Acute Vertigo in Adults

1. Overview

Acute vertigo is the illusion of movement, typically rotational, resulting from asymmetric vestibular system input. It represents a diagnostic challenge in emergency and primary care settings, with critical importance in distinguishing benign peripheral causes from life-threatening central pathology, particularly posterior circulation stroke. [1]

The acute vestibular syndrome (AVS)—defined as rapid-onset vertigo with nystagmus, nausea/vomiting, head motion intolerance, and gait instability—affects approximately 3.5% of emergency department visits in the United States. [2] Misdiagnosis rates for stroke presenting as isolated vertigo range from 10-35%, highlighting the clinical significance of accurate assessment. [3,4]

Key Clinical Message: The HINTS examination (Head Impulse, Nystagmus, Test of Skew) has superior sensitivity to early MRI for detecting posterior circulation stroke in acute vestibular syndrome, with sensitivity 96-100% versus 50-85% for diffusion-weighted MRI in the first 48 hours. [1,5] A negative head impulse test in a patient with acute continuous vertigo is concerning for central pathology.

Epidemiology

Prevalence and Incidence

• Vertigo accounts for approximately 4% of emergency department chief complaints [2]
• Annual incidence of vestibular neuritis: 3.5 per 100,000 population [6]
• BPPV lifetime prevalence: 2.4%, with peak incidence in 6th-7th decades [7,8]
• Meniere's disease prevalence: 190 per 100,000 (0.19%) [9]
• Posterior circulation stroke represents 5-10% of acute vertigo presentations in high-risk populations [3,4]

Risk Factors by Cause

---

2. Aetiology & Pathophysiology

Vestibular Anatomy

Peripheral Vestibular System

• Semicircular canals (3 per labyrinth): Detect angular acceleration in three orthogonal planes (horizontal, anterior, posterior)
• Otolith organs: Utricle (horizontal linear acceleration), saccule (vertical linear acceleration, gravity)
• Vestibular nerve (CN VIII): Transmits signals to vestibular nuclei in pons/medulla

Central Vestibular System

• Vestibular nuclei: Four nuclei in brainstem (medial, lateral, superior, inferior) integrate peripheral input
• Cerebellum: Flocculus and nodulus modulate vestibulo-ocular reflex (VOR); vermis coordinates truncal balance
• Cortical projections: Parieto-insular vestibular cortex (spatial orientation)
• Vestibulo-ocular reflex (VOR): Stabilizes gaze during head movement via CN III, IV, VI connections

Mechanism of Vertigo

Normal Vestibular Balance The brain receives matched input from bilateral vestibular organs. Any asymmetry creates the sensation of rotation toward the side of greater activity.

Peripheral Asymmetry

• Vestibular neuritis: Acute unilateral hypofunction → brain perceives rotation away from affected side
• BPPV: Displaced otoconia cause inappropriate excitation during head position change
• Meniere's disease: Endolymphatic hydrops creates episodic pressure-induced dysfunction

Central Asymmetry

• Stroke/TIA: Ischemia to vestibular nuclei, cerebellum, or cortical centers disrupts central processing
• Multiple sclerosis: Demyelination of vestibular pathways creates conduction asymmetry

Vestibular Compensation

Central neuroplasticity allows recovery from unilateral vestibular loss over days to weeks through:

• Recalibration of vestibular nuclei
• Enhanced reliance on visual and proprioceptive input
• Cerebellar adaptation

Clinical Implications:

• Vestibular suppressants (meclizine, benzodiazepines) delay compensation—limit use to 48-72 hours [13]
• Early mobilization and vestibular rehabilitation accelerate recovery [14,15]

---

3. Clinical Presentation

Classification of Dizziness

Peripheral vs Central Vertigo

---

4. Common Causes

Benign Paroxysmal Positional Vertigo (BPPV)

Epidemiology: Most common cause of vertigo (17-42% of all vertigo presentations). [7,8]

Pathophysiology: Displaced otoconia (calcium carbonate crystals) from utricle migrate into semicircular canals (most commonly posterior canal, 85-95%). Canal debris creates inappropriate endolymph flow with position change. [7]

Clinical Features:

• Brief episodes (less than 60 seconds) triggered by specific head positions (rolling in bed, looking up, bending forward)
• Latency of 2-5 seconds after position change
• Fatigability with repeated maneuvers
• No hearing loss or tinnitus
• Positive Dix-Hallpike test (see Investigations)

Variants by Canal:

Vestibular Neuritis

Epidemiology: Second most common peripheral cause. Incidence 3.5 per 100,000. Peak age 40-50 years. [6]

Pathophysiology: Presumed viral inflammation of vestibular nerve (superior division most common), causing acute unilateral vestibulopathy. Seasonal clustering supports viral etiology. [6,10]

