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VNG (Videonystagmography) Report — Detailed Graph Analysis & Diagnosis

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🔍 SECTION-BY-SECTION GRAPH ANALYSIS

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1. SACCADE TESTING

A. Horizontal Saccades — 0.3 Hz

B. Horizontal Saccades — 0.45 Hz

C. Random Frequency/Amplitude Horizontal Saccades

D. Vertical Saccades — 0.3 Hz ⚠️ ABNORMAL

• Markedly reduced velocities — well below the 400°/s normal threshold
• Very poor precision (~20–33%) — extremely hypometric (undershooting)
• Severely prolonged latencies — >500 ms
• Asymmetry between right and left eye on vertical axis

E. Vertical Saccades — 0.45 Hz ⚠️ ABNORMAL

F. Hemifield Saccades

• Left Hemifield (rightward gaze target): Velocity ~474/395°/s (RE/LE); Precision 68.48/85.34%; Latency ~287–294 ms
• Right Hemifield (leftward gaze target): Velocity ~372/363°/s; Precision 77.62/76.72%; Latency ~254/250 ms

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2. SMOOTH PURSUIT TESTING ⚠️ SIGNIFICANTLY ABNORMAL

Horizontal Smooth Pursuit

Vertical Smooth Pursuit

• Horizontal gain at 0.2 Hz is only 0.30–0.39 (normal ≥0.8)
• Horizontal gain at 0.4 Hz is only 0.12–0.18 (normally ~0.6–0.7)
• Vertical pursuit gain is even more severely impaired (0.09–0.26)
• The impairment is symmetric bilaterally and affects both horizontal and vertical planes

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3. OPTOKINETIC TEST (OKN)

• Horizontal OKN is normal (gain ≈ 1.0)
• Vertical OKN is markedly elevated (gains 1.3–2.0), suggesting abnormal velocity storage or vertical canal/otolith pathway dysfunction
• Fast phase was absent in the left-to-right and vertical directions; present in right-to-left (145–152°) which is within expected range

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4. NYSTAGMUS TESTING

A. Spontaneous in Light — NORMAL

B. Spontaneous in Dark — NORMAL

C. High-Frequency Head Shake ⚠️ ABNORMAL

D. Hyperventilation — NORMAL

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5. GAZE TESTING

Gaze with Fixation (Fixation Suppression Active)

• Center, Left, Right, Down: All parameters normal (all values "–")
• Gaze Up with Fixation: ⚠️ Left eye shows SPV –4.36°/s, amplitude –1.48°, frequency 1.34 Hz → upward gaze nystagmus on left eye

Gaze Without Fixation (Eyes in Darkness) ⚠️ MULTIPLE ABNORMALITIES

• The nystagmus is predominantly vertical/mixed direction
• It appears in multiple gaze positions — this is direction-changing positional nystagmus or gaze-evoked nystagmus without fixation
• The fact that fixation suppresses the nystagmus in most positions supports a peripheral-to-central mixed etiology
• Right gaze without fixation shows bidirectional components (horizontal + vertical on left eye), which leans central

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6. DIX-HALLPIKE POSITIONAL TESTING

Dix-Hallpike Right

• Sit Head Right: No nystagmus (normal baseline)
• Supine Head Extended + Right: ⚠️ ABNORMAL
  • Right Eye: SPV –8.47°/s, Amplitude –3.02°, Frequency 1.07 Hz
  • Left Eye: SPV –7.22°/s, Amplitude –4.87°, Frequency 0.85 Hz
  • Vertical nystagmus present bilaterally in this position
• Return to Sit: No nystagmus (fatigable)

Dix-Hallpike Left

• Sit Head Left (first): Left eye: SPV –4.37°/s, Amplitude –2.48°, Frequency 0.80 Hz (mild)
• Supine Head Extended + Left: ⚠️ ABNORMAL
  • Right Eye: SPV –6.01°/s, Amplitude –4.08°, Frequency 0.75 Hz
  • Left Eye: SPV –5.27°/s, Amplitude –4.86°, Frequency 0.54 Hz
• Nystagmus is bilateral and predominantly vertical (downbeat component)

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7. YACOVINO POSITIONAL TEST (Cupulolithiasis/Central Positional Nystagmus)

• Strong persistent downbeat nystagmus elicited in the Yacovino maneuver
• SPV reaches –19.74°/s at maximal head extension — this is highly significant
• Yacovino sign (downbeat nystagmus in this position) is classically associated with central positional nystagmus from the cerebellum, specifically the nodulus and uvula
• The persistence (not fatiguing) and bilateral nature strongly favor central etiology

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8. McCLURE-PAGNINI POSITIONAL TEST (Horizontal Canal BPPV)

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🧠 INTEGRATED DIAGNOSTIC IMPRESSION

Summary of Key Findings

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📋 DIAGNOSIS

Primary Diagnosis:

Central Vestibular Dysfunction — Strongly Suggestive of Cerebellar Pathology (Likely Involving Posterior Fossa / Cerebellar Flocculus-Nodulus Complex)

Supporting Evidence:

1. Severely impaired vertical saccades (velocity 113–238°/s; normal >400°/s) with poor precision — this is a hallmark of central vestibular or cerebellar pathology, particularly involving the fastigial nucleus or posterior vermis
2. Bilaterally symmetric, severely reduced smooth pursuit in all directions (gain as low as 0.09) — characteristic of cerebellar or brainstem lesion affecting the flocculus
3. Positive Yacovino test with strong downbeat positional nystagmus — classic for nodulus/uvula cerebellar lesion or anterior canal pathology
4. Post-head-shake vertical nystagmus — indicative of central canal/otolith imbalance, not peripheral
5. Nystagmus not suppressed consistently by fixation in multiple gaze directions — favors central over peripheral
6. No spontaneous nystagmus in light/dark and negative McClure-Pagnini — argues against acute unilateral peripheral vestibulopathy or BPPV

Differential Diagnoses to Consider:

1. Cerebellar degenerative disease (e.g., spinocerebellar ataxia, multiple system atrophy — cerebellar type)
2. Posterior fossa mass lesion (e.g., vestibular schwannoma, cerebellar tumor — though these often also show caloric asymmetry)
3. Episodic ataxia type 2 (EA2) — presents with downbeat nystagmus, cerebellar findings
4. Downbeat nystagmus syndrome (may be idiopathic cerebellar; associated with Mg/vitamin deficiencies, medications like lithium, anticonvulsants)
5. Cervical-cerebellar syndrome / Arnold-Chiari malformation — Chiari I classically causes downbeat positional nystagmus
6. Demyelinating disease (Multiple Sclerosis with brainstem plaques)
7. Vascular (vertebrobasilar insufficiency or cerebellar infarct/TIA given patient age 55)

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🏥 RECOMMENDED NEXT STEPS

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⚠️ CLINICAL NOTE

This report reflects findings from a 55-year-old male. The combination of severely impaired smooth pursuit, impaired vertical saccades, and positive Yacovino test with downbeat positional nystagmus constitutes a central vestibular/cerebellar pattern that requires urgent neurological workup. These findings are not consistent with a benign peripheral vestibular disorder (BPPV, vestibular neuritis, or Menière's disease) and should prompt MRI of the posterior fossa as a priority.

This analysis is provided for clinical decision support. Final diagnosis must be correlated with clinical examination findings, patient history, and additional investigations by the treating clinician.