Dizziness
Dizziness is a nonspecific symptom encompassing sensations of lightheadedness, unsteadiness, presyncope, or vertigo, arising from cardiovascular, neurological, vestibular, or systemic causes.
Dizziness — Definition, Epidemiology, Risk Factors, Anatomy, Aetiology, Pathophysiology, Classification and Clinical Features
"Dizziness" is one of the most imprecise words in medicine. Patients use it to describe at least four fundamentally different sensations, and your first job is to figure out which one they mean. Getting this wrong sends you down the completely wrong diagnostic pathway.
Dizziness = a non-specific umbrella term for any subjective sensation of disturbed spatial orientation or impaired stability. It is not a diagnosis — it is a symptom that must be subcategorised before any meaningful workup can begin.
The word itself comes from Old English dysig = "foolish, stupid" — originally describing a muddled mental state.
1.1 The Four Subtypes of "Dizziness"
| Subtype | Patient's description | What it actually is | Key mechanism |
|---|---|---|---|
| Vertigo | "The room is spinning" / "I'm spinning" | An illusion of rotational or linear movement | Asymmetric vestibular input (peripheral or central) |
| Presyncope / Lightheadedness | "I feel faint, like I'm about to pass out" | Impending loss of consciousness | ↓ global cerebral perfusion (↓CO, ↓BP, hypoglycaemia) |
| Disequilibrium | "I feel off-balance, unsteady on my feet" | Impaired balance without head sensation | Sensory (proprioceptive / visual / vestibular) or motor (cerebellar / extrapyramidal) deficit |
| Non-specific / psychogenic dizziness | "I feel light-headed, weird, floaty, spaced out" | Ill-defined sensation, often chronic | Anxiety, hyperventilation, somatisation, depression, PPPD |
Careful history to determine if the problem is vertigo or pseudovertigo (giddiness, faintness or disequilibrium) [1].
Clinical Pearl
The single most important question in dizziness is: "What exactly do you mean by dizzy?" Ask the patient to describe the sensation without using the word "dizzy." Offer prompts: "Do you feel the room spinning? Do you feel like you're about to faint? Do you feel off-balance when you walk?" This one question determines the entire diagnostic direction.
Common Exam Mistake
Students often conflate "vertigo" with "dizziness." Vertigo is a subset of dizziness — specifically, an illusion of movement (usually rotational). Not all dizziness is vertigo, and not all vertigo is peripheral. Always subcategorise first.
2. Epidemiology
- Dizziness is one of the most common presenting complaints in primary care and emergency medicine [2]:
- Lifetime prevalence: ~20–30% of the general population
- Accounts for ~5% of all primary care visits and ~4% of Emergency Department presentations
- Prevalence increases markedly with age: ~30% of those > 65 years have experienced significant dizziness
- Vertigo specifically:
- 1-year prevalence: ~5% in the general population
- BPPV alone affects ~2.4% of the population at some point in their lives
- Vestibular neuritis / acute vestibulopathy: incidence ~3.5/100k/year
- Sex: Female > Male for most vestibular causes (~2:1 for BPPV, Ménière's disease)
- Why? Hormonal factors (oestrogen affects inner ear fluid homeostasis), higher prevalence of migraine in women, and possibly different otoconia composition
- Age:
- Young adults: anxiety–hyperventilation, vestibular neuritis, vestibular migraine, BPPV
- Middle-aged: Ménière's disease (peak 40–60y), vestibular migraine
- Elderly: postural hypotension, BPPV (most common single cause in the elderly), cerebrovascular disease, multifactorial dizziness [1]
- "Dizziness is often multifactorial, especially in the elderly" [1]
- Ageing population → rising prevalence of multifactorial dizziness, postural hypotension, polypharmacy-related dizziness
- High prevalence of cerebrovascular risk factors (hypertension, DM, smoking) → vertebrobasilar insufficiency is an important consideration
- Stroke is the 2nd–3rd leading cause of death in HK [3] — always consider posterior circulation stroke in acute vestibular syndrome
3. Anatomy and Physiology of Balance
Understanding the anatomy is essential because the clinical approach to dizziness is fundamentally anatomical — you are localizing where the problem is.
3.1 The Three Sensory Inputs for Balance
The brain maintains spatial orientation and postural stability by integrating information from three sensory systems. A mismatch between these systems is what produces the sensation of dizziness.
This is the primary system for detecting head movement and position relative to gravity.
Peripheral vestibular apparatus (located in the petrous temporal bone):
| Structure | What it detects | How |
|---|---|---|
| 3 Semicircular canals (horizontal/anterior/posterior) | Angular (rotational) acceleration of the head | Endolymph flow deflects the cupula in the ampulla → bends hair cells → changes firing rate of CN VIII |
| Utricle | Linear acceleration + static head tilt in the horizontal plane | Otoconia (calcium carbonate crystals) on gelatinous membrane exert shearing force on hair cells |
| Saccule | Linear acceleration + static head tilt in the vertical plane | Same otolithic mechanism as utricle |
- The vestibular nerve (part of CN VIII = vestibulocochlear nerve; "vestibulo" = balance, "cochlear" = hearing) projects to the vestibular nuclei in the brainstem (at the pontomedullary junction).
Key reflexes mediated by the vestibular system:
- Vestibulo-ocular reflex (VOR): stabilises gaze during head movement → eyes move equal and opposite to head. This is what the head impulse test tests.
- Vestibulo-spinal reflex (VSR): maintains upright posture and balance
Central vestibular pathways:
- Vestibular nuclei → cerebellum (vestibulocerebellum = flocculonodular lobe) → modulates vestibular reflexes [4]
- Vestibular nuclei → thalamus → cortex (temporo-parietal junction) → conscious perception of movement
- Vestibular nuclei → medial longitudinal fasciculus (MLF) → CN III, IV, VI nuclei → coordinated eye movements
- Provides spatial reference frame — tells the brain "this is up, this is the horizon"
- Visual–vestibular mismatch → motion sickness, visual vertigo
- Joint position sensors (especially cervical spine, ankles) and muscle spindles
- Travels via the dorsal column–medial lemniscal (DCML) pathway
- Loss → sensory ataxia (positive Romberg sign, because removing visual compensation unmasks the proprioceptive deficit)
The cerebellum, particularly the vestibulocerebellum (flocculonodular lobe) and the spinocerebellum (vermis), integrates all three inputs and calibrates motor output [4].
- Midline (vermis/flocculonodular) lesions → nystagmus, truncal ataxia, gait disturbance
- Hemispheric lesions → limb ataxia, dysmetria, intention tremor, dysdiadochokinesia
- Cervical proprioceptors contribute to spatial orientation
- Cervical dysfunction/spondylosis is listed as a probability diagnosis [1] — cervicogenic dizziness arises from abnormal proprioceptive input from degenerative cervical joints/muscles
Risk factors vary by the underlying cause but can be broadly grouped:
4.1 General Risk Factors for Dizziness
| Category | Specific Factors | Mechanism |
|---|---|---|
| Age | Elderly (> 65y) | Multisensory decline (vestibular hair cell loss, ↓proprioception, ↓visual acuity), postural hypotension, polypharmacy, cerebrovascular disease |
| Medications | Antihypertensives, antidepressants, aspirin/salicylates, glyceryl trinitrate, benzodiazepines, major tranquillisers, antiepileptics, antibiotics (aminoglycosides) [1] | Postural hypotension (antihypertensives, GTN), vestibulotoxicity (aminoglycosides), CNS depression (BZD, neuroleptics), cerebellar toxicity (phenytoin, carbamazepine) |
| Cardiovascular | HTN, AF, aortic stenosis, heart failure | ↓CO → ↓cerebral perfusion, or embolic events |
| Cerebrovascular | DM, smoking, dyslipidaemia, previous stroke/TIA | Vertebrobasilar insufficiency, posterior circulation stroke [1][3] |
| Psychiatric | Anxiety, depression, panic disorder | Hyperventilation → ↓PaCO₂ → cerebral vasoconstriction; somatisation |
| Recent infection | Recent URTI [1] | Post-viral vestibular neuritis / acute vestibulopathy |
| Head injury | Post head injury [1] | Post-traumatic BPPV (otoconia displacement), labyrinthine concussion, postconcussion syndrome |
| Metabolic | Anaemia, hypoglycaemia, dehydration | ↓O₂ delivery, ↓cerebral perfusion |
| Vestibular risk factors | Migraine history, motion sickness susceptibility, prior vestibular episode | Vestibular migraine, recurrent BPPV |
High Yield – Drug-Induced Dizziness
"Commonly prescribed drugs, especially antihypertensives, antidepressants, aspirin and salicylates, glyceryl trinitrate, benzodiazepines, major tranquillisers, antiepileptics and antibiotics, can cause dizziness." [1]
Always take a thorough drug history in any dizzy patient. In the elderly, polypharmacy is the single most correctable cause of dizziness.
5. Aetiology (with Pathophysiology)
This is the core of the clinical approach. Organised by Murtagh's framework and supplemented with senior notes [1][2][5].
5.1 Probability Diagnoses (Common Causes)
These are what you should think of first in a dizzy patient:
Probability diagnosis: [1]
- Anxiety–hyperventilation
- Postural hypotension
- Simple faint — vasovagal
- Acute vestibulopathy (V) — viral illness
- Benign paroxysmal positional vertigo (V)
- Motion sickness (V)
- Post head injury (V)
- Cervical dysfunction/spondylosis
Note: V = vertigo
- Pathophysiology: Anxiety triggers sympathetic activation → rapid, shallow breathing → "hyperventilation" → excessive CO₂ blowing off → ↓PaCO₂ (respiratory alkalosis) → cerebral vasoconstriction (CO₂ is a potent cerebral vasodilator, so ↓CO₂ = ↓cerebral blood flow) → lightheadedness, paraesthesia (perioral, fingertips), chest tightness, palpitations
- Alkalosis also causes ↑protein-bound Ca²⁺ → ↓ionised Ca²⁺ → neuromuscular excitability → tetany, carpopedal spasm
- Clinical picture: chronic / episodic non-specific dizziness ("floaty, spaced out"), often with associated panic symptoms; resolves with slow breathing / paper bag rebreathing
- Context: very common in young adults, F > M, often with known anxiety/panic disorder
- Definition: ↓SBP ≥ 20 mmHg or ↓DBP ≥ 10 mmHg within 3 minutes of standing from supine
- Pathophysiology: On standing, ~500–1000 mL of blood pools in the lower extremities and splanchnic bed due to gravity → normally compensated by baroreceptor reflex → ↑sympathetic tone → vasoconstriction + ↑HR → maintains BP. If this reflex is impaired → ↓cerebral perfusion → presyncope/syncope
- Causes:
- Drugs (most common correctable cause): antihypertensives, diuretics, α-blockers, vasodilators, TCAs, phenothiazines, antiparkinsonian drugs
- Autonomic neuropathy: diabetes (commonest cause of autonomic neuropathy — postural tachycardia with lightheadedness, dizziness, presyncope [6]), Parkinson's disease, MSA, amyloidosis
- Hypovolaemia: dehydration, haemorrhage, adrenal insufficiency
- Prolonged bed rest / deconditioning: especially in elderly hospitalised patients
- Pathophysiology: An exaggerated autonomic (Bezold-Jarisch) reflex:
- Trigger (prolonged standing, emotional stress, pain, heat) → venous pooling → ↓venous return → ↓stroke volume
- Heart contracts vigorously on an under-filled ventricle → mechanoreceptors in LV wall are activated
- Paradoxical vagal activation ("vasovagal") → ↓HR (cardioinhibitory) and/or ↓SVR (vasodepressor) → ↓BP → ↓cerebral perfusion → presyncope or syncope
- Prodrome (vagal activation): nausea, lightheadedness, sweating, pallor, tunnel vision [2][5]
- Episode: usually when standing, associated with situational trigger (cough, eating, drinking cold liquid, urination…), usually brief (in minutes), pallor [2][5]
- Recovery: relatively rapid with recumbency, no postictal confusion (cf. seizures)
- The name tells you: "vestibular" = balance system, "neuritis" = nerve inflammation, "labyrinthitis" = inner ear labyrinth inflammation
- Pathophysiology: Viral infection (often preceded by recent URTI [1]) → inflammation and damage to the vestibular nerve (usually the superior division) or labyrinth → sudden unilateral loss of vestibular input → asymmetric tonic vestibular firing → brain interprets the mismatch as rotation → severe acute vertigo
- The intact side has a higher baseline firing rate → the brain perceives rotation towards the intact side
- Commonly attributed to HSV-1 reactivation (analogous to Bell's palsy)
- Vestibular neuritis = vertigo only (vestibular nerve affected, cochlea spared)
- Labyrinthitis = vertigo + hearing loss ± tinnitus (labyrinth involved → both vestibular and cochlear components)
- "A sudden attack of vertigo in a young person after a recent URTI suggests vestibular neuronitis" [1]
- Break down the name: "benign" = not dangerous, "paroxysmal" = sudden attacks, "positional" = triggered by head position, "vertigo" = spinning sensation
- Pathophysiology — Canalithiasis theory (the accepted mechanism):
- Otoconia (calcium carbonate crystals) dislodge from the utricle (due to degeneration, trauma, or idiopathic reasons) and migrate into one of the semicircular canals (most commonly the posterior canal, ~80%)
- With certain head movements (rolling over in bed, looking up, bending forward), the displaced otoconia move within the canal due to gravity → this deflects the cupula → generates an abnormal signal of rotation → brief but intense vertigo
- Because the otoconia settle within seconds, the vertigo is brief (< 60 seconds per episode) and fatigable (repeated positioning → diminishing response, because the otoconia gradually disperse)
- Clinical pattern: paroxysmal, positional, brief, fatigable — the name IS the clinical description
- Epidemiology: most common cause of vertigo overall; incidence increases with age, F > M; associated with head trauma, prior vestibular neuritis, osteoporosis (↑otoconia degeneration)
- Pathophysiology: Sensory conflict theory — the vestibular system signals movement (e.g., on a boat), but visual input says "not moving" (e.g., reading below deck) → sensory mismatch → the brain interprets this as possible neurotoxin ingestion (an evolutionary protective mechanism) → triggers nausea and vomiting via the chemoreceptor trigger zone (CTZ) and vomiting centre
- Key receptors involved: H₁ (histamine) and mACh (muscarinic) in the vestibular nuclei [7]
- Treatment targets these receptors: antihistamines (cinnarizine, dimenhydrinate), anticholinergics (hyoscine/scopolamine)
- Mechanism: Trauma → dislodges otoconia → post-traumatic BPPV (most common); or labyrinthine concussion, perilymphatic fistula, temporal bone fracture → direct vestibular damage
- Part of the post-concussion syndrome: dizziness + headache + cognitive difficulties + fatigue lasting weeks to months after mild TBI
- Pathophysiology: Cervical proprioceptors (especially C1-C3 facet joints and deep neck muscles) provide important input to the vestibular nuclei. Degenerative changes, muscle spasm, or injury to the cervical spine → abnormal proprioceptive signalling → mismatch with vestibular and visual input → vague dizziness/unsteadiness (not true vertigo)
- Typically in middle-aged to elderly patients with cervical osteoarthritis
- Dizziness is often associated with neck pain and movement
5.2 Serious Disorders Not to Be Missed
Serious disorders not to be missed: [1]
- Neoplasia/cancer:
- Acoustic neuroma
- Posterior fossa tumour
- Other brain tumours, primary or secondary
- Intracerebral infection (e.g. abscess)
- Cardiovascular:
- Arrhythmias
- Myocardial infarction
- Aortic stenosis
- Cerebrovascular:
- Vertebrobasilar insufficiency
- Brain stem infarct (e.g. PICA thrombosis)
- Multiple sclerosis
- "Acoustic" = hearing nerve (misnomer — actually arises from vestibular portion of CN VIII), "neuroma" = nerve tumour; more correctly called vestibular schwannoma ("Schwann" cells = cells that myelinate peripheral nerves)
- Pathophysiology: Benign tumour of Schwann cells on the vestibular portion of CN VIII → grows slowly in the cerebellopontine angle (CPA) → progressive unilateral vestibular dysfunction
- Because it grows slowly, the brain compensates for the gradual vestibular asymmetry → patients rarely get acute vertigo; instead they get progressive unilateral hearing loss (sensorineural) + tinnitus + mild unsteadiness
- As it enlarges: compresses CN V (facial numbness), CN VII (facial weakness), cerebellum (ataxia), brainstem (↑ICP signs)
- Association: NF2 (bilateral vestibular schwannomas) [8]
- Consider MRI, especially if acoustic neuroma or other tumour suspected [1]
- Any tumour in the posterior fossa (cerebellum, brainstem, CPA) can cause vertigo/disequilibrium [1][8]
- Mechanism: direct compression or infiltration of vestibular nuclei, cerebellar peduncles, or vestibular nerve; ± obstructive hydrocephalus (4th ventricle obstruction) → ↑ICP → headache, N/V, papilloedema [9]
- Metastatic brain tumours (lung, breast, melanoma most common) [8] may present with dizziness as part of posterior fossa involvement
- Mechanism: Space-occupying lesion → mass effect + surrounding oedema + ↑ICP → dizziness, headache, focal deficits, ± fever
- Posterior fossa abscess → direct vestibular/cerebellar dysfunction
These cause dizziness via ↓cardiac output → ↓cerebral perfusion → presyncope/syncope [2][5]:
| Cause | Mechanism | Key features |
|---|---|---|
| Arrhythmias | Tachy- or bradyarrhythmia → ↓effective CO → ↓cerebral perfusion | Palpitations, sudden onset, may occur in any position, brief |
| Myocardial infarction | ↓LV function → ↓CO; or arrhythmia as complication | Chest pain, diaphoresis, SOB, risk factors for IHD |
| Aortic stenosis | Fixed obstruction to LVOT → cannot ↑CO with exertion → exertional syncope | Exertional dizziness/syncope, crescendo-decrescendo murmur, narrow pulse pressure |
| Cause | Mechanism | Key features |
|---|---|---|
| Vertebrobasilar insufficiency (VBI) | Atherosclerosis of vertebral/basilar arteries → ↓posterior circulation blood flow → transient ischaemia of brainstem, cerebellum, occipital cortex | Episodes of vertigo + other posterior circulation symptoms (diplopia, dysarthria, dysphagia, drop attacks, visual field defects) — the "5 D's" |
| Brainstem infarct (e.g. PICA thrombosis) | PICA (posterior inferior cerebellar artery) supplies the lateral medulla → occlusion = lateral medullary syndrome (Wallenberg) | Acute vertigo, nystagmus, ipsilateral facial pain/numbness, Horner's syndrome, contralateral body pain/temperature loss, dysphagia, hoarseness |
- Why PICA stroke is a mimicker of vestibular neuritis: Both present with acute vertigo + nausea + nystagmus. The key differences are: (a) central signs like skew deviation, direction-changing nystagmus, inability to walk, other brainstem signs; (b) HINTS exam (Head Impulse, Nystagmus, Test of Skew) — peripheral causes have a positive head impulse test (catch-up saccade), while central causes have a negative head impulse test (VOR intact because the lesion is central, not at the vestibular nerve/labyrinth).
Must Know for Exams — PICA Stroke vs Vestibular Neuritis
An acute vestibular syndrome (sudden vertigo + nausea + nystagmus + unsteadiness) has only TWO major diagnoses:
- Vestibular neuritis (peripheral — safe)
- Posterior circulation stroke (central — dangerous)
The HINTS exam at the bedside is more sensitive than early MRI (within 24–48h) for distinguishing these. A normal (negative) head impulse test in acute vestibular syndrome is concerning for stroke, not reassuring.
