absent-minded. Symptoms include irritability, irritability, and social withdrawal. Individuals with Alzheimer's disease depression are more likely than individuals with major depressive disorder to show a decrease in their enjoyment of socializing or traditional activities, but they are less likely to express guilt or to feel suicidal or to attempt suicide.

Geriatric medicine

Dementia results from cognitive impairment, due to damage to the brain. Most cases of dementia are classified as Alzheimer's disease. Signs of dementia generally include, but are not limited to, a decline in short-term memory, a decline in problem-solving skills, a decline in sensory perception skills, and changes in personality. Dementia appears gradually, and the course of the disease extends over several years or more. In Alzheimer's disease, it progresses through several stages in conjunction with levels of regressive development. Occupational therapists work with older adults in a variety of settings, treating dementia as a condition that affects occupational functioning. Occupational therapists educate family members, stakeholders, and even patients in the early stages. Occupational therapists assess people with dementia to identify areas of strength and functional decline that require therapeutic intervention. Although cognitive performance therapy is unlikely to improve cognitive function, the patient can improve through compensation or adaptation. Occupational therapists also help caregivers to help them cope with these difficulties. In the community, a therapist can help people with dementia live safely in their homes for as long as possible through environmental assessment and adaptation. They may also provide medical services, such as fall prevention and educational care courses, and help people with dementia maintain remaining functions for as long as possible. This can be done in different ways based on: • Health promotion: By focusing on strengths and maintaining them for as long as possible, and enhancing medical services from caregivers, therapists can enrich patients’ lives by increasing performance in their preferred activities. • Treatment: Although cognitive skills are not expected to be cured, there is a possibility of restoring physical skills. • Maintenance: The therapist identifies what works well in the daily routine of people with dementia, and provides support to ensure that the person’s skills are maintained for as long as possible. • Modification: This is perhaps the most widely used intervention for people with dementia because it involves a safe and supportive environment through adaptation and compensation. In the early stages of dementia, the patient has difficulty with executive skills. He or she may be referred to occupational therapy for assessment of driving, work, home safety and therapeutic intervention. Specialists can help patients by working on those tasks that are considered important. In the middle stages, the specialist focuses on home safety and getting the patient to do activities and tasks that are personally meaningful. During the later stages, the patient has difficulty with basic activities of daily living. Enhancing function, encouraging relationships and social participation, and finding ways for those with dementia to enjoy life are keys to a successful occupational therapy intervention. Providing education for all family members, caregivers, and patients, and building on the strengths of the patient, will enable people with dementia and caregivers to support them in living life to the fullest.

Geriatric medicine

The biochemistry of Alzheimer's disease, one of the most common causes of dementia in old age, is still not fully understood. Alzheimer's disease is thought to be a disease of protein misfolding resulting from the accumulation of the abnormally folded protein amyloid beta in the brains of those affected by the disease. Amyloid beta, a short peptide, is an abnormal protein by-product of the nucleoprotein amyloid, a membrane protein, whose function is unclear, but it is thought to play a role in neuronal development. Presenilins are components of the proteolytic complexes involved in the processing and degradation of amyloid precursor proteins. Amyloid beta monomers are normally soluble, and contain short regions of beta sheets and a polypropylene dimer structure in solution, although they are large alpha helices in tissues. At high concentrations they undergo a dramatic conformational change to form a tertiary structure rich in beta sheets that aggregate to form amyloid fibrils, which are deposited outside neurons in formations Dense, known as senile plaques or neuritic plaques. Less dense deposits are diffuse occlusions and sometimes in the walls of small blood vessels in the brain in a process called vascular amyloid dysfunction. Alzheimer's disease is also considered a tau-related disease, resulting from abnormal aggregation of this protein, a microtubule-associated protein expressed in neuronal cells that normally stabilizes microtubules in the cytoskeleton. Like most microtubule-associated proteins, tau is controlled by phosphorylation, but in Alzheimer's patients, highly phosphorylated tau aggregates into double helices, which in turn aggregate into clumps within the cell body, known as amyloid plaque-associated neurofibrillary tangles. Although little is known about the process of fimbriae assembly, it has recently been identified that prolyl isomerase—a protein in the parafilin family—accelerates the aggregation of abnormal tau. Neuroinflammation is also involved in the complex cascade that causes Alzheimer's disease and its symptoms. With medical evidence The pathophysiological analysis of the immunological changes in Alzheimer's disease documents increased concentrations of inflammatory cytokines in the blood and cerebrospinal fluid. Whether this inflammation is a cause or a consequence of Alzheimer's disease is not fully understood, but inflammation in the brain, including increased susceptibility of resident microglia to amyloid deposits, is implicated in the pathological progression of Alzheimer's disease. At the macroscopic level, Alzheimer's disease is characterized by a loss of neurons and synapses in the cerebral cortex and some subcortical regions, leading to gross atrophy in the affected areas, including degeneration in the temporal and parietal lobes, parts of the frontal cortex, and the cingulate gyrus. Both amyloid deposits and neurofibrillary tangles are clearly visible under microscopic examination in the brains of people with Alzheimer's disease. These deposits are dense, insoluble deposits of protein and cellular material outside and around neurons. Tangles are insoluble, twisted fibers that accumulate inside the cell. Although many older adults develop some tangles, the brains of Alzheimer’s patients have significantly higher levels of these tangles and at different locations in the brain. The biochemical events that lead to the accumulation of amyloid-beta and tau are fundamental to understanding Alzheimer’s disease. A delicate balance of production enzymes regulates the accumulation of amyloid-beta. The activity of alpha-proteinase inhibits the aggregation of amyloid-beta. Recently, the relationship between cholinergic neuronal activity and alpha-proteinase activity, which can inhibit amyloid-beta, has been highlighted in the brains of Alzheimer’s patients. Alzheimer’s disease has been defined as a proteinaceous or protopathic disease due to the accumulation of abnormally folded amyloid-beta proteins in the brains of patients. Abnormal amyloid-beta accumulation can be detected using cerebrospinal fluid analysis and subsequently using positron emission tomography. Although Alzheimer’s shares pathophysiological mechanisms with prion diseases, it does not Amyloid-beta is a short peptide, a secondary protein of the membrane protein amyloid of unclear function but thought to be involved in neuronal development. Prenicillin is a component of a protein complex involved in the processing and degradation of secondary membrane amyloid. Although beta-amyloid monomers are harmless, they undergo a dramatic conformational change at high enough concentrations to form a tertiary structure rich in beta sheets that aggregate to form amyloid fibrils that deposit outside neurons in dense formations known as senile plaques or neuritic plaques, in less dense clumps such as diffuse plaques, and sometimes in the walls of small blood vessels in the brain in a process called amyloid angiopathy or cerebral angiopathy. Alzheimer's disease is also considered a tau-related disease, resulting from abnormal aggregation of this protein, a microtubule-associated protein expressed in neurons that normally stabilizes microtubules in the cytoskeleton. Like most microtubule-associated proteins, tau is controlled by Phosphorylation, however, in Alzheimer's patients, the highly phosphorylated tau protein aggregates into double helices, which in turn aggregate into clumps within the cell body, known as neurofibrillary tangles associated with amyloid plaques. Levels of the neurotransmitter acetylcholine are decreased. Levels of other neurotransmitters, such as serotonin, norepinephrine, and somatostatin, are also frequently decreased. Replenishment of acetylcholine with its antagonists is an FDA-approved treatment. An alternative approach to stimulating M1-M3 acetylcholine receptors has been proposed, through the development of slower dissociation agonists, as next-generation cholinergics in Alzheimer's disease. Although the overall histopathological features of Alzheimer's disease in the brain are well characterized, three main hypotheses have been advanced regarding the underlying cause. The oldest hypothesis suggests that a deficiency in cholinergic signaling initiates the development of the disease. Alternatively, two alternative hypotheses suggest that either tau or beta-amyloid initiates the disease. In sequence. While researchers have not identified a clear causative pathway resulting from any of the three molecular hypotheses to explain the gross anatomical changes observed in advanced Alzheimer's disease, variants of the beta-amyloid hypothesis of molecular initiation have become dominant among the three possibilities: The oldest hypothesis for the etiology of Alzheimer's disease is the "cholinergic hypothesis." It states that Alzheimer's disease begins as a deficiency in the production of acetylcholine, a vital neurotransmitter. Early therapeutic research was based on this hypothesis, including the restoration of "cholinergic nuclei." The possibility of cell replacement therapy has been investigated on the basis of this hypothesis. All first-generation anti-Alzheimer's drugs are based on this hypothesis and work to preserve acetylcholine by inhibiting acetylcholinesterase. These drugs, while sometimes helpful, have not led to a cure. In all cases, they have only treated the symptoms of the disease and have not stopped or reversed it. These findings and other research have led to the conclusion that acetylcholine deficiency may not be a cause Directly, it is the result of extensive brain tissue damage, and the damage is so widespread that cell-replacement therapies are likely to be impractical. More recently, cholinergic effects have been proposed as a possible causative factor for the formation of plaques and tangles that lead to generalized neuroinflammation. Newer hypotheses focus on the effects of the enveloped and aggregated proteins, amyloid beta and tau. Two positions were described slightly as the B and Tau views in one scientific publication. In it, it was suggested that Tauians believe that tau protein abnormalities initiate the disease cascade, while Bists believe that beta-amyloid deposits are the causative agent. The hypothesis that tau is the primary causative agent was long rejected because of the observation that amyloid plaque deposition does not correlate well with neuronal loss. A mechanism for neurotoxicity has been proposed based on loss of tau protein that helps to inhibit the cytoskeleton. However, no consensus has been reached on whether tau is phosphorylated or caused by the formation of abnormal helical filament aggregates. Support for The tau hypothesis also derives from the existence of other diseases known as tauopathies in which the same protein is misfolded. However, the majority of researchers support the alternative hypothesis that amyloid is the primary causative factor. The amyloid hypothesis is initially compelling because the gene for the beta-amyloid precursor APP is located on chromosome 21, and patients with trisomy 21—commonly known as Down syndrome—who have an extra gene copy commonly show Alzheimer’s-like disorders by age 40. The traditional formulation of the amyloid hypothesis points to the cytotoxicity of mature aggregated fibroins, which are thought to be the toxic form of the protein responsible for disrupting the calcium ion balance in the cell and thus inducing apoptosis. This hypothesis is supported by the observation that higher levels of amyloid beta, which is known to form fibrils more rapidly in vitro, are associated with earlier onset and greater cognitive impairment in mouse models and with the diagnosis of Alzheimer’s in humans. However, the mechanisms of calcium influx, or proposals for alternative cytotoxic mechanisms, by mature fibrils are not clear. A 1994 study showed that isoprenoid changes in Alzheimer’s disease are different from those occurring during normal aging, and therefore do not This disease can be considered a consequence of premature aging. During aging the human brain shows a gradual increase in dodehol levels, a decrease in ubiquinone levels, but relatively unchanged concentrations of cholesterol and dodehyde phosphate. In Alzheimer's disease, the situation is reversed with decreased dodehyde levels and increased ubiquinone levels. Dodehyde phosphate concentrations are also increased, while cholesterol remains unchanged. The increase in the sugar carrier dodecyl phosphate may reflect increased glycosylation rate in the affected brain and an increase in the endogenous antioxidant oxynone in an attempt to protect the brain from oxidative stress, for example caused by lipid peroxidation. Rubrin, previously identified in Russia, is neuroprotective in a rat model of Alzheimer's disease. Oxidative stress appears to be a major factor in the pathogenesis of Alzheimer's disease. Excessive oxidative stress is thought to play a critical role in the accumulation and deposition of beta-amyloid in the disease. Alzheimer's patients have elevated levels of oxidative DNA damage in both nuclear and mitochondrial DNA, but mitochondrial DNA has approximately 10 times more strands than nuclear DNA. Aged mitochondria may be a critical factor in the origin of neurodegeneration in Alzheimer's disease. Even individuals with mild cognitive impairment, the stage between normal aging and early dementia, have increased oxidative damage in both nuclear and mitochondrial DNA in the brain.

Geriatric medicine

Protein aggregation or protein aggregation or protein clumping is a biological phenomenon that lies in a protein formation error that results in aggregation, meaning the accumulation of protein clumps, either inside or outside cells. 2. The aggregation of these proteins often results in a harmful toxic effect, meaning that the aggregation of these proteins may appear in a large group of diseases known as amyloidosis, including other diseases such as amyotrophic lateral sclerosis, Alzheimer's, Parkinson's, and Brion's disease. 3 During the stages of protein synthesis, folds occur that make the formed protein a three-dimensional structure and become biologically active only when formed in that form. The folding stage in the process of protein formation occurs due to the repellent property of water molecules. The presence of parts of the protein that are attractive or loving and parts that are repellent or repellent is a reason for the protein to be in its biological state so that the outer part of the protein becomes attractive to water and the inner part repels water. However, some misfoldings may occur during the process of protein formation or misfoldings in a previously manufactured protein in an impromptu accident. In such cases, the cell may not be able to help refold the protein to its normal shape or may not be able to disassemble the previously defective protein, so it begins to clump inside it. During this process, the water-repellent part of the protein becomes exposed and interacts with repulsive parts of other defective proteins, and thus these proteins clump together. Protein clumping can occur for several reasons. Some people may have genetic mutations that make them more susceptible to misfolding during protein formation and make it prone to clumping. In contrast, a defect in the process of refolding the defective protein known as or a defect in the disassembly of the defective protein can lead to protein clumping. It seems that many diseases are accompanied by protein clumping with age, as the cell becomes less able to filter out defective proteins and thus they clump. It is worth mentioning that there are several new studies that assume that protein aggregation is a second step by the cell as a response to the imbalance in the protein cycle. Away from harm or mere coincidence, there has been a pioneering study that has shown that the aggregation of proteins that are clumped due to errors in their folding or their high tendency to aggregation occurs in an organized process by the cell and are placed in specific places for them, and this depends on the quality of the parts that control the repair of these damages, including the HSP and the co-chaperone. In addition, it has been shown that eukaryotic cells have the ability to sort damaged proteins into two separate groups based on the quality of control. 1- The control group in the quality of the nucleolar juxta-nucleolar 2- The control group in the insoluble protein deposit. The existence of two separate groups is due to the existence of two different ways of dealing and interacting with different types of misfolded and clumped proteins. The second type of control group acts as a site for the aggregation of non-objectin proteins such as huntingtin protein. Under difficult conditions such as high temperature, the cellular work of quality control becomes unable to keep up with the work, so the observable protein begins to aggregate into the first control group, which is the juxtanuclear group, and eventually begins to disintegrate, which means that the aggregation is an organized and controlled process by the cell. According to one theory, protein aggregation is a cause of aging, and this theory may seem testable given that there are ways to delay aging. Therefore, if the increase in protein aggregation is not related to aging, then slowing down the aging process will not result in any change in the rate of collateral damage of protein aggregation over time. However, aging is associated with a decline in the protection system from protein aggregation damage. To solve the problem, different methods were found to examine the toxicity of protein aggregation in C-elegans. Through these studies, it was shown that reducing the work of one of the most important regulatory pathways, including insulin growth factor signaling 2S, may result in protection from neurodegeneration associated with the toxicity of the aggregated protein. The validity of this approach has been demonstrated in mammals by reducing the regulatory pathway in insulin growth factor-1 activity, which resulted in greater protection from Alzheimer's disease in mice in terms of behavior and the organic chemistry associated with the defect in the disease. Although there is an idea that the aggregation of fully formed proteins may be toxic, new research has shown that incomplete and clumped proteins are more toxic. The hydrophobic parts of these clumped proteins may cause interaction with other components of the cell and cause damage to them. One theory about how cellular damage occurs by clumped proteins suggests that it occurs due to disruption of the cell wall. It is known that clumped proteins in laboratory tubes are able to destabilize the manufactured lipid bilayer, which is similar to that found in living cells, thus leading to increased disintegration of the cell wall.

https://ar.wikipedia.org/wiki/%D8%AE%D8%B1%D9%81

Geriatric medicine

Dementia, mental decline, or dementia is a disorder that manifests as a group of related symptoms, which usually appear when the brain is damaged by injury or disease. Symptoms include progressive impairments in memory, thinking, and behavior, which negatively impact a person's ability to function and perform daily activities. Aside from memory impairment and disturbances in thinking patterns, the most common symptoms include emotional problems, difficulties with language, and decreased motivation. Symptoms can be described as occurring on a continuum over several stages. Consciousness is not affected. Dementia ultimately has a significant impact on the individual, caregivers, and social relationships in general. A diagnosis of dementia requires noting a change from a person's usual mental functioning, and a cognitive decline greater than that caused by normal aging. Many diseases and injuries to the brain, such as stroke, can lead to dementia. However, the most common cause is Alzheimer's disease, a neurodegenerative disorder. The International Classification of Diseases classifies dementia as a neurocognitive disorder with several forms or subcategories. Dementia is listed as an acquired brain syndrome, characterized by a decline in cognitive function, and contrasted with neurodevelopmental disorders. Dementia subtypes may be based on a known disorder, such as Parkinson's disease; Huntington's disease; vascular disease, vascular dementia—vascular brain injury, including stroke, often leads to vascular dementia; Lewy body disease; frontotemporal lobar degeneration; or a number of other medical conditions, including HIV infection, which causes HIV-related dementia; and prion diseases. Easily reversible dementias include hypothyroidism, vitamin B12 deficiency, and Lyme disease. Diagnosis is usually based on history and cognitive testing using imaging. Blood tests may be done to rule out other possible reversible causes, such as an underactive thyroid or vitamin B12 deficiency, and to determine the subtype. One commonly used cognitive test is the Mini Medical Status Examination. The biggest risk factor for developing dementia is old age, but dementia is not a normal part of aging. Dementia has two main forms, considering its causes, which are: Alzheimer's disease can be diagnosed based on the following symptoms according to the criteria of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders issued by the American Psychiatric Association (DSM-4), which are summarized as follows: A. A continuous decline in cognitive abilities represented by each of the following: B. The cognitive impairment mentioned in both A and 2) leads to a clear impairment in social or professional functions, and represents a clear decline compared to the level at which these functions were before that. C. The course of the condition is characterized by a gradual appearance of symptoms and a continuous deterioration in cognitive abilities. D. The cause of the cognitive impairment mentioned in both A and 2) must not be any of the following: E. This deterioration in cognitive abilities does not occur only during cases of delirium. F. This deterioration in cognitive abilities cannot be explained by cases of another mental disorder such as: depression or schizophrenia. Dementia resulting from multiple cerebral infarction can be diagnosed based on the following symptoms according to the criteria of the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders issued by the American Psychiatric Association (DSM-4), which are summarized as follows: A. A continuous decline in cognitive abilities represented by each of the following: B. The cognitive impairment mentioned in both A and 2) leads to a clear impairment in social or professional functions, and represents a clear decline compared to the level of these functions before that. C. Specific neurological symptoms and signs known to doctors indicate damage or dysfunction in specific areas of the brain, and the doctor sees that they are related to the deterioration of cognitive abilities. D. This deterioration in cognitive abilities does not only occur during cases of delirium. Dementia has multiple causes, which we summarize as follows: Dementia occurs in different forms depending on its cause. However, the final result, regardless of the cause, is often damage to brain cells. Successive studies have found that there is a severe deficiency in the nerve fluid called acetylcholine, in addition to the appearance of changes in brain cells indicating their fibrosis and damage. The risk of developing dementia generally increases with age, especially after the age of 65. The incidence of dementia is estimated at about 2% between the ages of 65-69, increasing to 5% between 75-79, then reaching 20% between the ages of 85-89, and 50% among those over the age of 90. Alzheimer's disease is the most common form of dementia, and occurs in women three times more often than in men. Multiple infarct dementia occurs more often in men because men are more likely to suffer from causes of infarctions such as atherosclerosis and high blood pressure. The prevalence of this type of dementia varies from one society to another due to prevailing dietary patterns, unlike Alzheimer's, which is equally prevalent in several societies around the world. The World Health Organization estimates that there are about 10 million new cases of dementia annually. There are a number of organic and psychological diseases that resemble dementia. Some organic diseases were previously mentioned when discussing the causes. Other conditions that resemble dementia are: Treatment of dementia varies according to its causes. There are some cases of dementia that are curable, such as cases resulting from vitamin deficiency, malnutrition, hypothyroidism, etc., because these causes can be treated, and then mental abilities can return to normal as they were. As for the drugs used in cases of dementia, they are as follows: Cases of dementia that cannot be treated are considered chronic cases. If left untreated, the patient's mental abilities continue to deteriorate until he loses the ability to take care of his simplest affairs, such as eating and drinking... He may also lose the ability to control his exits, and may go out at inappropriate times and be exposed to harm or loss, especially when the patient's physical condition helps him move and walk, which requires constant monitoring and closing the doors. These cases require a great effort from his family, which may be at the expense of their work and other aspects of their lives. In most cases, dementia cases that have no known treatable cause cannot be cured. Therefore, the course of these cases is characterized by slow or rapid deterioration until death, within a period ranging from 5-10 years. However, the drugs used to treat Alzheimer's disease may contribute to reducing the acceleration of deterioration in mental ability or may lead to stopping it for a period that may be long or short, depending on various personal and therapeutic factors estimated by the treating physician.

Geriatric medicine

Wilma Sue Tilton Griffin, born January 25, 1934, is an American neuroscientist best known for her contributions to the role of neuroinflammation in the pathogenesis of Alzheimer's disease and other neurodegenerative conditions. She devised a "cellular cycle" by which interleukin-1 and other paracrine factors cooperate with each other to create a "feed-forward" collaboration, thus creating a hypothesis for a progressive disease. Griffin is the Alexa and William T. Dillard Professor in Aging Research and Director of Research at the Donald W. Reynolds Institute on Aging at the University of Arkansas for Medical Sciences. She is also the founding editor of the journal Neuroinflammation. Griffin grew up in western Arkansas and attended high school in Fort Smith. After graduation, she moved with her parents to Los Alamos, New Mexico, where she worked for the Atomic Energy Commission and met and married her husband, Edmund Griffin. Ed was also a native Arkansas native and worked at the Los Alamos National Laboratory helping to determine the biological effects of ionizing radiation. The couple had two sons, Edmund II and Clay. Sue Griffin received her BS and MS degrees in nutrition from the University of Tennessee at Knoxville. In 1974, she received her Ph.D. in physiology from the University of Rochester School of Medicine. After receiving her Ph.D., Griffin was a fellow at the University of Texas Southwestern Medical Center. In 1986, Griffin moved to her home state of Arkansas to take a position in the Department of Pediatrics at the University of Arkansas for Medical Sciences, where her laboratory was already located at Arkansas Children’s Hospital. Although ostensibly committed to the neurological abnormalities in Down syndrome, her laboratory pursued a link between the condition and Alzheimer’s disease. In 1989, Griffin published an article demonstrating that the immune system, interleukin-1, was elevated in both Down syndrome and Alzheimer’s disease. This represented one of the first published links between Alzheimer’s and Parkinson’s disease. Griffin went on to explain how this inflammation contributes to the formation of amyloid plaques, neurofibrillary tangles, and Lewy bodies in the brain in Alzheimer’s and Parkinson’s disease, as well as its association with genetic variations that confer a higher risk of Alzheimer’s in some individuals. In 2016, Griffin received the Alzheimer’s Association’s Lifetime Achievement Award at its international conference. In 2018, she was inducted into the Arkansas Women’s Hall of Fame.

Geriatric medicine

Amyloid-related imaging abnormalities (ARIAs) are abnormalities observed on neuroimaging in patients with Alzheimer's disease, associated with amyloid-modifying therapies, specifically human monoclonal antibodies such as adecanemab. There are two types of these abnormalities, ARIA-E and ARIA-H. This phenomenon was first observed in clinical trials of bapineuzumab. ARIA-E refers to cerebral edema, which is the breakdown of the tight junctions of endothelial cells of the blood-brain barrier and the resulting accumulation of fluid. In a double-blind trial of the human monoclonal antibody solenizumab, 16 patients, or 0.78%, developed ARIA-E. An additional seven patients developed ARIA-E during an open-label extension of the clinical trial. Side effects of ARIA-E depend on the severity and location of the edema. Symptoms can include headache, mental status changes, confusion, vomiting, nausea, tremor, and gait abnormalities. Aria-H refers to cerebral microbleeds, which accompany small cerebral hemorrhages, usually hemosiderosis. Microbleeds are usually seen as small, round, slightly indented lesions that are small hemosiderin deposits. Some studies define microbleeds as less than or equal to 10 mm, while others define them as less than 5 mm. The prevalence of microbleeds in healthy older adults is about 6%, but this value increases to between 50% and 80% in older adults with cerebrovascular disease.

Geriatric medicine

Mild cognitive impairment (MCI) is a neurological disorder characterized by cognitive impairment that is greater than expected for a person's age and education level, but not severe enough to interfere with basic daily activities. MCI may occur as a transitional stage between normal aging and dementia, particularly Alzheimer's disease. This disorder includes both memory-related and non-memory-related manifestations. The cause of MCI is still not clearly known, and its prevention and treatment are equally unknown. MCI can present with a range of symptoms, but it is mainly divided into two types: According to some experts, MCI can result from brain changes induced during the early stages of Alzheimer's disease and other forms of dementia. However, the direct causes of this disorder are still unclear. The risk factors for MCI are the same as those for dementia: aging and the genetic cause of Alzheimer's disease or senility, in addition to another risk factor, cardiovascular disease. In patients with mild cognitive impairment, increased oxidative DNA damage was observed in the nuclei and mitochondria of brain neurons. Increases in 8-hydroxyguanine, a substance known to cause DNA damage, were found in the frontal and temporal lobes of patients with mild cognitive impairment and in mitochondrial DNA of the temporal lobe compared with age-matched controls. The number of oxidized DNA bases was increased in the brains of patients with this disorder. These findings suggest that oxidative DNA damage occurs in the earliest diagnosable stages of Alzheimer's disease and may therefore play an important role in the study of the pathogenesis of this disease. The diagnosis of mild cognitive impairment requires expert clinical judgment, in addition to a detailed clinical evaluation that includes clinical approach, neuroradiology, blood tests, and neuropsychological evaluation to rule out alternative differential diagnoses. Mild cognitive impairment is diagnosed when: There is evidence that people with mild cognitive impairment with amnesia may be in the transitional phase of Alzheimer's disease even though they do not meet the neuropathological criteria for a diagnosis of Alzheimer's disease; people in this presumed transitional phase have widespread amyloid deposits in the neocortex and neurofibrillary tangles in the medial temporal lobe. On the other hand, many people develop neurofibrillary tangles without amyloid, a pattern called primary age-related tauopathy. There is emerging evidence that MRI can detect degeneration, including progressive loss of gray matter in the brain, ranging from mild cognitive impairment to overt Alzheimer's disease. An imaging technique known as Pittsburgh B positron emission tomography is used to visualize areas of beta-amyloid peptide in living specimens using a radiocarbon marker that selectively binds to these deposits. 18F positron emission tomography (PET) using florbetapine is a promising method for predicting the future progression of mild cognitive impairment to Alzheimer’s disease dementia, but further study is needed to prove the diagnostic test’s accuracy in larger trials. These methods could be of great help in facilitating clinical research into treatments. The prevalence of mild cognitive impairment varies by age. The prevalence of the disorder in several age groups is as follows: 6.7% in 60-64 age groups, 8.4% in 65-69 age groups, 10.1% in 70-74 age groups, 14.8% in 75-79 age groups, and 25.2% in 80-84 age groups. After two years of follow-up, the overall prevalence of dementia among people with mild cognitive impairment aged 65 and over appears to be 14.9%. Globally, about 16% of the world’s population over the age of 70 has some form of mild cognitive impairment.

Geriatric medicine

Appreciation therapy or appreciation therapy is a method and attitude for dealing with people with dementia, which can be used particularly in elderly care as well as in social life in general. Appreciation therapy is, on the one hand, the respectful, non-ignorant, appreciative attitude developed for dealing with people with dementia, and is based in particular - according to Carl Rogers - on the basic attitudes of client-centered therapy aimed at accepting the behavior of people with dementia as correct for them. On the other hand, appreciation is a special form of social communication characterized by acceptance and non-correction and attempts to understand and discern the needs of the person concerned. Appreciation therapy was developed by Naomi Vail, a social worker who assumed that disoriented older people are struggling to navigate the messy issues in their lives. According to her, users of the appreciation method should make it their job to support these people in this process. While Nicole Richard, a German gerontologist, developed appreciation therapy as part of a national working group and called her method integrative appreciation, her approach does not see the practitioner as making it his job to care for and accompany people with dementia in the process of coping with “unfinished business”, but rather to accept them as they are and their current state of mind. According to Richard, this means that people become calmer because they feel understood. Appreciation therapy uses a number of specific techniques, but has drawn criticism from researchers who dispute the evidence for some of the beliefs and values of appreciation therapy, and the appropriateness of these techniques, because there is insufficient evidence to prove that such methods are effective for people with dementia.

