VNG Interpretation - Kamal Sachdeva (57M) | 08-Jul-2026

COMPLETE FINDINGS SUMMARY

1. SACCADES (Pages 2-3)

• Latency: 250-330 ms (mildly prolonged)
• Precision: 72-84% (borderline to mildly reduced, especially LE downward at 72.85%)
• Velocities within acceptable range

2. SMOOTH PURSUIT (Pages 4-5) - ABNORMAL

• Normal gain = 0.8-1.0
• All gains are markedly reduced (0.22 - 0.66) - severely degraded pursuit
• Asymmetry: Rightward gain is consistently much worse than leftward gain (66.67% asymmetry at 0.2 Hz; 40.91% at 0.4 Hz), always biased toward leftward (L)
• The waveforms show catch-up saccades superimposed on sinusoidal target, confirming saccadic pursuit

• Marked upward-downward asymmetry: Downward gain is approximately 2x upward gain
• Upward pursuit severely impaired (gain 0.28-0.34); downward is also reduced but less so
• Gain asymmetry 42-62% in the Downward direction (meaning downward >> upward)

3. OPTOKINETIC NYSTAGMUS (Pages 6-7)

• Horizontal OKN gains: normal bilaterally (>1.0)
• Vertical OKN gains: reduced (0.61-0.76; normal >0.8), especially bottom-to-top
• Vertical OKN asymmetry consistent with the vertical pursuit abnormality
• No significant horizontal OKN asymmetry

4. GAZE TESTING (Pages 8-12) - NORMAL

• No gaze-evoked nystagmus in any direction (center, left, right, up, down)
• Both with and without fixation: no nystagmus recorded
• Gaze holding is intact

5. SPONTANEOUS NYSTAGMUS (Page 13) - NO CLINICALLY SIGNIFICANT NYSTAGMUS

• In Light (with fixation): No organized nystagmus. Traces show occasional small drift but no sustained rhythmic nystagmus pattern. Table confirms all parameters are "-"
• In Dark (without fixation): Low-amplitude irregular movements visible in the dark traces. No clear directional, high-velocity spontaneous nystagmus. The system did not auto-detect any nystagmus above threshold.

6. HEAD SHAKE TEST (Page 14) - NO POST-HEAD-SHAKE NYSTAGMUS

• The shaking phase shows vigorous head movement artifact (gray-shaded zone, first 10 seconds)
• After shaking ends (~10 seconds onward): no clear post-head-shake nystagmus is observed
• Traces return to baseline without a clear unidirectional nystagmus burst
• No vertical cross-axis nystagmus observed

7. POSITIONAL TESTING (Pages 15-17)

• Multiple position changes recorded
• No sustained nystagmus in any static position
• Eye movement reflects only position change transients, then settles to baseline
• No positional nystagmus

8. SUPINE ROLL TEST - McClure-Pagnini (Pages 18-20) - NEGATIVE

• Supine First, Right Lateral, Supine Second positions tested
• No geotropic or apogeotropic horizontal nystagmus observed on roll to either side
• No horizontal canal BPPV pattern

9. DIX-HALLPIKE RIGHT (Pages 21-22)

• Hallpike maneuver performed to the right
• The traces show head movement ("Pitch Forward" label, then extension "Right")
• No paroxysmal upbeat-torsional nystagmus pattern typical of posterior canal BPPV
• The eye traces show some movement artifact at position change but no sustained crescendo-decrescendo nystagmus
• Negative Dix-Hallpike right

10. DIX-HALLPIKE LEFT (Pages 23-24)

• "Yaw Left", "Extension Left", "Pitch Forward", "Hallpike" labels visible in sequence
• Similarly, no paroxysmal nystagmus characteristic of posterior canal BPPV
• Negative Dix-Hallpike left

OVERALL INTERPRETATION

Primary Finding: Central Oculomotor Abnormality

DIAGNOSIS / DIFFERENTIAL DIAGNOSIS

Primary (Most Likely): Central Vestibular / Cerebellar-Pontine Pathway Dysfunction

1. Severely degraded smooth pursuit in all directions (gain 0.22-0.66)
2. Asymmetric pursuit - rightward horizontal gain significantly lower than leftward
3. Grossly impaired upward vertical pursuit (gain 0.28-0.34) with relatively preserved downward
4. Vertical OKN reduction (bottom-to-top more affected)
5. No spontaneous nystagmus
6. No positional or paroxysmal nystagmus

Differential Diagnosis (ranked by likelihood given this VNG pattern):

• Saccadic pursuit is the hallmark of cerebellar dysfunction
• Globally reduced pursuit gain with cerebellar flocculus/paraflocculus involvement
• Asymmetric pursuit suggests possible lateralized cerebellar/cerebellar peduncle involvement
• Impaired vertical OKN is consistent

• The rightward horizontal pursuit deficit is consistent with an ipsilateral pontine lesion (the pursuit pathway for rightward pursuit uses right PPRF/pontine circuits)
• A right-sided lesion could also impair the upward pursuit pathways
• Causes: lacunar infarct, demyelination (MS), pontine glioma

• Subacute onset with globally degraded pursuit and saccadic pursuit
• Should be considered especially if there is a known malignancy

• PSP classically shows vertical > horizontal pursuit abnormality and particularly downward saccade slowing
• The upward pursuit deficit fits partially, but the absence of downward saccade abnormality makes PSP less likely here
• Still worth considering in a 57-year-old male

• Demyelinating plaques in the pontine or cerebellar pathways can produce asymmetric saccadic pursuit
• Internuclear ophthalmoplegia (INO) would be expected but wasn't clearly demonstrated here

• Posterior circulation TIA/stroke affecting the cerebellum or brainstem
• Especially right PICA territory or basilar artery territory

What is NOT supported by this VNG:

• BPPV: Dix-Hallpike and supine roll both negative. No paroxysmal nystagmus.
• Unilateral peripheral vestibular hypofunction (e.g., vestibular neuritis, Meniere's disease): No spontaneous nystagmus, no head-shake nystagmus, and the pattern of central oculomotor dysfunction does not fit a peripheral lesion.
• Bilateral peripheral vestibulopathy: While pursuit is poor, the OKN is preserved horizontally, making bilateral peripheral loss less likely.

RECOMMENDATIONS

1. MRI brain with posterior fossa protocol (thin-slice cerebellum, brainstem, with gadolinium) - to rule out structural lesion (infarct, demyelination, tumor)
2. Neurology referral for full cerebellar/extrapyramidal examination
3. Paraneoplastic antibody panel (anti-Yo, anti-Hu, anti-Ri) if no structural cause found
4. Consider Video Head Impulse Test (vHIT) to assess individual semicircular canal function (not performed in this VNG)
5. Caloric testing if available - notably absent from this report, would have provided quantitative canal function data