- Pathophysiology: Autoimmune demyelination of CNS white matter → lesions in brainstem (vestibular nuclei, MLF), cerebellar peduncles, or vestibular nerve root entry zone → vertigo/disequilibrium
- Vertigo is a presenting symptom in ~5–10% of MS; occurs at some point in ~30–50%
- Internuclear ophthalmoplegia (INO) — a classic MS finding — arises from an MLF lesion and causes impaired adduction on the side of the lesion + nystagmus of the abducting eye; this is a central oculomotor sign
- Typically young adult (20–40y), F > M, relapsing-remitting course
5.3 Other Important Aetiologies (Not in Murtagh's List but Clinically Important)
- "Ménière" = Prosper Ménière, French physician who first described it
- Pathophysiology: Endolymphatic hydrops — excess endolymph accumulates in the membranous labyrinth (cochlea and vestibular apparatus) → distension → disrupts normal hair cell function → episodic vertigo + fluctuating hearing loss + tinnitus + aural fullness
- The episodes are thought to occur when the distended Reissner's membrane ruptures → mixing of endolymph (high K⁺) and perilymph (high Na⁺) → potassium-mediated depolarisation and then paralysis of hair cells → acute vertigo + hearing loss
- Clinical triad (classic): episodic vertigo (20 min to hours) + fluctuating low-frequency sensorineural hearing loss + tinnitus (± aural fullness)
- Unilateral initially (becomes bilateral in ~30% over time)
- The second most common cause of episodic vertigo (after BPPV); increasingly recognised
- Pathophysiology: Migraine-associated cortical spreading depression and trigeminal-vascular activation may modulate vestibular nuclei processing → episodic vertigo with or without headache
- Key features: recurrent episodic vertigo (5 min to 72h) in a patient with migraine history; may have migrainous features (photophobia, phonophobia, visual aura) during attacks; headache may or may not accompany the vertigo
- Often overlaps with Ménière's disease clinically; important to consider in young/middle-aged women with episodic vertigo and a migraine history
- "Commonly prescribed drugs, especially antihypertensives, antidepressants, aspirin and salicylates, glyceryl trinitrate, benzodiazepines, major tranquillisers, antiepileptics and antibiotics, can cause dizziness" [1]
- Aminoglycosides (gentamicin, streptomycin): directly toxic to vestibular hair cells → bilateral vestibulopathy → oscillopsia (visual blurring with head movement because VOR is lost bilaterally) + chronic disequilibrium
- Phenytoin, carbamazepine: cerebellar toxicity → nystagmus, ataxia, slurred speech [4]
- Loop diuretics (furosemide): ototoxicity at high doses, especially with concurrent aminoglycosides
- The modern terminology for what was previously called "chronic subjective dizziness" or "phobic postural vertigo"
- Pathophysiology: After an initial vestibular insult (e.g., BPPV episode, vestibular neuritis), maladaptive central processing persists even after the peripheral lesion has resolved → chronic non-specific dizziness worsened by upright posture, active/passive motion, and complex visual stimuli
- Essentially a functional disorder of vestibular processing — the hardware has recovered but the software hasn't recalibrated
- Important because it's very common and treatable (with vestibular rehabilitation ± SSRIs)
- Anaemia: ↓O₂ carrying capacity → ↓O₂ delivery to brain → dizziness, especially with exertion or postural change [10]
- "Acute/severe: SOB (esp on exertion), palpitation, dizziness/syncope (may be postural)" [10]
- Hypoglycaemia: glucose is the brain's primary fuel → ↓glucose → neuroglycopenia → dizziness, confusion, tremor, sweating (adrenergic response)
- Dehydration / hypovolaemia: ↓circulating volume → ↓preload → ↓CO → ↓cerebral perfusion
- "Orthostatic hypotension due to central/peripheral sympathetic denervation" and "Postural tachycardia with lightheadedness, dizziness, presyncope" are manifestations of diabetic autonomic neuropathy [6]
- Mechanism: chronic hyperglycaemia → metabolic/osmotic neurotoxicity → damage to autonomic nerve fibres → impaired baroreceptor reflex → postural hypotension
- Hyperviscosity-related symptoms: headache, dizziness, blackouts [11]
- Mechanism: ↑RBC mass → ↑blood viscosity → ↓cerebral blood flow and ↓oxygen delivery despite polycythaemia → dizziness
6. Classification
Dizziness can be classified in multiple ways. The most clinically useful frameworks:
| Type | Examples |
|---|---|
| Vertigo | BPPV, vestibular neuritis, Ménière's, vestibular migraine, central causes |
| Presyncope/Syncope | Vasovagal, cardiac arrhythmia, aortic stenosis, orthostatic hypotension |
| Disequilibrium | Peripheral neuropathy, cerebellar disease, Parkinson's disease, bilateral vestibulopathy |
| Non-specific | Anxiety/hyperventilation, depression, PPPD, polypharmacy, metabolic |
This is the single most important clinical distinction within vertigo:
| Feature | Peripheral Vertigo | Central Vertigo |
|---|---|---|
| Lesion site | Inner ear or CN VIII | Brainstem, cerebellum, vestibular nuclei |
| Onset | Sudden, often severe | May be sudden or gradual |
| Nystagmus | Unidirectional, horizontal-torsional; suppressed by visual fixation | Direction-changing or purely vertical/torsional; NOT suppressed by fixation |
| Hearing loss / tinnitus | May be present (labyrinthitis, Ménière's) | Usually absent (unless AICA stroke) |
| Brainstem signs | Absent | Present (diplopia, dysarthria, dysphagia, crossed sensory/motor deficits, Horner's) |
| Head impulse test | Positive (abnormal) — catch-up saccade | Negative (normal) — VOR intact |
| Severity of vertigo | Often very severe | May be moderate; sometimes imbalance > vertigo |
| Examples | BPPV, vestibular neuritis, Ménière's, labyrinthitis | Posterior circulation stroke, MS, cerebellar tumour, vestibular migraine |
| Timing pattern | Duration | Causes |
|---|---|---|
| Episodic, seconds | < 1 min | BPPV (positional trigger) |
| Episodic, minutes to hours | Minutes to 24h | Ménière's disease, vestibular migraine, TIA |
| Acute, persistent | Days to weeks | Vestibular neuritis, posterior circulation stroke, MS relapse |
| Chronic | Weeks to months | PPPD, bilateral vestibulopathy, acoustic neuroma (progressive unsteadiness), cerebellar degeneration |
| Mechanism | Proportion | Examples |
|---|---|---|
| Cardiac syncope | 15% | Arrhythmic (10%): tachy/bradyarrhythmia; Structural (5%): AS, HCM, PE |
| Neurocardiogenic syncope | 60% | Vasovagal, situational (micturition, cough, defaecation, carotid sinus hypersensitivity) |
| Postural hypotension | 15% | Drugs, autonomic neuropathy, hypovolaemia |
| Unexplained | ~10% |
7. Clinical Features
7.1 History — The Key Questions
"Careful history to determine if the problem is vertigo or pseudovertigo (giddiness, faintness or disequilibrium). Check for neurological symptoms, aural symptoms and visual symptoms. Recent history of respiratory infection or head injury. Drug history including illicit drugs and alcohol (?acute intoxication)." [1]
The approach should be systematic:
- "Describe the sensation without using the word 'dizzy'"
- Spinning → vertigo
- About to faint → presyncope
- Off-balance → disequilibrium
- Vague/floaty → non-specific
- Episodic or continuous?
- Duration of each episode: seconds (BPPV), minutes-hours (Ménière's, vestibular migraine), days (vestibular neuritis, stroke), chronic (PPPD, acoustic neuroma)
- First episode or recurrent?
- Positional: turning head, rolling in bed, looking up → BPPV
- Exertional: suggests cardiac cause (aortic stenosis, HCM) or cardiac arrhythmia
- Standing up: orthostatic hypotension
- Situational: coughing, micturition, swallowing → situational syncope
- Emotional stress, prolonged standing, hot environment: vasovagal
- Head movement (any): cervicogenic, bilateral vestibulopathy
- Valsalva / loud noise: superior semicircular canal dehiscence (Tullio phenomenon)
| Symptom category | Symptoms | Suggests |
|---|---|---|
| Aural | Hearing loss, tinnitus, aural fullness | Ménière's disease, labyrinthitis, acoustic neuroma |
| Neurological | Diplopia, dysarthria, dysphagia, limb weakness, numbness, facial droop | Central cause: stroke, MS, posterior fossa tumour [1] |
| Cardiac | Palpitations, chest pain, exertional component | Arrhythmia, MI, aortic stenosis |
| Autonomic | Nausea, sweating, pallor before episode | Vasovagal (prodrome) |
| Psychiatric | Anxiety, hyperventilation, panic, depersonalisation | Anxiety/hyperventilation, PPPD |
| Headache | Migraine features (photophobia, phonophobia, aura) | Vestibular migraine |
| Preceding URTI | Fever, rhinorrhoea, cough 1–2 weeks prior | Vestibular neuritis [1] |
Antihypertensives, antidepressants, aspirin/salicylates, GTN, benzodiazepines, major tranquillisers, antiepileptics, antibiotics [1], plus alcohol and illicit drugs
7.2 Symptoms by Aetiology with Pathophysiological Basis
| Symptom | Pathophysiological basis |
|---|---|
| Brief (< 60s) spinning vertigo | Displaced otoconia deflect cupula on positional change → abnormal rotational signal → brain perceives movement that isn't happening |
| Triggered by specific positions (rolling over, looking up, bending down) | Gravity moves the otoconia within the canal only in specific head orientations relative to gravity |
| Nausea (± vomiting) | Vestibular input to CTZ and vomiting centre via vestibular nuclei |
| No hearing loss | Cochlea is not involved — otoconia are in the semicircular canals |
| Fatigability (repeated positioning → less vertigo) | Otoconia disperse with repeated movement, reducing the abnormal cupular deflection |
| Symptom | Pathophysiological basis |
|---|---|
| Sudden severe rotational vertigo, constant for hours to days | Acute unilateral loss of vestibular nerve function → tonic firing asymmetry → perception of rotation |
| Nausea, vomiting (often severe) | Vestibular nuclear connections to CTZ and vomiting centre |
| Spontaneous horizontal-torsional nystagmus (beating away from lesion) | Intact side has higher firing → drives slow phase towards lesion; fast phase (nystagmus direction) towards intact side |
| Imbalance (falls/leans towards affected side) | Loss of vestibulospinal reflex on affected side → reduced postural tone ipsilaterally |
| Worsened by head movement | Any movement accentuates the asymmetric vestibular input |
| No hearing loss (vs labyrinthitis) | Vestibular nerve is affected, but cochlear nerve is spared |
| Symptom | Pathophysiological basis |
|---|---|
| Episodic vertigo (20 min – hours) | Endolymphatic hydrops → distortion and periodic rupture of Reissner's membrane → K⁺ intoxication of hair cells → acute vestibular dysfunction |
| Fluctuating low-frequency hearing loss | Hydrops initially affects the cochlear apex (which transduces low frequencies) → distortion of basilar membrane mechanics |
| Tinnitus (roaring quality) | Abnormal hair cell stimulation from endolymphatic pressure changes |
| Aural fullness | Increased endolymphatic pressure → mechanical distension felt as "blocked ear" sensation |
| Nausea/vomiting during attacks | Vestibular → CTZ pathway |
| Symptom | Pathophysiological basis |
|---|---|
| Lightheadedness, feeling "about to faint" | ↓cerebral perfusion (↓BP and/or ↓HR) → insufficient blood to RAS |
| Nausea, sweating, pallor (prodrome) [2][5] | Vagal activation: parasympathetic stimulation → ↑GI motility (nausea), cholinergic sweating; ↓sympathetic → peripheral vasodilatation → pallor |
| Tunnel vision, "greying out" | Retinal ischaemia (retinal cells very sensitive to hypoperfusion) |
| LOC if complete syncope, spontaneous recovery | RAS hypoperfusion → LOC; recumbency restores cerebral perfusion → consciousness returns |
| Symptom | Pathophysiological basis |
|---|---|
| Sudden onset, in any position [2][5] | Arrhythmia or obstruction occurs regardless of posture (cf. vasovagal which needs standing) |
| ± preceded by palpitation, chest pain [2][5] | Palpitation = awareness of arrhythmia; chest pain = myocardial ischaemia |
| Usually brief (< 1 min) [2][5] | If the arrhythmia self-terminates, perfusion returns quickly |
| Extreme "death-like" pallor [2][5] | Profound ↓CO → maximal sympathetic vasoconstriction to redirect blood centrally → extreme cutaneous pallor |
| ± associated with exertion (esp LVOT obstruction) [2][5] | Aortic stenosis/HCM: fixed obstruction cannot accommodate ↑CO demand during exercise → exertional syncope |
| Symptom | Pathophysiological basis |
|---|---|
| Acute vertigo | Ischaemia of vestibular nuclei (brainstem) or cerebellum |
| Diplopia | CN III, IV, or VI nuclei ischaemia (all in brainstem) |
| Dysarthria | Ischaemia of lower cranial nerve nuclei (CN IX, X, XII) or cerebellar connections |
| Dysphagia | CN IX, X nuclei ischaemia |
| Drop attacks (sudden falls without LOC) | Reticular formation or vestibulospinal tract ischaemia |
| Crossed deficits (ipsilateral face, contralateral body) | Classic brainstem lesion pattern — cranial nerve nuclei (ipsilateral) + long tracts (contralateral, as they cross below) |
7.3 Signs with Pathophysiological Basis
"Key examination: General examination including gait; Cardiovascular, auditory and neurological examinations; Hallpike manoeuvre and Epley test; Forced hyperventilation test" [1]
| Sign | What it suggests | Why |
|---|---|---|
| Postural hypotension (↓SBP ≥ 20 / ↓DBP ≥ 10 on standing) | Orthostatic hypotension | Impaired baroreceptor reflex → insufficient vasoconstriction on standing |
| Pallor | Anaemia, vasovagal | ↓Hb → pale conjunctivae/palmar creases; sympathetic vasoconstriction → pallor |
| Irregular pulse | Arrhythmia (eg AF) | Irregular ventricular response → variable stroke volume → intermittent ↓CO |
| Sign | What it suggests | Why |
|---|---|---|
| Ejection systolic murmur (crescendo-decrescendo, RUSB, radiating to carotids) | Aortic stenosis | Fixed LVOT obstruction → turbulent flow across narrowed valve |
| Slow-rising pulse, narrow pulse pressure | Aortic stenosis | Prolonged ejection time, reduced stroke volume |
| Irregular pulse | AF, other arrhythmias | Irregular atrial impulses → variable R-R interval |
| Sign | What it suggests | Why |
|---|---|---|
| Unilateral sensorineural hearing loss | Acoustic neuroma, Ménière's, labyrinthitis | Damage to cochlear nerve (schwannoma), cochlear hair cells (hydrops, inflammation) |
| Tuning fork tests: Rinne +ve (AC > BC) but Weber lateralises to good ear | SNHL on affected side | Damage to cochlea/cochlear nerve → reduced ability to transduce sound on that side |
| Test / Sign | Positive finding | What it means | Pathophysiological basis |
|---|---|---|---|
| Hallpike (Dix-Hallpike) manoeuvre [1] | Upbeating torsional nystagmus with latency (~2-5s), lasting < 60s, with vertigo, fatigable on repetition | BPPV (posterior canal) | Gravity moves otoconia in posterior canal → deflects cupula → excitatory signal → characteristic nystagmus pattern |
| Head impulse test (HIT) | Corrective saccade (catch-up eye movement after rapid head turn towards affected side) | Peripheral vestibular lesion (vestibular neuritis) | VOR is impaired on the affected side → eyes cannot stay on target during head turn → must make a catch-up saccade |
| Head impulse test — Normal (no saccade) | In context of acute vestibular syndrome | Central cause (stroke!) | VOR pathway passes through brainstem; if lesion is central (not at nerve/labyrinth), the VOR arc may be intact → normal HIT despite vertigo |
| Spontaneous nystagmus — unidirectional, horizontal-torsional, suppressed by fixation | Present | Peripheral vestibular lesion | Tonic asymmetry → slow drift towards lesion, fast corrective phase away |
| Spontaneous nystagmus — direction-changing, purely vertical, or not suppressed by fixation | Present | Central cause | Central processing abnormality → gaze-evoked or direction-changing patterns |
| Test of skew | Vertical skew deviation (one eye higher than the other) | Central cause (brainstem) | Disruption of otolithic-ocular pathways (utriculo-ocular projections cross in brainstem) → vertical misalignment |
| Romberg test — positive | Falls with eyes closed | Sensory ataxia (proprioceptive loss) | Removing visual compensation unmasks reliance on damaged proprioceptive input |
| Romberg test — negative but wide-based ataxic gait | Gait ataxia without worsening on eye closure | Cerebellar ataxia | Cerebellum coordinates motor output; it doesn't depend on visual input in the way the proprioceptive system does |
| Unterberger/Fukuda stepping test | Rotation > 45° towards one side while marching in place | Peripheral vestibular hypofunction on that side | Vestibulospinal asymmetry → deviation towards the weaker side |
| Forced hyperventilation test [1] | Reproduces the patient's dizziness | Hyperventilation / anxiety | Hyperventilation → ↓PaCO₂ → cerebral vasoconstriction → dizziness |
| Cerebellar signs (DANISH: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Scanning dysarthria, Hypotonia) | Present | Cerebellar lesion | Loss of cerebellar error correction → incoordination, overshooting, inability to perform rapid alternating movements |
The HINTS Exam — High Yield for Acute Vestibular Syndrome
Head Impulse, Nystagmus, Test of Skew
In acute vestibular syndrome (sudden vertigo + nystagmus + N/V + unsteadiness), a "benign" HINTS pattern (positive head impulse + unidirectional nystagmus + no skew deviation) = peripheral (vestibular neuritis).
A "dangerous" HINTS pattern (normal head impulse + direction-changing nystagmus OR skew deviation) = central (stroke!).
HINTS performed by an experienced clinician is > 98% sensitive for posterior circulation stroke — better than MRI in the first 24-48 hours (MRI can be falsely negative early in posterior fossa strokes due to DWI artefact).
"Key investigations: FBE, blood glucose, audiometry, ECG, ?Holter monitor. Other tests according to history and examination. Consider MRI, especially if acoustic neuroma or other tumour suspected." [1]
| Investigation | What it screens for | Rationale |
|---|---|---|
| FBE (Full Blood Examination / CBC) | Anaemia (↓Hb → dizziness from ↓O₂ delivery), polycythaemia (↑viscosity → dizziness) | |
| Blood glucose | Hypoglycaemia (neuroglycopenia → dizziness, confusion) | |
| Audiometry | Sensorineural hearing loss (Ménière's, acoustic neuroma, labyrinthitis) | |
| ECG | Arrhythmias (AF, heart block, long QT, Brugada), ischaemia (ST changes) | |
| Holter monitor | Paroxysmal arrhythmias not captured on single ECG | |
| MRI brain (with gadolinium) | Acoustic neuroma, posterior fossa tumour, MS plaques, stroke | "Consider MRI, especially if acoustic neuroma or other tumour suspected" [1] |
| Lying-standing BP | Orthostatic hypotension | |
| CT brain | Acute haemorrhagic stroke, mass lesion (if MRI not immediately available) | |
| CT/MR angiography | Vertebrobasilar stenosis, dissection | |
| Vestibular function tests (calorics, VEMP, videonystagmography) | Peripheral vs central vestibular lesion | |
| Blood tests: U&E, Ca²⁺, TFTs, B12, ESR/CRP | Metabolic causes (hyponatraemia, hypercalcaemia, hypothyroidism, B12 deficiency, GCA) | |
| Tilt table test | Vasovagal syncope (confirm neurocardiogenic mechanism) | |
| Echocardiography | Structural heart disease (aortic stenosis, HCM, valvular disease) |
High Yield Summary
Definition: Dizziness is a non-specific symptom that must be subcategorised into vertigo (illusion of movement), presyncope (feeling faint), disequilibrium (off-balance), or non-specific dizziness (floaty, vague). The first step is always to clarify what the patient means.
