Ménière’s disease has no single established cause. Genetic susceptibility, viral infections, autoimmune activity and autonomic dysregulation may converge on several interconnected processes, including abnormal accumulation of endolymph in the membranous labyrinth, inflammation, impaired inner-ear circulation, oxidative stress and injury to auditory and vestibular neurons. This biological complexity helps explain why interventions aimed at a single pathway can produce inconsistent results in a condition whose severity and course vary considerably among patients. Current management is correspondingly staged, beginning with lifestyle modification, dietary sodium restriction, diuretics and betahistine, followed by intratympanic corticosteroids or gentamicin and, in severe cases, surgery. The review notes that the evidence for some conservative measures remains equivocal, while intratympanic gentamicin can control vertigo while carrying a risk of permanent ototoxicity.

The pathological feature drawing the most mechanistic attention is endolymphatic hydrops, an abnormal accumulation of endolymph that is associated with Ménière’s disease but neither unique to it nor sufficient on its own for diagnosis. Endolymph is produced mainly by the cochlear stria vascularis and normally removed through the endolymphatic sac, a specialized structure involved in fluid regulation and metabolic-waste clearance. Aquaporin 2, a membrane protein that transports water, is expressed in the sac and vestibular end organs and helps regulate endolymph volume. Pathological studies have reported congenital malformation, inflammation-related fibrosis and age-related degeneration in the endolymphatic sac, all of which could impair reabsorption. In rodent models in which the endolymphatic duct was surgically obstructed, aquaporin 2 expression fell, consistent with reduced water clearance and hydrops. Whether changing this protein can prevent or reverse human disease remains unknown, but it provides a measurable target for mechanistic research.

Herbal experiments reviewed by the authors connect TCM interventions with several processes implicated in Ménière’s disease. In guinea pigs with surgically induced hydrops, the herbal formula Wendan decoction improved neurovestibular function, reduced labyrinthine swelling and preserved outer hair cells compared with untreated animals. Assays also found reduced aquaporin 2 expression in inner-ear tissue. Because the intervention lowered rather than raised a protein associated with water transport, the authors interpret the result as consistent with the formula supporting endolymph absorption and fluid balance. This provides a possible biological interpretation of the traditional category “phlegm-dampness,” but the review stresses that an animal experiment does not directly validate a classical theory or demonstrate clinical benefit in people. The study also used surgical induction of hydrops, so its findings may not reproduce the heterogeneous biological triggers of human disease.

The same preclinical work points to an anti-inflammatory pathway. Wendan decoction reduced activation of the mitogen-activated protein kinase, or MAPK, pathway and lowered the release of proinflammatory cytokines in experimental inner-ear models. Other botanical preparations, including Ginkgo biloba extract, have suppressed tumor necrosis factor alpha and interleukin-1 beta in laboratory studies. These mediators can activate NF-κB signaling, recruit immune cells and damage the blood-labyrinth barrier, which helps isolate inner-ear tissues from systemic immune activity. Persistent inflammation can also promote reactive oxygen species, mitochondrial dysfunction and programmed cell death in sensory hair cells and neurons. Experimental reports of an anti-inflammatory action by acupuncture add another possible mechanism, possibly involving vagal and cholinergic pathways, although these explanations remain hypotheses requiring direct confirmation in humans. The review also proposes a longer-term neuroprotective role for interventions that reduce oxidative stress and apoptosis, but that possibility is based principally on experimental pathways rather than demonstrated protection of human hearing or vestibular function.

Human evidence is more developed, though still methodologically uneven, for acupuncture. A 2024 meta-analysis of six randomized controlled trials reported that acupuncture alone or combined with conventional therapy performed better than conventional therapy alone for overall efficacy. Other pooled analyses found reductions in Dizziness Handicap Inventory scores, improvements in Tinnitus Handicap Inventory scores, less ear fullness on visual analogue scales and better pure-tone audiometry thresholds. These findings point to effects on both perceived disability and measured hearing, but the review does not establish a reliable treatment effect or a consistent clinical benefit across patients. Trials tend to be small, acupuncture protocols vary and sham controls are inconsistent. Ménière’s disease also has a fluctuating course, and the substantial placebo response described in the review makes it difficult to distinguish specific effects from nonspecific improvement and natural variation.

That placebo problem is unusually important for interpreting results. Reviews cited in the article report reductions in vertigo-attack frequency of roughly 50 percent or more in placebo groups of some studies. An uncontrolled observation or a trial without credible blinding can therefore appear favorable even when the intervention’s specific effect is small. Herbal trials face similar problems: small samples, subjective endpoints, short follow-up, inadequate controls and inconsistent preparation or dosing. One reported study of modified Banxia Baizhu Tianma decoction recorded a 94.74 percent overall response rate, but the review says that the numerical result cannot be separated from bias, natural symptom fluctuation and placebo or other nonspecific effects without a properly controlled comparison. The response rate therefore should not be read as proof that the formula prevents attacks, protects hearing or changes the long-term course of disease. A substantial placebo response is a property of the evidence context, not evidence that an intervention is ineffective, but it raises the threshold needed to demonstrate a specific therapeutic effect.

Several other TCM ingredients have biological effects relevant to the disorder, although most have not been tested adequately in patients with Ménière’s disease. Gastrodia elata contains gastrodin, which has shown anticonvulsant, sedative, neuroprotective and microcirculation-related effects in experimental research. Pinellia ternata supplies alkaloids with antiemetic activity, while Alisma species contain triterpenoids with diuretic effects. Ginkgo biloba extracts have been investigated for blood flow, oxidative stress and tinnitus, and preclinical work reports effects on cochlear microcirculation through platelet aggregation and endothelial nitric oxide production. These properties are compatible with the pathways proposed in the review, including improved cochleovestibular circulation and reduced oxidative injury. Compatibility is not proof that isolated effects translate into meaningful changes in vertigo frequency, hearing loss or disease progression in humans. The clinical evidence for these individual constituents remains more limited than the mechanistic literature.

The review’s proposed research program calls for multicentre, adequately powered randomized controlled trials with standardized herbal preparations or clearly specified acupuncture protocols. For herbal studies, researchers should control batch variability, report preparation methods, use appropriate placebos and assess blinding where feasible. Acupuncture trials should employ carefully designed sham procedures, measure the success of blinding and standardize acupoint selection, stimulation parameters and treatment duration. Objective measures—including delayed gadolinium-enhanced inner-ear magnetic resonance imaging for hydrops, comprehensive audiometry, the video head impulse test and vestibular evoked myogenic potentials—should be combined with symptom scales. The authors also argue that molecular, immunological and imaging data may eventually help distinguish biological subgroups, while cautioning that MRI-detected hydrops is a structural feature rather than an etiological category. Proposed inflammatory, vascular or genetic profiles remain research concepts, and the review does not establish that they can yet guide the selection of a specific TCM regimen.