Geriatric medicine

Sundowning syndrome or sundowning syndrome is a well-known psychological and behavioral syndrome or phenomenon in the elderly, in which there is an increase in symptoms of delirium, hyperactivity, and possibly hallucinations, delusions, and unusual behavioral symptoms in some patients suffering from any form of dementia. It is more common in Alzheimer's disease, as studies indicate that 20-45% of people with Alzheimer's disease suffer from sundowning syndrome. The term "sundowning" refers to the appearance of these symptoms at sunset and the onset of night. The real causes of sundowning syndrome are not yet known, but it is believed that it occurs as a result of some factors such as: Treatment is done in consultation with a specialist doctor and by modifying some of the patient's behavior such as:

Geriatric medicine

Early-onset Alzheimer's disease, also called early-onset Alzheimer's disease or early-onset AD, is the term used for cases of Alzheimer's disease diagnosed before the age of 65. It is an uncommon type of Alzheimer's disease, accounting for 5-10% of all cases of Alzheimer's disease. About 13% of cases of early-onset Alzheimer's disease are familial Alzheimer's disease, where a genetic predisposition leads to the disease. Other forms of Alzheimer's disease share the same characteristics as late-onset Alzheimer's disease. Little is understood about how the disease begins. Nonfamilial early-onset Alzheimer's disease can develop in people in their 30s or 40s, but it is very rare. Most people with early-onset Alzheimer's are in their 50s or early 60s. History of Alzheimer's disease: The symptoms of Alzheimer's disease are distinct in the nosology of the disease as they were first identified by Emil Kraepelin, and the symptoms of neurological diseases were observed by Alois Alzheimer in 1906. In this sense, the disease was discovered by Emil Kraepelin and Alois Alzheimer, who worked in Emil Kraepelin's laboratory. Because of the importance of Kraepelin's disease to the basics of neurological diseases, Emil Kraepelin decided that the disease would be called Alzheimer's disease. Familial Alzheimer's disease: Familial Alzheimer's disease, or early-onset familial Alzheimer's disease, is an uncommon form of Alzheimer's disease that usually occurs in early life, defined by age 65 and is inherited by genetic factors, and is defined by genes, and other characteristics such as the age at which the disease appears. It accounts for approximately half of cases of early-onset Alzheimer's disease. Requires Familial Alzheimer's disease is a disease in which at least one person has a first-degree relative with Alzheimer's disease. Non-familial Alzheimer's disease is referred to as "sporadic Alzheimer's disease", where the risk factors in the genes are small and not varied. In the case of early familial Alzheimer's disease, estimates indicate only 0.035 of all Alzheimer's diseases. It has provided a useful model for studying various aspects of the disease. Currently: The mutations of the familial early Alzheimer's disease gene have led the vast majority of animal models to the discovery and development of therapeutics in Alzheimer's disease. Clinical symptoms Alzheimer's disease is the most common cause of dementia and often appears late in life. It is an inevitable fate, generally within ten years of the first signs. An early sign of Alzheimer's disease is unusual memory loss. Especially when remembering new events and the names of people and things, logopenic primary progressive aphasia. As the disease progresses, the patient develops serious problems, accompanied by mood swings and an inability to perform complex activities such as driving a car. In the later stages, the patient loses the ability to remember how to do simple things such as combing his hair and will then need constant care. Anatomically, diseases Familial Alzheimer's disease is virtually indistinguishable from other forms of the disease. Amyloid deposits can be seen in parts of the brain tissue. This amyloid protein forms plaques and neurofibrillary tangles that progress through the brain. The plaques are very rare and are unique to Alzheimer's disease; this may occur when there are mutations in the gene that produces a functional but defective protein, rather than the products of a nonfunctional gene that are usually the result of mutations. The underlying neurobiology of the disease has only recently been understood. Researchers have mapped the inflammatory pathways involved in the development and progression of the relapsing features of Alzheimer's disease. Key molecules involved in these pathways include microglial cells, amyloid beta, and proinflammatory aggregates. Amyloid beta is a small fragment of a larger protein called amyloid leader protein. When amyloid leader protein reacts, it is broken down into other protein fragments. One of the fragments produced in this process is β-amyloid. β-amyloid is more sticky than any other fragment produced from the amyloid precursor protein and because of this property it begins to accumulate in the brain. The accumulation is caused by genetic variations and abnormalities in neurobiology. Finally, the fragments form small units. Then fibers, beta-amyloid fragments, and finally plaques. The presence of β-amyloid plaques in the brain prompts the body to recruit and activate astrocytes. This is normally a beneficial response. However, not with Alzheimer’s because beta-amyloid plaques stimulate glial cells to release oxygen free radicals. Free radicals are normally effective against abnormal cells. But free radicals cannot distinguish between normal and abnormal cells. Free radicals destroy beta-amyloid plaques but also destroy surrounding healthy tissue. As more tissue dies, glial cells release chemokines and stoichioids. These aggregates recruit more glial cells which means more free radicals. This uncontrolled response and inflammatory response contribute to the neurodegenerative development of Alzheimer's disease. Genetics Familial Alzheimer's disease is caused by mutations in at least one of three genes: presenilin 1, presenilin 2, and amyloid precursor proteins. Mutations in other genes in the study. Presenilin 1 The presenilin 1 gene was identified by Sherrington in 1995 and several mutations have been identified. Mutations in this gene definitely cause familial Alzheimer's disease type 3, usually in people under 50 years of age. This protein has been identified as part of an enzyme complex that cleaves beta-amyloid from APP. The gene contains 14 exons and the estimated coding area is 60 kb, as reported by Rogev M. 1997 and Del Vivero 1999. The protein that the gene encodes is an integral membrane protein. As mentioned by Koichi 2002, Notch1 ps1 is thought to have a role in somitogenesis in the embryo. It also acts on amyloid precursor protein, which gives a possible role in the pathogenesis of FAD. Homologs of PS1 have been found in plants, invertebrates, and other vertebrates. Some of the mutations in the genes, of which there are more than 90, include: His163Arg, Ala246Glu, Leu286Val, and Cys410Tyr. The most common mutation is Glu318Gly and this predisposes individuals to familial Alzheimer's disease, with a study by Tadi finding an incidence of 8.7% in patients with familial presenilin 2: The presenilin 2 gene is very similar in structure and function to presenilin 1. Located on the chromosome, mutations in this gene cause flavin adenine dinucleotide type IV. This gene was discovered by Rudolf Tanzi and Jerry Schellenberg in 1995. A subsequent study by Kovacs in 1996 showed that presenilin 1 and 2 proteins were expressed in similar amounts, and in similar organelles, in mammalian neurons. Levi-Lahd reported that presenilin 2 contained 12 exons, 10 of which were coding exons, and that the original basal transcript encoded a 448 amino acid peptide, with 67% homology. For presenilin 1, this protein is known to be part of the plaque enzyme complex that degrades amyloid beta peptide. Mutations of APP have not been studied as much as for presenilin 1, but distinct allelic variants have been known. These include Asn141Ile, which was first identified by Rudolf Tanzi and Jerry Schellingberg in families in Wolga, Germany, with early familial Alzheimer's disease. One of these studies of Nucleol found amyloid angiogenesis in affected individuals in the family. This phenotype may be explained by Tomita's study, suggesting that Asn141Ile mutations alter amyloid beta-peptide metabolism, causing increased deposition of the protein in plaques. Other allelic variants are Met239Val, which was identified by the Italian Rogge, who also suggested earlier that this gene might be homologous to presenilin 1, and Asp439Ala mutations in exon 12 of the gene, which were suggested by Liu to alter the endoproteolytic activity of presenilin 2. Amyloid beta-peptide Amyloid beta-peptide mutations are located on the long arm of chromosome 21, which causes Alzheimer's disease. Familial. PathophysiologyFollowing β-secretase cleavage, amyloid beta peptide is cleaved by a membrane-bound protein complex called γ-secretase to generate amyloid beta. Presenilin 1,2 are the intermediate enzymes in the complex with nicastrin, IPH1 and presenilin 1. Cleavage of alpha-secretase from amyloid beta peptide, which prevents amyloid beta production, is the most common event in amyloid beta peptide processing. Twenty-one allelic mutations have been identified in the amyloid beta gene. These ensure early-onset Alzheimer's disease, all of which occur in a region within amyloid beta peptide that encodes the amyloid beta domain. Genetic testingGenetic testing is available for individuals and relatives with symptoms. Early-onset Alzheimer's disease has devastating effects on the careers, caregivers, and family members of the affected individual. Many affected individuals are within the age range of caregivers of children. Children of people with pre-puberty suffer physically and emotionally and their parents are unable to care for them. Those who work lose their ability to do their jobs and are forced into early retirement, and when it is predictable the employee should discuss their future with their employers regarding the loss of skills. Those forced into early retirement may not have access to the full range of benefits available to those who retire at the minimum age set by the government. With some jobs, a mistake can have serious consequences for a large number of people, and cases of distress have been reported in people with early-onset Alzheimer's. People with Alzheimer's lose the ability to meet their own needs, such as managing money.

https://ar.wikipedia.org/wiki/%D9%87%D9%88%D8%BA%D9%88%D9%8A

Geriatric medicine

The Hoogeweg is a model gated village under the supervision of the Hoogeweg Nursing Home in Weesp, the Netherlands. It was specifically designed to be a pioneering care facility for elderly people with dementia. Hoogeweg is different from traditional care homes because it uses 24-hour reminiscence therapy, which means that residents with dementia are more active and require less medication. The place has been compared to the one in the movie “The Truman Show”. Caregivers, doctors and nurses work around the clock to provide the necessary care for residents throughout the day. The Hoogeweg complex is a village with a square, a supermarket, a hairdresser, a theatre, a bar, a café and a restaurant, in addition to twenty-three homes. In 2018, four homes were added to Hoogeweg. Each home reflects a common and familiar style for the six or seven people who live there. The seven homes available are: The doctors and nurses strive to make the experience as real as possible for the residents. Residents shop at the supermarket and help with preparation and cooking as if they were at home. Carers wear casual day clothes rather than clinic clothes and fit into a role appropriate to the comfort of dementia patients; in working class households, carers act in their natural role or may be nurses, while in aristocrats/upper class households, nurses act as servants. Lifestyles include different forms of music, a wide variety of interior design styles, food and table settings. Residents in each house have their own large bedroom and meet with other residents to share the living room, kitchen and dining room. There are no locks on the doors and residents are free to walk around the village, including the choice of visiting the supermarket or café. The village has a staff of 250. There is no ‘fake reality’ or ‘hyper reality’. The institution provides a place of normality where residents are supported by well-trained staff. When residents become confused, the staff have many ways of making them feel comfortable. At the same time, the staff will not deceive patients if asked directly and will tell them honestly that the residents are in a place to receive the care that their condition requires. Because of the nature of Alzheimer’s disease and dementia, residents can remember the distant past but not the present, so even honest answers given by staff will be forgotten in a short time. The first ideas for the village came about in 1922 when the management team of the traditional nursing home Hugowi met after discussing the future of their parents with Alzheimer’s disease and decided that they did not want to put them through hospital-like care. After a series of research and brainstorming sessions in 1993, they concluded that normality should prevail in all aspects of care in the nursing home. This vision was called “Normal Living in Small Space for People with Dementia.” Among other things, they decided that people generally prefer to be surrounded by like-minded people with similar backgrounds and experiences and interact with them.

Geriatric medicine

HIV-associated neurocognitive disorder (HIV-ASCD) is a neurological disorder associated with HIV and AIDS, including neurological disorders of varying severity. HIV-associated neurocognitive disorder is associated with metabolic encephalopathy caused by HIV infection, fueled by immune activation by macrophages and microglia, as these cells are actively infected by the virus and secrete neurotoxins produced by humans and viruses. The main features of HIV-associated neurocognitive disorder are disabling cognitive impairment accompanied by motor impairment, speech problems and behavioral changes. Cognitive impairment is characterized by mental slowness, memory problems and poor concentration. Motor symptoms include loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and reduced emotional and spontaneous responses. At the histopathological level, it is characterized by infiltration of monocytes and macrophages into the central nervous system, neuroglial degeneration, myelin sheath pallor, dendritic cell damage and neuronal loss. HAD typically occurs years after HIV infection and is associated with low CD4+ T-cell levels and high plasma viral load. It is sometimes considered the first sign of AIDS onset. The prevalence is 10–24% in Western countries and has been observed in only 1–2% of infections returning to India. With the advent of highly active antiretroviral therapy (HAART), the incidence of HAD has declined in developed countries, although its prevalence is increasing. HAART has the potential to suppress or delay the onset of HAD in HIV-infected individuals, as well as improve mental function in those with pre-existing HIV-associated dementia. Dementia occurs when an individual develops a progressive and severe neurocognitive deficit that significantly interferes with daily functioning. The patient subsequently loses the ability to work and may be unable to care for themselves. Before the condition progresses to this degree, a patient can be considered to have mild neurocognitive disorder. HIV-associated cognitive deficits affect the domains of attention, memory, verbal fluency, and visuospatial construction. For memory in particular, decreased activity in the hippocampus alters the basis of memory encoding and affects a number of mechanisms including long-term consolidation. The severity of deficits in different domains varies depending on whether a patient is treated with H-A-R-T or monotherapy. Studies have shown that patients experience cognitive deficits with dysfunction in fronto-striatal circuits including associated parietal regions, which may play a role in the observed deficits in visuospatial function. In addition to cognitive deficits, the development of psychological dysfunction can be observed. For example, HIV-infected patients have high rates of clinical depression and alexithymia, which is the difficulty in processing or recognizing one’s own emotions. Patients also have difficulty recognizing facial expressions. The severity of cognitive deficits is exacerbated in later stages of HIV infection if a patient is not treated with a combination of highly active antiretroviral therapies. Early HIV patients show mild difficulties with concentration and attention. In advanced HIV-associated dementia, speech impairment, motor dysfunction, and disturbances in thinking and behavior can be observed. In particular, slower motor speeds have been associated with enlargement of the right putamen. HIV-associated neurocognitive disorder can be diagnosed using clinical criteria after other etiological possibilities have been considered and ruled out. The severity of neurocognitive disorder correlates with CD4, suggesting that early treatment to prevent HIV-induced immunosuppression may help prevent the development of HIV-associated neurocognitive disorders. Mother-to-child transmission during pregnancy is the most common form of HIV infection in children and has been associated with an increased risk of death and developmental delay. Neurological disease has been observed in children with AIDS as a result of HIV-1 infection. HIV-1 can infect the central nervous system of newborns with HIV within weeks of initial infection, causing neurological damage and cell death. Although neuronal dysfunction is associated with HIV infection of the CNS, the pathogenesis of the neurological disorders remains unclear. The main cells infected by HIV-1 in the nervous tissue include microglia, astrocytes, and macrophages, while neurons are rarely infected. Susceptibility to HIV-1 infection, along with viral replication in neurons and glia, is a function of cell differentiation, and is more likely to occur in immature progenitor cells than in differentiated cells. Several resolvable signals, such as cytokines, have been proposed to modulate susceptibility and contribute to viral latency or viral replication during organ development. In fact, cells during CNS development are under the control of environmental factors that provide guidance signals to neuronal cell targets. By regulating the survival, differentiation, and maintenance of specific functions of neuronal and glial progenitor cells, these extracellular signals can influence various stages of CNS development as well as mediate viral-cell interactions in the developing brain. In addition to cytokine production, HIV-1-infected monocytes and astrocytes are capable of producing a number of soluble mediators, including viral proteins such as gp120 and Tat, which can exert deleterious effects on both developing and mature neural tissues. Furthermore, molecules such as platelet-activating factor and prostaglandins, produced by functional interactions between microglia/macrophages and astrocytes, have been shown to mediate cellular damage in primary neuronal cultures and neuronal cell lines with an immature phenotype. Together, these observations suggest that the mechanism by which the virus modulates CNS development and induces immature brain disease depends on the modulation of the production of soluble bioactive compounds. Several mediators that may exert neurotoxic effects have been identified in several model systems, including inflammatory cytokines, viral proteins and neurotoxic metabolites. As a result, the complex interplay between different mediating factors may modify the function of developing and mature cells, responsible for neurological disorders, and influence their survival.

Geriatric medicine

Frontotemporal dementia, also known as frontotemporal degeneration, or frontotemporal neurocognitive disease, is a disease that includes several types of dementia involving the frontal and temporal lobes. Frontotemporal dementias are broadly defined as language or behavioral disorders. The three main subtypes or variant syndromes include the behavioral variant, formerly known as Pick's disease, and two variants of primary progressive aphasia, the semantic variant and the afluent variant. Two rare subtypes of frontotemporal dementia exist, called interneuronal interneuronal inclusion disease and basal body inclusion disease. Other related disorders include corticobasal syndrome and frontotemporal dementia with amyotrophic lateral sclerosis, also called FTD-ALS or FTD-MND. Frontotemporal dementia is a predominantly early-onset syndrome associated with frontotemporal lobar degeneration, characterized by progressive neuronal loss involving mostly the frontal or temporal lobes, with a typical loss of more than 70% of spindle neurons, while other types of neurons remain intact. Frontotemporal dementia was first described by Arnold Pick in 1892, and was initially called Pick's disease, a term now reserved only for the behavioral variant of frontotemporal dementia that shows the presence of Pick bodies and Pick cells. Second only to Alzheimer's disease in prevalence, frontotemporal dementia actually accounts for about 20% or less of degenerative dementias found at autopsy. Signs and symptoms typically appear in late adulthood, are most common between the ages of 45 and 65, and affect men and women roughly equally. Common signs and symptoms include significant changes in social and interpersonal behavior, apathy, blunted emotions, and deficits in expressive and receptive language. There is currently no cure for frontotemporal dementia, but treatments may help relieve symptoms. Frontotemporal dementia is early-onset and most often occurs before age 65, but can begin earlier, occurring after this age in 20%-25% of cases. It is the most common type of early-onset dementia. The International Classification of Diseases (ICD) classifies it as a disorder that affects the mental and behavioral aspects of the human being. Report the gradual onset of behavioral changes or language deficits and their progression several years before presenting to a neurologist.

Geriatric medicine

Progressive supranuclear palsy, also known as Steele-Richardson-Olszewski syndrome, is a degenerative disease involving the gradual loss and deterioration of cells in areas of the brain. The condition causes symptoms including imbalance, slowed movement, difficulty moving the eyes, and dementia. Progressive supranuclear palsy is similar to other neurodegenerative diseases such as Parkinson's and Alzheimer's. The cause of the condition is not yet certain, but it is related to the buildup of a type of protein called tau in the brain. Medications such as levodopa and amantadine may help in some cases. Supranuclear palsy affects approximately six people in every 100,000 people, and symptoms usually begin in people between the ages of 60 and 70. Males are slightly more likely to be affected than females. No association has been found between supranuclear palsy and any particular race, location, or occupation. The initial symptoms in two-thirds of cases are loss of balance, lurching forward when moving, walking quickly, bumping into objects or people, and frequent falls. Dementia is also the first symptom in one-fifth of cases. Other common early symptoms include personality changes and general slowing of movement, in addition to visual symptoms. Later symptoms and signs are dementia, slowing of speech, difficulty swallowing, and difficulty moving the eyes, especially in a vertical direction. The latter symptom explains some of the falls experienced by these patients, as they are unable to look up or down. Other signs include poor eyelid function, facial muscle contraction with head tilted backwards, neck muscle spasms, sleep disturbances, urinary incontinence, and constipation. Visual symptoms are of particular importance in the diagnosis of this disorder. Patients often complain of difficulty reading due to the inability to see well. It is worth noting here that the eye disorders experienced by these patients are mainly related to voluntary eye movement and the inability to make vertical saccadic movements, which are often worse with downward saccadic movements. Patients complain of difficulty looking down due to neck formation, followed by upper gaze palsy, which is corrected when the examiner rotates the patient's head up and down as part of the glioblastoma test. The involuntary eye movements may be close to normal, as in Bell's phenomenon, and on close inspection, eye movements called "square-wave tremors" are visible when the patient fixates at a distance. These are subtle movements, which can be mistaken for nystagmus, but they are rapid in nature. Although healthy individuals also make square-wave tremors, patients with PNP make slower square-wave tremors with smaller vertical movements. Evaluation of these square-wave tremors and decreased vertical movement is particularly useful in diagnosing PNP because these movements distinguish PNP patients from other Parkinson's patients. Convergence difficulties, where the eyes converge when focusing on a nearby object such as the pages of a book, are typical. Because the eyes have difficulty converging to focus at short distances, the patient may complain of diplopia when reading. Primary Pathology: The cause of PNP is not known. Less than 1% of people with PSP have a family history of the disorder, meaning that a genetic factor is unlikely. A variant in the tau gene called haplotype H1, located on chromosome 17, has been linked to PSP. Almost all people with PSP have received a copy of this variant from their parents, but two-thirds of the general population have received a copy of this variant! So it seems that the H1 haplotype is necessary but not sufficient to cause PSP. Other genes and environmental toxins are being investigated as other contributing factors to PSP. Mitochondria and complex I inhibitors are particularly implicated in PSP-like brain lesions. Affected brain cells include both neurons and glial cells. Neurofibrillary tangles, which are clumps of tau protein, are a normal part of the internal structure of brain cells. These tangles are often different from those seen in Alzheimer's disease, but may be structurally similar when they occur in the cerebral cortex. Its chemical composition is usually different, similar to the tangles seen in corticobasal atrophy. The presence of tau protein chains in astrocytes or in astrocyte bundles is also a diagnostic factor. Unlike globular neurofibrillary tangles, they may be more widespread in the cortex. Lewy bodies are seen in some cases, but it is not clear whether this is a distinct or independent process. In some cases, PSP can coexist with cortical atrophy, Parkinson's disease, and/or Alzheimer's disease, especially in older patients. The main areas of the brain affected are: MRI is often performed to diagnose PSP. MRI may show atrophy of the midbrain with preservation of the pons, giving the "hummingbird" and Mickey Mouse signs. Progressive supranuclear palsy is often misdiagnosed as Parkinson's disease because it presents with slowed movements and difficulty walking, and in these symptoms it is similar to progressive supranuclear palsy as it is one of a group of diseases referred to as Parkinsonian syndromes. Both Parkinson's and progressive supranuclear palsy begin in late middle age and involve slowed and rigid movement. However, there are several distinguishing features between them. Tremor is very common in people with Parkinson's disease, but rare in people with progressive supranuclear palsy. Difficulty speaking and swallowing are more common and severe in progressive supranuclear palsy, and the abnormal eye movements of progressive supranuclear palsy are essentially absent in people with Parkinson's disease. Poor response to levodopa can help distinguish between Parkinson's and progressive supranuclear palsy. Patients with Richardson type of progressive supranuclear palsy tend to stand upright or with a hunched back, unlike the forward-bending posture seen in other Parkinsonian disorders. Frequent falls are also more common with progressive supranuclear palsy, especially Richardson type. Progressive supranuclear palsy can be misdiagnosed as Alzheimer's disease because of behavioral changes. Chronic traumatic encephalopathy (CTEP) shows many similarities to PSP. There is no cure for PSP, and treatment is primarily supportive. PSP is often divided into two subgroups, Richardsonian PSP, which is the classic type, and parkinsonian PSP, in which a short-term response to levodopa can be obtained. Dyskinesia is an occasional but rare complication of treatment. Amantadine is also sometimes helpful. After a few years, PSP tends to take on the characteristics of Richardson's disease. Botox can be used to treat neck dystonia and blepharospasm, but this can worsen dysphagia. Two studies have suggested that rivastigmine may help with cognitive aspects, but the authors of both studies suggest using large sample sizes. There is some evidence that the hypnotic zolpidem may improve motor and eye function, but these studies have been small. Patients with PSP typically seek or are referred to occupational therapy, speech-language pathologists for speech changes, and physical therapy for balance and gait problems and history of frequent falls. Reports of rehabilitation in PSP are lacking in scientific evidence, and currently the majority of research on this topic consists of reports involving only a small number of patients. Reports of rehabilitation programs for patients with PSP include limb coordination activities, balancing on incline boards, gait training, strength training with progressive resistance exercises, isokinetic exercises, and neck muscle stretching. While some reports suggest that physical therapy can provide improvements in balance and gait for patients with PSP, the results cannot be generalized to all patients with PSP, as each report only involved one or two patients. However, the observations obtained from these case studies may be useful in helping to guide future research on the effectiveness of balance and gait training programs in the rehabilitation of patients with PSP. Individuals with progressive supranuclear palsy are often referred to occupational therapists to help manage their condition and to help promote independence. Treatment may include teaching them to use transportation. A walker, especially one that leans forward, is recommended because of their tendency to fall backwards frequently. Using an appropriate mobility aid can help reduce the risk of falls and make the individual safer in the community. Due to balance problems and irregular movements, individuals need to spend time learning how to get around safely in their homes and in the community. This may include getting up from a sitting position and then sitting in a chair safely. Due to the progressive nature of the disease, most individuals eventually lose the ability to walk and will eventually need to use a wheelchair for mobility. This is often followed by severe difficulty swallowing, at which point death is often only a matter of months. Although some symptoms can respond to some measures, no cure has been found for progressive supranuclear palsy. The average age of onset is 63 and the average survival time from onset is 7 years, with wide variation between patients. In these patients, pneumonia is a common cause of death. Progressive supranuclear palsy was first described by neurologists John Still, John Richardson, and Jerzy Olszowski in 1963.

Geriatric medicine

Post-chemotherapy cognitive impairment describes the cognitive impairment that can result from chemotherapy, with approximately 20% to 30% of people undergoing chemotherapy experiencing some level of cognitive impairment after treatment. This phenomenon was first discovered in an evaluation of a large group of breast cancer survivors who complained of problems with memory, fluency, and other mental abilities. Although the causes of post-chemotherapy cognitive impairment have been debated, recent studies have confirmed that post-chemotherapy cognitive impairment is a real, measurable side effect of chemotherapy and is seen in some patients. While any cancer patient may experience temporary cognitive impairment during chemotherapy, patients with PCCI continue to experience these symptoms long after chemotherapy is complete. PCCI is most often seen in patients treated for breast cancer, ovarian cancer, prostate cancer, and other reproductive cancers, as well as other cancers that require aggressive chemotherapy. The clinical significance of PCCI is significant, given the growing population of long-term cancer survivors, many of whom have been treated with aggressive doses of chemotherapy drugs, or have had chemotherapy as an adjunct to other forms of treatment. In some patients, fear of PCCI may influence treatment decisions. The magnitude of chemotherapy-related cognitive changes and their impact on activities of daily living is uncertain. The body systems most affected by chemotherapy drugs include visual and semantic memory, attention, and motor coordination. These effects may affect a chemotherapy patient’s ability to understand and make decisions about treatment, perform at school or work, and can reduce quality of life. Survivors often report difficulty multitasking, understanding what they have just read, following the development of a conversation, and recalling words. Breast cancer survivors treated with chemotherapy may have more difficulty performing tasks than survivors treated with surgery. The brains of cancer survivors treated with chemotherapy physically shrank, while the brains of people treated with surgery alone did not. Cognitive impairment after chemotherapy comes as a surprise to many cancer survivors. Often, survivors think their lives will return to normal once the cancer is gone, only to find that the lingering effects of post-chemotherapy cognitive impairment are hampering their efforts. Working, communicating with loved ones, and doing everyday tasks—all of these can be extremely difficult for a brain with a weakened mind. Although post-chemotherapy cognitive impairment seems temporary, it can be long-lasting, with some cases lasting 10 years or more.

