Research Data for paper: Evidence for peripheral neuroinflammation after acute whiplash

<b>Data for paper published in Pain. March 2025.</b>Data is arranged by figure, with each Excel tab corresponding to a different figure. It includes MRI T2-signal ratios for the C5-C8 roots of the brachial plexus (Figure 3), C5-C8 dorsal root ganglia (Figure 4), and the median nerve at the carpal tunnel (Figure 5) in whiplash-associated disorder grade 2 (WADII) participants and healthy control subjects. It also includes measures of heightened nerve trunk mechanosensitivity (Figure 6), blood serum concentrations of inflammatory mediators (Figure 7), and dermatomal changes and quantitative sensory testing (Figure 8) in the same individuals. Data for Figure 9 is separated into WADII participants with and without heightened nerve mechanosensitivity.<b>Abstract</b>Whiplash injury is associated with high socioeconomic costs and poor prognosis. Most people are classified as having whiplash-associated disorder grade II (WADII), with neck complaints and musculoskeletal signs, in the absence of frank neurological signs. However, evidence suggests that there is a subgroup with underlying nerve involvement in WADII, such as peripheral neuroinflammation. This study aimed to investigate the presence of neuroinflammation in acute WADII using T2-weighted magnetic resonance imaging of the brachial plexus, dorsal root ganglia and median nerve, and clinical surrogates of neuroinflammation: heightened nerve mechanosensitivity (HNM), raised serum inflammatory mediators, and somatosensory hyperalgesia. One hundred twenty-two WADII participants within 4 weeks of whiplash and 43 healthy controls (HCs) were recruited. Magnetic resonance imaging T2 signal ratio was increased in the C5 root of the brachial plexus and the C5-C8 dorsal root ganglia in WADII participants compared with HCs but not in the distal median nerve trunk. Fifty-five percent of WADII participants had signs of HNM. Inflammatory mediators were also raised compared with HCs, and 47% of WADII participants had somatosensory changes on quantitative sensory testing. In those WADII individuals with HNM, there was hyperalgesia to cold and pressure and an increased proportion of neuropathic pain. Many people with WADII had multiple indicators of neuroinflammation. Overall, our results present a complex phenotypic profile for acute WADII and provide evidence suggestive of peripheral neuroinflammation in a subgroup of individuals. The results suggest that there is a need to reconsider the management of people with WADII.