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analyse_media
analyse_media
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Finding Sources
Finding Sources
Running Command
cd /tmp/workspace/attachments/7fed6a26-a204-4e70-add8-44b37ba2676f && python3 -c " import pdfplumber with pdfplumber.open('Habiba VNG.pdf') as pdf: print(f'Total pages: {len(pdf.pages)}') for i, page in enumerate(pdf.pages): print(f'\n===== PAGE {i+1} =====') text = page.extract_text() if text: print(text) tables = page.extract_tables() if tables: for j, t in enumerate(tables): print(f'--- TABLE {j+1} ---') for row in t: print(row) "
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Full Clinical Interpretation - Ms. Habiba Hasan (Age 68F)
Patient Summary
| Detail | Value |
|---|---|
| Name | Ms. Habiba Hasan |
| Age / Sex | 68 years / Female |
| Complaints | Vertiginous feeling, dizziness on and off, imbalance while walking x 2 years; long-standing migraine |
| Vitals | BP 120/80, Pulse 73, SpO2 97% - all normal |
| Prior Imaging | MRI Brain normal, MRA Brain normal, Left Vertebral Artery (VA) Hypoplasia noted |
| Neurologist's working diagnosis | ? Vestibular Migraine |
| VNG done | July 31, 2026 (Priority Hearing Care) |
VNG Report - Test-by-Test Interpretation
1. Saccades (Page 2)
| Parameter | Right Eye | Left Eye | Normal |
|---|---|---|---|
| Horizontal Velocity | 556.87 °/s | 504.53 °/s | >200 °/s |
| Horizontal Precision | 96.06% | 95.03% | >85% |
| Horizontal Latency | 336 ms | 344 ms | 150-250 ms |
| Vertical Velocity | 335.70 °/s | 454.83 °/s | >150 °/s |
| Vertical Precision | 93.75% | 99.03% | >85% |
| Vertical Latency | 293 ms | 300 ms | 150-250 ms |
Interpretation: Saccadic velocities and precision are within normal range. However, saccadic latencies are mildly prolonged bilaterally (both horizontal and vertical latencies exceed 300 ms; normal upper limit ~250 ms). This mild prolongation can indicate subtle central processing delay (prefrontal-brainstem pathways) but can also be a non-specific finding in older patients. No saccadic dysmetria (no overshoot/undershoot). Overall: borderline/mildly abnormal latency, otherwise normal saccades.
2. Smooth Pursuit (Page 3)
| Direction | Right Eye Gain | Left Eye Gain | Normal |
|---|---|---|---|
| Horizontal - Rightward | 0.50 | 0.48 | ≥0.70 |
| Horizontal - Leftward | 0.65 | 0.65 | ≥0.70 |
| Vertical - Upward | 0.26 | 0.25 | ≥0.60 |
| Vertical - Downward | 0.19 | 0.17 | ≥0.60 |
Interpretation: This is the most significant abnormality in the entire VNG.
- Horizontal pursuit gain is reduced bilaterally (0.48-0.65; normal ≥0.70), indicating impaired smooth pursuit.
- Vertical pursuit gain is severely reduced bilaterally (0.17-0.26; normal ≥0.60), indicating markedly impaired vertical smooth pursuit.
Reduced smooth pursuit - especially symmetrically and more severely in the vertical plane - is a central sign. It localizes to the cerebellum (flocculus/paraflocculus), brainstem (pontine/mesencephalic pursuit pathways), or diffuse cerebral involvement. This is not a peripheral vestibular finding. In the context of this patient, it strongly suggests central vestibular dysfunction.