Probability diagnoses (Murtagh) [1]: Anxiety–hyperventilation, postural hypotension, vasovagal, acute vestibulopathy (vestibular neuritis), BPPV, motion sickness, post-head injury, cervical dysfunction/spondylosis
Serious not to miss [1]: Acoustic neuroma, posterior fossa tumour, brain tumours, intracerebral infection (abscess), arrhythmias, MI, aortic stenosis, vertebrobasilar insufficiency, brainstem infarct (PICA thrombosis), multiple sclerosis
Peripheral vs Central vertigo: Peripheral = unidirectional nystagmus suppressed by fixation, positive HIT, ± hearing loss. Central = direction-changing/vertical nystagmus not suppressed, negative HIT, brainstem signs, skew deviation. Use HINTS in acute vestibular syndrome.
Key exam manoeuvres [1]: Hallpike manoeuvre, Epley test, forced hyperventilation test, plus cardiovascular, auditory, and neurological exams.
Key investigations [1]: FBE, blood glucose, audiometry, ECG, ?Holter monitor, consider MRI
Always check drug history — polypharmacy is the most correctable cause in the elderly.
Syncope classification [2][5]: Cardiac (15%) — most dangerous (30% mortality), Neurocardiogenic (60%) — most common, Postural hypotension (15%), Unexplained (10%).
Red flags for central cause: sudden onset with brainstem symptoms (5 D's), direction-changing nystagmus, negative HIT, skew deviation, inability to walk, new headache, cardiovascular risk factors for stroke.
Active Recall - Dizziness: Definition, Epidemiology, Aetiology and Clinical Features
[1] Lecture slides: murtagh merge.pdf (Dizziness/vertigo section, pp. 35–37) [2] Senior notes: Ryan Ho Cardiology.pdf (Section 2.4 Syncope, p. 63) [3] Senior notes: Ryan Ho Neurology.pdf (Section 3.2 Cerebrovascular Diseases, p. 74) [4] Senior notes: Ryan Ho Neurology.pdf (Section 5.1.3 Cerebellar Syndrome, p. 117) and Ryan Ho Fundamentals.pdf (Section 3.4.8, p. 333) [5] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.4 Syncope, p. 208) [6] Senior notes: Ryan Ho Endocrine.pdf (Diabetic autonomic neuropathy, p. 98) [7] Senior notes: maxim.md (PONV pathophysiology, section 622) [8] Senior notes: maxim.md (Brain tumours, section 771) [9] Senior notes: Ryan Ho Opthalmology.pdf (Papilloedema, p. 90) [10] Senior notes: Ryan Ho Haemtology.pdf (Approach to Anaemia, p. 10) [11] Senior notes: Ryan Ho Haemtology.pdf (Polycythaemia Vera, p. 76)
Differential Diagnosis of Dizziness
The differential diagnosis of dizziness is one of the broadest in medicine because "dizziness" is a symptom, not a disease. Your job is to narrow the field rapidly by first sub-categorising the complaint (vertigo vs presyncope vs disequilibrium vs non-specific), then applying Murtagh's diagnostic framework to ensure nothing dangerous is missed.
Think of it this way: the differential is enormous before you talk to the patient, but after a careful history and a few bedside tests, it should shrink to 2–3 realistic possibilities. That's the power of the structured approach.
Murtagh's framework is designed for primary care and emergency presentations. It forces you to consider common things first, then systematically rule out the dangerous and the sneaky [1].
2. The Complete Differential — Murtagh's Categories
These account for the vast majority of presentations. When you hear hoofbeats, think horses first.
Probability diagnosis: [1]
- Anxiety–hyperventilation
- Postural hypotension
- Simple faint — vasovagal
- Acute vestibulopathy (V) — viral illness
- Benign paroxysmal positional vertigo (V)
- Motion sickness (V)
- Post head injury (V)
- Cervical dysfunction/spondylosis
| Diagnosis | Type of dizziness | Why it's common | Key distinguishing feature |
|---|---|---|---|
| Anxiety–hyperventilation | Non-specific / lightheadedness | Prevalence of anxiety disorders (~5–10% population); hyperventilation → ↓PaCO₂ → cerebral vasoconstriction → dizziness | Chronic/episodic, a/w perioral paraesthesia, chest tightness, panic symptoms; reproduced by forced hyperventilation test [1] |
| Postural hypotension | Presyncope | Very common in elderly (polypharmacy, autonomic decline, dehydration); drugs are the most correctable cause [1] | Occurs on standing; documented by lying-standing BP (↓SBP ≥ 20 or ↓DBP ≥ 10) |
| Simple faint — vasovagal | Presyncope → syncope | Accounts for ~60% of all syncope [2][3]; exaggerated Bezold-Jarisch reflex | Prodrome of nausea, sweating, pallor; situational trigger; rapid recovery on recumbency |
| Acute vestibulopathy — viral illness | Vertigo (acute, persistent) | Post-viral vestibular neuritis is the most common cause of acute vestibular syndrome; "sudden vertigo in a young person after recent URTI" [1] | Acute onset severe vertigo lasting days, positive HIT (catch-up saccade), unidirectional nystagmus, no hearing loss |
| BPPV | Vertigo (episodic, seconds) | Most common cause of recurrent vertigo overall; incidence ↑ with age | Brief (< 60s), positional, fatigable; diagnostic Hallpike manoeuvre [1] with upbeating torsional nystagmus |
| Motion sickness | Vertigo + nausea | Sensory conflict (vestibular vs visual input); almost universal susceptibility to some degree | Clear relationship to motion; resolves when motion stops |
| Post head injury | Vertigo / mixed | Post-traumatic BPPV from otoconia displacement; labyrinthine concussion; post-concussion syndrome | Temporal relationship to head trauma |
| Cervical dysfunction/spondylosis | Disequilibrium / vague dizziness | Very common degenerative condition in middle-aged/elderly; cervical proprioceptors contribute to balance | A/w neck pain and stiffness; dizziness worsens with neck movement; no true vertigo |
Clinical Pearl — BPPV is the Most Common Vertigo
BPPV is the single most common cause of vertigo in both young and old. It's also the most satisfying to diagnose (Dix-Hallpike manoeuvre) and treat (Epley manoeuvre) at the bedside — a "one-stop" diagnosis and cure in many cases.
These are the diagnoses that will kill or permanently disable your patient if you miss them. Always actively exclude these.
Serious disorders not to be missed: [1]
- Neoplasia/cancer: acoustic neuroma, posterior fossa tumour, other brain tumours (primary or secondary)
- Intracerebral infection (e.g. abscess)
- Cardiovascular: arrhythmias, myocardial infarction, aortic stenosis
- Cerebrovascular: vertebrobasilar insufficiency, brain stem infarct (e.g. PICA thrombosis)
- Multiple sclerosis
| Diagnosis | Type of dizziness | Why it's serious | Key red flags |
|---|---|---|---|
| Acoustic neuroma | Progressive unsteadiness (rarely acute vertigo) | CPA mass → progressive CN VIII compression → sensorineural hearing loss; if large → brainstem/cerebellar compression | Unilateral progressive SNHL + tinnitus in a middle-aged patient; consider MRI [1]; a/w NF2 if bilateral [5] |
| Posterior fossa tumour / other brain tumours | Disequilibrium ± vertigo | Mass effect, ↑ICP, direct cerebellar/brainstem involvement; metastases common (lung, breast, melanoma) [5] | Progressive headache (worse AM, with Valsalva), N/V, papilloedema, cerebellar signs, focal neurological deficits |
| Intracerebral infection (abscess) | Disequilibrium ± vertigo | SOL with surrounding oedema → ↑ICP + focal deficits; posterior fossa abscess mimics cerebellar tumour | Fever + progressive neurological deficit + headache; risk factors (otitis media, sinusitis, immunosuppression, congenital heart disease) |
| Arrhythmias | Presyncope / syncope | Cardiac syncope carries ~30% mortality [2][3]; sudden ↓CO from tachy-/bradyarrhythmia → ↓cerebral perfusion | Sudden onset in any position, ± palpitations, brief (< 1 min), extreme pallor [2][3]; abnormal ECG; FHx of sudden death |
| Myocardial infarction | Presyncope / lightheadedness | ↓LV function → ↓CO; may also trigger arrhythmia; in elderly/DM, dizziness may be an "angina equivalent" [4] | Chest pain, diaphoresis, risk factors for IHD; ECG changes, elevated troponin |
| Aortic stenosis | Exertional presyncope / syncope | Fixed LVOT obstruction → cannot ↑CO with exercise → exertional cerebral hypoperfusion | Exertional dizziness/syncope, ejection systolic murmur radiating to carotids, narrow pulse pressure |
| Vertebrobasilar insufficiency | Vertigo (episodic, with brainstem symptoms) | Posterior circulation TIA; herald of brainstem stroke | Vertigo + the "5 D's" (Diplopia, Dysarthria, Dysphagia, Drop attacks, Dystaxia) + visual field defects; vascular risk factors |
| Brainstem infarct (e.g. PICA thrombosis) | Vertigo (acute, persistent, severe) | Lateral medullary syndrome (Wallenberg); a deadly mimicker of vestibular neuritis | Acute vertigo + brainstem signs (ipsilateral Horner's, facial numbness, contralateral body pain/temp loss, dysphagia); negative HIT (central pattern); direction-changing/vertical nystagmus |
| Multiple sclerosis | Vertigo / disequilibrium (episodic or progressive) | Demyelination of brainstem/cerebellar pathways; vertigo is presenting symptom in ~5–10% of MS | Young adult (20–40y), F > M; relapsing-remitting course; INO (MLF lesion); other demyelinating symptoms (optic neuritis, sensory symptoms, Lhermitte's sign) [7] |
Must Know — Posterior Circulation Stroke Mimics Vestibular Neuritis
The single most dangerous diagnostic pitfall in dizziness is misdiagnosing a posterior circulation stroke as vestibular neuritis. Both present with acute vertigo + nausea + nystagmus. The HINTS exam distinguishes them:
- Peripheral (safe): Positive HIT (catch-up saccade) + unidirectional nystagmus + no skew
- Central (stroke!): Negative HIT (normal VOR) OR direction-changing nystagmus OR skew deviation
If any one of the three HINTS components is "central," treat as stroke until proven otherwise. HINTS is > 98% sensitive — better than MRI within 48 hours for posterior fossa strokes.
These are diagnoses that are frequently overlooked — either because they're atypical presentations of common diseases, or because clinicians simply don't think of them.
Pitfalls (often missed): [1]
- Ear wax – otosclerosis
- Arrhythmias
- Hyperventilation
- Alcohol and other drugs (incl. illicit, e.g. cocaine)
- Cough or micturition syncope
- Vertiginous migraine / migrainous vertigo
- Parkinson disease
- Meniere syndrome (overdiagnosed)
Rarities: [1]
- Addison disease
- Neurosyphilis
- Autonomic neuropathy
- Hypertension
- Subclavian steal
- Perilymphatic fistula
- Shy–Drager syndrome
| Diagnosis | Why it's a pitfall | Mechanism of dizziness | How to catch it |
|---|---|---|---|
| Ear wax (cerumen impaction) | Easily overlooked; clinicians jump to complex diagnoses | Impacted cerumen against tympanic membrane → altered proprioceptive/pressure input ± conductive hearing loss → mild disequilibrium | Otoscopy — always look in the ears! Simple syringing may cure the "dizziness" |
| Otosclerosis | Gradual onset, may present as vague unsteadiness rather than classical hearing loss | Abnormal bone remodelling around stapes footplate → progressive conductive hearing loss; if involves cochlea (cochlear otosclerosis) → SNHL + vestibular symptoms | Progressive hearing loss in young adult; family history (AD inheritance); audiometry |
| Arrhythmias (repeated here because easily missed) | Paroxysmal arrhythmias may not be captured on a single ECG; patients may describe it only as "dizzy" | Intermittent ↓CO → transient cerebral hypoperfusion | ECG, Holter monitor [1]; ask about palpitations; consider loop recorder |
| Hyperventilation | Patients may not recognise they are hyperventilating; may present with "cardiac" symptoms (chest pain, palpitations) | ↓PaCO₂ → cerebral vasoconstriction + ↓ionised Ca²⁺ | Forced hyperventilation test [1] reproduces symptoms; look for perioral/digital paraesthesia, carpopedal spasm [4] |
| Alcohol and drugs (incl. illicit, e.g. cocaine) [1] | Patients may not volunteer substance use; clinicians may not ask | Alcohol: direct vestibulotoxicity + cerebellar toxicity; cocaine: vasospasm → cerebral ischaemia; many drugs → orthostatic hypotension/CNS depression | Always ask about alcohol, illicit drugs, and OTC medications |
| Cough or micturition syncope | Situational triggers may be embarrassing or not volunteered | Cough syncope: prolonged vigorous cough → ↑intrathoracic pressure → ↓venous return → ↓CO; micturition syncope: post-void vasovagal reflex (splanchnic blood pooling + vagal activation) | Careful history: "Do you feel dizzy when coughing / after urinating?" |
| Vertiginous migraine / migrainous vertigo (now called "vestibular migraine") | Vertigo without headache leads to misdiagnosis as Ménière's or anxiety; one of the most commonly missed diagnoses in dizziness clinics | Migraine pathophysiology modulates vestibular nuclei → episodic vertigo ± migrainous features | History of migraine; vertigo episodes (5 min–72h) with photophobia/phonophobia/visual aura; Meniere syndrome is overdiagnosed [1] — many "Ménière's" cases are actually vestibular migraine |
| Parkinson disease | Early PD may present with dizziness from orthostatic hypotension (autonomic dysfunction) before classical motor features are obvious [6] | Dopamine depletion in hypothalamus → autonomic dysfunction → postural hypotension → presyncope/dizziness; "worsened by levodopa/DA" [6] | Look for subtle tremor, bradykinesia, rigidity; lying-standing BP; ask about constipation, anosmia, REM sleep behaviour disorder |
| Meniere syndrome — overdiagnosed [1] | Clinicians overdiagnose Ménière's in any patient with episodic vertigo; true Ménière's requires the full triad (vertigo + hearing loss + tinnitus/aural fullness) | Endolymphatic hydrops | Insist on documented fluctuating low-frequency SNHL on audiometry before diagnosing; consider vestibular migraine as the more common alternative |
Rarities explained:
| Rarity | Mechanism of dizziness |
|---|---|
| Addison disease | Cortisol deficiency → ↓vascular tone + ↓mineralocorticoid → hypovolaemia and hypotension → presyncope; also hyponatraemia (↑ADH from hypocortisolaemia) [8] |
| Neurosyphilis | Treponema pallidum invades CNS → meningovascular syphilis (cerebrovascular ischaemia) or tabes dorsalis (posterior column degeneration → sensory ataxia) or otosyphilis (cochleo-vestibular damage) |
| Autonomic neuropathy | Damage to autonomic nerves (DM most common cause [9]) → impaired baroreceptor reflex → orthostatic hypotension → presyncope; "postural tachycardia with lightheadedness, dizziness, presyncope" [9] |
| Hypertension | Usually does NOT cause dizziness; however, severe/malignant HTN → hypertensive encephalopathy with headache, dizziness, visual disturbance; also antihypertensive overtreatment → orthostatic hypotension |
| Subclavian steal | Stenosis of subclavian artery proximal to vertebral artery origin → exercising ipsilateral arm "steals" blood from vertebrobasilar circulation via retrograde flow in vertebral artery → posterior circulation ischaemia → vertigo + arm claudication; BP discrepancy between arms |
| Perilymphatic fistula | Abnormal communication between middle ear and inner ear → perilymph leakage → vestibular dysfunction; triggered by Valsalva, straining, barotrauma, or surgery; Tullio phenomenon (vertigo induced by loud sounds) |
| Shy-Drager syndrome (now called Multiple System Atrophy — MSA, cerebellar type) | Progressive neurodegenerative disease with severe autonomic failure (orthostatic hypotension, urinary incontinence) + cerebellar/parkinsonian features → dizziness from both autonomic and cerebellar dysfunction |
These are common medical conditions that can "masquerade" as dizziness — i.e., dizziness may be the presenting complaint but the underlying cause is something else entirely.
Masquerades checklist: [1]
- Depression
- Diabetes (hyper and hypoglycaemia)
- Drugs (several)
- Anaemia
- Thyroid disorder (possible)
- Spinal dysfunction
- UTI (possible)
| Masquerade | Mechanism of dizziness | How to detect |
|---|---|---|
| Depression | Psychomotor retardation, poor concentration → subjective "dizziness"; somatisation; also a/w hyperventilation; commonly coexists with anxiety | Screen with PHQ-9; look for low mood, anhedonia, sleep disturbance, appetite change |
| Diabetes — hypoglycaemia | Neuroglycopenic symptoms: hunger, paraesthesia, seizures, focal weakness, clouding of vision, ↓consciousness [10]; adrenergic symptoms: palpitation, sweating, anxiety, tremor | Blood glucose [1]; Whipple's triad [10]; check drug history (insulin, sulfonylureas) |
| Diabetes — hyperglycaemia | Osmotic diuresis → dehydration → hypovolaemia → orthostatic hypotension; also diabetic autonomic neuropathy [9] | Blood glucose, HbA1c; lying-standing BP |
| Drugs (several) | Multiple mechanisms: orthostatic hypotension, CNS depression, vestibulotoxicity, cerebellar toxicity | "Commonly prescribed drugs, especially antihypertensives, antidepressants, aspirin and salicylates, glyceryl trinitrate, benzodiazepines, major tranquillisers, antiepileptics and antibiotics, can cause dizziness" [1] |
| Anaemia | ↓O₂ carrying capacity → ↓O₂ delivery to brain; "acute/severe: SOB, palpitation, dizziness/syncope (may be postural)" [11] | FBE [1]; look for pallor; ask about menorrhagia, melena, dietary history |
| Thyroid disorder | Hypothyroidism: ↓metabolic rate → ↓CO, ↓cerebral perfusion; hyperthyroidism: AF → irregular CO → dizziness; thyrotoxic crisis → cardiovascular collapse | TFTs; look for thyroid-related symptoms (weight changes, heat/cold intolerance, bowel habit changes) |
| Spinal dysfunction | Cervical spondylosis → abnormal proprioceptive input to vestibular nuclei → vague dizziness/disequilibrium (see probability diagnoses above) | Neck ROM, cervical spine tenderness, neurological exam of UL |
| UTI (possible) | In elderly: UTI → sepsis/systemic inflammation → delirium with dizziness/unsteadiness; also dehydration from fever | Urinalysis, urine culture; particularly relevant in elderly with new-onset confusion + dizziness |
"Is the patient trying to tell me something? Very likely. Consider anxiety and/or depression." [1]
The Elderly Dizzy Patient — Almost Always Multifactorial
"Dizziness is often multifactorial, especially in the elderly" [1]. In an 80-year-old on 8 medications with cataracts, peripheral neuropathy, cervical spondylosis, and mild depression — the "dizziness" isn't from one cause. It's the cumulative effect of degraded visual, vestibular, proprioceptive, cardiovascular, and central processing systems, compounded by polypharmacy. Your management must address all contributing factors, not just one.
