TY - GEN
T1 - Temporally Distinct Neural Responses to Pain in ASD: Evidence for Altered Cognitive Pain Modulation and Relationships to Self-Injurious Behaviors
T2 - 2016 International Meeting for Autism Research
AU - Failla, Michelle D.
AU - Moana-Filho, E. J.
AU - Essick, G.
AU - Baranek, G. T.
AU - Rogers, B.
AU - Cascio, C. J.
N1 - NV - Perspectives on Pain in ASD: Perception, Physiology, and Behavior
PY - 2016
Y1 - 2016
N2 - Background: There is a prevalent assumption that individuals with autism spectrum disorders (ASD) are less sensitive to pain. Yet, this assertion is not well supported by empirical evidence. Importantly, communication deficits make assessing pain through verbal reports particularly challenging in ASD. Objective markers of pain, such as neural responses obtained with neuroimaging, have been suggested as a means of clarifying the pain experience in vulnerable populations. Previous work has identified a neural pain signature (somatosensory cortices, insula, anterior cingulate) using functional magnetic resonance imaging (fMRI) that differentiates pain from innocuous stimulation. Objectives: The goal of this study was to determine whether the temporal or spatial properties of the neural pain signature differ in individuals with ASD, and if so, what possible modulators outside the identified neural pain signature contribute to these differences. We also sought to explore whether differences in the signature relate to self-injurious behaviors that are thought to arise from aberrant pain processing in ASD. Methods: Participants included 16 adults with ASD and 16 adults without ASD in a typical comparison group. Self-injurious behaviors were assessed with the Repetitive Behavior Scale-Revised; participants with ASD were categorized by presence or absence of self-injurious behaviors. Neural response to sustained heat pain was assessed with fMRI using a block design. For each trial, heat was applied to the right lateral calf for 21 seconds (15 seconds at target temperature, 3 second ramp up/down) followed by 39 seconds rest period. Results: The two groups had similar pain ratings and pain thresholds, in addition to similar neural pain signature responses during acute pain. Yet, there was a highly exaggerated suppression of the neural pain signature in ASD during intermediate and late phases of sustained pain (Z>2.3, p
AB - Background: There is a prevalent assumption that individuals with autism spectrum disorders (ASD) are less sensitive to pain. Yet, this assertion is not well supported by empirical evidence. Importantly, communication deficits make assessing pain through verbal reports particularly challenging in ASD. Objective markers of pain, such as neural responses obtained with neuroimaging, have been suggested as a means of clarifying the pain experience in vulnerable populations. Previous work has identified a neural pain signature (somatosensory cortices, insula, anterior cingulate) using functional magnetic resonance imaging (fMRI) that differentiates pain from innocuous stimulation. Objectives: The goal of this study was to determine whether the temporal or spatial properties of the neural pain signature differ in individuals with ASD, and if so, what possible modulators outside the identified neural pain signature contribute to these differences. We also sought to explore whether differences in the signature relate to self-injurious behaviors that are thought to arise from aberrant pain processing in ASD. Methods: Participants included 16 adults with ASD and 16 adults without ASD in a typical comparison group. Self-injurious behaviors were assessed with the Repetitive Behavior Scale-Revised; participants with ASD were categorized by presence or absence of self-injurious behaviors. Neural response to sustained heat pain was assessed with fMRI using a block design. For each trial, heat was applied to the right lateral calf for 21 seconds (15 seconds at target temperature, 3 second ramp up/down) followed by 39 seconds rest period. Results: The two groups had similar pain ratings and pain thresholds, in addition to similar neural pain signature responses during acute pain. Yet, there was a highly exaggerated suppression of the neural pain signature in ASD during intermediate and late phases of sustained pain (Z>2.3, p
M3 - Other contribution
CY - Baltimore, MD, USA.
ER -