Geriatric medicine

Cerebellar cognitive-affective syndrome, also called Schmahmann syndrome, is a condition resulting from lesions of the cerebellum. It refers to a group of disorders in the cognitive domains of executive function, spatial perception, language and other effects of cerebellar damage. Executive function disorders include problems with planning, task switching, abstract thinking, verbal fluency and working memory, and are often accompanied by perseveration, distractibility and inattention. Language problems include dysarthria, agrammatic aphasia and mild nomenclature aphasia. Spatial perception disorders result in poor visuospatial organization and poor visuospatial memory. Personality changes are manifested by emotional blunting or inappropriate behavior. These cognitive impairments result in an overall decline in intellectual function. This syndrome challenges the traditional view that the cerebellum is solely involved in the regulation of motor functions. The cerebellum is now thought to be responsible for the regulation of a wide range of motor and nonmotor functions. The non-motor disturbances seen in CCAS are also thought to result from dysfunctional connections between the cerebellum and the cerebral cortex and limbic system. CCAS has been diagnosed in both children and adults. The precise manifestations of the disease vary from individual to individual, likely reflecting the precise location of the cerebellar damage. Researchers have subsequently expanded on the affective component of the syndrome, i.e., the neuropsychiatric manifestations. They have reported numerous cases in which patients with single cerebellar damage exhibit vagueness, hyperactivity, impulsivity, disinhibition, anxiety, stereotyped and ritualistic behaviors, irrational thinking, lack of empathy, aggression, irritability, obsessive and ruminative behaviors, dysphoria and depression, tactile defensiveness and sensory overload, apathy, infantile behavior, and an inability to understand social boundaries and identify hidden motives. CCAS can be identified by a pattern of disturbances that includes executive function, visuospatial perception, language performance, and changes in emotions and personality. The low number of diagnosed cases may reflect a lack of awareness of the syndrome in the medical and scientific community. The nature and diversity of symptoms are also challenging. Levels of depression, anxiety, emotional dysregulation, and dysregulation of emotions vary from patient to patient. Symptoms of cerebellar-cognitive-affective syndrome are often quite severe after acute injury in adults and children, but tend to decrease over time. This supports the view that the cerebellum plays a role in regulating cognitive processes. There are a number of psychiatric disorders that have been linked to cerebellar dysfunction and that are similar to the symptoms of CCAS. Cerebellar lesions have been suggested to play a role in some features of psychiatric disorders, such as schizophrenia, depression, bipolar disorder, attention deficit hyperactivity disorder, developmental dyslexia, Down syndrome, and fragile X syndrome. Schmahmann's dysmetropia hypothesis has been applied to these psychiatric disorders. In schizophrenia, dysfunction of the corticocortico-thalamo-cerebellar circuit has been suggested, which in turn causes problems with emotional behaviors and emotional cognition. Postmortem studies have supported this idea, showing smaller anterior portions of the cerebellar vermis and lower Purkinje cell density in cerebellar vermis in patients with schizophrenia. There is also ample evidence to support the hypothesis that symptoms of some psychiatric disorders are due to cerebellar dysfunction. One study found that people with schizophrenia had smaller inferior cerebellar vermis and decreased asymmetry between the cerebellar hemispheres compared with controls. People with ADHD were also found to have smaller posterior inferior lobes compared with controls. Other studies have reported a correlation between cerebellar vermis size and ADHD severity. A PET study of people with dyslexia showed reduced cerebellar activity during motor tasks compared with controls. The pathogenesis of these psychiatric disorders may be better understood by studying CCAS. The symptoms of CCAS vary depending on the many possible causes, but all cases present with a cluster of central symptoms regardless of the cause. Causes of CCAS include cerebellar agenesis, dysplasia, or hypoplasia, stroke, tumors, cerebellar inflammation, trauma, and neurodegenerative diseases. CCAS can also be seen in children with prenatal, early postnatal, or developmental lesions. In these cases, the cerebellum is affected by lesions that cause cognitive and emotional deficits. The severity of CCAS varies depending on the location and extent of the lesion. In the original report describing the syndrome, patients with bilateral hemispheric infarction, pancerebellar disease, or large unilateral posterior inferior cerebellar artery infarction had greater cognitive impairment than patients with small right PICA infarction, small right anterior internal cerebellar artery infarction, or superior cerebellar artery territory. In general, patients with posterior cerebellar damage or bilateral lesions have the most severe symptoms, while patients with frontal lobe lesions have less severe symptoms. In children, patients with astrocytoma have performed better on neuropsychological tests than their peers with medulloblastoma. When diagnosing a patient with CCAS, medical professionals must remember that there are many different causes of the syndrome. Current treatments for CCAS focus on relieving symptoms. One treatment used is cognitive behavioral therapy, which involves making the patient aware of his or her cognitive problems. For example, many patients with CCAS have difficulty multitasking. With CBT, the patient must recognize this problem and focus on one task at a time. This technique is also used to relieve some motor symptoms. In a case study of a patient with CCAS resulting from a stroke, the patient showed improvements in mental function and attention with reality orientation therapy and attention training. Reality orientation therapy consists of repeated exposure to past event cues, such as images. Attention training consists of visual and auditory tasks that improve attention. The patient had difficulty applying these skills to “real life” situations. His family's help at home played a significant role in restoring his ability to perform activities of daily living. The family motivated the patient to perform basic tasks and set a regular schedule for him to follow. Transcranial magnetic stimulation has been suggested as a potential treatment option for cerebellar psychopathology. One study used TMS on the cerebellar vermis of a population of patients with schizophrenia. After stimulation, patients showed increased happiness, alertness, and energy, along with decreased sadness. Neuropsychological testing after stimulation showed improved working memory, attention, and visuospatial skills. Exercises to relieve motor symptoms are another treatment for CCAS. These exercises have also been shown to be helpful in treating cognitive symptoms. Medications used to relieve disorders caused by traumatic brain injury in adults have been suggested as a treatment option for CCAS. Bromocriptine, a direct D2 agonist, has been shown to help with executive function and spatial learning abilities. Methylphenidate, in turn, helps with attention and inhibition disorders. Neither of these medications have yet been tested in CCAS patients. It is also possible that some CCAS symptoms improve over time without formal treatment. In the original report of the syndrome, four patients with the syndrome were re-examined one to nine months after their initial neuropsychological evaluation. Three of them showed improvement in their symptoms without any formal treatment, with executive function being the only deviation from the norm. The symptoms worsened over time in the last patient. This patient experienced cerebellar atrophy and deterioration in visuospatial abilities, conceptual formation, and verbal memory. None of the above treatments has been tested in a large enough sample to determine their effect on patients with CCAS. Further research is needed on CCAS treatments.

Geriatric medicine

Cognitive vulnerability in the context of cognitive psychology is a false belief, cognitive bias, or thought pattern that predisposes an individual to psychological problems. Vulnerability is present before symptoms of a psychological disorder begin to manifest. After an individual has experienced a stressful experience, cognitive vulnerability is a maladaptive response that increases the likelihood of developing a psychological disorder. In psychopathology, there are multiple perspectives through which the origins of cognitive vulnerability are viewed, a pathway that includes cognitive schema models, hopelessness models, and attachment theory. Attention bias is one mechanism that leads to the defective cognitive bias that leads to cognitive vulnerability. The perception of a level of threat depends on the urgency or intensity of the threshold. Anxiety is not a selective orientation. Initial or "distal" causes contribute to cognitive vulnerability, ultimately leading—through immediate or proximate causes—to the emergence of individual symptoms of the disorder. Current cognitive and emotional responses call up past assumptions and assumptions leading to compensatory and protective behavior that in turn reinforces false beliefs or other cognitive exposures. Communication with caregivers defines a specific attachment process. When secure attachment is disrupted and becomes insecure, maladaptive models are initiated, increasing the risk for depression. Working models construct sensory perceptions of relationships with others. Cognitive vulnerability occurs through maladaptive cognitive processes in the formation of relationships and attachments. Predisposition contributes to vulnerability. The term predisposition refers to the tendency to develop disorders. In the relationship between predisposition and stress, latent vulnerability is activated when an individual experiences events as stressful. In the psychological context, vulnerability refers to an increased tolerance for emotional distress and some types of psychopathology. Vulnerability can be a combination of genetic and learned experiences or an interaction between them. Vulnerability leads to coping with something unpleasant and manifests as symptoms of a variety of psychological disorders. Vulnerability predisposes individuals to a disorder, but it does not cause it. Predisposition to a particular psychological disorder is based on the subjective perception of an event by the individual. Selective mood-matching cues become entrenched over long periods. Emotional stimuli that are consistent with emotional concerns create an overall effect on symptoms associated with depression. Depression is related to selective orienting. Attention is blocked to emotional cues that do not fit the internal arrangement of a schema and that could harm the individual, ultimately leading to shared anxiety. When individuals at risk for depression are asked to recall specific events, they explain the overall order of events. Associative and reflective processing mechanisms come into play when cognitive vulnerability turns into depression. The dual-processing model is applicable in personality and social psychology but does not fit clinical phenomena. Negative self-evaluation bias provides the basis for cognitive vulnerability to depression. A spiral is created that creates forms of distress. This negative associative processing maintains a state of dysphoric mood. As the dysphoric mood escalates, the cognitive resources needed to combat the distress through reflective processing are depleted. Irrelevant tasks and intrusive thoughts come to mind when the upset mood and depleted cognitive resources further contribute to the escalation of the mood. The feedback loop in the dual processing model lies between self-referential cognition and the upset. The feedback loop results in an inability to apply reflective processing to correct negative biases.

Geriatric medicine

Corticobasal degeneration is a rare neurodegenerative disease that affects both the cerebral cortex and the basal ganglia. The onset of symptoms of CBD typically occurs between the ages of 50 and 70 years, and the average duration of the disease is six years. It presents with significant motor and cognitive impairments, and is classified as one of the Parkinson-plus syndromes. The disease is difficult to diagnose, as its symptoms are similar to those of other disorders, such as Parkinson's disease, progressive supranuclear palsy, and Lewy body disease, and a definitive diagnosis is only made after neuropathological testing. Because CBD is a progressive disease, a standard set of diagnostic criteria can be used that center on the progression of the disease. These core features include problems with cortical processing, basal ganglia dysfunction, and a sudden and devastating onset of symptoms. Cognitive and psychiatric dysfunction, while present in CBD, are less common and lack sufficient evidence to be considered a common marker of the disease. Although corticobasal degeneration is characterized by a wide range of symptoms, they vary in prevalence. In a study of 147 people with CBD, all patients had at least one parkinsonian sign, 95% had two, and 93% showed some higher level of dysfunction. In a separate study of 14 patients, recorded 3 years after symptom onset, many patients had a wide range of motor symptoms. Seventy-one percent had bradykinesia, 64% had apraxia, and 43% reported limb dystonia, although 36% of cognitive impairment patients had dementia. In another study of 36 patients, half had an alien arm and 27% had gait abnormalities. Here we can see why CBD is so difficult to diagnose. While it is possible to distinguish the disease as a distinct form from other similar diseases, its different symptom clusters create a difficult diagnostic trajectory. Some of the most common symptoms in patients with CBD are specific movement disorders and problems with cortical processing. These symptoms are the first signs of the disease. Each of these associated motor complications appears asymmetrically, with symptoms not being uniform across the body. For example, a person with alien hand syndrome in one hand may not have symmetrical symptoms in the other hand. Notable movement disorders and cortical dysfunctions associated with CBD include: The presence of parkinsonism as a clinical symptom of CBD creates a number of complications that prevent the development of unique diagnostic criteria for the disease. Other diseases in which parkinsonism is a fully diagnostic feature include Parkinson's disease and progressive supranuclear palsy. Parkinsonism in CBD is largely localized to the extremities, such as the arm, and is often characterized by asymmetry. It has been suggested that it most often occurs in the nondominant hand. The most common motor dysfunctions associated with parkinsonism include rigidity, bradykinesia, and gait disturbance, with limb rigidity being the most typical parkinsonian manifestation in CBD. Although relatively subtle, rigidity sometimes leads to disturbances in gait and coherent movements. Bradykinesia in CBD is characterized by a marked slowing of specific limb movements. In a companion study, 71% of patients with CBD showed bradykinesia three years after their initial diagnosis. Alien hand syndrome has been shown to be prevalent in approximately 60% of patients diagnosed with CBD. This disorder involves a person’s failure to control their hand movements, due to the sensation that their limb is “alien.” Alien limb movements are a response to external stimuli and cannot occur in isolation or without stimulation. The alien limb is characterized by its characteristic appearance in CBD, with the patient displaying a persistent tactile stalking sign. This “mitgehen” is a relative feature of CBD, where the patient’s hand seeks to catch up with the examiner’s hand when both hands are in direct contact. A rarer form of alien hand syndrome has been observed in CBD, where the person’s hand displays an avoidance response to external stimuli. In addition, sensory impairment, manifested by numbness or tingling sensations in the extremities, may occur concomitantly with alien hand syndrome, both of which are considered evidence of cortical dysfunction. Alien hand syndrome, like most motor disorders, occurs asymmetrically in those diagnosed with corticobasal degeneration. IMA, although clearly present in CBD, is often atypical, due to the slowness of movement and rigidity associated with these disorders. IMA symptoms in CBD are characterized by the inability to repeat or mimic certain movements with or without achieving goals. This type of IMA is most prevalent in the hands and arms, while IMA in the lower extremities causes gait disturbances. CBD patients who present with IMA symptoms have difficulty initiating walking, with the feet appearing to be planted on the ground. This can lead to stumbling and difficulty maintaining balance. IMA is associated with deterioration in the premotor cortex, parietal association areas, white matter association tracts, thalamus and basal ganglia. Some CBD patients have limb movement apraxia, which manifests as dysfunction in fine movements, mostly performed by the hands and fingers.

Geriatric medicine

Semantic dementia is a progressive neurodegenerative disorder characterized by loss of semantic memory in verbal and nonverbal domains. The most common symptom is in the verbal domain and is characterized by a progressive primary aphasia. Patients with semantic dementia sometimes exhibit surface dyslexia, a relatively selective impairment in reading low-frequency words with unusual or unusual correspondences. Semantic dementia is one of three clinical syndromes associated with anterolateral temporal lobar degeneration. Semantic dementia is a clinically specific syndrome, but it is most often associated with temporal lobe atrophy and is therefore sometimes called lobar variant anterolateral temporal lobar degeneration. The condition was first described by Arnold Pick in 1904 but in modern times its features were identified by Professor Elizabeth Warrington in 1975 but it was not given the name semantic dementia until 1989. The association with temporal lobe atrophy was noted by Professor John Hodges and colleagues in 1992 in a classic description of the clinical and neuropsychological features. Semantic dementia patients often complain of word-finding difficulties. Clinical symptoms include aphasia with fluency, anomia, poor understanding of word meanings and associative visual agnosia. As the disease progresses, behavioural and personality changes similar to those seen in frontotemporal dementia are common, although cases of 'pure' semantic dementia with few late behavioural symptoms have been described. Patients perform poorly on tests of semantic knowledge. The published tests include verbal and non-verbal tasks, for example, The Warrington Concrete and Abstract Word Synonym Test, and The Pyramids and Palm Trees task. The scans will also reveal deficits in picture naming and fluency. Structural MRI shows a distinctive pattern of atrophy in the temporal lobes with greater medial than superior and greater anterior than posterior temporal lobe atrophy. This distinguishes it from Alzheimer's disease. Analyses based on the pooling of independent MRI and FDG-PET studies have confirmed these findings by identifying alterations in the medial temporal poles and amygdala as hotspots of disease - brain regions discussed in the context of cognitive, semantic information processing and social cognition. Based on these imaging modalities, semantic dementia can be separated from other subtypes of frontotemporal lobar degeneration, frontotemporal dementia and progressive aphasia. The majority of patients with SS dementia will have ubiquitin-positive, TDP-43-positive, and tau-negative inclusions, although other pathologies have been described less frequently, notably tau-positive Pick's disease and Alzheimer's disease. Of all the frontotemporal lobar degeneration syndromes, SS dementia is the least likely to occur in families and is usually sporadic. There is currently no known cure for this condition. Supportive care is essential for a highly debilitating problem.

https://ar.wikipedia.org/wiki/%D8%AE%D8%B1%D9%81_%D9%88%D8%B9%D8%A7%D8%A6%D9%8A

Geriatric medicine

Vascular dementia, also known as vascular occlusion or vascular cognitive impairment, is a dementia caused by problems with the blood vessels that supply blood to the brain, usually as a series of secondary strokes that lead to progressive cognitive decline. Vascular dementia is the second most common form of dementia after Alzheimer's disease in older adults. The term refers to a syndrome consisting of an interaction of cerebrovascular diseases and risk factors that lead to changes in the structure of the brain that lead to changes in cognition. Early screening and accurate diagnosis are very important, and vascular dementia is at least relatively preventable. Although the cerebral changes in the brain are permanent, a person with vascular dementia can show periods of stability or even mild improvement. Also, to diagnose vascular dementia, a concurrent relationship between cognitive decline and stroke must be demonstrated. Some of the main early signs of this disease are: single infarcts in specific areas of the brain, multiple brain lesions, and hemorrhagic lesions. Vascular lesions can be the result of diffuse cerebrovascular disease, such as microangiopathies, or focal lesions, but are usually the result of both. Mixed dementia is diagnosed when patients have evidence of both Alzheimer's dementia and cerebrovascular disease, either clinically or based on neuroimaging evidence of brain lesions. In practice, vascular dementia and Alzheimer's disease often coexist, especially in older patients. Cerebrovascular dementia is sometimes caused by amyloid angiopathy, which involves the accumulation of beta-amyloid plaques in the walls of cerebral arteries, leading to collapse and rupture of the vessels. Since amyloid plaques are a hallmark of Alzheimer's disease, vascular dementia may occur as a result. However, amyloid angiopathy can also occur in people who have had no previous dementia and some beta-amyloid plaques are known to be present in normal older adults. Differentiating between vascular dementia syndromes can be difficult, given the many overlaps in clinical presentation and the overlap in the underlying diseases. In particular, vascular dementia may be accompanied by Alzheimer's disease. Patients with vascular dementia develop cognitive impairment after multiple cerebrovascular events, which may be acute or subacute, such as mild cognitive impairment. Symptoms of dementia may develop gradually or abruptly after each small stroke, and some people may show improvement between strokes but show signs of deterioration after a number of silent strokes. Rapid deterioration of the condition may lead to death from stroke, heart disease, or infections. Advanced symptoms such as hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflex, loss of coordination, pseudobulbar palsy, gait disturbance, and dysphagia may be noted. Symptoms typically resemble those of other types of dementia, but primarily include cognitive decline and memory impairment severe enough to interfere with daily living activities, and may be accompanied by focal neurological signs and brain imaging findings consistent with cerebrovascular disease. Patients have irregular cognitive deficits, tend to have more free recall and fewer overlapping memories than patients with Alzheimer's disease. Patients may present with stuttering and aphasia in severe cases or in patients with infarctions in Wernicke's or Broca's areas of the brain. In microangiopathy, the frontal lobes are most often affected. Early onset lethargy is more suggestive of vascular dementia because it occurs in the later stages of Alzheimer's disease. Consequently, patients with vascular dementia tend to have poorer performance than those with Alzheimer's disease in frontal lobe functions such as verbal fluency, and they tend to show more conservative behavior, and may exhibit slower processing ability, difficulty switching between situations, and poorer summarization of ideas. The incidence is highest in the fourth to seventh decades, and 80% of affected individuals have a history of hypertension. Patients will present with a series of behavioral, motor, cognitive, and behavioral signs and symptoms. A significant proportion will present with affective symptoms, and these changes usually appear within 5–10 years. If the frontal lobes are affected, patients will become lethargic and apathetic. They may also have problems with attention, orientation, and urinary incontinence. Although atherosclerosis of the major cerebral arteries is common in vascular dementia, smaller vessels and arteries are primarily affected. Rare genetic disorders that cause vascular lesions have other patterns of presentation. As a rule, they tend to appear earlier in life and are more aggressive. In addition, infectious diseases such as syphilis can damage the arteries, cause strokes, and cause bacterial brain inflammation. Risk factors for vascular dementia include age, high blood pressure, smoking, high cholesterol, diabetes, and brain disease. Other factors include geographic location, genetic susceptibility, and previous strokes. Further strokes should be prevented with treatment, either surgically or by medication, to reduce the chance of multiple strokes. Several specific diagnostic criteria can be used to diagnose vascular dementia, including: Diagnostic and Statistical Manual of Mental Disorders criteria, International Classification of Diseases criteria, National Institute of Neurological Disorders and Stroke criteria, Alzheimer's Disease Treatment and Diagnosis Center criteria, and . Recommended tests for cognitive impairment include blood tests, chest x-rays, electrocardiograms, and some types of neuroimaging, preferably with a functional or metabolic function test rather than a CT scan or MRI. When gamma imaging and positron emission tomography of the brain are available as diagnostic tools, they can be used to confirm the diagnosis of multilesional dementia in conjunction with evaluations that include a mental status examination. In a person with pre-existing dementia, gamma imaging has the advantage of distinguishing multilesional dementia from Alzheimer's disease, compared with the use of standard mental testing and medical history. Advances have led to the proposal of new diagnostic criteria. Blood tests typically include a complete blood count, liver function tests, thyroid function tests, serum lipids, erythrocyte sedimentation rate, C-reactive protein, syphilis serology, serum calcium, fasting glucose, urea and electrolytes, vitamin B-12, and folic acid. HIV antibody testing and serology may be performed in selected patients. A gross examination of the brain may reveal significant lesions and damage to the arteries. Accumulation of various materials such as fatty cysts and blood clots is visible on microscopic waves. The white matter is most commonly affected, with marked atrophy and tissue loss, as well as arterial calcification. Microstrokes may also be present in the grey matter, sometimes in large numbers. In rare cases, infarcts in the hippocampus or thalamus are the cause of dementia. The main aim of treatment is to prevent further cerebral vascular lesions. This includes the administration of antiplatelet drugs and the control of major vascular risk factors such as high blood pressure, high cholesterol, smoking and diabetes. Some of the responsibilities of the management body in the treatment of dementia include referral to community services, adjudication and decision-making regarding legal and ethical issues, and consideration of the stress on carers. Some cholinesterase inhibitors such as galantamine have shown benefit in various randomised controlled trials. However, their use is not yet licensed. Behavioural and emotional symptoms are of particular importance in this group of patients and deserve special attention. Because these problems, if they develop, tend to be resistant to treatment with conventional psychotherapy, and in many cases lead to hospitalization and placement in long-term care. Several studies have been conducted to determine how long patients with dementia can survive. The studies have often been limited and small, leading to contradictory results on the relationship between mortality rates for a particular type of dementia and the gender of the patient. In 2015, a very large study conducted in the Netherlands found that patients’ mortality within one year after referral to the clinic was 3-4 times higher than in the general population. The mortality rate for patients hospitalized for dementia was higher than for patients hospitalized for cardiovascular disease. Patients with vascular dementia have been found to have survival rates similar to or worse than those of patients with Alzheimer’s disease. Also, a very large Swedish study in 2014 found that the disease had a worse prognosis in males and older patients. Unlike Alzheimer's disease, which only weakens the patient to the point that he succumbs to bacterial infections such as pneumonia, vascular dementia is a direct cause of death due to potentially fatal interruption of blood supply to the brain. Vascular dementia is the second most common type of dementia in the United States and Europe in the elderly, but it is more common in parts of Asia. The prevalence of the disease is 1.5% in Western countries and about 2.2% in Japan. It accounts for 50% of all dementias in Japan, 20% to 40% in Europe and 15% in Latin America. The incidence of dementia is 9 times higher in patients who have had a stroke than in those who have not had one. 25% of stroke patients show the first signs of dementia within one year after their stroke. The relative risk of developing dementia is 5.5% within 4 years of a stroke. One study found that in the United States specifically, the prevalence of vascular dementia in individuals over the age of 71 was 2.43%, and another study found that the prevalence of dementia doubles with every 5.1 years of age.

Geriatric medicine

Binzwanger disease, also known as subcortical leukoencephalopathy, is a form of vascular dementia caused by damage to the white matter of the brain. The atrophy of the white matter can occur as a result of a number of conditions, such as chronic hypertension and aging. The disease is characterized by loss of memory and intellectual function, along with changes in mood, which surround what is known as the executive functions of the brain. The disease usually occurs between the ages of 54 and 66, with early symptoms being mental decline or stroke. Otto Binzwanger first described the disease in 1894, and Alois Alzheimer used the term "Binzwanger disease" in 1902. However, Olszewski is credited with much of the modern investigation of the disease, which began in 1962. Symptoms include mental decline, language impairment, transient ischemic attacks, and ataxia, a movement disorder that includes gait abnormalities, slow movements, and postural changes. These symptoms are often accompanied by multiple falls, seizures, fainting, and bladder control. Since Binswanger disease affects the speed of information processing and causes poor concentration, the ability to perform daily tasks such as managing money and preparing meals can become extremely difficult. Binswanger disease is a type of subcortical vascular dementia caused by atrophy of the brain's white matter. However, atrophy of the white matter alone is not sufficient; evidence of subcortical dementia is also necessary. Histological findings include diffuse and patchy loss of axons and myelin with widespread neuroglial damage, tissue death due to infarction or loss of blood supply to the brain, and changes in the neuroplasticity of the arteries. The pathogenesis may lie in damage from severe atherosclerosis. The onset of the disease is usually between the ages of 54 and 66 years and the first symptom is usually mental decline or stroke. The vessels supplying the subcortical white matter branch off from vessels supplying the basal ganglia, the basal capsule, and the thalamus. Chronic hypertension is known to cause changes in the smooth wall tone of blood vessels as well as changes in vessel diameter. Consequently, arteries can become permeable, leading to a breach of the blood-brain barrier. Binzwanger disease has been shown to target vessels in this subcortical region, excluding the microcirculatory vessels and capillaries, which is why Alzheimer's disease differs from Binzwanger disease. Binzwanger disease has no cure and has been shown to be the most severe form of vascular dementia, but the best way to address vascular risk factors that contribute to poor brain perfusion is to treat the underlying cause, such as chronic hypertension or diabetes. The current Alzheimer's drug donepezil has also been shown to help Binzwanger disease.

Geriatric medicine

Clouded consciousness is a term used in medicine to denote a milder and less severe impairment of the organization of the general level of consciousness than delirium. A patient with clouded consciousness experiences a subjective sense of mental clouding, described as "foggy." The term clouded consciousness has referred to the same basic pathophysiological features of delirium since it was proposed by the physician George Greiner in 1817. Historically, the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) has used the term in its definition of delirium. However, both the DSM-III and DSM-IV replaced the term "clouded consciousness" with "disorder of consciousness" to make it easier to understand, but it is essentially the same thing. Clouded consciousness on the spectrum of disorder of consciousness may be less severe than delirium, and clouded consciousness may be synonymous with borderline delirium. Borderline delirium differs from ordinary delirium in that it is generally less severe; it lacks the severity of onset and duration, and the sleep-wake cycle and motor changes are relatively stable. The clinical features of borderline delirium include inattention, thought process distortions, comprehension distortions, and language distortions, but the clinical features do not reach full-blown delirium. Patients with borderline delirium have similar survival rates in intensive care units to those with a score of 0 on the delirium scale, but they require more care than patients with a score of 0. Patients with borderline delirium have lower rates of functional independence after discharge from the hospital than the general population, but they are still more independent than patients with full-blown delirium. There is no specific, definitive standardized test in clinical practice, so diagnosis is based on the clinician's subjective impression. The DSM-IV-TR directs clinicians to record manifestations of borderline delirium under the diverse category of "cognitive disorders not elsewhere classified." The abstract, pictorial model of clouding of consciousness centers on the presence of a part of the brain that regulates the "general level" of consciousness, which is responsible for awareness of self and the environment. Various causes can disrupt this organizing part of the brain, which in turn can disrupt the "general level" of consciousness. The general activation of consciousness is referred to as “alertness” or “wakefulness.” The clouding of consciousness is not necessarily accompanied by drowsiness; the patient may be awake but his awareness and perception of reality are clouded. Ironically, sufferers respond that they are “awake, but otherwise, not.” Lipofsky points out that the decline in “alertness” as used here is not exactly synonymous with drowsiness; one is a stage on the way to coma, the other on the way to sleep, two very different things. The sufferer experiences a subjective sense of mental clouding described in the patient’s own words as a “foggy sensation.” One sufferer describes it in the following words: “I thought everything was blurry, somehow… the outlines were blurry.” Others may describe a feeling of detachment from everything. Sufferers compare their overall experience to that of a dream; as in dream consciousness, attention, orientation to time and space, perception, and awareness are disturbed. Barbara Schildkrout, a board-certified psychologist and clinical instructor in psychiatry at Harvard Medical School, described her own experience of clouding consciousness, or what she also called “mental fog,” after taking a single dose of the antihistamine chlorpheniramine for a cottonwood allergy during a cross-country road trip. Schildkrout described feeling detached from everything, as if in a “dream state,” and feeling uncertain about her judgment, that her consciousness was frozen, and that she had no sense of time. Clouding consciousness is different from depersonalization, although people with both conditions describe their experiences as similar to dreaming. Standard psychological tests provide little evidence of a relationship between clouding consciousness and depersonalization. Clouding consciousness affects performance on almost any cognitive task. “It should be obvious that cognition is not possible without a reasonable degree of alertness,” one of the authors says. Cognitive functions include perception, memory, learning, executive functions, language, reasoning abilities, voluntary motor control, attention, and mental speed. The extent of impairment and impairment is variable because inattention can impair many cognitive functions. Sufferers may complain of forgetfulness, "confusion," or "inability to think straight." Borderline delirium is distinct from mild cognitive impairment, despite similarities, the main difference being that mild cognitive impairment is a dementia-like disorder; it does not involve disturbances in alertness. The concept of "slowed cognitive activity" implies the same terms and symptoms as "mental clouding."

Geriatric medicine

Postoperative cognitive impairment is a decline in cognitive function that may persist from one to 12 months after surgery, or longer. In some cases, it may persist for several years after major surgery. Postoperative cognitive impairment is different from the onset of delirium. Its causes are under investigation and it typically occurs in older patients and those with pre-existing cognitive impairment. The causes of postoperative cognitive impairment are not understood. It does not appear to be caused by decreased oxygen or blood flow to the brain. It may be mediated by the body's inflammatory response to surgery. Postoperative cognitive impairment is common after cardiac surgery, and recent studies have now demonstrated that postoperative cognitive impairment is also present after major noncardiac surgery, although at a lower incidence. The risk of neurological dementia increases with age, and the type of surgery is also important as there is a very low incidence associated with minor surgery. Postoperative cognitive impairment is common in adult patients of all ages upon discharge from hospital after major noncardiac surgery, but only the elderly are at high risk for long-term cognitive problems. Patients with postoperative cognitive impairment are at increased risk of death in the first year after surgery. Research interest has increased since the early 2000s, especially as more elderly patients are able to undergo successful minor and major surgical procedures. Postoperative cognitive impairment has been studied by several institutions since the inception of the study, which was based in Eindhoven, the Netherlands, and Copenhagen, Denmark. This study found no causal relationship between cerebral hypoxia and hypotension and postoperative cognitive impairment. Age, duration of anesthesia, preoperative complications, and postoperative infections were found to be associated with postoperative cognitive impairment. The body's inflammatory response to surgery is likely to play an important role, at least in elderly patients. Several research initiatives in recent years have evaluated whether measures taken before, during, and after surgery can reduce the potentially harmful effects of inflammation. For example, anti-inflammatory agents can be given before surgery. During surgery, inflammation can be modulated by temperature control, the use of local rather than general anesthesia, or the use of beta-blockers. After surgery, optimal pain management and infection control are important. Several studies have shown positive effects of variable importance when a multidisciplinary, multifactorial approach is taken for the elderly patient during pre-, peri- and postoperative care.

