ابعاد کنترل روانشناختی والدین: ارتباطات با پرخاشگری فیزیکی و رابطه پیش دبستانی در روسیه

In this study, short echo time 1H-magnetic resonance spectroscopy (MRS) was applied for quantification of neurometabolites using the LC Model algorithm in Taiwanese adolescents with attention-deficit hyperactivity disorder (ADHD). Proton magnetic resonance spectra were acquired bilaterally on the prefrontal area (part of the anterior cingulate gyrus and part of the medial frontal gyrus) in 15 adolescents with ADHD (average age of 13.88 years) and 22 controls (average age of 14.85 years). Absolute metabolite levels and ratios relative to creatine plus phosphocreatine (Cr + PCr) were obtained to be compared between groups. Results showed that adolescents with ADHD had significantly lower mean right prefrontal levels of Cr + PCr as compared with the controls. No significant differences between groups were noted in the remainder of the prefrontal metabolites. As for the group comparison of relative ratios, the N-acetylaspartate/Cr + PCr ratio was significantly higher in the right prefrontal regions of ADHD adolescents. This finding provides evidence of a right prefrontal neurochemical alteration in ADHD adolescents, which is consistent with current ADHD theory of prefrontal neuropathology with developmental mechanism. In addition, it highlights the importance of the method in interpretation of MRS findings in the context of ADHD.

Attention-deficit hyperactivity disorder (ADHD) is the most common neuropsychiatric disorder in children with a worldwide prevalence reported to be 5.2% (Polanczyk et al., 2007). It is defined by persistent, developmentally inappropriate, cross-situational, impaired levels of inattention, impulsiveness and hyperactivity (American Psychiatric Association, 2000). Deficits in ADHD are hypothesized to be due to the impairment of fronto-striatal–cerebellar networks, which are found to be abnormal in children with ADHD in neuroimaging studies (Durston, 2003, Seidman et al., 2005 and Konrad et al., 2006). Meta-analysis of structural imaging studies of ADHD reported the most frequently replicated findings as smaller volumes of the total brain, the right frontal cortex and white matter, the cerebellum and striatal subcortical structures (Durston, 2003, Konrad et al., 2006, Seidman et al., 2005 and Valera et al., 2007). Neurochemically, dysregulation of dopamine and norepinephrine systems plays the central role in the pathophysiology model of ADHD. This is initially suggested by the action of drugs for the disorder, which increase the synaptic availability of these neurotransmitters, and by animals showing that lesions in dopamine pathways create animal models of ADHD (Biederman and Faraone, 2005). In this regard, proton magnetic resonance spectroscopy (1H-MRS) has been considered to be a suitable tool in investigating the neuropathology of ADHD because it allows the reliable and noninvasive in vivo measurement of neurometabolites, such as N-acetylaspartate (NAA), the glutamatergic resonance (glutamate and glutamine or GLu + GLn), creatine plus phosphocreatine (Cr + PCr), choline compounds (glycerophosphorylcholine and phosphorylcholine, GPC + PC) and myo-inositol (Ins). A recent meta-analysis reviewed 16 MRS studies of ADHD ( Perlov et al., 2008) and revealed significant changes of choline compounds in left striatum (effect size: 0.66) and right frontal lobes (effect size: 0.52) of ADHD children as compared with normal children. ADHD begins in childhood and may persist into adult life in a substantial subgroup. However, most of the available MRS studies of ADHD were focused on childhood, and only two studies reporting neurometabolites ratios addressed subjects with average age in the adolescent range (Jin et al., 2001 and Sun et al., 2005) . In these two studies, single-voxel 1H-MRS was applied to investigate the basal ganglia of adolescents with ADHD, yielding a decreased NAA/Cr ratio in bilateral striatum (Jin et al., 2001) and right lenticular nucleus (Sun et al., 2005). Given that not all the children with ADHD will be clinically affected as adolescents, one could speculate that adolescents/adult patients with ADHD represent a distinct subpopulation, possibly with a different neurobiological or environmental underpinning. Hence, scientific investigations of neurochemical substrates for ADHD beyond childhood are needed to determine the nature of neurobiological alterations. In a recent study of 31 psychostimulant-naïve children (age range 6.1–10 years) using in vivo 31P spectroscopy methods, Stanley et al. reported a group × age interaction in the prefrontal cortex (PFC) and inferior parietal region, with relatively older psychostimulant-naive ADHD children showing significantly lower PFC and higher inferior parietal membrane phospholipids precursor levels (Stanley et al., 2008). This finding would provide support for a developmental mechanism targeting a bottom-up dysfunction of the basal ganglia impairing the fine-tuning of prefrontal function so that PFC alterations were not apparent until the onset of fine-tuning processes in the PFC of children with ADHD. In this study, we applied short echo time 1H-MRS for quantification of neurometabolites of the prefrontal area in ADHD adolescents and compared their spectra with healthy adolescents. The method of single-voxel spectroscopy allowed us to obtain both ratios and absolute levels of neurometabolites in a defined region of interest. Based on previous studies, we hypothesized that in ADHD adolescents, alterations in neurometabolites would be observed in the prefrontal areas as these subjects have already reached adolescence.