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VNG Report - Full Diagnostic Analysis
Patient: Ms. Anuradha | Female, Age 35 | ID: CCDA00371 | Date: 28-May-2026
Facility: Priority Hearing Care Pvt. Ltd.
Summary of Findings by Test Module
1. Saccades (Rapid Eye Movements)
| Parameter | Recorded Values | Normal Reference |
|---|
| Velocity (horizontal) | 373-773 °/s | > 275-400 °/s |
| Latency (horizontal) | 170-223 ms | 180-200 ms (up to 260 ms acceptable) |
| Precision (accuracy) | 59-83% | 80-134% |
| Velocity (vertical) | 330-463 °/s | > 275 °/s |
| Precision (vertical) | 60-83% | 80-134% |
Interpretation:
- Saccade velocities are within or above acceptable ranges for most frequencies - no hypometric or slow saccades of concern.
- Precision (accuracy) scores are repeatedly reduced, particularly in the vertical plane and at some horizontal frequencies (values of 59-66% are well below the normal floor of 80%). Reduced precision indicates consistent undershooting or overshooting of visual targets (dysmetria).
- Latencies are mostly within normal limits, with slight prolongation at higher frequencies.
- Reduced saccadic accuracy is a recognized indicator of cerebellar or central pathway dysfunction, particularly involving the vermis and flocculus.
2. Smooth Pursuit (Tracking)
| Direction/Frequency | Gain (Right Eye) | Gain (Left Eye) | Normal Range |
|---|
| Horizontal 0.2 Hz | 0.32-0.42 | 0.28-0.45 | 0.9-1.0 |
| Horizontal 0.4 Hz | 0.31-0.34 | 0.14-0.30 | 0.9-1.0 |
| Horizontal 0.6 Hz | 0.20-0.27 | 0.18-0.22 | 0.9-1.0 |
| Vertical 0.2 Hz | 0.11-0.26 | 0.19-0.30 | 0.9-1.0 |
| Vertical 0.4 Hz | 0.13-0.19 | 0.14-0.29 | 0.9-1.0 |
| Vertical 0.6 Hz | 0.14-0.21 | 0.14-0.17 | 0.9-1.0 |
Interpretation:
- Smooth pursuit gain is severely and bilaterally reduced across all tested frequencies and in both horizontal and vertical planes.
- Normal gain should be 0.9-1.0 at low frequencies. Gains of 0.11-0.45 represent a profound deficit - the patient's eyes are tracking at only 11-45% of target velocity.
- Severely reduced bilateral smooth pursuit gain strongly suggests central vestibular pathology, specifically involving the cerebellum (flocculus/paraflocculus) or brainstem pursuit pathways. This is not a pattern typical of peripheral vestibular disease.
- The vertical pursuit is as impaired as horizontal, which further points toward a central lesion rather than peripheral (peripheral disease predominantly affects horizontal systems).
3. Optokinetic Nystagmus (OKN)
| Stimulus | Direction | Gain RE | Gain LE |
|---|
| 10° Left-to-Right | - | 0.94 | 0.95 |
| 10° Right-to-Left | - | 0.95 | 1.13 |
| 10° Top-to-Bottom | Fast Phase ~114-122° | 1.01 | 1.17 |
| 10° Bottom-to-Top | - | 1.16 | 1.10 |
| 20° Left-to-Right | - | 0.98 | 0.79 |
| 20° Right-to-Left | Fast Phase 205° (RE only) | 0.85 | 0.99 |
| 20° Top-to-Bottom | Fast Phase ~107-111° | 0.26 | 0.36 |
Interpretation:
- OKN gains at 10° and most 20° stimuli are largely preserved (near 1.0), which is somewhat paradoxical given the severely impaired smooth pursuit.
- However, the Top-to-Bottom 20° test shows markedly reduced gain (0.26-0.36), suggesting a directional (downward) OKN asymmetry.
- The presence of fast phase directions in the Top-to-Bottom tests (normal OKN should suppress fast phases at steady-state) may indicate subtle velocity storage dysfunction or a central pathway abnormality.
- The dissociation between near-normal OKN and severely impaired smooth pursuit is itself a recognized pattern pointing toward central dysfunction, as these two subsystems partially share circuitry but are not identical.
