Kindly provide the detailed report with diagnosis ?
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cd /tmp/workspace/attachments/819c04bc-a264-4d1f-a546-160791dea7c7/ && python3 -c " import pdfplumber with pdfplumber.open('upasana vng.pdf') as pdf: print(f'Total pages: {len(pdf.pages)}') for i, page in enumerate(pdf.pages): text = page.extract_text() print(f'--- PAGE {i+1} ---') print(text) print() "
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VNG videonystagmography BPPV interpretation Dix-Hallpike positive diagnosis
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I now have all the data I need to provide a comprehensive diagnostic report. Let me compile it.
Videonystagmography (VNG) Report - Detailed Analysis & Diagnosis
Patient: Upasana Dewan | Age: 62 years | Gender: Female
Patient ID: CCDA00404 | Date of Test: 17-Jul-2026
Clinic: Priority Hearing Care Pvt. Ltd.
SUMMARY OF TEST FINDINGS
1. Saccade Testing (Eye Speed & Accuracy)
| Parameter | Right Eye | Left Eye | Normal Range |
|---|---|---|---|
| Horizontal Velocity | 449 °/s | 537 °/s | 200-700 °/s |
| Horizontal Precision | 89% | 93.6% | >80% |
| Latency | 244 ms | 244 ms | <250 ms |
| Vertical Velocity | 427 °/s | 364 °/s | 200-700 °/s |
| Vertical Precision | 86.8% | 82.8% | >80% |
| Vertical Latency | 283 ms | 272 ms | <250-300 ms |
Interpretation: Saccades are within normal limits bilaterally for velocity and precision. No saccadic dysmetria or slowing is present. This is a normal finding and does not suggest cerebellar or brainstem pathology.
2. Smooth Pursuit (Tracking Ability)
| Direction | Right Eye Gain | Left Eye Gain | Normal |
|---|---|---|---|
| Rightward | 0.86 | 0.90 | >0.80 |
| Leftward | 0.92 | 0.96 | >0.80 |
| Upward | 0.85 | 0.86 | >0.80 |
| Downward | 0.65 | 0.62 | >0.80 |
Interpretation: Horizontal smooth pursuit is normal bilaterally. However, downward vertical smooth pursuit is mildly reduced (gain ~0.63-0.65 vs. normal >0.80) in both eyes. Reduced vertical pursuit gain, particularly in the downward direction, may reflect age-related decline (patient is 62 years) or mild central pathway involvement. This warrants clinical correlation.
3. Optokinetic Testing (OKN)
| Stimulus Direction | Right Eye Gain | Left Eye Gain | Normal |
|---|---|---|---|
| Left-to-Right | 0.90 | 0.94 | >0.80 |
| Right-to-Left | 0.81 | 0.84 | >0.80 |
| Top-to-Bottom | 0.93 | 0.87 | >0.80 |
| Bottom-to-Top | 0.99 | 0.93 | >0.80 |
Interpretation: All optokinetic responses are within normal limits in all four directions. No asymmetry. This reflects intact cortical and brainstem visual tracking pathways.
4. Spontaneous Nystagmus
| Condition | Nystagmus Present | SPV | Notes |
|---|---|---|---|
| In Light | None | - | Normal |
| In Dark | Yes (Right Eye) | 1.85 °/s | Frequency: 0.46 Hz, Amplitude: 1.83° |
Interpretation: No spontaneous nystagmus in light (with fixation) - this indicates normal fixation suppression. A low-level horizontal nystagmus is present in darkness in the right eye (SPV 1.85 °/s). This is borderline - values <2 °/s are considered subclinical. While this may represent a very mild residual vestibular asymmetry, it is not clinically significant on its own, especially given the age of the patient.
- No nystagmus was induced by head-shake or hyperventilation, which argues against active peripheral vestibular neuritis or perilymph fistula.
5. Gaze Testing
| Position | Nystagmus | SPV |
|---|---|---|
| Center (with fixation) | None | - |
| Left, Right, Up, Down (with fixation) | None | - |
| Center (without fixation) | None | - |
| Right (without fixation) | None | - |
| Left (without fixation) | Yes (Right Eye) | 3.76 °/s, Amplitude 5.02°, Freq 0.38 Hz |
| Down (without fixation) | Yes (Right Eye) | 3.61 °/s, Amplitude 2.17°, Freq 0.77 Hz |
| Up (without fixation) | Yes (Left Eye) | 1.19 °/s, Amplitude -0.99°, Freq 0.75 Hz |
Interpretation: Gaze-evoked nystagmus is present in the dark (without fixation) in eccentric positions - leftward, downward, and upward gaze. The fact that this is suppressed with fixation is a peripheral feature. The presence of gaze-evoked nystagmus in multiple directions without fixation suggests central compensation is ongoing but the vestibular system is not fully symmetric. The pattern seen here - particularly the direction-specific gaze nystagmus that resolves with fixation - is more consistent with a recovering peripheral lesion or residual vestibular asymmetry than a central lesion.
