A controlled study comparing visual function in patients treated with vigabatrin and tiagabine

Krauss, Gregory L.

doi:10.1136/jnnp.74.3.339

Cited by 40 publications

(26 citation statements)

References 23 publications

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“…Abnormal EOGs in VGB-treated patients implicate the retinal pigment epithelium and the retinal pigment epithelial-outer segment complex (9,(18)(19)(20). Abnormal ERGs implicate both the central and peripheral cone and rod systems (5,8,11,12,(19)(20)(21)(22). The findings are consistent with Müller and amacrine cell dysfunction (8,11,18,19).…”

supporting

confidence: 74%

“…Some reports describe visual field constriction that may be more severe nasally (8,9), but central visual loss also may develop (10). In accordance with these observations, ophthalmoscopy can show optic nerve pallor, macular irregularities, and peripheral retinal abnormalities (9,11,12). The VFDs may or may not depend on the cumulative VGB dose and duration of therapy (5,6,7,13).…”

supporting

confidence: 49%

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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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supporting

confidence: 74%

supporting

confidence: 49%

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

Izumi¹,

Ishikawa

Benz³

et al. 2004

Epilepsia

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“…Paradoxically some conditions require treatment in order to pass driving criteria which then are failed because of iatrogenic VF loss, for example hippocampal surgery or vigabatrin therapy in the treatment of epilepsy [2, 26, 27, 80, 100, 119, 123, 145, 154, 155, 173]. These hazards need to be discussed with the patient prior to the intervention.…”

Section: Disorders With Pcsmentioning

confidence: 99%

“…Vigabatrin has been associated with VF constriction in approximately 40% of treated patients [2, 100, 145, 173]. Driving licences have been withdrawn on the basis of vigabatrin-related VF loss [130, 153].…”

Section: Disorders With Pcsmentioning

confidence: 99%

Central and Paracentral Visual Field Defects and Driving Abilities

Petzold¹,

Plant²

2005

Ophthalmologica

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“…51,52 Concentric field defects similar to those associated with vigabatrin treatment, another drug that increases synaptic concentrations of GABA, have not been shown to occur with tiagabine. 53,54 Tiagabine undergoes hepatic metabolism via the cytochrome P450 system. The half-life is 5-8 h, which is reduced to 2-3 h in patients also taking hepatic enzymeinducing AEDs, therefore, the potential for drug interactions exist.…”

Section: Tiagabine (Gabitril®)mentioning

confidence: 99%

New generation anticonvulsants for the treatment of epilepsy in children

Donner

Snead

2006

NeuroRX

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Summary:In the last 12 years, 10 new anticonvulsants have been approved by the U.S. Food and Drug Administration and, as a result, the treatment options for children and adults with epilepsy have been expanded considerably. These new generation antiepileptic drugs offer equal efficacy with improved tolerability, pharmacokinetic properties, and side effect profiles compared with the traditional drugs. With many new medications available, the clinician treating children with epilepsy must be well versed in the application of these drugs to their patient population. This manuscript will review the indications, mechanism of action, pharmacokinetics, adverse effects, and dosing of the new generation of anticonvulsant medications.

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A controlled study comparing visual function in patients treated with vigabatrin and tiagabine

Cited by 40 publications

References 23 publications

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

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

Central and Paracentral Visual Field Defects and Driving Abilities

New generation anticonvulsants for the treatment of epilepsy in children

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