Dizziness and Vertigo¶
Chapter 24 | Part 2: Cardinal Manifestations and Presentation of Diseases
KEY CLINICAL POINTS¶
- Dizziness encompasses vertigo (illusion of motion), light-headedness, faintness, and imbalance—patient descriptions are often unreliable for diagnosis
- Key diagnostic questions: Is it dangerous (arrhythmia, TIA/stroke)? Is it vestibular? If vestibular, is it peripheral or central?
- Head impulse test is the most useful bedside test—normal result in acute vertigo suggests central cause and possible stroke
- BPPV is the most common cause of recurrent vertigo, diagnosed by Dix-Hallpike maneuver, treated with Epley repositioning maneuver
- Vestibular suppressant medications should be limited to first few days of acute vestibular syndrome to avoid impeding central compensation
1. DEFINITION & OVERVIEW¶
Dizziness is an imprecise symptom describing a variety of common sensations. Proper characterization is essential for diagnosis and management.
1.1 Terminology¶
- Vertigo: Sense of spinning or motion; may be physiological (during/after head rotation) or pathological (vestibular dysfunction). Implies acute asymmetry of vestibular inputs.
- Light-headedness: Classically refers to presyncopal sensations from brain hypoperfusion, but patients use this term imprecisely.
- Faintness: Presyncopal sensation.
- Imbalance/Disequilibrium: Instability without vertigo; may occur with bilateral vestibular loss.
- Oscillopsia: Illusion that the visual scene is moving; occurs with bilateral vestibular hypofunction during head movement.
1.2 Pathophysiology of Vestibular Symptoms¶
- Acute unilateral vestibular lesion: Causes vertigo due to sudden imbalance in vestibular inputs from the two labyrinths.
- Bilateral vestibular lesions: Cause imbalance and oscillopsia during head movement due to loss of vestibulo-ocular reflex (VOR), but NOT vertigo.
- Symmetric bilateral vestibular hypofunction: Causes imbalance but no vertigo because there is no asymmetry of input.
2. ETIOLOGY & CLASSIFICATION¶
Dizziness has multiple etiologies that must be systematically differentiated through history, examination, and appropriate testing.
Features of Peripheral vs Central Vertigo¶
| Feature | Peripheral Vertigo | Central Vertigo |
|---|---|---|
| Nystagmus direction | Unidirectional, fast phases beat away from lesioned ear | May change direction with gaze (gaze-evoked nystagmus) |
| Nystagmus character | Horizontal-torsional; mixed vertical-torsional in BPPV | Pure vertical or pure torsional nystagmus is central sign |
| Visual fixation effect | Nystagmus inhibited by fixation | Nystagmus NOT suppressed by fixation |
| Head impulse test | Abnormal (catch-up saccade toward affected side) | Often normal despite acute vertigo |
| Hearing loss | Unilateral sensorineural loss suggests peripheral | Usually absent unless lesion at CN VIII root entry zone |
| Associated symptoms | Ear pain, pressure, fullness, tinnitus | Diplopia, dysarthria, numbness, limb ataxia |
2.1 Vestibular Causes¶
Peripheral Disorders (affect labyrinth or vestibular nerve): - Benign paroxysmal positional vertigo (BPPV) - Vestibular neuritis - Ménière's disease - Vestibular schwannoma - Herpes zoster oticus (Ramsay Hunt syndrome) - Labyrinthitis Central Disorders (affect brainstem or cerebellar vestibular pathways): - Cerebellar infarct or hemorrhage - Brainstem stroke/TIA - Multiple sclerosis - Cerebellar degeneration - Tumors of posterior fossa
2.2 Non-Vestibular Causes¶
Presyncopal Dizziness: - Cardiac dysrhythmias - Orthostatic hypotension - Medication effects - Vasovagal episodes Other Causes: - Gait disorders (loss of proprioception, parkinsonism) - Anxiety disorders - Peripheral polyneuropathy (impaired proprioception)
3. CLINICAL APPROACH TO THE PATIENT¶
A systematic approach using history and physical examination can often determine the etiology without extensive testing.
