What could be the reason for left eye recordings and provide the full detailed report on VNG WITH DIAGnOSIS ?
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Videonystagmography (VNG) Report — Full Interpretation
Patient: Birmati Devi | Age: 74F | ID: CCDA00356 | Date: 30-Apr-2026
PART 1: WHY IS THE LEFT EYE RECORDING ABNORMAL OR ABSENT?
Across nearly every subtest in this VNG, the left eye channel shows either absent data (–), minimal signal, or highly degraded waveforms compared to the right eye. The possible reasons are:
Technical / Procedural Causes (Most Likely)
| Cause | Explanation |
|---|---|
| Poor infrared camera fit/positioning | The VNG goggle's left camera may have been misaligned, too far from the eye, or slipped during testing — the most common cause of unilateral missing data |
| Ptosis of the left eyelid | At age 74, age-related ptosis is common and can partially or fully occlude the pupil from the infrared sensor |
| Left eye kept closed or squinting | Patient discomfort, photophobia, or poor cooperation with the left camera |
| Eyelash/makeup artifact | Mascara, eyelashes, or heavy periorbital tissue blocking the pupil tracker |
| Pupil tracking failure | If the patient's left pupil is small (miosis), the software may fail to lock on — common in elderly patients under bright conditions |
Clinical / Pathological Causes (Must Be Ruled Out)
| Cause | Explanation |
|---|---|
| Left internuclear ophthalmoplegia (INO) | A lesion in the left medial longitudinal fasciculus causes impaired adduction of the left eye — producing asymmetric saccade velocities (RE fast, LE slow) |
| Third nerve palsy (CN III) left | Would reduce left eye movement across all directions |
| Left hemispheric or brainstem lesion | Central ocular motor pathway lesion affecting left eye conjugate movements |
| Visually impaired left eye | Significant cataract, macular degeneration, or severe refractive error in the left eye at age 74 is common and can reduce corneal reflex intensity for the VNG tracker |
Clinical note: Given that the right eye data is robust and internally consistent, the most probable explanation in this 74-year-old is a technical recording failure of the left eye camera (ptosis, camera slippage, or pupil-tracking failure), rather than a true monocular ocular motor deficit. However, clinical correlation with direct ophthalmologic examination is recommended to exclude CN III palsy, cataract, or severe ptosis.
PART 2: FULL DETAILED VNG REPORT WITH INTERPRETATION
1. SACCADES (0.3 Hz — Horizontal & Vertical)
| Parameter | Right Eye | Left Eye | Normal Reference |
|---|---|---|---|
| H Velocity | 579.55°/s | 165.90°/s | >200°/s (for 20° target) |
| H Precision | 91.37 | 11.15 | >85% |
| H Latency | 327.06 ms | 354.29 ms | 150–250 ms |
| V Velocity | 461.28°/s | 374.45°/s | >150°/s |
| V Precision | 99.52 | 38.08 | >85% |
| V Latency | 314.29 ms | 533.33 ms | 150–250 ms |
Interpretation — Right Eye:
- Horizontal saccade velocity is normal to brisk at 579.55°/s
- Precision of 91.37% is within normal limits
- Latency of 327 ms is mildly prolonged (normal <250 ms) — may reflect age-related slowing (normal in elderly >60 years) or mild attentional delay
Interpretation — Left Eye:
- Horizontal precision of only 11.15% is severely degraded — strongly suggests a recording artifact rather than a true neurological deficit (near-zero precision means the eye tracking system could not lock on)
- Latency of 533 ms for vertical is grossly prolonged — again consistent with tracking failure
- Left eye saccade data is unreliable/uninterpretable
Saccade Conclusion: Right eye saccade velocities are normal. Mildly prolonged latency bilaterally may reflect age-related changes or mild frontal lobe slowing. No definitive hypometria or intrusive saccades observed in the right eye tracings.
2. SMOOTH PURSUIT (0.2 Hz — Horizontal & Vertical)
| Parameter | Right Eye | Left Eye | Normal (age-adjusted) |
|---|---|---|---|
| H Rightward Gain | 0.97 | 0.31 | >0.6 (age >60: >0.5) |
| H Leftward Gain | 0.95 | 0.42 | >0.6 |
| V Upward Gain | 0.78 | 0.38 | >0.6 |
| V Downward Gain | 0.93 | 0.21 | >0.6 |
Interpretation — Right Eye:
- Horizontal gains of 0.97 and 0.95 are excellent — smooth pursuit is intact and age-appropriate
- Vertical upward gain of 0.78 is mildly reduced (normal downward > upward in elderly); downward gain 0.93 is normal
- Right eye pursuit waveforms show a smooth sinusoidal pattern tracking the target accurately
Interpretation — Left Eye:
- All gains are markedly reduced (0.21–0.42) — again this is consistent with camera/tracking failure since the right eye pursues normally
- A true bilateral smooth pursuit deficit would show degraded gain bilaterally
Smooth Pursuit Conclusion: Normal smooth pursuit in the right eye. Reduced upward pursuit gain (0.78) may represent early age-related or cerebellar change but is not clinically significant in isolation. Left eye data unreliable.
