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🧠 Vestibular System, Dizziness & Vertigo — A Complete Guide

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PART 1: WHAT IS DIZZINESS?

The challenge in diagnosis is that patients often cannot distinguish between these, and the words they choose do not reliably indicate the underlying cause.

— Harrison's Principles of Internal Medicine 22E

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PART 2: THE VESTIBULAR SYSTEM — ANATOMY & PHYSIOLOGY

Where Is It?

What Does It Contain?

• Oriented in three planes (horizontal, anterior, posterior)
• Detect angular (rotational) head movement
• Filled with endolymph fluid
• Paired left and right — normally respond symmetrically

• Utricle — detects head tilt and vertical linear acceleration (e.g., going up in an elevator). Contains otoliths (calcium carbonate crystals on hair cells).
• Saccule — detects vertical linear motion

How Does the Signal Travel?

Inner Ear (Labyrinth)
        ↓
CN VIII (Vestibulocochlear nerve)
        ↓
Enters brainstem below the pons, anterior to cerebellum
        ↓
4 Vestibular Nuclei (brainstem)  ←→  Cerebellum
        ↓                  ↓
Medial Longitudinal    Vestibulospinal Tract
Fasciculus (MLF)       (to limb muscles)
        ↓
Eye muscles (VOR)      Postural muscles

• The MLF connects vestibular nuclei to the eye muscles → controls eye movements to compensate for head motion
• The vestibulospinal tract connects to limb motor neurons → maintains posture and balance
• Autonomic connections → explain why vertigo causes sweating, nausea, and vomiting
• Cerebral cortex connections → conscious perception of motion and spatial orientation

The Three Systems That Maintain Balance

Any disease that causes a mismatch of information from any two of these three systems may give rise to symptoms of vertigo.

— Rosen's Emergency Medicine

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PART 3: WHERE IN THE BODY CAN DIZZINESS COME FROM?

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🔴 A. PERIPHERAL VESTIBULAR CAUSES (Inner Ear / Vestibular Nerve)

1. Benign Paroxysmal Positional Vertigo (BPPV)

• Most common cause of recurrent vertigo
• Caused by displaced otoconia (calcium carbonate crystals) that have broken free from the utricular macula and floated into one of the semicircular canals (usually the posterior canal)
• When the head position changes, gravity moves the crystals through the canal → triggers sudden vertigo
• Onset: Sudden, lasts <1 minute (typically 15–20 sec)
• Triggers: Lying down, rolling in bed, looking up, rising from supine
• Nystagmus pattern: Upward + torsional (toward the affected ear)
• Treatment: Repositioning maneuvers (Epley maneuver)

Modified Epley Maneuver (Treatment for BPPV):

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2. Vestibular Neuritis

• Sudden acute unilateral vestibular lesion (likely viral, possibly reactivation of herpes simplex)
• Causes: constant vertigo, nausea, vomiting, oscillopsia (visual scene appears to move), imbalance
• Unlike BPPV, vertigo persists even when the head is still
• Represents an acute asymmetry of input from the two labyrinths — the brain interprets this as constant rotation
• Duration: Hours to days
• Nystagmus: Horizontal-torsional, unidirectional, fast phase beating away from the affected ear
• Treatment: Vestibular suppressants acutely (meclizine), then vestibular rehabilitation. Steroids considered. Avoid prolonged suppressant use — it impedes central compensation.

3. Labyrinthitis

• Like vestibular neuritis but also involves cochlear (hearing) function
• Causes: vertigo + sensorineural hearing loss

4. Ménière's Disease (Endolymphatic Hydrops)

• Caused by excess endolymph fluid in the inner ear
• Classic triad: Episodic vertigo + low-frequency hearing loss + tinnitus + ear fullness/pressure
• Attacks last minutes to hours
• Hearing loss is a key distinguishing feature (not seen in BPPV or vestibular neuritis)
• Audiometry shows asymmetric low-frequency hearing loss during attacks
• Treatment: Diuretics + sodium restriction → middle ear injections (steroids or gentamicin) → surgery (endolymphatic sac decompression) if refractory

5. Vestibular Schwannoma (Acoustic Neuroma)

• Slow-growing benign tumor at the cerebellopontine angle, compressing CN VIII
• Causes slowly progressive unilateral sensorineural hearing loss + vestibular hypofunction
• Typically no vertigo — the deficit develops so slowly that the brain compensates as it goes
• Diagnosis: MRI of internal auditory canals
• Head impulse test shows deficient response toward the affected side