3. Optokinetic Test (OKN) (Pages 4-5)
| Direction | Gain | Normal |
|---|---|---|
| Left-to-Right | 1.05 / 1.04 | 0.80-1.20 |
| Right-to-Left | 0.94 / 0.91 | 0.80-1.20 |
| Top-to-Bottom | 0.89 / 1.11 | 0.80-1.20 |
| Bottom-to-Top | 0.81 / 0.97 | 0.80-1.20 |
| Fast Phase Direction | None recorded | - |
Interpretation: OKN gains are normal in all four directions. No directional preponderance or asymmetry. The absence of fast-phase nystagmus during OKN is consistent with the intact caloric response (peripheral canal function not severely disrupted).
4. Nystagmus Testing (Pages 6-7)
Spontaneous Nystagmus - In Light:
- No nystagmus detected (all parameters "-"). Normal.
Spontaneous Nystagmus - In Dark:
- Horizontal (Right Eye): SPV 6.94 °/s, Amplitude 5.97°, Frequency 1.20 Hz
- Vertical (both eyes): SPV -6.69 / -6.21 °/s, Amplitude -6.10 / -5.85°
- Fast Phase Direction: 45.62° (oblique/mixed direction)
Interpretation: There is spontaneous nystagmus in the dark that is suppressed in light (absent in light condition). This is a key finding:
- Nystagmus present in dark but suppressed by visual fixation = consistent with peripheral vestibular cause (fixation suppresses peripheral nystagmus).
- However, the nystagmus has a mixed/oblique direction (45.62°, combining horizontal and vertical components). Pure horizontal nystagmus points to peripheral origin; vertical or torsional components suggest central pathology or vestibular migraine.
- The SPV of ~7 °/s is mild (pathological threshold is typically ≥5 °/s in dark).
This represents a low-grade spontaneous vestibular nystagmus, mostly suppressible with fixation, with a mixed direction - a pattern seen in vestibular migraine.
Head Shake Nystagmus (High Frequency):
- Horizontal: No nystagmus
- Vertical: SPV -8.01 / -9.12 °/s, Amplitude -6.08 / -6.91°, Frequency 0.72 Hz bilaterally
Interpretation: Post-head-shake vertical nystagmus is present. Vertical head-shake nystagmus is a central sign - it implies asymmetric cerebellar/brainstem processing of vestibular signals. This further supports a central vestibular component. It can be seen in vestibular migraine, cerebellar disease, and brainstem lesions.
Hyperventilation Nystagmus:
- All parameters "-". No nystagmus provoked. This argues against a demyelinating lesion (MS) or acoustic neuroma, where hyperventilation-induced nystagmus is classically seen.
5. Gaze Testing (Pages 8-12)
With Fixation (Center, Left, Right, Up, Down): All parameters "-" (no gaze-evoked nystagmus). Normal.
Without Fixation (in darkness):
- Center-without fixation: Vertical nystagmus bilaterally (SPV -6.13 / -6.96 °/s). Fast phase 58.41°. This confirms the dark spontaneous nystagmus is real.
- Left-without fixation: Horizontal nystagmus right eye only (SPV 8.47 °/s, Amplitude 7.32°) - this is a left-beating nystagmus appearing in left gaze without fixation, suggesting left canal hypofunction.
- Up-without fixation: Vertical nystagmus right eye (SPV -8.59 °/s, Amplitude -9.66°). Significant downbeat component in upgaze.
- Right-without fixation: No nystagmus.
- Down-without fixation: Vertical nystagmus left eye only (SPV -4.31 °/s, Amplitude -2.08°). Mild.
Interpretation: No gaze-evoked nystagmus with fixation (ruling out significant cerebellar/brainstem gaze palsy). However, direction-changing nystagmus appears in different gaze positions without fixation - again suggesting central vestibular dysfunction (peripheral nystagmus is direction-fixed, not direction-changing).
6. Positional Testing - Dix-Hallpike (Pages 13-15)
| Position | Nystagmus |
|---|---|
| DH Right (sitting head right) | No nystagmus (SPV "-") |
| DH Right (supine head ext. + right) | No nystagmus |
| DH Left (sitting head left) | No nystagmus |
| DH Left (supine head ext. + left) | No nystagmus |
Interpretation: All Dix-Hallpike positions are NEGATIVE. No positional nystagmus provoked. This effectively rules out Benign Paroxysmal Positional Vertigo (BPPV) as the cause.