Clinical Features:

• Acute onset of severe, continuous vertigo lasting days
• Often preceded by viral upper respiratory infection (30-50% cases) [10]
• Nausea, vomiting, gait instability
• No hearing loss (differentiates from labyrinthitis)
• Positive head impulse test toward affected side
• Unidirectional horizontal-torsional nystagmus (fast phase away from lesion)
• Symptoms improve over days to weeks with central compensation

Labyrinthitis

Similar to vestibular neuritis but with cochlear involvement:

• Acute vertigo PLUS hearing loss and/or tinnitus
• May be viral or bacterial (secondary to otitis media, meningitis)
• Same management as vestibular neuritis plus treatment of underlying infection

Meniere's Disease

Epidemiology: Prevalence 0.19%. Peak age 40-60 years. [9,12]

Pathophysiology: Endolymphatic hydrops (increased endolymph volume) causes episodic rupture of membranous labyrinth, mixing endolymph and perilymph. [12]

Clinical Features (Classic Triad):

1. Episodic vertigo: 20 minutes to 12 hours (typically 2-4 hours)
2. Fluctuating low-frequency sensorineural hearing loss (progresses over time)
3. Tinnitus (low-pitched roaring)
4. Aural fullness in affected ear

Natural History: Progressive hearing loss with decreased vertigo frequency over years as vestibular function declines bilaterally.

Posterior Circulation Stroke (Most Critical)

Epidemiology: 10-20% of posterior circulation strokes present with isolated vertigo without other neurological signs. [3,4] Misdiagnosis rate: 10-35%. [4]

High-Risk Territories:

Risk Factors (same as general stroke risk):

• Age > 60, hypertension, diabetes, atrial fibrillation, smoking, hyperlipidemia, prior stroke/TIA [11]
• Vertebral artery dissection: Young patient with neck pain/trauma

---

5. The HINTS Examination

HINTS = Head Impulse, Nystagmus, Test of Skew

The HINTS examination is the most critical bedside test for distinguishing peripheral from central causes in acute vestibular syndrome (continuous vertigo with nystagmus). [1,5]

Sensitivity and Specificity

HINTS examination for stroke (in AVS):

• Sensitivity: 96-100% [1,5,16]
• Specificity: 94-96% [1,16]

Early MRI (DWI) for posterior stroke (first 48h):

• Sensitivity: 50-85% (false negative common) [5,17]

Key Point: HINTS examination is MORE SENSITIVE than MRI in the first 48 hours. [1,5]

HINTS Components

1. Head Impulse Test (HIT)

Technique:

1. Patient fixates on examiner's nose
2. Examiner rapidly rotates patient's head ~15-20° to one side then returns to center
3. Observe for corrective saccade (refixation movement)
4. Repeat to opposite side

Interpretation:

CRITICAL: In acute vestibular syndrome, a negative (normal) head impulse test is DANGEROUS and suggests central pathology. [1,18]

2. Nystagmus Direction

Observe nystagmus in primary gaze and with lateral gaze (left, right).

Interpretation:

Fixation Suppression: Peripheral nystagmus decreases with visual fixation; central nystagmus does not.

3. Test of Skew (Alternate Cover Test)

Technique:

1. Patient fixates on distant target
2. Cover one eye for 2-3 seconds
3. Uncover and observe for vertical refixation movement
4. Repeat covering opposite eye

Interpretation:

INFARCT Mnemonic (Central Features)

Impulse Negative (normal HIT = dangerous)
Fast phase Alternating (direction-changing nystagmus)
Refixation on Cover Test (skew deviation)

If ANY of these features present → high concern for central cause (stroke) [1]

HINTS Limitations

• Only valid in acute vestibular syndrome (continuous vertigo with nystagmus)
• NOT for episodic vertigo (e.g., BPPV, TIA)
• Requires examiner training and experience
• Cannot be performed in uncooperative or severely ill patients

---

6. Differential Diagnosis

By Timing and Duration

Episodic, Positional (Seconds)

• BPPV (most common)
• Orthostatic hypotension

Episodic, Spontaneous (Minutes to Hours)

• Meniere's disease (20 min - 12 hours)
• Vestibular migraine (minutes to hours)
• Posterior circulation TIA (minutes, rarely > 24h)
• Panic attack

Continuous (Days)

• Vestibular neuritis
• Labyrinthitis
• Stroke (sudden onset, persistent)
• Multiple sclerosis (may be subacute)

Dangerous Mimics

---

7. Investigations

Step-by-Step Clinical Approach

Step 1: Clarify Dizziness Type

• True vertigo (rotation) vs presyncope vs disequilibrium vs lightheadedness

Step 2: Determine Timing Pattern

• Brief positional (BPPV) vs episodic spontaneous (Meniere's, migraine, TIA) vs continuous (neuritis, stroke)

