Visual function in epilepsy patients treated with initial valproate monotherapy

Sorri, Iiris; Rissanen, Eeva; Mäntyjärvi, Maija; Kälviäinen, Reetta

doi:10.1016/j.seizure.2005.04.010

Cited by 20 publications

(18 citation statements)

References 13 publications

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“…With regard to use of additional AEDs, McCoy et al 15 detected a significantly higher percentage of retinal toxicity in a group of patients treated with vigabatrin in combination with other AEDs and questioned whether vigabatrin alone was responsible for the defects. However, in other studies, monotherapy with GABAergic drugs such as valproate 21 or tiagabine 22 did not cause VFDs. In the present study, two children treated with vigabatrin monotherapy had severe VFDs.…”

Section: Discussionmentioning

confidence: 82%

Does vigabatrin treatment for infantile spasms cause visual field defects? An international multicentre study

Riikonen

Rener-Primec

Carmant

et al. 2014

Develop Med Child Neuro

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AEDAntiepileptic drug ERG Electroretinography GABA Gamma-aminobutyric acid VFD Visual field defect AIM The aim of this study was to examine whether vigabatrin treatment had caused visual field defects (VFDs) in children of school age who had received the drug in infancy.METHOD In total, 35 children (14 males, 21 females; median age 11y, SD 3.4y, range 8-23y)were examined by static Humphrey perimetry, Goldmann kinetic perimetry, or Octopus perimetry. The aetiologies of infantile spasms identified were tuberous sclerosis (n=10), other symptomatic causes (n=3), or cryptogenic (n=22).RESULTS Typical vigabatrin-attributed VFDs were found in 11 out of 32 (34%) children: in one out of 11 children (9%) who received vigabatrin for <1 year (group 1), in three out of 10 children (30%) who received vigabatrin for 12 to 24 months (group 2), and in seven out of 11 children (63%) who received vigabatrin treatment for longer than 2 years (group 3). VFDs were mild in five and severe in six children. Patients with tuberous sclerosis were at higher risk of VFDs (six out of 10 children). The mean cumulative doses of vigabatrin were 140.5, 758.8, and 2712g in group 1, 2, and 3, respectively.INTERPRETATION VFDs were found in 34% of the cohort of children in this study. The rate of VFD increased from 9% to 63% as duration of treatment increased. The results of this study showed that the risk-benefit ratio should always be considered when using vigabatrin.

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Section: Discussionmentioning

confidence: 82%

Does vigabatrin treatment for infantile spasms cause visual field defects? An international multicentre study

Riikonen

Rener-Primec

Carmant

et al. 2014

Develop Med Child Neuro

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“…49,50 One study reports a concentric visual field defect in a 22-year-old patient. 51 In contrast, Sorri et al 52 found that VPA therapy was not associated with visual field defects after 8.4 Ϯ 5.1 years of treatment. Furthermore, morphologic retinal alterations (modifications of retinal nerve fiber layer or macular thickness) have not been reported in patients after 1 year of VPA treatment.…”

Section: Discussionmentioning

confidence: 93%

Valproic Acid–Mediated Neuroprotection and Regeneration in Injured Retinal Ganglion Cells

Biermann¹,

Grieshaber²,

Goebel

et al. 2010

Invest. Ophthalmol. Vis. Sci.

111

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“…[23] In a cross-sectional study involving 18 patients who had been taking valproate monotherapy for 2-20 years, only minor abnormalities in colour vision were discovered in two patients. [118] Short wavelength-sensitive cones seemed to be affected by the antiepileptic drug. This uncommon effect is mostly subclinical and does not require monitoring.…”

Section: Abnormal Colour Perceptionmentioning

confidence: 99%

“…Visual acuity, both subjective and objective, was preserved. [118] 7.9 Impaired Contrast Sensitivity…”

Section: Abnormal Colour Perceptionmentioning

confidence: 99%

Ocular Adverse Effects of Common Psychotropic Agents

Richa¹,

Yazbek²

2010

CNS Drugs

178

143

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All psychotropic medications have the potential to induce numerous and diverse unwanted ocular effects. Visual adverse effects can be divided into seven major categories: eyelid and keratoconjunctival disorders; uveal tract disorders; accommodation interference; angle-closure glaucoma; cataract/pigmentary deposits in the lens and cornea; retinopathy; and other disorders. The disorders of the eyelid and of the keratoconjunctiva are mainly related to phenothiazines and lithium. Chlorpromazine, at high dosages, can commonly cause abnormal pigmentation of the eyelids, interpalpebral conjunctiva and cornea. It can also cause a more worrisome but rarer visual impairment, namely corneal oedema. Lithium can rarely lead to a bothersome eye irritation by affecting sodium transport. Uveal tract problems are mainly associated with tricyclic antidepressants (TCAs), typical antipsychotics, topiramate and selective serotonin reuptake inhibitors (SSRIs). TCAs, typical antipsychotics and SSRIs can all cause mydriasis that is often transient and with no major consequences, but that can promote closure of angles in susceptible patients. Topiramate has been frequently associated with a number of significant ocular symptoms including acquired myopia and angle-closure glaucoma. Problems with accommodation are related to TCAs and to low-potency antipsychotics. TCAs cause transient blurred vision in up to one-third of patients. Angle-closure glaucoma is a serious condition that has been mainly associated with TCAs, low-potency antipsychotics, topiramate and, to a lesser extent, SSRIs. When patients with narrow angles are given TCAs, they all appear to experience induction of glaucomatous attacks. Antipsychotics and SSRIs may lead to an added risk of developing angle-closure glaucoma, but only in predisposed eyes. Topiramate can lead to an allergic-type reaction whereby structures of the lens and ciliary body are displaced, which results in angle-closure glaucoma. Cataractous changes can result from antipsychotics, mainly from high dosages of chlorpromazine or thioridazine. These two drugs, when used at high dosages and for prolonged periods, frequently cause lenticular opacifications. Retinopathy has been shown to be related to high dosages of typical antipsychotics, mainly chlorpromazine and thioridazine. The frequency of occurrence of retinal effects seems to be proportional to the total amount of drug used over a long period of time. Other visual problems of special concern are the ocular dystonias, other eye movement disorders, and decreased ability to perceive colours and to discriminate contrast. Ocular dystonias can occur with antipsychotics (especially high-potency ones), carbamazepine (especially in polytherapy), topiramate and, rarely, with SSRIs. Disturbance in various eye movements is frequently seen with benzodiazepines, antiepileptic drugs and lithium. Impairment in the perception of colours and the discrimination of contrasts has been shown to occur not uncommonly with carbamazepine and lorazepam. Thus, typical antipsycho...

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Visual function in epilepsy patients treated with initial valproate monotherapy

Abstract: The use of VPA in the treatment of epilepsy is not associated with visual field defects similar to vigabatrin, but may induce abnormalities in colour vision.

Cited by 20 publications

References 13 publications

Does vigabatrin treatment for infantile spasms cause visual field defects? An international multicentre study

Does vigabatrin treatment for infantile spasms cause visual field defects? An international multicentre study

Valproic Acid–Mediated Neuroprotection and Regeneration in Injured Retinal Ganglion Cells

Ocular Adverse Effects of Common Psychotropic Agents

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