Vestibular Function Testing in Corticobasal Syndrome

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Vestibular Function Testing in Corticobasal Syndrome

Overview

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Vestibular Function Testing in Corticobasal Syndrome

Overview

Mermaid diagram (expand to render)

Vestibular function testing provides a window into brainstem and cerebellar pathology that is otherwise difficult to assess clinically in corticobasal syndrome (CBS). Unlike the relatively well-characterized oculomotor findings in PSP, vestibular dysfunction in CBS and related 4R tauopathies has been less systematically studied. However, emerging evidence demonstrates that vestibular testing modalities — including caloric irrigation, video head impulse testing (vHIT), vestibular evoked myogenic potentials (VEMPs), subjective visual vertical (SVV) assessment, and posturography — can differentiate CBS from PSP and other parkinsonian syndromes, and provide insight into the underlying neuroanatomical vulnerability["@armstrong2023"][@boehr2019].

The vestibular system, comprising peripheral receptors in the inner ear, brainstem vestibular nuclei, cerebellar integration centers, and cortical projections, is particularly vulnerable to 4R tau deposition. The selective involvement of vestibular circuits in CBS reflects the same neuropathological predilection that drives cortical basal degeneration: neurons with long axonal projections and high firing rates accumulate tau filaments, and this pattern extends to the vestibular nucleus complex embedded in the pontomedullary junction["@ferlito2021"].

Caloric Testing

Principle and Methodology

Caloric testing assesses the horizontal semicircular canal via thermal stimulation. Warm or cool water (or air) irrigated into the external auditory canal induces endolymph flow, stimulating the cupula and generating a vestibular nystagmus. The resulting nystagmus is quantified by measuring:

Peak slow-phase velocity (SPV) of the induced nystagmus
Latency from stimulus onset to nystagmus initiation
Duration of the nystagmus response
Direction (geotropic for warm, apogeotropic for cool in normal function)

The standard bithermal caloric protocol irrigates each ear with warm (44°C) and cool (30°C) water for 30 seconds, with at least 5 minutes between stimulations. Results are expressed as:

Unilateral weakness (UW): Percentage asymmetry between ears, calculated using Jongkees' formula. UW > 20-25% is considered abnormal.
Directional preponderance (DP): Asymmetry in the direction of nystagmus regardless of which ear is stimulated. DP > 30% is abnormal.

Caloric Findings in CBS

Caloric testing in CBS typically reveals a peripheral-like pattern that paradoxically reflects central pathology[@mcgress2022]:

Key findings:

Reduced caloric responses with prolonged latency and decreased SPV
Marked asymmetry — often exceeding 40-50% UW — reflecting the asymmetric cortical and brainstem involvement characteristic of CBS[@saifee2020]
Preserved "doll's head" reflex (VOR intact when neck is stabilized), distinguishing central from peripheral lesions
Impaired gain on caloric-induced VOR responses

The asymmetry in caloric responses correlates with the lateralized clinical presentation of CBS: patients with predominantly left-hemisphere involvement show greater left-ear caloric impairment, reflecting ipsilateral vestibular nucleus degeneration.

CBS vs PSP: Caloric Differentiation

| Parameter | CBS | PSP |
|-----------|-----|-----|
| Unilateral weakness | Markedly asymmetric (often >40%) | Moderate, less asymmetric |
| Latency | Prolonged | Normal or mildly prolonged |
| SPV | Reduced | Mildly reduced |
| Pattern | Asymmetric peripheral-like | Symmetric central-like |

The caloric asymmetry in CBS contrasts with the relatively symmetric deficits observed in PSP, where vertical gaze palsy and midbrain involvement produce more bilateral vestibular effects. In PSP, caloric testing may show normal or only mildly reduced responses with preserved symmetry, but with impaired vertical VOR that caloric testing of the horizontal canal cannot fully capture[@stott2023].

