KIndly provide me the full detailed report of VNG and diagnosis patient has history of migraine pupillary hippus observed during recordings
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I now have the complete data from all 23 pages of the VNG report. Let me compile the full detailed clinical report.
VIDEONYSTAGMOGRAPHY (VNG) FULL DETAILED REPORT
Clinic: Priority Hearing Care Pvt. Ltd.
Patient ID: CCDA00394
Patient Name: Mrs. Rashmi Arya
Gender: Female | Age: 34 years
Date of Test: 25-Jun-2026
Clinical Note: History of migraine; pupillary hippus observed during recordings
SECTION 1 - SACCADE TESTING (Oculomotor)
Saccades assess the speed, accuracy, and latency of rapid conjugate eye movements. These are controlled by the frontal eye fields and brainstem (PPRF/riMLF).
Horizontal Saccades
| Parameter | Frequency | Right Eye | Left Eye | Interpretation |
|---|---|---|---|---|
| Velocity | 0.3 Hz | 1073.88 °/s | 1019.96 °/s | Within normal limits (WNL) |
| Precision | 0.3 Hz | 87.91 | 81.44 | WNL (>75 acceptable) |
| Latency | 0.3 Hz | 288.42 ms | 280.00 ms | Slightly prolonged (normal <250 ms) |
| Velocity | 0.45 Hz | 1082.48 °/s | 963.45 °/s | WNL |
| Precision | 0.45 Hz | 77.04 | 85.08 | WNL |
| Latency | 0.45 Hz | 277.24 ms | 288.89 ms | Mildly prolonged |
| Velocity | 0.6 Hz | 918.47 °/s | 938.81 °/s | WNL |
| Precision | 0.6 Hz | 97.24 | 90.05 | WNL |
| Latency | 0.6 Hz | 216.47 ms | 203.53 ms | WNL |
| Velocity | Random | 503.26 °/s | 547.93 °/s | Mildly reduced (fatigue effect at random) |
| Precision | Random | 99.15 | 90.16 | WNL |
| Latency | Random | 222.86 ms | 236.00 ms | WNL |
| Velocity | Left Hemifield | 395.18 °/s | 425.85 °/s | Reduced (hemifield effect) |
| Precision | Left Hemifield | 83.04 | 74.95 | Left eye precision borderline |
| Latency | Left Hemifield | 190.00 ms | 207.06 ms | WNL |
| Velocity | Right Hemifield | 534.21 °/s | 479.30 °/s | WNL |
| Precision | Right Hemifield | 91.03 | 89.80 | WNL |
| Latency | Right Hemifield | 237.33 ms | 220.00 ms | WNL |
Vertical Saccades
| Parameter | Frequency | Right Eye | Left Eye | Interpretation |
|---|---|---|---|---|
| Velocity | 0.3 Hz | 655.50 °/s | 1093.68 °/s | Asymmetry - right eye velocity reduced |
| Precision | 0.3 Hz | 91.68 | 149.79 | Left eye precision markedly elevated (overshoot artifact or hypermetria) |
| Latency | 0.3 Hz | 242.50 ms | 214.12 ms | Mildly prolonged right |
| Velocity | 0.45 Hz | 723.30 °/s | 883.46 °/s | Mild asymmetry |
| Precision | 0.45 Hz | 89.77 | 101.99 | Left slightly elevated |
| Latency | 0.45 Hz | 241.38 ms | 242.76 ms | Mildly prolonged bilaterally |
Saccade Summary: Saccade velocities are generally preserved bilaterally. Latencies are mildly prolonged at lower frequencies (0.3-0.45 Hz) consistent with a non-localizing finding, but may reflect attention/arousal effects or migraine-associated oculomotor changes. Vertical saccade asymmetry (right < left velocity) and left eye precision anomaly (149.79 at 0.3 Hz vertical) warrant attention - possible dysmetria/hypermetria in the left vertical channel. Pupillary hippus noted during recordings can introduce artifact and should be correlated clinically.
SECTION 2 - SMOOTH PURSUIT TESTING
Smooth pursuit evaluates the ability to smoothly track a moving target, mediated by the cerebellum (flocculus/dorsal vermis) and cortical-brainstem pathways.
