8 research outputs found
HIGH Pain-related percent signal change in representative brain regions across three groups in both run 1 and run 2.
<p>Bars represent mean ± SEM.</p
HIGH-pain related brain activations, overlaid on the MNI152 standard brain.
<p>HIGH-pain related brain activations, overlaid on the MNI152 standard brain.</p
Brain structures exhibiting a significant genotype effect for HIGH pain in the second run.
<p>For descriptive purposes, the significant cluster was partitioned in subclusters by further applying a voxelwise threshold of z = 2.3. Subclusters with a N<sub>voxels</sub>≥20 are described.</p><p>Abbreviations: cx = cortex, g. = gyrus, HF = hippocampal formation, PAG = periaqueductal gray.</p
Descriptive statistics for the three genotype groups studied.
<p>Descriptive statistics for the three genotype groups studied.</p
Average expectancy scores in all original groups, across all ERS assessment points
<p>. Means ± SEM are shown for N = 35. Time 1 occurs after verbal suggestion but prior to the conditioning phase in the conditioning groups, and prior to the matched variable pain phase in the no- conditioning group. Time 2 occurs immediately after the conditioning/variable pain phase, and Time 3 occurs after testing.</p
Average Pain Ratings for all Groups.
<p>Mean (SD) ratings of pain intensity and unpleasantness for each audio type before and after the conditioning/variable pain phase for both cohorts. Note that all pre- pain stimuli occurred in silence (i.e. pre- ratings for music and sound are given for the corresponding skin spot of stimulation). One outlier subject has been removed from the original music conditioning group (as noted in text).</p><p>Average Pain Ratings for all Groups.</p
Average pain intensity and unpleasantness changes, all original groups.
<p>N = 35. Shown here are pre (baseline) minus post (testing) pain difference scores (mean ± SEM); positive values indicate analgesia. Panel A displays Pain Intensity, panel B displays Pain Unpleasantness.</p