When a Withdrawal Aid Mimics a Brainstem Lesion: Gabapentin-associated Transient Ophthalmoplegia.

Abstract

Gabapentin is frequently used as a benzodiazepine-sparing agent for the management of mild to moderate alcohol withdrawal and is generally considered well-tolerated. Although neurological adverse effects have been reported, objective ocular motor abnormalities associated with gabapentin use during alcohol withdrawal are rarely described. Recognition of such effects is important to guide evaluation and management. We report a 60-year-old man admitted to a residential treatment program for alcohol use disorder who developed acute diplopia and transient ophthalmoplegia shortly after initiation of gabapentin for mild alcohol withdrawal. The patient had no history of withdrawal seizures or delirium tremens and presented with a low CIWA-Ar score. Gabapentin was initiated at a total daily dose of 1800 mg using a fixed-dose taper. Within 24 hours, he developed diplopia, gaze-evoked nystagmus, and mild gait ataxia. Neurological examination revealed unilateral ophthalmoplegia, while neuroimaging and laboratory evaluation were unremarkable. Gabapentin was discontinued, and symptoms resolved completely within 24 hours without recurrence. The temporal relationship between gabapentin initiation and symptom onset, along with rapid resolution after discontinuation, supports a medication-induced neurological effect rather than alcohol withdrawal-related encephalopathy or structural neurological disease. The findings localize to cerebellar-brainstem pathways and are consistent with gabapentin's known effects on voltage-gated calcium channels. Gabapentin remains a useful option for mild to moderate alcohol withdrawal; however, rapid dose escalation may increase the risk of reversible neurological adverse effects. New-onset diplopia or ocular motor abnormalities should prompt medication review and appropriate neurological evaluation to ensure patient safety.