Approach to Vertigo — A Clinical Framework

Vertigo is a symptom, not a diagnosis. It is also one of the most frequently mismanaged presentations in clinical medicine — not because it is rare, but because the word “dizzy” covers an enormous range of physiological phenomena, and many clinicians begin treatment before establishing what the symptom actually is. The first task is always to characterise the symptom precisely. The second is to determine whether it arises from a peripheral (labyrinthine or vestibular nerve) lesion or a central (brainstem, cerebellum) one. These two steps take most patients out of danger and most diagnoses out of uncertainty.

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Vertigo is Not Dizziness

Before anything else, establish what the patient means. Four categories cover almost all presentations:

True vertigo: An illusion of movement — the room spinning, the patient spinning, or things tilting and falling. This is the hallucination of angular or linear motion that does not correspond to actual movement. It implies vestibular pathology — peripheral or central.

Presyncope: A feeling of impending fainting or blackout, lightheadedness, greyout of vision. This is a circulatory symptom — orthostatic hypotension, cardiac arrhythmia, vasovagal events. It has nothing to do with the vestibular system.

Disequilibrium: A sense of unsteadiness or imbalance without a rotary component, often worse when walking or standing. Usually a sensorimotor or cerebellar problem — peripheral neuropathy, cerebellar ataxia, Parkinson’s, bilateral vestibular failure. Not a spinning sensation.

Nonspecific dizziness: Floating, woolly-headed, or vaguely “off” sensations that fit none of the above. This category includes anxiety-driven symptoms, hyperventilation, visual vertigo, and persistent postural-perceptual dizziness (PPPD).

These categories do not always present cleanly — patients mix descriptors and the translation into clinical categories requires careful listening. But the distinction between true vertigo and the others is the most important first step, because it determines whether the vestibular system is involved at all.

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The Single Most Important Distinction: Peripheral vs Central

Once true vertigo is established, the diagnostic priority is peripheral versus central. This distinction determines urgency: central vertigo can be a posterior circulation stroke, and the window for thrombolysis is time-limited.

Feature	Peripheral	Central
Onset	Often sudden	Sudden or gradual
Severity of vertigo	Usually intense	Variable; often milder
Nausea/vomiting	Common, often severe	Variable
Hearing loss/tinnitus	May be present	Usually absent
Neurological symptoms	Absent	Often present
Nystagmus direction	Unidirectional, horizontal-torsional	May be bidirectional, vertical, or direction-changing
Fixation suppression	Nystagmus suppressed by fixation	Nystagmus NOT suppressed by fixation
Head impulse test	Abnormal (corrective saccade)	Normal
Falls	May occur	Often pronounced, unable to stand

This table is a guide, not a rule — there is overlap. The HINTS examination (below) is the most reliable clinical tool for distinguishing the two at the bedside in acute vestibular syndrome.

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The History — Four Questions That Do Most of the Work

A structured history narrows the differential in most cases before the patient stands up for examination.

1. What is the time course?

Seconds to two minutes, position-triggered, episodic: BPPV. The brief, position-triggered, fatigable episodes of posterior or horizontal canal BPPV are distinctive. See the BPPV article for full characterisation.

Minutes to hours, episodic, with auditory symptoms: Menière’s disease. Attacks typically last 20 minutes to 4 hours. Fluctuating sensorineural hearing loss, tinnitus (often low-frequency roaring), and aural fullness are the triad. Between attacks, the patient may be entirely symptom-free.

Days, continuous, following viral prodrome, no auditory symptoms: Vestibular neuritis. A single prolonged episode of vertigo with severe nausea and vomiting, made worse by head movement, following a viral illness. Hearing is unaffected (distinguishing it from labyrinthitis). Improves over days to weeks.

Days, continuous, with hearing loss: Labyrinthitis. Same presentation as vestibular neuritis but with concurrent sensorineural hearing loss, indicating that the cochlear nerve is also inflamed.

Seconds to minutes, with position change, and accompanied by neurological symptoms: Central positional vertigo — posterior fossa lesion until proved otherwise.

Acute, continuous, with neurological symptoms: Posterior circulation stroke or TIA. A clinical emergency.

2. Are there auditory symptoms?

Hearing loss and tinnitus localise the problem to the cochlea or cochlear nerve and suggest a labyrinthine or CN VIII lesion. Their presence in the context of vertigo points toward Menière’s disease, labyrinthitis, sudden SNHL with vestibular involvement, or an acoustic neuroma eroding CN VIII. Their absence in acute prolonged vertigo suggests vestibular neuritis or a central cause.

