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

On the basis of a large material of organic dementia, accumulated during a 20 year long prospective study, certain basic structural changes in dementia, mainly of Alzheimer's type (DAT) viz. the topography of lesions, the amyloid angiopathy and white matter changes are discussed with respect to their relevance for modern etiologic and pathogenetic theories and implications for the clinical picture and treatment in DAT. The topographic pattern and its evolution appears to be a relevant basis for the symptomatology and the picture shown by PET and regional cerebral blood flow studies. It lends some support to theories implicating the spread of a causative agent via olfactory pathways. The amyloid depositions, particularly those in the vessels present, both with regard to amount and topography, features which to some extent validate the modern etiological gene theories but which in other respects lend little or no support to the etiologic or pathogenetic importance ascribed to amyloid. The white matter changes, common in DAT and of an incomplete infarction type, may blur the DAT clinic and also serve to block axonal transport through the white matter and cause dysfunction or death of neurons dependent upon routes involved. It might thus influence therapeutic measures such as administration of transmitter substitutes or their precursors and the outgrowth or efficacy of transplanted cholinergic replacement neurons.
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PMID:Structural changes in ageing and dementia of Alzheimer's type with special reference to recent etiologic and therapeutic theories. 269 Jan 4

Brain biopsies from two patients with non-hereditary cerebral hemorrhages and eighty autopsied cases with the clinical diagnosis of dementia are presented. The biopsied cases, both males aged 64 and 59, had a sudden onset of cerebral hemorrhage, mild progressive dementia and cystatin C cerebral amyloid angiopathy. Of the autopsied cases 59 had senile plaques and cerebral amyloid angiopathy was also found in 36 of them. Both senile plaques and the blood vessel amyloid stained positively with beta-protein antibodies, and five of them also showed a positive reaction to cystatin C antibodies. These cystatin C positive cases were three males aged 76, 80 and 83, and one female 93 years old and the fifth case was a female aged 47 with Down's syndrome.
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PMID:Dementia with non-hereditary cystatin C angiopathy. 269 Jan 11

Three operated cases of lobar intracerebral hemorrhage (LICH) related to cerebral amyloid angiopathy (CAA) were studied clinicopathologically. They constituted about 8% of all LICH cases (n = 37) operated upon in our institute (DUSM) during the past 3 years. Case 1, 2 and 3 aged 71, 67 and 73 years, respectively. There were 2 males (Cases 1 & 2) and 1 female (Case 3). Only one case (Case 3) had both hypertension and dementia before hemorrhage. In all 3 cases, neurologic symptoms deteriorated after admission. The hematoma involved the right temporo-parietal in 1 (Case 1), the right parieto-occipital in 1 (Case 2) and the left fronto-parietal region in 1 (Case 3). Case 1 developed a new hematoma in the right occipital lobe on the day following surgery. On CT, the hematoma was multilobular in shape and located very superficially extending to the subarachnoid space in all cases. There was no abnormal enhancement in and around the hematoma upon contrast infusion. Angiography showed only an avascular mass sign in case. At surgery, the hematoma was extruded onto the cortical surface in all cases. The surgical outcome was good in 2 (Cases 1 & 2) and fair in 1 (Case 3). Removed hematomas, solid nodular tissues and adjacent brain tissues were examined histologically using hematoxylin and eosin, Azan-Mallory, elastica van Gieson, silver and Congo red stains. Arteries in the hematoma wall, the subarachnoid space and the adjacent brain parenchyma were intensely stained with Congo red and showed birefringence on polarized light.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lobar intracerebral hemorrhage secondary to cerebral amyloid angiopathy: a clinicopathologic study of three operated cases]. 269 77

Main causes of dementia in the elderly are vascular dementia and Alzheimer's dementia. Vascular dementia is related to both amounts and localization of lesions. Recently incidence of diffuse vascular leukoencephalopathy (Binswanger type, leukoaraiosis) and amyloid angiopathy are increasing. In Alzheimer's protein chemistry of amyloid (beta protein, A4 protein) revealed its precursor APP and its gene (chromosome 21), which produces protease inhibitor in the brain of Alzheimer and Down's brains. APP is considered as an membrane protein (receptor) and appears abundantly in the cerebral cortex. Immunohistochemical study showed that beta protein is observed also in normal aged brain. On the other hand, tau protein (main component of Alzheimer's neurofibrillary tangle, PHF) appeared as abnormal sprouting of neurites in Alzheimer's brain. The latter may related to dementia and neural death. In Alzheimer's dementia, several neurotransmitters, including acetylcholine, are reduced in the brain and related structural changes are observed. Recently olfactory bulb and mucosal changes are remarked as one of pathogenesis of this disease. Delayed neuronal death is a new phenomenon of nerve cell death of vascular origin and should be studied in human vascular dementia.
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PMID:[Approach to the dementia research]. 269 99

Amyloid protein in Icelandic patients with hereditary cerebral amyloid angiopathy (CAA) is a variant of cystatin C. Immunoreactivities of the cystatin C and other amyloid proteins were investigated in CAA and other senile amyloid deposits in the Japanese sporadic aged cases including patients with dementia of Alzheimer type, and compared with those in Icelandic hereditary CAA. Compared with positive reaction of cystatin C in Icelandic hereditary CAA, no immunoreactivity of cystatin C was found in senile amyloid deposits of the Japanese aged including CAA. Immunoreactivity of the amyloid beta protein was negative in Icelandic hereditary CAA, for which CAA and senile plaque amyloid in the Japanese senile brains were positive. Our data suggest that the cystatin C amyloid would be present only in hereditary CAA, but not in the CAA and other senile amyloid deposits of the sporadic aged cases.
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PMID:Absence of the cystatin C amyloid in the cerebral amyloid angiopathy, senile plaque, and extra-CNS amyloid deposits of aged Japanese. 278 31

