Vestibular Function Testing

Vestibular function testing provides objective, quantitative assessment of the vestibular end organs and their central connections when the bedside examination is insufficient for diagnosis, when quantification is needed for monitoring disease progression or treatment response, or when medicolegal documentation is required. The vestibular testing laboratory has evolved significantly over the past two decades, with video head impulse testing (vHIT) and vestibular evoked myogenic potentials (VEMPs) joining the traditional caloric test and rotary chair to create a comprehensive assessment battery that can evaluate each semicircular canal and each otolith organ independently. Understanding when to order each test, how to interpret results, and how findings correlate with specific clinical conditions is essential for neurologists managing vestibular disorders.

Bottom Line

  • Caloric testing: Gold standard for detecting unilateral vestibular hypofunction; tests only the horizontal canal at low frequencies; Jongkees formula with >25% asymmetry is abnormal
  • Video head impulse test (vHIT): Tests individual semicircular canals at high (physiologic) frequencies; quantifies VOR gain; detects covert saccades invisible at bedside; complementary to (not a replacement for) caloric testing
  • Cervical VEMP (cVEMP): Assesses saccule and inferior vestibular nerve function; absent in vestibular neuritis affecting the inferior division; enhanced amplitude and low threshold in superior canal dehiscence syndrome (SCDS)
  • Ocular VEMP (oVEMP): Assesses utricle and superior vestibular nerve function; absent in superior vestibular neuritis; enhanced in SCDS
  • Rotary chair: Gold standard for bilateral vestibulopathy; sinusoidal testing across multiple frequencies; useful for ototoxicity monitoring
  • Posturography: Evaluates sensory integration for balance (visual, vestibular, somatosensory); identifies functional/malingering patterns; does not localize lesions
  • No single test evaluates the entire vestibular system: A comprehensive assessment often requires combining caloric, vHIT, VEMPs, and audiometry to fully characterize the pattern and extent of vestibular damage

Videonystagmography / Electronystagmography (VNG/ENG)

VNG (using infrared video goggles) has largely replaced ENG (using periorbital electrodes) as the standard vestibular test battery. VNG provides superior spatial resolution and real-time visualization of eye movements. The battery typically includes three components: oculomotor evaluation, positional testing, and caloric testing.

Oculomotor Evaluation

SubtestWhat It AssessesNormal ResponseAbnormal Findings
Saccade testingAccuracy, velocity, and latency of rapid eye movementsAccurate, fast saccades with normal latencyHypometric (cerebellar), slow (brainstem/basal ganglia), hypermetric (cerebellar), increased latency (cortical/frontal)
Smooth pursuitAbility to track a slowly moving targetSmooth tracking with gain near 1.0Saccadic pursuit (broken into catch-up saccades) — cerebellar, medication effect, aging, inattention
Optokinetic nystagmus (OKN)Combined pursuit and vestibular processingSymmetric OKN in both directionsAsymmetric OKN — parietal lesion (ipsilateral pursuit deficit); absent OKN — widespread cortical or cerebellar pathology
Gaze testingAbility to maintain stable eccentric gazeNo nystagmus in eccentric gaze positionsGaze-evoked nystagmus — cerebellar, medication (anticonvulsants, benzodiazepines); rebound nystagmus — cerebellar
Spontaneous nystagmusBaseline vestibular tone asymmetryNo nystagmus with fixation or withoutSpontaneous nystagmus — peripheral (suppressed by fixation) or central (not suppressed)

Positional Testing

  • Static positional testing: Head in various positions (supine, head right, head left, head hanging) for 30–60 seconds each; nystagmus recorded with and without fixation
  • Dix-Hallpike and supine roll: Performed within the VNG suite with goggles recording; provides permanent documentation of nystagmus direction, latency, duration, and fatigue
  • Interpretation: Direction-fixed positional nystagmus (same direction in all positions) is usually peripheral; direction-changing positional nystagmus is concerning for central pathology but can also occur with horizontal canal BPPV

Caloric Testing

The caloric test remains the gold standard for detecting unilateral peripheral vestibular hypofunction. It evaluates each horizontal semicircular canal independently by inducing endolymph convection currents through thermal stimulation.

