Module 12 of 12

Clinical Correlates & Vestibular Testing

How physiological lesions map onto vHIT, caloric testing, and VEMP, and onto the major vertigo syndromes.

Each diagnostic test probes a specific limb of vestibular physiology. Reading a test result well means knowing which structure it interrogates.

Doctors test the balance system in a few different ways — checking how the eyes respond to quick head turns, to warm or cool water in the ear, and to sound. Each test looks at a different part of the system.

The video head impulse test assesses VOR performance at high frequencies and identifies a deficient semicircular canal. Caloric testing evaluates the horizontal canal and reveals side-to-side asymmetry. Vestibular evoked myogenic potentials assess otolith function — cervical VEMP for the saccule, ocular VEMP for the utricle ¹³.

Mapping physiology to disease: benign paroxysmal positional vertigo reflects displaced otoconia within a canal; vestibular neuritis is an acute unilateral afferent hypofunction; endolymphatic hydrops disturbs the fluid homeostasis of Module 3; central syndromes implicate the brainstem and cerebellar circuits of Module 10. Treatment leans on plasticity — vestibular rehabilitation therapy recalibrates reflex pathways through tailored gaze-stabilization exercises³⁴.

Nystagmus. A slow vestibular drift in one direction is interrupted by a rapid corrective saccade. The direction the fast phase beats names the nystagmus. Pattern and behaviour with gaze localise the cause.

Downbeat nystagmus — points to a cerebellar / craniocervical lesion (often Chiari, or floccular).

Head impulse test. Normally the eye velocity mirrors the head, keeping gain near 1 with no corrective saccade. When the canal is deficient the eye lags, and a visible catch-up saccade appears once the head impulse ends — a localising sign of peripheral hypofunction.

Caloric test. Warm and cool irrigations of each ear induce nystagmus whose peak slow-phase velocity reflects horizontal-canal function. A symmetric butterfly indicates intact canals; a small-amplitude side signals a unilateral peripheral weakness.

Pure-tone audiogram. All thresholds at or below 25 dB HL.

cVEMP pathway. A loud acoustic click excites saccular hair cells; the signal travels via the inferior vestibular nerve and medial vestibulospinal tract to inhibit the ipsilateral sternocleidomastoid, generating the biphasic P13-N23 myogenic response.

The Dix-Hallpike provokes posterior-canal BPPV. The patient sits, the examiner turns the head 45° toward the suspect ear, then lays the patient back rapidly with the head hanging extended. A latent, fatigable upbeat-torsional nystagmus confirms the diagnosis.

Disease mechanisms at a glance

Acute vestibular neuritis. Inflammation of one vestibular nerve silences afferent input on the affected side, leaving the intact side unopposed. The resting asymmetry drives a unidirectional spontaneous nystagmus beating away from the lesion, the head impulse test is abnormal toward the lesion, and hearing is spared.

Canalithiasis. Otoconia displaced from the utricular macula enter a semicircular canal — most often the posterior canal — and settle gravitationally. When the head moves, the debris drifts through the endolymph, abnormally deflecting the cupula and producing the brief, position-triggered vertigo of BPPV.

Two pathologies underlie BPPV. In canalithiasis, free-floating otoconia drift through the endolymph and briefly deflect the cupula — characteristically with a latency and a vertigo lasting under a minute. In cupulolithiasis, debris adheres to the cupula itself, making it gravity-sensitive and producing a sustained, persistent nystagmus on positioning.

The Epley manoeuvre treats posterior-canal BPPV by sequentially rotating the head so otoconia migrate around the canal and exit into the utricle. Each position is held until nystagmus settles before the next step.

Endolymphatic hydrops. When endolymph homeostasis is disturbed the membranous compartment distends, raising pressure on both cochlear and vestibular sensors. The resulting fluctuating hearing, tinnitus, fullness, and episodic vertigo define Ménière’s syndrome.

A vestibular schwannoma arises on the vestibular branch of CN VIII within the internal auditory canal. Because it grows slowly, the brain compensates for vestibular asymmetry, so the dominant complaints are unilateral progressive hearing loss and tinnitus rather than vertigo.

Superior canal dehiscence is a bony gap in the roof of the superior semicircular canal. The third mobile window allows sound and pressure to deflect the canal endolymph, producing the Tullio phenomenon (sound-induced vertigo) and an autophony of internal sounds.

Vestibular migraine does not destroy the vestibular periphery. Instead, cortical spreading depression and trigeminovascular activation sensitise central vestibular pathways, producing episodic vertigo that may occur with, before, or apart from headache.

Bilateral vestibulopathy. With both sides equally reduced there is no asymmetry to drive a spontaneous nystagmus, but the VOR fails on every head movement. Vision bounces with the head — oscillopsia — and balance becomes visually dependent, sharply worse in the dark.

Medial longitudinal fasciculus. Internuclear ophthalmoplegia — failed adduction, abducting-eye nystagmus.

From physiology to the bedside

The diagnostic toolkit is rooted in VOR dynamics and eye-head interaction; interpreting it well is simply applied vestibular physiology ¹⁸. The clinical cases and conditions sections work through these patterns in detail.