3. Differential Organised by Dizziness Subtype
This is the clinically practical way to use the differential — once you've subcategorised the symptom, you apply the appropriate differential.
| Category | Peripheral (inner ear / CN VIII) | Central (brainstem / cerebellum) |
|---|---|---|
| Episodic, seconds | BPPV | — |
| Episodic, minutes–hours | Ménière's disease | Vestibular migraine, VBI/TIA |
| Acute persistent (days) | Vestibular neuritis, labyrinthitis | Posterior circulation stroke (PICA), MS relapse, cerebellar haemorrhage |
| Chronic/progressive | Acoustic neuroma [1], bilateral vestibulopathy (aminoglycosides), otosclerosis [1] | Posterior fossa tumour [1], cerebellar degeneration, MS [1] |
| Positional | BPPV | Central positional vertigo (rare — 4th ventricle tumour, Chiari malformation) |
| Trauma-related | Post-head injury BPPV [1], labyrinthine concussion, perilymphatic fistula [1] | Post-traumatic brainstem lesion |
| Drug-related | Aminoglycosides (bilateral vestibulopathy), alcohol [1] | Phenytoin/carbamazepine (cerebellar toxicity), alcohol [1] |
| Mechanism | Proportion | Causes | Key distinguishing features |
|---|---|---|---|
| Neurocardiogenic (60%) [2][3] | Most common | Vasovagal, cough/micturition syncope [1], carotid sinus hypersensitivity | Prodrome (nausea, sweating, pallor); situational trigger; when standing; quick recovery |
| Cardiac (15%) [2][3] | Most dangerous | Arrhythmias [1], MI [1], aortic stenosis [1], PE, HCM, aortic dissection | Sudden onset, any position, ± palpitations/chest pain, brief, extreme pallor; ± exertional [2] |
| Orthostatic hypotension (15%) [2][3] | Very common in elderly | Drugs [1], autonomic neuropathy [9], hypovolaemia, Addison's [1], Shy-Drager/MSA [1], Parkinson's [1][6] | On standing; documented BP drop; identifiable cause |
| Metabolic | Variable | Hypoglycaemia [1][10], anaemia [1][11], hyperventilation | Context-dependent (diabetic medications, blood loss, anxiety) |
| System | Causes | Why it causes imbalance |
|---|---|---|
| Sensory (proprioceptive) | Peripheral neuropathy (DM, B12 deficiency, alcohol), spinal dysfunction [1], dorsal column disease (tabes dorsalis) | Loss of joint position sense → Romberg positive; wide-based gait worsened by eye closure |
| Vestibular | Bilateral vestibulopathy (aminoglycosides, bilateral Ménière's), chronic unilateral vestibular loss | Impaired vestibular input → oscillopsia + unsteadiness |
| Cerebellar | Posterior fossa tumour [1], cerebellar stroke, MS [1], chronic alcohol, drugs (phenytoin) | Loss of motor coordination → truncal/limb ataxia; Romberg negative; wide-based gait NOT worsened by eye closure |
| Motor | Parkinson disease [1][6], normal pressure hydrocephalus | PD: rigidity + postural instability; NPH: triad of gait apraxia + dementia + urinary incontinence |
| Visual | Cataracts, macular degeneration, refractive error | Loss of visual spatial reference → instability, especially in low light |
| Multifactorial | Elderly with multiple contributing factors [1] | Cumulative degradation of all sensory and motor systems |
| Category | Causes | Mechanism |
|---|---|---|
| Psychiatric | Anxiety–hyperventilation [1], depression [1], panic disorder [12], PPPD, somatoform disorder [12] | Hyperventilation → ↓PaCO₂ → cerebral vasoconstriction; somatisation; maladaptive central vestibular processing |
| Metabolic | Hypoglycaemia [1][10], hyperglycaemia [1], hyponatraemia [13], hypercalcaemia, thyroid disorder [1] | Variable: neuroglycopenia, osmotic shifts, altered neuronal excitability |
| Haematological | Anaemia [1][11], polycythaemia vera [14] | Anaemia: ↓O₂ delivery; PV: hyperviscosity → ↓cerebral blood flow |
| Drug-related | Multiple drugs [1], alcohol [1] | Multiple mechanisms (see Section 2.3) |
| Infective | UTI in elderly [1], systemic sepsis | Delirium, dehydration, hypotension |
When evaluating any dizzy patient, actively look for these red flags that point towards serious pathology:
| Red flag | Suggests |
|---|---|
| New headache (especially progressive, worse AM, with Valsalva) | Posterior fossa tumour, ↑ICP [5] |
| Brainstem symptoms (diplopia, dysarthria, dysphagia, facial numbness, Horner's) | Posterior circulation stroke, brainstem lesion [1] |
| Sudden onset at rest/during exertion + palpitations + chest pain | Cardiac syncope — 30% mortality [2][3] |
| Negative head impulse test in acute vestibular syndrome | Central cause (stroke) — NOT peripheral |
| Direction-changing or purely vertical nystagmus | Central cause |
| Progressive unilateral hearing loss | Acoustic neuroma [1] |
| New focal neurological deficit | Stroke, MS, tumour, abscess |
| Exertional syncope | Aortic stenosis, HCM, pulmonary hypertension [1] |
| Family history of sudden cardiac death | Inherited arrhythmia (Long QT, Brugada, HCM) |
| Recent head trauma with worsening symptoms | Expanding subdural haematoma, diffuse axonal injury |
Here is a practical bedside algorithm integrating the Murtagh framework with modern vestibular neurology:
| Feature | BPPV | Vestibular neuritis | Ménière's | Vestibular migraine | Posterior circulation stroke | Cardiac syncope | Vasovagal |
|---|---|---|---|---|---|---|---|
| Type | Vertigo | Vertigo | Vertigo | Vertigo | Vertigo ± brainstem Sx | Presyncope/syncope | Presyncope/syncope |
| Duration | Seconds | Days | 20 min–hours | 5 min–72h | Minutes–days | Seconds–minutes | Seconds–minutes |
| Trigger | Position change | None (post-URTI) | Spontaneous | Migraine triggers | Spontaneous | Any position, ± exertion | Standing, situational |
| Hearing loss | No | No | Yes (fluctuating, low-freq) | No (usually) | Rare (if AICA) | No | No |
| Nystagmus | Upbeating torsional | Unidirectional horiz-torsional | Horizontal | Variable | Direction-changing/vertical | None | None |
| HIT | Normal (if not acute) | Positive (catch-up saccade) | Normal between attacks | Normal | Negative (normal = bad!) | N/A | N/A |
| Brainstem signs | No | No | No | No | Yes | No | No |
| Key test | Dix-Hallpike [1] | HINTS | Audiometry | Clinical criteria | MRI/CTA | ECG, Holter [1] | Tilt table |
High Yield Summary — Differential Diagnosis of Dizziness
-
First step: Subcategorise → Vertigo vs Presyncope vs Disequilibrium vs Non-specific
-
Probability diagnoses [1]: Anxiety–hyperventilation, postural hypotension, vasovagal, vestibular neuritis, BPPV, motion sickness, post-head injury, cervical spondylosis
-
Serious not to miss [1]: Acoustic neuroma, posterior fossa tumour, brain tumour, intracerebral abscess, arrhythmias (30% mortality!), MI, aortic stenosis, VBI, brainstem infarct (PICA), MS
-
Pitfalls [1]: Ear wax, arrhythmias, hyperventilation, alcohol/drugs, cough/micturition syncope, vestibular migraine (commonly missed), Parkinson's (autonomic features), Ménière's (overdiagnosed)
-
Masquerades [1]: Depression, diabetes (hypo/hyperglycaemia), drugs, anaemia, thyroid disorder, spinal dysfunction, UTI
-
Acute vestibular syndrome: The critical DDx is vestibular neuritis (peripheral) vs posterior circulation stroke (central) → use HINTS exam (more sensitive than early MRI)
-
Syncope: Cardiac (15%, most dangerous) vs Neurocardiogenic (60%, most common) vs Orthostatic (15%)
-
In the elderly: Always think multifactorial, check all medications, lying-standing BP, FBE, glucose
Active Recall - Differential Diagnosis of Dizziness
References
[1] Lecture slides: murtagh merge.pdf (Dizziness/vertigo section, pp. 35–37) [2] Senior notes: Ryan Ho Cardiology.pdf (Section 2.4 Syncope, p. 63) [3] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.4 Syncope, p. 208) [4] Senior notes: Ryan Ho Cardiology.pdf (Chest Pain approach, pp. 55–56) [5] Senior notes: maxim.md (Brain tumours, section 771) [6] Senior notes: Ryan Ho Neurology.pdf (Parkinson disease clinical features, p. 121) [7] Senior notes: Ryan Ho Opthalmology.pdf (Optic neuritis, p. 92) [8] Senior notes: Ryan Ho Endocrine.pdf (Adrenal insufficiency, p. 71) [9] Senior notes: Ryan Ho Endocrine.pdf (Diabetic autonomic neuropathy, p. 98) [10] Senior notes: Ryan Ho Endocrine.pdf (Hypoglycaemia, p. 94) [11] Senior notes: Ryan Ho Haemtology.pdf (Approach to Anaemia, p. 10) [12] Senior notes: Ryan Ho Psychiatry.pdf (Panic disorder / GAD, pp. 173, 179) [13] Senior notes: Ryan Ho Chemical Path.pdf (SIADH / hyponatraemia, p. 10) [14] Senior notes: Ryan Ho Haemtology.pdf (Polycythaemia Vera, p. 76)
Diagnostic Criteria, Diagnostic Algorithm and Investigation Modalities for Dizziness
There is no single diagnostic criterion for "dizziness" — because dizziness is a symptom, not a disease. Instead, the diagnostic approach has two sequential goals:
- Subcategorise the symptom (vertigo vs presyncope vs disequilibrium vs non-specific) — this is done by history
- Diagnose the underlying cause within that subcategory — this requires specific diagnostic criteria and investigations for each candidate diagnosis
The implication is that you need to know the diagnostic criteria for the individual conditions that cause dizziness. I'll cover the most important ones below, followed by the overall diagnostic algorithm and a comprehensive review of investigation modalities.
2. Diagnostic Criteria for Key Causes of Dizziness
BPPV is a clinical diagnosis — no blood test or imaging is needed. The diagnostic gold standard is the Dix-Hallpike manoeuvre (for posterior canal BPPV, which accounts for ~80% of cases) and the supine roll test (for horizontal canal BPPV).
Dix-Hallpike Manoeuvre — Diagnostic Criteria for Posterior Canal BPPV:
| Feature | Description | Why this feature occurs |
|---|---|---|
| Latency | Nystagmus begins 2–5 seconds after achieving the test position | Time for otoconia to settle under gravity and deflect the cupula |
| Direction | Upbeating + geotropic torsional (top pole of eye beating towards the ground) | Excitatory stimulation of the posterior canal → specific nystagmus pattern dictated by the plane of the posterior SCC |
| Duration | Nystagmus lasts < 60 seconds (typically 10–30s) | Otoconia settle → cupula returns to neutral → signal ceases |
| Vertigo | Patient reports spinning during nystagmus | Cupular deflection generates false rotational signal |
| Fatigability | Repeated testing → diminishing response | Otoconia disperse with repeated repositioning |
| Reversibility | Nystagmus reverses direction when patient sits back up | Otoconia flow in opposite direction on return to upright |
A positive Hallpike manoeuvre [1] with these characteristic features confirms posterior canal BPPV. No further investigation is needed.
Exam Pitfall — Atypical Dix-Hallpike
If the Dix-Hallpike produces no latency (immediate onset), does not fatigue, is purely downbeating or direction-changing, or lasts > 60 seconds — think central positional vertigo (e.g., posterior fossa tumour, Chiari malformation). This mandates urgent neuroimaging.
Vestibular neuritis is also a clinical diagnosis. The key bedside tool is the HINTS exam (Head Impulse, Nystagmus, Test of Skew), used specifically in the context of an acute vestibular syndrome (acute onset continuous vertigo + nausea/vomiting + nystagmus + gait unsteadiness lasting > 24h).
HINTS Criteria — Peripheral (Vestibular Neuritis) vs Central (Stroke):
| HINTS component | Peripheral pattern (vestibular neuritis) | Central pattern (stroke) | Why |
|---|---|---|---|
| Head Impulse | Positive (abnormal): catch-up saccade when head turned towards affected ear | Negative (normal): no saccade, eyes stay on target | Peripheral: VOR arc disrupted at labyrinth/nerve → eyes lag behind. Central: VOR arc intact (lesion in brainstem/cerebellum, not at nerve level) |
| Nystagmus | Unidirectional, horizontal-torsional, beating away from lesion; suppressed by visual fixation | Direction-changing (gaze-evoked), or purely vertical/torsional; NOT suppressed by fixation | Peripheral: tonic asymmetry → unidirectional drift. Central: gaze-holding dysfunction → direction-changing patterns |
| Test of Skew | Absent (no vertical misalignment) | Present (skew deviation — one eye higher) | Skew deviation = disruption of otolithic–ocular pathways that cross in the brainstem → indicates brainstem lesion |
Rule: If any ONE component is "central," the pattern is considered dangerous → treat as stroke until proven otherwise.
The HINTS exam, when performed by a trained clinician in acute vestibular syndrome, has sensitivity > 98% and specificity ~96% for posterior circulation stroke — superior to MRI-DWI within the first 24–48 hours (DWI can be falsely negative early in posterior fossa strokes due to susceptibility artefact from adjacent bone).
AAO-HNS 2020 Diagnostic Criteria for Definite Ménière's Disease:
| Criterion | Detail |
|---|---|
| A | ≥ 2 spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours |
| B | Audiometrically documented low- to mid-frequency sensorineural hearing loss in the affected ear on at least one occasion before, during, or after one of the episodes of vertigo |
| C | Fluctuating aural symptoms (hearing, tinnitus, or fullness) in the affected ear |
| D | Not better accounted for by another vestibular diagnosis |
- Meniere syndrome is overdiagnosed [1] — the key requirement that many clinicians miss is criterion B: you need audiometric documentation of low-frequency SNHL. Without it, many of these patients actually have vestibular migraine.
ICHD-3 / Bárány Society Diagnostic Criteria (2012):
| Criterion | Detail |
|---|---|
| A | ≥ 5 episodes of vestibular symptoms of moderate or severe intensity, lasting 5 minutes to 72 hours |
| B | Current or previous history of migraine (with or without aura) per ICHD criteria |
| C | ≥ 1 migraine feature with ≥ 50% of vestibular episodes: (1) headache with ≥ 2 of: unilateral, pulsating, moderate-severe, aggravated by routine physical activity; (2) photophobia and phonophobia; (3) visual aura |
| D | Not better accounted for by another vestibular or ICHD diagnosis |
Consensus Definition (AAS/AHA/ESH):
| Criterion | Value |
|---|---|
| SBP drop | ≥ 20 mmHg |
| OR DBP drop | ≥ 10 mmHg |
| Timing | Within 3 minutes of standing from supine |
Why these thresholds? They represent the point at which cerebral autoregulation becomes insufficient to maintain adequate perfusion in most individuals, correlating with symptom onset.
Measurement protocol: Supine BP after 5 minutes of rest → standing BP at 1 minute and 3 minutes.
Syncope itself is diagnosed clinically (transient LOC + loss of postural tone + spontaneous recovery). The critical question is cardiac vs non-cardiac cause:
| Feature | High risk (admit/investigate urgently) | Low risk (may discharge) |
|---|---|---|
| History | Syncope during exertion or supine; new-onset chest pain/SOB/abdominal pain before syncope; FHx of sudden cardiac death < 40y; palpitation preceding syncope | Classic vasovagal prodrome; specific situational trigger; young patient; known long-standing recurrent episodes with same features |
| Examination | New murmur; unexplained low SBP; rectal exam suggesting GI bleed; persistent bradycardia < 40 bpm | Normal cardiovascular exam |
| ECG | Acute ischaemia; new bundle branch block; Brugada pattern; long QT (QTc > 460ms); SVT/VT; high-degree AV block; pacemaker malfunction | Normal ECG |
Cardiac syncope carries ~30% mortality [2][3] — always actively look for cardiac red flags.
No specific "diagnostic criteria" exist in the way that BPPV has the Dix-Hallpike. Instead, the diagnosis rests on:
- Clinical presentation: acute vestibular syndrome + central HINTS pattern ± brainstem signs
- Neuroimaging: MRI with DWI is the gold standard (sensitivity 80–95% after 24h; lower in first 24h for posterior fossa) [15][16]; CT brain is primarily to rule out haemorrhage (sensitivity for ischaemic stroke < 50% in first 24h) [15]
- Vascular imaging: CT angiography or MR angiography to identify site of vascular occlusion/stenosis [17]
This algorithm integrates history, examination, bedside tests, and investigations into a practical flow. The philosophy is: history first → bedside tests → targeted investigations.
4. Investigation Modalities — Comprehensive Guide
Here we systematically cover every investigation relevant to dizziness, organised from bedside tests through bloods to advanced imaging. For each, I explain what it tests, the key findings, and the interpretation — i.e., why each test is ordered and what the result tells you.
