Now I have sufficient information to provide a comprehensive VNG interpretation and clinical analysis. Let me synthesize all the data.
VNG Report Analysis — Mala Rajodia, 43F | 22-Apr-2026
Clinical Summary (from history provided)
| Feature | Detail |
|---|
| Migraine history | >10–15 years |
| Vertigo character | Rotational (objects spinning around patient) |
| Triggers | Position change (karwat/rolling over), lights turning off |
| Sound sensitivity | Loud sounds irritating (car door slam) — hyperacusis/phonophobia |
| Smell sensitivity | Even mild fragrances (cucumber, muskmelon) trigger headache |
| No hearing loss, no anxiety/depression meds | |
VNG Test-by-Test Interpretation
1. Saccades
| Parameter | Finding | Interpretation |
|---|
| Velocity (Horiz 0.3 Hz) | RE 516 °/s, LE 528 °/s | Normal range |
| Precision (all trials) | 35–64 | Reduced (normal >70–80%) — hypometric saccades |
| Latency | 192–316 ms | Borderline prolonged (normal <200 ms ideally) |
| Vertical saccades | Similar reduced precision | Bilateral |
Interpretation: Bilateral saccadic hypometria with mildly prolonged latency. This pattern — where precision is consistently below normal bilaterally in both horizontal and vertical planes — points toward a central/cerebellar or vestibulo-cerebellar pathway dysfunction, rather than a pure peripheral lesion. Isolated BPPV does not affect saccades.
2. Smooth Pursuit
| Frequency | Horizontal Gain | Vertical Gain |
|---|
| 0.2 Hz | 0.53–0.78 | 0.52–0.56 |
| 0.4 Hz | 0.11–0.23 | 0.26–0.44 |
| 0.6 Hz | 0.08–0.15 | 0.22–0.43 |
Interpretation: Smooth pursuit gain is severely reduced horizontally at higher frequencies (0.4 and 0.6 Hz). Normal gain is ≥0.7–0.8 at these frequencies. Vertical pursuit is mildly reduced. This pattern of frequency-dependent smooth pursuit breakdown is characteristic of:
- Vestibular migraine (most common in this demographic with this history)
- Cerebellar dysfunction
- Central vestibular disorders
Pure peripheral disorders (BPPV, vestibular neuritis) do not significantly impair smooth pursuit.
3. Optokinetic Testing (OKN)
| Direction | Gain | Comment |
|---|
| Horizontal 10°–20° | 0.70–0.94 | Normal |
| Horizontal 40°–60° | 0.39–0.66 | Mildly reduced with increasing velocity |
| Vertical (Top→Bottom, Bottom→Top) | 0.07–0.20 at 20°–60° | Severely reduced |
Critical finding: Vertical OKN gain is severely impaired (0.07–0.20; normal ≥0.70), while horizontal OKN is relatively preserved at lower speeds. Asymmetric vertical OKN suppression is a central sign, pointing strongly to a brainstem or cerebellar vestibular pathway abnormality. The fast phase direction deviations recorded (56–69° for top-to-bottom, 254–257° for bottom-to-top) also suggest direction-specific asymmetry.
4. Spontaneous Nystagmus (Light and Dark)
No spontaneous nystagmus recorded in either condition (all values dash/absent).
This effectively rules out active unilateral peripheral vestibular loss (which would show nystagmus in darkness). It also argues against active Menière's disease during the testing session.
5. Head Shake / Hyperventilation Nystagmus
No nystagmus provoked — negative head-shake test, negative hyperventilation-induced nystagmus.
6. Gaze Testing
No gaze-evoked nystagmus in any direction (center, left, right, up, down — both with and without fixation).
This rules out significant gaze-holding failure (e.g., Alexander's law nystagmus) at rest.