Geriatric medicine

Dementia prevention is the attempt to avoid developing dementia. Although there is no cure for dementia, there are ways to reduce the risk of developing dementia, including lifestyle changes and medications. Efforts to prevent dementia include trying to reduce risk factors for vascular disease, including diabetes, high blood pressure, obesity, smoking, and physical inactivity. “Use it or lose it” can be applied to the brain when it comes to dementia. Being mentally active helps keep your brain in shape for years to come. Reading, playing cards, board games, and playing a musical instrument are all examples of activities that can delay the onset and slow the progression of both Alzheimer’s and vascular dementia. The risk of developing dementia decreases with the frequency of these activities, and slower cognitive decline is associated with increased mental activity early in life and later in life. In addition to leisure activities, mentally demanding tasks may help prevent dementia, especially during the 30s, 40s, and 50s. Mental activity can help prevent dementia by building up “brain reserve”: additional connections between nerve cells that are more resistant to the deterioration associated with dementia. Since vascular dementia is the second most common form of dementia, reducing the risk of cerebrovascular disease also reduces the risk of dementia. Thus, exercising, having good cholesterol in the blood, maintaining a healthy weight and ideal blood pressure reduce the risk of dementia. An active lifestyle can reduce the risk by half compared to a sedentary life. And physical activity does not only affect the blood vessels, it can stimulate new neurons in the brain, in addition to releasing a substance that protects them. A protein known as neurotrophic factor (NDF) is known to be important for the growth, plasticity and survival of nerve cells. Regular exercise can boost levels by 2-3 times. Some studies suggest that high blood pressure is a cause of Alzheimer’s disease and other dementias, because it can cause blood vessel damage through constriction. Obesity increases the risk of any type of dementia and Alzheimer’s disease in particular. The effect of alcohol on the risk of dementia is represented by a J-curve, with higher alcohol consumption increasing the risk of dementia. While low alcohol consumption may be protective. However, low alcohol consumption may not protect against vascular dementia and cognitive decline in general. Moderate alcohol consumption may reduce the risk of vascular disease and dementia because it can increase levels of HDL cholesterol in the blood, impair blood clotting factors such as fibrinogen, and may provide some protection against heart attacks and mini-strokes that can damage the brain. The effect of omega-3 fatty acids in preventing dementia is also uncertain. Vegetables and nuts may be beneficial because of their high unsaturated fat content. Non-fish meats, on the other hand, increase the risk of Alzheimer’s disease because of their high saturated fat content. However, fish consumption should be limited due to concerns about mercury poisoning, which can worsen symptoms of dementia. Niacin is also believed to be effective in preventing dementia, and research has shown that those with the highest levels of niacin in their blood are believed to be at lower risk of developing dementia or cognitive decline. Niacin is involved in DNA synthesis and repair, nerve cell signaling, improves blood circulation and reduces cholesterol levels, and it is recommended that patients take 100-300 mg of niacin daily to benefit from its positive effects on the brain. There is evidence that there is a relationship between cognitive decline and homocysteine status, as well as B vitamins status, particularly vitamins B12, B6 and folic acid B9. In particular, a deficiency of vitamin B12 and/or folic acid can cause an increase in plasma homocysteine levels, which in turn leads to toxicity of the blood vessels and nervous system. Vitamin D deficiency has also been linked to cognitive impairment and dementia. However, the effect of vitamin D on cognitive impairment remains questionable. Sleeping more than nine hours a day may be associated with an increased risk of dementia. Poor sleep may also increase the risk of dementia by increasing the deposition of amyloid beta protein. Being neurotic increases the risk of Alzheimer's disease, a type of dementia. Neuroticism is associated with increased brain atrophy and cognitive impairment later in life, while conscientiousness has a protective effect against brain atrophy. High blood pressure is a risk factor for vascular dementia. Thus, lowering blood pressure with blood pressure-lowering medications may have a positive effect in preventing dementia, as may physical activity. However, one study failed to prove a link between high blood pressure and dementia. This study, published in July 2008 in The Lancet Neurology, found that blood pressure-lowering medications did not reduce the incidence of dementia to a statistically significant degree. Analysts of this and other studies suggested that further research could prove this. Diabetes is a risk factor for vascular dementia, and can be inhibited by antihyperglycemic agents. In addition, rosiglitazone improves memory and thinking abilities in people with early-stage Alzheimer's disease. The mechanism of this effect may be that the drug reduces insulin resistance and, therefore, the need for less insulin to metabolize it. Insulin in the bloodstream is the trigger for the production of amyloid beta, so lower levels of insulin in the bloodstream will lead to lower levels of these proteins. This leads to less amyloid plaque formation, which is closely associated with Alzheimer's disease and is seen in it. Estrogen may help prevent dementia, but not in the presence of dementia, when cognitive function is already impaired. This hormone increases blood flow to the brain and is an anti-inflammatory agent, which enhances the activity of synapses in the brain. This hormone may also help increase brain activation in areas affected by dementia, most commonly the hippocampus. There is limited evidence on the effects of estrogen that does not allow for a clear recommendation for estrogen supplementation, but it suggests that the timing of estrogen supplementation may be important, with early postmenopausal use preferred over later in life. NSAIDs have the potential to overcome risk factors for Alzheimer’s and Parkinson’s disease. The length of time needed to prevent dementia varies, but based on most studies, it is usually two to ten years. One study showed that these treatments must be used in a way that is appropriate to the patient’s clinical condition, and that so-called “baby aspirin” doses are ineffective in preventing and treating dementia. Alzheimer’s disease causes inflammation of neurons, which is caused by deposits of amyloid beta peptides in neurofibrillary tangles. These deposits irritate the body by causing the release of cytokines and acute phase proteins, for example, causing inflammation. As these substances accumulate over the years, they contribute to the effects of Alzheimer’s disease. NSAIDs prevent the formation of such inflammatory substances, preventing the effects from worsening. There is no vaccine for dementia yet. The explanation is that a vaccine could activate the body’s own immune system to fight the amyloid beta plaques in Alzheimer’s disease. One hurdle to overcome is an overreaction of the immune system, which causes inflammation of the brain.

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Geriatric medicine

Delirium is a state of decreased cognitive function. It is a complex symptom in which a person becomes confused and has significant changes in behavior and mental state. Signs of delirium include problems with attention, awareness, emotions, and muscle control. Many medical conditions can cause delirium. People with delirium often recover completely after treatment for the condition that caused it. However, recovery does not always occur. Signs of delirium usually come and go during the day. There may be periods when a person shows no signs of delirium. Signs of delirium appear quickly. They may develop over hours or days. The main sign of delirium is a decreased ability to understand and perceive situations and surroundings. A person with delirium may have difficulty staying focused on a topic. Symptoms of delirium: Delirium occurs when the brain is no longer able to function properly. This may be due to infection, toxins, severe pain, or substance abuse. Doctors know of factors that can increase the risk of developing delirium. These factors are called "risk factors." Older people, those in hospitals or long-term care facilities, are at higher risk for delirium. Malnutrition is another risk factor for delirium. A person is also more likely to develop delirium if they are dehydrated. People with long-term or severe illnesses, as well as those with life-threatening illnesses, are also more likely to develop delirium. HIV and AIDS are examples of these diseases. Other risk factors include: Treatment for delirium depends on several things. To do this, the doctor must determine what caused the delirium. For example, stopping certain medications can treat the condition and make the delirium symptoms go away. It may also take a long time for the person to recover, either at home or in care facilities. Sometimes delirium does not last long, sometimes it goes away after a few hours, and sometimes it lasts longer, up to weeks, months, or years. Supportive care, such as relaxation and rest, can help with treatment and start the recovery process. Examples of permanent care include: The injured person’s healthy mental state must also be maintained, and this can be done through:

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Geriatric medicine

Donepezil, sold under the brand name Aricept among others, is a medication used to treat Alzheimer's disease. It appears to produce a small improvement in mental function and ability to function. However, use has not been shown to affect the progression of the disease. Treatment should be stopped if no benefit is seen. It is taken by mouth. Common side effects include nausea, difficulty sleeping, aggression, diarrhea, feeling tired, and muscle spasms. Serious side effects may include irregular heartbeat, urinary retention, and seizures. Donepezil acts as an acetylcholinesterase inhibitor. Donepezil was approved for medical use in the United States in 1996. In the United Kingdom, donepezil costs the NHS about £8.44 per person as of 2019. The total cost in the United States is about $1.38. In 2016, donepezil was the 98th most prescribed medication in the United States, with more than 7 million prescriptions. There is no evidence that donepezil or other similar medications alter the course or progression of Alzheimer's disease. Studies lasting 6 to 12 months have shown modest benefits in improving cognition or behavior. The National Institute for Health and Care Excellence recommends donepezil as an option for treating mild to moderate Alzheimer's disease. However, the person should be monitored frequently, and if there is no significant benefit, the drug should be discontinued. In 2006, the FDA also approved donepezil for the treatment of moderate to severe dementia in Alzheimer's disease. The most common side effects in clinical trials that led to discontinuation were nausea, diarrhea, and vomiting. Other side effects included difficulty sleeping, muscle cramps, and loss of appetite. Most side effects were seen in patients taking the 23 mg dose compared with the 10 mg or lower dose. Side effects were also less common with continued use. Donepezil should be used with caution in people with heart disease, conduction disorders, chronic obstructive pulmonary disease, asthma, cardiac arrhythmias, and sick sinus syndrome. People with peptic ulcer disease should be careful when taking NSAIDs because of the increased risk of gastrointestinal bleeding. Slow heart rate and fainting have also been seen in people with heart problems. These symptoms may occur more frequently when starting treatment or increasing the dose of donepezil. Although seizures are rare, people with a predisposition to seizures should be treated with caution. Donepezil reversibly binds and blocks the activity of cholinesterase, thereby preventing the hydrolysis of acetylcholine. This increases the concentrations of acetylcholine in acetylcholine-dependent synapses. The exact mechanism of action of donepezil in Alzheimer's disease remains incompletely understood. Alzheimer's disease is certainly caused by a significant deficiency of acetylcholine, and it is generally accepted that the symptoms of Alzheimer's disease are related to this cholinergic deficit, particularly in the cerebral cortex and other brain regions. The hippocampal formation is noted to play an important role in the control of attention, memory, and learning. The severity of acetylcholine-dependent neuronal loss in the central nervous system has been found to correlate with the severity of cognitive impairment. In addition to its role as an acetylcholine inhibitor, donepezil has been found to act as a potent σ receptor agonist, and has been shown to produce specific anticancer effects in animals primarily through this action. Research into the development of donepezil began in 1983 at Eisai, and in 1996 Eisai received FDA approval for donepezil under the brand name Aricept, which it co-marketed with Pfizer. The marketing team at Eisai was led by Hachiro Sugimoto. As of 2011, Aricept was the world's best-selling Alzheimer's disease treatment. The first generic became available in November 2010 with the USFDA approval of a formulation prepared by Ranbaxy Laboratories. In April 2011, a second generic formulation, by Wockhardt, received preliminary marketing approval from the USFDA. Donepezil has been tested in the treatment of other cognitive disorders, including dementia and vascular dementia, but has not yet been approved for these indications. Donepezil has also been found to improve sleep apnea in patients with Alzheimer's disease. It also improves movement in patients with mild Alzheimer's disease. Donepezil has also been studied in patients with mild cognitive impairment, schizophrenia, attention deficit disorder, CADASIL syndrome associated with coronary artery bypass surgery, multiple sclerosis-related disability, and Down syndrome. A three-year National Institutes of Health study in patients with mild cognitive impairment reported that donepezil was superior to placebo in delaying progression to dementia during the first 18 months of the study, but this was not sustained through 36 months. In a secondary analysis, a subgroup of individuals with the apolipoprotein E4 genotype showed sustained benefits with donepezil throughout the study. Donepezil has not been indicated for the prevention of dementia at this time.

Geriatric medicine

Rivastigmine, sold under the brand name Exelon, is a cholinergic agent used to treat mild to moderate Alzheimer's dementia or dementia due to Parkinson's disease. The drug can be taken orally or by transdermal patch; the latter form reduces the incidence of side effects, including nausea and vomiting. The drug is excreted in the urine, and appears to have relatively few drug interactions. Rivastigmine was developed by Marta Weinstock-Rosin of the Department of Pharmacology at the Hebrew University of Jerusalem and sold to Novartis by Yissum Commercial Development. It is a semisynthetic derivative of physostigmine. It has been available in capsule and liquid formulations since 1997. In 2006 it became the first product approved worldwide for the treatment of mild to moderate dementia due to Parkinson's disease; in 2007, rivastigmine transdermal patches became the first patches for the treatment of dementia. Rivastigmine tartrate is a white, lipophilic, hydrophilic crystalline powder. It is available in several forms: capsules, solutions, and skin patches. Like any cholinesterase inhibitor, it requires a gradual increase in dose over several weeks, a phase called titration. Oral doses of rivastigmine should be titrated by 3 mg/day increments every 2-4 weeks. Oral administration begins with a dose of 1.5 mg twice daily followed by an increase in dose of 1.5 mg per dose after 4 weeks. The dose should be increased to the point where side effects are tolerable. Patients should always be reminded to take it with food. For transdermal patches, the initial dose is 4.6 mg/day and is increased to 9.5 mg per day after 4 weeks if side effects are tolerable for the patient. Patients should be reminded to change the patch daily and to change the sites of application. It is preferable to apply it to the upper back and trunk. Rivastigmine is category B for pregnancy, and there is insufficient information to monitor its risks for breastfeeding. In cases of overdose, atropine is given to treat bradycardia. Dialysis is ineffective because of the drug's half-life. Rivastigmine, a cholinesterase inhibitor, inhibits both butyriccholinesterase and acetylcholinesterase, meaning it works by inhibiting the cholinesterase enzymes that break down acetylcholine transporters in the brain. The U.S. Food and Drug Administration has approved rivastigmine in its various forms to treat mild to moderate Alzheimer's dementia and mild to moderate Parkinson's-related dementia. It has been used by approximately 6 million patients. Rivastigmine has shown significant therapeutic effects on cognitive, functional, and behavioral problems associated with Alzheimer's and Parkinson's dementia. The drug has shown real, satisfactory results in patients with both types of dementia by increasing their sense of independence, and these results have been particularly evident in the most severe cases. For example, the presence of hallucinations is an indication of a strong response to the drug in patients with Alzheimer's and Parkinson's. These effects reflect inhibition of butyric cholinesterase and suggest additional benefits over selective acetylcholinesterase inhibitors. Patients with multi-infarct dementia show modest improvements in executive and behavioral functions. In patients with schizophrenia, there is no strong evidence to support their use. Rivastigmine is similar in efficacy to donepezil and tarcine. Doses less than 6 mg/day may be ineffective. The effects of these drugs in various types of dementia, including Alzheimer's dementia, are modest, and it remains unclear which enzyme inhibitor is best for Parkinson's dementia, despite studies on rivastigmine. Side effects may include nausea, vomiting, decreased appetite, and weight loss. The strong effect of rivastigmine leads to more nausea and vomiting during the titration phase of the oral medication, which encourages taking the medication with food. However, rates of nausea and vomiting are significantly reduced when rivastigmine patches are used once daily. Patients and caregivers should be aware of the signs of potential toxicity and when to call their doctor. A rash can occur with both the skin patch and the oral medication, and a doctor should be contacted immediately. The patient should monitor for severe itching, redness, swelling, or blistering at the patch site. In this case, the patient should remove the patch, rinse the affected area, and call their doctor immediately. In a large clinical trial of rivastigmine patches in 1,195 patients with Alzheimer's disease, the target dose of the patches, which is 9.5 mg/24 hours, achieved similar results to the higher dose of rivastigmine capsules, but with one-third the risk of nausea and vomiting. The drug is well absorbed when given orally, with a bioavailability of 40% at a dose of 3 mg. The pharmacokinetics follow a linear dose relationship up to 3 mg/12 h and become nonlinear at higher doses. The drug is eliminated in the urine. The concentration of the drug in plasma reaches its peak in about 1 h, and in the cerebrospinal fluid within 1.4-3.8 h. When taken as a transdermal patch, its kinetics are smoother compared to capsules with a peak concentration and less fluctuations. The patches at a dose of 9.5 mg/24 h show a comparison of the amount of exposure to the drug between them and capsules that reach the maximum permissible dose of 12 mg/24 h. This compound cannot cross the blood-brain barrier, and its plasma protein binding reaches 40%. The main route of metabolism of the drug is via the degradation of the enzyme cholinesterase, and when eliminated, it avoids the liver and therefore cytochrome p450 is not affected by its presence. It has few drug interactions because it is not exposed to cytochrome P450, which is a metabolic pathway for many other drugs.

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Geriatric medicine

Solnezumab is a monoclonal antibody being researched by Eli Lilly for use as a neuroprotective agent in patients with Alzheimer's disease. The drug initially received much media coverage as a scientific breakthrough, but failed to show promising effects in phase 3 clinical trials. Solnezumab has been used safely in combination with other licensed Alzheimer's treatments, such as acetylcholine esterase inhibitors or memantine, in clinical trials. In addition to Alzheimer's disease, there are other diseases in which beta amyloid is involved, such as Down syndrome and cerebral amyloid angiopathy, for which solenezumab may be used. However, its use in these conditions has not yet been studied. No safety concerns have been identified in any of the studies conducted. Some patients experienced reactions to the drug that resolved on their own. Other adverse reactions that have occurred, such as headache or hematoma, were not considered to be related to the treatment. Some anti-beta-amyloid antibodies have caused amyloid-related imaging abnormalities, which has not occurred with solanezumab.

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Geriatric medicine

Memantine is a medication used to treat moderate to severe Alzheimer's disease. Memantine is used as a second-line treatment after acetylcholinesterase inhibitors such as donepezil. Treatment should only be continued if positive effects are seen. The medication is taken by mouth. Common side effects include headache, constipation, drowsiness, and dizziness. Severe side effects may include blood clots, psychosis, and heart failure. It is thought to work by blocking NMDA receptors. Memantine was approved for medical use in the United States in 2003. A monthly supply in the United Kingdom costs the National Health Service about £1.60 per person as of 2019. In the United States, the wholesale cost of this amount is about US$5.50. Memantine was the 147th most prescribed drug in the United States in 2016, with more than 4 million prescriptions. Memantine is used to treat moderate to severe Alzheimer's disease, especially in people who cannot tolerate or are contraindicated in taking acetylcholinesterase inhibitors. One guideline recommends that memantine or an acetylcholinesterase inhibitor be considered in people with early to moderate dementia. Memantine has been associated with moderate improvement with little positive effect on cognition, mood, behavior, and ability to perform daily activities in moderate to severe Alzheimer's disease. There has been no evidence of improvement in mild cases of the disease. Memantine is generally well tolerated. Common adverse drug reactions include confusion, dizziness, drowsiness, headache, insomnia, agitation, and/or hallucinations. Less common side effects include vomiting, anxiety, hypertonia, cystitis, and increased libido. Like other N-methyl-D-aspartate receptor antagonists, memantine acts as a dissociative agent when used in supra-therapeutic doses. Memantine also appears to lack most of the psychoactive effects that recreational users typically seek, such as euphoria or hallucinations. Dysfunction of glutamate neurotransmission, manifested by excitotoxicity, is hypothesized to be one of the etiologies of Alzheimer's disease. Targeting the glutamic acid pathway, particularly N-methyl-D-aspartate (NMDA) receptors, offers a new approach to treatment in light of the limited efficacy of existing drugs targeting the acetylcholine system. Memantine is a low-affinity, non-competitive antagonist. With a higher affinity for Mg2+ ions, memantine is unable to suppress the influx of Ca2+ ions for a long time, especially from extrasynaptic receptors, which form the basis of excitatory activity in synapses. However, the low affinity, non-competitive nature, and rapid kinetics of memantine at the level of NMDA receptors preserve the function of the receptors in synapses, where they can still be activated by the physiological release of glutamic acid after depolarization of postsynaptic neurons. The interaction of memantine with NMDA receptors plays a key role in the symptomatic improvement produced by the drug in Alzheimer's disease. However, there is no evidence to date that memantine's ability to protect against NMDA receptor-mediated excitotoxicity has a disease-modifying effect in Alzheimer's disease, although this has been suggested in animal models. Memantine acts as a non-competitive antagonist at serotonin 5-HT3 receptors, with potency similar to that of NMDA receptors. Many serotonin antagonists act as antiemetics, but the clinical significance of this serotonergic activity in the treatment of Alzheimer's disease remains unknown. Memantine acts as a non-competitive antagonist at various acetylcholine receptors in a mode of action that may be similar to that at NMDA and serotonin receptors, but its accuracy is difficult to ascertain due to the rapid sensitivity of acetylcholine receptor responses in these experiments. It should be noted that memantine is an antagonist at the alpha7 acetylcholine receptor, which may contribute to the initial worsening of cognitive function during memantine treatment in the first treatment. The alpha7 acetylcholine receptor rapidly responds to competitive stimuli, which may explain the cognitive-enhancing effect of chronic memantine treatment. The number of nicotinic receptors in the brain has also been shown to decrease in Alzheimer's disease, even in the absence of a general decline in the number of neurons, and nicotinic receptor agonists are seen as interesting targets for anti-Alzheimer's drugs. Memantine acts as a dopamine receptor agonist with an affinity equal to or slightly higher than that of NMDA receptors. Memantine was first manufactured and patented by Eli Lilly and Company in 1968 as a diabetes drug, but was ineffective at lowering blood sugar. Memantine was later discovered to have a central nervous system effect, and was produced by Merz for the treatment of dementia in Germany; NMDA receptors were discovered after trials had already begun. The drug was first marketed as a dementia treatment in Germany in 1989 under the name Axura. Some effects on the central nervous system were discovered at Children's Hospital in Boston in the United States in 1995. In 2000, Mrs. entered into a partnership with Forest to develop an Alzheimer's drug in the United States under the name Namenda. In 2000, Mrs. entered into a partnership with Suntory for the Japanese market and with Lundbeck for other markets including Europe; the drug was originally marketed by Lundbeck under the name Ebixa. Sales of the drug reached $1.8 billion in 2014. Namenda cost $269 to $489 per month in 2012. In February 2014, with the July 2015 patent expiration of memantine, Actavis, which acquired Forest, announced that it was launching an extended-release form of memantine that could be taken once daily instead of twice daily as needed, and that it intended to stop selling the short-acting IR version in August 2014 and withdraw its marketing authorization. This was a mechanism to thwart generic competition called "product hopping." However, the supply of the XR version ran out, so Actavis extended the deadline until it was gone from the market. In September 2014, New York Attorney General Eric Schneiderman filed a lawsuit to force Actavis to continue selling the IR version on antitrust grounds. In December 2014, a New York judge granted his request and issued an injunction, preventing Actavis from withdrawing the short-acting IR version until generic versions could be launched. Actavis appealed the ruling, and in May a panel of the Second Circuit Court of Appeals upheld the appeal, and in June Actavis asked to have its case heard by a full Second Circuit panel. Actavis’s request was denied in August 2015. There is research into the use of memantine in the treatment of attention deficit hyperactivity disorder, but the evidence is not yet conclusive. There is also research into its use in the treatment of migraines.

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Geriatric medicine

Huperzine A is an alkaloid naturally occurring in pure huperzine and in varying amounts from other huperzine species. Huperzine A has been studied as a treatment for neurological conditions such as Alzheimer's disease, but a meta-analysis of these studies concluded that they were of poor methodological quality and the results should be interpreted with caution. Huperzine inhibits the breakdown of the neurotransmitter acetylcholine by the enzyme acetylcholinesterase. It is commonly sold over-the-counter as a dietary supplement and is marketed as a cognitive enhancer to improve memory and concentration. Huperzine A is extracted from the huperzine spike plant. Huperzine A is a reversible inhibitor of acetylcholinesterase and NMDA receptors that cross the blood-brain barrier. Acetylcholinesterase is the enzyme that catalyzes the breakdown of acetylcholine at synapses and some neurotransmitters that perform the same function. A complex of huperzine A with radiolabeled acetylcholine crystals has been determined at 10 . Huperzine A has been studied for several years as a potential treatment for diseases characterized by neurodegeneration, particularly Alzheimer's disease. A 2013 meta-analysis found that this compound may be effective in improving cognitive function, medical status, and activities of daily living in individuals with Alzheimer's disease. However, due to the poor size and quality of the clinical trials reviewed, it is not recommended for use as a treatment for Alzheimer's disease unless further high-quality studies confirm its beneficial effects. Huperzine A is also marketed as a dietary supplement with claims of improving memory and mental function. Huperzine A may cause mild cholinergic side effects such as nausea, vomiting, and diarrhea. It is not recommended for use during pregnancy and lactation due to a lack of adequate safety data. Huperzine A may have additive effects if taken with medications that cause bradycardia, such as beta-blockers, which may reduce heart rate. In theory, there may be potential additive cholinergic effects if taken with other acetylcholinesterase inhibitors or cholinergic agents. Two scalable and efficient macro recipes from Huberzin A.

Geriatric medicine

Every year on September 21, World Alzheimer's Day is celebrated. The story began in 1984 in Washington, DC, where a group of Alzheimer's disease experts presented a single dream and vision: "A better life for people with dementia and their families." In the 25 years since, the vision has not changed, nor has the passion wavered, as the number of members of the Alzheimer's Association has doubled from four members to more than 75 international Alzheimer's associations. Alzheimer's International believes that the key to winning the battle against dementia lies in a unique combination of global solutions and local knowledge. It works locally, empowering national associations to strengthen their roles in providing care and support to Alzheimer's patients and their families. At the global level, attention has focused on this epidemic and a campaign to change policies has been launched by governments and the World Health Organization. Around 35 million people worldwide suffer from Alzheimer's disease, which is being celebrated on World Alzheimer's Day today. This number is expected to rise to 115 million by 2050, according to estimates from the German Alzheimer's Association. There are around 1.2 million Germans suffering from some form of dementia. Since 1994, Alzheimer's organizations have been organizing activities on September 21st every year to draw attention to this widespread disease and to its sufferers, who are a burden on their families and on health systems in various countries. The slogan for World Alzheimer's Day 2011 is Faces of Dementia This article is a personal translation of part of the World Alzheimer's Day overview found in the first reference

Geriatric medicine

Memory disorders result from damage to the neuroanatomical structures responsible for storing, retaining, and retrieving memories. Memory disorders may occur gradually, including Alzheimer's disease, or immediately, including those caused by head injury. Agnosia is the inability to recognize specific elements of objects, people, or sounds. Agnosia typically results from brain damage or neurological disorders. Treatment for agnosia varies depending on the location and cause of the damage. Recovery from agnosia is possible depending on the severity of the disorder and the severity of the brain damage. Agnosia can be diagnosed in more specific types, including: associative visual agnosia, stereopsis, auditory agnosia, auditory verbal agnosia, prosopagnosia, morphognosia, topographic disorientation, visual agnosia, and others. Alzheimer's disease is a type of progressive, degenerative, and fatal brain disease that involves the loss of connections between cells in the brain. Alzheimer's is the most common type of dementia. Alzheimer's disease (AD) affects approximately 1-5% of the world's population. The prevalence of AD is disproportionate between the sexes, with women being more affected. Evidence suggests that women with AD experience a greater degree of cognitive impairment than men with AD of the same age, and show a faster rate of cognitive decline. Amnesia is an abnormal mental state that affects memory and learning among other cognitive functions in an alert, responsive patient. There are two types of amnesia: anterograde amnesia and retrograde amnesia, which show damage to the hippocampus and medial temporal lobe. Individuals with anterograde amnesia have difficulty learning and retaining information when exposed to it after brain damage. Individuals with retrograde amnesia generally experience loss of memories for specific experiences or semantic information that is independent of context. Traumatic brain injury (TBI) is often the result of brain damage caused by an external force, and may lead to the development of amnesia depending on the severity of the injury. Head injury may result in temporary or permanent amnesia. In some cases, post-traumatic amnesia develops without retrograde amnesia, but this is more common in cases of penetrating brain lesions. Damage to the anterior temporal or frontal regions can be associated with the development of heterogeneous retrograde amnesia. Studies have shown that patients who have suffered a head injury have an accelerated state of forgetting of information learned during PTA. However, forgetting rates have returned to normal after PTA. Traumatic brain injury, as mentioned above, is associated with memory impairment; however, Alzheimer’s disease also carries several risks when it comes to aging. There is evidence to support a high rate of falls among the elderly, which is one of the leading causes of death associated with TBI in individuals aged 75 years or older. Looking at the graph on the right, it can be seen that falls account for only 28% of all TBI-related causes, indicating that the elderly constitute a significant portion of this proportion. Another factor associated with TBI and aging is the relationship between the duration of the injury and the age at which it occurred. It is estimated that the need for assistance after a TBI increases with age. In some cases, individuals have reported a distorted memory of images or sounds experienced specifically shortly before the injury, during the period of regaining consciousness, or during the conscious transition period between the actual injury and the onset of the TBI. As a result, this issue has raised controversy regarding the possibility that PTSD symptoms may be a result of severe head injury and memory loss. Patients in a study by McMillan reported experiencing “windows” of emotional distress that precipitated the development of PTSD. These “windows” included recalling events close to the impact, traumatic events that occurred immediately after the injury, or “islands” of memory. Brain injuries may also develop as a result of a stroke caused by anoxia that damages the site of the cerebrovascular accident. The effects of a stroke on both the right and left hemispheres of the brain include both short-term memory disturbances and difficulty acquiring and retaining new information.