Caloric Testing: Technique and Interpretation

  • Technique:
    • Patient supine with head elevated 30° (to place horizontal canal in vertical orientation, maximizing convection)
    • Water irrigation (gold standard): warm (44°C) and cool (30°C) water in each ear (4 irrigations total); air caloric as alternative if TM perforation
    • Each irrigation lasts ~30–60 seconds; nystagmus recorded for ~90–120 seconds post-irrigation
    • Measure peak slow-phase velocity (SPV) of the induced nystagmus
  • Expected response (COWS mnemonic): Cold → Opposite (nystagmus fast phase away from irrigated ear); Warm → Same (nystagmus fast phase toward irrigated ear)
  • Jongkees formula for unilateral weakness (UW):
    • UW = [(RC + RW) – (LC + LW)] / (RC + RW + LC + LW) × 100%
    • RC = right cool, RW = right warm, LC = left cool, LW = left warm (all as peak SPV values)
    • UW >25% = significant unilateral vestibular hypofunction on the weaker side
  • Directional preponderance (DP):
    • DP = [(RW + LC) – (LW + RC)] / (RC + RW + LC + LW) × 100%
    • DP >30% = significant; indicates asymmetric spontaneous vestibular drive (may reflect central compensation or acute vestibular imbalance)
  • Bilateral vestibular weakness: Total caloric response (sum of all 4 SPV values) <20°/sec indicates bilateral vestibulopathy

Limitations of Caloric Testing

  • Tests only the horizontal semicircular canal — does not evaluate posterior or superior canals, or the otolith organs
  • Tests only the very low frequency range (~0.003 Hz) — a patient can have normal calorics but abnormal high-frequency VOR (detected by vHIT)
  • Anatomic variations in the temporal bone and external auditory canal can affect heat transfer, producing false results
  • Cannot be performed with tympanic membrane perforation (use air caloric) or middle ear disease
  • Patient alertness affects results — the patient must perform alerting tasks (serial subtractions, conversation) to prevent habituation

Video Head Impulse Test (vHIT)

vHIT uses lightweight video goggles with a high-speed camera (typically 250 Hz) to precisely measure eye movements during rapid head impulses, providing quantitative assessment of the VOR for each individual semicircular canal.

Technique

  • Equipment: Lightweight goggles with infrared camera and gyroscope (measures head velocity); patient fixates on a wall target at ~1 m distance
  • Horizontal canals: Tested by horizontal head impulses (as in bedside HIT); head is turned in the plane of the horizontal canals
  • Vertical canals: LARP (left anterior / right posterior) and RALP (right anterior / left posterior) planes; the examiner turns the head diagonally in the plane of the canal pair being tested
  • Parameters measured: VOR gain (ratio of eye velocity to head velocity at a specific time point, typically at 60–80 ms) and corrective saccades (overt and covert)

Interpretation

ParameterNormalAbnormalClinical Significance
VOR gain (horizontal)≥0.8 (ratio of eye/head velocity)<0.7 definitively abnormal; 0.7–0.8 borderlineReduced gain indicates hypofunction of the ipsilateral horizontal canal
VOR gain (vertical)≥0.7 (LARP/RALP planes)<0.6 abnormalReduced gain indicates hypofunction of the specific canal tested
Overt saccadesAbsentCorrective saccades occurring AFTER the head impulseVisible at bedside; indicate VOR deficit on the tested side
Covert saccadesAbsentCorrective saccades occurring DURING the head impulseNOT visible at bedside (too fast for the examiner to see); detected only by vHIT; partially compensate for VOR deficit
Gain asymmetry<10%>10–15%Asymmetry suggests unilateral hypofunction even if absolute gains are borderline