Diagnostic Approach by Episode Duration¶
| Duration | Common Causes | Key Features |
|---|---|---|
| Seconds | BPPV, orthostatic hypotension | Provoked by position changes relative to gravity |
| Minutes | Posterior circulation TIA, vestibular migraine | Vascular risk factors; associated neurologic symptoms |
| Hours | Vestibular migraine, Ménière's disease | Migraine features; aural symptoms in Ménière's |
| Days | Vestibular neuritis, cerebellar/brainstem stroke | Continuous vertigo; differentiate with head impulse test |
3.1 Key Diagnostic Questions¶
- Is it dangerous? (e.g., arrhythmia, TIA/stroke)
- Is it vestibular?
- If vestibular, is it peripheral or central?
3.2 History Taking¶
Episode Characteristics: - First attack vs recurrent - Duration of episodes - Provoking factors - Accompanying symptoms Timing Classification: - Seconds: BPPV, orthostatic hypotension (provoked by position change) - Minutes: Consider posterior circulation TIA (also migraine) - Hours: Vestibular migraine, Ménière's disease - Days: Vestibular neuritis, central lesion Associated Symptoms: - Unilateral hearing loss, ear pain, pressure, fullness, tinnitus → Peripheral cause - Double vision, numbness, limb ataxia, dysarthria → Brainstem/cerebellar lesion
4. PHYSICAL EXAMINATION¶
The neurologic examination is essential, with focus on eye movements, vestibular function, and hearing.
4.1 Ocular Motility Assessment¶
Range of Movement: - Check if equal in each eye - Peripheral disorders (CN palsies, muscle weakness) → disconjugate Pursuit and Saccades: - Poor smooth pursuit → central pathology - Dysmetric saccades (inaccurate) → cerebellar pathology Cover Test for Alignment: - Alternate covering eyes while patient fixates on target - Watch for corrective saccades - Vertical misalignment → brainstem or cerebellar lesion Spontaneous Nystagmus: - Jerk nystagmus: slow drift (slow phase) alternating with rapid saccade (quick/fast phase) - If easily seen in light → likely central cause - Downbeat nystagmus: fast phases downward → cerebellar pathology - Gaze-evoked nystagmus: direction changes with gaze → cerebellar pathology - Peripheral lesions → unidirectional horizontal nystagmus
4.2 Head Impulse Test¶
Most useful bedside test of peripheral vestibular function Technique: 1. Patient fixates on examiner's nose 2. Examiner holds patient's head and performs small-amplitude (~20°) rapid rotations to left and right 3. Observe for catch-up saccades Interpretation: - Normal VOR: Eyes remain fixed on target during head rotation - Deficient VOR: Rotation followed by catch-up saccade in opposite direction Clinical Significance: - Unilateral hypofunction: Catch-up saccades after rotation toward weak side - Bilateral hypofunction: Catch-up saccades after rotations in both directions - CRITICAL: Normal head impulse test in acute vertigo suggests CENTRAL cause
4.3 Dix-Hallpike Maneuver¶
Indication: All patients with episodic dizziness, especially if provoked by positional change Technique: 1. Patient seated with head turned 45° to one side 2. Examiner holds back of head 3. Lower patient rapidly to supine with head extended 20° backward below horizontal 4. Watch eyes for 15-20 seconds 5. If negative, return to sitting and repeat with head turned to opposite side Positive Test (Posterior Canal BPPV): - Transient upbeating-torsional nystagmus - Latency 1-5 seconds before onset - Duration typically 15-30 seconds - May reproduce patient's symptoms Enhanced Sensitivity: Use Frenzel goggles or infrared video goggles to detect subtle nystagmus (prevents visual fixation suppression)
4.4 Dynamic Visual Acuity¶
Functional test of vestibular function Technique: 1. Measure visual acuity with head still (near card or Snellen chart) 2. Measure visual acuity while examiner rotates head back and forth (~1-2 Hz) Abnormal Result: Drop of >1 line during head motion indicates vestibular dysfunction
5. INVESTIGATIONS & ANCILLARY TESTING¶
Choice of tests should be guided by history and examination findings.