4. Spontaneous Nystagmus
| Condition | Horizontal | Vertical |
|---|
| In Light | Absent | Absent |
| In Dark (Left Eye) | Absent | SPV: -2.95°/s, Amplitude: -4.53°, Freq: 0.61 Hz |
| Head Shake Test | Absent | Absent |
Interpretation:
- No spontaneous nystagmus in light (fixation suppresses it, as expected).
- Low-velocity downbeat-direction spontaneous nystagmus in the dark (left eye vertical, SPV ~3°/s). Downbeat nystagmus - even subtle - is a central sign strongly associated with lesions at the cervicomedullary junction, cerebellum (especially flocculus/nodulus), or foramen magnum region.
- Head-shake nystagmus is absent (negative), which somewhat reduces likelihood of significant unilateral peripheral hypofunction.
5. Gaze Testing
| Gaze Position | Fixation | Without Fixation |
|---|
| Center | Normal | Normal |
| Left | Normal | Normal |
| Right | Normal | Right Eye: SPV 8.18°/s, Amplitude 7.46°, Freq 0.57 Hz |
| Up | Normal | Normal |
| Down | Normal | Normal |
Interpretation:
- Gaze-evoked nystagmus is present in right gaze without fixation (right eye, SPV 8.18°/s). Gaze-evoked nystagmus that appears only without fixation - and is directional (toward the direction of gaze, i.e., right-beating in right gaze) - is a recognized sign of cerebellar or central pathway dysfunction.
- Normal gaze with fixation indicates some degree of intact fixation suppression.
6. Dix-Hallpike Positional Testing
Right-side Dix-Hallpike:
- Sitting head right: Bilateral horizontal slow-phase velocity (-6 to -8°/s), vertical SPV 3.93°/s right eye, fast phase 234°, freq 1.63 Hz - nystagmus provoked
- Supine head ext. & right: Horizontal SPV -3.97°/s right eye, vertical SPV -8.62°/s, fast phase 105.7°, freq 2.02 Hz - nystagmus provoked
- Return to sit: Horizontal SPV 4.19°/s, freq 0.72 Hz
Left-side Dix-Hallpike:
- Sitting head left: Bilateral horizontal SPV (-3 to -5°/s), freq 0.82-1.01 Hz - nystagmus provoked
- Supine head ext. & left: Left eye vertical SPV -16.37°/s, amplitude -6.13°, freq 1.13 Hz - significant nystagmus provoked
Interpretation:
- Positional nystagmus is provoked bilaterally with both right and left Dix-Hallpike maneuvers.
- The fast phase directions (105°, 234°) are oblique/mixed (not purely torsional-vertical), which is atypical for classic posterior semicircular canal BPPV.
- Bilateral provocation raises concern for cupulolithiasis, canal conversion, or central positional nystagmus rather than simple unilateral BPPV.
- The relatively high SPV on the left (up to -16.37°/s) in the supine extended position suggests significant left-sided positional response.
7. Yacovino and McClure-Pagnini Positional Tests
These tests target the anterior (superior) semicircular canal and horizontal canal BPPV/cupulolithiasis, respectively.
Yacovino (Anterior Canal / Central Test):
- Supine head flex 45°: Left eye vertical SPV 0.63°/s, freq 0.97 Hz - mild
- Supine end position: Right eye vertical SPV -17.62°/s, amplitude -6.81°, freq 1.15 Hz - strong downward vertical nystagmus
McClure-Pagnini (Horizontal Canal Roll):
- Sit-to-supine: Right eye combined horizontal/vertical nystagmus, fast phase 165°, freq 2.67 Hz
- Right lateral: Bilateral, both eyes, fast phase ~130-132°, freq 1.84 Hz bilaterally - strong symmetric response
- Supine head neutral: Left eye vertical SPV -16.84°/s, freq 1.00 Hz - persistent vertical nystagmus in neutral position
- Left lateral: Left eye vertical SPV -3.62°/s, freq 1.03 Hz
Interpretation:
- The Yacovino test showing strong downbeat vertical nystagmus in the final supine position is characteristic of anterior canal BPPV or central anterior canal pathology (the Yacovino maneuver was designed specifically to elicit anterior canal involvement).
- Persistent vertical nystagmus in supine neutral head position (McClure-Pagnini) is a central sign - true peripheral BPPV should resolve when the head is neutral. This "geotropic/apogeotropic" persistent nystagmus without clear direction reversal raises central concern.