These are your first-line tools and often the most powerful. A careful bedside assessment can diagnose BPPV, vestibular neuritis, and even rule out posterior circulation stroke with greater accuracy than early MRI.
| Test | How to perform | Positive finding | Interpretation | Condition diagnosed |
|---|---|---|---|---|
| Hallpike (Dix-Hallpike) manoeuvre [1] | Patient sits → rapidly laid supine with head hanging 30° below table edge, turned 45° to one side. Observe eyes for 30s. Repeat to other side | Upbeating torsional nystagmus with 2-5s latency, < 60s, with vertigo; fatigable on repetition | Displaced otoconia in posterior SCC stimulated by gravity → pathognomonic | Posterior canal BPPV |
| Supine roll test | Patient supine → rapidly turn head to one side, then the other | Horizontal nystagmus; geotropic (towards ground) or apogeotropic (away from ground) | Canalithiasis (geotropic, stronger to affected side) vs cupulolithiasis (apogeotropic, stronger to unaffected side) | Horizontal canal BPPV |
| Head impulse test (HIT) | Patient fixates on examiner's nose → examiner delivers rapid, small-amplitude, unpredictable head rotations to each side | Corrective saccade (eyes lag then "catch up") when head turned towards affected side | VOR deficit on that side → peripheral vestibular lesion; normal HIT in acute vertigo = red flag for central cause | Peripheral vs central vestibular lesion |
| Test of skew (alternate cover test) | Cover one eye, then quickly switch cover to other eye. Observe for vertical refixation movement | Vertical correction (one eye higher than the other) | Brainstem otolithic pathway disruption → central sign | Central vestibular lesion (stroke) |
| Nystagmus assessment | Observe eyes in primary gaze, then eccentric gaze. Use Frenzel goggles (remove fixation) if available | Characterise: direction, suppression by fixation, gaze-dependence | Unidirectional + fixation-suppressed = peripheral; Direction-changing or not fixation-suppressed = central | Peripheral vs central |
| Forced hyperventilation test [1] | Ask patient to breathe rapidly and deeply for 2–3 minutes | Reproduces the patient's dizziness and associated symptoms (paraesthesia, lightheadedness) | ↓PaCO₂ → cerebral vasoconstriction → symptoms; confirms anxiety/hyperventilation as cause | Hyperventilation syndrome |
| Romberg test | Stand with feet together, eyes open → then eyes closed | Falls or significant sway with eyes closed but stable with eyes open | Removing visual compensation unmasks proprioceptive deficit → positive = sensory ataxia. Negative with wide-based gait = cerebellar ataxia | Sensory ataxia vs cerebellar ataxia |
| Unterberger/Fukuda stepping test | March in place with eyes closed for 50 steps | Rotation > 45° to one side | Vestibulospinal asymmetry → the patient rotates towards the weaker (hypoactive) vestibular side | Unilateral vestibular hypofunction |
| Lying-standing BP | Supine BP after 5 min rest → standing BP at 1 min and 3 min | ↓SBP ≥ 20 or ↓DBP ≥ 10 within 3 min | Impaired baroreceptor reflex / hypovolaemia / drug-induced | Orthostatic hypotension |
| Gait assessment [1] | Observe walking, turning, tandem (heel-to-toe) walk | Wide-based, unsteady, veering, high-stepping, shuffling, etc. | Pattern identifies aetiology: wide-based = cerebellar; shuffling = PD; high-stepping = foot drop/sensory; veering = unilateral vestibular | Multiple conditions |
High Yield — Frenzel Goggles
Frenzel goggles (high-dioptre lenses that blur the patient's vision while allowing the examiner to observe the eyes under magnification) are invaluable because they remove visual fixation. Peripheral nystagmus is suppressed by fixation, so Frenzel goggles make it more visible. Central nystagmus is not suppressed, so it's equally visible with or without goggles. If goggles aren't available, having the patient close their eyes then quickly open them, or using an ophthalmoscope to observe one eye while the other is covered, can serve as a rough substitute.
Key investigations: FBE, blood glucose, audiometry, ECG, ?Holter monitor. Other tests according to history and examination. [1]
| Investigation | What it tests | Key findings | Interpretation / Why order it |
|---|---|---|---|
| FBE (Full Blood Examination / CBC) [1] | Red cells, white cells, platelets | ↓Hb: anaemia; ↑Hb/Hct: polycythaemia [14]; ↑MCV: B12/folate def, alcohol, MDS [18]; ↑WCC: infection | Anaemia → ↓O₂ delivery → dizziness/presyncope [19]. Polycythaemia vera → hyperviscosity → dizziness [14]. Must-do in every dizzy patient as it catches the "masquerade" of anaemia |
| Blood glucose [1] | Plasma glucose | ↓glucose (< 3.9 mmol/L in diabetics, < 2.8 mmol/L in non-diabetics): hypoglycaemia; ↑glucose: DM → osmotic diuresis → dehydration | Hypoglycaemia → neuroglycopenia → dizziness, confusion [20]. Hyperglycaemia → dehydration/autonomic neuropathy → orthostatic dizziness |
| U&E (Urea, Creatinine, Electrolytes) | Renal function, Na⁺, K⁺ | ↓Na⁺ (hyponatraemia): confusion, dizziness, seizures; ↑K⁺: arrhythmia risk [21]; ↑urea/Cr: renal failure → uraemic encephalopathy | Hyponatraemia is a common cause of non-specific dizziness, especially in elderly on thiazides. K⁺ and Mg²⁺ abnormalities predispose to arrhythmia |
| Calcium (Ca²⁺) | Total and ionised Ca²⁺ | ↑Ca²⁺ (hypercalcaemia): lethargy, confusion, dizziness, polyuria; ↓Ca²⁺: paraesthesia, tetany, dizziness | Hypercalcaemia → CNS depression + dehydration → dizziness |
| TFTs (Thyroid Function Tests) | TSH, fT4 | ↑TSH ↓fT4: hypothyroidism → ↓CO, ↓metabolic rate; ↓TSH ↑fT4: hyperthyroidism → AF, anxiety | Thyroid disorder is a Murtagh masquerade [1]. Hypothyroidism → sluggish circulation → dizziness. Hyperthyroidism → AF → palpitations + dizziness; also causes anxiety-type symptoms |
| HbA1c | Glycaemic control over 2–3 months | ≥ 6.5% (48 mmol/mol): DM | Identifies undiagnosed DM → leads to investigation for autonomic neuropathy as cause of orthostatic dizziness [9] |
| Vitamin B12 / Folate | Nutritional status, haematopoiesis | ↓B12: macrocytic anaemia + subacute combined degeneration (posterior + lateral column) → sensory ataxia + disequilibrium | B12 deficiency → demyelination of dorsal columns → proprioceptive loss → disequilibrium (Romberg +ve) |
| ESR / CRP | Inflammatory markers | ↑↑ESR (> 50 mm/h): GCA; ↑CRP: infection, inflammation | ESR > 50 in elderly patient with new headache + dizziness → must exclude GCA (temporal arteritis) urgently [22]; also screens for infection |
| Iron studies (Ferritin, TIBC, serum Fe) | Iron deficiency | ↓ferritin, ↑TIBC, ↓serum iron: IDA | Chronic iron deficiency anaemia is the most common cause of anaemia worldwide → dizziness on exertion |
| Cortisol / ACTH | Adrenal function | ↓cortisol ± ↑ACTH (primary) or ↓ACTH (secondary): adrenal insufficiency | Addison disease [1] is a rare but dangerous cause of dizziness → hypotension, hypovolaemia, hyponatraemia [20] |
| Investigation | What it tests | Key findings | Interpretation / When to order |
|---|---|---|---|
| ECG [1] | Cardiac rhythm and conduction | Arrhythmias (AF, VT, SVT, heart block), ischaemic changes (ST depression/elevation), long QT (QTc > 460ms), Brugada pattern, RBBB, S₁Q₃T₃ (PE), LVH (hypertensive heart disease, HCM/AS) | First-line in any patient with presyncope/syncope or palpitations. Cardiac syncope carries ~30% mortality [2][3] — the ECG is your screening tool |
| Holter monitor (ambulatory ECG) [1] | Paroxysmal arrhythmias over 24–72h or 7 days | Captures intermittent arrhythmia not seen on single ECG: paroxysmal AF, intermittent heart block, non-sustained VT | Order when history suggests arrhythmia [1] but resting ECG is normal. Symptom-rhythm correlation is the goal [2][23] |
| External loop recorder | Longer-term rhythm monitoring (weeks) | Patient-activated recording at time of symptoms | When events are too infrequent for Holter. Provides symptom-rhythm correlation over weeks [2][23] |
| Implantable loop recorder (ILR) | Very long-term monitoring (18–36 months) | Automatically detects and records arrhythmias | Unexplained recurrent syncope after initial workup is non-diagnostic. Battery lasts 18–36 months [2][23] |
| Echocardiography | Structural heart disease | Aortic stenosis (calcified AV, ↓AVA, ↑gradient), HCM (asymmetric septal hypertrophy, SAM), DCMP (↓EF), valvular disease, RV strain (PE) | Order when murmur detected, exertional syncope, or suspicion of structural cardiac disease [2][23] |
| Tilt-table test | Neurocardiogenic reflex | Positive = reproduction of syncope with ↓HR (cardioinhibitory) and/or ↓BP (vasodepressor) during 70° head-up tilt for 30–40 min ± isoproterenol/sublingual GTN provocation [2][3] | Indicated for recurrent unexplained syncope after cardiac causes excluded. Confirms predisposition to vasovagal syncope. Important: "suggestive of tendency/predisposition to reflex syncope only" [3] — result must be interpreted in clinical context |
| Carotid sinus massage | Carotid sinus hypersensitivity | Positive = sinus pause > 3 seconds (cardioinhibitory) and/or ↓SBP > 50 mmHg (vasodepressor) [2][3] | Recommended for undiagnosed syncope > 40y [3]. C/I: MI, TIA, stroke in past 3 months, carotid bruit [3] |
| Electrophysiological study (EPS) | Inducible arrhythmias | Inducible VT, abnormal AV conduction, accessory pathway | Reserved for high suspicion of malignant arrhythmia: CAD with LV dysfunction, cardiomyopathy, BBB, suspected WPW [2][23] |
| Investigation | What it tests | Key findings | Interpretation / When to order |
|---|---|---|---|
| Audiometry (pure tone audiogram) [1] | Hearing thresholds at different frequencies | Low-frequency SNHL (characteristic trough at 250–1000 Hz): Ménière's disease. Asymmetric high-frequency SNHL: acoustic neuroma. Conductive hearing loss: otosclerosis, cerumen impaction | Audiometry [1] is essential when aural symptoms (hearing loss, tinnitus, aural fullness) accompany dizziness. Mandatory for Ménière's diagnosis (criterion B requires audiometric documentation) |
| Tympanometry | Middle ear function | Type B (flat): middle ear effusion/cerumen. Type C: eustachian tube dysfunction. Type As: otosclerosis (reduced compliance) | Helps distinguish conductive from sensorineural causes of hearing loss |
| Otoacoustic emissions (OAE) | Outer hair cell function | Absent in cochlear damage, present in retrocochlear (neural) lesion | Helps differentiate cochlear (Ménière's) from retrocochlear (acoustic neuroma) pathology |
| Auditory brainstem response (ABR) | CN VIII and brainstem auditory pathway integrity | Prolonged wave I–V interpeak latency or absent waves: retrocochlear lesion (acoustic neuroma, MS) | Screening test for acoustic neuroma; largely superseded by MRI but still used when MRI is contraindicated |
These are specialised tests usually performed in ENT/neurology vestibular clinics.
| Investigation | What it tests | Key findings | Interpretation |
|---|---|---|---|
| Videonystagmography (VNG) / Electronystagmography (ENG) | Records eye movements during various tasks (spontaneous nystagmus, positional, caloric, smooth pursuit, saccades) | Spontaneous nystagmus direction/amplitude; positional nystagmus; gaze-evoked nystagmus; saccade abnormalities | Comprehensive vestibular and oculomotor assessment; identifies peripheral vs central patterns; documents nystagmus objectively |
| Caloric testing | Individual horizontal SCC function by thermal stimulation | Reduced response on one side (canal paresis > 25%): unilateral vestibular hypofunction; bilateral absence: bilateral vestibulopathy | The only test that stimulates each labyrinth independently — "COWS" mnemonic: Cold = Opposite, Warm = Same (direction of fast-phase nystagmus). Absent bilateral caloric response + oscillopsia → bilateral vestibulopathy (e.g., aminoglycoside toxicity) |
| Video head impulse test (vHIT) | VOR function across all 6 SCCs | Reduced VOR gain (< 0.8) + overt/covert saccades on head impulse towards affected side | Quantitative version of bedside HIT; can test all 6 canal planes; detects covert saccades invisible to naked eye |
| Vestibular evoked myogenic potentials (VEMPs) | Otolith organ function | cVEMP (cervical): saccule function via inferior vestibular nerve. oVEMP (ocular): utricle function via superior vestibular nerve. Absent or reduced amplitude = otolith dysfunction; ↓threshold = superior SCC dehiscence | Useful for: vestibular neuritis (localise superior vs inferior nerve), Ménière's, superior canal dehiscence syndrome |
| Rotatory chair testing | VOR function across a range of frequencies | Reduced gain at low frequencies: bilateral vestibular hypofunction | Most useful for confirming bilateral vestibulopathy |
"Consider MRI, especially if acoustic neuroma or other tumour suspected" [1]
| Modality | What it shows | Key findings for dizziness | When to order |
|---|---|---|---|
| CT brain (non-contrast) | Haemorrhage, large mass lesions, bone | Hyperdense lesion: acute haemorrhage (ICH, SAH, cerebellar haemorrhage). Hypodense lesion: established infarct (but sensitivity for ischaemic stroke < 50% in first 24h [15]). Normal CT does NOT exclude ischaemic stroke | First-line in acute vestibular syndrome if MRI unavailable; primary role is to exclude haemorrhage [15] |
| MRI brain (with gadolinium) [1] | Soft tissue detail — infarction, demyelination, tumours | DWI restriction: acute ischaemic stroke (bright on DWI, dark on ADC). Enhancing CPA mass: acoustic neuroma [1]. Periventricular/juxtacortical T2 lesions: MS (Dawson's fingers) [24]. Posterior fossa mass: tumour, metastasis [1] | "Consider MRI, especially if acoustic neuroma or other tumour suspected" [1]. Also for: central vestibular syndrome (stroke), progressive unilateral SNHL, chronic unexplained vertigo, MS suspicion |
| MRI DWI (diffusion-weighted imaging) | Cytotoxic oedema from acute ischaemia | Restricted diffusion (bright DWI + dark ADC map) within minutes of onset — "very sensitive for small and early infarcts" [16] | Acute vestibular syndrome with central HINTS → urgent DWI to confirm posterior circulation stroke. Caveat: sensitivity in posterior fossa may be lower in first 24h due to susceptibility artefact from bone → if negative but high clinical suspicion, repeat MRI in 3–5 days |
| CT angiography (CTA) | Vascular anatomy — stenosis, occlusion, dissection, aneurysm | Vertebral/basilar artery stenosis or occlusion: VBI or posterior circulation stroke. Carotid stenosis. Dissection (intimal flap, luminal narrowing) [17] | Acute stroke workup; suspected VBI; suspected arterial dissection (neck pain + vertigo + Horner's) |
| MR angiography (MRA) | Same as CTA but without radiation or iodinated contrast | Same as CTA | Alternative to CTA; preferred for follow-up or when contrast is contraindicated |
| CT temporal bone (high-resolution) | Temporal bone anatomy | SCC dehiscence (superior canal dehiscence syndrome); cholesteatoma; otosclerosis; mastoiditis; temporal bone fracture | Suspected perilymphatic fistula, superior SCC dehiscence, chronic ear disease |
| MR venography (MRV) | Cerebral venous sinuses | Venous sinus thrombosis (absent flow signal in affected sinus) | Headache + papilloedema + dizziness → exclude cerebral venous sinus thrombosis (CVST) as cause of ↑ICP [25] |
MRI Sensitivity for Posterior Fossa Stroke — A Critical Caveat
MRI-DWI is excellent for supratentorial strokes (sensitivity > 99%) but its sensitivity for posterior fossa strokes is lower in the first 24–48 hours (~80–85%), largely due to susceptibility artefact from the petrous bone. This means a negative MRI does NOT definitively exclude a posterior fossa stroke in the acute setting. If clinical suspicion remains high (central HINTS pattern, vascular risk factors), repeat MRI in 3–5 days. This is why HINTS at the bedside can paradoxically be more sensitive than early imaging.
| Investigation | Indication | Findings |
|---|---|---|
| Lumbar puncture | Suspected CNS infection (meningitis, encephalitis), IIH, neurosyphilis, MS (oligoclonal bands) | ↑opening pressure (IIH [25]); ↑WCC + protein (infection); oligoclonal bands + ↑IgG (MS [24]); positive VDRL/FTA-ABS (neurosyphilis) |
| EEG (Electroencephalogram) | Differentiating seizure from syncope when history is unclear | Epileptiform discharges (seizure); normal between episodes (syncope) |
| Nerve conduction studies / EMG | Suspected peripheral neuropathy causing disequilibrium | ↓conduction velocity (demyelinating neuropathy); ↓amplitude (axonal neuropathy) → identifies cause of proprioceptive loss |
| Dopaminergic SPECT/PET | Suspected Parkinson's disease with dizziness from autonomic dysfunction | ↓dopamine transporter uptake in basal ganglia → confirms Parkinsonism (does not distinguish IPD from MSA/PSP) [22] |
| Temporal artery biopsy | Suspected GCA (elderly, new headache, ↑↑ESR, jaw claudication + dizziness) | Granulomatous inflammation with giant cells → diagnostic. Must order urgently (< 24–48h) [22]; can be falsely negative due to skip lesions |
| Finding | Points towards |
|---|---|
| Dix-Hallpike: classic upbeat-torsional nystagmus with latency | BPPV (posterior canal) |
| HINTS: +ve HIT, unidirectional nystagmus, no skew | Vestibular neuritis (peripheral) |
| HINTS: -ve HIT, direction-changing nystagmus, OR skew | Posterior circulation stroke (central) |
| Orthostatic BP drop ≥ 20/10 | Orthostatic hypotension |
| ECG: AF, long QT, heart block, Brugada | Cardiac syncope |
| Audiometry: low-frequency SNHL | Ménière's disease |
| Audiometry: asymmetric high-frequency SNHL | Acoustic neuroma |
| MRI: CPA enhancing mass | Vestibular schwannoma (acoustic neuroma) |
| MRI-DWI: restricted diffusion in posterior fossa | Posterior circulation ischaemic stroke |
| MRI: periventricular T2 lesions (Dawson's fingers) | Multiple sclerosis |
| CT: hyperdense lesion in cerebellum/brainstem | Cerebellar/brainstem haemorrhage |
| FBE: ↓Hb | Anaemia → dizziness from ↓O₂ delivery |
| FBE: ↑Hb/Hct | Polycythaemia → hyperviscosity → dizziness |
| Blood glucose < 3.9 | Hypoglycaemia → neuroglycopenia |
| ESR > 50 in elderly with headache | GCA → urgent temporal artery biopsy |
| Forced hyperventilation test: reproduces symptoms | Anxiety / hyperventilation syndrome |
| Tilt-table: ↓HR and/or ↓BP with syncope | Vasovagal (neurocardiogenic) syncope |
High Yield Summary — Diagnosis of Dizziness
-
BPPV: Diagnosed by Dix-Hallpike manoeuvre [1] — no imaging needed if classic. Atypical features → MRI to exclude central cause.
-
Vestibular neuritis vs stroke: HINTS exam in acute vestibular syndrome is > 98% sensitive for posterior circulation stroke — better than early MRI. Peripheral = +ve HIT, unidirectional nystagmus, no skew. Central = any one central sign → urgent MRI + CTA.
-
Ménière's disease: Requires audiometric documentation of low-frequency SNHL (AAO-HNS 2020). Without it, consider vestibular migraine. Meniere syndrome is overdiagnosed [1].
-
Orthostatic hypotension: Lying-standing BP with ≥ 20/10 drop within 3 minutes.
-
Cardiac syncope: ECG [1] is first-line. Holter monitor [1] for paroxysmal arrhythmias. Echocardiogram if structural disease suspected. Tilt-table for recurrent unexplained syncope. Cardiac syncope carries ~30% mortality [2][3].
-
First-line bloods: FBE, blood glucose [1], plus U&E, Ca²⁺, TFTs, B12 to screen for metabolic masquerades.
-
Neuroimaging: MRI with gadolinium [1] when suspecting acoustic neuroma, posterior fossa tumour, MS, or stroke. CT brain for acute haemorrhage exclusion. CTA for vascular pathology.
-
Key bedside tests: Dix-Hallpike, HINTS, forced hyperventilation test, lying-standing BP, Romberg, gait — these often give you the diagnosis before any lab or imaging result.
