Lacosamide-induced myoclonus in patients with acute symptomatic metabolic seizures: A case series

Fluid and electrolyte imbalances are common causes of seizures and admissions to intensive care units. This case series describes three female patients who experienced their first seizures. Case 1 was a 64-year-old woman with status epilepticus and severe hypocalcemia (6.8 mg/dL), who presented with generalized tonic–clonic (GTC), focal motor, and myoclonic seizures. Case 2 was a 70-year-old woman with cluster seizures, diagnosed with hypocalcemia (7 mg/dL) and hypomagnesemia (1.2 mg/dL), who also experienced GTC seizures. Case 3 was a 77-year-old woman with status epilepticus, diagnosed with dehydration, hyponatremia (120 mEq/dL), hypocalcemia (8 mg/dL), and hypokalemia (2 mEq/dL), who experienced complex partial seizures. Hospital management included intravenous fluids, electrolyte replacement, and antiseizure medications (ASMs) such as midazolam, levetiracetam, and phenytoin. Lacosamide, administered either to manage focal seizures or as an adjuvant ASM, induced myoclonic jerks, which resolved upon its discontinuation. After discharge, the patients received oral mineral and vitamin supplements and continued ASMs (levetiracetam, oxcarbazepine, and carbamazepine) for more than 3 months without seizure recurrence. In conclusion, this series emphasizes the potential for lacosamide to induce myoclonus in patients with electrolyte imbalances, potentially due to its specific action on sodium channels in the motor cortex.