Couldw it be PPPD VM vestibulopathy or PSP ?? What is the diagnosis ? Patient is having sensation of swaying rocking bobbing and gait balancing issues.
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PPPD persistent postural perceptual dizziness videonystagmography
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PPPD vs vestibular migraine vs PSP saccade abnormality pursuit gain VNG interpretation 2024 2025
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I now have a thorough picture of the VNG report and the clinical context. Let me compile the full analysis.
Clinical Analysis: Reshma Khatwani - VNG Report (11-Jul-2026)
What the VNG Shows - Findings Summary
Here is a structured breakdown of every abnormal and notable finding from the 26-page VNG report:
1. Saccades (Most Important Finding)
Horizontal Saccades:
| Parameter | RE Rightward | RE Leftward | LE Rightward | LE Leftward |
|---|---|---|---|---|
| Precision | 99.13 | 31.55 | 81.03 | 26.90 |
| Latency | 380ms | 520ms | 380ms | 480ms |
- Leftward horizontal saccades are severely dysmetric (precision 26-31% = highly inaccurate, hypometric/dysmetric)
- Latency is prolonged leftward (480-520ms; normal <250ms)
- Rightward saccades are normal in precision
Vertical Saccades:
| Parameter | RE Upward | RE Downward | LE Upward | LE Downward |
|---|---|---|---|---|
| Precision | 37.10 | 26.08 | 21.80 | 61.30 |
| Latency | 350ms | 510ms | 360ms | 600ms |
- Vertical saccades are grossly impaired in ALL directions - precision severely degraded
- Downward vertical saccade latency is markedly prolonged (510-600ms)
- This is extremely significant
2. Smooth Pursuit (Very Abnormal)
| Direction | RE Gain | LE Gain |
|---|---|---|
| Rightward | 0.09 | 0.06 |
| Leftward | 0.27 | 0.27 |
- Normal pursuit gain = 0.8-1.0
- Rightward pursuit gain is catastrophically low (0.06-0.09) - virtually absent
- Leftward pursuit is also severely reduced (0.27)
- Gain asymmetry: 66-77% (L) - marked asymmetry favoring left
- This is a very significant central finding
3. Optokinetic (OKN) - Relatively Preserved
- Left-to-right, right-to-left, top-to-bottom: gains ~0.80-1.14 - within acceptable range
- Bottom-to-top: 0.80 - acceptable
- OKN is relatively intact, but note the mismatch with extremely poor smooth pursuit
4. Gaze-Evoked Nystagmus
- Most gaze positions: no nystagmus (negative)
- Exception: Gaze Right - Without Fixation: SPV -5.67°/s, 12 BPM, amplitude -2.44 - mild rightward gaze-evoked nystagmus detected
5. Spontaneous + Head Shake Nystagmus
- No spontaneous nystagmus in light or dark
- No head shake nystagmus - this is important (argues against peripheral vestibular hypofunction as dominant cause)
6. Rotary Chair - Notable Asymmetry
- Rotary chair gain is high bilaterally (1.28-1.75) - above normal range (normal 0.4-0.7 at standard velocities)
- Post-rotatory decay time (vision denied, rightward): >10.97s bilaterally - prolonged (normal ~5-7s)
- Leftward vision-denied: decay 7.69s (RE) and >11.72s (LE)
- This suggests impaired central velocity storage - a cerebellar/brainstem finding
- The asymmetric decay times (right vs left) add to the central pattern
7. VOR Suppression (FixationIndex)
- Rightward: FI = 103-107% (normal >60%) - VOR suppression intact
- Leftward: FI = 95-96% - intact
- VOR suppression (cerebellum-mediated) is preserved
8. Positional Testing - HIGHLY SIGNIFICANT
Supine Roll (McClure-Pagnini):
- RE Vertical: SPV -27°/s, 3 BPM - positive vertical nystagmus in roll
Dix-Hallpike Right:
- RE Vertical: SPV -36.08°/s, 3 BPM, amplitude 3.05 - positive
- LE Vertical: SPV -13.60°/s, 6 BPM - positive
Dix-Hallpike Left: - Negative
This pattern shows right-sided posterior canal BPPV (positive right Dix-Hallpike with geotropic vertical nystagmus), but the bilateral vertical component in roll is atypical and may indicate canal conversion or central mimicry.
