Visual field defects associated with vigabatrin therapy

Citation
Mc. Lawden et al., Visual field defects associated with vigabatrin therapy, J NE NE PSY, 67(6), 1999, pp. 716-722
Citations number
39
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
ISSN journal
00223050 → ACNP
Volume
67
Issue
6
Year of publication
1999
Pages
716 - 722
Database
ISI
SICI code
0022-3050(199912)67:6<716:VFDAWV>2.0.ZU;2-4
Abstract
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.