Skip to main content
SpringerLink
Log in

Visual field constriction and electrophysiological changes associated with vigabatrin

  • Published:
Documenta Ophthalmologica Aims and scope Submit manuscript

Abstract

Purpose: We investigated functional, morphological and electrophysiological changes in patients under anti-epileptic therapy with vigabatrin (VGB), a GABA aminotransferase inhibitor. Methods: 20 epileptic patients treated with vigabatrin (age range 25–66 years) were enrolled in this study. The referrals were made by the treating neurologist, based on suspected or known visual field changes in these patients. Two patients had vigabatrin monotherapy, 18 patients were treated with vigabatrin in combination with other antiepileptic drugs. None of the patients reported visual complaints. Patients were examined with psychophysical tests including colour vision (Farnsworth D15), dark adaptation threshold, Goldmann visual fields and Tuebingen Automated Perimetry (90°). A Ganzfeld ERG and an EOG following the ISCEV standard protocol were also obtained. Additionally, all patients were examined with the VERIS multifocal ERG including recordings of multifocal oscillatory potentials. Results: Visual acuity, anterior and posterior segments, colour vision and dark adaptation thresholds were normal in all patients. Of 20 patients, 18 presented visual field constriction. All patients with visual field defects revealed altered oscillatory potentials waveforms in the ERG, especially in those patients with marked visual field defects. Multifocal oscillatory potentials were also delayed in those patients. In some patients a delayed cone single flash response (6/20), a reduced mERG amplitude (12/20) and a reduced Arden ratio (9/20) were found. Conclusions: The present data indicate an effect of vigabatrin on the inner retinal layers. Since abnormalities of the oscillatory potentials were seen in all patients with visual field defects a dysfunction of GABA-ergic retinal cell transmission might be assumed.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Eke T, Talbot JF, Lawden MC. Severe persistent visual field constriction associated with vigabatrin. Br Med J 1997; 314: 180–181

    Google Scholar 

  2. Harding GFA. Severe persistent visual field constriction associated with vigabatrin. Four possible explanations exist. Br Med J 1997; 314: 1694

    Google Scholar 

  3. Blackwell N, Hayllar J, Kelly G. 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. Wilson EA, Brodie MJ. Chronic refractory epilepsy may have role in causing these unusual lesions. Br Med J 1997, 314: 1693

    Google Scholar 

  5. Wong IC, Mawer GE, Sander JW. Severe persistent visual field constriction associated with vigabatrin. Reaction might be dose dependent. Br Med J 1997; 314: 1694

    Google Scholar 

  6. MacKenzie R, Klistorner A. Severe persistent visual field constriction associated with vigabatrin. Asymptomatic as well as symptomatic defects occur with vigabatrin. Br Med J 1998; 316: 233

    Google Scholar 

  7. Harding GFA. Severe persistent visual field constriction associated with vigabatrin. Benefit:risk ratio must be calculated for individual patients. Br Med J 1998; 316: 232–3

    Google Scholar 

  8. Rao GP, Fat FA, Kyle G, Leach JP, Chadwick DW, Batterbury M. Study is needed of visual field defects associated with any long term antiepileptic drug. Br Med J 1998; 317: 206

    Google Scholar 

  9. Baulac M, Nordmann JP. Lanoé Y. Severe visual field constriction and side effects of GABA-mimetic antiepileptic agents. Lancet 1998; 352:546

    Google Scholar 

  10. Daneshvar H, Racette L, Coupland SG, Kertes PJ, Guberman A, Zackon D. Symptomatic and asymptomatic visual field loss in patients taking vigabatrin. Ophthalmology 1999; 106: 1792–8

    Google Scholar 

  11. Miller NR, Johnson MA, Paul SR. Girkin CA, Perry JD, Endres M, Krauss GL. Visual dysfunction in patients receiving vigabatrin - clinical and electrophysiologic findings. Neurology 1999; 53(9): 2082–7

    Google Scholar 

  12. Vanhatalo S, Pääkkönen L. Visual field constriction in children treated with vigabatrin. Neurology 1999; 52: 1713–4

    Google Scholar 

  13. Kälviäinen R, Nousiainen I. Mäntyjärvi M, Nikoskelainen E, Partanen J, Partanen K, Riekkkinen P. Vigabatrin, a gabaergic antiepileptic drug, causes concentric visual field defects. Neurology 1999; 53: 922–6

    Google Scholar 

  14. Lawden MC, Eke T, Degg C, Harding GF, Wild JM. Visual field defects associated with vigabatrin therapy. J Neurol Neurosurg Psychiatry 1999; 716–22

  15. Wild JM, Martinez C, Reinshagen G, Harding GF. Characteristics of a unique visual field defect attributed to vigabatrin. Epilepsia 1999; 40(12): 1784–94

    Google Scholar 

  16. Besch D, Safran NB, Matter MA, Asenbauer C, Dennig D, Zrenner E, Schiefer U. What is specific about vigabatrin-induced visual field defects? Submitted to Ann Neurol.

