Visual and auditory evoked potentials during long-term vigabatrin treatment in children and adolescents with epilepsy

• Published in: Clinical neurophysiology Vol. 111; no. 12; pp. 2150 - 2154
• Main Authors: Zgorzalewicz, M, Galas-Zgorzalewicz, B
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.12.2000; Elsevier Science
• Subjects: Adolescent; Biological and medical sciences; Brain-stem auditory evoked potentials; Child; Children; Electrodiagnosis. Electric activity recording; Electroencephalography; Epilepsy; Epilepsy - drug therapy; Epilepsy - physiopathology; Evoked potentials; Evoked Potentials, Auditory - drug effects; Evoked Potentials, Auditory - physiology; Evoked Potentials, Visual - drug effects; Evoked Potentials, Visual - physiology; Female; Humans; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Nervous system; Vigabatrin; Vigabatrin - therapeutic use; Visual evoked potentials; Visual evoked potentials; Children; Vigabatrin; Evoked potentials; Brain-stem auditory evoked potentials; Epilepsy; Human; Nervous system diseases; Visual evoked potential; Anticonvulsant; Cerebral disorder; Electrodiagnosis; Treatment; Auditory evoked potential; Central nervous system disease; Adolescent; Child; Age
• ISSN: 1388-2457; 1872-8952
• DOI: 10.1016/S1388-2457(00)00453-3

Objectives: The aim of the study was to estimate the effects of Vigabatrin (VGB) as add-on therapy on visual (VEP) and brain-stem (BAEP) evoked potentials. Method: The investigation covered 100 epileptic patients from 8 to 18 years of age. The treatment included therapy with carbamazepine (CBZ) or valproate acid (VPA) using slow release formulations of these AEDs. Combination therapy was administered using add-on VGB in the recommended dose 57.4±26.5 mg/kg body mass/day. VEP and BAEP evoked potentials were recorded by means of Multiliner (Toennies, Germany). The obtained values were compared with age matched control group. Results: Compared to control groups, significant differences in epileptic groups emerged in latencies of the peak III, V along with the interpeak intervals I–III of BAEP. Also VEP studies showed the reduction of N75/P100 and P100/N145 amplitudes. Conclusions: Adding VGB did not significantly increase the percentage of pathological abnormalities observed from EPs. Our electrophysiological studies demonstrate abnormalities in EPs parameters due to subclinical toxicity induced by AEDs. Major alterations produced bitherapy of VPA-SR + VGB and minor SR formulations of CBZ or VPA.