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I now have sufficient clinical context to provide a comprehensive interpretation of Mr. B R Saini's VNG report. Let me compile the full detailed analysis.
Videonystagmography (VNG) Report — Detailed Interpretation
Patient: Mr. B R Saini | Age: 76 years | Gender: Male
Patient ID: CCDA00354 | Date: 27-Apr-2026
Clinic: Priority Hearing Care Pvt. Ltd.
1. SACCADE TEST
1a. Horizontal Saccades
| Frequency | Parameter | Right Eye | Left Eye | Interpretation |
|---|---|---|---|---|
| 0.3 Hz | Velocity | 602.54 °/s | 1157.19 °/s | Asymmetric — Left eye hypometric/dysmetric |
| 0.3 Hz | Precision | 68.69 | 107.59 | Left eye overshooting (>100 = dysmetric) |
| 0.3 Hz | Latency | 203.33 ms | 193.33 ms | Both within borderline normal (≤200–250 ms) |
| 0.45 Hz | Velocity | 540.61 °/s | 2080.05 °/s | Grossly elevated left eye velocity — artifact or dysmetria |
| 0.45 Hz | Precision | 71.87 | 164.45 | Left eye severely overshooting |
| 0.45 Hz | Latency | 208.00 ms | 190.77 ms | Borderline normal |
Findings: There is a marked inter-ocular asymmetry in saccadic velocity and precision, with the left eye showing extremely high velocity values (1157–2080 °/s) and precision values far exceeding 100, indicative of saccadic dysmetria (overshoot) of the left eye. Normal horizontal saccade peak velocity for a 20° target is approximately 400–600 °/s; values exceeding 700–800 °/s, especially asymmetrically, suggest either a monocular tracking abnormality, ocular muscle disorder, or a recording artifact from that eye. The right eye velocities are within the normal-to-low range (540–602 °/s). Saccade latency is borderline prolonged bilaterally (>200 ms; normal <200 ms).
1b. Vertical Saccades
| Frequency | Parameter | Right Eye | Left Eye | Interpretation |
|---|---|---|---|---|
| 0.3 Hz | Velocity | 148.08 °/s | 1681.19 °/s | Right eye severely reduced; left grossly elevated |
| 0.3 Hz | Precision | 20.19 | 168.12 | Right eye hypometric; left severely dysmetric |
| 0.3 Hz | Latency | 295.00 ms | 255.00 ms | Prolonged bilaterally |
| 0.45 Hz | Velocity | 167.09 °/s | 2348.39 °/s | Right eye markedly slow; left excessively fast |
| 0.45 Hz | Precision | 18.97 | 240.31 | Right eye severely hypometric; left severely dysmetric |
| 0.45 Hz | Latency | 456.67 ms | 341.67 ms | Markedly prolonged bilaterally |
Findings: Vertical saccades are severely abnormal. The right eye vertical saccade velocity is markedly reduced (148–167 °/s; normal vertical saccade velocity ~200–400 °/s) with very low precision scores (18–20, indicating hypometria/undershooting). The latencies are significantly prolonged (295–457 ms for right eye; normal <250 ms). This pattern of slow, hypometric vertical saccades with prolonged latency raises concern for supranuclear or central oculomotor pathology. In elderly patients this pattern can be seen in progressive supranuclear palsy (PSP), cerebellar disorders, or brainstem lesions. The extreme left-eye velocity figures likely reflect recording artifact.
2. SMOOTH PURSUIT TEST
2a. Horizontal Smooth Pursuit
| Frequency | Direction | Right Eye | Left Eye | Normal Range |
|---|---|---|---|---|
| 0.2 Hz | Rightward Gain | 0.56 | 0.05 | ≥0.7–0.8 |
| 0.2 Hz | Leftward Gain | 0.48 | 0.03 | ≥0.7–0.8 |
| 0.4 Hz | Rightward Gain | 0.50 | 0.07 | ≥0.5–0.6 |
| 0.4 Hz | Leftward Gain | 0.57 | 0.12 | ≥0.5–0.6 |
Findings: The right eye smooth pursuit gain is reduced bilaterally at 0.2 Hz (0.48–0.56; normal ≥0.7–0.8 for 0.2 Hz). The left eye gains are essentially zero (0.03–0.12), indicating virtual absence of smooth pursuit in the left eye. This could reflect a monocular ocular motor deficit or recording issue with the left eye sensor. The right eye shows reduced smooth pursuit gain consistent with age-related decline or a central (cerebellar/brainstem) process.
