| 제목 |
Find the missing link between brain network analyses and the empirical therapeutic target in CPSP |
| 소속 |
Yonsei University College of Medicine, Department of Rehabilitation Medicine and Research Institute1 |
| 저자 |
Na Young Kim 1*†, Seung Been Hong1, Yong Wook Kim1 |
Objective
Central post-stroke pain (CPSP) is the neuropathic pain owing to cerebrovascular lesion at any level of the somatosensory pathway of the brain. However, many other brain regions seem to be implicated in the symptom. The underlying mechanisms of developing and improving CPSP remain poorly understood. In this study, we examined brain regions functionally connected to lesions causing CPSP. We also hypothesized that the strength of connectivity would be correlated with changes of brain metabolism and the empirical therapeutic target of non-invasive brain stimulation.
Method
For lesion mapping and metabolism analyses, 43 subjects with thalamic intracerebral hemorrhage were included. 20 of 43 patients were diagnosed with CPSP. Brain 18F-FDG PET-CT was performed and preprocessed using SPM 12. Left-sided lesions were flipped to all lesions on the same(right) side of the brain. All lesions were traced onto the patient’s CT, then transformed to atlas space using an affine warp. For connectivity analyses, we used a normative dataset of 1000 subjects from the Brain Genomics Superstruct Project on whom resting state functional MRI had been obtained. Three analyses were performed: First, we computed functional connectivity between each lesion and regions showing hypometabolism in CPSP group. Second, we calculated the functional connectivity between each lesion and all other brain voxels. The strength of connectivity between CPSP and non-pain group was statistically compared using FSL PALM. A voxel-based FWE-corrected p < 0.05 was considered statistically significant. A positive finding from lesion-network analyses was used as a mask to analyze the difference in metabolism. Third, we investigate the relationship among the lesion network map, the changes of brain metabolism and the empirical therapeutic target of non-invasive brain stimulation for neuropathic pain (hand knob area).
Result
The functional connectivity between each lesion and regions showing hypometabolism in CPSP group is significantly decreased in CPSP group (Figure 1B). Various brain regions including primary motor cortex showed significant positive correlation with lesions causing CPSP (Figure 2A). These areas had significantly reduced metabolism in CPSP group, compared to non-pain group (Figure 2B). Regions showing significant positive correlation with lesions causing CPSP overlap regions showing hypometabolism in CPSP group in the empirical therapeutic target of non-invasive brain stimulation for neuropathic pain (hand knob area, Figure 3).
Conclusion
Our results suggest that the brain connectivity of lesions causing CPSP is related to the change of brain metabolism. Our finding also matched the target of effective non-invasive brain stimulation, suggesting relevance to find an optimal treatment target for CPSP. These result lend insight into the causal neuroanatomical substrate of CPSP and may be useful to establish alternative treatments.
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(A) Regions where brain glucose metabolism is significantly decreased in patients with CPSP. (B) The functional connectivity between each lesion and regions shown in (A) is significantly decreased in CPSP group compared to non-pain group.
(A) Regions that are significantly more functionally connected to lesions causing CPSP. (B) Brain glucose metabolism is significantly decreased in these areas in CPSP group, compared to non-pain group.
Regions showing significant hypometabolism in CPSP group (blue) and regions showing significant positive correlation with lesions causing CPSP (red) overlap (purple) in the hand knob area (yellow-white), the empirical therapeutic target of non-invasive brain stimulation for neuropathic pain.
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