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Biomedical subjects

I Nousiainen

Publications and source records attributed to I Nousiainen.

8 recordsLinked to original sources
PubMed2001

No reversion in vigabatrin-associated visual field defects.

Sixty adult patients with partial epilepsy who have been treated with vigabatrin for 7 months to 14 years as mono- or add-on therapy were examined with repeated kinetic Goldmann perimetries to evaluate the prevalence, risk factors, and long-term outcome of vigabatrin-associated visual field defects. A follow-up examination was performed after 4 to 38 months (mean, 15 +/- 7) in 55 patients, 29 of whom had discontinued vigabatrin therapy. Neither reversion nor progression in visual field constriction was observed.

Adult↗
PubMed2001

Reversed visual field constrictions in children after vigabatrin withdrawal--true retinal recovery or improved test performance only?

While vigabatrin-associated visual field constrictions have been generally considered irreversible, some case reports have raised the hope of partial improvement after drug withdrawal in occasional patients. Here we describe seven children with epilepsy, whose visual field constrictions, as demonstrated by the kinetic perimetry (Goldmann), attenuated or recovered after discontinuation of vigabatrin therapy. While this improvement may be largely due to better performance in later test sessions, we want to raise the possibility that some visual field recovery may be possible at least in young patients.

Adolescent↗
PubMed2001

Visual field defects with vigabatrin: epidemiology and therapeutic implications.

Vigabatrin is an antiepileptic drug (AED) that acts as a selective irreversible inhibitor of gamma-aminobutyric acid (GABA) transaminase. In 1997, 3 cases of severe symptomatic and persistent visual field constriction associated with vigabatrin treatment were described. During 1997 to 1998, similar concentric visual field constrictions were described in patients with drug-resistant epilepsy who were receiving vigabatrin concurrently with other AEDs. However, a study of patients treated with vigabatrin monotherapy alone showed that there was a causal relationship between vigabatrin treatment and the specific bilateral concentric visual field constriction. The Marketing Authorisation Holders survey (involving 335 vigabatrin recipients aged >14 years) indicated that 31% of patients [95% confidence interval (CI) 26 to 36%] had a visual field defect attributable to vigabatrin, compared with a 0% incidence of visual field defects (upper 95% CI 3%) in an unexposed control group. Other studies in adults have given similar overall prevalences, with a total of 169 of 528 patients diagnosed with vigabatrin-associated field defects (32%, 95% CI 28 to 36%). Male gender seems to be associated with an increase in the relative risk of visual field loss of approximately 2-fold. The pattern of defect is typically a bilateral, absolute concentric constriction of the visual field, the severity of which varies from mild to severe. Data gathered so far suggest that the cumulative incidence increases rapidly during the first 2 years of treatment and within the first 2 kg of vigabatrin intake, stabilising at 3 years and after a total vigabatrin dose of 3 kg. The prevalence of vigabatrin-associated field defects seems to be lower in children, but there are also methodological problems and greater variability in the assessment of visual fields in children. There is particular concern that the increased risk of the visual field defects will outweigh the benefit of the drug in patients who could be controlled with other AEDs. Vigabatrin should currently be used only in combination with other AEDs for patients with resistant partial epilepsy when all other appropriate drug combinations have proved inadequate or have not been tolerated. Regular visual field testing should be performed before the start of treatment and at regular intervals during treatment. Patients with pre-existent visual field defects due to other causes should not be treated with vigabatrin. Currently, the benefits of treating infantile spasms with vigabatrin monotherapy seem to outweigh the risks, but further prospective studies and follow-up of children receiving treatment are needed to evaluate the place of vigabatrin in this indication.

Animals↗
PubMed2000

Color vision in epilepsy patients treated with vigabatrin or carbamazepine monotherapy.

PURPOSE: To investigate color vision in epilepsy patients treated with vigabatrin or carbamazepine monotherapy and to evaluate the association between vigabatrin-induced visual field defects and dyschromatopsia. DESIGN: Nonrandomized comparative trial. PARTICIPANTS: Thirty-two epilepsy patients treated with vigabatrin monotherapy, 18 patients treated with carbamazepine monotherapy, and 47 age-matched healthy controls were examined. MAIN OUTCOME MEASURES: Color vision was examined with Standard Pseudoisochromatic Plates 2 (SPP2) screening test, Farnsworth-Munsell 100 (FM 100) hue test, and Color Vision Meter 712 anomaloscope. RESULTS: Abnormal color perception was found in 32% of the epilepsy patients treated with vigabatrin monotherapy and 28% of the epilepsy patients treated with carbamazepine monotherapy. The total error score in the Farnsworth-Munsell 100 hue test was abnormally high in the vigabatrin monotherapy patients who had concentrically constricted visual fields and a statistically significant correlation was found between the temporal visual field extents and the age-adjusted Farnsworth-Munsell 100 total error score in vigabatrin monotherapy patients (R = .533, P = 0.003 in the right eye, R = .563, P = 0.001 in the left eye). Four of 31 (12%) vigabatrin monotherapy patients, and 1 of 18 (6%) carbamazepine monotherapy patients had a blue axis in Farnsworth-Munsell 100 hue test. In the anomaloscope, there were a few pathologic findings in both groups. In the SPP2 screening test, a few plates were not seen in both groups. CONCLUSIONS: Both examined antiepileptic drugs, vigabatrin and carbamazepine, cause acquired color vision defects. The abnormal color perception seems to be associated with constricted visual fields in the vigabatrin monotherapy patients. The duration of carbamazepine therapy correlates with high FM100 total error score. The best method for detecting dyschromatopsia in patients treated with vigabatrin or carbamazepine was the Farnsworth-Munsell 100 hue test. The SPP2 screening test does not seem to be useful in clinical practice.