vHIT vs. Caloric Testing: Complementary, Not Interchangeable

  • Different frequency ranges: Caloric tests very low-frequency VOR (~0.003 Hz); vHIT tests high-frequency VOR (5–7 Hz, the physiologic range)
  • Dissociation is possible: A patient may have an abnormal caloric (low-frequency deficit) but normal vHIT (high-frequency VOR preserved) — this pattern is common in Ménière disease and vestibular migraine
  • Reverse dissociation: Abnormal vHIT with normal caloric is less common but can occur in early gentamicin toxicity
  • Complete vestibular testing requires both: For comprehensive assessment, caloric testing and vHIT provide complementary information across the frequency spectrum
  • vHIT advantages: Tests all 6 canals (3 pairs); rapid (<10 min); well-tolerated; detects covert saccades; quantitative and reproducible
  • vHIT limitations: Requires experienced examiner; artifacts from goggle slippage can produce falsely low gains; less sensitive than caloric for mild hypofunction

Vestibular Evoked Myogenic Potentials (VEMPs)

VEMPs are short-latency electromyographic responses evoked by loud sound or vibration stimuli that assess otolith organ (saccule and utricle) function. There are two types: cervical VEMP (cVEMP) and ocular VEMP (oVEMP).

Cervical VEMP (cVEMP)

ParameterDetail
What it assessesSaccule function and the inferior vestibular nerve
Reflex pathwaySaccule → inferior vestibular nerve → vestibular nuclei → medial vestibulospinal tract → ipsilateral SCM motor neurons (otolith-spinal reflex)
Recording siteIpsilateral sternocleidomastoid (SCM) muscle; patient must tonically activate SCM (head turn or head lift)
StimulusLoud air-conducted sound (clicks or tone bursts, typically 500 Hz, 95–100 dB nHL) or bone-conducted vibration
WaveformBiphasic inhibitory potential: p13 (positive at ~13 ms) and n23 (negative at ~23 ms)
Key measuresAmplitude (p13–n23), amplitude asymmetry ratio, threshold

Ocular VEMP (oVEMP)

ParameterDetail
What it assessesUtricle function and the superior vestibular nerve
Reflex pathwayUtricle → superior vestibular nerve → vestibular nuclei → contralateral oculomotor nucleus → inferior oblique muscle (otolith-ocular reflex)
Recording siteContralateral inferior oblique muscle (electrodes beneath the eye); patient gazes upward ~30°
StimulusSame as cVEMP; bone-conducted vibration at Fz (forehead) is often preferred for oVEMP
WaveformInitial negative potential: n10 (negative at ~10 ms) followed by p15 (positive at ~15 ms)
Key measuresAmplitude (n10), amplitude asymmetry ratio, threshold

Clinical Applications of VEMPs

ConditioncVEMP FindingsoVEMP FindingsClinical Significance
Superior canal dehiscence syndrome (SCDS)Enhanced amplitude; decreased threshold (≤75 dB nHL)Enhanced amplitude; decreased thresholdVEMPs are the most sensitive laboratory test for SCDS; low threshold is the hallmark finding
Vestibular neuritis (superior division)Normal (saccule/inferior nerve spared)Absent or reduced on affected sidePattern confirms selective superior vestibular nerve involvement
Vestibular neuritis (inferior division)Absent or reduced on affected sideNormalLess common; isolated inferior vestibular nerve involvement
Ménière diseaseEnhanced early in disease; absent in late stagesVariable; may be reducedReflects endolymphatic hydrops affecting saccule; progressive loss over time
Vestibular schwannomaAbsent or delayed on tumor sideAbsent or reduced on tumor sideSchwannoma compresses vestibular nerve; VEMPs may be abnormal before hearing loss
Bilateral vestibulopathyBilaterally absent or reducedBilaterally absent or reducedSupports diagnosis when caloric and vHIT are also bilaterally abnormal

VEMP Limitations and Pitfalls

  • Conductive hearing loss: Reduces air-conducted VEMP amplitudes; must use bone-conducted stimuli if middle ear disease is present
  • Age effect: VEMP amplitudes decline with age (particularly cVEMP after age 60); age-matched normative data are essential
  • SCM activation for cVEMP: Inadequate SCM contraction reduces cVEMP amplitude; EMG monitoring and normalization for muscle activation level are important
  • Asymmetry ratio is more reliable than absolute amplitude: Intersubject amplitude variability is high; asymmetry ratio >35–40% is generally considered abnormal

Rotary Chair Testing

Rotary chair testing evaluates the VOR across a range of frequencies by rotating the patient on a motorized chair in darkness, measuring the resulting eye movements.

