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Original Article
Characteristics of uncompensated acute unilateral vestibulopathy and preliminary clinical characteristics of patients with direction-changing positional nystagmus: a retrospective observational study
Yu Jung Park1,*orcid, Eun Jeong Jo1,*orcid, Sang Hyub Kim2orcid, Sang Yoon Kim3orcid, Ji Eun Choi1orcid, Jae Yun Jung1orcid, Min Young Lee1orcid
Research in Vestibular Science 2026;25(1):38-44.
DOI: https://doi.org/10.21790/rvs.2025.028
Published online: March 13, 2026

1Department of Otolaryngology-Head and Neck Surgery, Dankook University Hospital, Cheonan, Korea

2Cham ENT Clinic, Seosan, Korea

3Department of Radiology, Dankook University College of Medicine, Cheonan, Korea

Corresponding author: Min Young Lee Department of Otolaryngology-Head and Neck Surgery, Dankook University College of Medicine, 119 Dandae-ro, Dongnam-gu, Cheonan 31116, Korea. E-mail: eyeglass210@gmail.com
*These authors contributed equally to this study as co-first authors.
• Received: September 1, 2025   • Revised: January 3, 2026   • Accepted: February 11, 2026

© 2026 Korean Balance Society

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Objectives:
    Vestibular compensation supports recovery after acute unilateral vestibulopathy (UVP). A subset of patients develops direction-changing positional nystagmus (DCPN), which may reflect atypical central adaptation. The objective was to preliminarily investigate clinical characteristics of UVP patients with persistent vestibular weakness presenting with DCPN.
  • Methods:
    Seventeen patients with persistent unilateral weakness on video head impulse test (mean 41 days post-onset) were analyzed retrospectively. Three exhibited DCPN (DCNp group) and were compared with 14 without DCPN (CONTROLp group) using vestibular testing and magnetic resonance imaging white matter hyperintensity (WMH) grading.
  • Results:
    The DCNp group showed reduced spontaneous and head-shaking nystagmus amplitudes (p<0.05) and selectively decreased gains in the contralesional anterior and ipsilesional posterior canals (p<0.05). Periventricular WMH burden was significantly higher in the DCNp group (mean 3.0 vs. 1.8; p=0.001), while deep WMH did not differ.
  • Conclusions:
    DCPN in UVP is linked to canal-specific gain asymmetry and increased periventricular WMH, suggesting impaired central compensation possibly influenced by cerebrovascular microstructural changes.
Vestibular compensation is a crucial neuroplastic mechanism that facilitates recovery following acute unilateral vestibulopathy (UVP), such as vestibular neuritis. This process helps restore balance, gaze stability, and functional ability by enabling central nervous system adaptation to asymmetric vestibular input. Effective compensation not only alleviates symptoms like vertigo and dizziness but also promotes long-term stability; however, prolonged or maladaptive compensation may lead to persistent imbalance or masking of residual deficits [1].
In some cases, patients exhibit direction-changing positional nystagmus (DCPN), which can complicate the differential diagnosis of vestibular disorders [2]. While such nystagmus is often associated with benign paroxysmal positional vertigo, it may also result from central lesions or atypical vestibular recovery processes. The involvement of brain white matter lesions further influences these clinical presentations, as disruptions in pathways responsible for vestibular processing and compensation can lead to abnormal nystagmus patterns and delayed recovery.
To monitor and evaluate the progression of vestibular function during the compensation process, tools such as the video head impulse test (vHIT) are invaluable. The vHIT allows for serial follow-up assessments of vestibulo-ocular reflex gain, providing insights into the dynamic neurological recovery and guiding appropriate management strategies [3]. Understanding the intricate relationship between peripheral vestibular damage, central compensation, neuroanatomical alterations, and the utilization of follow-up tools like the vHIT is essential for accurate diagnosis and effective treatment of vestibular dysfunctions.
The objective of current study was to investigate the serial vHIT outcomes and related clinical features of UVP patients with persistent vestibular weakness uniquely presenting with DCPN during compensation process.
Ethics Statement
This study was approved by the Institutional Review Board of Dankook University Hospital (No. 2025-06-011-001) and was conducted in accordance with the Declaration of Helsinki. The requirement for informed consent was waived due to the retrospective nature of the study.
Subjects
We retrospectively reviewed patients who were diagnosed with acute UVP at Dankook University Hospital between March 1, 2016 and February 28, 2024. A total of 115 patients were initially screened based on prior studies [4]. All vestibular tests were conducted by the same examiner using standardized procedures. No formal sample size calculation was performed because all patients who met the inclusion criteria between 2016 and 2024 were included.
Inclusion criteria were (1) acute onset vertigo with a clinical diagnosis of UVP, (2) unilateral weakness demonstrated on both the vHIT and bithermal caloric testing, and (3) patients who underwent at least two vestibular function tests (vHIT or caloric) during the study period. Exclusion criteria included the presence of Ménière disease, other neurological disorders (e.g., stroke, demyelinating disease, tumor), psychiatric illness, or inability to complete vestibular testing. Patients who met the criteria of definitive or possible Ménière disease were excluded. All the patients showed continuous vestibular symptoms and did not show episodic ear symptoms.
From this cohort, 17 patients met the criteria of persistent unilateral weakness on vHIT gain at follow-up (average 41 days after onset) and were classified as uncompensated UVP patients (Fig. 1, Table 1). Among them, three patients demonstrated atypical videonystagmographic findings characterized by DCPN (DCNp group), while the remaining 14 patients were classified as the CONTROLp group.
Demographically, the DCNp group (n=3) had a higher mean age (67.6 years) compared to the CONTROLp group (59.9 years) and showed a female predominance (2:1), while the CONTROLp group had a balanced sex ratio. Comorbidities such as hypertension and diabetes were observed in some CONTROLp patients, whereas none were found in the DCNp group.
Vestibular Function tests