6. Bilateral Vestibular Hypofunction

• Both labyrinths lose function (simultaneously or sequentially)
• No vertigo (no asymmetry) — instead: loss of balance, especially in the dark + oscillopsia while walking
• Causes: aminoglycoside ototoxicity (especially gentamicin), neurofibromatosis type 2, autoimmune disease, meningitis, peripheral neuropathy
• Romberg sign positive; bilateral abnormal head impulse test

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🟠 B. CENTRAL VESTIBULAR CAUSES (Brainstem / Cerebellum)

1. Posterior Circulation Stroke / TIA

• Strokes in the vertebrobasilar territory affect the medulla, pons, midbrain, cerebellum
• May present as isolated acute vertigo — mistaken for peripheral disease
• Key arteries involved:
  • PICA (posterior inferior cerebellar artery) — branch of vertebral artery → Wallenberg syndrome
  • AICA (anterior inferior cerebellar artery) — branch of basilar artery
• Wallenberg Syndrome (Lateral Medullary Syndrome):
  • Vertigo + nausea/vomiting + ataxia
  • Loss of pain/temperature on same-side face, opposite-side body
  • Hoarseness, dysphagia
  • Horner syndrome (ipsilateral ptosis, miosis, anhidrosis)
• A normal head impulse test in a patient with new-onset constant vertigo = red flag for stroke (not peripheral)

2. Vestibular Migraine

• Most common cause of episodic vertigo that is often underdiagnosed
• Vertigo occurs during or (more often) without the headache phase
• Duration: minutes to hours; some patients have prolonged disequilibrium lasting days
• Features: motion sensitivity, sensitivity to visual motion, photophobia, phonophobia, visual aura
• Treatment: Standard migraine prophylaxis medications

3. Multiple Sclerosis (MS)

• Vertigo is the presenting symptom in 7–10% of MS patients; appears in one-third over disease course
• Can cause horizontal, rotary, or vertical nystagmus
• Nystagmus may persist after vertigo resolves
• Key finding: Internuclear ophthalmoplegia (INO) — on lateral gaze, the adducting eye barely moves while the abducting eye moves normally → caused by demyelination of the MLF

4. Cerebellar Hemorrhage

• Medical emergency
• Sudden severe vertigo + severe headache + vomiting + true ataxia (dysmetria)
• May have ipsilateral CN VI palsy

5. Other Central Causes

• Brain tumors (especially posterior fossa)
• Superficial siderosis
• Meningeal infection or tumor

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🟡 C. CARDIOVASCULAR / SYSTEMIC CAUSES (Pre-syncope / Near-syncope)

Faintness and syncope should always be considered when evaluating patients with brief dizziness or dizziness that occurs with upright posture.

— Harrison's Principles of Internal Medicine 22E

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🟢 D. NON-VESTIBULAR NEUROLOGICAL CAUSES

• Sensory neuropathy — loss of proprioception in the feet (common in diabetes, B12 deficiency) removes ground-sense input
• Parkinsonism — gait and postural instability
• Cerebellar ataxia — poor pursuit, dysmetric saccades, true limb ataxia
• Normal pressure hydrocephalus — magnetic gait + cognitive decline + urinary incontinence

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🔵 E. PSYCHIATRIC / FUNCTIONAL CAUSES

Persistent Postural-Perceptual Dizziness (PPPD)

• Formerly called: phobic postural vertigo, chronic subjective dizziness
• Chronic dizziness persisting after a vestibular, neurological, or psychiatric trigger event
• Aggravated by: upright posture, movement, visual stimuli, complex visual patterns (shopping malls, crowds, movies)
• Not due to ongoing structural vestibular disease — it is a functional neurological disorder
• Strong association with anxiety and panic disorder
• Treatment: vestibular rehabilitation, SSRIs/SNRIs, cognitive behavioral therapy

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PART 4: PERIPHERAL vs. CENTRAL VERTIGO — KEY DIFFERENCES

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PART 5: NYSTAGMUS — THE CARDINAL SIGN

• Slow phase: drift of eyes toward the side of the lesion (vestibular drive)
• Fast phase (quick phase): rapid saccadic correction back to midline (cortical reset)
• Direction named by fast phase (by convention)

• Unidirectional horizontal: peripheral lesion (fast phase beats away from the sick ear)
• Direction-changing with gaze: central lesion
• Downbeat nystagmus (fast phase toward nose): cerebellar pathway lesion
• Vertical/torsional at rest: central lesion
• Mixed vertical-torsional, transient: BPPV (posterior canal)