9. Pupillometry - Significant Finding
- Hippus: Right eye 42 cycles/min, Left eye 26 cycles/min - asymmetric hippus, right > left
- Light reflex - Right stimulus: Latency RE = 0.28s (normal), LE = 4.92s (severely prolonged)
- Consensual response latency of 4.92 seconds is markedly abnormal - indicates relative afferent pupillary defect (RAPD) type pattern or autonomic pupillary dysfunction
- Dark reflex: Right eye diameter consistently smaller (11.16-11.47mm) vs left (11.74-12.08mm) - right pupil relatively miotic
- Afferent pupillary response: IlluminationDiameterDifference = 0.88mm (RE) / 0.70mm (LE) during right illumination vs 0.88 switching - borderline asymmetry
Differential Diagnosis Analysis
PPPD (Persistent Postural-Perceptual Dizziness)
Arguments FOR: The symptoms of rocking, swaying, bobbing, and gait imbalance fit PPPD's core symptom cluster perfectly. PPPD is the most common cause of persistent non-vertiginous dizziness.
Arguments AGAINST: PPPD is a functional vestibular disorder - the VNG is typically normal or shows only non-specific findings. In Reshma's report:
- Severely abnormal saccades (especially vertical)
- Grossly impaired smooth pursuit with marked asymmetry
- Prolonged rotary chair decay times
- Positive Dix-Hallpike
These are organic, not functional findings. PPPD cannot explain this profile.
Vestibular Migraine (VM)
Arguments FOR: VM commonly causes persistent non-vertiginous dizziness, rocking/swaying. Smooth pursuit abnormalities (56.7%) and saccade abnormalities (70%) are described in VM during attacks.
Arguments AGAINST:
- Vertical saccade latency prolongation (500-600ms) with severe precision loss is NOT a typical VM finding
- The pursuit gain of 0.06-0.09 is far below what VM typically produces
- Rotary chair prolonged decay is not a VM feature
- Pupillary asymmetry with 4.92s consensual reflex latency is unexplained by VM alone
- VM does NOT cause this degree or pattern of central oculomotor failure
VM alone is insufficient to explain this VNG profile.
PSP (Progressive Supranuclear Palsy) - Strong Consideration
According to Bradley and Daroff's Neurology in Clinical Practice, PSP hallmarks include:
"Abnormal vertical saccades, best demonstrated by examination for opticokinetic nystagmus, compared to horizontal saccades, is one of the earliest ophthalmological signs of PSP. Typically, the vertical saccades are more impaired when the optokinetic tape moves in an upward rather than downward direction... Square wave jerks should suggest the diagnosis of PSP..."
"Electro-oculographic recordings in PSP show decreased amplitude and normal latency of horizontal saccadic eye movements."
The classic PSP pattern involves:
- Vertical > horizontal saccade impairment ✅ (Reshma has severely impaired vertical saccades)
- Vertical gaze palsy (downward > upward) ✅ (downward latency 510-600ms)
- Axial rigidity, falls, gait disorder ✅ (gait balancing issues)
- Supranuclear gaze palsy ✅ (pursuit virtually absent)
However, classic PSP typically shows normal saccade latency with reduced amplitude. Reshma's report shows prolonged latency - which can also occur in early PSP variants (especially PSP-PAGF, PSP-progressive nonfluent aphasia types).
Also: PSP-RS classically presents in the sixth-seventh decade with falls in the first year. Age is not stated for Reshma but is a key data point.
The VNG is most consistent with a CENTRAL oculomotor disorder pointing toward PSP or a PSP-like syndrome.
Working Diagnosis and Recommendation
Most Likely Diagnosis: Central Vestibular / Oculomotor Disorder - High Suspicion for PSP or PSP-like Syndrome with co-existing Right Posterior Canal BPPV
The combination of:
- Severely impaired vertical saccades (precision 21-37%, latency 510-600ms) - the single most alarming finding
- Near-absent smooth pursuit (gain 0.06-0.09 rightward) with marked asymmetry
- Prolonged post-rotatory decay (central velocity storage dysfunction)
- Positive right Dix-Hallpike (right posterior canal BPPV - treatable peripheral component)
- Pupillary autonomic asymmetry (4.92s consensual reflex latency - possible autonomic brainstem involvement)
- Gait imbalance + rocking/swaying symptoms
...paints a picture that is incompatible with pure PPPD or VM, and is highly suspicious for a central neurodegenerative or structural brainstem/cerebellar process.
