VNG Report Interpretation — Kamal Sachdeva (57M, 08-Jul-2026)

PATIENT SUMMARY

• Age/Sex: 57 years, Male
• Complaints: Episodic vertigo since Feb 2023; recurrent episodes (Jan 2026, June 2026), each lasting seconds, with spinning sensation, sense of falling, unsteadiness, anxiety, and transient BP rise
• Provocation: Positional changes - head turning side to side, bending forward, lying-to-sitting
• Relief: Keeping head still
• Co-morbidities: Bilateral cataracts, hypertension (on medication), thyroid disorder (on medication)

SECTION-BY-SECTION INTERPRETATION

1. SUBJECTIVE / CLINICAL TESTS

2. SACCADES

Horizontal Saccades (0.3 Hz and 0.45 Hz)

Vertical Saccades (0.3 Hz and 0.45 Hz)

3. SMOOTH PURSUIT TRACKING

Horizontal Pursuit

Vertical Pursuit

4. OPTOKINETIC RESPONSES (OKN)

5. GAZE TESTS

• No gaze-evoked nystagmus with fixation in any direction - this partially argues against a brainstem gaze-holding defect (which would typically produce direction-changing gaze nystagmus with fixation).
• Left-beating nystagmus in left gaze without fixation is a low-intensity finding. This may represent a subtle Alexander's Law phenomenon where a spontaneous left-beating nystagmus is enhanced in the direction of its fast phase (left gaze) and suppressed by fixation. This is consistent with a left peripheral direction-fixed spontaneous nystagmus suppressed by vision.

6. SPONTANEOUS NYSTAGMUS

• No spontaneous nystagmus in light - fixation suppresses it. This supports a peripheral origin where fixation suppression is intact.
• Left-beating nystagmus in dark - indicates a resting vestibular tone imbalance with the left side being the more active side (the fast phase beats toward the left, meaning the right side has relative hypofunction OR the left has relative hyperfunction). The direction being consistent (left-beating) is more typical of peripheral vestibular asymmetry.
• No head-shake nystagmus - the absence here argues against a significant high-frequency unilateral vestibular hypofunction (head-shake nystagmus typically appears in significant peripheral lesions). This could mean: (a) the asymmetry is mild, (b) compensation has occurred, or (c) the pathology is central.

7. POSITIONAL TESTS

Head Position Test

• Slight left-beating nystagmus in pitch backward position
• No nystagmus in other positions

Dix-Hallpike Maneuver

McClure-Pagnini (Supine Roll Test)

1. Left-beating nystagmus on BOTH right and left Dix-Hallpike - Classic BPPV of the posterior canal produces direction-changing nystagmus (right-beating upbeat torsional on right DHP; left-beating downbeat torsional on left DHP). The finding of same-direction (left-beating) nystagmus on both sides is atypical for standard posterior canal BPPV.
2. No accompanying dizziness during any positional maneuver - Typical BPPV produces intense, reproducible vertigo with the nystagmus. Absence of subjective vertigo during Dix-Hallpike is a yellow flag for central origin (central positional nystagmus often has minimal or no subjective vertigo).
3. Direction-consistent (left-beating) nystagmus in multiple positions rather than position-specific paroxysmal nystagmus - suggests a persistent, direction-fixed positional nystagmus that is more characteristic of central or peripheral cupulolithiasis than typical canalithiasis BPPV.
4. McClure-Pagnini: Leftward beats in supine, rightward in sitting - the transition is noted; this pattern does not clearly fit right- or left-lateral canal BPPV. Normal lateral canal BPPV would show geotropic or apogeotropic nystagmus that is clearly lateralizing.

