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Aims: Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder with an etiopathogeny not fully understood. According to the prevailing view, the main factors contributing to the disorder are prefrontal dopamine deficiency and central dopaminergic dysfunction, but the factors/ mechanisms involved in the brain dysfunction and its consequences are not well known. We suggest that changes in oxidative metabolism and cellular immunity may be involved. In this study, we aimed to investigate whether there are associations between ADHD and changes in serum levels of nitric oxide synthase (NOS), xanthine oxidase (XO), glutathione S-transferase (GST) and paraoxonase-1 (PON-1) activities, which are important markers of oxidative stress, and adenosine deaminase (ADA) activity, marker of cellular immunity. Methods:The study sample consisted of 35 child or adolescent patients diagnosed with ADHD according to DSM-IV-TR criteria. Thirty-five healthy subjects were also included in the study as controls. Venous blood samples were collected, and NOS, XO, GST, PON-1 and ADA activities were measured.Results: NOS, XO and ADA activities of the patients were significantly higher than those of the controls. GST and PON-1 activities of the patients were significantly lower than those of the controls.Conclusions: Changes in oxidative metabolism and cellular immunity may have a role in the etiopathogenesis of ADHD.Key words: attention-deficit/hyperactivity disorder, cellular immunity, oxidative stress. A TTENTION-DEFICIT/HYPERACTIVITY DISOR-DER (ADHD) consists of a persistent pattern of inattention, hyperactivity and impulsivity.1 ADHD is relatively common, affecting an estimated 5-10% of school-aged children, depending on the definition and study.2 ADHD is usually identified in childhood and persists into adulthood in about 60% of individuals with childhood onset. 3The cause and pathophysiology of ADHD is incompletely understood. Research into the neurobiology and genetics of ADHD is robust and continues to break new ground regarding both methodological approaches and substantive findings. 4 A number of reviews that have addressed the neurobiology of ADHD have focused on imaging and genetics. Relatively little attention has been given to factors/ mechanisms involved in the brain dysfunction and its consequences, 5 such as the oxidative metabolism and the immune system response, very important in cellular pathology. Free radicals, such as the superoxide anion and hydroxyl radicals, are reactive chemical species generated during the normal metabolic processes and, in excess, can damage lipids, proteins and DNA of neuronal and non-neuronal cells.6 Cellular immunity may contribute to the occurrence of the disorder by injuring neuronal cells, similar to oxidative metabolism.Associations between brain cells and behavior may be direct; for example, brain cells may play a role in the cause of psychiatric disorder as serving in

These results suggest that the prevalence of parasomnias was high in the 9- and 10-year-old age groups. Parasomnias are associated with a history of physical illness and neurobehavioral abnormalities.

The purpose of this study was to estimate striatal dopamine (D2) receptor availability in non-drug treated children with attention-deficit-hyperactivity disorder (ADHD) before and after methylphenidate therapy, and to examine correlations between severity of symptoms and response rates to stimulant medication with levels of striatal D2 receptor binding. Nine children (six males, three females; mean age 9.8 years, SD 2.3 years) with ADHD participated. All underwent iodobenzamide (123I IBZM) brain SPECT within 2 hours following intravenous injection of 123I IBZM before and 3 months after methylphenidate therapy. A semiquantitative approach was used to generate indices of specific D2 receptor binding in the basal ganglia. Specific binding ratios at baseline were higher than the previously reported specific binding values obtained in studies using young healthy adults. D2 availability reduced significantly (paired t-test,p<0.05) as a function of methylphenidate therapy in patients with ADHD in all four regions of the striatum. When the relation between therapy response and D2 availability was investigated, we observed that the higher the baseline D2 levels were, the higher the response rate was (detected as the percentage reduction of hyperactivity scores and Conners Teacher Rating Scale scores), while no such trend was observed between the initial D2 binding levels and the response in attention-deficit scores. Results indicate that in non-drug treated children with ADHD, higher D2 receptor availability is observed at baseline which is down-regulated back to reported near-normal values after methylphenidate therapy. The effect of methylphenidate on D2 receptor levels in patients with ADHD is similar to that observed in healthy adults; a down-regulation phenomenon within 0 to 30%. In addition, initially higher values of D2 availability seem to indicate better response to methylphenidate therapy in ADHD.

The etiology of autism is unclear, however autism is considered as a multifactorial disorder that is influenced by neurological, environmental, immunological and genetic factors. Growth factors, including epidermal growth factor (EGF), play an important role in the cellular proliferation and the differentiation of the central and peripheral nervous system. In this study we hypothesized that EGF may play a role in the pathophysiology of autism and examined serum EGF levels in children with autism. We measured serum levels of EGF in the 27 autistic children and 28 age- matched normal controls. The serum levels of EGF in the subjects with autism were significantly higher than those of normal control subjects. However, there were no correlations between serum EGF levels and clinical variables in the subjects with autism. This is the first report demonstrating the increased serum levels of EGF in children with autism. This study suggests that increased levels of EGF might have an importance in the pathophysiology of autism.