¹Hospital Universitario 12 de Octubre, Psychiatry, Madrid, Spain, ²Hospital Universitario de La Princesa, Psychiatry, Madrid, Spain

Background: Disulfiram is a widely prescribed aversive agent for the treatment of Alcohol Use Disorder (AUD). Although generally well tolerated, rare but potentially serious adverse effects have been described, including peripheral and optic neuropathy, with an estimated annual incidence of approximately 1 per 15,000 treated patients. Disulfiram-induced neuropathy may present as sensory, motor, or sensorimotor polyneuropathy, optic neuritis, or, in severe cases, quadriplegia. The risk appears to be dose-related and associated with prolonged exposure, particularly at doses ≥500 mg/day. Importantly, it may be underrecognized in clinical practice, as symptoms can be misattributed to alcoholic neuropathy.

Aims & Objectives: To describe the sociodemographic and clinical characteristics of patients with AUD who developed confirmed disulfiram-induced peripheral and/or optic neuropathy in an alcohol treatment programme at a tertiary care hospital.

Method: We conducted a descriptive study including all patients diagnosed with AUD (n=10) who attended the Alcohol Treatment Programme at a tertiary care hospital in Madrid, Spain, during 2025 and received a confirmed diagnosis of disulfiram-induced neuropathy. Diagnosis was established based on clinical presentation, temporal association with disulfiram exposure, exclusion of alternative etiologies (including diabetes mellitus, vitamin B12 deficiency, and other known causes of neuropathy), and specialist neurological and/or ophthalmological assessment when indicated. Clinical records were reviewed to obtain demographic, substance use, treatment, and outcome data.

Results: Eighty per cent of patients were male, with a mean age of 60 years (SD 6.2). The mean duration of alcohol consumption was 44 years (SD 6.5), and the mean reported daily alcohol intake was 254 grams, ranging from 50 to 800 g/day. All patients were active tobacco users. Regarding disulfiram dosage, 50% were receiving 500 mg/day and 50% 250 mg/day at the time of symptom onset. The most common presentation was peripheral sensory neuropathy (70%), followed by optic neuropathy (20%) and combined peripheral and optic involvement (10%). The mean duration of disulfiram treatment prior to neuropathy onset was 49 months (SD 62.8), indicating substantial variability in time to presentation. Following discontinuation of disulfiram, only 10% of patients achieved full recovery, 50% experienced partial improvement, and 40% had persistent neurological symptoms at follow-up.

Discussion & Conclusions: In this case series, disulfiram-induced neuropathy predominantly occurred in patients with long-standing AUD, prolonged exposure to disulfiram, and frequent use of higher doses. The most common manifestation was peripheral sensory neuropathy. Although some degree of clinical improvement was observed after drug discontinuation, complete recovery was uncommon, and persistent sequelae were frequent. Given the potential for irreversible damage and the possibility of diagnostic confusion with alcoholic neuropathy, clinicians should maintain a high index of suspicion, particularly in patients receiving doses ≥500 mg/day or long-term treatment. Use of the lowest effective dose (preferably ≤250 mg/day) and regular neurological and ophthalmological monitoring may facilitate early detection and improve outcomes.