Step 3: Assess for Red Flags (see Red Flags section)

Step 4: Bedside Vestibular Examination

Bedside Tests

Dix-Hallpike Maneuver (for BPPV)

Indication: Suspected BPPV (brief positional vertigo)

Technique:

1. Patient seated, head turned 45° to side being tested
2. Rapidly lie patient supine with head extended 20° off table edge
3. Maintain position for 30-60 seconds, observe for nystagmus and ask about vertigo
4. Return to sitting, observe for reversal nystagmus
5. Wait 1-2 minutes, repeat on opposite side

Positive Test (Posterior Canal BPPV):

• Latency: 2-5 seconds after lying down
• Nystagmus: Up-beating and torsional (toward affected ear)
• Fatigability: Decreases with repeated maneuvers
• Vertigo: Matches nystagmus direction and timing

Sensitivity: 79-83% for posterior canal BPPV [7,19]
Specificity: 95% [19]

False Negatives: Anterior canal BPPV, horizontal canal BPPV, debris may have settled

Supine Roll Test (for Horizontal Canal BPPV)

Technique:

1. Patient supine, head flexed 30°
2. Rapidly turn head 90° to one side
3. Observe for horizontal nystagmus
4. Return to center, repeat to opposite side

Positive Test:

• Horizontal nystagmus (geotropic or apogeotropic)
• Indicates horizontal canal BPPV (5-15% of BPPV)

HINTS Examination

(Described in detail above—only for acute vestibular syndrome)

Neurological Examination

Complete cranial nerve assessment:

• CN V: Facial sensation (may be lost in AICA stroke)
• CN VII: Facial movement (AICA stroke, Ramsay Hunt syndrome)
• CN VIII: Hearing (Rinne, Weber), vestibular function (HIT)
• CN IX, X: Palate elevation, gag (medullary stroke)
• CN XI, XII: SCM/trapezius strength, tongue protrusion

Cerebellar testing:

• Finger-nose-finger: Dysmetria
• Heel-shin: Ataxia
• Rapid alternating movements: Dysdiadochokinesia
• Gait: Wide-based, truncal ataxia (inability to walk = red flag)
• Romberg: Tests proprioception (not specific for vertigo)

Motor/Sensory:

• Crossed sensory loss (face vs body) suggests lateral medullary syndrome
• Unilateral weakness suggests stroke

Laboratory Studies

Generally not required for diagnosis of peripheral vertigo but consider in selected cases:

Neuroimaging

When to Image (MRI Brain with DWI)

Imaging Modality Choice:

CRITICAL POINT: MRI-DWI can be falsely negative in first 24-48 hours for small posterior fossa strokes. If clinical suspicion high (concerning HINTS), admit for observation and repeat imaging. [5,17]

Audiometry

Indication: Hearing loss present (Meniere's, labyrinthitis, AICA stroke, acoustic neuroma)

Pure tone audiometry: Low-frequency sensorineural hearing loss in Meniere's disease [12]

Specialist Vestibular Testing (Outpatient)

• Videonystagmography (VNG): Quantifies vestibular function
• Caloric testing: Assesses lateral semicircular canal function
• Vestibular evoked myogenic potentials (VEMP): Otolith function
• Electrocochleography: Endolymphatic hydrops (Meniere's)

---

8. Red Flags (Life-Threatening Central Causes)

Critical Features Requiring Urgent Evaluation

ABCD² Score (TIA Risk Stratification)

If transient vertigo resolved, consider posterior circulation TIA:

Score interpretation (2-day stroke risk):

• 0-3: Low risk (1%)
• 4-5: Moderate risk (4%)
• 6-7: High risk (8%)

Note: ABCD² developed for anterior circulation TIA; less validated for posterior circulation but provides framework.

---

9. Management

BPPV Management

Canalith Repositioning Maneuvers

Epley Maneuver (Posterior Canal BPPV)

Success rate: 70-80% after single treatment; up to 90-95% after 2-3 treatments. [7,19,20]

Technique:

1. Start seated, head turned 45° toward affected ear
2. Step 1: Rapidly lie back to Dix-Hallpike position (head extended), wait 30-60 seconds
3. Step 2: Turn head 90° to opposite side (now 45° away from affected ear), wait 30-60 seconds
4. Step 3: Roll entire body onto side, nose pointing down, wait 30-60 seconds
5. Step 4: Slowly sit up

Post-maneuver instructions (evidence mixed, but commonly recommended):

• Sleep with head elevated 30-45° for 1-2 nights [7]
• Avoid rapid head movements for 24-48 hours
• May repeat maneuver if symptoms recur

