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VNG Report Interpretation

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Overview of Tests Performed

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1. Saccades

• Horizontal saccade velocities are within normal limits (>200 °/s for horizontal is acceptable).
• Horizontal precision at 0.3 Hz is very good (92/90); at 0.45 Hz it drops to 71–73, which is at the lower edge of normal (normal ≥80 is ideal, but 70s can be acceptable with faster targets).
• Horizontal latency of 328 ms at 0.3 Hz is mildly prolonged (normal typically <250–280 ms). This suggests some cortical/attentional delay in initiating eye movements, or possibly a central issue.
• Vertical saccade velocities are mildly reduced, particularly the left eye at 0.3 Hz (168 °/s). Normal vertical saccade velocities are generally ≥200 °/s. This asymmetry (right eye 210 vs left eye 169 °/s) warrants attention.

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2. Smooth Pursuit

• Horizontal pursuit at 0.2 Hz is mildly impaired (leftward gain 0.70/0.72 is below normal; normal gain ≥0.80 is expected at this frequency).
• Horizontal pursuit at 0.4 Hz is significantly impaired (gains 0.38–0.55; expected ≥0.70 at this frequency). This is a consistent bilateral finding.
• Vertical pursuit is impaired at both frequencies, with gains in the 0.48–0.77 range — below expected normal (≥0.80 at 0.2 Hz).
• Bilateral smooth pursuit impairment, affecting both horizontal and vertical planes and worsening at higher frequencies, is a pattern characteristic of central nervous system dysfunction (cerebellum, brainstem, or diffuse cerebral pathology). It can also occur with sedating medications, fatigue, or lack of attention, so clinical correlation is essential.

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3. Optokinetic Nystagmus (OKN)

• OKN is normal at low velocity (10°) in horizontal and vertical directions.
• At 20° stimulus velocity, horizontal OKN gains drop significantly (0.53–0.62; normal ≥0.80).
• Vertical OKN at 20° is severely impaired, especially Top-to-Bottom (0.19/0.11) and Bottom-to-Top (no measurable response).
• This velocity-dependent OKN impairment mirrors the smooth pursuit findings and again points to central pathway involvement — particularly the parieto-occipital pursuit pathway and/or brainstem/cerebellar circuits.

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4. Spontaneous & Gaze Nystagmus

• No significant spontaneous or gaze-evoked nystagmus is present in light or dark conditions, which is a reassuring finding.
• The very low-amplitude nystagmus detected in the left eye during eccentric gaze without fixation (SPV < 3 °/s) is of borderline significance. Slow phase velocities < 5–6 °/s in eccentric gaze without fixation are generally considered physiological or of minimal clinical significance.
• Negative head shake nystagmus argues against a significant unilateral peripheral vestibular deficit at the time of testing.

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5. Positional Testing

Dix-Hallpike (for posterior/anterior canal BPPV):

McClure-Pagnini (for horizontal canal BPPV):

Head Position Tests:

• Positional nystagmus is clearly provoked with Dix-Hallpike maneuvers bilaterally and in specific head positions (Yaw Left, Roll Left).
• The nystagmus is predominantly vertical and horizontal, appears in multiple positions, and shows reversal on returning to upright — all features that need to be interpreted with the clinical context.
• The bilateral positional provocation without a clearly lateralized, purely torsional-upbeat pattern that extinguishes within 30–60 seconds makes classical posterior canal BPPV less certain. However, BPPV — particularly canal conversion or bilateral BPPV — remains possible.
• The pattern of nystagmus provoked in Yaw Left position (horizontal nystagmus, SPV 22 °/s) raises the possibility of horizontal canal BPPV affecting the left side.
• Central positional nystagmus cannot be excluded given the bilateral involvement, mixed planes, and the concurrent smooth pursuit and OKN impairment.

