Objective-To estimate the prevalence of visual field defects in patients ta
king the anticonvulsant drug vigabatrin and to characterise the features of
visual dysfunction found.
Methods-Thirty three unselected patients attending neurology and epilepsy c
linics were identified as taking vigabatrin and asked to attend for neuro-o
phthalmic evaluation. A control group of 16 patients with epilepsy unexpose
d to vigabatrin was also evaluated. Visual fields were examined by static p
erimetry using a Humphrey field analyser. Patients underwent detailed ophth
almic examination, various blood tests, and brain MRI where necessary. Visu
al evoked responses (VERs), electro-oculograms (EOGs), and electroretinogra
ms (ERGs) were recorded.
Results-Of 31 assessable patients treated with vigabatrin, 16 (52%) had def
initely abnormal visual fields, nine (29%) had fields that were inconclusiv
e, four (13%) had normal fields, and two (6%) proved unable to cooperate wi
th testing. In four patients some plausible cause was found for the field a
bnormality leaving 12 patients (39%) in whom a definite bilateral field def
ect was found, possibly caused by vigabatrin treatment. Of 16 control patie
nts none had definitely abnormal fields, 12 (75%) had normal fields, and fo
ur (25%) had fields that were inconclusive. The field defects associated wi
th vigabatrin treatment showed a characteristic pattern of concentric perip
heral field loss with temporal and macular sparing. The VERs and ERGs were
normal. The EOG Arden Index was reduced in patients taking vigabatrin, alth
ough this returned towards normal when vigabatrin was stopped, even in the
presence of persistent field defects. Multifocal ERGs recorded in two patie
nts were abnormal, showing marked reduction in amplitude of the peripheral
focal ERG.
Conclusions-Treatment with vigabatrin was associated with a high prevalence
of peripheral visual field defects. This seemed to be the result of a toxi
c effect of vigabatrin on the retina and seemed to persist if the drug was
withdrawn.