Video head impulse test

The patients sat in a bright examination room and fixated on a stationary point 1 meter ahead. The vHIT (ICS impulse, GN Otometrics) goggles were then fitted onto the examiner, and the test was performed. The head rotation angle was between 10° and 20°, with a maximum angular velocity of 100°/sec to 250°/sec. The test was repeated at least 10 times for each semicircular canal. During the lateral canal test, the examiner stood behind the patient, holding both sides of the patient’s jaw, and rotated the head to the right or left. For the vertical canals, the head was turned 30° to 40° to either the right (left anterior right posterior) or left (right anterior left posterior), and the head was moved quickly up and down. A positive result in the vHIT was defined as a gain less than 0.8 for the horizontal semicircular canal and less than 0.7 for the vertical semicircular canals [5].

Video nystagmography test

The video nystagmography test (System 2000, Micromedical Technologies Inc.) was used to record and measure eye movements. The test included assessments of spontaneous nystagmus, head-shaking nystagmus, Dix-Hallpike test, head roll test, and bow and lean test, to observe the resulting eye movements. The direction of nystagmus was recorded according to the fast component.
Spontaneous nystagmus was evaluated while the patient was seated, with video goggles worn to monitor eye movements. For head-shaking nystagmus test, the patient wore video goggles and was asked to tilt their head forward by 30°, then shake their head left and right approximately 20 to 30 times at a frequency of 2 Hz, to observe the presence and direction of nystagmus. In the Dix-Hallpike test, the patient's head was turned 45° to the right or left, then lowered 20° downward from the horizontal position, and maintained for 30 seconds. Afterward, the patient was asked to sit up, and nystagmus was observed for about 30 seconds. The head roll test involved placing the patient in the supine position on the examination table with the head flexed forward by 30°. The head was then rotated 90° to the right, back to the center, then to the left, and back to the center, each position held for approximately 30 seconds to observe for induced nystagmus. The bow and lean test assessed nystagmus that appears when the patient tilts their head forward between 90° and 120°, and when they lean their head backward between 45° and 60°.

