Persistent pain is experienced by over 50% of people who sustain a traumatic brain injury (TBI) and over 30% experience significant pain as early as six weeks after injury. Although neuropathic pain is a common consequence after CNS injuries, little attention has been given to neuropathic pain symptoms after TBI. MRS studies in subjects with TBI show decreased brain concentrations of <i>N</i>-acetylaspartate (NAA), a marker of neuronal density and viability. Although decreased brain NAA has been associated with neuropathic pain associated with spinal cord injury (SCI) and diabetes, this relationship has not been examined after TBI. The primary purpose of this study was to test the hypothesis that lower NAA concentrations in brain areas involved in pain perception and modulation would be associated with greater severity of neuropathic pain symptoms. Participants with TBI underwent volumetric MR spectroscopy, pain and psychosocial interviews. Cluster analysis of the Neuropathic Pain Symptom Inventory subscores resulted in two TBI subgroups: The Moderate Neuropathic Pain (n=17; 37.8%), with significantly (p=0.038) lower insular NAA than the Low or no Neuropathic Pain group (n=28; 62.2%), or age- and sex-matched controls (n=45; p<0.001). A hierarchical linear regression analysis controlling for age, sex, and time post-TBI showed that pain severity was significantly (F=11.0; p<0.001) predicted by a combination of lower insular NAA/Cr (p<0.001), lower right insular gray matter fractional volume (p<0.001), female sex (p=0.005), and older age (p=0.039). These findings suggest that neuronal dysfunction in brain areas involved in pain processing is associated with pain after TBI.
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 24 January 2019.
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