Study of visual field and vigabatrin treatment in children

INTRODUCTION: Concentric visual field defects have been described in association with vigabatrin, a GABA mimetic antiepileptic agent. Few cases have been reported in children. METHODS: A systematic ophthalmological examination was performed in 14 children treated with vigabatrin for seizures. A manual kinetic perimetry test (Goldmann) was done in 11 cases. The ERG was recorded in the 3 cases where perimetry could not be done. RESULTS: All children were asymptomatic. The mean age was 9.6 years. The mean duration of vigabatrin treatment was 41 months. The visual field was abnormal when central and peripheral fields were constricted. A visual field defect was discovered in 6 cases: 4 were severe, 2 were mild. When vigabatrin treatment was stopped, 1 case became worse, 1 case was slightly better, and 1 case remained stationary. A disturbed ERG was found in 3 children (depressed b-wave, raised a/b ratio). CONCLUSION: The visual field defects discovered in children treated with vigabatrin are similar to those described in adults. The incidence and progression of visual field constriction in children with and after vigabatrin treatment are not yet well known. Children treated with vigabatrin should therefore have systematic and regular ophthalmological perimetry, and ERG examinations.     

Visual field and electrophysiological abnormalities due to vigabatrin

The purpose of this study was to determine the electrophysiological changes in patients using the anti epileptic drug vigabatrin and to correlate these findings with the previously reported risk for visual field loss in these patients. In 1998 the neurologists of both involved hospitals referred all patients on vigabatrin medication for ophthalmological examination to the outpatients clinics. Of the 33 patients whom were referred to our outpatient clinics, four had to be dropped from the study because of disability to perform the examinations the remaining 29 patients were included in the study. Standard ophthalmological investigations were carried out, and contrast sensitivity, visual field (Humphrey 30-2 and Esterman or Octopus 32), colour vision (panel D15), ERG and EOG according to ISCEV standards were tested. 18 patients continued the medication and 11 stopped taking the drug during the study. Nine of the patients who stopped the drug were followed during at least half a year afterwards, this group will be described in the combined article `Electro ophthalmic recovery after withdrawal from vigabatrin' (Graniewski and Van der Torren, this issue). The electro-ophthalmological findings in the group of 29 patients were correlated with the visual fields and the daily and cumulative dosages of vigabatrin. Of the patients, 32% showed no visual field constriction at all; from these patients 64% had EOG and/or ERG changes. Of the patients with slight to marked visual field constriction, 90% presented EOG and/or ERG changes. Significant correlation between daily dosages of vigabatrin and visual field defects was shown as well as between visual field defects and rod and cone b wave amplitude reductions. Cumulative vigabatrin dosages presented a significant correlation with EOG ratio and ERG rod b-wave amplitude. Conclusively EOG and ERG testing were found to be even an more accurate way to monitor the direct vigabatrin effect on the outer retina and is possible different from the visual field testing.     

Vigabatrin: longterm follow-up of electrophysiology and visual field examinations

BACKGROUND: To report the results of repeated electrophysiological and visual field examinations in patients with vigabatrin-associated visual field loss (VGB-VFL) and the relationship between these electrophysiological findings, the cumulative dose of vigabatrin and the extent of visual field loss. METHODS: Twenty-two eyes of 11 patients with VGB-VFL were studied. All patients underwent surgery for therapy-resistant epilepsy. Repeated electro-oculograms (EOGs) and flash electroretinograms (ERGs) were made and the cumulative dose of vigabatrin and the visual field loss were recorded after a period of 37-47 months. RESULTS: The visual field loss was stable in patients who had stopped vigabatrin at the time of the first examination. There was a slight increase in VFL in patients who continued vigabatrin. During the second EOG and ERG, abnormalities in scotopic and photopic a-wave latencies and in scotopic b-wave amplitude were found in more than 50% of patients. Only b-wave latency became normal, while EOG, a-wave latency, a-wave amplitude and b-wave amplitude stayed abnormal. The amount of VFL and the cumulative dose of vigabatrin were statistically correlated with the b-wave amplitude, mainly photopic, found during the first and second examinations. CONCLUSION: After 4 years, EOG, flash ERG and visual field loss had not improved in patients with VGB-VFL. The statistically significant correlation found during the first examination between the amount of VFL and the cumulative dose of vigabatrin with the (mainly photopic) b-wave amplitude remained constant.     

