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Lata VNG Detailed Report

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VNG Report Summary — Lata | CCDA00454 | 54F | 11-May-2026

Head Shake Nystagmus (from video + VNG data)

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VNG Results at a Glance

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Overall Impression

Recommendations

1. Epley Manoeuvre (right side) — first-line CRP treatment
2. Specialist review — correlate with imaging (MRI posterior fossa)
3. Continue Vestibular Rehabilitation Exercises (Brandt-Daroff → gaze stabilization → balance training)
4. Fall prevention counselling
5. Follow-up VNG at 4–6 weeks post-repositioning

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Detailed VNG Analysis — Lata | CCDA00454 | 54F | 11-May-2026

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PATIENT CONTEXT

• First vertigo episode 20 years ago post two-wheeler fall (head trauma)
• Second major head trauma 7th April 2026 → vertigo 2 days later
• Positional triggers (rolling, looking up/down, lying↔sitting)
• Symptoms while watching moving objects (10–15 years) → OKN pathway involvement
• Ear fullness/pressure > right ear
• Thyroid medication + antidepressants (both can mildly suppress vestibular gain)
• Unterberger's: >30° deviation right → right vestibular asymmetry

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1. SACCADE TESTING

Horizontal Saccades (0.3 Hz & 0.45 Hz)

Vertical Saccades

• Velocity: Bilateral vertical saccade velocities are comfortably within normal range (300–315°/s). Symmetric between right and left eyes — no internuclear ophthalmoplegia (INO), no skew deviation pattern.
• Precision: Excellent — 92–97% bilaterally. No dysmetria.
• Latency: Mildly prolonged (~292–312 ms vs. the 150–250 ms ideal range). At age 54 with history of head trauma and medication use, this is within acceptable limits. Does not suggest frontal lobe or basal ganglia pathology at this level.
• Overall: Saccade system intact. No brainstem saccade generator pathology.

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2. SMOOTH PURSUIT TRACKING

Horizontal Pursuit

Vertical Pursuit

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3. OPTOKINETIC NYSTAGMUS (OKN)

Horizontal OKN

Vertical OKN

1. L→R 10° being normal (0.98–1.00) while R→L 10° is reduced (0.75–0.78): This horizontal OKN asymmetry (better leftward stimulus response vs. rightward stimulus) suggests relative dysfunction of the right NOT/accessory optic system. The NOT mediates the reflex OKN response to visual field motion ipsilateral to each hemisphere. Right NOT or right hemisphere parieto-occipital dysfunction would reduce gain for rightward stimulus.
2. Velocity-dependent reduction (10° better than 20°): At higher stimulus velocities, cortical pursuit pathways dominate. The progressive reduction at 20° reflects the same smooth pursuit limitation seen above — floccular/cortical pathway dysfunction.
3. Vertical OKN: Bottom-to-Top 20° being completely absent and Top-to-Bottom 20° nearly absent (RE 0.15) with left eye non-responsive is the most striking OKN finding. Vertical OKN is mediated primarily by the interstitial nucleus of Cajal (INC) and the posterior commissure — structures in the mesencephalon. Severe vertical OKN reduction disproportionate to horizontal can indicate:
   • Posterior fossa / mesencephalic dysfunction (old head trauma)
   • Nodulus/uvula dysfunction (controls vertical VOR and OKN)
   • Bilateral otolith pathway dysfunction
4. Oblique fast phase direction (63°–65°) in T→B OKN: Fast phase at 63–65° is oblique (45° = pure diagonal; 90° = pure vertical). A vertical OKN stimulus producing an oblique fast phase indicates a torsional component to the nystagmus, suggesting otolith-ocular coupling dysfunction — the same pathway implicated in BPPV-related nystagmus.
5. Patient symptoms during OKN: Spinning sensation and head heaviness = confirms active vestibulo-ocular mismatch, particularly when large visual fields move. This is consistent with long-standing visual-vestibular conflict (symptoms of watching moving objects for 10–15 years).

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4. SPONTANEOUS NYSTAGMUS

• In an uncompensated acute peripheral lesion, spontaneous nystagmus in dark (removed fixation suppression) would be expected.
• Absence confirms that the vestibular system is centrally compensated — the brainstem/cerebellum has adapted to the right-sided asymmetry over time. This is consistent with a chronic or recurrent condition (20-year history) rather than an acute unilateral peripheral loss.
• This also argues against active Menière's disease or acute labyrinthitis at the time of testing.
• The fact that the right-sided asymmetry only emerges on provocative testing (head shake, positional) means the deficit is present but compensated at rest.

