An Unusual Mechanism of Stroke in Neurobrucellosis: Middle Cerebral Artery Infarction Secondary to Direct Abscess Compression - A Case Report and Literature Review.

Abstract

Introduction: Brucellosis is a zoonotic infection that remains endemic across the Middle East, Central Asia, the Mediterranean basin, and parts of Africa and Latin America. Neurobrucellosis (NB) develops in fewer than 5% of cases and constitutes the most severe systemic complication. Cerebrovascular involvement is uncommon and most often attributed to small-vessel vasculitis, immune-mediated endarteritis, or septic embolization. Ischemic stroke caused by direct mechanical compression of an intracranial artery by a Brucella abscess has not been previously reported.

Case presentation: A 47-year-old previously healthy male with occupational livestock exposure presented with sudden onset of left-sided weakness, facial droop, and global aphasia. Initial imaging demonstrated an acute right middle cerebral artery (MCA) territory infarct, and standard ischemic stroke management was initiated. Over the next 24 h, intermittent low-grade fever, persistent confusion, and focal motor seizures emerged despite levetiracetam. Subsequent magnetic resonance imaging showed a 2.5 cm rim-enhancing lesion in the right temporal lobe with central diffusion restriction, consistent with a pyogenic abscess. Magnetic resonance angiography demonstrated focal occlusion of the anterior segment of the right MCA, immediately adjacent to the abscess. Cerebrospinal fluid showed lymphocytic pleocytosis (36 cells/mm³, 85% lymphocytes) and elevated protein (112 mg/dL). Serum Brucella IgG returned positive on day 20, confirming neurobrucellosis. Triple antimicrobial therapy with intravenous ceftriaxone, oral doxycycline, and oral rifampicin produced gradual neurological improvement, and the patient was discharged on long-term oral therapy.

Conclusion: This case illustrates a novel cerebrovascular mechanism in NB, in which mass effect from a peri-vascular abscess produced ischemic stroke. Coexisting perilesional inflammation likely contributed through a vasculitic component, and the two mechanisms are not mutually exclusive. The absence of systemic brucellosis features delayed recognition and underscores the protean clinical presentation of NB. Brucellosis warrants consideration in the differential diagnosis of acute ischemic stroke when imaging reveals concurrent intracranial infectious lesions, particularly in endemic regions. Early antimicrobial therapy is critical to limit progression and improve neurological outcomes.