• Cold water → nystagmus to Opposite side
• Warm water → nystagmus to Same side
• If nystagmus is reduced/absent on one side → vestibular lesion on that side

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PART 6: CLINICAL APPROACH — 3 KEY QUESTIONS

1. Is it dangerous? (arrhythmia? TIA/stroke?)
2. Is it vestibular?
3. If vestibular — is it peripheral or central?

Timing & Triggers Framework (Most Useful Clinically):

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PART 7: IMPORTANT CLINICAL SIGNS (HINTS Exam)

A normal head impulse test in a patient with new-onset constant vertigo is a red flag for a central (stroke) cause — the absence of a catch-up saccade means the vestibular nerve is intact, and the lesion is likely central.

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PART 8: TREATMENT OVERVIEW

Vestibular suppressant medications should be avoided beyond the first few days in vestibular neuritis — they interfere with central compensation and recovery.

— Harrison's Principles of Internal Medicine 22E

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SUMMARY: Every System That Can Make You Dizzy

INNER EAR         → BPPV, vestibular neuritis, Ménière's, labyrinthitis, schwannoma
VESTIBULAR NERVE  → Schwannoma, neuritis, ototoxicity
BRAINSTEM/PONS    → Stroke (AICA/PICA), MS, Wallenberg syndrome
CEREBELLUM        → Hemorrhage, infarct, tumor, ataxia
CORTEX/MIGRAINE   → Vestibular migraine, PPPD
EYES              → Diplopia (breaks visual-vestibular match)
PROPRIOCEPTION    → Sensory neuropathy (DM, B12 deficiency)
HEART             → Arrhythmia, orthostatic hypotension, aortic stenosis
BLOOD VESSELS     → Vertebrobasilar insufficiency (TIA/stroke)
PSYCHOLOGY        → Anxiety, panic disorder, PPPD
MEDICATIONS       → Antihypertensives, aminoglycosides, anticonvulsants, alcohol

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📋 Complete Vestibular Testing Guide

Written from the Perspective of Neurology, Neuro-Otology & ENT/Otolaryngology

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INTRODUCTION — Why Testing Matters

1. Site-of-lesion localization — peripheral (inner ear / CN VIII) vs. central (brainstem / cerebellum)
2. Functional assessment — how well is the patient using their remaining vestibular function?
3. Compensation status — is the brain adapting to the deficit or not?

No single test is sufficient. The vestibular test battery must be interpreted in light of the full history, symptom duration, and medical background of the patient.

— Cummings Otolaryngology

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SECTION A — BEDSIDE CLINICAL EXAMINATION

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🔵 TEST 1: SPONTANEOUS NYSTAGMUS OBSERVATION

• Examine first with Frenzel goggles (self-illuminated magnifying goggles that prevent visual fixation) or infrared video goggles — these prevent fixation suppression of peripheral nystagmus
• Observe the eyes in primary gaze, then lateral gaze (left and right), then vertical (up and down)

Peripheral nystagmus is inhibited by visual fixation. Central nystagmus is not. This is a key distinguishing feature. — Harrison's Principles of Internal Medicine 22E

Abnormal nystagmus is the cardinal sign of inner ear disease and the principal objective evidence of vestibular dysfunction. — Rosen's Emergency Medicine

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🔵 TEST 2: HEAD IMPULSE TEST (HIT) / HEAD THRUST TEST

1. Examiner stands face-to-face with the patient
2. Both hands placed on either side of the patient's head
3. Patient fixates on the examiner's nose
4. Head is rapidly (unexpectedly) rotated ~10–20° to one side at high velocity (~1000–4000°/s/s)
5. Observe whether the eyes stay on target or slip with the head

If the head impulse test is normal in a patient with acute constant vertigo, a peripheral lesion is unlikely. A central cause (stroke) must be considered. — Harrison's Principles of Internal Medicine 22E

Eliciting a positive head impulse test indicates a benign peripheral cause such as vestibular neuritis. — Rosen's Emergency Medicine

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🔵 TEST 3: DIX-HALLPIKE MANEUVER (Hallpike / Nylen-Barany Test)

1. Patient sits upright on examination table
2. Examiner turns patient's head 45° toward the side being tested
3. Patient is rapidly moved from sitting → supine with head hanging over edge of table (~20–30° below horizontal)
4. Eyes are observed carefully for nystagmus after a brief latency period
5. Patient is brought back to sitting; test repeated to the other side

