Ghozy, Sherief A.

ABSTRACT Sudden sensorineural hearing loss (SSNHL) is most often idiopathic or related to benign conditions such as Meniere's disease. However, SSNHL caused by vertebrobasilar ischemia is rare and may precede life‐threatening neurological deficits. We present the case of a 67‐year‐old male with hypertension and hyperlipidemia who developed acute vertigo, left‐sided hearing loss, dysarthria, right facial droop, and right‐sided weakness. Initial non‐contrast CT was unremarkable, but computed tomography angiography (CTA) revealed a near‐occlusive thrombus in the mid‐basilar artery. MRI showed an acute infarct in the left cerebellum within the anterior inferior cerebellar artery (AICA) distribution, which supplies the internal auditory artery. Subsequent audiometry confirmed bilateral SSNHL, more severe on the left. The patient was outside the thrombolysis window but underwent cerebral angiography, which confirmed chronic left vertebral occlusion and high‐grade basilar stenosis. He was started on dual antiplatelet therapy and high dose statin therapy and discharged to rehabilitation with residual vertigo and hearing loss. This case emphasizes that SSNHL and vertigo can be early signs of posterior circulation stroke. High‐grade basilar stenosis affecting AICA flow may compromise perfusion to the auditory and vestibular systems. Clinicians should maintain a high index of suspicion for vertebrobasilar ischemia in patients presenting with audiovestibular symptoms, even in the absence of classic stroke findings. Early imaging with MRI and CTA is critical for diagnosis. Recognizing these atypical presentations enables timely management and may reduce long‐term neurologic impairment.

Brain arteriovenous malformations (bAVMs) are a notable cause of intracranial hemorrhage, strongly associated with severe morbidity and mortality. Contemporary treatment options include surgery, stereotactic radiosurgery, and endovascular embolization, each of which has limitations. Hence, development of pharmacological interventions is urgently needed. The recent discovery of the presence of activating Kirsten rat sarcoma ( KRAS ) viral oncogene homologue mutations in most sporadic bAVMs has opened the door for a more comprehensive understanding of the pathogenesis of bAVMs and has pointed to entirely novel possible therapeutic targets. Herein, we review the status quo of genetics, animal models, and therapeutic approaches in bAVMs.