Lamotrigine May Aggravate or Provoke Atypical Absence Seizures in Cryptogenic and Symptomatic Epilepsies in Children
Abstract number :
3.123
Submission category :
Year :
2001
Submission ID :
2803
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
E. Liukkonen, MD, Pediatric Neurology, Hospital for Children and Adol., Helsinki Univ., Helsinki, Finland; E. Gaily, MD, Pediatric Neurology, Hospital for Children and Adol., Helsinki Univ., Helsinki, Finland; R. Paetau, MD, Pediaric Neurology, Hospital f
RATIONALE: Lamotrigine (LTG) is now a widely used antiepileptic drug in localization related as well as generalized epilepsies in childhood. The mechanism of action is mainly via sodium channels, similarly to carbamazepine, oxcarbazepine and phenytoin. There are reports on seizure aggravation on carbamazepine, oxcarbazepine and phenytoin, but only a few concerning LTG. We describe four children whose seizures were exacerbated while on LTG.
METHODS: All patients were cared for by the authors in 1999-2000. Three children had a video-EEG recording before LTG, and all four while on LTG and after LTG discontinuation. Trough LTG level measurements were available in three cases.
RESULTS: Two children had CP syndrome and hydrocephaly due to prematurity and intraventricular hemorrhage. One child had an unspecified retardation-malformation syndrome with abnormal MRI. One child had no antecedent events and normal MRI. Seizures at onset of epilepsy (mean age 4.2 years, range, 1.4-8.5 years) were psychomotor (PM) in three patients (with secondary generalization in two), and right sided clonic with occasional generalization in one patient. Two children had rare atypical absences (AAs) before LTG. LTG was introduced at mean age of 7.5 years (range, 6.3-10.4 years) as an adjunctive to valproate with slow dosage increments as suggested by the manufacturer. Within a couple of months all children experienced clinical worsening (developmental, behavioral and/or motor) combined with exacerbation of PM seizures in one and AA seizures two. AAs emerged as a new seizure type in one child. Two patients had non-convulsive status epilepticus. AAs were documented in three children with video-EEG during LTG treatment. One child developed continuous spike and wave discharge in sleep (CSWS). Mean LTG blood level was 41 umol/l (range 37-46 umol/l). After discontinuation of LTG, absence seizures disappeared in two and were reduced by 50-80 per cent in two patients. CSWS also disapppeared.
CONCLUSIONS: Also atypical absences, usually regarded as one of the most favourable target seizure types for LTG, may be provoked or exacerbated by LTG.
Disclosure: Consulting - UCB Pharma. Other - Invited to participate meetings on epilepsy by GlaxoSmithKline.