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5. HIGH-FREQUENCY HEAD SHAKE NYSTAGMUS (HSN)

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6. GAZE TESTS

• No gaze-evoked nystagmus (GEN): Rules out cerebellar gaze-holding failure (flocculus, nucleus prepositus hypoglossi). Pure floccular lesions produce GEN; its absence confirms the smooth pursuit/OKN deficits noted above are not from a complete floccular lesion.
• No Alexander's law violation: In peripheral vestibular lesions, spontaneous nystagmus increases in the direction of the fast phase (Alexander's law). The absence of any gaze-evoked nystagmus even without fixation confirms complete central compensation.
• No rebound nystagmus: No cerebellar rebound nystagmus detected.
• No fixation-suppression failure: The fixation suppression index is effectively normal — the cerebellum is suppressing any residual vestibular drive when fixation is provided.

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7. HEAD POSITION TESTS

Yaw Positions

• Left-beating in left yaw = geotropic nystagmus in this position → consistent with right horizontal canal BPPV (cupulolithiasis pattern) or right HC hypofunction.

Pitch Positions

Roll Positions

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8. DIX-HALLPIKE TEST

Right Dix-Hallpike

• V-SPV RE = 16.99°/s — this is the strongest nystagmus velocity recorded in the entire study
• Fast phase direction 279.47° ≈ straight left (270° = left; 279° = slightly upward-left)
• RE frequency 2.31 Hz — higher than the supine position, consistent with reversal nystagmus on return to sitting
• LE V-SPV = -6.78°/s (downward slow phase = upward fast phase in left eye) with 0.99 Hz

Left Dix-Hallpike

• Residual right-sided posterior canal debris stimulated even in left DH position (as the right posterior canal is still partially gravity-dependent in this position)
• Possible right anterior canal minor component (anterior canal BPPV produces down-beating nystagmus in the ipsilateral DH position)
• No symptoms reported for left DH — further distinguishing this from left-canal pathology

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9. McCLURE-PAGNINI (ROLL TEST)

Right Lateral

1. Right horizontal canal BPPV — cupulolithiasis (debris attached to cupula → tonic deflection → ageotropic nystagmus, typically sustained)
2. Right horizontal canal hypofunction — the dependent (right) ear stimulation should produce rightward nystagmus; left-beating in right lateral = right side weaker

Left Lateral: No nystagmus, No symptoms.

Supine Neutral (post both): No nystagmus — confirming position-dependence.

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10. SUBJECTIVE VISUAL VERTICAL (SVV)

• Clockwise trial +3°: Exceeds the ±2° normal limit. The rod is tilted 3° to the right of true vertical but the patient perceives it as vertical — this means her perceived vertical is shifted clockwise (rightward tilt), consistent with right otolithic hypofunction.
• Anti-clockwise trial -1°: Within normal range, but the perceived direction is "Clockwise" — i.e., even when approaching from the other side, the patient's perception drifts rightward.
• Blank Background +1°: Without visual context cues, the deviation persists at +1° rightward.

1. Concurrent right utricular otoconia displacement (utricular BPPV contributing)
2. Chronic right utricular deafferentation from repeated head trauma
3. Saccular asymmetry

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INTEGRATED ANALYSIS & TOPOGRAPHIC LOCALISATION

Site of Lesion Map

Diagnosis Hierarchy

1. Primary (Definitive): Right Posterior Canal BPPV — Canalolithiasis type
   • Classic provocation pattern; symptom-matched; reversal nystagmus; 1 Hz frequency; unilateral DH
2. Secondary (Probable): Right Utricular Hypofunction / Otolith Dysfunction
   • SVV deviation; cross-coupled HSN; pitch-forward left-torsional nystagmus; roll-position nystagmus
3. Tertiary (Possible): Right Horizontal Canal Positional Component
   • Mild horizontal canal nystagmus in McClure-Pagnini and yaw-left position
4. Background (Likely chronic/old): Bilateral posterior fossa/floccular dysfunction from prior head trauma
   • Symmetric reduction in vertical OKN and higher-frequency smooth pursuit; not acute

