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Washington University Experience | VASCULAR | Congophilic Angiopathy (CAA) | 25A0 Case 25 History

25A0 Case 25 History
Case 25 History ---- This 71-year-old woman remained CDR 0, no dementia from 1997-2005. In April 2001, she had an episode of right hand and arm numbness plus headache thought to be a TIA and was started on Plavix. In April 2004, she experienced right-sided weakness which was thought to be a small left posterior frontal infarct. In October 2005, she was admitted to a hospital with altered mental status and slight right facial drooping. A brain CT showed a left temporal lobe hemorrhage. The main finding was aphasia – word finding and word substitution. A source reported that there was a problem with her memory which was sudden in onset. She continued to live independently until she was found on her apartment floor, flailing her arms and semi-conscious in January 2010. After 12 days in the hospital, she was sent to a rehab facility for 6 weeks. On April 13, she was sent to the hospital with a “massive stroke”. The family was told that the entire right side of her brain was involved. She was given comfort measures only until she died 5 days later with a diagnosis of vascular dementia. ---- At autopsy her estimated whole brain weight was 1,080 g. She had the neuropathology of Alzheimer disease and Lewy bodies were demonstrated in the substantia nigra. Remote infarcts/microinfarcts with admixed hemosiderin were found in multiple sites, including cerebral cortex, subcortical white matter and basal ganglia. Patchy subarachnoid hemorrhage, subacute-remote, consisting of hemosiderin laden macrophages, small vessel disease, arteriolosclerosis and cerebral amyloid angiopathy (severe) were also identified. The histopathology is consistent with the neuropathological diagnosis of Alzheimer's disease (AD) by Khachaturian criteria; 'probable' AD by the CERAD criteria and there is an 'intermediate' probability that the dementia is caused by AD according to the NIA-Reagan Institute criteria. Vascular pathology consisted of moderate to severe cerebral arteriolosclerosis, focal mild white matter pallor with relative axonal loss, and remote infarcts in the frontal and temporal lobes, scattered remote microinfarcts in multiple areas and severe cerebral amyloid angiopathy.



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