Autistic Disturbances of Affective Contact: Are Cognitive Accounts Sufficient?

Background: It is now well established that individuals with Autism Spectrum Disorder (ASD) experience often very marked difficulties in multiple aspects of reciprocal emotional communication. Controlled laboratory experiments show that such individuals either experience difficulties in identifying the emotional expressions of others or that they deploy qualitatively different perceptual processes in order to do so. In naturalistic settings individuals with ASD tend to direct few emotional expressions at others and when others direct such expressions at them, they often react atypically or not at all. Despite the consistency with which these abnormalities are demonstrated, there is, to date, no consensus as to what the cause of this facet of the ASD phenotype might be. Some argue that socio-emotional disturbances are the result of abnormalities in the development of mentalising abilities, whilst others believe that the core problem lies in the development of relatively basic emotional processes. The only consensus that has emerged over the past few years is that abnormalities of the amygdala most likely play a role in the socio-emotional characterisation of the ASD phenotype.

Objectives: To suggest that recently accumulating evidence from studies assessing emotional processes outside the immediate context of social cognition may help to resolve the debate regarding the developmental origin of socio-emotional disturbances in ASD.

Methods: First, we will demonstrate that it is difficult (if not impossible) to resolve the developmental debate surrounding the socio-emotional disturbances characterising ASD on the basis of evidence from studies that assess the emotional competencies of individuals with ASD solely within the reciprocal social context. We then present an overview of how the concept of ‘emotion’ is currently operationalised outside the field of ASD in order to highlight a consensus that emotional experiences and behaviours are the result of the interplay between physiological response mechanisms and cognition. Finally, we note that this interplay is known to involve the amygdala at a neural level, establishing a parallel between neural frameworks of emotion and neural frameworks of ASD. On the basis of this overview we conclude that studies of how physiological and cognitive aspects of emotional experiences are integrated in ASD are essential in order to arrive at an understanding of the causes of the clinically defining manifestations of this disorder.

Results: We provide an overview of the few studies that have examined how physiological aspects of emotional experiences influence cognition and behaviour in ASD and conclude that the evidence from these studies suggests that also outside the reciprocal social context, individuals with ASD are characterised by abnormalities in emotional processes.

Conclusions: We will conclude that purely cognitive explanations are inadequate to account for the observation that ASD is characterised by abnormalities in emotional processes outside the social domain and that, as a result, the suitability of such explanations for the socially relevant emotional deficits of ASD is questionable. We present an alternative theoretical framework that we believe is neurologically and developmentally plausible and that could potentially explain not only the social but also the non-social characteristics of the ASD phenotype.