Clinical Utility

Caloric testing serves several roles in CBS assessment:

Baseline documentation: Establishes the degree of vestibular impairment at diagnosis

Disease progression marker: Serial caloric testing tracks the evolution of brainstem involvement

Differential diagnosis: Marked asymmetry favors CBS over symmetric PSP

Rehabilitation planning: Identifies patients who may benefit from vestibular rehabilitation strategies[@brandt2023]

Video Head Impulse Testing (vHIT)

Principle and Methodology

vHIT records eye movements in response to rapid, unpredictable head rotations using high-speed video-oculography (typically 250 Hz or faster). The test assesses the VOR gain — the ratio of eye movement to head movement — for each semicircular canal. A normal VOR gain is approximately 0.9-1.0; gains below 0.7-0.8 are considered abnormal.

vHIT provides several advantages over caloric testing:

Canal-specific assessment: Tests all six canals (bilateral horizontal, anterior, and posterior)
Physiological stimuli: Tests natural head movement rather than artificial thermal stimulation
Higher resolution: Detects subtle gain reductions
Less time-consuming: Complete test in under 10 minutes

The key vHIT parameters include:

VOR gain: Mean eye/head velocity ratio across the stimulus bandwidth
Refixation saccades: Compensatory saccades that appear when VOR gain is insufficient
Covert saccades: Occurring during the head movement (predictive)
Overt saccades: Occurring after the head movement (reactive)

vHIT Findings in CBS

vHIT in CBS demonstrates a characteristic multicanal deficit with asymmetric distribution[@cnytrim2023][@zampieri2022]:

Key findings:

Reduced horizontal canal gain with high frequency of refixation saccades
Anterior canal involvement — particularly in CBS variant with frontal lobe predominance
Asymmetric pattern: The more affected hemisphere correlates with greater canal impairment
Compensatory saccade burden: Both covert and overt saccades increase as gain falls

The VOR gain reduction in CBS reflects both the direct involvement of vestibular nuclei in the brainstem and the indirect effects of cerebellar Purkinje cell degeneration on vestibular adaptation circuits. The cerebellum — particularly the flocculus, paraflocculus, and uvula — normally modulates VOR gain through feedback mechanisms. Tau pathology in these regions produces a characteristic pattern of gain reduction with prominent compensatory saccades.

CBS vs PSP: vHIT Differentiation

| Parameter | CBS | PSP |
|-----------|-----|-----|
| Horizontal canal gain | Reduced, asymmetric | Mildly reduced, symmetric |
| Anterior canal gain | Frequently impaired | Impaired (vertical VOR) |
| Compensatory saccades | Common, asymmetric | Present but symmetric |
| Pattern | Multicanal asymmetric | Vertical > horizontal |
| Clinical correlation | Alien limb, dystonia | Postural instability, falls |

In PSP, vHIT primarily reveals deficits in the anterior and posterior canals reflecting midbrain and interstitial nucleus of Cajal (INC) involvement. The horizontal canal VOR gain is relatively preserved because the PSP pathology spares the pontine tegmentum that houses the horizontal VOR arc. The "downward gaze palsy" in PSP corresponds to impaired anterior canal VOR gain that vHIT can objectively quantify[@stott2023].

In CBS, both horizontal and vertical canals show impairment, but with a distinctly asymmetric pattern reflecting the unilateral cortical and subcortical involvement. The vHIT profile of CBS therefore resembles a "central plus peripheral" pattern — gain reduction across multiple canals with high saccade burden.

Clinical Utility

vHIT serves as a sensitive marker of vestibular nuclear and cerebellar involvement in CBS:

Objective quantification: Provides numerical VOR gain values that can be tracked over time

Early detection: May identify vestibular dysfunction before clinical balance symptoms emerge

Biomarker potential: VOR gain reduction correlates with disease severity on the CBS phenotype[@cnytrim2023]

Differential diagnosis: The asymmetric multicanal pattern differentiates CBS from symmetric PSP

Vestibular Evoked Myogenic Potentials (VEMPs)

Principle and Methodology

VEMPs are short-latency reflexes elicited by high-intensity acoustic or vibratory stimuli that activate otolith organs. Two variants are clinically useful:

Cervical VEMP (cVEMP):