Ancillary Testing by Clinical Scenario¶
| Clinical Scenario | Recommended Tests |
|---|---|
| Any suspected vestibular disorder | Audiometry |
| Suspected peripheral vestibulopathy | VNG, caloric testing, vHIT |
| Unilateral hearing loss or vestibular hypofunction | MRI internal auditory canals with gadolinium |
| Suspected central cause | MRI brain with posterior fossa protocol |
| Acute vertigo with vascular risk factors | MRI/MRA brain, evaluate for stroke |
| Otolith dysfunction suspected | Vestibular evoked myogenic potentials (VEMPs) |
5.1 Audiometry¶
Indicated in all suspected vestibular disorders - Unilateral sensorineural hearing loss → supports peripheral disorder (vestibular schwannoma) - Predominantly low-frequency hearing loss → characteristic of Ménière's disease - Hearing may improve between attacks in Ménière's disease but permanent loss eventually occurs
5.2 Vestibular Function Testing¶
Videonystagmography (VNG): - Records spontaneous nystagmus - Measures positional nystagmus Caloric Testing: - Compares responses of two horizontal semicircular canals - Reduced response indicates peripheral hypofunction on that side Video Head-Impulse Testing (vHIT): - Measures integrity of each of the six semicircular canals Vestibular Evoked Myogenic Potentials (VEMPs): - Assess otolith (utricle and saccule) reflexes Saccade and Pursuit Recordings: - Evaluate central ocular motor function
5.3 Neuroimaging¶
MRI with Gadolinium of Internal Auditory Canals: - Indicated for unexplained unilateral hearing loss or vestibular hypofunction - Rule out vestibular schwannoma MRI Brain (Including Posterior Fossa): - Indicated when central vestibular disorder suspected - Acute vestibular syndrome with vascular risk factors → evaluate for stroke even without specific central signs
6. SPECIFIC VESTIBULAR DISORDERS¶
Treatment should be driven by the underlying diagnosis. Generic vestibular suppressants are often unhelpful and may prolong recovery.
Comparison of Major Vestibular Disorders¶
| Disorder | Episode Duration | Key Features | Treatment |
|---|---|---|---|
| BPPV | Seconds (15-30s) | Provoked by position change; Dix-Hallpike positive | Epley repositioning maneuver |
| Vestibular Neuritis | Days | Constant vertigo; abnormal head impulse test | Supportive; limit suppressants; rehab |
| Vestibular Migraine | Minutes to hours | Migraine history; photophobia; motion sensitivity | Migraine prophylaxis; antiemetics |
| Ménière's Disease | Hours | Low-frequency hearing loss; aural symptoms | Diuretics; Na restriction; injections |
| Vestibular Schwannoma | None (chronic) | Progressive hearing loss; no vertigo | MRI surveillance vs surgery |
| Bilateral Vestibulopathy | None (chronic) | Oscillopsia; imbalance in dark; Romberg+ | Vestibular rehabilitation |
6.1 Vestibular Neuritis (Acute Prolonged Vertigo)¶
Definition: Acute unilateral vestibular lesion causing constant vertigo Symptoms: - Constant vertigo (persists with head still, unlike BPPV) - Nausea and vomiting - Oscillopsia - Imbalance Pathophysiology: Sudden asymmetry of vestibular inputs simulating continuous head rotation Key Diagnostic Consideration: Distinguish from central causes (cerebellar/brainstem stroke) Features Suggesting Central Cause: - Normal head impulse test in acute vertigo - Diplopia, weakness, numbness, dysarthria - Direction-changing nystagmus - Pure vertical or torsional nystagmus IMPORTANT: Older patients with vascular risk factors presenting with acute vestibular syndrome should be evaluated for stroke even without specific central signs
6.2 Vestibular Neuritis Treatment¶
Prognosis: Most patients recover spontaneously Pharmacologic Treatment: - Glucocorticoids: Role uncertain; studies have yielded disparate results - Antivirals: No proven benefit; not typically given unless evidence of herpes zoster oticus (Ramsay Hunt syndrome) - Vestibular suppressants: May reduce acute symptoms but should be AVOIDED after first several days to prevent impeding central compensation Non-Pharmacologic Treatment: - Early mobilization and resumption of normal activity - Vestibular rehabilitation therapy accelerates improvement
6.3 Benign Paroxysmal Positional Vertigo (BPPV)¶
