There is no clear understanding of the mechanisms causing persistent pain in patients with whiplash-associated disorder (WAD). The aim of this systematic review was to assess the evidence for nerve pathology and neuropathic pain in patients with WAD. EMBASE, PubMed, CINAHL (EBSCO), and MEDLINE were searched from inception to September 1, 2020. Study quality and risk of bias were assessed using the Newcastle–Ottawa Quality Assessment Scales. Fifty-four studies reporting on 390,644 patients and 918 controls were included. Clinical questionnaires suggested symptoms of predominant neuropathic characteristic in 34% of patients (range 25%-75%). The mean prevalence of nerve pathology detected with neurological examination was 13% (0%-100%) and 32% (10%-100%) with electrodiagnostic testing. Patients independent of WAD severity (Quebec Task Force grades I-IV) demonstrated significantly impaired sensory detection thresholds of the index finger compared with controls, including mechanical (SMD 0.65 [0.30; 1.00] P < 0.005), current (SMD 0.82 [0.25; 1.39] P = 0.0165), cold (SMD −0.43 [−0.73; −0.13] P = 0.0204), and warm detection (SMD 0.84 [0.25; 1.42] P = 0.0200). Patients with WAD had significantly heightened nerve mechanosensitivity compared with controls on median nerve pressure pain thresholds (SMD −1.10 [−1.50; −0.70], P < 0.0001) and neurodynamic tests (SMD 1.68 [0.92; 2.44], P = 0.0004). Similar sensory dysfunction and nerve mechanosensitivity was seen in WAD grade II, which contradicts its traditional definition of absent nerve involvement. Our findings strongly suggest a subset of patients with WAD demonstrate signs of peripheral nerve pathology and neuropathic pain. Although there was heterogeneity among some studies, typical WAD classifications may need to be reconsidered and include detailed clinical assessments for nerve integrity.

对于颈椎扭伤相关疾病 (WAD) 患者持续性疼痛的机制尚无明确的了解。本系统评价的目的是评估 WAD 患者神经病理学和神经性疼痛的证据。 EMBASE、PubMed、CINAHL (EBSCO) 和 MEDLINE 的检索时间从开始到 2020 年 9 月 1 日。研究质量和偏倚风险使用纽卡斯尔-渥太华质量评估量表进行评估。纳入了 54 项研究，涉及 390,644 名患者和 918 名对照者。临床调查问卷表明 34% 的患者（范围 25%-75%）具有主要神经病理特征的症状。通过神经系统检查检测到的神经病理学的平均患病率为 13% (0%-100%)，通过电诊断测试检测到的神经病理学平均患病率为 32% (10%-100%)。与 WAD 严重程度无关的患者（魁北克工作组 I-IV 级）表现出与对照组相比，食指的感觉检测阈值显着受损，包括机械 (SMD 0.65 [0.30; 1.00] P < 0.005)、电流 (SMD 0.82 [0.25) ; 1.39] P = 0.0165），冷（SMD -0.43 [-0.73; -0.13] P = 0.0204）和热检测（SMD 0.84 [0.25; 1.42] P = 0.0200）。与正中神经压痛阈值（SMD -1.10 [-1.50; -0.70]， P < 0.0001）和神经动力学测试（SMD 1.68 [0.92; 2.44]， P = 0.0004）对照组相比，WAD 患者的神经机械敏感性显着升高。 WAD II 级患者也出现类似的感觉功能障碍和神经机械敏感性，这与缺乏神经受累的传统定义相矛盾。我们的研究结果强烈表明，一部分 WAD 患者表现出周围神经病理学和神经性疼痛的迹象。 尽管一些研究之间存在异质性，但典型的 WAD 分类可能需要重新考虑，并包括对神经完整性的详细临床评估。