Neurotoxicity of antituberculous drugs in a patient without active tuberculosis

Abstract

Three months after the beginning of an antituberculous regimen with Isoniazid (INH, 5 mg/kg daily), Ethambutol (20 mg/kg daily), Rifampicin (675 mg daily) and vitamin B₆ a 56-year-old patient presented with a mild sensory polyneuropathy and a bilateral retrobulbar neuritis which progressed to a severe optic atrophy. Multiple hyperintense foci were detected with NMR-imaging in the cerebral white matter suggestive of central demyelination. INH and Ethambutol are known for their neurotoxic effects but the suggestion was made that neurologic signs may not be due to drug neurotoxicity but could be induced by immunological processes initiated by the tubercle bacillus. In the patient reported the suspected tuberculosis of the urogenital tract could not be proved histologically. Most likely his neurological symptoms were therefore caused by the administration of INH and Ethambutol. Patients with a low serum zinc level and a slow acetylation of INH are reported to be at special risk, both factors being present in the authors' patient.

Key Words:

• neurotoxicity
• antituberculous drugs
• optic atrophy
• encephalopathy