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1. Introduction

The acute vestibular syndrome

The acute vestibular syndrome (AVS) is the sudden, persistent onset of vertigo lasting hours to days, with nystagmus, head-motion intolerance, nausea, vomiting, and unsteadiness of gait. It is one of the most common presentations of posterior circulation stroke — and one of the most commonly missed.

The clinical question at the bedside is sharp and binary: is this patient's acute vertigo peripheral (vestibular neuritis, labyrinthitis) or central (cerebellar or brainstem stroke)?

Why HINTS

HINTS is a three-step oculomotor exam — Head Impulse, Nystagmus, Test of Skew — that, in trained hands, has been reported to be more sensitive for stroke than early MRI with diffusion-weighted imaging within the first 24–48 hours of symptom onset³. The protocol relies on features that are immediately observable at the bedside, requires no equipment, and takes under two minutes to complete.

When HINTS applies

HINTS was developed and validated for patients with the continuousacute vestibular syndrome. It is not appropriate for episodic positional vertigo (use Dix-Hallpike), for vertigo of less than several hours' duration, for patients without nystagmus at the time of examination, or for patients with normal head impulse and no spontaneous nystagmus — they are likely outside the protocol's validated domain.

Operator dependency

The validation studies were performed by neuro-otologists with subspecialty expertise³. Reported sensitivity and specificity in less experienced hands are substantially lower. Video head impulse testing (vHIT) reduces operator dependency for the impulse component but is not always available at the bedside⁸. The strongest evidence supports HINTS-plus — the original three plus assessment for new auditory symptoms — interpreted by trained clinicians^10,1.

2. Anatomy & physiology of the VOR

The peripheral labyrinth

Each labyrinth contains three semicircular canals (horizontal, anterior, posterior) oriented in roughly orthogonal planes, and two otolith organs (utricle and saccule). Angular acceleration of the head deflects the cupula of the canal aligned with the plane of motion. Linear acceleration and head tilt deflect the otolith maculae.

The vestibular nerve

The vestibular nerve has two anatomically and functionally distinct divisions. The superior division innervates the horizontal and anterior canals, and the utricle. The inferior division innervates the posterior canal and the saccule. Superior vestibular neuritis is far more common than inferior, and the pattern of head-impulse abnormality and oVEMP / cVEMP findings follows the division involved.

The three-neuron VOR arc

The vestibulo-ocular reflex stabilises gaze during head movement. Its shortest pathway has just three neurons: primary afferent from the canal to the vestibular nucleus; vestibular nucleus to contralateral abducens nucleus; abducens to lateral rectus, with an MLF branch to the medial rectus of the opposite eye. The horizontal VOR arc is the substrate of the head-impulse test.

Central VOR connections relevant to HINTS

The vestibular nuclei project to the cerebellar flocculus and nodulus, which calibrate VOR gain and adapt it to context. Lesions of these structures — common in posterior circulation stroke — can produce direction-changing gaze-evoked nystagmus and abnormal smooth pursuit while leaving the brainstem VOR arc intact. This is why a normal head impulse in acute vestibular syndrome is a central red flag.

Otolith pathways and the test of skew

Skew deviation reflects an imbalance in the otolith-ocular pathway between the utricle, vestibular nuclei, interstitial nucleus of Cajal, and the ocular motor nuclei. Because this pathway crosses the brainstem, skew is sensitive to brainstem lesions but can occasionally be seen in severe peripheral utricular disease — a recognised pitfall of the test.

3. Examination technique

Head Impulse

Stand facing the patient at arm's length. Ask the patient to fixate on your nose and to relax their neck muscles. Place your hands on either side of the head, just above the ears. Tilt the head 30° forward to bring the horizontal semicircular canals into the plane of testing. Apply a small, rapid, unpredictable head turn of approximately 10–20° amplitude with a peak velocity of about 150–250°/s.

If the VOR is intact, the eyes stay locked on your nose throughout the head turn. If the VOR is impaired on the side of the head rotation, the eyes are dragged with the head and the patient generates a visible corrective saccade back to your nose at the end of the movement. The corrective saccade is the positive finding².

Nystagmus

Assess spontaneous nystagmus in primary gaze and in eccentric gaze (left, right, up, down). Note the direction of the fast phase, whether it changes with gaze direction, and whether it has vertical or pure torsional components. Peripheral pattern: unidirectional, horizontal-torsional, fast phase beating away from the affected ear, suppressed by visual fixation. Central pattern: direction-changing on lateral gaze, vertical, pure torsional, or not suppressed by fixation.

