Correlation between nystagmus intensity and vestibular–ocular reflex gain in benign paroxysmal positional vertigo: A prospective,clinical study

Abstract

BACKGROUND:

Video head impulse test (vHIT) and videonystagmography (VNG) provide significant benefits in evaluating benign paroxysmal positional vertigo (BPPV) and determining the semicircular canal localization of the otoconia.

OBJECTIVE:

This study aimed to investigate the relationship between vestibular–ocular reflex (VOR) gains measured via vHIT and the slow-phase velocity (SPV) of nystagmus in patients with the posterior semicircular canal (PSCC)-BPPV.

METHODS:

Sixty-two patients were included in this study and divided into the study (n = 32, patients with isolated PSCC-BPPV) and control (n = 30, age- and sex-matched healthy individuals) groups. While VOR gains were measured with vHIT in both groups and compared between groups, the SPV values of nystagmus observed during the Dix-Hallpike maneuver in the study group were recorded using VNG and compared with the VOR gains of the study group.

RESULTS:

There were significant differences in posterior canal VOR gains between the study and control groups (p < 0.001 and p < 0.01, respectively). Although the affected PSCC had decreased VOR gains versus the control group, it was still within the normal range. However, there was no significant relationship between the VOR gains of the affected PSCC and the SPV of the nystagmus.

CONCLUSIONS:

vHIT can help detect semicircular canal dysfunction in patients with PSCC-BPPV. The SPV values of nystagmus on VNG during the Dix–Hallpike maneuver do not correlate with the level of VOR gain.

Keywords

Benign paroxysmal positional vertigo vestibular function tests head impulse test vestibulo–ocular reflex semicircular canals

1 Introduction

Benign paroxysmal positional vertigo (BPPV) is an inner ear disease characterized by recurrent episodes of positional vertigo. BPPV occurs in 11–64 out of 100,000 patients with a female-to-male ratio of 2:1–3:1 [3 , 30]. Two different theories have been proposed in the pathophysiology of the disease: cupulolithiasis [34] and canalithiasis [18]. In cupulolithiasis, the debris or otoconia consisting of fragmented endolymph particles and calcium carbonate crystals adhere to the cupula. In canalithiasis, the cupula is displaced by the hydrodynamic attraction of the freely moving otoconia in the canal. In both cases, abnormal nystagmus and vertigo occur when the head moves in the plane of the canal [18]. Since the most frequently involved canal in BPPV is the posterior canal (85% –95% of cases), the definition was created considering the posterior semicircular canal (PSCC) [31]. This etiology is also valid in lateral semicircular canal BPPV (LSCC-BPPV), which accounts for 5% –30% of cases [7]. Anterior semicircular canal BPPV (ASCC-BPPV) is seen in only 2% of cases; multicanal BPPV; and bilateral multicanal BPPV are the other less common types of BPPV [3].

Videonystagmography (VNG), a measurement tool that records eye movements due to vestibular stimuli, provides great benefits in determining the semicircular canal localization of the otoconia according to the nature of the nystagmus in BPPV [21]. Activation of embedded sensory hair cells in semicircular canals with head motion induces a slow compensatory eye movement [5, 35]. When the slow compensatory eye movement moves away from the center, the eyes are returned to the central position with rapid correction of the movement. These slow compensatory and fast corrective eye movements constitute the components of nystagmus [5]. Slow eye movements cause the slow phase of nystagmus, and rapid eye movements cause the fast phase. The nystagmus intensity is defined as the slow-phase velocity (SPV), which VNG measures.

The video head impulse test (vHIT) documents the vestibular–ocular reflex (VOR) generated in each semi-circular canal by the stimulation generated by head movements through a video camera system [21]. It allows measuring the VOR gain in each of the six semi-circular canals [1]. The VOR is based on the principle of stability of the eyes against head movements and occurs when stimuli from the semicircular canals reach the extraocular muscles. A recent meta-analysis found that posterior canal VOR gain was significantly reduced compared to the contralateral healthy side and in healthy controls. Regarding this, vHIT can be valuable as a supporting test in diagnosing BPPV, especially for PSCC-BPPV [14].

