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Detailed VNG Analysis & Diagnosis - Udal Singh (Male, 74 yrs)

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Clinical History (from Handwritten Note)

• Chief Complaint: Vertigo since 19th May - spinning sensation
• Vomiting - 3-4 minutes duration episodes
• Attacks last for seconds also
• No change with position (no positional dependency noted by clinician)
• H/o few episodes around May; no longer present
• No H/o PICA (posterior inferior cerebellar artery - ruling out Wallenberg syndrome)
• No H/o ambulance or overt fainting during attacks
• Gait imbalance during nights (last portion of note partially cut off, but mentions nocturnal gait issues and possible phone phobia - likely "photophobia" during attacks)

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VNG Test-by-Test Analysis

1. Saccades

• Horizontal saccade velocities are within normal limits; precision is good
• Latency is mildly prolonged bilaterally - right eye horizontal latency (264 ms) is borderline; left eye (340 ms) is clearly prolonged
• Vertical saccade velocity is mildly reduced (both eyes < 150°/s normal threshold) and vertical latency is markedly prolonged (>497 ms)
• Prolonged latency + reduced vertical velocity = mild saccadic dysmetria/slowing, which can reflect cerebellar or brainstem involvement, but must be interpreted with the full test battery

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2. Smooth Pursuit

• Horizontal pursuit is within normal limits (gain 0.70-0.85 is acceptable especially at age 74)
• Vertical pursuit is significantly impaired - particularly downward (0.34-0.42) and upward (0.56-0.62) pursuit gains are below normal threshold of 0.7
• Selective impairment of vertical smooth pursuit (especially downward) is a red flag for central pathology - specifically brainstem/cerebellar dysfunction. In an elderly patient, this raises concern for PSP (progressive supranuclear palsy) or posterior fossa pathology, though isolated central vestibulopathy is also possible

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3. Optokinetic Nystagmus (OKN)

• All OKN gains are within normal range (0.85-1.09)
• No significant asymmetry in horizontal or vertical OKN
• Intact OKN reflexes suggest the cortical and subcortical pathways for visual-vestibular interaction are largely functioning
• Fast phase directions noted in vertical OKN (57.16° and 55.53° for top-to-bottom; 292.66° for bottom-to-top right eye) suggest mildly oblique nystagmus responses but within acceptable limits

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4. Spontaneous Nystagmus

• No spontaneous nystagmus detected in either condition
• This argues against an acute, active unilateral peripheral vestibular lesion (which would typically show direction-fixed spontaneous nystagmus, especially in darkness)
• Normal finding at this stage could indicate a compensated or intermittent vestibular lesion

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5. Head Shake Nystagmus & Hyperventilation

• Head Shake Nystagmus: No nystagmus evoked
• Hyperventilation Nystagmus: No nystagmus evoked

• Absence of head shake nystagmus makes significant unilateral peripheral weakness less likely (a positive HSN - nystagmus beating away from lesion side - is a sensitive indicator of unilateral weakness)
• Negative hyperventilation nystagmus reduces likelihood of acoustic neuroma / vestibular schwannoma (which characteristically shows hyperventilation-induced nystagmus)

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6. Gaze Testing

• Upward gaze nystagmus (right eye, SPV 7.35°/s at 1.28 Hz) is a significant finding
• Gaze-evoked nystagmus that is direction-specific (upbeat on upgaze) is a strong indicator of central vestibular pathology - specifically cerebellar or brainstem (particularly affecting the flocculus/paraflocculus, or the medial longitudinal fasciculus)
• A tiny residual nystagmus at center without fixation (SPV 0.61°/s) is at the very threshold of clinical significance but suggests mild vestibular tone imbalance
• The combination of upward gaze nystagmus + impaired vertical smooth pursuit is characteristic of central vestibular syndrome

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7. Positional Tests (Dix-Hallpike)

• The Dix-Hallpike test is essentially negative for classic posterior canal BPPV
• A classic positive BPPV Dix-Hallpike shows: geotropic torsional-vertical nystagmus, latency of 5-20 seconds, duration <60 seconds, fatigable with repeat testing
• The trivial left eye horizontal nystagmus (SPV 1.79°/s) on initial right head turn is non-diagnostic for BPPV - it is below the typical threshold (>5-10°/s) and lacks the characteristic torsional component
• BPPV is not confirmed by this test battery

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8. Static Head Positions (Positional Head Position Tests)

• Pitch Backward is the most abnormal position - significant mixed horizontal-vertical nystagmus (right eye vertical SPV 15.55°/s is markedly elevated)
• Positional nystagmus elicited by pitch backward and yaw left that is:
  • Direction-changing across positions (horizontal in one, vertical in another)
  • Persistent (not fatiguing rapidly)
  • Multi-directional across different positions
  • These features are characteristic of central positional nystagmus, not peripheral BPPV
• Persistent nystagmus in pitch backward and yaw left positions without a clear BPPV pattern suggests involvement of the vestibulocerebellum (nodulus/uvula) or brainstem connections - K.J. Lee's Essential Otolaryngology, p. 351

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9. Subjective Visual Vertical (SVV)

• The clockwise trials showing a consistent +6° rightward tilt represent a significant SVV deviation
• SVV deviation indicates otolith pathway disruption (utricular or its central connections)
• A consistent rightward tilt (especially in clockwise trials) suggests dysfunction on the right side of the otolith-ocular pathway
• In combination with the other findings, this supports a right-sided utricular or central otolith pathway lesion
• The variability between clockwise (+6°) and anticlockwise (-5°) trials suggests some inconsistency, possibly due to patient effort/cooperation or fluctuating central compensation

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Summary of Abnormal Findings

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Diagnosis

Primary Diagnosis:

Supporting Evidence:

1. Gaze-evoked nystagmus (upbeat on upgaze) - hallmark of central vestibular pathology
2. Impaired vertical smooth pursuit (particularly downward) - cerebellar/brainstem dysfunction
3. Central positional nystagmus - persistent, direction-changing across positions, particularly marked in pitch backward (SPV 15.55°/s)
4. Abnormal SVV (+6°) - otolith pathway involvement
5. Negative Dix-Hallpike - effectively excludes posterior canal BPPV
6. Negative head shake and hyperventilation tests - against simple peripheral vestibulopathy or acoustic neuroma

Differential Diagnoses (in order of likelihood):

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Clinical Correlation & Recommendations

Urgent Investigations Needed:

1. MRI Brain with contrast (posterior fossa protocol) - to exclude:
   • Cerebellar infarct or hemorrhage
   • Brainstem infarct (especially dorsal medulla/pons)
   • Posterior fossa tumor
   • Demyelinating plaques
2. MRA (Magnetic Resonance Angiography) of the posterior circulation - vertebrobasilar system assessment
3. Neurology / Neuro-otology referral - urgent, given the central VNG pattern

Additional Workup:

• VEMP (Vestibular Evoked Myogenic Potentials) - cervical and ocular, to further characterize otolith dysfunction
• Audiogram - baseline hearing assessment
• Vascular risk factor assessment - HbA1c, lipids, ECG, BP monitoring (given age and posterior circulation risk)

Key Point for the Treating Clinician:

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Disclaimer: This analysis is for educational and clinical support purposes. Final diagnosis must be confirmed by a qualified neurologist or neuro-otologist with correlation of full clinical history, examination findings, and imaging.