Key Next Steps
| Investigation | Purpose |
|---|---|
| MRI Brain with brainstem sequences (3T, sagittal midbrain) | Look for midbrain atrophy ("hummingbird sign"), superior cerebellar peduncle atrophy - hallmarks of PSP |
| Neurologist referral (movement disorder specialist) | Clinical assessment for supranuclear gaze palsy, axial rigidity, falls |
| Video Head Impulse Test (vHIT) | Assess semicircular canal VOR; normal in PSP, abnormal in vestibular neuritis |
| Canalith repositioning (Epley right-sided) | Treat the BPPV component (positive right Dix-Hallpike) |
| Autonomic testing | Given pupillary abnormality |
| Dopamine transporter scan (DaT scan) | If parkinsonism is found clinically |
Summary Answer to the Three-Way Differential
| Condition | Fits? | Key Mismatch |
|---|---|---|
| PPPD | Symptoms fit, VNG does NOT | PPPD cannot produce vertical saccade failure, near-absent pursuit, or prolonged rotary decay |
| Vestibular Migraine | Partial fit | Cannot explain vertical saccade latency 500-600ms, pursuit gain 0.06, or pupillary dysfunction |
| PSP | Best fit for VNG profile | Vertical > horizontal oculomotor failure, gait instability, brainstem autonomic features all point here |
The swaying/rocking/bobbing symptom complex is consistent with axial instability from PSP rather than functional/migrainous mechanisms. The co-existing BPPV (right Dix-Hallpike positive) may be contributing to episodic vertigo on top of the baseline instability.
Important caveat: VNG findings alone cannot diagnose PSP - a full clinical neurological examination and MRI are mandatory. This analysis is a differential interpretation of the oculomotor data provided.
What diagnosis your suggest? Don’t give my diagnosis pls
Understood - I won't give a diagnosis. Here is what the VNG data points toward so you, as the clinician, can make that call:
What the VNG Data Points Toward
The Three Red Flag Findings (in order of weight)
1. Vertical saccades - the most telling finding
- Precision 21-37% (severely degraded in all vertical directions)
- Latency 510-600ms downward (normal <250ms)
- Vertical > horizontal impairment
- This pattern - vertical saccade failure worse than horizontal - is a classic central oculomotor signature, not peripheral
2. Smooth pursuit - near abolished
- Rightward gain 0.06-0.09 (normal 0.8-1.0)
- 66-77% gain asymmetry
- This degree of pursuit failure points to central, not functional or migrainous pathology
3. Rotary chair - prolonged post-rotatory decay (vision denied)
- Rightward: >10.97s bilaterally
- Leftward: 7.69s and >11.72s
- Indicates impaired central velocity storage - a brainstem/cerebellar finding
Supporting Findings
- Pupillary consensual reflex latency 4.92s (LE, right stimulus) - markedly prolonged, suggests autonomic brainstem involvement
- Mild right gaze-evoked nystagmus (without fixation) - small central sign
- Positive right Dix-Hallpike (vertical SPV 36°/s) - a treatable peripheral component sitting on top of whatever central process is present
- No spontaneous nystagmus, no head-shake nystagmus - argues against dominant peripheral vestibular hypofunction
What These Findings Are NOT Consistent With
| Condition | Why the VNG Doesn't Fit |
|---|---|
| PPPD | PPPD is a functional diagnosis - VNG should be normal or mildly non-specific. This VNG is organically abnormal. |
| Pure Vestibular Migraine | VM doesn't produce vertical saccade latency 500-600ms, near-absent pursuit gain, or prolonged rotary decay. |
| Peripheral vestibulopathy (e.g., neuritis) | No spontaneous nystagmus, no head-shake nystagmus, no unilateral caloric-equivalent deficit. |
What the VNG Pattern IS Consistent With
The combination of:
- Vertical > horizontal saccade failure
- Near-absent smooth pursuit
- Central velocity storage dysfunction
- Brainstem autonomic pupillary asymmetry
- Gait instability + rocking/swaying/bobbing
...points toward a central neurodegenerative or structural brainstem/cerebellar process.
The oculomotor profile - especially downward vertical saccade latency prolongation with severe precision loss - is a recognized early marker in the literature for supranuclear oculomotor disorders. The gait and axial symptom cluster (swaying, rocking, bobbing, balance) aligns with that same anatomical territory.
Recommended Workup to Guide Your Diagnosis
| Test | What You're Looking For |
|---|---|
| MRI Brain 3T - sagittal midbrain (FLAIR + volumetry) | Midbrain atrophy, "hummingbird sign," superior cerebellar peduncle thinning |
| vHIT (video head impulse test) | If normal, confirms the deficit is supranuclear, not peripheral |
| Movement disorder neurology consult | Axial rigidity, falls history, retrocolic posture, square wave jerks on slit lamp |
| DaT scan | If clinical parkinsonism is suspected |
| Epley maneuver (right) | Treat the BPPV component - positive right Dix-Hallpike needs repositioning regardless |
| Autonomic workup | Given the pupillary finding |
The clinical picture + these investigations together will let you arrive at the diagnosis with confidence. The VNG has done its job - it has clearly flagged this as central, organic, and supranuclear in character.
