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In this cross-sectional study, we investigated screen use habits, problematic internet use (PIU), and screen-psychopathology relationship in a clinical sample of children and adolescents. The study included 277 children and adolescents (129 [46.4%] girls) aged between 6-17 years referred to a psychiatry outpatient setting for various reasons. All parents completed the Strengths and Difficulties Questionnaire (SDQ), while adolescents also completed the Internet Addiction Test (IAT). The mean screen time was 3.85 (SD = 2.72) hours per day. Longer screen times were found among children and adolescents with specific psychiatric disorders compared to those with no psychiatric symptoms; especially among those with internalizing disorders (i.e., an anxiety disorder and/or depression), but also with attention deficit/hyperactivity disorder and/or conduct disorder. Longer screen time may be related with more functioning impairments. Based on the IAT, 2.1% of adolescents may have PIU. The findings from this study suggest that children and adolescents with psychiatric symptoms may have prolonged screen times. This needs to be taken into account during diagnostic and therapeutic procedures. C1 [Basay, Burge Kabukcu; Basay, Omer; Akdogan, Cemre; Karaisli, Seyma; Satilmis, Merve; Gozen, Burcu; Sekerci, Naci Bahadir; Co, Omerbasaygmail] Pamukkale Univ, Med Fac, Child & Adolescent Psychiat Dept, Denizli, Turkey.

Attention-deficit/hyperactivity disorder (ADHD) is a prevalent neurodevelopmental disorder. Its etiology is not clearly understood yet, but neurobiological, genetic and environmental factors are shown to play a role. The relationship between ADHD and miRNAs has been studied quite recently, and few studies have been conducted up to now. In this study, peripheral blood expression levels of miR-5692b, miR-let-7d, miR-124-3p, miR-4447 and miR-107 of 30 children and adolescents with combined type ADHD were compared to 30 healthy controls to understand the roles of these miRNAs in the ADHD etiopathogenesis. Compared to controls, levels of miR-5692b (p = 0.006) were found higher and levels of miR-let-7d (p = 0.017) were found lower in the ADHD group. There was no significant difference in terms of miR-124-3p, miR-4447, and miR-107 levels between the groups. In conclusion, our findings support other studies suggesting the importance of miRNAs in the pathogenesis of ADHD. Regarding the regulatory role of miRNAs in gene regulation, their contribution to etiopathogenesis and heterogeneity of ADHD should be investigated further. C1 [Aydin, Sezai Ustun] Denizli State Hosp, Child & Adolescent Psychiat Clin, Denizli, Turkey. [Basay, Burge Kabukcu] Pamukkale Univ, Sch Med, Dept Child & Adolescent Psychiat, Denizli, Turkey. [Cetin, Gokhan Ozan] Pamukkale Univ, Sch Med, Dept Med Genet, Denizli, Turkey. [Aydin, Aysegul Gungor] Pamukkale Univ, Sch Med, Dept Anat, Denizli, Turkey. [Tepeli, Emre] Next Genet Ctr, Istanbul, Turkey.

Objective Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder that negatively affects different areas of life. We aimed to evaluate the associations between the Va166Met polymorphism of brain-derived neurotrophic factor (BDNF) and ADHD and to assess the effect of the BDNF polymorphism on the neurocognitive profile and clinical symptomatology in ADHD. Methods Two hundred one ADHD cases and 99 typically developing subjects (TD) between the ages of 8 and 15 years were involved in the study. All subjects were evaluated using a complete neuropsychological battery, Child Behavior Checklist, the Teacher's Report Form (TRF) and the DSM-IV Disruptive Behavior Disorders Rating Scale-teacher and parent forms. Results The GG genotype was significantly more frequent in the patients with ADHD than in the TD controls, and the GG genotype was also significantly more frequent in the ADHD-combined (ADHD-C) subtype patients than in the TDs. However, there were no significant associations of the BDNF polymorphism with the ADHD subtypes or neurocognitive profiles of the patients. The teacher-assessed hyperactivity and inattention symptom count and the total score were higher, and the appropriately behaving subtest score of the TRF was lower in the GG genotypes than in the GA and AA (i.e., the A-containing) genotypes. Conclusion We found a positive association between the BDNF gene Va166Met polymorphism and ADHD, and this association was observed specifically in the ADHD-C subtype and not the ADHD-predominantly inattentive subtype. Our findings support that the Va166Met polymorphism of BDNF gene might be involved in the pathogenesis of ADHD. Furthermore Va166Met polymorphism of BDNF gene may be more closely associated with hyperactivity rather than inattention.

