Suspected induction of epileptic negative myoclonus after lacosamide initiation

Older voltage-gated sodium channel (VGSC) blockers, such as carbamazepine and phenytoin, can increase interictal epileptiform abnormalities and induce new seizure types. However, we could find no reports for lacosamide (LCM), a newer VGSC blocker, behaving similarly in pediatric patients. We describe three pediatric patients who experienced epileptic negative myoclonus (ENM) following LCM administration. One patient had self-limited epilepsy with centrotemporal spikes; the others had focal epilepsy. In all cases, interictal electroencephalography (EEG) showed unilateral or bilateral independent spike-and-wave discharges in the central region before LCM initiation. Concomitant medications at the time of LCM initiation included levetiracetam (Case 1), levetiracetam and valproate (Case 2), and valproate (Case 3). After LCM initiation, all patients experienced brief unilateral upper extremity muscle tone loss during wakefulness. Electromyography confirmed momentary interruption of muscle activity, time-locked to the spike-and-wave discharges in the bilateral centrotemporal region. Hence, we determined that the movement was ENM. In addition, the interictal EEG worsened and showed bilateral synchronous spike-and-waves in all cases. ENM disappeared after the discontinuation of LCM. LCM can induce ENM, and the exacerbation seen in EEG due to LCM may have induced ENM. Patients should be monitored carefully for worsening of EEG findings or inducing other types of seizures.