In BPPV, otoliths displaced from the utricle to the SCC impinge on the cupula and cause cupula deformation. These free-floating otoliths in the SCC also disrupt the endolymphatic flow and ultimately impair the VOR. As Wu et al. stated, SPV, a slow-phase nystagmus marker, is expected to be higher when cupula deformation is more substantial [41]. In our study, we aimed to investigate whether there is a relationship between high SPV value and a decrease in VOR gain and, therefore, whether the decrease in VOR gain is associated with cupula deformation.

2 Materials and methods

The study was approved by the Selcuk University Clinical Trials Ethics Committee (approval number: 2019/54). The study was carried out in a university hospital between April 2019 and July 2020 and written informed consent was obtained from all patients who agreed to participate in the study. All participants included in the study were thoroughly examined by an otolaryngologist.

2.1 Participants and study groups

A total of 62 patients were included in the study. Thirty-two patients (25 females, 7 males) with isolated PSCC-BPPV were included in the study group, and 30 healthy individuals (21 females, 9 males) were included in the control group. The patients in the study group were those whose clinical symptoms had recently started and were diagnosed with isolated PSCC-BPPV by a positive Dix-Hallpike test. We included only first-episode patients, as different results may be obtained in vHIT with recurrent, unresponsive, or prolonged forms of BPPV [8]. Patients considered to have PSCC-BPPV but had reduced VOR gain in other canals were excluded from the study group. The control group consisted of patients who applied with complaints other than otological and vestibular symptoms, such as nasal septum deviation or chronic pharyngitis. Control group patients were similar to the gender and age (±5 years) distribution of the study group patients. We excluded participants with a history of neuro-otological disease, an orthopedic disease that prevents neck movements, or any disease or surgery that causes impaired eye movements from both groups.

2.2 Interventions and outcome measures

Dix–Hallpike test was performed with VNG (Visual Eyes 4-Channel VNG, Spectrum 9.1, Micromedical Technologies Inc., IL, USA) on patients in the study group. Eye movements detected by video recording glasses were recorded in a computer database. VNG values of patients diagnosed with PSCC-BPPV were also recorded. Our patients’ up-beating (UB) torsional nystagmus had two components: an upward-beating vertical component and a torsional component. Unfortunately, the torsional component cannot be recorded via VNG since the movements of the eyes are recorded in vertical and horizontal planes. The mean slow-phase velocity (SPV) value of these two components was recorded as UB and right-beating (RB) or left-beating (LB) according to the affected side (Fig. 1). For the Dix-Hallpike positioning test, patients were seated with their heads rotated 45 degrees towards the tested ear and then laid down with their heads hanging from the table at a 20–degree angle. According to the Consensus Document of the Committee for the Classification of Vestibular Disorders of the Bárány Society, patients with positional nystagmus that occurs after a latency of one or several seconds with the Dix-Hallpike maneuver or the Semont diagnostic maneuver are considered PSCC-BPPV canalithiasis [39]. In PSSC-BPPV cupulolithiasis, positional nystagmus is elicited with a brief or no latency, and nystagmus is expected to last longer than 1 minute. However, the duration of a positional vertigo attack is usually less than 1 minute because patients tend to turn their heads to a position where vertigo and nystagmus cease. The time may be longer when the head is in a provocative position [39]. For this reason, we ended the maneuver in less than 1 minute in order not to cause discomfort in our patients who developed positional vertigo attacks due to the maneuver. We differentiated canalithiasis and cupulolithiasis in these patients according to the latency period.

Fig. 1

VNG (VisualEyes 4 Channel VNG, Spectrum 9.1. Micromedical Technologies Inc., IL, USA) of a right-sided PSCC-BPPV patient. Geotrophic rotatory nystagmus seen with horizontal component (SPV 14°/s) and vertical component (SPV 13°/s).

