Bodily self disturbances: a new clinical marker of persistent postural-perceptual dizziness

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 and defined by established diagnostic criteria, PPPD typically follows peripheral or central otoneurological disorders. However, the mechanisms underlying the transition from these disorders 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 neurological disorders, but not yet systematically investigated in PPPD. We characterized bodily self disturbances in PPPD by assessing depersonalization-derealization symptoms in a large cross-sectional study (n = 455), including 100 patients with PPPD, 180 patients with other otoneurological disorders, and 175 healthy controls. Depersonalization-derealization symptoms were assessed using the Cambridge Depersonalization Scale, alongside measures of anxiety, depression, dizziness-related impairment, and PPPD symptom severity. PPPD patients exhibited markedly elevated depersonalization-derealization symptoms compared to both other otoneurological disorders and healthy controls (all P < 0.001). Notably, 20% of PPPD patients met the threshold for clinical depersonalization-derealization, compared with 7.2% of other otoneurological disorders and <1% of controls. Depersonalization-derealization severity in PPPD overlapped with levels observed in other functional neurological disorders but remained lower than in primary dissociative disorders. Factor analyses identified three depersonalization-derealization 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 ({superscript 2} = 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 tenfold 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. These findings identify depersonalization-derealization 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 pathophysiological models.