Abstract Body: Objectives: To investigate the correlation between iron deposition changes in the lesioned thalamic nuclei and the presence and severity of central post-stroke pain (CPSP) after thalamic infarction using quantitative susceptibility mapping (QSM) technique.

Methods: We consecutively enrolled patients with unilateral chronic thalamic infarction with radiological examination conformed . Detailed and multidimensional pain characteristics measured as follows: Douleur Neuropathique 4 (DN4) questionnaire for validation of neuropathic pain diagnosis, Short-Form McGill Pain Questionnaire (SF-MPQ) for comprehensive representation of pain experience, Present Pain Intensity index (PPI) for current pain severity upon examination, and Visual Analogue Scale (VAS) for overall pain feeling since symptom onset. Age- and sex-matched stoke-free healthy controls were recruited simultaneously. High resolution structural image 3D-T1 BRAVO and QSM sequences were obtained with 3.0T MRI. The voxel-lesion-symptom-mapping (VLSM) was used to determine lesioned thalamic nuclei at the high risk for CPSP. Then ipsilateral QSM values of the whole thalamus and subregions were compared with contralateral side and healthy controls. Partial correlation analysis were performed to explore the relationship between QSM value and pain severity.

Results: Finally, 28 CPSP patients, 33 non-CPSP patients and 55 healthy controls were included in the study. Our results indicated no significant difference in overall QSM values of the whole thalamus among the groups. The VLSM results showed lesion involving ventral posterolateral nuclei (VPL) was highly orrelaed with occurance of CPSP (p_FWE=0.0092.). The QSM values of each subnuclei in the thalamus ipsilateral to infarction were lower compared with the contralateral side and healthy controls (p<0.001). Nonetheless, the QSM values in ipsilateral VPL were higher in CPSP patients campared with non-CPSP patients(p=0.003). Notably, the QSM values in the ipsilateral VPL were significantly correlated to pain severity (all p<0.05).

Conclusions: The study showed that altered iron deposition in the VPL nuclei is associated with the occurrence and severity of CPSP following thalamic infarction. Aberrant iron deposition after ischemic thalamus stroke may play an important role in the pathogenesis of CPSP.

Key words: Thalamic infarction; Central post-stoke pain; Iron deposition; VLSM; Quantitative susceptibility mapping