Overall, the review positions acupuncture and herbal medicine as testable components of an integrative model rather than replacements for established care. Acupuncture has the larger body of clinical studies and shows preliminary associations with symptom relief and some audiometric improvement. Herbal prescriptions have more detailed laboratory and animal findings involving aquaporin expression, MAPK and NF-κB signaling, microcirculation, oxidative stress and apoptosis, but those results do not establish efficacy in people. The review’s proposed multi-tiered sequence—an immediate anti-inflammatory and fluid-regulatory effect, medium-term vestibular compensation and long-term neuroprotection—is a mechanistic framework for testing, not a demonstrated treatment trajectory. Until adequately powered, standardized and long-term trials confirm both clinical effects and relevant mechanisms, firm clinical recommendations would go beyond the available evidence.

Subject of Research: Evaluation of acupuncture and herbal medicine as adjunctive treatments for Ménière’s disease

Article Title: Bridging mechanistic evidence and clinical perspectives: traditional Chinese medicine in Menière's disease

Article References: Ye, S., & Zhu, Z. (2026). Bridging mechanistic evidence and clinical perspectives: traditional Chinese medicine in Menière's disease. Frontiers in Neurology, 17, Article 1915230. https://doi.org/10.3389/fneur.2026.1915230

Image Credits: AI Generated

DOI: 10.3389/fneur.2026.1915230

Keywords: Ménière’s disease, traditional Chinese medicine, acupuncture, herbal medicine, endolymphatic hydrops, aquaporins, vertigo, hearing loss, tinnitus, clinical evidence, Bridging, mechanistic

The report, authored by Antonio Denia-Lafuente and Belén Lombardero of the Unidad de Oído y Vértigo at Hospital Universitario Nuestra Señora del Rosario, follows a 56-year-old woman with a lifelong history of CN, migraine, and episodic vertigo across five years of clinical visits. The patient arrived at the emergency department after three days of severe headache followed by vertigo, persistent imbalance, nausea, and bilateral tinnitus that was more pronounced in the left ear, without hearing loss. A neurological workup, including brain computed tomography, revealed spontaneous left-beating nystagmus and findings consistent with episodic migraine. She received vestibular sedatives and rizatriptan benzoate and was referred for further evaluation.

Her history was striking. She had experienced episodes of vertigo lasting two to three days for approximately 27 years, sometimes while in bed, and tinnitus in the left ear for the previous three years. Since reaching menopause, these episodes had been associated with migraines, sometimes preceding them, with photophobia and phonophobia, and occasionally antedated by bilateral ear pressure and tinnitus, especially in the left ear. She described fluctuating, non-permanent hearing loss, frequent spatial disorientation in open spaces, and a history of childhood strabismus. Her Dizziness Handicap Inventory (DHI) score of 60 indicated a substantial impact on daily life.

Clinical and videonystagmography examination using an Interacoustics VN415 system revealed a high-frequency, horizontal, jerk, left-beating nystagmus in primary gaze, which intensified in left gaze and changed direction, decreasing in right gaze. The CN limited standard vestibular assessment, including observation of spontaneous nystagmus, head shaking, vibration-induced nystagmus, and head impulse tests, as well as videonystagmography. Despite this, the right Dix-Hallpike test with VNS elicited, after two to three seconds, intense mixed upbeat and right-torsional nystagmus lasting about 18 seconds with severe vertigo. The patient was diagnosed with CN, vestibular migraine, and right posterior canalolithiasis benign paroxysmal positional vertigo (BPPV) — a diagnosis of BPPV in a patient with CN that the authors report for the first time.

The technical heart of the report lies in the vHIT recordings. The video head impulse test measures the vestibulo-ocular reflex (VOR), the rapid eye movement that stabilizes gaze when the head turns, by tracking eye motion during brief, passive head rotations at high frequencies. Each of the six SCCs can be probed individually. In this patient, the CN waveform conditioned the recorded lateral VOR eye movements: with spontaneous nystagmus suppression disabled, the system registered a low acceptance rate and frequent rejections, so results were reported with suppression enabled, showing a normal acceptance and rejection rate. Lateral HIMP revealed reduced gain values and impaired bilateral horizontal VOR generation, while vertical canal VOR gains remained normal for each SCC, without refixation saccades.

Perhaps the most intriguing finding was the spectrum of compensatory saccades — rapid corrective eye movements that substitute for a deficient VOR — observed during passive head impulses. These included very early saccades with near-zero latency or occurring at the onset of head acceleration, early covert saccades during head acceleration, and covert saccades occurring during the deceleration phase of the impulse, at approximately 100 to 140 milliseconds. These responses were predominantly rightward and frequently exhibited a double-peaked saccadic pattern. To the authors’ knowledge, very early saccades during passive head impulses have not been specifically characterized in the literature, and only a few studies have reported early saccades in vestibular lesions under these conditions.

The authors believe that repeated use of the passive HIMP protocol trained this patient to detect and reduce retinal slip errors by gradually increasing the number of saccades, adjusting their latency during the deceleration phase, and improving gaze stability and functional recovery. Over the five-year follow-up, the saccadic response shifted from a dispersed pattern to a clustered organization of covert saccades, compatible with compensated vestibular deficits, with consistently low gains. The authors suggest that congenital nystagmus does not interfere with vertical VOR function, allowing normal and abnormal vestibular response patterns to be observed, which they emphasize as important for routine study.

The SHIMP protocol — the suppression head impulse test, which removes compensatory saccades and generates anticompensatory saccades instead — proved essential for accurate interpretation. SHIMP VOR gains were comparable on both sides at two visits but remained below HIMP values, and saccade analysis showed low bilateral anticompensatory amplitudes, greater to the left, with 5 percent rightward covert compensatory saccades at three months that were absent at two years nine months. The presence of SHIMP anticompensatory saccades in a difficult-to-assess lateral VOR can be a very useful sign of vestibular function, and anticompensatory saccade generation through training can promote vestibular compensation and functional recovery.

Functionally, the patient’s trajectory was one of gradual improvement. At three months, positional tests were normal; at two years nine months, they revealed left posterior canalolithiasis, which was resolved with an Epley maneuver after a mild COVID-19 infection. At four years three months, after another mild COVID-19 infection, a right Dix-Hallpike test revealed posterior canalolithiasis, again resolved with an Epley maneuver. At four years six months, her symptoms had improved, with a DHI score of 30. At four years eight months, she reported being satisfied using both pairs of glasses, with a DHI score of 28 and a Visual Function Questionnaire (VFQ-25) score of 91 percent. At five years, she reported better global steadiness, no vertigo, greater visual stability, and fewer headaches, with a DHI score of 20.

