TY - GEN
T1 - Aberrant processing of pain in autism spectrum disorder: FMRI evidence for immediate suppression of pain networks in ASD
T2 - 45th Annual Meeting of the Society for Neuroscience
AU - Failla, Michelle D.
AU - Moana-Filho, E. J.
AU - Essick, G.
AU - Cascio, C.
N1 - NV - Pain Imaging and Perception
PY - 2015
Y1 - 2015
N2 - Individuals with autism spectrum disorders (ASD) exhibit aberrant behavioral responses to noxious stimulation compared to neurotypical controls, yet little is known regarding mechanisms of sensory processing in ASD. Thus, we investigated neural patterns of pain processing in ASD by applying a noxious heat stimulus (49°C) to the right calf during functional MRI. Subjects included 17 adults with ASD and 16 neurotypical controls. ADOS and ADI-R were administered to confirm ASD diagnosis and to estimate symptom severity. Sensory processing in daily life was assessed with the Sensory Profile Questionnaire. Blood oxygenation level-dependent (BOLD) signal in response to noxious heat was assessed with a whole brain and region of interest (ROI) approach. ROIs related to pain processing were selected based on previous literature: 5 mm spheres were created surrounding the peak voxel within the left primary somatosensory cortex (SI), left secondary somatosensory cortex (SII), and the left insular cortex in the control group. Mean activation was calculated for all voxels within the ROI. There were no differences in calf heat pain thresholds between the two groups (p=0.551). In whole brain analysis, individuals with ASD had hypoactivation in response to noxious heat, with controls exhibiting greater activation in cerebellum, thalamus, left putamen, left insula, and left premotor cortex compared to those with ASD. In ROI analysis, the ASD group had significantly less mean activation in the left SI (p=0.047), SII (p=0.004) and insula (p=0.002) ROIs. Additionally, BOLD response time series also differed between groups. The time course of BOLD responses in controls exhibited sustained activation during stimulus presentation, yet individuals with ASD had an early peak followed by an immediate undershoot. This pattern was consistent within left SI, left SII, and left insula ROIs. Left insula mean activation during noxious heat correlated with calf heat pain threshold (r=0.39, p=0.04) across groups. Mean activation in S1 correlated with restricted and repetitive behaviors (RRB) as measured on the ADOS (r=-0.54, p=0.04). A negative correlation between SI activation and RRB fits with hypotheses that RRB may be a compensatory behavior for sensory hypo-responsiveness in ASD. Importantly, activation patterns of an immediate peak followed by possible active suppression in areas involved in pain processing may indicate suppression of pain networks immediately following onset of a painful stimulus in ASD. Future studies are needed to characterize pain processing in ASD, including neural networks for pain and general sensory salience, as they relate to behavioral symptoms.
AB - Individuals with autism spectrum disorders (ASD) exhibit aberrant behavioral responses to noxious stimulation compared to neurotypical controls, yet little is known regarding mechanisms of sensory processing in ASD. Thus, we investigated neural patterns of pain processing in ASD by applying a noxious heat stimulus (49°C) to the right calf during functional MRI. Subjects included 17 adults with ASD and 16 neurotypical controls. ADOS and ADI-R were administered to confirm ASD diagnosis and to estimate symptom severity. Sensory processing in daily life was assessed with the Sensory Profile Questionnaire. Blood oxygenation level-dependent (BOLD) signal in response to noxious heat was assessed with a whole brain and region of interest (ROI) approach. ROIs related to pain processing were selected based on previous literature: 5 mm spheres were created surrounding the peak voxel within the left primary somatosensory cortex (SI), left secondary somatosensory cortex (SII), and the left insular cortex in the control group. Mean activation was calculated for all voxels within the ROI. There were no differences in calf heat pain thresholds between the two groups (p=0.551). In whole brain analysis, individuals with ASD had hypoactivation in response to noxious heat, with controls exhibiting greater activation in cerebellum, thalamus, left putamen, left insula, and left premotor cortex compared to those with ASD. In ROI analysis, the ASD group had significantly less mean activation in the left SI (p=0.047), SII (p=0.004) and insula (p=0.002) ROIs. Additionally, BOLD response time series also differed between groups. The time course of BOLD responses in controls exhibited sustained activation during stimulus presentation, yet individuals with ASD had an early peak followed by an immediate undershoot. This pattern was consistent within left SI, left SII, and left insula ROIs. Left insula mean activation during noxious heat correlated with calf heat pain threshold (r=0.39, p=0.04) across groups. Mean activation in S1 correlated with restricted and repetitive behaviors (RRB) as measured on the ADOS (r=-0.54, p=0.04). A negative correlation between SI activation and RRB fits with hypotheses that RRB may be a compensatory behavior for sensory hypo-responsiveness in ASD. Importantly, activation patterns of an immediate peak followed by possible active suppression in areas involved in pain processing may indicate suppression of pain networks immediately following onset of a painful stimulus in ASD. Future studies are needed to characterize pain processing in ASD, including neural networks for pain and general sensory salience, as they relate to behavioral symptoms.
M3 - Other contribution
CY - Chicago, IL, USA
ER -