Vertigo
Exam Tips
- Start with symptom language: confirm true rotational illusion before labelling as vertigo.
- Use timing and triggers: brief positional attacks strongly suggest BPPV; continuous acute vestibular syndrome needs urgent central cause exclusion.
- In acute vestibular syndrome, dangerous signs are normal head impulse, direction-changing nystagmus, skew deviation, or focal neurology.
- Romberg helps detect instability but does not reliably distinguish peripheral from central vertigo.
- Dix-Hallpike is high yield for OSCEs; mention contraindication/caution in significant cervical spine disease or unstable cardiovascular status.
- Name safety-net advice explicitly: return urgently for new weakness, diplopia, dysarthria, severe headache, inability to stand, or persistent worsening symptoms.
Definition
Vertigo is a symptom complex in which the patient experiences an illusory sensation of movement (usually spinning), either of self or surroundings, despite no true motion. It is distinct from non-rotatory dizziness (for example presyncope or light-headedness) and should trigger diagnostic localisation to peripheral vestibular structures or central brainstem/cerebellar pathways.
Pathophysiology
Normal balance depends on concordant input from the vestibular labyrinth, vision, and proprioception, integrated in vestibular nuclei and cerebellum. Vertigo occurs when there is asymmetry or mismatch in vestibular signalling: peripheral causes include abnormal endolymph mechanics (BPPV canalithiasis; Meniere endolymphatic hydrops), vestibular nerve/labyrinth inflammation (vestibular neuritis/labyrinthitis), or ototoxic hair-cell injury; central causes include ischemia, demyelination, migraine-related brainstem network dysfunction, or posterior fossa mass lesions. The vestibulo-ocular reflex (VOR) generates nystagmus when vestibular tone is unbalanced (see Figure: VOR pathway and semicircular canal planes in standard neuro-otology diagrams; see Figure: Dix-Hallpike canal provocation sequence in OSCE ENT texts).
Risk Factors
- Recent upper respiratory tract infection or otitis (suggesting vestibular neuritis/labyrinthitis)
- Migraine history or family history of migraine
- Head trauma (risk of BPPV, labyrinthine concussion, or central injury)
- Direct ear trauma/barotrauma (risk of perilymphatic fistula)
- Cardiovascular risk factors: hypertension, diabetes, smoking, atrial fibrillation, previous ischemic heart disease
- Ototoxic or dizziness-inducing drugs (for example aminoglycosides, loop diuretics such as furosemide, antidepressants, antipsychotics)
- Older age, multimorbidity, and polypharmacy
- Excess alcohol intake/intoxication
Clinical Features
Symptoms
- True spinning/rotatory sensation, often worsened by head movement
- Nausea and vomiting
- Positional episodes when rolling in bed or looking up/down (typical of BPPV)
- Hearing loss, tinnitus, aural fullness, or otorrhoea (otological clues)
- Headache, visual disturbance, diplopia, dysarthria, dysphagia, limb sensory or motor symptoms (central red flags)
- Gait unsteadiness and functional limitation (walking, driving, work)
Signs
- Nystagmus on eye examination (direction and gaze effect help localisation)
- Positive Dix-Hallpike with transient positional vertigo and characteristic nystagmus in posterior canal BPPV
- Abnormal head impulse test suggesting unilateral peripheral vestibular hypofunction
- Direction-changing gaze-evoked nystagmus, skew deviation (alternate cover), or severe truncal ataxia suggesting central pathology
- Romberg instability (supports vestibular/proprioceptive dysfunction but does not reliably separate central from peripheral causes)
- Focal neurological deficits (cranial nerve abnormality, cerebellar signs, facial asymmetry)
Investigations
Management
Lifestyle Modifications
- Urgently refer same day/emergency pathway if central red flags (new focal neurology, severe truncal ataxia, persistent acute vestibular syndrome with concerning exam)
- Use diagnosis-directed treatment rather than non-specific long-term vestibular suppressants
- For BPPV, perform canalith repositioning manoeuvres (for example Epley) and provide recurrence advice
- Hydration, short-term fall-risk reduction, and driving/work safety counselling during active symptoms
- Vestibular rehabilitation exercises after acute phase, especially for persistent imbalance
- For Meniere-pattern symptoms, consider salt reduction and trigger management (caffeine/alcohol moderation) alongside specialist follow-up
Pharmacological Treatment
Short-term vestibular suppressant/antiemetic
- Prochlorperazine 5-10 mg orally 2-3 times daily (or buccal 3 mg twice daily)
- Cyclizine 50 mg orally up to 3 times daily when needed
Use the lowest effective dose for the shortest duration (typically 24-72 hours in acute severe vertigo/nausea). Avoid prolonged use because it may delay central vestibular compensation. Prochlorperazine is generally avoided in Parkinson's disease, carries extrapyramidal/QT-prolongation risk, and causes sedation; cyclizine has anticholinergic adverse effects and caution in angle-closure glaucoma and urinary retention.
Meniere symptom control (specialist or shared-care context)
- Betahistine 16 mg three times daily, adjusted to response (commonly 24-48 mg/day in divided doses)
Evidence is mixed but widely used in UK practice for recurrent Meniere-type vertigo. Use caution in peptic ulcer disease and asthma; review efficacy regularly and stop if no meaningful benefit.
Cause-specific therapy
- If vestibular migraine is diagnosed, use standard migraine preventives (for example propranolol or topiramate) according to comorbidity and contraindications
- If bacterial labyrinthitis/otitis media is present, treat infection per local antimicrobial guidance
Do not mask possible stroke with repeated antiemetics without reassessment. Aminoglycosides are ototoxic and should be prescribed only with clear indication and monitoring.
Surgical / Interventional
- Intratympanic therapies or endolymphatic sac procedures for refractory Meniere disease under ENT specialist care
- Surgical repair for confirmed perilymphatic fistula when persistent or severe
- Posterior canal occlusion or vestibular nerve section in highly selected, refractory unilateral peripheral disease
Complications
- Falls and fall-related injury
- Loss of independence and reduced quality of life
- Driving and occupational impairment
- Anxiety, panic symptoms, and social avoidance/phobia
- Missed posterior circulation stroke if central red flags are not recognised early
Prognosis
Outcome is determined by the underlying diagnosis. Many peripheral causes (for example BPPV and vestibular neuritis) improve substantially over days to weeks with repositioning or vestibular compensation, although recurrence is common (especially BPPV and Meniere-pattern disease). Central causes carry higher morbidity and require urgent diagnosis and condition-specific management.
Sources & References
💊BNF Drug References(1)
- Cinnarizine with dimenhydrinate[management.pharmacological]
✅NICE Guidelines(1)
- Vertigo[overview]
📖Textbook References(13)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 940, 941)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 273, 274)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1817, 1818)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 272, 273)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 942)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 941, 942)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 631)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 941)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 630)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 630, 631)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 941)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 494, 495)[context]
- Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 493, 494, 495)[context]