A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features was reported. A 33-year-old woman showed a progressive dementia followed by apallic state at the relatively early stage, and died of cardiac failure at the age of 45. Neurological examination disclosed chorea, myoclonus, rigidity, pyramidal sign, and generalized convulsion. Neuropathologically, extensive senile changes such as senile plaques, neurofibrillary tangles, and granurovascular degenerations were observed in the brain, chiefly in the cerebral cortex and limbic system. The present case was characterized by a severe neuronal loss in the subcortical gray matter such as the caudate nucleus, dentate nucleus, substantia nigra, and thalamus as well as a marked myelin loss and axonal damages in the cerebral white matter. This case suggested a combination of multisystemic degeneration and a primary degeneration of the cerebral white matter. The additional peculiar aspects in this case were the senile plaques and amyloid angiopathy in the cerebellar cortex, and the senile plaques and grumose degeneration in the cerebellar dentate nucleus. In the clinicopathological standpoint, the apallic state in this case could be attributed to a severe degeneration of the cerebral white matter in addition to the cerebral cortical deterioration. Furthermore, the occurrence of chorea and myclonus might be contributed to the severe degeneration of the caudate nucleus and to the degeneration of the dentate nucleus, particularly to the grumose degeneration, respectively.
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PMID:[A case of familial juvenile Alzheimer's disease with apallic state at the relatively early stage and various neurological features--a clinicopathological study]. 279 15

We describe the pathologic findings in 17 persons with dementia, 12 of whom exhibited leuko-araiosis on computed tomographic scan. The presence of white matter pallor was confirmed on autopsy in 11 of these 12 cases, 9 with Alzheimer's disease and 2 with multi-infarct dementia. Two further patients, 1 with Alzheimer's disease and 1 with multi-infarct dementia, proved to have white matter changes on pathologic examination. White matter pallor coexisted with cerebral amyloid angiopathy in the brains of the patients with Alzheimer's disease. The presence of severe white matter pallor in patients with Alzheimer's disease correlated with early death, while the presence of cortical scars was associated with prolonged survival. Because early death in patients with Alzheimer's disease has been linked with severe pathologic and chemical changes, the presence of white matter pallor may be further evidence of a particularly severe process in patients with early onset of Alzheimer's disease.
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PMID:Neuropathologic correlates of leuko-araiosis. 280 72

Alzheimer's disease is a degenerative brain disorder with a progressive dementia which develops in middle or late life. The pathological findings of this disease are characterized by neurofibrillary tangles, senile plaques and cerebrovascular amyloidosis. However, cerebral hemorrhage caused by amyloid angiopathy rarely occurs. A 71-year-old woman, who had been suffering from an impairment of her cognitive ability for the past several months, suddenly developed a severe headache with vomiting and gait disturbance. Brain CT disclosed a hemorrhagic lesion in the right parieto-occipital region. In the following two years she had experienced two episodes of the similar subcortical hemorrhage which occurred in the right parietal lobe and bilateral parieto-occipital regions. She died at the age of 73. Histopathological examinations of the brain revealed a decreased number of neurons with diffuse distribution of senile plaques and neurofibrillary tangles in the neocortex and hippocampus. Severe cerebrovascular amyloid deposits were also seen. Immunostaining for amyloid was carried out using a monoclonal antibody to amyloid beta protein. The senile plaque and cerebrovascular amyloid was strongly immunoreactive to anti-beta protein antibody. Cerebral amyloid angiopathy is commonly seen in the brains with Alzheimer's disease and severe cerebrovascular degeneration secondary to heavy amyloid deposits may cause recurrent subcortical hemorrhages in the patients with this disorder.
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PMID:[An Alzheimer's disease case showing recurrent subcortical hemorrhage: an autopsy findings with immunohistochemical studies of cerebral amyloid deposits]. 280 20

Twenty-five patients with vascular dementia, 18 patients with senile dementia of Alzheimer type (SDAT) and 17 normal persons were examined by magnetic resonance imaging. Lesions of high signal intensity were always recognizable and were frequently very marked in patients with vascular dementia, while they were absent or mild in patients with pure SDAT and in non-demented patients without vascular disease. The possible nature of this disease as well as the role played in determining the type of dementia are discussed.
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PMID:Lesions of high signal intensity at magnetic resonance imaging in vascular dementia. 298 May 4

Single photon emission computed tomography (SPECT) is becoming an increasingly important part of routine clinical nuclear medicine. By providing tomographic reconstructions in multiple planes through the patient, SPECT expands the clinical applications in nuclear medicine as well as providing better contrast, edge definition and separation of target from background activities. Imaging techniques have been developed for the evaluation of regional cerebral blood flow using radiolabeled amines. Thus cerebral functional imaging can be used in the diagnosis of acute cerebral infarction, cerebral vascular disease, dementia and epilepsy. SPECT plays a complementary role in the evaluation of coronary artery disease, particularly when it is coupled with thallium-201 and exercise testing. SPECT extends our diagnostic capabilities in additional areas, such as liver and bone scintigraphy as well as tumor imaging with gallium-67.
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PMID:Single photon emission computed tomography. 299 98


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