At the bedside

Differential diagnosis & HINTS

Two questions decide everything. First: is this central or peripheral? Then, if central: is it stroke or something slower? Both are answered mostly by the history and a careful oculomotor examination.

Central versus peripheral

The first fork is the highest-stakes one. A handful of features separate a benign peripheral vestibulopathy from a dangerous central lesion — no single one is decisive, but the pattern usually is.1

Bedside features: peripheral vs central
Feature	Peripheral	Central
Nystagmus	Unidirectional, horizontal-torsional; suppressed by fixation	Vertical / torsional / direction-changing; fixation does not suppress
Head impulse test	Abnormal (catch-up saccade) on the affected side	Often normal — a red flag in acute vestibular syndrome
Skew deviation	Absent	May be present
Gait	Unsteady but able to walk	Often cannot stand or walk unaided
Hearing	May be affected (e.g. labyrinthitis, Ménière’s)	Usually spared — except AICA infarction
Other signs	None	Diplopia, dysarthria, dysphagia, weakness, numbness, Horner’s

The HINTS interpreter

In a genuine acute vestibular syndrome, the three-step HINTS battery is more sensitive than early MRI for stroke.2,3 Set each finding below and read off the verdict. Remember the rule: any one central feature is enough to call the pattern dangerous.

HINTS interpreter

for a true acute vestibular syndrome

Head Impulse

Nystagmus

Test of Skew

✓ Peripheral

Reassuring (peripheral) pattern

Abnormal head impulse + unidirectional nystagmus + no skew is the benign peripheral triad, consistent with vestibular neuritis — but only when a true AVS is present and there are no other red flags.

Remember the danger mnemonic INFARCT — Impulse Normal, Fast-phase Alternating, Refixation on Cover Test. HINTS only applies to a genuine acute vestibular syndrome with spontaneous nystagmus; outside that setting it can mislead.

The reassuring peripheral triad — abnormal head impulse, unidirectional nystagmus, no skew — is only valid when there is a true continuous AVS with spontaneous nystagmus. HINTS does not apply to episodic or positional vertigo, and a benign pattern never overrides other red flags or a worsening course.1

Stroke versus multiple sclerosis

Once a cause looks central, age, tempo, the company the vertigo keeps, and a few targeted tests usually separate the time-critical vascular event from the slower demyelinating one.

Stroke vs multiple sclerosis at a glance
Feature	Stroke	Multiple sclerosis
Onset	Sudden, maximal at onset	Subacute, over hours to days
Course	Monophasic, constant	Relapsing, evolves and recurs
Typical age	> 50 years	20–40 years
Sex skew	Either	Female 2–3 : 1
Risk factors	Vascular — hypertension, diabetes, hyperlipidaemia, smoking	Autoimmune predisposition; prior demyelinating events
Nystagmus	Vertical/torsional, direction-changing, non-fatigable, fixation-resistant	Upbeat, downbeat or gaze-evoked; INO common
Associated signs	Hemiparesis, diplopia, dysarthria, Horner's, crossed sensory loss	Optic neuritis, INO, Lhermitte's sign, sensory symptoms
MRI	DWI-bright acute infarct in brainstem/cerebellum	T2/FLAIR plaques — periventricular, juxtacortical, infratentorial, cord
CSF	Usually normal	Oligoclonal bands in ~85–95%
Priority	Time-critical reperfusion / antithrombotic therapy	Steroids for the relapse, then disease-modifying therapy

MRI and CSF seal the distinction: a DWI-bright posterior-fossa infarct points to stroke, while T2/FLAIR plaques in characteristic sites with oligoclonal bands point to MS under the 2017 McDonald criteria.6,7

Diagnostic pitfalls

The false-negative MRI. Up to ~20% of small posterior-fossa infarcts are missed on DWI in the first 24–48 hours; persistent or progressive symptoms justify repeat imaging.4
Isolated vertigo as stroke. Cerebellar and brainstem infarcts can present with vertigo and nothing else, and are repeatedly mislabelled as neuritis.5
HINTS misuse. Applied outside continuous AVS, or by an untrained examiner, it misleads — and a normal head impulse in a truly vertiginous patient is a stroke red flag, not reassurance.
MS mimics. An isolated brainstem plaque can imitate vestibular migraine, BPPV or PPPD, and a clinically isolated syndrome may not yet meet criteria — both need follow-up and repeat imaging.8

Future directions

Several developments aim to close the diagnostic gap in central vertigo: advanced MRI (diffusion-tensor and susceptibility-weighted imaging) for small or atypical lesions; blood biomarkers — serum neurofilament light chain in MS, and ischaemia markers in stroke — to support early triage;9 machine-learning analysis of videonystagmography and video head-impulse data; and tele-HINTS, delivering expert oculomotor assessment remotely to under-served settings.

Key points

Decide central vs peripheral first; in AVS, HINTS is more sensitive than early MRI for stroke.
Any one central feature — normal head impulse, direction-changing nystagmus, or skew — makes the pattern dangerous.
Stroke is sudden, older, vascular, monophasic; MS is subacute, younger, autoimmune, relapsing.
MRI (DWI vs T2/FLAIR plaques) and CSF oligoclonal bands separate stroke from MS.
Beware the false-negative early MRI and the misuse of HINTS outside acute vestibular syndrome.