31476
PAIN Peception in Adults with High Functioning Autism Spectrum Disorder: Subjective Vs. Objective Measures
Pain research in autism spectrum disorder (ASD) is scarce, with limited methodology, resulting in a paucity of knowledge comprising conflicting findings on the pain sensitivity profile of individuals with ASD. Overall neural hyper-responsiveness that underpins the ASD pathology is one of the manifestations of the excitatory/inhibitory (E/I) imbalance, which may also account for pain hyper-sensitivity. Yet, difficulties in communicating socially appropriate responses to pain may cause underestimated judgment of pain by selves or others, and indeed pain hypo-sensitivity is suggested to characterize individuals with ASD.
Objectives:
To explore the pain sensitivity profile in individuals with ASD using both subjective (i.e. self-report) and objective (i.e. cortical event-related potentials) responses to experimental pain stimuli. Specifically, to investigate whether the two measures differ (i) in people with ASD compared to typically developed controls, and (ii) in the within group correlations between subjective and objective measures.
Methods:
This study included 24 high functioning individuals diagnosed with ASD based on the ADOS-2, and 24 healthy controls (CTRL), aged mean (SD): 28 (11); 26 (4); (p>0.05), respectively, with verbal performance and full-scale estimate of 80 and above on the IQ Wechsler Abbreviated Scale of Intelligence® - Second Edition (WASI®-II). Psychophysical testing comprised of phasic noxious heat stimuli that were delivered to the dominant volar forearm (572.5mm2 thermode, PATHWAY system, MEDOC, Ramat Yishai, Israel) at 49°C, and 52°C, using a stimuli train of 20 repetitions (ISIs of 8 to 12 sec.) for each intensity. Pain ratings were obtained after each stimulus using a 0-100 numerical pain scale (NPS). Contact heat-evoked potentials (CHEPs) were recorded simultaneously and the N2 and P2 amplitudes, considered an objective tool for assessment of central pain transmitting pathways and pain quantification, was extracted for each participant.
Results:
Increase pain ratings in-line with temperature rise were found in both groups. Groups differed across the 2 temperature trains of stimuli. The ASD group reported lower NPS ratings in comparison to controls [CTRL vs. ASD: Mean (SD); 49°C: 37.59 (22.25) vs. 26.15 (18.98); p=0.05 , 52°C: 52.88 (25.63) vs. 34.97 (23.29); p=0.01]. In contrast, greater N2-P2 amplitude (µV), at Cz location in response to 52°C stimuli, was found in ASD vs. the control group [CTRL vs. ASD; Mean (SD); 29.98 (16.93) vs. 40.24 (14.15); p=0.01]. Moreover, an interaction was found between group X pain ratings on P2 amplitude (p=0.03); while controls demonstrated a significant association between pain ratings and P2 amplitude (r= 0.66; p=0.05), the ASD group did not (r=0.20; p=0.48).
Conclusions:
This is the first study exploring self-report pain ratings and evoked potentials during experimental heat pain stimuli. Our exploratory findings point at a mismatch between the individual’s subjective pain reports and the neurophysiological responses. While behaviorally individuals with ASD demonstrate pain hypo-sensitivity, the brain responses imply neural hyper-responsiveness. This finding confirms our hypothesis that E/I imbalance may also shape the pain processing in ASD.