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Videonystagmography (VNG) Report - Detailed Analysis & Diagnosis

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Summary of All Test Findings

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1. SACCADE TESTING

• Latency is significantly prolonged in both eyes bilaterally (normal: 150-250 ms; patient: 327-469 ms). This reflects delayed initiation of saccadic eye movements.
• Precision is markedly elevated in the left eye (up to 143.49%; normal ~80-100%). Values >100% indicate hypermetria - the eyes overshoot their targets. Right eye also shows values above 100% at lower frequencies. Hypermetria is a sign of cerebellar vermis dysfunction.
• Velocities are high-normal to elevated, which can accompany hypermetric saccades.
• Conclusion: Bilateral saccadic dysmetria (predominantly hypermetria) with prolonged latency - suggesting central cerebellar pathology (cerebellar vermis involvement).

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2. SMOOTH PURSUIT TESTING

• Smooth pursuit gain is severely reduced bilaterally in both horizontal and vertical directions (all values well below 0.8, most below 0.5).
• The left eye shows extremely low gain (0.05-0.28), consistently worse than the right eye.
• The defect is bilateral and symmetric to asymmetric, with the left eye worse.
• Conclusion: Severely impaired smooth pursuit - bilateral symmetric-to-asymmetric defect. Symmetric bilateral impairment indicates diffuse cortical, basal ganglia, or cerebellar dysfunction. The asymmetry (left eye worse) may point to a focal element involving the left cerebellar hemisphere, brainstem, or left parieto-occipital region.

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3. OPTOKINETIC NYSTAGMUS (OKN) TESTING

• Horizontal OKN gains are normal bilaterally (0.92-1.04).
• Vertical OKN gains are borderline low (0.74-0.87), especially bottom-to-top and top-to-bottom.
• No significant asymmetry in horizontal OKN, making a unilateral central lesion less likely for this parameter.
• Conclusion: OKN is largely preserved horizontally; mild reduction in vertical OKN. This partially contrasts with the severely impaired smooth pursuit, which may suggest the defect is not a simple global cerebellar or cortical lesion but may involve more specific pathways.

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4. SPONTANEOUS NYSTAGMUS

• Spontaneous nystagmus is present in both light and dark conditions in the left eye.
• SPV in dark (6.26°/s) exceeds the threshold of 4°/s (the standard pathological threshold for horizontal spontaneous nystagmus without fixation).
• The nystagmus increases in the dark (from 3.21 to 6.26°/s), which is characteristic of peripheral vestibular nystagmus where fixation partially suppresses the nystagmus. This is Alexander's Law behaviour.
• The negative sign of the slow phase velocity indicates the fast phase is directed to the right (rightward nystagmus), suggesting a left peripheral vestibular weakness (lesion side = opposite to fast phase direction).
• Conclusion: Left-beating spontaneous nystagmus (fast phase right) - consistent with a left peripheral vestibular hypofunction.

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5. HEAD SHAKE TEST

• Post-head-shake vertical nystagmus was induced (in the right eye, SPV 19.53°/s). This is notable.
• Normal head shake induces brief horizontal nystagmus in peripheral vestibular disease. The presence of vertical (rather than horizontal) post-head-shake nystagmus is a central sign - indicating cerebellar or brainstem dysfunction.
• This finding is strongly suggestive of a central vestibular lesion.

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6. GAZE TESTING

• Nystagmus is absent with fixation (all gaze positions) - this indicates fixation suppression is working, a peripheral feature.
• Without fixation, nystagmus is elicited in left and right gaze positions - indicating direction-changing gaze-evoked nystagmus without fixation.
• Direction-changing nystagmus that appears only in eccentric gaze without fixation (but not with fixation) can represent unmasked peripheral spontaneous nystagmus (Alexander's Law) rather than true gaze-evoked nystagmus.
• The complete absence of gaze nystagmus with fixation speaks against a purely central gaze-holding defect.

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7. POSITIONAL TESTING

Dix-Hallpike Test (for Posterior Canal BPPV):

• Dix-Hallpike Left (Supine Head Ext. & Left): Both eyes show nystagmus (-2.21°/s right, -4.50°/s left) at 0.65 and 0.77 Hz. This is a positive Dix-Hallpike on the left side.
• The absence of classic upbeat-torsional nystagmus pattern (VNG cannot show torsional component) requires clinical correlation. However, the presence of positional nystagmus with left Dix-Hallpike is suspicious for left posterior canal BPPV but must be correlated clinically.
• Dix-Hallpike Right showed minimal, borderline nystagmus only in the sitting position (1.99°/s), not meeting clear criteria.

McClure-Pagnini Roll Test (for Horizontal Canal BPPV):

• Nystagmus is present in supine neutral and sit-to-supine positions, with left-eye nystagmus (fast phase rightward) in supine and left lateral nystagmus in the right eye.
• The pattern of nystagmus in the supine position (SPV 3.91-4.44°/s) is consistent with horizontal canal involvement or persistent positional nystagmus.
• This pattern may represent horizontal canal BPPV (canalith repositioning) or positional nystagmus of central origin given the other central findings.

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8. SUBJECTIVE VISUAL VERTICAL (SVV)

• Normal SVV deviation is within ±2-3° of true vertical.
• The clockwise trial shows 6° deviation to the right - this is outside the normal range and represents a significant SVV tilt.
• On blank background, the deviation is -1° (borderline normal), suggesting the abnormality is modulated by visual context.
• An SVV tilted to the right (ipsilesional tilt in the left direction) may suggest left otolithic (utricular or saccular) dysfunction or a lesion affecting the left otolithic pathways.
• This supports a left-sided vestibular lesion.