2b. Vertical Smooth Pursuit
| Frequency | Direction | Right Eye | Left Eye | Normal Range |
|---|---|---|---|---|
| 0.2 Hz | Upward Gain | 0.34 | 0.06 | ≥0.6–0.7 |
| 0.2 Hz | Downward Gain | 0.32 | 0.04 | ≥0.6–0.7 |
| 0.4 Hz | Upward Gain | 0.18 | 0.04 | ≥0.4–0.5 |
| 0.4 Hz | Downward Gain | 0.20 | 0.06 | ≥0.4–0.5 |
Findings: Vertical smooth pursuit gain is markedly reduced in both eyes (right eye 0.18–0.34; normal ≥0.4–0.7). This is more than what is expected from normal aging alone. Significantly reduced vertical smooth pursuit, especially downward pursuit, is a hallmark of central oculomotor pathology (cerebellar/brainstem involvement or PSP). The left eye again shows near-absent tracking.
3. OPTOKINETIC TEST (OKN)
| Stimulus Direction | Right Eye Gain | Left Eye Gain | Normal |
|---|---|---|---|
| Left to Right 10° | 1.00 | 0.96 | ~1.0 |
| Right to Left 10° | 1.13 | 2.37 | ~1.0 |
| Top to Bottom 10° | — | 0.75 | ~1.0 |
| Bottom to Top 10° | 0.94 | 0.95 | ~1.0 |
Findings: OKN responses are largely within normal limits for horizontal stimuli. The right-to-left gain is slightly elevated for the left eye (2.37). Vertical OKN is essentially absent for the right eye (no response recorded for Top-to-Bottom), with only the left eye showing 0.75. Bottom-to-top is symmetric and normal. The absent/asymmetric vertical OKN corroborates central involvement, specifically brainstem/pretectal pathology (downward OKN abnormality is associated with pretectal lesions).
4. SPONTANEOUS NYSTAGMUS
In Light
- No nystagmus recorded — all parameters negative.
In Dark
- No nystagmus recorded — all parameters negative.
Interpretation: No spontaneous nystagmus in either light or darkness. This is a normal finding and argues against an acute peripheral vestibular lesion at the time of testing.
5. HIGH-FREQUENCY HEAD SHAKE TEST
- No post-head shake nystagmus recorded.
- Normal finding — no evidence of a significant uncompensated unilateral vestibular hypofunction.
6. HYPERVENTILATION-INDUCED NYSTAGMUS
- Right Eye: No response
- Left Eye: Vertical nystagmus — Slow Phase Velocity: 13.63 °/s, Amplitude: 6.06°, Frequency: 0.89 Hz
Findings: The left eye shows hyperventilation-induced vertical nystagmus. This is an abnormal finding. Hyperventilation-induced nystagmus is known to occur with vascular compression of the 8th nerve (vestibular nerve), demyelinating disease (acoustic neuroma/vestibular schwannoma), or perilesional vestibular or cerebellar pathology. A slow-phase velocity of 13.63 °/s is clinically significant (threshold >5 °/s is considered significant).
7. GAZE TEST
With Fixation (Center, Left, Right, Up, Down)
- No nystagmus in any gaze direction with fixation.
- Normal finding — no gaze-evoked nystagmus with visual fixation.