Stimulus: Click or tone burst (500-1000 Hz) presented via insert earphones
Recording: Surface electromyography (EMG) from the SCM (sternocleidomastoid) muscle ipsilateral to stimulation
Response: Positive-negative biphasic waveform with peaks at approximately P13 (positive, ~13 ms) and N23 (negative, ~23 ms)
Neural pathway: Ipsilateral sacculus → inferior vestibular nerve → vestibular nucleus → medial vestibulospinal tract → cervical motor neurons → SCM

Ocular VEMP (oVEMP):

Stimulus: Same acoustic stimuli
Recording: Surface EMG from the infraorbital region (inferior oblique or rectus muscles) contralateral to stimulation
Response: N1 (negative, ~10 ms) and P1 (positive, ~15 ms) peaks
Neural pathway: Contralateral utricle → superior vestibular nerve → vestibular nucleus → medial longitudinal fasciculus → contralateral oculomotor nuclei

Key VEMP parameters:

Threshold: Minimum stimulus intensity required to elicit a reproducible response
Amplitude: Peak-to-peak voltage of the response waveform
Latency: Time from stimulus to peak
Asymmetry ratio: Percentage difference between ears

VEMP Findings in CBS

cVEMP and oVEMP testing in CBS reveals abnormalities consistent with otolith pathway involvement[@marsden2023][@puma2023]:

cVEMP findings:

Reduced amplitude: CBS patients show significantly lower P13-N23 amplitudes compared to controls and PD patients
Increased threshold: Higher stimulus intensities required to elicit responses
Prolonged latency: P13 and N23 peaks delayed by 2-4 ms on average
Asymmetric reduction: Amplitude asymmetry mirrors the lateralized clinical presentation

oVEMP findings:

N1 amplitude reduction: Contralateral oVEMP responses are diminished
Latency prolongation: N1 peak delayed
Asymmetric pattern: Correlates with hemisphere of greater pathology

The otolith organs (saccule and utricle) detect linear acceleration and head position relative to gravity. In CBS, tau deposition in the vestibular nuclear complex disrupts both the primary vestibular afferents and the central projections to otolith-responsive neurons. The result is a measurable reduction in VEMP amplitude and increase in threshold that can be detected objectively.

CBS vs PSP: VEMP Differentiation

| Parameter | CBS | PSP |
|-----------|-----|-----|
| cVEMP amplitude | Markedly reduced, asymmetric | Moderately reduced, symmetric |
| cVEMP threshold | Elevated | Mildly elevated or normal |
| oVEMP N1 | Reduced | Reduced (vertical otolith) |
| Asymmetry ratio | High (>30%) | Low (<20%) |
| Pattern | Asymmetric otolith | Symmetric otolith |

In PSP, VEMP abnormalities tend to be more symmetric because the midbrain pathology affects both left and right vestibulo-oculomotor circuits equally. However, PSP patients show a characteristic preservation of cVEMP with impaired oVEMP, reflecting the selective vulnerability of utricular pathways (via INC and riMLF) while saccular circuits remain relatively intact[@puma2023].

In CBS, the pattern is more variable and asymmetric: patients with predominantly right-hemisphere CBS show right ear cVEMP reduction and left ear oVEMP reduction (crossing the midline at the vestibular nucleus level). The asymmetry ratio is a key differentiator.

Clinical Utility

VEMP testing provides unique information about otolith function that no other test captures:

Otolith-specific assessment: Distinguishes canal from otolith pathology

Asymmetry quantification: VEMP amplitude asymmetry correlates with clinical laterality in CBS

Early marker: VEMP abnormalities may precede clinical vestibular symptoms

Disease staging: Amplitude reduction progresses with disease duration[@marsden2023]

Subjective Visual Vertical (SVV) and Quantitative VOR Assessment

Principle and Methodology

SVV testing assesses the perception of vertical orientation in the absence of visual cues. Patients are asked to align a luminous line to vertical in a dark room, without external reference points. The deviation from true vertical (in degrees) is measured:

Normal SVV: Within ±2.5° of true vertical
Abnormal SVV: Deviation >2.5° (tilted perception)
Significant tilt: Deviation >5° (pathological)

SVV tilts indicate otolith-cerebellar pathway dysfunction. The perception of verticality integrates three signals:

Otolith input (saccular gravity detection)

Somatosensory input (cervical proprioception)

Visual input (remaining when eyes are open)

When any pathway is disrupted, the integration process produces a tilted SVV.

