Lamotrigine therapy of epilepsy in tuberous sclerosis

Citation
Dn. Franz et al., Lamotrigine therapy of epilepsy in tuberous sclerosis, EPILEPSIA, 42(7), 2001, pp. 935-940
Citations number
24
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EPILEPSIA
ISSN journal
00139580 → ACNP
Volume
42
Issue
7
Year of publication
2001
Pages
935 - 940
Database
ISI
SICI code
0013-9580(200107)42:7<935:LTOEIT>2.0.ZU;2-K
Abstract
Purpose: Lamotrigine (LTG), a newer antiepileptic drug (AED), has activity against both partial-onset and generalized seizures. Its reported benefits for behavior, and its effectiveness in Lennox-Gastaut syndrome and other fo rms of refractory epilepsy, make it a logical choice for treatment of epile psy in tuberous sclerosis complex (TSC). We present our experience with LTG therapy of epilepsy in 57 patients with TSC. Methods: Patients fulfilled the diagnostic criteria for clinically definite TSC. LTG was initiated and increased until improvement in seizure frequenc y was noted, intolerable side effects occurred, or maximal doses were reach ed. Seizure frequency and behavioral changes were recorded during LTG thera py and compared with those prior to the introduction of LTG. Results: Twenty-four (42%) were seizure free, and 21 (37%) had a > 50% redu ction in seizure frequency. Eighteen (32%) had subjectively improved behavi or and/or alertness with daily activities. Thirty-eight (67%) had no change in this regard, whereas one (2%) became worse. Responders were more likely to not have a history of infantile spasms, and to have experienced only pa rtial seizures (p < 0.05). Otherwise no phenotypic correlations with respon se were apparent. Conclusions: Among patients with TSC and epilepsy, LTG was effective and we ll tolerated, including as initial monotherapy. Improved alertness and beha vior were apparent in many patients. The incidence of side effects is simil ar to that reported for other pediatric populations with symptomatic partia l epilepsy. The usefulness of LTG in TSC may relate to an underlying defect of glutamatergic neurotransmission in partial epilepsy.