Abstract 466: Acute Aphasia Following Middle Meningeal Artery Embolization ‐ A Case Report

Objectives To describe a rare complication of acute ischemic stroke (AIS) following middle meningeal artery (MMA) embolization for recurrent traumatic subdural hematoma (SDH). This event may represent an infrequent procedure‐related complication due to distal embolization or ischemia arising from failure of collateral vessels. Introduction Traumatic and chronic SDH are common intracranial disorders in the elderly. Risk factors include cerebral atrophy, coagulopathy, and antiplatelet or anticoagulant therapy. Tearing of bridging veins is the classic mechanism; however, in chronic SDH, trauma‐induced injury to dural border cells has also been implicated. These injuries trigger inflammation, fibrosis, and angiogenesis, forming a neo‐membrane. The outer neo‐membrane is highly vascular and prone to micro bleeding and thrombosis. Therefore, in addition to surgical evacuation, adjunctive therapies such as corticosteroids and MMA embolization have emerged as promising strategies. Case Presentation A 75‐year‐old man with hypertension, diabetes mellitus, atrioventricular block s/p permanent pacemaker, and traumatic acute‐on‐chronic SDH s/p recent left frontal craniectomy and left MMA embolization presented with global aphasia and right upper motor neuron (UMN) facial weakness four days after the embolization.On neurological examination, he had global aphasia (expressive and receptive) and a right facial droop; motor and sensory examinations were otherwise intact. Non‐contrast head CT showed expected postoperative changes at the left anterofrontal convexity without enlargement of the SDH or new midline shift. CT angiography of the head and neck showed no stenosis, occlusion, or other vasculopathy. An electroencephalogram (EEG) showed no epileptiform discharges or seizure activityHe had previously been taking aspirin 81 mg daily for cardiovascular benefit but was held given risks considering the SDH, but was resumed at discharge once cleared by neurosurgery. He had been discharged previously on levetiracetam 1000 mg twice daily, which was continued. MRI Brain was deferred due to device‐related constraints including an incompatible pacemaker and the patient's preference. Device interrogation demonstrated atrial pacing without arrhythmia, including no atrial fibrillation or flutter. He remained stable during hospital course and was discharged to home with outpatient speech therapy. Discussion The patient's persistent global aphasia and right facial weakness following MMA embolization are most consistent with a clinical diagnosis of acute ischemic. The absence of arrhythmia on device interrogation, lack of significant extracranial or intracranial stenosis on CTA, and unremarkable echocardiogram make a cardioembolic or large‐vessel etiology less likely. Instead, the temporal relationship to the embolization procedure raises the possibility of procedure‐related ischemia.Potential mechanisms include distal embolization of embolic material used in the MMA embolization, unintentional migration through fragile collateral channels, or compromise of cortical collateral supply, particularly around Broca's area. Although MMA embolization has been increasingly adopted due to its favorable safety profile, reported complications have included cranial nerve palsies, scalp necrosis, and very rarely ischemic stroke. This case emphasizes that even with technically successful embolization, vigilance for delayed ischemic complications is warranted. While the diagnosis of stroke remains clinical, the case contributes to the growing awareness of rare but significant ischemic complications of MMA embolization. Recognition of these risks may inform future procedural refinements, peri‐procedural monitoring strategies, and decision‐making regarding the timing of resumption of antiplatelet therapy.