Abstract
Neuropathic pain has been found to be related to profound reorganization in the function and structure of the brain. We previously demonstrated changes in local brain activity and functional/metabolic connectivity among selected brain regions by using neuroimaging methods. The present study further investigated large-scale metabolic brain network changes in 32 Sprague–Dawley rats with right brachial plexus avulsion injury (BPAI). Graph theory was applied in the analysis of 2-deoxy-2-[18F] fluoro-D-glucose (18F-FDG) PET images. Inter-subject metabolic networks were constructed by calculating correlation coefficients. Global and nodal network properties were calculated and comparisons between pre- and post-BPAI (7 days) status were conducted. The global network properties (including global efficiency, local efficiency and small-world index) and nodal betweenness centrality did not significantly change for all selected sparsity thresholds following BPAI (p > 0.05). As for nodal network properties, both nodal degree and nodal efficiency measures significantly increased in the left caudate putamen, left medial prefrontal cortex, and right caudate putamen (p < 0.001). The right entorhinal cortex showed a different nodal degree (p < 0.05) but not nodal efficiency. These four regions were selected for seed-based metabolic connectivity analysis. Strengthened connectivity was found among these seeds and distributed brain regions including sensorimotor area, cognitive area, and limbic system, etc. (p < 0.05). Our results indicated that the brain had the resilience to compensate for BPAI-induced neuropathic pain. However, the importance of bilateral caudate putamen, left medial prefrontal cortex, and right entorhinal cortex in the network was strengthened, as well as most of their connections with distributed brain regions.
Highlights
Brachial plexus avulsion injury (BPAI) is a serious peripheral nerve injury causing partial or total loss of motor, sensory, and autonomic functions [1]
brachial plexus avulsion injury (BPAI)-induced neuropathic pain is a specific type of deafferentation pain, the mechanism of which may be distinct from acute pain [29]. 2-deoxy-2-[18F] fluoro-D-glucose (18F-FDG) is a widely used marker for detecting glucose metabolic rates in the brain
Our previous study has revealed a specific pattern of brain metabolic changes following unilateral BPAI
Summary
Brachial plexus avulsion injury (BPAI) is a serious peripheral nerve injury causing partial or total loss of motor, sensory, and autonomic functions [1]. We have previously revealed changed regional brain activities following BPAI-induced neuropathic pain in rats by 18F-FDG PET images [14,15,16]. Studies showed that chronic pain was related to reorganization over the whole brain and connectivity among distributed brain regions [18,19,20]. Graph theory was applied for the inter-subject metabolic network analysis in SD rats with unilateral BPAI. Graph theoretical approaches provided a method for analyzing functional correlations among all the brain regions and the whole brain network efficiency. It allowed us to explore the entire assembling of the network Both global and local topologic features were employed to quantify changes following BPAI. We provided a more global view of information flow in the brain by longitudinally comparing pre- and post-BPAI status which would be inapplicable in human researches
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