A 63 year old patient who reported a visual acuity (VA) deficit in the right eye (OD) of several months' evolution.
His personal history included post-traumatic epilepsy of ten years' duration, arterial hypertension and type II diabetes mellitus.
He had been treated with 1.5 g vigabatrin and 200 mg carbamazepine daily since the trauma.
VA was 0.3 in the OD and 0.8 in the left eye with correction.
Anterior biomicroscopy and tonometry were normal.
Ophthalmoscopy revealed pallor of both papillae and a macular epiretinal membrane in the OD.

Computerised Humphrey 30/2 white-white and blue-yellow perimetry showed severe concentric campimetric reductions in both eyes (Humphrey instruments, model 745, Carl Zeiss Inc).

She had no family history of interest, so hereditary optic neuropathy was ruled out.
The anamnesis and analytical determinations of mean corpuscular volume, vitamins B1, B6, B12 and folic acid ruled out nutritional aetiology.
A diagnosis of retinotoxicity due to vigabatrin was established and the patient was referred to the neurology department.
At one year of follow-up, the loss of campimetry and VA persisted.