Bithermal caloric test

The bithermal caloric test (VISUALEYES Spectrum, Micromedical Technologies Inc.) was performed after the participant wore video goggles and rested in a supine position with a pillow to maintain approximately 30° head elevation. During the test, warm (44 °C) and cold (30 °C) water were alternately irrigated into each ear, and nystagmus was recorded and analyzed based on the responses. The canal paresis (CP) value was determined using Jongkee formula, which utilizes the maximum velocity of the slow component of nystagmus [6]. A CP value exceeding 25% was considered indicative of unilateral vestibular weakness.
Image Analysis and Statistics
All magnetic resonance imaging (MRI) tests were conducted using a 3 T scanner (Signa HDxt, GE Medical system) with an eight channel head coil. White matter lesions were assessed by a single professional radiologist (SYK) according to the prior published references [7-9]. Deep white matter hyperintensities and periventricular white matter hyperintensities (PVWMH) were classified into four groups (0 to 3). The grading for PVWMH is as follows: (1) Grade 0: No lesions; (2) Grade 1: “Caps” or pencil-thin linings around the ventricles; (3) Grade 2: A smooth “halo” or band of hyperintensity around the ventricles; and (4) Grade 3: Irregular periventricular lesions extending into the deep white matter.
All data were analyzed by GraphPad Prism ver.8 (GraphPad Software) and IBM SPSS ver.26 (IBM SPSS Corp.). A Shapiro-Wilk normality test was used to determine whether the data were parametric or nonparametric. Significant differences between groups were statistically analyzed using t-test in cases of a parametric distribution, and Mann-Whitney U-test in cases of a nonparametric distribution. Fischer exact test was used for the cross-table analysis. A p-value less than 0.05 was considered statistically significant.
Characteristics and Demographics
A total of 17 patients diagnosed with acute UVP were included in this study. All patients presented with acute vertigo and demonstrated unilateral weakness on the vHIT and increased CP on bithermal caloric testing. Follow-up assessments conducted after an average of 41 days (range, 14 to 120 days) revealed that all patients continued to exhibit unilateral weakness of vHIT gain in the affected lateral semicircular canal, classifying them as persistent vHIT weak patients.
Among these, three patients exhibited unusual videonystagmographic findings characterized by positional direction-changing nystagmus. Specifically, two patients showed no spontaneous nystagmus initially but developed apogeotropic, DCPN later, while one displayed spontaneous torsional nystagmus during the Dix-Hallpike test. Based on these findings, these three patients were categorized into the DCNp (direction-changing nystagmus positive) group, with the remaining 14 forming the CONTROLp group. All patients in the DCNp group did not complain positional symptoms.
The DCNp group tended to be older (average age, 67.6 years) compared to the CONTROLp group (average age, 59.9 years), although this difference was not statistically significant. Gender distribution differed as well, with the CONTROLp group displaying an equal male-to-female ratio, while the DCNp group was predominantly female (2:1). There was no statistical difference of interval between two vHIT test between two groups (CONTROLp group, 43 days; DCNp group, 31 days). In terms of systemic health, some control patients had comorbidities like hypertension or diabetes, whereas none were identified in the DCNp group.
Vestibular Function Tests and Imaging Studies
Initial vestibular function tests revealed that the CONTROLp group had larger mean spontaneous and head-shaking nystagmus amplitudes than the DCNp group (4.5° vs. 1.0°, p=0.04; 5.9° vs. 0.6°, p=0.01). The CP percentage was high in both groups (approximately 70%–76%) with no significant difference.
