On 10/16/18, a 5-year-old male castrated Bernese Mountain Dog presented to the Cornell University Hospital for Animals’ Emergency Service for an acute onset inability to rise. About one year prior to presentation, the patient had a fibrocartilaginous embolism diagnosed following magnetic resonance imaging. Although the dog returned to voluntary ambulation, he never regained L6-S3 spinal cord segment function or sensation and remained incontinent. Residual neurologic deficits localized to an L6-S3 myelopathy and the patient also had chronic recurrent urinary tract infections and presumed antibiotic induced diarrhea. On presentation to the Emergency Service the patient was anxious, hyperthermic, and tachypneic with clinical signs suggestive of distributive shock; these problems were addressed immediately. General physical exam was otherwise unremarkable and neurologic exam revealed clinical signs consistent with a central vestibular lesion. Principal differentials for the dog’s central vestibular lesion, considering signalment and history, included: metronidazole toxicity, thromboembolic event, and neoplasia. Based on the dog’s need for supportive care and further diagnostic investigation, he was hospitalized for transfer to the Neurology Service. To treat presumptive metronidazole toxicity, given his history of chronic metronidazole administration and client-directed provision of additional doses of metronidazole, an intravenous dose of diazepam was administered on admission to the intensive care unit. Additional diagnostics performed were unremarkable and the dog’s clinical signs rapidly improved over the next 36 hours. He was discharged to the care of his owner two days after initial presentation. Diazepam, combined with discontinuation of metronidazole and provision of supportive care, is currently the recommended treatment for metronidazole toxicity (Gwaltney-Brant, 2018). It is posited that metronidazole mediates toxicity through the benzodiazepine binding sites of gamma-aminobutyric acid (GABA) receptors within the central vestibular nuclei and cerebellum. Thus, administration of diazepam may displace the metronidazole molecule from the GABA receptor. While this mechanism is not yet confirmed, dogs that received diazepam following metronidazole overdose recovered significantly faster than dogs that did not (Evans, 2003).