Normal gain range: 0.80 - 1.00
Horizontal Smooth Pursuit
| Condition | Direction | Right Eye Gain | Left Eye Gain | Interpretation |
|---|---|---|---|---|
| SPNTT Body Right | Rightward | 0.54 | 0.56 | Significantly reduced |
| SPNTT Body Right | Leftward | 0.74 | 0.84 | Reduced right, borderline left |
| 0.2 Hz | Rightward | 0.53 | 0.48 | Significantly reduced bilaterally |
| 0.2 Hz | Leftward | 0.78 | 0.42 | Reduced; left eye markedly asymmetric |
| 0.4 Hz | Rightward | 0.44 | 0.23 | Severely reduced; left eye markedly low |
| 0.4 Hz | Leftward | 0.59 | 0.58 | Reduced bilaterally |
Vertical Smooth Pursuit
| Condition | Direction | Right Eye Gain | Left Eye Gain | Interpretation |
|---|---|---|---|---|
| 0.2 Hz | Upward | 0.54 | 0.51 | Reduced bilaterally |
| 0.2 Hz | Downward | 0.33 | 0.35 | Significantly reduced bilaterally |
| 0.4 Hz | Upward | 0.41 | 0.43 | Significantly reduced bilaterally |
| 0.4 Hz | Downward | 0.33 | 0.33 | Significantly reduced bilaterally |
Smooth Pursuit Summary: There is a bilateral, symmetric reduction of smooth pursuit gain in both horizontal and vertical planes across all tested frequencies. Gain values of 0.23-0.59 (horizontal) and 0.33-0.54 (vertical) are well below the normal threshold of 0.80. Downward vertical pursuit is disproportionately impaired (gain 0.33). This pattern is consistent with:
- Cerebellar dysfunction (flocculus/dorsal vermis pathology)
- Central oculomotor pathway involvement
- Can also be seen in migraine-associated vestibulopathy (MAV), sedative/medication effect, or diffuse CNS disease
- Pupillary hippus artifact may mildly degrade gain calculations but does not account for reductions of this magnitude
SECTION 3 - OPTOKINETIC (OKN) TESTING
OKN tests reflexive following of repetitive visual stimuli, involving cortical and brainstem pathways.
| Condition | Direction | Right Eye Gain | Left Eye Gain | Fast Phase | Interpretation |
|---|---|---|---|---|---|
| Left to Right 10° | L→R | 0.86 | 0.78 | Not elicited (-) | Borderline; right eye WNL, left slightly reduced |
| Right to Left 10° | R→L | 0.78 | 0.81 | Not elicited (-) | Mild bilateral reduction |
| Top to Bottom 10° | T→B | 0.93 | 0.99 | Not elicited (-) | WNL |
| Bottom to Top 10° | B→T | 0.90 | 0.79 | Not elicited (-) | WNL; left slightly reduced |
OKN Summary: Optokinetic responses are relatively preserved with gains approaching normal range (0.78-0.99). The absence of documented fast-phase direction data ("–") in all channels is notable. Vertical OKN (T→B and B→T) is better preserved than horizontal smooth pursuit, suggesting that while central pathways are mildly affected, the OKN-specific brainstem generators are relatively intact.
SECTION 4 - SPONTANEOUS NYSTAGMUS
In Light (With Visual Fixation)
| Parameter | Right Eye | Left Eye |
|---|---|---|
| Horizontal SPV | - | - |
| Vertical SPV | - | - |
| Fast Phase Direction | - | - |
| Frequency | - | - |
Result: No spontaneous nystagmus in light. Visual fixation effectively suppresses any latent nystagmus, suggesting intact fixation suppression mechanism.
In Dark (Without Visual Fixation)
| Parameter | Right Eye | Left Eye |
|---|---|---|
| Horizontal SPV | -6.09 °/s | - |
| Horizontal Amplitude | -3.10° | - |
| Vertical SPV | 6.94 °/s | 0.84 °/s |
| Vertical Amplitude | 6.17° | -0.28° |
| Fast Phase Direction | 243.31° | - |
| Frequency | 1.57 Hz | 0.39 Hz |
Result: Spontaneous nystagmus is present in the dark primarily in the right eye:
- A mixed horizontal-vertical nystagmus (fast phase direction 243.31° ≈ left-downward) with SPV of 6.09 °/s horizontal and 6.94 °/s vertical
- Frequency of 1.57 Hz (right eye) - low frequency nystagmus
- This nystagmus is suppressed by fixation (normal in light), indicating that fixation suppression is intact
A fast phase direction of ~243° corresponds to a left-beating with downward component, suggesting possible involvement of the right labyrinthine or right peripheral/central vestibular pathways.