The Dix–Hallpike maneuver was performed for ASCC-BPPV, whereas the supine roll test was performed for LSCC-BPPV. Patients with isolated decreased PSCC VOR gain in vHIT were included in the study. Patients with multiple channel involvement of PSCC-BPPV with ASCC-BPPV or LSCC-BPPV and patients with ASCC-BPPV and LSCC-BPPV were excluded from the study.

The vHIT video system (Ulmer II, Synapsys 3.1.0.8, Synapsys, Marseille, France) was used to evaluate the VOR (Fig. 2). The VOR gain was obtained by dividing the eye velocity by the head velocity using the data analysis program. The patient was placed in a sitting position 1 meter away from the camera and asked to look at the points determined on the device. Before starting the test, the camera was calibrated to ensure the visibility of the patient’s eye and to detect pupils by the device’s software. The device’s software only records vertical and horizontal eye movements. During the test, the patient looks at three predetermined points, and eye movements are recorded while the patient makes sudden head movements in the horizontal and vertical planes. The same audiologist performed passive head movements at a rate of ≥100°/sec and around 20°–30°. Horizontal canal VOR gains were evaluated by moving the head to the right and left along the plane while the patient was looking at the midpoint of the plane. Vertical canals were evaluated by aligning the patient’s head with the right anterior, left posterior, and left anterior, right posterior and giving up-down impulses. Patients diagnosed with PSCC-BPPV were treated with canalith repositioning maneuvers. Accordingly, the ipsilateral Epley maneuver was conducted for PSCC canalithiasis on the affected side, and the Semont release maneuver was conducted for PSCC cupulolithiasis on the affected side. Patients in both study and control groups underwent vHIT measurements for each SCC on both sides.

Fig. 2

Vhıt (Ulmer II, Synapsys 3.1.0.8, Synapsys, Marseille, FRANCE) results of a patient with abnormal PSCC-VOR gain presented in the figure. VOR gains of all semicircular canals were shown above each box. The mean value of the vestibulo-ocular reflex (VOR) gain (eye velocity/head velocity) and corresponding standard deviation (σ) was reported for each canal. A selective deficient VOR gain for the right posterior semicircular canal (0.66) was detected.

2.3 Statistical analysis

The Statistical Package for the Social Sciences (version 16; SPSS Inc., Chicago, USA) was used for statistical evaluation. The Mann–Whitney U test was used to compare the VOR gains between groups. Since the data in the analysis were not normally distributed according to the Kolmogorov–Smirnov test, a comparison of VOR gains and SPV values in the study group was made using the Spearman correlation analysis. P-values <0.05 were considered statistically significant.

3 Results

Of the patients in the study group, 25 (78.1%) were female, and 7 (21.9%) were male (mean age 50.1±12.2 years); 21 (70%) of the patients in the control group were female, and 9 (30%) were male (mean age 50.3±11.4 years). While 19 (59.4%) patients in the study group had right ear involvement, 13 (40.6%) had left ear involvement (Table 1). All patients had unilateral PSCC-BPPV. Among the patients in the study group, the right posterior canal mean VOR gain was 0.85±0.12 in patients with right-sided PSCC-BPPV, while the mean left posterior canal VOR gain in patients with left-sided PSCC-BPPV was 0.87±0.16. Among the patients in the control group (60 ears), the mean VOR gain for the right posterior SCC was 0.95±0.04, while the mean VOR gain for the left posterior SCC was 0.98±0.04. There was a significant difference in both right and left posterior channel VOR gains between the BPPV and control groups (p < 0.001 and p < 0.01, respectively) (Table 2). UB torsional nystagmus was observed in patients in the study group. According to the affected side, LB and RB were accepted as horizontal components, and UB was the vertical component. The mean and standard deviation of horizontal nystagmus SPV (12.03°/s±6.43°/s) and vertical nystagmus SPV (11.90°/s±6.23°/s) were recorded at each position. As indicated by the Spearman correlation analysis, the VOR gains of the posterior SCC were not significantly correlated to the SPV of the nystagmus in patients with PSCC-BPPV [Spearman correlation coefficient for the horizontal component r = –.173 (p = 0.345) and Spearman correlation coefficient for the vertical component r = –.293 (p = 0.103)]. The vHIT results and VNG findings in all canal planes of the patients in the study and control groups are presented in Table 3.

