Electrical status epilepticus during slow-wave sleep (ESES) is an epilepsy syndrome with sleep-induced epileptic discharges and acquired impairment of cognition or behavior. Since the disease’s original description in 1971, no clear consensus has emerged on diagnostic criteria or optimal treatment. The treatment of ESES can be challenging, often including numerous antiepileptic drugs, immunomodulatory agents, and even surgical interventions. There is little evidence to guide treatment because only retrospective studies and case reports on the efficacy of treatment of ESES are present in literature. In this paper, we aim to analyze the etiopathogenesis of ESES in the new genetic era and to evaluate the treatment modalities in accordance with the genetic data and electroclinic spectrum of ESES.

Background: Vitamin B12 deficiency occurs primarily as a result of insufficient dietary intake in children in developing countries. Vitamin B12 deficiency produces a cluster of neurological symptoms in children. Aim: The aim of this study was to describe the vitamin B12 status of patients who were admitted with neurological symptoms and to evaluate the clinical response to vitamin B12 treatment. Materials and Methods: This study was conducted on children who had vitamin B12 deficiency presented with neurological findings from January 2014 to October 2016. Patients with serum vitamin B12 levels lower than 300 pg/mL received intramuscular or oral vitamin B12 treatment. Results: Three hundred and fifty-one patients presenting with neurologic symptoms and who had low serum vitamin B12 deficiency were analyzed. Our study population was composed mainly of adolescent age. The most common symptom with respect to age was headache. In infant patients, most common symptoms were seizure and developmental delay. Conclusion: Early diagnosis and vitamin B12 treatment are advocated to avoid long-term injury. Our study shows that patients with serum vitamin B12 levels lower than 300 pg/mL showed clinical improvement of neurological symptoms after receiving vitamin B12 treatment.

Congenital myasthenic syndromes (CMS) are neuromuscular transmission disorders caused by mutations in genes encoding neuromuscular junction proteins. CMS due to choline acetyltransferase (CHAT) gene is characterized by episodic apnea. We report a case of a 12-month-old female patient presented with recurrent episodic apnea carrying a mutation in CHAT gene, p.I336T. Furthermore, we describe the genetic and clinical findings in 44 CMS patients due to CHAT mutations in the literature up to date. Episodes of apnea and respiratory insufficiency are the hallmarks of CHAT mutations. Clinical manifestations usually provoked by infections and fever. CMS due to CHAT mutations are rare, but it is important to diagnosis. Early diagnosis and appropriate treatment can improve morbidity and mortality.

Bell’s palsy is the most common cause of acute peripheral facial nerve paralysis, but the optimal dose of corticosteroids in pediatric patients is still unclear. This retrospective study aimed to evaluate the efficacy of low-dose corticosteroid therapy compared with high-dose corticosteroid therapy in children with Bell’s palsy. Patients were divided into 2 groups based on the dose of oral prednisolone regimen initiated. The severity of idiopathic facial nerve paralysis was graded according to the House-Brackmann Grading Scale. The patients were re-assessed in terms of recovery rate at the first, third, and sixth months of treatment. There was no significant difference in complete recovery between the 2 groups after 1, 3, and 6 months of treatment. In our study, we concluded that even at a dose of 1 mg/kg/d, oral prednisolone was highly effective in the treatment of Bell’s palsy in children.