vHIT assessments showed that both groups exhibited reduced gain in the ipsilesional lateral semicircular canal, with the CONTROLp group averaging 0.37 and the DCNp group 0.49. Importantly, the DCNp group demonstrated significantly smaller gains in the contralesional anterior canal and ipsilesional posterior canal at baseline compared to CONTROLp (p=0.004 and p=0.03). Although the difference in anterior canal gain diminished over time, the disparity in the ipsilesional posterior canal gain persisted significantly (p=0.02) (Fig. 2).
Neuroimaging evaluations were performed 4.1 days after onset, and interval between MRI and vHIT was 6.7 days in average. There was no statistical difference in both time points between groups. Neuroimaging evaluations revealed no significant difference in deep white matter hyperintensity grades between the groups. However, the DCNp group had a significantly higher grade of PVWMH compared to the CONTROLp group (average grade of 3 vs. 1.8, respectively; p=0.001), suggesting potential neuroanatomical correlates influencing recovery and nystagmus patterns (Fig. 3).
This study evaluated acute UVP patients with persistent low vHIT gain, identifying a subgroup characterized by DCPN. While their demographic profile did not differ significantly from other persistent low-gain patients, this subgroup exhibited possibility of unique vestibular and neuroimaging features: reduced gains in the contralateral anterior and ipsilateral posterior canals, and a higher burden of PVWMH.
DCPN is an atypical finding in unilateral peripheral vestibulopathy, more commonly associated with central vestibular or cerebellar dysfunction [10]. The selective involvement of the contralesional anterior and ipsilesional posterior canals suggests that compensatory mechanisms after unilateral loss may not be uniform across all canal planes. According to Ewald’s first law, nystagmus direction aligns with endolymph flow within the stimulated canal; thus, the asymmetric gain reduction observed here may reflect altered intercanal coupling, possibly mediated by central adaptive processes or subclinical structural changes in vestibular pathways.
The observed PVWMH burden is particularly noteworthy. While often attributed to aging, PVWMH reflects microangiopathy, gliosis, and perivascular changes that can disrupt subcortical-cortical connectivity [7-9]. Such changes may compromise central vestibular compensation by affecting white matter tracts involved in vestibular integration, including the vestibulo-thalamo-cortical pathways. This could manifest as persistent canal asymmetry or atypical nystagmus profiles despite peripheral recovery.
Clinically, these findings raise two important considerations. First, DCPN in UVP should prompt evaluation for subtle central contributions, particularly in older adults or those with vascular risk factors. Second, the association with PVWMH highlights the potential role of cerebrovascular health in vestibular compensation. Targeted rehabilitation strategies, and potentially interventions to improve cerebral microvascular function, may be warranted in this subgroup. However, this study holds several limitations which are retrospective design, very small DCNp sample (n=3), potential referral/selection bias, and unmeasured confounding. Because this was a small, single-center retrospective study, caution should be used when generalizing these results to other populations. Given the exploratory nature and the small sample size, no formal correction for multiple testing was performed. Therefore, future study compensating these limitations are necessary. Future studies should explore whether the observed canal-specific gain reduction represents a transient maladaptation or a marker of incomplete central compensation. Longitudinal neuroimaging, combined with quantitative vestibular testing, may help clarify whether PVWMH burden predicts persistent imbalance, abnormal nystagmus evolution, or poorer recovery trajectories.

