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Full Detailed Analysis Report

Patient: Ms. Anuradha | Age/Sex: 35/F | Date: 28-May-2026

Facility: MAX Super Speciality Hospital, Vaishali (MRI) & Priority Hearing Care Pvt. Ltd. (VNG)

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REPORT 1: MRI BRAIN PLAIN

Technique

Detailed Findings

MRI Impression

1. No significant intracranial abnormality - the brain, brainstem, cerebellum, ventricles, and CSF spaces are all normal.
2. Focal subgaleal soft tissue thickening, right parietal region - with calcifications and prominent flow voids on T2Wt - suggestive of benign etiology, query scalp haemangioma.

Clinical Interpretation of MRI Findings

• Subgaleal location - situated between the galea aponeurotica and the pericranium
• Multiple foci of calcification - phleboliths (calcified thrombi within vascular channels) are a classical feature of venous-type haemangiomas/vascular malformations
• Prominent flow voids on T2WI - flow voids indicate high-flow or large vascular channels within the lesion, consistent with a vascular neoplasm or malformation

1. Scalp cavernous haemangioma (most likely) - benign vascular tumor; typically soft, compressible, may enlarge with Valsalva; calcifications (phleboliths) common
2. Venous vascular malformation - slow-flow lesion; phleboliths classic; often present since childhood
3. Arteriovenous malformation (AVM) of scalp - high-flow voids, pulsatile; less likely given "benign" appearance
4. Calcified dermoid/epidermoid cyst - usually lacks prominent flow voids
5. Ossifying fibromyxoid tumor or calcified lipoma - less likely given the flow void characteristics

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REPORT 2: VIDEONYSTAGMOGRAPHY (VNG)

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TEST 1: SACCADE TEST

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TEST 2: SMOOTH PURSUIT TEST

• Central vestibular dysfunction (cerebellar pathology, brainstem lesion) - most clinically important cause
• Medication effect (sedatives, anticonvulsants, benzodiazepines) - must be excluded
• Fatigue, inattention, or poor cooperation during testing - can reduce gain at all frequencies
• Migraine-associated vestibulopathy - may produce central-pattern smooth pursuit abnormalities
• Note: The normal MRI brain makes a structural cerebellar/brainstem lesion less likely, though functional or early demyelinating disease is not excluded by a plain MRI without contrast.

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TEST 3: OPTOKINETIC TEST (OKN)

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TEST 4: SPONTANEOUS NYSTAGMUS

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TEST 5: GAZE TEST

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TEST 6: POSITIONAL TESTING (Dix-Hallpike & McClure-Pagnini)

Dix-Hallpike Right

Dix-Hallpike Left

Yacovino Test (for anterior canal / cupulolithiasis)

McClure-Pagnini (for horizontal canal BPPV)

• Dix-Hallpike right: Positive - torsional-vertical nystagmus evoked with right head-down position with fast phase direction ~105° (upbeat-torsional toward lower ear) - consistent with right posterior semicircular canal BPPV
• Dix-Hallpike left supine: Strong vertical nystagmus evoked (SPV -16.37 °/s) - may indicate left posterior canal BPPV or a central positional nystagmus component
• McClure-Pagnini right lateral: Geotropic horizontal nystagmus bilaterally - consistent with horizontal/lateral canal BPPV (canalithiasis type)
• Yacovino supine end: Downbeat nystagmus (SPV -17.62 °/s) - the Yacovino sequence is used for anterior canal BPPV; a downbeat response at the "supine end" position raises the possibility of anterior canal BPPV or a central (midline cerebellar/anterior vermis) process
• High SPVs in positional testing (up to 17 °/s) indicate strong vestibular responses, not necessarily pathological in isolation

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TEST 7: SUBJECTIVE VISUAL VERTICAL (SVV)

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INTEGRATED DIAGNOSTIC SYNTHESIS

Primary Diagnoses

• The strongest finding: Positive Dix-Hallpike right with torsional-vertical nystagmus consistent with right posterior semicircular canal BPPV
• McClure-Pagnini geotropic horizontal nystagmus suggests concomitant horizontal canal BPPV (canalithiasis subtype)
• Possible left posterior canal involvement based on Dix-Hallpike left findings
• BPPV is the most common cause of vertigo in a 35-year-old female (Cummings Otolaryngology)

• Severely reduced smooth pursuit gain bilaterally (all frequencies, both H and V)
• Reduced downward OKN at 20° bilaterally
• Gaze-evoked nystagmus on right gaze (without fixation)
• Spontaneous vertical nystagmus in darkness
• Downbeat nystagmus on Yacovino supine-end position
• High-velocity positional nystagmus on left DH supine and McClure-Pagnini supine

• Subgaleal vascular lesion with calcifications (phleboliths) and T2 flow voids
• Clinically unrelated to vestibular symptoms
• Requires clinical correlation; Doppler US or contrast MRI of lesion may be done electively

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Summary Table

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Recommendations

1. Canalith Repositioning Maneuver (CRM): Epley maneuver for right posterior canal BPPV; Gufoni or Barbecue roll maneuver for horizontal canal BPPV - should be performed promptly as first-line treatment.
2. Further MRI: Contrast-enhanced MRI Brain + posterior fossa protocol, or MRI with diffusion-weighted imaging to evaluate for central pathology (demyelination, early cerebellar lesion) given the prominent central VNG features despite normal plain MRI.
3. Medication Review: Confirm no use of sedatives, anticonvulsants, or vestibular suppressants that could reduce smooth pursuit gain.
4. Audiology Assessment: Pure tone audiogram and tympanometry to complete the vestibular workup.
5. Neurotology / Neurology Consultation: Given the combination of BPPV and central VNG features in a 35-year-old woman, a specialist evaluation is warranted, particularly to evaluate for vestibular migraine (very common in young women) or early demyelinating disease.
6. Scalp Lesion: Clinical examination of the right parietal scalp lesion; Doppler ultrasound for further characterization; no urgent intervention required unless symptomatic.