Semont Maneuver (Alternative for Posterior Canal)

• Rapid side-to-side movements from one lateral position to opposite
• Similar efficacy to Epley [19]

Horizontal Canal BPPV: Log roll maneuver (barbecue rotation) or Gufoni maneuver

Recurrence: 15-20% per year; patients can be taught self-treatment [7,8]

Surgical Option (rare): Posterior canal occlusion for refractory BPPV unresponsive to repositioning

Vestibular Neuritis/Labyrinthitis Management

Acute Symptom Management (First 48-72 hours)

Vestibular Suppressants (⚠️ LIMIT TO 48-72 HOURS—delay compensation) [13,14]

Antiemetics

Corticosteroids (for Vestibular Neuritis)

Methylprednisolone taper (most evidence) [21]:

• Regimen: 100 mg PO daily × 3 days, then taper over 3 weeks (e.g., 80-60-40-20-10 mg every 3-5 days)
• Benefit: Modest improvement in vestibular function recovery (NNT ~7-10) [21]
• Timing: Most effective if started within 72 hours of symptom onset
• Evidence: Cochrane review shows improved vestibular function at 1-12 months, but unclear clinical significance [21]

Antivirals: No proven benefit (acyclovir, valacyclovir studied); not routinely recommended [21]

Vestibular Rehabilitation Therapy (VRT)

CRITICAL for recovery: Accelerates central compensation and improves functional outcomes. [14,15,22]

Indications: All patients with vestibular neuritis after acute phase (> 48-72h)

Components:

• Habituation exercises: Repeated exposure to provocative movements
• Gaze stabilization: VOR adaptation exercises
• Balance training: Static and dynamic balance challenges

Timing: Begin as soon as patient tolerates (48-72h after onset)

Referral: Physical therapy with vestibular rehabilitation expertise

Outcomes: Significantly faster recovery versus natural compensation alone [14,15,22]

Meniere's Disease Management

Acute Attack

• Vestibular suppressants (meclizine, dimenhydrinate) PRN
• Antiemetics (ondansetron)
• Reassurance (attacks are self-limited)

Preventive/Long-term Management

Lifestyle Modifications [12]:

• Low-sodium diet: less than 1.5-2 g/day (reduces endolymphatic pressure)
• Avoid caffeine, alcohol, tobacco
• Adequate hydration
• Stress management

Medical Therapy [12,23]:

Interventional (Refractory Cases):

• Intratympanic gentamicin: Chemical labyrinthectomy (controlled vestibular ablation)
• Intratympanic dexamethasone: Preserve hearing, less effective than gentamicin
• Endolymphatic sac surgery: Limited evidence
• Vestibular nerve section: For intractable vertigo with serviceable hearing
• Labyrinthectomy: For intractable vertigo with non-serviceable hearing

Prognosis: Natural history shows decreased vertigo frequency over years as bilateral vestibular function declines; progressive hearing loss common.

Central Vertigo (Stroke) Management

If central cause suspected or confirmed:

ACUTE STROKE PROTOCOL
1. NIL PER OS (aspiration risk with dysphagia)
2. IV access, continuous monitoring
3. STAT neurology/stroke team consultation
4. MRI brain with DWI (or CT if MRI contraindicated/unavailable)
5. CT/MR angiography (if dissection suspected)
6. Consider IV thrombolysis if within window (4.5h) and eligible
7. Blood pressure management per stroke protocol
8. Admit stroke unit or ICU
9. Swallow assessment before oral intake
10. If MRI initially negative but high suspicion, admit for observation and repeat imaging at 24-48h

Posterior Circulation Stroke Specific Concerns:

• Cerebellar stroke edema: Risk of brainstem compression, herniation
• Neurosurgery consultation: If large cerebellar infarct (may require decompressive suboccipital craniectomy)
• Anticoagulation/antiplatelet: Per stroke guidelines (e.g., aspirin 300 mg loading, then 75-100 mg daily)

---

10. Disposition

Admission Criteria

Admit to Hospital:

• Suspected or confirmed central cause (stroke, MS flare, tumor)
• Unable to tolerate oral intake (intractable vomiting, dehydration)
• Severe symptoms requiring IV medications unresponsive to initial treatment
• Unable to ambulate safely
• Uncertain diagnosis with red flags or concerning features
• Vascular risk factors + atypical presentation
• Need for serial neurological exams

ICU/Stroke Unit:

• Confirmed posterior circulation stroke (especially cerebellar)
• Hemodynamic instability
• Decreased level of consciousness
• Risk of herniation (large cerebellar stroke)

Safe Discharge Criteria (Peripheral Vertigo)

Requirements:

• ✅ Clear peripheral diagnosis (BPPV with typical Dix-Hallpike, vestibular neuritis with positive HIT)
• ✅ HINTS reassuring (if performed)
• ✅ Symptoms controlled with oral medications
• ✅ Able to ambulate safely (with assistance device if needed)
• ✅ Able to tolerate oral fluids and medications
• ✅ Reliable follow-up arranged (PCP, ENT, or neurology)
• ✅ No red flags present
• ✅ Patient understands return precautions

Discharge Medications (BPPV):

• Meclizine 25 mg PO q8h PRN severe symptoms × 3 days only
• Ondansetron 4 mg PO q8h PRN nausea × 3 days

Discharge Medications (Vestibular Neuritis):

• Meclizine 25 mg PO q8h PRN severe symptoms × 2-3 days only (EMPHASIZE time limit)
• Ondansetron 4 mg PO q8h PRN nausea × 3 days
• Consider methylprednisolone taper (if presenting within 72h of symptom onset)

Follow-up Recommendations

Return Precautions

Instruct patient to return immediately if:

• New or worsening headache
• Weakness or numbness in face, arm, or leg
• Difficulty speaking or swallowing
• Double vision
• New or worsening hearing loss
• Severe imbalance (unable to walk)
• Symptoms persistently worsening despite treatment
• Fever (suggests bacterial labyrinthitis)

---

11. Special Populations

Elderly Patients (Age > 65)

Considerations:

• Higher stroke risk: Lower threshold for imaging even with "typical" peripheral features [3,11]
• Multifactorial dizziness: Often combination of vestibular, visual, proprioceptive, and cardiovascular factors
• Polypharmacy: Review medications (antihypertensives, sedatives, anticholinergics)
• Fall risk: High risk of injury; ensure safe disposition with assistive devices
• Slower compensation: Vestibular rehabilitation especially important

Vascular Risk Factors

Patients with HTN, DM, AF, smoking, prior stroke:

• Lower threshold for HINTS examination and neuroimaging
• Even "typical BPPV" may warrant imaging if multiple risk factors
• Consider posterior circulation TIA even if symptoms resolved
• Aggressive risk factor modification (antiplatelet, statin, BP control)

Pregnancy

Physiological changes: BPPV may be more common due to hormonal changes, fluid shifts

Medication safety:

• Safe: Meclizine (Category B), ondansetron (Category B, though avoid in 1st trimester if possible)
• Avoid: Benzodiazepines (Category D), promethazine (use with caution)

Imaging: MRI without gadolinium generally safe after 1st trimester if needed for stroke concern

Pediatric Vertigo (Brief Mention)

• Less common in children
• Consider benign paroxysmal vertigo of childhood (episodic vertigo in toddlers, often migraine precursor)
• Vestibular migraine more common than Meniere's in children
• Otitis media-related labyrinthitis more common than in adults

---

12. Prognosis & Outcomes

BPPV

• Immediate success with Epley: 70-80% symptom resolution [19,20]
• Recurrence rate: 15-20% per year [7,8]
• Long-term: Excellent prognosis with treatment; may recur but treatable
• Untreated: 20-30% spontaneous resolution over weeks to months (but unnecessary suffering)

Vestibular Neuritis

• Acute symptoms: Peak 24-48h, then gradual improvement over days to weeks
• Central compensation: Most patients significantly improved by 6-8 weeks
• Persistent symptoms: 20-30% have residual dizziness/imbalance at 1 year [6,10]
• Vestibular rehabilitation: Significantly improves recovery rate and functional outcomes [14,15,22]
• Recurrence: less than 2% (rare)

Meniere's Disease

• Natural history: Variable, unpredictable attack frequency
• Hearing loss: Progressive, often bilateral (30-50% develop bilateral disease over 10-20 years) [12]
• Vertigo: Attack frequency tends to decrease over years as vestibular function declines
• Functional impact: Significant impact on quality of life during active phase

Posterior Circulation Stroke

• Mortality: 10-20% for cerebellar stroke (higher if herniation occurs) [11]
• Functional recovery: Variable depending on size and location
• Recurrence: 5-10% annual stroke risk without treatment; reduced with antiplatelet/anticoagulation and risk factor management

---

13. Clinical Pearls

Diagnostic Pearls

1. HINTS examination is more sensitive than MRI in first 48 hours for posterior circulation stroke [1,5]
2. Negative head impulse test is DANGEROUS in acute vestibular syndrome—suggests central pathology [1,18]
3. Vertical nystagmus is ALWAYS central—never seen in peripheral vertigo [18]
4. BPPV vertigo is BRIEF (less than 60 seconds)—if prolonged (minutes-hours), it's not BPPV [7]
5. Can walk independently = likely peripheral; cannot sit/stand = concerning for central [18]
6. Hearing loss + vertigo + facial palsy = AICA stroke until proven otherwise (mimics peripheral)
7. Neck pain + vertigo in young patient = vertebral dissection (requires angiography)