Why OKN is Globally Reduced (not just one direction)

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CLINICAL RED FLAGS TO MONITOR

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TREATMENT PRIORITY SEQUENCE

1. Immediate: Epley manoeuvre (right posterior canal) — highest level evidence (Cochrane Class A)
2. Short-term: Brandt-Daroff habituation exercises for residual otolith dysfunction
3. Concurrent: Gaze stabilisation VRT for floccular/OKN pathway deficit
4. Investigate: MRI brain (posterior fossa, internal auditory canals) to exclude central pathology contributing to vertical OKN failure and downward smooth pursuit reduction
5. Thyroid review: Ensure thyroid function is optimally controlled (hypothyroidism → endolymphatic pressure → can mimic/worsen BPPV)
6. Follow-up VNG at 6 weeks: Expect resolution of DH nystagmus post-Epley; monitor OKN recovery and SVV normalisation

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Head Shake Test — Eye Analysis (Visual + Video)

What You're Seeing on Screen

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Phase-by-Phase Eye Behaviour

🟡 t=1–8s — Baseline / Pre-Shake (Eyes at Rest)

• Both eyes are looking upward and slightly left — pupils are positioned toward the upper-nasal quadrant of the iris
• The left eye (left panel) shows the pupil displaced upward, with more sclera visible below
• The right eye (right panel) has the pupil positioned slightly upward and medially
• This is the resting orbital position before the head shake begins — notable that even at baseline, both eyes are not perfectly centred, suggesting a tonic upward and leftward deviation at rest
• This is a clinically meaningful baseline finding: it suggests a persistent upward gaze bias, consistent with the left up-beating nystagmus pattern documented in the VNG data

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🔴 t=9–19s — Head Shake Phase (Active Head Movement)

• The frames from t=9–19s show significant motion blur and tracking artifact — the goggle cameras are capturing the eyes during the active horizontal head shaking
• Key observation: even during the shake, both pupils can be seen making rapid, conjugate horizontal oscillations
• At t=10s and t=11s the eyes show marked upward displacement with sclera visible inferiorly on both sides — the eyes are being driven upward during the shake, consistent with VOR-related superior rectus activation
• The left eye (left panel) shows more upward displacement than the right — this asymmetry during the shake itself hints at the left-sided compensatory dominance

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🟠 t=20–35s — Critical Post-Shake Period (Nystagmus Window)

• Left Eye (left panel): Pupil is positioned toward the medial (nasal) side — more sclera visible on the temporal (outer) side of the iris. The upper eyelid crease shows a slight downward tilt on the lateral side suggesting torsion
• Right Eye (right panel): Pupil is near central but slightly medial, with the gaze directed slightly upward
• Both eyes are conjugate (moving together) — the medial drift in both = slow phase going right, confirming the fast phase (nystagmus beat) is directed LEFT
• The upward position of both pupils (more sclera below than above) = upward slow phase is occurring (downward drift), so fast phase beats UPWARD

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🟡 t=35–55s — Nystagmus Decay Phase

• t=40s: The eyes are still showing slight upward deviation. The left eye pupil still appears medially biased. Nystagmus is decaying but residual drift persists.
• t=45–50s: Pupils begin to return toward centre. The asymmetry between eyes is reducing. Slow phase velocity is decelerating — consistent with velocity storage discharge following head shake.
• t=55s: Eyes look more centred. Left eye pupil now closer to geometric centre of the iris. Right eye centred. Nystagmus has largely resolved.

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🔵 t=57–63s — Return to Baseline

• Both eyes centred, no visible positional drift
• Pupil positions symmetric bilaterally
• t=64s: Camera moves away (end of recording)

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Pupil Position Map — Key Moments

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What This Clinically Means

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Summary in Plain Terms

After shaking her head, Lata's eyes beat leftward and upward — they drift slowly to the right and downward (slow phase) and then jump quickly back left and up (fast phase, the nystagmus beat direction). This tells us her right ear's balance organ is weaker than the left. The upward component is an extra clue that the gravity-sensing part (utricle) of the right ear is also affected. The eyes keep doing this for about 30 seconds before settling — which is longer than normal, showing significant underlying right vestibular asymmetry.