Vertigo & Dizziness

Introduction

Dizziness is one of the most common presenting complaints in medicine and one of the most diagnostically challenging. Patients use the word "dizzy" to describe a spectrum of sensations — from true spinning vertigo to light-headedness, unsteadiness, or a feeling of impending faint. Accurate diagnosis depends almost entirely on the history, as the examination may be normal between episodes. Before reaching for prochlorperazine, invest time in a careful, structured history.

It is useful to remember that the human balance system has three components: vestibular input (accounting for approximately 15% of balance function in each ear — approximately 30% total bilaterally), proprioceptive input from joints, muscles, and tendons of the lower limbs and spine (approximately 35%), and visual input (approximately 35%). Disruption to any of these — particularly in elderly patients in whom all three may be sub-optimal simultaneously — causes disequilibrium. This is why a multifactorial approach is often needed in older patients, and why input from a falls clinic or elderly care physician can be invaluable.

Step 1: Characterise the Dizziness

The first and most important question to ask is: "What do you mean by dizzy?"

• True vertigo — the illusion of movement. The patient typically describes the room spinning around them, or a sensation of being on a merry-go-round. They may feel that they are tilting, falling, or rotating. This is caused by asymmetric vestibular input to the brain and implies a peripheral or central vestibular pathology. True vertigo is the key symptom in ENT-relevant causes of dizziness.
• Pre-syncope (light-headedness) — the patient feels as though they are about to faint, with a "greying out" of vision, weakness, or sweating. This is typically caused by reduced cerebral perfusion — hypotension (postural or otherwise), cardiac arrhythmia, or vasovagal episodes. The world does not spin; it simply goes dark. This is not an ENT problem.
• Dysequilibrium (unsteadiness) — an impairment of balance and gait without a sensation of spinning. Most common in elderly patients with multifactorial cause (proprioceptive loss, visual impairment, cerebellar atrophy, medication side-effects). Best managed in a falls clinic.
• Psychogenic / non-specific dizziness — anxiety, hyperventilation, and panic attacks can all produce a non-specific floating or dizzy sensation. Consider this in younger patients with no objective neurological or audiological findings and a history of anxiety.

Step 2: Take a Detailed Vertigo History

Duration of Episodes — The Key Diagnostic Question

The single most useful piece of information in a vertigo history is how long each episode lasts:

Associated Symptoms

• Hearing loss and tinnitus — fluctuating low-frequency sensorineural hearing loss plus tinnitus with episodic vertigo suggests Meniere's disease. Gradual progressive unilateral SNHL with tinnitus but without episodic vertigo suggests an acoustic neuroma. Note the Lermoyez variant of Meniere's disease — hearing and tinnitus paradoxically improve at the onset of the vertiginous attack, then worsen afterwards.
• Aural fullness — a pressure or blocked sensation in the ear is characteristic of Meniere's disease.
• Preceding viral illness — a flu-like illness or URTI in the weeks before acute, severe, sustained vertigo suggests vestibular neuronitis (no hearing loss) or labyrinthitis (with hearing loss and/or tinnitus).
• Positional trigger — does the vertigo come on with specific head movements? BPPV sufferers classically describe vertigo on rolling over in bed, sitting up from lying, or looking upward. There may be a history of recent head trauma or a prolonged period lying in one position (e.g., dental chair, hairdresser).
• Headache, photophobia, nausea — vestibular migraine can present with vertigo, and these patients often have a history of migraines or a family history. May be misdiagnosed as Meniere's disease. Migraine without headache ("silent migraine") can present purely with vertigo.
• Vertigo in cold air or induced by loud noise — Hennebert's sign (vertigo on pressure changes, e.g., sneezing, coughing, or cold wind on the ear) and Tullio's phenomenon (vertigo induced by loud sound) are very specific symptoms suggesting a perilymph fistula (a tear in the round or oval window membrane, allowing perilymph to leak into the middle ear). These patients require urgent ENT specialist assessment.
• Neurological symptoms — diplopia (double vision), dysarthria (slurred speech), dysphagia (difficulty swallowing), facial numbness, limb weakness or incoordination, or new headache should immediately raise concern for a central (posterior fossa) cause. A posterior inferior cerebellar artery (PICA) infarct (Wallenberg's syndrome) can present with sudden-onset vertigo mimicking a peripheral vestibular event — but will have additional features on HINTS exam.

