Lacosamide (LCM), a novel antiseizure medication (ASM), is believed to exert its anticonvulsant action through selective enhancement of slow inactivation of voltage-gated sodium channels. LCM is indicated for the treatment… Click to show full abstract
Lacosamide (LCM), a novel antiseizure medication (ASM), is believed to exert its anticonvulsant action through selective enhancement of slow inactivation of voltage-gated sodium channels. LCM is indicated for the treatment of focal seizures, and has recently been demonstrated to be efficacious as an adjunctive therapy for primary generalised tonic-clonic seizures (GTCS) [1]. Genetic generalised epilepsies (GGEs) comprise 15–20% of all epilepsies, and are usually easy to treat with broad‐spectrum ASM [2, 3]. Myoclonic and absence seizures in GGEs seem to be more vulnerable to aggravation by some ASMs. The older sodium channel blockers (SCBs) such as phenytoin (PHT), carbamazepine (CBZ), oxcarbazepine (OCBZ), and lamotrigine (LTG), may worsen myoclonic seizures [2]. Here we report a case series of patients who experienced an exacerbation of generalised myoclonic seizures following initiation of LCM in light of the existing literature.
               
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