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Some authors draw a connection between the dopaminergic pathways and emotional perception. The present study is based on that association and addresses the question whether methylphenidate and the resulting amelioration of the disturbed dopamine metabolism lead to an improvement of the facial affect recognition abilities in children with attention-deficit/hyperactivity disorder (ADHD).
A computer test was conducted on 21 participants, aged 7–14 years and with a diagnosis of ADHD – some with comorbid oppositional defiant disorder – conducted the FEFA (Frankfurt Test and Training of Facial Affect), a computer test to examine their facial affect recognition abilities. It consists of two subtests, one with faces and one with eye pairs. All participants were tested in a double-blind cross-over study, once under placebo and once under methylphenidate.
Results and Discussion
The collected data showed that methylphenidate leads to amelioration of facial affect recognition abilities, but not on a significant level. Reasons for missing significance may be the small sample size or the fact that there exists some overlapping in cerebral connections and metabolic pathways of the site of action of methylphenidate and the affected dopaminergic areas in ADHD. However, consistent with the endophenotype concept, certain gene locations of the dopaminergic metabolism as both an aetiological factor for ADHD and the deficient facial affect recognition abilities with these individuals were considered. Consulting current literature they were found to be not concordant. Therefore, we conclude that the lacking significance of the methylphenidate affect on facial affect recognition is based on this fact.
Psychopathological, neuropsychological and genetic findings indicate an association between ASD Spectrum Disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). The goal of this study was to compare the neuropsychological profiles of attention functions in children with ADHD and with ASD and without comorbid ADHD. The hypothesis was that either ADHD and autistic children with comorbid ADHD symptoms were more impaired in inhibition and sustained attention performance and that all individuals with ASD show more deficits in divided attention.
Children aged 6 to 18 years old with ADHD (n = 30) or ASD with (n = 21) and without comorbid ADHD (n = 20) and 30 healthy children were included consecutively. Psychopathology was evaluated using the KIDDIE-SADS and symptom checklists for ADHD and ASD according to DSM-IV. Assessed neuropsychological functioning included inhibition, sustained as well as divided attention and alertness tasks.
Age and IQ-corrected z-scores were used. Statistically significant group effects were found for the variables sustained attention median (F = 3.2, = .02), hits (F = 3.3, p = .02) and false alarms (F = 3.9, p = .01), divided attention hits (F = 3.3, p = .02), errors (F = 3.1, p = .03) and false alarms (F = 3.3, p = .03) and alertness false alarms (F = 2.9, p = .04). Pearson Correlations revealed associations between ADHD symptoms and sustained attention in the ADHD group and between ADHD symptoms and inhibition in the ASD+ group.
Our hypothesis was partly confirmed as ADHD children showed more deficits in sustained attention and ASD children in divided attention tasks. However there was no evidence that children with ASD and comorbid ADHD symptoms have a specific profile in comparison to pure ASD children.