Test of Skew

Have the patient fixate on your nose. Alternately cover one eye, then the other, releasing each cover for about a second before switching. Watch the uncovered eye as it takes up fixation. A vertical refixation movement — even a small one — is a positive skew, and a central red flag in acute vestibular syndrome.

Pitfalls and quality control

Predictable impulses let smooth pursuit and visual fixation compensate — vary timing and direction. Insufficient velocity (below ~100°/s) does not challenge the VOR. Covert saccades happen during the impulse and can be missed at the bedside; video head impulse testing (vHIT) captures these⁸. Always observe nystagmus with and without fixation — Frenzel lenses or video-Frenzel goggles are useful.

HINTS-plus and audiometric testing

HINTS-plus adds new hearing loss as a central red flag. AICA territory infarction can involve the labyrinthine artery and present with peripheral-pattern HINTS but acute sensorineural hearing loss. In the setting of acute vestibular syndrome, new audiometric loss should prompt urgent posterior fossa imaging even when the three core HINTS findings look peripheral^10,1.

4. Normal findings

Normal head impulse

In a healthy subject the VOR generates an equal-and-opposite eye movement for any head rotation, so the eyes remain locked on the target throughout the impulse. There is no overt or covert corrective saccade. On video head impulse testing (vHIT) the VOR gain — peak eye velocity divided by peak head velocity — is approximately 0.9–1.0 for the horizontal canal.

Normal nystagmus pattern

In primary gaze and during fixation there should be no spontaneous nystagmus. With fixation removed, a small amount of physiologic spontaneous nystagmus may be visible. End-point or end-gaze nystagmus — small, exhaustible, symmetric beats in extreme lateral gaze — is a normal variant and should not be confused with pathological gaze-evoked nystagmus.

Absent skew

On alternate cover testing the uncovered eye should not make a vertical refixation movement. Some patients have a small phoria; this is not the same as a vertical skew deviation and is generally well-compensated.

Quantitative norms — vHIT

Published normative ranges for the horizontal canal VOR gain cluster around 0.9–1.0, with most laboratories using a lower limit of normal around 0.8. Vertical canal gains tend to run slightly lower (~0.7–0.9). Specific cut-offs depend on device and recording protocol⁸.

5. Vestibular neuritis

Clinical picture

Sudden-onset, prolonged vertigo with horizontal-torsional nystagmus, head-motion intolerance, nausea, and gait unsteadiness. Hearing is spared (distinguishing it from labyrinthitis). Symptoms peak in 24 hours and improve over days to weeks as central compensation develops¹¹.

HINTS signature — peripheral pattern

Abnormal head impulse toward the affected side; unidirectional horizontal-torsional nystagmus, fast phase away from the affected ear; absent skew. This is the reassuring triad in acute vestibular syndrome when complete and unambiguous^3,10.

Superior vs inferior vestibular neuritis

Superior vestibular neuritis is far more common and produces the classic findings above plus an abnormal oVEMP and normal cVEMP. Inferior vestibular neuritis is rarer, may produce posterior-canal head-impulse findings, an abnormal cVEMP, and a normal oVEMP.

Mimics and caveats

The peripheral HINTS pattern does not exclude AICA stroke involving the labyrinthine artery — which can present with peripheral HINTS plus acute sensorineural hearing loss. This is the rationale for HINTS-plus^10,1.

6. Posterior circulation stroke

Why HINTS matters here

Posterior circulation strokes are commonly misdiagnosed as peripheral vertigo in emergency departments. The bedside HINTS protocol, when performed by trained clinicians, has been reported to be more sensitive than diffusion-weighted MRI in the first 24–48 hours of symptoms — DWI can be falsely negative in small brainstem and cerebellar infarcts during this window^3,9,4.

The INFARCT mnemonic

Impulse Normal, Fast-phase Alternating, Refixation on Cover Test. Any one of these in a patient with acute vestibular syndrome is a central red flag³.

Territory-specific features

PICA (lateral medullary / Wallenberg). Ipsilateral Horner, ipsilateral facial / contralateral body sensory loss, dysphagia, hoarseness, ipsilateral limb ataxia. Central HINTS plus brainstem signs.

AICA. Can mimic peripheral vestibulopathy when the labyrinthine artery is involved — peripheral HINTS plus acute sensorineural hearing loss^1,10. Facial weakness, ipsilateral deafness, cerebellar ataxia.

Cerebellar (non-AICA/PICA). Isolated vertigo and ataxia are possible. Skew may be absent; reliance on impulse and nystagmus components is critical⁹.

