This observational analysis reveals altered brain function in neuropathic pain due to carpal tunnel syndrome, suggesting new insights into management strategies.
Abnormal central pain sensitization is a possible explanation for persistent neuropathic pain after carpal release. However, its exact mechanism remains unclear. This study examined the cortical patterns in chronic neuropathic pain secondary to recurring median neuropathy. Forty-nine patients with recurrent painful carpal tunnel syndrome (CTS) and 22 age- and sex-matched controls were enrolled. Multimodal MRI, including structural, blood oxygenation level-dependent (BOLD), and 3D pseudo-continuous arterial spin labeling (pCASL) were employed. Cerebral blood flow (CBF) and seed-based functional connectivity (FC) were analyzed. Global and regional CBF in several brain regions in the recurring CTS group decreased. Significant between-group differences were found in CBF maps involving the frontal gyrus and insula, which exhibited an inverse correlation with central sensitization scores. Increased brain connectivity was noted in recurrent CTS patients and was negatively correlated with symptom severity. Individuals with chronic neuropathic pain secondary to recurrent median nerve entrapment manifested maladaptive brain networks in cortical regions involving sensory, cognitive, and affective processing. Our findings may highlight new avenues for cortical biomarkers and potential mechanisms underlying central sensitization in persistent pain after peripheral neuropathy, which may facilitate innovative targeted management strategies for those who respond poorly to concurrent treatment regimes.
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Feng et al. (2025) studied this question.
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