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🧠 Complete VNG Analysis & Diagnosis

Patient: Laxmi Narayan | 75 yr/M | Date: 09-May-2026

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CLINICAL SUMMARY (From Prescriptions + History)

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VNG FULL ANALYSIS (Parameter by Parameter)

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1. SACCADE TEST

• Bilaterally prolonged saccade latency — strongly suggests central (cerebellar/cortical frontal lobe) origin
• Saccade velocity preserved (rules out severe brainstem/INO), but accuracy (precision) is bilaterally low, indicating cerebellar dysmetria of saccades
• This is the hallmark of cerebellar saccadic dysfunction — the cerebellum (vermis, fastigial nucleus) normally corrects saccade accuracy

🔑 Key: Saccadic dysmetria (hypometria) + prolonged latency = central oculomotor dysfunction, cerebellar pattern

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2. SMOOTH PURSUIT TEST

• Severely reduced bilateral smooth pursuit gain — all values well below 0.9
• Reduction is symmetric (both eyes, both directions, both horizontal and vertical)
• Gain drops further at higher frequencies (0.4 Hz) — shows central tracking failure
• This is not peripheral — peripheral lesions do not cause bilateral symmetric smooth pursuit failure
• Location: Cerebellar (paraflocculus, vestibulocerebellum), pontine nuclei, or cortical (but given DDK affected, cerebellar most likely)

🔑 Key: Bilateral symmetric smooth pursuit gain <0.5 at 0.2 Hz = Central — cerebellar/brainstem

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3. OPTOKINETIC TEST (OKN)

• Horizontal OKN gain is relatively preserved (0.79–1.09) — better than smooth pursuit at same speeds
• Vertical OKN gain reduced (0.81–1.06, with absent fast phase in left eye for Top→Bottom)
• The asymmetry in vertical OKN fast phase (present only in right eye for vertical) suggests unilateral defect in the saccadic generator for vertical OKN — a subtle central finding
• No OKAN (optokinetic after-nystagmus) data, but the velocity storage mechanism can be inferred as partially impaired

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4. SPONTANEOUS NYSTAGMUS

• No spontaneous nystagmus in light (fixation suppresses it — normal)
• Low-amplitude spontaneous nystagmus in dark (SPV 2.05°/s, amplitude 2.09°) in the right eye only
• SPV >2°/s in dark is borderline significant — suggests a slight right-sided vestibular asymmetry OR a central low-grade spontaneous nystagmus
• The fact it is absent in light (well fixation-suppressed) means it is not strongly peripheral

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5. HEAD SHAKE NYSTAGMUS

• Post–head shake nystagmus (HSN) present with both horizontal AND vertical components
• Horizontal component: leftward slow-phase (fast phase ~222–226°, i.e., toward lower-left) = subtle left-beating HSN → indicates right vestibular deficit (per HSN rule: nystagmus beats away from the lesion)
• Vertical component > horizontal → this is the critical finding — a predominantly vertical or oblique HSN is a central sign (peripheral HSN is purely horizontal)
• Fast phase direction ~222–226° = SW quadrant (left-downward) → mixed horizontal + downbeat component

🔑 Central finding: Vertical/oblique head-shake nystagmus → central vestibular pathology (cerebellar or brainstem)

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6. HYPERVENTILATION NYSTAGMUS

• Nystagmus provoked by hyperventilation — beats toward 344° (upper-right area)
• Hyperventilation-induced nystagmus (HVIN) is significant if SPV >5°/s; here it is borderline (2.05–2.95°/s)
• However, in the context of central disease, HVIN can unmask vestibular nerve or demyelinating lesions
• Low amplitude, but directionally consistent with right vestibular asymmetry

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7. GAZE TEST (With & Without Fixation)

• Gaze-evoked nystagmus (GEN) without fixation, especially in upgaze and rightward gaze
• Upgaze nystagmus without fixation (SPV 1.72–2.10°/s, FPD 315° = upper-left direction) — upbeat component, direction-changing in different gaze positions
• Rightward gaze nystagmus without fixation (H-SPV -4.01 to -5.52°/s, FPD 221° = leftward) — left-beating nystagmus on right gaze
• Down-gaze with fixation: V-SPV 5.43°/s — present even with fixation, which is more significant
• This pattern of direction-changing gaze-evoked nystagmus = central sign (cerebellar/brainstem)

🔑 Key: Bidirectional gaze-evoked nystagmus = central vestibular pathology. In peripheral disease, nystagmus is unidirectional and suppressed by fixation.

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8. POSITIONAL TEST — DIX-HALLPIKE

Right Dix-Hallpike (Supine Head Ext. + Right)

Left Dix-Hallpike (Supine Head Ext. + Left) — Two recordings:

• Nystagmus is present bilaterally with both right and left Dix-Hallpike
• The frequencies are high (1.5–2 Hz) and SPVs are moderate
• Geotropic pattern (nystagmus towards ground with both sides during roll test) + bilateral Dix-Hallpike positivity is atypical for classic BPPV
• This could represent cupulolithiasis OR — more importantly — central positional nystagmus (which can mimic BPPV but lacks the typical latency, fatigability, and torsional specificity)

⚠️ Central positional nystagmus: No latency (appears immediately), non-fatigable, variable direction, seen in posterior fossa/cerebellar lesions

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9. McCLURE-PAGNINI (SUPINE ROLL) TEST

🔑 Direction-consistent positional nystagmus across multiple positions = CENTRAL, not BPPV

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10. HEAD POSITION TEST (Yaw/Pitch/Roll)