8. CALORIC TEST

OVERALL PATTERN SYNTHESIS

IMPRESSION AND DIFFERENTIAL DIAGNOSIS

Primary Impression: (?) Central Vestibulopathy (as reported)

• Profoundly reduced smooth pursuit in all planes
• Mildly impaired vertical saccade precision
• Direction-consistent positional nystagmus without subjective vertigo
• Non-lateralizing McClure-Pagnini

Differential Diagnosis (in order of probability)

1. Cerebellar/Brainstem Central Vestibulopathy (MOST LIKELY based on VNG pattern)

• Severely impaired smooth pursuit - hallmark of cerebellar/pontine involvement
• Bilateral and biplanar pursuit defect (not unilateral)
• Vertical OKN mildly reduced - implicates the cerebellar vermis
• Vertical saccade precision mildly impaired
• Positional nystagmus without subjective vertigo (classic central behavior)
• Direction-fixed nystagmus across multiple positions

• Cerebellar atrophy / degenerative (age-related or toxic)
• Small vessel ischemia (posterior circulation) given age 57, hypertension
• Thyroid-related cerebellar dysfunction (hypothyroid cerebellar ataxia is well-recognized)
• Medication effect - some antihypertensives (calcium channel blockers, beta-blockers) can impair pursuit

2. Benign Paroxysmal Positional Vertigo (BPPV) - ATYPICAL or CUPULOLITHIASIS VARIANT

• Clear positional provocation of symptoms
• Short-duration episodes (seconds)
• Unterberger's left deviation
• Positional nystagmus on both Dix-Hallpike and roll tests

• No subjective vertigo during provocative testing
• Same-direction nystagmus (left-beating) on both right and left Dix-Hallpike (typical BPPV changes direction)
• Cannot exclude cupulolithiasis variant or multi-canal BPPV
• The severely impaired smooth pursuit is NOT explained by BPPV alone - BPPV does not cause pursuit abnormalities

3. Vestibular Migraine

• Episodic vertigo with variable duration
• Positional sensitivity
• Anxiety during episodes

• No headache history documented
• History spans 3 years with infrequent, brief episodes
• VNG pattern (profound pursuit defect) is more consistent with structural/cerebellar pathology than typical vestibular migraine

4. Right-Sided Peripheral Vestibular Hypofunction (Partial/Compensated)

• Left-beating spontaneous nystagmus in dark (fast phase toward left = right side hypoactive)
• Unterberger's left deviation (if right side is weak, patient deviates toward the weaker side - but Unterberger's actually deviates TOWARD the weaker side, which here is LEFT, suggesting LEFT hypofunction - this is discordant with the nystagmus direction)

5. Thyroid-Related Vestibulo-Cerebellar Dysfunction

• Known thyroid disorder on medication
• Hypothyroidism is associated with cerebellar ataxia, impaired smooth pursuit, and vestibular symptoms
• Thyroid disease can cause endolymphatic changes affecting inner ear function
• If thyroid medication is suboptimal, subclinical hypothyroidism may impair central vestibular processing

RECOMMENDATIONS

1. MRI Brain with posterior fossa protocol (DWI, FLAIR, T2) - to rule out ischemia, cerebellar atrophy, demyelination, or mass lesion given the central VNG pattern
2. Caloric Testing - not performed; essential to quantify unilateral vestibular hypofunction and complete the VNG battery
3. Review thyroid function (TSH, Free T4) - thyroid dysfunction can cause both cerebellar and inner ear vestibular symptoms
4. Neurology/Neurotology consultation - the central VNG pattern warrants neuro-otological evaluation
5. Medication review - assess whether antihypertensive medications (particularly beta-blockers, calcium channel blockers) are contributing to smooth pursuit impairment
6. Canalith Repositioning Maneuver (CRM) - may be attempted cautiously given the positional component, though the atypical positional nystagmus pattern (no dizziness, same-direction on bilateral DHP) warrants caution; not the first priority
7. Vestibular rehabilitation / Habituation exercises - as already recommended; appropriate alongside further workup
8. Follow-up VNG - after thyroid optimization and medication review, to reassess smooth pursuit and determine if improvement occurs

KEY CLINICAL SUMMARY