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Aim: The purpose of this study was to compare HMGB‐1, TLR4, IL‐1β, IL‐1R1, and TNF‐α levels in patients with mild and severe epilepsy with those in a healthy control group. Methods: Children aged 4–17 years, diagnosed with epilepsy for at least three years and with no progressive neurological disease, metabolic disease or infection, were selected for the study. The severe epilepsy group consisted of 28 children with at least one episode a week despite receiving three or more antiepileptic drugs. The mild epilepsy group consisted of 29 children with no seizures in the previous year, receiving only one antiepileptic drug, while 27 healthy children were selected as the control group. HMGB‐1, TLR4, IL‐1R1, TNF‐α and IL‐1β levels were investigated in these three groups. The MRI findings and clinical characteristics of the patients in the epilepsy group were also compared with these markers. Results: HMGB‐1, TLR4, TNF‐α, and IL‐1β levels in the severe epilepsy group were higher than in the control group and the mild epilepsy group (p<0.05), and were higher in the mild epilepsy group than in the control group (p<0.05). IL‐1R1 was also higher in the severe epilepsy group than in the control group (p<0.05). Conclusion: In this first report to identity a possible correlation between HMGB‐1, TLR4, IL‐1β, IL‐1R1, and TNF‐α levels and severity of epilepsy, our data demonstrates that the serum level of these cytokines is higher in cases of drug‐refractory epilepsy.

Anti-epileptic drugs may induce atherogenesis by affecting the thyroid hormones. According to the current data, the effects of thyroid hormones on vascular system may be independent of other biochemical markers. Epileptic patients using anti-epileptic drugs must be followed closely for arterial stiffness, and also for the development and progression of atherosclerosis.

Levetiracetam (LEV) efficacy in the treatment of chorea in Huntington disease, paroxysmal nonkinesigenic dyskinesia, paroxysmal kinesigenic choreoathetosis, and dyskinetic cerebral palsy was reported in some studies. We described a case of a child with Sydenham chorea treated with LEV. A 7.5-year-old male patient presented with chorea, orofacial dyskinesia, speech impairment, and irritability. Echocardiographic examination revealed mitral insufficiency. Sydenham chorea was diagnosed after excluding other diseases causing chorea. Although his choreiform movements were decreased substantially with haloperidol treatment, speech impairment, orofacial dyskinesia, and light chorea were continued. Therefore, on day 9, LEV was added, and his complaints resolved in a few days. The severity of the chorea according to the Universidade Federal de Minas Gerais Sydenham's Chorea Rating Scale decreased from 47 to 5 points after LEV treatment. Thus, on day 13, the dose of haloperidol was reduced and gradually discontinued within 4 days. Symptoms did not reoccur. The follow-up at 1.5 months revealed recurrence of complaints due to discontinuation of LEV by parents. Signs and symptoms were regressed completely within 1 week after LEV retreatment. We suggest that LEV with fewer adverse effects comparing to other drugs may be considered to be a good alternative in the treatment of Sydenham chorea.

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Our study supports the recent idea that IL-6 and IL-17A are cytokines involved in the pathogenesis of infantile spasm.

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