HINTS vs neuroimaging — operational reality

Early MRI DWI sensitivity for posterior circulation stroke is approximately 80% in the first 24–48 hours, with reported sensitivity as low as ~50% for small infarcts. A negative DWI does not exclude posterior stroke in this window³. HINTS by a trained examiner with HINTS-plus audiometric assessment, followed by appropriately timed MRI, is the current best-evidence approach^10,4.

7. Vestibular migraine

Clinical picture

Recurrent episodes of vertigo lasting minutes to 72 hours, often with migrainous headache, photophobia, phonophobia, or visual aura. Diagnosis is by the Bárány Society / International Headache Society criteria, not by HINTS^5,6.

HINTS during an attack

Between attacks the exam is typically normal. During an attack, oculomotor findings are heterogeneous — central or peripheral features may appear, and direction-changing nystagmus has been described. The clinical context (recurrent attacks, migraine features, return to baseline between episodes) distinguishes vestibular migraine from acute vestibular syndrome.

Why HINTS is not the right tool here

HINTS was developed and validated specifically for the continuousacute vestibular syndrome³. Episodic vertigo — vestibular migraine, BPPV, Ménière's — falls outside its validated domain. Applying HINTS to these patients can produce misleading results.

8. MS & brainstem demyelination

Clinical picture

Demyelinating disease can produce isolated vertigo, but classical brainstem MS attacks combine vestibular symptoms with other ocular motor findings — internuclear ophthalmoplegia, gaze palsies, skew, vertical or torsional nystagmus, and cerebellar signs.

HINTS signature — central pattern

Head impulse typically normal (the peripheral apparatus is intact); nystagmus often vertical, gaze-evoked direction-changing, or with INO features; skew may be present, especially with brainstem plaques.

Internuclear ophthalmoplegia

INO is caused by a lesion in the medial longitudinal fasciculus on the side of the impaired adducting eye. On lateral gaze the ipsilateral adducting eye is slow or fails to cross the midline, while the contralateral abducting eye shows dissociated nystagmus. Bilateral INO in a young patient should raise strong suspicion of MS.

Imaging and workup

MRI of the brain and craniocervical junction with FLAIR and post-contrast T1 sequences. Look for periventricular, juxtacortical, infratentorial, and spinal cord lesions. CSF examination for oligoclonal bands. The McDonald criteria are the diagnostic framework; HINTS findings alone are insufficient¹².

9. Ménière's disease

Clinical picture

Spontaneous attacks of vertigo lasting 20 minutes to 12 hours, with low- to medium-frequency sensorineural hearing loss documented on audiometry in the affected ear, plus fluctuating aural symptoms — hearing change, tinnitus, or aural fullness — in the same ear. Two or more such attacks meet criteria for definite Ménière's disease⁷.

HINTS during an attack

Peripheral pattern: abnormal head impulse on the affected side, unidirectional horizontal-torsional nystagmus, absent skew. HINTS-plus is positive — the aural symptoms count as auditory change. In a first-ever attack the picture can mimic AICA stroke with labyrinthine artery involvement; the discriminators are the audiometric profile (low-frequency) and the stereotyped recurrence on subsequent attacks.

Why HINTS is not the diagnostic framework

Ménière's is episodic; HINTS is validated for the continuous acute vestibular syndrome³. The diagnostic framework is the Bárány Society / Japan Society for Equilibrium Research / EAONO / AAO-HNS / Korean Balance Society 2015 consensus, which is built on history, audiogram, and aural symptoms⁷.

10. Benign paroxysmal positional vertigo

Clinical picture

Brief attacks of spinning vertigo, seconds to under a minute, provoked by specific head movements: lying down, rolling over in bed, looking up, or bending forward. Between episodes, asymptomatic or only mildly unsteady. No hearing loss, no tinnitus, no continuous vertigo, no central oculomotor abnormality between episodes¹³.

Why HINTS is the wrong tool

HINTS is validated for continuous acute vestibular syndrome³. BPPV is the opposite phenotype: episodic, positional, brief, with a well-patient between attacks. Applying HINTS yields uninformative findings. The right bedside tests are the Dix-Hallpike manoeuvre for posterior or anterior canal BPPV and the supine roll test for horizontal canal BPPV¹³.

Dix-Hallpike

Sit the patient on the couch with the head turned 45° toward the tested ear. Quickly move them to supine with the head extended approximately 20° below the horizontal. Watch the eyes for at least 30 seconds. Posterior canal canalolithiasis produces a short-latency, fatigable, upbeating torsional nystagmus toward the dependent ear, lasting under one minute, with reproduction of the vertigo.

Treatment

Canalith repositioning manoeuvres — the Epley for posterior canal and the Lempert / barbecue roll for horizontal canal — use gravity to walk the otoconia back into the utricle and are highly effective in a single session.