• Positive on one side only: The downward ear = the affected side → start treatment on that side
• Nystagmus persisting >90 seconds: Consider central positional nystagmus (fixed otolith lesion or CNS pathology)
• If both sides seem positive: may have bilateral BPPV; repeat carefully

• Patient with acute vestibular syndrome (constant vertigo at rest) — this is inconsistent with BPPV; provocative testing may worsen symptoms and mislead diagnosis

Clinicians should diagnose posterior semicircular canal BPPV when vertigo associated with torsional, upbeating nystagmus is provoked by the Dix-Hallpike maneuver. This is a strong recommendation in clinical guidelines.

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🔵 TEST 4: SUPINE ROLL TEST (Log Roll / Pagnini-McClure Test)

1. Patient lies supine (face up)
2. Head rapidly rolled 30° to the right → observe nystagmus
3. Return to neutral; then head rapidly rolled 30° to the left → observe nystagmus

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🔵 TEST 5: HINTS EXAMINATION (Bedside Stroke Screen)

Component 1 — Head Impulse Test (H)

Component 2 — Nystagmus Pattern (N)

Component 3 — Test of Skew (T)

• Perform alternate cover test: alternately cover each eye while patient fixates on a target
• Look for vertical realignment of the uncovered eye

HINTS should only be used in patients with a first-ever episode of constant vertigo (acute vestibular syndrome) — not in episodic or positional vertigo. It requires experience to perform correctly. — Rosen's Emergency Medicine

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🔵 TEST 6: ROMBERG TEST

1. Patient stands with feet together, hands crossed over chest
2. Eyes open first → then eyes closed
3. Observe for excessive sway or falling

This test does not localize the lesion — vestibular deficits, cerebellar lesions, and peripheral neuropathy can all cause a positive Romberg. — Cummings Otolaryngology

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🔵 TEST 7: FUKUDA STEPPING TEST (Unterberger Test)

1. Patient marches in place for 50 steps, eyes closed, arms outstretched
2. Observe for rotation (turning clockwise or counterclockwise)

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🔵 TEST 8: OCULAR MOTILITY EXAMINATION

INO (adducting eye weak + abducting eye nystagmus) is virtually pathognomonic of multiple sclerosis affecting the brainstem. — Rosen's Emergency Medicine

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🔵 TEST 9: DYNAMIC VISUAL ACUITY (DVA) TEST

• Patient reads an eye chart first with head still (static acuity)
• Then patient tries to read while head is oscillated by the examiner (or self)
• Loss of >2 lines of acuity during head movement = abnormal

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🔵 TEST 10: CEREBELLAR FUNCTION TESTS

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🔵 TEST 11: ORTHOSTATIC VITAL SIGNS

• Systolic BP drop ≥20 mmHg OR diastolic drop ≥10 mmHg within 3 minutes of standing
• Often accompanied by symptoms of lightheadedness or near-faint

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SECTION B — ENT / OTOSCOPY EXAMINATION

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🟢 TEST 12: OTOSCOPY

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🟢 TEST 13: TUNING FORK TESTS

Weber Test

• 512 Hz tuning fork placed on the midline of skull (forehead or vertex)
• Ask: "Does the sound go to one side or stay in the middle?"

Rinne Test

• Fork placed on mastoid bone (bone conduction) → when no longer heard, moved to external ear (air conduction)

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SECTION C — LABORATORY / ANCILLARY TESTS

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🟡 TEST 14: PURE TONE AUDIOMETRY (PTA)

Audiometry should be performed whenever a vestibular disorder is suspected. Unilateral SNHL supports a peripheral vestibular disorder such as vestibular schwannoma. — Harrison's Principles of Internal Medicine 22E

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🟡 TEST 15: VIDEONYSTAGMOGRAPHY (VNG) / ELECTRONYSTAGMOGRAPHY (ENG)

a) Spontaneous Nystagmus Recording

• Eyes open in darkness (goggles eliminate fixation)
• Identifies residual spontaneous nystagmus not visible at bedside
• Clinically significant spontaneous nystagmus suggests incomplete compensation or active peripheral lesion

b) Positional Nystagmus Testing

• Patient moved into various positions (supine, left lateral, right lateral, Hallpike positions)
• Records nystagmus characteristics in each position
• Differentiates BPPV from other positional disorders

c) Caloric Testing — THE KEY VNG SUBTEST

• Warm water (44°C) and cold water (30°C) are instilled into each external ear canal, one at a time (4 irrigations total)
• Temperature difference sets up convection currents in the endolymph → stimulates the horizontal canal
• Resulting nystagmus is recorded

