What is the nature of face processing impairment in autism?
Autism is a neurodevelopmental disorder, characterised by social, imaginative and communicative impairments with unusual/restricted behaviours (APA, 1994). One such impairment is in the ability to process faces. Face processing is essential for one’s social development (Tronick, 1978). It provides vital information, with a core set of facial expressions universally recognised (Ekman, 1999). Research has shown that individuals with autistic spectrum disorder (ASD) process faces; they have impaired emotional recognition and abnormal eye fixation. They use different strategies from typically developing (TD) individuals, such as featural processing. Some believe there is a neural basis for this problem; others argue that differences in methodology of testing produce different results. This essay outlines some of these arguments and discusses the nature of face processing impairment in autism.
Very early on, babies preferentially attend to faces. Within a few days, babies can differentiate their mother’s face to that of strangers and have the ability to imitate facial gestures posed by another person (Meltzoff and Moore, 1977; Bushnell et al. 1986). These milestones may vary for ASD individuals.
Studies have confirmed the robustness and universality of the still-face paradigm (Tronick, 1978; Kisilevsky et al, 1998; Segal et al, 1995). However, ASD infants didn’t respond the same when unfamiliar faces were used, failing to form the generalised expectation about a stranger’s social behaviour (Nadel et al, 2000). This can provide an insight into why ASD individuals may avoid strangers, interacting only with close family members (Lord, 1984). It can also explain why face processing impairments may affect social development.
ASD individuals have deficits in facial emotion recognition (Gepner et al, 1996; Hobson et al, 1988). Polijac et al (2000) found that scorers with high autism-spectrum quotients (AQ), which strongly correlate with autism, were less able to identify facial expressions correctly. Furthermore, ASD children performed worse than TD controls when labelling, identifying and finding odd facial and emotional displays (Tantam et al, 1989; Gross, 2004; Hubert et al, 2007). These studies support an impaired perception of facial emotional recognition.
Certain areas of the brain are responsible for face processing, including the fusiform gyrus (FFG), superior temporal sulcus (STS), and amygdala. In TD individuals, studies using fMRI have shown increased activation in the right FFG when exposed to human faces; in comparison to the decreased activation seen in ASD individuals (Kanwisher et al, 1999; Critchley et al, 2000). Furthermore, their FFG contains less GABBA receptors with smaller and fewer neurons (Oblak et al, 2010; Van Kooten et al, 2008). These could contribute to a facial processing deficit.
Brain damaged patients and animal studies have shown that damage or removal of STS can impair eye gaze direction, an important social cue (Akiyama et al, 2006; Campbell et al, 1990). This suggests that a neural basis underlies the face processing deficit in autism, thus causing a social deficit e.g. lack of social interest or impaired theory of mind. (Schultz, 2005; Baron Cohen, 1997).
Amygdala differences can also have an effect. High functioning autistic individuals, who performed poorly on facial recognition tasks and eye gaze, also possessed a larger amygdala. Amygdala size may also affect the severity of symptomatology, thus explaining individual differences (Howard et al, 2000). Some had increased grey matter volume with less activation compared to controls. (Sparks et al, 2002; Baron-Cohen et al, 2000; Abell et al, 1999).
The above studies provide strong evidence that the specific mechanisms for face recognition may be impaired in ASD individuals. These may underlie their social impairments.
- Quote paper
- Sanum Ghafoor (Author), 2014, The Nature of Face Processing Impairment in Autism, Munich, GRIN Verlag, https://www.grin.com/document/377437