Treatment Pearls

1. Limit vestibular suppressants to 48-72 hours—prolonged use delays central compensation [13,14]
2. Epley maneuver is curative for BPPV—success rate 70-80% after single treatment [19,20]
3. Early mobilization and vestibular PT accelerate recovery from vestibular neuritis [14,15,22]
4. Corticosteroids for vestibular neuritis: modest benefit if started within 72h [21]
5. Betahistine widely used for Meniere's in Europe/Asia but not FDA-approved in US; evidence mixed [23]

Disposition Pearls

1. When in doubt, admit—missing a stroke is high-stakes
2. HINTS positive for peripheral (abnormal HIT, unidirectional nystagmus, no skew) + no red flags = safe discharge with close follow-up
3. Vascular risk factors matter—lower threshold for imaging in elderly, diabetics, hypertensives
4. Clear return precautions are essential—headache, focal deficits, worsening symptoms
5. Arrange vestibular PT before discharge for vestibular neuritis—improves outcomes

---

14. Common Exam Questions

Viva/OSCE Questions

Q1: "A 65-year-old patient presents with acute onset vertigo and vomiting. Describe your approach."

Model Answer: "I would approach this systematically. First, I would take a focused history to confirm this is true vertigo (rotational sensation), determine timing (acute continuous versus episodic), identify triggers (positional versus spontaneous), and screen for red flags (headache, focal neurological symptoms, neck pain). I would assess vascular risk factors (age, hypertension, diabetes, atrial fibrillation).

On examination, I would perform a complete neurological examination including cranial nerves, cerebellar testing, and gait assessment. For acute continuous vertigo with nystagmus—acute vestibular syndrome—I would perform the HINTS examination to distinguish peripheral from central causes.

Key red flags suggesting stroke include: negative (normal) head impulse test, direction-changing or vertical nystagmus, skew deviation, severe truncal ataxia, and focal neurological deficits. If HINTS suggests central pathology or red flags present, I would initiate stroke protocol with urgent neurology consultation and MRI brain with DWI. If peripheral features with no red flags, I would consider diagnoses like vestibular neuritis or labyrinthitis, treat symptomatically with vestibular suppressants (limited duration) and antiemetics, and arrange close follow-up with vestibular rehabilitation."

Q2: "What is the HINTS examination and why is it important?"

Model Answer: "HINTS stands for Head Impulse test, Nystagmus direction, and Test of Skew. It is a bedside oculomotor examination used to distinguish peripheral from central causes in acute vestibular syndrome (continuous vertigo with nystagmus).

The HINTS examination has sensitivity of 96-100% for posterior circulation stroke, which is superior to MRI-DWI sensitivity of 50-85% in the first 48 hours. This makes it the most important initial diagnostic test.

A concerning HINTS examination for stroke includes: negative (normal) head impulse test, direction-changing or vertical nystagmus, or skew deviation. The INFARCT mnemonic helps remember central features: Impulse Negative, Fast phase Alternating, Refixation on Cover Test.

Importantly, HINTS is only valid for acute vestibular syndrome with continuous vertigo and nystagmus—it should not be used for episodic vertigo like BPPV or TIA."

Q3: "Describe how to perform and interpret the Dix-Hallpike maneuver."

Model Answer: "The Dix-Hallpike maneuver tests for posterior canal BPPV. With the patient seated, I turn their head 45 degrees toward the side being tested. I then rapidly move them to a supine position with their head extended 20 degrees off the edge of the examination table, maintaining the 45-degree head turn. I observe for up to 60 seconds for nystagmus and ask about vertigo.

A positive test shows: latency of 2-5 seconds after lying down, up-beating and torsional nystagmus toward the affected (lowermost) ear, accompanying vertigo, and fatigability with repeated testing. The nystagmus is suppressed by visual fixation.

If positive, I would perform the Epley maneuver for treatment, which has 70-80% success after a single treatment. The sensitivity of Dix-Hallpike is 79-83% and specificity is 95% for posterior canal BPPV."

Q4: "What are the key differences between vestibular neuritis and labyrinthitis?"

Model Answer: "Both are acute peripheral vestibulopathies, but they differ in cochlear involvement. Vestibular neuritis affects only the vestibular nerve, presenting with acute severe vertigo, nausea, vomiting, and gait instability, but with normal hearing. Labyrinthitis affects both vestibular and cochlear structures, presenting with the same vertigo symptoms plus hearing loss and/or tinnitus.

