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videonystagmography smooth pursuit saccade normative values interpretation
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VNG vestibular testing saccades smooth pursuit interpretation
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VNG Report - Detailed Analysis & Diagnosis
Patient: Chander Singh Rawat | Age: 74 years | Male | Date: 05-Jun-2026
Facility: Priority Hearing Care Pvt. Ltd. | ID: CCDA00378
1. SACCADE TESTING (Eye Movement Accuracy & Speed)
Saccades test the integrity of the brainstem saccadic burst generators and cerebellar pathways.
Horizontal Saccades
| Parameter | Right Eye | Left Eye | Normal Range (Adult) |
|---|---|---|---|
| Velocity (0.3 Hz) | 461 °/s | 477 °/s | 300-700 °/s |
| Latency (0.3 Hz) | 223 ms | 242 ms | 150-250 ms |
| Velocity (0.45 Hz) | 322 °/s | 164 °/s | 300-700 °/s |
| Velocity (0.6 Hz) | 471 °/s | 542 °/s | Normal |
| Velocity (Random Amp) | 395 °/s | 450 °/s | Normal |
Findings: Horizontal saccade velocities are largely within acceptable ranges for a 74-year-old. Latencies are borderline prolonged, particularly at 0.3 Hz (right 223 ms, left 242 ms), but this is consistent with age-related slowing. The 0.45 Hz left eye velocity (164 °/s) is notably reduced, raising a question of asymmetry, though this may reflect tracking artifact at that frequency.
Vertical Saccades - KEY ABNORMALITY
| Parameter | Right Eye | Left Eye |
|---|---|---|
| Velocity (0.3 Hz) | 357 °/s | 708 °/s |
| Precision (0.3 Hz) | 60.81 | 105.13 |
| Latency (0.3 Hz) | 313 ms | 307 ms |
| Velocity (0.45 Hz) | 336 °/s | 714 °/s |
| Precision (0.45 Hz) | 60.20 | 83.09 |
| Velocity (Random Amp) | 129 °/s | 531 °/s |
| Precision (Random Amp) | 59.86 | 218.96 |
| Velocity (Random Freq Amp) | 241 °/s | 583 °/s |
| Precision (Random Freq Amp) | 63.90 | 164.53 |
Critical Finding: There is a marked, consistent left eye velocity hypermetria and precision overshoot across all vertical saccade paradigms. Precision values > 100 indicate saccadic overshoot (hypermetria). The left eye overshoots vertical targets, while the right eye falls within or slightly below normal. This right-left eye velocity asymmetry in vertical saccades is a significant oculomotor abnormality. The right eye random amplitude vertical velocity (129 °/s) is also notably reduced.
Significance: Saccadic hypermetria of the left eye and hypometria of the right eye in vertical tracking suggests cerebellar involvement (fastigial nucleus or vermis dysfunction causes dysmetric saccades). Bilateral but asymmetric vertical saccade abnormalities with extremely high left eye velocities (1313 °/s in random frequency vertical) are highly anomalous and suggest artifact or a genuine binocular disconjugacy.
Hemifield Saccades
| Test | Right Eye | Left Eye |
|---|---|---|
| Left Hemifield Velocity | 385 °/s | 1250 °/s |
| Left Hemifield Precision | 88.07 | 175.35 |
| Up Hemifield RE Velocity | 155 °/s | 1054 °/s |
| Up Hemifield RE Precision | 51.64 | 220.19 |
| Down Hemifield RE Velocity | 260 °/s | 950 °/s |
The extreme left-eye velocities (up to 1250-1313 °/s) are physically implausible for normal saccades and indicate either left-eye tracking artifact/calibration error or a genuinely pathological finding. The right-eye velocities remain in range, suggesting the left eye recording may be unreliable for vertical and up/down hemifield testing.
2. SMOOTH PURSUIT TESTING - SIGNIFICANT ABNORMALITY
Smooth pursuit gain is the ratio of eye velocity to target velocity. Normal gain is approximately 0.8-1.0. Gains below 0.7 are abnormal.