6. Positional Testing (Dix-Hallpike Maneuver) - KEY FINDING
Dix-Hallpike Right (Supine Head Extended & Right):
- Vertical SPV: 8.64 °/s (RE) / 6.30 °/s (LE)
- Amplitude: 1.64° / 1.16°
- Frequency: 1.73 Hz / 1.52 Hz
Dix-Hallpike Left (Supine Head Extended & Left): - MOST SIGNIFICANT FINDING
- Horizontal SPV (LE): 13.99 °/s
- Horizontal Amplitude (LE): 3.90°
- Vertical SPV (LE): -9.70 °/s (downward)
- Vertical Amplitude (LE): -5.00°
- Fast Phase Direction (LE): 52.03° (upward-torsional)
- Frequency: 1.88 Hz
Interpretation: The Dix-Hallpike Left position provokes a clearly positive response - nystagmus with both horizontal and vertical (torsional) components in the left eye, with a fast phase direction at 52.03° (consistent with upward-torsional nystagmus toward the affected side). The right-sided Dix-Hallpike also shows some activity but at lower velocity.
According to K J Lee's Essential Otolaryngology, the classic features of BPPV on the Hallpike maneuver are: (1) rotational, geotropic nystagmus that crescendos then decrescendos; (2) latency of onset; (3) short duration (<1 minute); and (4) fatigues on repeated testing. The pattern here - with the left Dix-Hallpike being more positive and showing upward-torsional fast phase nystagmus - is consistent with Left Posterior Semicircular Canal (PSCC) BPPV.
7. Static Positional Testing (Head Yaw, Pitch, Roll)
All head position tests (Yaw Right/Left, Pitch Forward/Backward, Roll Right/Left) showed no significant nystagmus. This supports a positional/positioning disorder rather than a sustained positional nystagmus syndrome.
8. Subjective Visual Vertical (SVV)
| Trial | Direction | Deviation | Normal |
|---|---|---|---|
| Clockwise stimulus | AntiClockwise | +7° (Right) | ±2-3° |
| AntiClockwise stimulus | Clockwise | -2° (Left) | ±2-3° |
| Blank background | Clockwise | 0° | ±2-3° |
Interpretation: The clockwise trial shows a 7° rightward deviation, which is outside the normal range of ±2-3°. The SVV measures the perceived upright position and is controlled by the otolith organs (utricle and saccule). A significant deviation on one trial (especially with the blank background showing 0°) may indicate some otolith asymmetry, but the inconsistency across trials reduces its significance. Clinical correlation is required. The blank background result (0°) is reassuring.
OVERALL DIAGNOSTIC IMPRESSION
Primary Diagnosis:
Benign Paroxysmal Positional Vertigo (BPPV) - Left Posterior Semicircular Canal (Left PC-BPPV)
The most significant finding is a positive Dix-Hallpike test on the LEFT side, demonstrating upward-torsional nystagmus with horizontal components (SPV 13.99 °/s horizontal, 9.70 °/s vertical, fast phase at 52.03°) consistent with canalolithiasis of the left posterior semicircular canal.
Supporting evidence:
- No spontaneous nystagmus in light (peripheral pattern)
- No fixation failure (peripheral, not central)
- Nystagmus suppressed by visual fixation
- Normal saccades and OKN (central pathways intact)
- No head-shake nystagmus
- Mildly asymmetric dark spontaneous nystagmus (residual peripheral asymmetry)
Secondary / Additional Findings:
-
Mildly Reduced Downward Vertical Smooth Pursuit (gain ~0.63) - possibly age-related; cannot exclude a very mild central contribution. Recommend clinical correlation and follow-up.
-
Low-level Spontaneous Nystagmus in Dark (SPV 1.85 °/s, right eye) - subclinical; may represent mild compensated vestibular asymmetry.
-
SVV Deviation (7° right on clockwise trial) - suggests possible minor otolithic dysfunction; inconsistent across trials, so clinical significance is limited.
RECOMMENDED MANAGEMENT
-
Epley Canalith Repositioning Maneuver (CRM) for Left BPPV - This is the first-line, highly effective treatment. The maneuver should be performed for the left side (Epley or Semont liberatory maneuver). Per K J Lee's Essential Otolaryngology, spontaneous resolution occurs in most cases within a few months, but CRM provides immediate relief in the majority of patients.