Table 1
Demographic features of both BPPV (study) group and control group and Dix –Hallpike side of BPPV group

BPPV group Control Group

n % n %

Sex

Female 25 78.1 21 70.0

Male 7 21.9 9 30.0

Age (Mean) 50.1±12.2 50.3±11.4

Dix –Hallpike

Right positive 19 59.4

Left positive 13 40.6

	BPPV group	Control Group
	n	%	n	%
Sex
Female	25	78.1	21	70.0
Male	7	21.9	9	30.0
Age (Mean)	50.1±12.2		50.3±11.4
Dix –Hallpike
Right positive	19	59.4
Left positive	13	40.6

BPPV: Benign paroxysmal positional vertigo.

Table 2

Comparison of VOR gains for PSCC between the BPPV (study) and control groups

VOR Gain	BPPV group		Control group
	Median	Q1–Q3	Median	Q1–Q3	p
RP SCC	0.86	0.81–0.94	0.96	0.92–0.99	0.001^**
LP SCC	0.93	0.78–0.99	0.98	0.96–1.02	0.01^*

^*p < 0.05; ^**p < 0.001. VOR: vestibulo-ocular reflex, PSCC: posterior semicircular canal, BPPV: Benign paroxysmal positional vertigo, RP: right posterior, LP: left posterior.

Table 3

The vHIT and VNG results in all canal planes for the control and study group patients

