Abstract
Background: Spinal cord injury (SCI) and its accompanying changes of brain structure and function have been widely studied and reviewed. Debilitating chronic neuropathic pain (NP) is reported in 53% of SCI patients, and brain changes have been shown to be involved with the presence of this secondary complication. However, there is yet a synthesis of current studies that investigated brain structure, resting connectivity, and metabolite changes that accompanies this condition.Methods: In this review, a systematic search was performed using Medical Subject Headings heading search terms in PubMed and SCOPUS to gather the appropriate published studies. Neuroimaging studies that investigated supraspinal structural, resting-state connectivity, and metabolite changes in SCI subjects with NP were included. To this end, voxel-based morphometry, diffusion tensor imaging, resting-state functional MRI, magnetic resonance spectroscopy, and PET studies were summarized and reviewed. Further inclusion and exclusion criteria allowed delineation of appropriate studies that included SCI subgroups with and without NP.Results: A total of 12 studies were eligible for qualitative synthesis. Overall, current studies that investigated NP-associated changes within the SCI cohort show primarily metabolite concentration alterations in sensory-pain processing regions, alongside bidirectional changes of brain structure. Moreover, in comparison to healthy controls, there remains limited evidence of structural and connectivity changes but a range of alterations in metabolite concentrations in SCI subjects with NP.Conclusions: There is some evidence suggesting that the magnitude and presence of NP following SCI results in both adaptive and maladaptive structural plasticity of sensorimotor regions, alongside altered metabolism of brain areas involved with descending pain modulation, pain perception (i.e., anterior cingulate cortex) and sensory integration (i.e., thalamus). However, based on the fact that only a few studies investigated structural and glucose metabolic changes in chronic SCI subjects with NP, the underlying mechanisms that accompany this condition remains to be further elucidated. Future cross-sectional or longitudinal studies that aim to disentangle NP related to SCI may benefit from stricter constraints in subject cohorts, controlled subgroups, improved pain phenotyping, and implementation of multimodal approaches to discover sensitive biomarkers that profile pain and optimize treatment in SCI subjects with NP.
Highlights
RationaleSpinal cord injury (SCI) has severe consequences for the individual, commonly causing distinct motor and sensory deficits below the level of lesion, attributed to the damage of the corresponding efferent and afferent neural pathways
There is some evidence suggesting that the magnitude and presence of neuropathic pain (NP) following SCI results in both adaptive and maladaptive structural plasticity of sensorimotor regions, alongside altered metabolism of brain areas involved with descending pain modulation, pain perception and sensory integration
Future cross-sectional or longitudinal studies that aim to disentangle NP related to SCI may benefit from stricter constraints in subject cohorts, controlled subgroups, improved pain phenotyping, and implementation of multimodal approaches to discover sensitive biomarkers that profile pain and optimize treatment in SCI subjects with NP
Summary
RationaleSpinal cord injury (SCI) has severe consequences for the individual, commonly causing distinct motor and sensory deficits below the level of lesion, attributed to the damage of the corresponding efferent and afferent neural pathways. The pathophysiology of NP involves a complex interaction of neuronal changes, inflammation, glial–neuron interactions, supraspinal and spinal sensitization, and alterations in endogenous pain modulation [see reviews: [5,6,7,8,9]] Consequences of these mechanistic changes are chronic alterations of nociceptive pathways and pain processing regions within the central nervous system, i.e., spinal cord, brainstem, and the brain. Gray matter volume in chronic low back pain [16] and connectivity changes in fibromyalgia subjects [17], respectively, were shown to be reversed concurrently following pain treatment [16, 17] Together, these studies suggest that changes of structural and functional plasticity within the brain accompany those who experience chronic pain [see reviews: [18, 19]]. There is yet a synthesis of current studies that investigated brain structure, resting connectivity, and metabolite changes that accompanies this condition
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