The value of electrophysiology results in patients with epilepsy and vigabatrin associated visual field loss

PURPOSE: To determine the value of electrophysiological findings in patients with temporal lobe epilepsy and to relate these findings to the amount of concentric contraction of the visual field and the use of vigabatrin. METHODS: Electro-retinograms and electro-oculograms were done on 30 patients, operated for temporal lobe epilepsy. The patients were divided into three groups: (A) concentric contraction of the visual field associated with a history of vigabatrin medication (15 patients), (B) normal visual field with vigabatrin use (11 patients) and (C) normal visual field without vigabatrin medication (4 patients). RESULTS: Electrophysiological abnormalities were found in 50% of the patients in group A. The Arden ratio of the EOG was lowered in 57%. Abnormalities in the ERG were found: b-wave implicit time photopic F was prolonged (50%), b-wave amplitudes scotopic B (53%), C (73%) and G (50%) and photopic H (50%) were diminished. The amount of visual field loss and the total dose of vigabatrin used, showed only slight correlation with the ERG and EOG. The use of vigabatrin during the ERG and EOG recording in group A, gave a higher b-wave amplitude scotopic G in 64% of cases. The a-wave implicit times scotopic G (73%) and photopic G (59%) and H (73%) were shortened in group B. CONCLUSION: EOG was abnormal in 57% in group A. ERG abnormalities could only be found in 50% of group A, mainly in the inner retina. Since also the total dose of vigabatrin and the amount of visual field loss did not really show a correlation with the electrophysiological findings and results of literature are not unanimous, electrophysiology does not appear at present to be a good method to detect patients with, or at risk of, vigabatrin associated visual field loss. Regularly performed visual field examination remains the cornerstone in screening.     

Retinal dysfunction in patients treated with vigabatrin

PURPOSE: To present the current knowledge of vigabatrin influence on the retinal function and to introduce a case report of toxic retinopathy diagnosed in our laboratory, in patient treated with vigabatrin. MATERIAL AND METHODS: A review study based on other authors', concerning the role of diagnostic tests like: perimetry, flash electroretinography (ERG), multifocal electroretinography (mfERG), electrooculography (EOG) in patients treated with vigabatrin and presentation of toxic retinopathy in drug-resistant epileptic patient treated with vigabatrin. RESULTS: In vigabatrin treated patients a functional or structural retinal changes may occur, what can be measured by electrophysiological and visual field testing. Irreversible abnormalities of visual field and ERG tests results prove the toxic character of retinopathy in presented vigabatrin treated patient. CONLUSIONS: ERG tests and visual field assessment should be performed in patients treated with vigabatrin. Initial abnormalities occurrence should be a signal for considering the change of therapy.     

The effects of vigabatrin on electrophysiology and visual fields in epileptics: a controlled study with a discussion of possible mechanisms

Purpose: To compare the visual electrophysiology and visual fields of patients taking vigabatrin to those of a control group of epileptics on other anti-epileptic drugs (AEDs). Methods: Fourteen epileptics treated with vigabatrin and 10 control patients treated with other AEDs underwent ERG and EOG. Goldmann visual fields were performed and analysed using standard software to measure areas contained within I4e isopters. Results: The cone and rod b-waves of the ERG, the oscillatory potential amplitudes and Arden indices were reduced in vigabatrin-treated subjects and the oscillatory potentials delayed. The Arden indices were reduced due to an increased dark trough. The areas contained within the I4e isopter of vigabatrin treated subjects were reduced compared to the control group and these areas correlated well with oscillatory potential amplitudes and b-wave amplitudes in the vigabatrin group only. Conclusions:The use of vigabatrin is associated with a reduction of the ERG cone b-wave amplitude and oscillatory potentials which correlates with visual field loss. The Arden ratio is reduced in subjects taking vigabatrin but may recover after cessation. However, visual loss may persist in the presence of a recovered EOG. These findings suggest further effects of the drug than those mediated by GABA receptors, and support the contention that the cause of the field loss may be at least in part due to retinal effects. Possible mechanisms are discussed.     