Gender	Age	Direction	SPV	Diagnosis	RA SCC	RL SCC	RP SCC	LA SCCC	LL SCC	LP SCC
Study Group
M	43	R	6RB 7UB	RIGHT POST. CAN. BPPV	0.98	0.93	0.89	0.96	0.92	0.95
F	55	R	5RB 5UB	RIGHT POST. CAN. BPPV	0.78	0.88	0.68	0.78	0.82	0.88
F	59	R	14RB 19UB	RIGHT POST. CUP. BPPV	0.95	0.87	0.83	1.04	0.97	0.87
F	51	R	16RB 11UB	RIGHT POST. CUP. BPPV	0.97	0.90	0.86	0.99	0.88	0.98
F	51	R	32RB 22UB	RIGHT POST. CUP. BPPV	1.12	0.96	0.83	1.11	0.85	0.89
F	66	R	16RB 16UB	RIGHT POST. CUP. BPPV	0.94	0.98	0.64	0.95	0.98	0.84
M	67	R	9RB 9UB	RIGHT POST. CUP. BPPV	0.95	0.79	0.84	0.95	0.88	0.90
M	49	R	14RB 11UB	RIGHT POST. CAN. BPPV	0.95	0.80	1.01	0.96	0.88	0.98
F	42	R	13RB 11UB	RIGHT POST. CAN. BPPV	0.77	0.92	0.78	0.73	0.87	0.89
F	63	R	6RB 7UB	RIGHT POST. CAN. BPPV	0.93	0.94	0.90	1	0.82	0.89
F	21	R	7RB 8UB	RIGHT POST. CAN. BPPV	1.01	0.98	0.94	0.96	0.96	0.94
F	53	R	7RB 6UB	RIGHT POST. CAN. BPPV	0.99	0.85	0.81	0.91	0.92	0.83
F	33	R	10RB 9UB	RIGHT POST. CAN. BPPV	0.98	0.95	1.02	0.91	0.89	0.99
M	46	R	7RB 11UB	RIGHT POST. CAN. BPPV	0.97	0.87	0.92	0.82	0.81	0.86
F	57	R	8RB 8UB	RIGHT POST. CAN. BPPV	0.93	0.82	0.58	0.81	0.86	0.77
F	24	R	4RB 7UB	RIGHT POST. CUP. BPPV	0.99	0.98	0.95	0.99	1	0.93
F	52	R	8RB 7UB	RIGHT POST. CUP. BPPV	1.06	0.94	0.91	0.94	0.93	0.97
M	40	R	5RB 5UB	RIGHT POST. CAN. BPPV	1.09	0.93	0.96	1.05	0.87	0.95
F	49	R	13RB 24UB	RIGHT POST. CUP. BPPV	0.97	0.82	0.85	0.96	0.81	0.95
F	51	L	16LB 27UB	LEFT POST. CUP. BPPV	1.12	0.96	0.83	1.11	0.85	0.59
F	62	L	10LB 10UB	LEFT POST. CAN. BPPV	1.03	0.91	0.96	0.93	0.91	0.76
F	57	L	9LB 8UB	LEFT POST. CAN. BPPV	0.99	0.92	1.0	1.05	0.92	1
F	53	L	29LB 9UB	LEFT POST. CAN. BPPV	0.99	0.91	0.99	1.02	0.94	0.94
F	58	L	16LB 8UB	LEFT POST. CAN. BPPV	0.89	0.94	0.87	0.91	1.02	0.97
F	33	L	9LB 10UB	LEFT POST. CAN. BPPV	1.01	0.99	0.98	1.01	0.99	1.02
F	57	L	16LB 14UB	LEFT POST. CAN. BPPV	1.02	0.96	0.89	0.99	0.96	0.93
F	28	L	13LB 18UB	LEFT POST. CAN. BPPV	0.99	0.99	0.97	1.01	0.96	0.92
F	64	L	21LB 14UB	LEFT POST. CUP. BPPV	1.01	0.84	0.77	0.90	0.86	0.55
F	60	L	8LB 6UB	LEFT POST. CAN. BPPV	0.93	0.89	0.93	1.01	0.92	0.94
F	45	L	17LB 17UB	LEFT POST. CUP. BPPV	0.86	0.84	0.91	0.95	0.84	0.91
M	60	L	10LB 10UB	LEFT POST. CUP. BPPV	1.08	1	1.03	1.06	1.04	1.04
M	57	L	11LB 27UB	LEFT POST. CAN. BPPV	0.86	0.91	0.83	0.90	0.81	0.79
Control Group
F	51				0.93	0.91	1.04	0.98	0.94	1.01
F	42				0.90	1	0.97	1.03	0.95	0.96
F	36				0.98	0.95	0.96	1.07	0.96	0.93
F	28				1.03	1.04	0.92	1.02	1.04	0.98
F	30				0.97	0.94	0.97	0.97	0.98	0.94
M	38				1.03	0.96	0.92	1	0.95	0.96
F	52				1.06	0.94	0.91	0.97	0.96	0.97
M	38				1.01	0.98	0.98	0.99	0.97	1
F	24				0.99	0.98	0.95	0.99	1	0.93
M	46				1.01	1.02	0.92	1.05	1.03	0.92
M	48				0.94	1.1	0.93	1.01	1.02	0.98
F	22				1	1.04	0.97	0.91	1.01	0.95
M	28				0.99	0.99	0.97	1.01	0.96	0.92
F	34				0.97	0.95	0.97	0.95	0.96	0.92
M	57				1.02	0.96	0.89	0.99	1	0.93
F	48				1	0.98	1.01	1.01	1.01	0.98
F	33				1.01	0.99	1.02	1.01	1.05	0.94
F	58				0.92	0.94	0.89	0.95	1.02	0.97
M	60				1.08	1.03	1.03	1.06	1.04	1.04
F	50				0.99	0.92	0.87	0.92	0.88	0.88
F	23				0.95	1	0.93	0.92	0.99	0.95
F	49				1.01	0.90	0.92	0.98	0.97	0.99
M	42				1.01	0.98	0.95	1.03	0.91	1.01
F	48				1.01	0.94	0.87	1	0.94	0.86
F	36				0.92	0.98	0.94	0.94	0.99	0.93
M	57				0.99	0.92	1	1.05	0.92	1
F	29				1.08	1	1.01	1.05	0.96	1.02
M	46				1.06	1	1.02	1.04	1.05	0.98
F	32				1.06	0.99	0.95	0.96	1.02	0.95
F	26				0.88	0.94	0.97	0.98	0.98	0.99

vHIT: Video head impulse test, VNG: videonystagmography.