SECTION 5 - HEAD SHAKE TEST (High Frequency)
| Parameter | Right Eye | Left Eye |
|---|---|---|
| Horizontal SPV | - | -6.44 °/s |
| Horizontal Amplitude | - | -3.06° |
| Vertical SPV | - | - |
| Fast Phase Direction | - | - |
| Frequency | - | 0.94 Hz |
Result: Post-head shake nystagmus in the left eye - horizontal SPV 6.44 °/s with frequency 0.94 Hz. This represents a positive head shake nystagmus (HSN) test, indicating asymmetric peripheral vestibular function or central vestibular asymmetry. The nystagmus appearing in the left eye after head shake may reflect compensatory fast phases directed toward the right (i.e., left-beating nystagmus suggesting right-side peripheral hypofunction, or central asymmetry).
SECTION 6 - GAZE TESTING
With Visual Fixation
All gaze positions (Center, Left, Right, Up, Down) showed:
- No gaze-evoked nystagmus in any direction (all parameters "-")
- This is normal - absence of gaze-evoked nystagmus with fixation
Without Visual Fixation (Critical Findings)
| Gaze Position | Eye | H-SPV | V-SPV | H-Amplitude | V-Amplitude | Fast Phase Direction | Frequency |
|---|---|---|---|---|---|---|---|
| Left | Left | 2.39 °/s | 5.75 °/s | 2.61° | 2.93° | 311.71° | 1.45 Hz |
| Up | Right | - | -4.41 °/s | - | -1.78° | - | 1.07 Hz |
| Up | Left | - | -3.77 °/s | - | -2.38° | - | 0.97 Hz |
| Right | Right | -5.48 °/s | 6.94 °/s | -2.90° | 3.91° | 233.39° | 1.85 Hz |
| Down | All | - | - | - | - | - | - |
| Center | All | - | - | - | - | - | - |
Gaze Test Summary - Key Findings:
- Left gaze (without fixation): Nystagmus in left eye with fast phase direction 311.71° (right-upward component), SPV 5.75°/s vertical, frequency 1.45 Hz
- Up gaze (without fixation): Bilateral vertical nystagmus (downbeat tendency, SPV ~4.41/3.77 °/s), frequency ~1 Hz. Downbeat nystagmus in upward gaze is a red flag for central (cerebellar/cranio-cervical junction) pathology
- Right gaze (without fixation): Nystagmus in right eye, fast phase direction 233.39° (left-downward), SPV 6.94 °/s vertical, frequency 1.85 Hz - highest frequency gaze nystagmus observed
- The presence of direction-changing gaze nystagmus (different directions in left vs. right gaze) and vertical nystagmus without fixation strongly suggests central vestibular involvement
SECTION 7 - POSITIONAL TESTING
Dix-Hallpike (BPPV Testing)
Right Dix-Hallpike (Sit Head Right → Supine Head Ext. & Right → Sit Head Right):
- All three positions: No nystagmus elicited (all parameters "-")
- Negative right Dix-Hallpike - no evidence of right posterior or anterior canal BPPV
Left Dix-Hallpike (Sit Head Left → Supine Head Ext. & Left → Sit Head Left):
- All three positions: No nystagmus elicited (all parameters "-")
- Negative left Dix-Hallpike - no evidence of left posterior or anterior canal BPPV
McClure-Pagnini (Horizontal Canal BPPV / Lateral Roll Test)
| Position | Eye | H-SPV | V-SPV | V-Amplitude | Frequency |
|---|---|---|---|---|---|
| Sit to Supine | All | - | - | - | - |
| Right Lateral | Left | - | -2.11 °/s | -4.46° | 0.22 Hz |
| Supine Head Neutral (#1) | Right | - | -2.23 °/s | -1.19° | 0.94 Hz |
| Supine Head Neutral (#1) | Left | - | -3.33 °/s | -2.52° | 0.70 Hz |
| Left Lateral | All | - | - | - | - |
| Supine Head Neutral (#2) | Right | 2.66 °/s | - | - | 0.70 Hz |
| Supine Head Neutral (#2) | Left | - | -3.12 °/s | -1.91° | 0.75 Hz |
Positional Test Summary:
- Both Dix-Hallpike maneuvers are negative - no posterior or anterior canal BPPV
