The authors evaluated basic sleep architecture and non-rapid eye movement (NREM) sleep alterations in drug-naïve attention-deficit/hyperactivity disorder (ADHD) children without psychiatric or other comorbidities. This cross-sectional case-control study included 28 drug-naïve children with ADHD and 15 healthy controls. This subjective studies revealed that children with ADHD had a worse sleep quality and increased daytime sleepiness. Polysomnography data showed that the sleep macrostructure was not significantly different in children with ADHD. Sleep microstructure was altered in ADHD children by means of reduced total cyclic alternating pattern rate and duration of cyclic alternating pattern sequences. This reduction was associated with a selective decrease of A1 index during stage 2 NREM. SpO2 in total sleep was slightly decreased; however, the incidence of sleep disordered breathing showed no significant difference. The authors suggest that cyclic alternating pattern scoring would provide a further insight to obtain a better understanding of the sleep structure in children with ADHD.

Background/Aims: Monocarboxylate transporter 8 (MCT8) is essential for thyroid hormone (TH) transport in the brain. Mutations in MCT8 are associated with the Allan-Herndon-Dudley syndrome (AHDS), characterized by severe psychomotor retardation and altered serum thyroid parameters. Here we report two novel mutations in MCT8 and discuss the clinical findings. Case Report and Results: We describe 4 males with AHDS from two unrelated families varying in age from 1.5 to 11 years. All 4 patients presented with typical clinical signs of AHDS, including severe psychomotor retardation, axial hypotonia, lack of speech, diminished muscle mass, increased muscle tone, hyperreflexia, myopathic facies, high T3, low T4 and rT3, and normal/mildly elevated TSH levels. Comparison of patients at different ages suggests the progressive nature of AHDS. Genetic analyses identified a novel missense MCT8 mutation (p.G495A) in family 1 and a 2.8-kb deletion comprising exons 3 and 4 in family 2. Functional analysis of p.G495A revealed impaired TH transport varying from 20 to 85% depending on the cell context. Conclusion: Herewe report 4 AHDS patients in unrelated Turkish families harboring novel MCT8 mutations. Despite the widely different mutations, the clinical phenotypes are very similar and findings support the progressive nature of AHDS.

Lactococcus lactis cremoris infections are very rare in humans. It is recognized as a commensal organism of mucocutaneous surfaces of cattle, and is occasionally isolated from human mucocutaneous surfaces. We report a brain abscess caused by L. lactis cremoris in an immunocompetent child. A 19-month-old female patient was admitted with fever and vomiting. Brain computed tomography (CT) revealed brain abscess. L. lactis cremoris was isolated from culture of the abscess material. The patient was treated with pus drainage from brain abscess and antibiotics including vancomycin and meropenem. The patient recovered completely. To our knowledge, this is the first report of a L. lactis cremoris infection in children.

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A 14-year-old male presented with paresthesias on the right upper and lower extremities, headache, and vomiting. In addition to worsening paresthesia and weakness on the right side of his body, blurred vision, fever, and skin lesions developed. He also had skin lesions characterized with 3-10 mm papules with a white atrophic center surrounded by pink rim mostly on the trunk and lower extremities. Brain magnetic resonance imaging showed chronic subdural effusion and encephalomalacia of the left cerebral hemisphere. Cerebrospinal fluid (CSF) examination revealed increased protein levels. Electromyography was consistent with diffuse polyradiculoneuropathy. Skin biopsy confirmed the diagnosis of a rare vasculopathy: Degos disease. A case presenting with chronic subdural effusion, encephalomalacia, elevated CSF protein, and polyradiculopathy should be carefully examined for skin lesions, which may suggest the diagnosis of Degos disease.