{'fraction_non_alphanumeric': 0.027577937649880094, 'fraction_numerical': 0.005595523581135092, 'mean_word_length': 5.764864864864865, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Amiodarone‐induced gait unsteadiness is revealed to be bilateral vestibulopathy

A 73-year-old man presented with persisting unsteadiness of gait and motioninduced vertigo for 3 years, worsened in darkness and on uneven ground. Symptoms began 6 months after the initiation of antiarrhythmic therapy with amiodarone (200 mg/day). With progressing gait unsteadiness, further neurological work-up had been initiated, revealing a mixed axonal demyelinating sensorimotor polyneuropathy. Clinical vestibular testing was not performed at that time. As a drug-related polyneuropathy was considered, amiodarone was discontinued. Within weeks of the withdrawal, symptoms initially partially improved, but then remained stable. His medical history was significant for ventricular extrasystoles, thoracic aortic aneurysm, status post-renal cell carcinoma, status postesophageal carcinoma, arterial hypertension and hyperlipoproteinemia. The patient never received ototoxic drugs. Clinical examination revealed a bilateral pathological head-impulse test. Vestibular testing showed profoundly pathological responses bilaterally in the video head-impulse test and calorimetry (Fig. 1). Audiometry detected bilateral symmetric high-frequency hearing loss. Laboratory tests were within normal ranges. Repeated high-resolution magnetic imaging excluded any pathologies such as cerebellar/brainstem infarction or atrophy. There was no evidence of a central vestibular or cerebellar disorder. Compared with liver, pulmonary and thyroid side-effects, neurological adverse reactions of amiodarone are less well-known and probably under-reported [1–3]. Earlier reports frequently described amiodarone-induced gait ataxia, but did not clearly define the type of gait disorder summarized under this term. Interestingly, a cerebellar syndrome was clinically suspected in only a minority of the cases [1]. Although gait unsteadiness is one of the key clinical features of bilateral vestibulopathy, vestibular function tests were not performed in any of the previous studies. Ototoxic drugs are one of the most common reasons for bilateral vestibulopathy [4], and amiodarone has been reported to accumulate in neural tissue and cause the formation of lysosomal inclusion bodies [5]. The main risk factor for the development of neurotoxic effects seems to be treatment duration [2]. Based on the findings that time course and intensity of symptoms were linked to intake and discontinuation of amiodarone, treatment duration and the