BackgroundRecent studies have not paid a great deal of attention to comorbid attention-deficit/hyperactivity disorder (ADHD) symptoms in autistic children even though it is well known that almost half of children with autism spectrum disorder (ASD) suffer from hyperactivity, inattention and impulsivity. The goal of this study was to evaluate and compare executive functioning (EF) profiles in children with ADHD and in children with ASD with and without comorbid ADHD.MethodsChildren aged 6 to 18 years old with ADHD (n = 20) or ASD (High-Functioning autism or Asperger syndrome) with (n = 20) and without (n = 20) comorbid ADHD and a typically developing group (n = 20) were compared on a battery of EF tasks comprising inhibition, flexibility, working memory and planning tasks. A MANOVA, effect sizes as well as correlations between ADHD-symptomatology and EF performance were calculated. Age- and IQ-corrected z scores were used.ResultsThere was a significant effect for the factor group (F = 1.55; dF = 42; p = .02). Post-hoc analysis revealed significant differences between the ADHD and the TD group on the inhibition task for false alarms (p = .01) and between the ADHD group, the ASD+ group (p = .03), the ASD- group (p = .02) and the TD group (p = .01) for omissions. Effect sizes showed clear deficits of ADHD children in inhibition and working memory tasks. Participants with ASD were impaired in planning and flexibility abilities. The ASD+ group showed compared to the ASD- group more problems in inhibitory performance but not in the working memory task.ConclusionOur findings replicate previous results reporting impairment of ADHD children in inhibition and working memory tasks and of ASD children in planning and flexibility abilities. The ASD + group showed similarities to the ADHD group with regard to inhibitory but not to working memory deficits. Nevertheless the heterogeneity of these and previous results shows that EF assessment is not useful for differential diagnosis between ADHD and ASD. It might be useful for evaluating strengths and weaknesses in individual children.
Difficulties initiating and maintaining sleep may be transient or persistent. In practice, children and adolescents should be included in the diagnostic and therapeutic process.
Psychopathological, genetic and neuropsychological findings indicate an association between autism and attention deficit/hyperactivity disorder (ADHD). The goal of this study was to assess possible differences in facial affect recognition in children with autism (with and without comorbid ADHD), with ADHD and healthy controls. Children aged 6-18 years old with DSM-IV-diagnosis ADHD (n=30) or autism (n=40) were included consecutively in the study. Facial affect recognition was assessed with a computer-based program used for teaching emotion processing called the Frankfurt Test and Training of Social Affect (FEFA) using faces and eye-pairs as target material. Additionally three attention-tasks (Sustained attention, Inhibition, Set-Shifting) were administered. Approximately 52% of the autistic children met the criteria for the comorbid diagnosis of ADHD. A MANOVA with post-hoc Scheffé tests revealed a significant difference in the recognition of faces and eye pairs between the group ADHD and controls (P=0.009). Children with autism and ADHD also differed significantly from healthy participants in the recognition of eye-pairs (P=0.009). Neither correlations with PDD nor with ADHD symptom scores were able to explain these results. Sustained attention and inhibition deficits had a significant influence on emotion recognition in children with ADHD. Our findings imply that the ability of facial affect recognition is reduced in children suffering from ADHD symptoms, both in autistic and pure ADHD children. ADHD symptoms need to be taken into account in future studies assessing emotion recognition in autistic children and adolescents.
We treated a 13-year-old boy for life-threatening self-injurious behavior (SIB) and severe Kanner's autism with deep brain stimulation (DBS) in the amygdaloid complex as well as in the supra-amygdaloid projection system. Two DBS-electrodes were placed in both structures of each hemisphere. The stimulation contacts targeted the paralaminar, the basolateral (BL), the central amygdala as well as the supra-amygdaloid projection system. DBS was applied to each of these structures, but only stimulation of the BL part proved effective in improving SIB and core symptoms of the autism spectrum in the emotional, social, and even cognitive domains over a follow up of now 24 months. These results, which have been gained for the first time in a patient, support hypotheses, according to which the amygdala may be pivotal in the pathogeneses of autism and point to the special relevance of the BL part.
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