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🟡 TEST 16: VIDEO HEAD IMPULSE TEST (vHIT / VHIT)

• High-speed infrared camera (250–500 fps) tracks eye movements during rapid passive head rotations in all 6 canal planes
• Computer measures VOR gain (eye velocity / head velocity ratio)
• Detects both overt saccades (visible, after head stops) and covert saccades (during head movement — only detectable by machine)

vHIT is being utilized in emergency departments as part of a clinical algorithm to distinguish central causes of acute vestibular syndrome from peripheral causes. It expands caloric testing by covering all six semicircular canals. — Cummings Otolaryngology

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🟡 TEST 17: ROTARY CHAIR TESTING (Rotational Chair)

• Patient sits in a motorized chair in complete darkness, rotating at various speeds and frequencies
• VOR is measured: gain (amplitude), phase (timing lag), and symmetry

Persistent asymmetry (bias) in slow-phase eye velocity responses during rightward vs. leftward rotation strongly suggests the peripheral lesion is physiologically uncompensated. — Cummings Otolaryngology

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🟡 TEST 18: VESTIBULAR EVOKED MYOGENIC POTENTIALS (VEMP)

a) Cervical VEMP (cVEMP) — Tests the SACCULE

• Patient turns head to one side (activating the sternocleidomastoid / SCM muscle)
• Loud clicks (95–105 dB) delivered to the ear via headphones
• SCM muscle EMG is recorded
• Normally: an inhibitory potential at 13 ms followed by excitatory potential at 21 ms after the stimulus

b) Ocular VEMP (oVEMP) — Tests the UTRICLE

• Loud clicks delivered; small electrodes under the eyes record the response from the contralateral inferior oblique and inferior rectus muscles
• Normal: excitatory potential at 10 ms, inhibitory potential at 16 ms

• Helps localize lesion to inferior vs. superior vestibular nerve division
• Detects otolith organ dysfunction missed by caloric/rotary chair
• Particularly useful in diagnosing Ménière's disease and superior semicircular canal dehiscence (SSCD)

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🟡 TEST 19: DYNAMIC POSTUROGRAPHY (Computerized Dynamic Posturography / CDP)

Dynamic posturography provides information about balance system function that is not available through other vestibular testing modalities. It is primarily a test of functional capability rather than site-of-lesion evaluation. — Cummings Otolaryngology

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🟡 TEST 20: ELECTROCOCHLEOGRAPHY (ECoChG)

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🟡 TEST 21: AUDITORY BRAINSTEM RESPONSE (ABR / BAER)

• Wave I = cochlear nerve
• Wave III = cochlear nucleus / pons
• Wave V = inferior colliculus

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🟡 TEST 22: OTOACOUSTIC EMISSIONS (OAEs)

• Transient OAEs (TEOAEs): Presence indicates outer hair cells are functioning; absent in hearing loss >30 dB
• Distortion Product OAEs (DPOAEs): Provides frequency-specific information

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SECTION D — NEUROIMAGING

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🔴 TEST 23: MRI BRAIN WITH GADOLINIUM (Internal Auditory Canals)

• Unexplained unilateral sensorineural hearing loss
• Unexplained unilateral vestibular hypofunction
• Suspected vestibular schwannoma (acoustic neuroma)
• Central vestibular syndrome suspected (abnormal HINTS, direction-changing nystagmus, neurological signs)
• Posterior fossa lesion suspected

MRI is the diagnostic modality of choice for posterior fossa lesions, as well as for vestibular schwannoma and MS. Gadolinium contrast is required to detect schwannomas. — Rosen's Emergency Medicine

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🔴 TEST 24: CT SCAN OF TEMPORAL BONE

Superior canal dehiscence (absence of overlying bone on the superior semicircular canal) causes a unique syndrome: vertigo triggered by loud sounds (Tullio phenomenon) or pressure changes, plus low-frequency conductive hearing loss with normal tympanograms.

