Metronidazole‐induced vertigo

A 57-year-old female patient was treated with metronidazole due to paralytic ileus. Two weeks later, she presented with vertigo after being given a cumulative dose of 25 g. On physical examination, she revealed gaze-induced bidirectional nystagmus without other neurologic finding. Laboratory findings, including white blood cell count and cerebrospinal fluid (CSF) test, were all normal. Facial nerve stimulation studies show decreased compound muscle action potentials on both sides. Blink reflex studies, auditory brainstem response, and pure tone audiometry were within normal limits. Videonystagmography and vestibular function revealed central vestibulopathy. Brain magnetic resonance imaging (MRI) demonstrated symmetric high signal intensity in dorsal medulla (Fig. 1A) and inferior colliculus (Fig. 1B) on T2-weighted fluidattenuated inversion recovery imaging (T2WFLAIR). Her vertigo resolved in 2 weeks after cessation of metronidazole. Follow-up of brain MRI showed no previous brain lesions (Fig. 1C and D). Metronidazole, a 5-nitroimidazole compound, is a good choice for treating anaerobic and protozoa-related infections. However, in rare cases, it can adversely induce peripheral neuropathy or encephalopathy [1] due to its cellular penetration to CSF. Metronidazole-induced encephalopathy (MIE) is one serious but rare side effect. The exact mechanism of the neurotoxicity is yet to be clarified. Rao and Mason [2] reported that catecholamine neurotransmitters can induce 5-nitroimidazole drugs to produce semiquinone radicals and nitro anion radicals, which may contribute to neural damage. Graves et al.’s [3] study stated that MIE will occur if a daily dose of 1.6 g is used for an average duration of 79 days. However, our patient received 1.5 g daily for 14 days, which was originally considered to be within the