Documenta Ophthalmologica

, Volume 104, Issue 2, pp 181–188 | Cite as

Visual field and electrophysiological abnormalities due to vigabatrin

  • Kors van der Torren
  • Hellen S. Graniewski-Wijnands
  • B.C.P. Polak


The purpose of this study was to determine the electrophysiological changes in patients using the anti epileptic drug vigabatrin and to correlate these findings with the previously reported risk for visual field loss in these patients. In 1998 the neurologists of both involved hospitals referred all patients on vigabatrin medication for ophthalmological examination to the outpatients clinics. Of the 33 patients whom were referred to our outpatient clinics, four had to be dropped from the study because of disability to perform the examinations the remaining 29 patients were included in the study. Standard ophthalmological investigations were carried out, and contrast sensitivity, visual field (Humphrey 30-2 and Esterman or Octopus 32), colour vision (panel D15), ERG and EOG according to ISCEV standards were tested. 18 patients continued the medication and 11 stopped taking the drug during the study. Nine of the patients who stopped the drug were followed during at least half a year afterwards, this group will be described in the combined article `Electro ophthalmic recovery after withdrawal from vigabatrin' (Graniewski and Van der Torren, this issue). The electro-ophthalmological findings in the group of 29 patients were correlated with the visual fields and the daily and cumulative dosages of vigabatrin. Of the patients, 32% showed no visual field constriction at all; from these patients 64% had EOG and/or ERG changes. Of the patients with slight to marked visual field constriction, 90% presented EOG and/or ERG changes. Significant correlation between daily dosages of vigabatrin and visual field defects was shown as well as between visual field defects and rod and cone b wave amplitude reductions. Cumulative vigabatrin dosages presented a significant correlation with EOG ratio and ERG rod b-wave amplitude. Conclusively EOG and ERG testing were found to be even an more accurate way to monitor the direct vigabatrin effect on the outer retina and is possible different from the visual field testing.

EOG ERG cumulative dosages vigabatrin 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Eke T, Talbot JF, Lawden MC. Severe persistent visual field constriction associated with vigabatrin. Br Med J 1997; 314: 180–1.Google Scholar
  2. 2.
    Wilton LV, Stephens MOB, Mann RD. Visual field defect associated with vigabatrin: observational cohort study. Pharmacol. Epidemiol. Drug Safety 1999; 8: S9–14.Google Scholar
  3. 3.
    Blackwell N. Severe persistent visual field constriction associated with vigabatrin. Patients taking vigabatrin should have regular visual field testing. Br Med J 1997; 314: 1694.Google Scholar
  4. 4.
    Harding GF. Severe persistent visual field constriction associated with vigabatrin. Four possible explanations exist. Br Med J 1997; 314: 1694.Google Scholar
  5. 5.
    Lawden MC, Eke T, Degg C, Harding GFA, Wild JM. Visual field defects associated with vigabatrin therapy. J Neurol Neurosurg Psychiatry 1999; 67: 716–22.Google Scholar
  6. 6.
    Hardus P, Verduin WM, Postma G, Stilma JS, Berenschot TTJM, van Veelen CWM. Long-term changes in visual fields of patients with temporal lobe epilepsy using vigabatrin. In press.Google Scholar
  7. 7.
    Neal MJ, Cunningham JR, Shah MA, Yazulla S. Immunocytochemical evidence that vigabatrin in rats causes GABA accumulation in glial cells of the retina. Neurosci Lett 1989; 98: 29–32.Google Scholar
  8. 8.
    Gottlob I, Wundsch L, Tuppy FK. The rabbit electroretinogram: effect of GABA and its antagonists. Vis Res 1988; 2: 203–10.Google Scholar
  9. 9.
    Euler T, Wassle H. Different contributions of GABAa and GABAc receptors to rod and cone bipolar cells in rat retinal slice preparation. J Neurophys 1998; 79: 1384–95.Google Scholar
  10. 10.
    Qqian H, Malchow RL, Chappell RL, Ripps H. The GABA receptors of skate Muller cells. Brain Res J 1996; 37: 222–3.Google Scholar
  11. 11.
    Bayer A, Thiel H-J, Zrenner E, Paulus W, Ried S. Schmidt D. Colour vision deficiencies and enhanced sensitivity to glare in epileptic patients treated with carbamazepine and phenytoin: ocular side effects of antiepileptic drug. Nervenarz 1995; 66: 89–96.Google Scholar
  12. 12.
    Arndt CF, Derambure P, Defoort-Ohellemes S, Hache JC. Outer retinal dysfunction in patients treated with vigabatrin. Neurology 1999; 52: 1201–5.Google Scholar
  13. 13.
    Daneshvar H, Racette L, Coupland S, Kertes PJ, Gubermann A, Zackon D. Symptomatic and asymptomatic visual loss in patients taking vigabatrin. Ophthalmology 1999; 106: 1792–8.Google Scholar
  14. 14.
    Krauss GL, Johnson MA, Miller NR. Vigabatrin associated retinal cone system dysfunction. Electroretinogram and ophthalmic findings. Neurology 1998; 50: 614–8.Google Scholar
  15. 15.
    Mustafa BA. Diversity of GABA receptors in the vertebrate outer retina. Trends Neurosci 1995; 18: 118–20.Google Scholar

Copyright information

© Kluwer Academic Publishers 2002

Authors and Affiliations

  • Kors van der Torren
    • 1
  • Hellen S. Graniewski-Wijnands
    • 2
  • B.C.P. Polak
    • 3
  1. 1.Department of OphthalmologyAlbert Schweitzer HospitalDordrechtThe Netherlands
  2. 2.Leiden University Medical CenterLeidenThe Netherlands
  3. 3.Vrije Universiteit AmsterdamUniversity HospitalAmsterdamThe Netherlands

Personalised recommendations