Technique

  • Setup: Patient seated in a motorized rotational chair in a light-tight enclosure; eye movements recorded with VNG goggles or EOG electrodes
  • Sinusoidal harmonic acceleration (SHA): Chair oscillates sinusoidally at frequencies from 0.01 to 0.64 Hz (or higher); measures VOR gain, phase, and symmetry at each frequency
  • Step velocity testing: Rapid rotation to a constant velocity (e.g., 60°/s); measures the decay of per-rotational nystagmus (time constant) and post-rotational responses
  • Visual-vestibular interaction: VOR in light, VOR suppression (fixation on a chair-mounted target during rotation)

Interpretation

ParameterNormalClinical Significance of Abnormality
VOR gainFrequency-dependent; increases from ~0.3 at 0.01 Hz to ~0.6–0.8 at 0.64 HzBilaterally reduced gain across all frequencies = bilateral vestibulopathy; the gold standard test for this diagnosis
PhaseSlight phase lead at low frequencies, approaches 0 at higher frequenciesIncreased phase lead = peripheral vestibular dysfunction (velocity storage deficit)
SymmetrySymmetric responses in both directions (<5–10% asymmetry)Asymmetry reflects unilateral vestibular imbalance; correlates with directional preponderance
Time constant~15–20 seconds (per-rotational nystagmus decay)Shortened = bilateral vestibulopathy; prolonged = velocity storage hyperactivity (rare)
VOR suppressionFixation suppresses VOR to near-zeroFailure to suppress VOR = central (cerebellar) pathology

When Rotary Chair Is Most Useful

  • Bilateral vestibulopathy: The single best test for confirming bilateral vestibular loss; caloric testing shows bilateral weakness but rotary chair quantifies residual function across frequencies
  • Ototoxicity monitoring: Serial rotary chair testing during gentamicin or cisplatin therapy can detect progressive bilateral VOR loss before symptoms develop
  • Compensation assessment: Phase and symmetry changes over time reflect central compensatory processes after unilateral loss
  • Pediatric vestibular testing: Better tolerated by children than caloric testing; requires no water irrigation
  • Limitation: Stimulates both labyrinths simultaneously during rotation — cannot identify unilateral hypofunction as effectively as caloric or vHIT (which test ears independently)

Computerized Dynamic Posturography (CDP)

CDP evaluates postural stability by measuring sway on a force platform under systematically varied sensory conditions. The most widely used protocol is the Sensory Organization Test (SOT).

Sensory Organization Test (SOT)

ConditionSurfaceVisual SurroundSensory Input Available
1FixedFixedVision + somatosensory + vestibular
2FixedEyes closedSomatosensory + vestibular (vision removed)
3FixedSway-referenced (moves with patient)Somatosensory + vestibular (vision inaccurate)
4Sway-referenced (moves with patient)FixedVision + vestibular (somatosensory inaccurate)
5Sway-referencedEyes closedVestibular ONLY
6Sway-referencedSway-referencedVestibular ONLY (vision inaccurate, somatosensory inaccurate)

Interpretation Patterns

  • Vestibular pattern: Falls/excessive sway on conditions 5 and 6 (vestibular-only conditions); conditions 1–4 relatively preserved; consistent with bilateral vestibular hypofunction or uncompensated unilateral loss
  • Somatosensory pattern: Falls on conditions 3, 4, 5, 6 (all conditions with sway-referenced platform); suggests peripheral neuropathy or somatosensory deficit
  • Visual preference pattern: Poor performance whenever visual input is inaccurate (conditions 3 and 6); patient is overly reliant on vision; seen in visual vertigo and some PPPD patients
  • Aphysiologic pattern: Falls on simple conditions (1 and 2) but performs better on more difficult conditions (5, 6) — this paradoxical pattern suggests functional/non-organic dizziness or symptom exaggeration