  17. Backstrom JT, Hinkle RI, Flicker MR. Manufacturers have started several studies. Br Med J 1997; 314: 1694–5

    Google Scholar 

  18. Arndt, CF, Derambure P, Defoort S, Hache JC. Is visual impairment related to vigabatrin reversible? Epilepsia 1999; 40(Suppl): 256

    Google Scholar 

  19. Versino M, Veggiotti P. Reversibility of vigabatrin-induced visual-field defect. The Lancet 1999; 354: 486

    Google Scholar 

  20. Butler WH, Ford GP, Newberne JW. A study of the effects of vigabatrin on the central nervous system and retina of sprague dawley and lister-hooded rats. Toxicol Pathol 1987; 15:143: 148

    Google Scholar 

  21. Butler WH. The neuropathology of vigabatrin. Epilepsia 1989; 30: 515–7

    Google Scholar 

  22. Gibson JP, Yarrington JT, Loudy DE. Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor. Toxicol Pathol 1990; 18: 225–38.

    Google Scholar 

  23. French J, Mosier M, Walker S, Somerville K, Sussman N. A double-blind placebo controlled study of vigabatrin 32 g/day in patients with uncontrolled complex partial seizures. Neurology 1996; 46: 54–61

    Google Scholar 

  24. Cocito J, Maffini M, Loeb C. MRI findings in epileptic patients on vigabatrin for more than five years. Seizure 1992; 1: 163–5

    Google Scholar 

  25. Mauguiere F, Chauvel P, Dewailly J, Dousse N. No effect of long-term vigabatrin treatment on central nervous system conduction in patients with refractory epilepsy: results of a multicenter study of somatosensory and visual evoked potentials. PMS Study Multicenter Group. Epilepsia 1997; 38: 301–8

    Google Scholar 

  26. Rüther K, Pung T, Keliner U, Schmitz B, Hartmann C, Seeliger M. Electrophysiologic evaluation of a patient with peripheral visual field contraction associated with vigabatrin. Arch Ophthalmol 1998; 116: 817–9

    Google Scholar 

  27. Krauss GL, Johnson MA, Miller NR. Vigabatrin associated retinal cone system dysfunction. Electroretinogram and ophthalmologic findings. Neurology 1998; 50: 614–8

    Google Scholar 

  28. Arndt CF, Derambure P, Defoort-Dhellemmes S, Hache JC. Outer retinal dysfunction in patients treated with vigabatrin. Neurology 1999; 52: 1201–5

    Google Scholar 

  29. Bayer A, Zrenner E, Reid S, Schmidt D. Effects of anticonvulsant drugs on retinal function. Psychophysical and electrophysiological findings on patients with epilepsy. Invest Ophthalmol Vis Sci 1990; 31(Suppl):427

    Google Scholar 

  30. Bayer AU, Thiel HJ, Zrenner E, Paulus W. Ried S, Schmidt D. Disorders of color reception and increased glare sensitivity in phenytoin and carbamazepine therapy: ocular side effects of anticonvulants. Nervenarzt 1995; 66: 89–96

    Google Scholar 

  31. Dietrich TJ, Friedrich M, Selig B, Benda N, Schiefer U. Application of video display units for campimetric purposes –luminance characteristics and calibration procedures. In: Wall M, Heijl A, eds. Perimetry Update 1996/1997. Amsterdam/New York: Kugler Publications, 1997: 471

    Google Scholar 

  32. Dietrich TJ, Schiefer U, Benda N, Selig B. Autokinetische Perimetrie bei Patienten mit Retinitis pigmentosa. Ophthalmologe 1997; 94(Suppl 1): 141

    Google Scholar 

  33. Schiefer U, Dietrich TJ. Benda N. Autokinetische Perimetrie/Kampimetrie – Prinzip und Einsatzbeispiele. Ophthalmologe 1997; 94(Suppl 1): 176

    Google Scholar 

  34. Marmor MF, Arden GB, Nilsson SE, Zrenner E. Standard for clinical electroretinography. Arch Ophthalmol 1989; 107: 816–9