Geriatric medicine

Dissociative identity disorder, formerly known as multiple personality disorder, is a mental disorder characterized by the presence of at least two distinct and relatively permanent personalities, often accompanied by difficulties in remembering events that cannot be explained by the normal process of forgetting. These states appear alternately in a person's behavior, and vary from person to person. Dissociative identity disorder is often associated with borderline personality disorder, post-traumatic stress disorder, depression, substance abuse disorder, self-harm, and stress. Childhood trauma is thought to be the cause of dissociative identity disorder. In about 90% of cases, there was a history of childhood abuse, while other cases are linked to experiences of war or health problems during childhood. Genetic factors are also thought to play a role. An alternative hypothesis is that dissociative identity disorder is a by-product of techniques used by some therapists, particularly those who use hypnosis. Before making a diagnosis, it is important to make sure that the condition is not due to drug use, seizures, childhood fantasy play, or religious practices. Treatment includes Generally supportive care and psychological counseling. The condition often persists without treatment. It is thought to affect about 2% of the general population and 3% of those admitted to hospitals for mental health problems in Europe and North America. DID is diagnosed six times more often in females than in males. The number of cases has risen dramatically in the second half of the 20th century, along with the number of identities claimed by patients. DID is controversial in both psychiatry and the legal system. It has been used in some cases as a rarely successful model for the insanity defense. A large proportion of patients diagnosed with DID are clustered around a small number of clinicians who support the hypothesis that DID can be induced by treatment. Typical symptoms of the disorder may vary by location and according to how the disorder is portrayed by the media. Dissociation, the term under which dissociative disorders, including DID, fall, lacks a generally agreed-upon, precise, empirical definition. A wide range of diverse experiences have been described as dissociative, ranging from the ordinary failure to Attention is ultimately impaired by the breakdown of memory processes that characterize dissociative disorders. It is therefore not known whether there is a common origin for all that fall under dissociative experience, or whether the range of moderate to severe symptoms is a product of different etiologies and biological structures. Other terms used in the literature, including personality, personality state, identity, ego state, and amnesia, have also not been agreed upon. There are several competing models that incorporate some non-dissociative symptoms while excluding dissociative symptoms. The most widely used model of dissociation depicts DID as severe dissociation that is persistent at one end and flux at the other, although this model is still being tested. Some terminology has been proposed in relation to dissociation, and psychiatrist Paulette Gillig has drawn a distinction between the terms “ego state” and “alter egos,” which are commonly used in discussions of DID. Elert Nijenhuis and colleagues have proposed a distinction between personalities responsible for daily functioning and those that emerge from survival states. Van der Hart and colleagues have used the term “structural dissociation.” "Personality" to distinguish dissociations attributed to traumatic and pathological causes, which in turn are divided into primary, secondary, and tertiary. According to this hypothesis, primary dissociation involves "a normal personality part" and "an emotional personality part", secondary dissociation involves "a normal personality part" and at least two "emotional personality parts", and tertiary dissociation, unique to dissociative identity disorder, is described as having at least two "normal personality parts" and "two emotional personality parts". Others have suggested that dissociation can be separated into two distinct forms, affective detachment and fragmentation, arguing that fragmentation, in which there is a failure to control normally controllable actions and processes, is most prominent in dissociative identity disorder. Efforts have been made to distinguish normal from pathological dissociation through psychometrics, but they have not been generally accepted. DID, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, involves "the presence of two or more distinct personalities", The DSM symptoms include loss of identity in relation to multiple personalities or states, loss of sense of time, self, and level of consciousness. The clinical presentation of the disorder varies in each individual, and the level of functioning can vary from severely impaired to adequate. Symptoms of dissociative amnesia are included under the diagnosis of DID, but they can also be diagnosed separately. Individuals with DID may experience distress from both the symptoms of DID and the consequences of associated symptoms. The majority of patients with DID report sexual and/or physical abuse, although the accuracy of these reports is debated. The multiple personalities or identities may be unaware of each other, and the fragmentation of knowledge and memories results in a chaotic personal life. Individuals with DID may be reluctant to discuss symptoms because of their association with abuse, shame, and fear. Patients with DID may frequently and strongly experience time disturbances. The number of changes varies widely, with Most patients identify with fewer than ten, although over 4,500 have been reported. The average number of alterations has increased recently over the past few decades, from two or three to now an average of about 16. However, it is unclear whether this is due to a true increase in alterations, or simply that the psychiatric community has become more accepting of a high number of alterations. The primary identity, usually the patient's given name, tends to be "passive, dependent, guilty, and depressed" with other personalities or alterations that are more active, aggressive, or hostile, and usually contain more complete memories. Most identities are of ordinary people, although fantastical, mythical, famous, and animal alterations have been reported. Most cases of dissociative identity disorder have comorbid mental disorders, with an average of 8 DSM-I diagnoses and 4.5 DSM-II diagnoses. The psychiatric history frequently contains multiple previous diagnoses of various disorders and failed treatments. The most common presenting complaint of dissociative identity disorder is depression, with headaches being a neurological symptom. Common. Comorbid disorders can include substance abuse, eating disorders, anxiety, post-traumatic stress disorder, and personality disorders. A significant percentage of those diagnosed with dissociative identity disorder meet DSM axis II criteria for personality disorders such as borderline personality disorder; A significant minority met criteria for avoidant personality disorder and other personality disorders, with about half meeting criteria for borderline personality disorder specifically. On the other hand, the data support a high level of psychotic symptoms in DID, and that both individuals diagnosed with schizophrenia and those diagnosed with DID have a history of trauma. Individuals diagnosed with DID also appear to be more susceptible to hypnosis than clinical patients. The large number of symptoms displayed by individuals diagnosed with DID has led some clinicians to suggest that, rather than being a separate disorder, the diagnosis of DID is actually an indication of the severity of other disorders the patient is diagnosed with. The DSM-IV showed that self-mutilation, impulsivity, and rapid changes in interpersonal relationships "could justify a consensus diagnosis of borderline personality disorder." Stephen Leinen and colleagues have suggested that the significant overlap between BPD and DID may be a contributing factor to the development of drug-induced DID. These are suggestions of subtle changes by therapists who suggest a diagnosis of DID that provide an explanation for the behavioral instability, self-mutilation, mood swings, and unpredictable behaviors that patients experience. In 1993, a group of researchers reviewed both DID and BPD, concluding that DID was an additional manifestation of BPD, with no tests or clinical descriptions able to distinguish between the two. Their conclusions about the empirical evidence for DID were reiterated by a second group, who still believe that the diagnosis exists, but while the knowledge to date has not justified DID as a separate diagnosis, it has also not disproved its existence. Reviews of medical records and psychological tests have shown that the majority of DID patients could be diagnosed with BPD instead, although a third could not, suggesting that DID does exist but could be overdiagnosed. Between 50 and 66% of patients also meet criteria for BPD, Approximately 75% of patients with borderline personality disorder also meet criteria for dissociative identity disorder, with significant overlap between the two conditions in terms of personality traits, cognitive and daily functioning, and assessments by clinicians. Both groups also report higher rates of physical and sexual abuse than the general population. Patients with borderline personality disorder also score high on measures of schizophrenia. Even using very strict criteria, it can be difficult to distinguish between dissociative disorders and borderline personality disorder, although the presence of comorbid anxiety disorders can help. The cause of DID is unknown and widely debated, with debate occurring among proponents of different hypotheses: that DID is a reaction to trauma; that DID is caused by inappropriate psychotherapeutic techniques that cause the patient to assume the role of a patient with DID; More recent hypotheses include memory processes that allow for the possibility that trauma-induced dissociation can occur after childhood in DID, as it does in PTSD. It has been suggested that all trauma-induced and stress-related disorders could be placed into a single category that would include both DID and PTSD. Disturbed or altered sleep has also been suggested to play a role in dissociative disorders in general and DID in particular. Changes in environments also significantly affect the patient with DID. Research is needed to determine the prevalence of the disorder in those who have never been in treatment, and prevalence rates across cultures. These central issues related to the epidemiology of DID remain largely unaddressed despite decades of research. Debates about the causes of DID also extend to disagreements about how to assess and treat the disorder. People diagnosed with DID often report having been subjected to physical and sexual abuse, particularly during early or middle childhood. Others reported an early loss, serious medical illness, or other traumatic event. They also reported more historical psychological trauma than those diagnosed with any other mental illness. Severe sexual, physical, or psychological abuse in childhood has been suggested as an explanation for the development of the illness; Awareness, memories, and emotions of traumatic events and actions are erased from consciousness, and alternate personalities or subpersonalities are formed with different memories, emotions, and behavior. Dissociative identity disorder is characterized by extreme distress or attachment disorders. It can be interpreted as post-traumatic stress disorder in adults and can become dissociative identity disorder when it occurs in children, perhaps because of their greater use of fantasy as a coping mechanism. Perhaps because of developmental changes and a greater sense of coherence about their past before the age of six, experiencing trauma at its most intense can result in personality disorders and dissociative symptoms that are diverse, yet complex. A particular relationship between childhood abuse, disturbed attachments, and lack of social support is thought to be essential components of dissociative identity disorder. Others have proposed explanations that include incomplete childhood upbringing and the innate ability of children in general to dissociate memories and experiences from consciousness. The separation of early trauma from the etiology of dissociation has been explicitly rejected by those who support the early trauma model. However, a 2012 review of an article supports the hypotheses that Recent or current trauma can influence individuals' appraisals more than more recent trauma, altering past experience and resulting in dissociative states. Giesbrecht et al. have suggested that there is no real empirical evidence linking early trauma with schizophrenia, and instead suggest that problems are neuropsychological processes, such as increased fragmentation in responses to certain emotions and contexts, that explain dissociative characteristics. A middle-ground postulates that trauma, in some cases, alters neural mechanisms associated with memory. Evidence is growing that dissociative disorders are associated with a history of trauma and "specific neural mechanisms." It has also been suggested that there may be a real but more modest link between trauma and DID, with early trauma causing increased fantasy tendencies, which in turn may make individuals more sensitive to the social cognitive influences surrounding the development of DID. The suggestion that DID results from childhood trauma has increased demand for the diagnosis among health care providers, patients, and the public because it lends credence to the idea that child abuse has serious, lasting effects. There is very little empirical evidence to support the schizophrenia-related hypothesis. With trauma, there is no research showing that schizophrenia is consistently associated with long-term memory disturbances. The model of schizophrenia and dissociative disorders following widespread stress is controversial. It has been hypothesized that symptoms of DID can be created by a therapist using memory therapy techniques on suggested individuals. Referred to as the social cognitive model, it proposes that DID is caused by a person's conscious or unconscious behavior in specific ways reinforced by culturally constructed stereotypes, and the therapist inadvertently provides cues through inappropriate therapeutic techniques. This behavior is reinforced by media depictions of DID. Proponents of the social cognitive model note that bizarre dissociative symptoms are rarely present prior to intensive treatment by DID professionals who, through elicitation, talk to, and identify changes, shape, or perhaps create a diagnosis. While proponents note that DID is accompanied by real distress and grief symptoms, and can be reliably diagnosed using DSM criteria, they are skeptical of the trauma causality proposed by proponents. Characteristics of people diagnosed with DID Contributing These concerns and those regarding the validity of recovered memories of trauma. Skeptics note that a subset of clinicians are responsible for diagnosing the majority of individuals with DID. Psychologist Nicholas Spanos and others have suggested that in addition to treatment-induced conditions, DID may be the result of alternative identities, although others have disagreed, citing lack of motivation to create or maintain separate identities and alleged history of abuse. Other evidence that treatment can cause DID includes the lack of children diagnosed with DID, the dramatic rise in diagnosis rates after 1980, the absence of evidence of increased rates of child abuse, the disorder most likely to occur in individuals undergoing psychotherapy, particularly involving hypnosis, the presence of bizarre alternative identities, and an increase in the number of alternative identities over time. These diverse therapeutic and cultural causes occur in the context of pre-existing mental illness, particularly borderline personality disorder, which is a common comorbidity with DID. In addition, the manifestations of the illness can vary across cultures, Like Indian patients who switch personalities after a period of sleep, which is common in how DID is presented by the media in that country. Treatment-induced cases of DID are argued to be closely related to false memory syndrome, a concept and term coined by members of the False Memory Syndrome organization in response to memories of alleged abuse that have been exposed by a range of controversial treatments of unproven efficacy. Such memories can be used to make false claims of child sexual abuse. There is little agreement between those who see treatment as a cause and trauma as a cause. Proponents of treatment as a cause of DID suggest that the small number of physician diagnoses and a disproportionate number of cases provide evidence for their position, although it has been argued that diagnoses at higher rates in a particular country, such as the United States, may be due to greater awareness of DID. Lower rates in other countries may be due to less diagnostic recognition. However, false memory syndrome itself is not considered a valid diagnosis by mental health professionals. It has been described as a "non-psychiatric term created by A private organization whose stated goal is to support accused parents, critics argue that the concept has no empirical support, and further describe the False Memory Syndrome organization as an advocacy group that has distorted and misrepresented the research on memory. DID is rarely diagnosed in children, although the average age of onset is three years. This fact is cited as a reason to doubt the validity of DID. Proponents of both pathogenesis models believe that the discovery of DID in a child who has never undergone treatment would critically undermine the social cognitive model (SCM). Conversely, if children were found to develop DID only after undergoing treatment, it would challenge the trauma-mediated model. In 2011, approximately 250 cases of DID in children were identified, although the data do not provide clear evidence for either theory. While the children were diagnosed with DID prior to treatment, many were presented to clinicians by parents who themselves had been diagnosed with DID; Others were influenced by the appearance of DID in popular culture or by being diagnosed with mania due to hearing voices, a symptom found in DID. No studies have looked at children with DID who were not previously in treatment, but by examining the children of those previously in treatment for DID. An analysis of children's diagnoses reported in scientific publications found that 44 single-patient case studies were regularly distributed, but in articles referring to a group of patients, four studies accounted for the majority of the reports. The initial theoretical description of DID was that dissociative symptoms were ways of coping with acute stress, but this belief has been challenged by data from multiple research studies. Proponents of the trauma-origin hypothesis have stated that the high correlation of reported childhood physical and sexual abuse by adults with DID supports the association between trauma and DID. However, the association of poor treatment and DID has been questioned for several reasons. Studies reporting an association usually rely on self-report rather than Independent corroboration, and these results can be distorted by selection or conversion errors. Most studies of trauma and schizophrenia are cross-sectional rather than longitudinal, which means that researchers cannot attribute cause, and studies that avoid recall error have failed to support such a causal association. In addition, studies rarely control for the many comorbid disorders associated with DID, or family disharmony. The common association of DID with childhood abuse is relatively recent, occurring only after the publication of Sybil in 1973. The most recent example of a "multiple" is Chris Costner Sizemore, whose life was depicted in the book and film The Three Faces of Eve, which revealed no history of child abuse. DID can be diagnosed in the fourth revision of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders using the diagnostic criteria found in the section on dissociative disorders. DID is difficult to diagnose primarily because there is no universally accepted definition. The criteria require that two or more separate identities or personality states repeatedly control an adult, accompanied by loss of recollection of important information, and that no cause is alcohol, drugs, medications, or other medical conditions such as partial seizures. The diagnostic criteria for the disorder in children also specify that the symptoms should not be confused with imaginative play. Diagnosis is usually made by a clinically trained mental health professional, such as a psychiatrist. The psychologist, through clinical assessment and interviews with the patient's family and friends, and taking into account other supportive tools. Some personal assessments and interviews designed specifically for differentiation can also be used in the assessment. Since most symptoms are self-reported, and since they are intangible and unobservable, there is a degree of subjectivity in the diagnosis. Sufferers are often reluctant to seek treatment, especially since their symptoms may not be taken seriously; Dissociative disorders have thus come to be referred to as "disappearance diseases." The diagnosis has been criticized by proponents of the treatment-as-causal or social cognitive hypothesis as being culture-bound and often triggered by health care. Social cues involved in the diagnosis can play a significant role in shaping the patient's behavior and characteristics, such that symptoms in one context may be associated with DID, while in another setting or time the diagnosis may be something other than DID. Other researchers disagree, arguing that the condition's existence and inclusion in the DSM are supported by multiple lines of reliable evidence, with diagnostic criteria that allow it to be distinguished from conditions that are mistaken for such. A large proportion of cases are therefore diagnosed by specific health care providers, and those symptoms that are generated in non-clinical research subjects and given appropriate indications have been suggested as evidence that a small number of clinicians specializing in DID are responsible for the development of alters through treatment. Perhaps because of its scarcity of understanding, dissociative disorders were not initially included in the Structured Clinical Interview in the DSM. The Structured Clinical Interview for DSM-IV, designed to make psychiatric diagnoses more rigorous and reliable. Instead, soon after the publication of the Structured Clinical Interview (SCID), a free system for dissociative disorders was published. This interview takes about 30 to 90 minutes, depending on the subject's experiences. An alternative diagnostic tool, the Dissociative Disorders Interview Schedule, also exists, but the SCID-D is generally considered better. The DDIS is a highly structured interview that distinguishes between the different DSM-IV diagnoses. The DDIS can usually be completed in 30 to 45 minutes. Other questionnaires include the Dissociative Experiences Scale (DES), the Perceptual Changes Scale, the Dissociative Experiences Questionnaire, the Dissociative Experiences Questionnaire, and the Mini-SCIDD. All are related except the Mini-SCIDD, and all include comprehension, a normal part of personality that involves narrowing or widening of attention. The DES provides a quick way to screen people, so the more time-consuming structured interview can be used in groups who have achieved High scores on the DES. Depending on where the cutoffs are placed, people who would later be diagnosed may be mistakenly avoided. An early recommended cutoff was 15–20. The reliability of the DES in nonclinical samples has been questioned. People with DID are diagnosed with five to seven comorbid disorders at a rate much higher than other mental illnesses. Because of the overlapping symptoms, differential diagnoses include schizophrenia, bipolar disorder, epilepsy, borderline personality disorder, and Asperger syndrome. Delusions or auditory hallucinations can be mistaken for formal speech by other personalities. Persistence and stability of identities and behavior, amnesia, or dissociative or hypnotic measurements and reports from family members or other caregivers detailing a history of such changes can help distinguish DID from other conditions. A diagnosis of DID takes precedence over any of the other dissociative disorders. Other. Distinguishing DID from malingering is of interest when there is financial or legal gain, and factitious disorder may be considered if there is a history of seeking help and attention. Individuals who state that their symptoms are due to external spirits or entities entering their bodies are generally diagnosed with dissociative disorder not otherwise specified rather than DID because of the lack of identity or personality states. Most people who present to the emergency department and are unaware of their names are generally in a psychotic state. Auditory hallucinations are also common in DID, and complex visual hallucinations can also occur. Those with DID generally have adequate reality testing; They may have the positive Schneiderian symptoms of schizophrenia but lack the negative symptoms. They can perceive any voice they hear as coming from inside their head. In addition, individuals with psychosis are much less susceptible to hypnosis than those with DID. The difficulties in differential diagnosis are greater in children. DID must be distinguished, or identified if it is comorbid, from a variety of disorders including mood disorders, psychosis, anxiety disorders, post-traumatic stress disorder, personality disorders, perceptual disorders, neurological disorders, epilepsy, somatoform disorder, factitious disorder, malingering, other dissociative disorders, and trance states. An additional aspect of the controversy over diagnosis is that there are many forms of schizophrenia and amnesia, which can be common in both stress and nonstress states and can be attributed to less controversial diagnoses. Individuals who fake or imitate DID due to factitious disorder will typically exaggerate symptoms, lie, and blame bad behavior on the symptoms and often exhibit mild distress about their apparent diagnosis. In contrast, a true DID patient is characterized by confusion, distress, and shame about their symptoms and history. The condition can be underdiagnosed due to skepticism and lack of awareness among mental health professionals, made difficult by the lack of specific and precise criteria for diagnosing DID as well as by the lack of prevalence rates due to the failure to systematically test a representative, selective population. A specific relationship between DID and BPD has been postulated many times, with different clinicians noting significant overlap between symptoms and patient behaviors and suggesting that some cases of DID may arise "from a substrate of borderline features." Reviews of DID patients and their medical records have concluded that the majority of those diagnosed with DID may also meet criteria for either BPD or more generally for borderline personality. The DSM-5 elaborates on cultural background as an influence on some clinical presentations of DID. Many characteristics of DID can be influenced by cultural background. Individuals with this disorder may present with unexplained neurological symptoms, such as non-epileptic seizures, paralysis, or sensory loss, in cultural settings where such symptoms were common. Similarly, in settings where standardized ownership is common, divided identities may take the form of possessive spirits, gods, demons, animals, or mythical figures. Cultural exchange or prolonged contact between cultures may shape the characteristics of other identities. The possessive form of DID can be distinguished from culturally acceptable possessions in that the possessive form of DID is involuntary, distressing, uncontrollable, and often recurrent or persistent; involves conflict between the individual and the family, social, or work environment; It appears in times and places that break the norm of culture or religion. The DSM-II used the term hysterical neurosis, dissociative type. It described the potential for changes in the patient's conscious state or identity, and included symptoms of "amnesia, sleepwalking, fugues, and multiple personalities." The DSM-III combined the diagnosis with the four major dissociative disorders using the term "multiple personality disorder." The DSM-IV made more changes to DID than any other dissociative disorder, and renamed it dissociative identity disorder. The name was changed for two reasons. First, the change emphasized that the primary problem was not multiple personalities, but rather the lack of a single, unified identity and emphasized "identities as information-processing centers." Second, the term "personality" was used to refer to "distinct patterns of beliefs, feelings, moods, and behaviors of the entire individual," whereas for a patient with DID, the shifts between identities and behavior patterns are the personality. For this reason, the revised DSM-IV referred to "Distinct identities or personal states" rather than personalities. The diagnostic criteria were also changed to indicate that while the patient could name and personally make the alters, they lacked an independent objective existence. The changes also included increased amnesia as a symptom, which was not included in the DSM-III because, despite being a core symptom of the condition, patients could experience "amnesia about amnesia" and fail to report it. Amnesia was replaced when it became clear that the risk of a false negative diagnosis was low because the amnesia was core to DID. The ICD-10 placed the diagnosis in the category of "dissociative disorders", in the subcategory of "other dissociative disorders", but went on to record the condition as multiple personality disorder. The revised DSM-IV criteria for DID have been criticized for failing to capture the clinical complexity of DID, reducing the usefulness of diagnosing individuals with DID and resulting in a high rate of false negatives and a large number of diagnoses of dissociative disorder not otherwise specified (DDNOS). To exclude possession, and to include only two of the core symptoms of DID while failing to address the symptoms of hallucinations, trance-like states, somatoform, depersonalization and derealization. Arguments have been made to allow diagnosis by the presence of some, but not all, of the features of DID rather than the current focus. The two exclusive features are the two less common and observable ones. The DSM-IV-TR criteria have also been criticized for being tautological, for using undefined and imprecise language, and for using tools that give a false sense of validity and empirical certainty to the diagnosis. The DSM-5 redefined DID in 2013, summarizing changes such as: Several changes to the criteria for DID were made in the DSM-5. First, Criterion A was expanded to include the phenomenon of possession-form specifically and functional neurological symptoms to account for more diverse presentations of the disorder. Second, Criterion A now specifically states that the identity shift can be observed by others or self-reported. Third, according to Criterion B, individuals with DID may have recurrent gaps in recall of everyday events, not just traumatic experiences. Other textual changes clarify the nature and course of the identity dissociation. DID is among the most controversial of the dissociative disorders, and among the most controversial of the disorders in the DSM-IV-TR DSM-IV-TR. The initial conflict was between those who believed that DID was caused by traumatic stressors that forced the mind to split into multiple identities, each with a separate set of memories, and those who believed that DID symptoms were artificially produced by specific psychotherapeutic practices or by having patients play a role they believed was app

Geriatric medicine

Amnesia is a memory disorder that involves distorted memories of past events. It is generally considered a normal physiological phenomenon that occurs in most people occasionally. However, it becomes a pathological condition when it occurs repeatedly, and the pathological condition is usually associated with People with mood disorders such as depression or mania and those with schizophrenia, paranoia or other types of delirium. Treatment is done by identifying the cause of the illness and treating it.

Geriatric medicine

Dissociative fugue, or psychogenic fugue, formerly known as fugue state, is a rare schizophrenic disorder that causes amnesia of personal identity, including memories, personality, and other distinguishing features of the individual, but it is treatable. The condition may last days, months, or perhaps longer, and is usually accompanied by symptoms such as unplanned travel or wandering, and sometimes the creation of a new identity. According to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), this disorder is one aspect of dissociative amnesia. Memories can usually be restored as they were after recovery from the fugue state, and no further treatment is required. In addition, a fugue episode is not classified as a mental disorder if it is due to taking psychotropic drugs, exposure to physical trauma, dissociative identity disorder, flatulence, dementia, or if it is a general medical condition. A series of long-term traumatic episodes causes fugue states, which are common in victims of childhood sexual abuse who learn over time to separate the memory of the abuse. Symptoms of dissociative fugue include mild confusion, and once the person recovers from the fugue state, they may develop depression, feelings of sadness, shame, and discomfort. People with the disorder have also experienced post-fugue anger. Loss of identity may also be a symptom of the fugue state. A doctor may suspect dissociative fugue when a person appears confused about their identity, feels confused about their past, or denies in interviews their new identity or denies the existence of one or both identities. The doctor also reviews symptoms and performs a physical examination to rule out any physical disorders that could contribute to or cause amnesia. Sometimes, dissociative fugue can only be diagnosed when the person regains their previous identity before the fugue and is distressed by finding themselves in unfamiliar circumstances, and sometimes by realizing “lost time.” The diagnosis is usually made retrospectively, i.e., the doctor reviews the history and collects information that documents the patient’s condition before they traveled and left their home country and before establishing their alternative life. Functional amnesia can also be specific to a particular case, which differs from all forms and types of trauma or experiences of violence in general, in which the person suffers from severe amnesia as a result of being exposed to a specific trauma. All of the following cause specific amnesia: committing murders or committing or being exposed to a violent crime such as rape and torture, or experiencing anti-violence work or attempting suicide. Or being in car accidents or disasters, and he noted that caution should be exercised when diagnosing cases of psychogenic amnesia when there are convincing motives to pretend to have a memory deficit for legal or financial reasons, and although a small proportion of cases of psychogenic amnesia can be explained in this way, it is generally accepted that true cases are not rare, and both general amnesia and amnesia specific to a particular condition are often distinguished from organic amnesia syndrome in that the ability to store memories and new experiences in them remains the same, and usually a concerted effort is made to help the person regain his identity and history, due to the very sensitive nature of amnesia in such cases, which are sometimes dramatic as well, and sometimes this will help to resolve the matter automatically when treated with certain treatments. The cause of the fugue state is related to dissociative amnesia, which has a number of other subtypes: selective amnesia, generalized amnesia, persistent amnesia, organized amnesia, as well as the subtype "dissociative fugue". Unlike retrograde amnesia, dissociative amnesia is not due to the direct physiological - i.e., functional - effects of a substance or to a neurological or other general health condition; it is a complex neuropsychological process. The emergence of a defensive personality in a person suffering from dissociative fugue is considered by some to be a rational fear of the situation; Because this person may have recently experienced a recurrence of an event or person that was a traumatic event in their life. Accordingly, the term “fugue state” may carry a slight semantic distinction from “dissociative fugue,” as the former indicates a greater degree of “movement.” For the purposes of this article, a “fugue state” occurs during an “enactment” of a “dissociative fugue.” The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) defines “dissociative fugue” as: The Merck Manual defines “dissociative fugue” as: One or more episodes of amnesia in which a person is unable to recall some or all of his or her past, either with the loss of his or her identity or with the formation of a new identity, which occurs with sudden, unexpected travel intended to be away from home. To support this definition, dissociative amnesia is also defined as: The inability to recall important personal information, usually of a traumatic or stressful nature, for a period so long that it cannot be explained by ordinary forgetfulness. The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV-TR) states that the period of fugue may last from days to months, and recovery is usually rapid, but some cases are resistant to treatment, and the individual often experiences only one episode.