Posturography: Strengths and Limitations

  • Strengths: Identifies the sensory strategy a patient uses for balance; quantifies fall risk; useful for rehabilitation planning; helps identify functional/non-organic dizziness; objectively tracks progress
  • Limitations: Does not localize the lesion (peripheral vs. central); does not identify the specific vestibular pathology; influenced by patient effort and anxiety; expensive equipment; not available at all centers
  • Medicolegal role: Aphysiologic patterns on CDP provide objective evidence of symptom exaggeration in disability and litigation cases

Audiometry in Vestibular Disorders

Audiometric testing is an essential component of the vestibular evaluation, as specific patterns of hearing loss point to particular diagnoses and localize pathology.

ConditionAudiometric PatternKey Features
Ménière diseaseLow-frequency sensorineural hearing loss (SNHL)Fluctuating early in disease; progressive; unilateral (becomes bilateral in 30–50% over decades); may have “peak” configuration (trough at 250–500 Hz, recovery at 1–2 kHz)
Vestibular schwannomaAsymmetric high-frequency SNHLUnilateral or asymmetric (>15 dB difference at 2+ frequencies); speech discrimination disproportionately poor relative to pure-tone loss; ABR shows prolonged I–III or I–V interpeak latencies
Superior canal dehiscenceLow-frequency conductive hearing loss (air-bone gap) with normal tympanometry“Third window” effect: bone conduction thresholds may be supranormal (<0 dB); air-bone gap closes at higher frequencies; mimics otosclerosis but tympanometry and stapedial reflexes are normal
Vestibular neuritisNormal hearingSpares cochlear function; if hearing loss is present, consider labyrinthitis (viral) or AICA stroke
Vestibular migraineNormal or mild bilateral high-frequency SNHLNo progressive low-frequency loss (differentiates from Ménière); mild changes may occur during attacks
LabyrinthitisUnilateral SNHL (variable frequencies)Hearing loss accompanies vestibular neuritis; viral or bacterial etiology; bacterial requires urgent treatment
Bilateral vestibulopathyMay be normal or show bilateral SNHLIf SNHL present, consider ototoxicity (aminoglycosides — high-frequency loss) as the common etiology for both

When to Order Audiometry

  • All patients presenting with vertigo or dizziness (baseline assessment)
  • Any patient with subjective hearing loss, aural fullness, or tinnitus
  • Asymmetric symptoms suggesting unilateral pathology (to screen for schwannoma)
  • Follow-up for Ménière disease (documenting progression of hearing loss)
  • Before and during ototoxic drug therapy (aminoglycosides, cisplatin)
  • After acute vestibular syndrome to differentiate vestibular neuritis (normal hearing) from labyrinthitis (hearing loss) or AICA stroke (hearing loss)

Auditory Brainstem Response (ABR)

  • Purpose: Evaluates neural conduction along the auditory pathway from the cochlear nerve through the brainstem; useful as a screening tool for retrocochlear pathology when MRI is unavailable or contraindicated
  • Key waves: Wave I (distal CN8), wave III (cochlear nucleus/SOC), wave V (lateral lemniscus/inferior colliculus); interpeak latencies (I–III, III–V, I–V) are the primary measures
  • Vestibular schwannoma: Prolonged I–III or I–V interpeak latency; absent wave V; interaural latency difference >0.2 ms for wave V is abnormal; sensitivity ~90% for tumors >1 cm, but lower for small intracanalicular tumors
  • Limitations: Cannot detect small intracanalicular schwannomas reliably; MRI with gadolinium is the gold standard imaging test and has largely replaced ABR for schwannoma screening in most centers
  • Intraoperative monitoring: ABR is used during CPA surgery to monitor auditory nerve function in real time and preserve hearing