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6. Subjective Visual Vertical (SVV)

• The blank background result (+2°) is within normal limits (±2–3°).
• The −9° anticlockwise deviation is abnormal (normal ≤ ±2.5–3°). Pathological SVV tilt (>3°) suggests utricular dysfunction or involvement of the graviceptive pathway (utricle → inferior vestibular nerve → brainstem).
• The inconsistency between conditions (clockwise shows 5° vs blank 2°) may reflect attentional variability or a subtle tilt perception deficit that is context-dependent.
• Abnormal SVV is seen in acute peripheral vestibular lesions (labyrinthitis, vestibular neuritis), otolithic disorders, and brainstem/thalamic lesions.

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Summary and Clinical Impression

Clinical Impression:

1. Positional vestibular dysfunction is present, consistent with BPPV — most likely involving the posterior or horizontal canal, possibly bilateral. The dominant side is the left based on Dix-Hallpike left and Yaw Left results.
2. Smooth pursuit and OKN impairment (bilateral, velocity-dependent) raises a concern for a central vestibular/cerebellar component. This pattern should prompt clinical correlation with symptoms, neurological examination, and consideration of neuroimaging (MRI brain with posterior fossa focus) if not already done.
3. Abnormal SVV suggests additional utricular (otolithic) pathway involvement.

Recommendations:

• Canalith Repositioning Maneuver (Epley or Semont) if BPPV is confirmed clinically
• Neurological evaluation and MRI brain (posterior fossa/cerebellum) given the central pursuit/OKN pattern
• Vestibular rehabilitation therapy
• Reassessment of caloric or rotational chair testing if central pathology is suspected

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Disclaimer: This interpretation is based solely on the data provided in the VNG report. Final clinical diagnosis must be made by the treating physician with full clinical history, physical examination, and additional investigations as appropriate. The report form itself shows the impression field as blank — a clinician's formal conclusion is still required.

• No anxiety/depression medications
• No hearing loss history
• Phonophobia — loud sounds cause irritation (car door slamming)
• Spinning sensation (vertigo)
• Dizziness triggered by switching lights off
• Position change-induced dizziness (turning in bed)
• Oscillopsia — feels surroundings are spinning (external vertigo)
• Strong fragrance allergy + headache from even mild fragrances (cucumber/muskmelon smell)
• Migraine history >10–15 years

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COMPLETE VNG ANALYSIS — Mala Rajodia, 43F, 22 April 2026

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1. SACCADES

• Velocities are generally preserved (no hypometria or hypersaccadia)
• Precision is globally reduced across all frequencies — this is the dominant finding. Normal precision should be ≥70. Scores of 35–65 indicate dysmetric saccades (mixture of undershooting/overshooting), consistent with cerebellar or pursuit pathway dysfunction
• Latency prolongation at 0.3 Hz (RE 275 ms) and 0.6 Hz (both eyes 291–316 ms) — indicates delayed saccade initiation, consistent with cortical/frontal lobe or attentional/cerebellar involvement
• Velocity asymmetry at 0.6 Hz horizontal (RE 284 vs LE 379 °/s) — 25% asymmetry, clinically significant, may suggest right-sided efferent pathway (PPRF/MLF) involvement
• Vertical saccade velocity asymmetry at 0.3 Hz (RE 386 vs LE 303 °/s) — suggests possible right-eye supranuclear or internuclear pathway advantage

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2. SMOOTH PURSUIT

• Leftward pursuit at 0.2 Hz is the only near-normal value (0.73–0.78) — all other gains are significantly reduced
• Progressive deterioration with increasing frequency (velocity) in both planes — classic frequency-dependent pursuit degradation
• Horizontal rightward pursuit is disproportionately impaired across all frequencies vs. leftward — possible asymmetry implicating contralateral (left) pursuit pathway
• Vertical downward pursuit is particularly impaired (0.22 at 0.6 Hz) — downward pursuit is mediated by posterior fossa pathways; this raises concern for posterior fossa/cerebellar dysfunction
• The overall pattern is bilateral, symmetric, frequency-dependent pursuit failure consistent with central vestibular/cerebellar dysfunction, strongly associated with vestibular migraine in this clinical context