Without Fixation
| Gaze Position | Right Eye Finding | Left Eye Finding |
|---|---|---|
| Center | No nystagmus | No nystagmus |
| Left | Vertical SPV 8.53 °/s, amplitude 3.12°, freq 1.11 Hz | Horizontal SPV 2.95 °/s, amplitude 1.23° |
| Right | Horizontal SPV −3.14 °/s; Vertical SPV 4.59 °/s, freq 1.55 Hz | Horizontal SPV −4.11 °/s; Vertical SPV 3.73 °/s, freq 1.17 Hz; Fast phase dir 223.11° |
| Up | No nystagmus | No nystagmus |
| Down | Vertical SPV 4.98 °/s, freq 0.76 Hz | Horizontal SPV −2.91 °/s; Vertical SPV 5.20 °/s, freq 1.36 Hz; Fast phase dir 252.92° |
Key Findings:
- Nystagmus appears in multiple eccentric gaze positions without fixation (left, right, down) but is suppressed with fixation — indicating central adaptation with intact fixation suppression.
- The fast phase directions (243°, 223°, 252°) are oblique/downward-beating, suggesting a torsional-vertical nystagmus component.
- Gaze-evoked nystagmus without fixation in multiple directions is a feature of central vestibular pathology (cerebellar, brainstem).
8. POSITIONAL TESTING
Dix-Hallpike Test — Right Side
| Position | Horizontal SPV | Vertical SPV | Fast Phase Direction | Freq |
|---|---|---|---|---|
| Sit Head Right | No nystagmus | No nystagmus | — | — |
| Supine Head Ext. & Right | H: +13.98 / +12.15 °/s | V: −19.27 / −21.12 °/s | 52.86° / 56.89° | 1.75 / 1.69 Hz |
| Return to Sit | No nystagmus | — | — | — |
Findings on Right Dix-Hallpike: A robust nystagmus is provoked in the supine head extended and right position, with both horizontal and vertical components (fast phase directed at ~52–57°, i.e., upper-beating oblique nystagmus). This nystagmus resolves on return to sitting. The fast phase direction of ~52° (upward/geotropic direction) is consistent with right posterior semicircular canal BPPV (canalolithiasis) — the hallmark of which is upward-torsional nystagmus on Dix-Hallpike to the affected side.
Dix-Hallpike Test — Left Side
| Position | Horizontal SPV | Vertical SPV | Fast Phase Direction | Freq |
|---|---|---|---|---|
| Sit Head Left | No nystagmus | — | — | — |
| Supine Head Ext. & Left | — | V: −3.64 °/s (RE only) | — | 1.15 Hz (RE) |
| Return to Sit | No nystagmus | — | — | — |
Findings on Left Dix-Hallpike: Only a very mild, low-velocity vertical nystagmus is seen in the right eye during supine head-extended left position (SPV 3.64 °/s, amplitude 3.42°). This is below the typical diagnostic threshold (SPV <6 °/s is borderline). This likely represents residual/compensating activity rather than a left posterior canal BPPV.
McClure-Pagnini (Roll) Test — Horizontal Canal BPPV Assessment
| Position | R Eye Vertical SPV | L Eye Horizontal SPV | Fast Phase Dir | Freq |
|---|---|---|---|---|
| Right Lateral | −12.01 °/s | −15.24 °/s (V); +8.63 °/s (H) | 60.54° (LE) | 0.73 / 1.86 Hz |
| Supine Neutral (1) | −14.09 °/s (RE vertical) | — | — | 0.53 Hz |
| Left Lateral | +9.30 °/s (RE vertical) | — | — | 0.81 Hz |
| Supine Neutral (2) | No nystagmus | — | — | — |
Findings: Nystagmus is present in both lateral positions of the roll test (right lateral and left lateral), with persistent vertical nystagmus in the supine-neutral position after right lateral testing. The nystagmus in both lateral positions suggests either bilateral horizontal canal BPPV (canalolithiasis or cupulolithiasis) or a central positional nystagmus. The persistent nystagmus in the neutral supine position is also atypical. The direction-changing nature of this positional nystagmus (geotropic in right lateral, ageotropic pattern in left lateral) warrants clinical correlation to differentiate BPPV from a central cause.
9. SUBJECTIVE VISUAL VERTICAL (SVV)
| Condition | Deviation | Time Taken | Direction |
|---|---|---|---|
| Clockwise rotation | +6° (Right) | 34 s | Anti-clockwise |
| Anti-clockwise rotation | −3° (Left) | 13 s | Anti-clockwise |
| Blank background | −1° (Left) | 10 s | Anti-clockwise |
Findings:
- The SVV during clockwise rotation showed a significant rightward tilt of 6° (normal SVV deviation ≤2–3° in static condition). A static/blank background deviation of −1° (Left) is within normal limits.