Past History, Medications, and Background

Always ask about:

• Previous ear surgery, infections, or hearing problems
• History of cardiovascular disease (poor left ventricular function, previous strokes, atrial fibrillation)
• Current medications — many drugs cause dizziness (antihypertensives including atenolol, aminoglycosides, loop diuretics, benzodiazepines, tricyclics, anticonvulsants)
• Diabetes — causes peripheral neuropathy (impaired proprioception) and autonomic dysfunction (postural hypotension)
• History of temporal bone trauma

Step 3: Examination

General Assessment

A structured examination should assess all contributors to balance:

• Lying and standing blood pressure (postural hypotension) — a drop of greater than 20 mmHg systolic or 10 mmHg diastolic within 3 minutes of standing is significant and suggests postural hypotension as a contributing or primary cause.
• Visual acuity — poor vision impairs the visual component of balance
• Cardiovascular examination — pulse rhythm (atrial fibrillation), murmurs, signs of heart failure
• Ear examination — otoscopy may reveal cholesteatoma, haemotympanum, previous surgery, or middle ear effusion, all of which can cause or contribute to dizziness
• Full cranial nerve examination — focusing on cranial nerves V (facial sensation), VII (facial movement), and VIII (hearing and vestibular function)
• Cerebellar examination — finger-nose test (past-pointing/dysmetria), dysdiadochokinesis, gait assessment, Romberg's test

Romberg's Test

The patient stands with their feet together and arms outstretched. They first do this with their eyes open (to assess proprioception and cerebellar function while allowing visual compensation) and then with their eyes closed (removing the visual contribution to balance). Stand behind and beside the patient, ready to catch them if they fall — do not allow them to injure themselves.

If the patient is stable with eyes open but falls with eyes closed, this is a positive Romberg's test — it indicates a failure of either proprioceptive or vestibular input (the visual system was compensating and its removal unmasked the deficit). If the patient falls with eyes open, this suggests a cerebellar lesion (cerebellar ataxia is not dependent on visual input). The side of the fall in a positive Romberg's test tends to be the side of the abnormal vestibular system.

Unterberger's (Fukuda Stepping) Test

After performing Romberg's test, the patient stands with feet together and arms extended forwards, and is then asked to march on the spot with high knee lifts with their eyes closed. Normal individuals maintain their position. Patients with a unilateral vestibular deficit will rotate more than 30 degrees or walk forward more than 1 metre towards the affected side (the intact contralateral vestibular system "pushes" them towards the weaker side). When they open their eyes, they are often surprised to find they have moved significantly from their starting position.

Dix-Hallpike Test (for BPPV)

The Dix-Hallpike test (also called the Hallpike test) is the diagnostic test for benign paroxysmal positional vertigo (BPPV). It should be performed on each side:

1. Explain the test to the patient — tell them they may feel temporarily dizzy but that it is safe and diagnostic
2. Instruct the patient to keep their eyes open and focused on your nose throughout the manoeuvre, regardless of dizziness
3. Sit the patient on the examination couch with their legs extended, arms crossed on the chest
4. Holding the patient's head firmly with both hands, turn it 45 degrees to the side being tested
5. Swiftly lower the patient to the supine position, extending the neck so that the head hangs over the end of the couch at approximately 20–30 degrees below horizontal (the Hallpike position)
6. Maintain this position for at least 30 seconds, observing the eyes carefully for nystagmus
7. A positive test produces a brief latency of 5–20 seconds (the time for crystals to move within the semicircular canal) followed by a burst of geotropic rotatory nystagmus (the fast phase beats towards the ground — i.e., towards the affected ear) that lasts less than 60 seconds. The nystagmus is fatigable (diminishes with repeated testing) and the patient typically experiences vertigo at the same time.
8. Sit the patient up again (further nystagmus in the reverse direction may occur) and wait for them to settle before testing the other side

A negative Dix-Hallpike does not exclude BPPV — the test may be negative if the crystals (otoliths/canalith) have spontaneously repositioned, or if the wrong side is being tested. Non-geotropic nystagmus on Dix-Hallpike, or nystagmus that does not fatigue, should raise concern for a central cause.