4 Discussion

BPPV, the most common peripheral vestibular disease, occurs due to two different etiologies: canalolithiasis and cupulolithiasis [18, 34]. The most important clinical difference caused by these two different etiologies in patients is the time of occurrence of nystagmus during the positioning test. Nystagmus occurs late in canalithiasis after the latency period, whereas in cupulolithiasis, it occurs early without a latent period and significant fatigue. In addition, nystagmus is paroxysmal in canalolithiasis, while it is persistent (>1 minute) in cupulolithiasis [20]. The etiology of 62.5% of the patients with BPPV in our study was canalithiasis, and 37.5% was cupulolithiasis.

When VNG is used in conjunction with the Dix-Hallpike maneuver, it provides valuable information for diagnosing BPPV and helps identify which SCC is affected by identifying nystagmus characteristics [7]. vHIT is also the first proposed method to evaluate each SCC function by measuring VOR gain [29]. In typical PSCC-BPPV, otoliths moving inside the ampullary arm cause a characteristic torsional UB nystagmus during the Dix–Hallpike maneuver [2 , 39]. Sometimes, debris can be located in the distal portion of the non-ampullary tract of the PSCC, resulting in apogeotropic posterior canal paroxysmal positional vertigo, which is characterized by torsional down-beating nystagmus [9 , 38]. Identifying the affected canal may be challenging since the same oculomotor responses are observed in non-ampullary arm PSCC-BPPV and contralateral anterior canal canalolithiasis [10]. The routine use of vHIT in patients with positional down-beating nystagmus will be beneficial as in other peripheral vestibular disorders because it can localize debris in the labyrinth to demonstrate the pathophysiology of nystagmus.

Positional nystagmus may occur to stabilize the eyes after a change of position in total darkness [4]. The SPV range for positional nystagmus in normal subjects is around ≈2.5°/sec and can be up to 5°/sec, with only 5% of individuals exceeding 11°/sec [26, 37]. In the study of Lopez-Escamez et al., the SPV of the vertical and horizontal components of positional nystagmus recorded in patients with vertigo was higher than these values. For PC BPPV patients, the vertical component SPV value was 33.20°/s±16.57°/s (13.5–81.1), and the horizontal component SPV value was 16.089°/s±11.89°/s (3, 2 –25.2) [28]. In our patients, the mean and standard deviation of horizontal nystagmus SPV was 12.03°/s±6.43°/s, and the mean and standard deviation of vertical nystagmus SPV was 11.90°/s±6.23°/s. In line with these values, although the nystagmus pattern of PSCC-BBBV is up-beating torsional nystagmus, we found the SPV of the horizontal component above the expected mean values in our patients.

This study aimed to determine the relationship between nystagmus degrees obtained using VNG and vHIT findings. Although the SPV value in VNG is quantitative evidence of nystagmus in patients with BPPV, we found that it was unrelated to the degree of loss of function in SCCs. Fallahnezad et al. [16] found that 55.17% of patients with PSCC-BPPV had reduced posterior canal VOR gains on the side of the affected ear. Also, Karawani et al. showed a significant reduction in PSCC VOR gain during the acute phase of PSCC BPPV attack [24]. However, in the study by Califano et al., which analyzed 150 patients, there was no significant difference in the mean VOR gains of all semicircular canals between the study and control groups [8]. Particularly in the pretreatment phase, the mean VOR gain of the affected PSCC was not significantly different compared to the control group. At the same time, it was significantly lower than the mean VOR gain of the healthy contralateral PSCC. The same study found that PSCC VOR gain was not significantly affected in patients with typical PSCC BPPV, except for a subgroup of 10 patients (6.7%). The authors attributed the VOR gain deficit in this group to the influence of canalolithiasis effects on ampullar receptor stimulation and a reduction in age-related PSCC VOR gain [23]. Since we did not separate our patients according to age groups in our study and did not classify them into canalithiasis and cupulolithiasis, our evaluations on this subject are limited, which is a limitation for our study.

