This study determined the stability of self-reported clinical pain characteristics and pain-induced interference with sleep and daily activities in people with spinal cord injury. The study followed up a previous survey that identified clinical pain patterns (i.e., neuropathic pain below the level of injury; upper-limb pain in tetraplegia; and severe, persistent pain). A confirmatory factor analysis (CFA) of the present study's data confirmed the previously observed pain patterns. The CFA also confirmed positive correlations between the surveys on individual pain characteristics (i.e., number of pain locations [r = 0.63, p < 0.001], number of descriptors [r = 0.61, p < 0.001], pain intensity [r = 0.68, p < 0.001], and temporal aspects [r = 0.47, p < 0.001]). Despite an overall stable clinical picture of pain, "aching" pain (p < 0.001) and sleep interference caused by pain (p < 0.001) significantly increased over time.

Persistent pain is a common reason for reduced quality of life after a spinal cord injury (SCI). Biomarkers of neuropathic pain may facilitate translational research and the understanding of underlying mechanisms. Research suggests that pain and affective distress are anatomically and functionally integrated in the anterior cingulate cortex and can modulate sensory and affective aspects of pain. We hypothesized that severe neuropathic pain with a significant psychosocial impact would be associated with metabolite concentrations (obtained by magnetic resonance spectroscopy) in the anterior cingulate cortex, indicating neuronal and/or glial dysfunction. Participants with SCI and severe, high-impact neuropathic pain (SCI-HPI; n = 16), SCI and moderate, low-impact neuropathic pain (SCI-LPI; n = 24), SCI without neuropathic pain (SCI-noNP; n = 14), and able-bodied, pain-free control subjects (A-B; n = 22) underwent a 3-T magnetic resonance imaging brain scan. Analyses revealed that the SCI-HPI group had significantly higher levels of myoinositol (Ins) (P < .000), creatine (P = .007), and choline (P = .014), and significantly lower levels of N-acetyl aspartate/Ins (P = .024) and glutamate-glutamine (Glx)/Ins (P = .003) ratios than the SCI-LPI group. The lower Glx/Ins ratio significantly discriminated between SCI-HPI and the A-B (P = .006) and SCI-noNP (P = .026) groups, displayed excellent test-retest reliability, and was significantly related to greater pain severity, interference, and affective distress. This suggests that the combination of lower glutamatergic metabolism and proliferation of glia and glial activation are underlying mechanisms contributing to the maintenance of severe neuropathic pain with significant psychosocial impact in chronic SCI. These findings indicate that the Glx/Ins ratio may be a useful biomarker for severe SCI-related neuropathic pain with significant psychosocial impact.

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