Electroretinographic (ERG) responses in pediatric patients using vigabatrin

The antiepileptic drug vigabatrin is known to cause retinal and visual dysfunction, particularly visual field defects, in some patients. Electroretinography (ERG) is used in an attempt to identify adverse effects of vigabatrin (VGB) in patients who are not candidates for conventional perimetry. We report data from 114 pediatric patients taking VGB referred for clinical evaluation; median age at test was 22.9 (2.4 to 266.1) months, and median duration of VGB use was 9.7 (0.3 to 140.7) months. Twenty-seven of them were tested longitudinally (3 to 12 ERG tests). ERG responses to full-field stimuli were recorded in scotopic and photopic conditions, and results were compared to responses from healthy control subjects. We found that abnormalities of photoreceptor and post-receptor ERG responses are frequent in these young patients. The most frequently abnormal scotopic parameter was post-receptor sensitivity, log σ, derived from the b-wave stimulus-response function; the most frequently abnormal photopic parameter was the implicit time of the OFF response (d-wave) to a long (150 ms) flash. Abnormal 30-Hz flicker response amplitude, previously reported to be a predictor of visual field loss, occurred infrequently. For the group as a whole, none of the ERG parameters changed significantly with increasing duration of VGB use. Four of the 27 patients tested longitudinally showed systematic worsening of log σ with duration of VGB use. In a subset of patients who underwent perimetry (N = 39), there was no significant association of any ERG parameter with visual field defects. We cannot determine whether the ERG abnormalities we found were due solely to the effects of VGB. We caution against over-reliance on the ERG to monitor pediatric patients for VGB toxicity and recommend further development of a reliable test of peripheral vision to supplant ERG testing.     

Vigabatrin and retinal changes

Purpose: Vigabatrin is an effective antiepileptic drug but visual field constriction (VFC) is found to be a severe side-effect. The aims have been to investigate whether visual field constriction (VFC) is related to changes in the electroretinography (ERG). Methods: Twenty patients with localisations related epilepsy of whom one half had received vigabatrin were subjected to examination without informing about the treatment given. The eye examination included Goldmann perimetry and ERG. Results: All the patients had normal visual acuity. A total of three patients (30%) in the vigabatrin group and none in the control group were found to have VFC. In the vigabatrin group ERG examination were normal in one case, in five cases there were changes scotopic, photopic and in the oscillatory potentials (OP), while the remaining four had changes in two of these parameters. OPs were abnormal in eight of 10 patients. Of the three patients with VFC all had changes in ERG. The four patients with the most severe abnormalities in ERG had received high daily doses of vigabatrin (4 – 6 mg) in a period. In the control group no abnormality was observed in five cases, and in the remaining five changes were present in one or two of the potentials. Conclusion: It is found that 30% of patients treated with vigabatrin, develop VFC, and none in the control group. Similarly more patients in the vigabatrin group had changes in the ERG as compared to the control group, and the number of abnormal potentials are significantly higher among patients with VFC compared to those without. But the finding of abnormal ERG results is not synonymous with VFC, and this is important to bear in mind when examining patients that cannot cooperate to a VF examination. An individual sensitivity to vigabatrin is supposed, but severe ERG changes occurred in all patients having had high daily doses slant4 g.     

Visual field defects in patients taking vigabatrin

PURPOSE: To investigate visual field loss in patients on long-term treatment with the antiepileptic drug vigabatrin, recently reported to cause visual disturbances. METHODS: Eighteen patients taking vigabatrin for 0.5-9.5 years were examined with automated perimetry up to 60 degrees from fixation using the Humphrey Field Analyser. Five patients with epilepsy receiving other medications served as controls. Patients found to have a visual field defect underwent ophthalmologic examination. RESULTS: Among the 18 patients in the vigabatrin group, visual field defects categorised as mild were revealed in 6 right eyes (33%) and 8 left eyes (44.4%), while defects categorised as severe were found in 9 right eyes (50%) and 8 left eyes (44.4%). The majority of the defects (66.7% in the right eye) were peripheral constriction with nasal predominance. The location of the defects was confirmed in 8 patients also tested with Kowa AP340 perimetry. CONCLUSION: According to our results, visual field defects among the patients on vigabatrin therapy may occur more frequently than previously recognised.     

