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I now have comprehensive information from both textbooks and clinical sources. Here is the full VNG report:
Full VNG (Videonystagmography) Report
What is VNG?
Videonystagmography (VNG) is a complete diagnostic system for recording, analyzing, and reporting eye movements using infrared video goggle technology. It evaluates vestibular (inner ear) function, differentiates peripheral from central lesions, and identifies unilateral versus bilateral involvement. It has largely replaced ENG (electronystagmography) because it directly records eye movements rather than measuring them indirectly through corneoretinal potentials.
SECTION 1 - OCULOMOTOR (CENTRAL) TESTS
These tests assess non-vestibular eye movement pathways. Any abnormality in these tests points to a central (CNS) lesion.
1A. Saccade Test
Purpose: Assesses rapid refixation eye movements controlled by the frontal cortex, basal ganglia, cerebellum, and brainstem.
Parameters measured:
| Parameter | Normal Value | Abnormal |
|---|---|---|
| Latency | < 200-260 ms | > 260 ms |
| Velocity | > 275 °/s | < 275 °/s |
| Accuracy (gain) | 80-134% | < 80% or > 134% |
Interpretation:
- Delayed latency (>260 ms): Frontal/frontoparietal cortex or basal ganglia lesion (more significant if unilateral)
- Reduced velocity (<275°/s): Brainstem or cerebellar pathology
- Hypometria (undershoot): Cerebellar flocculus lesion
- Hypermetria (overshoot): Cerebellar vermis lesion
- Abnormal saccades = always central; never peripheral
1B. Smooth Pursuit (Tracking) Test
Purpose: Assesses the ability to smoothly follow a moving target; controlled by the vestibulocerebellum, ipsilateral cerebellar hemisphere, brainstem, and parieto-occipital cortex.
Parameter measured:
| Parameter | Normal Value | Abnormal |
|---|---|---|
| Gain (eye velocity / target velocity) | 0.9 - 1.0 (for targets <20°/s) | < 0.9 |
Interpretation:
- Symmetric defect: Diffuse cortical, basal ganglia, or cerebellar dysfunction (also seen with sedating medications)
- Asymmetric/unilateral defect: Focal lesion in the ipsilateral cerebellar hemisphere, brainstem, or parieto-occipital region
- Saccadic pursuit (broken pursuit) = central pathology
1C. Optokinetic (OPK) Test
Purpose: Measures nystagmus generated by a large moving visual field (moving stripes or patterns).
Normal: Symmetric gain in both directions (rightward and leftward stimulation).
Interpretation:
- Asymmetric OPK: Central lesion; the response is reduced in the direction toward the side of the lesion
- Absent OPK: Severe bilateral central dysfunction
- Use of OKAN (Optokinetic After-Nystagmus): nystagmus persisting after stimulation stops reflects velocity storage in the vestibular nuclei (brainstem)
SECTION 2 - VESTIBULAR TESTS
2A. Spontaneous Nystagmus Test
Purpose: Detects nystagmus present at rest, recorded without visual fixation, with the patient in a neutral head-upright position.
Normal: No nystagmus, or intensity < 4°/s (horizontal) or < 7°/s (vertical) in the absence of fixation.
Interpretation - Peripheral pattern:
- Horizontal or horizontal-torsional direction
- Follows Alexander's Law (nystagmus intensifies when gazing in the direction of the fast phase)
- Suppressed by fixation (intensity reduces by ≥50% with visual fixation)
- Direction-fixed (does not change direction with change in gaze position)
- Associated with intact fixation suppression
Interpretation - Central pattern:
- Present with fixation and not significantly increased by removing fixation
- Direction-changing nystagmus in a single gaze position
- Pure vertical nystagmus (up-beat or down-beat)
- Failure of fixation suppression
2B. Gaze Nystagmus Test
Purpose: Detects nystagmus that appears or changes in different gaze directions (eyes deviated to the right, left, up, or down).
Normal: Minimal or no nystagmus in any gaze direction. Square-wave jerks of 0.5-5° at 20-30 per minute are considered normal.
Interpretation:
| Finding | Significance |
|---|---|
| Direction-changing nystagmus | Central lesion |
| Gaze-evoked nystagmus (bilateral) | Cerebellum or brainstem |
| Macro square-wave jerks (5-15°) | Brainstem or cerebellar pathology |
| Macro saccadic oscillations | Cerebellar pathology |
| Ocular flutter / opsoclonus | Brainstem or cerebellar pathology |
| Rebound nystagmus | Cerebellar lesion |
2C. Positional Test (Static)
Purpose: Detects nystagmus triggered by sustained static head positions. The patient is moved slowly into at least 4 positions and held there for ≥30 seconds each:
- Sitting
- Supine (head elevated 30° - caloric test position)
- Head right
- Head left
- Body right / Body left (if needed)
Normal: No significant nystagmus in any position (threshold < 4°/s horizontal or < 7°/s vertical).
Interpretation - Peripheral:
- Direction-fixed nystagmus
- Fatigues with repeated testing
Interpretation - Central:
- Direction-changing nystagmus in a single head position
- Non-fatiguing nystagmus
- Pure vertical nystagmus
2D. Positioning Test (Dynamic) - Dix-Hallpike and Roll Test
Purpose: Detects nystagmus triggered by rapid head movement into a specific position. The most common: Dix-Hallpike maneuver (for posterior canal BPPV).
Normal response: No nystagmus.
