Key result
Subjects with neuropathic pain after spinal cord injury exhibited intact pain inhibition comparable to healthy controls, but demonstrated an inverse relationship between conditioned pain modulation efficiency and intrinsic connectivity of supraspinal regions.
Why the study?
Differences in conditioned pain modulation efficiency in relation to resting-state functional connectivity between individuals with neuropathic pain after spinal cord injury and healthy controls were unexplored.
Cross-Sectional (n=26)
No
Subjects with neuropathic pain after spinal cord injury demonstrate intact endogenous pain inhibition, but exhibit altered intrinsic brain connectivity relationships with pain modulation efficiency compared to healthy controls.
Answers are grounded in this paper and cite their sources.
Intact pain inhibition in SCI neuropathic pain cautions against assuming endogenous deficits; leaves open supraspinal connectivity as a hypothesis-generating biomarker.
Endogenous pain modulation in humans is frequently investigated with conditioned pain modulation (CPM) and deficient pain inhibition is a proposed mechanism that contributes to neuropathic pain (NP) after spinal cord injury (SCI). Recent studies have combined CPM testing and neuroimaging to reveal neural correlates of CPM efficiency in chronic pain. This study investigated the unexplored differences in CPM efficiency in relation to resting-state functional connectivity (rsFC) between 13 SCI-NP subjects and 13 age- and sex-matched healthy controls (HC). Psychophysical readouts were analyzed to determine CPM efficiency within and between cohorts. To explore group differences of rsFC in relation to CPM efficiency, seed-to-voxel rsFC analyses were performed within pain modulatory regions, e.g., ventrolateral periaqueductal gray (vlPAG) and amygdala. Overall, pain inhibition was not deficient in SCI-NP subjects and was greater in those with more intense NP. In addition, in SCI-NP greater pain inhibition was associated with weaker rsFC between the vlPAG and amygdala with the visual and frontal cortex, respectively, but with stronger rsFC in HC. Taken together, SCI-NP subjects present with intact pain inhibition, but can be differentiated from HC by an inverse relationship between CPM efficiency and intrinsic connectivity of supraspinal regions. Specifically, abnormal neural plasticity could be related to weaker pain modulatory function in SCI-related NP.
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Huynh et al. (2022) conducted a cross-sectional in Neuropathic pain after spinal cord injury (n=26). Neuropathic pain after spinal cord injury vs. Healthy controls was evaluated on Sham-corrected conditioned pain modulation (CPM) effect (p=0.283). Subjects with neuropathic pain after spinal cord injury exhibited intact pain inhibition comparable to healthy controls, but demonstrated an inverse relationship between conditioned pain modulation efficiency and intrinsic connectivity of supraspinal regions.
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