Glossary

The 2017 American Academy of Neurology practice guideline on cervical and ocular VEMP testing. Rates evidence as Level B for SCD diagnosis and Level C-negative for routine use in Ménière's, vestibular migraine, and BPPV.

No reproducible VEMP at the highest tolerated stimulus intensity. Implies severe receptor or nerve dysfunction — but inadequate muscle contraction must be excluded first.

The recording electrode placed over the muscle of interest (SCM belly for cVEMP, infraorbital ridge for oVEMP). Picks up the differential signal that becomes the displayed waveform.

Sound delivered through the ear canal (insert earphone or headphone). The default route for clinical VEMP testing; subject to attenuation by conductive hearing loss.

Stimulus delivery alternating compression and rarefaction of the diaphragm to cancel stimulus artefact. Recommended for clinical VEMP recording.

The peak-to-peak voltage of the VEMP, measured in microvolts (µV). Reduced or absent amplitudes suggest receptor or peripheral nerve dysfunction.

The portion of each averaged sweep displayed for measurement, typically 0–50 or 0–100 ms post-stimulus, with a 10-ms pre-stimulus baseline.

Peak-to-peak amplitude larger than the lab-specific upper limit. Most characteristically seen on the affected side in SCD (third-window effect).

Hearing one's own voice as too loud or reverberant. A classic symptom of SCD, resulting from altered transmission of body-generated sounds through the third window.

Electronic filter that passes frequencies between a high-pass and low-pass cut-off. Typical VEMP settings are 5–30 Hz high-pass and 1000–3000 Hz low-pass; the oVEMP often uses a lower high-pass.

Mechanical stimulus delivered via a vibrator placed at Fz (midline forehead) or the mastoid. Bypasses the middle ear, so unaffected by conductive hearing loss. Particularly effective for evoking the oVEMP.

Brief vertigo triggered by head position change due to otoconia displaced from the utricle into a semicircular canal (most commonly the posterior canal). VEMP has no role in diagnosis but oVEMP abnormalities are common in recurrent cases.

Stimulation of the horizontal semicircular canal by warm and cool irrigation of the ear canal. Tests the superior vestibular nerve — complementary to VEMP, which tests the otolith branches.

A 100-microsecond rectangular pulse delivered through earphones. An older alternative to the tone burst; has a broader frequency spectrum but is less frequency-selective.

Abnormal sensitivity to one's own internal sounds (footsteps, heartbeat, eye movements). Pathognomonic of third-window disorders.

Raw cVEMP P1–N1 amplitude divided by mean rectified pre-stimulus EMG. Reduces variability due to differences in muscle contraction strength.

Cervical vestibular evoked myogenic potential — a brief inhibitory modulation of tonic sternocleidomastoid EMG, recorded ipsilateral to the stimulated ear. Tests the saccule and the inferior vestibular nerve.

Decibels normal hearing level — a clinical reference scale calibrated against the threshold of normal-hearing young adults. Most VEMP protocols use 95–100 dBnHL stimuli (≈ 120 dB SPL).

A visual bar on the recording system that shows the patient how strongly their SCM is contracting. Helps maintain consistent muscle activation during cVEMP recording.

Procedure to compensate for variable underlying SCM contraction in cVEMP recording. The raw P1–N1 amplitude is divided by the mean rectified pre-stimulus EMG, producing the 'corrected amplitude' used for between-subject comparison.

Distension of the endolymphatic compartment of the inner ear. Considered the histopathological substrate of Ménière's disease; produces reduced VEMP amplitudes and a frequency-tuning shift.

Bedside VEMP stimulus delivered with a tendon hammer or reflex hammer at the midline forehead. A simple, rapid way to elicit oVEMPs without specialised equipment.

The dependence of VEMP amplitude on stimulus frequency. Normal otolith organs are tuned to 500 Hz; tuning shifts can be diagnostically informative.

