Lawden M C, Eke T, Degg C, Harding G F, Wild J M
Department of Neurology, Leicester Royal Infirmary, Leicester, UK.
J Neurol Neurosurg Psychiatry. 1999 Dec;67(6):716-22. doi: 10.1136/jnnp.67.6.716.
To estimate the prevalence of visual field defects in patients taking the anticonvulsant drug vigabatrin and to characterise the features of visual dysfunction found.
Thirty three unselected patients attending neurology and epilepsy clinics were identified as taking vigabatrin and asked to attend for neuro-ophthalmic evaluation. A control group of 16 patients with epilepsy unexposed to vigabatrin was also evaluated. Visual fields were examined by static perimetry using a Humphrey field analyser. Patients underwent detailed ophthalmic examination, various blood tests, and brain MRI where necessary. Visual evoked responses (VERs), electro-oculograms (EOGs), and electroretinograms (ERGs) were recorded.
Of 31 assessable patients treated with vigabatrin, 16 (52%) had definitely abnormal visual fields, nine (29%) had fields that were inconclusive, four (13%) had normal fields, and two (6%) proved unable to cooperate with testing. In four patients some plausible cause was found for the field abnormality leaving 12 patients (39%) in whom a definite bilateral field defect was found, possibly caused by vigabatrin treatment. Of 16 control patients none had definitely abnormal fields, 12 (75%) had normal fields, and four (25%) had fields that were inconclusive. The field defects associated with vigabatrin treatment showed a characteristic pattern of concentric peripheral field loss with temporal and macular sparing. The VERs and ERGs were normal. The EOG Arden Index was reduced in patients taking vigabatrin, although this returned towards normal when vigabatrin was stopped, even in the presence of persistent field defects. Multifocal ERGs recorded in two patients were abnormal, showing marked reduction in amplitude of the peripheral focal ERG.
Treatment with vigabatrin was associated with a high prevalence of peripheral visual field defects. This seemed to be the result of a toxic effect of vigabatrin on the retina and seemed to persist if the drug was withdrawn.
评估服用抗惊厥药物氨己烯酸的患者视野缺损的患病率，并描述所发现的视觉功能障碍特征。
在神经内科和癫痫门诊就诊的33例未经过挑选的患者被确定为正在服用氨己烯酸，并被要求前来接受神经眼科评估。还对16例未接触过氨己烯酸的癫痫患者组成的对照组进行了评估。使用Humphrey视野分析仪通过静态视野检查法检查视野。必要时，患者接受详细的眼科检查、各种血液检查和脑部磁共振成像。记录视觉诱发电位（VERs）、眼电图（EOGs）和视网膜电图（ERGs）。
在31例可评估的服用氨己烯酸的患者中，16例（52%）视野明显异常，9例（29%）视野结果不确定，4例（13%）视野正常，2例（6%）无法配合检查。在4例患者中发现了一些可能导致视野异常的原因，剩下12例患者（39%）发现明确的双侧视野缺损，可能是由氨己烯酸治疗引起的。16例对照患者中，无一例视野明显异常，12例（75%）视野正常，4例（25%）视野结果不确定。与氨己烯酸治疗相关的视野缺损呈现出一种特征性模式，即周边视野呈同心性丧失，颞侧和黄斑区保留。VERs和ERGs正常。服用氨己烯酸的患者EOG Arden指数降低，尽管在停药后该指数恢复正常，即使存在持续性视野缺损。对2例患者记录的多焦ERGs异常，显示周边局部ERG振幅明显降低。
氨己烯酸治疗与周边视野缺损的高患病率相关。这似乎是氨己烯酸对视网膜产生毒性作用的结果，并且在停药后似乎仍然存在。