From the patient’s perspective, at two years nine months she reported that before coming to the office, she missed work at least twice a month on days when she had disabling vertigo and that, after treatment, she has not missed work again. At four years eight months and at five years, progressive improvement persisted, with a marked reduction in vertigo and greater visual stability, which contributed to improved balance and well-being. The authors conclude that vestibular function assessment in CN and vertigo using vHIT and VNS enables accurate diagnosis and successful management of the most common vertigo syndromes, and they recommend an updated binocular vision study in these patients. The findings support the value of vHIT and videonystagmoscopy, providing new perspectives for assessing and managing the most frequent vertigo syndromes in CN and vertigo.

Subject of Research: Vestibular function assessment with vHIT and videonystagmoscopy in congenital nystagmus and vertigo

Article Title: Vestibular function assessment using the video head impulse test and videonystagmoscopy in congenital nystagmus and vertigo: a long-term case report

Article References: Denia-Lafuente, A., & Lombardero, B. (2026). Vestibular function assessment using the video head impulse test and videonystagmoscopy in congenital nystagmus and vertigo: a long-term case report. Frontiers in Audiology and Otology, 4, Article 1917636. https://doi.org/10.3389/fauot.2026.1917636

Image Credits: AI Generated

DOI: 10.3389/fauot.2026.1917636

Keywords: congenital nystagmus, vertigo, video head impulse test, videonystagmoscopy, semicircular canals, vestibulo-ocular reflex, BPPV, vestibular migraine, saccades, vestibular rehabilitation, case report, Dix-Hallpike test

Obstructive sleep apnea, or OSA, is defined by repeated interruptions or reductions of breathing during sleep, each lasting more than ten seconds and occurring at least five times per hour. The condition is extraordinarily common and extraordinarily underdiagnosed. An estimated 80 to 90 percent of affected adults do not know they have it, and recent estimates place the prevalence in the United States at 32.4 percent, roughly 83.7 million people, a dramatic rise from figures recorded in the 1990s. Severity is graded by the apnea-hypopnea index, with mild disease involving 5 to 15 breathing events per hour, moderate disease 15 to 30, and severe disease 30 or more.

The review’s central question is what happens to the vestibular system, the network of fluid-filled semicircular canals and otolith organs in the inner ear that detects head motion and gravity. Vestibular dysfunction shows up objectively as a reduced vestibulo-ocular reflex gain on the video head impulse test, asymmetrical or absent vestibular-evoked myogenic potentials, or weakened caloric responses. Subjectively, it manifests as dizziness, vertigo, oscillopsia, imbalance, and a heightened risk of falls and accidents that can uproot daily life.

The evidence linking OSA to these deficits is striking. In one study, all 32 patients with moderate-to-severe OSA showed decreased vestibulo-ocular reflex gain compared with healthy controls, and patients with the most severe disease had a significantly higher fall-risk index than those with mild disease or controls. Both ocular and cervical vestibular-evoked myogenic potentials appear significantly lower in OSA patients than in healthy people, indicating damage across the semicircular canals, the saccule and the utricle. A meta-analysis from February 2025 quantified the risk: adults with OSA were significantly more likely to show abnormal vestibular testing, with an odds ratio of 4.8 for abnormal caloric tests, 7.9 for absent cervical vestibular-evoked potentials, and 6.2 for absent ocular vestibular-evoked potentials.

Why would a breathing disorder attack the inner ear? The review lays out three converging mechanisms. The ischemic theory holds that intermittent hypoxia, surging sympathetic tone, and endothelial dysfunction, including elevated levels of the vasoconstrictor endothelin, starve the labyrinth of blood. Because the inner ear is fed exclusively by terminal branches of the anterior inferior cerebellar artery with no collateral circulation, vasospasm or pressure swings can quickly translate into localized oxygen deprivation, and laboratory studies confirm that vestibular hair cells and the vestibular nucleus are vulnerable to hypoxia and reactive oxygen species.

The inflammation theory adds a second assault. Chronic inflammation in OSA releases pro-inflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6, which can trigger apoptosis in vestibular hair cells and atrophy of the stria vascularis. Inflammation also activates monocytes, creating microvascular perfusion deficits within the inner ear that may locally ischemize the vestibular neuroepithelium. A third, anatomical explanation notes that the nasopharynx and oropharynx, the very segments that collapse in OSA, are crucial to eustachian tube function; repetitive mechanical stress and high negative intrathoracic pressure can disrupt middle ear pressure, disturb the endolymph and perilymph, and mechanically stimulate vestibular receptors. Recent work even links semicircular canal dysfunction to altered heart rate variability, implicating autonomic dysregulation as a mediator of the vertigo-apnea connection.

The clinical consequences ripple through three classic vestibular syndromes. Benign paroxysmal positional vertigo, the most common cause of vertigo worldwide, arises when calcium carbonate otoconia dislodge into the semicircular canals, producing brief, violent spinning triggered by head movements. Patients with OSA show significantly higher rates of BPPV than healthy controls, and a 2021 study concluded that BPPV is not a random occurrence in these patients but a systemic consequence of sleep-disordered breathing, although no study has yet screened for BPPV specifically within OSA populations.

Meniere’s disease, a chronic disorder marked by vertigo, hearing loss, tinnitus and aural fullness thought to stem from endolymphatic hydrops, is similarly entangled with sleep apnea. A 2025 study found a staggering 75 percent prevalence of OSA among Meniere’s patients, with moderate-to-severe apnea associated with greater hearing loss. A nine-year longitudinal cohort of more than one million South Koreans showed that adults aged 45 to 64 with OSA had twice the incidence of subsequent Meniere’s disease. Shared risk factors such as obesity, hypertension and metabolic syndrome, along with intermittent hypoxia stressing the blood-labyrinthine barrier, likely explain the association, while fragmented sleep worsens tinnitus.

Vestibular migraine, the leading cause of episodic non-positional vertigo, completes the triad. Among 130 patients with severe OSA, 10.8 percent had vestibular migraine, and OSA was significantly overrepresented in vestibular migraine groups compared with controls. Obesity links the two conditions biologically, and the review’s authors suggest that treating OSA may itself relieve vestibular migraine, an intriguing therapeutic hypothesis that deserves further study.