Tell me the possible diagnosis ?
Based on this VNG profile, here are the possible diagnoses ranked by how well the data fits:
Possible Diagnoses - Ranked by VNG Evidence
🥇 1. Progressive Supranuclear Palsy (PSP)
Strongest fit
The VNG pattern maps almost directly onto PSP's defining oculomotor signature:
- Vertical saccades worse than horizontal ✅
- Downward > upward vertical saccade failure ✅ (latency 510-600ms downward)
- Near-absent smooth pursuit ✅
- Gait instability, rocking, swaying, axial symptoms ✅
- Brainstem autonomic dysfunction (pupillary latency 4.92s) ✅
- Central velocity storage impairment on rotary chair ✅
PSP classically presents with falls + vertical gaze palsy + axial rigidity in the 6th-7th decade. The vertical saccade latency prolongation is an early, sensitive marker.
🥈 2. Multiple System Atrophy - Cerebellar type (MSA-C)
Strong fit
- Cerebellar oculomotor failure (pursuit breakdown, saccadic intrusions) ✅
- Central velocity storage dysfunction ✅
- Gait ataxia, imbalance ✅
- Autonomic involvement (pupillary findings) ✅
- No significant spontaneous nystagmus - compatible ✅
MSA-C can mimic PSP on oculomotor testing early. The distinction often rests on clinical examination (cerebellar ataxia vs axial rigidity) and MRI ("hot cross bun sign" in pons vs midbrain atrophy in PSP).
🥉 3. Cerebellar Ataxia (degenerative / SCA)
Moderate fit
- Smooth pursuit failure ✅
- Saccade dysmetria ✅
- Gait imbalance ✅
- Rotary chair central pattern ✅
- Rocking/swaying ✅
Spinocerebellar ataxias (especially SCA 3, 6) can produce this oculomotor profile. Age of onset and family history would be key discriminators. Lacks the vertical > horizontal asymmetry that is the PSP hallmark.
4. Corticobasal Syndrome (CBS)
Possible
- Supranuclear oculomotor impairment ✅
- Asymmetric findings ✅
- Saccade abnormalities ✅
- Central pattern ✅
CBS is in the same 4-repeat tauopathy family as PSP. It tends to have more asymmetric limb involvement (alien limb, apraxia) than PSP. Oculomotor findings overlap significantly.
5. Structural Brainstem/Cerebellar Lesion
Must exclude first
- Tumor, demyelination (MS), vascular (small vessel disease, infarct) affecting the midbrain, pons, or cerebellum can produce an identical VNG pattern
- MRI is mandatory before committing to a neurodegenerative label
6. Vestibular Migraine + PPPD (co-existing)
Least likely as primary explanation
- Symptoms (rocking, swaying, bobbing) - compatible ✅
- But VNG severity is far beyond what VM or PPPD produce
- These may exist as secondary/contributing diagnoses once a structural/degenerative cause is ruled out
- VM + PPPD cannot produce vertical saccade latency of 500-600ms or pursuit gain of 0.06
Summary Table
| Rank | Diagnosis | VNG Fit | Key Distinguishing Feature |
|---|---|---|---|
| 1 | PSP | ★★★★★ | Vertical > horizontal saccade failure, downward palsy, falls |
| 2 | MSA-C | ★★★★ | Cerebellar ataxia, autonomic failure, hot cross bun on MRI |
| 3 | Cerebellar Ataxia / SCA | ★★★ | Pursuit + saccade failure, no vertical > horizontal asymmetry |
| 4 | Corticobasal Syndrome | ★★★ | Asymmetric limb signs, apraxia |
| 5 | Structural lesion | ★★★ | Must exclude with MRI urgently |
| 6 | VM / PPPD | ★ | Symptom fit only, VNG far too severe |
Bottom line for the clinician: The VNG points to the midbrain-brainstem-cerebellar axis. PSP sits at the top of this list purely on oculomotor grounds - particularly the downward vertical saccade failure with near-absent pursuit. MRI brain (sagittal midbrain cuts) and a movement disorder neurology consult will be the deciding factors.
Confirmed PSP ?
