Introduction: Autism Spectrum Disorders (ASD) are defined by behavioral measures and characterized by deficits in 3 domains: social skills, communication, and repetitive and/or stereotypic behaviors (Minshew and Williams, 2007). Although none of the criteria used to diagnose ASD involve perceptual deficits, individuals with autism often demonstrate abnormal responses to stimulation of the skin. However, the literature about ASD and pain is limited, and hypo- and hypersensitivity to noxious stimuli have both been reported in autistic subjects (Bursch et al., 2004). This on-going study aims to assess the brain response of autistic subjects and neurotypic controls to non-noxious and noxious skin heating by means of functional magnetic resonance imaging (fMRI). Methods: Seven high-functional autistic adult subjects and four controls have participated in the study to date. Prior to imaging, heat pain thresholds were determined for each subject. For each fMRI run, a thermal stimulus was delivered six times to the dorsal calf of the subjects, using the protocol illustrated in Fig. 1. Four autistic subjects provided two runs of data, one for non-noxious (38ºC) and one for noxious heat (49ºC), while the remaining subjects provided twice this amount of data. The acquired data was processed using FMRIB software library (FSL) 4.1, and skin-heating and group-dependent effects were evaluated using fixed effects models. Results: The heat pain thresholds determined prior to the fMRI scan are described in Table 1.The noxious heat stimuli revealed evoked activity in primary and secondary somatosensory cortex (SI and SIl, respectively). A peculiar finding was that, for 4 autistic subjects, in most of SII, insula, and anterior cingulate cortex the time course of the hemodynamic response (MR percent signal change) was very different than all other subjects (3 autistic and all controls). The latter subjects’ evoked response was sustained (see Aut2 and control in Fig 2); whereas, the aberrant response for the 4 autistic subjects initially increased, then appeared to be suppressed before the stimulus was turned off (see Aut1 in Fig. 2). This difference in the time course was not observed in response to the non-noxious warm stimuli (38ºC), suggesting its specificity to painful stimulation. Conclusions: The presence of this aberrant cortical processing of noxious stimulation in 4 autistic individuals demands further investigation. For these subjects, the onset of heat pain appeared to activate a suppressive mechanism that obtunded the cortical neural response until the noxious stimulation was terminated. This did not appear to elevate the heat pain thresholds exhibited by the subjects.
|Original language||English (US)|
|Media of output||Poster|
|Place of Publication||San Francisco, CA. USA.|
|State||Published - 2009|