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VNG Report - Detailed Analysis: Nirupma Saxena

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SECTION 1 - SACCADES

Horizontal Saccades (0.3 Hz)

• Latency is prolonged bilaterally (normal <250 ms; both eyes >300 ms). This indicates delayed saccadic initiation, which can be seen with aging, cerebral white matter disease, or mild central dysfunction.
• The right eye precision at 78.31% is slightly hypometric (undershooting), while the left eye at 112.44% is slightly hypermetric (overshooting). The left eye hypermetria is particularly noteworthy and may suggest cerebellar dysfunction affecting gain calibration.
• Velocities are within acceptable range.

Vertical Saccades (0.3 Hz)

• Vertical saccadic velocities are reduced, particularly in the left eye (102°/s is low-normal to abnormal for vertical saccades).
• Both precision values are significantly hypometric (under 70% and under 55%), indicating prominent vertical saccadic undershoot bilaterally. This is an important central indicator.
• Latency again prolonged bilaterally.
• Reduced vertical saccade velocity with hypometria strongly suggests central pathology (cerebellar, midbrain, or pontine involvement).

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SECTION 2 - SMOOTH PURSUIT

• All smooth pursuit gains are markedly reduced (normal >0.7 for horizontal, >0.6 for vertical in younger patients; adjusted cutoff for age 72 is approximately >0.55 horizontally, but these values are far below even age-adjusted norms).
• Gain values of 0.21-0.43 indicate severely impaired smooth pursuit in all directions.
• Bilateral, symmetric, multi-directional smooth pursuit breakdown is a central sign, most commonly associated with cerebellar or cerebro-cerebellar pathway dysfunction.
• Peripheral vestibular lesions do NOT typically cause this degree of smooth pursuit impairment.
• At age 72, some decline in pursuit is expected, but gains this low are pathological and indicate central involvement.

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SECTION 3 - OPTOKINETIC TEST (OKN)

• Horizontal OKN gains are relatively preserved (0.90-1.38), with the left eye showing slightly higher gain which may reflect a compensatory asymmetry.
• Vertical OKN gains (0.60-0.91) are mildly reduced but more preserved than smooth pursuit gains.
• The OKN and smooth pursuit dissociation (OKN better preserved) is not uncommon with central pathology, as OKN can be driven partly by non-cortical pathways.

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SECTION 4 - SPONTANEOUS NYSTAGMUS

In Light:

• Horizontal SPV: none recorded
• Vertical SPV: none recorded
• No spontaneous nystagmus in light - normal finding

In Dark:

• All parameters: none recorded
• No spontaneous nystagmus in dark - this actually argues against acute peripheral vestibular decompensation

High-Frequency Head Shake (HST):

• Right Eye Horizontal SPV: -8.53°/s, Amplitude: -0.93°, Frequency: 1.12 Hz
• Left eye: no response recorded

• A post-head-shake horizontal nystagmus is present in the RIGHT eye (-8.53°/s is a significant slow-phase velocity; abnormal threshold typically >5°/s).
• The negative sign indicates that the slow phase is leftward (so fast phase/nystagmus beats rightward) following head shake.
• This indicates a left-sided peripheral vestibular asymmetry - the slower/weaker side is on the LEFT. After head shaking, nystagmus beats toward the side with higher vestibular tone (the stronger, RIGHT side).
• This is a classic Head Shake Nystagmus (HSN) pattern for left peripheral hypofunction.

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SECTION 5 - GAZE TEST (DETAILED)

5A. Gaze with Fixation (All Positions: Center, Left, Up, Right, Down)

5B. Gaze WITHOUT Fixation (Eyes Open in Dark / Frenzel-equivalent)

• Vertical SPV of -5.96°/s in the right eye (no horizontal component)
• Frequency 0.62 Hz
• This represents a downbeat component in primary gaze when fixation is removed - a significant central sign

• Horizontal SPV of +5.64°/s in right eye (fast phase toward RIGHT while gazing LEFT = beating toward midline/right, consistent with Alexander's Law if primary vestibular nystagmus is right-beating)
• This is consistent with a peripheral vestibular asymmetry with right-beating nystagmus that enhances on leftward gaze (Alexander's Law - nystagmus enhanced in direction of fast phase)

• Bilateral vertical downward slow phase (-3.21°/s right eye, -3.94°/s left eye)
• Nystagmus present bilaterally on upward gaze - upbeat nystagmus on upgaze (eyes drift down, fast phase upward)
• Bilateral involvement with upward gaze nystagmus is a significant central finding