Clinical Decision-Making: Which Tests to Order

Clinical ScenarioRecommended TestsRationale
Acute vestibular syndrome (suspected peripheral)Audiometry; consider vHIT if bedside HIT uncertainAudiometry to rule out labyrinthitis/AICA; vHIT quantifies VOR loss and detects covert saccades
Recurrent episodic vertigo (suspected Ménière)Audiometry; VNG with caloric; consider ECoG, VEMPsLow-frequency SNHL supports diagnosis; caloric may show UW; ECoG for hydrops; VEMPs for saccular function
Recurrent episodic vertigo (suspected VM)Audiometry; MRI brain/IACRule out Ménière (audiometry) and structural lesions (MRI); vestibular testing often normal interictally
Asymmetric hearing lossAudiometry; MRI with IAC (gadolinium); ABR if MRI unavailableRule out vestibular schwannoma; >15 dB asymmetry at ≥2 frequencies warrants MRI
Suspected bilateral vestibulopathyRotary chair; caloric testing; vHIT (all 6 canals); VEMPs; audiometryRotary chair is gold standard; caloric confirms bilateral weakness; vHIT quantifies canal-specific loss; audiometry for ototoxicity-related hearing loss
Suspected SCDSVEMPs (cVEMP + oVEMP); audiometry; high-resolution CT temporal boneEnhanced VEMPs with low threshold; air-bone gap with normal tympanometry; CT confirms dehiscence
Chronic dizziness / PPPDCDP/posturography; VNG with caloric; audiometryCDP identifies sensory strategy and aphysiologic patterns; VNG/caloric to rule out uncompensated peripheral loss; audiometry for completeness
Medicolegal / disability assessmentFull battery: VNG, caloric, rotary chair, vHIT, VEMPs, CDP, audiometryComprehensive documentation; CDP helps identify exaggeration; multiple tests provide cross-validation

Emerging and Advanced Testing

Electrocochleography (ECoG)

  • Purpose: Detects endolymphatic hydrops in suspected Ménière disease
  • Measure: Summating potential to action potential ratio (SP/AP ratio); elevated ratio (>0.4–0.5) suggests endolymphatic hydrops
  • Technique: Transtympanic (needle on promontory — most sensitive) or extratympanic (tympanic membrane surface electrode)
  • Limitations: Sensitivity varies (60–80%); may be normal interictally; invasive transtympanic approach limits availability

MRI Hydrops Imaging

  • Technique: 3D-FLAIR MRI 4–24 hours after intratympanic or intravenous gadolinium injection
  • Principle: Gadolinium enters perilymph but not endolymph, allowing visualization of endolymphatic space expansion
  • Clinical utility: Directly visualizes hydrops; increasingly used in research and clinical practice; may differentiate Ménière from vestibular migraine

Subjective Visual Vertical (SVV)

  • Purpose: Assesses otolith (primarily utricle) function; the patient aligns a luminous bar to perceived vertical in darkness
  • Abnormal: Tilt >2–2.5° from true vertical; tilts toward the lesion side in acute peripheral vestibulopathy; may tilt away from lesion in central otolithic lesions (brainstem)
  • Time course: Maximally abnormal in the acute phase; normalizes over weeks as central compensation occurs; persistent deviation suggests ongoing vestibular imbalance or central pathology
  • Clinical role: Quick bedside or office test; complements VEMPs in assessing otolith function; available as a smartphone application for point-of-care use

Vestibular Test Patterns by Condition

ConditionCaloricvHITcVEMPoVEMPAudiometry
Vestibular neuritis (superior div.)UW ipsilateralHorizontal + anterior canal reduced gainNormalAbsent/reduced ipsilateralNormal
Vestibular neuritis (inferior div.)Normal (or mild UW)Posterior canal reduced gainAbsent/reduced ipsilateralNormalNormal
Ménière diseaseUW ipsilateral (may be normal early)Normal (caloric-vHIT dissociation)Enhanced early; absent lateVariableLow-frequency SNHL
Vestibular schwannomaUW ipsilateralMay be normal (slow deafferentation)Absent/reducedAbsent/reducedAsymmetric high-frequency SNHL
SCDSNormal or enhanced ipsilateralNormalEnhanced, low thresholdEnhanced, low thresholdLow-frequency ABG, normal tympanometry
Bilateral vestibulopathyBilateral weaknessBilaterally reduced gain (all 6 canals)Bilaterally reduced/absentBilaterally reduced/absentNormal or bilateral high-frequency SNHL
Vestibular migraineNormal or mild UWNormal interictallyVariableVariableNormal or mild bilateral SNHL

