Otolin-1 for differentiating central and peripheral causes of acute continuous dizziness
6 affiliations
- 1Department of Emergency Medicine, Jeroen Bosch Hospital, 's-Hertogenbosch, the Netherlands.
- 2Department of Vascular Surgery, University Medical Center Utrecht, Utrecht, the Netherlands.
- 3Department of Neurology, Haga Hospital, The Hague, the Netherlands.
- 4Department of Neurology, Maasstad Hospital, Rotterdam, the Netherlands.
- 5Department of Neurology, St. Antonius Hospital, Nieuwegein, the Netherlands.
- 6Department of Neurology, Haaglanden Medical Center, The Hague, the Netherlands.
Abstract
Background: Patients with isolated acute-onset continuous dizziness (iAOCD) are commonly seen at the emergency department (ED). Distinguishing peripheral vestibular disorders from central causes remains challenging. Existing diagnostic tools, including bedside examination and neuroimaging, have important limitations. Otolin-1, an inner ear–specific glycoprotein, has been proposed as a biomarker of peripheral vestibular pathology. This study evaluated whether otolin-1 could serve as a diagnostic biomarker for this differentiation. Methods: This study analyzed samples from a prospective multicenter cohort of adult patients who were seen at the ED with acute onset, continuous dizziness without focal neurological deficits. Patients were included within 24 hours of symptom onset. Otolin-1 plasma concentrations were measured using an enzyme-linked immunosorbent assay. Final diagnoses (central versus peripheral) were determined by an expert panel based on clinical assessment, diffusion-weighted magnetic resonance imaging and 3-month follow-up. Results: We analyzed 245 patients (179 peripheral, 66 central). Median otolin-1 concentrations did not differ significantly between peripheral and central causes (517.6 [IQR 443.7–592.8] pg/mL vs 487.9 [424.9–644.4] pg/mL; p = 0.349). No significant differences were observed in hyperacute (<4.5 hours after symptom onset) or acute (4.5–24 hours after symptom onset) subgroups. Similarly, otolin-1 concentrations did not differ between central iAOCD and specific peripheral diagnoses. Substantial overlap in concentration ranges was observed across all comparisons. Receiver operating characteristic analysis similarly showed no useful discrimination (AUC 0.539, 95% CI 0.455–0.623). Conclusions: Otolin-1 does not differentiate between central and peripheral causes of iAOCD in the ED setting. Although biologically linked to inner ear pathology, otolin-1 lacks sufficient discriminatory value as a stand-alone diagnostic biomarker.
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BibTeX
@article{klokman2026otolin1,
title = {{Otolin-1 for differentiating central and peripheral causes of acute continuous dizziness}},
author = {Vincent W Klokman and Merel J J Verhagen and Adriaan A J Ros and Karlijn F de Laat and Korné Jellema and Dominique P V de Kleijn and Kim E Jie},
journal = {PLOS One},
year = {2026},
month = oct,
doi = {10.1371/journal.pone.0361036},
url = {https://doi.org/10.1371/journal.pone.0361036},
note = {CC BY},
}
RIS
TY - JOUR
TI - Otolin-1 for differentiating central and peripheral causes of acute continuous dizziness
AU - Vincent W Klokman
AU - Merel J J Verhagen
AU - Adriaan A J Ros
AU - Karlijn F de Laat
AU - Korné Jellema
AU - Dominique P V de Kleijn
AU - Kim E Jie
PY - 2026
DA - 2026/10/22
JO - PLOS One
DO - 10.1371/journal.pone.0361036
UR - https://doi.org/10.1371/journal.pone.0361036
AB - Background: Patients with isolated acute-onset continuous dizziness (iAOCD) are commonly seen at the emergency department (ED). Distinguishing peripheral vestibular disorders from central causes remains challenging. Existing diagnostic tools, including bedside examination and neuroimaging, have important limitations. Otolin-1, an inner ear–specific glycoprotein, has been proposed as a biomarker of peripheral vestibular pathology. This study evaluated whether otolin-1 could serve as a diagnostic biomarker for this differentiation. Methods: This study analyzed samples from a prospective multicenter cohort of adult patients who were seen at the ED with acute onset, continuous dizziness without focal neurological deficits. Patients were included within 24 hours of symptom onset. Otolin-1 plasma concentrations were measured using an enzyme-linked immunosorbent assay. Final diagnoses (central versus peripheral) were determined by an expert panel based on clinical assessment, diffusion-weighted magnetic resonance imaging and 3-month follow-up. Results: We analyzed 245 patients (179 peripheral, 66 central). Median otolin-1 concentrations did not differ significantly between peripheral and central causes (517.6 [IQR 443.7–592.8] pg/mL vs 487.9 [424.9–644.4] pg/mL; p = 0.349). No significant differences were observed in hyperacute (<4.5 hours after symptom onset) or acute (4.5–24 hours after symptom onset) subgroups. Similarly, otolin-1 concentrations did not differ between central iAOCD and specific peripheral diagnoses. Substantial overlap in concentration ranges was observed across all comparisons. Receiver operating characteristic analysis similarly showed no useful discrimination (AUC 0.539, 95% CI 0.455–0.623). Conclusions: Otolin-1 does not differentiate between central and peripheral causes of iAOCD in the ED setting. Although biologically linked to inner ear pathology, otolin-1 lacks sufficient discriminatory value as a stand-alone diagnostic biomarker.
SN - 1932-6203
ER -