Adult↗
PubMed2000

Contrast and glare sensitivity in epilepsy patients treated with vigabatrin or carbamazepine monotherapy compared with healthy volunteers.

BACKGROUND/AIM: Many antiepileptic drugs have influence on visual functions. The aim of this study was to investigate possible changes in contrast sensitivity, macular photostress, and brightness acuity (glare) tests in patients with epilepsy undergoing vigabatrin (VGB) or carbamazepine (CBZ) monotherapy compared with healthy volunteers. METHODS: 32 patients undergoing VGB therapy, 18 patients undergoing CBZ therapy, and 35 healthy volunteers were asked to participate in an ophthalmological examination. In the previous study, visual field constrictions were reported in 40% of the patients treated with VGB monotherapy. In the present study, these VGB and CBZ monotherapy patients were examined for photopic contrast sensitivity with the Pelli-Robson letter chart and brightness acuity and macular photostress with the Mentor BAT brightness acuity tester. RESULTS: Contrast sensitivity with the Pelli-Robson letter chart showed no difference between these groups and normal subjects (ANOVA: p= 0.534 in the right eye, p= 0.692 in the left eye) but the VGB therapy patients showed a positive correlation between the contrast sensitivity values and the extents of the visual fields in linear regression (R = 0.498, p = 0.05 in the right eye, R = 0.476, p = 0. 06 in the left eye). Macular photostress and glare tests were equal in both groups and did not differ from normal values. CONCLUSION: The results of this study indicate that carbamazepine therapy has no effect on contrast sensitivity. Vigabatrin seems to impair contrast sensitivity in those patients who have concentrically constricted in their visual fields. Neither GBZ nor VGB affect glare sensitivity.

Adult↗
PubMed1999

Vigabatrin, a gabaergic antiepileptic drug, causes concentric visual field defects.

OBJECTIVE: To determine whether there is a causal link between vigabatrin treatment and concentric visual field defects and to evaluate the prevalence of these visual field constrictions. BACKGROUND: While the GABAergic antiepileptic drug (AED) vigabatrin was being clinically developed, only rare cases (less than 1:1000) of symptomatic visual field constriction and retinal disorders were reported. During 1997 to 1998, concentric visual field constrictions were described in case reports of mostly drug-resistant epilepsy patients receiving vigabatrin concurrently with other AEDs. METHODS: Ophthalmologic tests including Goldmann perimetry were performed on 32 adult patients on long-term successful vigabatrin monotherapy (treatment duration 29 to 119 months) and on 18 patients on carbamazepine monotherapy (treatment duration 32 to 108 months). Eighteen healthy adults served as controls. RESULTS: None of the patients complained about vision problems when asked to participate into the study. Thirteen out of the 32 (40%) epilepsy patients treated with vigabatrin monotherapy had concentrically constricted visual fields (9% severely, 31% mildly constricted), whereas none of the carbamazepine monotherapy patients or normal controls presented with a visual field defect (chi-square test, p = 0.0001). The extents of the visual fields were significantly constricted in vigabatrin group as compared with the visual fields of the patients in carbamazepine group or healthy controls (analysis of variance, Scheffe F-test, significant at 99%). CONCLUSIONS: The use of vigabatrin seems to increase the risk of a unique and specific pattern of bilateral, mainly asymptomatic visual field constriction. This risk should be considered when using vigabatrin. Visual field testing should also be performed before treatment and during routine follow-up for patients on vigabatrin.

Adolescent↗
PubMed1988

Refraction and accommodation in diabetic school children.

Refraction and accommodation of 61 diabetic children (aged 9 to 16 years) and 92 non-diabetic children (aged 10 to 16 years) were studied. Myopia was found in 36.1% of the diabetic children and in 29.3% of the non-diabetic children. The difference was not statistically significant. In the diabetic children, the age of the onset of myopia and the progression of myopia were the same as in the usual myopia at school age. The refraction curve of the diabetic children was less peaked than that of the non-diabetic children; a greater number of low myopic refractions were observed, and the low hyperopic refractions were more evenly distributed in the curve of the diabetic children. The mean accommodation of the diabetic children was 9.9 D +/- 2.2, and in the non-diabetic children it was 11.8 D +/- 2.6. The difference was statistically significant. The accommodation of both the diabetic and non-diabetic girls was lower than that of the boys. The accommodation in the myopic diabetic children was statistically significantly lower than the accommodation in the hyperopic diabetic children.

Accommodation, Ocular↗