Different brain responses during empathy in autism spectrum disorders versus conduct disorder and callous-unemotional traits.

BACKGROUND: Deficits in empathy are reported in autism spectrum disorders (ASD) and also underlie antisocial behavior of individuals with conduct disorder and callous-unemotional traits (CD/CU+). Many studies suggest that individuals with ASD are typically impaired in cognitive aspects of empathy, and individuals with CD/CU+ typically in affective aspects. In the current study, we compared the neural correlates of cognitive and affective aspects of empathy between youth with ASD and youth with CD/CU+. METHODS: Functional magnetic resonance imaging (fMRI) was used to assess boys with ASD (N = 23), boys with CD/CU+ (N = 23), and typically developing (TD) boys (N = 33), aged 15-19 years. Angry and fearful faces were presented and participants were asked to either infer the emotional state from the face (other-task; emotion recognition) or to judge their own emotional response to the face (self-task; emotional resonance). RESULTS: During emotion recognition, boys with ASD showed reduced responses compared to the other groups in the ventromedial prefrontal cortex (vmPFC). During emotional resonance, the CD/CU+ and ASD groups showed reduced amygdala responses compared to the TD controls, boys with ASD showed reduced responses in bilateral hippocampus, and the CD/CU+ boys showed reduced responses in the inferior frontal gyrus (IFG) and anterior insula (AI). CONCLUSION: Results suggest differential abnormal brain responses associated with specific aspects of empathic functioning in ASD and CD/CU+. Decreased amygdala responses in ASD and CD/CU+ might point to impaired emotion processing in both disorders, whereas reduced vmPFC responses suggest problems in processing cognitive aspects of empathy in ASD. Reduced IFG/AI responses, finally, suggest decreased emotional resonance in CD/CU+.

A complex chromosome 7q rearrangement identified in a patient with mental retardation, anxiety disorder, and autistic features.

We have characterized a de novo complex rearrangement of the long arm of chromosome 7 in a female patient with moderate mental retardation (MR), anxiety disorder, and autistic features. G-banding suggested a de novo paracentric inversion 46,XX,inv(7)(q31.3q34). However, SNP-array analysis, showed a +/-10 Mb, 7q21.11-q21.3 deletion in the paternal chromosome. Subsequent FISH analysis with BAC/PAC clones in the 7q21-q35 region confirmed this deletion. However, the expected paracentric inversion turned out to be an intra-chromosomal insertion of the 7q31.31-q35 fragment into band 7q21.3, disrupting the predicted gene C7orf58 in band 7q31.31. Seven other patients have been previously reported with a deletion of 7q21.1-q21.3. Although there is an overlap in phenotype between our patient and these patients, none of them has been described with anxiety disorder and/or autistic features. Therefore we suggest that disruption of the C7orf58 gene might contribute to the anxiety disorder, and autistic features in our patient.