Funding/Support

This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2020R1A6A1A03043283; NRF-2021R1I1A3047407) and Bio&Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT) [RS-2023-00220408]. The Dankook Biomed Animal Facility was supported through the Research-Focused Department Promotion & Interdisciplinary Convergence Research Project as a part of the Support Program for University Development for Dankook University in 2025.

Conflicts of Interest

No potential conflict of interest relevant to this article was reported.

Availability of Data and Materials

All data generated or analyzed during this study are included in this published article. For other data, these may be requested through the corresponding author.

Authors’ Contributions

Conceptualization, Methodology: Lee MY, Jung JY, Choi JE; Data curation, Formal analysis, Investigation: Park YJ, Choi JE, Kim SY; Project administration, Supervision, Visualization: Lee MY; Writing–original draft: Lee MY, Park YJ, Choi JE, Kim SH; Writing–review & editing: All authors. All authors read and approved the final manuscript.

Fig. 1.
Flow diagram summarizing patient selection. DCPN, direction-changing positional nystagmus.
rvs-2025-028f1.jpg
Fig. 2.
Video head impulse (vHIT) test gain comparisons. vHIT gains between groups were compared at two different time points, at baseline and follow-up. The DCNp group demonstrated smaller gains in the contralesional anterior canal and ipsilesional posterior canal at baseline compared to CONTROLp. At follow-up, the difference in anterior canal gain diminished over time, the disparity in the ipsilesional posterior canal gain persisted significantly. X-axis values indicated the gains of each respective semicircular canal (SCC). Mean value of CONTROLp baseline contralesional anterior canal was 0.897 (95% confidence interval [CI], 0.749–1.045). Mean value of DCNp baseline contralesional anterior canal was 0.737 (95% CI, 0.687–0.767). Mean value of CONTROLp baseline ipsilesional posterior canal was 0.699 (95% CI, 0.589–0.809). Mean value of DCNp baseline ipsilesional posterior canal was 0.46 (95% CI, 0.113–0.751). Mean value of CONTROLp follow-up ipsilesional posterior canal was 0.692 (95% CI, 0.538–0.846). Mean value of DCNp follow-up ipsilesional posterior canal was 0.517 (95% CI, 0.325–0.664). Error bar represents standard errors. DCNp group, three patients with direction-changing positional nystagmus (DCPN); CONTROLp group, 14 patients without DCPN. Mann-Whitney U-test was used for statistical analysis (*p<0.05; ***p<0.001).
rvs-2025-028f2.jpg
Fig. 3.
Periventricular white matter hyperintensity (PVWMH) scores. The DCNp group had a significantly higher grade of PVWMH (average grade of 3) compared to the CONTROLp group (average grade of 1.8). Mean value of CONTROLp PVWMH grade was 1.8 (95% confidence interval [CI], 1.009–2.591). Mean value of DCNp PVWMH grade was 3 (95% CI, 0.853–4.155). Error bar represents standard errors. DCNp group, three patients with direction-changing positional nystagmus (DCPN); CONTROLp group, 14 patients without DCPN. Mann-Whitney U-test was used for statistical analysis (***p<0.001).
rvs-2025-028f3.jpg
Table 1.
Detailed information of individual patients
Group Age (yr) Sex Averaged PTA (dB HL) better hearing Initial SN Initial HSN DCNP Caloric CP (%) Interval between vHITs Onset SSNHL
CONTROLp 52 Female 18 3 7 0 73 20 14 No
CONTROLp 76 Female 40 0 4 0 100 90 7 Yes
CONTROLp 56 Male Not done 4 3 0 73 21 6 No
CONTROLp 67 Male 78 0 0 0 58 14 2 No
CONTROLp 51 Male Not done 11 10 0 60 40 0 No
CONTROLp 69 Male 58 5 5 0 75 40 0 No
CONTROLp 84 Female 58 0 6 0 44 30 90 No
CONTROLp 79 Male 10 4 9 0 63 120 6 No
CONTROLp 52 Female 16 21 9 0 83 60 1 No
CONTROLp 56 Male 13 10 19 0 61 28 1 No
CONTROLp 33 Female Not done 5 2 0 81 42 6 No
CONTROLp 57 Female 2 0 4 0 43 30 90 No
CONTROLp 65 Female 18 0 5 0 78 27 90 No
CONTROLp 42 Male 24 0 0 0 100 45 17 No
DCNp 72 Female 16 0 0 B)  PH ageotrophic 100 21 90 No
DCNp 68 Male 8 0 0 B) PH ageotrophic 100 55 30 No
DCNp 63 Female 21 3 2 B) DH geotropic torsional  30 17 1 No

PTA, pure tone audiometry (average of 0.5, 1, 2, and 4 kHz); HL, hearing level; SN, spontaneous nystagmus; HSN, head shake nystagmus; DCPN, direction-changing positional nystagmus; CP, canal paresis; vHIT, video head impulse; SSNHL, sudden sensory neural hearing loss; PH, positional head; DH, Dix-Hallpike.

CONTROLp group, 14 patients without DCPN; DCNp group, three patients with DCPN.

