Itraconazole-Induced Motor Sensory Polyneuropathy in a Young Indian Male: An Unusual Case

Itraconazole, a widely prescribed triazole antifungal agent, is generally well tolerated but can rarely cause neurotoxicity. Motor-sensory polyneuropathy secondary to itraconazole use is an exceptionally uncommon and underrecognized adverse effect. Although reversibility has been reported in several cases, delayed diagnosis or continued exposure may result in persistent neurological impairment. This case report aims to highlight a rare but clinically significant adverse effect-motor-sensory polyneuropathy-associated with prolonged itraconazole use in an otherwise healthy young adult.

We report the case of a 21-year-old previously healthy Indian male student who developed progressive weakness and sensory disturbances in both lower limbs, more pronounced on the left side, after two months of oral itraconazole therapy for onychomycosis. He presented with intermittent headaches for 20 days and worsening lower limb weakness over five days. Neurological examination revealed decreased power in the lower limbs (3/5 in the right lower limb and 2/5 in the left lower limb) and impaired sensation in all upper and lower limbs. Cerebrospinal fluid analysis and brain MRI were normal. Laboratory investigations excluded metabolic, infectious, and autoimmune causes. Nerve conduction studies confirmed motor-sensory polyneuropathy. Based on the clinical course, temporal association, and exclusion of other causes, itraconazole-induced neuropathy was diagnosed. The drug was discontinued, and supportive physiotherapy was initiated. The patient showed significant improvement during hospitalization and at one-month follow-up (5/5 in the right lower limb and 4+/5 in the left lower limb).

This case emphasizes the importance of considering itraconazole-induced neuropathy in patients presenting with new-onset neurological symptoms, particularly when there is a clear history of recent itraconazole use. Early recognition and prompt withdrawal of the drug are crucial to prevent permanent neurological deficits and achieve functional recovery.