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SECTION E — BLOOD AND ROUTINE LABORATORY TESTS

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SECTION F — COMPLETE TEST RESULT SUMMARY TABLE

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STANDING ALGORITHM — Emergency / Clinical Decision

1. Is nystagmus present? (use Frenzel goggles)
   • Direction-changing / vertical / pure torsional → Central (stop, image)
   • Unidirectional → proceed to Step 2
2. Head Impulse Test
   • Positive (saccade) + unidirectional nystagmus → Peripheral (vestibular neuritis)
   • Negative (no saccade) + any nystagmus → Central (stroke)
3. Can patient walk/stand independently?
   • No → Central until proven otherwise
   • Yes + peripheral signs → Peripheral vestibular cause

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QUICK REFERENCE: WHICH TEST FOR WHICH CONDITION

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📖 FULL VNG INTERPRETATION — A Complete Learner's Guide

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WHAT IS VNG?

• The patient wears infrared goggles/cameras that record eye movements in real time
• Cameras capture the pupil and corneal reflections at high speed
• Eye movements are plotted on a graph (position or velocity vs. time)
• Results are analyzed by a trained audiologist or neuro-otologist

It is always important to review the original recordings and not rely on the interpretations of others or automated readings of data tracings. — Cummings Otolaryngology

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THE VNG BATTERY — 9 SUBTESTS IN 2 CATEGORIES

VNG BATTERY
│
├── OCULOMOTOR SUBTESTS (tests the BRAIN — central pathways)
│     1. Saccade Testing
│     2. Smooth Pursuit Testing
│     3. Optokinetic Testing (OKN)
│     4. Gaze / Fixation Testing
│
└── VESTIBULAR SUBTESTS (tests the INNER EAR / CN VIII)
      5. Spontaneous Nystagmus
      6. Gaze-Evoked Nystagmus
      7. Positional Nystagmus Testing
      8. Positioning Nystagmus (Dix-Hallpike / Supine Roll)
      9. Bithermal Caloric Testing ← THE MOST IMPORTANT SUBTEST

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PART 1 — OCULOMOTOR SUBTESTS

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🔵 SUBTEST 1: SACCADE TESTING

What Are Saccades?

How the Test is Done:

• Patient sits in front of a light bar or screen
• Random dots/lights appear at various positions (left/right, 5° to 30°)
• Patient jumps eyes to each new target as quickly as possible
• Head is kept still

What is Measured:

How to Read the Saccade Tracing:

Normal saccade trace looks like this:
         ________
        |        |
________|         |_______
   target         target
(Steps = sharp, quick, accurate)

Abnormal patterns:
Undershoot (hypometria):  ___/¯¯¯  (eye falls short, makes correction)
Overshoot (hypermetria):  ¯¯¯\___ (eye goes too far, corrects back)
Slow saccades:            /¯¯¯¯¯\ (reduced velocity - "round top")

Interpreting Saccade Results:

Key rule: If saccades are abnormal but caloric test is normal → central pathology is highly likely. — K.J. Lee's Essential Otolaryngology

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🔵 SUBTEST 2: SMOOTH PURSUIT TESTING

What Is Smooth Pursuit?

How the Test is Done:

• A dot moves slowly and sinusoidally back and forth on the screen
• Frequency: 0.2–0.7 Hz, amplitude: ±20° (total arc of 40°)
• Patient follows the dot without moving their head

What is Measured: Pursuit Gain

• Gain = eye velocity / target velocity
• Normal gain = 0.8–1.0 (eyes keep up smoothly with the target)

How to Read the Pursuit Tracing:

NORMAL (gain ~1.0) — eyes mirror the target:
Target:  /\/\/\/\/\/\
Eyes:    /\/\/\/\/\/\   ← Perfect smooth tracking

ABNORMAL (saccadic pursuit) — catch-up saccades appear:
Target:  /\/\/\/\/\/\
Eyes:    /\/|/\/|/\/|   ← Staircase pattern with saccades

ABNORMAL (reduced gain) — eyes lag behind:
Target:  /\/\/\/\/\/\
Eyes:    /\__/\__/\__   ← Flat, lagging

Interpreting Pursuit Results:

"Saccadic pursuit" — a staircase pattern — is characteristic of cerebellar disease and also occurs with the decreased pursuit gain of normal aging. — Cummings Otolaryngology

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🔵 SUBTEST 3: OPTOKINETIC TESTING (OKN)

What Is the Optokinetic Reflex?