Active Recall - Diagnostic Criteria, Algorithm and Investigations for Dizziness
References
[1] Lecture slides: murtagh merge.pdf (Dizziness/vertigo section, pp. 35–37) [2] Senior notes: Ryan Ho Cardiology.pdf (Section 2.4 Syncope, pp. 62–66) [3] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.4 Syncope, pp. 207–211) [9] Senior notes: Ryan Ho Endocrine.pdf (Diabetic autonomic neuropathy, p. 98) [14] Senior notes: Ryan Ho Haemtology.pdf (Polycythaemia Vera, p. 76) [15] Senior notes: Ryan Ho Diagnostic Radiology.pdf (CT in stroke, p. 40) [16] Senior notes: Ryan Ho Diagnostic Radiology.pdf (MRI in acute stroke, p. 50) [17] Senior notes: Ryan Ho Diagnostic Radiology.pdf (CT Angiography, p. 43) [18] Senior notes: Ryan Ho Haemtology.pdf (MDS, p. 82) [19] Senior notes: Ryan Ho Haemtology.pdf (Approach to Anaemia, p. 10) [20] Senior notes: Ryan Ho Endocrine.pdf (Hypoglycaemia, p. 94; Adrenal insufficiency, p. 71) [21] Senior notes: Ryan Ho Chemical Path.pdf (Hyperkalaemia, p. 14) [22] Senior notes: Ryan Ho Neurology.pdf (GCA, p. 65; PD diagnosis, p. 122) [23] Senior notes: Ryan Ho Fundamentals.pdf (Palpitations workup, p. 207) [24] Senior notes: Ryan Ho Neurology.pdf (MS investigations, p. 136) [25] Senior notes: Ryan Ho Neurology.pdf (IIH, p. 158)
Management of Dizziness — Algorithm and Treatment Modalities
The management of dizziness is cause-specific — there is no single "dizziness pill." Once you have subcategorised the symptom and identified the underlying aetiology (as discussed in previous sections), treatment follows logically. The overall strategy can be summarised in three tiers:
- Emergency stabilisation — ABC, recognise and treat life-threatening causes (stroke, cardiac syncope, arrhythmia)
- Definitive treatment of the specific cause — canalith repositioning for BPPV, thrombolysis for stroke, pacemaker for heart block, etc.
- Symptom control and rehabilitation — vestibular suppressants (short-term only), vestibular rehabilitation therapy (long-term), lifestyle modifications
Golden Rule of Dizziness Management
Vestibular suppressant drugs (antihistamines, benzodiazepines, anticholinergics) should be used only for acute symptom relief in the first 48–72 hours. Prolonged use delays central vestibular compensation and converts an acute problem into a chronic one. The brain needs the mismatch signal to recalibrate — if you suppress it, it never learns.
3. Treatment of Specific Causes
3.1 BPPV — Canalith Repositioning Manoeuvres
BPPV is the most satisfying condition in dizziness management because it has a bedside cure with ~80% success rate in a single session.
- Principle: Use gravity-assisted sequential head positioning to guide the displaced otoconia out of the posterior semicircular canal back into the utricle (where they can be reabsorbed or remain harmlessly)
- Procedure: 5 sequential positions, each held for 30–60 seconds:
- Dix-Hallpike position (head turned 45° to affected side, lying back)
- Turn head 90° to opposite side
- Roll body to face the floor (nose pointing down)
- Sit up slowly with head still turned
- Return head to neutral
- Success rate: ~80% after single treatment; ~95% after 2–3 treatments
- Post-manoeuvre: traditionally patients were told to sleep upright for 48 hours — this is no longer recommended (no evidence of benefit)
- Contraindications: severe cervical spine disease, carotid stenosis, unstable cardiac disease, high-grade vertebrobasilar stenosis
- Principle: Repeated positional changes to habituate the vestibular system and disperse otoconia
- Procedure: Patient sits → rapidly lies on one side → holds 30s (or until dizziness resolves) → sits up → lies on opposite side. Repeat 5× each side, 3× daily
- Indication: Adjunct to or alternative if Epley is unsuccessful or not tolerated; also useful for self-treatment of recurrences
- Lempert (BBQ roll) manoeuvre: 360° sequential head rotation towards the unaffected ear while supine → guides otoconia out of the horizontal canal
- Gufoni manoeuvre: alternative for horizontal canal BPPV
Key Point — No Role for Medication in BPPV
Vestibular suppressant drugs (betahistine, meclizine, etc.) are NOT effective for BPPV and should not be used as primary treatment. Canalith repositioning is the definitive treatment. The only role for a short-acting suppressant might be to reduce nausea enough to allow the manoeuvre to be performed, but this should be the exception not the rule.
Management has three phases: acute symptom control → early mobilisation → vestibular rehabilitation.
| Phase | Timing | Treatment | Rationale |
|---|---|---|---|
| Acute symptom control | First 24–72h only | Vestibular suppressants (see Section 4 below): prochlorperazine 5–10 mg PO/IM TDS or dimenhydrinate 50 mg PO TDS or meclizine 25 mg PO TDS. Anti-emetics for nausea/vomiting. IV fluids if dehydrated | Reduce the severity of vertigo and vomiting in the most distressing acute phase. Must be stopped after 48–72h to allow central compensation |
| Corticosteroids | Start within 72h of onset | Methylprednisolone tapering course (100 mg/d → taper over 3 weeks) or prednisolone 1 mg/kg/d × 5 days then taper | Evidence is mixed but some studies show improved vestibular function recovery if started early. Why? If viral inflammation of vestibular nerve, steroids ↓inflammation → ↓nerve damage. Not universally recommended but commonly given in practice |
| Vestibular rehabilitation therapy (VRT) | Start as soon as acute symptoms allow (ideally within 1 week) | Gaze stabilisation exercises (VOR adaptation), balance training, habituation exercises, supervised by physiotherapist | The most important treatment. Central vestibular compensation requires neural plasticity — the brain must recalibrate to function with asymmetric vestibular input. VRT provides the graded sensory mismatch stimuli that drive this adaptation |
Why Must Vestibular Suppressants Be Stopped Early?
Vestibular suppressants work by dampening the vestibular signal mismatch that reaches the cortex (via H₁, mACh, and GABA receptors). This provides symptom relief but prevents the very mismatch signal that the brain needs to recalibrate. Prolonged suppressant use → delayed central compensation → chronic dizziness → the patient ends up with PPPD (persistent postural-perceptual dizziness). Maximum 48–72 hours, then stop and start rehabilitation.
Management follows a stepwise approach from conservative to interventional:
| Step | Treatment | Mechanism / Rationale | Evidence / Notes |
|---|---|---|---|
| Step 1: Lifestyle | Dietary sodium restriction (< 1.5–2 g/day), adequate hydration, avoid caffeine, alcohol, tobacco | ↓Na intake → ↓endolymphatic volume → ↓hydrops. Caffeine and alcohol are vestibulotoxic and can trigger attacks | First-line. Up to 60% of patients improve with lifestyle measures alone |
| Step 2: Diuretics | Betahistine 16–48 mg TDS (most commonly used; not available in US). Alternatively, hydrochlorothiazide 25 mg or acetazolamide | Betahistine: H₁ agonist + H₃ antagonist → ↑cochlear blood flow + ↓endolymph production. Thiazides: ↓total body fluid → ↓endolymph. Acetazolamide: CA inhibitor → ↓endolymph secretion | Betahistine widely used in HK/Europe though evidence from Cochrane is equivocal. Thiazides have moderate evidence. Often tried for 3–6 months |
| Step 3: Intratympanic therapy | Intratympanic dexamethasone (if refractory) or Intratympanic gentamicin (if very refractory) | Dexamethasone: anti-inflammatory, modulates ion transport in inner ear. Gentamicin: vestibulotoxic — selectively ablates vestibular hair cells → eliminates vertigo but risks hearing loss | Gentamicin is very effective for vertigo control (~80–90%) but carries ~30% risk of further hearing loss. Reserved for severe refractory cases with poor hearing |
| Step 4: Surgery | Endolymphatic sac decompression (hearing-preserving) or Vestibular neurectomy (selective CN VIII section) or Labyrinthectomy (destroys all inner ear function) | Sac decompression: ↓endolymphatic pressure. Neurectomy: eliminates vestibular input while preserving cochlear function. Labyrinthectomy: total vestibular ablation (only if hearing already lost) | Surgery is last resort. Labyrinthectomy is definitive but results in total unilateral deafness |
| Acute attacks | Vestibular suppressants (prochlorperazine, dimenhydrinate) + anti-emetics + bed rest | Symptom relief during the acute episode | Short courses only; same principle as vestibular neuritis — don't use chronically |
Treatment follows the same principles as migraine management [26][27]:
| Modality | Treatment | Details |
|---|---|---|
| Trigger avoidance | Dietary (alcohol, chocolate, tyramine, caffeine), hormonal (OCP, menstrual), emotional (stress), sleep (irregular), others (weather, fluorescent lights) [27] | Diary to identify personal triggers |
| Acute (abortive) treatment | Simple analgesics (paracetamol, NSAIDs) for mild attacks. Triptans (sumatriptan, zolmitriptan) for moderate-severe. Anti-emetics (metoclopramide, domperidone — D₂ blockers that also help headache) [27] | Triptans: 5HT₁B/₁D agonists → vasoconstriction + ↓trigeminal neurotransmission. C/I: IHD, stroke, CAD, uncontrolled HTN [27] |
| Prophylaxis (if frequent: ≥ 2 attacks/month or very disabling) | β-blockers (propranolol, metoprolol). Antidepressants (amitriptyline, venlafaxine). Anticonvulsants (topiramate, valproate). CCB (verapamil, flunarizine). CGRP antagonists (erenumab, fremanezumab) [27] | No specific RCTs for vestibular migraine prophylaxis — extrapolated from migraine guidelines. Propranolol and amitriptyline are most commonly used first-line |
| Vestibular rehabilitation | Balance training, habituation exercises | Useful as adjunct, particularly for inter-ictal unsteadiness and to prevent PPPD |
Treatment targets the underlying mechanism — improving venous return, expanding blood volume, or enhancing vasoconstrictor tone:
| Approach | Treatment | Mechanism | Notes |
|---|---|---|---|
| Drug review [1] | Reduce/stop offending drugs (antihypertensives, diuretics, α-blockers, TCAs, vasodilators) | Remove the iatrogenic cause of impaired vasoconstriction / volume depletion | First and most important step. "Commonly prescribed drugs… can cause dizziness" [1]. Always reassess the risk-benefit of each medication |
| Volume expansion | ↑oral fluid intake (2–3 L/day), ↑dietary salt (6–10 g/day unless HF/CKD) | ↑intravascular volume → ↑preload → ↑CO → maintains BP on standing | C/I in heart failure and severe renal disease |
| Physical measures | Compression stockings (thigh-high, 30–40 mmHg), abdominal binder; sleep with head of bed elevated 10–15°; rise slowly; physical counterpressure manoeuvres (crossing legs, squatting) | Compression: ↓venous pooling in lower extremities and splanchnic bed. Head elevation: stimulates RAAS overnight → ↑plasma volume. Counterpressure: manually ↑venous return | Non-pharmacological measures should always be tried first |
| Fludrocortisone | 0.1–0.3 mg PO daily | Mineralocorticoid → ↑renal Na⁺ and water retention → ↑blood volume + sensitises peripheral α-adrenoceptors to NE | S/E: hypokalaemia, supine hypertension, ankle oedema, HF exacerbation. C/I: HF, severe renal impairment |
| Midodrine | 2.5–10 mg PO TDS (avoid taking within 4h of bedtime) | α₁-adrenergic agonist → peripheral vasoconstriction → ↑SVR → ↑BP | S/E: supine hypertension (must avoid supine position within 4h of dose), piloerection, urinary retention. C/I: severe heart disease, acute renal failure, phaeochromocytoma |
| Droxidopa | 100–600 mg TDS | Norepinephrine prodrug → converted to NE → ↑sympathetic vasoconstriction | Used in neurogenic orthostatic hypotension (Parkinson's, MSA, autonomic failure). S/E: headache, dizziness, supine HTN |
Management is primarily non-pharmacological — the key is education and trigger avoidance [2][3]:
| Modality | Treatment | Mechanism / Rationale |
|---|---|---|
| Education and reassurance | Explain the benign nature; identify and avoid triggers (prolonged standing, dehydration, heat, alcohol) | Patients are often very anxious after syncope — reassurance is therapeutic |
| Recognition of prodrome | Teach patients to recognise early warning signs (lightheadedness, nausea, sweating, visual dimming) and immediately lie down or assume counterpressure position | Early intervention prevents full syncope by maintaining cerebral perfusion |
| Physical counterpressure manoeuvres | Leg crossing + tensing, squatting, hand grip (isometric exercises when prodrome begins) | ↑venous return → ↑CO → maintains BP → aborts the faint |
| Adequate hydration and salt intake | 2–3 L fluid/day, ↑dietary salt | ↑blood volume → ↑preload → harder to trigger the reflex |
| Compression garments | Waist-high compression stockings (30–40 mmHg) | ↓venous pooling → ↑venous return |
| Tilt training | Progressive standing against a wall for increasing durations | Desensitisation of the vasovagal reflex over time — evidence is modest but some patients benefit |
| Pharmacological (if refractory) | Midodrine (α₁-agonist): best evidence among drugs. Fludrocortisone: volume expansion. β-blockers (controversial, no longer routinely recommended). SSRIs (some evidence for ↓recurrence) | Reserved for frequent, recurrent, disabling episodes unresponsive to non-pharmacological measures |
| Tilt-table test [2][3] | Diagnostic (not treatment), but useful in recurrent unexplained cases | Confirms neurocardiogenic mechanism; guides management |
| Permanent pacemaker | Dual-chamber pacing with rate-drop response algorithm | Only for highly selected patients with documented prolonged asystole (> 3 seconds) during syncope on ILR, and predominantly cardioinhibitory pattern. Not effective for vasodepressor-type |
Treatment is cause-specific — this is cardiology territory and potentially life-saving:
| Cause | Treatment | Key points |
|---|---|---|
| Arrhythmias [1] | Bradycardia: atropine 0.5 mg IV (first-line for acute symptomatic bradycardia; max 3 mg) → temporary pacing (TCP then TVP) → permanent pacemaker for 3° HB, Mobitz II [28][29]. Tachycardia: rate/rhythm control per ACLS (amiodarone, cardioversion for unstable VT; adenosine for SVT; rate control for AF) [30] | "If haemodynamically unstable, give atropine followed by pacing" [28][29]. Pacemaker indications: symptomatic bradycardia, complete heart block, Mobitz II |
| Myocardial infarction [1] | ACS protocol: dual antiplatelet + anticoagulant + statin + β-blocker + ACEI/ARB. Revascularisation: PCI for STEMI, PCI/CABG for NSTEMI based on risk stratification [30] | Dizziness/syncope may be the presenting complaint of MI, especially in elderly/diabetics ("angina equivalent" [30]) |
| Aortic stenosis [1] | Symptomatic severe AS → surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI). Medical management (diuretics, cautious vasodilators) is temporising only | Exertional syncope in AS = high-risk → warrants urgent cardiology referral. Medical therapy alone carries poor prognosis (50% 2-year mortality if symptomatic) |
This is a neurological emergency [1]. Treatment follows the acute ischaemic stroke pathway:
| Phase | Treatment | Details |
|---|---|---|
| Acute stroke pathway | IV thrombolysis (alteplase 0.9 mg/kg, 10% bolus then 90% over 60 min) if within 4.5 hours of symptom onset. Endovascular thrombectomy if large vessel occlusion within up to 24 hours (based on perfusion imaging) | Same eligibility criteria as anterior circulation stroke. BP must be ≤ 185/110 before thrombolysis [26] |
| General measures | ABC, maintain SpO₂ > 94%, blood glucose 7.8–10.0 mmol/L, permissive hypertension (do not lower BP unless > 220/120 in non-thrombolysis patients) [26], fever control | BP should be CAREFULLY LOWERED since some degree of elevation may be necessary to maintain cerebral blood flow to ischaemic regions [26] |
| Cerebellar stroke with mass effect | Urgent neurosurgery: suboccipital decompressive craniectomy ± external ventricular drain (EVD) for obstructive hydrocephalus | Posterior fossa has very limited space → even a small infarct with oedema can compress the brainstem → fatal if not decompressed |
| Secondary prevention | Antiplatelet (aspirin + clopidogrel for 21 days then monotherapy), statin, BP control, glycaemic control, smoking cessation, AF management (anticoagulation if cardioembolic) | Long-term strategy to prevent recurrence |
| Approach | Indication | Details |
|---|---|---|
| Watch and wait (observation with serial MRI) | Small tumours (< 1–1.5 cm), elderly patients, minimal symptoms | Many vestibular schwannomas grow very slowly (~1–2 mm/year); serial MRI every 6–12 months |
| Stereotactic radiosurgery (Gamma Knife) | Small-medium tumours (< 2.5–3 cm), patients unfit for surgery | Focused radiation to arrest growth; ~90–95% tumour control rate; hearing preservation ~50–70% |
| Microsurgical excision | Large tumours (> 3 cm), brainstem compression, rapid growth | Definitive removal; risk of facial nerve (CN VII) injury |
| Condition | Treatment | Rationale |
|---|---|---|
| Anxiety–hyperventilation [1] | Reassurance (the most therapeutic intervention). Breathing retraining (slow diaphragmatic breathing). CBT (cognitive behavioural therapy). ± SSRI/SNRI if GAD or panic disorder diagnosed [31] | Address the underlying anxiety; correct the hyperventilation pattern; SSRIs modulate serotonergic tone in amygdala → ↓anxiety |
| PPPD | Vestibular rehabilitation therapy (core treatment). CBT. SSRI/SNRI (sertraline 50–200 mg or venlafaxine 75–225 mg) | PPPD is a maladaptive central processing disorder — VRT retrains the vestibular processing; SSRIs may modulate the serotonergic component of vestibular processing and reduce the associated anxiety |
| Depression [1] | Antidepressants + psychotherapy per depression guidelines. Address underlying dizziness if identifiable organic cause | Depression can present as dizziness (Murtagh masquerade) [1] |
| Somatic symptom disorder | Therapeutic alliance, scheduled visits, CBT, ± SSRI [31] | Avoid excessive investigation; validate symptoms; "high health care utilization: doctor-shopping" [31] |
| Cause | Treatment | Key principle |
|---|---|---|
| Anaemia [1] | Treat underlying cause (iron supplementation for IDA, B12/folate for megaloblastic, transfusion if acute/severe) | Dizziness resolves as Hb normalises and O₂ delivery improves |
| Hypoglycaemia [1] | Oral carbohydrates if conscious (15–20 g glucose); IV dextrose (D50 40 mL stat → D10 drip) if unconscious; IM glucagon 1 mg if no IV access [20] | Correct neuroglycopenia → symptoms resolve within minutes |
| Thyroid disorder [1] | Levothyroxine for hypothyroidism; antithyroid drugs (carbimazole/PTU) or radioactive iodine or surgery for hyperthyroidism | Correct the metabolic derangement |
| Drug-induced [1] | Medication review and adjustment — reduce dose, switch to alternative, or stop offending drug | "Commonly prescribed drugs… can cause dizziness" [1] — this is the single most correctable cause of dizziness in the elderly |
| Hyponatraemia | Fluid restriction (SIADH), saline replacement (hypovolaemic), treat underlying cause | Correct slowly (≤ 8–10 mmol/L per 24h) to avoid osmotic demyelination syndrome |
These drugs are used for acute symptomatic relief only (first 48–72 hours). They target the receptors involved in vestibular signal transmission:
| Drug class | Examples | Mechanism | Indications | Key S/E | C/I |
|---|---|---|---|---|---|
| Antihistamines (H₁ blockers) | Meclizine 25 mg TDS, cinnarizine 25 mg TDS, dimenhydrinate 50 mg TDS, promethazine 25 mg TDS | Block H₁ receptors in vestibular nuclei → ↓vestibular signal transmission + anticholinergic properties → also ↓CTZ activation | Acute vertigo, motion sickness | Sedation (anti-H₁ in CNS), dry mouth (anticholinergic), blurred vision, urinary retention | Glaucoma, BPH (anticholinergic effects), elderly (↑falls risk from sedation) |
| Anticholinergics | Hyoscine (scopolamine) patch/PO | Block muscarinic (mACh) receptors in vestibular nuclei and vomiting centre → ↓vestibular signal and ↓emesis | Motion sickness (best prophylaxis), acute vertigo | Dry mouth, blurred vision, constipation, urinary retention, sedation, confusion (esp elderly) | Glaucoma, BPH, elderly with dementia |
| Phenothiazines | Prochlorperazine (Stemetil) 5–10 mg PO/IM TDS | D₂ antagonist at CTZ + H₁ blocker → anti-emetic + mild vestibular suppression | Acute vertigo with prominent N/V, Ménière's attacks | Extrapyramidal S/E (acute dystonia — especially in young), sedation, postural hypotension | Parkinson's disease (D₂ antagonism worsens PD), children < 10 kg (dystonia risk) |
| Benzodiazepines | Diazepam 2–5 mg PO/IV BD-TDS, lorazepam 0.5–1 mg PO/SL BD | GABA_A receptor positive allosteric modulator → ↓vestibular nuclei excitability + anxiolytic + muscle relaxant | Acute severe vertigo (especially if anxious); vestibular neuritis first 48h | Sedation, respiratory depression, dependence, cognitive impairment, ↑falls risk | Respiratory failure, myasthenia gravis, alcohol intoxication, severe hepatic impairment |
| Betahistine | Betahistine 16–48 mg TDS | H₁ agonist (↑cochlear blood flow) + H₃ antagonist (↑histamine release in vestibular nuclei — paradoxically aids compensation) | Ménière's disease (long-term), chronic vestibular symptoms | Generally well-tolerated; GI upset, headache | Phaeochromocytoma (histamine release → catecholamine surge), active peptic ulcer |
| Corticosteroids | Prednisolone 1 mg/kg/d taper, methylprednisolone IV taper, intratympanic dexamethasone | Anti-inflammatory → ↓vestibular nerve oedema (vestibular neuritis), ↓inner ear inflammation (Ménière's) | Vestibular neuritis (systemic), Ménière's (intratympanic) | Hyperglycaemia, GI upset, insomnia, adrenal suppression (if prolonged), osteoporosis | Active infection (relative), DM (monitor glucose), psychosis |
Drug Breakdown — Betahistine
"Beta" + "histine" = related to histamine. Betahistine is a structural analogue of histamine that acts as an H₁ agonist and H₃ antagonist:
- H₁ agonism → vasodilation of cochlear vessels → ↑cochlear blood flow → may ↓endolymphatic hydrops
- H₃ antagonism → blocks the autoinhibitory H₃ presynaptic receptor → ↑histamine release in vestibular nuclei → paradoxically helps vestibular compensation (histamine is involved in central vestibular processing)
This is why betahistine is the most commonly prescribed long-term vestibular drug for Ménière's disease, particularly in Europe and Hong Kong. It is not a vestibular suppressant in the same way antihistamines are — it is more of a "vestibular modulator."