The Head Impulse Test (HIT)

The head impulse test (HIT) assesses the vestibulo-ocular reflex (VOR). The patient is asked to fix their gaze on a stationary target (your nose). Their head is then rapidly and unexpectedly rotated to one side by approximately 15–20 degrees. In a normal VOR, the eyes stay fixed on the target because the VOR generates a compensatory eye movement in the opposite direction to the head rotation — the patient's gaze remains on target.

In a peripheral vestibular lesion (e.g., vestibular neuronitis), the VOR is impaired on the affected side. When the head is rotated towards the affected side, the eyes are initially dragged with the head and then make a corrective saccade back to the target. This visible corrective saccade (a "catch-up saccade") is the positive HIT and indicates a peripheral vestibular deficit. A normal HIT (no corrective saccade) in a patient with acute vertigo and nystagmus is a red flag for a central cause.

HINTS Exam — Peripheral vs Central Vertigo

In a patient presenting with acute continuous vertigo with nystagmus, the HINTS (Head Impulse, Nystagmus, Test of Skew) battery is a highly validated bedside tool that distinguishes peripheral from central causes:

The HINTS battery has been shown in studies (Kattah et al., Stroke 2009) to be more sensitive than early MRI for detecting posterior fossa infarction in acute vertigo. A central HINTS result (normal HIT + direction-changing nystagmus or vertical skew) should prompt urgent neurological assessment and MRI/CT of the posterior fossa.

Investigations

• Pure tone audiogram (PTA) — invaluable in the workup of vertigo. Low-frequency sensorineural hearing loss is characteristic of Meniere's disease. Progressive unilateral SNHL with tinnitus suggests acoustic neuroma. Age-related presbyacusis is common in elderly patients and may contribute to dysequilibrium.
• Tympanometry — assesses middle ear function; may reveal effusion or abnormal Eustachian tube function
• MRI of the internal auditory meati and posterior fossa — indicated if an acoustic neuroma is suspected, if there are any central features, or if the diagnosis remains unclear after clinical assessment. MRI is superior to CT for assessing the posterior fossa and intracranial compartment.
• CT head — faster and more widely available than MRI; useful acutely when posterior fossa haemorrhage or large infarct is suspected, though it is insensitive for early posterior fossa ischaemic stroke.
• Electrocardiogram (ECG) — if cardiac arrhythmia is suspected as a cause of presyncope
• Caloric testing and vestibular function tests — performed in specialist vestibular clinics; caloric testing provides objective assessment of horizontal semicircular canal function in each ear, useful for confirming unilateral vestibular hypofunction
• Electrocochleography (ECoChG) — can support the diagnosis of Meniere's disease by detecting endolymphatic hydrops (increased summating potential to action potential ratio)

Causes and Management

Benign Paroxysmal Positional Vertigo (BPPV)

BPPV is the most common cause of recurrent vertigo, accounting for approximately 20–30% of all cases. It is caused by the displacement of calcium carbonate crystals (otoconia/otoliths) from the utricular macula into one of the semicircular canals — most commonly the posterior semicircular canal (90% of cases). When the head is moved into certain positions, the displaced crystals move within the fluid-filled canal, causing aberrant deflection of the cupula and a brief but intense burst of vertigo and nystagmus.

Key features: very brief vertigo (seconds only) triggered by specific head movements (rolling over in bed, looking up, bending forward); positive Dix-Hallpike test with characteristic geotropic rotatory nystagmus; no hearing loss; no tinnitus; fatigable nystagmus. There may be a history of preceding minor head trauma or a period of prolonged recumbency.

