Cases Neurology ® Clinical Practice Acute peripheral vestibulopathy in a cocaine addict Cracking the vestibular nucleus Anteneh M. Feyissa, MD, MSc Todd Masel, MD Stephen P. Busby, MD A previously healthy 58-year-old man developed vertigo, imbalance, nausea, and vom- iting shortly after smoking cocaine. He denied hearing loss, double vision, limb weakness, or sensory loss. Examination showed left-beating horizontal nystagmus with a torsional component, skew deviation, and positive right-sided head-impulse test. His urine tested positive for cocaine. Autoimmune workup, lipid panel, and echocardiog- raphy were unremarkable. MRI revealed acute right medial vestibular nucleus (VN) infarction (figure, A and B) and subcortical T2 hyperintensities (figure, C). Cerebral angiography was unremarkable. Presenting symptoms responded to meclizine and ondansetron, resolving by the third day. Our patient presented with signs and symptoms consistent with acute peripheral vestibulop- athy (APV), albeit for the skew deviation, in the context of acute right VN infarction. This un- usual occurrence may be related to the VN’s role in relaying and central processing of peripheral vestibular signals. 1 The exact mechanism of cocaine-induced ischemic stroke Figure Isolated vestibular nucleus infarction after cocaine consumption Brain MRI shows an acute infarct (arrows) that selectively involved the right vestibular nucleus at the pontomedullary junction level on diffusion-weighted imaging (A) and apparent diffusion coefficient mapping (B). Fluid-attenuated inversion recovery image depicting periventricular and subcortical white matter hyperintensities (C). Department of Neurology, University of Texas Medical Branch at Galveston, Galveston, TX. Funding information and disclosures are provided at the end of the article. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp. Correspondence to: amfeyiss@utmb.edu 532 © 2014 American Academy of Neurology