Failure to deactivate in autism: The co-constitution of self and other

Ahmanson-Lovelace Brain Mapping Center, Department of Psychiatry and Biobehavioral Sciences, NeuroPsychiatric Institute, Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Trends in Cognitive Sciences (Impact Factor: 21.97). 11/2006; 10(10):431-3. DOI: 10.1016/j.tics.2006.08.002
Source: PubMed


A new brain imaging study demonstrates that patients with autism have a strikingly different pattern of brain activity compared with control subjects. During cognitive tasks, cortical areas known as the "default state" network--areas that have been implicated in both self-referential processing and processing of socially relevant information--typically reduce their brain activity. In patients with autism, such a reduction was not observed. This new finding indicates that a core deficit in autism might be related to the construal of a sense of self in its relationship with others and will certainly generate exciting new research on the neurobiology of autism.

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    • "e l s e v i e r . c o m / l o c a t e / n e u b i o r e v conceptualizations of the brain basis of ASD have taken a systemslevel approach, and proposed that ASD may be explained by abnormalities in the mirror neuron system (Oberman and Ramachandran, 2007; Williams et al., 2001), the default-mode network (Kennedy and Courchesne, 2008; Kennedy et al., 2006), or both (Iacoboni, 2006). These conceptualizations, however, have primarily focused on specific brain systems and have largely ignored the critical interactions between multiple distinct brain systems, which may be important for understanding the neurobiology of a complex neurodevelopmental disorder such as ASD. "

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    • "This seemingly inconsistency can be understood if we hypothesize that the positive pole of dipoles in the parietal cortex that underwent OT modulations pointed to the frontal lobe, though this speculation should be examined in future research. The right parietal cortex plays a role in recognition of one's own face (Uddin, Molnar- Szakacs, Zaidel, & Iacoboni, 2006) and the LPP has been shown to be sensitive to evaluative categorization processes, with the LPP amplitude reflecting the extent to which a particular categorization process involves context updating (Cacioppo, Crites, Gardner, & Berntson, 1994). Thus our results suggest that OT treatment may weaken self-related processing in both early encoding of stimulus self-relevance and late evaluative processes. "
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    ABSTRACT: Oxytocin (OT) influences how humans process information about others and modulates their social behavior. Whether OT affects the processing of information about oneself remains unknown. Using a double-blind, placebo-controlled within-subject design, we recorded event-related potentials (ERPs) from adults during trait judgments about oneself and a celebrity and during judgments on word valence, after intranasal OT or placebo administration. Differential ERP amplitudes during self- or celebrity-judgments relative to valence-judgments were calculated to assess neural processing of self and others, respectively. We found that, relative to placebo treatment, OT treatment reduced the differential amplitudes of a fronto-central positivity at 220-280ms (P2) during self- vs. valence-judgments but did not affect the differential P2 amplitude during other- vs. valence-judgments. OT vs. placebo treatment tended to reduce the differential amplitude of a late positive potential at 520-1000ms (LPP) during self-judgments but to increase the differential LPP amplitude during other-judgments. Moreover, the OT effects on the differential P2 and LPP amplitudes to self- vs. celebrity-judgments were positively correlated with a measure of interdependence of self-construals. Our findings provide evidence for OT effects on the neural correlates of self-referential processing that may vary across individuals with different levels of interdependence of self-construals.
    Biological psychology 08/2013; 94(2). DOI:10.1016/j.biopsycho.2013.08.003 · 3.40 Impact Factor
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    • "Functional MRI has shown that witnessing the emotions of others triggers neural activations in brain regions (insula and cingulate cortex) normally associated with feeling similar emotions oneself (Bastiaansen et al., 2009; Lamm et al., 2011), and witnessing what others do and sense recruits one's own motor and somatosensory cortices (Pineda, 2008; Keysers and Gazzola, 2009; Caspers et al., 2010; Keysers et al., 2010). The strength of these so called vicarious neural activations is predicted by interindividual differences in trait-empathy (Singer et al., 2004; Gazzola et al., 2006; Jabbi et al., 2007) and they are therefore thought to represent a neural marker for empathy (Singer et al., 2004; Iacoboni, 2006; Pineda, 2008; Bastiaansen et al., 2009; Keysers and Gazzola, 2009). These neural markers for empathy have been investigated in several psychiatric disorders, autism in particular (Dapretto et al., 2006; Decety and Moriguchi, 2007; Dinstein et al., 2008; Minio- Paluello et al., 2009), but surprisingly, not directly in psychopathy. "
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    ABSTRACT: Psychopathy is a personality disorder associated with a profound lack of empathy. Neuroscientists have associated empathy and its interindividual variation with how strongly participants activate brain regions involved in their own actions, emotions and sensations while viewing those of others. Here we compared brain activity of 18 psychopathic offenders with 26 control subjects while viewing video clips of emotional hand interactions and while experiencing similar interactions. Brain regions involved in experiencing these interactions were not spontaneously activated as strongly in the patient group while viewing the video clips. However, this group difference was markedly reduced when we specifically instructed participants to feel with the actors in the videos. Our results suggest that psychopathy is not a simple incapacity for vicarious activations but rather reduced spontaneous vicarious activations co-existing with relatively normal deliberate counterparts.
    Brain 08/2013; 136(Pt 8):2550-62. DOI:10.1093/brain/awt190 · 9.20 Impact Factor
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