Treatment — The Epley Manoeuvre: The Epley canalith repositioning manoeuvre is the definitive treatment for posterior canal BPPV. The principle is to move the displaced otolithic crystals through a series of carefully sequenced head positions so that they exit the affected semicircular canal and return to the utricle, where they can do no further harm. The manoeuvre involves four positions, each held for 30 seconds to allow the crystals to settle:

1. Dix-Hallpike position on the affected side (head turned 45 degrees towards the affected ear, neck extended over the end of the couch)
2. Head rotated 90 degrees to the opposite side (now turned 45 degrees away from the affected ear), still supine
3. The patient rolls onto their side (shoulder and head rotate together so the face is now pointing towards the floor, 45 degrees below horizontal)
4. The patient is brought back to sitting, with the head slightly chin-tucked

Each step takes approximately 30 seconds. Some practitioners tap the affected mastoid bone (as described in the original Epley technique) to help dislodge adherent crystals. The manoeuvre is highly effective, with 60–80% of patients experiencing resolution after a single manoeuvre and up to 90% after repeat treatments. Post-Epley activity restrictions (avoiding lying flat for 48 hours) are no longer considered necessary. Tapping the mastoid in the affected side is sometimes done at each position change to help dislodge adherent crystals.

Horizontal canal BPPV (approximately 10% of BPPV cases) is treated with the Barbecue Roll manoeuvre rather than the Epley. If symptoms persist despite repeated Epley manoeuvres, referral to a specialist vestibular physiotherapist should be arranged. The Brandt-Daroff exercises can also be taught to patients to perform at home between clinic visits.

Vestibular Neuronitis and Labyrinthitis

Vestibular neuronitis is an acute, often severe, episode of vertigo caused by inflammation of the vestibular nerve — most commonly presumed to be viral (HSV-1 reactivation is the leading hypothesis). The patient presents with sudden onset of severe continuous vertigo, nausea, and vomiting, typically following a viral illness. There is no hearing loss and no tinnitus (the cochlea is not involved). Nystagmus is typically unidirectional, beating away from the affected (damaged) ear, and is suppressed by visual fixation. The HIT is positive (abnormal) towards the affected side.

Labyrinthitis differs from neuronitis in that it involves the cochlea as well as the vestibular system — there is accompanying sensorineural hearing loss and/or tinnitus in addition to vertigo. The clinical picture is otherwise similar.

Management:

• Acute phase — prochlorperazine (Stemetil) 12.5 mg intramuscularly for acute nausea/vomiting; subsequently 5 mg orally three times daily as a vestibular sedative to reduce the acute symptoms. Prochlorperazine is a dopamine antagonist that acts centrally on the chemoreceptor trigger zone; it reduces vestibular sensation and nausea. It should be used for the shortest period necessary — typically 5–7 days maximum — as prolonged use of vestibular sedatives slows vestibular compensation.
• Vestibular rehabilitation (Cawthorne-Cooksey exercises) — after the acute phase, these structured exercises promote central vestibular compensation by encouraging the brain to adapt to the reduced vestibular input from the damaged side. Exercises progress from eye and head movements in bed to complex dynamic activities. They should be encouraged as soon as the acute vomiting has settled. Referral to a specialist vestibular physiotherapist is helpful.
• Prognosis — most patients make a good recovery over weeks to months as the brain compensates for the vestibular imbalance. Some residual unsteadiness may persist, particularly in older patients.

Meniere's Disease

Meniere's disease (endolymphatic hydrops) is characterised by the classic triad of:

1. Episodic vertigo lasting 20 minutes to several hours (not seconds as in BPPV, not days as in neuronitis)
2. Fluctuating low-frequency sensorineural hearing loss (worse during attacks, better between them — initially)
3. Tinnitus and aural fullness in the affected ear

The underlying pathophysiology is endolymphatic hydrops — distension of the endolymphatic compartment of the inner ear with excess endolymph, which is thought to periodically rupture the Reissner's membrane, causing the characteristic attacks. The cause of the hydrops is unknown.

Meniere's disease is a clinical diagnosis, supported by PTA findings (low-frequency SNHL that fluctuates) and electrocochleography (if available). Bilateral Meniere's disease occurs in approximately 30–40% of patients over time. ENT specialist referral is required for diagnosis confirmation, audiometric monitoring, and management planning.