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Integrated Diagnostic Summary

Key Abnormalities:

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Diagnosis

Primary Diagnosis:

Specific Components:

• Spontaneous nystagmus with fast phase to the right (Alexander's Law pattern, fixation suppression intact)
• SVV tilted right (6°), consistent with left utricular dysfunction
• Positive Dix-Hallpike Left - suspicious for left posterior semicircular canal BPPV
• Persistent positional nystagmus in supine and lateral positions

• Severely impaired bilateral smooth pursuit (all frequencies, all directions) - gain values as low as 0.05
• Bilateral saccadic hypermetria with prolonged latency - indicates cerebellar vermis dysfunction
• Post-head-shake vertical nystagmus - this is a hard central sign, not seen in peripheral lesions
• The combination of hypermetric saccades + impaired smooth pursuit strongly localizes to the cerebellum (vermis and hemispheres)

Differential Diagnosis to Consider:

1. Vestibular Neuritis (left side) with incidental cerebellar atrophy or degenerative change
2. Cerebellar ataxia with peripheral vestibulopathy (e.g., spinocerebellar ataxia variants)
3. Multiple System Atrophy (MSA-C) - cerebellar subtype with peripheral autonomic involvement
4. Vertebrobasilar insufficiency - affecting both peripheral and central vestibular structures
5. Left posterior canal BPPV superimposed on pre-existing central vestibular disease

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Recommended Next Steps

1. MRI Brain with diffusion and FLAIR sequences - to evaluate cerebellum (vermis, hemispheres), brainstem (pons, medulla), and posterior fossa for structural lesion, infarct, demyelination, or atrophy
2. Caloric Testing (Bithermal) - not performed in this report; essential to quantify the degree of left canal paresis and confirm peripheral hypofunction
3. Video Head Impulse Test (vHIT) - to assess individual semicircular canal function and differentiate peripheral from central origin
4. Canalith Repositioning Maneuver (Epley, left side) - if clinical examination confirms left posterior canal BPPV
5. Neurology/Neuro-otology referral - given the central signs
6. Audiometry - baseline hearing assessment in this age group
7. Vestibular Evoked Myogenic Potentials (VEMPs) - to assess utricular and saccular function, corroborating the SVV findings

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Note: This report is based on data extracted from the VNG tracing (Patient ID CCDA00392, dated 19-Jun-2026). The absence of caloric test data limits a complete peripheral vestibular assessment. Clinical correlation with the patient's symptoms (vertigo, dizziness, imbalance, oscillopsia), neurological examination, and imaging is essential for definitive diagnosis and management.

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REVISED DEFINITIVE DIAGNOSIS

Patient: Kusum Lata Singh | 59F | ID: CCDA00392 | Date: 19-Jun-2026

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Exact Primary Diagnosis:

VESTIBULAR MIGRAINE (VM)

with Otolithic Dysfunction causing Vestibular Drop Attacks

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Why the Previous Diagnosis Was Incomplete

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How Every Finding Now Fits Vestibular Migraine

VNG Findings Explained Through the VM Framework

Key distinction: In a fixed cerebellar lesion (e.g., infarct, atrophy), OKN would also be severely abnormal and symptoms would be constant - not episodic. This patient's OKN is normal, pointing against a structural cerebellar lesion and toward a functional/episodic migrainous disruption of the cerebellum and brainstem.

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The Falls: Explained

Mechanism: Otolithic Crisis (Tumarkin-like Vestibular Drop Attack) in the context of Vestibular Migraine

• Falls ~10 times/month
• Triggered by bending forward
• No loss of consciousness
• No warning (sudden)

• SVV deviation of 6° on clockwise rotation - confirms left utricular dysfunction
• Spontaneous nystagmus fast phase rightward - left vestibular system is the affected side
• Persistent positional nystagmus in supine/neutral positions - chronic otolithic membrane instability

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Barany Society Diagnostic Criteria - FULFILLED

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Final Complete Diagnosis

Primary: Vestibular Migraine (Barany/IHS criteria) Subtype: With otolithic dysfunction and vestibular drop attacks (Tumarkin-type mechanism) Affected side: Left vestibular system (left utricular pathway) VNG pattern: Central-type positional nystagmus + bilateral oculomotor dysfunction (smooth pursuit + saccades) + left spontaneous nystagmus - all consistent with interictal/ictal VM

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Clinical Explanation to Patient

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Urgent Recommendations

1. Neurologist / Neuro-otologist referral - for vestibular migraine management (topiramate, valproate, amitriptyline, or propranolol as prophylaxis; vestibular suppressants for acute episodes)
2. MRI Brain + posterior fossa MRI - mandatory to exclude structural lesion (especially if central signs persist between attacks)
3. Fall prevention counseling - avoid rapid bending forward; use handrails; home safety assessment (10 falls/month at age 59 is a serious injury risk)
4. Caloric testing + vHIT - to quantify left canal paresis
5. VEMP (cVEMP + oVEMP) - to formally document utricular/saccular dysfunction on the left
6. Vestibular Rehabilitation Therapy (VRT) - to improve central compensation and reduce fall frequency
7. Migraine diary - to document temporal correlation between migraine attacks and vestibular/fall episodes