Abstract Details

Title Clinical Presentation and Pathological Findings of Cerebral Amyloid Angiopathy-Related Inflammation Caused by COVID-19 Infection: A Case Report and Literature Review

Topic Infectious Disease

Presentation(s) P1 - Poster Session 1 (11:45 AM-12:45 PM)

Poster/Presentation
Number 10-001

Objective To compare the clinical and pathological characteristics of cerebral amyloid angiopathy-related inflammation (CAA-ri) potentially induced by COVID-19 infection with the known features of typical CAA-ri cases.

Background CAA-ri associated with COVID-19 infection is an exceedingly rare phenomenon, with limited information available regarding its clinical manifestations, pathological findings, therapeutic responsiveness, and prognosis.

Design/Methods We present a case report of a patient who developed parkinsonism following COVID-19 infection, with an accompanying literature review detailing the clinical course, diagnostic process, pathological findings, and response to immunotherapy.

Results A 79-year-old woman presented with subacute dementia and gait disturbance associated with parkinsonism one month post-COVID-19 infection. Brain magnetic resonance imaging (MRI) revealed diffuse T2-weighted hyperintensities predominantly in the subcortical white matter of the left temporal and occipital lobes, alongside multiple cerebral microbleeds that had been present for two years. Dopamine transporter single-photon emission computed tomography (DAT-SPECT) showed no significant dopaminergic impairment. Pathological examination of an occipital lobe biopsy disclosed vascular amyloid-β deposits accompanied by perivascular inflammatory infiltrates composed of CD3-positive T lymphocytes, findings characteristic of CAA-ri. Notably, granulomatous inflammation was absent. Based on the MRI and pathological features, a diagnosis of CAA-ri was confirmed. The patient underwent three courses of intravenous methylprednisolone pulse therapy, followed by oral prednisone, which resulted in significant improvement in cognitive function, parkinsonism, and MRI findings. A literature review identified only one similar case of CAA-associated inflammatory angiitis occurring after COVID-19 infection. Additionally, other CAA-ri cases with parkinsonism, though unrelated to COVID-19 infection, were documented, implicating the cerebral cortex as the primary site of pathology.

Conclusions This case underscores critical insights: 1) neuroinflammation, possibly induced by COVID-19 infection, may precipitate the onset of CAA-ri; and 2) the clinical and pathological characteristics of CAA-ri following COVID-19 infection may be comparable to those of typical CAA-ri, with a favorable response to immunotherapy.

Authors/Disclosures
Yasushi Shiba, MD PRESENTER	Dr. Shiba has nothing to disclose.
Akira Takekoshi	Akira Takekoshi has nothing to disclose.
Akio Kimura, MD (Gifu University Graduate School of Medicine)	Dr. Kimura has nothing to disclose.
Hiroshi Shimizu, MD, PhD	Dr. Shimizu has nothing to disclose.
Takayoshi Shimohata, MD, FAAN (Department of Neurology, Gifu University)	Dr. Shimohata has nothing to disclose.

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