Abstract TMP27: Structural Network Dysfunction and Aberrant Structural-Functional Connectivity Coupling Correlate With Central Post-Stroke Pain of Thalamic Origin

Abstract

Introduction and Hypothesis: As the most frequent subtype of central post-stroke pain (CPSP), CPSP of thalamic origin can often be refractory to treatments and affect long-term prognosis of thalamic-stroke patients, while the mechanism remains unclear. We assumed that post-thalamic stroke CPSP might be a brain network disorder and aimed to investigate brain network alterations in post-thalamic stroke CPSP patients and explore whether these changes underlie clinical symptoms. Methods: A total of 92 participants were finally enrolled, of whom 62 were chronic thalamic stroke patients (26 had CPSP) and 30 were healthy controls. Using graph theory approaches, we compared the structural and functional brain network topological characteristics and structural-functional connectivity (SC-FC) couplings at multi-modular levels among the groups, and further explored their potential relationships with pain severity. Results: Distinct SC topological changes were found in CPSP patients, characterized as a higher clustering coefficient (Cp), global efficiency (Eg), local efficiency (Eloc), and lower characteristic path length (Lp) and normalized characteristic path length (Lambda) values than that in non-CPSP group. No significant differences were found in the FC network among the three groups. CPSP patients had significantly lower SC-FC couplings at the global and the structural Hub-modular levels. Further, we found significant and various correlations between pain severity and structural Lp, Eloc, global and Hub-modular SC-FC couplings. Results: These results indicated that thalamic stroke-induced distinct structural network dysfunction and SC-FC decoupling may be a novel neural mechanism for CPSP. It may provide new insights for future targeted neuromodulation therapies and individualized rehabilitative strategies in CPSP patients.