Visual field constriction and electrophysiological changes associated with vigabatrin

Purpose: We investigated functional, morphological and electrophysiological changes in patients under anti-epileptic therapy with vigabatrin (VGB), a GABA aminotransferase inhibitor. Methods: 20 epileptic patients treated with vigabatrin (age range 25–66 years) were enrolled in this study. The referrals were made by the treating neurologist, based on suspected or known visual field changes in these patients. Two patients had vigabatrin monotherapy, 18 patients were treated with vigabatrin in combination with other antiepileptic drugs. None of the patients reported visual complaints. Patients were examined with psychophysical tests including colour vision (Farnsworth D15), dark adaptation threshold, Goldmann visual fields and Tuebingen Automated Perimetry (90°). A Ganzfeld ERG and an EOG following the ISCEV standard protocol were also obtained. Additionally, all patients were examined with the VERIS multifocal ERG including recordings of multifocal oscillatory potentials. Results: Visual acuity, anterior and posterior segments, colour vision and dark adaptation thresholds were normal in all patients. Of 20 patients, 18 presented visual field constriction. All patients with visual field defects revealed altered oscillatory potentials waveforms in the ERG, especially in those patients with marked visual field defects. Multifocal oscillatory potentials were also delayed in those patients. In some patients a delayed cone single flash response (6/20), a reduced mERG amplitude (12/20) and a reduced Arden ratio (9/20) were found. Conclusions: The present data indicate an effect of vigabatrin on the inner retinal layers. Since abnormalities of the oscillatory potentials were seen in all patients with visual field defects a dysfunction of GABA-ergic retinal cell transmission might be assumed.     

Visual electrophysiological effect of a GABA transaminase blocker

Vigabatrin is an antiepileptic drug for the treatment of partial seizures. The anticonvulsant effect is achieved by irreversible inhibition of the enzyme GABA-transaminase which catalyses the inactivation of GABA. Vigabatrin has been associated with visual field loss and electrophysiological abnormalities. The purpose of the study was to determine any alterations in normal volunteers of the visual field and the visual electrophysiology resulting from a short exposure to vigabatrin. A three-way, double-blind study of placebo, carbamazepine and vigabatrin was undertaken at baseline and on days two, four and nine. Seven subjects completed all three cycles and 14 subjects (six females and eight males; mean age 27.3 years SD 6.7) completed at least one cycle. Static threshold automated perimetry comprised Humphrey Visual Field Analyzer Programs 30-2 and 30/60-2. Electro-oculography and electroretinograms were performed with undilated pupils using the Medelec Ganzfeld stimulator GS2000. The visual field was unaffected by placebo, carbamazepine or vigabatrin. The group mean amplitudes and latencies for the scotopic ERG, 30Hz flicker ERG and the oscillatory potentials remained unchanged for any cycle. The group mean photopic ERG b-wave latency increased from baseline (p < 0.05); no significant change occurred with carbamazepine or placebo. The group mean Arden Index for vigabatrin decreased from baseline to day 9 (p <; 0.01); no significant differences were present for carbamazepine or placebo. Vigabatrin has a rapid effect on both the photopic ERG and the EOG; however, the changes merely reflect alterations in retinal GABA levels secondary to concomitant blocking of GABA transaminase by existing vigabatrin therapy. This revised version was published online in July 2006 with corrections to the Cover Date.     

Pattern ERG and psychophysical functions in Best's disease

The aim of the study was to asses the neurosensory retinal function in 12 patients (24 eyes) with different stages of Best's disease, by determining how pattern and full field flash ERG responses were related to visual acuity, stage of disease and extent of visual field loss. All patients had typically abnormal EOG responses and normal full field-flash ERG responses. Patients were stratified in two groups according to visual acuity. In the first group 12 eyes with visual acuity better than 0.5, all amplitudes and latencies of PERG P50 and N95 responses were in the normal range. Small central scotoma was detected by static perimetry in four of these eyes. In the second group of 12 eyes with visual acuity 0.5 or less, PERG showed reduced both P50 and N95 amplitudes in five eyes, and N95 solely, in two eyes. All patients had central scotomas detected by static perimetry. Progression of the disease, seen in deterioration of visual acuity and progression of central visual field defects, corresponded well with reduction of both PERG P50 and N95 amplitudes. There was no correlation found between visual acuity and EOG responses. Our results show that in Best's distrophy, pattern ERG is getting abnormal with progression of the disease, indicating relative preservation of neurosensory retina in initial stages of the disease. In contrast to EOG - being abnormal in all the patients regardless of the stage of disease - and full field-flash ERG - being normal in most of the patients - PERG gives opportunity for electrophysiological determination of the progression of the disease.     