7. Positional Testing - Head Positions (Yaw, Pitch, Roll) (Pages 16-18)
All slow phase velocities are "-" (no positional nystagmus) in:
- Yaw Right / Yaw Left
- Pitch Forward / Pitch Backward
- Roll Right / Roll Left
Interpretation: No positional nystagmus in any static head position. No cupulolithiasis or canalithiasis variant of BPPV. Rules out central positional nystagmus in static positions.
8. Subjective Visual Vertical (SVV) (Page 19)
| Trial | Deviation |
|---|---|
| Clockwise | +2° (Right) |
| Anticlockwise | -2° (Left) |
| Blank Background | -1° (Left) |
Interpretation: SVV deviations of ±2° are within the normal range (normal ±2.5°). This means otolith function (utricle) is essentially intact bilaterally, and there is no significant utricular lesion or lateralized otolith dysfunction. Normal SVV argues against acute unilateral vestibular neuritis or a static otolith lesion.
Summary of VNG Findings
| Test | Finding | Significance |
|---|---|---|
| Saccades | Mildly prolonged latency, otherwise normal | Minor/non-specific |
| Smooth Pursuit (Horizontal) | Reduced gain bilaterally | Central sign |
| Smooth Pursuit (Vertical) | Severely reduced gain bilaterally | Central sign |
| OKN | Normal all directions | Normal |
| Spontaneous Nystagmus (dark) | Present, suppressed by fixation, mixed direction | Peripheral/central mixed |
| Head-Shake Nystagmus | Vertical post-head-shake nystagmus | Central sign |
| Hyperventilation | No nystagmus | Against MS/schwannoma |
| Gaze Testing (with fixation) | Normal (no gaze-evoked nystagmus) | - |
| Gaze Testing (no fixation) | Direction-changing nystagmus in various positions | Central sign |
| Dix-Hallpike | NEGATIVE bilaterally | BPPV excluded |
| All positional tests | Negative | BPPV excluded |
| Subjective Visual Vertical | Normal (±2°) | Otolith function intact |
DIAGNOSIS
Primary Diagnosis: Vestibular Migraine (Central Vestibular Dysfunction)
This is the most consistent diagnosis given the following convergence of evidence:
Clinical features supporting Vestibular Migraine (ICHD-3 / Barany Society criteria):
- Long-standing migraine history (explicitly stated)
- Episodic vertiginous symptoms for 2 years, on and off
- Imbalance and lightheadedness
- No photophobia, no phonophobia (as noted on handwritten sheet) - these are absent between attacks, which is compatible; they typically occur during attacks
- Floaters noted (+) - visual symptoms are a migraine feature
- No LOC / no LOV
- Normal MRI Brain - no structural lesion
- Age and sex (migraine-associated vestibular disorders are common in middle-aged women)
- No hearing loss mentioned - arguing against Meniere's disease
- Nausea present
VNG features supporting Central/Vestibular Migraine:
- Bilaterally reduced smooth pursuit (especially vertical) - most consistent with migrainous cerebellar/brainstem dysfunction; the cerebellum is hyperperfused/dysfunctional during migraine attacks
- Vertical post-head-shake nystagmus - central brainstem/cerebellar sign
- Direction-changing nystagmus without fixation - central pattern
- Negative Dix-Hallpike - excludes BPPV
- Normal SVV - no fixed otolith lesion
- Nystagmus suppressible by fixation - partially peripheral pattern, consistent with the overlap pattern seen in vestibular migraine
- Negative hyperventilation - argues against demyelination or nerve compression
As stated in Harrison's Principles of Internal Medicine 22E (2025): "Vestibular migraine is a common yet undiagnosed cause of episodic vertigo. Vertigo sometimes precedes a typical migraine headache but more often occurs without headache or with only a mild headache... motion sensitivity and sensitivity to visual motion are common. Even in the absence of headache, other migraine features may be present."