7. Dix-Hallpike Testing — KEY FINDING
| Position | Finding |
|---|
| Right DH (all positions) | No nystagmus — all values negative |
| Left DH — Sit Head Left (first recording) | Vertical RE: SPV 5.77 °/s, amplitude 4.96°, frequency 0.59 Hz |
| Left DH — Sit Head Left (return) | Horizontal RE: SPV 6.44 °/s, amp 5.37°; Vertical RE: SPV 5.50, amp 4.49°, freq 1.44 Hz; Left Eye Vertical: SPV 8.48°/s, amp 6.31°, freq 0.69 Hz; Fast Phase Direction 320.12° |
Interpretation of Left Dix-Hallpike positional nystagmus:
- Nystagmus is geotropic/mixed with both vertical and horizontal (torsional) components
- Fast phase direction ~320° (upper-left) is consistent with the expected nystagmus of left posterior canal BPPV (upbeat + left torsional with left ear down in DH)
- However, the slow phase velocities are mild (5–8 °/s; classical BPPV typically >10–15 °/s)
- The nystagmus appears to persist rather than fatigue within the short recording window shown
McClure-Pagnini (roll test): No horizontal nystagmus provoked in lateral positions — argues against horizontal canal BPPV.
8. Subjective Visual Vertical (SVV)
| Trial | Deviation | Direction |
|---|
| All 3 trials (CW, CCW, Blank) | 90° (Right) | AntiClockwise rotation |
This is a striking finding. Normal SVV deviation is ≤2–3°. A 90° deviation is massively abnormal. This indicates profound utricle/otolith dysfunction — the patient's perceived vertical is rotated 90° from true vertical. This level of SVV tilt is seen in:
- Severe acute unilateral utricle dysfunction
- Vestibular migraine with central otolithic involvement
- Rarely in thalamic or brainstem strokes
Given the absence of spontaneous nystagmus and preserved horizontal OKN, an acute stroke is less likely. The combination of 90° SVV with migraine history and central smooth pursuit/OKN findings strongly points to vestibular migraine with central pathway involvement.
Overall VNG Impression
Primary Diagnosis: Vestibular Migraine (VM)
This patient meets diagnostic criteria per Barany Society/IHS:
- ✅ At least 5 episodes of vestibular symptoms of moderate/severe intensity (spinning, position-induced vertigo)
- ✅ Current/prior migraine history (>10–15 years)
- ✅ Migraine features during vestibular episodes — phonophobia (loud sound irritation), osmophobia (fragrance-triggered headache), photophobia (lights-off triggering dizziness)
Supporting VNG Evidence for VM:
- Impaired smooth pursuit (especially horizontal at 0.4–0.6 Hz) — central pattern
- Severely impaired vertical OKN — central vestibular pathway sign
- Bilateral saccadic hypometria — cerebellar/central involvement
- No spontaneous nystagmus — argues against active peripheral lesion
- Massively abnormal SVV (90° right tilt) — severe otolithic dysfunction, consistent with VM
Secondary Finding: Left Posterior Canal BPPV (mild/equivocal)
- Mild positional nystagmus on left Dix-Hallpike with appropriate direction
- SPV mild (5–8 °/s), possibly subclinical
- Note: BPPV and VM frequently co-exist — Cummings Otolaryngology states: "Meniere disease and benign paroxysmal positional vertigo are commonly associated with migraine."
Recommended Management
Vestibular Migraine
- Lifestyle modification first — sleep hygiene, dietary triggers (caffeine, chocolate, processed cheese, strong fragrances as triggers), hydration, regular meals
- Vestibular/migraine diary — track triggers, episode frequency
- Pharmacotherapy options:
- Prophylaxis: Propranolol (beta-blocker), Amitriptyline (TCA), Topiramate, Valproate, Venlafaxine
- Acute: Triptans during vestibular attacks with headache
- Vestibular rehabilitation — helps with central compensation
BPPV (if symptomatic)
- Left Epley maneuver (for left posterior canal)
- Patient can be reassured — canalith repositioning is highly effective
Further Workup to Consider
- MRI brain with FLAIR (given central VNG signs and 90° SVV) — to rule out cerebellar/brainstem pathology
- Audiometry — baseline despite no current hearing complaints
- ENT/Neurotology referral recommended given complexity
Reference: Cummings Otolaryngology Head and Neck Surgery — Chapter 168, Vestibular Migraine; Vestibular Disorders Associated With Migraine