J Neurol (2014) 261:2025–2027 DOI 10.1007/s00415-014-7487-4

LETTER TO THE EDITORS

Successful treatment of refractory absence status epilepticus with lacosamide Ulrik Sodemann • Harald Settergren Møller Morten Blaabjerg • Christoph Patrick Beier



Received: 30 April 2014 / Revised: 1 September 2014 / Accepted: 1 September 2014 / Published online: 9 September 2014 Ó Springer-Verlag Berlin Heidelberg 2014

Dear Sirs, Lacosamide is a novel anticonvulsant agent approved as add-on therapy in patients with partial and secondary generalized seizures [1]. It is occasionally used in patients with status epilepticus (SE) due to the availability of a formulation allowing intravenous application [2]. Lacosamide demonstrated broad anticonvulsant effects in murine seizure models of generalized seizures, complex partialonset seizures, and SE. The principal mode of action is the enhancement of sodium channel slow activation [3]. Whether lacosamide also modulates the collapsing response mediator protein 2 (CRMP-2) remains controversial [1, 3]. The effectiveness of lacosamide in patients with idiopathic generalized epilepsy has not yet been established. A few case reports, however, suggest that these patients may benefit from Lacosamide and a pilot study found this treatment to be safe [4, 5]. It remains unknown whether Lacosamide is effective in patients with juvenile absence epilepsy (JAE), or absence status epilepticus (ASE). We report the case of a 64-year-old male patient who was admitted to Department of Neurology at Odense University Hospital after increasing frequency of absences, U. Sodemann  H. S. Møller  M. Blaabjerg  C. P. Beier (&) Department of Neurology, Odense University Hospital and Clinical Institute, University of Southern Denmark, Sdr. Boulevard 19, 5000 Odense C, Denmark e-mail: [email protected] U. Sodemann e-mail: [email protected] H. S. Møller e-mail: [email protected] M. Blaabjerg e-mail: [email protected]

eventually resulting in confusion and inability to communicate. Apart from JAE with onset at childhood, and typical interictal EEG, he had no relevant previous medical record. His medication included lamotrigine (400 mg/day), topiramate (400 mg/day) and levetiracetam (2500 mg/day). According to his wife the patient had an excellent compliance. The latest seizure (absence) was 6 months prior to admission. On admission, he appeared confused, was neither able to speak nor corporate. ASE was suspected. Physical examination, emergency laboratory tests, and electrocardiography were normal. The patient was admitted to the observation ward and the ictal EEG revealed bilateral synchronous paroxysmal spike-polyspike-wave discharges at 3 Hz (Fig. 1a). Intravenous diazepam (10 mg) induced a rapid but short lasting effect. The patient additionally received 1 g levetiracetam intravenously. After 3 h, confusion reoccurred. Additional 5 mg intravenous diazepam induced sleep, but 20 min later, the patient had generalized tonic epileptic seizure for 30 s and remained somnolent and confuse thereafter. ASE was again suspected and we therefore administrated a loading dose of 400 mg intravenous lacosamide over a period of 30 min, followed by a maintenance therapy with lacosamide 200 mg b.i.d. No changes in blood pressure, heart rate, temperature, laboratory tests, or ECG were observed during or after the administration of lacosamide. Loading with lacosamide resulted in a rapid and complete recovery of the patient, who was alert and orientated less than 2 h later. A control EEG showed intermittent rhythmic slowing in the pre-mid-temporal area but no epileptic discharges (Fig. 1b). The patient was discharged with lamotrigine 400 mg/day, levetiracetam 2500 mg/day, topiramate 400 mg/day and lacosamide 400 mg/day. During the follow-up, no seizures occurred but the patient suffered from non-specific dizziness related to his antiepileptic treatment.

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J Neurol (2014) 261:2025–2027

Fig. 1 Representative parts of the patient’s EEG before (a) and after (b) lacosamide treatment

We here provide the first evidence that lacosamide may be effective in patients with JAE and ASE. In contrast to the only previous case report [6], lacosamide i.v. treatment resulted in a prompt clinical response in this heavily pretreated patient with ASE. Intravenous treatment with lacosamide was safe and without relevant acute systemic side effects. The good but only transient response of ASE to benzodiazepines is well established, while good control with adequate doses of drugs with established efficacy, mainly valproate, has been documented [7]. We did not use intravenous valproate because the patient previously experienced side effects. Loading with levetiracetam remained ineffective due to the high pretreatment. It remained essentially unknown, why the patient developed an ASE. Unfortunately, we did not investigate the plasma concentrations of topiramate, lamotrigine, and levetiracetam before treating the patient’s ASE. The patient was treated in our Epilepsy Clinic for many years. Inadherence to the treatment therefore appears unlikely. However, this would hardly affect the main message of our case report, i.e. that lacosamide was instantly effective in this patient with ASE. This case report complements data of a pilot study and case reports suggesting that intravenous

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lacosamide treatment of patients with idiopathic, generalized epilepsy is safe and do not increase the rate of absences or myoclonic jerks [4, 5]. In summary, we provide first evidence that lacosamide may be effective in patients with ASE, and lacosamide may therefore be a safe and possibly effective anticonvulsive agent for patients with ASE refractory to standard treatment. Conflicts of interest Christoph P. Beier is member of a scientific advisory board of UCB. The other authors do not have conflicts of interest. Ethical standards The author hereby declares that the research documented in the submitted manuscript has been carried out in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki.

References 1. Kellinghaus C, Berning S, Besselmann M (2009) Intravenous lacosamide as successful treatment for nonconvulsive status epilepticus after failure of first-line therapy. Epilepsy Behav 14:429–431 2. Hofler J, Trinka E (2013) Lacosamide as a new treatment option in status epilepticus. Epilepsia 54:393–404

J Neurol (2014) 261:2025–2027 3. Mantegazza M, Curia G, Biagini G, Ragsdale DS, Avoli M (2010) Voltage-gated sodium channels as therapeutic targets in epilepsy and other neurological disorders. Lancet Neurol 9:413–424 4. Wechsler R, Leroy R, Beller C, Doty P (2013) Open-label pilot study of adjunctive lacosamide for patients with uncontrolled primary generalized tonic-clonic seizures. Neurology 80(Meeting Abstracts 1):PD4.010

2027 5. Afra P, Adamolekun B (2012) Lacosamide treatment of juvenile myoclonic epilepsy. Seizure-Eur J Epilepsy 21:202–204 6. D’Orsi G, Pacillo F, Trivisano M, Pascarella MG, Ferrara MA, Specchio LM (2014) Lacosamide in absence status epilepticus. Seizure 23:397–398 7. Treiman DM, Meyers PD, Walton NY et al (1998) A comparison of four treatments for generalized convulsive status epilepticus. N Engl J Med 339:792–798

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Successful treatment of refractory absence status epilepticus with lacosamide.

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