VRT is arguably the single most important treatment modality across all chronic vestibular conditions. It is evidence-based, non-pharmacological, and addresses the root problem — impaired central compensation.
| Component | Exercises | Mechanism | Indication |
|---|---|---|---|
| Gaze stabilisation | VOR adaptation exercises: fixate on a target while moving the head (×1 and ×2 viewing) | Drives neural plasticity in the VOR pathway → recalibrates the VOR gain for the new asymmetric input | Unilateral vestibular loss (vestibular neuritis), bilateral vestibulopathy |
| Habituation | Repeated exposure to movements and positions that provoke dizziness (in a graded, controlled manner) | Repeated exposure → ↓central response to the abnormal signal (habituation, a form of neural adaptation) | BPPV (residual), PPPD, chronic dizziness, motion sensitivity |
| Balance training | Standing exercises on unstable surfaces, tandem walking, single-leg stance, with/without visual input, eyes open → eyes closed | Challenges the postural control system → promotes sensory reweighting (↑reliance on intact systems, ↓reliance on damaged system) | All vestibular disorders, falls prevention in elderly, sensory ataxia |
| Walking exercises | Guided walking with head turns, walking on different surfaces | Integrates vestibular, visual, and proprioceptive input in a real-world functional context | All vestibular disorders |
Evidence: Cochrane review shows VRT is effective and safe for unilateral peripheral vestibular dysfunction, with moderate-to-strong evidence for reducing symptoms, improving function, and improving quality of life.
"Dizziness is often multifactorial, especially in the elderly" [1]. The approach must address all contributing factors simultaneously:
| Factor | Intervention |
|---|---|
| Medication review [1] | Reduce polypharmacy; stop/reduce antihypertensives, sedatives, anticholinergics where safe |
| Orthostatic hypotension | Lying-standing BP; drug review, compression stockings, salt/fluid, ± midodrine/fludrocortisone |
| Visual impairment | Ophthalmology referral; correct refractive errors; cataract surgery |
| Hearing loss | Hearing aids; audiological rehabilitation |
| Peripheral neuropathy | Glycaemic control; B12 supplementation; physiotherapy |
| Cervical spondylosis | Physiotherapy; gentle neck exercises; avoid sudden neck movements |
| Deconditioning | Graded exercise programme; vestibular rehabilitation |
| Falls prevention | Home hazard assessment; walking aids; strength and balance training; hip protectors |
| Depression/anxiety | Screen and treat; SSRIs if indicated; CBT; social support |
| Cognitive impairment | Assess for dementia; simplify medication regimens; carer support |
| Cause | First-line treatment | Second-line / Refractory | Key drug to remember |
|---|---|---|---|
| BPPV | Epley manoeuvre [1] | Brandt-Daroff exercises; repeat Epley; surgical canal occlusion (very rare) | None (medication NOT first-line) |
| Vestibular neuritis | Short-term suppressants + corticosteroids + early VRT | Prolonged VRT; ± betahistine | Prednisolone (early); prochlorperazine (acute N/V only) |
| Ménière's disease | Salt restriction + betahistine + lifestyle | Diuretics; intratympanic steroids/gentamicin; surgery | Betahistine 16–48 mg TDS |
| Vestibular migraine | Trigger avoidance + acute abortive Rx | Prophylaxis: propranolol / amitriptyline / topiramate | Propranolol (prophylaxis); sumatriptan (acute) |
| Orthostatic hypotension | Drug review [1] + fluid/salt + physical measures | Midodrine; fludrocortisone | Midodrine 2.5–10 mg TDS |
| Vasovagal syncope | Education + trigger avoidance + counterpressure | Midodrine; pacemaker (if documented asystole) | Midodrine (if pharmacotherapy needed) |
| Cardiac arrhythmia | Per ACLS / cardiology guidelines | Permanent pacemaker; ICD; ablation | Atropine (acute bradycardia) [28][29] |
| Posterior circulation stroke | Acute stroke pathway: thrombolysis ± thrombectomy | Decompressive surgery if cerebellar mass effect | Alteplase 0.9 mg/kg (within 4.5h) |
| Acoustic neuroma | Watch and wait (small) | Gamma Knife radiosurgery; microsurgery (large) | None (surgical management) |
| Anxiety/hyperventilation | Reassurance + breathing retraining + CBT | SSRI/SNRI | Sertraline / escitalopram |
| PPPD | VRT + CBT + SSRI/SNRI | Prolonged multidisciplinary rehabilitation | Sertraline 50–200 mg |
| Drug-induced | Medication review [1] | Switch/reduce/stop offending agents | — |
| Multifactorial (elderly) | Comprehensive multidisciplinary approach | Address each contributing factor | — |
High Yield Summary — Management of Dizziness
-
BPPV: Epley manoeuvre [1] is the definitive treatment (~80% cure in one session). Medications are NOT first-line.
-
Vestibular neuritis: Short-term suppressants (≤ 72h only!) → corticosteroids → early vestibular rehabilitation (the most important intervention). Prolonged suppressant use delays compensation and causes chronicity.
-
Ménière's disease: Stepwise — lifestyle (salt, caffeine, alcohol) → betahistine/diuretics → intratympanic steroids/gentamicin → surgery.
-
Vestibular migraine: Same as migraine — trigger avoidance + abortive Tx (triptans) + prophylaxis (propranolol, amitriptyline, topiramate, CGRP antagonists).
-
Orthostatic hypotension: Drug review first [1] → fluids/salt/compression → midodrine/fludrocortisone.
-
Vasovagal syncope: Education, trigger avoidance, counterpressure manoeuvres; pharmacotherapy (midodrine) or pacemaker only if refractory with documented asystole.
-
Cardiac causes: Treat the underlying arrhythmia/structural disease per cardiology guidelines — potentially life-saving.
-
Posterior circulation stroke: Neurological emergency — acute stroke pathway (thrombolysis ± thrombectomy).
-
Anxiety/PPPD: Reassurance, CBT, SSRI/SNRI, vestibular rehabilitation.
-
Elderly multifactorial: Address ALL contributing factors — drug review, vision, hearing, neuropathy, exercise, falls prevention, mood.
-
Universal principle: Vestibular rehabilitation therapy is beneficial in almost all chronic vestibular conditions.
Active Recall - Management of Dizziness
References
[1] Lecture slides: murtagh merge.pdf (Dizziness/vertigo section, pp. 35–37) [2] Senior notes: Ryan Ho Cardiology.pdf (Section 2.4 Syncope and neurocardiogenic syncope, pp. 63–66) [3] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.4 Syncope, pp. 208–211) [20] Senior notes: Ryan Ho Endocrine.pdf (Hypoglycaemia management, p. 94) [26] Senior notes: felixlai.md (Ischaemic stroke management, sections 1697–1704) [27] Senior notes: Ryan Ho Neurology.pdf (Migraine treatment, pp. 59–63) [28] Senior notes: Ryan Ho Cardiology.pdf (Bradyarrhythmia management, p. 88) [29] Senior notes: Ryan Ho Critical Care.pdf (Symptomatic bradyarrhythmia management, p. 41) [30] Senior notes: Ryan Ho Cardiology.pdf (Post-MI arrhythmia management, p. 139) [31] Senior notes: Ryan Ho Psychiatry.pdf (Anxiolytics and SSD, pp. 60, 202)
Complications of Dizziness and Its Underlying Causes
Dizziness itself is a symptom, not a disease — so when we talk about "complications," we must think on two levels:
- Complications arising from the symptom of dizziness itself (regardless of cause) — falls, injuries, functional impairment, psychological impact
- Complications of the specific underlying conditions that present as dizziness — these are cause-specific and range from benign to life-threatening
Understanding complications matters because they often determine prognosis, guide management urgency, and inform patient counselling. Let me walk through these systematically.
1. Complications of Dizziness as a Symptom (Universal)
These complications apply to any cause of dizziness and are mediated by the core problem: impaired spatial orientation and/or cerebral perfusion.
- Mechanism: Dizziness impairs balance and postural control → falls, especially in the elderly
- Vertigo → sudden loss of spatial orientation → patient loses balance and falls unpredictably
- Presyncope/syncope → ↓cerebral perfusion → LOC → uncontrolled fall with no protective reflexes
- Disequilibrium → chronic unsteadiness → recurrent stumbles and falls
- Consequences of falls:
- Fractures: hip fracture (the most feared — carries ~20–30% 1-year mortality in elderly), Colles' fracture (falling on outstretched hand), vertebral compression fractures
- Head injuries: subdural haematoma (especially in elderly on anticoagulants — the bridging veins are fragile), traumatic brain injury, concussion
- Soft tissue injuries: lacerations, bruising, sprains
- Scale of the problem: Dizziness is one of the top risk factors for falls in the elderly. Among community-dwelling adults > 65y, ~30% fall each year, and dizziness is an independent predictor.
Clinical Pearl — The Vicious Cycle of Falls
Fall → injury (e.g., hip fracture) → hospitalisation → deconditioning + delirium → worsened dizziness → ↑falls risk. This is the falls cascade that makes dizziness in the elderly a geriatric emergency to address proactively. "Dizziness is often multifactorial, especially in the elderly" [1] — and falls prevention must be a core component of management.
When dizziness progresses to syncope (LOC), the risk is amplified because the patient collapses without protective reflexes (cf. a conscious person who can brace for impact):
- Sudden collapse → head strike → traumatic brain injury, facial lacerations
- During driving → motor vehicle accident (potentially fatal for patient and others)
- During hazardous activity → drowning (swimming), burns (cooking), workplace injuries (operating machinery)
Cardiac syncope carries ~30% mortality [2][3] — the mortality isn't just from the underlying arrhythmia/AS/MI, but also from the injuries sustained during the syncopal fall.
- Fear of falling (ptophobia): After an episode of dizziness or a fall, many patients (especially elderly) develop an intense fear of falling → self-imposed activity restriction → deconditioning → worsened balance → ↑falls risk → vicious cycle
- Anxiety and depression: Chronic dizziness is strongly associated with the development of anxiety disorders (panic disorder, agoraphobia) and depression [1]
- "Is the patient trying to tell me something? Very likely. Consider anxiety and/or depression" [1]
- The relationship is bidirectional: anxiety causes dizziness (hyperventilation), and dizziness causes anxiety (fear of undiagnosed illness, fear of falls, activity limitation)
- Social isolation: Avoidance of activities (shopping, socialising, exercise) due to dizziness → loneliness, depression, loss of independence
- Reduced quality of life: Chronic dizziness consistently ranks as one of the most disabling symptoms in patient surveys — often more distressing than chronic pain
- Cognitive impairment: Particularly in elderly patients with multifactorial dizziness — the combination of polypharmacy, deconditioning, depression, and social isolation accelerates cognitive decline
- Impaired activities of daily living: Difficulty with ambulation, transfers, housework
- Inability to drive: Particularly relevant in syncope (many jurisdictions have legal driving restrictions after a syncopal episode) and in chronic severe vertigo
- Occupational disability: Inability to work, especially in jobs requiring balance (construction, roofing), driving, or operating heavy machinery
- Economic impact: Lost productivity, healthcare utilisation costs, need for home care or residential care
Dizziness often prompts the use of vestibular suppressants, which carry their own complications:
- Sedation → ↑falls risk, impaired cognition, ↓driving ability
- Prolonged vestibular suppressant use → delayed central compensation → chronic dizziness → progression to PPPD (persistent postural-perceptual dizziness)
- Why? The brain needs the vestibular mismatch signal to recalibrate its balance processing. Suppressants dampen this signal → the brain never learns to compensate → the dizziness becomes self-perpetuating
- Anticholinergic burden (from antihistamines, anticholinergics) → dry mouth, urinary retention, constipation, confusion (especially in elderly)
- Drug interactions: Adding a vestibular suppressant to an already polymedicated elderly patient → synergistic sedation and hypotension
2. Complications of Specific Underlying Conditions
BPPV is the most benign of the vertigo causes — no structural damage occurs. However:
| Complication | Mechanism | Frequency | Notes |
|---|---|---|---|
| Recurrence | Otoconia re-dislodge into the SCC (ongoing degeneration, especially in elderly/osteoporosis) | 15–20% recurrence per year; 50% lifetime recurrence | Patients should be taught Brandt-Daroff exercises for self-management of recurrences |
| Residual dizziness | After successful canalith repositioning, some patients have persistent vague unsteadiness for days to weeks | 30–60% after Epley | Due to transient otolith dysfunction and/or anxiety; resolves spontaneously or with vestibular rehabilitation |
| Canal conversion | Otoconia migrate from posterior canal into horizontal canal during repositioning manoeuvre | ~5–10% during Epley | Requires supine roll test and Lempert/BBQ manoeuvre for the horizontal canal |
| Falls and injuries | As above (section 1.1) — during acute vertigo episodes | Variable | Particular risk in elderly patients with early-morning attacks (rolling over in bed → vertigo → fall out of bed) |
| Progression to PPPD | Maladaptive central processing after the acute event | ~15–25% of BPPV patients develop chronic non-specific dizziness | Treated with vestibular rehabilitation + CBT ± SSRI |
| Complication | Mechanism | Frequency | Management |
|---|---|---|---|
| Incomplete vestibular compensation | Brain fails to fully recalibrate to asymmetric vestibular input → persistent unsteadiness | 30–40% have residual symptoms at 1 year | Vestibular rehabilitation therapy is the treatment — this is why early VRT is so important |
| PPPD (chronic subjective dizziness) | Maladaptive central processing: the "software" never recalibrates despite peripheral "hardware" recovery | 10–25% | VRT + CBT + SSRI/SNRI |
| Secondary BPPV | Vestibular neuritis damages the utricle → otoconia degenerate and dislodge into the SCC | 10–15% within first year | Standard BPPV treatment (Epley manoeuvre) |
| Anxiety and depression | Sudden, severe, prolonged vertigo is a terrifying experience → conditioned fear response → avoidance behaviour | Common (up to 50%) | Reassurance, CBT, ± pharmacotherapy |
| Bilateral sequential involvement | Second ear affected later (rare in viral vestibular neuritis; consider autoimmune or vascular cause if occurs) | < 2% | Investigate for alternative aetiology (autoimmune inner ear disease) |
| Complication | Mechanism | Frequency | Clinical significance |
|---|---|---|---|
| Progressive hearing loss | Repeated endolymphatic hydrops → cumulative damage to cochlear hair cells → permanent SNHL | Almost universal in long-standing disease | Initially low-frequency and fluctuating; becomes flat, severe, and permanent over years |
| Bilateral involvement | Endolymphatic hydrops develops in the contralateral ear | ~30% over 10–20 years | Devastating — bilateral fluctuating hearing loss + vertigo; hearing aids/cochlear implants needed |
| "Burnt-out" Ménière's | End-stage: complete vestibular ablation from repeated damage → no more vertigo attacks, but permanent hearing loss + chronic imbalance | Late disease | Vertigo stops (no functioning vestibular organ to generate mismatch), but the price is profound hearing loss |
| Drop attacks (Tumarkin crises) | Sudden mechanical distortion of otolith organs by hydrops → acute loss of vestibular tone → sudden fall without LOC or vertigo | 5–10% | Extremely dangerous — patient falls suddenly with no warning and no protective reflexes → high injury risk |
| Psychological impact | Unpredictable attacks → anxiety, agoraphobia, depression, social isolation | Very common | Drives significant disability even between attacks |
| Complication | Mechanism | Clinical context |
|---|---|---|
| Traumatic injuries | Fall from syncope without protective reflexes (see section 1.2) | Any syncope; more severe in cardiac syncope (sudden onset) |
| Sudden cardiac death | Underlying arrhythmia (VT/VF, complete heart block) or structural disease (severe AS, HCM) that caused the syncope also causes fatal arrhythmia | Cardiac syncope carries ~30% mortality [2][3] — this is the most dangerous complication of the dizziness-syncope spectrum |
| Recurrent syncope | Failure to identify and treat the underlying cause | Especially vasovagal (40–50% recurrence at 4 years), cardiac, orthostatic hypotension |
| Driving accidents / occupational injuries | Syncope while driving or operating machinery | Many jurisdictions mandate driving cessation for 6–12 months after syncope (varies by cause and local law) |
| Aspiration | LOC → loss of airway protective reflexes → aspiration of gastric contents | Especially if associated vomiting (which is common in vasovagal syncope prodrome) |
This is the most feared complication of what may initially present as "just dizziness." The complications of posterior circulation stroke mirror stroke complications in general [32][33]:
| Category | Complications | Mechanism |
|---|---|---|
| Cerebral | Cerebral oedema → ↑ICP → herniation (tonsillar herniation in posterior fossa is rapidly fatal as it compresses the brainstem); haemorrhagic transformation (30–40% of ischaemic strokes); seizures; obstructive hydrocephalus (4th ventricle obstruction) | "Posterior cranial fossa infarct with oedema → obstruction of CSF drainage → hydrocephalus ± coning → death" [33] |
| Neurological deficits | Permanent vertigo/imbalance; diplopia; dysarthria; dysphagia; ataxia; facial numbness; Horner's syndrome; locked-in syndrome (basilar artery occlusion) | Irreversible neuronal death in brainstem/cerebellar territories |
| Aspiration pneumonia | Dysphagia from brainstem lesion (CN IX, X) → aspiration of food/saliva → pneumonia | "Infections: bronchopneumonia, aspiration pneumonia" [33] — this is one of the leading causes of death post-stroke |
| DVT / PE | Immobilisation → venous stasis (Virchow's triad) | "DVT, PE" [33] — VTE prophylaxis is essential |
| Pressure sores | Immobilisation → sustained pressure on skin → ischaemic necrosis | "Pressure sores: reposition weak limbs, frequent turning" [33] |
| Post-stroke depression | Multifactorial: neurochemical changes from stroke + reaction to disability + social isolation | "Prevalence of depression observed at any time after stroke = 29%" [32]; "depression at 3 months is correlated with poor outcome at 1 year" [32] |
| UTI | Bladder dysfunction from brainstem lesion + catheterisation | Common source of post-stroke infection and delirium |
| Contractures and frozen shoulder | Immobilisation → muscle shortening + joint capsule fibrosis | "Prolonged immobilization: pressure sores, contractures, frozen shoulder, shoulder subluxation" [33] |
| Cardiac complications | Stroke → sympathetic surge → MI, arrhythmias; also pre-existing CVS disease (same risk factors) | "CVS disturbances" [33] |
Why Posterior Fossa Strokes Are Particularly Dangerous
The posterior cranial fossa is a tight, rigid space (bounded by the tentorium cerebelli above and the foramen magnum below). Even a small infarct with modest oedema can:
- Compress the brainstem → respiratory arrest, coma, death
- Obstruct the 4th ventricle → obstructive hydrocephalus → rapid ↑ICP → herniation
This is why cerebellar/brainstem strokes require immediate neurosurgical assessment for possible suboccipital decompressive craniectomy and/or external ventricular drain (EVD) [33]. Time is even more critical than in supratentorial strokes.
