Document Type

Article

Publication Date

12-2010

Comments

This article has been peer reviewed. It is the authors' final version prior to publication in Epilepsy Research Volume 92, Issues 2-3, December 2010, Pages 170-176. The published version is available at DOI: 10.1016/j.eplepsyres.2010.09.004. Copyright © Elsevier Inc.

Abstract

Purpose:

Vigabatrin can cause retinopathy, resulting in bilateral visual field constriction. Previous analyses of results from a prospective, observational study assessing vigabatrin-induced visual field constriction (described below) employed a partially subjective interpretation of static perimetery. In an effort to affirm these previous findings through more objective, quantitative methodology, we now report data from a subset analysis of refractory partial epilepsy patients in the study who underwent Goldmann kinetic perimetry.

Methods:

Patients aged ≥8 years with refractory partial seizures were enrolled and grouped: those receiving vigabatrin for ≥6 months (Group I); those who had received vigabatrin for ≥6 months and then had discontinued for ≥6 months (Group II); and those naïve to vigabatrin (Group III). Patients underwent static or kinetic perimetry or both every 4–6 months for ≤3 years. For kinetic perimetry, the temporal and nasal visual fields were measured along the horizontal meridian with the largest (V4e, IV4e) and smallest (I2e, I1e) isopters, respectively.

Results:

Of 735 patients enrolled, 341 had Goldmann perimetry data. Of these, 258 received vigabatrin. Sixteen percent of vigabatrin-exposed patients had moderate visual field defects (30°–60° retained temporal vision), and 3% had severe defects (<30° retained temporal vision). Visual function questionnaire results indicated a weak correlation between visual field constriction severity and visual symptoms.

Conclusions:

These results affirm both an analysis of the same study based primarily on static perimetry and findings from cross-sectional studies. The present analysis verifies that visual field constriction, when it occurs, is most often mild or moderate and is not associated with symptoms of abnormal visual function. The clinical decision to prescribe vigabatrin should be based on a benefit-risk analysis for each individual patient.

Figure1.TIF (140 kB)
Figure 1. Distribution of patients who underwent kinetic perimetry.

Figure2A.TIF (895 kB)
Figure 2. Cumulative distribution of degrees in the (A) temporal visual field at final perimetry in vigabatrin-exposed (n=258) and vigabatrin-naïve patients (n=83) and (B) nasal visual field at final perimetry in vigabatrin-exposed (n=256) and vigabatrin-naïve (n=81) patients.

Figure2B.TIF (926 kB)
Figure 2. Cumulative distribution of degrees in the (A) temporal visual field at final perimetry in vigabatrin-exposed (n=258) and vigabatrin-naïve patients (n=83) and (B) nasal visual field at final perimetry in vigabatrin-exposed (n=256) and vigabatrin-naïve (n=81) patients.

Figure3A.TIF (1303 kB)
Figure 3. Severity of visual field defect at last kinetic perimetry in (A) vigabatrin-exposed and (B) vigabatrin-naïve patients. Unimpaired: >80° monocular temporal field retained; Mild: 60°–80° monocular temporal field retained; Moderate: 30°–60° monocular temporal field retained; Severe: <30° monocular temporal field retained. Measurements are of largest isopter tested at final Goldmann perimetry.

Figure3B.TIF (1354 kB)
Figure 3. Severity of visual field defect at last kinetic perimetry in (A) vigabatrin-exposed and (B) vigabatrin-naïve patients. Unimpaired: >80° monocular temporal field retained; Mild: 60°–80° monocular temporal field retained; Moderate: 30°–60° monocular temporal field retained; Severe: <30° monocular temporal field retained. Measurements are of largest isopter tested at final Goldmann perimetry.

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