Geriatric medicine

False memory or false memory is a psychological phenomenon in which a person remembers things that did not actually happen. False memory is often considered in legal cases regarding child sexual abuse. The phenomenon was first discussed by Pierre Janet and Sigmund Freud. Much of the work in proving it has been attributed to Elizabeth Loftus, since she first published a research project on the issue in 1974. False memory syndrome is a distinct syndrome from false memory in that it affects a person's daily life. False memories do not fundamentally affect a person's life. False memory syndrome occurs because a person believes that the memory is true. However, research differs on whether false memory syndrome is a mental disorder, and it has therefore also been excluded from the Diagnostic and Statistical Manual of Mental Disorders. False memory syndrome is an important part of psychological research because of its associations with a wide range of mental illnesses such as post-traumatic stress disorder. False memory syndrome is one of the unfortunate outcomes of pseudoscience approaches to psychotherapy. The academic literature describes false memories as having the same characteristics as other memories, so that we cannot distinguish false memories from real memories that actually happened. But there is a way to check them, which is to look for supporting evidence for any memory you want to check. Some people are more likely to generate false memories than others. These are people with low IQs, children and adolescents, as well as people with mental illnesses such as schizophrenia, which make it difficult for them to engage with reality. Basically, anyone who has difficulty distinguishing reality from fantasy is more likely to generate false memories. However, in a study conducted by Julia Shaw on “non-pathological” adults, she found that there were no differences in the personality of people who did not generate false memories compared to those who did. The participants in the study were subjected to several tests on several levels, including: exposure to fantasy matters, compliance, personality, as well as tests for gender, age, and education level, and she found no differences. This does not mean that there are no weaknesses, which may exist. It is certainly possible for anyone to have false memories. The implications of false memory research for the criminal justice system are enormous. It has cast doubt on the memories of suspects, victims, witnesses, and even police officers and lawyers. Memories are now invalidating many cases. It has shown that we cannot rely on them because they are inherently unreliable. It calls into question the very basis of evidence used in criminal trials. It suggests that someone may have been convicted of a crime on the basis of evidence that requires reliance solely on memory. It also shows the weaknesses of techniques that can help generate false memories, and it forces us to rethink police practice. False memory is a psychological phenomenon where a person remembers things that did not actually happen. There are some similar false memories that are sometimes shared by multiple people. For example, a fairly common false memory is that the name of the bear's name was spelled Bernstein. Another reported example is the widespread false memory of the 1990 film Shazam starring the comedian Sinbad as a genie. These false memories may be the product of a confluence of factors, such as the performer wearing a genie costume during a 1994 television screening of Sinbad the Sailor, as well as the 1996 film Kazaam featuring a genie played by Shaquille O'Neal. A 2010 study examined people who were familiar with the clock at Bologna Centrale railway station, which was damaged in the 1980 Bologna massacre. In the study, 92% falsely remembered that the clock had been stopped since the bombing; in fact, the clock was repaired shortly after the attack but stopped again 16 years later as a symbolic celebration. In 2010, this phenomenon of collective false memory was dubbed the "Mandela Effect" by self-described paranormal consultant Fiona Broome, referring to a false memory she said was of South African leader Nelson Mandela's death in the 1980s but which she claims is shared by "probably thousands" of others. Broome has speculated about alternative facts as an explanation, but most commentators suggest that these are instead examples of false memories formed by similar factors affecting multiple people, such as social reinforcement of incorrect memories, or false news reports and misleading images influencing the formation of memories based on them.

Geriatric medicine

Repressed memories are memories that have been unconsciously blocked as a result of the memory being associated with a high level of stress or trauma. The theory posits that although the individual cannot recall the memory, they are still affected by it without being aware of it, and that these memories can later resurface in the conscious realm. The ideas about repressed memories hiding trauma from consciousness were an important part of Sigmund Freud's work in psychoanalysis. The existence of repressed memories is a highly controversial topic in psychology. Although some studies have concluded that they can occur in varying degrees, many studies doubt their existence entirely. Some psychologists support the theory of repressed memories and claim that repressed memories can be recovered through therapy, but most psychologists argue that false memories are created by a combination of actual memories and external influences. One study concluded that repressed memories were cultural symptoms due to the lack of written evidence of their existence before the 19th century, but its findings were disputed by some psychologists and a 1786 work discussing repressed memory was eventually recognized despite the fact that Others, besides their hypotheses. According to the American Psychological Association, it is not possible to distinguish between repressed memories and false memories without supporting evidence. The term repressed memory is sometimes equated with the term "dissociative amnesia," which is defined by the Diagnostic and Statistical Manual of Mental Disorders as: "The inability to recall personal information." According to the Mayo Clinic, amnesia refers to any condition in which memories stored in long-term memory are partially or completely forgotten, usually due to brain injury. According to proponents of the existence of repressed memories, such memories can be retrieved years or decades after the event on their own due to being triggered by a certain smell or taste or by a hint during psychotherapy. It was initially claimed that there was no documented literature on repressed memories or dissociative amnesia before the 1980s. The concept of repressed memory originated with Sigmund Freud in 1896 in his article "Concerning the Aetiology of Hysteria." One of the studies published in his article involved a young woman named Anna, among whom was Her many illnesses caused her to suffer from severe paralysis on the right side of her body, and Freud stated that her symptoms were related to psychological trauma. The traumatic memories had become disconnected from her conscious area and she was harming herself. Freud used hypnosis to treat Anna and she reportedly gained slight movement on her right side. Freud's theory of repressed memory was integrated into his philosophy of psychoanalysis, and repressed memory remained a controversial topic within Freud's psychoanalytic philosophy. Some research suggests that memories of child sexual abuse and other traumatic events may be forgotten. The spontaneous retrieval of traumatic memories has been demonstrated, and recovered memories of child abuse have been demonstrated. Van der Wessler's research shows that traumatic memories are initially retrieved as scattered mental traces. These traces are the emotional and sensory components of the traumatic experience. The level of emotional significance of the memory is directly related to the validity of the memory. Studies of self-reports of memory show that memories of unusually important events are consistently accurate and stable over time. Time. The effects of traumatic experiences appear to be qualitatively different from those of nontraumatic events. Traumatic memories may be encoded differently from memories of ordinary events. Another possibility is that traumatic events are pushed out of consciousness until later events trigger them as a psychological response. For example, a high percentage of female and other psychiatric patients have reported a history of childhood sexual abuse. Another clinical study found that patients who had experienced incest reported higher rates of suicide attempts, negative identity formation, and more interpersonal disturbances. There is considerable evidence that the difficulty with traumatic memories for most people is their inability to forget rather than their removal from consciousness. Retrospective studies rely critically on the ability of the mind to recall accurate memories. It has been suggested that repression may be one of the methods individuals use to deal with traumatic memories, pushing them out of consciousness to allow the child to maintain an attachment to a person on whom they depend for survival. Memories of events are a mixture of emotionally charged reality, mixed with With interpretation, and filled with fantasy and doubt about its veracity. For example, one study was conducted in which victims of a documented incident of child abuse were re-interviewed many years later, and 38% of the women denied any memory of the abuse. Arguments against the existence of “traumatic amnesia” have noted that many manipulations can be used to implant false memories. A classic experiment in memory research, conducted by Elizabeth Loftus, has become widely known as “Lost in the Mall.” In this experiment, three accounts of real childhood events written by family members were given in a shopping mall and a fourth was entirely false. A quarter of the subjects reported remembering the fictional event, giving extensive incidental details in a detailed manner. This experiment inspired many, including Porto, who was able to convince about half of his subjects that they had survived a vicious animal attack in childhood. Such experimental studies have been criticized in particular about whether the results are really relevant to traumatic memories and psychological conditions. However, these studies have raised public concern about the treatment of recovered memories due to sexual abuse. Previous. When memories are retrieved after a long period of amnesia, especially when unusual means are used to secure the memory, it is now widely agreed that the memories are likely to be false—that is, the events that occurred did not happen. Nevertheless, many therapists believe in the veracity of the recovered memories they hear from their clients. In a nonrandomized study by Loftus and Herzog of 16 physicians, 13 of them said that they always believed in their clients. The most common basis for this belief was bodily memories or the patient's symptoms. The mechanism by which these phenomena occur is poorly understood, and at this stage it is impossible to distinguish true from false memories without other corroborating evidence. True and false memories can be recovered using memory-working techniques, but there is no evidence that they can be distinguished. Some believe that memories retrieved under hypnosis are especially likely to be false. According to the Council on Scientific Affairs of the American Medical Association, memories obtained during hypnosis can include false memories, and appear to be less reliable than non-hypnotic retrieval. Neuroscientist Donald Hebb was the first to distinguish between short-term and long-term memory. According to current theories in neuroscience, things we notice are stored in short-term memory for up to a few minutes. This memory is based on the electrical activity of the neural circuits and can be easily destroyed by interruption or interference. Memories are stored for longer periods in long-term memory. The information stored in long-term memory depends on its importance. Traumatic events are likely to be important for the adaptive value they have for future avoidance behavior, and hormones released during stress play a role in determining which memories are retained. Amnesia is a partial or complete loss of memory that goes beyond mere forgetting. It is often temporary and involves only part of a person's experience. Amnesia is often caused by a brain injury such as a blow to the head, or by psychological trauma. Anterograde amnesia is a failure to remember new experiences that occurs after brain damage, and retrograde amnesia is the loss of memories of events that occurred before the trauma or injury. For a memory to become permanent, there must be a steady change in the strength of the memory. The connection between certain nerves in the brain. Anterograde amnesia can occur because this consolidation process is disrupted, and retrograde amnesia can occur either from damage to the memory storage site or from a malfunction in the mechanisms by which memories are retrieved from their stores. Specific types of amnesia are recognized, including: Childhood amnesia: This is the normal inability to remember events from the first three years of life. Sigmund Freud observed that humans not only remember everything from birth to three years of age, but also have fragmentary memories of anything that happens from three to seven years of age. There are several theories about why this happens. Some believe that the development of language is important for the effective storage of long-term memories, while others believe that early memories do not last long because the brain is still developing. Fugue: This is a rare condition caused by a stressful event. A form of amnesia associated with recovered memories is dissociative amnesia, which is caused by a psychological cause rather than direct brain damage, and is usually about traumatic or extremely stressful events. This is usually seen as a gap in recalling aspects of a person's life history but with Severe acute trauma such as during war, and there can be a sudden acute onset of symptoms. The "traitor trauma" theory suggests that in the case of child abuse dissociative amnesia is an adaptive response, and that they may need to remain unaware of the trauma, not to reduce suffering but to enhance survival. When stress interferes with memory, some memory may be retained by a system that records emotional experience but has no symbolic location in time or space. Traumatic memories are initially retrieved as scattered mental traces of the emotional and sensory elements of the traumatic experience. Psychiatrist Bessel van der Kolk has divided the effects of trauma on memory functions into four groups: Traumatic amnesia: This includes loss of memories of traumatic experiences. The younger the individual, the longer the traumatic event, and the greater the chance of amnesia. The subsequent retrieval of memories after traumatic amnesia is well documented in the literature with documented examples from natural disasters and accidents, combat soldiers, victims of kidnapping and torture in concentration camps, victims of physical and sexual abuse, and those who have committed murder. -Global amnesia: This makes it difficult for a person to create an accurate account of their current and past history. The combination of lack of autobiographical memory and persistent dissociation and emotional schemas involving victimization, helplessness, and betrayal likely makes these individuals vulnerable to constructing explanations for their trauma-related effects that may have little to do with remembering the actual facts of their lives. -Dissociative processes: This refers to memories being stored in fragments rather than as a single mass. - Sensory motor regulation of traumatic memories. The inability to integrate traumatic memories appears to be associated with post-traumatic stress disorder. When there is inappropriate retrieval between neurological situations, changes in the stress response system may occur, some of which may be irreversible and cause pathological responses that may include amnesia, learning disabilities, and other maladaptive symptoms. In an animal study, high levels of cortisol can damage the hippocampus, which may cause deficits in short-term memory. In humans, MRI studies have shown reduced hippocampal volume in veterans and adults with PTSD, and survivors of repeated childhood sexual or physical abuse. The existence of repressed memory recovery is not accepted by mainstream psychology nor clearly proven, and some experts in the field of human memory feel that there is no reliable scientific support for the concept of repressed memories. One research report suggests that a distinction should be made between spontaneously recovered memories and memories recovered during therapy. A criticism of Loktos is that recovered memories can The American Psychiatric Association's Working Group on Investigating Memories of Child Abuse has made conclusions that contradict those of other professional organizations. The Working Group made five major conclusions: 1. Controversies about adult memories should not be allowed to obscure the fact that child sexual abuse is a complex and widespread problem in America that has historically been under-recognized. 2. Most people who were sexually abused as children remember all or part of what happened to them. 3. Long-forgotten memories of abuse can be recalled. 4. It is also possible to construct false memories that are convincing for events that did not occur. 5. There are gaps in our knowledge about the processes that lead to accurate and inaccurate memories of childhood abuse. Many critics believe that memories may be false and distorted. Psychologist Elizabeth Loftus questions the concept of repressed memories and whether they can be accurate. Loftus focuses on techniques that therapists use to help patients recover their memories. These techniques include age regression, guided imagery, Body work, and hypnosis. Loftus's research suggests that repressed memories face problems such as memory alteration. Recovered memory therapy is a group of psychotherapeutic methods based on recalling previously forgotten memories of abuse. The term "recovered memory therapy" is not listed in the Diagnostic and Statistical Manual of Mental Disorders or used by mainstream formal psychotherapy. Patients who retract their claims after reporting their recovered memories may suffer from post-traumatic stress disorder due to the trauma of the false memories.

Geriatric medicine

In psychology, false memory syndrome is a condition in which an individual's identity and social relationships are affected by false memories of trauma, which are factually incorrect reassemblies that the individual strongly believes. The term was coined in part by Peter J. Fried when explaining what he called a false accusation after his daughter Jennifer Fried accused him of sexual assault, and his later work The Basis of False Memory Syndrome helped popularize the concept. The concept that individuals are capable of forming false memories and that external influences may be involved in the formation of such memories is widely accepted among scholars. However, false memory syndrome has not been classified as a psychiatric disorder in any medical manual, including the tenth revision of the International Classification of Diseases and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. False memory syndrome is likely a result of recovered memory therapy, which is also one of the terms defined by the False Memory Syndrome Foundation in the early 1990s, and refers to a group of therapeutic approaches that can induce the process of confabulation. Psychologist Elizabeth Loftus is considered the most prominent and influential figure in the development of this theory. Human memory is highly suggestive and novel, and a wide variety of frightening, embarrassing, and harmless memories can be created through a variety of techniques—including guided imagery, hypnosis, and suggestion by others. Although not all individuals exposed to these techniques have been successfully recreated, experiments suggest that they can be recreated in a significant number of people, who will actively defend the existence of these false events, even after being informed that they are false and deliberately planted. Questions about the possibility of false memories have generated a tremendous interest in the suggestibility of human memory, allowing for a dramatic increase in knowledge about how memories are encoded, stored, and retrieved, culminating in a series of groundbreaking experiments such as the Lost in the Mall experiment. In the Roediger and McDermott experiment, the researchers presented a group of subjects with a list of items to study. When asked to recall these items, subjects were more likely to recall some of the nonexistent words with linguistic relevance than the studied items, creating false memories. Despite its widespread replication, this experiment remains controversial, as it is possible that subjects tended to store the linguistically related items from the word list conceptually rather than as a language, which would explain the errors in word recall without creating false memories. Susan Clancy found that subjects who claimed to be victims of alien abduction were more likely to remember the linguistically related words than to remember the control set of words in the experiment. The Lost in the Mall experiment is a research method designed to implant a false memory of being lost in a shopping mall as a child in order to discuss the ability to create a “memory” of a nonexistent event when discussing the false event. In her initial study, Elizabeth Loftus found that 25% of subjects developed a “memory” of a previously nonexistent event. Extensions and perversions of the mall-lost technique showed that an average of one-third of study participants could be convinced that they had experienced things that were not real in their childhood, even when those things involved traumatic or impossible experiences. Experimental researchers demonstrated the ability to modify memory cells in the hippocampus of mice to create artificial false memories.

Geriatric medicine

Wernicke-Korsakoff syndrome is a co-occurrence of two brain disorders: Wernicke encephalopathy and Korsakoff syndrome. Because of the close relationship between these disorders, people with either condition are diagnosed with Wernicke-Kosakoff syndrome as a single syndrome. The primary cause of this type of brain disorder is thiamine deficiency, which in turn can cause a group of disorders including beriberi, Wernicke encephalopathy and Korsakoff psychosis, which may occur together or separately. Wernicke-Korsakoff syndrome is usually a secondary result of alcohol abuse, which in turn can cause significant changes in vision, movement disorders and memory impairment. Alcoholics are the most common people to develop Wernicke encephalopathy and Wernicke-Korsakoff syndrome, and only about 20% of these cases are diagnosed before death. Failure to diagnose and thus treat this type of condition is the main cause of death in about 20% of cases. While 75% of patients may suffer from permanent brain damage associated with this syndrome. As for those affected, 25% of them need the intervention of the concerned institutions for the long term to provide them with the necessary and effective care. This syndrome appears as a result of the presence of two disorders with the same name - Wernicke's encephalopathy and Korsakoff's psychosis. This syndrome includes two stages: an acute stage of Wernicke's encephalopathy followed by the development of a chronic stage of Korsakoff's syndrome. This type of disorder is characterized by the presence of three symptoms: These three symptoms result from a severe deficiency of an essential coenzyme in the body, which is vitamin D. The above-mentioned changes in the psychological state occur in about 82% of the general symptoms that patients suffer from as a whole, and this ranges from confusion and apathy, inability to concentrate and decreased ability to act immediately in situations that require it. The condition may end in a coma or death if these symptoms are left untreated. In about 29% of patients, eye disorders are represented by nystagmus and paralysis of the lateral rectus muscles or other muscles in the eye. While there is a smaller percentage of patients The syndrome is characterized by a marked decrease in the normal reaction time required for visual stimuli in addition to swelling of the optic disc, which may often be accompanied by retinal hemorrhage. Finally, symptoms involving unstable posture and gait may occur in about 23% of patients and are due to dysfunction of the cerebellum and vestibular system. In addition to the symptoms mentioned, the person with the syndrome suffers from a clear state of stupor, low blood pressure, high heart rate, low body temperature, seizures and progressive hearing loss. The syndrome is described as an acute onset of severe memory impairment without any obvious impairment in the person's thinking or learning abilities. The Diagnostic and Statistical Manual of Mental Disorders lists a set of criteria for diagnosing Korsakoff syndrome, which includes a set of symptoms, the most important of which are the following: In addition to the presence of one of these symptoms: In addition, the DSM-IV indicates that the daily activities and functions of the affected person will be affected by memory deficits, and that the phase in which the affected person loses memory must occur outside of times when the individual is in a state of delirium, intoxication or trying to quit The criteria used to diagnose the syndrome maintain the need for evidence that the amnesia in the sufferer is the result of alcohol use. Although alcohol is considered the main cause of Korsakoff syndrome as mentioned above, other conditions have been proven to be the cause, including: Thiamine deficiency, which is caused by malnutrition due to many conditions such as stomach cancer, anorexia nervosa and gastrectomy. Wernicke-Korsakoff syndrome has been diagnosed on a large scale. In 1947, 52 patients were diagnosed in a hospital in Singapore where the prisoners’ diets contained less than 1 mg of thiamine per day. Thus, such cases have provided an opportunity to understand the nature of the effects of this syndrome on the cognitive and perceptual abilities of the sufferer as a whole. In this particular case, the sufferer suffers from insomnia, anxiety, difficulties in concentration, loss of memory for the recent past, and a gradual decline in psychological status, including confusion, contemplation and hallucinations. In other cases, the syndrome has caused other cognitive symptoms, including: severe speech impairment, Dizziness, and a heavy head. In addition, some patients have been observed to suffer from a loss of ability to concentrate and the inability of others to attract the attention of these patients due to their distraction. In a study conducted in 2003 by Brand on the cognitive effects caused by the syndrome, researchers used a neuropsychological test battery that included tests of intelligence, data processing speed, memory, executive function, and cognitive estimation. Researchers found that patients with Wernicke-Korsakoff syndrome showed significant impairment in all aspects of the tests of this battery, but most notably on cognitive estimation tasks. This task requires subjects to estimate physical qualities such as size, weight, quantity, and time for a particular item. Patients with this syndrome performed poorly on these tasks compared to the normal group. Patients found that estimates related to time were more difficult for them than estimates related to quantity, which were easier for them to estimate. In addition, the study included a category for classifying “odd” answers, meaning any answer that was very far from the normal range of expected responses. Patients with the syndrome gave answers that could fall into this category, including answers such as 15 seconds or one hour for the estimated length of a shower, or 4 kg or 15 tons for a car. Memory loss in patients with Wernicke-Kosakoff syndrome includes both retrograde amnesia and anterograde amnesia. Retrograde amnesia is represented by the inability of patients with the syndrome to recall memories or recognize information related to recent public events, while anterograde amnesia is represented by the patient's inability to perform tasks related to the ability to encode or remember words or faces as well as semantic learning tasks. Patients with the syndrome have also shown difficulties in the ability to memorize, as evidenced by their performance deficits on the Wisconsin Card Sorting Test. Retrograde amnesia associated with Wernicke-Kosakoff syndrome can extend for a period ranging from twenty to thirty years under a chronological gradient, such that the patient can retrieve past memories better than recent memories. It has been widely agreed that the brain bodies responsible for the memory impairment associated with the syndrome are the mammillary bodies and the thalamic regions. Despite the memory deficits mentioned above, unconscious memory functions appear to be almost intact in patients with the syndrome. This has been demonstrated by psychological preparation tests. Other studies have shown deficits in recognition memory and motivational and reward retrieval in patients with Wernicke-Korsakoff syndrome. Deficits in motivational and reward functions were demonstrated by Oskar-Berman and Pulaski who presented patients with reinforcements for some stimuli but not others, and then asked patients to discriminate rewarding stimuli from non-rewarding stimuli. Patients with the syndrome showed significant deficits on this task. Researchers have also successfully demonstrated deficits in recognition memory by having patients make a yes/no decision as to whether a stimulus was familiar or novel, and patients in this study showed significant deficits in their ability to perform this task as well. Spontaneous compromises refer to incorrect memories that the patient believes to be correct, and may arise spontaneously without any provocation. Enriched distortions can occur when the patient is committed to providing a response, which may occur in test settings. Spontaneous compromises that are displayed in WKS are thought to result from a deficit in source memory, where they are unable to recall spatial and contextual information of the event, and thus may They use old or inappropriate memory traces to fill in the inaccessible information. It has also been suggested that this behavior may be due to executive dysfunction where they are unable to inhibit incorrect memories or are unable to divert their attention from the incorrect response. Wernicke-Korsakoff syndrome is commonly found in alcoholics and is caused by a deficiency of thiamine. It is generally agreed that the encephalitis in Wernicke syndrome is caused by severe thiamine deficiency. Thiamine pyrophosphate is the active metabolic form of thiamine and plays an important role as a cofactor or enzyme in glucose metabolism. The enzymes that depend primarily on pyrophosphate are found in the citric acid cycle, also known as the Krebs cycle, where they catalyze the oxidation of pyruvate, alpha-ketoglucoate, and branched-chain amino acids. Therefore, what increases glucose metabolism will certainly exacerbate clinical thiamine deficiency. As mentioned earlier, Wernicke-Korsakoff syndrome in the United States is particularly prevalent in those who are malnourished. Alcoholics, long-term IV patients without vitamin B1 supplements, patients undergoing gastric bypass surgery, or hunger strikers. In some areas, thiamine deficiency has been noted in severe malnutrition, particularly in diets high in white rice, which is a thiamine-deficient food. The neurological disease resulting from thiamine deficiency is called beriberi. In people with subclinical thiamine deficiency, a large dose of glucose can precipitate the onset of overt encephalopathy. Wernicke-Korsakoff syndrome in alcoholics is associated with atrophy/infarction of certain brain regions, especially the mammillary bodies. Other regions include the anterior region of the thalamus, the medial hypothalamus, the basal forebrain, the medial and lateral Rajesh nuclei, and the cerebellum. One isolated study has linked susceptibility to this syndrome to inherited deficiency of transketolase, an enzyme that requires thiamine as a cofactor. The fact that gastrointestinal surgery contributes to the development of Wernicke-Korsakoff syndrome was demonstrated by a study of three patients who had recently undergone gastrectomy. These patients later developed Wernicke-Korsakoff syndrome but were not alcoholics and had no history of food deprivation or malnutrition. Wernicke-Korsakoff syndrome developed within two to twenty years after surgery. There were minor dietary changes that contributed to the development of Wernicke-Korsakoff syndrome but in general the underlying cause was poor absorption of thiamine from the gastrointestinal tract. Therefore, it is important to ensure that patients who undergo gastrectomy are fully aware of proper dietary habits and to monitor the amount of thiamine they consume. In addition, early diagnosis of Wernicke-Korsakoff syndrome, if it develops, is very important. Strong evidence indicates that ethanol directly interferes with the absorption of thiamine in the gastrointestinal tract. Ethanol also disrupts the storage of thiamine in the liver and the conversion of thiamine to its active isotope. The role of alcohol consumption in the development of Wernicke-Korsakoff syndrome has been experimentally agreed upon. Wernicke-Korsakoff syndrome was demonstrated by using rats that were exposed to alcohol and reduced their thymine levels by providing them with a diet containing little thymine. In particular, scientific studies have shown that clinical symptoms of neurological problems resulting from thymine deficiency develop faster in rats that consumed alcohol and a diet deficient in thymine than in rats that did not consume alcohol. In another study, rats that were chronically and continuously fed alcohol were found to have significantly reduced thymine stores in the liver compared to rats that were given alcohol regularly and under supervision. This provides an explanation for why thymine deficiency and Wernicke-Korsakoff syndrome are higher in alcoholics who suffer from liver cirrhosis. The brain atrophy associated with Wernicke-Korsakoff syndrome occurs in the following areas: mammillary bodies, thalamus, central gray, walls of the third ventricle, floor of the fourth ventricle, cerebellum and frontal lobe. In addition to the observed destruction in these areas, there are some reports of damage to the cerebral cortex, although it has been noted that this may be due to direct toxic effects. Alcoholic thymine deficiency has been linked to the underlying cause of Wernicke-Korsakoff syndrome. The amnesia associated with this syndrome is due to atrophy of the diencephalic regions, similar to the amnesia seen in cases of midtemporal lobe injury. It has been suggested that memory impairment can occur as a result of damage to any part of the mammillary-thalamic pathway, which explains how Wernicke-Korsakoff syndrome develops in patients with damage to the thalamus or mammillary bodies. The diagnosis of Wernicke-Korsakoff syndrome is based on clinical impression and is sometimes confirmed by formal neuropsychological evaluation. The encephalopathy associated with Wernicke syndrome presents with ataxia, nystagmus, and Korsakoff psychosis with retrograde and anterograde amnesia. Often, because of the thymine deficiency and resulting cerebral edema in Korsakoff syndrome, patients have marked regression of the mammillary bodies. Thymine is an important coenzyme essential for carbohydrate metabolism and is also Regulator of the osmotic gradient. Thiamine deficiency may cause swelling of the intracellular space and local disturbance of the blood-brain membrane. The blood-brain membrane is sensitive to changes in electrolytes and pressure and cerebral edema can be toxic. This occurs in Wernicke syndrome particularly in the mammillary bodies, the midbrain, the tectum of the midbrain and the central gray. Affected patients may also have aversion to sunlight and may wish to stay indoors with the lights off. The mechanism of this degeneration is unknown, but it supports the current neurological theory that the mammillary bodies play a role in various “memory circuits” within the brain. An example of a memory circuit is the Papez circuit. Axial image shows signal in the central gray matter and the tectum of the midbrain. Axial image shows signal indicating limited diffusion in the dorsal thalamus. Axial FLAIR MRI shows signal in the dorsal thalamus, which is common in Wernicke syndrome-associated encephalopathy. This patient was nearly comatose when he was started on intravenous thiamine; he responded well but was left with some deficits associated with the syndrome. Korsakoff. The appearance of Wernicke's encephalopathy is a medical emergency, and thiamine should be started immediately if symptoms of the disease are suspected; This is because thiamine prevents the disease from developing into Wernicke-Korsakoff syndrome and reduces the severity of the disease. Treatment can alleviate the disability resulting from the disease and its symptoms, but it cannot return the patient to normal or reverse the existing deficiencies. At least 80% of patients continue to show symptoms of Wernicke-Korsakoff syndrome despite continuing treatment. Patients suffering from Wernicke encephalopathy should be given the minimum dose of thiamine hydrochloride (which is equivalent to 500 mg intravenously over 30 minutes for two to three days. If the patient does not respond, treatment should be stopped immediately. As for patients who respond to treatment, thiamine hydrochloride is continued, but with a modification in the amount and duration of the dose to 250 mg for three to five days intravenously or intramuscularly. In addition, another method used in treatment is the use of a banana bag, which is a bag containing vitamins and minerals in addition to thiamine) given intravenously. As previously explained, Korsakoff syndrome is often associated with Wernicke-Korsakoff encephalopathy unless Wernicke-Korsakoff encephalopathy is treated promptly with thiamine (this will prevent the disease from developing into Korsakoff syndrome), so the appropriate dose of thiamine must be given at the appropriate time. On the other hand, a study on Wernicke-Korsakoff syndrome showed that adherence to thiamine (this led to significant improvements in mental status after only two to three weeks of treatment, which gives hope that Wernicke-Korsakoff encephalopathy does not necessarily develop into Wernicke-Korsakoff syndrome. At the same time, in order to reduce the risk of developing Wernicke-Korsakoff syndrome, it is important to limit the consumption of alcohol and alcoholic beverages and follow a healthy diet in order to meet the body's needs for proper nutrition, which works together with thiamine (this will reduce the chance of developing Wernicke-Korsakoff syndrome). This method may also help in getting rid of alcohol addiction in people who are unable to quit alcoholism. Internationally, the prevalence of Wernicke-Korsakoff encephalopathy is relatively stable, anywhere between Zero and two percent. However, there are certain groups that have higher rates of Wernicke-Korsakoff syndrome, especially homeless people, the elderly, and mentally ill patients in institutions. In addition, studies indicate that the prevalence of Wernicke-Korsakoff syndrome is not related to the rate of alcohol consumption per capita. For example, in France, a country well known for its wine consumption and production, the prevalence of the disease was only 0.4% in 1994, while in Australia the prevalence of the disease was 2.8%. Carl Wernicke discovered Wernicke encephalopathy in 1881. During his first diagnosis of the disease, he noted the following symptoms: paralysis of eye movements, ataxia, and mental confusion. He also noted bleeding in the gray matter around the third and fourth ventricles in the cerebral aqueduct. In addition, he noted brain atrophy after dissecting a patient with the disease. On the other hand, Wernicke believed that the bleeding was caused by inflammation, so he called the disease epidural hemorrhagic myelitis. Later, he found that The cause of Wernicke's encephalopathy and Korsakoff's syndrome is the same. Sergei Korsakoff was a Russian physician after whom "Korsakoff's syndrome" was named. In the late 19th century, Korsakoff was following long-term alcoholic patients and began to notice a decline in their memory function. At the 13th International Medical Congress in Moscow in 1897, Korsakoff presented a report entitled: "A special form of mental illness with degenerative neuritis." It was after this report that the term "Korsakoff's syndrome" was coined. Although Wernicke's encephalopathy and Korsakoff's syndrome were discovered separately, they are usually referred to under the same name, Wernicke-Korsakoff syndrome, due to the fact that they are part of the same cause and because the onset of Korsakoff's syndrome usually follows Wernicke's encephalopathy if left untreated. A famous case study was written about by Oliver Sacks, in the story "The Lost Sailor," in his book "The Man Who Mistook His Wife for a Hat."