That therapeutic angle is where the story turns hopeful. Continuous positive airway pressure, the gold standard OSA treatment, keeps the airway splinted open with a steady stream of pressurized air, maintaining consistent oxygen levels and reducing oxidative stress and inflammation. Early evidence suggests CPAP may benefit vestibular function directly: a pilot study of 20 Meniere’s patients with concomitant OSA found that CPAP alone helped control dizziness and vertigo with potential hearing benefit, and CPAP use in migraine sufferers dramatically reduced attack frequency from 5.8 to 0.1 days per month alongside shorter, less painful attacks and less medication use. A 12-month study tracking vestibulo-ocular reflex gain before and after CPAP found no significant improvement yet, hinting that longer treatment windows may be needed. The authors’ prescription is twofold: patients with OSA, especially those with Meniere’s disease or BPPV, should undergo systematic vestibular screening, and anyone with unexplained balance problems should be evaluated for hidden sleep apnea. In a condition that already affects more than 80 million Americans silently, the spinning room may be the clue nobody thought to chase.

Subject of Research: The impact of obstructive sleep apnea on vestibular dysfunction, vertigo syndromes, and balance

Article Title: Vestibular dysfunction in patients with obstructive sleep apnea: from physiopathology to treatment

Article References: Jihène, M., Selima, J., Aymen, S., & Melek, D. (2026). Vestibular dysfunction in patients with obstructive sleep apnea: from physiopathology to treatment. Frontiers in Sleep, 5, Article 1750104. https://doi.org/10.3389/frsle.2026.1750104

Image Credits: AI Generated

DOI: 10.3389/frsle.2026.1750104

Keywords: obstructive sleep apnea, vestibular dysfunction, vertigo, Meniere's disease, benign paroxysmal positional vertigo, vestibular migraine, CPAP, inner ear, intermittent hypoxia, balance disorders, vestibulo-ocular reflex, fall risk

The review is organized around how patients actually present: acute, episodic, or persistent symptoms. In the acute category, the authors highlight a newly characterized entity called the acute imbalance syndrome, or AIS, defined as an acute vestibular syndrome without nystagmus. Among emergency department consultations for vertigo or dizziness, roughly ten percent meet criteria for the acute vestibular syndrome, and about one fifth of those patients ultimately turn out to have suffered a stroke. Crucially, nearly half of central cases present as AIS rather than the classic nystagmus-associated form. Lesion-symptom mapping in stroke patients shows that AIS lesions cluster in the anterior cerebellar lobe, disrupting networks for posture and gait control, while the classic syndrome with nystagmus involves the posterior cerebellar and flocculonodular lobes and their vestibulo-ocular reflex circuits. This anatomical split means clinicians must choose their bedside tests carefully: when no nystagmus is present, algorithms such as STANDING are the appropriate choice.

For acute unilateral vestibulopathy, often called vestibular neuritis, the epidemiological picture has shifted. A Japanese nationwide survey estimated the annual incidence at about 7.1 per 100,000, double the figure recorded in 1993, likely reflecting better recognition of dizziness as the presenting symptom. About twenty percent of patients experience prodromal dizziness hours to days before the full syndrome, and involvement of both divisions of the vestibular nerve predicts more intense, longer-lasting symptoms and a higher risk of secondary functional dizziness. Delayed post-contrast 3D-FLAIR MRI now visualizes inflammatory enhancement of the labyrinth in roughly half of patients, offering an objective window into the disease process. The video head-impulse test remains the first instrumental examination, with a vestibulo-ocular reflex gain below 0.7 on the affected side serving as the recommended cut-off to separate peripheral from central lesions.

Treatment of vestibular neuritis still rests on three pillars, but each has been refined. Symptomatic drugs such as dimenhydrinate should be limited to one to three days. Steroids remain guideline-endorsed, although a recent placebo-controlled trial showed no effect on peripheral vestibular recovery, a result the authors attribute to a total steroid dose only a quarter of that used in the landmark 2004 randomized trial, leaving the question genuinely open. Physiotherapy has emerged as the strongest evidence-based intervention: a recent randomized trial found that an individualized program including rapid head rotations, performed three times daily for eight weeks, was probably the most effective approach, while isolated eye movements in a static head position show no benefit. In animal work, betahistine enhanced central compensation in a dose-dependent fashion, an effect amplified by combination with the MAO-B inhibitor selegiline, setting the stage for human trials.

Perhaps the most consequential advances concern the emergency department, where the stakes are highest. Vertical or torsional spontaneous nystagmus, though present in only about fifteen percent of acute vestibular syndrome patients, is highly predictive of a central cause, with specificity approaching 98 percent. Adding new-onset hearing loss to the HINTS battery mainly helps detect strokes of the anterior inferior cerebellar artery, raising stroke sensitivity by nearly eighteen percentage points in that subgroup. The four-step STANDING algorithm has now been validated repeatedly: after a single training session, interns achieved a sensitivity of about 85 percent and specificity of about 90 percent for dangerous central causes, and in a multicenter Italian study of isolated acute vertigo, trained emergency physicians using STANDING substantially outperformed standard care, while also reducing unnecessary head CT scans. A meta-analysis further showed that moderately trained non-specialists reach sensitivity comparable to subspecialists, though with somewhat lower specificity, and that as little as six hours of structured training suffices for successful implementation.

Technology is now entering the acute workflow. Machine learning models applied to video head-impulse data from all six semicircular canals distinguished stroke from vestibular neuritis with an accuracy of 87.8 percent, matching blinded expert clinicians and clearly beating simple gain cut-offs. A meta-analysis of horizontal canal data across 905 patients reported sensitivity of 85 percent and specificity of 84 percent for stroke detection, with a negative likelihood ratio useful for ruling out the disease. A separate retrospective model combining saccade gains, pursuit asymmetries, age and hypertension differentiated posterior circulation stroke from peripheral disease with sensitivity and specificity above 82 percent. The authors caution, however, that radiographic conjugate gaze deviation on CT or MRI cannot by itself separate peripheral from central causes and does not replace bedside examination.

In episodic vertigo, the review champions a provocative renaming: benign paroxysmal positional vertigo should become peripheral paroxysmal positional vertigo, because the condition is often not benign at all. Delayed diagnoses, atypical presentations in the elderly, high recurrence rates, fear of falling and residual dizziness in up to seventy percent of successfully treated patients all argue against the label. When the supine roll test is performed correctly, with the head raised twenty-five degrees and the whole body turned, horizontal canal variants account for nearly forty percent of cases, far more than previously appreciated. On the therapy side, the Semont Plus maneuver, which moves the head at least 150 degrees to the affected side based on biophysical modeling, halved the mean time to symptom freedom compared with the classic Semont maneuver and outperformed the Epley maneuver in randomized trials. For Menière’s disease, six 2023 Cochrane analyses rated the evidence for most established treatments as low or very low, but a phase 1 study showed that combining betahistine with selegiline increases the drug’s bioavailability a hundredfold, and a properly powered placebo-controlled trial is planned.

