Search

Exercise interventions in mental disorders have evidenced a mood-enhancing effect. However, the association between physical activity and affect in everyday life has not been investigated in adult individuals with ADHD, despite being important features of this disorder. As physical activity and affect are dynamic processes in nature, assessing those in everyday life with e-diaries and wearables, has become the gold standard. Thus, we used an mHealth approach to prospectively assess physical activity and affect processes in individuals with ADHD and controls aged 14–45 years. Participants wore accelerometers across a four-day period and reported their affect via e-diaries twelve times daily. We used multilevel models to identify the within-subject effects of physical activity on positive and negative affect. We split our sample into three groups: 1. individuals with ADHD who were predominantly inattentive (n = 48), 2. individuals with ADHD having a combined presentation (i.e., being inattentive and hyperactive; n = 95), and 3. controls (n = 42). Our analyses revealed a significant cross-level interaction (F(2, 135.072)=5.733, p = 0.004) of physical activity and group on positive affect. In details, all groups showed a positive association between physical activity and positive affect. Individuals with a combined presentation significantly showed the steepest slope of physical activity on positive affect (slope_inattentive=0.005, p <0.001; slope_combined=0.009, p <0.001; slope_controls=0.004, p = 0.008). Our analyses on negative affect revealed a negative association only in the individuals with a combined presentation (slope=-0.003; p = 0.001). Whether this specifically pronounced association in individuals being more hyperactive might be a mechanism reinforcing hyperactivity needs to be empirically clarified in future studies. [ABSTRACT FROM AUTHOR]

Background: Previous studies of conduct disorder (CD) have reported structural and functional alterations in the limbic system. However, the white matter tracts that connect limbic regions have not been comprehensively studied. The uncinate fasciculus (UF), a tract connecting limbic to prefrontal regions, has been implicated in CD. However, CD-related alterations in other limbic tracts, such as the cingulum and the fornix, have not been investigated. Furthermore, few studies have examined the influence of sex and none have been adequately powered to test whether the relationship between CD and structural connectivity differs by sex. We examined whether adolescent males and females with CD exhibit differences in structural connectivity compared with typically developing controls. Methods: We acquired diffusion-weighted magnetic resonance imaging data from 101 adolescents with CD (52 females) and 99 controls (50 females). Data were processed for deterministic spherical deconvolution tractography. Virtual dissections of the UF, the three subdivisions of the cingulum [retrosplenial cingulum (RSC), parahippocampal and subgenual cingulum], and the fornix were performed and measures of fractional anisotropy (FA) and hindrance-modulated orientational anisotropy (HMOA) were analysed. Results: The CD group had lower FA and HMOA in the right RSC tract relative to controls. Importantly, these effects were moderated by sex – males with CD significantly lower FA compared to male controls, whereas CD and control females did not differ. Conclusions: Our results highlight the importance of considering sex when studying the neurobiological basis of CD. Sex differences in RSC connectivity may contribute to sex differences in the clinical presentation of CD. [ABSTRACT FROM AUTHOR]

Attention deficit hyperactivity disorder is one of the most frequent neuropsychiatric disorders in childhood. Transcranial magnetic stimulation studies based on muscle responses (motor-evoked potentials) suggested that reduced motor inhibition contributes to hyperactivity, a core symptom of the disease. Here we employed the N100 component of the electroencephalographic response to transcranial magnetic stimulation as a novel marker for a direct assessment of cortical inhibitory processes, which has not been examined in attention deficit hyperactivity disorder so far. We further investigated to what extent affected children were able to regulate motor cortical inhibition, and whether effects of age on the electroencephalographic response to transcranial magnetic stimulation were compatible with either a delay in brain maturation or a qualitatively different development. N100 amplitude evoked by transcranial magnetic stimulation and its age-dependent development were assessed in 20 children with attention deficit hyperactivity disorder and 19 healthy control children (8–14 years) by 64-channel electroencephalography. Amplitude and latency of the N100 component were compared at rest, during response preparation in a forewarned motor reaction time task and during movement execution. The amplitude of the N100 component at rest was significantly lower and its latency tended to be shorter in children with attention deficit hyperactivity disorder. Only in controls, N100 amplitude to transcranial magnetic stimulation was reduced by response preparation. During movement execution, N100 amplitude decreased while motor evoked potential amplitudes showed facilitation, indicating that the electroencephalographic response to transcranial magnetic stimulation provides further information on cortical excitability independent of motor evoked potential amplitudes and spinal influences. Children with attention deficit hyperactivity disorder showed a smaller N100 amplitude reduction during movement execution compared with control children. The N100 amplitude evoked by transcranial magnetic stimulation decreased with increasing age in both groups. The N100 reduction in children with attention deficit hyperactivity disorder at all ages suggests a qualitative difference rather than delayed development of cortical inhibition in this disease. Findings further suggest that top-down control of motor cortical inhibition is reduced in children with attention deficit hyperactivity disorder. We conclude that evoked potentials in response to transcranial magnetic stimulation are a promising new marker of cortical inhibition in attention deficit hyperactivity disorder during childhood. [ABSTRACT FROM AUTHOR]