Geriatric medicine

Korsakoff syndrome is a brain disorder caused by a deficiency of thiamine in the brain. The condition is named after the Russian neurologist who discovered it, Sergei Korsakoff. There are six main symptoms of Korsakoff syndrome: As mentioned earlier, these symptoms appear as a result of a deficiency of thiamine, which leads to dysfunction of the thalamus, and in some cells in the hypothalamus. In addition, it leads to neuronal loss, such as the destruction of neurons in the central nervous system, bleeding in parts of the hypothalamus, and even dysfunction of the hypothalamic nucleus. It was previously thought that anyone with the disease would eventually need constant care. However, with appropriate treatment, there is a clear chance that the patient may remain independent and maintain a good quality of life. Treatment involves replacing or supplementing thiamine in the blood intravenously or by injection into the muscle, along with proper nutrition and fluids. However, as for the memory loss and brain dysfunction, they cannot usually be treated by supplementing with thiamine. There are some cases where improvement has begun to appear, and with appropriate treatment within two years, although progress in treatment is slow, if the treatment is not correct. These symptoms mentioned above usually appear due to vitamin deficiency due to chronic drinking of alcohol. Alcohol is usually an indicator of poor nutrition, which in addition to inflammation in the stomach tissues, leads to thiamine deficiency. In addition, there is also malnutrition, repeated intentional vomiting, intermittent eating, a result of chemotherapy, in addition to mercury poisoning. Due to thiamine deficiency, the hypothalamus begins to decay, leaving a defect in the data that is over a short period until it affects long-term memories. The best way to prevent Korsakoff's disease is to avoid thiamine deficiency, and this is seen by avoiding chronic alcohol consumption, especially in Western countries. There was a suggestion in the United States to add thiamine to alcohol, but this method did not work, and the disease continued to appear. In this case, you see that the best way is to avoid drinking. There is a famous case study written by the writer Oliver Sacks, in the story “The Lost Sailor”, in his book “The Man Who Mistook His Wife for a Hat”, and also used by the writer Mohamed Ibrahim Mahrous in his novel “The Devil’s Mirrors” where the hero was afflicted with this syndrome.

Geriatric medicine

Face forgetting is a Greek word composed of two parts "προσωπον" meaning face and "αμνησια" meaning to forget. Face forgetting is a selective neural impairment in the ability to learn new faces. There is a special neural network for processing faces as opposed to other non-face objects. It is also a deficit in the part of this neural network responsible for encoding perceptions as memories. Prosopagnosia manifests itself in patients as an inability to recognize people they have previously encountered based on their faces. In this way, prosopagnosia is easily mistaken for prosopagnosia. Prosopagnosia is defined as the inability to perceive or recognize faces and is also a deficit that occurs early in the neural network during the processing of facial stimuli. Prosopagnosia occurs when the brain attempts to encode processed facial stimuli into memory. A person with prosopagnosia cannot even recognize the faces of family members over a lifetime. People with prosopagnosia have a memory for facial stimuli they learned before the onset of their condition or for facial stimuli they have encountered repeatedly over long periods of time. Currently, there are only two cases of prosopagnosia that have been diagnosed, and this is likely due to the fact that prosopagnosia can be misdiagnosed as prosopagnosia based on symptoms. Some clinicians have even recognized the differences between deficits in face perception and facial memory encoding and have classified the deficits as subcategories of prosopagnosia. This lack of consistency within the scientific community in classifying patients with facial memory encoding deficits is one reason why the diagnosis of this condition is rare. Most of the current information about how face forgetting occurs in the brain is speculative and has not been proven due to the lack of studies on the condition. A correct diagnosis of face forgetting may occur when doctors are able to tell the difference between prosopagnosia and face forgetting. Face forgetting can be genetic or acquired as a result of accidental brain damage. The exact cause of face forgetting has not been investigated because there are only two known cases. Each group of doctors who have studied currently diagnosed face forgetting has proposed slightly different explanations for why. Dr. Tippett's group described face forgetting as a "dissociation between learning mechanisms and domain-specific representations"—in other words, a general dysfunction in the brain's ability to encode a representative face stimulus into memory. Dr. Williams's group hypothesized that face forgetting is caused by the inability of the fusiform face area to maintain a stable representation of new faces long enough to be encoded into memory. This conclusion is based in part on the patient's different responses to familiar and unfamiliar faces within the fusiform face area as seen in blood oxygenation responses recorded during functional magnetic resonance imaging tests. Visual stimuli are processed within the brain by several biological neural networks. Given the importance of the ability to recognize faces and associate information with others, humans have developed a distinct neural network for processing facial stimuli. Since the discovery of this distinct network, the anatomical structures involved have been studied in depth. Initial processing of visual stimuli occurs in the prefrontal cortex, the posterior parietal cortex, and the precuneus. The stimuli are then identified as facial processing and more precisely. The stimuli occur within the fusiform face area, the occipital lobe, and the face-selective area of the superior temporal sulcus. The fusiform face area serves low-level tasks such as distinguishing between details and similar known objects. The occipital lobe and the superior temporal sulcus serve higher-level processing tasks such as associating a person’s identity with their face and processing emotions based on the arrangement of facial features, respectively. Once facial stimuli are processed, they are encoded into memory. This involves several brain structures including the temporal lobe and the hippocampus. The storage and retrieval of these memories involves the same regions as the fusiform face area and the occipital cortex. The frontal and posterior parietal cortex performed the primary processing tasks. The following criteria are used to diagnose patients with acquired face amnesia: In acquired face amnesia, face recognition must match the timing of the lesion; that is, faces encountered before the lesion are recognized as familiar, while faces encountered after the lesion are considered unfamiliar. Face memory and recognition tests are essential to ensure an accurate diagnosis of prosopagnosia and prosopagnosia. Several face memory and recognition tests have been developed and used by researchers in the past, including the Warrington Face Recognition Memory Test, the Benton Face Recognition Test, and the Cambridge Face Recognition and Face Memory Test, which were developed to address the shortcomings of the first two tests. The Warrington Face Recognition Memory Tests contain a wealth of information about non-internal facial features. The Benton Face Recognition Test allows the test taker to rely on features that match the strategies used, such as the hairline and eyebrows, rather than recognizing the facial configuration. The Cambridge Face Recognition Test allows participants to look at a target face and then rank 6 other faces according to their similarity to the target face. People with prosopagnosia will fail this test, while people with prosopagnosia will pass it, making this test a hallmark for differentiating between the two disorders. The Cambridge Face Memory Test gives participants 20 seconds to look at a set of target faces. Participants are then shown one of the test cases from the first set of target faces, and are given a score based on how many target faces they can correctly recognize from the test cases. The test is repeated using different target faces with different levels of Gaussian noise. A person with normal face processing abilities on this test will score an average of 80%, while a person with poor face processing or face memory will score less than 50%. Face forgetting was first proposed as a distinct neurological disorder in 1996. Doctors observed a patient who appeared to have prosopagnosia after a temporal lobe injury. This initial patient was unable to recognize faces of people he encountered after the injury but had no problem recognizing faces of people he had previously known. This discrepancy led doctors to view the deficit as involving encoding facial memories rather than just perception. This was the first case of acquired face forgetting. More than a decade later, another group of scientists came across a similar patient. The group initially thought the patient had prosopagnosia based on her symptoms. However, after further investigation, they discovered that the problem was not with face recognition, because the patient had been able to pass the Cambridge Face Recognition Test but had shown an inability to remember facial stimuli based on poor scores on the Cambridge Face Memory Test. Upon this discovery, the doctors found research that had been done on the initial case of prosopagnosia and reached the same diagnosis. After this case, the criteria for diagnosing prosopagnosia were refined from a list of specific symptoms to a more formal scale that required a normal score on the Face Recognition Test and a significantly low score on the Face Memory Test. In the second case of prosopagnosia, the patient reported a lifelong deficit in the ability to remember faces. This suggests that damage to the neural network vital to face processing could be genetic or accidental brain damage. There are many implications for the field of neuroscience that the discovery of face forgetting supports. Within the biological neural network involved in processing visual stimuli is a special network for face processing. This neural network is present from birth, as evidenced by newborns who show a predisposition to follow face-like patterns. Normal infants are able to recognize familiar faces, as evidenced by the fact that infants react differently when people approach them depending on whether they are familiar or not. Based on evolutionary theory, for a unique biological neural network to arise and be inherited, some survival or fitness advantage must be present. It has been suggested that the ability to recognize faces is important for seeing another person as friend or foe. This network specializes over time to become more adept at distinguishing facial features between familiar people, ethnic groups, and age groups. This has led to a phenomenon known as the interracial effect, where people are much better at distinguishing between faces of people from the same group. Other implications of face forgetting include a division of labor within the brain. People with acquired face forgetting are able to recognize familiar faces before brain damage occurs. This implies a division of labor between primary memory encoding and information storage and also suggests that these tasks are performed in different regions within the brain. Face forgetting is characterized as a deficit in encoding facial memories, while prosopagnosia is a deficit in recognizing facial information. The fact that there are multiple divisions of labor within the neural network vital for face processing and other neural networks in general makes it difficult to distinguish between disorders such as face forgetting and face forgetting.

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Geriatric medicine

Twilight sleep or twilight state is a state of amnesia characterized by loss of pain sensation without loss of consciousness, caused by injections of morphine and hyoscine, and was used especially to relieve the pain of childbirth. In 1899, Dr. Schneiderlin recommended the use of hyoscine and morphine as an anesthesia for surgery and began to use it intermittently for this purpose. This combination has been shown to be effective in easing and facilitating childbirth, and was first proposed by Richard von Steinbeckel in 1902 and then developed by Carl Gauss in Freiburg, Germany from 1903. The method was known as the "Dämmerschlaf" or "Freiburg method". The method spread slowly to different clinics, and was experimented with with different dosages and ingredients. In 1915 the Canadian Medical Association Journal reported that "the method is really still in a state of development and improvement." In 1915, the New York Times published an article about twilight sleep and the work of Hannah Rion, or Mrs. Frank Fair Peck, who had recently written a book called The Truth About Twilight Sleep. In the article, Rion said that the consensus of 69 medical reports she had recently reviewed was that "the combination of scopolamine and morphine is not dangerous to children." It was initially seen as the dawn of a new era, which was described as "a new age for women in the entire human race." Early on, women in the United States formed the National Twilight Sleep Association, which advocated for its expanded use. Articles in The New York Times and Reader's Digest praised it, but the campaign eventually waned after one of its leaders died of childbirth hemorrhage. The drug combination did not relieve pain; it did create amnesia, for example: women who had gone through childbirth did not remember the pain. The drug remained widely used in the United States until 1960, when chemophobia grew and women began to desire natural childbirth without chemicals, which led to its abandonment.

Geriatric medicine

Henry Gustav Molaison, known by his abbreviation "HM", was an American patient who suffered from memory disorders as a result of undergoing many surgeries to treat his epilepsy. His case was studied from late 1957 until his death in 2008. His case played an important role in developing theories and facts that link brain functions and memory, and developing a mental system for behavior and habits. His case also contributed to understanding some concepts of psychology that were concerned with human behavior. He was receiving treatment at a health care center in Winder Lock, where he was examined and monitored by doctors and scientists. Henry Molaison was born on February 26, 1926, and suffered from chronic epilepsy that later led him to fall off a bicycle due to convulsions at the age of seven. He had suffered from this epilepsy for many years and the matter worsened significantly when he was sixteen. Therefore, he underwent surgery under the supervision of neurosurgeon William Beecher Scoville to treat and remove the disease. After examining the two sides of the brain during the patient's epilepsy, the doctor suggested removing parts of them. On August 25, 1953, at the age of 27, Molaison underwent surgery in which parts of his brain were removed, including the cerebral cortex, which secretes painkillers and is responsible for memory. The center responsible for memory became ineffective due to the destruction of part of it as a result of damage to part of the cerebral cortex, which are nerve cells responsible for entering and storing memories, and due to damage to the front part of the cerebral cortex. After the success of the main goals of the surgery, which was to control epilepsy, doctors confirmed that Molaison was suffering from amnesia, as he remembered most of his past, but he could not remember most current events. According to some scientists, he had lost the ability to keep up with the present, but some researchers objected to that, because Molaison could not remember any events that happened during the two years before the surgery, while he could remember events that happened to him eleven years ago, which means that he had a major memory disorder. Although he retains long-term memory, he can, for example, learn chess and play it professionally; but he cannot remember when he learned it. Molaison learned to solve puzzles and crosswords late in life, and could solve all paragraphs that contained information or events prior to 1953. He would activate his old memories with new information and games, for example, adding information about a person by comparing it with a person he could remember from his past. Henry Molaison died on December 2, 2008. Molaison's studies revolutionized the understanding of the organization of human memory. They provided extensive evidence to reject old theories, and to form new theories about human memory, particularly about the underlying neural processes and structures. His case was first published in the journal Science in 1957 by Scoville and Brenda Milner. His studies played an important role in developing theories that explain the link between brain function and memory, and in developing cognitive neuropsychology, the branch of psychology that aims to understand how brain structure and function relate to specific psychological processes. His brain is kept at the University of San Diego, where it is being studied in the histology labs and has been kept since December 4, 2009, to facilitate and contribute information and studies to researchers and scientists.

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Geriatric medicine

Tauopathy is a neurodegenerative disease characterized by the accumulation of tau protein in tangles in the human brain. These tangles result from hyperphosphorylation of a microtubule protein known as tau, which causes the protein to dissociate from microtubules and form insoluble aggregates. The mechanism of tangle formation is not yet well understood, and whether tangles are a primary cause of Alzheimer's disease or play an important role is unknown. Neurofibrillary tangles were first described by Alois Alzheimer in one of his patients with Alzheimer's disease. Tangles are considered a secondary neuropathy. AD is also classified as amyloidosis because of the presence of senile plaques. When tau becomes hyperphosphorylated, the protein dissociates from microtubules in axons. Tau then disperses and the protein begins to aggregate, eventually forming the neurofibrillary tangles seen in Alzheimer's patients. Microtubules are also disrupted when tau dissociates. The combination of neurofibrillary tangles and unstable microtubules leads to disruption of processes such as axonal transport and neuronal communication. The degree of NFT involvement in AD is determined by Braak stages. Braak stages I and II are used when NFT involvement is confined primarily to the transientis cortices of the brain, stages III and IV when there is also involvement of limbic regions such as the hippocampus, and V and VI when there is widespread involvement of the cerebral cortex. This should not be confused with the degree of involvement of the senile plaque, which progresses differently. In both Pick's disease and cortical degeneration, tau proteins are deposited as inclusion bodies within swollen or "swollen" neurons. Retrograde grain disease, another type of dementia, is characterized by an abundance of agglutinin-like grains and coiled bodies on microscopic examination of brain tissue. Some consider it a variant of Alzheimer's disease. It may coexist with other diseases such as progressive supranuclear palsy and cortical degeneration, as well as Pick's disease. Tauopathies often overlap with synucleinopathies, possibly because of the interaction between synuclein and tau proteins. Non-Alzheimer's disease synucleinopathies are sometimes grouped together as a "Pick complex" because of their association with frontotemporal dementia, or frontal lobar degeneration.

Geriatric medicine

Ideopregnancy is a neurological disorder characterized by the inability to conceptualize, plan, and execute complex sequential motor actions to use a tool or interact with various objects in daily life. Ideopregnancy is defined as the inability of an individual to plan the movements involved in interacting with an object, due to the inability to perceive the purpose of that object. The hallmarks of this disorder include a failure to understand the sequential organization of voluntary movements. The patient loses his or her knowledge or idea of what an object represents. The disorder was first described 100 years ago, when physician Arnold Beck described a patient with object apraxia. The patient made a number of mistakes, such as combing his hair with the wrong side of a comb or putting a gun in his mouth. Since then, many researchers and clinicians have encountered similar cases of this unique disorder. Ideopregnancy has been described under many names, such as apraxia of use, conceptual apraxia, tool apraxia, or tool-related semantic amnesia. The term apraxia was first coined by Steinthal in 1871, when it was used to describe disorders of motor planning rather than of visual, linguistic, or symbolic perception. Lippmann was the first to test such patients in his laboratory. These tests were known as multiple-object tasks, or MOTs. Each task required the patient to use more than one object; the researcher described the task to the patient and asked him or her to perform the task as described. Lippmann provided patients with all necessary objects, such as a candle and a matchbox, which were placed in front of the patient. He then observed the patients to see how they reacted to each object. In the matchbox case, one patient placed the entire box in front of the wick, rather than a single match. Another opened the box and pulled out a single match, but placed it on the unlit wick. Another struck the candle with the ignition surface of the matchbox. As such, Lipman was able to observe a discontinuity in the subjects’ actions with respect to everyday objects as well as the categorization of errors they made: misassignment of actions, incorrect use of objects, neglect, confusion, and sequencing errors. Although affected individuals failed to perform simple tasks using the multiple items provided, they were able to accurately identify objects involved in simple tasks. For example, they could match a given sequence of pictures with the correct category, such as the process of making coffee, buttering bread, or making tea. These patients could also successfully identify objects when the researcher verbally described the function of a tool. Another test involved matching the object with its appropriate function. Finally, the fact that patients were able to identify the actions of a particular tool across sequences of pictures provided evidence that they fully understood the use of the objects. Thus, the deficit was not that patients lacked knowledge of how to use the object; they had a full understanding of the function of each tool. Rather, the problem was due to a defect in execution, when they attempted to interact with these tools in order to carry out their functions.

Geriatric medicine

Constructional apraxia is characterized by difficulty or loss of the ability to build, assemble, or draw objects. It is a neurological disorder in which a person is unable to perform a task or movement despite understanding it, having the will to complete it, and having the physical ability to do so. Constructional apraxia may result from parietal lobe lesions following stroke or may be a sign of Alzheimer's disease. The inability to copy or draw a picture correctly is a core disability in patients with constructional apraxia. The disorder shows qualitative differences between patients with left hemisphere damage, right hemisphere damage, and Alzheimer's disease. Patients with left hemisphere damage tend to memorize elements, oversimplify the features of a drawing, and neglect details when drawing from memory. In addition, patients with left hemisphere damage are less likely to be able to arrange the parts of their drawing systematically. Patients with right hemisphere damage have difficulty correctly reproducing the spatial relationships of complex shapes. Drawing elements are often scattered, moved to different locations or directions, or are diagonal on the page. As a result, patients with right-hemisphere damage tend to produce distorted or asymmetric drawings characterized by hemispatial neglect, that is, neglect of elements on one side of the model. Patients with right-hemisphere damage were previously thought to be twice as likely to make errors on 3D construction tasks as those with left-hemisphere damage. This inaccurate finding was attributed to a selection bias, as researchers excluded people with severe left-hemisphere lesions because they had debilitating language impairment. However, studies included people with severe right-hemisphere lesions. Subsequent research has provided evidence that there is no significant difference in performance on 3D construction tasks between right-hemisphere and left-hemisphere patients. Alzheimer's patients with constructional apraxia have unique symptoms. Drawings contain reduced angles, spatial distortions, lack of perspective, and numerous simplifications, which are uncommon in patients with both left and right hemispheric damage. Developmental disturbances appear early in the disease and worsen over time; however, patients with advanced Alzheimer's disease may be able to perform some developmental tasks. Automatic drawing is affected early on, as it relies heavily on semantic memory; simplifications in drawing may therefore occur as a result of impaired access to semantic knowledge. As Alzheimer's disease progresses, the patient's ability to copy objects deteriorates and the patient is more likely to be unable to draw figures correctly due to motor loss of routine memories. In 1934, Carl Kleist characterized developmental apraxia as a disorder "of formative activities such as assembling, building, and drawing, in which the spatial form of the products is impaired, without apraxia of the individual movements." Over the following years, the definition of developmental apraxia has diversified. Some have considered it an executive processing command, while others have seen it as a visual-spatial disorder. As a result of the conflicting definitions, apraxia of construction has become an umbrella term to describe any type of constructional disorder. Contemporary researchers remain skeptical about the appropriateness of the term "apraxia" to describe this disorder.

Geriatric medicine

Apraxia of speech is an acquired disorder that causes difficulty in speaking, as a result of a defect in the transmission of commands from the brain to the muscles of the mouth. Developmental verbal dyskinesia is also known as childhood apraxia of speech. It is the inability of a child to perform the verbal movements necessary for speaking during the learning period. Although the causes of apraxia of speech and developmental verbal dyskinesia differ, they have similar characteristics and treatment. Especially when it comes to sequencing and producing sounds. The Lefelt model describes the process of speaking through three stages: conception, formulation, and articulation. According to the Lefelt model, apraxia of speech affects the articulation stage. The affected person does not actually have difficulty with language, but rather the difficulty lies in producing language in an understandable sound form. Interestingly, this difficulty is limited to vocal speech only, but body language is not affected, which confirms that the defect is in the part of the brain responsible for sending signals to the muscles of the mouth to perform a specific movement. The most obvious symptoms of this disease are the presence of errors in articulation and phonation. Some of the accompanying symptoms include effort in speaking, self-correction of errors, difficulty initiating speech, abnormal tension, and instability in pronunciation. Wirtz described five symptoms that appear in an individual with apraxia of speech. Stuttering is the process of finding the right mouth position to produce the desired sound. When the patient tries to pronounce a word, it takes longer or he pronounces it repeatedly or in a low voice. In some cases, the patient can pronounce the word easily and spontaneously, but when asked to pronounce a specific word, he makes an effort and struggles to pronounce the word. The patient is aware of his pronunciation errors and tries to correct them for himself. This is because he is able to understand speech more than he expresses it. When pronouncing the same word repeatedly with different examples, the person with apraxia of speech has some difficulty in using and maintaining the same pronunciation similar to the previous pronunciation. The person with apraxia of speech may make some mistakes on some days or may seem as if he is losing the ability to pronounce certain sounds at some times. Articulation also becomes more difficult when a word or phrase requires some organization in the way it is articulated, such that the tongue and lip movements must be in a specific order to move between sounds. For example, the word "baby" requires less organization of the mouth than the word "dog"; if "dog" is said, it requires both tongue and lip movements to articulate. Speech production becomes more difficult for people with apraxia of speech, resulting in more speech errors. Errors in completing speech gestures are likely to increase as the length of the utterance increases. Since multi-syllable words are difficult, people with apraxia of speech use simple words with a limited range of vowels and consonants. Speech-language pathologists diagnose apraxia of speech through specific tests that measure the oral mechanics of speech. The oral mechanics test includes tasks such as pursing lips, blowing, licking the lips, and lifting the tongue, and also includes an examination of the mouth. A complete examination also includes observing the patient while he or she is eating and speaking. Speech-language pathologists do not agree on a specific set of characteristics that constitute a diagnosis of apraxia of speech, so any of the characteristics from the above section can be used for diagnosis. Patients may be required to perform other daily tasks such as reading, writing, and speaking with others. In cases involving brain damage, brain MRIs can also help identify damaged areas of the brain. Differential diagnosis must be used to rule out other similar or alternative disorders. Although other disorders such as expressive apraxia, conductive apraxia, and dysarthria involve symptoms similar to apraxia of speech, the disorders must be distinguished in order to treat patients properly—while apraxia of speech involves motor organization or the processing stage of speech, aphasia disorders may involve other linguistic processes. According to Ziegler et al., this difficulty in diagnosis stems from the unknown causes and function of the disorder, making it difficult to establish specific criteria for defining apraxia of speech. However, he specifically states that orofacial apraxia, dysarthria, and aphasia are three distinct disorders that cause individuals to have symptoms that are often similar to those of a person with apraxia of speech, and that speech-language pathologists must properly rule out close associations before giving apraxia of speech as a diagnosis. In this way, apraxia of speech is a diagnosis of exclusion, generally defined when all other similar speech production disorders have been ruled out. Apraxia of speech and expressive aphasia are often confused as the same disorder because they often occur together in patients. Although both disorders come with symptoms such as difficulty producing sounds due to damage to the language parts of the brain, they are not the same. The main difference between these disorders is the ability to understand spoken language. Patients with apraxia are able to fully understand speech, whereas patients with aphasia are not always fully able to understand the speech of others. Conduction aphasia is another speech disorder that is similar, but not the same as apraxia of speech. Although patients with conduction aphasia have full understanding of speech, like those with apraxia of speech, there are differences between the two disorders. Patients with conduction aphasia are usually able to speak fluently, but they do not have the ability to repeat what they hear. Dysarthria, in turn, is another motor speech disorder characterized by difficulty articulating sounds. Difficulty in adequate articulation does not occur in the preparation of motor movements, as occurs with apraxia of speech. Rather, dysarthria is due to inability or weakness of the muscles of the mouth, face, and respiratory system. "Apraxia of speech may be caused by dysfunction of the parts of the brain that control muscle movement and speech," but the specific area of the brain in which apraxia of speech occurs is controversial. Many patients with damage to the left subcortical structures, the insula, and Broca's area have been diagnosed with apraxia of speech. It is usually caused by vascular lesions, but apraxia of speech can also arise as a result of tumors and injuries. Stroke-associated apraxia of speech is the most common form of acquired apraxia of speech, accounting for about 60% of all cases of acquired apraxia of speech reported. It is one of several possible disorders that can result from stroke, but only about 11% of stroke cases involve this disorder. Damage to the brain's nerve connections, especially the synapses, during a stroke can lead to acquired apraxia of speech. Most stroke-related apraxia of speech is mild, but in severe cases, motor function of the tongue may be lost and must be re-learned. Because most patients with this type of apraxia of speech are at least 50 years old, few recover completely to their previous level of speech production. Other brain disorders and injuries that can lead to apraxia of speech include dementia, progressive neurological disorders, and traumatic brain injury. In cases of brief apraxia of speech, the patient may recover and regain the ability to speak as before. Cases of acquired apraxia of speech require treatment, and the type of treatment varies depending on the patient's condition. Treatment usually involves seeing a speech pathologist. In severe cases of apraxia of speech, the patient may need several therapy sessions each week, and the number of sessions may decrease as the patient's condition improves. One of the basic types of treatment is repetition; the goal of this treatment is to obtain a large amount of meaningful speech or desired use of speech. There are several methods for treating apraxia of speech. The linguistic approach is a treatment method that uses sound and sequencing rules, and focuses on mouth position when forming sounds. The movement programming approach involves training the patient in the mouth movements and transitions necessary to produce sounds. Research on the treatment of apraxia has identified four main categories: articulation movement, rhythmic rate control, reorganization, and alternative and incremental communication. One study described the use of electroplatography to treat patients with severe acquired apraxia of speech. Electroplatography is a computer-based tool for assessing and treating speech problems. This program allows the patient to see the position of the mouth when speaking so that he or she can achieve the correct position. Speech problems often reappear within two years of treatment, and this study demonstrated that electroplatography therapy allows the patient to see previous mouth position problems when speaking and thus helps him or her improve them. Studies are ongoing to explore different approaches to treating apraxia of speech. Some suggestions made by ASHA include combining objective evidence for treatment, rationale, knowledge and experience of the therapist, and the needs and goals of the patient. The term apraxia was first defined by Hugo Karl Lippmann in 1908 as “the inability to perform a complex task due to weakness of the muscles”. In 1969 Frederick Darley coined the term apraxia of speech and replaced Lippmann’s definition with “the inability to perform the structure of the tongue, lips, and larynx”. Paul Burka also defined dysarthria in 1862 and renamed it aphasia, a disorder involving difficulty in articulation despite intact language skills and muscle function.

