a 21-year - old man has been treated for a seizure disorder in the department of neurology since he was 15 years old . at the age of nine years the beginning of his seizures was a visual aura , right side hemianopsia , usually accompanied by a headache , and then he stares vacantly and does not respond to verbal commands . when he was 13 years old , he had started to take an unknown species of antiepileptic drug . but because of the bankruptcy of the hospital he was treated in , he stopped the medication when he was 14 years old . he suffered a generalized tonic - clonic seizure under the drug withdrawal state . just after the seizure he visited another hospital . valproic acid ( vpa ) monotherapy did not change the seizure frequency under poor drug compliance . he heard that there were no abnormal findings on the two eegs checked in that hospital . the patient visited the pediatric department of our hospital when he was 15 years old . there were no abnormal findings in the brain mri taken at that age ; vgb was added on and vpa was tapered ; his prescription was adjusted to high dosage of vgb ( 3,500 mg / day ) by a pediatrician . five months after his visit to the pediatric department , he suffered another complex partial seizure , and the pediatrician in charge referred the patient to the department of neurology . since then , he had been seizure free for four years and eight months while taking 3,000 mg / day of vgb . however , he had another complex partial seizure starting with visual aura when he was 20 years old ; that was his last seizure . eegs were recorded periodically in our hospital after the use of vgb since the first visit in the pediatric department . in eight of the consecutive nine eegs recorded over approximately four years , the diffuse bursts of 22.5 hz spike - and - wave complexes were observed repetitively ( fig . the occurrences of the abnormal discharges in each eeg were several to frequent during the 30 min recording . in another eeg recorded five months after the last seizure at when he was 20 years old , the generalized epileptiform discharges were also observed intermittently . just after that eeg recording , 600 mg / day of vpa the patient s prescription at that time was 600 mg / day of vpa plus 1,000 mg / day of vgb . in the eeg recorded under that medication , several clusters of spikes on the occipital area of the left hemisphere there was no burst of the 22.5 hz spike - and - wave complexes on that eeg . when the patient was 21 years old , four months after the eeg recording , another eeg was recorded ; no epileptiform discharges were observed in that eeg . the mechanism of vgb induced - seizure aggravation is thought to associate with gabaergic system that vgb may act antiepileptic role . in the thalamocortical circuit , nucleus reticularis thalami neurons ( nrts ) the inhibitory impulses produced by the firing of nrts keep tcrs in an inhibitory state . the overactivation of the gabab receptors of the tcrs , resulting from the exceedingly active state of nrts , changes the spindle waves to the spike - and - wave - complexes.6 enhancement of gabaergic transmission could show both preventive and aggravating effects to seizures depending on the site of action . the systemic or local gabaergic stimulation by drugs increased the occurrences of seizures and the duration of spike - and wave discharges in pharmacological and genetic animal models of absence seizures.7,8 in the microinjection study with the genetic absence epilepsy rats from strasbourg ( gaers ) , the injection of vgb into tcrs increased spontaneous cortical spike - and - wave discharges but the injection into nrts inhibits the discharges . this may be because the inhibition of nrts reduces the tendency of synchronization of tcrs , but the enhanced inhibition of tcrs by vgb may make the tcrs in a more synchronized state.1,9 worsening of seizures induced by vgb has been reported usually in the patients with generalized epilepsy.2,3 vgb also could induce de novo absence seizures or absence status epilepticus with generalized epileptiform discharges in patients with partial seizures.4,5 in addition , myoclonic jerks with generalized polyspike and wave complexes in eeg were observed during vgb therapy in focal epilepsy.10 however all of seizures induced by vgb , in both of the aggravated cases and the de novo cases , subsided after the discontinuation of vgb or switching from vgb to other antiepileptic drugs.4,5,10 the vgb - induced generalized spike - and - wave complexes had been observed for about four years in this patient , who had focal epilepsy ; there was no clinically definitive provocation of primary generalized seizures . after the introduction of vpa and reduction of vgb , there was disappearance of the generalized epileptiform discharges completely . the pattern of epileptiform discharges on that eeg was focal type , which confined to the occipital area of the left hemisphere . the use of vgb may chronically induce generalized epileptiform discharges without the induction of primary generalized seizures in the patients with focal epilepsy . regardless that it is not clear whether the discontinuation of vgb , the introduction of vpa or a combination of both disappear the generalized epileptiform discharges in this case . the discontinuation of vgb would be helpful to suppress the generalized epileptiform discharges in such cases .
vigabatrin ( vgb ) may aggravate clinical seizures and epileptiform discharges especially in the patients with generalized epilepsy . 
 this report is about the repetitive appearance of generalized spike - and - wave complexes in a patient with focal epilepsy . 
 though there were constant appearances of the generalized epileptiform discharges on the consecutive electroencephalograms ( eegs ) taken over approximately four years under vgb monotherapy , clinical provocation of primary generalized seizures was not occurred . 
 because of the repetitive observations of the generalized epileptiform discharges , valproic acid was added and the tapering of vgb was started . on the eeg taken during the tapering period of vgb and another eeg after the discontinuation of vgb , the generalized epileptiform discharges were completely disappeared . through observation in this case 
 , we suggests that the use of vgb could induce generalized epileptiform discharges without clinical seizure induction for long term period .