Summary: Attention-deficit/hyperactivity disorder (ADHD) is one of the most common child psychiatric disorders. Previous studies have reported a blunted cortisol response to challenging situations and a decreased cortisol awakening response (CAR) in children with ADHD. As ADHD often is comorbid with oppositional defiant disorder (ODD), conduct disorder (CD), or anxiety disorder (AnxD), and changes in hypothalamic–pituitary–adrenal (HPA) axis activity have also been reported for these disorders, the present study aimed to compare the CAR in children with ADHD with and without comorbid disorders. Data on the CAR were obtained in 128 children with ADHD (aged 6–13 years) and in 96 control children (aged 6–12 years). Children with ADHD+ODD showed an attenuated CAR (area under the curve, AUC) compared to children with ADHD without ODD/CD and control children. Findings point towards either disinhibition or pervasive underarousal in children with ADHD+ODD, and seem to be specific for children with ADHD+ODD, as the attenuated CAR–AUC was not observed in children with ADHD without comorbid disorders or children with ADHD+CD or ADHD+AnxD. In addition, current adverse parenting conditions, family conflicts, and acute life events were associated with mean increase in CAR, emphasizing the role of psychosocial risk factors in mediating HPA axis activity in children with ADHD. [Copyright &y& Elsevier]

Abstract: Although attention-deficit/hyperactivity disorder (ADHD) is highly heritable, environmental conditions play an important role in its manifestation during childhood development. Here, we report the results of an investigation on the interaction of adverse childhood environment with a functional polymorphism of the serotonin transporter promoter gene (5-HTTLPR) and its impact on ADHD psychopathology in young adult delinquents. Standardized instruments were used to assess childhood and current ADHD and adverse childhood environment in 184 male delinquents. Each subject was genotyped for 5-HTTLPR long (L) and small (S) alleles. Logistic regression analysis revealed independent effects of high childhood environmental adversity and the 5-HTTLPR LL-genotype on self-reported childhood ADHD and on persistent ADHD. In addition, a significant gene by environment interaction was found, indicating that carriers of at least one 5-HTTLPR short allele are more sensitive to childhood environment adversity than carriers of the LL-genotype. The results support prior findings of association between ADHD and 5-HTTLPR LL-genotype and adverse childhood environment, and they underline the need for further investigation of gene by environment interaction with respect to ADHD. [Copyright &y& Elsevier]

