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Attention-deficit/hyperactivity disorder without comorbidity is associated with distinct atypical patterns of cerebral microstructural development.

ABSTRACT: Differential core symptoms and treatment responses are associated with the pure versus comorbid forms of attention-deficit/hyperactivity disorder (ADHD). However, comorbidity has largely been unaccounted for in neuroimaging studies of ADHD. We used diffusional kurtosis imaging to investigate gray matter (GM) and white matter (WM) microstructure of children and adolescents with ADHD (n = 22) compared to typically developing controls (TDC, n = 27) and examined whether differing developmental patterns are related to comorbidity. The ADHD group (ADHD-mixed) consisted of subgroups with and without comorbidity (ADHD-comorbid, n = 11; ADHD-pure, n = 11, respectively). Age-related changes and group differences in cerebral microstructure of the ADHD-mixed group and each ADHD subgroup were compared to TDC. Whole-brain voxel-based analyses with mean kurtosis (MK) and mean diffusivity (MD) metrics were conducted to probe GM and WM. Tract-based spatial statistics analyses of WM were performed with MK, MD, fractional anisotropy, and directional (axial, radial) kurtosis and diffusivity metrics. ADHD-pure patients lacked significant age-related changes in GM and WM microstructure that were observed globally in TDC and had significantly greater WM microstructural complexity than TDC in bilateral frontal and parietal lobes, insula, corpus callosum, and right external and internal capsules. Including ADHD patients with diverse comorbidities in analyses masked these findings. A distinct atypical age-related trajectory and aberrant regional differences in brain microstructure were detected in ADHD without comorbidity. Our results suggest that different phenotypic manifestations of ADHD, defined by the presence or absence of comorbidity, differ in cerebral microstructural markers.

SUBMITTER: Adisetiyo V

PROVIDER: S-EPMC3972353 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:To determine comorbidity patterns in treatment-seeking substance use disorder (SUD) patients with and without adult attention deficit hyperactivity disorder (ADHD), with an emphasis on subgroups defined by ADHD subtype, taking into account differences related to gender and primary substance of abuse.Data were obtained from the cross-sectional International ADHD in Substance use disorder Prevalence (IASP) study.Forty-seven centres of SUD treatment in 10 countries.A total of 1205 treatment-seeking SUD patients.Structured diagnostic assessments were used for all disorders: presence of ADHD was assessed with the Conners' Adult ADHD Diagnostic Interview for DSM-IV (CAADID), the presence of antisocial personality disorder (ASPD), major depression (MD) and (hypo)manic episode (HME) was assessed with the Mini International Neuropsychiatric Interview-Plus (MINI Plus), and the presence of borderline personality disorder (BPD) was assessed with the Structured Clinical Interview for DSM-IV Axis II (SCID II).The prevalence of DSM-IV adult ADHD in this SUD sample was 13.9%. ASPD [odds ratio (OR)?=?2.8, 95% confidence interval (CI)?=?1.8-4.2], BPD (OR?=?7.0, 95% CI?=?3.1-15.6 for alcohol; OR?=?3.4, 95% CI?=?1.8-6.4 for drugs), MD in patients with alcohol as primary substance of abuse (OR?=?4.1, 95% CI?=?2.1-7.8) and HME (OR?=?4.3, 95% CI?=?2.1-8.7) were all more prevalent in ADHD(+) compared with ADHD(-) patients (P?<?0.001). These results also indicate increased levels of BPD and MD for alcohol compared with drugs as primary substance of abuse. Comorbidity patterns differed between ADHD subtypes with increased MD in the inattentive and combined subtype (P?<?0.01), increased HME and ASPD in the hyperactive/impulsive (P?<?0.01) and combined subtypes (P?<?0.001) and increased BPD in all subtypes (P?<?0.001) compared with SUD patients without ADHD. Seventy-five per cent of ADHD patients had at least one additional comorbid disorder compared with 37% of SUD patients without ADHD.Treatment-seeking substance use disorder patients with attention deficit hyperactivity disorder are at a very high risk for additional externalizing disorders.

Project description:ObjectiveThe neurobiological basis of inattentiveness, a core feature of attention-deficit/hyperactivity disorder (ADHD), is not yet well understood. Structural abnormalities in thalamus, especially the pulvinar nuclei, have recently been reported in ADHD. Pulvinar nuclei maintain reciprocal connections with cortical/subcortical areas, and play a central coordinating role during visual attention processing. The objective of this study was to test the hypothesis that children and young adolescents with ADHD would show atypical pulvinar-cortical functional pathways during sustained attention performance, and that these functional abnormalities would be associated with the inattentive symptoms of the disorder.MethodVisual attention task-based functional magnetic resonance imaging (fMRI) data from 22 children and young adolescents with ADHD and 22 demographically matched, normal control subjects were analyzed. Cortical activation maps and temporal correlations of activity patterns between pulvinar nuclei and the remainder of brain were constructed for each participant. Correlations between activation magnitude of pulvinar and diagnostic measures were calculated in subjects with ADHD.ResultsCompared to controls, subjects with ADHD showed significantly reduced pulvinar activations bilaterally, significantly decreased functional connectivity between bilateral pulvinar and right prefrontal regions, and significantly increased connectivity between the right pulvinar and bilateral occipital regions. In addition, the activation magnitude in the left pulvinar was negatively correlated with the DSM-IV inattentive index in ADHD group.ConclusionsAllied with previous evidence of structural abnormalities in pulvinar, the current data suggest that inappropriate development of pulvinar may lead to disrupted functional circuits for visual attention processing, and that these disruptions contribute significantly to the pathophysiological mechanisms of the inattentiveness symptoms in ADHD.

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Attention-deficit/hyperactivity disorder without comorbidity is associated with distinct atypical patterns of cerebral microstructural development.

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