    Google Scholar 

  35. Marmor ML, Zrenner E. Standard for clinical electroretinography (1999 update). Doc Ophthalmol 1999; 97: 143–56

    Google Scholar 

  36. Marmor ML, Zrenner E. Standard for clinical electro-oculography. Arch Ophthalmol 1993; 111: 601–4

    Google Scholar 

  37. Sutter EE, Tran D. The field topography of ERG components in man. I. The photopic luminance response. Vis. Res 1992; 32: 433–46

    Google Scholar 

  38. Wu S, Sutter EE. A topographic study of oscillatory potentials in man. Vis Neurosci 1995; 12: 1013–25

    Google Scholar 

  39. Kurtenbach A, Langrova H, Zrenner B. Multifocal oscillatory potentials in Type 1 diabetics without retinopathy. Invest Ophthalmol Vis Sci (in press)

  40. Martinez C, Rietbrock S. Visual field defects: pattern and epidemiology. ISCEV Feb. 2000, Sydney.

  41. Besch D, Safran AB, Kurtenbach A, Apfelstedt-Sylla E, Dietrich TJ, Asenbauer C, Dennig D, Zrenner B, Schiefer U. Visual field defects and inner retinal dysfunction associated with vigabatrin. Invest Ophthalmol Vis Sci 2000; 41(4): 4743

    Google Scholar 

  42. Crofts K, Brennan R, Kearney P, O'Connor G. Vigabatrin induced optic neuropathy. J Neurol 1997; 10: 666–7

    Google Scholar 

  43. Mirchandani GR, Abi-Saab W, Mattson RH, Kross JD. Garbapentin and Vigabatrin enhance promoted GABA release in rat hippocampus in vivo. Epilepsia 1999, 40: 138

    Google Scholar 

  44. Sills GJ, Patsalos PN, Butler B, Ratnaraj N, Brodie MJ. Concentration-related pharmacodynamic study of vigabatrin and tiagabine in rat brain and eye. Epilepsia 1999; 40: 244

    Google Scholar 

  45. Beran RG, Currie J, Dandbach J, Plunkett M. Visual field restriction with new antiepileptic medication. Epilepsia 1998; 39(Suppl 2): 6

    Google Scholar 

  46. Kälviäinen R, Nousiainen I, Mäntyjarvi M, Riekkkinen P. Absence of concentric visual field defects in patients with initial tiagabine monotherapy. Epilepsia 1999; 40(Suppl): 259

    Google Scholar 

  47. Duckett T, Brigell M, Ruckh S. Electroretinographic changes are not associated with loss of function in pediatric epileptic patients following treatment with vigabatrin. Vis Sci 1998; 39(4): 973

    Google Scholar 

  48. Harding GFA, Robertson KA, Edson AS, Barnes P, Wild J. Visual electrophysiological effect of a GABA transaminase blocker. Doc Ophthalmol 1999; 97: 179–88

    Google Scholar 

  49. Brown KT. The electroretinogram: Its components and their origin. Vis Res 1968; 8: 633–77

    Google Scholar 

  50. Peachey NS, Alexander KR, Fishman GA. Rod and cone system contributions to oscillatory potentials: an explanation for the conditioning flash. Vis Res 1987; 27: 859–66

    Google Scholar 

  51. Neal MJ, Cunningham JR, Shah MA, Yazulla S. Immunocytochemical evidence that vigabatrin in rats cause GABA accumulation in glial cells of the retina. Neurosci Lett 1988; 98: 29–32

    Google Scholar 

  52. Pow DV, Rogers M. GABA transamination regulates neuronal glutamate content in the retina. Neuroreport 1996; 7: 2683–6

    Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Neuro-Ophthalmology and Pathophysiology of Vision, University Eye Hospital, D-72076, Tübingen, Germany

    Dorothea Besch, Anne Kurtenbach, Eckart Apfelstedt-Sylla, Bettina Sadowski, Eberhart Zrenner & Ulrich Schiefer

  2. Seelbergstr. 9, D-70372, Stuttgart, Germany

    Dieter Dennig

  3. Department of Neurology, University of Tübingen, Hoppe-Seyler-Str. 3, D-72076, Tübingen, Germany

    Christiane Asenbauer

Authors
  1. Dorothea Besch
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Anne Kurtenbach
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Eckart Apfelstedt-Sylla
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Bettina Sadowski
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Dieter Dennig
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Christiane Asenbauer
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Eberhart Zrenner
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Ulrich Schiefer
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Besch, D., Kurtenbach, A., Apfelstedt-Sylla, E. et al. Visual field constriction and electrophysiological changes associated with vigabatrin. Doc Ophthalmol 104, 151–170 (2002). https://doi.org/10.1023/A:1014644307518

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1023/A:1014644307518

Search

Navigation