3. OPTOKINETIC NYSTAGMUS (OKN)
| Direction | Right Eye Gain | Left Eye | Normal |
|---|---|---|---|
| Left→Right | 1.05 | — | 0.7–1.2 |
| Right→Left | 0.91 | — | 0.7–1.2 |
| Top→Bottom | 0.98 | — | 0.7–1.2 |
| Bottom→Top | 1.04 | — | 0.7–1.2 |
Interpretation:
- OKN responses in the right eye are entirely normal in all four directions (0.91–1.05)
- Left eye again unrecorded
- Symmetric OKN gain (L→R: 1.05 vs R→L: 0.91) — asymmetry <25% is within normal limits
- Fast phase direction is unreported for most subtests, suggesting absence of pathological fast phases
- No evidence of OKN asymmetry that would suggest a parieto-occipital or brainstem lesion
OKN Conclusion: Normal.
4. SPONTANEOUS NYSTAGMUS (Light & Dark)
| Condition | Right Eye | Left Eye |
|---|---|---|
| In Light (SPV) | — | — |
| In Dark (SPV) | — | — |
Interpretation:
- No spontaneous nystagmus detected in either light or darkness in either eye
- Absence of spontaneous nystagmus in light is expected (fixation suppresses peripheral nystagmus)
- Absence in darkness means no active unilateral vestibular deafferentation at time of testing
- This argues against an acute peripheral vestibular lesion (e.g., acute vestibular neuritis)
Spontaneous Nystagmus Conclusion: Normal (absent — appropriate).
5. HIGH-FREQUENCY HEAD SHAKE & HYPERVENTILATION NYSTAGMUS
| Test | Right Eye | Left Eye |
|---|---|---|
| Head Shake SPV | — | — |
| Hyperventilation SPV | — | — |
Interpretation:
- No post-head-shake nystagmus (HSN): Absence of HSN argues against a significant unilateral peripheral vestibular hypofunction (HSN typically appears when >20% caloric asymmetry is present)
- No hyperventilation-induced nystagmus: Absence argues against a vestibular schwannoma (which classically produces nystagmus toward the lesion side with hyperventilation) or demyelinating lesion
Conclusion: Normal.
6. GAZE TESTS (Fixation & Without Fixation)
With Fixation (all positions): No nystagmus recorded in any gaze position — normal.
Without Fixation — Noteworthy Findings:
| Position | Eye | Component | Value |
|---|---|---|---|
| Left gaze, no fixation | Right | Vertical SPV | 5.23°/s, Amplitude 8.24°, Frequency 0.43 Hz |
| Up gaze, no fixation | Right | Vertical SPV | 0.52°/s (borderline) |
| Down gaze, no fixation | Right | Horizontal SPV | 13.60°/s, Amplitude 4.74°, Frequency 0.90 Hz |
Interpretation:
- Left gaze without fixation (SPV 5.23°/s): This exceeds the normal threshold of 4°/s and represents a low-level positional/gaze-evoked nystagmus when fixation is removed. This is a non-localizing finding that can indicate:
- Compensated peripheral vestibular lesion (direction-fixed nystagmus suppressed by fixation)
- Cerebellar or brainstem dysfunction (gaze-evoked nystagmus without fixation)
- Down gaze without fixation (Horizontal SPV 13.60°/s): This is above the normal threshold and represents the most significant gaze finding. Horizontal nystagmus in down gaze without fixation suggests:
- Peripheral vestibular imbalance with positional modulation
- Central positional nystagmus (particularly if direction changes with head position)
- The fact that nystagmus is suppressed with fixation in all gaze positions is a reassuring sign pointing toward peripheral etiology
Gaze Test Conclusion: Mild gaze-evoked nystagmus without fixation, most prominent in down gaze (SPV 13.6°/s) and left gaze (SPV 5.23°/s). Fixation suppression is intact — supports peripheral vestibular origin.
