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VNG (Videonystagmography) Report - Full Analysis with Diagnosis
Patient: Balraj Bedi
Patient ID: CCDA00473
Age/Sex: 72 years / Male
Date of Testing: 26-May-2026
Clinic: Priority Hearing
CLINICAL HISTORY SUMMARY
- Episodic vertigo for 6 months; episodes last 2-3 minutes
- Symptoms: spinning/rotating sensation, unsteadiness, blackout, sensation of falling, nausea, fatigue, double vision
- Triggered by: positional changes (lying-to-sitting, rolling to left side, turning head left), viewing moving objects
- Requires support to stand/walk during episodes
- No photophobia or phonophobia
- Comorbidities: Cervical spondylitis, Hypertension, Parkinson's disease, Diabetes mellitus
- Pure Tone Audiometry: Bilateral mild sensorineural hearing loss
VNG TEST FINDINGS - SYSTEMATIC REVIEW
1. SACCADES (Eye Movement Initiation & Speed)
| Parameter | Right Eye | Left Eye | Normal Reference |
|---|
| Velocity (0.3 Hz H) | 472.48°/s | 174.99°/s | >300°/s |
| Precision (0.3 Hz H) | 31.14 | 12.54 | >70% |
| Latency (0.3 Hz H) | 466.67 ms | 440.00 ms | <200 ms |
| Velocity (0.45 Hz H) | 1145.22°/s | 854.90°/s | >300°/s |
| Precision (0.45 Hz H) | 81.47 | 67.81 | >70% |
| Latency (0.45 Hz H) | 514.78 ms | 406.96 ms | <200 ms |
| Velocity (0.3 Hz V) | 310.17°/s | 244.71°/s | >300°/s |
| Latency (0.3 Hz V) | 345.00 ms | 440.00 ms | <200 ms |
| Velocity (0.45 Hz V) | 485.61°/s | 289.09°/s | >300°/s |
| Latency (0.45 Hz V) | 520.00 ms | 490.00 ms | <200 ms |
Interpretation: Saccade latencies are markedly prolonged bilaterally (normal <200 ms) in both horizontal and vertical planes. Precision is also reduced, particularly for the left eye and at lower frequencies. Prolonged latency with hypometric saccades is a hallmark finding of central oculomotor dysfunction, consistent with the patient's known Parkinson's disease (basal ganglia and frontal eye field impairment).
2. SMOOTH PURSUIT
| Parameter | Right Eye | Left Eye | Normal Gain |
|---|
| 0.2 Hz H - Rightward | 0.51 | 0.38 | ≥0.7 |
| 0.2 Hz H - Leftward | 0.53 | 0.63 | ≥0.7 |
| 0.4 Hz H - Rightward | 0.65 | 0.24 | ≥0.7 |
| 0.4 Hz H - Leftward | 0.21 | 0.32 | ≥0.7 |
| 0.2 Hz V - Upward | 0.27 | 0.51 | ≥0.7 |
| 0.2 Hz V - Downward | 0.61 | 0.57 | ≥0.7 |
| 0.4 Hz V - Upward | 0.05 | 0.12 | ≥0.7 |
| 0.4 Hz V - Downward | 0.33 | 0.43 | ≥0.7 |
Interpretation: Smooth pursuit gain is diffusely and severely reduced across all directions and frequencies, particularly at higher frequencies (0.4 Hz) and in the vertical (upward) plane. This indicates bilateral saccadic pursuit - the smooth tracking system is broken up by catch-up saccades. This pattern strongly suggests central cerebellar/brainstem or basal ganglia pathology. In the context of Parkinson's disease, this is a well-recognised finding due to dopaminergic deficiency affecting the frontal pursuit areas and cerebellum. A gain of 0.05 (upward, 0.4 Hz) is critically low.