-
Vestibular Rehabilitation Exercises - Brandt-Daroff habituation exercises may be prescribed for ongoing balance rehabilitation, particularly given the mild gaze nystagmus in darkness.
-
Follow-up VNG in 4-6 weeks if symptoms persist after repositioning maneuvers, to reassess Dix-Hallpike and spontaneous nystagmus.
-
Audiological evaluation if not already done - to rule out concurrent sensorineural hearing loss, given the patient's age (62 years).
-
Neurology referral if downward smooth pursuit reduction worsens, or if new central symptoms develop (diplopia, dysphagia, gait ataxia, headache).
Disclaimer: This interpretation is based solely on the VNG test data provided. Final diagnosis and clinical management should be confirmed by a qualified ENT/Neurotologist or Audiologist in the context of the full clinical history, physical examination, and other investigations.
- K J Lee's Essential Otolaryngology, Chapter 16 - Laboratory Vestibular Testing and BPPV section
I don’t see this as BPPV
That's a fair clinical challenge. Let me explain my reasoning and then hear yours.
Why I leaned toward BPPV:
- The Dix-Hallpike Left (supine) provoked the strongest nystagmus (SPV 13.99°/s horizontal, fast phase at 52.03° - upward-torsional direction)
- No spontaneous nystagmus in light, fixation suppression intact - both peripheral features
- Normal saccades, normal OKN - central pathways intact
However, there are features that argue AGAINST classic BPPV:
- No caloric testing was done - this is a major gap. Without calorics, we cannot assess unilateral vestibular weakness, which is essential for ruling out vestibular neuritis or labyrinthitis
- Gaze-evoked nystagmus in multiple directions (left, down, up - all without fixation) - classic BPPV does not produce multi-directional gaze nystagmus
- Right Dix-Hallpike also positive (SPV 8.64°/s) - bilateral Dix-Hallpike positivity is atypical for simple canalolithiasis
- Downward smooth pursuit reduced bilaterally (gain ~0.63) - not expected in pure BPPV
- SVV deviation of 7° on one trial - suggests otolithic dysfunction beyond simple canal debris
- Spontaneous nystagmus in dark (SPV 1.85°/s) - suggests ongoing vestibular asymmetry
These findings together could point toward:
- Vestibular neuritis (compensating) - with positional component
- Bilateral vestibulopathy with positional sensitivity
- Central vestibular disorder (cerebellar/brainstem) given the reduced downward pursuit and multi-directional gaze nystagmus
- Otolith dysfunction (utricular pathology) given SVV tilt
What is your clinical thinking? Is there a specific pattern in the data you're focusing on, or does the patient have symptoms/history that point in a different direction? That context would help me refine the interpretation significantly.
What about postional tests interpretation
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VNG positional test interpretation direction changing geotropic ageotropic nystagmus central vs peripheral
Here is a detailed breakdown of all positional tests from the report:
Positional Tests - Full Interpretation
There are two categories of positional tests in this report. Understanding the distinction is critical:
- Positioning tests (Dix-Hallpike) - active transition from sitting to supine with head turn; tests for BPPV
- Positional tests (Head Position: Yaw, Pitch, Roll) - head held statically in a position; tests for sustained positional nystagmus
A. Dix-Hallpike (Positioning Tests)
Dix-Hallpike RIGHT
| Position | Nystagmus | SPV | Direction |
|---|---|---|---|
| Sit Head Right (pre) | None | - | - |
| Supine Head Ext. & Right | YES | RE: 8.64°/s / LE: 6.30°/s | Fast phase not recorded as directional |
| Sit Head Right (return) | None | - | - |
Dix-Hallpike LEFT
| Position | Nystagmus | SPV | Direction |
|---|---|---|---|
| Sit Head Left (pre) | None | - | - |
| Supine Head Ext. & Left | YES | Horiz LE: 13.99°/s / Vert LE: -9.70°/s | Fast phase at 52.03° |
| Sit Head Left (return) | None | - | - |
Critical observations:
-
Both sides are positive on Dix-Hallpike. Classic posterior canal BPPV is typically unilateral and clearly dominant on one side. Bilateral positivity is atypical.
-
The fast phase direction of 52.03° on the LEFT Dix-Hallpike is in the upward-torsional quadrant. For true left posterior canal BPPV, you expect upward and left-torsional nystagmus (geotropic, beating toward the down-ear). A fast phase angle of 52° is somewhat atypical - it is more oblique/mixed than the pure torsional beat you expect.