The present report describes the cases of a 17-year-old male patient and a 13-year-old female patient who developed acute dystonia following the administration of low-dose aripiprazole (5 mg/day) after the cessation of atomoxetine treatment. Although aripiprazole-induced dystonia has been previously reported in the literature, it is rare, and most of these cases were associated with doses higher than 5 mg/day. Furthermore, both of the patients in the present study discontinued atomoxetine prior to the initiation of aripiprazole treatment; thus, this report also discussed the possible mechanisms underlying the manifestation of dystonia from the perspective of neurotransmitter activity.

Objective: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social interactions and behavioral problems. Various genetic and environmental factors, including oxidative stress, are claimed to play a role in the etiopathogenesis of ASD. In this study, we aimed to examine the status of oxidative metabolism in ASD and the association between oxidative parameters and ASD symptom severity and subtype of ASD. Method: Thirty-three children and adolescents diagnosed with ASD (16 children diagnosed with autistic disorder, 13 children with pervasive developmental disorder not otherwise specified, and 4 children with Asperger syndrome) according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) and 28 healthy controls, aged 2-17 years, were recruited in this study. Total oxidant status (TOS) and total antioxidant status (TAS) were evaluated using Rel Assay Kit in children and adolescents. The oxidative stress index (OSI) was calculated by dividing the TOS values by the TAS values. Autistic symptoms for these patients were scored on the Childhood Autism Rating Scale (CARS). Results: In patients with ASD, TAS was statistically significantly lower and OSI statistically significantly higher than in healthy controls. There were no statistically significant differences in TOS between the ASD and control groups. There were no statistically significant differences between the subtypes of ASD in terms of oxidative stress parameters. In addition, TAS, TOS, and OSI values did not differ statistically significantly between the patients' CARS groups, and were not associated with the CARS scores of the patients. Conclusion: Our findings suggest that oxidative imbalance is present in ASD and that oxidative stress may play a role in the etiopathogenesis of ASD. Therefore, it is suggested that antioxidants may have beneficial effects on ASD and may be a new therapeutic target in treating ASD.

Objective: Attention deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder. Thus, the present study aimed to determine the effects of a single dose of methylphenidate (Mph) on neurometabolite levels according to polymorphisms of the catechol-O-methyltransferase (COMT) gene. Methods: This study evaluated the neurometabolite levels including N-acetylaspartate (NAA), creative (Cr), and choline (Cho) of ADHD patients, before and after treatment with Mph (10 mg) according to the presence of COMT polymorphisms. The spectra were obtained from the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), cerebellum, and striatum. Results: The NAA levels of the val/val and val genotype carriers (val/val and val/met genotypes) increased in the DLPFC and ACC, respectively, following Mph treatment. The NAA/Cr ratio was lower in the DLPFC of val carriers than in the met/met genotype carriers prior to Mph administration. The Cho levels of the val/met genotype and val carriers increased in the striatum following Mph treatment. Following Mph treatment, the Cr levels of the met/met genotype carriers were higher than those of the val/met genotype and val carriers, Additionally, after Mph treatment, there was a significant increase in Cr levels in the DLPFC of the met/met genotype carriers but a significant decrease in such levels in the striatum of val/val genotype carriers. Conclusion: These findings suggest that polymorphisms of the COMT gene can account for individual differences in neurochemical responses to Mph among ADHD patients. Therefore, further studies are needed to fully characterize the effects of the Val158met polymorphism of the COMT gene on treatment outcomes in patients with ADHD.

Objective: To investigate the neurometabolite level changes according to synapsin III gene rs133945G>A and rs133946C>G polymorphisms by using magnetic resonance spectroscopy (MRS) in patients with attention-deficit hyperactivity disorder (ADHD). Methods: Fifty-seven adults diagnosed with ADHD were recruited for the study. The participants were examined by single-voxel H-1 MRS when medication naive and 30 minutes after oral administration of 10 mg methylphenidate (Mph). Those who had been on a stimulant discontinued the medication 48 hours before MRS imaging. Spectra were taken from the anterior cingulate cortex, dorsolateral prefrontal cortex, striatum, and cerebellum, and N-acetylaspartate (NAA), choline, and creatine levels were examined. For genotyping of the synapsin III gene polymorphisms, DNA was isolated from peripheral blood leukocytes. The effects of age, sex, and ADHD subtypes were controlled in the analyses. Results: After a single dose of Mph, choline levels increased significantly in the striatum of rs133945G>A polymorphism-GG genotypes (P=0.020) and NAA levels rose in the anterior cingulate cortex of rs133946C>G polymorphism-CG genotypes (P=0.014). Both rs133945G>A and rs133946C>G polymorphisms were found to statistically significantly affect the alteration of NAA levels in response to Mph in dorsolateral prefrontal cortex with two-way repeated measure of analysis of variance. Post hoc comparisons revealed a significant difference between CG and GG genotypes of rs133946C>G polymorphisms after Bonferroni adjustment (P=0.016). Conclusion: Synapsin III gene polymorphisms may be affecting the changes in neurometabolite levels in response to Mph in adult ADHD patients. Future studies are needed to confirm our findings.