Horizontal Smooth Pursuit
| Frequency | RE Rightward | RE Leftward | LE Rightward | LE Leftward |
|---|---|---|---|---|
| 0.2 Hz | 0.63 | 0.82 | 0.12 | 0.47 |
| 0.4 Hz | 0.51 | 0.60 | 0.31 | 0.65 |
| 0.6 Hz | 0.46 | 0.42 | 0.30 | 0.35 |
| SPNTT Body Right | 0.57 | 0.66 | 0.08 | 0.14 |
| SPNTT Body Left | 0.46 | 0.70 | 0.08 | 0.05 |
Vertical Smooth Pursuit
| Frequency | RE Upward | RE Downward | LE Upward | LE Downward |
|---|---|---|---|---|
| 0.2 Hz | 0.32 | 0.53 | 0.06 | 0.58 |
| 0.4 Hz | 0.25 | 0.39 | 0.06 | 0.32 |
| 0.6 Hz | 0.21 | 0.48 | 0.05 | 0.10 |
Critical Findings:
- Left eye smooth pursuit gain is severely reduced across ALL frequencies and directions, especially upward (gain 0.05-0.06) and during body rotation (gain 0.05-0.14). This is a consistent, reproducible finding across multiple paradigms.
- Right eye smooth pursuit gain is also reduced (0.21-0.82), which is below the expected range (0.8-1.0), especially for upward (0.21-0.32) and at higher frequencies (0.42-0.46 at 0.6 Hz).
- Bilateral smooth pursuit gain reduction is the pattern of a central oculomotor disorder, not peripheral vestibular disease.
- The right eye vertical upward gain (0.21-0.32) is particularly low, consistent with the known pattern of downbeat nystagmus/cerebellar degeneration where upward pursuit is most severely affected.
Interpretation: Severely abnormal smooth pursuit, worse for upward pursuit and worse for the left eye, strongly indicates a central lesion affecting the pursuit pathways - most likely the cerebellum (flocculus/paraflocculus) or the dorsal pons (nucleus of the optic tract, dorsal terminal nucleus, DLPN).
3. OPTOKINETIC NYSTAGMUS (OKN) TESTING
OKN tests the ability to generate reflexive nystagmus to a moving visual field. Normal gain is approximately 0.8-1.0.
| Direction | RE Gain | LE Gain | Normal |
|---|---|---|---|
| Left to Right (10°) | 1.00 | 1.05 | ~1.0 |
| Right to Left (10°) | 0.90 | 0.92 | ~1.0 |
| Top to Bottom (10°) | 1.02 | 1.09 | ~1.0 |
| Bottom to Top (10°) | 0.65 | 0.65 | ~1.0 |
| Left to Right (20°) | 0.68 | 0.76 | ~1.0 |
| Right to Left (20°) | 0.90 | 0.91 | ~1.0 |
Key Finding: The "Bottom to Top" (upward) OKN gain is 0.65 bilaterally - significantly reduced compared to all other OKN directions (which are normal or near-normal). This specific pattern of reduced upward OKN gain is consistent with a lesion affecting the anterior vermis/flocculus of the cerebellum or the brainstem pathways mediating upward gaze pursuit/OKN. It mirrors the finding of defective upward smooth pursuit.
4. SPONTANEOUS NYSTAGMUS
| Condition | Horizontal SPV | Vertical SPV | Result |
|---|---|---|---|
| In Light | - | - | None |
| In Dark | - | - | None |
No spontaneous nystagmus in light or dark. This argues against an active acute peripheral vestibular lesion.
5. PROVOCATIVE NYSTAGMUS TESTS
Head Shake (High Frequency)
- Right eye SPV: -5.72 °/s, Amplitude -2.77°, Frequency 0.84 Hz
- Left eye SPV: -3.86 °/s, Amplitude -1.28°, Frequency 0.88 Hz
Finding: Low-amplitude nystagmus noted after high-frequency head shake bilaterally. Head shake nystagmus (HSN) suggests possible dynamic vestibular asymmetry but with low slow-phase velocities (< 6 °/s), this is only mildly abnormal. HSN > 5 °/s (right eye: 5.72 °/s) can indicate a subtle horizontal canal imbalance.
