The presence and prognosis of nerve pathology following whiplash injury: a prospective cohort study.

Whiplash-associated disorders (WADs) affect 20-50 million individuals globally each year, with ≤50% developing persistent pain. WAD grade II (WADII) is the most common type and is characterized by neck symptoms and musculoskeletal signs without apparent nerve injury on routine diagnostic testing. However, emerging evidence suggests that nerve pathology might be present in some people with WADII. This longitudinal cohort study aimed to investigate comprehensively the presence, temporal patterns and prognostic value of nerve pathology and neuropathic pain in acute WADII. A prospective longitudinal cohort study was conducted with 129 acute participants with WADII (median age 36.0 years, 58% female) and 36 healthy controls (median age 39.0 years, 61% female). Participants with WADII were recruited within 4 weeks of injury from local emergency departments. Data collection included bedside neurological assessments, quantitative sensory testing, intraepidermal nerve fibre density and serum neurofilament light chain concentrations. Follow-up assessments were conducted 6 months after injury. Signs of neuropathic pain were present in 65% (84/129) acutely and persisted in 32% (21/66) 6 months post-injury. Bedside neurological assessment revealed that somatosensory loss-of-function was present in 54% (70/129) acutely, reducing to 25% (17/67) 6 months post-injury. Quantitative sensory testing demonstrated significantly reduced cold, warm, thermal sensory limen, mechanical and vibration detection thresholds in acute WADII compared with controls (d > 0.47). Acute loss-of-function in at least one quantitative sensory testing parameter was present in 67.6% (85/126) of WADII. At 6 months, participants with WADII showed persistent hypoaesthesia to warm, thermal sensory limen and mechanical detection thresholds, and decreased mechanical pain and pressure pain sensitivity compared with controls (d > 0.44). These functional neurological changes were accompanied by elevated serum neurofilament light chain levels in acute WADII compared with controls [d = -0.52 (95% confidence interval -0.94, -0.10)]. Intraepidermal nerve fibre densities at the index finger were not significantly different between groups. However, dermal myelin basic protein+/protein gene product+ myelinated nerve bundles at the index finger were reduced 6 months post-injury in WADII compared with controls [d = 0.69 (0.26, 1.11)]. Multivariable linear regression suggested that bedside tests for hypoaesthesia at the index finger were prognostic for whiplash-related upper quadrant pain 6 months post-injury (r2 = 0.13, P = 0.02). In conclusion, two-thirds of participants with acute WADII initially exhibited signs of neuropathic pain and nerve pathology. At the 6-month follow-up, neuropathic pain persisted in one-third of participants with WADII, and nerve pathology persisted in two-thirds. These findings challenge the traditional musculoskeletal classification of WADII and underscore the need for targeted neurological assessments and treatment.