To the best of our knowledge, this is the first study to explore the risk factors for residual dizziness in BPPV patients following successful repositioning maneuvers and to thoroughly analyze the relationship between lipid-related indicators and residual dizziness. We found that whether suffering from limb weakness, hypertension, nausea, or limb arteriosclerosis, medication treatment, DHI scores, HADS scores, TC, LDL, and HDL distributions were significantly different between the groups with and without residual dizziness. Moreover, the results of the multivariate logistic regression analysis further revealed that sleep disorders, medication treatment, hypertension, TG, and TC were all significant risk factors for residual dizziness (P < 0.05). Simultaneously, we further revealed the mediating effect (9.1%) of total cholesterol blood concentration between sleep disorders and residual dizziness.
Our study found that the more severe the sleep disorders were before repositioning, the less effective the maneuver was, and the higher the probability of residual dizziness. This finding aligns with another single-center retrospective study on sleep disorders in BPPV patients, which reported that BPPV patients experienced sleep disorders before the diagnosis of BPPV, suggesting it as a significant risk factor (22). In BPPV, the detachment and displacement of otoliths can mechanically stimulate the semicircular canal's ampullary ridge, leading to vertigo (23, 24). Regarding the potential mechanisms, some researchers believe that dysfunction in the central nervous system (CNS) increases the excitability of the trigeminal caudate nucleus, solitary tract nucleus, and vestibular nucleus, resulting in vertigo (25, 26). Others propose that abnormal trigeminal neurovascular pathways cause asymmetric release of neurotransmitters, such as serotonin and norepinephrine, on both sides of the vestibule, also leading to vertigo (27). Therefore, residual dizziness and sleep disorders in BPPV patients may have a bidirectional causal relationship. This finding needs further exploration in future prospective cohort studies.
Similarly, our results align with a previous meta-analysis, which suggested that hypertension and hyperlipidemia are risk factors for the recurrence of BPPV (28). This implies that these factors may also contribute to residual dizziness in BPPV patients even after successful repositioning maneuvers. Our findings indeed support this view, showing that higher levels of TG (OR: 1.05, 95% CI: 1.02–1.12), TC (OR: 1.12, 95% CI: 1.05–1.26), and hypertension (OR: 3.33, 95% CI: 2.90–4.22) are significantly associated with residual dizziness. This finding is also consistent with a cross-sectional study from Germany, which reported that hypertension and hyperlipidemia were independently associated with residual dizziness in BPPV patients (2, 29). The reason for this lies in the anatomical positioning of the SCC, which is at the lowest point in the vestibular apparatus when a person is standing (18, 30). Von Brevern et al. discovered that BPPV predominantly affects the right labyrinth, likely due to the common habit among most patients of sleeping on their right side (2, 18). Theoretically, hypertension acts as a vascular risk factor, suggesting that ischemia might be a common predisposing factor for BPPV. However, our study did not identify any association between BPPV and other recognized vascular risk factors, including smoking and alcohol consumption (P > 0.05) (17).
BPPV patients exhibit higher TC levels, and elevated TC levels have been identified as a risk factor for the occurrence of BPPV. The relationship between TC levels and BPPV has not been thoroughly explored in previous research. Elevated TC levels or hyperlipidemia can cause vascular damage in the inner ear, potentially leading to BPPV (31). Additionally, a recent study discovered an association between the three rs2074880 genotypes of the CACNA1A (Calcium Voltage-Gated Channel Subunit Alpha1 A) gene and elevated cholesterol levels in patients with BPPV (9, 32). Our study results also revealed the mediating role of TC levels in the relationship between sleep disorders and residual dizziness in BPPV patients. This finding highlights the importance of TC levels as a crucial intermediary factor. Elevated cholesterol levels, which are often a consequence of sleep disorders, can cause vascular damage in the inner ear, thus exacerbating dizziness symptoms. This mediating effect of TC levels suggests that managing cholesterol may help mitigate the impact of sleep disorders on residual dizziness (33, 34). For example, interventions aimed at reducing cholesterol levels could potentially disrupt the pathway linking sleep disturbances to dizziness, thereby improving patient outcomes (9, 35, 36). Such evidence underscores the need for comprehensive treatment approaches that address both sleep quality and lipid management in BPPV patients to effectively reduce residual dizziness (37, 38).
Several limitations of this study should be noted: (I) the sample size was relatively small, necessitating further validation and support from future research; (II) all the BPPV patients included were from a single location, which could restrict the generalizability of our findings; (III) the retrospective analysis period of this study was relatively short. Future research should utilize large-scale prospective cohort studies to further elucidate the risk factors for residual dizziness in BPPV patients and the interactions between these factors (39–41).