- The symmetric bilateral response in right lateral roll is unusual and may reflect bilateral horizontal canal involvement or a central velocity storage abnormality.
8. Subjective Visual Vertical (SVV)
| Trial | Deviation | Direction |
|---|
| Clockwise trial | +1° Right | Normal |
| Anti-clockwise trial | -3° Left | Borderline |
| Blank background | -1° Left | Normal |
Interpretation:
- SVV deviation should be within ±2°. The -3° left deviation in the anti-clockwise condition is borderline, suggesting a very mild left-sided utricular or otolith pathway dysfunction.
- Overall SVV findings are near-normal; the otolith (utricular) function appears largely intact.
Overall Diagnostic Impression
Primary Findings (Clinically Significant Abnormalities):
- Severely reduced bilateral smooth pursuit gain (all frequencies, both planes) - the most striking finding
- Reduced saccade precision/accuracy (dysmetria) in vertical plane
- Downbeat spontaneous nystagmus in darkness
- Gaze-evoked nystagmus in right gaze (without fixation)
- Bilateral positional nystagmus with atypical fast-phase directions
- Strong downbeat vertical nystagmus on Yacovino testing
- Persistent vertical nystagmus in head-neutral supine position
Pattern Recognition:
The constellation of:
- Bilaterally reduced smooth pursuit (all directions)
- Saccadic dysmetria (low precision)
- Downbeat nystagmus in darkness
- Gaze-evoked nystagmus
- Central-pattern positional responses
...is a central vestibular syndrome, most consistent with cerebellar/vestibulocerebellar dysfunction, particularly involving the flocculus, nodulus, and/or uvula of the cerebellum. These structures are the primary controllers of smooth pursuit, gaze holding, and velocity storage. Pathology here produces exactly the pattern seen.
Differential Diagnosis (Most to Least Likely):
| Rank | Diagnosis | Supporting Evidence |
|---|
| 1 | Cerebellar vestibulopathy (floccular/nodular syndrome) | Severely reduced smooth pursuit, downbeat nystagmus, gaze-evoked nystagmus, saccadic dysmetria |
| 2 | Central positional vertigo (anterior canal or cerebellar origin) | Bilateral Dix-Hallpike provocation, Yacovino downbeat response, atypical nystagmus direction |
| 3 | Brainstem vestibular pathway disease | Smooth pursuit + OKN dissociation, gaze-holding failure |
| 4 | Bilateral peripheral vestibular hypofunction with superimposed central signs | Bilateral positional responses; less likely given the central oculomotor pattern |
| 5 | Medication effect / toxic | Bilateral smooth pursuit reduction can occur with sedatives, anticonvulsants - must be excluded |
Recommended Next Steps
- Neuroimaging - MRI brain with gadolinium with focus on the posterior fossa, cerebellum, and cervicomedullary junction (to rule out structural causes: demyelination, Arnold-Chiari malformation, cerebellar atrophy, posterior fossa tumor, or vascular lesion)
- Caloric testing - This report does not include caloric irrigation results, which would quantify peripheral vestibular function in each ear separately; essential to complete the vestibular assessment
- Neurology/Neuro-otology referral - Given the central pattern, a neurological evaluation is warranted
- Medication review - Rule out pharmacological causes (anticonvulsants, benzodiazepines, lithium, alcohol)
- Video head impulse test (vHIT) - To assess semicircular canal gain in high-frequency range
- Vestibular evoked myogenic potentials (VEMPs) - To evaluate otolith and saccular function
- Posturography / balance platform testing - Functional assessment of balance system integration
Important Note: This analysis is a clinical interpretation of the raw VNG data for educational and informational purposes only. A formal diagnosis must be made by a qualified audiologist, neurologist, or neuro-otologist who has examined the patient, reviewed the full clinical history, and correlated these findings with physical examination and additional investigations. The report from Priority Hearing Care does not contain an "Impression" section - this analysis fills that gap based on the objective data, but formal clinical sign-off is required.
Reference sources: Cummings Otolaryngology Head and Neck Surgery (9780323612173); StatPearls - VNG/ENG Testing (NCBI NBK599515); British Society of Audiology - Vestibular Assessment Recommended Procedure 2023