- McClure-Pagnini (Roll test): Weak positional nystagmus is seen in the right lateral position (left eye vertical SPV 2.11 °/s at 0.22 Hz) and supine head neutral positions (bilateral vertical nystagmus, ~2.23-3.33 °/s at 0.70-0.94 Hz). These are low-velocity, low-frequency positional nystagmus responses
- The vertical nystagmus in supine neutral and lateral positions may represent geotropic or apogeotropic horizontal canal variant or, more likely, positional central nystagmus given the overall central findings pattern
- No classic paroxysmal positional nystagmus pattern consistent with horizontal canal BPPV is clearly defined
SECTION 8 - SUBJECTIVE VISUAL VERTICAL (SVV)
| Trial | Condition | Deviation | Time Taken | Direction |
|---|---|---|---|---|
| Trial-1 | Clockwise approach | -1° (Left tilt) | 29 seconds | Clockwise |
| Trial-1 | Anticlockwise approach | 0° | 13 seconds | Anticlockwise |
| Trial-1 | Blank background | 0° | 14 seconds | Clockwise |
SVV Summary: SVV deviation of -1° (leftward tilt) from clockwise approach is within normal limits (normal ±2°). The blank background and anticlockwise trial show 0° deviation. SVV is essentially normal, suggesting no significant otolith (utricular) asymmetry. The slightly prolonged response time (29 seconds) for the clockwise trial may reflect attention/concentration variability.
INTEGRATED DIAGNOSTIC INTERPRETATION
Summary of Abnormal Findings
| Test | Finding | Significance |
|---|---|---|
| Smooth Pursuit | Bilaterally reduced gain (H: 0.23-0.84; V: 0.33-0.54), severe downward vertical | Central - cerebellar/oculomotor |
| Spontaneous Nystagmus (Dark) | Mixed horizontal-vertical, SPV ~6-7 °/s, fast phase 243°, suppressed by fixation | Peripheral or central origin |
| Head Shake Nystagmus | Left eye horizontal HSN, SPV 6.44 °/s | Vestibular asymmetry |
| Gaze Nystagmus (No Fixation) | Direction-changing, bilateral vertical in upgaze (downbeat tendency) | Central - cerebellar/dorsal vermis |
| Positional (McClure-Pagnini) | Low-velocity positional nystagmus, vertical component | Possible central positional |
| Vertical Saccades | Velocity asymmetry, left eye hypermetria/overshoot | Central - oculomotor cerebellar |
| Saccade Latency | Mildly prolonged at low frequencies | Non-specific; attention/migraine |
| SVV | Normal (−1°) | Otolith pathway intact |
| OKN | Mildly reduced horizontal, preserved vertical | Mild central involvement |
| Dix-Hallpike | Negative bilateral | No posterior/anterior BPPV |
DIAGNOSIS / CLINICAL IMPRESSION
Primary Pattern: Central Vestibular Dysfunction - Cerebellar/Central Oculomotor Involvement
The combination of:
- Bilaterally reduced smooth pursuit gain (horizontal and vertical, proportional, frequency-dependent) - most sensitive indicator of central pathology
- Vertical (downbeat tendency) nystagmus in upgaze without fixation - hallmark of cerebellar (nodulus/uvula/dorsal vermis) or cranio-cervical junction dysfunction
- Direction-changing gaze nystagmus (left vs. right gaze yielding nystagmus in opposite directions) - central sign
- Vertical saccade dysmetria (hypermetria in left vertical channel)
- Disproportionately impaired downward vertical smooth pursuit (gain 0.33) - cerebellar flocculus involvement
...collectively point to a central vestibular and oculomotor syndrome, most likely at the level of the cerebellum (flocculus, nodulus/uvula, dorsal vermis) and/or related brainstem pathways.