The ICHD/Barany Society diagnostic criteria (from Scott-Brown's Otorhinolaryngology) are met:
- ≥5 episodes of vestibular symptoms, moderate-severe intensity (2 years of intermittent episodes ✓)
- Current/prior migraine history ✓
- Migraine features (nausea, visual symptoms/floaters) during episodes ✓
- Not better explained by another vestibular diagnosis (BPPV excluded, no Meniere's features) ✓
Contributory / Secondary Finding: Left Vertebral Artery Hypoplasia
MRA Brain showed left VA hypoplasia (known from clinic letter). This is important context:
- Left VA hypoplasia can cause reduced blood flow to the posterior fossa (brainstem, cerebellum, inner ear via AICA/PICA)
- This vascular anomaly may lower the threshold for vestibular migraine attacks and contribute to the smooth pursuit abnormalities seen on VNG
- It may also independently contribute to vertebrobasilar insufficiency (VBI) symptoms, especially positional dizziness, although all positional tests were negative here
- The neurologist has wisely ordered MRA Neck Vessels to assess the full vertebrobasilar tree, which is appropriate
Differential Diagnoses (Less Likely)
| Diagnosis | For | Against |
|---|---|---|
| BPPV | Common in this age group | Dix-Hallpike completely negative |
| Meniere's Disease | Episodic vertigo | No low-freq hearing loss, no aural fullness/tinnitus, SVV normal |
| Vestibular Neuritis | Peripheral nystagmus in dark | Bilateral smooth pursuit deficit (central), nystagmus direction-changing, 2-year duration, no acute onset |
| Cerebellar Stroke/TIA | Smooth pursuit deficit, vertical nystagmus | MRI Brain normal, no acute symptoms, no gaze-evoked nystagmus |
| MS | Central signs | No hyperventilation nystagmus, MRI normal |
Clinical Recommendations
The treating neurologist (Dr. KM Hassan) has prescribed appropriately:
| Medicine | Purpose | Comment |
|---|---|---|
| Flunarizine 10mg (Sibelium) once at night | Migraine prophylaxis; Ca-channel blocker also stabilizes vestibular system | First-line agent for vestibular migraine prevention |
| Ginkocer Plus (Ginkgo + betahistine combo) once daily | Improve cochlear/vestibular microcirculation | Useful given VA hypoplasia; improves posterior fossa perfusion |
| Betahistine 16mg (Vertin) SOS | Acute vestibular symptom relief | H1 agonist / H3 antagonist; reduces endolymphatic pressure |
| Crocin (Paracetamol + Caffeine) SOS | Acute migraine headache | Appropriate rescue |
Pending investigation: MRA of neck vessels - will assess for vertebral artery stenosis/hypoplasia along the full cervical course, carotid disease, and other vascular contributors.
VNG finding of note for follow-up: The bilaterally impaired vertical smooth pursuit should be re-assessed after 3-6 months of treatment. If it persists or worsens despite migraine prophylaxis, further cerebellar/brainstem evaluation may be warranted (repeat MRI with dedicated posterior fossa sequences).
In summary: Ms. Habiba's VNG is consistent with central vestibular dysfunction, characterized by bilaterally impaired smooth pursuit (most prominently vertical), vertical post-head-shake nystagmus, and direction-changing nystagmus without fixation - all with complete absence of positional nystagmus (negative Dix-Hallpike) and normal otolith (SVV). Combined with her 2-year history of episodic dizziness and long-standing migraine, the diagnosis is Vestibular Migraine (as the neurologist suspected), with Left VA Hypoplasia as a contributing vascular risk factor. BPPV is excluded. No evidence of Meniere's disease or a structural lesion.
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