The hypothesis was tested that weak theory of mind (ToM) and/or emotion recognition (ER) abilities are specific to subjects with autism. Differences in ToM and ER performance were examined between autistic (n = 20), pervasive developmental disorder—not otherwise specified (PDD-NOS) (n = 20), psychiatric control (n = 20), and normal children (n = 20). The clinical groups were matched person-to-person on age and verbal IQ. We used tasks for the matching and the context recognition of emotional expressions, and a set of first- and second-order ToM tasks. Autistic and PDD-NOS children could not be significantly differentiated from each other, nor could they be differentiated from the psychiatric controls with a diagnosis of ADHD (n = 9). The psychiatric controls with conduct disorder or dysthymia performed about as well as normal children. The variance in second-order ToM performance contributed most to differences between diagnostic groups.

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AIM To examine social information processing in children and adolescents with neurofibromatosis type 1 (NF1).METHOD Thirty-two children with NF1 (12 males, 20 females; mean age 12y 4mo, SD 4y) and 32 comparison children (12 males, 20 females; mean age 13y 1mo, SD 3y 11mo) completed face recognition, identification of facial emotions (IFE), and matching facial emotions (MFE) tasks. A series of general linear model analyses of variance were used to compare performance between children with NF1 and comparison children. RESULTSChildren with NF1 performed less accurately than comparison children in the face recognition task when faces were presented 'in profile' (p=0.05), when fearful expressions had to be identified in IFE (p=0.017), and across conditions in MFE (p=0.009). When quality of cognitive control (i.e. mean standardized scores on tasks measuring working memory and inhibitory control) was introduced to the analyses, differences in face recognition were no longer significant and differences in MFE were largely reduced (p=0.048). Differences in IFE between the comparison group and children with NF1 remained largely intact (fear: p=0.047).INTERPRETATION Children with NF1 have problems in social information processing, which, in part, appear to be caused by cognitive control deficits. Some of the deficits, however, appear to be caused by deficient bottom-up processing of social signals (e.g. fear recognition).Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder with an incidence of approximately 1 in every 3000 individuals. 1,2 Clinical manifestations of NF1 include café-au-lait spots, intertriginous freckling, Lisch nodules (i.e. pigmented iris hamartomas or freckling in the iris), neurofibromas (i.e. benign Schwann cell tumours, divided into four types: (1) focal or diffuse cutaneous, (2) subcutaneous, (3) spinal, and (4) nodular or diffuse plexiform neurofibromas, which develop from nerves and extend into surrounding structures, and which can transform into malignant tumours), optic pathway gliomas, and distinctive bone lesions (e.g. short stature or dystrophic scoliosis). 3 The NF1 gene is located on chromosome 17 (17q11.2). Neurofibromin, the protein product of this gene, inhibits Ras, which in turn stimulates cell proliferation and differentiation. Therefore, lack of neurofibromin might result in the inability to control the formation, migration, and differentiation of neurons. 4 Magnetic resonance imaging studies have shown widespread abnormalities in the brains of children with NF1, including T2 hyperintensities, reduced grey matter and increased white matter volumes, and reduced integrity of white matter. [5][6][7][8] Cognitive impairment is the most common complication in children with NF1. 9 Several studies reported deficits in specific cognitive domains, such as visuospatial skills or motor control, 10,11 whereas others provided evidence for more general executive function or cognitive control deficits affecting different cognitive domains when control demands increase. 12,13 Soc...

The findings do not support the hypothesis that ODD and ODD/ADHD children have a deficit in executive inhibitory control; rather, they emphasise that they have problems in regulating their behaviour under motivational inhibitory conditions.