The Nature of Face Processing Impairment in Autism

Face Recognition by Autistic People

Essay 2014 8 Pages

Psychology - Miscellaneous


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.

Emotional recognition

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.

Neural basis

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.

Atypical strategies

ASD individuals use atypical face processing strategies. They do not show inversion effects, like their TD-matched controls, when discriminating, sorting, and identifying inverted faces (O’Brien et al, 2014; Hobson et al, 1988; Langdell, 1978; Tantam et al, 1989). This suggests they are unaffected by the disruption in configural information (Boutsen and Humphreys, 2003).

Consequently, ASD individuals may rely on abnormal alternatives like feature-based strategies, thus resulting in enhanced processing for individual facial aspects (Tantam et al, 1989; Lahaie et al, 2006). They may not develop face expertise, nor process faces as special; rather, they process them in the same manner as objects (Hobson et al, 1988; O’Connor et al, 2005; Schultz, 2000).

Eye fixation

ASD individuals have diminished eye region fixation, a strong predictor of autism. They spend twice as long looking at the mouth region, but two times less time on the eye region, compared to controls. (Klin et al, 2002; Yi et al, 2013). ASD individuals focus less on the core internal features of the face and fixate on unimportant external features (Pelphrey et al, 2002; Trepagnier et al, 2002). They look more at the lower half of the face, often developing superior lip reading skills; possibly a compensatory mechanism for other impaired processing strategies (Schultz et al, 2000; Nadel et al, 2000).

Research using eye-tracking data has shown that high risk infants spend longer looking at stimuli of faces relative to other objects, suggesting it takes longer for them to process (Elsabbagh et al, 2013). This may be due to neural abnormalities causing slowed face processing speed (McPartland et al, 2004).

Other factors

Other factors may be involved. During face discrimination tasks, ASD adults had slower N170 responses; N170 is an ERP component thought to be important for face processing, suggesting a different basis for autism (O’Connor et al, 2005).

Research suggests face processing abilities in ASD individuals may follow a delayed developmental trajectory rather than a deficit. ASD adults performed similarly to TD children. Furthermore, ASD children performed similarly to developmentally delayed children and younger TD children (Greimel et al, 2014; Wilson et al, 2009).

There are some inconsistent findings. For example, Pierce & Redcay (2008) found normal FFG activity in ASD individuals, but only when viewing strangers’ faces were abnormalities present. Stimuli may affect results. Furthermore, some tasks may test memory rather than face processing. This is illustrated by ASD individuals who had worse recognition when faces had to be remembered over a delay than when they did not (Gepner et al, 1966).

Another potential methodological issue is the participants used. The severity of ASD individuals’ symptomatology differs. High functioning and low functioning autistic children both perform differently on face recognition tasks (Joseph and Tanaka, 2003; Wilson et al, 2009). Older ASD individuals may develop atypical strategies and these compensatory strategies may have camouflaged the perception deficit (Klin et al, 2002; Teunisse and de Gelder, 2001). Results using a single 9mm slice or 7mm sagittal slices will affect findings made, so technical differences should be considered (Schultz et al, 2009; Pierce et al, 2001). These factors make it difficult to be conclusive. Findings should be analysed carefully and not generalised.


ASD individuals have impaired facial emotional recognition; they use abnormal strategies in processing faces, including featural processing and abnormal eye fixation which may be compensating for other impaired processing strategies but which may also mask processing deficit. Abnormalities in the brain can impair face processing abilities, although no single region can be solely responsible.

Finally, methodology should be considered when understanding the nature of the face processing impairment in autism.


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Title: The Nature of Face Processing Impairment in Autism