title: Vigabatrin, a gabaergic antiepileptic drug, causes concentric visual field defects.
abstract: OBJECTIVE
  To determine whether there is a causal link between vigabatrin treatment and concentric visual field defects and to evaluate the prevalence of these visual field constrictions.
  
  
  BACKGROUND
  While the GABAergic antiepileptic drug (AED) vigabatrin was being clinically developed, only rare cases (less than 1:1000) of symptomatic visual field constriction and retinal disorders were reported. During 1997 to 1998, concentric visual field constrictions were described in case reports of mostly drug-resistant epilepsy patients receiving vigabatrin concurrently with other AEDs.
  
  
  METHODS
  Ophthalmologic tests including Goldmann perimetry were performed on 32 adult patients on long-term successful vigabatrin monotherapy (treatment duration 29 to 119 months) and on 18 patients on carbamazepine monotherapy (treatment duration 32 to 108 months). Eighteen healthy adults served as controls.
  
  
  RESULTS
  None of the patients complained about vision problems when asked to participate into the study. Thirteen out of the 32 (40%) epilepsy patients treated with vigabatrin monotherapy had concentrically constricted visual fields (9% severely, 31% mildly constricted), whereas none of the carbamazepine monotherapy patients or normal controls presented with a visual field defect (chi-square test, p = 0.0001). The extents of the visual fields were significantly constricted in vigabatrin group as compared with the visual fields of the patients in carbamazepine group or healthy controls (analysis of variance, Scheffe F-test, significant at 99%).
  
  
  CONCLUSIONS
  The use of vigabatrin seems to increase the risk of a unique and specific pattern of bilateral, mainly asymptomatic visual field constriction. This risk should be considered when using vigabatrin. Visual field testing should also be performed before treatment and during routine follow-up for patients on vigabatrin.
authors.affiliation: Department of Neurology, University Hospital of Kuopio, Finland. reetta.kalviainen@kuh.fi
authors.forename: R
authors.initials: R
authors.lastname: Kälviäinen
authors.forename: I
authors.initials: I
authors.lastname: Nousiainen
authors.forename: M
authors.initials: M
authors.lastname: Mäntyjärvi
authors.forename: E
authors.initials: E
authors.lastname: Nikoskelainen
authors.forename: J
authors.initials: J
authors.lastname: Partanen
authors.forename: K
authors.initials: K
authors.lastname: Partanen
authors.forename: P
authors.initials: P
authors.lastname: Riekkinen
mesh_terms: D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D000927:Anticonvulsants / Q000627:therapeutic use*; D002220:Carbamazepine / Q000627:therapeutic use; D004828:Epilepsies, Partial / Q000188:drug therapy*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D020888:Vigabatrin / Q000627:therapeutic use*; D058609:Visual Field Tests; D014794:Visual Fields / Q000187:drug effects*
chemical_list: D000927:Anticonvulsants; D002220:Carbamazepine; D020888:Vigabatrin