Practical Considerations

Optimizing Vestibular Test Interpretation

  • Clinical correlation is essential: No vestibular test result should be interpreted in isolation; always correlate with history, examination, and imaging findings
  • Timing matters: Test results change over time (compensation, disease progression); caloric weakness may partially recover months after vestibular neuritis; test at the appropriate clinical time point
  • Medication effects: Vestibular suppressants (meclizine, benzodiazepines) suppress caloric responses and may mask nystagmus; hold suppressants for ≥48 h before testing when safe to do so
  • Age-matched normative data: VOR gain, VEMP amplitudes, and caloric responses all decline with age; use age-appropriate reference ranges
  • Inter-test correlation: When caloric and vHIT results disagree (dissociation), the clinical context determines which is more relevant — caloric-vHIT dissociation is characteristic of Ménière and vestibular migraine
  • Cost-effectiveness: Not every patient needs a full vestibular test battery; tailor testing to the clinical question (see clinical decision-making table above)
  • Communication: Vestibular test reports can be complex; develop a working relationship with the audiologist/vestibular technologist to ensure high-quality testing and clear reporting

References

  1. Halmagyi GM, Chen L, MacDougall HG, Weber KP, McGarvie LA, Curthoys IS. The video head impulse test. Front Neurol. 2017;8:258.
  2. MacDougall HG, Weber KP, McGarvie LA, Halmagyi GM, Curthoys IS. The video head impulse test: diagnostic accuracy in peripheral vestibulopathy. Neurology. 2009;73(14):1134–1141.
  3. Rosengren SM, Colebatch JG, Young AS, Govender S, Welgampola MS. Vestibular evoked myogenic potentials in practice: methods, pitfalls, and clinical applications. Clin Neurophysiol Pract. 2019;4:47–68.
  4. Curthoys IS, Manzari L. Otolithic disease: clinical features and the role of vestibular evoked myogenic potentials. Semin Neurol. 2013;33(3):231–245.
  5. Furman JM, Redfern MS. Effect of aging on the otolith-ocular reflex. J Vestib Res. 2001;11(2):91–103.
  6. Shepard NT, Jacobson GP. The caloric irrigation test. Handb Clin Neurol. 2016;137:119–131.
  7. Baloh RW, Kerber KA. Clinical Neurophysiology of the Vestibular System. 4th ed. Oxford University Press; 2011.
  8. Welgampola MS, Colebatch JG. Characteristics and clinical applications of vestibular-evoked myogenic potentials. Neurology. 2005;64(10):1682–1688.
  9. Ward BK, Carey JP, Minor LB. Superior canal dehiscence syndrome: lessons from the first 20 years. Front Neurol. 2017;8:177.
  10. Jacobson GP, Newman CW, Kartush JM. Handbook of Balance Function Testing. 2nd ed. Plural Publishing; 2016.
  11. McGarvie LA, MacDougall HG, Halmagyi GM, Burgess AM, Weber KP, Curthoys IS. The video head impulse test (vHIT) of semicircular canal function — age-dependent normative values of VOR gain in healthy subjects. Front Neurol. 2015;6:154.
  12. Strupp M, Kim JS, Murofushi T, et al. Bilateral vestibulopathy: diagnostic criteria. J Vestib Res. 2017;27(4):177–189.
  13. Nashner LM, Peters JF. Dynamic posturography in the diagnosis and management of dizziness and balance disorders. Neurol Clin. 1990;8(2):331–349.
  14. Merchant SN, Adams JC, Nadol JB. Pathology and pathophysiology of idiopathic sudden sensorineural hearing loss. Otol Neurotol. 2005;26(2):151–160.
  15. Kingma H, van de Berg R. Anatomy, physiology, and physics of the peripheral vestibular system. Handb Clin Neurol. 2016;137:1–16.