Pain in Autism Spectrum Disorder.

Evidence to date of altered pain processing in Autism Spectrum Disorder (ASD) is largely reliant on case evidence and observations. The evidence suggests a hypo sensitivity to pain which is emphasised by the inclusion of this as a criterion in the DSM-5. However, this evidence has also yielded contradictory findings on hypersensitivity to pain and suffers with methodological flaws. The aim of this thesis was to experimentally investigate pain in ASD using robust psychophysical pain induction methods to expand our understanding of where in the pain process differences occurred that could account for the altered behaviours observed in the anecdotal evidence. Experiments 1 and 2 in Chapter 2 examined the processing of pain in people with autistic traits and those clinically diagnosed with ASD, using a comprehensive psychophysical test battery. Detection and pain thresholds were obtained for thermal and mechanical stimuli including vibration and pressure. Additional tests included a cold pressor, (Experiments 1 and 2). No consistent Quantitative Sensory Testing (QST) pattern of difference in relation to autistic trait severity or clinically diagnosed ASD, was observed. The Mechanical Detection Threshold exceeded that of a normal distribution of healthy individuals, as established by The German Research Network on Neuropathic Pain normative values (Backonja et al., 2013; Rolke, Baron, et al., 2006) for both autistic traits (Experiment 1) and clinically diagnosed ASD (Experiment 2) and differed to controls. Dynamic mechanical allodynia and paradoxical heat sensation were reported in a number of those with high autistic trait severity (Experiment 1) or clinically diagnosed ASD (Experiment 2), which does not typically occur in individuals otherwise considered healthy. Notably, there were a larger number of QST scores that fell outside the normal distribution (n = 48) in the clinically diagnosed ASD group (Experiment 2). A greater number of autistic individuals compared to controls, were found to show atypical patterns of pain response (n = 10). Indicating that there is a heterogeneity of pain response in ASD and that there may be subtypes with different pain responses. Experiment 3, Chapter 3, utilised a volitional joystick task to determine if there was a greater attenuation of pain avoidance behaviours by a valued reward in ASD. Individuals clinically diagnosed with ASD and controls, moved a joystick towards a target that resulted in the delivery of a nociceptive stimulus, which on 50% of occasions was paired with a reward. During choice-trials participants opted to make a safe movement (i.e., an opposing movement to the movement paired with pain in which there is no pain stimulus) or to make a movement towards a monetary reward whilst receiving a nociceptive stimulus. Reaction times were obtained for movements, as well as the number of choice trails. The ASD group were no different to controls at completing a painful yet rewarding movement and they also chose to negate the pain to receive a reward to the same degree as controls, suggesting that the ASD group’s fear avoidance and pain motivation processing is no different to controls. Experiment 4, Chapter 4, utilised the Facial Action Coding System and the Non-Communicating Adults Pain Checklist to code facial and behavioural responses to pain. The aim was to determine if the communication of pain in ASD differed to controls, or if there was a set of ASD specific pain behaviours. Participants were videoed during a cold pressor task and thermal heat stimuli (6 warm but not painful, 6 moderately painful, and 6 very painful). Painful facial expressions for cold and hot thermal stimuli were similar between the ASD group and controls. The ASD group showed expressions in the lower oblique cluster (comprised of muscles that pull the skin of the face upward at an oblique angle) more frequently. These expressions were also observed at a greater intensity in comparison to controls. In particular, Nasolabial Furrow Deepener and Lip Corner Puller occurred more frequently and at a greater intensity in the ASD group compared to controls. Controls were also more likely to show a neutral expression compared to the ASD group, indicating a masking mechanism is being employed by controls in the social context. It is possible that the social contagion or mimicry of expressions is focussed on the lower facial regions and therefore pain expression develops more so in this region for autistic individuals. Taken together, the findings from this thesis point towards greater intra-individual differences in the ASD group compared to controls, showing that there may be sub-groups in the autistic population who have altered pain experiences, or for whom pain expression might be more nuanced. Importantly, the results presented here do not support the DSM-5’s statement that an absence of the ability to feel pain is a defining feature of ASD