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3. OPTOKINETIC (OKN) TEST

• Horizontal OKN: Normal at low speeds (10–20°), begins to fail at 40°, markedly impaired at 60° — velocity-dependent failure mirroring smooth pursuit
• Vertical OKN: Catastrophic failure above 10° — even at 20°/s the gain drops to 0.16–0.20, and at 40–60°/s it is essentially absent
• Fast phase directions noted at 10° T→B (56.67° = oblique), 20° B→T (254–245°), 40° B→T (257°), 60° T→B (116°) — these anomalous fast phase directions (neither purely up nor down) suggest involuntary nystagmus contaminating the OKN response, consistent with central pathway disruption
• The disproportionate vertical OKN failure compared to horizontal strongly implicates posterior fossa/brainstem-cerebellar pathways (vertical OKN depends on pathways through the pretectum, flocculus, and NOT — nucleus of the optic tract)
• This pattern is highly characteristic of vestibular migraine with central sensitization

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4. SPONTANEOUS / GAZE NYSTAGMUS

• Center without fixation: Absent ✅
• Left without fixation: Very low amplitude, trace activity (scale shows −8°) — borderline, not clearly nystagmus
• Up without fixation: Absent ✅
• Right without fixation: Eye shows positional offset (~40–60°) but no clear nystagmus beats recorded
• Down without fixation: Apparent downward drift/offset visible — no clear nystagmus beats recorded

• No spontaneous, gaze-evoked, or head-shake nystagmus — argues strongly against active unilateral peripheral vestibular lesion (e.g., acute neuritis)
• The absence of gaze-evoked nystagmus in any direction with fixation is reassuring — no cerebellar floccular failure sign
• Minor baseline eye position variation without fixation is non-specific

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5. POSITIONAL TESTING

• Sit Head Right → Supine Head Extended Right: No nystagmus recorded (all dashes, SPV —)
• Return (Supine → Sit Head Right): No nystagmus recorded

• Sit Head Left (initial, at ~14–38 s timeframe): Vertical nystagmus recorded — Right eye vertical SPV 5.77 °/s, amplitude 4.96°, frequency 0.59 Hz — low-grade vertical nystagmus
• Supine Head Extended Left: No nystagmus recorded (all dashes)
• Return (Sit Head Left, second recording): Horizontal + vertical nystagmus — Right eye horizontal SPV 6.44 °/s, amplitude 5.37°; Vertical RE SPV 5.50 °/s, LE SPV 8.48 °/s, amplitude 6.31°; Fast phase direction 320.12° (upward-left); Frequency 1.44 Hz (RE), 0.69 Hz (LE)

• Sit → Supine: No nystagmus ✅
• Right Lateral: No nystagmus ✅
• Supine Head Neutral (first): No nystagmus ✅
• Left Lateral: No nystagmus ✅
• Supine Head Neutral (second): No nystagmus ✅

• Right DHP is completely negative — no posterior or horizontal canal BPPV on the right
• Left DHP supine position: Negative — the classic torsional upbeat nystagmus of posterior canal BPPV was NOT provoked in the head-down position
• Left DHP return (sitting back up): Low-amplitude mixed horizontal + vertical nystagmus, SPV 5.50–8.48 °/s with fast phase direction 320° (upward-leftward). This is below the clinical threshold of 15–20 °/s for BPPV and occurs on returning to sitting (not on going down) — this is atypical for classic posterior canal BPPV
• The low-amplitude, direction-changing, post-repositioning nystagmus is more consistent with central positional nystagmus or a very weak BPPV variant
• McClure-Pagnini (horizontal canal roll test): Completely negative — no horizontal canal BPPV
• The positional findings in this patient are significantly less prominent than in the prior patient and do not meet criteria for classic BPPV on either side

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6. SUBJECTIVE VISUAL VERTICAL (SVV)

1. Test validity issue: Patient likely did not understand the SVV task, rotating the bar 90° (to horizontal) instead of finding the vertical. This is the most probable explanation given the magnitude and consistency across all conditions
2. If genuine: 90° consistently rightward would suggest profound right-sided otolithic (utricular) dysfunction or significant CNS involvement — but this would be expected to correlate with severe spontaneous nystagmus and gait instability, which are absent here