3. OPTOKINETIC (OKN) TEST
| Direction | Right Eye Gain | Left Eye Gain | Normal |
|---|
| Left→Right (10°) | 1.08 | 1.15 | ~1.0 |
| Right→Left (10°) | 1.00 | 1.15 | ~1.0 |
| Top→Bottom (10°) | 1.33 | 1.05 | ~1.0 |
| Bottom→Top (10°) | 1.22 | 1.18 | ~1.0 |
| Left→Right (20°) | 1.05 | 1.10 | ~1.0 |
| Right→Left (20°) | 0.73 | 0.80 | ~1.0 |
| Top→Bottom (20°) | 0.29 | 0.25 | ~1.0 |
| Bottom→Top (20°) | 0.36 | unmeasurable | ~1.0 |
Interpretation: OKN gains are generally within normal range for horizontal and low-velocity stimuli. However, there is a marked asymmetry and reduction in the downward-moving OKN responses at 20° (Top-to-Bottom and Bottom-to-Top at 20° are severely reduced: 0.29/0.25). This vertical OKN asymmetry is further evidence of central pathology, as the vertical OKN pathway is mediated by the brainstem (interstitial nucleus of Cajal, nucleus of posterior commissure). An asymmetric or reduced vertical OKN suggests a lesion in the posterior fossa or high midbrain. The fast-phase directions noted (e.g., 53.09°, 63.49°, 282.29°, 305.75°) in some vertical OKN tests suggest oblique nystagmus components, which can occur with posterior fossa lesions.
4. SPONTANEOUS NYSTAGMUS
- In Light: No spontaneous nystagmus (Slow Phase Velocity = absent, Amplitude = absent)
- In Dark: No measurable spontaneous nystagmus recorded (values all absent/dashes)
Interpretation: Absence of spontaneous nystagmus in both light and darkness is noted. However, gaze traces in darkness show some non-specific irregular eye movements, which are consistent with poor fixation stability (a feature of Parkinson's disease and cerebellar dysfunction).
5. GAZE TEST
All gaze positions (Center, Left, Right, Up, Down) - both with and without fixation - showed:
- No definable slow-phase velocity
- No definable amplitude or frequency values
- Traces show irregular baseline movements (micro-oscillations) without a structured nystagmus pattern
Interpretation: No definite gaze-evoked nystagmus was recorded. However, the irregular eye movement traces in all positions (especially in the without-fixation condition) are consistent with gaze instability rather than true nystagmus. This further supports central/Parkinsonian involvement. Absence of gaze-evoked nystagmus makes an isolated peripheral lesion less likely as the sole cause.
6. DIX-HALLPIKE (Positional Tests)
Dix-Hallpike Right:
- Sit Head Right: Large amplitude horizontal and vertical eye movement deflections recorded (right horizontal up to 200°, left vertical down to -160°)
- Supine Head Ext. & Right: Large amplitude deflections (right horizontal up to 200°, left vertical -100°)
Dix-Hallpike Left:
- Sit Head Left: Large amplitude deflections (right horizontal ±150°, left vertical -90°)
- Supine Head Ext. & Left: Large amplitude deflections (right horizontal ±110°, left vertical -160°)
Head Position Tests (Static):
- Yaw Right, Yaw Left, Pitch Forward, Pitch Backward, Roll Right, Roll Left: Mild-to-moderate amplitude movements without definitive structured nystagmus pattern
Interpretation: The positional tests show large-amplitude eye movement deflections bilaterally on Dix-Hallpike maneuver, in both left and right head-down positions. The responses are bilateral and large - this is consistent with bilateral posterior semicircular canal BPPV or significant bilateral vestibular positional sensitivity. In the context of the clinical history (symptoms triggered by rolling left, turning head left, and lying-to-sitting transitions), left posterior SCC BPPV is the primary positional suspect, with right side also contributing (bilateral involvement possible given Parkinson's and age-related otoconia degeneration).
Per Adams and Victor's Principles of Neurology: "The dysfunctional ear is the one that is downward when vertigo is elicited... The induced vertigo and nystagmus last no more than 30 to 40 s." - Adams and Victor's Principles of Neurology, 12th Ed.
7. SUBJECTIVE VISUAL VERTICAL (SVV)
| Trial | Deviation | Direction |
|---|
| Clockwise Trial 1 | 90° Right | (Invalid - likely instrument artifact at 0s) |
| Clockwise Trial 2 | 9° Right | Clockwise |
| AntiClockwise Trial 1 | -10° Left | Clockwise |
| Blank Background Trial 1 | -2° Left | Clockwise |
Interpretation: Trial 1 (Clockwise, 90° deviation in 0 seconds) is almost certainly an instrument artifact or setup error. Discarding this, the valid SVV measurements show:
- SVV deviation of approximately 9° to the right in clockwise condition and 10° to the left in anticlockwise condition
- Normal SVV is within ±2-3°. Deviations exceeding ±2° are considered abnormal.
- The blank background deviation of -2° (Left) is at the upper limit of normal/borderline.
