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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study of senile degenerative lesions-including Alzheimer's neurofibrillary changes, senile plaques and amyloid angiopathy-the hippocampal area of the brain was examined by thioflavine T fluorescence microscopy in 146 consecutive autopsy patients over the age of 49. The incidence and quantity of neurofibrillary changes and senile plaques rose with age, and an approximate positive correlation in quantity was noted among the three kinds of degenerative change. The quantity of neurofibrillary lesions and senile plaques was significantly different between the demented and non-demented patients, but not between the severely and less severly demented patients. The cause of dementia was studied retrospectively, based on the extent of morphologic changes in the brain, thus classifying dementia into three types: degenerative, vascular, and mixed. Clinically, the mixed type resembled the vascular type with regard to major neurologic signs, and there was some similarity to the degenerative type with regard to mental features.
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PMID:Senile degenerative brain lesions and dementia. 5 Mar 38

More than 1400 necropsies performed on patients with either a nontraumatic cerebral hemorrhage (400 cases) or with dementia over the age of 55 (1010 cases), or both, have been reviewed. There were 15 cases in which a cerebral hemorrhage had occurred together with cerebral amyloid angiopathy all of whom had been demented. Eight of the 15 patients were hypertensive. The 7 non-hypertensives showing only the amyloid change included two cases of "atypical" Alzheimer's disease with acute neurological features, and 5 cases of senile dementia (aged 72 to 78 years) coupled with focal neurological disorders. In the hypertensive patients, aged 67 to 86 years, with a progressive dementing syndrome and acute neurological signs, multiple ball-like hemorrhages (7 cases) and/or cerebral hematomas (3 cases) were associated with a combination of amyloid and hyalinar (hypertensive) angiopathy, often affecting segments of the same pial and cortical vessels. From these data and recent reports on lethal cerebral hemorrhage occurring spontaneously or after neurosurgical procedures in demented old people, cerebral amyloid angiopathy, which is not necessarily associated with systemic amyloidosis or severe (pre)senile cerebral degeneration, may be considered a rare but important cause of cerebral hemorrhage in the aged. The "vascular" type of presenile dementia, occasionally complicated by focal cerebrovascular lesions or bleeds, is considered a variant of Alzheimer's disease. The mechanism leading to formation of cerebral amyloid is unknown.
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PMID:Cerebrovascular amyloidosis with cerebral hemorrhage. 6 54

Clinical and neuropathological findings of a 63-year-old male and a 25-year-old female with Down's syndrome are presented. Neuropathological examination of the older patient revealed intense features of Alzheimer's disease or senile dementia, including congophilic angiopathy and extensive mineral deposits in the globus pallidus and in the white matter of the cerebellum. In the hippocampus of the younger patient, plaque-like bodies and a few neurofibrillary tangles were found. From a survey of the cases hitherto reported in the literature it appears that among patients over 50 years of age it is common to encounter pathological features typical of Alzheimer's disease or senile dementia, that plaque-like bodies may occur in the second decade, neurofibrillary tangles in the third decade and a congophilic angiopathy in the fourth decade. The congophilic angiopathy is a frequent finding. Due to their high frequency, calcium or calciumlike deposits are regarded as important histopathological substrates of Down's syndrome. The clinical symptomatology of the long-surviving patients with Down's syndrome is that of a non-characteristic brain aging process and differs from that of the typical Alzheimer's disease. Organic dementia is not regularly found. Altogether, the anatomical findings in adult patients with Down's syndrome indicate a premature aging of the brain, which becomes more significant and widespread with increasing age.
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PMID:[Cerebral degeneration in Down's syndrome]. 15 70

Vascular disease is responsible for only a minority of cases of chronic dementia. Vascular dementia can be an end stage of a variety of mechansisms. Correct identification of the cause of the vascular disease is the key to successful treatment.
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PMID:Chronic vascular dementia. 26 61