Alhabib and Saliba reviewed all articles examining vHIT for different vestibular pathologies and determined VOR gain thresholds for each vHIT system [1]. They accepted the thresholds for abnormal gain as <0.79 for Eye SeeCam®, <0.80 for Otometrics LSC (Lateral semicircular canal)®, <0.70 for Otometrics VSC (Vertical semicircular canal)®, and <0.81 for Synapsis®, the system we used. In the present study, the mean VOR gain of the posterior canal was 0.85 and 0.87 for the right and left sides, respectively, which is not considered by the literature as an abnormal VOR gain value. On the other hand, they found a statistically significant difference in VOR gains between the BPPV and control groups (p < 0.001 for the right side and p < 0.01 for the left side). This discrepancy could be explained by the findings of Walther and Blödow [40], who claimed that vHIT would be abnormal if there were more than a 40% reduction in vestibular function. Thus, we can claim that our patients with PSCC-BPPV have abnormal VOR gains compared with normal vestibular systems; however, this decrease in function is not as much as in other vestibular disorders with severe SCC function loss.

Although a decrease in VOR gain was detected, no corrective saccade was observed in our patients. Consistent with our results, although Eza-Nunez et al. [15] and Fallahnezhad et al. [16] observed abnormal VOR gain in their studies, they did not detect any saccades. The authors stated that severe vestibular damage is required for corrective saccade formation.

Vestibular afferents with regular resting discharge constitute a system for signaling vestibular stimuli continuously, such as maintained head tilting, and we term these the static or sustained vestibular system. Also, vestibular afferents with irregular resting discharge constitute a system for signaling transient vestibular stimuli [13]. There is a difference between the behavior of regular (sustained) and irregular (transient) fibers. In fact, while nystagmus detected by VNG comes from the activation of type II hair cells and regular vestibular fibers, semicircular canal VOR gain, as detected in vHIT, reflects the activity of type I hair cells and irregular (transient) fibers. These two results come from the measurements of two distinct worlds. It may represent the most important factor leading to an insignificant correlation between SPV and VOR gain measures.

In a study by Ling et al. [27], 23 out of 44 patients with PSCC-BPPV, dizziness/vertigo developed during the Dix-Hallpike maneuver without nystagmus and any signs of VNG. Karawani et al. [24] found that three patients (9.1% of all patients), although the vHIT results were compatible with PSCC BPPV, no nystagmus was detected on VNG. In this study, we recruited patients with nystagmus, but in our clinical experience, we also see that some patients with BPPV do not have nystagmus despite the presence of vertigo on the Dix–Hallpike maneuver. As Huebner et al. [19] said, the diagnosis of BPPV may not involve visible nystagmus.

Nystagmus that occurs in a specific position, not with movement, as in dynamic positioning tests, is called positional nystagmus (PN) [22, 29]. Persistent PN, which can be difficult to distinguish from other types of PN and requires dynamic positional testing for differential diagnosis, may be seen after cupulolithiasis. For central PN, the absence of vertigo during the precipitating head position and the presence of persistent nystagmus usually make it easy to distinguish between BPPV and central PPV. However, it is not so easy to distinguish between BPPV and central PPV when paroxysmal nystagmus and dizziness are present [6]. It may also be misleading to decide by only looking at the direction of the nystagmus in differentiating paroxysmal CPN from BPPV [12]. It is known that different forms of PN may occur in anterior canal BPPV, horizontal canal BPPV, and migraine [11, 33]. Conversely, PN without vertigo may present as an atypical variant of non-central BPPV. To eliminate the confusion between these diagnoses, it is essential to evaluate the characteristics of nystagmus with positional tests, reveal the SCC involvement with vHIT, and evaluate whether the patient benefits from canalith repositioning maneuvers. Therefore, the detailed and correlated neuro-otological and vestibular test methods used in diagnosis and treatment will allow this disease to be successfully managed.