Vestibular migraine, the most common cause of recurrent spontaneous vertigo, is being reconceived as a broad spectrum rather than a narrow diagnosis. In a 2025 cross-sectional study of 2,801 newly diagnosed migraine patients, 68.4 percent reported vestibular symptoms, yet only 15.2 percent met formal diagnostic criteria. Therapeutically, the first adequately designed acute trial found rizatriptan ineffective against vertigo, but the INVESTMENT study, the first placebo-controlled trial of a CGRP monoclonal antibody in vestibular migraine, showed that galcanezumab improved disease-specific handicap and reduced dizzy days without serious adverse events, and a 2025 network meta-analysis ranked it as the current best preventive option. Meanwhile, delayed gadolinium-enhanced MRI revealed that endolymphatic hydrops occurs in vestibular migraine too, though typically bilateral, low-grade and vestibular-predominant, helping distinguish it from the pronounced, lateralized hydrops of Menière’s disease.

Genetics has transformed the understanding of chronic vestibular disorders. In bilateral vestibulopathy, biallelic RFC1 repeat expansions were found in eight percent of isolated cases, making RFC1 the most common monogenic cause, while FGF14 GAA expansions define the new spinocerebellar ataxia 27b. Quantitative vestibulo-ocular reflex testing now separates these entities at the bedside: a horizontal gain cut-off of 0.50 distinguished RFC1-related ataxia from SCA 27b with 91 percent specificity, and vHIT gains correlate with repeat size and disease duration, offering a progression biomarker. In so-called idiopathic downbeat nystagmus, FGF14 expansions were detected in roughly half of patients, and carriers showed an 80 percent response rate to 4-aminopyridine, compared with under five percent in RFC1 carriers whose disease involves neurodegeneration rather than reduced Purkinje cell excitability, a striking closure of the loop between genotype, mechanism and therapy.

The review closes with candid gaps. Functional dizziness, including persistent postural-perceptual dizziness, develops in roughly one in four patients after acute or episodic vestibular disorders, and new work on gaze behavior, maladaptive multisensory integration and illness-related cognitive appraisals is clarifying its mechanisms. Yet acute vestibular migraine episodes still evade emergency algorithms, evidence for thrombolysis and thrombectomy in posterior circulation stroke presenting as dizziness remains too thin for firm recommendations, and the authors emphasize that the field’s greatest unmet need is not new ideas but rigorous, placebo-controlled clinical trials with meaningful endpoints, together with systematic training so that the remarkable diagnostic knowledge of the last three years actually reaches the bedside.

Subject of Research: Recent advances in the diagnosis and treatment of vestibular and ocular motor disorders, including acute vestibular syndrome, positional vertigo, vestibular migraine and bilateral vestibulopathy

Article Title: An update on neuro-otology and neuro-ophthalmology – focusing on new developments in the last three years

Article References: Tarnutzer, A. A., Strupp, M. L., & Lehner, L. (2026). An update on neuro-otology and neuro-ophthalmology – focusing on new developments in the last three years. Journal of Neurology, 273(11), Article 657. https://doi.org/10.1007/s00415-026-14153-w

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14153-w

Keywords: vertigo, dizziness, vestibular disorders, stroke, HINTS, STANDING algorithm, vestibular migraine, Meniere's disease, bilateral vestibulopathy, vestibular neuritis, video head-impulse test, machine learning

The research, published in the Journal of Neurology, comes from the MobilE-TRA 2 cohort, a prospective observational study run at the German Center for Vertigo and Balance Disorders in Munich, a tertiary referral centre that sees more than 3,000 patients a year. The team, led by Sophia P. Schulze and Ralf Strobl of Ludwig-Maximilians-Universität München, followed 337 adults aged 60 and over who had been newly assessed for a vertigo, dizziness, or balance disorder. Just over half were women, and the average age was 71. Each participant underwent a full interdisciplinary work-up—structured medical history, neurological, ocular-motor, and neuro-otological examinations, and where clinically indicated, caloric testing, video head impulse testing, vestibular-evoked myogenic potentials, posturography, and audiometry. Then, at three and twelve months after receiving their individualised treatment recommendations, patients filled in postal questionnaires reporting how often they had actually implemented what had been prescribed. Follow-up rates were impressively high: 88.7 percent at three months and 87.2 percent at twelve.

The researchers drew a deliberate distinction between two categories of non-pharmacological recommendation. The first was specific exercises—balance, gait, or habituation exercises prescribed as part of vestibular rehabilitation, the standard therapy for many vestibular disorders. The second was lifestyle-related recommendations, a composite covering physical activity, general everyday movement, and weight control. This distinction matters because the two types demand different patterns of behaviour. Specific exercises need not be performed daily to be effective, whereas lifestyle changes depend on frequent, near-continuous implementation. Accordingly, the team applied different cut-offs on a five-point self-reported frequency scale, defining adherence to exercises as a score of two or higher and adherence to lifestyle recommendations as three or higher. The framework guiding the analysis was the World Health Organization’s multidimensional model of adherence, which sees the phenomenon as shaped by interacting social and economic, health system-related, condition-related, therapy-related, and patient-related factors.

The headline numbers look reassuring at first glance. Around 80 percent of participants were classified as adherent to each recommendation type at least once during follow-up—79.6 percent for specific exercises among the 216 who reported receiving them, and 80.4 percent for lifestyle recommendations among the 270 who received those. But the longitudinal analysis, using logistic generalised linear mixed-effects models with random intercepts to account for repeated measurements within each person, told a more nuanced story. Adherence to specific exercises dropped markedly between the three-month and twelve-month assessments, with an odds ratio of 0.28 (95 percent confidence interval 0.12 to 0.67). In plain terms, the odds of a patient still performing their prescribed vestibular exercises a year after their initial assessment were less than a third of the odds at three months. Adherence to lifestyle recommendations, by contrast, remained statistically stable over the same period.

Why do the exercises fall away while the lifestyle changes persist? The authors are careful not to interpret the decline as simple failure. In vestibular rehabilitation, symptoms often improve or resolve with treatment, and a patient whose dizziness has faded may genuinely need less practice. Previous research has also documented persistent barriers: symptom provocation during the exercises themselves—which can temporarily make people feel worse—along with time constraints, coexisting impairments, and insufficient guidance or feedback. People with vestibular disorders also report higher fear-avoidance beliefs and lower confidence during balance activities than healthy adults, which can make unsupervised home exercise feel risky. The decline may therefore reflect a mixture of successful recovery, waning motivation, and the well-known difficulty of sustaining self-managed home exercise that has been observed across physiotherapy and chronic disease populations more broadly.