- The wide spread (9°R to 10°L) across conditions suggests vestibular asymmetry and/or poor otolith-ocular reflex regulation, with possible contributions from the Parkinsonian postural control deficit.
- An abnormal SVV (particularly tilt toward one side consistently) would indicate otolith dysfunction (utricle/saccule) or thalamo-cortical vestibular pathway involvement.
COMPREHENSIVE DIAGNOSIS
Primary Diagnosis:
Bilateral Posterior Semicircular Canal Benign Paroxysmal Positional Vertigo (Bilateral PC-BPPV)
- Supported by: bilateral Dix-Hallpike positional responses with large deflections, episodic short-duration vertigo triggered by positional changes, clinical history of 2-3 minute episodes with head-movement provocation.
Secondary / Overlapping Diagnosis:
Central Vestibulo-Cerebellar / Basal Ganglia Oculomotor Dysfunction (Parkinson's Disease Related)
- Supported by: severely reduced smooth pursuit gain (bilateral, all directions), markedly prolonged saccade latencies (>400-520 ms bilaterally), reduced vertical OKN responses, and irregular gaze stability in darkness.
- Per K.J. Lee's Essential Otolaryngology: findings suggestive of central pathology include "abnormal saccades or saccadic pursuit results, especially with normal caloric results."
Contributing Factors:
- Parkinson's Disease - directly contributes to saccadic slowing, pursuit breakdown, impaired VOR cancellation, and postural instability
- Bilateral Mild Sensorineural Hearing Loss (on PTA) - suggests end-organ aging (presbycusis) with likely concurrent otoconia degeneration predisposing to BPPV
- Cervical Spondylitis - may exacerbate cervicogenic dizziness and limit head/neck movement during positional testing
- Hypertension and Diabetes - vascular and metabolic risk factors that can contribute to labyrinthine microvascular insufficiency
SUMMARY TABLE
| Test | Finding | Significance |
|---|
| Saccades | Prolonged latency bilaterally (>400 ms), reduced precision | Central - Parkinsonian/basal ganglia |
| Smooth Pursuit | Severely reduced gain bilaterally, all frequencies | Central - cerebellar/frontal |
| OKN | Reduced vertical OKN at 20°; horizontal preserved | Central - brainstem/posterior fossa |
| Spontaneous Nystagmus | Absent (light and dark) | Peripheral pathology less likely as primary |
| Gaze Nystagmus | Absent structured nystagmus; gaze instability | Central - non-specific |
| Dix-Hallpike | Bilateral large positional responses | Bilateral PC-BPPV |
| Head Position Tests | Mild responses without structured nystagmus | Consistent with BPPV |
| SVV | 9-10° deviation (borderline-abnormal); blank background borderline | Otolith/thalamo-cortical asymmetry |
CLINICAL RECOMMENDATIONS
-
Canalith Repositioning Maneuver (CRM): Epley maneuver for the left posterior SCC (primary symptomatic side). If bilateral BPPV confirmed, treat the more symptomatic side first, then the other after 48-72 hours.
-
Vestibular Rehabilitation Therapy (VRT): Gaze stabilisation exercises and balance retraining, modified for Parkinson's disease limitations (fall risk, rigidity).
-
Neurological Review: Given the significant central oculomotor findings (saccadic slowing, pursuit breakdown), urgent neurology review is recommended for re-evaluation and optimisation of Parkinson's disease management.
-
MRI Brain (with posterior fossa views): To exclude secondary BPPV causes and assess for any posterior fossa lesion contributing to the central VNG findings (particularly brainstem or cerebellar involvement).
-
Caloric Testing: The current VNG battery does not include bithermal caloric results (not present in the report). Caloric testing would be valuable to quantify unilateral canal weakness and complete the peripheral vestibular assessment.
-
Vascular Risk Factor Optimisation: Strict BP and glycaemic control given contributions of hypertension and diabetes to labyrinthine microvascular disease.
-
Fall Risk Assessment: This patient requires a formal falls risk assessment given Parkinson's disease, vertigo episodes, and bilateral vestibular involvement.
Note: This report is based on VNG data (videonystagmography) recorded on 26-May-2026 at Priority Hearing, supplemented by clinical history provided. The impression and signature fields on the cover page are blank - the treating clinician should review and countersign. Final clinical decisions should integrate this report with the full clinical examination and other investigations.
Sources: Adams and Victor's Principles of Neurology, 12th Ed. | K.J. Lee's Essential Otolaryngology | Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol.2