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

The cerebral amyloid angiopathy (CAA), morphologically characterized by amyloid deposition in the vessel walls which are altered to rigid tubes, is a chronic disease of the cortical and meningeal vessels and can cause intracerebral hemorrhages (1.5% of all intracerebral bleedings). We report the course of five surgically treated patients with lobar space-occupying intracerebral hemorrhages and CAA confirmed by histological examination. All patients were elderly (74-84 years), in good condition, and self-providing before the hemorrhage. There were no signs of dementia of the Alzheimer's type. In four cases, CT showed a hematoma in the parieto-occipital, and in one case in the temporo-parietal, region. After surgical evacuation, two patients recovered, one patient remained in bad condition, and two patients died from recurrent hemorrhage within two weeks. Spontaneous intracerebral hemorrhage of lobar localization in an elderly patient strongly suggests CAA. The prognosis seems to be poor in cases with recurrent hemorrhage, the other patients presented an uneventful course, comparable with patients operated on for intracerebral bleeding of other origin. Further investigations are necessary to elucidate the prognosis of this entity.
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PMID:Amyloid angiopathy--a rare cause of intracerebral hemorrhage. 179 45

A 54-year-old man died after a subcortical dementia that had developed over 7 years with focal neurological signs and a stepwise course. Clinical and radiological features were similar to those of Binswanger's disease but there was no vascular risk factor, especially no hypertension. Three similar cases had occurred in the family affecting the patient's mother, her brother and sister, suggesting an autosomal dominant hereditary disease. Postmortem examination disclosed an arteriopathic leukoencephalopathy. The white matter was mainly affected in the periventricular areas of the frontal and parietal lobes with myelin loss and pallor, sparing the U fibers. The vascular changes involved the small vessels and were not arteriosclerotic. There was severe thickening of the internal lamina and degradation products of the elastic fibers. There was no amyloid. This vascular leukoencephalopathy was different from Binswanger's disease and amyloid angiopathy. We think that the vascular lesions could correspond to a genetically transmitted specific degenerative pathology of the small arteries of the brain.
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PMID:[Familial subcortical dementia with arteriopathic leukoencephalopathy. A clinico-pathological case]. 185 35

The pathohistologic study was conducted on the brain of a dementia patient caused by simple cerebral amyloid angiopathy and the neural cell counts of cerebral cortices was compared with that of two normal subjects of same age. Medium to small arteries and capillaries of leptomeninges and cortices exhibited amyloid deposits. The occipital lobe was predominantly affected. 53.3% of medium to small arteries and 25.3% capillaries showed the abnormality. Decrease of neural cells also varied considerably. The occipital lobe was involved most severely and 54.8% neural cells lost in this lobe. The increase of amyloid deposits was closely related to the severity of ischemic lesion and loss of neurons. The findings in this patient indicated that the pathogenesis of dementia caused by cerebral amyloid angiopathy might be more complicated. The possible mechanism might be that the deposition of amyloid destroyed the structure of cerebral vasculature and lead to the impairment of autoregulation. These pathologic changes resulted in hypoperfusion which caused ischemic changes and loss of neurons and dementia.
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PMID:[The relationship of hypoperfusion and dementia caused by cerebral amyloid angiopathy]. 188 25

The coexistence of cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD) should be considered in the differential diagnosis of cases with acute onset of dementia when other causes have been excluded. We report clinical and neuropathological findings in a 78-year-old man who developed dementia of acute onset with an apparent rapid course three months before his death. Postmortem microscopic examination of the brain revealed senile (neuritic) plaques and neurofibrillary tangles in the hippocampus and cerebral cortex. CAA affected vessels of the neocortex and leptomeninges, most severely in the frontal and parietal areas.
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PMID:Alzheimer's disease, cerebral amyloid angiopathy, and dementia of acute onset. 191 6

In cerebral amyloid angiopathy, the contractile elements of the leptomeningeal and cortical arteries are replaced by noncontractile amyloid beta protein. The incidence of amyloid angiopathy increases with advancing age. It is associated with Alzheimer's disease and spontaneous cerebral hemorrhage. The latter can have the characteristic acute computed tomographic appearance of a hematoma at the cortex-white matter junction with extension of blood into the subarachnoid, subdural, and intraventricular spaces. Multiple hemorrhages are frequent. Additional bleeding can occur after evacuation of the hematoma, and postoperative hemorrhage can occur after cortical biopsy. To elucidate the role of surgery in this condition, we have reviewed 20 consecutive operated cases of cerebral amyloid angiopathy. A first group of 8 patients with senila dementia underwent cortical biopsy without resultant hemorrhage. A second group of 6 patients in good clinical condition had delayed evacuation of a spontaneous cerebral hematoma from cerebral amyloid angiopathy because of the radiological misdiagnosis of a hemorrhage within a tumor. One patient died of a pulmonary embolism, and another had subsequent multiple hemorrhages that were ultimately fatal. A third group of 6 patients in poor neurological condition had the acute evacuation of a spontaneous cerebral hematoma to relieve intracranial hypertension. All died or were severely disabled. One had repeated hemorrhages which added a progressively more severe organic dementia onto an initial hemiplegia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surgical considerations in cerebral amyloid angiopathy. 196 1