BPPV - Posterior Canal (Dix-Hallpike):
- Upbeat-torsional nystagmus toward the affected (lower) ear
- Latency of 2-20 seconds
- Duration < 60 seconds
- Fatigues with repeated testing
BPPV - Horizontal Canal (Roll Test):
- Geotropic or ageotropic horizontal nystagmus
- Geotropic: canalolithiasis (more intense toward the affected ear)
- Ageotropic: cupulolithiasis (beats away from the affected ear)
2E. Bithermal Caloric Test
Purpose: The most clinically important component. Independently stimulates each horizontal semicircular canal (SCC) by irrigating the external auditory canal with warm and cool water or air.
Patient position: Supine, head elevated 30° (places horizontal SCC in the vertical plane for maximum stimulation).
Stimulus:
- Water: 30°C (cool) and 44°C (warm) for 30 seconds each ear
- Air (used with TM perforation): 24°C (cool) and 58°C (warm) for 60 seconds each ear
Mnemonic - COWS: Cold Opposite, Warm Same (refers to the direction of the fast phase of nystagmus)
Physiological mechanism:
- Cool irrigation → endolymph drops → ampullofugal flow → hair cell inhibition → slow drift toward the irrigated ear → fast phase AWAY from irrigated ear
- Warm irrigation → endolymph rises → ampullopetal flow → hair cell excitation → slow drift away from irrigated ear → fast phase TOWARD the irrigated ear
Calculations:
Unilateral Weakness (UW%):
UW% = [(RW + RC) - (LW + LC)] / (RW + RC + LW + LC) × 100%
- Abnormal: >20-25% (laboratory dependent; some use 15-30%)
- Indicates weakness on the side with the lower combined response
- Suggests peripheral vestibular hypofunction on the weaker side
Directional Preponderance (DP%):
DP% = [(RW + CL) - (LW + CR)] / (RW + CR + LW + CL) × 100%
- Abnormal: >30% (some use 25-50%)
- Clinical significance is debated; roughly half are peripheral, ~5% central
Fixation Index (FI%):
- Abnormal: >60% (some use 50-60%)
- Measures failure of visual fixation to suppress caloric nystagmus
- Failure of fixation suppression = central lesion
Reference values summary:
| Finding | Threshold | Interpretation |
|---|---|---|
| Unilateral weakness | >20-25% | Peripheral vestibular hypofunction (side of weaker response) |
| Bilateral weakness | Total each ear <12°/s | Bilateral vestibular hypofunction |
| Directional preponderance | >30% | Peripheral or central; clinical significance debated |
| Fixation suppression failure | FI >60% | Central lesion |
| Hyperactive response | >140°/s per ear | Cerebellar disinhibition (check for TM perforation/mastoid cavity first) |
Practical considerations:
- Perform otoscopy before ordering caloric testing
- Water is contraindicated if TM perforation is present; use air instead
- Excess cerumen must be removed prior to testing, as it impedes accuracy
- Bilateral caloric hypofunction does not confirm bilateral complete vestibular loss; supplement with rotary chair or vHIT
SECTION 3 - OVERALL INTERPRETATION SUMMARY
Findings Suggesting PERIPHERAL Pathology:
- Unilateral caloric weakness
- Bilateral caloric weakness with history of labyrinthine disease or ototoxicity
- Fatiguing, direction-fixed positional nystagmus
- Spontaneous nystagmus suppressed by fixation
- Intact fixation suppression response
- Horizontal-torsional nystagmus following Alexander's Law
Findings Suggesting CENTRAL Pathology:
- Spontaneous/positional nystagmus with normal calorics
- Direction-changing nystagmus in a single head/gaze position
- Failure of fixation suppression (FI >60%)
- Bilateral reduced/absent calorics without prior labyrinthine disease or ototoxicity
- Abnormal saccades or saccadic pursuit (especially with normal calorics)
- Hyperactive caloric responses (loss of cerebellar inhibition)
- Pure vertical nystagmus (upbeat or downbeat)
SECTION 4 - COMMON DIAGNOSES AND VNG PATTERNS
| Diagnosis | Key VNG Findings |
|---|---|
| BPPV (posterior canal) | Positive Dix-Hallpike: upbeat-torsional nystagmus, latency 2-20s, duration <60s, fatigable; normal calorics |
| BPPV (horizontal canal) | Positive roll test: geotropic or ageotropic horizontal nystagmus |
| Unilateral peripheral vestibular hypofunction (e.g. neuritis, labyrinthitis) | UW >25% on affected side; direction-fixed spontaneous nystagmus toward healthy ear; intact fixation suppression |
| Bilateral vestibular hypofunction | Bilateral caloric weakness; total each ear <12°/s; no spontaneous nystagmus |
| Central vestibular lesion (e.g. posterior fossa tumor, infarct, MS) | Abnormal OPK/pursuit/saccades; direction-changing positional nystagmus; failure of fixation suppression; normal or asymmetric calorics |
| Cerebellar ataxia | Dysmetric saccades (hypermetria), broken pursuit, gaze-evoked nystagmus, abnormal OPK |
SECTION 5 - IMPORTANT LIMITATIONS
- VNG evaluates only the horizontal semicircular canal via calorics (low frequency, ~0.003 Hz); higher-frequency canals require rotary chair or vHIT
- Bilateral caloric hypofunction does not confirm bilateral complete loss; supplement with rotary chair or vHIT
- Many medications (sedatives, antivertigo drugs, anticonvulsants) suppress nystagmus - patients must stop these prior to testing
- The test is performed in an isolated frequency range; the true vestibular deficit may be underestimated
Sources: K.J. Lee's Essential Otolaryngology (9781260122237); StatPearls - VNG/ENG Testing (NCBI NBK599515); Mekki S. - Role of VNG in Assessment of the Dizzy Patient; Canadian Academy of Audiology - VNG Interpretation Workshop
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