身体自我障碍：持续性姿势-知觉性头晕的一种新临床标志物

文献信息

中文摘要

背景与目的： 持续性姿势-知觉性头晕（PPPD）是最常见的慢性神经耳科疾病之一，影响在神经科和专科头晕门诊就诊的成人中的15%-20%。PPPD被归类为一种具有既定诊断标准的功能性前庭障碍，通常继发于外周或中枢耳神经科疾病。然而，向慢性知觉性头晕过渡的机制仍不清楚。除适应不良的姿势控制和视觉依赖外，理论模型还涉及多感觉整合改变和预测加工受损。这些机制可能延伸至身体自我障碍，这一维度在功能性神经障碍中日益受到认识，但尚未在PPPD中进行系统研究。
方法： 我们通过在一项大型横断面研究（n = 455）中评估人格解体-现实解体（DD）症状，来刻画PPPD中的身体自我障碍，包括100例PPPD患者、180例其他耳神经科疾病患者和175名健康对照。DD症状使用剑桥人格解体量表评估，同时测量焦虑、抑郁、头晕相关损害和PPPD症状严重程度。
结果： 与其他耳神经科疾病和健康对照相比，PPPD患者的DD症状显著升高。值得注意的是，20%的PPPD患者达到临床DD阈值，而其他耳神经科疾病患者为7.2%，对照组<1%。PPPD中的DD严重程度与其他功能性神经障碍中观察到的水平重叠，但仍低于原发性分离障碍。因子分析识别出3个DD维度：身体自我障碍、认知与情感疏离以及麻木。只有身体自我障碍——涵盖自我定位、能动性、身体归属感和第一人称视角的紊乱——能够稳健地将PPPD与其他耳神经科疾病区分开来（η2 = 0.20，p < 0.001）。该维度预测PPPD诊断（比值比 = 1.40，p < 0.001），并显示出显著的判别能力（AUC = 0.66）。身体自我障碍最高十分位者的PPPD odds增加近十倍。结构方程模型证实PPPD对身体自我障碍有直接效应，部分由抑郁症状中介，但独立于年龄、性别、偏头痛和焦虑。
讨论： 这些发现将DD确定为PPPD表型中一个此前未被认识的组成部分，并确立身体自我障碍作为PPPD的一种新临床标志物，从而细化表型分型并为病理生理模型提供信息。

英文摘要

BACKGROUND AND OBJECTIVES: Persistent Postural-Perceptual Dizziness (PPPD) is among the most prevalent chronic neuro-otologic disorders, affecting 15%-20% of adults seen in neurology and specialized dizziness clinics. Classified as a functional vestibular disorder with established diagnostic criteria, PPPD typically follows peripheral or central otoneurological disorders. However, the mechanisms underlying the transition to chronic perceptual dizziness remain unclear. Beyond maladaptive postural control and visual dependence, theoretical models implicate altered multisensory integration and disrupted predictive processing. Such mechanisms may extend to disturbances of the bodily self, a dimension increasingly recognized in functional neurologic disorders, but not yet systematically investigated in PPPD.
METHODS: We characterized bodily self disturbances in PPPD by assessing depersonalization-derealization (DD) symptoms in a large cross-sectional study (n = 455), including 100 patients with PPPD, 180 patients with other otoneurological disorders, and 175 healthy controls. DD symptoms were assessed using the Cambridge Depersonalization Scale, alongside measures of anxiety, depression, dizziness-related impairment, and PPPD symptom severity.
RESULTS: Patients with PPPD exhibited markedly elevated DD symptoms compared with both other otoneurological disorders and healthy controls. Notably, 20% of patients with PPPD met the threshold for clinical DD, compared with 7.2% of other otoneurological disorders and <1% of controls. DD severity in PPPD overlapped with levels observed in other functional neurologic disorders but remained lower than in primary dissociative disorders. Factor analyses identified 3 DD dimensions: bodily self disturbances, cognitive and affective detachment, and numbing. Only bodily self disturbances, capturing disruptions in self-location, agency, body ownership, and first-person perspective, robustly differentiated PPPD from other otoneurological disorders (η2 = 0.20, p < 0.001). This dimension predicted PPPD diagnosis (odds ratio = 1.40, p < 0.001) and showed significant discriminative ability (AUC = 0.66). Individuals in the highest decile of bodily self disturbances had nearly ten-fold increased odds of PPPD. Structural equation modelling confirmed a direct effect of PPPD on bodily self disturbances, partially mediated by depressive symptoms but independent of age, sex, migraine, and anxiety.
DISCUSSION: These findings identify DD as a previously unrecognized component of the PPPD phenotype and establish bodily self disturbances as a novel clinical marker for PPPD, refining phenotyping and informing pathophysiologic models.