A 32 year-old diabetic woman presented with an acute coma followed by epileptic seizures, aphasia and constructive apraxia. No ischemic lesion was demonstrated by CT scan and carotid angiograms. The other investigations showed sensorineural hearing loss, retinal degeneration, calcifications of the basal ganglia and lactic acidosis. The follow-up was marked by pseudo-dementia with personality disorders, memory deficits, behavioural changes, migrainous and epileptic features. Although there was no sign of muscular deficiency, a muscular biopsy showed characteristic ragged-red fibers and mitochondrial abnormalities at electron microscopy. The muscular biopsy enables us to classify this case as a mitochondrial encephalopathy similar to the MELAS syndrome. The stroke-like episodes are probably caused by a specific angiopathy involving the mitochondria of brain vessels.
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PMID:[Mitochondrial encephalopathy affecting only the central nervous system]. 196 61

A review is presented of diseases of the central nervous system associated with amyloid deposition. The name amyloid is given to substances with particular physical characteristics which are independent of the chemical constitution of the proteins in the substance. Ideally, a classification of amyloid diseases should be based on the chemical composition of the amyloid deposits; this has only been partially realized. The best documented group of diseases with amyloid deposition in the central nervous system is the group of 'cerebral beta amyloid diseases', characterized by the deposition of beta-protein. This group includes: Alzheimer's disease, sporadic cerebral amyloid angiopathy, Down's syndrome, Parkinson-dementia of Guam, hereditary cerebral hemorrhage with amyloidosis-Dutch type and age-related asymptomatic amyloid angiopathy.
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PMID:Amyloid in central nervous system disease. 196 19

The differential diagnosis of the dementia syndrome may pose a difficult clinical problem, since the most common dementia, Alzheimer's disease (AD), is marked by normal laboratory tests. Neuroimaging has played an important role in evaluating the demented patient, and its uses are growing. Computed tomography (CT) is useful for excluding reversible and treatable causes of dementia, such as subdural hematoma and tumor. More recently, magnetic resonance imaging (MRI) has improved our ability to diagnose vascular disease and may show the presence of cerebral infarcts and white matter disease not visible on CT. Single photon emission computed tomography (SPECT) and positron emission tomography (PET), techniques that visualize such cerebral functions as glucose metabolism and blood flow, may provide positive evidence supportive of the diagnosis of AD.
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PMID:MRI, CT, SPECT, PET: their use in diagnosing dementia. 199 19

Elevated plasma lipid and lipoprotein levels are associated with an increased risk of cardiovascular disease in middle-aged men and women. It is still not clear, however, whether lipid and lipoprotein abnormalities continue to be risk factors for cardiovascular disease in the elderly population. It is not even clear what normal lipid values are in the elderly, and whether diet or drug therapy should be advised on the basis of lipid values established in middle-aged populations. Ischemic heart disease does remain the leading cause of death in the elderly, and there is now preliminary evidence from epidemiologic studies that relative elevations of levels of lipid and lipoprotein fractions in an elderly population might be associated with an independent and increased risk of coronary heart disease, stroke, and possibly dementia. Intervention studies are about to begin that will assess various lipid-and lipoprotein-modifying therapies and their ability to reduce vascular disease risk in the elderly.
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PMID:Lipids, vascular disease, and dementia with advancing age. Epidemiologic considerations. 199 50

Vascular dementia is the second most common type of dementia in the elderly after the dementia of Alzheimer's disease. Six forms of vascular dementia have been described: multi-infarct dementia, lacunar dementia, Binswanger's subcortical encephalopathy, cerebral amyloid angiopathy, white-matter lesions associated with dementias, and single-infarct dementia. Each is described. Severe dementia is found in 5% of persons over age 65 and in 15% to 20% of persons over age 80 years. Alzheimer's disease accounts for 50% to 60% of cases of severe dementia and vascular dementia for 10% to 20%; 20% of the patients have both disorders. The incidence of vascular dementia, which seems to be declining, is about 7/1,000 persons/year. Hypertension is the most powerful risk factor for all vascular dementias. Vascular dementias can be accurately diagnosed by using clinical and mental state examinations, Diagnostic and Statistical Manual of Mental Disorders criteria, ischemic scores, and computed tomography or magnetic resonance imaging. The most successful treatment of vascular dementia is the prevention of cerebral infarcts. Study of the incidence of vascular dementias and their treatment will be included in the European Trial on Systolic Hypertension in the Elderly (SYST-EUR) of 3,000 elderly hypertensive patients.
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PMID:Hypertension and the risk of dementia in the elderly. 200 54


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