Abstracts

APPARENT INDUCTION OR EXACERBATION OF PRIMARY GENERALIZED SEIZURES AFTER INITIATION OF OXCARBAZEPINE

Abstract number : 2.230
Submission category :
Year : 2002
Submission ID : 878
Source : www.aesnet.org
Presentation date : 12/7/2002 12:00:00 AM
Published date : Dec 1, 2002, 06:00 AM

Authors :
David E. Mandelbaum, Steven L. Kugler, Jan B. Wollack, Elizabeth C. Wenger. Pediatrics and Neurology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ

RATIONALE: In 1983 Shields and Saslow reported new onset of generalized seizures after initiating carbamazepine (CBZ) therapy (Neurology. 33:1487-9, 1983). We now report three cases in which treatment with oxcarbazepine (OXC) appears to have induced onset of, or exacerbated, generalized seizures. After review of these case reports participants will be aware of this possible complication.
METHODS: Review of clinical history and EEG[ssquote]s in children with focal seizures treated with oxcarbazepine who had onset of generalized seizures for the first time after oxcarbazepine was started.
RESULTS: Patient #1 had a history of complex partial seizures since age 3 years refractory to phenytoin, primidone, valproate, lorazepam, felbatol, phenobarbital, and CBZ. Her EEG revealed left frontal epileptiform activity. At age 13 years, while still on phenobarbital and CBZ, treatment with OXC was initiated and CBZ was discontinued. Approximately 3 months later she was noted to have new onset of eye fluttering episodes. An EEG revealed generalized 3.5 cps spike and slow wave activity. After discontinuation of OXC the eye fluttering ceased.
Patient #2 had onset of left sided focal seizures at 3 months of age refractory to phenobarbital, CBZ, lamotrigine, phenytoin, gabapentin, and valproate. Multiple EEGs revealed no epileptiform activity. At age 5 years OXC was added to valproate with good seizure control. The valproate was discontinued and within 2 months she had onset of frequent generalized convulsive seizures. An EEG revealed frequent bursts of generalized spike and slow wave activity. The OXC was discontinued and treatment with zonisamide was initiated, with improvement of the seizures.
Patient #3 had a history of eye fluttering episodes with altered responsiveness since age 8 years, and onset of generalized convulsive seizures at age 10. An EEG at that time revealed epileptiform discharges in the left frontal region. The eye flutters persisted on phenytoin. Switching to OXC resulted in a marked increase in eye fluttering episodes, as well as clumsiness and confusion. A repeat EEG done 6 weeks after the initial EEG revealed frequent, generalized 3 cps spike and slow wave discharges. Discontinuation of OXC and treatment with valproate resulted in a marked improvement in overall level of functioning and decreased, though not complete resolution of, eye fluttering. Further improvement was achieved by addition of ethosuximide.
CONCLUSIONS: It appears that OXC induced or exacerbated primary generalized epileptiform activity in these patients, as evident by both clinical and EEG findings. Of additional interest is the fact that this occurred in patients 1 and 2 even though prior treatment with CBZ did not result in this complication.
(Disclosure: Grant - Novartis, Ortho-McNeil, Consulting - GlaxoSmithKline, Novartis, Elan, UCB Pharma, Ortho-McNeil, Honoraria - Elan, UCB pharma)