| Complication | Mechanism | Significance |
|---|---|---|
| Progressive sensorineural hearing loss | Compression of cochlear nerve fibres by growing tumour | The most common presenting symptom; progressive and unilateral |
| Facial nerve (CN VII) palsy | Tumour compression or surgical damage during resection | CN VII runs in close proximity to CN VIII in the CPA and IAC; facial weakness is a dreaded complication of surgery (5–30% depending on tumour size and surgical approach) |
| Trigeminal nerve (CN V) involvement | Large tumour compresses CN V at CPA | Facial numbness, absent corneal reflex → risk of corneal ulceration (loss of protective blink) |
| Brainstem compression | Large tumour (> 3 cm) compresses pons/medulla | Obstructive hydrocephalus (4th ventricle), cerebellar ataxia, cranial nerve palsies, potentially fatal |
| Obstructive hydrocephalus | Tumour obstructs CSF flow at 4th ventricle | ↑ICP → headache, N/V, papilloedema, altered consciousness |
| Complications of treatment | Surgery: facial nerve injury, CSF leak, meningitis, hearing loss. Radiosurgery: radiation-induced oedema, delayed facial nerve neuropathy, rarely malignant transformation | Treatment itself carries morbidity — this is why "watch and wait" is appropriate for small, minimally symptomatic tumours |
| Cause | Specific complications | Why |
|---|---|---|
| Arrhythmias [1] | Sudden cardiac death (VF, VT → cardiac arrest); thromboembolism (AF → LA thrombus → stroke); heart failure (tachycardia-mediated cardiomyopathy from sustained tachyarrhythmia) | Arrhythmias can be immediately life-threatening or cause slow cardiac deterioration |
| Myocardial infarction [1] | Cardiogenic shock (↓CO from LV dysfunction); mechanical complications (papillary muscle rupture → acute MR, VSD, free wall rupture); arrhythmias (VT/VF); heart failure | MI presenting as dizziness may be undertreated if not recognised as an "angina equivalent" |
| Aortic stenosis [1] | Sudden cardiac death (if symptomatic severe AS, 50% 2-year mortality without valve replacement); heart failure (LVH → diastolic then systolic dysfunction); endocarditis | Exertional syncope in AS is a red flag for impending sudden death → urgent cardiology referral |
| Complication | Mechanism |
|---|---|
| Falls and fractures | ↓BP on standing → presyncope → falls (see section 1.1) |
| Supine hypertension (from treatment) | Fludrocortisone / midodrine raise baseline BP → patient may be hypertensive when lying down → ↑risk of end-organ damage. This is the main treatment-related complication |
| Cerebral hypoperfusion (chronic) | Repeated episodes of orthostatic hypotension → transient cerebral ischaemia → may contribute to cognitive decline and white matter disease over time |
| Cardiac ischaemia | In patients with coexisting IHD, ↓BP episodes can provoke demand ischaemia |
| Complication | Mechanism |
|---|---|
| Chronicity and disability | PPPD can persist for months to years → significant functional impairment, lost work days, reduced QoL |
| Somatisation and doctor-shopping | Repeated presentations with unexplained dizziness → unnecessary investigations (CT, MRI, blood tests) → radiation exposure, healthcare costs, incidental findings that generate further anxiety |
| Iatrogenic harm | Chronic vestibular suppressant prescriptions (BZDs, antihistamines) → sedation, dependence, falls, delayed compensation |
| Comorbid psychiatric disorders | Depression (30–60%), panic disorder, agoraphobia → further functional decline |
| Hyperventilation → tetany | Severe respiratory alkalosis → ↓ionised Ca²⁺ → carpopedal spasm, perioral tingling → further panic → more hyperventilation (positive feedback loop) |
Post head injury [1] can lead to prolonged complications:
| Complication | Mechanism | Frequency |
|---|---|---|
| Post-concussion syndrome | Neurobiological (axonal injury, neuroinflammation) + psychogenic factors → persistent headache (25–78%), dizziness, sleep disturbance, neuropsychiatric symptoms [34] | 10–30% after mild TBI |
| Post-traumatic BPPV | Trauma dislodges otoconia → BPPV; may be bilateral (cf. spontaneous BPPV which is usually unilateral) | Most common cause of post-traumatic vertigo |
| Perilymphatic fistula | Trauma causes a breach in the oval or round window membrane → perilymph leakage → vestibular dysfunction + hearing loss | Rare but important; worsened by Valsalva/straining |
| Chronic subdural haematoma | Especially in elderly patients on anticoagulants — initial head injury from fall may seem trivial → slow accumulation of blood over weeks → progressive headache, confusion, dizziness, focal deficits | Must consider in any elderly patient with progressive dizziness weeks after a fall |
Multiple sclerosis [1] presenting with dizziness may progress to:
| Complication | Mechanism |
|---|---|
| Progressive neurological disability | Accumulating demyelinating lesions → spasticity, weakness, cerebellar ataxia, visual loss, cognitive decline |
| Internuclear ophthalmoplegia (INO) | MLF lesion → impaired adduction + contralateral abducting nystagmus → diplopia and dizziness with lateral gaze |
| Brainstem syndromes | Multiple lesions in brainstem → complex combinations of cranial nerve palsies, vertigo, ataxia |
| Trigeminal neuralgia | Demyelination at trigeminal root entry zone → paroxysmal severe facial pain |
| Severity | Complication | Associated conditions |
|---|---|---|
| Life-threatening | Sudden cardiac death | Cardiac arrhythmias, aortic stenosis |
| Brainstem herniation | Posterior circulation stroke, posterior fossa tumour, cerebellar haemorrhage | |
| Fatal arrhythmia post-MI | MI presenting as dizziness | |
| Traumatic brain injury from fall | Any cause of syncope | |
| Serious | Stroke (ischaemic) | AF, VBI, carotid disease |
| Hip fracture | Falls from any dizziness cause (elderly) | |
| Aspiration pneumonia | Posterior circulation stroke (dysphagia) | |
| Progressive hearing loss | Ménière's disease, acoustic neuroma | |
| Post-stroke depression | Posterior circulation stroke | |
| Moderate | Chronic dizziness / PPPD | Vestibular neuritis, BPPV (incomplete compensation) |
| Anxiety and depression | Any chronic dizziness | |
| BPPV recurrence | BPPV | |
| Drug side effects | Vestibular suppressant overuse | |
| Mild | Residual unsteadiness | Post-vestibular neuritis |
| Social isolation | Chronic dizziness | |
| Driving restriction | Syncope |
High Yield Summary — Complications of Dizziness
Universal complications of dizziness (any cause):
- Falls → fractures (hip fracture: 20–30% 1-year mortality in elderly), head injuries, soft tissue injuries
- Syncope-related injuries (driving accidents, drowning, workplace injuries)
- Psychological: anxiety, depression, fear of falling → activity restriction → deconditioning → vicious cycle
- Functional disability: impaired ADLs, inability to drive/work, social isolation
- Iatrogenic: prolonged vestibular suppressant use → delayed compensation → PPPD; anticholinergic burden in elderly
Condition-specific complications to remember:
- BPPV: Benign but high recurrence (50% lifetime); residual dizziness; progression to PPPD
- Vestibular neuritis: Incomplete compensation (30–40%); secondary BPPV (10–15%); PPPD
- Ménière's disease: Progressive hearing loss; bilateral involvement (30%); Tumarkin drop attacks; "burnt-out" phase
- Cardiac syncope: 30% mortality [2][3]; sudden cardiac death; traumatic injury from uncontrolled fall
- Posterior circulation stroke: Brainstem herniation; obstructive hydrocephalus; aspiration pneumonia; post-stroke depression (29%); DVT/PE; pressure sores
- Acoustic neuroma: CN VII palsy (from tumour or surgery); brainstem compression; hydrocephalus
- Post-concussion: Post-concussion syndrome; post-traumatic BPPV; chronic subdural haematoma (elderly)
Active Recall - Complications of Dizziness
References
[1] Lecture slides: murtagh merge.pdf (Dizziness/vertigo section, pp. 35–37) [2] Senior notes: Ryan Ho Cardiology.pdf (Section 2.4 Syncope, p. 63) [3] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.4 Syncope, p. 208) [9] Senior notes: Ryan Ho Endocrine.pdf (Diabetic autonomic neuropathy, p. 98) [32] Senior notes: felixlai.md (Stroke complications and prognosis, sections 1710) [33] Senior notes: Ryan Ho Neurology.pdf (Stroke complications and management, pp. 80–82) [34] Senior notes: Ryan Ho Neurology.pdf (Post-concussion syndrome, p. 205)
High Yield Summary
Definition: Dizziness is a non-specific symptom that must be subcategorised into vertigo (illusion of movement), presyncope (feeling faint), disequilibrium (off-balance), or non-specific dizziness (floaty, vague). The first step is always to clarify what the patient means.
Probability diagnoses (Murtagh) [1]: Anxiety–hyperventilation, postural hypotension, vasovagal, acute vestibulopathy (vestibular neuritis), BPPV, motion sickness, post-head injury, cervical dysfunction/spondylosis
Serious not to miss [1]: Acoustic neuroma, posterior fossa tumour, brain tumours, intracerebral infection (abscess), arrhythmias, MI, aortic stenosis, vertebrobasilar insufficiency, brainstem infarct (PICA thrombosis), multiple sclerosis
Peripheral vs Central vertigo: Peripheral = unidirectional nystagmus suppressed by fixation, positive HIT, ± hearing loss. Central = direction-changing/vertical nystagmus not suppressed, negative HIT, brainstem signs, skew deviation. Use HINTS in acute vestibular syndrome.
Key exam manoeuvres [1]: Hallpike manoeuvre, Epley test, forced hyperventilation test, plus cardiovascular, auditory, and neurological exams.
Key investigations [1]: FBE, blood glucose, audiometry, ECG, ?Holter monitor, consider MRI
Always check drug history — polypharmacy is the most correctable cause in the elderly.
Syncope classification [2][5]: Cardiac (15%) — most dangerous (30% mortality), Neurocardiogenic (60%) — most common, Postural hypotension (15%), Unexplained (10%).
Red flags for central cause: sudden onset with brainstem symptoms (5 D's), direction-changing nystagmus, negative HIT, skew deviation, inability to walk, new headache, cardiovascular risk factors for stroke.
High Yield Summary — Differential Diagnosis of Dizziness
-
First step: Subcategorise → Vertigo vs Presyncope vs Disequilibrium vs Non-specific
-
Probability diagnoses [1]: Anxiety–hyperventilation, postural hypotension, vasovagal, vestibular neuritis, BPPV, motion sickness, post-head injury, cervical spondylosis
-
Serious not to miss [1]: Acoustic neuroma, posterior fossa tumour, brain tumour, intracerebral abscess, arrhythmias (30% mortality!), MI, aortic stenosis, VBI, brainstem infarct (PICA), MS
-
Pitfalls [1]: Ear wax, arrhythmias, hyperventilation, alcohol/drugs, cough/micturition syncope, vestibular migraine (commonly missed), Parkinson's (autonomic features), Ménière's (overdiagnosed)
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Masquerades [1]: Depression, diabetes (hypo/hyperglycaemia), drugs, anaemia, thyroid disorder, spinal dysfunction, UTI
-
Acute vestibular syndrome: The critical DDx is vestibular neuritis (peripheral) vs posterior circulation stroke (central) → use HINTS exam (more sensitive than early MRI)
-
Syncope: Cardiac (15%, most dangerous) vs Neurocardiogenic (60%, most common) vs Orthostatic (15%)
-
In the elderly: Always think multifactorial, check all medications, lying-standing BP, FBE, glucose
High Yield Summary — Diagnosis of Dizziness
-
BPPV: Diagnosed by Dix-Hallpike manoeuvre [1] — no imaging needed if classic. Atypical features → MRI to exclude central cause.
-
Vestibular neuritis vs stroke: HINTS exam in acute vestibular syndrome is > 98% sensitive for posterior circulation stroke — better than early MRI. Peripheral = +ve HIT, unidirectional nystagmus, no skew. Central = any one central sign → urgent MRI + CTA.
-
Ménière's disease: Requires audiometric documentation of low-frequency SNHL (AAO-HNS 2020). Without it, consider vestibular migraine. Meniere syndrome is overdiagnosed [1].
-
Orthostatic hypotension: Lying-standing BP with ≥ 20/10 drop within 3 minutes.
-
Cardiac syncope: ECG [1] is first-line. Holter monitor [1] for paroxysmal arrhythmias. Echocardiogram if structural disease suspected. Tilt-table for recurrent unexplained syncope. Cardiac syncope carries ~30% mortality [2][3].
-
First-line bloods: FBE, blood glucose [1], plus U&E, Ca²⁺, TFTs, B12 to screen for metabolic masquerades.
-
Neuroimaging: MRI with gadolinium [1] when suspecting acoustic neuroma, posterior fossa tumour, MS, or stroke. CT brain for acute haemorrhage exclusion. CTA for vascular pathology.
-
Key bedside tests: Dix-Hallpike, HINTS, forced hyperventilation test, lying-standing BP, Romberg, gait — these often give you the diagnosis before any lab or imaging result.
High Yield Summary — Management of Dizziness
-
BPPV: Epley manoeuvre [1] is the definitive treatment (~80% cure in one session). Medications are NOT first-line.
-
Vestibular neuritis: Short-term suppressants (≤ 72h only!) → corticosteroids → early vestibular rehabilitation (the most important intervention). Prolonged suppressant use delays compensation and causes chronicity.
-
Ménière's disease: Stepwise — lifestyle (salt, caffeine, alcohol) → betahistine/diuretics → intratympanic steroids/gentamicin → surgery.
-
Vestibular migraine: Same as migraine — trigger avoidance + abortive Tx (triptans) + prophylaxis (propranolol, amitriptyline, topiramate, CGRP antagonists).
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Orthostatic hypotension: Drug review first [1] → fluids/salt/compression → midodrine/fludrocortisone.
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Vasovagal syncope: Education, trigger avoidance, counterpressure manoeuvres; pharmacotherapy (midodrine) or pacemaker only if refractory with documented asystole.
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Cardiac causes: Treat the underlying arrhythmia/structural disease per cardiology guidelines — potentially life-saving.
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Posterior circulation stroke: Neurological emergency — acute stroke pathway (thrombolysis ± thrombectomy).
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Anxiety/PPPD: Reassurance, CBT, SSRI/SNRI, vestibular rehabilitation.
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Elderly multifactorial: Address ALL contributing factors — drug review, vision, hearing, neuropathy, exercise, falls prevention, mood.
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Universal principle: Vestibular rehabilitation therapy is beneficial in almost all chronic vestibular conditions.
High Yield Summary — Complications of Dizziness
Universal complications of dizziness (any cause):
- Falls → fractures (hip fracture: 20–30% 1-year mortality in elderly), head injuries, soft tissue injuries
- Syncope-related injuries (driving accidents, drowning, workplace injuries)
- Psychological: anxiety, depression, fear of falling → activity restriction → deconditioning → vicious cycle
- Functional disability: impaired ADLs, inability to drive/work, social isolation
- Iatrogenic: prolonged vestibular suppressant use → delayed compensation → PPPD; anticholinergic burden in elderly
Condition-specific complications to remember:
- BPPV: Benign but high recurrence (50% lifetime); residual dizziness; progression to PPPD
- Vestibular neuritis: Incomplete compensation (30–40%); secondary BPPV (10–15%); PPPD
- Ménière's disease: Progressive hearing loss; bilateral involvement (30%); Tumarkin drop attacks; "burnt-out" phase
- Cardiac syncope: 30% mortality [2][3]; sudden cardiac death; traumatic injury from uncontrolled fall
- Posterior circulation stroke: Brainstem herniation; obstructive hydrocephalus; aspiration pneumonia; post-stroke depression (29%); DVT/PE; pressure sores
- Acoustic neuroma: CN VII palsy (from tumour or surgery); brainstem compression; hydrocephalus
- Post-concussion: Post-concussion syndrome; post-traumatic BPPV; chronic subdural haematoma (elderly)
Diarrhoea
Diarrhoea is the passage of three or more loose or watery stools per day, or more frequently than is normal for the individual, resulting from increased intestinal secretion, decreased absorption, or altered motility.
Dyspepsia
Dyspepsia is a symptom complex of recurrent epigastric pain or discomfort, often accompanied by bloating, nausea, early satiety, or postprandial fullness, originating from the gastroduodenal region.