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        Characteristics of uncompensated acute unilateral vestibulopathy and preliminary clinical characteristics of patients with direction-changing positional nystagmus: a retrospective observational study
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      Characteristics of uncompensated acute unilateral vestibulopathy and preliminary clinical characteristics of patients with direction-changing positional nystagmus: a retrospective observational study
      Image Image Image
      Fig. 1. Flow diagram summarizing patient selection. DCPN, direction-changing positional nystagmus.
      Fig. 2. Video head impulse (vHIT) test gain comparisons. vHIT gains between groups were compared at two different time points, at baseline and follow-up. The DCNp group demonstrated smaller gains in the contralesional anterior canal and ipsilesional posterior canal at baseline compared to CONTROLp. At follow-up, the difference in anterior canal gain diminished over time, the disparity in the ipsilesional posterior canal gain persisted significantly. X-axis values indicated the gains of each respective semicircular canal (SCC). Mean value of CONTROLp baseline contralesional anterior canal was 0.897 (95% confidence interval [CI], 0.749–1.045). Mean value of DCNp baseline contralesional anterior canal was 0.737 (95% CI, 0.687–0.767). Mean value of CONTROLp baseline ipsilesional posterior canal was 0.699 (95% CI, 0.589–0.809). Mean value of DCNp baseline ipsilesional posterior canal was 0.46 (95% CI, 0.113–0.751). Mean value of CONTROLp follow-up ipsilesional posterior canal was 0.692 (95% CI, 0.538–0.846). Mean value of DCNp follow-up ipsilesional posterior canal was 0.517 (95% CI, 0.325–0.664). Error bar represents standard errors. DCNp group, three patients with direction-changing positional nystagmus (DCPN); CONTROLp group, 14 patients without DCPN. Mann-Whitney U-test was used for statistical analysis (*p<0.05; ***p<0.001).
      Fig. 3. Periventricular white matter hyperintensity (PVWMH) scores. The DCNp group had a significantly higher grade of PVWMH (average grade of 3) compared to the CONTROLp group (average grade of 1.8). Mean value of CONTROLp PVWMH grade was 1.8 (95% confidence interval [CI], 1.009–2.591). Mean value of DCNp PVWMH grade was 3 (95% CI, 0.853–4.155). Error bar represents standard errors. DCNp group, three patients with direction-changing positional nystagmus (DCPN); CONTROLp group, 14 patients without DCPN. Mann-Whitney U-test was used for statistical analysis (***p<0.001).
      Characteristics of uncompensated acute unilateral vestibulopathy and preliminary clinical characteristics of patients with direction-changing positional nystagmus: a retrospective observational study
      Group Age (yr) Sex Averaged PTA (dB HL) better hearing Initial SN Initial HSN DCNP Caloric CP (%) Interval between vHITs Onset SSNHL
      CONTROLp 52 Female 18 3 7 0 73 20 14 No
      CONTROLp 76 Female 40 0 4 0 100 90 7 Yes
      CONTROLp 56 Male Not done 4 3 0 73 21 6 No
      CONTROLp 67 Male 78 0 0 0 58 14 2 No
      CONTROLp 51 Male Not done 11 10 0 60 40 0 No
      CONTROLp 69 Male 58 5 5 0 75 40 0 No
      CONTROLp 84 Female 58 0 6 0 44 30 90 No
      CONTROLp 79 Male 10 4 9 0 63 120 6 No
      CONTROLp 52 Female 16 21 9 0 83 60 1 No
      CONTROLp 56 Male 13 10 19 0 61 28 1 No
      CONTROLp 33 Female Not done 5 2 0 81 42 6 No
      CONTROLp 57 Female 2 0 4 0 43 30 90 No
      CONTROLp 65 Female 18 0 5 0 78 27 90 No
      CONTROLp 42 Male 24 0 0 0 100 45 17 No
      DCNp 72 Female 16 0 0 B)  PH ageotrophic 100 21 90 No
      DCNp 68 Male 8 0 0 B) PH ageotrophic 100 55 30 No
      DCNp 63 Female 21 3 2 B) DH geotropic torsional  30 17 1 No
      Table 1. Detailed information of individual patients

      PTA, pure tone audiometry (average of 0.5, 1, 2, and 4 kHz); HL, hearing level; SN, spontaneous nystagmus; HSN, head shake nystagmus; DCPN, direction-changing positional nystagmus; CP, canal paresis; vHIT, video head impulse; SSNHL, sudden sensory neural hearing loss; PH, positional head; DH, Dix-Hallpike.

      CONTROLp group, 14 patients without DCPN; DCNp group, three patients with DCPN.


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