The historical events in the evolution of Alzheimer's disease are reviewed, including the initial description by Alois Alzheimer and the subsequent controversy regarding the nosological specificity of this entity. The similarity of senile dementia and Alzheimer's disease is emphasized. The basis for the modern concept of Alzheimer's disease as premature or accelerated aging is included in the review. The pathological correlates of the major categories of adult dementia have been described. The traditional criteria of neurofibrillary tangles and senile plaques have been re-evaluated using the current insight into these changes afforded by electron microscopy and biochemistry. The significance of amyloid has been described because it occurs within the senile plaque and also as the essential component of congophilic angiopathy. The new information regarding neuronal cell counts and the loss of choline acetyltransferase has been evaluated in terms of an indication of a pathogenic mechanism of Alzheimer's disease. The current understanding of normal pressure hydrocephalus, Creutzfeldt-Jakob disease, and multi-infarct dementia has been described. Brain biopsy in dementia has been described as having diagnostic, research, pathogenic, and prognostic value. The precautions involving the performance and handling of the biopsy have been stressed, particularly because these procedures involve conditions of possible slow virus etiology. The polemic for Alzheimer's disease as aging or slow virus infection has been summarized. At this time a consideration seems justified that Alzheimer's disease is an age-related, slow virus disease due to a hitherto unknown immune defect. Aging as an etiological agent must be clarified before Alzheimer's disease, in any form, can be considered to be an inevitable consequence of longevity.
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PMID:Adult dementia: history, biopsy, pathology. 37 82

Fifty-two patients presenting with dementia were divided into a group in whom clinical features suggested an ischaemic basis (multi-infarct dementia) and a group in whom a primary degenerative process seemed more likely. Focal EEG changes and angiographic evidence of ischeamic areas and atheromatous disease of intracranial vessels were more common in the "ischaemic" than in the primary degenerative group. CBF was significantly reduced in the former but the regional pattern was equally distorted in the two groups. These findings strengthen the belief that the ischaemic score can identify those patients whose dementia is associated with vascular disease.
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PMID:Multi-infarct dementia. 43 Jan 4

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.
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PMID:Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease). 56 79

In three cases of cerebral amyloid angiopathy there was also a chronic cerebral vasculitis characterized by segmental fibrinoid necrosis, chronic adventitial inflammatory infiltrates, obliterative "endarteritis" and hyaline arteriolar change, resembling rheumatoid vasculitis. Two of these cases had rheumatoid arthritis, and one had unspecified "arthritis" at the onset of dementia. Both vasculitis and amyloidosis involved the leptomeningeal and cerebral cortical vessels. In the two autopsy-verified cases, the vascular disease was limited to the brain. In the third case, only a brain biopsy was available. Amyloid-containing neuritic plaques were present in the cerebral cortex in all three cases, but they were abundant only in one, which also showed numerous Alzheimer tangles.
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PMID:Cerebral amyloid angiopathy: possible relationship to rheumatoid vasculitis. 57 77

The clinico-pathological features of five patients with vascular amyloid restricted to the central nervous system are presented. In three normotensive patients, intracerebral hemorrhage was the dramatic manifestation of amyloid angiopathy. In two other cases, one of amyloid in an arteriovenous malformation, the other of amyloid following therapeutic radiation, amyloid deposition was asymptomatic. Clinically, amyloid angiopathy must be considered in the different diagnosis of intracerebral hemorrhage, independent of the presence of dementia. Pathologically, a factor common to the syndrome of cerebrovascular amyloid appears to be locally increased vascular permeability resulting from a variety of previous tissue injuries.
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PMID:Vascular amyloid in the aging central nervous system. Clinico-pathological study and literature review. 59 96

Senile dementia of the Alzheimer type is becoming one of the most common of the malignant diseases as our society ages. Currently, research has identified several pathophysiological changes, including the bihelical filament and the loss of the enzyme choline acetyltransferase from the cortex. Although genetic factors play some role in this disease, the important environmental risk factors have not yet been identified and there is, at present, no specific treatment. The second most common cause of dementia, cerebrovascular disease, produces dementia only when there is destruction of brain tissue, as in individuals who have multiple strokes or who have hypertensive vascular disease leading to multiple lacunae. In both multi-infarct dementia and in the lacunar state, hypertension appears to play a greater role than it does in other forms of vascular disease. Many of the other causes of dementia, including normal pressure hydrocephalus, CNS infections or tumors, metabolic disorders produced by thiamine or vitamin B12 deficiency or thyroid dysfunction, are often reversible. Every patient, whatever the age, with a developing dementia deserves a thorough workup to identify these treatable disorders.
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PMID:Dementias. 75 96


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