The critical exception: a posterior circulation stroke affecting the anterior inferior cerebellar artery (AICA) supplies both the labyrinthine artery (to the cochlea and labyrinth) and the posterior fossa. AICA territory strokes can therefore present with acute vertigo AND hearing loss, mimicking labyrinthitis or Menière’s. This is one of the most dangerous mimics in acute vestibular medicine.

3. Are there neurological symptoms?

Diplopia, dysarthria, dysphagia, facial numbness, limb weakness or incoordination, headache, or altered consciousness accompanying vertigo should always raise the question of posterior fossa pathology. These symptoms have no place in peripheral vestibular disease. Their presence is a red flag that mandates urgent imaging.

4. What triggers or worsens the vertigo?

• Specific head positions (lying down, rolling over, head tilt) → BPPV
• Head movement in any direction, worse with all movement → vestibular neuritis (acute phase), or central
• Loud sounds or pressure changes worsening vertigo → superior semicircular canal dehiscence (Tullio phenomenon)
• Standing from sitting → postural hypotension (not vertigo at all)
• Crowded or visually complex environments → PPPD

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The HINTS Examination — For Acute Vestibular Syndrome

The HINTS examination (Head Impulse, Nystagmus, Test of Skew) is applied specifically to the patient with acute vestibular syndrome — acute onset continuous vertigo with nausea and vomiting, first-time presentation. This is the clinical scenario where stroke masquerading as vestibular neuritis is the danger, and HINTS is more sensitive than MRI-DWI in the first 24–48 hours for detecting posterior circulation stroke in this context (Kattah et al., Stroke 2009; Newman-Toker et al., Acad Emerg Med 2013).

The mnemonic works in a counterintuitive direction: a reassuring result in peripheral disease, a concerning result in central disease.

H — Head Impulse Test (HIT)

The examiner stands in front of the seated patient and holds the patient’s head, asking them to keep their eyes fixed on the examiner’s nose. The head is rapidly rotated about 15–20° to one side (a small, fast impulse). The sign being sought is a corrective saccade — when the head moves rapidly toward the damaged labyrinth, the vestibulo-ocular reflex (VOR) on that side is impaired, so the eyes cannot maintain fixation during the movement and a catch-up saccade is visible as the head decelerates.

Abnormal HIT (corrective saccade visible): indicates impaired VOR on the tested side — a peripheral lesion (vestibular neuritis, labyrinthitis). This is a reassuring sign — it points to peripheral disease.

Normal HIT (no corrective saccade, eyes stay fixed): the VOR is intact. In a patient with acute vertigo, a normal head impulse test means the peripheral vestibular system is working — the cause is central until proved otherwise. This is the dangerous finding.

N — Nystagmus

Observe the nystagmus direction with the patient looking straight ahead, then in each direction of gaze.

Unidirectional horizontal-torsional nystagmus (same direction in all gaze positions): peripheral. Nystagmus is suppressed by fixation — asking the patient to fix on a stationary target reduces it.

Direction-changing nystagmus (changes direction with gaze direction — gaze-evoked nystagmus): central. Nystagmus is NOT suppressed by fixation.

Pure vertical nystagmus (purely downbeat or purely upbeat): central. This pattern is never produced by a peripheral lesion.

T — Test of Skew

Cover one eye and then rapidly uncover it, looking for a vertical corrective movement of the newly uncovered eye. This is the cover-uncover test for vertical skew deviation.

Vertical skew deviation present: the covered eye drifts vertically (usually upward) and corrects when uncovered — an abnormal ocular motor sign indicating central pathology (brainstem lesion).

No vertical deviation: peripheral.

Interpreting HINTS Together

The combination that distinguishes peripheral from central:

Finding	Peripheral (safe)	Central (dangerous)
Head impulse test	Abnormal (corrective saccade)	Normal
Nystagmus	Unidirectional, suppressed by fixation	Direction-changing or pure vertical
Test of skew	Negative	Positive

A “benign HINTS” (abnormal HIT + unidirectional nystagmus + negative skew) points to peripheral vestibular neuritis. A “dangerous HINTS” (normal HIT, or direction-changing nystagmus, or positive skew) should prompt urgent MRI. The HINTS examination should be performed by a clinician trained in vestibular examination — the head impulse test in particular requires specific technique to interpret reliably.