Epidemiology: Most common cause of recurrent vertigo Episode Characteristics: - Duration: Brief (<1 minute, typically 15-20 seconds) - Always provoked by head position changes relative to gravity - Common triggers: Lying down, rising from supine, looking upward, rolling over in bed Pathophysiology: - Free-floating otoconia (calcium carbonate crystals) dislodged from utricular macula - Otoconia move into semicircular canal (usually posterior) - Head position change causes otoconia movement → vertigo and nystagmus Canal Involvement: - Posterior canal (most common): Upbeating-torsional nystagmus (upper poles beat toward affected lower ear) - Horizontal canal: Horizontal nystagmus when lying with either ear down - Superior/Anterior canal: Rare
6.4 BPPV Diagnosis and Treatment¶
Diagnosis: Dix-Hallpike maneuver (see Examination section) Treatment - Epley Maneuver for Posterior Canal BPPV: Step 1: Patient seated, turn head 45° toward affected ear Step 2: Keeping head turned, lower patient to head-hanging position. Hold ≥ 30 seconds and until nystagmus disappears Step 3: Without lifting head, turn it 90° toward the other side. Hold 30 seconds Step 4: Rotate patient onto their side while turning head another 90° so nose points down 45°. Hold 30 seconds Step 5: Patient sits up on side of table After Maneuver: Repeat to confirm successful treatment Refractory Cases: Patients can be taught home variant of maneuver
6.5 Vestibular Migraine¶
Epidemiology: Common but underdiagnosed cause of episodic vertigo Clinical Features: - Vertigo may precede typical migraine headache OR occur without headache or with only mild headache - Patients with frequent past migraines may present later with vestibular migraine predominating - Duration: Minutes to hours; some patients have prolonged disequilibrium (days to weeks) - Motion sensitivity and sensitivity to visual motion (movies) common - Associated features: Photophobia, phonophobia, visual aura (even without headache) Treatment: - Migraine prophylactic medications (see Chap. 441) - Antiemetics for acute attacks - Note: Controlled study data generally lacking
6.6 Ménière's Disease¶
Definition: Inner ear disorder associated with excess endolymph (endolymphatic hydrops) Triad of Symptoms: 1. Episodic vertigo 2. Fluctuating low-frequency sensorineural hearing loss 3. Aural symptoms: Pain, pressure, fullness in affected ear; tinnitus Key Distinguishing Features: - Aural symptoms distinguish from other peripheral vestibulopathies and vestibular migraine - Audiometry during attack: Asymmetric low-frequency hearing loss - Hearing may improve between attacks initially - Permanent hearing loss may eventually occur Pathophysiology: Excess endolymphatic fluid; exact mechanism unclear
6.7 Ménière's Disease Treatment¶
Evaluation: Refer to otolaryngologist Initial Treatment: - Diuretics - Sodium restriction Refractory Cases: - Intratympanic glucocorticoid injections - Intratympanic gentamicin injections (partial ablation) Surgical Options (rarely required): - Endolymphatic sac decompression and shunting - Vestibular nerve section (full ablation) - Labyrinthectomy (full ablation)
6.8 Vestibular Schwannoma¶
Terminology: Also called acoustic neuroma; tumors at cerebellopontine angle Clinical Features: - Slowly progressive unilateral sensorineural hearing loss - Slowly progressive vestibular hypofunction - NO vertigo because gradual deficit allows central compensation - Diagnosis often delayed until hearing loss is noticed Examination Findings: - Deficient head impulse response (rotation toward affected side) - Nystagmus not prominent Diagnosis: MRI of internal auditory canals with gadolinium IMPORTANT: All patients with unexplained unilateral hearing loss or vestibular hypofunction require MRI
6.9 Bilateral Vestibular Hypofunction¶
Symptoms: - No vertigo (vestibular loss is bilateral and symmetric) - Loss of balance, especially in dark (where vestibular input most critical) - Oscillopsia during head movement (walking, riding in car) Causes: - Idiopathic and progressive - Neurodegenerative disorders - Ototoxic medications (most commonly gentamicin and other aminoglycosides) - Bilateral vestibular schwannomas (neurofibromatosis type 2) - Autoimmune disease - Superficial siderosis - Meningeal infection or tumor - Peripheral polyneuropathy (combined with impaired proprioception) - Sequential unilateral processes (vestibular neuritis, Ménière's affecting both ears) Examination Findings: - Diminished dynamic visual acuity - Abnormal head impulse responses in BOTH directions - Positive Romberg sign - Reduced caloric responses bilaterally Treatment: Vestibular rehabilitation therapy
7. MANAGEMENT PRINCIPLES¶
Treatment should be diagnosis-specific. Generic symptomatic treatment with vestibular suppressants is often unhelpful.