4.1 Limitations

Our assumption that the cupular dynamics in cupulolithiasis are entirely different from that of canalolithiasis may have caused bias in our results. In fact, we can detect a normal or near-normal PSCC VOR gain in the case of free-floating particles, as they should not change the high-frequency inputs, although we would expect a lower VOR gain value or other VOR trace abnormalities due to persistent cupular bending in patients with cupulolithiasis. Similarly, persistent down-beating nystagmus due to ASC or non-ampullary arm PSSC-BPPV might lead to a reduction in VOR gain for the involved canal as a result of positional/transient canalith jam acting as a low pass filter for endolymphatic movements, allowing low-frequency movements while preventing high-acceleration inputs [10, 36].

The other limitation of our study is that although the patients applied to our clinic with the complaint of acute vertigo, we did not set a standard for the time from the onset of vertigo to the time they applied to our clinic. In addition, more impaired VOR gain values may have been obtained in long-term or resistant disease forms due to central adaptation. Moreover, the lack of additional vestibular examinations, such as caloric testing or VEMP, may have resulted in the failure to detect inner ear defects that could cause PSCC VOR gain abnormalities in some of our patients.

5 Conclusion

To our knowledge, this is the first study to compare the SPV of nystagmus with VOR gains in patients with PSCC-BPPV. vHIT and Dix-Hallpike tests can help diagnose BPPV quickly. In addition, vHIT may also be valuable in evaluating semicircular canals and upper and lower vestibular nerve functions, especially in peripheral vestibular diseases such as BPPV. Also, it could be helpful in the so-called “apogeotropic” or posterior canal BPPV when partial or total canal jam could justify the positional down-beating nystagmus clinical scenario [10].

Acknowledgements

Ethics declarations

Ethics approval and consent to publish: This study protocol was reviewed and approved by Selcuk University Faculty of Medicine Clinical Researches Ethics Committee, on April 2019 by approval number 2019/54. Written informed consent was obtained for participation in this study. All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. This study was registered in the Clinical Trial Registry with number NCT05141734.

Conflict of interest

The authors have no conflicts of interest to declare.

Funding

There is no funding relevant to this study. This work was conducted in the Selcuk University Faculty of Medicine Department of Otorhinolaryngology by using Department sources.

Authors’ contributions

Conceiving and designing the study; or collecting the data; or analyzing and interpreting the data; Merih Onal, Ahmet Aygun, Harun Karakayaoglu, Bahar Colpan, Ozkan Onal

Writing the manuscript or providing critical revisions that are important for the intellectual content; Merih Onal, Ozkan Onal

Approving the final version of the manuscript; Merih Onal, Ozkan Onal, Bahar Colpan

Data Availability Statement

All data generated or analysed during this study are included in this article. Further enquiries can be directed to the corresponding author.

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Correlation between nystagmus intensity and vestibular–ocular reflex gain in benign paroxysmal positional vertigo: A prospective,clinical study

Abstract

BACKGROUND:

OBJECTIVE:

METHODS:

RESULTS:

CONCLUSIONS:

Keywords

1 Introduction

2 Materials and methods

2.1 Participants and study groups

2.2 Interventions and outcome measures

3 Results

Table 1 Demographic features of both BPPV (study) group and control group and Dix –Hallpike side of BPPV group BPPV group Control Group n % n % Sex Female 25 78.1 21 70.0 Male 7 21.9 9 30.0 Age (Mean) 50.1±12.2 50.3±11.4 Dix –Hallpike Right positive 19 59.4 Left positive 13 40.6

4.1 Limitations

5 Conclusion

Acknowledgements

Ethics declarations

Conflict of interest

Funding

Authors’ contributions

Data Availability Statement

References

Table 1
Demographic features of both BPPV (study) group and control group and Dix –Hallpike side of BPPV group

BPPV group Control Group

n % n %

Sex

Female 25 78.1 21 70.0

Male 7 21.9 9 30.0

Age (Mean) 50.1±12.2 50.3±11.4

Dix –Hallpike

Right positive 19 59.4

Left positive 13 40.6