Full-field ERG and visual fields in patients 5 years after discontinuing vigabatrin therapy

Purpose In numerous studies vigabatrin medication has been associated with visual field constriction and alterations in the full-field electroretinogram (ff-ERG), but it is not clear whether these changes are reversible or not. The purpose of this study was to examine patients with visual field loss and reduced ff-ERG several years after discontinuing vigabatrin therapy, in order to investigate reversibility. Methods Eight patients with visual field constriction and reduced cone responses measured by 30 Hz flicker ERG were examined with Goldmann perimetry and ff-ERG 4-6 years after discontinuing medication. The results were compared with investigations conducted during medication, 4-6 years previously. Statistical analysis was also used to compare the ff-ERG results of the patients, during treatment and at follow-up, with a group of 70 healthy subjects. Results Visual field constriction remained 4-6 years after discontinuing vigabatrin therapy. The amplitude of the 30 Hz flicker response also remained reduced on follow-up both compared with the results during treatment and with the control group. Moreover, the amplitude of the isolated rod response and the combined rod-cone response were decreased in the patients compared with the control group, during vigabatrin treatment as well as on follow-up. On follow-up, oscillatory potentials (OPs) also were registered, showing reduced amplitudes in patients compared with controls. The within subject comparison showed no significant changes. Conclusion Vigabatrin attributed visual field constriction and reduced ff-ERG responses remain several years after discontinuing vigabatrin therapy, indicating drug-induced permanent retinal damage.     

Vigabatrin-associated loss of vision: rarebit perimetry illuminates the dose-damage relationship

PURPOSE: The utility of vigabatrin in the treatment of epilepsy is partially offset by its retinal toxicity. The relationship between dosage and damage is obscure. This may be due to perimetric shortcomings. The new technique of rarebit ('microdot') perimetry might be more informative. METHODS: Twelve patients who had been treated with vigabatrin for various durations were examined by manual, kinetic perimetry and by rarebit perimetry. RESULTS: Rarebit results differed significantly between patients and normal controls and rarebit deficits were directly proportional to cumulated vigabatrin doses (correlation coefficients were - 0.92 in the nasal field and - 0.82 in the temporal field). Manual perimetry results were less clearly related to dosage (r = - 0.54 and r = - 0.73, respectively). CONCLUSION: Rarebit perimetry indicates that each treated subject will develop visual loss and that visual loss will be proportional to the accumulated dose. Conventional perimetry is less well suited to detecting and quantifying vigabatrin-associated visual loss.     

Vigabatrin-induced visual dysfunction in Chinese patients with refractory epilepsy

PURPOSE: Bilateral visual field constriction has been reported following the use of the antiepileptic drug (AED) vigabatrin. The incidence of retinal toxicity is variable and there are limited data in Asian populations. The authors report the results of ophthalmologic examination in Chinese patients taking this drug. METHODS: The authors identified two groups of patients with refractory epilepsy: one group on vigabatrin and another cohort of patients taking other AEDs. The authors recorded the medical history and performed visual acuity testing, intraocular pressure measurement, slit lamp biomicroscopy, and conventional automated perimetry with Humphrey Visual Field Analyzer II in all patients. RESULTS: Eighteen patients--8 men and 10 women--with a mean age of 23.8 years who were taking vigabatrin were reviewed. Length of treatment with this drug ranged from 13 months to 5 years and the mean daily dosage was 1581 mg. None of the patients in either group had a history of coexisting optic nerve diseases or other neurotoxic drug use. Twenty of 36 (55.6%) eyes of the vigabatrin users showed significant bilateral visual field defects with 80% showing a concentric pattern, compared with none in the control group. CONCLUSIONS:The authors confirmed a high prevalence of visual field constriction associated with vigabatrin in Chinese patients. The use of alternative novel techniques such as measurement of the retinal nerve fibre layer thickness and perimetry may detect early retinal damage and result in even higher incidences. Visual field monitoring is recommended in patients who continue to take this drug.     

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

PURPOSE: 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 < 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 anti-convulsants. 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.     

