Illusion Of Infarction : Amyloid-related Imaging Abnormalities Mimicking Posterior Circulation Stroke
Ameya Kale1, Stephanie Lontok3, Melisha Budhathoki2, Alia Tewari2, Pooja Jethwani2, Priya Narwal2
1Neurology, UConn Health, 2UConn Health, 3University of Connecticut
Background:
Amyloid-related imaging abnormalities (ARIA) are MRI findings associated with anti-amyloid therapy (AAT) in Alzheimer’s disease. ARIA arises from vascular inflammation and increased permeability, resulting in vasogenic edema (ARIA-E) or microhemorrhage/siderosis (ARIA-H). Most often asymptomatic, ARIA can present with acute onset headache, vision changes and gait impairment, mimicking subacute infarction on CT, posing diagnostic challenges.
Design/Methods:
Case report
Results:
A 78-year-old woman with hypertension and mild cognitive impairment due to Alzheimer’s pathology presented with 2 days of visual disturbance, reading difficulty, headache, and unsteady gait, three weeks after starting lecanemab. Pre-infusion MRI showed moderate white matter disease and two microhemorrhages; she was heterozygous for ApoE gene (3/4). On examination, she had right homonymous hemianopia (NIHSS 2) with elevated blood pressure. CT demonstrated left parieto-occipital hypodensity, and CTA revealed high-grade stenosis of a left posterior cerebral artery (PCA) branch, raising concern for subacute infarct. Aspirin and permissive hypertension were initiated. MRI instead showed left occipital, parietal, and temporal, sulcal hyperintensity and enhancement, with slight right occipital edema, and a new punctate focus of susceptibility, consistent with moderate ARIA-E and mild ARIA-H. Aspirin was discontinued, blood pressure lowered, and she received three days of IV methylprednisolone followed by prednisone taper. Hemianopia resolved within 3 days. Lecanemab was withheld. Follow-up MRI at 1 month showed decreased edema without new hemorrhage. At 2 months, neuropsychological testing revealed new visuospatial and visual learning deficits.
Conclusions:
This case highlights that careful identification of vasogenic edema that crosses vascular territories is crucial to differentiate ARIA from stroke. Risk factors include ApoE4 genotype, baseline microhemorrhages, elevated blood pressure, and early treatment phase. Recognition is essential as treatment differs from ischemic stroke, involving corticosteroids, AAT cessation, and MRI surveillance. ARIA may result in lasting functional impairment. Anticoagulation is contraindicated due to bleeding risk, while safety of antiplatelet agents remains uncertain.
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