Combined Amyloid Vascular Changes and Argyrophilic Plaques in the Central Nervous System

Neumann, Meta A.

doi:10.1097/00005072-196007000-00005

Cited by 53 publications

(11 citation statements)

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“…This was in contrast with the other cases of severe CAA coexisting with AD where such lesions were found occasionally in a pari o f the vessels with CAA: Similar cases of dementia characterized by severe CAA with perivascular plaque formation have been reported [9,[24][25][26][27][28][29][30][31]. The reported cases were familial [24-26, 29, 30] or nonfamilial [9,27,28,31]; NFT were present [9,[24][25][26][29][30][31] or absent [27,28]. Some have been discussed as atypical AD [26,31], and others as the other entities including 'primary idiopathic cerebrovascular amyloidosis' [28].…”

Section: Discussionmentioning

confidence: 66%

Vascular Variant of Alzheimer's Disease Characterized by Severe Plaque-Like β Protein Angiopathy

Yamada

Itoh²,

Suematsu³

et al. 1997

Dement Geriatr Cogn Disord

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In the neuropathological investigations of 32 demented patients with severe cerebral amyloid angiopathy (CAA), we found an unusual case, a 90-year-old woman, presenting with the pathology of atypical Alzheimer''s disease (AD). The case showed severe plaque-like angiopathy, in which all the senile plaques except for some diffuse plaques were formed around amyloid β(/A4) protein-laden vessels. Analysis of the amyloid β protein precursor gene from the patient revealed no mutation. Our results have indicated that, among demented patients with severe CAA, there is the vascular variant of AD characterized by severe plaque-like β protein angiopathy.

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Section: Discussionmentioning

confidence: 66%

Vascular Variant of Alzheimer's Disease Characterized by Severe Plaque-Like β Protein Angiopathy

Yamada

Itoh²,

Suematsu³

et al. 1997

Dement Geriatr Cogn Disord

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“…1 The patient was a 46-year-old woman who had severe amyloid angiopathy and numerous senile plaques and who died of a lobar hemorrhage in the left parietal lobe. This case, however, was also complicated by the presence of a vascular malformation.…”

Section: Discussionmentioning

confidence: 99%

Autopsy study of incidence and distribution of cerebral amyloid angiopathy in Hisayama, Japan.

Masuda

Tanaka

Ueda

et al. 1988

Stroke

150

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The incidence of cerebral amyloid angiopathy in a general population was evaluated in brains of 400 consecutive autopsies of residents of Hisayama, Japan (November 1971-October 1983). Six samples taken from frontal lobe, parietal lobe, temporal lobe, occipital lobe, hippocampus, and basal ganglia of the same side of each brain were stained with both hematoxylin and eosin and Congo red. The specimens were surveyed microscopically with polarized light for deposition of amyloid in the vascular wall. In 26 cases with brain hemorrhage, the region surrounding the hemorrhagic sites was further examined to study the probable causal relation between cerebral amyloid angiopathy and brain hemorrhage. Cerebral amyloid angiopathy was found in 40 of 218 men (18.3%) and 51 of 182 women (28.0%). The incidence increased with age in both sexes. The frontal lobe was most frequently affected (66 cases), followed by parietal lobe (65), occipital lobe (49), temporal lobe (44), and hippocampus (32); the putamen was never affected. The incidence of cerebral amyloid angiopathy did not correlate with blood pressure or with the severity of cerebral atherosclerosis. Among the 26 cases in which there was brain hemorrhage, only one cerebellar hemorrhage, in an 85-year-old man, was attributed to cerebral amyloid angiopathy. This case showed four microaneurysms in vessels, with cerebral amyloid angiopathy surrounding the hemorrhagic site. Thirty similar lesions were observed in eight cases without brain hemorrhage. Cerebral amyloid angiopathy may play an etiologic role in the development of brain hemorrhage through formation of angionecrosis and microaneurysm.

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“…Recently, additional sections were prepared from the brains of the 60 cases, and stained with haematoxylin-eosin, Congo-red, periodic-acid-Schiff and Bodian methods. Sections examined were frontal lobe (areas 8,9), parietal lobe (area 7), temporal lobe (area 20, 21), occipital lobe (area 17, 18), insula, Ammon's horn and parahippocampal gyrus, basal ganglia, thalamus, pons, medulla and cerebellum (cortex, dentate nucleus), as well as areas around the haematomas. In seven cases, the haemorrhage was considered to be due to amyloid angiopathy.…”

Section: Cases and Methodsmentioning

confidence: 99%

Amyloid angiopathy and lobar cerebral haemorrhage.

Ishii¹,

Nishihara²,

Horie³

1984

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Seven cases of lobar cerebral haemorrhage due to amyloid angiopathy were found among 60 necropsy cases of intracerebral haemorrhage. Clinically five patients were demented and two had hypertension. Immediately after the onset of stroke there was a high incidence of headache and vomiting, followed by nuchal rigidity. Amyloid angiopathy was most prominent in the cerebral cortex and the leptomeninges. Senile Recently, additional sections were prepared from the brains of the 60 cases, and stained with haematoxylin-eosin, Congo-red, periodic-acidSchiff and Bodian methods. Sections examined were frontal lobe (areas 8, 9), parietal lobe (area 7), temporal lobe (area 20, 21), occipital lobe (area 17, 18), insula, Ammon's horn and parahippocampal gyrus, basal ganglia, thalamus, pons, medulla and cerebellum (cortex, dentate nucleus), as well as areas around the haematomas. In seven cases, the haemorrhage was considered to be due to amyloid angiopathy. A representative case is described below.A 78-year-old man (case 1), a retired mining engineer who had been living alone since his retirement, was admitted to a local hospital because of burns on his hands and legs. He (fig 1). Microscopically, the most striking finding was severe deposition of amyloid in the wall of small arteries and arterioles in the cerebral cortex and the leptomeninges (fig 2). Also present was prominent drusige Entartung (plaque-like degeneration), namely amyloid deposit in the capillary wall with infiltration into the adjacent brain parenchyma ( fig 3). These changes were observed throughout the cerebral cortex. Amyloid deposits were also noted in the Ammon's horn, the basal ganglia, the thalamus and the cerebellar cortex, but to a lesser extent than in the cerebral cortex There was no amyloid in the~~~~~~~~~~~~~~~~~~~~~~. 5,10Protected by copyright.

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Combined Amyloid Vascular Changes and Argyrophilic Plaques in the Central Nervous System

Cited by 53 publications

References 0 publications

Vascular Variant of Alzheimer's Disease Characterized by Severe Plaque-Like β Protein Angiopathy

Vascular Variant of Alzheimer's Disease Characterized by Severe Plaque-Like β Protein Angiopathy

Autopsy study of incidence and distribution of cerebral amyloid angiopathy in Hisayama, Japan.

Amyloid angiopathy and lobar cerebral haemorrhage.

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