The Neurohospitalist · 2026
Fulminant Amyloid-β-Related Angiitis after Tenecteplase: A Biopsy-Confirmed Cause of Post-Thrombolysis Neurologic Deterioration.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Schweitzer Christina, Durai Kalkini, Kadakia Shreeja, Zeigler Grant, Pham Khoa
Аннотация
BACKGROUND: Amyloid-β-related angiitis (ABRA) is a rare steroid-responsive inflammatory vasculopathy that can mimic or complicate acute cerebrovascular disease. Its interaction with thrombolytic therapy is poorly understood. We report a biopsy-confirmed case of fulminant ABRA temporally associated with intravenous tenecteplase.
CASE DESCRIPTION: An 86-year-old man presented with acute painless monocular vision loss and received tenecteplase for presumed central retinal artery occlusion. Initial imaging showed no hemorrhage. Within 24 hours, he developed progressive encephalopathy with a large left frontal lobar hemorrhage, additional contralateral lobar hemorrhages, and diffuse subarachnoid hemorrhage requiring surgical evacuation. Pathology demonstrated Congo red-positive amyloid deposition with transmural lymphocytic and macrophage-predominant inflammation and fibrinoid necrosis, confirming ABRA. MRI showed progressive vasogenic edema, new punctate infarcts, increasing cortical microbleeds, and convexity subarachnoid hemorrhage. Infectious evaluation was negative. High-dose corticosteroids led to gradual neurologic improvement.
CONCLUSIONS: Thrombolysis may unmask or exacerbate inflammatory cerebral amyloid angiopathy, causing multifocal hemorrhage, ischemia, and rapid decline. In older patients with unexpected post-thrombolysis deterioration and evolving lobar hemorrhage, edema, and microbleeds, ABRA should be considered, as early immunosuppression may improve outcomes.
CASE DESCRIPTION: An 86-year-old man presented with acute painless monocular vision loss and received tenecteplase for presumed central retinal artery occlusion. Initial imaging showed no hemorrhage. Within 24 hours, he developed progressive encephalopathy with a large left frontal lobar hemorrhage, additional contralateral lobar hemorrhages, and diffuse subarachnoid hemorrhage requiring surgical evacuation. Pathology demonstrated Congo red-positive amyloid deposition with transmural lymphocytic and macrophage-predominant inflammation and fibrinoid necrosis, confirming ABRA. MRI showed progressive vasogenic edema, new punctate infarcts, increasing cortical microbleeds, and convexity subarachnoid hemorrhage. Infectious evaluation was negative. High-dose corticosteroids led to gradual neurologic improvement.
CONCLUSIONS: Thrombolysis may unmask or exacerbate inflammatory cerebral amyloid angiopathy, causing multifocal hemorrhage, ischemia, and rapid decline. In older patients with unexpected post-thrombolysis deterioration and evolving lobar hemorrhage, edema, and microbleeds, ABRA should be considered, as early immunosuppression may improve outcomes.