Abstract
Current theoretical models of autism spectrum disorders (ASD) have proposed that impairments in the processing of social/emotional information may be linked to amygdala dysfunction. However, the extent to which amygdala functions are compromised in ASD has become a topic of debate in recent years. In a jittered functional magnetic resonance imaging study, sub-threshold presentations of anxious faces permitted an examination of amygdala recruitment in 12 high functioning adult males with ASD and 12 matched controls. We found heightened neural activation of the amygdala in both high functioning adults with ASD and matched controls. Neither the intensity nor the time-course of amygdala activation differed between the groups. However, the adults with ASD showed significantly lower levels of fusiform activation during the trials compared to controls. Our findings suggest that in ASD, the transmission of socially salient information along sub-cortical pathways is intact: and yet the signaling of this information to structures downstream may be impoverished, and the pathways that facilitate subsequent processing deficient.
Highlights
The autism spectrum disorders (ASD) are a complex group of disorders defined by deficits in social interaction, communication and a pattern of circumscribed interests and repetitive behaviours
We found greater activation in the amygdala and fusiform, bilaterally, to anxious compared to neutral faces [Right Amygdala (20, 23. 215) 254 voxels: t(1359)–2.62, p,0.026; Left Amygdala (222 27 220) 810 voxels: t(1359) = 3.035, p,0.011
In the present pilot work we found that the presentation of backward-masked anxious faces was associated with heightened neural activation of the amygdala in both high functioning adults with ASD and matched controls
Summary
The autism spectrum disorders (ASD) are a complex group of disorders defined by deficits in social interaction, communication and a pattern of circumscribed interests and repetitive behaviours [1] Fundamentally neurobiological in origin, ASD is marked by early developmental onset [2] and is among the most heritable of psychiatric disorders [3,4].Often considered core to ASD are the impairments in social interaction as other symptoms are observed more heterogeneously and share traits with a range of neuropsychiatric disorders such as primary language delay disorders and mental retardation syndromes [5]. The amygdala has long been accepted as the fast-acting, social appraisal centre of the limbic system. It plays a critical role in emotional arousal to fearful [7,8], threatening and uncertain external events [9,10]. There is converging evidence that the amygdala plays a central role in the perception, interpretation and recognition of emotion in faces [7,11,12,13,14,15] and may function to signal the social salience of emotional displays [16,17]. Several current theoretical models of autism link social and emotional impairments of the syndrome to amygdala dysfunction [6,18,19]. A number of postmortem studies have shown increased cell packing density in the amygdalae of individuals with autism [21,22]
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