Geriatric medicine

Topographic disorientation is the loss of an individual's ability to orient themselves in their surroundings, sometimes as a result of focal brain damage. This inability results from the inability to use spatial information meaningfully or the failure to use specific cognitive strategies for orientation, such as the ability to form a mental representation of the environment, also known as a perceptual map. Topographic disorientation may occur as part of a syndrome of visuospatial cognitive dysfunction. Topographic disorientation represents the inability to find one's way through an environment as a result of cognitive dysfunction. Numerous studies have investigated topographic disorientation using case studies of a number of patients who have lost the ability to selectively find their way in a wide-ranging motor environment. Several dozen case reports of topographic disorientation have emerged over the past century. Studying these individuals helps to understand the complex, multi-component behavior of navigation. Topographic disorientation can be a lifelong disability, as it may result from a stroke, or it may occur as part of a progressive disease. Disorders that frequently accompany topographic disorientation include hemispatial neglect, total color blindness, prosopagnosia, and Alzheimer's disease. Developmental topographic disorientation refers to the loss of orientation since childhood despite the absence of brain damage, neurological disorder, or general cognitive deficit. Individuals with developmental topographic disorientation do not have the ability to generate a mental representation of the environment and therefore cannot use this information when trying to orient themselves. Developmental topographic disorientation should not be confused with the impaired sense of direction in healthy individuals; individuals with developmental topographic disorientation experience daily loss in very familiar surroundings, such as their home or neighborhood. Egocentric disorientation is characterized by the loss of the ability to represent the location of objects relative to the self. This is usually due to lesions in the posterior parietal lobe. Patients have no difficulty recognizing and naming people or objects. These patients have an inability to accurately reach visual objects or the self. In a case study by Stark and colleagues, a patient known as “JW” described an inability to accurately reach visual targets despite her intact vision. The patient had no difficulty recognizing and naming objects presented to her, but she failed to indicate the locations of specific targets via visual, auditory, or proprioceptive input. Her loss of the egocentric spatial representation system resulted in her failure to locate herself in space. The patient's turning in the wrong direction when greeted by a person not facing her was the most significant indicator of her deficit.

Geriatric medicine

Anomia is a mild, fluent form of aphasia in which the individual fails to recall words and cannot express the words they want to say. Anomia is a disorder of expressive language. The most common disorder in aphasia is anomia. Some loss of naming is present in all aphasias. People with aphasia who show anomia can sometimes describe an object in detail, using hand gestures to describe how the object is used, but they cannot find the appropriate word to name it. Anomia is a type of aphasia characterized by problems retrieving words, names, and numbers. Speech is fluent and receptive language is intact in people with anomia. Patients sometimes use verbosity to avoid a name they cannot recall or to express a word they cannot remember. Sometimes patients can retrieve a name when given cues or clues. In addition, patients can speak with correct grammar, but the main problem is finding the appropriate word to identify a person or object. Sometimes patients may know what an object does, but cannot name it. For example, if a patient is shown an orange and asked what it is called, the person may be fully aware that it can be peeled and eaten, and that these actions can be described in words or actions – yet the patient cannot recall the word “orange” as the name for the object. Sometimes, when a person with this problem is multilingual, they may become confused about their own language while trying to find the right word. There are three main types of anomia or loss of anomia: Anomia can be hereditary or result from damage to different parts of the parietal or temporal lobe of the brain as a result of an accident, stroke or brain tumor. Although the exact causes are not known, several researchers have found contributing factors to anomia. It is known that people with damage to the left hemisphere of the brain are more likely to develop anomia. Broca’s area, the brain’s speech production center, has been linked to problems with speech execution, with functional magnetic resonance imaging now commonly used to study anomia patients. Other experts believe that lesions to Wernicke's area, the speech-comprehension area of the brain, are linked to anomia because patients cannot understand the words they hear. Although many experts believe that lesions to Broca's area or Wernicke's area are the primary causes of anomia, current studies show that lesions to the left parietal lobe are the primary focus of anomia. A study was conducted using a word repetition test as well as functional magnetic resonance imaging to see the highest level of activity and the location of the lesion in brain tissue. Fredrickson and others suggested that lesions to Broca's area or Wernicke's area were not the sole source of anomia in these patients. Thus, the original model of anomia, which assumed that the lesion occurred in the surface gray matter of the brain, was shown to be incorrect, and the lesion was found to occur in the white matter deep within the brain in the left hemisphere. More specifically, the damage was to a part of a nerve pathway called the arcuate fasciculus, whose mechanism is unknown, although it is known to connect the back of the brain to the front and vice versa. New data suggest that although the main function of the arcuate fasciculus is not to connect Broca’s area and Wernicke’s area, lesions in the pathway cause speech problems because the areas of speech comprehension and speech production are connected to the pathway. Some studies have found that in right-handed people, the language center is located in the left hemisphere in 99 percent of cases, so naming aphasia occurs almost exclusively in left-handed people. In left-handed people, the language center is located in the left hemisphere in about 60 percent of cases, so naming aphasia can occur in right-handed people. The best way to determine whether naming aphasia has occurred is to use oral tests in combination with imaging. Using two tests seems to be most effective, because either test alone can give false positives. For example, the oral test is used to see if there is a speech disorder, whether the problem is in speech comprehension or speech production. Alzheimer’s patients have speech problems associated with dementia or primary progressive aphasia, which can include loss of naming. Imaging testing, often using MRI, is ideal for visualizing the lesion or monitoring brain deterioration. However, imaging alone cannot diagnose anomia because the lesions may not be deep enough to affect the white matter or the arcuate fasciculus. However, it is very difficult to associate anomia with a specific brain injury site. Therefore, a combination of speech tests and imaging has the highest sensitivity and specificity. It is important to perform a hearing test first if the patient cannot clearly hear the words or sentences required in the speech repetition test. In speech tests, the person is asked to repeat a sentence with common words. If the person cannot recognize the words but can describe them, there is a high probability that he or she has anomia. However, to be completely sure, the test is performed while the patient undergoes fMRI and the exact locations of the lesions and the areas activated by speech are identified. There are simpler and cheaper options, so speech repetition tests with lesion location are the main method for diagnosing anomia. There is no cure for anomia. However, there are some habits that can help improve word-finding skills. Although anomia patients may have difficulty retrieving many types of words such as common nouns, proper nouns, verbs, etc. Several studies have shown that word or name therapy has shown promising results in rehabilitation research. The therapy involves visual aids, such as pictures, and the patient is asked to identify the object or activity. However, if this is not possible, the same picture is shown to the patient surrounded by words related to the object or activity. Positive reinforcement is provided throughout the process. Word-finding abilities are shown to increase during therapy, however, word recognition declines after two weeks of rehabilitation. Thus, rehabilitation needs to be ongoing for word-finding abilities to improve. Studies have shown that verbs are more difficult to retrieve or repeat, even with rehabilitation. Other approaches to treating anomia include naming therapy by circumlocution, in which the patient uses circumlocution to help them name rather than being asked to name the item in the picture. The results suggest that patients do better at naming objects appropriately during therapy because naming therapy by circumlocution strengthens the weak link between meanings and speech sounds in patients with anomia. Anomia can often be challenging or demanding for family and friends of patients. One way to overcome this is through computer-based therapy, which is particularly effective when used in conjunction with clinical therapy. Lehmann et al. provided computer-assisted therapy sessions for patients with anomia, in addition to traditional word list therapy sessions. Some patients received levodopa, which is known to help relieve symptoms, while others received a placebo. The researchers found that the drug had no significant effect on improvement with the list therapy, but all patients improved after the computer-assisted therapy sessions, and they concluded that this form of therapy was effective in increasing naming abilities in patients with anomia. In addition, one study looked at the effects of transcranial direct current stimulation on the temporoparietal cortex, a brain region associated with language. Electrical stimulation was shown to enhance language training outcomes in patients with chronic aphasia. Many different populations suffer from anomia. For example, deaf patients who have had a stroke may exhibit errors in meaning or words, much like patients with anomia. The researchers have dubbed this subtype sign anomia. Multilingual patients typically have a greater degree of anomia in only one of their languages. However, there is conflicting evidence about which language is most affected, the first or second language. Research on children with anomia has indicated that children who receive treatment are often able to return to normal language abilities, aided by neuroplasticity. However, research on children with anomia due to head injury shows that even many years after the injury, some deficits in word retrieval can still be observed. These residual symptoms can cause academic difficulties later on. The condition can be extremely frustrating for both those with and without anomia. Although an anomia sufferer may know the specific word, he or she may be unable to retrieve it, making it extremely difficult for everyone in the conversation. Positive reinforcement is helpful. Although there is not much literature on anomia, there are several nonfiction books about living with aphasia. One such book is The Man Who Lost His Language by Sheila Hill. It is the story of Sheila Hill’s husband, John Hill, a scientist who suffered from sedation and lost the ability to form speech. In her book, Sheila Hill explains the symptoms and mechanisms behind aphasia and speech formation, and adds emotional elements about dealing with someone with aphasia and how to be patient with speech and communication.

Geriatric medicine

Alcohol-related dementia is a form of dementia caused by long-term excessive consumption of alcoholic beverages, resulting in neurological damage and impaired cognitive function. Alcohol-related dementia is a broad term currently preferred by clinicians. Many experts use the terms alcoholic dementia to describe a specific form of ARD, characterized by impaired executive function. Another form of ARD, known as wet brain, is characterized by short-term memory loss and thiamine deficiency. Patients with ARD often have symptoms of both forms, i.e. impaired ability to plan, apathy, and memory loss. ARD may coexist with other forms of dementia. The diagnosis of ARD is widely recognized but rarely applied, due to the lack of specific diagnostic criteria. In many non-medical settings, the terms wet brain and alcohol-related dementia are often used interchangeably, creating considerable confusion. Additionally, the term persistent alcohol-induced dementia is another non-specific name that is sometimes used. Signs and Symptoms Alcohol-related dementia presents as a global decline in intellectual function with memory not specifically affected, but it can occur with other forms of dementia, resulting in a wide range of symptoms. Some individuals with alcohol-related dementia have damage to the frontal lobes of their brain that causes disinhibition, loss of planning and executive functions, and disregard for the consequences of their behavior. Other types of alcohol-related dementia, such as Korsakoff syndrome, damage specific areas of the brain, with changes in memory, primarily short-term memory loss, being the main symptom. Most presentations of alcohol-related dementia fall somewhere along the spectrum between global dementia and Korsakoff psychosis, and may include symptoms of both. Individuals with alcohol-related dementia may have memory problems, language impairment, and an inability to perform complex motor tasks such as dressing. Excessive alcohol consumption also damages the nerves in the arms and legs, i.e. peripheral neuropathy, as well as the cerebellum, which controls coordination, leading to the development of cerebellar ataxia. These patients often have problems with their limbs and may appear unsteady on their feet. Alcohol-related dementia can cause a variety of psychological problems including psychosis, depression, anxiety, and personality changes. People with alcoholic dementia often experience apathy, related to damage to the frontal lobe, which can mimic depression. People with alcoholism are more likely to develop depression than people without alcoholism, and it can be difficult to differentiate between depression and alcoholic dementia. Alcohol directly affects brain cells in the frontal part of the brain, leading to poor judgment, difficulty making decisions, and lack of insight. Long-term alcohol abuse often leads to poor nutritional status that damages parts of the brain due to vitamin deficiencies. These problems can also cause personality changes in some people. Samar Alkhazaleh 💜💜: Ridley, Nicole J; Draper, Brian; Withall, Adrienne . "Alcohol-related dementia: an update of the evidence". Alzheimer's Research & Therapy. 5: 3. doi:10.1186/alzrt157. ISSN 1758-9193. PMC 3580328. PMID 23347747.

Geriatric medicine

Visuospatial dysgnosia is the loss of a sense of "place" in relation to oneself, one's surroundings, objects, and each other. Visuospatial dysgnosia is often associated with topographic agnosia. The same symptoms of the syndrome rarely occur in every patient. Some examples of symptoms that may occur include: Studies have identified the brain region that, if damaged, causes visuospatial dysgnosia: the temporoparietal-occipital region. Lesions are most commonly found in the angular gyrus of the right hemisphere, and are usually unilateral, meaning that they occur in one hemisphere. Unilateral lesions produce more complex cognitive signs such as loss of object naming, prosopagnosia, alexia, apraxia of wearing, and memory deficits in addition to the symptoms of visuospatial dysgnosia. Visuospatial dysgnosia shares many symptoms with Balint syndrome and may be present simultaneously. Visuospatial dysgnosia, along with Balint syndrome, is associated with Alzheimer's disease as an early sign of the disease. Generally, memory loss is the first symptom of Alzheimer's disease, but visual impairment or visuospatial impairment is the presenting symptom in some cases and is common in later stages of the disease. In 1979, David J. Cogan published a lengthy paper describing 17 cases of visuospatial impairment. Here are some examples of patients with visuospatial impairment from Cogan's study: It is clear that visuospatial impairment does not present in the same way, although all of these cases were diagnosed with the disease in conjunction with other comorbidities. For patients with visuospatial impairment, input information can be augmented by adding tactile, kinesthetic, or verbal perceptual input. This is achieved with a general occupational therapy approach of teaching clients with intellectual impairment to use the most effective appropriate perceptual input, which may enable them to complete a task.

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Geriatric medicine

Agnosia is the inability to perceive oneself, a condition in which a person suffers from a certain disability and is unaware of the existence of this disability. The disease was named by neurologist Joseph Babinski in 1914. Agnosia results from damage to the nerves in the right hemisphere of the brain. This condition is different from the state of denial that results from a psychological state when receiving any calamity, whether death or otherwise. Both are associated with damage to the right hemisphere of the brain. Agnosia is sometimes accompanied by a condition which is a type of neglect in which they deny ownership of their limbs. The causes of this condition are not yet known. A study has revealed that agnosia is a multifaceted phenomenon. It can manifest with a number of neurological symptoms including motor deficits, sensory deficits, spatial deficits, memory deficits, and language deficits due to an anatomical-functional defect in the insular control system. Agnosia is relatively common after many brain injuries such as strokes and traumatic brain injuries. However, it can occur in conjunction with almost any neurological deficit. It is more common in acute than chronic cases and is more evident in the assessment of cases with lesions targeting the right hemisphere than the left, but is not associated with global brain confusion, intellectual flexibility, other major intellectual disorders, or sensory or cognitive deficits. Agnosia can be selective, meaning that a person with multiple impairments may appear unaware of one impairment while being fully aware of the rest. For example, agnosia in hemiplegia can occur with full awareness of unilateral spatial visual neglect or vice versa. The phenomenon of double separation can be an indication of impairments related to a specific part of the brain that is involved in sensory perception, meaning that brain damage can selectively affect the process of self-monitoring of motor or mental functions. This condition does not appear to be directly related to sensory deficits and is thought to be the result of damage to higher-level neurocognitive processes involved in integrating sensory information with processes that support bodily or spatial representation. Agnosia is thought to be related to unilateral spatial neglect, a condition that often occurs after damage to the nondominant cerebral hemisphere, in which sufferers appear unable to perceive anything on a specific part of their body. There are several studies that show that balance stimulation can temporarily improve both unilateral spatial neglect syndrome and left hemiplegia. There have been some cases of right hemisphere agnosia following left hemisphere failure or damage, but the incidence of this condition has not been estimated. This condition is associated with Alzheimer's disease and is often presented with poor cognition in the disorder and the insistence that he is healthy and that there is no disorder in him. Agnosia can occur as part of receptive aphasia, a condition that causes poor speech comprehension and the production of fluent but incomprehensible sentences. Patients with receptive aphasia cannot correct their phonological problems and are often angry and frustrated with people who talk about their inability to understand and comprehend. Agnosia is assessed clinically by giving patients a special questionnaire to assess their scientific mental state of their problems. However, there is no complete questionnaire for this disease and there is no benefit in revealing the nature of the disease from the information taken from these questionnaires. Differences exist among patients who are not aware of their psychological problems from questionnaires, but a reluctance to participate in web-based questionnaires has been observed. For example, patients with agnosia due to hemiplegia may find excuses for not doing manual work despite not admitting it and being paralyzed in the upper limbs. Similar situations can occur in patients with agnosia due to mental disorders after brain damage resulting from accidents when monitoring their errors while performing memory and attention tasks and when predicting the results of their performance before performing them. The condition can occur in patients with dementia and patients with agnosia resulting from cognitive impairments related to dementia when they are prompted with words similar to dementia, which shows that the pre-attentional stage is being processed directly and knowledge about their memory problems is being acquired. Interestingly, patients with agnosia may overestimate their performance when asked direct questions. When evaluating the etiology of the disease in patients with stroke, computed tomography is used to determine the location and extent of damage in different areas of the brain. Stroke patients with agnosia have been associated with lesions in the superior lateral lobes and thalamus when compared to patients with mild or no agnosia. In contrast, after a stroke, people with moderate agnosia have a higher risk of lesions in the basal ganglia than those with severe agnosia. Although agnosia is a term used to describe the inability to recognize neurological damage after stroke or traumatic brain injury, the same term is used to describe the impaired insight of people with anorexia nervosa. They do not seem to be able to recognize that they have a mental illness. There is evidence that dissociative agnosia may be caused by a frontal lobe disorder. E. Voller-Touré, a psychologist and schizophrenia researcher, notes that among schizophrenic and bipolar patients, agnosia is the most common cause of medication nonadherence. There is no long-term treatment for agnosia. As with unilateral ignoring, reflex thermography is known to help alleviate the lack of awareness of neurological damage, but its mechanism of action is unknown. It is speculated that the reason lies in the fact that attention is drawn to a specific direction, which stimulates the balance system, which temporarily affects perception. Most cases recover with time, but some may never recover. In the event of non-response, patients are subjected to cognitive behavioral therapy sessions to teach them to adapt to their unresponsive limbs. Another method of treatment is to use patients’ predictions of how they will respond to a certain action before it is performed and compare them with the actual results to develop their insight. The difficulty in neurorehabilitation is that patients are unable to understand that they have a problem in the first place and therefore do not seek treatment. In the acute phase of the injury, little can be done except to create a therapeutic relationship between the patient and the therapist in order to get to the causes of confusion and anger. Since the severity of the condition changes over time, it is difficult to use a single treatment method in all cases. For psychiatric patients, studies have shown that the severity of the condition is significantly associated with irregularity in treatment and re-admission due to the severity of the condition. 15% of patients with severe cases require psychological coercion in order to maintain regular use of medications. Agnosia is significantly associated with mental problems that can interfere with the ability to adhere to treatment.

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Geriatric medicine

Apraxia or motor agnosia is a motor disorder resulting from brain damage. The patient has difficulty planning a sequence of events to perform a movement or when asked to perform a task, even though the command is understandable and the patient intends to do it. It is a disorder in the motor planning process that does not cause a disturbance in coordination, sensory loss, or a failure to understand simple commands, but rather results from damage to specific areas of the brain. A distinction must be made between ataxia and ataxia, which is the inability to coordinate voluntary muscle movements; aphasia, which is a language disorder in comprehension, or both; loss of the will to perform an action or make an appropriate decision; contralateral displacement of sensation, which is the state of sensation in one of the limbs when the opposite limb is stimulated; and developmental apraxia, which affects the planning and coordination of movement. There are several types of apraxia, including: Each of these types may be detected in simple, uncomplicated stages. If the person fails to execute commands, you can perform the movement yourself and ask him to imitate it, or give him a tool and ask him to use it. Apraxia of speech includes the loss of the previously acquired ability to speak. It affects both children and adults who have acquired speech abilities before the disease, and affects the person's voluntary speech, and occurs as a result of stroke, tumor, diseases or nerve injuries. It may be accompanied by language disorders and is called aphasia. Symptoms include inconsistent verbal errors, the patient's groping and searching for oral movements in order to adopt the correct speaking position, an increase in verbal errors with the increase in the length of words and phrases, and the patient finds pronouncing vowels easier than consonants, and single consonants easier than mixtures. He also stutters, pronouncing consonants at the end of the word is easier than those at the beginning, as the letters at the beginning of the word may be affected by expected errors, and if the patient begins his speech with a vowel, the process of continuing the speech will continue more automatically. Fricatives and consonant-stop fricatives are the most difficult phonemes that the patient has a problem producing. Apraxia of speech may sometimes accompany oral apraxia, and may also accompany peripheral apraxia. Verbal developmental apraxia occurs in children who do not have difficulties with range or strength of joint movement, but rather results from a defect in coordination and motor planning. Apraxia is most often caused by damage to the left hemisphere of the brain, usually in the frontal and parietal lobes. The damage may be due to stroke, acquired brain injury, or neurodegenerative diseases such as Alzheimer's disease, dementia, Parkinson's disease, or Huntington's disease. Agnosia can also be caused by damage to other areas of the brain, including the right hemisphere. Ideomotor apraxia is usually caused by decreased blood flow to the left hemisphere of the brain, particularly the parietal area and the premotor area, and is often found in people with basal ganglia cortical degeneration. Ideomotor apraxia results in functional impairment in daily activities similar to that seen in late-stage dementia, and has been observed in people with damage to the left hemisphere near the area associated with aphasia. More studies are needed on ideomotor apraxia due to brain damage. The presence of damage to the frontal and temporal lobes explains the difficulty in motor planning in people with ideomotor apraxia and the difficulty in distinguishing it from aphasia. Constructional apraxia is caused by damage to the right posterior parietal lobe and may be caused by brain injury, disease, tumor, or other causes of brain damage. Although qualitative and quantitative studies are available, there is little consensus on the ideal method for assessing apraxia. Disadvantages of previous methods include their failure to meet psychometric standards and study designs that are difficult to translate into practice. The Upper Limb Apraxia Test is one method for assessing upper limb apraxia by quantitatively and significantly measuring gestural movements. In contrast to previous studies of apraxia assessment, the validity and reliability of the Upper Limb Apraxia Test has been extensively studied. This test includes subtests in which the patient is asked to imitate necessary gestural movements, such as “Walk away” and “Show me how to use a hammer.” A complete assessment of apraxia often includes discrimination testing, which is knowing which tasks are performed well and which are performed poorly, and recognition, which is pointing to the intended object or tool with a gesture. However, there may not be a strong correlation between the results of the formal test and the reality of performance in daily life or activities of daily living. For a comprehensive assessment of apraxia, it should include formal testing, standardized measurement of activities of daily living, observation of daily routines, the patient completing questionnaires, and targeted interviews with the patient and his relatives. As mentioned above, apraxia should not be confused with aphasia, but they often coexist, and for this reason it has been said that if a patient shows symptoms of apraxia, it should be assumed that he also has some degree of aphasia. Treatment of apraxia includes speech therapy, occupational therapy, and physical therapy. To date, treatment has received little attention for several reasons, including the tendency of the disease to disappear spontaneously in brief cases, in addition to the voluntary, spontaneous, dissociative nature of the tasks by which a person is judged to have apraxia, as the patient retains the ability to perform them despite the disease if taught to do so. However, research suggests that individuals with apraxia have less functional independence in their daily lives, which is evidence that treatment is rarely used. However, a review of apraxia treatment to date found that although treatment is in its early stages, there are specific aspects that should be included in treatment. One such approach is rehabilitative therapy, which has a positive impact on apraxia and activities of daily living. Rehabilitative therapy consists of 12 different contextual cues used to teach sufferers how to perform similar gestures under different contextual conditions. Other studies recommend different models of gesture therapy, whereby the patient is instructed to make gestures with a gradual relaxation of the commands from the therapist. There is no agreed-upon ideal treatment method for treatment because each case is different, but a series of therapy sessions with the support of family and friends is best. Because each person responds to treatment differently, some patients will improve significantly while others will improve less. The primary goal of treatment is to treat speech motor planning rather than voice level. The course of apraxia varies from patient to patient, with some patients improving significantly with treatment while others see only very little improvement. Some people with apraxia may benefit from devices that help with communication, but many become unable to function independently. People with gait apraxia or limb movement apraxia should avoid activities that could cause injury to themselves or others. Occupational therapy, physical therapy, and play therapy are effective ways to support and assist the patient and form an integrated apraxia treatment team in conjunction with a speech-language pathologist. People with limb apraxia have problems directing their movements, so it is difficult to treat apraxia caused by stroke or brain injury. There is no effective medication for apraxia.

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Geriatric medicine

Phonoma is a type of agnosia or loss of knowledge, which involves disturbance in the perception of familiar sounds and impairment of phonemic discrimination abilities that the affected person is not completely disabled by. Phonoma is an auditory agnosia, an acquired auditory processing disorder resulting from brain damage. Other auditory agnosia include cortical deafness and auditory verbal agnosia, also known as pure-word deafness. Since people with phonoma do not have aphasia, it has been proposed that the structures of language comprehension are functionally separate from this sensory perception of the identity of the person speaking it. Phonoma is the auditory equivalent of prosopagnosia. Unlike phonoma, studies of phonoma have not been pursued to a large extent. Phonoma was first described in a study by Van Lancker and Cantor in 1982. Participants in the study were asked to identify which of four names or faces matched the voice of a specific famous person. However, the participants were unable to complete the task. There have since been two studies of patients with phonoma. The clinical and radiological findings with CT scans in these cases indicated that perception of familiar sounds was impaired by damage to the inferior and parietal regions of the right hemisphere, while sound discrimination was impaired by damage to the temporal lobe of one hemisphere. These studies also showed evidence of a double dissociation between sound recognition and sound discrimination. Some patients can discriminate normally but perceive the object worse; others can perceive more normally than they discriminate. Patients do not fare badly in either case. Associative phonagnosia is a form of phonagnosia that develops with dementia or other central nervous system disorders. Some research has raised questions about other phonagnosia-related disorders. Recent studies have shown that phonagnosia also causes problems in the perception of familiar instrument sounds. As with voices, they also showed a deficit in the discrimination of sounds from different instruments. Despite the inability, phonagnosia affects this area very little in phonagnosia. In the case of sound discrimination, it is a complete agnosia, but this is not the case for musical instrument sounds, because some of them can be correctly identified. The controversy has increased, as not all cases of phonagnosia show these symptoms, nor do all researchers agree that these symptoms should be attributed to the damage that causes phonagnosia. There has been increased controversy over the fact that separate areas of the brain are used to process information about language and music. This has led some researchers to doubt that this impairment is a clear symptom of the disorder. Again, more research is needed to reach a clearer conclusion. The hallmark of phonagnosia is that they can correctly perceive emotions from sounds when someone speaks to them. They can match specific emotions with facial expressions. Although surprising, these findings are felt by those with a heightened sense of self, as the limbic system, which is responsible for expressing emotions and detecting others’ emotions, is a separate system within the brain. The limbic system consists of several brain structures, including the hippocampus, amygdala, anterior thalamic nucleus, septum, limbic cortex, and fornix. While there is currently no cure or treatment for phonagnosia, it is clear that more research is needed to find a cure for the disorder. There is no cure for this disorder due to lack of knowledge. Further research will reveal vital information needed to develop effective treatments and therapies. The condition is severe and worsens as the disease progresses. QR and KL participated in a study of auditory and visual tasks with brain MRI. QR had only a deficit in phoneme recognition, while KL had an associative form of phonagnosia. The auditory and visual deficits could then be compared with the patient’s brain MRI. The MRI for qualitative research, a patient with frontotemporal dementia, often shows behavioral and bilateral frontotemporal variability with atrophy of the right anterior temporal lobe, but extending into the temporal lobe and including the superior temporal fissure. The cognitive MRI showed bilateral anterior temporal lobe atrophy, with more damage on the right side and in the inferior temporal cortices. The clinical diagnosis of patient KL showed a temporal variant of frontotemporal lobar degeneration with progressive atrophy of the right temporal lobe. There has been a recent study of developmental phonagnosia. KH is a 60-year-old woman who showed all the symptoms of a phonological impairment, but no associated brain damage. In addition, KH had suffered from an inability to recognize sounds throughout her life, making her the first case of developmental phonagnosia. The study of KH turned the world’s research on phonagnosia on its head because it was thought that phonagnosia resulted only after damage to the parietal and temporal lobes. The discovery that phonagnosia could arise without structural damage suggested that the disorder could be the result of a cognitive abnormality. Given the novelty of this study, little research has been done on cognitive-based theories. Areas of interest lie in the neural connections between different regions of the parietal lobe, as well as those within the temporal lobe. Developmental phonagnosia, as the name suggests, develops as the brain develops in the womb and throughout childhood. Researchers have suggested that neurons do not make the necessary connections to correctly identify familiar and unfamiliar sounds. However, solid theories and research studies have not been formulated to test these individuals at their developmental stage.