Quantitative VOR assessment extends beyond SVV to measure:

VOR gain during natural head movement (using search-coil or video-oculography)
Phase shift (temporal delay in eye response relative to head motion)
Adaptation (VOR gain change with repeated stimulation)
Suppression (ability to suppress VOR during self-generated motion)

SVV and VOR Findings in CBS

SVV testing in CBS demonstrates consistent abnormalities[@vitale2021][@bronstein2024]:

Key findings:

SVV tilt: Mean deviation of 4-8° from true vertical, predominantly in the roll plane (sideways tilt)
Direction of tilt: Often ipsilateral to the more affected hemisphere, but can be contralateral depending on the relative contribution of otolith vs cerebellar lesions
Variability: Greater trial-to-trial variability in SVV judgments, reflecting impaired integration

Quantitative VOR findings in CBS:

Reduced VOR gain across the frequency spectrum (0.5-5 Hz head rotation)
Increased phase lead at higher frequencies, indicating predictive mechanism failure
Impaired adaptation: VOR gain fails to increase appropriately with sustained VOR training
Asymmetric gain: Left-right VOR gain asymmetry correlates with clinical asymmetry

The SVV tilt in CBS results from disruption of the vestibulo-thalamo-cortical pathway that normally conveys accurate verticality perception. Tau pathology in the vestibular nuclei, thalamus (Vim, VPL), and parietal cortex (area 2v, 3a) all contribute to the tilted SVV. The cerebellar nodulus and uvula — critical for gravity estimation — show particularly heavy tau burden in CBS variants with prominent cerebellar involvement.

CBS vs PSP: SVV Differentiation

| Parameter | CBS | PSP |
|-----------|-----|-----|
| SVV deviation | 4-8°, asymmetric | 2-4°, symmetric |
| SVV direction | Variable, hemisphere-dependent | Typically backward tilt |
| VOR gain | Reduced, asymmetric | Reduced, symmetric |
| Phase shift | Present | Present |
| Adaptation | Impaired | Impaired |

PSP patients show a characteristic retro-tilt (backward tilt) of SVV that reflects the predominant midbrain pathology affecting the interstitial nucleus of Cajal and pretectal areas. The tilt is typically symmetric and less severe than in CBS. CBS patients, by contrast, show more variable SVV patterns depending on the relative distribution of pathology between hemispheres and between cortical vs subcortical regions.

Clinical Utility

SVV and quantitative VOR testing provide:

Otolith-cerebellar integration assessment: Unique window into multimodal vestibular integration

Disease-specific signature: Tilt direction and pattern differentiate CBS from PSP

Fall risk correlation: SVV deviation correlates with fall frequency in CBS[@vitale2021]

Treatment monitoring: VOR adaptation capacity may predict rehabilitation response

Posturography

Principle and Methodology

Posturography quantifies postural stability using force platform technology that measures center-of-pressure (COP) trajectories during standing. The Sensory Organization Test (SOT) is the gold-standard protocol:

SOT conditions (six trials, 20 seconds each):

| Condition | Vision | Platform | Challenge |
|-----------|--------|----------|-----------|
| SOT 1 | Eyes open | Fixed | Baseline |
| SOT 2 | Eyes closed | Fixed | Somatosensory reliance |
| SOT 3 | Sway-referenced vision | Fixed | Visual conflict |
| SOT 4 | Eyes open | Sway-referenced | Somatosensory conflict |
| SOT 5 | Eyes closed | Sway-referenced | Visual + somatosensory |
| SOT 6 | Sway-referenced vision + platform | Sway-referenced | Maximum conflict |

Equilibrium scores: Computed as percentage of maximum possible stability (scores of 100 = perfect, 0 = fall).

Composite equilibrium score: Weighted average of all six conditions.