• Yaw Left: L eye H-SPV 21.54°/s, FPD 344° (upper-right) — strong right-beating nystagmus with head turned left = right canal paresis finding OR apogeotropic horizontal canal pattern
• Pitch Forward: V-SPV 13.48°/s (vertical nystagmus on head pitch) — anterior/posterior canal pathology or central
• Roll Right: H-SPV -15.75°/s, FPD 167–225° — strongest positional response throughout the test

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11. SUBJECTIVE VISUAL VERTICAL (SVV)

• SVV tilted -14° in one condition — significant deviation (normal ≤2.5°)
• SVV tilt indicates otolith (utricle) dysfunction or central (brainstem/cerebellar) tilted internal vertical estimate
• A 14° deviation is substantial — suggests either right otolith (utricular) dysfunction (causing leftward tilt of perceived vertical) OR — given all other central signs — a central graviceptive pathway disturbance
• This correlates with the Romberg tilt to right and subjective push sensation

🔑 SVV deviation + push sensation = Ocular tilt reaction (OTR) spectrum — strongly suggests graviceptive pathway involvement (utricle → inferior olive → cerebellum or brainstem)

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VNG SUMMARY TABLE

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MRI RECOMMENDATIONS & EXPECTED FINDINGS

What to Order:

• T1 with/without contrast
• T2/FLAIR
• DWI (to rule out acute infarct)
• SWI (microbleeds, vascular)
• 3D FIESTA/CISS (inner ear, cranial nerves)
• T2 sagittal midline (cerebellar vermis)

Expected Findings in this Patient:

1. Cerebellar atrophy — particularly vermis and flocculonodular lobe (gait ataxia + positional nystagmus)
2. Pontocerebellar atrophy — if DDK is bilateral
3. Microangiopathic white matter changes (given age 75, hypertension risk)

• Bilateral white matter hyperintensities (vascular/Binswanger) — can cause central imbalance
• Posterior fossa tumor (rare at this age — meningioma, ependymoma)
• MSA-C (Multiple System Atrophy – Cerebellar type): "hot cross bun sign" in pons on T2
• SCA (Spinocerebellar Ataxia): cerebellar >> brainstem atrophy

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DIAGNOSIS

Working Diagnosis:

CENTRAL VESTIBULAR SYNDROME — CEREBELLAR ORIGIN

With secondary bilateral peripheral vestibular asymmetry (right > left)

Differential Diagnoses (in order of probability):

⚠️ RED FLAG — Look at the Prescription:

• Fear of voiding urine, hesitancy in passing urine → autonomic urinary dysfunction
• Disturbed sleep, decreased confidence → autonomic/central

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CORRELATION: Clinical Signs → Anatomical Localization

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MANAGEMENT PLAN

Immediate:

1. MRI Brain with gadolinium — posterior fossa focus (urgent)
2. Neurology referral — to rule out MSA-C, NPH, SCA
3. CT Brain if MRI not immediately available (to rule out hemorrhage/mass)

Investigations:

• Blood: CBC, LFT, RFT, thyroid (TSH), B12, folate, HbA1c, VDRL
• Genetic panel: SCA1/2/3/6/7 (if family history or younger onset)
• Urodynamics / urological evaluation (given urinary symptoms)
• VEMP (cVEMP + oVEMP) — to assess otolith function directly
• vHIT — to assess semicircular canal VOR (not done here)

Vestibular Rehabilitation:

• Gaze stabilization exercises (smooth pursuit + saccade retraining)
• Balance training (static + dynamic, Cawthorne-Cooksey modified)
• Fall prevention program — high priority (conscious falls, face-down)

Medication:

• Current Restonorm (clonazepam 0.5 mg HS) — appropriate for anxiety + can reduce vestibular excitability at night
• Betahistine — limited value in central disease but may help peripheral component
• Vitamin D + Calcium — fall prevention in elderly
• Avoid vestibular suppressants (meclizine, cinnarizine) — counterproductive in cerebellar disease

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FINAL DIAGNOSTIC IMPRESSION

VNG IMPRESSION:
1. CENTRAL OCULOMOTOR DYSFUNCTION
   - Bilateral saccadic dysmetria with prolonged latency
   - Severely reduced bilateral smooth pursuit (cerebellar pattern)
   - Bidirectional gaze-evoked nystagmus without fixation
   
2. CENTRAL POSITIONAL NYSTAGMUS
   - Direction-consistent across positions (not BPPV)
   - Bilateral Dix-Hallpike positive (no fatigability pattern)
   
3. VERTICAL/OBLIQUE HEAD-SHAKE NYSTAGMUS
   - Indicates central vestibular pathology
   
4. OTOLITH DYSFUNCTION
   - SVV deviated -14° (right > left utricular)
   - Push sensation, Romberg tilt right
   
5. MILD RIGHT PERIPHERAL VESTIBULAR ASYMMETRY
   - Yaw-Left: strong right-beating nystagmus (right canal/nerve)
   - Head-Shake: horizontal component leftward (right loss)

CONCLUSION:
Central Vestibular Syndrome, cerebellar pattern
DDx: Cerebellar degeneration, MSA-C, NPH
Recommend: MRI Brain (posterior fossa), Neurology referral

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⚕️ Clinical Note: This patient is a 75-year-old male with conscious falls (face-down, knowing he is about to fall) — this is classic cerebellar gait ataxia (not syncopal, not vestibular drop attacks). The complete VNG shows a consistent central cerebellar pattern. The urinary hesitancy documented by the psychiatrist is a critical additional clue pointing toward MSA-C. MRI is urgently needed.