OBJECTIVE: Although the unfavorable effects of early antiepileptic drugs, valproic acid, and carbamazepine (CBZ) on cognitive functions and visual functions have been investigated, the unfavorable effects of levetiracetam (LEV) on cognitive and visual functions remain unknown. The aim of the present study is to investigate whether there is a difference between the adverse effects by comparing the P300 and P100 latencies of LEV with epileptic patients using CBZ or sodium valproate (VPA) and healthy subjects. METHOD: A control group of 20 healthy subjects and 53 patients receivingmonotherapy with CBZ (n = 15), VPA (n = 14), and LEV (n = 24) who admitted to neurology policlinic for investigation and treatment were enrolled in this study. Visual evoked potentials and event-related evoked potentials were studied according to these groups. Standard "oddball paradigm" (unpredictable stimuli series) was used to obtain P300. RESULTS: The P300 latencies of epileptic patients receiving CBZ, VPA, and LEV were longer compared with the control group, and the differences were statistically significant (P = 0.001, 0.001, and 0.03, respectively). The P300 latency of patients receiving LEV was significantly shorter than the group receiving CBZ and VPA with statistically significant difference (P < 0.01 for both). The P300 amplitude was lower in the groups receiving CBZ, VPA, and LEV compared with the control group, and the difference was statistically significant (P < 0.05). CONCLUSIONS: The present study shows that LEV disrupts P300 latency less than VPA and CBZ and does not prolong P100 as much as them.
RCT Entities:
OBJECTIVE: Although the unfavorable effects of early antiepileptic drugs, valproic acid, and carbamazepine (CBZ) on cognitive functions and visual functions have been investigated, the unfavorable effects of levetiracetam (LEV) on cognitive and visual functions remain unknown. The aim of the present study is to investigate whether there is a difference between the adverse effects by comparing the P300 and P100 latencies of LEV with epilepticpatients using CBZ or sodium valproate (VPA) and healthy subjects. METHOD: A control group of 20 healthy subjects and 53 patients receiving monotherapy with CBZ (n = 15), VPA (n = 14), and LEV (n = 24) who admitted to neurology policlinic for investigation and treatment were enrolled in this study. Visual evoked potentials and event-related evoked potentials were studied according to these groups. Standard "oddball paradigm" (unpredictable stimuli series) was used to obtain P300. RESULTS: The P300 latencies of epilepticpatients receiving CBZ, VPA, and LEV were longer compared with the control group, and the differences were statistically significant (P = 0.001, 0.001, and 0.03, respectively). The P300 latency of patients receiving LEV was significantly shorter than the group receiving CBZ and VPA with statistically significant difference (P < 0.01 for both). The P300 amplitude was lower in the groups receiving CBZ, VPA, and LEV compared with the control group, and the difference was statistically significant (P < 0.05). CONCLUSIONS: The present study shows that LEV disrupts P300 latency less than VPA and CBZ and does not prolong P100 as much as them.