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.