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Common Diagnoses at a Glance

Diagnosis	Key features	Duration of episode	Hearing affected
BPPV	Positional, brief, fatigable	Seconds (<60 sec)	No
Vestibular neuritis	Continuous, post-viral, no hearing loss	Days to weeks	No
Labyrinthitis	Continuous, post-viral, with SNHL	Days to weeks	Yes
Menière’s disease	Episodic attacks, low-frequency SNHL, tinnitus, aural fullness	20 min – 4 hours	Yes (fluctuating)
Posterior circulation stroke	Sudden onset, neurological signs, normal or dangerous HINTS	Continuous	Sometimes (AICA)
Acoustic neuroma	Gradual progressive SNHL + tinnitus; vertigo usually mild	Chronic/progressive	Yes

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Investigations

Pure tone audiogram: Mandatory in any vertigo patient where a cochlear or retrocochlear lesion is possible. A unilateral SNHL in the context of vertigo requires investigation for Menière’s disease or acoustic neuroma.

Tympanometry: To assess middle ear pressure and Eustachian tube function — relevant where eustachian tube dysfunction or middle ear disease may be contributing.

MRI internal auditory meati with gadolinium: First-line imaging for acoustic neuroma, labyrinthitis, or unexplained unilateral SNHL. MRI (not CT) is the appropriate modality.

MRI brain/posterior fossa: Urgently in any patient with central features on HINTS, neurological symptoms, or unexplained acute severe vertigo in a vascular risk patient.

Caloric testing / videonystagmography (VNG): For objective documentation of unilateral vestibular hypofunction — useful in work-up of vestibular neuritis, Menière’s disease, and bilateral vestibular failure, but not required acutely.

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Key Numbers

Parameter	Value
HINTS sensitivity for posterior circulation stroke	>99% in experienced hands
DWI-MRI sensitivity for stroke (first 24–48 hours)	~83% (HINTS outperforms MRI-DWI in this window)
BPPV episode duration	<60 seconds
Menière’s attack duration	20 minutes to 4 hours
Vestibular neuritis recovery	Days to weeks; most patients compensate fully within 6 weeks

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Frequently Asked Questions

How do I distinguish Menière’s disease from a vestibular migraine? This is one of the most challenging differentials in neurotology. Both produce episodic vertigo lasting minutes to hours. Vestibular migraine often occurs in patients with a personal or family history of migraine, may be accompanied by headache or migrainous phenomena (photophobia, phonophobia, visual aura), and does not consistently produce the fluctuating low-frequency SNHL characteristic of Menière’s disease. Audiometry during an attack is helpful — a true Menière’s attack produces documented low-frequency hearing change. The distinction matters because management differs.

My patient has had a “dizzy spell” — should I prescribe prochlorperazine? Not before characterising the symptom. Prochlorperazine (and other vestibular suppressants including betahistine in the acute phase) provide symptomatic relief but delay vestibular compensation — the central nervous system’s adaptation to a unilateral vestibular lesion. In a patient with vestibular neuritis, early mobilisation and vestibular rehabilitation accelerate recovery. In a patient with BPPV, vestibular suppressants are ineffective because the cause is mechanical. Prescribing prochlorperazine as a reflex response to any dizziness complaint is poor practice.

Can anxiety cause true vertigo? Not true vestibular vertigo — anxiety causes hyperventilation-related lightheadedness, presyncope, and spatial disorientation, which patients often describe as dizziness. However, persistent postural-perceptual dizziness (PPPD) is a recognised functional vestibular disorder in which anxiety and autonomic arousal produce genuine perceptual symptoms including motion sensitivity, visual triggers, and imbalance — often following an acute peripheral vestibular event. It is not anxiety causing vertigo, but anxiety perpetuating a vestibular adaptation failure. Distinguishing this from residual organic disease requires vestibular function testing and clinical judgement.

When is vertigo a neurological emergency? Acute vertigo with any of the following requires urgent neurological evaluation and imaging: neurological symptoms (diplopia, dysarthria, dysphagia, limb weakness, facial numbness), normal head impulse test (dangerous HINTS), direction-changing or purely vertical nystagmus, vertical skew deviation, severe headache, vascular risk factors in an older patient, inability to stand at all. Do not discharge without considering the posterior circulation.