BACKGROUND: The aim of this study is to verify if (1) there is a link between hypovitaminosis D and benign paroxysmal positional vertigo, (2) the number of benign paroxysmal positional vertigo relapses decreases after vitamin D supplementation; and (3) benign paroxysmal positional vertigo response to physical therapy improves after hypovitaminosis D correction. METHODS: We enrolled 26 patients with benign paroxysmal positional vertigo and 24 subjects, who never suffered from vertigo, as a control group. All benign paroxysmal positional vertigo patients underwent physical therapy, once a week, until benign paroxysmal positional vertigo resolution. All participants were subjected to a dosage of serum 25(OH) vitamin D. In patients with hypovitaminosis D, we prescribed cholecalciferol. After 3 months of therapy, all patients were asked to undergo a second dosage of serum 25(OH) vitamin D. For each patient, we counted the number of maneuvers required to resolve each episode of benign paroxysmal positional vertigo before and after vitamin D supplementation. RESULTS: Our results suggest that (1) there is a relationship between vitamin D deficiency and the onset of BPPV and (2) hypovitaminosis correction is able to reduce both the number of patients relapsing and the number of relapses per patient. CONCLUSIONS: We have not found a significant effect of vitamin D supplementation as regards the responsivity of benign paroxysmal positional vertigo to physical therapy. Cite this article as: Pecci R, Mandalà M, Marcari A, et al. Vitamin D insufficiency/deficiency in patients with recurrent benign paroxysmal positional vertigo. J Int Adv Otol. 2022;18(2):158-166.

Due to its mechanical pathogenesis, benign paroxysmal positional vertigo treatment is mainly physical: when posterior semicircular canal is involved, Semont's maneuver is reported as one of the most effective liberating procedures. In the case of a canalolithiasis, the efficacy of the maneuver is corroborated by the appearance of some nystagmus findings during its performance. Liberating nystagmus, that can occur in the second position of Semont's maneuver and whose direction is congruous with the excitation of the affected posterior semicircular canal has proven to be a favorable prognostic sign. On the other hand, in clinical experience, we've frequently verified the appearance of another nystagmus during the execution of the maneuver: upon reaching the third position, when replacing the patient seated, a torsional down beating nystagmus, with the torsional component “congruous” with the stimulation of the vertical semicircular canals of the affected side, can often be appreciated. Such a sign can occur with or without having had the previous liberating nystagmus in the second position and is almost always associated with an intense vertigo and/or body pulsion. In this study, we describe the incidence and characteristics of the congruous torsional down beating nystagmus that can arise by assuming the third position of Semont's maneuver in a cohort of patients treated for posterior semicircular canal benign paroxysmal positional vertigo due to canalolithiasis. In the best of our knowledge, such a sign has never been described and explained before. On the basis of the pathophysiology and of the possible canal receptors stimulation during the different phases of Semont's maneuver, we formulated different hypothesis on how such a nystagmus can be generated. We observed that such a sign, when elicited, has a very good prognostic meaning for healing purposes, even better than that of liberating nystagmus. Therefore, congruous torsional down beating nystagmus should always be checked when performing Semont's maneuver because it could help in predicting success of physical treatment and in managing patients.

Finding a vertical nystagmus, especially when looking straight ahead, should alert the neurologist/neuro-otologist for other signs of cerebellar or brainstem dysfunction. Upbeat nystagmus (UBN) is a relatively uncommon neuro-otological finding that clinicians may encounter in patients presenting with vertigo. This phenomenon is closely linked to central vestibular dysfunction, making it essential for healthcare providers to recognize and interpret it promptly. Accurate identification of UBN can significantly aid in directing patients toward the appropriate diagnostic and therapeutic pathways. As our understanding of UBN’s pathophysiology has advanced, the clinical significance of this sign has become increasingly evident. It is now recognized that UBN can occur as an isolated finding or more frequently as part of a broader spectrum within defined clinical syndromes. This expanded knowledge has also opened the door to various therapeutic approaches tailored to the underlying cause. In our study, we want to provide as accurate a picture as possible about the origins and clinical presentations of UBN.

Benign paroxysmal positional vertigo (BPPV) is the peripheral vestibular disorder that is most frequently encountered in routine neuro-otological practice. Among the three semicircular canals, the lateral semicircular canal (LSC) is the second most frequently interested in the pathological process. In most cases, LSC BPPV is attributable to a canalithiasis or cupulolithiasis mechanism. The clinical picture of LSC BPPV is that of positional nystagmus and vertigo evoked by turning the head from the supine to the side lateral position. With such a movement, a horizontal positional (and often also paroxysmal) direction-changing nystagmus is generated. Depending on whether the pathogenetic mechanism is that of canalithiasis or cupulolithiasis and depending on where the dense particles are located, LSC BPPV direction-changing positional nystagmus is geotropic or apogeotropic on both lateral sides. Due to its mechanical nature, BPPV is effectively treated by means of physical therapy. In the case of a LSC BPPV, one of the most effective therapies is the forced prolonged position (FPP), in which the patient is invited to lie for 12 h on the lateral side on which vertigo and nystagmus are less intense, to move the canaliths out from the canal (or to shift them inside of the canal from one tract to another) exploiting the force of gravity. Despite its efficacy, FPP is not always well tolerated by every patient, and it cannot be done during the diagnostic session because of its duration. The present study aimed to verify the efficacy of a different forced position, shortened forced position (SFP), with respect to the original FPP. SFP treatment would allow patients to more easily bear the forced position and physicians to control the outcome almost immediately, possibly enabling them to dismiss patients without vertigo. After 1 h of lying on the side where vertigo and nystagmus are the less intense, 38 out of 53 (71.7%) patients treated with SFP were either healed or improved. Although the outcomes are not as satisfying as those of the original FPP, SFP should be considered as a therapeutic prospect, especially by those physicians who work in collaboration with emergency departments or otherwise encounter acute patients to cure them of vertigo as soon as possible.

Objective: Cochlear receptors are sensitive to vibratory stimuli. Based on this sensibility, bone-anchored hearing aids have been introduced to correct unilateral or bilateral conductive or mixed hearing loss and unilateral deafness. The vestibular system is also sensitive to the vibratory stimulus and this type of response is used in clinics to test its functionality. Being aware of this double separated sensibility, we wondered whether bone vibration, which activates the acoustic receptors of patients with bone conduction aids, can also influence the functionality of the vestibular system. Methods: To this end, we recruited 12 patients with a bone-anchored hearing aid and evaluated their vestibular function with and without an activated vibratory acoustic device. Results: Our results show that the vibratory stimulus delivered by the bone conduction aid also reaches and stimulates the vestibular receptors; this stimulation is evidenced by the appearance or modification of some nystagmus findings during bedside vestibular testing. Despite this, none of these patients complained of dizziness or vertigo during prosthesis use. Nystagmus that appeared or changed during acoustic vibratory stimulation through the prosthesis was almost all predominantly horizontal, unidirectional with respect to gaze or body position, inhibited by fixation, and most often consistent with vestibular function tests indicating peripheral vestibular damage. Conclusions: The findings of sound-evoked nystagmus seem to indicate peripheral rather than central vestibular activation. The occurrence of some predominantly horizontal and high-frequency induced nystagmus seems to attribute the response mainly to the utricle and lateral semicircular canal.