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

被引:29
作者
Comaish I.F. [1 ]
Gorman C. [1 ]
Brimlow G.M. [2 ]
Barber C. [2 ]
Orr G.M. [1 ]
Galloway N.R. [1 ]
机构
[1] Department of Ophthalmology, Queen's Medical Centre, Nottingham
[2] Department of Medical Physics, Queen's Medical Centre, Nottingham
关键词
Electrophysiology; Lateral inhibition; Oscillatory potentials; Vigabatrin; Visual fields;
D O I
10.1023/A:1014603229383
中图分类号
学科分类号
摘要
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.
引用
收藏
页码:195 / 212
页数:17
相关论文
共 70 条
[1]  
Meldrum B.S., The role of glutamate in epilepsy and other CNS disorders, Neurology, 44, 11 SUPPL. 8, (1994)
[2]  
De Luka S.R., Protic S., Vrbaski S.R., Gamma aminobutyric acid - Its function, disorders and their sequelae, Med Pregl, 51, 7-8, pp. 319-324, (1998)
[3]  
Frumkes T.E., Nelson R., Functional role of GABA in cat retina: I. Effects of GABA(A) agonists, Vis Neurosci, 12, 4, pp. 641-650, (1995)
[4]  
Frumkes T.E., Nelson R., Pflug R., Functional role of GABA in cat retina: II. Effects of GABA(A) antagonists, Vis Neurosci, 12, 4, pp. 651-661, (1995)
[5]  
Gibson K.M., Hoffmann G.F., Hodson A.K., Bottiglieri T., Jakobs C., 4-Hydroxybutyric acid and the clinical phenotype of succinic semialdehyde dehydrogenase deficiency, an inborn error of metabolism, Neuropediatrics, 29, 1, pp. 14-22, (1998)
[6]  
De Biase D., Et al., Chemistry of the inactivation of 4-aminobutyrate aminotransferase by the antiepileptic drug vigabatrin, J Biol Chem, 266, 30, pp. 20056-20061, (1991)
[7]  
Loscher W., Horstermann D., Differential effects of vigabatrin, gamma-acetylenic acid, and valproate on levels of various amino acids in rat brain regions and plasma, Naunyn Schmiedebergs Arch Pharmacol, 349, 3, pp. 270-278, (1994)
[8]  
Bernasconi R., Klein M., Martin P., Christen P., Hafner T., Portet C., Schmutz M., Gamma-vinyl GABA: Comparison of neurochemical and anticonvulsant effects in mice, J Neural Transm, 72, 3, pp. 213-233, (1988)
[9]  
Sidhu R.S., Et al., Low-dose vigabatrin (gamma-vinylGABA)-induced damage in the immature rat brain, Exp Neurol, 144, 2, pp. 400-405, (1997)
[10]  
Mackenzie R., Klistorner A., Severe persistent visual field constriction associated with vigabatrin: Asymptomatic as well as symptomatic defects occur with vigabatrin, Br Med J, 316, (1998)