Residual dizziness after BPPV management: exploring pathophysiology and treatment beyond canalith repositioning maneuvers

Abstract

Despite the high success rate of canalith repositioning maneuvers (CRMs) in the treatment of benign paroxysmal positional vertigo (BPPV), a growing number of patients report residual dizziness symptoms that may last for a significant time. Although the majority of BPPV cases can be explained by canalolithiasis, the etiology is complex. Consideration of the individual patient's history and underlying pathophysiology of BPPV may offer the potential for treatment approaches supplementary to CRMs, as well as a promising alternative for patients in whom CRMs are contraindicated. This article provides a summary of the possible underlying causes of BPPV and residual dizziness, along with suggestions for potential management options that may be considered to relieve the burden of residual symptoms.

Keywords: benign paroxysmal positional vertigo; holistic; pathophysiology; residual dizziness; vestibular compensation.

Figure 1

Illustration of the mechanisms involved in BPPV and the potential interventions to address each mechanism. H, Histamine; VOR, Vestibular ocular reflex; and VSR, Vestibulospinal reflex. Otoconial debris may fall into a semicircular canal or attach to the cupula (4). Otoconial debris within the semicircular canals alters the tonic discharge of the affected labyrinth during BPPV, thereby inducing a central adaptation to rebalance the activity of vestibular nuclei to reduce peripheral asymmetry and the symptoms of vertigo (11, 12).

Figure 2

The current potential management approaches that may be considered based on known and proposed mechanisms of BPPV. H, Histamine; VOR, Vestibular ocular reflex; and VSR, Vestibulospinal reflex. Appropriate canalith repositioning maneuvers (CRMs) to remove the otolith from the semicircular canal provide relief from symptoms and positional nystagmus in up to 92% with ≥1 CRMs (36). Vitamin D deficiency is associated with microcirculatory dysfunction (59, 118). The biologically active form of vitamin D is involved in the upregulation of epithelial Ca2+ channel transporters that helps maintain low endolymph Ca²⁺, retain the capacity to dissolve exfoliated otoconia, and prevent abnormal otoconia (55).^† Betahistine increases local vestibular blood flow (56)^† and is involved in the regulation of intracellular calcium, which helps to reduce/delay otoconial detachment (51).^† Betahistine also facilitates central vestibular compensation by enhancing the rebalancing of the neuronal activity of the vestibular nuclei complexes on both sides (50, 64)^† and (67).^‡ Betahistine also improves brain arousal, a crucial factor for functional recovery/behavioral adaptation, through general upregulation of histamine (15, 50, 58).^† Gaze stabilization and vestibular rehabilitation exercises facilitate central compensation and reduce symptoms of dizziness and vertigo (1, 61).^{‡ †}Evidence from animal studies. ^‡Evidence from clinical studies.

Figure 3

Potential treatment approaches based on known and proposed mechanisms of BPPV. Large ticks represent the mechanisms supported by clinical evidence; small boxes represent potential benefits based on mechanisms with evidence from animal studies or proposed mechanisms. ¹Explanations and advice from the ENT specialist about what to expect during CRM and the expected trajectory for symptom resolution post-CRM may benefit anxious/stressed patients. ²Only for patients with diagnosed vitamin D insufficiency. ³Conditions that may affect the microcirculations, such as hypertension and dyslipidemia. ⁴Patients with orthostatic hypotension, vascular risk factors associated with microcirculatory effects, and brain atrophy may be at greater risk of BPPV. ^*Betahistine is recommended for use in patients with Ménière’s disease. BPPV, Benign paroxysmal positional vertigo; CRM, Canalith repositioning maneuver; and ENT, Ear, nose, and throat.