Published: October 1999


Vigabatrin and Visual Field Defects

This article is more than five years old. Some content may no longer be current.

Prescriber Update 19: 30-33
October 1999

Medsafe Editorial Team

Vigabatrin (Sabril™) causes visual field constriction in around 30% of users. Most cases are asymptomatic because vigabatrin affects the peripheral fields but does not impair central visual acuity. The effects appear to be irreversible, or incompletely reversible, in all cases after discontinuation of vigabatrin.
Patients using vigabatrin who have a developmental age of > 10 years should have baseline threshold visual field testing and follow-up at 6-monthly intervals. Visual field testing is not usually possible before a developmental age of 12 years, but in some centres a method which has not been validated for defects caused by vigabatrin and which is based on visual evoked potentials is available for younger children. Patients should be instructed to report any new problems with vision such as blurring, double vision and signs of peripheral vision impairment.
Vigabatrin is indicated for epilepsy which is not adequately controlled by other agents. Use should occur only after a careful risk-benefit assessment, including a comparison of the risks and benefits of alternative agents. Each patient currently using vigabatrin should be reviewed to ascertain whether the risk-benefit assessment supports continued use of this medication.

Vigabatrin causes visual field constriction in about 30% of users

In 1997 the first reports of visual field defects (VFDs) with vigabatrin (Sabril™) were published.1 At that time, it was not clear whether the association was causal or coincidental. However, recently published controlled studies have found high rates of VFDs in epileptic patients treated with vigabatrin. VFDs were not detected or were less severe, or less frequent, in those treated with other antiepileptic medication.2,3 VFDs do not appear to be a class effect since another GABAergic antiepileptic agent, tiagabine (Gabitril, Sanofi-Synthelabo; approved in New Zealand but not yet marketed) has not been associated with VFDs in controlled clinical trials.3

Some studies have found rates of VFDs for vigabatrin as high as 50%.4 At present the best estimate of rate is around 30%. The defects may occur as early as during the first month of therapy.5 It may be that the rate of occurrence continues to increase with duration of therapy. The effects appear to be irreversible, or incompletely reversible, in all cases after discontinuation of vigabatrin.

Most cases are not symptomatic and central visual acuity is not affected

In most cases the visual field constriction caused by vigabatrin is not symptomatic, and hence the problem can be overlooked if active monitoring is not performed. The pattern of defect is a concentric constriction of the visual field of both eyes with a more marked effect on the nasal fields than on the temporal fields. Central visual acuity is not impaired.1

Indicated where other agents are ineffective

Vigabatrin is indicated for:

  • The treatment of epilepsy not satisfactorily controlled by other antiepileptic medicines.
  • The management of infantile spasms (West syndrome).
  • Monotherapy for the treatment of partial seizures and secondarily generalised tonic-clonic seizures.

Treatment with vigabatrin is reimbursed in New Zealand only when it is initiated by a neurologist, paediatric neurologist or any other prescriber approved in writing by the relevant Health Funding Authority budget holding manager, and PHARMAC's entry criteria for the patient are met.

Use only after careful risk-benefit assessment and comparison with alternatives

Because of the high rate of VFDs with vigabatrin and their apparent irreversibility, vigabatrin should be used only after a careful risk-benefit assessment and if other therapies have failed to control seizures. Patients already taking vigabatrin should be assessed for its appropriateness in the light of the high risk of developing VFDs. If other treatment options are known to be effective or are untried, consideration should be given to switching therapy. If seizures are better controlled with vigabatrin than with alternatives, it may be acceptable to risk some visual field constriction.

Because of its effectiveness in the treatment of infantile spasms, vigabatrin can continue to be regarded as first line therapy in this indication. The risk of VFDs is low in these patients because use is only short term. Nevertheless, the decision to use vigabatrin should be made only by an appropriate specialist. For epilepsy in children, vigabatrin may be advantageous because it is associated with less cognitive impairment than some other antiepileptics.

If the use of vigabatrin is being considered, the risk of VFDs, the consequences of these effects and their possible irreversibility should be discussed with patients, and with the parent or guardian in the case of a child. The discussion should also cover the benefits of vigabatrin and the benefits and risks of alternative antiepileptic therapy. The patient, parent or guardian should be able to make an informed choice together with the prescribing specialist.

Patients on vigabatrin should have 6-monthly visual field testing

If a decision is made to prescribe vigabatrin, patients over the developmental age of ten years should be referred to an ophthalmologist, or an optometrist with threshold visual field testing equipment, for formal threshold visual field testing prior to commencing therapy. Follow-up testing should be performed at 6-monthly intervals. It is not usually possible to conduct visual field testing in children much before the developmental age of 12 years. For children from 3 years of age, a method based on visual evoked potentials is available in some centres, but its effectiveness in detecting VFDs caused by vigabatrin has not been validated.

Patients should be instructed to report any new problems with vision. Signs such as blurred or double vision or peripheral vision disturbances as evidenced by bumping into furniture or people. Patients developing visual symptoms should be referred to an ophthalmologist or optometrist for further evaluation.

If a VFD is identified, the benefit of continued treatment with vigabatrin should be weighed against the risk of the VFD progressing. If a decision is made to continue vigabatrin, it may be appropriate to monitor visual fields more frequently.

During the week of 18 October, Hoechst Marion Roussel sent letters about this subject to neurologists and paediatricians, general practitioners and ophthalmologists and optometrists. Medsafe worked with the company to finalise the letters.

  1. Eke T, Talbot JF, Lawden MC. Severe persistent visual field constriction associated with vigabatrin. BMJ 1997;314:180-1.
  2. Schmitz B, Jokiel B, Schmidt T, et al. Visual field defects under treatment with vigabatrin, carbamazepine, and valproate; a prospective study. Epilepsia 1999;40(Suppl.2):257.
  3. Kälviäinen R, Nousiainen I, Mäntjyärvi M, Riekkinen Sr. P. Absence of concentric visual field defects in patients with initial tiagabine monotherapy. Epilepsia 1999;40(Suppl.2):259.
  4. Lawden MC, Eke T, Degg C, et al. Visual field constriction associated with vigabatrin treatment. Epilepsia1999;40(Suppl.2):257.
  5. Update on visual field constriction with vigabatrin. Aust Adv Drug Reactions Bull 1999;18:3.


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