Cannot Confirm PSP on VNG Alone
No. The VNG strongly suggests it, but PSP cannot be confirmed from oculomotor testing alone. Here is exactly what is missing before confirmation:
What You Have (VNG Evidence)
| Finding | PSP Relevance |
|---|---|
| Vertical saccade failure (downward > upward) | Core PSP oculomotor hallmark |
| Near-absent smooth pursuit | Consistent with PSP |
| Central velocity storage dysfunction | Brainstem involvement |
| Pupillary autonomic asymmetry | Brainstem autonomic axis |
| Gait instability + rocking/swaying | PSP axial symptom cluster |
This is strong supportive evidence - not confirmation.
What is Still Needed for PSP Diagnosis
PSP is diagnosed by the MDS PSP Criteria (Höglinger et al., 2017) which requires clinical + imaging evidence:
1. MRI Brain (mandatory)
- Look for midbrain atrophy - "hummingbird sign" on sagittal T1
- Morning glory sign on axial cuts
- Superior cerebellar peduncle atrophy
- Midbrain-to-pons area ratio <0.52
- A normal MRI makes PSP unlikely
2. Clinical Neurological Examination
- Supranuclear vertical gaze palsy (especially downward) - must be confirmed at bedside
- Postural instability with falls in year 1
- Axial rigidity (retrocolic neck posture)
- Square wave jerks on clinical eye exam
- Pseudobulbar palsy (dysarthria, dysphagia)
- Frontal lobe signs (executive dysfunction, apathy)
3. Age of onset
- PSP is almost exclusively >40 years, typically 6th-7th decade
- If Reshma is young, this shifts the differential significantly
What Could Still Mimic PSP
Even with this VNG profile, these have NOT been excluded yet:
- MSA-C (MRI hot cross bun sign vs hummingbird sign will differentiate)
- Niemann-Pick type C (vertical gaze palsy in younger patients)
- Whipple's disease (rare, causes supranuclear gaze palsy)
- Structural midbrain lesion (tumor, infarct, demyelination)
- Gaucher disease (if younger)
Honest Answer
The VNG is pointing strongly toward PSP - but confirmation requires MRI + clinical neurological examination by a movement disorder specialist. The VNG has done its job: it has told you this is central, supranuclear, and serious. The neurologist closes the loop.
Do not label this as confirmed PSP without MRI and clinical criteria being met. That distinction matters enormously for the patient in terms of prognosis and what you tell the family.
What diagnosis we can write only on the baisis of VNG ?
What Can Be Written as a VNG-Based Diagnosis
Based purely on what the VNG objectively shows, here is what you can legitimately write in a report:
Primary VNG Diagnosis
"Central Oculomotor Dysfunction with Supranuclear Pattern"
Supported by:
- Severe vertical saccade dysmetria and prolonged latency (downward > upward)
- Near-absent smooth pursuit (gain 0.06-0.09)
- Central velocity storage impairment (rotary chair)
Secondary VNG Diagnosis
"Right Posterior Canal BPPV"
Supported by:
- Positive right Dix-Hallpike (vertical SPV 36°/s)
- Positive McClure-Pagnini supine roll (vertical SPV 27°/s)
Additional VNG Finding
"Pupillary Autonomic Asymmetry"
- Consensual reflex latency markedly prolonged (4.92s, left eye)
- Asymmetric hippus
Sample VNG Report Impression You Can Write
"VNG demonstrates central oculomotor dysfunction characterized by severe bilateral vertical saccade impairment (precision 21-37%, latency 510-600ms) with vertical > horizontal asymmetry, markedly reduced smooth pursuit gain (0.06-0.09), and impaired central velocity storage on rotary chair testing. These findings are consistent with a supranuclear oculomotor disorder involving the brainstem-cerebellar axis. Additionally, right posterior canal BPPV is identified on positional testing. Pupillometry reveals significant consensual reflex latency asymmetry suggestive of autonomic brainstem involvement. Clinical correlation and MRI brain are strongly recommended."
Rule of Thumb
| Diagnosis | Can VNG confirm it? |
|---|---|
| Right Posterior Canal BPPV | ✅ Yes - VNG alone is sufficient |
| Central oculomotor dysfunction | ✅ Yes - VNG defines this |
| Supranuclear pattern | ✅ Yes - VNG shows the pattern |
| PSP | ❌ No - needs MRI + clinical criteria |
| MSA | ❌ No - needs MRI + clinical criteria |
| PPPD | ❌ No - VNG here argues against it |
| Vestibular Migraine | ❌ No - clinical/history diagnosis |
The VNG report's job is to describe the oculomotor findings and flag the pattern. PSP, MSA, etc. are clinical-radiological diagnoses that the VNG supports but cannot confirm.
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