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.