One of the study’s most intriguing findings concerns who stuck with the exercises. Patients with greater perceived dizziness-related handicap at baseline—measured with the validated 25-item Dizziness Handicap Inventory, which scores the functional, physical, and emotional impact of dizziness from 0 to 100—were more likely to adhere to specific exercises, with an odds ratio of 1.03 per point (95 percent CI 1.00 to 1.06). This seems counterintuitive until one considers the psychology of symptom-driven motivation. People whose dizziness seriously disrupts their lives have a powerful, immediate reason to work at their rehabilitation. Those with mild or rapidly improving symptoms, on the other hand, may simply lose the incentive to continue. The same symptom burden can cut both ways, however: in other vestibulopathy subgroups, symptoms provoked by the exercises have been identified as a barrier to adherence. Symptom burden, the authors conclude, appears to influence adherence in ways that are highly context-specific.

The lifestyle recommendations obeyed a different logic altogether. Here, the strongest predictor was self-efficacy—a person’s belief in their own ability to perform specific behaviours, assessed with a three-item General Self-Efficacy Short Scale. Higher self-efficacy was associated with higher adherence (OR 1.65; 95 percent CI 1.02 to 2.66), while male gender was associated with lower adherence (OR 0.37; 95 percent CI 0.16 to 0.88). The self-efficacy finding aligns neatly with systematic reviews in physiotherapy, where low self-efficacy is consistently described as a barrier to home exercise, and with broader behavioural evidence linking confidence to health behaviour change. It also echoes earlier results from the same cohort, in which self-efficacy predicted functioning after specialised care. In a condition where patients must manage dizziness and unsteadiness while simultaneously changing daily habits, the belief that one can cope with difficult situations may be precisely the resource that sustains behaviour over time.

Perhaps the most methodologically interesting part of the study is what did not predict adherence. Drawing on behavioural economics, the team measured two further patient-related traits: time preferences, meaning how much people value future benefits relative to immediate rewards, and health-related risk attitudes, meaning willingness to take risks in health contexts. Both have been linked to health behaviours such as smoking, alcohol consumption, exercise, and diabetes self-management in previous research. Yet in this cohort, neither showed a statistically significant association with adherence to either recommendation type. The finding suggests that the psychological machinery behind keeping up vestibular exercises or lifestyle changes may differ from that behind other preventive health behaviours—or simply that the single-item measures used here lacked the sensitivity to detect weaker effects. Either way, it tempers the assumption that present-oriented, risk-tolerant patients are inevitably the ones who drift away from their treatment plans.

The study has honest limitations that shape how its results should be read. Adherence was self-reported and therefore vulnerable to recall and social desirability bias; the authors emphasise that the figures represent perceived implementation rather than objectively measured behaviour. Adherence measurement in VDB has never been standardised, and the category of specific exercises may have encompassed different exercise types across diagnostic subtypes, which ranged from benign paroxysmal positional vertigo and persistent postural-perceptual dizziness to Menière’s disease, vestibular migraine, and bilateral vestibulopathy. Diagnostic subtype could not be included in the multivariable models because several groups were too small, leaving open the possibility of residual confounding. Sensitivity analyses with alternative cut-offs shifted some estimates—for instance, under a stricter exercise cut-off, multimorbidity emerged as a barrier and self-efficacy as a stronger facilitator—so individual effect estimates warrant caution. Recruitment during the SARS-CoV-2 pandemic, when healthcare access was disrupted, may also have selected a more severely affected population, limiting transferability to primary care.

Even with those caveats, the practical message is clear and potentially actionable. Adherence in older adults with vertigo, dizziness, and balance disorders is not a single behaviour but at least two, with different time courses and different drivers. Exercises decay over the year after prescription, particularly among those whose symptoms were mild to begin with, while lifestyle changes persist—especially in patients with high self-efficacy, and less so in men. For clinicians, that argues against a one-size-fits-all follow-up schedule: patients with low self-efficacy, mild symptoms, or a recent exercise prescription may benefit most from booster contacts, feedback, and structured support in the months after their initial assessment, precisely when the data show adherence beginning to slip. For researchers, the study opens a direct question that it could not answer: why do patients stop? Larger cohorts, objective adherence measures, and primary-care replication will be needed to turn these observational patterns into interventions that keep older people steady on their feet.

Subject of Research: Adherence to non-pharmacological treatment recommendations in older adults with vertigo, dizziness, and balance disorders

Article Title: Adherence to treatment recommendations in older adults with vertigo, dizziness, and balance disorders: the MobilE-TRA 2 cohort study

Article References: Schulze, S. P., Katzenberger, B., Koller, D., Huppert, D., Grill, E., & Strobl, R. (2026). Adherence to treatment recommendations in older adults with vertigo, dizziness, and balance disorders: the MobilE-TRA 2 cohort study. Journal of Neurology, 273(10), Article 649. https://doi.org/10.1007/s00415-026-14195-0

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14195-0

Keywords: vertigo, dizziness, balance disorders, vestibular rehabilitation, treatment adherence, older adults, self-efficacy, geriatrics, cohort study, lifestyle modification, Dizziness Handicap Inventory, neurology

The stakes in this diagnostic puzzle could hardly be higher. Acute vestibular syndrome, defined as new-onset, severe and persistent vertigo or imbalance, makes up roughly 10 to 20 percent of all acute dizziness presentations to emergency departments. Posterior circulation stroke is life-threatening and demands urgent reperfusion therapy, while acute unilateral vestibulopathy, commonly known as vestibular neuritis, is a self-limiting inflammation of the vestibular nerve that resolves on its own. Yet these two conditions are among the most frequently misdiagnosed causes of dizziness, even by specialists. Focal neurological deficits, the classic red flags for stroke, are absent in as many as two-thirds of posterior circulation strokes, and early MRI can be falsely reassuring, missing about 15 percent of strokes when performed within the first 48 hours of symptom onset.

The traditional bedside answer to this problem is the HINTS examination, a three-step assessment comprising the head impulse test, nystagmus analysis and the test of skew. When performed by an experienced neuro-otologist, HINTS can exclude stroke with impressive accuracy, often outperforming early MRI. The catch is that frontline emergency clinicians, who are the ones actually evaluating these patients at 3 a.m., are rarely experts in the technique. Studies show they frequently avoid the examination, perform it incorrectly or misinterpret the results, particularly the subtle head impulse component. This gap between what is possible in expert hands and what happens in a busy emergency department is precisely what the Sydney team set out to close with algorithms rather than additional years of subspecialty training.