Both show positive head impulse test and unidirectional horizontal-torsional nystagmus. Management is similar with vestibular suppressants (limited to 48-72 hours), antiemetics, corticosteroids (if within 72 hours), and vestibular rehabilitation therapy. However, labyrinthitis may require additional investigation for the cause of cochlear involvement, especially if bacterial (secondary to otitis media or meningitis)."

Q5: "A patient with typical BPPV also has multiple vascular risk factors. Do they need imaging?"

Model Answer: "This requires clinical judgment. While typical BPPV with a positive Dix-Hallpike maneuver and brief positional symptoms usually does not require imaging, vascular risk factors (age > 60, hypertension, diabetes, atrial fibrillation) lower the threshold for considering imaging.

I would consider several factors: Is the presentation completely typical (brief less than 60 seconds, purely positional, positive Dix-Hallpike, no other symptoms)? Are there any atypical features or red flags? What is the patient's stroke risk burden?

For completely typical BPPV that resolves with Epley maneuver, even with risk factors, imaging may not be necessary but close follow-up is essential. However, if there are any atypical features, persistent symptoms despite appropriate treatment, or the patient has multiple high-risk features, I would have a low threshold for MRI to rule out central pathology. The key is 10-20% of posterior circulation strokes can present with isolated vertigo, and BPPV is common, so coexistence is possible."

MCQ/SBA Practice

Q1: A 45-year-old woman presents with acute severe vertigo of 24 hours duration. On examination, she has horizontal nystagmus to the right that does not change direction with gaze, a positive head impulse test to the left, and no skew deviation. What is the most likely diagnosis?

A) BPPV
B) Left vestibular neuritis
C) Right vestibular neuritis
D) Cerebellar stroke
E) Meniere's disease

Answer: B) Left vestibular neuritis

Explanation: Positive head impulse test indicates peripheral vestibulopathy. The corrective saccade occurs toward the affected (hypofunction) side. Nystagmus fast phase is away from the affected side. Continuous vertigo for 24 hours with positive HIT is classic for vestibular neuritis. Brief duration rules out BPPV; lack of hearing loss makes Meniere's less likely.

---

15. Evidence & Guidelines

Key Guidelines

1. American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS): Clinical Practice Guideline: Benign Paroxysmal Positional Vertigo (Update). 2017. [7]

   • Strong recommendation for Epley maneuver
   • Against routine imaging or vestibular testing for typical BPPV
   • Against routine medication use for BPPV

2. American Academy of Neurology: The rational clinical examination systematic review: Does this dizzy patient have stroke? [3]

   • HINTS examination for acute vestibular syndrome
   • MRI-DWI limitations in early posterior fossa stroke

3. Cochrane Reviews:

   • Epley maneuver for BPPV: OR 4.42 (95% CI 2.62-7.44) for symptom resolution [20]
   • Corticosteroids for vestibular neuritis: Improved vestibular function recovery but unclear clinical significance [21]
   • Betahistine for Meniere's disease: Insufficient high-quality evidence [23]

Performance Indicators (Quality Metrics)

---

16. Patient Education

Understanding Vertigo

• Vertigo is a symptom, not a disease—finding the cause is important
• Most causes are benign peripheral disorders (BPPV, vestibular neuritis) but distinguishing from stroke is critical
• BPPV can often be cured with simple repositioning maneuvers (Epley)
• Vestibular neuritis recovery takes days to weeks; early movement and exercises help
• Meniere's disease is a chronic condition requiring long-term management

Activity Guidelines

BPPV (after Epley maneuver):

• Sleep with head elevated 30-45° for 1-2 nights
• Avoid rapid head movements for 24-48 hours
• Symptoms may recur—can repeat Epley or see provider
• Safe to drive once symptoms resolved

Vestibular Neuritis:

• Early movement promotes recovery—avoid prolonged bed rest
• Start walking (with assistance if needed) as soon as tolerated
• Begin vestibular rehabilitation exercises early
• Gradual return to normal activities as tolerated

Medication Instructions

Vestibular Suppressants (Meclizine, Dimenhydrinate):

• ⚠️ Do NOT take for more than 2-3 days—delays your brain's natural recovery
• Causes drowsiness—do not drive or operate machinery
• Use only for severe symptoms; wean off as soon as possible
• The goal is to get OFF these medications, not stay on them

Warning Signs to Return to Emergency Department

Return immediately if you develop:

• New or severe headache
• Weakness or numbness in face, arm, or leg (especially one side)
• Difficulty speaking or slurred speech
• Difficulty swallowing or choking
• Double vision
• New or worsening hearing loss
• Unable to walk due to severe imbalance
• Symptoms getting worse instead of better
• Fever with ear pain (suggests infection)

Driving Restrictions

• Do NOT drive during acute vertigo episode
• Do NOT drive while taking meclizine, dimenhydrinate, or benzodiazepines
• Safe to resume driving once:
  • Symptoms resolved or well-controlled
  • Off sedating medications
  • Able to perform safe head checks and respond to visual stimuli

