Abstracts

Rationale: Lacosamide (LCM) is an antiepielptic drug (AED) which acts by enhancing slow inactivation of voltage-gated sodium channels resulting in stabilization of hyperexcitable neuronal membranes. The aim of this study was to report the first experiences of using LCM in patients with refractory partial seizures in Eskisehir, Turkey. Until now LCM was added to one to four concomitant AEDs in 15 patients with uncontrolled partial-onset seizures in our clinic. Methods: Eight of the patients were male and 7 were female. Fifteen epileptic patients with different etiologies (patients with Lenox-Gastaut Syndrome, Myoclonic Epilepsy with Ragged Red Fibers, Dandy -Walker Syndrome, sequelae of cerebral palsy, operated medullablastoma, encephalomalacic area in the left temporal region, cerebral infarction in the left occipital region, liver embryonal sarcoma operation, gliosis in the left temporal lobe, an autism spectrum disorder, frontal cortical-subcortical hyperintense lesions, frontal cortical dysplasia, a right frontal cortical-subcortical hyperintense lesion) were included in this report. All had partial-onset uncontrolled seizures. The seizure types of the patients were complex partial, secondary generalised partial seizures and complex partial seizures in accordance with myoclonias in one. All of the patients were taking three or more concomitant AEDs except one who received monotherapy. Four of the patients received 4 AEDs, 10 received 3 AEDs. Carbamazepine, clobazam, oxcarbazepine, lamotrigine, levetiracetam, phenobarbital, pregabalin, topiramate, valpropate and zonisamide were the drugs which were received as polytherapy in different combinations by each patient. The seizure frequency and severity were evaluated according to the diaries and the history of the patients. LCM was given twice 100-300 mg/day. Results: The mean age of the patients were 25.86 (19- 45). The mean duration time for taking LCM was 5.2 months. LCM therapy was started between January 2013- June 2014 in these patients. The seizure frequency and severity were reduced <50% in 4, >50% in 4 and 50% in 1 patient. No changes were reported in 2 of the patients yet. Only 1 of the patient reported some dizziness as an adverse reaction. Conclusions: In addition to its effects on slow sodium channels, LCM also binds to collapsing response mediator-2, a phosphoprotein which is primarily expressed in the nervous system and is involved in neuronal differentiation and control of axonal growth. As a result of its mechanism of action LCM could be added to different AED combinations. The results demonstrated the efficacy and tolerability of adjunctive LCM 200 and 300 mg/day and supported that LCM might be an advantageous option for the treatment of partial-onset seizures in patients with epilepsy. Because of its recent introduction, it is too early to ascertain the place of LCM in epilepsy treatment.