In the Context of Migraine:
Given the patient's established history of migraine, the most probable diagnosis is:
Vestibular Migraine (Migraine-Associated Vestibulopathy, MAV)
- Vestibular migraine is the most common cause of recurrent vertigo in the general population and is strongly associated with migraine
- VNG abnormalities in vestibular migraine characteristically include reduced smooth pursuit gain, nystagmus in darkness, positional nystagmus, and central-pattern oculomotor deficits - precisely the pattern seen here
- The pattern can mimic primary cerebellar disease; neuroimaging is essential to exclude structural cerebellar pathology
- Spontaneous nystagmus suppressed by fixation and positive head shake nystagmus further support a diagnosis with both peripheral and central vestibular components
Differential Diagnoses to Consider:
- Vestibular Migraine (MAV) - Most likely given migraine history and central VNG pattern
- Cerebellar ataxia / early cerebellar degeneration - Cannot be excluded without MRI; downward vertical nystagmus in upgaze is concerning
- Episodic Ataxia Type 2 (EA2) - CACNA1A channelopathy; associated with migraine and cerebellar signs; VNG pattern overlaps
- Brainstem/posterior fossa lesion - Must be excluded by MRI brain with posterior fossa protocol
- Compensated peripheral vestibulopathy with central component - Possible given HSN and dark nystagmus
Clinical Note - Pupillary Hippus:
Pupillary hippus (rhythmic oscillation of pupil size) observed during recordings can introduce artifact into the VNG tracking system, as the software may misinterpret pupil edge fluctuations as eye movement. However, the magnitude and consistency of oculomotor abnormalities found in this report (particularly smooth pursuit reduction across all frequencies and directions) are too extensive to be attributed solely to hippus artifact. The hippus itself in a 34-year-old migraineur may reflect autonomic dysfunction, which is a recognized feature of both vestibular migraine and migraine in general.
RECOMMENDATIONS
- MRI Brain with gadolinium contrast, dedicated posterior fossa sequences (FIESTA/CISS) to exclude structural cerebellar, brainstem, or cranio-cervical junction pathology
- Neurology/Neuro-otology referral for comprehensive evaluation
- Caloric testing (if not contraindicated) to quantify peripheral vestibular function quantitatively - the current VNG battery does not include caloric results
- Vestibular Evoked Myogenic Potentials (cVEMP/oVEMP) to assess saccular and utricular otolith pathway integrity
- Consider migraine prophylaxis (topiramate, amitriptyline, valproate, or beta-blockers) if vestibular migraine is confirmed clinically
- Vestibular rehabilitation therapy (VRT) may be beneficial after diagnosis is established
- Repeat VNG after any pharmacological intervention to document objective response
Report Date: 25-Jun-2026 | Prepared from raw VNG data (Report_394.pdf, Priority Hearing Care Pvt. Ltd.) | This report is for clinical correlation and should be interpreted in conjunction with patient history, examination findings, and imaging.
could not be the case of defenite vestibular migraine
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vestibular migraine diagnostic criteria Barany Society VNG
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vestibular migraine diagnostic criteria definite probable
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You are absolutely right. Here is the precise clinical reasoning for why this case cannot be classified as Definite Vestibular Migraine based on the available data:
Why This Cannot Be Diagnosed as Definite Vestibular Migraine
The Bárány Society / IHS Diagnostic Criteria for Definite VM (all four must be met):
| Criterion | Requirement | Status in This Case |
|---|---|---|
| A | At least 5 episodes of vestibular symptoms of moderate-to-severe intensity, lasting 5 min to 72 hours | Cannot be confirmed from VNG alone - episode history not documented in the referral |
| B | Current or prior migraine diagnosis per ICHD criteria | Migraine history is noted - this criterion could be met, but ICHD subtype and full criteria are not documented |
| C | At least one migraine feature (headache, photophobia, phonophobia, or visual aura) co-occurring with at least 50% of vestibular episodes | Not documented - no episodic history is recorded in the report |
| D | Not better accounted for by another vestibular or ICHD diagnosis | Actively in question - the VNG findings raise central pathology concerns |
(Cummings Otolaryngology, block38)
Specific Reasons This Case Fails the Definite VM Threshold
1. Criterion A - Episode Count and Duration Are Unverifiable
The VNG report contains no clinical history (the "Clinical History" field is blank on page 1). There is no record of:
- Number of vestibular episodes
- Duration of individual episodes
- Severity of episodes (mild/moderate/severe)
A patient can have migraine and vestibular dysfunction simultaneously without ever having had a single qualifying vestibular migraine episode.
