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The aim of this study was to investigate the relationship between autism spectrum disorders development and exposure to mono-(2-ethylhexyl)-phthalate (MEHP), di-(2-ethylhexyl)-phthalate (DEHP), and bisphenol A (BPA), 1 of the endocrine disruptors, among phthalates. The study included 48 children with autism spectrum disorder (27 boys, 21 girls) and 41 healthy subjects (24 boys, 17 girls) as controls. Serum MEHP, DEHP, and BPA levels were measured by using high-performance liquid chromatography. Children with autism spectrum disorder had significantly increased serum MEHP, DEHP, and BPA concentrations (0.47 +/- 0.14 mu g/ml, 2.70 +/- 0.90 mu g/ml, 1.25 +/- 0.30 ng/ml) compared to healthy control subjects (0.29 +/- 0.05 mu g/ml, 1.62 +/- 0.56 mu g/ml, 0.88 +/- 0.18 ng/ml) respectively (P = .000). The fact that higher serum MEHP, DEHP, and BPA were found levels in the autism spectrum disorder group compared to healthy controls suggests that endocrine disruptors may have a role in the pathogenesis of autism spectrum disorders.

The aim of this study was to compare the efficacy and safety of different oral chloral hydrate and dexmedetomidine doses used for sedation during electroencephalography (EEG) in children. One hundred sixty children aged 1 to 9 years with American Society of Anesthesiologists physical status I-II who were uncooperative during EEG recording or who were referred to our electrodiagnostic unit for sleep EEG were included to the study. The patients were randomly assigned into 4 groups. In groups D1 and D2, patients received oral dexmedetomidine doses of 2 and 3 µg/kg, respectively. In group C1 and C2, patients received oral chloral hydrate doses of 50 and 100 mg/kg, respectively. The induction time was significantly shorter in group C2 compared with other groups ( P = .000). The rate of adverse effects was significantly higher in group C2 compared with the dexmedetomidine groups (D1 and D2; P = .004). In conclusion, dexmedetomidine can be used safely for sedation during EEG in children.

Sjögren-Larsson syndrome is an autosomal-recessive hereditary disorder involving congenital ichthyosis, mental retardation, and spastic diplegia or tetraplegia. It is caused by the deficient activity of fatty aldehyde dehydrogenase. In this report, the authors describe 2 siblings with Sjögren-Larsson syndrome. Both the patients had generalized ichthyosis, and the older one had spastic paraplegia and mental retardation, and the fundus examination revealed foveal and parafoveal glistening dots. The authors report the large kinship with Sjögren-Larsson syndrome, which is a rare and most probably underdiagnosed syndrome.

Contrary to belief, neonatal hypoglycemia is relatively common and can cause more severe neurological sequelae than is currently believed. Prevention of hypoglycemic brain damage by hindering prolonged and profound neonatal hypoglycemia might contribute to psychomotor development. At Erciyes University, between December 1996 and 2005, of the patients who applied to Paediatric Neurology Department, 60 cases with a history of neonatal hypoglycemia were included in the study. The magnetic resonance imaging (MRI) scans and clinical records of all patients were reviewed retrospectively. It was noted that the sequelae with glucose levels of 0 0 to 40 were more serious and intense. The same results were also observed in cranial MRI evaluation. In conclusion, intractable epilepsy, mental motor retardation, cerebral palsy, and visual disturbance were found to be the most common and severe conditions affecting sufferers of neonatal hypoglycemia. In the first 3 days of life, the close monitoring of patients at risk is critical, and hospitalization of severe cases should be considered.