18 research outputs found

    The neurobiological link between OCD and ADHD

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    Comorbid anxiety and neurocognitive dysfunctions in children with ADHD

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    Item does not contain fulltextPrevious research established that children with ADHD and comorbid anxiety have a later age of ADHD onset, show less off-task and hyperactive behavior, and have more school problems than children with ADHD alone. Comorbid anxiety appears to ameliorate behavioral inhibition deficits, worsen working memory problems, and lengthen reaction times in ADHD. This study investigated the effect of comorbid anxiety on a broad range of neurocognitive functions and includes child-, parent- and teacher reports of anxiety. The sample consisted of 509 children in the age range 5-19 years, including 238 children with a diagnosis of ADHD combined subtype and 271 normal control children. Children were tested on a broad battery of neurocognitive tasks that proved highly sensitive to ADHD in previous work. Linear Structural Equation Modeling (SEM) was used to estimate the effect of comorbid anxiety on the neurocognitive functions. Child reported anxiety was associated with slower motor speed and response speed and better behavioral inhibition. Teacher reported anxiety was related to worse time production. Parent reported anxiety was not significantly associated with any of the neurocognitive functions. Compared to parent and teacher reports of anxiety, child reported comorbid anxiety shows foremost the largest associations with the neurocognitive dysfunctions observed in children with ADHD. This stresses the importance of including child self-reported anxiety assessments in clinical and research practice

    Is Clinical Anxiety a Risk or a Protective Factor for Executive Functioning in Youth with ADHD? A Meta-regression Analysis

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    Comorbidity rates between ADHD and anxiety disorders (AD) are high, but little is known about the nature of this co-occurrence. A dominant idea is that AD may intensify some (i.e., attention and working memory) and attenuate other (i.e., inhibition) ADHD symptoms. Results are mixed, potentially because of between-study differences. To investigate this further we performed a meta-regression analysis on 11 studies (n ‘ADHD-only’ = 695; n ‘ADHD + AD’ = 608), containing 35 effect sizes on attention, inhibition and working memory. Main results were: (1) no evidence of a negative effect of AD on attention and working memory; (2) better response inhibition in children with ADHD with AD than those with only ADHD (medium ES g = − .40); (3) medication moderated this association: the effect seemed limited to studies that included medication-naïve participants; (4) the difference between the two groups increased with age for attention and with proportion of boys for working memory ability. There was no effect of comorbid disruptive behavior disorder. In conclusion, AD seems to be a protective factor for inhibition problems as assessed with laboratory tasks in ADHD, especially in children who are medication naïve. Further, AD may have a protective function for attention in older children, and for working memory in boys with ADHD. It is therefore important to screen for AD when diagnosing ADHD, and to educate those with comorbid AD about the possible positive function of feeling anxious. Potential negative effects of ADHD medication on inhibition in children with comorbid AD should be considered

    Reduced cortical surface area in adolescents with conduct disorder

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    Children with conduct disorder (CD) are at increased risk of developing antisocial personality disorder and psychopathy in adulthood. Neuroimaging research has identified abnormal cortical volume (CV) in CD. However, CV comprises two genetically and developmentally separable components: cortical thickness (CT) and surface area (SA). Aim of this study is to explore the relationship between the cortical constituents of CV in boys with CD. We applied FreeSurfer software to structural MRI data to derive measures of CV, CT, and SA in 21 boys with CD and 19 controls. Relationships between these cortical measures were investigated. Boys with CD had significantly reduced CV and SA compared to non-CD boys in ventromedial and dorsolateral prefrontal cortex. We found no significant between-group differences in CT. Reduced prefrontal CV in boys with CD is associated with significantly reduced SA in the same regions. This finding may help to identify specific neurodevelopmental mechanisms underlying cortical deficits observed in CD.</p
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