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. 2024 May 24;15:1382196. doi: 10.3389/fneur.2024.1382196

Table 1.

Proposed and proven benefits of interventions for BPPV in addition to or after successful CRM*.

Benefit Intervention Mechanism(s) Action(s)
Reduce/delay otoconial detachment Vitamin D supplementation Maintain low endolymph Ca2+ to prevent abnormal otoconia (55).
  • The biologically active form of vitamin D is involved in the upregulation of epithelial Ca2+ channel transporters (55).

Betahistine Regulation of intracellular calcium (51).
  • Action on histamine receptors located in the vestibular periphery (51).

Maintain capacity to dissolve exfoliated otoconia Vitamin D supplementation Maintain low endolymph Ca2+ to retain capacity to dissolve exfoliated otoconia (55).
  • The biologically active form of vitamin D is involved in the upregulation of epithelial Ca2+ channel transporters (55).

Improve static components Betahistine Rebalancing of the vestibular nuclei neurons (51–53).
  • Improves (reduces) spontaneous resting activity imbalance between the bilateral vestibular nuclei complexes through actions on the histamine H1, H2, and H3 receptors (51).

  • Excitatory effects on the vestibular nuclei neurons (52, 53).

Improve labyrinthine microcirculation Betahistine Increases local vestibular blood flow (56).
  • Inverse agonism at H3 receptor by both betahistine and its major metabolite, aminoethylpyridine (56, 57).

  • Increased release of histamine (direct and indirect via H1 receptors) (58).

Management of vascular comorbidities Vascular comorbidities such as hypertension, dyslipidemia, obesity, and diabetes, may be risk factors for BPPV recurrence (59).
  • Patients with mild small vessel disease are more likely to suffer a peripheral vestibular disorder (60); their vascular risk factors should be considered in a comprehensive treatment plan, which may include referral to a vascular specialist.

  • High TC levels or hyperlipidemia can cause vascular damage in the inner ear, increasing the risk of BPPV (59).

  • Otolith detachment may be secondary to microvascular dysfunction (17).

Aid central vestibular compensation Gaze stabilization techniques Reduce symptoms of dizziness and vertigo (61).
  • Improve the gain of the vestibular ocular reflex; improve visual acuity during head movement (61).

Balance training Improved symptom resolution in posterior canalithiasis BPPV (62).
  • Dissolution and dispersion of otoconial debris and habituation of the pathologic response (62).

Betahistine†‡ Brain arousal, a crucial factor for functional recovery/behavioral adaptation, through general upregulation of histamine (15, 50, 58).
  • Cerebral H1 receptors that regulate sensorimotor activity (50, 58, 63).

Increase histamine turnover and release, and modulation of release of other neurotransmitters, particularly GABA that facilitate late-stage vestibular compensation (50, 64, 65).
  • Antagonistic action on both the presynaptic histamine H3 and postsynaptic histamine H1 receptors (50, 64, 66).

Promote vestibular compensation of both static and dynamic symptoms: mediation of the asymmetric activation of commissural inhibitory system at circuit level; actively promotes rebalancing of bilateral vestibular systems and vestibular compensation (58).
  • Partial H1 receptor agonism (47).

Enhance the rebalancing of the neuronal activity of the vestibular nuclei complexes on both sides (50, 64) and (67).
  • Increased histamine turnover and enhanced histamine release in the CNS (50, 64, 67).

  • H3 receptor antagonism (or H3 receptor inverse agonism) at the level of the secondary vestibular neurons (50, 64, 67).

*Current guidelines recommend against the routine treatment of patients with BPPV with vestibular suppressant medications such as antihistamines [dimenhydrinate, cinnarizine, meclizine, promethazine (54), and/or benzodiazepines (27)]. Vestibular suppressant medications (especially benzodiazepines) have the potential for significant harm and may produce drowsiness, cognitive deficits, and interference with driving or operating machinery. Benzodiazepines and antihistamines interfere with central compensation for a vestibular injury (27). Evidence from animal studies. Evidence from clinical studies. BPPV, Benign paroxysmal positional vertigo; Ca, Calcium; CNS, Central nervous system; CRM, Canalith repositioning maneuver; GABA, Gamma-aminobutyric acid; and TC, Total cholesterol.