• Heterogeneous results of cortisol stress response are reported in ADHD and MDD. • Blunted cortisol stress response is consistently reported for CD and/or ODD. • If altered, cortisol stress response in ADHD is driven by comorbidity with CD and/or ODD. • More, and sex-specific research is needed to clarify differences in cortisol stress response. • *ADHD = Attention-deficit/hyperactivity Disorder, CD = Conduct Disorder, MDD = Major Depressive Disorder, ODD = Oppositional Defiant Disorder. BERNHARD, A., J. S. Mayer, N. Fann, and C. M. Freitag. Cortisol response to acute psychosocial stress in ADHD compared to Conduct Disorder and Major Depressive Disorder: A systematic review. NEUROSCI BIOBEHAV REV XX(X) XXX-XXX, 2020. – Heterogeneous alterations of the cortisol stress response in Attention-deficit/hyperactivity Disorder (ADHD) were recently reported by a systematic literature review. To investigate the moderating effect of frequent psychiatric comorbidities, we systematically searched for studies on cortisol stress response to psychosocial stress in ADHD compared to Conduct Disorder (CD) and Major Depressive Disorder (MDD) following PRISMA guidelines. EBSCOhost and PubMed databases were searched in July 2020, employing relevant keywords. Nineteen studies met inclusion criteria. While blunted cortisol stress response was consistently reported in individuals with CD and/or Oppositional Defiant Disorder (ODD), alterations of cortisol stress response were less pronounced in ADHD. Consistently blunted cortisol stress response in ADHD was only found in children with comorbid CD/ODD. Results on cortisol stress response in children and adolescents with MDD were mixed, and no indication for influence of comorbid MDD on cortisol stress response in ADHD was found. Taken together, altered cortisol stress response in ADHD is driven by comorbidity with disruptive behavior disorders. Limitations of previous research and suggestions for future studies are discussed. [ABSTRACT FROM AUTHOR]

• Young adults with ADHD have an increased risk for co-morbid depression. • This systematic review specifies shared neurocognitive impairments of ADHD and MDD. • Impairments of executive functions and memory are candidate risk markers of MDD. • Shared neurocognitive risk mechanisms may mediate pathways from ADHD to MDD. • Low IQ may not confer risk for MDD among patients with ADHD. The risk for major depressive disorder (MDD) is considerably increased in young adults with attention-deficit/hyperactivity disorder (ADHD) but underlying mechanisms are poorly understood. This review explores ADHD-specific neurocognitive impairments as possible underlying mechanisms for ADHD-depression comorbidity. Two systematic literature searches were conducted in EBSCOhost, PubMED, and Cochrane Reviews databases according to PRISMA guidelines. The first search identified 18 meta-analyses of cross-sectional and longitudinal studies on cognitive dysfunctions in MDD across the lifespan. The second search identified six original studies on reaction time variability in MDD. During acute depression, children and adults showed cognitive deficits that overlapped with some of the ADHD-related impairments. Findings from remitted patients, high-risk individuals, and few prospective studies suggest that a subset of these shared impairments, specifically executive dysfunctions (selective attention, verbal fluency, working memory) and long-term memory problems, are candidate pre-existing risk markers of depression. We discuss if and how these specific neurocognitive mechanisms may mediate developmental pathways from ADHD to depression. If replicated by longitudinal studies, these findings may guide future prevention strategies. [ABSTRACT FROM AUTHOR]

Stress results in a variety of neuroendocrine, immune and behavioral responses and represents a risk factor for many disorders. Following exposure to stress, glucocorticoids are secreted from the adrenal cortex and act via the ligand-activated glucocorticoid receptor (GR). Several polymorphisms of the GR-encoding gene NR3C1 have been described and functionally investigated. However, the impact of these variants on complex diseases such as Attention-Deficit/Hyperactivity Disorder (ADHD) is still unclear. In this study, 251 children with ADHD, 19 affected and 35 unaffected siblings, and their parents were included in a family-based association study assessing seven common variants of NR3C1 ( TthIII I_rs10052957; NR3C1-I_rs10482605; ER22/23EK_rs6189/rs6190; N363S_rs56149945; Bcl I_rs41423247; GR-9beta_rs6198). A four-marker haplotype ( TthIII I-NR3C1-I-ER22/23EK) was nominally associated with ADHD. In addition, in index children with ADHD, associations with comorbid disorders, inattentive and hyperactive-impulsive symptoms were explored. N363S minor allele carriers were more likely to show comorbid conduct disorder (CD). In our study, NR3C1 variants moderately affected ADHD and had a significant effect on comorbid CD. Therefore, NR3C1 as an important gene of the hypothalamic–pituitary–adrenal axis seems to be particularly relevant for the pathophysiology of ADHD combined with comorbid CD. For a deeper understanding, investigations in larger samples of healthy, ADHD and CD individuals are warranted. [ABSTRACT FROM AUTHOR]