VNG Report Interpretation

1. SACCADES

2. SMOOTH PURSUIT

3. OPTOKINETIC NYSTAGMUS (OKN)

4. SPONTANEOUS NYSTAGMUS

5. GAZE TEST

6. DIX-HALLPIKE POSITIONAL TEST

7. McCLURE-PAGNINI (ROLL TEST)

8. SUBJECTIVE VISUAL VERTICAL (SVV)

OVERALL IMPRESSION

1. Downbeat nystagmus in darkness and post-head-shake (vertical slow phase velocity ~3–5°/s)
2. Upward gaze-evoked vertical nystagmus without fixation
3. Frequency-dependent smooth pursuit failure (prominent at 0.4 Hz, both planes)
4. Reduced vertical saccade velocity and precision
5. Central positional nystagmus on Dix-Hallpike and Roll test (non-fatiguing, high frequency, predominantly vertical)

• Neurological/neuro-otological consultation
• MRI brain with posterior fossa protocol (thin cuts through brainstem and cerebellum, with contrast) to exclude:
  • Cerebellar degeneration (e.g., spinocerebellar ataxia)
  • Arnold-Chiari malformation
  • Demyelinating disease
  • Vascular lesion (posterior inferior cerebellar artery territory)
• Vestibular rehabilitation may be considered after neurological evaluation

Updated VNG Interpretation — Revised with Clinical History

REVISED CLINICAL CONTEXT

• The VNG is being performed in the post-symptomatic/resolved phase
• Many findings that would appear alarming in isolation now need to be recontextualized
• The central findings on VNG must be weighed against the likelihood of a compensated or resolved peripheral vestibular event vs. a true central pathology

RE-INTERPRETATION OF KEY FINDINGS

Positional Tests (Dix-Hallpike & Roll Test)

• Low amplitude (SPV 5–10°/s)
• Predominantly vertical in character
• Present in both right and left head-down positions

This pattern is compatible with resolving/resolved Benign Paroxysmal Positional Vertigo (BPPV) — most likely posterior canal BPPV that has either:

• Undergone spontaneous resolution (common — ~50% resolve within 4 weeks), or
• Been previously treated and resolved

Downbeat Nystagmus in Dark / Post-Head-Shake

• SPV is low (~3–5°/s) — below the threshold considered clinically significant for active central pathology in many laboratories (typically >5°/s sustained)
• Post-head-shake vertical nystagmus after a history of vestibular event can reflect central compensation asymmetry rather than primary central pathology
• In an older patient (64 years) with a history of positional vertigo, residual subclinical vestibular asymmetry generating low-level nystagmus in dark is expected during the compensation phase

Smooth Pursuit Degradation at 0.4 Hz

• Age-related decline in smooth pursuit is well-documented in patients ≥60 years
• Pursuit gain of 0.40–0.50 at 0.4 Hz in a 64-year-old is at the lower limit of age-adjusted normal and does not in isolation confirm central pathology
• This finding should not be over-interpreted without neurological symptoms

Vertical Saccade Reduction at Higher Frequencies

• Similarly, mild reduction in vertical saccade precision (76–83%) and velocity (278–374°/s) at high frequencies can reflect physiological aging in a 64-year-old
• Horizontal saccades remain fully normal, which is reassuring against significant central brainstem pathology

REVISED OVERALL IMPRESSION

Resolved / Compensated BPPV (most likely posterior canal) with age-related background vestibulo-ocular changes.

CLINICAL RECOMMENDATIONS

Primary Recommendation

• Neurologically intact (no ataxia, no diplopia, no dysphagia, no headache, no focal neurological signs)
• Symptom-free and functioning well
• Without other risk factors for posterior fossa pathology

Follow-Up

1. Reassurance — findings are consistent with resolved BPPV with ongoing central compensation
2. Vestibular rehabilitation exercises (Brandt-Daroff or Cawthorne-Cooksey) to accelerate central compensation if any residual imbalance or unsteadiness persists
3. Repeat Dix-Hallpike clinically at the next visit — if nystagmus has completely resolved, this confirms the BPPV resolution
4. Monitor — if vertigo recurs, return for re-assessment; recurrence rate of BPPV is ~15–37% over 1 year
5. Neuroimaging (MRI posterior fossa) should be considered only if:
   • Vertigo recurs and does not respond to repositioning manoeuvres
   • New neurological symptoms appear (headache, diplopia, ataxia, dysarthria)
   • Downbeat nystagmus becomes persistent and symptomatic on future testing

SUMMARY FOR REPORT

VNG performed in a 64-year-old male with a 3-month history of now-resolved positional vertigo. The study shows no spontaneous nystagmus in light and good fixation suppression, indicating effective central compensation. Low-amplitude residual positional nystagmus is present on Dix-Hallpike and Roll test manoeuvres, consistent with post-resolution BPPV. Smooth pursuit and vertical saccade parameters show mild frequency-dependent reduction in keeping with age-related vestibulo-ocular changes in a 64-year-old. Subjective Visual Vertical is within normal limits. Overall findings are consistent with resolved/compensating BPPV with no definitive evidence of active central vestibular pathology in the current clinical context. Clinical correlation and follow-up are advised.