Hyperventilation
- Right eye vertical SPV: -4.86 °/s, frequency 0.87 Hz
- No horizontal nystagmus
Finding: Hyperventilation-induced nystagmus (HVIN) can suggest a demyelinating lesion (MS) near the VIII nerve or central pathways, or a partially compensated vestibular lesion. The vertical component in the right eye is noteworthy.
6. GAZE TESTING
| Position | With Fixation | Without Fixation |
|---|---|---|
| Center | No nystagmus | Mild vertical RE: SPV 1.97 °/s |
| Left | No nystagmus | No nystagmus |
| Right | No nystagmus | No nystagmus |
| Up | No nystagmus | Bilateral vertical: RE 1.87 °/s, LE 6.38 °/s |
| Down | No nystagmus | No nystagmus |
Key Finding: Vertical nystagmus in the upward gaze position (without fixation) - left eye SPV 6.38 °/s, right eye 1.87 °/s. This upward gaze-evoked nystagmus, specifically seen in the vertical component without fixation, is a central sign. The absence of fixation-suppressed nystagmus in right, left, and down gaze, but its presence on upward gaze, is consistent with a cerebellar or dorsal brainstem lesion.
7. DIX-HALLPIKE POSITIONAL TESTING
Dix-Hallpike Right
- Sitting, Head Right: No nystagmus
- Supine with Head Extended Right: Left eye vertical: SPV -4.77 °/s, Amplitude -1.91°, Frequency 1.21 Hz
- Return to Sitting: No nystagmus
Dix-Hallpike Left
- Sitting, Head Left: No nystagmus
- Supine with Head Extended Left: Left eye vertical: SPV +4.75 °/s, Amplitude 1.26°, Frequency 1.02 Hz
- Return to Sitting: No nystagmus
Finding: Low-amplitude vertical nystagmus is elicited by both right and left Dix-Hallpike maneuvers. Crucially:
- The nystagmus is purely vertical (no torsional component noted in the text extraction)
- It appears in the same left eye in both directions
- SPV values are low (< 5 °/s)
- It is non-direction-changing with head position in a typical BPPV pattern
Interpretation: Classic BPPV produces geotropic, direction-changing, torsional-vertical nystagmus. The presence of only vertical nystagmus (no torsional component) on bilateral Dix-Hallpike is more consistent with a central positional nystagmus than typical posterior canal BPPV. Central positional nystagmus does not fatigue, is often persistent, and lacks the typical latency.
8. McCLURE-PAGNINI (ROLL TEST) - Horizontal Canal Testing
All positions (Sit-to-Supine, Right Lateral, Supine Neutral, Left Lateral) showed no nystagmus across all positions and both eyes. This effectively rules out horizontal canal BPPV (cupulolithiasis or canalithiasis).
9. SUBJECTIVE VISUAL VERTICAL (SVV)
| Condition | Deviation | Direction |
|---|---|---|
| Clockwise starting | 6° rightward | (abnormal; normal ≤ 2.5°) |
| Anticlockwise starting | -10° leftward | (abnormal; normal ≤ 2.5°) |
| Blank Background | -2° (Left) | Borderline |
Critical Finding: The SVV shows a very large variability across trials - swinging from +6° (rightward tilt) to -10° (leftward tilt) depending on the starting direction. Normal SVV deviation is ≤ 2.5°. A unilateral peripheral utricular lesion would produce a consistent tilt toward one side. The inconsistent, direction-dependent deviation (6° right versus 10° left) is atypical for peripheral utricle disease and suggests either:
- Poor patient cooperation/understanding of the task
- Central otolith processing dysfunction with inconsistent graviceptive representation
DIAGNOSTIC SYNTHESIS
Summary of Key Abnormalities
| Finding | Clinical Significance |
|---|---|
| Severely reduced smooth pursuit gain bilaterally (worse left eye, worse upward) | Central oculomotor pathology |
| Reduced upward OKN gain (0.65) bilaterally | Anterior cerebellar/brainstem lesion |
| Vertical saccadic hypermetria of left eye | Cerebellar dysmetria |
| Upward gaze nystagmus without fixation | Central vestibular/cerebellar sign |
| Central positional nystagmus (bilateral Dix-Hallpike) | Central positional nystagmus |
| Mild post-head-shake nystagmus | Dynamic vestibular asymmetry |