The researchers recruited 294 consecutive patients presenting to the emergency department of Royal Prince Alfred Hospital between March 2018 and March 2023, all reviewed within seven days of symptom onset by a clinician with neuro-otology expertise. Of these, 163 had acute unilateral vestibulopathy and 131 had imaging-confirmed posterior circulation stroke. Each patient underwent a standardised history covering demographics, vertigo characteristics, aural symptoms, focal neurological complaints and cardiovascular risk factors, a detailed bedside examination, and a battery of modern vestibular function tests: video-nystagmography to quantify spontaneous nystagmus with visual fixation removed, the video head impulse test assessing all six semicircular canals, cervical and ocular vestibular-evoked myogenic potentials probing the saccule and utricle, and the subjective visual horizontal test of utricular function. In total, 203 variables fed the modelling pipeline.

Rather than building a single model that demanded every possible test, the team deliberately designed three tiers of data availability to mirror real-world clinical settings. Tier 1 simulated a fully equipped emergency department with neuro-otology support, using history, specialist examination, video-nystagmography, horizontal canal video head impulse testing and ocular vestibular-evoked myogenic potentials. Tier 2 represented a non-expert clinician with basic examination skills and access to the video head impulse test, deliberately excluding the bedside head impulse and test of skew that trip up inexperienced examiners. Tier 3 captured the most resource-limited scenario, relying on history and basic examination alone. The researchers trialled three gradient-boosted tree algorithms, XGBoost, LightGBM and CatBoost, using five-fold stratified cross-validation, and compared the results against HINTS applied by experts to the same evaluation sets.

The results were striking. The best Tier 1 model, built on CatBoost, identified stroke with 96.6 percent accuracy, with a 95 percent confidence interval of 93.3 to 99.9 percent. The Tier 2 model, requiring no specialist examination skills at all, matched HINTS almost exactly, achieving 94.6 percent accuracy, statistically indistinguishable from the expert-performed bedside algorithm. Even the minimalist Tier 3 model, working from history and basic examination alone, reached 88.8 percent accuracy, significantly outperforming a conventional logistic regression model trained on the same data. HINTS itself achieved 94.6 percent accuracy in this cohort, confirming that the machine learning approaches were operating at the ceiling of what expert clinical assessment can deliver.

Feature importance analysis revealed that the algorithms were, reassuringly, learning clinically sensible patterns. In the richest data tier, the bedside head impulse test was the single most influential variable, followed by the slow phase velocity of spontaneous nystagmus measured on video-nystagmography and the presence of focal neurological symptoms on history. In Tier 2, where the head impulse test was unavailable, focal neurological symptoms dominated, with video head impulse metrics effectively substituting for the bedside manoeuvre. In the history-only tier, age emerged as the most powerful predictor, reflecting its status as a recognised stroke risk factor. The dataset explained why focal symptoms carried such weight: 65.6 percent of stroke patients reported them, compared with just 3.0 percent of those with vestibulopathy.

Perhaps most intriguingly, the models handled some of the trickiest atypical cases better than HINTS. Two patients with vestibulopathy but no spontaneous nystagmus on video-oculography, and two with the misleading test-of-skew finding, were correctly classified by the tiered models in several instances where HINTS failed. Among the small handful of patients misclassified by every model were two atypical vestibulopathy cases and a pontine stroke with no focal signs, no nystagmus and an abnormal bedside head impulse test, a genuinely deceptive combination. The researchers also showed that lowering the probability threshold for flagging stroke could push sensitivity above 99 percent in the better-resourced tiers, an attractive trade-off given the far greater cost of missing a stroke than of over-investigating a benign vertigo case.

The study’s implications reach well beyond the algorithm itself. The video head impulse test can be performed at the bedside in about five minutes, is well tolerated even in acutely unwell patients, and yields an objective quantified result that is easier to interpret than the naked-eye equivalent, especially when vigorous spontaneous nystagmus obscures the examination. A Tier 2-style workflow, combining structured history, basic neurological examination and video head impulse testing, could therefore provide rapid risk stratification early in the diagnostic pathway, potentially reducing unnecessary neuroimaging and the complications of inappropriate reperfusion therapy. The authors even found that video-nystagmography could substitute for the head impulse test in their Tier 2 model with similar performance, opening another accessible route for non-specialist departments.

The researchers are careful to frame this as a proof-of-concept rather than a finished clinical tool. Their history and examination data were collected by experts, which may flatter the models’ real-world performance, and the HINTS comparison benefited from video-oculographic nystagmus assessment that most emergency departments lack. The cohort came from a single tertiary centre, vestibular migraine patients were excluded, and external validation on larger, multi-centre datasets remains essential before deployment. The team also notes that practical hurdles, from user interface design and offline functionality to patient consent, data privacy and clinician adherence, must be solved before any algorithm enters the emergency workflow. Still, the central message is hard to ignore: with nothing more than a structured history, a basic examination and, ideally, a five-minute video head impulse test, machine learning can now tell a dangerous stroke from a self-limiting ear problem with the accuracy of the world’s leading dizziness specialists.

Subject of Research: Machine learning differentiation of posterior circulation stroke from acute unilateral vestibulopathy in acute vestibular syndrome

Article Title: Separating stroke and acute unilateral vestibulopathy using history, examination and vestibular tests: a machine learning approach

Article References: Wang, C., Chaturvedi, K., Nham, B., Reid, N., Bradshaw, A. P., Rosengren, S. M., Black, D. A., Bein, K. J., Halmagyi, G. M., Braytee, A., Bharathy, G. K., Prasad, M., & Welgampola, M. S. (2026). Separating stroke and acute unilateral vestibulopathy using history, examination and vestibular tests: a machine learning approach. Journal of Neurology, 273(10), Article 573. https://doi.org/10.1007/s00415-026-13779-0

Image Credits: AI Generated

DOI: 10.1007/s00415-026-13779-0

Keywords: machine learning, stroke, acute vestibular syndrome, vestibular neuritis, HINTS, video head impulse test, emergency medicine, neurology, vertigo, diagnosis, XGBoost, CatBoost

The study, led by Huseyin Nezih Ozdemir, Iryna Klopotovska and Diego Kaski of the SENSE Research Unit in UCL’s Department of Clinical and Movement Neurosciences, was conducted at the National Hospital for Neurology and Neurosurgery in London between April 2025 and April 2026. Consecutive patients aged 18 and over arriving at the dizziness clinic underwent a structured ten-question interview before their clinical consultation. Crucially, the interviewer recorded answers about symptom timing, triggers, avoidance behaviours and behavioural responses before any diagnosis had been established. The final diagnoses were then made independently by a vestibular neurologist who was blinded to the interview responses, using established criteria from the Bárány Society and the International Classification of Headache Disorders. This design ensured that the behavioural data could not be contaminated by knowledge of the diagnosis.