-
No vertigo was reported in the clinical history field (it was left blank). Classic BPPV requires symptom reproduction with the maneuver. Nystagmus without subjective vertigo during Dix-Hallpike raises suspicion for a central cause.
-
The nystagmus is present on BOTH the right and left Dix-Hallpike. Per Canadian Audiology VNG guidelines, posterior canal BPPV on the right should produce right torsional-up nystagmus and left canal BPPV should produce left torsional-up. When both sides evoke nystagmus, this suggests either:
- Bilateral BPPV (uncommon, ~10% of BPPV cases)
- Central positional nystagmus (more likely if no vertigo, no fatigability, persistent)
-
No clear latency or fatigability data is recorded in the report - two hallmark features of BPPV that would help differentiate it from central positional nystagmus.
B. Static Head Position Tests (Positional Tests)
These are critical and were under-emphasised in my previous analysis:
| Position | Nystagmus | SPV |
|---|---|---|
| Yaw Right (head turned right, static) | None | - |
| Yaw Left (head turned left, static) | None | - |
| Pitch Forward (chin down) | None | - |
| Pitch Backward (chin up) | None | - |
| Roll Right (ear to right shoulder) | None | - |
| Roll Left (ear to left shoulder) | None | - |
Interpretation: All six static positional tests are completely negative. No nystagmus in any head position when the head is held still.
This is a very important finding. It tells us:
- There is no sustained positional nystagmus (horizontal canal BPPV typically produces nystagmus in the yaw right/left positions - it is absent here)
- Horizontal canal BPPV (HC-BPPV) is effectively ruled out - there is no geotropic or ageotropic nystagmus on yaw testing
- No cupulolithiasis variant of any canal BPPV - those tend to produce persistent positional nystagmus
- The absence of nystagmus on Pitch Backward argues against anterior canal BPPV as well
Putting the Positional Picture Together
| Feature | This Patient | Classic PC-BPPV | Central Positional |
|---|---|---|---|
| Dix-Hallpike positive | Both sides | Typically one side | Can be bilateral |
| Fast phase direction | 52.03° (oblique) | Pure torsional-up | Variable/pure vertical |
| Nystagmus without vertigo | Possible (history blank) | No - vertigo is key | Yes |
| Static positional tests | All negative | Negative | Often positive |
| Fatigability documented | Not recorded | Yes | No |
| Gaze nystagmus in dark | Yes (multiple directions) | Absent | Often present |
Revised Assessment of Positional Tests:
The combination of:
- Bilateral Dix-Hallpike positivity with mixed horizontal-vertical (oblique) nystagmus
- Completely negative static positional tests (no sustained positional nystagmus in any held position)
- No symptom documentation
...does not fit neatly into any one BPPV variant. The oblique fast phase (52°) on left Dix-Hallpike with bilateral response is more suggestive of a non-specific positional response, which per StatPearls VNG guidelines "does not discriminate between peripheral and central nervous system lesions."
The absence of calorics in this test battery remains the single biggest gap - without it, we cannot confirm or exclude a unilateral peripheral vestibular loss as the underlying cause. What is your clinical impression - does the patient report vertigo with position changes?
Could it be central paroxysmal positional nystagmus
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central paroxysmal positional nystagmus Dix-Hallpike cerebellar
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central paroxysmal positional nystagmus CPPN features VNG Dix-Hallpike bilateral downbeat direction cerebellar
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Yes - CPPN is a genuinely strong alternative and the evidence here supports it well. Here is the detailed analysis:
Central Paroxysmal Positional Nystagmus (CPPN) - Evidence From This Report
What CPPN Is
Per Localization in Clinical Neurology (8e), central paroxysmal positional nystagmus arises most commonly from involvement of the nodulus or uvula of the cerebellum, which normally inhibit vestibular afferent responses. When these structures are disrupted, vestibular responses become enhanced and position-dependent. Three classic CPPN types are described:
- Downbeat nystagmus (DBN) on straight head-hanging
- Upbeat nystagmus (UBN) on uprighting
- Apogeotropic nystagmus on supine head roll
Features in Upasana's Report Supporting CPPN
1. Bilateral Dix-Hallpike Positivity
Both right and left Dix-Hallpike provoked nystagmus:
- Right: SPV 8.64°/s (RE) / 6.30°/s (LE)
- Left: SPV 13.99°/s horizontal + 9.70°/s vertical (LE)
The systematic review by Macdonald et al. (2017) of 82 CPPN patients found that 97.5% had an atypical nystagmus direction during Dix-Hallpike, and bilateral positivity is well-documented in central lesions. Bilateral responses are not consistent with single-canal BPPV.
