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Structural network dysfunction and aberrant SC-FC coupling correlate with central post-stroke pain of thalamic

Chen Ye¹, Biqiu Tang², Junfeng Liu¹

¹Department of Neurology, West China Hospital, Sichuan University, Chengdu, China; Center of Cerebrovascular Diseases, West China Hospital, Sichuan University, Chengdu, China.

The Journal of Pain

|June 3, 2026

Summary

Central post-stroke pain (CPSP) after thalamic stroke shows distinct structural brain network changes and impaired structure-function coupling, correlating with pain severity. These findings offer new insights into treatment-resistant neuropathic pain.

Keywords:

Brain network topology Central post-stroke pain Graph theory Structural-functional connectivity coupling Thalamic stroke

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Area of Science:

Neuroscience
Neurology
Medical Imaging

Background:

Central post-stroke pain (CPSP) of thalamic origin is a frequent and treatment-resistant complication of thalamic stroke.
The underlying neural mechanisms of thalamic CPSP remain unclear, impacting patient prognosis.

Purpose of the Study:

To investigate brain network alterations in patients with CPSP following thalamic stroke.
To explore the relationship between these network changes and clinical pain symptoms.

Main Methods:

Observational study including 26 CPSP patients and 30 healthy controls (HCs).
Structural connectivity (SC) using diffusion spectrum imaging (DSI) and functional connectivity (FC) using resting-state fMRI.
Graph theory analysis of network topology and structural-functional connectivity (SC-FC) couplings.

Main Results:

CPSP patients exhibited altered SC topology (higher clustering coefficient, global/local efficiency; lower characteristic path length).
Significantly reduced SC-FC couplings were observed globally and at the structural Hub-modular level in CPSP patients.
Pain severity correlated with structural network metrics (path length, local efficiency) and SC-FC couplings.

Conclusions:

Thalamic stroke-induced structural network dysfunction and SC-FC decoupling represent a potential neural mechanism for CPSP.
Findings suggest network-based biomarkers and inform targeted neuromodulation and rehabilitation strategies for CPSP.