- The prolonged time taken for the clockwise trial (34 s vs. 10–13 s for others) may indicate difficulty perceiving the gravitational vertical, suggesting otolith dysfunction (particularly the utricle). Significant SVV deviation >2.5–3° is a marker of utricular dysfunction, which can be peripheral (e.g., otolith end-organ disease) or central (brainstem/thalamic pathology).
- The dynamic SVV tilt during clockwise rotation (6° rightward) may indicate right-sided utricular asymmetry.
OVERALL SUMMARY & CLINICAL INTERPRETATION
Key Abnormalities Identified:
| Domain | Finding | Significance |
|---|---|---|
| Saccades (Horizontal) | Bilateral prolonged latency; left eye dysmetria | Central/oculomotor |
| Saccades (Vertical) | Markedly reduced velocity & hypometria right eye; prolonged latency | Central — possible supranuclear pathology |
| Smooth Pursuit (H & V) | Reduced gain bilaterally, more severe for vertical | Central — cerebellar/brainstem |
| OKN | Absent downward right-eye response | Central — pretectal/brainstem |
| Spontaneous Nystagmus | Absent | Normal |
| Head Shake | No nystagmus | Normal |
| Hyperventilation | Left eye vertical nystagmus (SPV 13.63 °/s) | Abnormal — nerve/central lesion |
| Gaze Test (no fixation) | Multi-directional nystagmus (left, right, down gaze) | Central vestibular |
| Dix-Hallpike Right | Positive — upward oblique nystagmus (fast phase ~53°) | Right posterior canal BPPV |
| McClure-Pagnini | Bilateral positional nystagmus | BPPV vs. central positional nystagmus |
| SVV | Clockwise deviation +6° Right | Otolith (utricular) asymmetry — Right |
Clinical Impression
This VNG demonstrates a mixed picture:
-
Right Posterior Canal BPPV — The Dix-Hallpike right test is positive with upward-torsional nystagmus (fast phase ~53°, frequency 1.7 Hz, SPV ~19–21 °/s) consistent with right posterior semicircular canal canalolithiasis. This is the most common cause of episodic positional vertigo and is amenable to Epley canalith repositioning maneuver.
-
Central Oculomotor Abnormalities — Multiple findings indicate central nervous system involvement:
- Severely slow and hypometric vertical saccades with markedly prolonged latencies
- Globally reduced smooth pursuit (horizontal and vertical)
- Multi-directional gaze nystagmus without fixation
- Absent vertical OKN (right eye)
- These features together are most consistent with cerebellar or brainstem dysfunction. In a 76-year-old, etiologies include cerebellar atrophy, posterior fossa ischemic disease, or degenerative conditions such as progressive supranuclear palsy (PSP — classically causing slowed vertical saccades).
-
Hyperventilation-Induced Nystagmus — Suggests possible neurovascular compression, demyelinating process, or an irritative central lesion (vestibular nerve/nucleus level).
-
Utricular Asymmetry — Dynamic SVV deviation of 6° rightward during clockwise rotation points to right utricular hypofunction or asymmetry.
Recommended Next Steps
- Epley Maneuver for right posterior canal BPPV (most immediately treatable finding).
- MRI Brain with posterior fossa protocol (FLAIR, DWI, T2) to evaluate for cerebellar/brainstem pathology, lacunar infarcts, or posterior fossa lesion.
- Neurological consultation given the pattern of vertical saccade slowing and reduced smooth pursuit (rule out PSP or multisystem atrophy).
- Caloric testing (not included in this report) would complete the peripheral vestibular evaluation.
- Vestibular rehabilitation once BPPV is treated, to address residual central vestibular instability.
Disclaimer: This interpretation is based solely on the data provided in the VNG report. A complete clinical correlation including history, physical examination, neurological assessment, and caloric test results is essential for a definitive diagnosis. This report should be reviewed by the treating ENT/Neurootologist or neurologist.
— K J Lee's Essential Otolaryngology, p. 351
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