Benign paroxysmal positional vertigo (BPPV) is a clinical disorder characterized by recurrent positional vertigo [1]. BPPV is considered the most common vestibular disease with a prevalence of 10.7–64.0 cases per 100,000 population. The female- to-male ratio of BPPV patients has been reported to range from 2:1 to as much as 3:1 [2].

Otoconial debris that dislodges from the utricular macula can precipitate into the semicircular canals [3], and its movement in the endolymph produces push or pull forces on the cupula of the semicircular canal, thereby eliciting excitation or inhi-bition of the corresponding semicircular canals that results in the characteristic nystagmus (Fig. 1) [4]. Therefore, the diag-nosis of BPPV is made by identifying the characteristic positioning nystagmus during the Dix-Hallpike and supine head roll tests [5–7].

The vestibulo-ocular reflex (VOR) is a reflex between the vestibular system and ocular movement that stabilizes images during head movements by producing exquisite eye movements. A left head turn induces excitation of the left horizontal semi-circular canal, followed by excitation of the left vestibular nuclei and inhibition of the right vestibular nuclei. After that, exci-tation of the left oculomotor and right abducens nuclei and leading contraction of the left medial rectus and right lateral rectus muscle cause compensatory eye movement to the right side. The rotational VOR related to the plane of each semi-circular canal stabilizes vision during movement.

A previous study showed that disruption of the VOR in terms of caloric hypoexcitability was frequently identified in BPPV patients, especially in the cupulolithiasis type of horizonal canal BPPV. However, no association between symptom duration and caloric results was detected, probably due to the nonphysiologic nature of the caloric stimulation. Likewise, the authors supposed that the atypical dizziness in BPPV might result from the otolith in the endolymph affecting the flow of endolymph and dis-rupting the VOR. Nowadays, the video head impulse test (vHIT) allows the VOR to be easily measured objectively at physi-ologic stimulation speed [8].

To test this idea, we planned a prospective case-control study using vHIT to evaluate the possible alteration of the VOR in patients with horizontal canal BPPV (h-BPPV).

A total of 133 patients were diagnosed as h-BPPV, 75 with canalolithiasis and 58 with cupulolithiasis. Table 1 presents their demographic characteristics. The mean age was 56.5±12.5 years old; the male to female ratio was 1:2.02, and the right side affected was in 73 patients and the left in 60. The patients underwent an average of 2.2±1.8 sessions of the canalith re-position maneuver, and 29 patients suffered recurrent BPPV (13.9%).

The VOR gain was not significantly different in the h-BPPV and control group, whereas the asymmetry on vHIT was sig-nificantly higher in the h-BPPV group (p=0.013). A vHIT gain below 0.8 was seen in 3 patients (2.3%) in the hBPPV group and in 1 patient (1.3%) in the control group (Table 2). In a subgroup analysis, cupulolithiasis of hBPPV showed signifi-cantly elevated asymmetry (p=0.011) (Table 3). Other para-meters were not significantly different. There was also no sig-nificant difference in vHIT gain or vHIT asymmetry between the cupulolithiasis and canalolithiasis groups (Table 4).

This study assessed a possible alteration of the VOR in h-BPPV using vHIT. The results can be summarized as follows: (1) The asymmetry of the VOR was significantly increased in h-BPPV. (2) Cupulolithiasis of h-BPPV displayed the highest asymmetry, and (3) no decrease of VOR gain was evident in h-BPPV.

The VOR guarantees clear vision during head rotation. The rotational VOR produces a slow phase eye movement that compensates for horizontal, vertical and torsional head rotations. The ordinary rotational VOR compensates perfectly for both the direction and speed of horizontal and vertical head rotations. The eye movements remain well-aligned with the head in the direction of its rolling rotation.