• Most prominent nystagmus position
• Horizontal SPV: -4.86°/s (R), -7.99°/s (L) - LEFTWARD slow phase = right-beating nystagmus
• Vertical component: -4.29°/s in right eye
• Fast phase direction: 130.59° (oblique - combined horizontal + vertical)
• Frequency: 1.79 Hz (R), 1.25 Hz (L)
• This is the maximum intensity position for the primary vestibular nystagmus (right-beating, enhanced on rightward gaze)
• The oblique fast phase direction (130.59°) suggests a mixed horizontal-torsional component typical of peripheral vestibular nystagmus

• Minor left eye vertical nystagmus (1.11°/s, 1.05 Hz) - clinically borderline

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SECTION 6 - POSITIONAL TESTING

Dix-Hallpike Right (Testing Right Posterior Canal BPPV):

Dix-Hallpike Left (Testing Left Posterior Canal BPPV):

• Significant horizontal nystagmus elicited with LEFT Dix-Hallpike in the head-extended left supine position (both eyes; SPV up to -15°/s in left eye)
• The nystagmus has a negative horizontal slow phase (fast phase rightward) and is present bilaterally
• This is a LEFT-sided positional nystagmus elicited on left Dix-Hallpike - but the nystagmus characteristics (horizontal, bilateral, persistent) suggest Cupulolithiasis of the Left Horizontal Canal (geotropic or apogeotropic) rather than classical posterior canal BPPV (which would give upbeat-torsional nystagmus)
• The nystagmus persisting during the return-to-sit position also supports cupulolithiasis (prolonged, not brief paroxysmal)

Supine Straight Head Extension:

McClure-Pagnini (Testing Horizontal Canal BPPV):

Head Position Tests (Static Positional):

• Roll Left elicits the strongest nystagmus (left eye horizontal -9.51°/s) - right-beating on left lateral roll. This is characteristic of apogeotropic horizontal canal nystagmus (nystagmus beats AWAY from the ground = cupulolithiasis of horizontal canal)
• Pitch Backward generates bilateral vertical downbeat-like nystagmus, suggesting posterior/vertical canal involvement
• Direction-changing nystagmus with different head positions indicates multi-canal BPPV or cupulolithiasis

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SECTION 7 - SUBJECTIVE VISUAL VERTICAL (SVV)

• SVV on blank background: -1° (left tilt) - this is at the border of normal (±2° is normal). A 1° deviation is clinically insignificant in isolation.
• The significant dynamic SVV variations with rotation (+6° to -8°) suggest otolithic dysfunction affecting utricle processing
• However, static SVV near normal (-1°) suggests compensated or mild utricular dysfunction

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OVERALL DIAGNOSTIC IMPRESSION

Primary Diagnosis: Left Peripheral Vestibular Hypofunction with Superimposed Multi-Canal/Horizontal Canal BPPV

Supporting Evidence:

• Post-head-shake nystagmus: right-beating (SPV -8.53°/s) - indicates LEFT side weakness
• Gaze test without fixation: right-beating nystagmus enhanced on right gaze (Alexander's Law) - fixation completely suppresses it (peripheral pattern)
• No spontaneous nystagmus in light or dark (compensated/chronic rather than acute)

• Positive LEFT Dix-Hallpike with horizontal nystagmus (not the upbeat-torsional of posterior canal)
• Positive McClure-Pagnini Supine Head Neutral with bilateral horizontal nystagmus
• Roll Left producing the strongest horizontal nystagmus (apogeotropic = cupulolithiasis)
• Persistent positional nystagmus (lasting through the head extension sequence) suggests cupulolithiasis rather than canalolithiasis

• Severely reduced smooth pursuit gains bilaterally (0.15-0.43; far below normal even for age 72)
• Prolonged saccadic latencies bilaterally (>300 ms)
• Bilateral vertical saccadic hypometria (53-65%)
• Vertical downbeat component in center gaze without fixation (-5.96°/s)
• Bilateral upbeat nystagmus on upgaze without fixation
• These central signs cannot be explained by peripheral vestibular disease alone

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CLINICAL RECOMMENDATIONS

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SUMMARY TABLE

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Note: This analysis is based solely on the VNG data provided. Clinical correlation with the patient's history, audiometry, and neuroimaging is essential for definitive diagnosis and management planning.