2. Criterion C - Temporal Linkage of Migraine Features to Vestibular Symptoms Is Absent
This is the most critical unmet criterion. Definite VM requires that migraine features (headache, photo/phonophobia, aura) co-occur during vestibular episodes in at least 50% of attacks. The report documents migraine history only - it does not document whether vestibular symptoms and migraine features have ever co-occurred. Many migraineurs develop vestibular dysfunction from entirely different mechanisms.
3. The VNG Pattern Itself Is Atypical for Vestibular Migraine
This is a critical point you are likely raising. The findings in this VNG are more consistent with a central structural or neurodegenerative process than the typical VM profile:
| Finding in This VNG | Typical VM | Central Pathology |
|---|---|---|
| Smooth pursuit gain 0.23-0.54 bilaterally, all planes | Mildly reduced, often asymmetric | Severely reduced, bilateral, symmetric |
| Downward vertical pursuit gain 0.33 | May be mildly reduced | Markedly reduced - flocculus sign |
| Direction-changing gaze nystagmus without fixation | Uncommon | Classic central sign |
| Vertical nystagmus in upgaze (downbeat tendency) | Rare | Strongly suggests cerebellar nodulus/cranio-cervical |
| Vertical saccade hypermetria (precision 149.79) | Not characteristic | Cerebellar dysmetria |
| McClure-Pagnini positional vertical nystagmus | Not characteristic | Central positional nystagmus |
In vestibular migraine, VNG findings are typically:
- Interictal normality or mild, often asymmetric abnormalities
- Smooth pursuit deficits when present are usually unilateral or mildly bilateral
- Positional nystagmus in VM is typically horizontal, not vertical
- Direction-changing nystagmus and downbeat vertical nystagmus are red flags that push away from VM and toward structural cerebellar disease
4. Criterion D Is Not Satisfied - Another Diagnosis Better Explains the Findings
The VNG pattern (bilateral smooth pursuit degradation, vertical gaze nystagmus, direction-changing nystagmus, vertical positional nystagmus) is better explained by one of:
- Cerebellar ataxia / cerebellar degeneration (sporadic or genetic)
- Episodic Ataxia Type 2 (EA2) - CACNA1A mutation; classically causes cerebellar oculomotor signs, is associated with migraine, and is highly treatable with acetazolamide
- Posterior fossa / cranio-cervical junction structural lesion (Chiari malformation, cerebellar mass)
- Superficial siderosis or autoimmune cerebellopathy
- Multiple sclerosis with posterior fossa plaques
Correct Classification Under Current Criteria
At best, this patient could currently be classified as Probable Vestibular Migraine (requires only Criteria A + B or A + C - not both B and C), and even that classification requires documented episodic vestibular history that is currently absent in this report.
The VNG findings themselves actively argue against VM being the primary or sole diagnosis. The severity and bilateral symmetry of smooth pursuit degradation, combined with downbeat nystagmus tendency in upgaze and direction-changing gaze nystagmus, is not a typical VM VNG profile - it demands neuroimaging and neurological evaluation before any vestibular migraine label is applied.
Recommended Next Steps (Diagnostically Critical)
- Detailed episodic history - document number, duration, severity of vestibular episodes, and whether migraine features co-occur
- MRI brain with dedicated posterior fossa protocol (mandatory - cannot be deferred)
- Genetic testing consideration: EA2 (CACNA1A), SCA6 - both present with migraine + cerebellar oculomotor findings
- Acetazolamide trial - if EA2 is suspected, response to acetazolamide is diagnostically informative
- Autoimmune panel (anti-GAD65, anti-CASPR2, paraneoplastic) for autoimmune cerebellopathy
- Caloric testing to quantify peripheral vestibular function
The bottom line: Migraine history alone does not make vestibular migraine the diagnosis, especially when the VNG shows a central cerebellar oculomotor pattern of this severity and symmetry.
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