BPPV can be categorized into 2 types, canalolithiasis and cupulolithiasis. “Canalolithiasis” involves free-floating particles within a semicircular canal [9]. Canlolithiasis is mostly due to free-floating debris in the endolymph, which tends to gravitate towards the posterior canal, the most gravity-affected part of the vestibular labyrinth in both upright and supine positions. Once debris enters the posterior canal, the cupula barrier at the end of the canal prevents its exit and it can only prolapse at the end at the ampulla (the common crus) [7]. “Cupulolithiasis” involves particles adherent to the cupula of a semicircular canal [10]. Since particles adhere to the cupula, the vertigo is often severe and persists while the head is in the provoking position. When the head rotates toward the affected side, the cupula undergoes an ampullofugal (inhibitory) deflection causing ageo-tropic nystagmus. Turning the head in the opposite side creates an ampullopetal (stimulatory) deflection, resulting in stronger ageotropic nystagmus [7]. Ageotropic nystagmus is present in about 27% of patients with h-BPPV [11].

The present study was conducted to test the possibility that the presence of otoliths can affect the VOR. Studies have pointed to canal paresis in the caloric test in patients with BPPV by showing that unilateral caloric loss occurs in up to 36% of h-BPPV patients. They also showed that the side with the de-creased caloric response corresponded to the side with the highest-velocity horizontal positional nystagmus [12]. Another study demonstrated reversibility of the hypoexcitability in the caloric test after a liberatory maneuver [13,14].

It has been speculated that cupulolithiasis may affect the cupular deflection due to the weight of otoconia during the rotary chair test. However, the gain and time constant did not differ between cupulolithiasis and canalolithiasis [15]. This suggests that the otolith has little effect on the VOR. However, a recent polot study revealed that gain in the vHIT in the plane of the posterior semicircular canal was reduced in posterior semicircular canal BPPV, suggesting a possible otolithic influence on the VOR in different angle or velocity [2].

The caloric test, rotary chair test, and vHIT can assess the functioning of the VOR in response to different stimulus fre-quencies. The vHIT evaluates frequencies around 2.5 Hz using rapid and short head impulses, whereas the caloric test activates lower frequency bands around 0.003Hz [16]. The rotatory chair test generally evaluates frequencies around 0.01–1 Hz. In daily life, people usually experience head rotation frequencies ranging from 1 Hz to as high as 6 Hz [17]. Since the rotatory chair test and the caloric test cannot reflect the VOR at high fre-quency, these tests do not directly reflect the functional changes of patients' VORs in daily life. Thus, the vHIT test may better reflect the physiologic status of the VOR.

The present study showed that the vHIT gain was not significantly different between h-BPPV and control, whereas the asymmetry of vHIT was significantly elevated in h-BPPV patients. In addition, vHIT gain and asymmetry did not signifi-cantly differ between canalolithiasis and cupulolithiasis.

Interestingly, the asymmetry of vHIT was significantly ele-vated in cupulolithiasis. We assume that the otolith adhering to the cupula may influence the resting state of the cupula making it heavier, and lead to increased gain asymmetry. Ac-cordingly, the distorted input from the semicircular canal may then affect the velocity storage system that enhances VOR per-formance by CNS [18]. However, in canalolithiasis, gain asym-metry is not influenced by the presence of an otolith due to physical factors such as the weight or static friction [19]. Like-wise, the otolith is far from the cupula in canalolithiasis, so it probably cannot affect the VOR gain during head movement.

There are also numerous reports showing frequent occurrence of BPPV on the side of vestibular hypofunction [20,21]. Ab-normal caloric results are frequently seen in BPPV patients even after performing the canalith reposition maneuver [20,22]. It has been postulated that detachment of the otolith from utricle or saccule in BPPV might also have an adverse effect on the trans-itional VOR [23]. Although this study did not include patients with prior experience of vestibulopathy by history, the possible coexistence of vestibulopathy might interfere with interpretation of the results.

There are a few limitations to the present study. We could not perform other vestibular function tests including the caloric test, vestibular evoked myogenic potential, and rotary test, which could provide information on the specific functional status of the vestibular system. In addition, it might have been valuable to compare the result of the vHIT before and after treatment, since this could have provided more direct evidence concerning BPPV's influence on vHIT. In future studies, it would be advisable to examine how vHIT results change after BPPV treatment.

In conclusion, the study showed that the asymmetry of vHIT gain increased in the cupulolith type of hBPPV, thus demon-strating possible alteration of the VOR.