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Videonystagmography (VNG) - Full Detailed Interpretation

Patient Details

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1. SACCADE TESTING

Horizontal Saccades (0.3 Hz)

Horizontal Saccades (0.45 Hz)

Vertical Saccades (0.3 Hz)

Vertical Saccades (0.45 Hz)

• Velocities are preserved (brainstem excitatory burst neurons intact).
• Precision is inconsistent - undershooting at some frequencies and overshooting at others, indicating cerebellar dysmetria (the cerebellum fine-tunes accuracy; impaired cerebellar function produces both hypo- and hypermetric saccades).
• The markedly prolonged latencies at 0.45 Hz vertical (491-492 ms, nearly double normal) suggest central pathway slowing, possibly involving the superior colliculus or cortical-brainstem pathways, consistent with age-related central changes or an early central lesion.

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2. SMOOTH PURSUIT TESTING

Horizontal Smooth Pursuit

Vertical Smooth Pursuit

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3. OPTOKINETIC TESTING (OKN)

Horizontal OKN

Vertical OKN

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4. SPONTANEOUS NYSTAGMUS

In Light

In Dark

• There is persistent spontaneous nystagmus both in light and in dark, with SPV exceeding 2°/s (horizontal SPV ~3.2-3.5°/s; vertical SPV ~5.8-6.6°/s).
• The nystagmus is present even with fixation (in light), which is significant - peripheral nystagmus is typically suppressed by fixation, but this one is not fully suppressed, suggesting a central component.
• A combined horizontal and vertical component (fast phase at 235.91° = oblique/down-left direction) is consistent with a down-beat or torsional-vertical nystagmus pattern, raising concern for central (particularly cerebellar or craniocervical junction) pathology.
• The nystagmus does not worsen substantially in darkness (SPV similar in light and dark), further pointing away from a purely peripheral vestibular lesion.

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5. HEAD SHAKE TEST

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6. GAZE TESTING

With Fixation

Without Fixation (Eyes Open in Dark / Vision Removed)

• Nystagmus appears on left gaze - with fixation it is mild but measurable (vertical 3.12°/s); without fixation (vision removed), it is dramatically amplified (horizontal SPV 13.63°/s + vertical SPV 9.18°/s with fast phases at ~325° = upper-left direction).
• The fact that nystagmus dramatically increases without fixation during left gaze = failure of fixation suppression - a hallmark of central vestibular pathology.
• The gaze-evoked nystagmus on left gaze (but not right) may indicate right cerebellar or right brainstem neural integrator dysfunction (GEN typically appears in the direction of the damaged side when the lesion is peripheral, but central lesions can produce asymmetric GEN).

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7. POSITIONAL TESTING

Dix-Hallpike (for posterior canal BPPV)

McClure-Pagnini Test (for horizontal canal BPPV)

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8. SUBJECTIVE VISUAL VERTICAL (SVV)

• The blank-background SVV (the most clinically relevant) is -1°, which is within the normal range (±2.5°), suggesting no gross utricular asymmetry at rest.
• However, the anticlockwise condition shows -6° deviation - a 6° tilt is abnormal and suggests otolith dysfunction, possibly involving the left utricle or its central connections, as the SVV tilts toward the side of the lesion in acute unilateral otolith dysfunction.
• The disparity between conditions (3° right in CW vs. 6° left in ACW) suggests abnormal otolith-ocular integration under dynamic conditions.

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OVERALL INTERPRETATION & CLINICAL SYNTHESIS

Summary Table of Findings

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Final Clinical Impression

The VNG findings in this 77-year-old male demonstrate a predominantly CENTRAL vestibular disorder pattern.

1. Severely reduced smooth pursuit (gains <0.5) in all planes - most consistent with cerebellar or cortical-cerebellar pathway disease.
2. Spontaneous nystagmus not suppressed by fixation (present in both light and dark at similar velocities).
3. Oblique/directional spontaneous nystagmus with a combined horizontal-vertical component (fast phase 235.91°/325.17°) - this directionality suggests cerebellar or brainstem involvement rather than a simple peripheral horizontal canal lesion.
4. Left gaze nystagmus amplified without fixation (failure of fixation suppression) - a definitive central sign.
5. Saccade dysmetria (undershooting and overshooting) and markedly prolonged latency at higher frequencies - pointing to cerebellar dysmetria and central pathway slowing.
6. Reduced upward vertical OKN - a brainstem/cerebellar sign.

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Recommended Next Steps

1. MRI brain with posterior fossa protocol (gadolinium-enhanced) to evaluate the cerebellum, cerebellar vermis, flocculus, brainstem, and craniocervical junction - given the pattern of pursuit failure, oblique spontaneous nystagmus, and failure of fixation suppression.
2. Bithermal caloric testing (if not contraindicated) to assess peripheral vestibular function quantitatively.
3. Neurological review - assessment for cerebellar ataxia, cerebellar signs (dysmetria, dysdiadochokinesia), and posterior fossa pathology.
4. Vestibular-evoked myogenic potential (VEMP) - cVEMP and oVEMP to assess saccular and utricular otolith function separately.
5. Video Head Impulse Test (vHIT) - to assess all six semicircular canals individually for gain and corrective saccades.

Note: This interpretation is based on the numerical and textual data extracted from the VNG report. Clinical correlation with the patient's symptoms (vertigo, imbalance, oscillopsia, falls, neurological symptoms) and physical examination findings is essential for final diagnosis and management.