Vigabatrin-associated visual field constriction in a longitudinal series. Reversibility suggested after drug withdrawal

PURPOSE: To evaluate through a longitudinal study the effects on visual fields of long-term vigabatrin medication in patients with partial epilepsy and to discuss visual field screening strategies. METHODS: A total of 26 patients aged 14-68 years with a mean history of vigabatrin medication of 8.5 years (range 2-14 years) were followed by manual kinetic Goldmann perimetry (objects IV,4 and I,4) for 6-26 months (mean value 12.3 months). At time zero and at follow-up, each patient was assigned a "pooled" averaged value, as a linear percentage of normal isopter position, for the two objects as tested nasally and temporally in the five most horizontal meridians on the Goldmann chart. Twelve eyes from nine adults (age 24-60 years) served as controls. RESULTS: Constrictions were recorded in 24 of 26 patients at baseline. Averaged isopters ranged from 8% to 96% of the controls' averaged isopter positions. Median values of 71.5% and 60.5% for large and small objects, respectively, indicated that the smaller object was more sensitive to visual field constriction. There was no difference in the degree of constriction between nasal and temporal hemifields. Significant improvement in the visual field (mean gain 13.6% units) was seen in the eight patients who underwent full drug withdrawal. No similar improvement was seen in the 12 patients still on full dose or the six with reduced intake. CONCLUSIONS: Most Danish patients on long-term vigabatrin medication have suffered some visual field loss. Contrary to most clinical evidence so far, the present follow-up study indicates some reversibility of visual field loss after drug withdrawal. Kinetic Goldmann perimetry appears to be a fair alternative to computerized static perimetry techniques for screening and following vigabatrin-treated patients.     

Concentric changes in the visual field associated with GABA-mimetic antiepileptic agents]

Bilateral visual field constriction has been recently reported in patients treated with vigabatrin. It has been considered that vigabatrin, a GABA agonist antiepileptic drug, was specifically responsible for this visual field defect. We present four observations sharing the same characteristics of chronic tunnel vision. Three patients had had vigabatrin but the fourth one received other antiepileptic drugs, progabide, an agonist of post-synaptic GABA receptors, and phenobarbital which interferes with GABA-A receptors. It is thus possible to hypothesize a retinal toxicity triggered by chronically increased GABA transmission. If this is confirmed, an accurate incidence of symptomatic and asymptomatic visual field constriction with GABA-mimetic drugs should be established, as well as the patients' profiles which are more at risk. Patients currently under this type of treatment should be checked by both manual and automatic perimetry every six months to one year.     

Evaluation of the central visual field by the Friedmann Mark I analyzer and color vision in 85 patients with multiple sclerosis. Correlation with visual evoked potentials in 50 cases

Analysis of the visual field using Friedmann's analyser Mark I and color study in 85 multiple sclerosis patients. Static perimetry of the central visual field and test batteries (Ishihara plates, 15 Hue Standard, 15 Hue of Lanthony) for acquired color vision defects were performed in 85 multiple sclerosis patients (61 definite, 12 probable, 12 possible cases). Results in patients were compared to data obtained in 53 control subjects matched for age. 64% of the 85 patients and 52% of 48 patients with no history of optic nevritis showed visual field abnormalities and/or color vision defects. Comparison with VEP was available in 50 patients. While 10 patients had abnormal VEP and normal static perimetry and coloration tests, 5 patients had the reverse findings.     

Electro-ophthalmological recovery after withdrawal from vigabatrin

This study describes the effects of stopping of the anti-epileptic drug vigabatrin on the visual field and electrophysiological changes in one third of the group of patients which is described in the paper `Visual field and electrophysiological abnormalities due to vigabatrin' (Van der Torren and Graniewski, 2002). In 1997 several reports described the possible oculotoxic effect of vigabatrin followed by a reconsideration of this medication in epileptic patients. Vigabatrin was discontinued in one-third of the patients on chronic medication (mean duration 4.8 years). The visual field and electrophysiological examinations were repeated every 3 months if possible, otherwise at 6-month intervals. The EOG Arden index and the ERG rod b-wave showed a significant improvement when vigabatrin was discontinued. Repeated examinations of visual fields and electrophysiology shortly after discontinuation of the drug (between 1 and 3 months) and later on after 6 months and 1 year showed a recovery of the EOG Arden index and the ERG rod b-wave during this period. The visual fields did not change in either direction. Conclusion: the recovery effect is a strong argument for the hypothesis that the reduction in EOG and ERG b-wave is an oculotoxic effect. The electrophysiological improvement during 6 months or longer after discontinuation and the unchanged visual fields are an argument for the hypothesis that the visual field represents the irreversible intoxicating effect on the retina, whereas the electrophysiology represents a more direct effect on the retinal glial cells level.