---

17. References

1. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40(11):3504-3510. doi:10.1161/STROKEAHA.109.551234

2. Newman-Toker DE, Hsieh YH, Camargo CA Jr, Pelletier AJ, Butchy GT, Edlow JA. Spectrum of dizziness visits to US emergency departments: cross-sectional analysis from a nationally representative sample. Mayo Clin Proc. 2008;83(7):765-775. doi:10.4065/83.7.765

3. Kerber KA, Newman-Toker DE. Misdiagnosing dizzy patients: common pitfalls in clinical practice. Neurol Clin. 2015;33(3):565-575. doi:10.1016/j.ncl.2015.04.009

4. Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh YH, Newman-Toker DE. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ. 2011;183(9):E571-E592. doi:10.1503/cmaj.100174

5. Carmona S, Martínez C, Zalazar G, et al. The diagnostic accuracy of truncal ataxia and HINTS as cardinal signs for acute vestibular syndrome. Front Neurol. 2016;7:125. doi:10.3389/fneur.2016.00125

6. Strupp M, Magnusson M. Acute unilateral vestibulopathy. Neurol Clin. 2015;33(3):669-685. doi:10.1016/j.ncl.2015.04.012

7. Bhattacharyya N, Gubbels SP, Schwartz SR, et al. Clinical practice guideline: benign paroxysmal positional vertigo (update). Otolaryngol Head Neck Surg. 2017;156(3_suppl):S1-S47. doi:10.1177/0194599816689667

8. von Brevern M, Radtke A, Lezius F, et al. Epidemiology of benign paroxysmal positional vertigo: a population based study. J Neurol Neurosurg Psychiatry. 2007;78(7):710-715. doi:10.1136/jnnp.2006.100420

9. Alexander TH, Harris JP. Current epidemiology of Meniere's syndrome. Otolaryngol Clin North Am. 2010;43(5):965-970. doi:10.1016/j.otc.2010.05.001

10. Strupp M, Brandt T. Vestibular neuritis. Semin Neurol. 2009;29(5):509-519. doi:10.1055/s-0029-1241040

11. Caplan LR. Posterior circulation ischemia: then, now, and tomorrow. The Thomas Willis Lecture-2000. Stroke. 2000;31(8):2011-2023. doi:10.1161/01.str.31.8.2011

12. Basura GJ, Adams ME, Monfared A, et al. Clinical practice guideline: Ménière's disease. Otolaryngol Head Neck Surg. 2020;162(2_suppl):S1-S55. doi:10.1177/0194599820909438

13. Lacour M, van de Heyning PH, Novotny M, Tighilet B. Betahistine in the treatment of Meniere's disease. Neuropsychiatr Dis Treat. 2007;3(4):429-440.

14. Hillier SL, McDonnell M. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2011;(2):CD005397. doi:10.1002/14651858.CD005397.pub3

15. McDonnell MN, Hillier SL. Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2015;(1):CD005397. doi:10.1002/14651858.CD005397.pub4

16. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med. 2013;20(10):986-996. doi:10.1111/acem.12223

17. Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial management of cerebellar infarction. Lancet Neurol. 2008;7(10):951-964. doi:10.1016/S1474-4422(08)70216-3

18. Chen L, Lee W, Chambers BR, Dewey HM. Diagnostic accuracy of acute vestibular syndrome at the bedside in a stroke unit. J Neurol. 2011;258(5):855-861. doi:10.1007/s00415-010-5853-4

19. Fife TD, Iverson DJ, Lempert T, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2008;70(22):2067-2074. doi:10.1212/01.wnl.0000313378.77444.ac

20. Hilton MP, Pinder DK. The Epley (canalith repositioning) manoeuvre for benign paroxysmal positional vertigo. Cochrane Database Syst Rev. 2014;(12):CD003162. doi:10.1002/14651858.CD003162.pub3

21. Fishman JM, Burgess C, Waddell A. Corticosteroids for the treatment of idiopathic acute vestibular dysfunction (vestibular neuritis). Cochrane Database Syst Rev. 2011;(5):CD008607. doi:10.1002/14651858.CD008607.pub2

22. Lacour M, Dutheil S, Tighilet B, Lopez C, Borel L. Tell me your vestibular deficit, and I'll tell you how you'll compensate. Ann N Y Acad Sci. 2009;1164:268-278. doi:10.1111/j.1749-6632.2008.03731.x

23. Murdin L, Hussain K, Schilder AG. Betahistine for symptoms of vertigo. Cochrane Database Syst Rev. 2016;(6):CD010696. doi:10.1002/14651858.CD010696.pub2

---

Version History