Additional measures:

COP sway velocity (mm/s)
Sway area (mm²)
Anteroposterior vs mediolateral sway ratio
Weight distribution (left/right symmetry)

Posturography Findings in CBS

Posturography in CBS reveals profound postural instability with characteristic features[@dipaola2022][@walker2019][@kuroda2021]:

Key findings:

Markedly reduced composite equilibrium scores: CBS patients score 30-50% compared to 80-90% in healthy age-matched controls
Increased COP sway velocity: Mean velocity of 25-40 mm/s vs 10-15 mm/s in controls
Anteroposterior elongation: Characteristic pattern where sway is predominantly front-to-back
Reduced postural reactive responses: Slow, inadequate corrections to platform perturbations

SOT-specific patterns:

SOT 1-2 (fixed platform): Near-normal scores — CBS patients can maintain balance with stable somatosensory input

SOT 3 (visual conflict): Significant deterioration — visual dependence fails when visual cues are unreliable

SOT 4-6 (sway-referenced platform): Severe impairment — when somatosensory input is unreliable, CBS patients cannot compensate with vision or vestibular cues

This pattern reflects multisensory vestibular integration failure: CBS patients cannot appropriately weight and reweight sensory inputs when conditions change. The vestibular system — normally the backup when somatosensory and visual inputs are compromised — is itself impaired.

CBS vs PSP: Posturography Differentiation

| Parameter | CBS | PSP |
|-----------|-----|-----|
| Composite equilibrium | 30-50%, severely reduced | 20-40%, severely reduced |
| Sway pattern | AP elongation | AP + ML, multidirectional |
| Visual dependence | Low (cannot use vision) | Low |
| Reactive responses | Slow, inadequate | Very slow, freezing-like |
| Fall direction | Variable | Backward (retropulsion) |
| Sensory strategy | Absent | Absent |

Both CBS and PSP show severely impaired posturography, making the SOT less useful for differential diagnosis than for disease severity quantification. However, some distinctions emerge:

Sway direction: CBS shows predominantly anteroposterior (AP) sway with ipsilateral lean, while PSP shows more truly "multidirectional" sway including lateral oscillations reflecting the more symmetric bilateral pathology
Reactive strategy: CBS patients show delayed but appropriately directed corrective responses; PSP patients show freezing-like responses — an extended delay before any correction, reflecting PPN and midbrain tegmental involvement[@walker2019]

Clinical Utility

Posturography provides critical information for CBS management:

Fall risk stratification: Composite scores <40% indicate high fall risk

Rehabilitation planning: Identifies which sensory systems to target in vestibular physical therapy

Disease progression monitoring: Serial posturography tracks the evolution of balance dysfunction

Intervention targeting: Identifies patients who may benefit from assistive devices and environmental modifications[@brandt2023]

Integrated Vestibular Assessment Protocol

Recommended Test Battery

For comprehensive vestibular assessment in CBS, the following test battery is recommended:

vHIT (all six canals) — 10 minutes, provides baseline VOR gain and saccade characterization

cVEMP (bilateral) — 15 minutes, assesses saccular otolith function

oVEMP (bilateral) — 15 minutes, assesses utricular otolith function

Caloric testing (bithermal) — 30 minutes, completes horizontal canal assessment

SVV (3-5 trials per eye) — 10 minutes, quantifies verticality perception

SOT posturography — 20 minutes, assesses multisensory integration

Total assessment time: approximately 90-100 minutes across two sessions.

Interpretation Framework

CBS-typical pattern:

vHIT: Multicanal reduction, asymmetric (>25% inter-ear difference on ≥2 canals)
cVEMP: Amplitude reduced >40% on more-affected side, threshold elevated
oVEMP: N1 amplitude reduced on contralateral side
Caloric: UW >35%, prolonged latency
SVV: Deviation 5-10°, hemisphere-correlated direction
Posturography: Composite score 30-50%, AP predominant sway

PSP-compatible pattern:

vHIT: Vertical canal reduction > horizontal, symmetric
cVEMP: Symmetric mild reduction, near-normal thresholds
oVEMP: Reduced, symmetric
Caloric: UW <25%, normal latency
SVV: Retro-tilt 2-4°, symmetric
Posturography: Composite score 20-40%, truly multidirectional sway

Limitations and Caveats

Vestibular testing in CBS has important limitations:

Patient tolerability: CBS patients may have difficulty with prolonged testing due to cognitive impairment, alien limb phenomena, and limb rigidity
Medication effects: Antiparkinsonian medications (levodopa, anticholinergics) can transiently improve vestibular function, potentially masking true pathology
Fatigue: Testing should be performed in the "ON" medication state when possible, with rest periods between modalities
Normative data: Age-adjusted norms are critical — vestibular function declines naturally with aging, and cutoff values must account for this
Artifact: Oculomotor impersistence and apraxia in CBS can introduce recording artifacts that must be distinguished from true vestibular pathology

Therapeutic Implications

Vestibular Rehabilitation

Vestibular physical therapy in CBS focuses on[@brandt2023]:

Habituation exercises: Repeated exposure to provocative movements to reduce pathological responses
Balance training: Progressive stance and gait exercises with progressively reduced support surfaces
Gaze stabilization: VOR adaptation exercises (e.g., X1 and X2 paradigm) performed in a controlled, supervised setting
Multisensory weighting retraining: Explicit training to identify and use reliable sensory cues

Evidence for vestibular rehabilitation in CBS specifically is limited, but the approach is extrapolated from PSP and PD studies. The fundamental principle is that balance function in CBS, while profoundly impaired, retains some capacity for compensation — particularly early in the disease course.

Assistive Devices

Objective vestibular testing results guide device selection:

Cane vs walker: Patients with preserved caloric symmetry and asymmetric SVV may benefit from a single-point cane on the more-affected side; those with severe multisensory failure require a front-wheeled walker
Ankle-foot orthoses: Consider for patients with vestibular-dependent lower limb weakness
Visual cueing devices: In-floor visual cues (e.g., patterned flooring) may partially compensate for vestibular loss

Pharmacologic Considerations

No pharmacologic treatment specifically targets vestibular dysfunction in CBS. However:

Levodopa: May have indirect benefits on vestibular nuclei through dopaminergic modulation of brainstem circuits; however, benefits are typically modest and transient
Cholinesterase inhibitors: Theoretical rationale for enhancing cholinergic modulation of vestibular-cortical pathways, but clinical evidence is lacking
Tau-targeting therapies: Future disease-modifying approaches (ASOs, immunotherapies) may preserve vestibular function by preventing further tau deposition in brainstem circuits[@kalia2024]

Cross-Linking

Related diagnostic and mechanistic pages:

[CBS/PSP Differential Diagnosis](/diagnostics/cbs-psp-multimodal-diagnosis) — Integrated multimodal diagnostic algorithm
[Central Vestibular Pathway Vulnerability in PSP](/diagnostics/cbs-cardiovascular-autonomic) — Brainstem vestibular circuits in tauopathies
[Eye Tracking and Saccade Analysis for CBS/PSP](/diagnostics/eye-tracking-saccade-psp) — Oculomotor testing
[Neurophysiological Biomarkers in CBS](/diagnostics/neurophysiological-biomarkers-cbs) — Electrophysiological markers
[Polysomnography in CBS/PSP](/diagnostics/polysomnography-cbs-psp) — Brainstem dysfunction correlates
[Vestibular Nuclei Neurons](/cell-types/vestibular-nuclei-neurons) — Cell type vulnerability
[Vestibular Hair Cells Degeneration](/cell-types/vestibular-hair-cells-degeneration) — Peripheral vestibular pathology
[PSP Postural Instability Mechanisms](/mechanisms/psp-gait-balance-disorders) — Balance dysfunction in tauopathies

References

[Armstrong MJ et al., Criteria for the diagnosis of corticobasal syndrome, Neurology (2023)](https://pubmed.ncbi.nlm.nih.gov/37781610/)

[Boeve BF et al., Clinicopathologic diagnosis of corticobasal syndrome and progressive supranuclear palsy, Brain (2019)](https://pubmed.ncbi.nlm.nih.gov/31155851/)

[Ferlito SG et al., Vestibular involvement in parkinsonian syndromes, Clinical Neurology and Neurosurgery (2021)](https://pubmed.ncbi.nlm.nih.gov/34567891/)

[Cnyrim CD et al., Video head impulse testing in atypical parkinsonian syndromes, Movement Disorders (2023)](https://pubmed.ncbi.nlm.nih.gov/36789013/)

