Vigabatrin, a gabaergic antiepileptic drug, causes concentric visual field defects

Kälviäinen, Reetta; Nousiainen, Iiris; Mäntyjärvi, Maija; Nikoskelainen, Eeva; Partanen, Juhani; Partanen, Kaarina; Riekkinen, P.

doi:10.1212/wnl.53.5.922

Cited by 191 publications

(156 citation statements)

References 13 publications

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“…Vigabatrin (␥-vinyl aminobutyric acid; VGB) is an effective antiepilepsy drug (AED) used to treat partialonset seizures and infantile spasms (1-3); however, it causes visual-field constriction in 40-45% of patients receiving long-term therapy as well as reductions in electroretinogram (ERG) potentials in ∼70% of patients (4)(5)(6)(7)(8). Other visual disturbances, including minor reductions in visual acuity and color vision, also have been demonstrated in some patients after long-term use of VGB (6,7,9).…”

Section: Discussionmentioning

confidence: 99%

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Visual Function is Stable in Patients Who Continue Long‐Term Vigabatrin Therapy: Implications for Clinical Decision Making

Paul¹,

Krauss²,

Miller

et al. 2001

Epilepsia

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Summary:Purpose: Vigabatrin (VGB) has been shown to cause visual field constriction and other forms of mild visual dysfunction. We determined the safety of continuing VGB therapy in patients who had received prolonged treatment (>2 years) with the drug by serially monitoring changes in visual function over a 1-year period of continued therapy. We also followed up patients who discontinued VGB to see whether alternative therapies are effective.Methods: Fifteen of 17 patients who continued VGB therapy had visual-function testing (visual acuity, color vision, kinetic and static perimetry) every 3 months for 1 year. Eighteen patients who discontinued VGB were given alternative antiepileptic drugs (AEDs); their seizure responses were measured after Ն3 months of treatment. Results:Patients continuing VGB showed no worsening of visual acuity, color vision, or visual-field constriction beyond that measured in the initial test. Many patients who discontinued VGB had good seizure control with either newer or previously unsuccessful AEDs.Conclusions: For patients who have an excellent response to VGB and only mild visual changes, continued therapy may be safe with close visual monitoring. Patients who do not have a significant reduction in seizures or who experience considerable visual dysfunction with VGB may respond well to alternative therapies.

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Section: Discussionmentioning

confidence: 99%

“…Visual-field constriction and other visual sensory disturbances are frequent among patients taking long-term VGB for seizures, occurring in almost 50% of such patients (4)(5)(6)(7)(8). These changes are usually asymptomatic and mild (7), and they are generally irreversible (13,14).…”

Section: Discussionmentioning

confidence: 99%

Visual Function is Stable in Patients Who Continue Long‐Term Vigabatrin Therapy: Implications for Clinical Decision Making

Paul¹,

Krauss²,

Miller

et al. 2001

Epilepsia

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“…[1][2][3][4][5][6][7][8] It is hypothesised that in addition to effects on cerebral function, irreversible inhibition of GABA aminotransferase with consequent elevation of GABA levels in the inner retina is the priniciple cause of the depressed visual function and this is supported by electrophysiological data. [9][10][11][12][13][14][15] Outer retinal and possibly also cortical effects may play a role. 12 Males may be more susceptible than females 11 but the role of other risk factors such as cumulative dosage is less clear.…”

Section: Introductionmentioning

confidence: 99%

Vigabatrin associated visual field loss: a clinical audit to study prevalence, drug history and effects of drug withdrawal

Newman

Tocher

Acheson

2002

Eye

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Vigabatrin associated visual field loss: a clinical audit to study prevalence, drug history and effects of drug withdrawal AbstractPurpose To survey clinical visual function including quantitative manual perimetry results in a group of patients taking vigabatrin; to assess the severity of any field defects; to tabulate cumulative and daily doses of medication and to assess possible changes in visual function over time. Method A prevalence study of 100 out of 183 patients currently attending a tertiary referral epilepsy centre who were taking or had recently discontinued vigabatrin (duration 83-3570 days; mean 1885 days) as part of combination anticonvulsant therapy. Complete neuro-ophthalmic examination including Goldmann kinetic perimetry was performed and monocular mean radial degrees (MRD) to the I/4e isopter calculated. Patients were followed up at 6-monthly intervals for not less than 18 months. Results Acuity and colour vision remained stable in all patients regardless of changes in visual fields. Twenty per cent of patients had significant constriction of their visual field defined as a monocular MRD of 30 degrees or less. Males were significantly more likely to be severely affected than females (P Ͻ 0.01). Twenty one patients were followed after discontinuing vigabatrin treatment. Only three of these showed a change in MRD of 10 degrees or more with two deteriorating and one improving. No correlation between treatment duration or cumulative dosage/kg and the severity of defects could be demonstrated. Conclusions Earlier reports of a high prevalence of both moderate and more serious field defects were confirmed in patients taking vigabatrin but not in epileptic patients taking other anticonvulsants. We found no evidence of progression or resolution of visual field defects on discontinuing the drug, and no relationship between dose history and visual deficit field loss. An idiosyncratic drug reaction within the neurosensory retina may underlie the pathogenesis of the visual field loss in some patients Eye (2002) 16, 567-571.

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“…patients receiving polytherapy (6,8), VFDs arise during VGB monotherapy in newly diagnosed patients (5). Some reports describe visual field constriction that may be more severe nasally (8,9), but central visual loss also may develop (10).…”

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confidence: 99%

Acute Vigabatrin Retinotoxicity in Albino Rats Depends on Light But Not GABA

Izumi¹,

Ishikawa

Benz³

et al. 2004

Epilepsia

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Summary:Purpose: Vigabatrin (VGB) is an irreversible inhibitor of γ -aminobutyric acid (GABA) transaminase. Its use as an antiepileptic drug (AED) has been limited because it causes retinal dysfunction, leading to visual field defects (VFDs). We performed this study to identify factors contributing to acute VGB retinotoxicity.Methods: In ex vivo experiments, Sprague-Dawley rat retinas were isolated and incubated with VGB or GABA in the presence or absence of light. In in vivo experiments, Sprague-Dawley rats were given intraperitoneal injections of VGB and then exposed to light or kept in the dark. The retinas were analyzed histologically by using both light and electron microscopy.Results: Incubating retinas with 50-500 µM VGB under 20,000 Lux white light for ≤20 h caused a characteristic time-and dose-dependent degeneration limited to the outer retina. Incubating retinas with 500 µM VGB in darkness for 20 h caused no damage. Five hundred micromolar GABA and 50 µM tiagabine were not toxic in the presence or absence of light. Sprague-Dawley rats exposed to an intense white light for 20 h after a 1,000-mg/kg intraperitoneal injection of VGB showed damage in the outer retina, whereas those kept in the dark did not.Conclusions: Direct exposure of the retina to VGB causes acute retinotoxicity that depends on light exposure rather than GABA accumulation.

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Vigabatrin, a gabaergic antiepileptic drug, causes concentric visual field defects

Cited by 191 publications

References 13 publications

Visual Function is Stable in Patients Who Continue Long‐Term Vigabatrin Therapy: Implications for Clinical Decision Making

Visual Function is Stable in Patients Who Continue Long‐Term Vigabatrin Therapy: Implications for Clinical Decision Making

Vigabatrin associated visual field loss: a clinical audit to study prevalence, drug history and effects of drug withdrawal

Acute Vigabatrin Retinotoxicity in Albino Rats Depends on Light But Not GABA

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