Upward shift of peak VEMP frequency response — from 500 Hz toward 1 kHz — observed in endolymphatic hydrops. More specific to Ménière's than amplitude reduction alone.

Direct electrical stimulation of vestibular afferents via electrodes over the mastoid processes. Mostly research; bypasses receptor mechanisms and tests downstream pathways directly.

The system common-reference electrode, typically placed on the upper forehead. Reduces electrical interference between the patient and the amplifier.

The sensory receptor of the inner ear. Type I hair cells are flask-shaped and surrounded by a calyceal nerve ending; Type II hair cells are cylindrical with bouton endings. VEMP responses depend on Type I striolar hair cells.

Pressure-induced nystagmus or vertigo elicited by tragal pressure or pneumatic otoscopy. Suggests a third-window disorder.

Electrical resistance between an electrode and the skin, measured in ohms. Clean VEMP recording requires < 5 kΩ at every electrode; achieved with skin abrasion and conductive gel.

Small extraocular muscle that elevates and laterally rotates the eye. The oVEMP is recorded over the inferior oblique on the side contralateral to the stimulated ear.

The second division of the vestibular nerve. Carries afferents from the saccule and posterior semicircular canal. Generates the cVEMP via the vestibulo-collic reflex.

A measure of side-to-side VEMP amplitude asymmetry: IAR = |L − R| / (L + R) × 100. Values above 33–40% are generally considered abnormal.

Bony canal in the petrous temporal bone through which the cochlear and vestibular nerves and the facial nerve pass from the brainstem to the inner ear. The most common site of vestibular schwannoma.

A vestibular nerve fibre that fires with irregular interspike intervals at rest. Irregular afferents innervate striolar hair cells and respond preferentially to high-frequency stimuli, including sound and vibration — the population responsible for VEMP generation.

Originally devised for caloric responses, the formula (|L − R| / (L + R)) × 100 is also applied to VEMP amplitudes to compute the interaural asymmetry ratio.

The time from stimulus onset to a peak of the response, measured in milliseconds. Prolonged latency suggests slowed conduction (e.g. central demyelination, retrolabyrinthine lesion).

The sensory epithelium of an otolith organ, containing hair cells covered by a gelatinous layer in which the otoconia are embedded. Each otolith organ has one macula.

The fluid-filled epithelial structures inside the bony labyrinth, including the cochlear duct, three semicircular ducts, and the saccule and utricle.

Episodic vertigo with fluctuating low-frequency sensorineural hearing loss and tinnitus. Histopathological substrate is endolymphatic hydrops; VEMPs commonly show reduced amplitudes and a frequency-tuning shift on the affected side.

Chronic immune-mediated demyelinating disease of the CNS. Brainstem plaques can produce prolonged VEMP latencies, sometimes when MRI is normal — supporting VEMP's role as a complementary functional test.

The first negative peak of the VEMP. In the cVEMP, N1 occurs at approximately 23 ms after the stimulus (following P1). In the oVEMP, N1 is the EARLIER peak, at approximately 10 ms, preceding P1.

Tiny calcium carbonate crystals embedded in the otolith membrane above each macula. Their inertia is what allows the otolith organs to detect linear acceleration. Displaced otoconia in a semicircular canal cause BPPV.

Collective name for the saccule and utricle — the two gravity-sensing organs of the inner ear. Distinguished from the three semicircular canals, which sense rotation.

Ocular vestibular evoked myogenic potential — a brief excitatory response recorded over the inferior oblique muscle contralateral to the stimulated ear. Tests the utricle and the superior vestibular nerve.

The first positive peak of the cVEMP, occurring at approximately 13 ms after the stimulus. Together with N1, it defines the diagnostic cVEMP complex.

Age-related decline in vestibular function. Manifests as bilaterally reduced VEMP amplitudes and increased proportion of absent responses, particularly after the seventh decade.

