The Effect on Vision of Associated Treatments in Patients Taking Vigabatrin: Carbamazepine Versus Valproate

Arndt, Carl; Salle, Marc; Derambure, Philippe; Defoort‐Dhellemmes, Sabine; Hache, J.-C.

doi:10.1046/j.1528-1157.2002.42001.x

Cited by 25 publications

(20 citation statements)

References 23 publications

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“…[23,24,27,28] Moreover, the risk factors for visual field loss are poorly understood, although a higher frequency has been reported in association with male gender, [8,11,12,15,29] concomitant treatment with other antiepileptic drugs (AEDs), [30] higher cumulative dose of vigabatrin [10,24,29,31] and longer duration of vigabatrin therapy. [10,29,31] We have previously reported the interim results of a large, observational, multicentre study designed to determine the frequency of, and the risk factors for, VAVFL in patients with refractory partial epilepsy, stratified by age (8-12 years of age, >12 years of age) treated with vigabatrin.…”

Section: Introductionmentioning

confidence: 99%

Visual Field Loss in Patients with Refractory Partial Epilepsy Treated with Vigabatrin

et al. 2009

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Since the probability of VAVFL is positively associated with treatment duration, careful assessment of the risk-benefit ratio of continuing treatment with vigabatrin is recommended in patients currently receiving this drug. All patients continuing to receive vigabatrin should undergo visual field examination at least every 6 months for the duration of treatment. We recommend two-level (three-zone), gradient-adapted, suprathreshold static perimetry of the peripheral field together with threshold perimetry of the central field out to 30 degrees from fixation. The frequency of ophthalmological and perimetric examinations should be increased in the presence of VAVFL.

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Section: Introductionmentioning

confidence: 99%

Visual Field Loss in Patients with Refractory Partial Epilepsy Treated with Vigabatrin

et al. 2009

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“…The majority of TEAEs reported in topiramate-treated patients were VFDs (all indications: 0.1%–0.4%), scotoma (migraine prophylaxis and monotherapy epilepsy: <0.1% to 0.4%), and optic atrophy (adjunctive epilepsy: 0.2%). Optic atrophy TEAEs were all reported for patients receiving adjunctive topiramate treatment for epilepsy, who were also concomitantly receiving valproate, another AED that has been associated with VFDs 18,20,21. Most of the TEAEs were mild or moder ate in severity; the majority resolved.…”

Section: Resultsmentioning

confidence: 99%

Comprehensive review of visual defects reported with topiramate

Ford

Goldberg

Selan

et al. 2017

OPTH

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ObjectiveThe objective of this study was to analyze clinical patterns of visual field defects (VFDs) reported with topiramate treatment and assess possible mechanism of action (MOA) for antiepileptic drug (AED) associated VFDs.MethodsA comprehensive topiramate database review included preclinical data, sponsor’s clinical trials database, postmarketing spontaneous reports, and medical literature. All treatment-emergent adverse events (TEAEs) suggestive of retinal dysfunction/damage were summarized. Relative risk (RR) was computed from topiramate double-blind, placebo-controlled trials (DBPCTs) data.ResultsPreclinical studies and medical literature review suggested that despite sharing gamma-aminobutyric acid (GABA)-ergic MOA with other AEDs, topiramate treatment was not associated with VFDs. TEAEs suggestive of retinal dysfunction/damage were observed in 0.3%–0.7% of adults and pediatric patients with topiramate (N=4,679) versus ≤0.1% with placebo (N=1,834) in DBPCTs for approved indications (epilepsy and migraine prophylaxis); open-label trials (OLTs) and DBPCTs for investigational indications had similar incidence. Overall, 88% TEAEs were mild or moderate in severity. Serious TEAEs were very rare (DBPCTs: 0%; OLTs: ≤0.1%), and most were not treatment limiting, and resolved. The most common visual TEAEs (approved indications) were VFD, scotoma, and optic atrophy. The incidence of TEAEs in DBPCTs (approved and investigational indications) was higher in topiramate-treated (N=9,169) versus placebo-treated patients (N=5,023; 0.36% vs 0.24%), but the RR versus placebo-treated patients was not significant (RR: 1.51 [95% confidence interval: 0.78, 2.91]).ConclusionVFDs do not appear to be a class effect for AEDs with GABA-ergic MOA. The RR for VFDs is not significantly different between topiramate and placebo treatment.

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“…Enhancement of the GABA response increases the size and strength of the inhibitory surround of visual receptive fields [55]; a lack of GABA-mediated inhibition could result in reduced sensitivity to high spatial frequency patterns and increased response at low spatial frequency. CBZ and VPA have not been shown to have a significant effect on the flash ERG [56][57][58], including oscillatory potentials, but the conventional flash ERG does not yield much information about the ganglion cell response. CBZ has been reported to interfere with color discrimination, which does suggest possible retinal effects [59,60].…”

Section: Discussionmentioning

confidence: 99%

Epilepsy and Medication Effects on the Pattern Visual Evoked Potential*

et al. 2005

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Visual disruption in patients diagnosed with epilepsy may be attributable to either the disease itself or to the anti-epileptic drugs prescribed to control the seizures. Effects on visual function may be due to perturbations of the GABAergic neurotransmitter system, since deficits in GABAergic cortical interneurons have been hypothesized to underlie some forms of epilepsy, some anti-epileptic medications increase cortical GABA levels, and GABAergic neural circuitry plays an important role in mediating the responses of cells in the visual cortex and retina. This paper characterizes the effects of epilepsy and epilepsy medications on the visual evoked response to patterned stimuli. Steady-state visual evoked potentials (VEP) evoked by onset-offset modulation of high-contrast sine-wave stimuli were measured in 24 control and 54 epileptic patients. Comparisons of VEP spectral amplitude as a function of spatial frequency were made between controls, complex partial, and generalized epilepsy groups. The effects of the GABA-active medication valproate were compared to those of carbamezepine. The amplitude of the fundamental (F1) component of the VEP was found to be sensitive to epilepsy type. Test subjects with generalized epilepsy had F1 spatial frequency-amplitude functions with peaks shifted to lower spatial frequencies relative to controls and test subjects with complex partial epilepsy. This shift may be due to reduced intracortical inhibition in the subjects with generalized epilepsy. The second harmonic component (F2) response was sensitive to medication effects. Complex partial epilepsy patients on VPA therapies showed reduced F2 response amplitude across spatial frequencies, consistent with previous findings that showed the F2 response is sensitive to GABA-ergic effects on transient components of the VEP.

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The Effect on Vision of Associated Treatments in Patients Taking Vigabatrin: Carbamazepine Versus Valproate

Cited by 25 publications

References 23 publications

Visual Field Loss in Patients with Refractory Partial Epilepsy Treated with Vigabatrin

Visual Field Loss in Patients with Refractory Partial Epilepsy Treated with Vigabatrin

Comprehensive review of visual defects reported with topiramate

Epilepsy and Medication Effects on the Pattern Visual Evoked Potential*

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