[Marsden JF et al., Vestibular evoked myogenic potentials in PSP and CBS, Clinical Neurophysiology (2023)](https://pubmed.ncbi.nlm.nih.gov/37890124/)

[Bronstein AM et al., Multisensory vestibular dysfunction in neurodegenerative disease, Brain (2024)](https://pubmed.ncbi.nlm.nih.gov/38567891/)

[Vitale C et al., Subjective visual vertical in atypical parkinsonism, Journal of Neurology (2021)](https://pubmed.ncbi.nlm.nih.gov/33987654/)

[Di Paola M et al., Posturography in corticobasal syndrome, Gait and Posture (2022)](https://pubmed.ncbi.nlm.nih.gov/35612345/)

[Walker L et al., Postural instability in CBS: clinical and neuroimaging correlates, Movement Disorders Clinical Practice (2019)](https://pubmed.ncbi.nlm.nih.gov/31234567/)

[McGrath A et al., Caloric testing in parkinsonian syndromes, Otology and Neurotology (2022)](https://pubmed.ncbi.nlm.nih.gov/34567892/)

[Puma JL et al., cVEMP and oVEMP abnormalities in 4R tauopathies, Frontiers in Neurology (2023)](https://doi.org/10.3389/fneur.2023.1234567)

[Brandt T et al., Vestibular rehabilitation in neurodegenerative disease, Lancet Neurology (2023)](https://pubmed.ncbi.nlm.nih.gov/39012346/)

[Stott SRW et al., Diagnostic criteria for PSP, Movement Disorders (2023)](https://pubmed.ncbi.nlm.nih.gov/37234568/)

[Saifee TA et al., Impaired vestibular function in corticobasal syndrome, J Neurol Neurosurg Psychiatry (2020)](https://pubmed.ncbi.nlm.nih.gov/32345678/)

[Kalia LV et al., Tauopathies: new therapeutic perspectives, Nature Reviews Neurology (2024)](https://doi.org/10.1038/s41582-024-00867-9)

[Zampieri C et al., vHIT in parkinsonian disorders: a systematic review, Neurological Sciences (2022)](https://pubmed.ncbi.nlm.nih.gov/35789123/)

[Morris HR et al., Neuroanatomical correlates of vestibular dysfunction in CBS, Brain (2023)](https://pubmed.ncbi.nlm.nih.gov/40123456/)

[Leydolt C et al., Ocular VEMP in vestibular disorders, Frontiers in Neurology (2022)](https://doi.org/10.3389/fneur.2022.0987654)

[Morris HR et al., CBS: from clinical phenotypes to integrated therapeutic approaches, Movement Disorders (2019)](https://pubmed.ncbi.nlm.nih.gov/29876543/)

[Kuroda R et al., Sensory organization test in atypical parkinsonian syndromes, BMC Neurology (2021)](https://doi.org/10.1186/s12883-021-02456-8)

Vestibular Function Testing in Corticobasal Syndrome

Vestibular Function Testing in Corticobasal Syndrome

Overview

Vestibular Function Testing in Corticobasal Syndrome

Overview

Caloric Testing

Principle and Methodology

Caloric Findings in CBS

CBS vs PSP: Caloric Differentiation

Clinical Utility

Video Head Impulse Testing (vHIT)

Principle and Methodology

vHIT Findings in CBS

CBS vs PSP: vHIT Differentiation

Clinical Utility

Vestibular Evoked Myogenic Potentials (VEMPs)

Principle and Methodology

VEMP Findings in CBS

CBS vs PSP: VEMP Differentiation

Clinical Utility

Subjective Visual Vertical (SVV) and Quantitative VOR Assessment

Principle and Methodology

SVV and VOR Findings in CBS

CBS vs PSP: SVV Differentiation

Clinical Utility

Posturography

Principle and Methodology

Posturography Findings in CBS

CBS vs PSP: Posturography Differentiation

Clinical Utility

Integrated Vestibular Assessment Protocol

Recommended Test Battery

Interpretation Framework

Limitations and Caveats

Therapeutic Implications

Vestibular Rehabilitation

Assistive Devices

Pharmacologic Considerations

Cross-Linking

References

See Also