How the Test is Done:

• A large striped drum or full-field moving pattern is presented
• Moving at 30–60°/s, first in one direction then the other
• VNG records the resulting nystagmus

What is Measured:

• OKN gain = slow-phase eye velocity / stimulus velocity
• Symmetry between leftward and rightward stimulation

Interpreting OKN:

Slow-phase abnormalities on optokinetic tests parallel those detected with smooth-pursuit testing, whereas quick-phase abnormalities are correlated with saccade testing. — Cummings Otolaryngology

OKAN (Optokinetic After-Nystagmus):

• Relies on the velocity storage mechanism (vestibular nuclei + cerebellum)
• Reduced in bilateral peripheral vestibular loss
• Asymmetric in unilateral vestibular hypofunction (greater toward side of lesion)

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🔵 SUBTEST 4: GAZE / FIXATION TESTING

What Is Fixation Suppression?

How the Test is Done:

• Patient looks straight ahead (primary gaze) first with eyes open with fixation target, then in a darkened environment (goggles block light)
• Then patient looks 30° to the right, left, up, down

What is Measured:

• Fixation Index = nystagmus SPV with fixation / SPV without fixation
• Normal: fixation reduces or eliminates nystagmus

Interpreting Gaze/Fixation:

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PART 2 — VESTIBULAR SUBTESTS

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🟠 SUBTEST 5: SPONTANEOUS NYSTAGMUS (with and without fixation)

What It Tests:

How the Test is Done:

1. Patient looks straight ahead
2. Eyes OPEN with fixation target (light on)
3. Eyes in darkness (goggles, no fixation)
4. Record any nystagmus

How to Read the Tracing:

Normal: Flat line — no eye movement at rest
         _________________________

Abnormal: Regular sawtooth = spontaneous nystagmus present
         /|/|/|/|/|/|/|/|/|/|/|
         slow  fast  (jerk nystagmus)
         ← slow phase    ↑fast phase

Interpreting Spontaneous Nystagmus:

Alexander's Law — MUST KNOW for VNG:

The slow-phase velocity of peripheral nystagmus increases when the eyes look in the direction of the fast phase and decreases when looking away from it. — K.J. Lee's Essential Otolaryngology

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🟠 SUBTEST 6: GAZE-EVOKED NYSTAGMUS

What It Tests:

How Done:

Interpretation:

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🟠 SUBTEST 7: POSITIONAL NYSTAGMUS TESTING

What It Tests:

Positions Tested (Static Holds):

1. Supine (lying flat on back)
2. Right lateral (lying on right side)
3. Left lateral (lying on left side)
4. Head-right (supine, head turned right)
5. Head-left (supine, head turned left)

Types of Positional Nystagmus:

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🟠 SUBTEST 8: POSITIONING NYSTAGMUS (Dix-Hallpike / Supine Roll)

This is the DYNAMIC test — the patient is moved RAPIDLY into position.

Dix-Hallpike — Posterior Canal BPPV

• Latency: 3–10 seconds after positioning
• Upbeat + torsional nystagmus
• Duration: 5–30 seconds then stops
• Reversal on return to sitting
• Fatigues with repetition (diminishes each time test is repeated)

• No latency (begins immediately)
• No fatigability (stays just as strong with repeated testing)
• Purely vertical or torsional (not the mixed upbeat+torsional of BPPV)
• Persists >90 seconds in head-hanging position

PERIPHERAL BPPV (Hallpike tracing):
Time → 0  3s  5s         30s
        |  |___|          |
        |  /\  \          |___  ← resolves spontaneously
           peak  decay
        ↑ latency   ↑ fatigues

CENTRAL (Hallpike tracing):
Time →  0  1s     steady...
        |  |______________
        | immediate onset, no decay, persists

Supine Roll Test — Horizontal Canal BPPV

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🔴 SUBTEST 9: BITHERMAL CALORIC TESTING — THE HEART OF VNG

Principle: Why Does Temperature Cause Nystagmus?

• Warm (44°C) irrigation → endolymph near the ear rises (less dense) → ampullopetal flow (toward the ampulla) → hair cells excited → nystagmus toward the same (irrigated) ear → "W" in COWS
• Cold (30°C) irrigation → endolymph near the ear sinks (more dense) → ampullofugal flow (away from ampulla) → hair cells inhibited → nystagmus toward the opposite ear → "C" in COWS

COWS Mnemonic:

Cold → Opposite | Warm → Same

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The 4 Irrigations of Bithermal Caloric Testing:

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What is Measured: SPV (Slow Phase Velocity)

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Real VNG Caloric Tracing — What You Are Looking At:

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Jongkees Formulas — THE CALCULATIONS YOU MUST KNOW

