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VNG videonystagmography interpretation spontaneous nystagmus dark bilateral gaze diagnosis

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VNG spontaneous nystagmus dark slow phase velocity 15-20 degrees second diagnosis peripheral vestibular

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VNG Report Interpretation - Satish Bansal (73M, 03-Jun-2026)

Summary of Key Findings

1. Oculomotor Tests

Saccades (Horizontal)

Velocity: Right eye 500°/s, Left eye 1066°/s - asymmetric, but horizontal saccade velocities can vary; left eye velocity is elevated/noisy
Latency: ~247-274 ms (borderline prolonged; normal < ~200 ms)
Precision: Right 82, Left 134 - left eye overshooting (hypermetric saccades)

Smooth Pursuit (Horizontal)

Rightward gain: Right eye 0.16, Left eye 0.30 - severely reduced (normal ~0.8-1.0)
Leftward gain: Right 0.52, Left 0.88 - reduced on the right eye, near-normal on the left
This is a markedly abnormal smooth pursuit, particularly in the rightward direction
Vertical pursuit: gains 0.61-0.76 - mildly reduced but closer to normal

Optokinetic Test (OKN)

Generally symmetric and within acceptable range bilaterally (gains 0.67-1.13)
OKN relatively preserved compared to smooth pursuit - this asymmetry between OKN and pursuit can occur in central pathology

2. Spontaneous Nystagmus

In Light: No nystagmus - normal (fixation suppresses it)

In Dark:

Horizontal SPV: -17.12°/s (right eye), -16.56°/s (left eye) - significant left-beating nystagmus (negative SPV = slow phase to the right = fast phase to the LEFT)
Vertical SPV: -3.70 to -6.96°/s - also present
Frequency ~2.4-2.6 Hz
This is abnormal. SPV >6°/s in dark is clinically significant. The nystagmus is suppressed with fixation in light - this is a pattern consistent with peripheral vestibular lesion (intact fixation suppression).

Head-Shake Nystagmus:

Post-head-shake nystagmus present in left eye only (SPV -2.74°/s horizontal, -3.39°/s vertical)
This suggests vestibular asymmetry, typically peripheral

3. Gaze Tests

With Fixation (Center):

Right eye: no nystagmus
Left eye: SPV -5.48°/s (horizontal), -3.59°/s (vertical) - nystagmus persists with fixation in center gaze

Without Fixation (Center):

Both eyes: SPV ~-15°/s horizontal - persistent left-beating nystagmus suppressed by fixation

Gaze Left, Right, Down without fixation:

Nystagmus noted in multiple positions without fixation
Direction appears consistent (left-beating) across gaze positions - direction-fixed nystagmus, favoring a peripheral origin per Lee's Otolaryngology criteria

4. Positional Tests (Dix-Hallpike)

Dix-Hallpike Right (supine head extended & right):

Both eyes: horizontal SPV ~-5.6°/s, vertical SPV ~-6 to -7°/s
Fast phase direction ~140-141° - nystagmus present

Dix-Hallpike Left (supine head extended & left):

Horizontal SPV ~-5.7°/s (both eyes)
Nystagmus present bilaterally

Yaw Right (head turned right): Nystagmus present (horizontal SPV ~-6 to -7°/s)

Pitch Backward: Nystagmus present bilaterally (SPV -5.5 to -8.2°/s)

Roll Right: Nystagmus present bilaterally

The positional nystagmus is present in multiple head positions bilaterally - this pattern (multi-positional nystagmus, not isolated to a single canal position) is more consistent with central positional nystagmus or horizontal canal BPPV / cupulolithiasis, rather than the classic posterior canal BPPV which gives a brief, fatigable vertical-torsional response.

5. Subjective Visual Vertical (SVV)

Clockwise: 3° deviation to the right
Anti-clockwise: -3° deviation to the left
Blank background: -1° deviation (left)
Normal SVV is ±2-2.5°. The 3° deviation is borderline/mildly abnormal.

Overall Interpretation

Feature	Finding	Interpretation
Spontaneous nystagmus in dark	Left-beating, SPV ~16-17°/s	Significant peripheral vestibular asymmetry
Fixation suppression	Nystagmus suppressed in light	Favors peripheral origin
Smooth pursuit	Severely reduced (rightward especially)	Suggests central involvement (cerebellum/brainstem)
Saccades	Hypermetric left, prolonged latency	Central (cerebellar) component possible
Positional nystagmus	Multi-positional, bilateral	Central positional nystagmus OR horizontal canal BPPV
Head-shake nystagmus	Present (left eye)	Vestibular asymmetry
SVV	Mildly deviated (3°)	Mild otolith dysfunction

Clinical Diagnosis (VNG-based)

Primary: Left-sided peripheral vestibular hypofunction (most likely), evidenced by:

Persistent left-beating spontaneous nystagmus in dark with fixation suppression
Direction-fixed nystagmus pattern
Head-shake nystagmus indicating vestibular asymmetry (right > left vestibular tone)

Additional concern - Central component cannot be excluded, because:

Markedly impaired smooth pursuit (rightward gain 0.16 right eye, 0.30 left eye) is a central oculomotor sign (cerebellar/brainstem)
Hypermetric saccades and prolonged saccadic latency
Multi-directional positional nystagmus
Smooth pursuit asymmetry disproportionate to the degree of peripheral nystagmus

Differential diagnoses to consider:

Vestibular neuritis (left side) - most common cause of this pattern in adults; acute/subacute unilateral peripheral vestibular loss
Chronic unilateral vestibular hypofunction - possibly incompletely compensated
Combined central + peripheral lesion (e.g., cerebellopontine angle lesion, posterior fossa pathology) - given the abnormal smooth pursuit and saccades alongside peripheral-type nystagmus
Horizontal canal BPPV - could explain multi-positional nystagmus component

Note: This VNG was performed without caloric testing (no bithermal caloric data in the report). Caloric testing is the gold standard for quantifying unilateral canal paresis and would be essential for confirming the side and degree of vestibular weakness. An MRI of the posterior fossa/IAC should be strongly considered given the central oculomotor signs (abnormal smooth pursuit, saccadic hypermetria) in a 73-year-old patient, to rule out acoustic neuroma, cerebellar stroke, or other posterior fossa pathology.

This interpretation is based on the raw VNG data. Clinical correlation with symptoms (onset, duration, hearing loss, tinnitus, neurological signs) and a formal audiogram + caloric testing are recommended to complete the vestibular workup. - Cummings Otolaryngology; Lee's Essential Otolaryngology, p.351

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VNG smooth pursuit gain 0.16 saccadic hypermetria spontaneous nystagmus dark peripheral vs central vestibular diagnosis criteria

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Final VNG Diagnosis - Satish Bansal (73M)

The Evidence, Weighed Systematically

Findings that point PERIPHERAL:

Spontaneous nystagmus in dark: left-beating, SPV ~16-17°/s - suppressed with fixation in light (intact fixation suppression = peripheral hallmark per Bradley & Daroff Neurology, p.366; Lee's Otolaryngology p.351)
Direction-fixed nystagmus (consistently left-beating across all gaze positions without fixation)
Head-shake nystagmus (left-beating = asymmetry with right side dominant = left side weaker)

Findings that point CENTRAL:

Smooth pursuit gain rightward: 0.16 (right eye), 0.30 (left eye) - severely reduced; normal is 0.90-1.0 (StatPearls VNG/ENG). This is the single most important central sign.
Saccade latency ~247-274 ms - borderline abnormal (>260 ms = abnormal per StatPearls)
Left eye saccade precision 134.83 - at the upper limit of the normal range (80-134%); technically borderline hypermetric
Multi-positional nystagmus (present in nearly all head positions) - more consistent with central positional nystagmus than classic BPPV

Applying the Decision Framework

The critical interpretive rule from Lee's Otolaryngology (p.351) is:

"Abnormal saccades or saccadic pursuit results, especially with normal caloric results = central pathology"

However, the caloric test was NOT performed here, so the full peripheral vs. central distinction cannot be made definitively from VNG alone. That said:

Intact fixation suppression + direction-fixed nystagmus = peripheral vestibular tone imbalance (left side deficit)
Severely impaired smooth pursuit + borderline saccade latency = coexisting central (cerebellar/brainstem) dysfunction

The combination of peripheral-type spontaneous nystagmus WITH impaired central oculomotor tests in a 73-year-old is a well-recognized pattern of mixed peripheral + central vestibular pathology.

FINAL DIAGNOSIS

Primary Diagnosis:

Left-sided Peripheral Vestibular Hypofunction (likely chronic/sub-acute unilateral vestibular loss, left ear)

Evidence: Direction-fixed left-beating spontaneous nystagmus in dark (SPV 16-17°/s), suppressed by fixation, with head-shake nystagmus indicating right > left vestibular tone asymmetry.

Co-existing / Overlapping Finding:

Central Oculomotor Dysfunction (cerebellar or brainstem involvement cannot be excluded)

Evidence: Severely impaired smooth pursuit (rightward gain 0.16-0.30, normal 0.90-1.0), borderline prolonged saccade latency, multi-positional nystagmus.

Most Likely Unifying Clinical Diagnosis:

Chronic Left Vestibular Neuropathy with Central Compensation Failure - OR - Cerebellopontine Angle (CPA) / Retrocochlear Pathology (e.g., acoustic neuroma / vestibular schwannoma) which can simultaneously cause peripheral vestibular loss AND affect adjacent cerebellar/brainstem oculomotor pathways.

Mandatory Next Steps

Investigation	Reason
MRI Brain + IAC with contrast	Rule out acoustic neuroma, cerebellar infarct, MS plaque, posterior fossa tumour - high priority in a 73-year-old with mixed central/peripheral VNG signs
Bithermal caloric testing	Incomplete without it - needed to quantify left canal paresis (%)
Pure tone audiogram	Sensorineural hearing loss would further support left vestibulocochlear pathology
Neurology / Neuro-otology referral	Given the central oculomotor signs

Bottom line for the report impression: "VNG findings are consistent with left peripheral vestibular hypofunction (direction-fixed left-beating spontaneous nystagmus with intact fixation suppression, left directional preponderance on head-shake). Abnormal smooth pursuit (rightward gain 0.16-0.30) and borderline saccadic latency indicate additional central oculomotor dysfunction. Mixed peripheral + central pattern in a 73-year-old warrants urgent MRI of the posterior fossa and internal auditory canals with contrast to exclude retrocochlear/CPA pathology. Caloric testing is strongly recommended to quantify vestibular canal paresis."

Lee's Essential Otolaryngology, p.351; Bradley & Daroff's Neurology in Clinical Practice, p.366; StatPearls: VNG/ENG Testing

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