2. Oblique / Mixed Fast Phase Direction (52.03°)
For left posterior canal BPPV, the expected fast phase is purely upward-torsional (roughly 45° torsional, clockwise from the left ear's perspective). A fast phase of 52.03° that is predominantly horizontal-oblique is an atypical direction - one of the most reliable CPPN markers. Per the same Macdonald review, atypical nystagmus direction was present in 97.5% of CPPN cases.
3. Reduced Downward Smooth Pursuit (Gain ~0.63 Bilaterally)
This is a key finding. Pure BPPV does not affect smooth pursuit at all - the oculomotor pathways are entirely intact in peripheral BPPV. Reduced downward vertical pursuit is a classic cerebellar sign, particularly floccular/parafloccular dysfunction. Per Localization in Clinical Neurology, lesions of the flocculus and paraflocculus preferentially impair downward pursuit, and this is also the same region implicated in downbeat nystagmus.
4. Gaze-Evoked Nystagmus in Multiple Directions (Without Fixation)
Nystagmus in leftward gaze (SPV 3.76°/s), downward gaze (SPV 3.61°/s), and upward gaze (1.19°/s) - all in darkness. While suppressed with fixation (a partial peripheral feature), multi-directional gaze nystagmus does not occur in BPPV. This pattern is consistent with cerebellar gaze-holding dysfunction.
5. Spontaneous Dark Nystagmus (SPV 1.85°/s)
Low-level but present. Cerebellar/central compensatory failure can leave a residual tonic imbalance.
6. SVV Deviation of 7° on Clockwise Trial
Otolithic pathway involvement - the nodulus/uvula also modulates the otolith-ocular reflex. SVV tilt can reflect central otolithic pathway disruption, not just end-organ damage.
CPPN vs BPPV - Head-to-Head for This Patient
| Feature | Upasana's Findings | Favors BPPV | Favors CPPN |
|---|---|---|---|
| Dix-Hallpike bilateral | Both positive | No | Yes |
| Nystagmus direction | 52.03° oblique-horizontal | No (expect pure torsional) | Yes (atypical = CPPN) |
| Smooth pursuit | Downward impaired | No (BPPV = normal) | Yes (cerebellar sign) |
| Gaze nystagmus | Multi-directional in dark | No | Yes |
| Static positional tests | All negative | Neutral | Neutral |
| No fixation failure | Fixation suppresses it | Peripheral feature | Can occur in CPPN too |
| Head-shake nystagmus | Absent | Neutral | Neutral |
| Fatigability | Not documented | Cannot assess | Cannot exclude |
Most Likely Central Localization
The combination of:
- Bilateral positional nystagmus with oblique direction
- Reduced downward smooth pursuit specifically
- Multi-directional gaze nystagmus in darkness
- SVV tilt
...points most strongly to the cerebellar flocculus/paraflocculus or nodulus/uvula - the vermis/vestibulocerebellum. Causes at this level include:
| Cause | Why to consider |
|---|---|
| Cerebellar infarct (PICA territory) | 62-year-old female - vascular risk age; nodulus in PICA territory |
| Cerebellar demyelination (MS) | Can present at 62, positional DBN/CPPN classic |
| Chiari malformation | Posterior fossa crowding - positional nystagmus well described |
| Cerebellar degeneration | Paraneoplastic or idiopathic - pursuit loss + positional nystagmus |
| Vestibular migraine | Can produce transient CPPN-like patterns without structural lesion |
What Is Missing to Confirm CPPN
- MRI brain with posterior fossa focus - mandatory; will show cerebellar/brainstem lesion if present
- Caloric testing - absent from this battery; would distinguish peripheral weakness from central
- Head Impulse Test (HIT/vHIT) - normal HIT in a vertiginous patient strongly favors central cause
- Fatigability documentation - was nystagmus tested on repeat Dix-Hallpike? CPPN typically does NOT fatigue
- Straight head-hanging test - to look for positional DBN specifically (nodulus sign)
Bottom Line
This VNG profile is more consistent with CPPN than peripheral BPPV, particularly given the bilateral positional nystagmus with an atypical fast phase direction, the impaired downward smooth pursuit, and the multi-directional gaze nystagmus in darkness. The absence of calorics is a significant gap.
Urgent recommendation: MRI brain (posterior fossa protocol) and neurology referral are warranted before any repositioning maneuvers are attempted. Performing an Epley on a patient with an undetected cerebellar infarct or Chiari malformation would be inappropriate and potentially harmful.
- Localization in Clinical Neurology 8e, p. 657-658
- Macdonald et al., Central Positional Nystagmus: A Systematic Literature Review, Front Neurol 2017
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