Management of Meniere's disease is aimed at reducing the frequency and severity of attacks:

• Low-salt diet — reducing sodium intake to approximately 1,500 mg/day reduces endolymphatic pressure by decreasing sodium (and therefore water) retention in the inner ear
• Betahistine (Serc) 16 mg three times daily — the most widely used pharmacological treatment. Betahistine is a histamine analogue that acts on H1 and H3 receptors, improving inner ear microcirculation and reducing endolymphatic pressure. Evidence for its efficacy is mixed but it is generally well tolerated and is recommended by ENT UK and many clinical guidelines as first-line medical treatment
• Prochlorperazine 12.5 mg intramuscularly or 5 mg orally three times daily — for symptomatic relief during acute attacks of vertigo
• Diuretics — bendroflumethiazide or frusemide are sometimes used to reduce endolymph volume, though evidence is limited
• Intratympanic gentamicin — chemical ablation of the vestibular apparatus on the affected side using transtympanic gentamicin injections. This sacrifices vestibular function in the treated ear in exchange for control of vertigo attacks. It is reserved for patients with disabling vertigo who have already lost useful hearing in the affected ear. Specialist procedure only.
• Intratympanic dexamethasone — there is growing evidence for the use of intratympanic steroids in Meniere's disease, particularly for controlling acute attacks and reducing hearing fluctuation. Less destructive than gentamicin.
• Surgery — endolymphatic sac decompression, labyrinthectomy, or vestibular nerve section are reserved for refractory cases failing medical management. Vestibular nerve section preserves cochlear function while ablating vestibular function.
• Natural history — most patients improve significantly with time (over 10–15 years), with attacks becoming less frequent and less severe. However, progressive hearing loss occurs in many patients.

Acoustic Neuroma (Vestibular Schwannoma)

An acoustic neuroma is a benign, slow-growing tumour of the Schwann cells of the vestibular nerve (hence "vestibular schwannoma" is the more accurate term). It does not typically cause acute vertigo — more often it presents with gradual, unilateral sensorineural hearing loss and tinnitus. Vertigo may occur but tends to be a mild, chronic unsteadiness rather than episodic severe attacks. The gradual onset allows the brain to compensate over time.

Clinical suspicion should be raised by: gradual unilateral SNHL (particularly affecting speech discrimination more than pure tone thresholds); unilateral tinnitus; and unexplained unilateral vestibular hypofunction. MRI with gadolinium is the gold standard investigation.

Management options depend on tumour size and patient factors:

• Conservative management (watchful waiting) — with serial MRI scans every 6–12 months. Appropriate for small, slow-growing tumours, particularly in older patients or those with pre-existing poor hearing in the affected ear. Many acoustic neuromas do not increase in size over years of monitoring.
• Stereotactic radiosurgery (Gamma Knife) — highly focused single-fraction radiotherapy is effective for tumours under approximately 2.5–3 cm in size. It aims to halt tumour growth rather than eliminate the tumour. Facial nerve preservation rates are excellent. Preferred for many small-to-medium tumours.
• Microsurgery — surgical excision via a retrosigmoid, translabyrinthine, or middle fossa approach. Reserved for larger tumours, growing tumours causing mass effect, or those not suitable for radiosurgery. Facial nerve preservation is the priority; hearing preservation surgery is possible via certain approaches for small tumours with good residual hearing.

Central Causes of Vertigo — Do Not Miss

Central causes of vertigo originate in the cerebellum or brainstem and require urgent investigation. These include:

• Posterior fossa stroke (PICA, AICA infarct) — can mimic peripheral vestibular disease very closely. Key distinguishing features: central HINTS (normal head impulse test, direction-changing nystagmus, vertical skew), associated cranial nerve signs, cerebellar signs on examination, new severe headache ("the worst headache of my life"), older patient with vascular risk factors. Urgent CT/MRI is required.
• Cerebellar tumour — progressive unsteadiness, cerebellar signs, and imaging features
• Multiple sclerosis — vertigo may be a demyelinating episode; younger patient, other neurological episodes in history
• Vertebrobasilar insufficiency — particularly in older patients; vertigo provoked by neck movements