7. DIX-HALLPIKE POSITIONAL TESTING
Right Dix-Hallpike:
| Position | Nystagmus |
|---|---|
| Sit head right | None |
| Supine head extended + right | None |
| Return to sit | None |
→ Negative right Dix-Hallpike
Left Dix-Hallpike:
| Position | Nystagmus |
|---|---|
| Sit head left (initial) | None |
| Supine head extended + left | None |
| Return to sit head left | Right eye: Vertical SPV 7.90°/s, Amplitude 8.65°, Freq 0.44 Hz |
Interpretation:
- The left Dix-Hallpike return to sit provokes vertical nystagmus (SPV 7.90°/s, amplitude 8.65°, frequency 0.44 Hz) in the right eye
- The nystagmus appears on returning to the upright position (not on lying down), which is atypical for classic posterior canal BPPV
- This may represent:
- Cupulolithiasis variant of BPPV (persistent rather than transient nystagmus on provocation)
- Horizontal canal BPPV (geotropic or apogeotropic variant)
- Persistent positional nystagmus with a peripheral basis
- The amplitude of 8.65° and frequency of 0.44 Hz are consistent with the low-frequency slow nystagmus of cupulolithiasis
8. POSITIONAL TESTS — HEAD POSITIONS (Supine)
| Position | Nystagmus | Value |
|---|---|---|
| Yaw Right | None | — |
| Yaw Left | None | — |
| Pitch Forward | None | — |
| Pitch Backward | Right eye Horizontal SPV | 2.49°/s, Amplitude 1.76°, Freq 0.63 Hz |
| Roll Right | None | — |
| Roll Left | None | — |
Interpretation:
- Pitch backward (supine with neck extended) produces a low-level horizontal nystagmus (SPV 2.49°/s) — this is at the borderline of normal (<4°/s threshold) but notable given the pattern across multiple positions
- The horizontal component during neck extension could reflect otolithic stimulation or a low-level BPPV variant
- All other head positions: no nystagmus — reassuring
9. SUBJECTIVE VISUAL VERTICAL (SVV)
| Condition | Deviation | Normal |
|---|---|---|
| Clockwise rotation | +2° Right | ±2–3° |
| Anticlockwise rotation | –4° Left | ±2–3° |
| Blank background | –1° Left | ±2° |
Interpretation:
- Clockwise: +2° right — within normal limits
- Anticlockwise: –4° left — this is at the upper limit / mildly abnormal for SVV tilt
- Blank background: –1° left — essentially normal
- A consistent leftward tilt on SVV would suggest right otolithic dysfunction (utricle), as the SVV tilts toward the side of lesion (or away, depending on context). However, with inconsistent results across trials (right in CW, left in ACW), this is not definitively abnormal
- The SVV findings are inconclusive without multiple trials per condition
SVV Conclusion: Borderline findings — not definitively abnormal with single trials. Repeat testing with multiple trials recommended.
PART 3: OVERALL SUMMARY AND IMPRESSION
Key Abnormal Findings:
- Left eye recording failure across all subtests — technical or structural (ptosis/camera) cause most likely
- Gaze nystagmus without fixation — down gaze (SPV 13.6°/s) and left gaze (SPV 5.23°/s), suppressed with fixation
- Positional nystagmus on returning to sit from left Dix-Hallpike (SPV 7.90°/s) — suggests provokable positional nystagmus, possibly left-sided BPPV (cupulolithiasis)
- Saccade latency mildly prolonged (327–354 ms) — likely age-related
- Borderline SVV on anticlockwise condition
Normal Findings:
- No spontaneous nystagmus (light or dark)
- Normal smooth pursuit (right eye)
- Normal OKN (right eye, all directions)
- Normal gaze with fixation (all positions)
- Negative right Dix-Hallpike
- No head-shake or hyperventilation nystagmus
DIAGNOSTIC IMPRESSION
Primary Finding: Peripheral Vestibular Dysfunction — Likely Left-Sided BPPV (Cupulolithiasis variant)
The combination of:
- Nystagmus provoked on return to sitting from left Dix-Hallpike (suggesting left canal involvement)
- Gaze nystagmus without fixation (suppressed by fixation — peripheral pattern)
- Absent spontaneous nystagmus (rules out acute active vestibular deafferentation)
- Normal OKN and smooth pursuit (argues against central pathology)
...is most consistent with peripheral vestibular dysfunction, likely left-sided BPPV (possibly involving the posterior or horizontal semicircular canal, cupulolithiasis type).
Central pathology is less likely given: intact fixation suppression, normal smooth pursuit, symmetric OKN, and no direction-changing nystagmus with fixation. However, the absent left eye data limits full interpretation.
RECOMMENDATIONS
| Priority | Action |
|---|---|
| 1 | Repeat VNG with careful left eye camera fitting to obtain valid binocular data |
| 2 | Ophthalmology referral to assess for left ptosis, cataract, or monocular ocular motor deficit |
| 3 | Canalith Repositioning Maneuver (Epley or Semont) for suspected left-sided BPPV |
| 4 | Bithermal caloric testing (not present in this report) — essential for quantifying unilateral vestibular weakness |
| 5 | Vestibular rehabilitation given age and likely chronic compensated vestibular imbalance |
| 6 | MRI brain with IAC protocol if symptoms persist post-repositioning, to exclude schwannoma or cerebellar lesion |
Interpretation based on: K.J. Lee's Essential Otolaryngology (9th ed.) and Bradley & Daroff's Neurology in Clinical Practice. This report is for clinical correlation only and should be reviewed by the treating physician or audiologist.
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