fMRI of parents of children with Asperger Syndrome: A pilot study

Baron‐Cohen, Simon; Ring, Howard; Chitnis, Xavier; Wheelwright, Sally; Gregory, Lloyd J.; Williams, Steven; Brammer, Mick; Bullmore, Edward T.

doi:10.1016/j.bandc.2005.12.011

Cited by 120 publications

(89 citation statements)

References 21 publications

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“…In summary, then, we have established discriminating and statistically significant facial asymmetry in the ASD boys, especially in the supraorbital region, in comparison with appropriate controls. Because, preliminary data have suggested that unaffected firstdegree relatives of individuals with ASD share some of the same brain characteristics, 18 we next undertook similar analyses of affected and unaffected firstdegree relatives.…”

Section: Resultsmentioning

confidence: 99%

Face–brain asymmetry in autism spectrum disorders

et al. 2008

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The heterogeneity of autism spectrum disorders (ASDs) confounds attempts to identify causes and pathogenesis. Identifiable endophenotypes and reliable biomarkers within ASDs would help to focus molecular research and uncover genetic causes and developmental mechanisms. We used dense surface-modelling techniques to compare the facial morphology of 72 boys with ASD and 128 first-degree relatives to that of 254 unrelated controls. Patternmatching algorithms were able to discriminate between the faces of ASD boys and those of matched controls (AUC = 0.82) and also discriminate between the faces of unaffected mothers of ASD children and matched female controls (AUC = 0.76). We detected significant facial asymmetry in boys with ASD (P < 0.01), notably depth-wise in the supra-and periorbital regions anterior to the frontal pole of the right hemisphere of the brain. Unaffected mothers of children with ASD display similar significant facial asymmetry, more exaggerated than that in matched controls (P < 0.03) and, in particular, show vertical asymmetry of the periorbital region. Unaffected fathers of children with ASD did not show facial asymmetry to a significant degree compared to controls. Two thirds of unaffected male siblings tested were classified unseen as more facially similar to unrelated boys with ASD than to unrelated controls. These unaffected male siblings and two small groups of girls with ASD and female siblings, all show overall directional asymmetry, but without achieving statistical significance in two-tailed t-tests of individual asymmetry of ASD family and matched control groups. We conclude that previously identified right dominant asymmetry of the frontal poles of boys with ASD could explain their facial asymmetry through the direct effect of brain growth. The atypical facial asymmetry of unaffected mothers of children with ASD requires further brain studies before the same explanation can be proposed. An alternative explanation, not mutually exclusive, is a simultaneous and parallel action on face and brain growth by genetic factors. Both possibilities suggest the need for coordinated face and brain studies on ASD probands and their first-degree relatives, especially on unaffected mothers, given that their unusual facial asymmetry suggests an ASD susceptibility arising from maternal genes.

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Section: Resultsmentioning

confidence: 99%

Face–brain asymmetry in autism spectrum disorders

et al. 2008

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“…In support of this position, fMRI studies of ToM in autism have found differences in activity in STS and Broca's area [Baron-Cohen et al, 1999;Castelli, Frith, Happe, & Frith, 2002] suggesting that the mirror neuron system may be underactive during ToM function in autism. Baron-Cohen et al [2006] reported (as a preliminary finding) that Broca's area showed reduced activity during an empathic task in parents of children with autism compared to control parents, and also that this area was less active in male controls compared to female controls. Thus, they suggest that this area could be hypermasculinized in autism.…”

Section: Tests Of the Neurobiological Hypothesismentioning

confidence: 89%

Self–other relations in social development and autism: multiple roles for mirror neurons and other brain bases

2008

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Mirror neuron system dysfunction may underlie a self-other matching impairment, which has previously been suggested to account for autism. Embodied Cognition Theory, which proposes that action provides a foundation for cognition has lent further credence to these ideas. The hypotheses of a self-other matching deficit and impaired mirror neuron function in autism have now been well supported by studies employing a range of methodologies. However, underlying mechanisms require further exploration to explain how mirror neurons may be involved in attentional and mentalizing processes. Impairments in self-other matching and mirror neuron function are not necessarily inextricably linked and it seems possible that different sub-populations of mirror neurons, located in several regions, contribute differentially to social cognitive functions. It is hypothesized that mirror neuron coding for action-direction may be required for developing attentional sensitivity to self-directed actions, and consequently for person-oriented, stimulus-driven attention. Mirror neuron networks may vary for different types of social learning such as ''automatic'' imitation and imitation learning. Imitation learning may be more reliant on self-other comparison processes (based on mirror neurons) that identify differences as well as similarities between actions. Differential connectivity with the amygdala-orbitofrontal system may also be important. This could have implications for developing ''theory of mind,'' with intentional self-other comparison being relevant to meta-representational abilities, and ''automatic'' imitation being more relevant to empathy. While it seems clear that autism is associated with impaired development of embodied aspects of cognition, the ways that mirror neurons contribute to these brain-behavior links are likely to be complex.

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“…It has been suggested that these characteristics constitute a broader phenotype of autism which may represent an expression of the genetic liability for ASD. Several studies have reported biological differences in ASD parents versus controls, including increased whole blood serotonin Leboyer 1999); decreased plasma levels of reelin (Fatemi et al 2002); diminished size of the left hippocampus (Rojas et al 2004); altered local gray matter volumes (Peterson et al 2006) and decreased cortical activation (Baron-Cohen et al 2006). The biological findings are in need of replication and a structural imaging study not finding differences between parents and controls has been reported (Palmen et al 2005).…”

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confidence: 99%

Cortical Serotonin Type-2 Receptor Density in Parents of Children with Autism Spectrum Disorders

Goldberg

Anderson

Zwaigenbaum

et al. 2008

J Autism Dev Disord

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Parents (N = 19) of children with autism spectrum disorders (ASD) and adult controls (N = 17) underwent positron emission tomography (PET) using [(18)F]setoperone to image cortical serotonin type-2 (5-HT2) receptors. The 5-HT2 binding potentials (BPs) were calculated by ratioing [(18)F]setoperone intensity in regions of interest (ROI) to cerebellar intensity. Cortical 5-HT2 BPs were significantly lower in parents compared to controls and platelet 5-HT levels were significantly negatively correlated with cortical 5-HT2 BP in parents. Lower cortical 5-HT2 receptor density in parents of children with ASD is consistent with reports of diminished 5-HT2 expression and functioning in individuals with ASD. Further research should examine the relationship of reduced 5-HT2 receptor expression to underlying causation and to clinical and neurochemical correlates of autistic behavior.

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fMRI of parents of children with Asperger Syndrome: A pilot study

Cited by 120 publications

References 21 publications

Face–brain asymmetry in autism spectrum disorders

Face–brain asymmetry in autism spectrum disorders

Self–other relations in social development and autism: multiple roles for mirror neurons and other brain bases

Cortical Serotonin Type-2 Receptor Density in Parents of Children with Autism Spectrum Disorders

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