| Hyperventilation-induced vertical nystagmus | Possible demyelination or partic. lesion |
| Abnormal and inconsistent SVV | Central otolith dysfunction |
| No spontaneous nystagmus in light/dark | No active peripheral lesion |
| Negative Roll Test | No horizontal canal BPPV |
DIAGNOSIS
Primary Diagnosis:
Central Vestibulo-Oculomotor Dysfunction - Pattern Consistent with Cerebellar or Cervicomedullary/Dorsal Brainstem Pathology
The constellation of:
- Bilateral impaired smooth pursuit (most severe upward, consistent across frequencies)
- Deficient upward OKN (while horizontal OKN is preserved)
- Upward gaze nystagmus without fixation
- Central positional nystagmus (non-torsional, bilateral, low SPV)
- Vertical saccadic dysmetria (asymmetric hypermetria)
- Abnormal SVV with poor reproducibility
...is characteristic of a central vestibulocerebellar disorder, most specifically pointing to the cerebellar flocculus/paraflocculus and/or anterior vermis as the primary site of dysfunction. These structures are responsible for smooth pursuit modulation, OKN gain, vertical gaze holding, and saccadic calibration.
Differential Diagnoses to Investigate (in order of probability in a 74-year-old male):
| Priority | Diagnosis | Supporting Features |
|---|---|---|
| 1 | Cerebellar atrophy/degeneration (age-related or sporadic) | Age 74, bilateral symmetric smooth pursuit deficit, upward OKN deficit |
| 2 | Cerebrovascular disease (lacunar infarct - dorsal pons or cerebellum) | Age, common in males, hypertension risk |
| 3 | Multiple System Atrophy - Cerebellar type (MSA-C) | Progressive cerebellar signs with oculomotor involvement |
| 4 | Spinocerebellar Ataxia (SCA) | Hereditary, oculomotor abnormalities prominent early |
| 5 | Downbeat Nystagmus Syndrome | Upward pursuit deficit, upward OKN deficit (though no persistent DBN seen here) |
| 6 | Demyelinating disease (MS) | Hyperventilation-induced nystagmus, age is less typical |
Peripheral Component:
- No evidence of acute peripheral vestibular lesion (no spontaneous nystagmus in light/dark)
- Mild dynamic vestibular asymmetry suggested by head-shake test - may represent a subclinical peripheral contribution or central asymmetry
RECOMMENDED FURTHER EVALUATION
- MRI Brain with FLAIR and T2 (posterior fossa protocol) - to identify cerebellar atrophy, lacunar infarcts, or demyelinating plaques in the brainstem and cerebellum
- Neurology referral - for full cerebellar examination (finger-nose test, tandem gait, Romberg)
- Caloric test / Video Head Impulse Test (vHIT) - not reported in this VNG; needed to assess peripheral canal function quantitatively
- VEMP (cVEMP & oVEMP) - to assess otolith (saccule/utricle) and inferior/superior vestibular nerve integrity
- Genetic/metabolic workup - if MSA or SCA is suspected (SCA gene panel)
- Orthostatic blood pressure - if MSA suspected
- Audiogram - complete audiological evaluation in the context of the vestibular findings
CLINICAL NOTE
The left eye recording abnormalities (extreme velocities > 1000 °/s in some vertical saccade paradigms) may partly reflect a calibration artifact with the left eye goggle/infrared sensor. However, the smooth pursuit findings are robust, internally consistent, and reproducible across multiple frequencies and paradigms, making them the most clinically reliable indicators of pathology.
The right eye smooth pursuit deficits (particularly upward: gain 0.21-0.32) are themselves independently significant and support the central diagnosis even if left-eye recordings are considered unreliable.
This is a VNG technical analysis report. Final clinical diagnosis must be made by a qualified neurologist or neuro-otologist following a full clinical history, neurological examination, and appropriate imaging.
- Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol 2, Chapter 49 (nystagmus and vestibular oculomotor physiology)
- Cummings Otolaryngology - VNG/Caloric Testing section
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