Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Senile dementia of the Binswanger's type is a term used to describe a dementia syndrome characterized by onset in the sixth or seventh decade of life, subcortical neurologic deficits, psychiatric disorders and evidence of hypertension or systemic vascular disease. The status of senile dementia of the Binswanger's type as a distinct entity is a matter of some controversy. The array of neuroimaging abnormalities and clinical findings attributed to this condition overlap with a number of other neuropathologies. Leukoaraiosis, or attenuation of subcortical white matter, seen on computed tomographic scans or magnetic resonance imaging of the brain, is a hallmark of senile dementia of the Binswanger's type. The clinical findings associated with Binswanger's disease are varied but typically include a progressive dementia, depression and "subcortical" dysfunction such as gait abnormalities, rigidity and neurogenic bladder. Treatment is largely supportive and includes a discussion about advanced directives, social support and antidepressant therapy. Control of hypertension and aspirin prophylaxis may help prevent further progression of white matter disease.
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PMID:Senile dementia of the Binswanger's type. 986 80

Mental disorders due to cerebral microvascular disease have been known for over 100 years. Recently, an autosomal dominant form of cerebral arteriopathy (CADASIL) has been described in association with a Notch3 family gene on the short arm of chromosome 19. CADASIL causes subcortical lacunar infarction and dementia in over 80% of cases and depression in a large proportion of patients. Clinically, CADASIL may appear to be very similar to hypertensive microvascular disease (Binswanger's disease), a condition that is seen in the elderly. This article reviews the clinical, pathologic, and genetic features of CADASIL. CADASIL is of interest to neurologists and psychiatrists because it is the first syndrome of vascular dementia and depression with an identified gene. How the gene causes the widespread arteriopathy is not yet known. Insights gained from the study of CADASIL should help us better understand its etiology, as well as the options for treatment of the more common forms of microvascular disease seen in the elderly.
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PMID:CADASIL syndrome: a genetic form of vascular dementia. 987 28

Binswanger's disease(BD) in an effect of a vascular destruction of deep white matter structures following multiple infarcts leading to disturbances of perception functions, recent memory and characterological disorders. BD is a disease occurring in late 6th decade of life. Computerized tomography and magnetic resonance imaging demonstrate foci of microinfarcts which coexist with arterial hypertension, atheromatous lesions and general cerebral atherosclerosis. BD leads to dementia, certain Parkinson-like signs, pyramidal system involvement, depression, organic brain damage syndrome, dysbasia and sphincter control loss. Ten patients observed by the author are reported.
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PMID:[Binswanger's disease--diagnostic criteria and analysis of cases]. 1110 74

Small vessel disease (SVD) is responsible for brain chronic circular disorder, and accounts for 20%-30% cases of ischemic stroke as well as cerebral hemorrhage, and to a great extent, encephalopathy. Binswanger's disease and multiple small strokes, which are common in older people, are also closely associated with SVD. These disorders often cause decline in cognition, vascular dementia, impairment in gait and balance, mood depression, and urinary incontinence, and often brings great social and economic burdens. SVD-related encephalopathy increases the incidences of fall, disability and death in elderly people. With the aging of the society, more attention should be paid to the importance of early diagnosis and prophylactic treatment of SVD. Here the clinical manifestations and pathophysiology of SVD are reviewed.
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PMID:The clinical manifestations and pathophysiology of cerebral small vessel disease. 2050 5


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