Sporadic cerebral amyloid angiopathy is not a frequent cause of spontaneous brain hemorrhage.

Saved in:
Bibliographic Details
Title: Sporadic cerebral amyloid angiopathy is not a frequent cause of spontaneous brain hemorrhage.
Authors: Jellinger, K. A., Lauda, F., Attems, J.
Source: European Journal of Neurology. Aug2007, Vol. 14 Issue 8, p923-928. 6p. 4 Charts, 2 Graphs.
Subjects: Autopsy, Cerebral hemorrhage, Intracerebral hematoma, Apolipoproteins, Neurobehavioral disorders, Cerebrovascular disease
Abstract: The retrospective study of a consecutive autopsy series of 1100 elderly subjects (mean age 78.3 ± 6.8 SD years), revealed sporadic cerebral amyloid angiopathy (CAA) in 50.0% and in 95.7% of autopsy-confirmed cases of Alzheimer disease (AD). Apolipoprotein (APOE) ℇ 3/4 and ℇ 4/4 were significantly more frequent in AD than in controls, and were associated with more severe degrees of CAA. Spontaneous (non-traumatic) intracerebral hemorrhages (ICH) (excluding microbleeds and hemorrhagic infarctions) were seen in 5.4% and only in 3.3% of AD cases. CAA was found in 50.6% of brains without and in 42.4% with ICH, the latter showing a significantly higher frequency of severe degrees of CAA. ICH was related to CAA in 42.4%, whilst no such relation was seen in 57.6%. Patients with CAA were older, showed a higher frequency of clinical dementia and pathologically confirmed AD, but signs of hypertension (history and/or autopsy) occurred in 40%, compared with 80% in those with non-CAA-related ICHs. CAA-related ICH more frequently involved in cerebral lobes or hemispheres, whilst non-CAA-related ones were more often located in the basal ganglia and brainstem. The data of a lower prevalence of CAA in cases with than without ICH and of ICH with and without CAA do not support the concept that CAA represents the most important risk factor for ICH in the aged, probably because of other risk factors including hypertension. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neurology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
Description
Abstract:The retrospective study of a consecutive autopsy series of 1100 elderly subjects (mean age 78.3 ± 6.8 SD years), revealed sporadic cerebral amyloid angiopathy (CAA) in 50.0% and in 95.7% of autopsy-confirmed cases of Alzheimer disease (AD). Apolipoprotein (APOE) ℇ 3/4 and ℇ 4/4 were significantly more frequent in AD than in controls, and were associated with more severe degrees of CAA. Spontaneous (non-traumatic) intracerebral hemorrhages (ICH) (excluding microbleeds and hemorrhagic infarctions) were seen in 5.4% and only in 3.3% of AD cases. CAA was found in 50.6% of brains without and in 42.4% with ICH, the latter showing a significantly higher frequency of severe degrees of CAA. ICH was related to CAA in 42.4%, whilst no such relation was seen in 57.6%. Patients with CAA were older, showed a higher frequency of clinical dementia and pathologically confirmed AD, but signs of hypertension (history and/or autopsy) occurred in 40%, compared with 80% in those with non-CAA-related ICHs. CAA-related ICH more frequently involved in cerebral lobes or hemispheres, whilst non-CAA-related ones were more often located in the basal ganglia and brainstem. The data of a lower prevalence of CAA in cases with than without ICH and of ICH with and without CAA do not support the concept that CAA represents the most important risk factor for ICH in the aged, probably because of other risk factors including hypertension. [ABSTRACT FROM AUTHOR]
ISSN:13515101
DOI:10.1111/j.1468-1331.2007.01880.x