The cohort of 109 patients had a mean age of 55.3 years, and 71.5 percent were female. Thirty-three patients were diagnosed with vestibular migraine, thirty-three with persistent postural-perceptual dizziness, fourteen with benign paroxysmal positional vertigo and fifteen with orthostatic dizziness. Smaller groups included patients with central structural disorders such as posterior circulation stroke and other peripheral vestibular conditions including bilateral vestibular loss. When the researchers applied logistic regression to the interview data, four clear behavioural profiles emerged, each mapping closely onto the known biology of the underlying disorder.

The strongest single predictor belonged to vestibular migraine. Patients who reported that reading while travelling as a passenger in a vehicle brought on their dizziness were more than twenty times more likely to have vestibular migraine than any other diagnosis, with an odds ratio of 20.99. This finding fits with the idea that vestibular migraine reflects a heightened vulnerability to sensory conflict, the discordance between visual motion signals and vestibular input that occurs when the eyes track a page while the inner ear registers the movement of a car. It also builds on earlier work from the same group showing that motion sickness while reading in a moving car is highly predictive of the condition. For patients with persistent postural-perceptual dizziness, visually stimulating environments such as crowded, busy or visually complex settings were the strongest precipitating factor, carrying an odds ratio of 12.45, consistent with the disorder’s characteristic over-reliance on visual cues for spatial orientation.

The two remaining diagnoses produced equally distinctive patterns. For benign paroxysmal positional vertigo, head movements and positional changes were the dominant trigger, with an odds ratio of 11.51, exactly what would be expected from the abnormal movement of displaced calcium carbonate crystals, or otoconia, within the semicircular canals. Patients with orthostatic dizziness, by contrast, pointed to standing up quickly as their principal trigger, reflecting the transient drop in cerebral blood flow that occurs during orthostatic stress. In each case, the reported precipitant was not an arbitrary preference but a direct behavioural echo of the underlying mechanism: sensory conflict in vestibular migraine, visual dependence in persistent postural-perceptual dizziness, otoconial displacement in positional vertigo and cerebral hypoperfusion in orthostatic dizziness.

Avoidance behaviours proved just as diagnostic as triggers. Patients with vestibular migraine disproportionately avoided bright or noisy environments and sought refuge by resting in dark, quiet rooms, mirroring the visual and auditory hypersensitivity that characterises migraine more broadly. Those with persistent postural-perceptual dizziness avoided visually busy places such as supermarkets, crowded streets or scrolling screens, and notably reported trying to maintain their activity despite the symptoms, an effort to push through the persistent, physically non-disabling dizziness that defines the condition. Patients with benign paroxysmal positional vertigo reported deliberately avoiding quick head movements and staying still during attacks, an understandable strategy to prevent the violent, brief episodes of rotational vertigo that position changes provoke. Orthostatic dizziness patients avoided sudden standing and tended to sit or lie down slowly, a sensible countermeasure against orthostatic intolerance, although this particular association did not reach statistical significance, likely because of the smaller size of that subgroup.

Temporal patterns added a further layer of discrimination. Episodic dizziness was significantly associated with vestibular migraine, while patients with persistent postural-perceptual dizziness were far more likely to report continuous dizziness lasting days or longer, in keeping with the chronic nature of that disorder. Patients with benign paroxysmal positional vertigo characteristically reported brief episodes lasting seconds to minutes, matching its paroxysmal presentation. Although patients with positional vertigo and orthostatic dizziness tended to describe dizziness that comes and goes, these associations did not reach statistical significance, a limitation the authors attribute to the relatively small numbers in those diagnostic groups.

The clinical implications of the work are considerable. Because neuroimaging has limited utility in most cases of dizziness and definitive tests are lacking for many vestibular syndromes, diagnosis rests heavily on history taking, and patients’ descriptions of symptom quality are notoriously imprecise. Structured questions about avoidance and coping could capture dimensions of the patient’s experience that conventional symptom questions miss. Asking simply whether a patient avoids supermarkets, refrains from turning their head quickly, or retreats to a dark room when dizzy may sharpen diagnostic accuracy, shorten the long delays many patients experience before correct treatment, and potentially prevent progression to chronic dizziness. Beyond diagnosis, recognising these behaviours may help clinicians understand how the disorders impair daily and occupational functioning, since triggers such as bright environments or awkward head positions have been shown to interfere with work tasks and contribute to reduced productivity and absenteeism.

Perhaps the most intriguing aspect of the findings is that patients developed these behavioural signatures without any formal knowledge of disease mechanisms. The researchers argue that such adaptations arise intuitively through repeated symptom experience, which is precisely what makes them informative: they represent the body’s own experiment on the disorder, conducted over months or years. The behaviours therefore function as natural biomarkers, reflecting pathophysiology rather than clinical teaching. The authors also caution that avoidance behaviours can themselves contribute to disability, and identifying them may open the door to rehabilitation strategies that prevent deconditioning and fear-driven withdrawal from activity.

The study is not without limitations. The structured interview was not a validated instrument, several diagnostic subgroups were small, limiting statistical power for some response categories, and the single-centre design in a specialised London clinic may constrain generalisability. Larger cohorts will be needed to confirm the diagnostic value of these behavioural markers and to quantify their impact on patients’ functioning. Even so, the message is clear and potentially transformative for routine practice: when a patient says they feel dizzy, the clinician should ask not only what it feels like and when it happens, but what the patient does about it. The answers, this research suggests, may point directly to the diagnosis hiding behind one of medicine’s most vague and common complaints.

Subject of Research: Behavioural signatures as diagnostic clues in common vestibular disorders causing dizziness

Article Title: What patients do when they feel dizzy: behavioural signatures reveal diagnostic clues in common vestibular disorders

Article References: Ozdemir, H. N., Klopotovska, I., & Kaski, D. (2026). What patients do when they feel dizzy: behavioural signatures reveal diagnostic clues in common vestibular disorders. Journal of Neurology, 273(10), Article 587. https://doi.org/10.1007/s00415-026-14133-0

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14133-0

Keywords: dizziness, vestibular disorders, vestibular migraine, PPPD, BPPV, orthostatic dizziness, avoidance behaviour, coping strategies, behavioural adaptation, diagnosis, vertigo, neurology