Peak-to-peak amplitude smaller than the lab-specific lower limit. Suggests partial receptor or nerve dysfunction (e.g. Ménière's disease, presbyvestibulopathy).

An electrode placed on a relatively quiet site (e.g. medial clavicle for cVEMP, cheek for oVEMP) that provides the differential pair for the active electrode.

A vestibular nerve fibre with low resting variability that responds best to sustained head position and slow accelerations. Regular afferents innervate extrastriolar hair cells and contribute little to the VEMP.

One of the two otolith organs of the inner ear. Its macula lies in the vertical plane and detects vertical linear acceleration and gravity. The saccule is innervated by the inferior vestibular nerve and is the receptor that generates the cVEMP.

Absence of bone over the superior semicircular canal, creating a 'third window' in the inner ear. Causes sound- and pressure-induced vertigo, autophony, conductive hyperacusis, and characteristically augmented low-threshold VEMP responses.

The probability that a diagnostic test will be positive in a patient who has the disease. Reported VEMP sensitivities range from ~80% for SCD and schwannoma to ~50–70% for MS.

The probability that a diagnostic test will be negative in a patient who does not have the disease. VEMP specificity varies widely by condition and protocol — high-frequency oVEMP gives the best specificity for SCD.

Large strap-like neck muscle that flexes and rotates the head. The cVEMP is recorded as a brief inhibitory modulation of its tonic contraction.

A curved zone running across each otolith macula at which the kinocilium orientation of the hair cells reverses. Striolar hair cells are predominantly Type I and are innervated by irregularly-firing afferents that generate the VEMP response.

One of the two divisions of the vestibular nerve (CN VIII). Carries afferents from the utricle, superior semicircular canal, and horizontal semicircular canal. Generates the oVEMP via the vestibulo-ocular reflex.

Synchronous averaging of many time-locked stimulus presentations to extract the VEMP from ongoing background EMG. 100–250 sweeps are typically averaged per run.

Mechanism by which abnormal communication between the inner ear and surrounding structures (e.g. superior canal dehiscence) increases the inner ear's responsiveness to sound and pressure. Produces lowered VEMP thresholds and augmented amplitudes.

The lowest stimulus intensity that still produces a reproducible VEMP. A lowered threshold (e.g. < 70 dBnHL on cVEMP) is the most specific finding for SCD.

A short pulse of a pure tone — typically 500 Hz, 2-ms rise/fall, 2-ms plateau — used as the standard auditory stimulus for clinical VEMP testing.

Localising a vestibular lesion to a specific structure (saccule vs utricle, superior nerve vs inferior nerve) by combining VEMP with caloric and other tests. The combination resolves what 'a vestibular problem' actually means.

Sound-induced vertigo, oscillopsia, or eye movements — classically associated with third-window disorders such as SCD. Named after Pietro Tullio's 1929 experiments on pigeons.

One of the two otolith organs. Its macula lies in the horizontal plane and detects horizontal linear acceleration and head tilt. The utricle is innervated by the superior vestibular nerve and is the receptor that generates the oVEMP.

A common cause of episodic vertigo associated with a migraine diathesis. VEMP findings are heterogeneous — reduced amplitudes and increased asymmetry ratios are common but not diagnostic.

Acute unilateral vestibulopathy, usually presumed post-viral. May affect the superior division alone (most common), the inferior division alone, or both. VEMP/caloric pattern allows topographic localisation.

Benign tumour arising from the vestibular nerve sheath, usually within the internal auditory canal. VEMP sensitivity ~81%, specificity ~53%; useful adjunct but MRI remains the diagnostic standard.

Disynaptic reflex from saccular afferents through the inferior vestibular nucleus and medial vestibulospinal tract to the ipsilateral sternocleidomastoid. The cVEMP is its surface EMG representation.

Reflex that stabilises gaze during head movement. The oVEMP exploits a sound- and vibration-evoked component of the VOR mediated by utricular afferents to the contralateral inferior oblique.