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.