• RW = Right Warm SPV
• RC = Right Cold SPV
• LW = Left Warm SPV
• LC = Left Cold SPV

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Formula 1: UNILATERAL WEAKNESS (UW) / Canal Paresis (CP)

        [(RW + RC) - (LW + LC)]
UW% = ─────────────────────────── × 100
        (RW + RC + LW + LC)

• UW < 25% = Normal (both ears respond equally)
• UW ≥ 25% = Abnormal — Canal Paresis on the side with SMALLER total response
• If right side has smaller (RW+RC), then there is Right Canal Paresis

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Formula 2: DIRECTIONAL PREPONDERANCE (DP)

        [(RW + LC) - (LW + RC)]
DP% = ─────────────────────────── × 100
        (RW + RC + LW + LC)

• DP < 30% = Normal (nystagmus beats equally in both directions)
• DP ≥ 30% = Significant directional imbalance — the brain/vestibular system has a persistent bias toward one direction
• DP directed away from a peripheral lesion (the intact ear dominates)
• DP directed toward a central lesion (less reliable clinically)

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Worked Example — Step by Step:

• RW = 20°/s (right warm)
• RC = 14°/s (right cold)
• LW = 42°/s (left warm)
• LC = 38°/s (left cold)

[(20+14) - (42+38)]  ÷  (20+14+42+38)  × 100
= [34 - 80]  ÷  114  × 100
= -46  ÷  114  × 100
= -40%  → 40% RIGHT canal paresis

[(20+38) - (42+14)]  ÷  114  × 100
= [58 - 56]  ÷  114  × 100
= 2  ÷  114  × 100
= 1.7%  → Normal DP

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VNG Caloric Finding — "Caloric Inversion"

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VNG Caloric — Bilateral Weakness (BW):

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Hyperactive Caloric Response:

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Special Caloric Consideration — Fixation Suppression During Calorics:

• A fixation light is turned on
• Normally the caloric nystagmus reduces by >50% (peripheral suppression)
• Failure to suppress = Fixation Index <0.5 → central pathology (cerebellar flocculus damage)

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PART 3 — PUTTING IT ALL TOGETHER

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VNG Pattern Recognition — The 5 Essential Patterns

Pattern 1: UNILATERAL PERIPHERAL VESTIBULAR HYPOFUNCTION

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Pattern 2: BILATERAL PERIPHERAL VESTIBULAR HYPOFUNCTION

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Pattern 3: BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)

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Pattern 4: CENTRAL VESTIBULAR LESION

KEY RULE: Abnormal saccades or saccadic pursuit with normal caloric responses = central pathology until proven otherwise. — K.J. Lee's Essential Otolaryngology

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Pattern 5: UNCOMPENSATED PERIPHERAL LESION (Chronic / Rehabilitating)

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QUICK REFERENCE: PERIPHERAL vs. CENTRAL ON VNG

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COMMON CLINICAL SCENARIOS — VNG INTERPRETATION

🔎 Case 1:

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🔎 Case 2:

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🔎 Case 3:

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🔎 Case 4:

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🔎 Case 5:

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FACTORS THAT CAN AFFECT VNG ACCURACY — PITFALLS

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SUMMARY: HOW TO READ A VNG REPORT IN 5 STEPS

STEP 1 — OCULOMOTOR TESTS (Saccades, Pursuit, OKN, Fixation)
          Normal? → No central pathology
          Abnormal? → Central lesion likely regardless of caloric result

STEP 2 — SPONTANEOUS NYSTAGMUS
          Present? → Suppressed by fixation? (peripheral) / Not suppressed? (central)
          Direction? Fixed (peripheral) / Changing (central)

STEP 3 — POSITIONAL / POSITIONING TESTS
          Dix-Hallpike positive? → Check: latency, direction, fatigability → BPPV vs. central
          Static positions: direction-fixed vs. direction-changing

STEP 4 — CALORIC RESULTS
          Calculate UW% and DP%
          UW ≥25% → Canal paresis (which ear is weaker)
          Bilateral weakness → Think ototoxicity / autoimmune / degeneration
          Fixation suppression: Intact (peripheral) / Failed (central)

STEP 5 — INTEGRATE ALL FINDINGS → Pattern Recognition
          Peripheral pattern → counsel on diagnosis + treatment
          Central pattern → urgent neuroimaging (MRI-DWI)
          Mixed pattern → consider neuro-otology referral

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