7.1 Vestibular Suppressant Medications¶
Classes: - Antihistamines (meclizine, dimenhydrinate) - Benzodiazepines (diazepam, lorazepam) - Phenothiazines (promethazine, prochlorperazine) Indications: - Acute relief in first 1-3 days of vestibular neuritis - Acute Ménière's attacks IMPORTANT LIMITATION: - Should be AVOIDED after first several days of acute vestibular syndrome - Prolonged use impedes central compensation and recovery - Simply treating dizziness with suppressants is often unhelpful
7.2 Vestibular Rehabilitation¶
Indications: - Vestibular neuritis (accelerates recovery) - Bilateral vestibular hypofunction - Chronic uncompensated vestibulopathy - Post-surgical vestibular loss Components: - Gaze stabilization exercises - Balance training - Habituation exercises for motion sensitivity - Gradual return to normal activities
7.3 When to Refer¶
Otolaryngology: - Suspected Ménière's disease - Unilateral hearing loss - Refractory BPPV - Consideration for intratympanic injections or surgery Neurology: - Suspected central vestibular disorder - Vestibular migraine - Acute vestibular syndrome with central features Emergency Evaluation: - Acute vestibular syndrome with vascular risk factors - New diplopia, dysarthria, weakness, or numbness - Normal head impulse test with acute prolonged vertigo
8. KEY CLINICAL PEARLS¶
Clinical Pearls for Dizziness and Vertigo¶
| Pearl |
|---|
| Patient descriptions of dizziness (vertigo, light-headedness, imbalance) do not reliably indicate underlying etiology |
| Normal head impulse test in acute vertigo = HIGH suspicion for central lesion (possible stroke) |
| Pure vertical or pure torsional nystagmus = CENTRAL sign |
| Direction-changing gaze-evoked nystagmus = CEREBELLAR pathology |
| Unilateral hearing loss requires MRI to rule out vestibular schwannoma |
| Rolling over in bed triggering vertigo helps distinguish BPPV from orthostatic hypotension |
| Bilateral vestibular loss causes oscillopsia and imbalance, NOT vertigo |
| Vestibular suppressants should be limited to first 1-3 days to avoid impeding compensation |
| Low-frequency hearing loss pattern is characteristic of Ménière's disease |
| Older patients with vascular risk factors + acute vertigo need stroke evaluation even without focal deficits |
9. DIAGNOSTIC ALGORITHM¶
Step 1: Characterize the Episode - Duration: Seconds → Minutes → Hours → Days - Triggers: Position change? Spontaneous? - Associated symptoms: Hearing loss? Neurologic deficits? Step 2: Determine if Dangerous - Cardiac symptoms or arrhythmia risk → ECG, monitoring - Vascular risk factors + acute vertigo → Evaluate for stroke - Focal neurologic deficits → Urgent neuroimaging Step 3: Determine if Vestibular - Vertigo (spinning) suggests vestibular - Perform head impulse test and Dix-Hallpike Step 4: Peripheral vs Central - Peripheral: Unidirectional nystagmus, positive head impulse test, hearing symptoms - Central: Direction-changing nystagmus, NORMAL head impulse test, focal neurologic signs Step 5: Specific Diagnosis - Brief + positional → BPPV (confirm with Dix-Hallpike) - Hours + aural symptoms → Ménière's disease - Hours + migraine features → Vestibular migraine - Days + abnormal head impulse → Vestibular neuritis - Days + NORMAL head impulse or neurologic signs → Central lesion