Abstracts

RATIONALE: The objective of this study is to examine the effect of lamotrigine (LMG) therapy on epileptiform EEG patterns in children with refractory epilepsies. By the end of this presentation, the participants should be able to discuss the relationship between lamotrigine therapy and EEG abnormalities.
METHODS: Charts of 860 patients with epilepsy seen in Division of Epilepsy and Clinical Neurophysiology at Boston Children[scquote]s Hospital between 1997-2000 were retrospectively reviewed. Only patients who had taken LMG during this time period and had at least two years of follow-up after the commencement of LMG were included. Charts were reviewed for age of onset, seizure type, frequency, underlying possible etiology, neuroimaging studies, clinical response, side effects after starting LMG, concomitant AEDs, and other modes of therapy (VNS, ketogenic diet, epilepsy surgery). EEGs were examined for background activity (i.e. frequency of the reactive posterior rhythm), interictal epileptiform discharges (i.e. frequency and localization of spikes, sharp waves, and spike-waves). All the relevant demographic and clinical data during the two-year follow-up period were entered into a database and subsequently analyzed
RESULTS: LMG was prescribed in 77 patients during the period studied; in 30 of these patients EEGs prior to and after LMG were available for review (mean age: 11.9 years with a range of 4 months-25 years; mean age at seizure onset: 3.4 years with a range of 1 month to 10 years). All patients had severe pharmacoresistant epilepsy. Mixed types of seizures were seen in 65%; generalized seizures in 23.8%; and complex partial seizures in 10.3% of the patients. Prior to LMG therapy, the baseline EEG was abnormal because of slow background activity in 17.2%; localized spikes or sharp waves in 27.5%; generalized spikes, sharp waves, or spike-waves in 24.1% or both generalized and local epileptiform activity in 48.2%. EEG analysis during the two years of follow-up after starting LMG demonstrated improvement in the background pattern in 18.8% and increased background slowing in 2.2% of the patient. There was improvement in the interictal epileptiform pattern in 30% of the patients with either elimination or reduction of spikes, sharp waves, or spike-waves; whereas, interictal EEG spikes or sharp waves were increased or became generalized in 6.8% of the patients. To better understand the acute effects of LMG on the EEG, we examined changes in the EEGs in a subset of patients who had repeat studies performed within three months of LMG initial therapy. In the first three months after LMG therapy none of the patients showed a worsening pattern in background or epileptiform activity whereas improvement was noted in 28.5%. During the two years follow-up period, 52% of the patients had a [gt]50% reduction in seizures; 24% had a [lt]50% reduction, and 24 % had no change in seizure frequency. Exacerbation of seizures did not occur in any patients.
CONCLUSIONS: In this group of highly refractory pediatric patients with epilepsy, LMG therapy resulted in parallel improvements in interictal EEG background patterns and epileptiform activity and seizure control. Furthermore, our findings suggest that LMG does not acutely exacerbate EEG abnormalities.
[Supported by: a grant from Glaxo-Smith-Kline Pharmaceutical and a grant to GLH from NINDS (NS27984)]