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CLINICAL CORRELATION WITH SYMPTOMS

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INTEGRATED CLINICAL IMPRESSION

Primary Diagnosis: Vestibular Migraine (VM)

1. Smooth pursuit failure — bilateral, frequency-dependent, affecting both horizontal and vertical planes — is the single most characteristic VNG finding in VM. It reflects interictal central vestibular pathway dysfunction.
2. OKN velocity-dependent failure with disproportionate vertical OKN impairment — directly mirrors the smooth pursuit finding and confirms central (not peripheral) pathway involvement.
3. No significant spontaneous nystagmus — distinguishes from peripheral vestibular disorders and acute cerebellar lesions.
4. No significant head-shake nystagmus — argues against unilateral peripheral hypofunction.
5. Saccade precision deficits with frequency-dependent latency prolongation — consistent with cerebellar/brainstem microstructural changes seen in chronic migraineurs.
6. Mild, low-amplitude positional nystagmus on left DHP return — insufficient for classical BPPV diagnosis; consistent with central positional nystagmus seen in VM.
7. Negative roll test (McClure-Pagnini) — excludes horizontal canal BPPV.
8. Clinical history: Long-standing migraine (>10–15 years) + phonophobia + osmophobia (fragrance sensitivity causing headache) + oscillopsia + position-dependent and light-change-related dizziness = Bárány Society criteria for vestibular migraine are met.

Diagnostic Criteria Checklist (International Classification of Vestibular Disorders — ICVD 2012):

• ✅ At least 5 episodes of vestibular symptoms (moderate or severe intensity, 5 min–72 hrs)
• ✅ Current or previous history of migraine with or without aura (15+ year history)
• ✅ One or more migraine features during ≥50% of vestibular episodes (phonophobia, osmophobia/fragrance sensitivity)
• ✅ Not better explained by another vestibular diagnosis

Secondary Consideration: Superimposed Mild Left-sided Positional Vestibular Sensitivity

• The low-amplitude nystagmus on left DHP return (SPV 5.77–8.48 °/s, not exceeding 10 °/s) may represent a central positional component of VM rather than true BPPV
• Cannot fully exclude a very weak posterior canal variant BPPV (left) — though it does not reach diagnostic threshold

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RECOMMENDATIONS

Immediate / Clinical

1. Vestibular Migraine Management should be initiated:
   • Acute: Triptans or ergotamines for acute vestibular migraine attacks
   • Preventive: Propranolol, topiramate, amitriptyline, or valproate (neurology consultation for selection based on contraindications)
   • Lifestyle: Strict migraine trigger avoidance — fragrance-free environment, light regulation, regular sleep schedule, avoid dietary triggers
2. Fragrance/osmophobia management: Advise avoidance of all strong fragrances; note that even mild organic scents (cucumber, muskmelon) are triggering headache — this level of osmophobia suggests central sensitization and may respond to preventive migraine therapy
3. Vestibular Rehabilitation Therapy (VRT): Indicated for the interictal central pursuit/OKN deficits and oscillopsia. Gaze stabilization exercises are particularly useful in VM.
4. Canalith Repositioning (Epley/Semont): Not indicated in this case — the positional findings do not meet BPPV diagnostic criteria. Performing Epley in a vestibular migraine patient without confirmed BPPV may worsen symptoms.
5. Light adaptation strategies: Gradual light transitions rather than sudden light switches; may benefit from filtered lighting

Investigations

1. MRI Brain with posterior fossa protocol (gadolinium): Recommended given central pursuit/OKN findings — to exclude posterior fossa pathology (though VM is the most likely diagnosis)
2. Neurology/Headache specialist referral: For migraine classification, preventive therapy optimization
3. SVV repeat: After proper patient instruction — current result is likely invalid
4. Caloric testing (bithermal): Optional — to quantify any underlying peripheral vestibular asymmetry if treatment response is poor

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SUMMARY TABLE