The present report describes the cases of a 17 year old male patient and a 13 year old female patient who developed acute dystonia following the administration of low dose aripiprazole (5 mg/day) after the cessation of atomoxetine treatment. Although aripiprazole induced dystonia has been previously reported in the literature, it is rare, and most of these cases were associated with doses higher than 5 mg/day. Furthermore, both of the patients in the present study discontinued atomoxetine prior to the initiation of aripiprazole treatment; thus, this report also discussed the possible mechanisms underlying the manifestation of dystonia from the perspective of neurotransmitter activity.

OBJECTIVE: Attention deficit/hyperactivity disorder (ADHD) is a common neurodevelopmental disorder. Thus, the present study aimed to determine the effects of a single dose of methylphenidate (Mph) on neurometabolite levels according to polymorphisms of the catechol-O-methyltransferase (COMT) gene. METHODS: This study evaluated the neurometabolite levels including N-acetylaspartate (NAA), creatine (Cr), and choline (Cho) of ADHD patients, before and after treatment with Mph (10 mg) according to the presence of COMT polymorphisms. The spectra were obtained from the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), cerebellum, and striatum. RESULTS: The NAA levels of the val/val and val genotype carriers (val/val and val/met genotypes) increased in the DLPFC and ACC, respectively, following Mph treatment. The NAA/Cr ratio was lower in the DLPFC of val carriers than in the met/met genotype carriers prior to Mph administration. The Cho levels of the val/met genotype and val carriers increased in the striatum following Mph treatment. Following Mph treatment, the Cr levels of the met/met genotype carriers were higher than those of the val/met genotype and val carriers. Additionally, after Mph treatment, there was a significant increase in Cr levels in the DLPFC of the met/met genotype carriers but a significant decrease in such levels in the striatum of val/val genotype carriers. CONCLUSION: These findings suggest that polymorphisms of the COMT gene can account for individual differences in neurochemical responses to Mph among ADHD patients. Therefore, further studies are needed to fully characterize the effects of the Val158met polymorphism of the COMT gene on treatment outcomes in patients with ADHD.

Introduction: In this article, the COMT gene val(158)met polymorphism and attention-deficit hyperactivity disorder (ADHD)-related differences in diffusion-tensor-imaging-measured white matter (WM) structure in children with ADHD and controls were investigated. Patients and methods: A total of 71 children diagnosed with ADHD and 24 controls aged 8-15 years were recruited. Using diffusion tensor imaging, COMT polymorphism and ADHD-related WM alterations were investigated, and any interaction effect between the COMT polymorphism and ADHD was also examined. The effects of age, sex, and estimated total IQ were controlled by multivariate analysis of covariance (MANCOVA). Results: First, an interaction between the COMT val(158)met polymorphism and ADHD in the right (R) cingulum (cingulate gyrus) (CGC) was found. According to this, valine (val) homozygote ADHD-diagnosed children had significantly lower fractional anisotropy (FA) and higher radial diffusivity (RD) in the R-CGC than ADHD-diagnosed methionine (met) carriers, and val homozygote controls had higher FA and lower RD in the R-CGC than val homozygote ADHD patients. Second, met carriers had higher FA and axial diffusivity in the left (L)-uncinate fasciculus and lower RD in the L-posterior corona radiata and L-posterior thalamic radiation (include optic radiation) than the val homozygotes, independent of ADHD diagnosis. Third, children with ADHD had lower FA in the L-CGC and R-retrolenticular part of the internal capsule than the controls, independent of the COMT polymorphism. Conclusion: Significant differences reported here may be evidence that the COMT gene val(158)met polymorphism variants, as well as ADHD, could affect brain development. ADHD and the COMT polymorphism might be interactively affecting WM development in the R-CGC to alter the WM connectivity in children with val homozygote ADHD.