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Disclaimer: This analysis is based on the documented findings in the provided MRI and VNG reports. It is intended to assist clinical correlation and should be reviewed by the treating physician alongside the patient's history and physical examination findings. All treatment decisions must be made by a qualified healthcare professional.

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CORRECTED & REVISED VNG ANALYSIS REPORT

Patient: Ms. Anuradha | Age/Sex: 35/F | Date: 28-May-2026

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WHY THIS IS NOT BPPV - Critical Criteria Review

1. Latency of 1-15 seconds before nystagmus onset
2. Transient nystagmus - typically abates within 30-60 seconds
3. Fatigability - nystagmus diminishes with repeated maneuvers
4. Vertical-torsional nystagmus pattern (mixed, not pure vertical or pure horizontal)
5. Vertigo is prominent during the maneuver

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REVISED INTEGRATED ANALYSIS

TEST-BY-TEST RE-INTERPRETATION

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1. SPONTANEOUS NYSTAGMUS

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2. GAZE TEST

• Gaze-evoked nystagmus (GEN) on rightward gaze - suppressed by fixation, exposed without fixation
• GEN that changes direction with gaze direction is a hallmark of central vestibular/cerebellar dysfunction, specifically implicating the neural integrator (flocculus, nucleus prepositus hypoglossi, medial vestibular nucleus)
• Per Shambaugh's: GEN occurs with multiple sclerosis, cerebellar atrophy, and medication effects - NOT with peripheral vestibular disease
• The suppression by fixation confirms fixation suppression is intact (a reassuring finding, but does not make this peripheral)

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3. SMOOTH PURSUIT - GLOBALLY SEVERELY ABNORMAL

• Global reduction of smooth pursuit gain - bilateral, symmetric, all frequencies, both horizontal and vertical axes
• This pattern is pathognomonic of central vestibulo-cerebellar dysfunction
• Per KJ Lee's Otolaryngology: "Abnormal saccades or saccadic pursuit results, especially with normal caloric results = central pathology"
• Per Harrison's: "Poor pursuit... usually indicates central pathology, often involving the cerebellum"
• Differential for globally reduced pursuit: cerebellar disease, demyelination (MS), medication effect (sedatives/anticonvulsants), vestibular migraine with central features
• Downward pursuit is most severely impaired (gains 0.11-0.15) - points specifically to anterior cerebellar/floccular pathology or midbrain involvement

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4. OPTOKINETIC TEST - SELECTIVE DOWNWARD FAILURE

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5. POSITIONAL TESTING - REINTERPRETED AS CENTRAL POSITIONAL NYSTAGMUS

Critical observations across ALL positional tests:

• Vertical component: SPV -8.62 °/s, FPD 105.71° (upbeat-torsional direction)
• However, also present during sitting (before supine position) suggesting it is not purely position-dependent with latency
• Nystagmus present during both the going-down AND sitting-up phases - not the classic unidirectional BPPV pattern

• Pure vertical nystagmus: SPV -16.37 °/s, amplitude -6.13°
• Pure vertical (downbeat direction given negative SPV) = central positional nystagmus, not BPPV
• Per Goldman-Cecil: Central paroxysmal positional nystagmus is "often pure vertical"

• Downbeat vertical nystagmus: SPV -17.62 °/s, amplitude -6.81°
• The Yacovino sequence tests for anterior canal BPPV, but downbeat nystagmus in the supine-end position is specifically associated with anterior cerebellar vermis / nodulus pathology or central positional nystagmus
• Per Bradley & Daroff: "Downbeat nystagmus results from bilateral damage to the vestibulocerebellum (flocculus, paraflocculus, nodulus, and uvula)"

• Bilateral direction: FPD 132° bilaterally, SPV -5.89 to -9.11 °/s
• While geotropic horizontal nystagmus CAN be seen in horizontal canal BPPV, the bilateral symmetric nature and the presence in supine neutral position (SPV -16.84 °/s in left eye) is not consistent with BPPV
• Nystagmus in the supine neutral head position (no head turn) is a direct red flag for central positional nystagmus

• Mixed horizontal AND vertical nystagmus: H-SPV -5.79, V-SPV -2.94, FPD 165°
• Mixed-direction nystagmus during a simple positional change = central pattern

Red flags against BPPV (per Localization in Clinical Neurology, 8e):

• Positive on both right AND left Dix-Hallpike - classic central red flag ✓
• Direction-changing nystagmus across positions ✓
• No fatigability described / persistent across repeated positions ✓
• Nystagmus present in supine head neutral (no canal stimulation) ✓
• Pure vertical nystagmus on DH left and Yacovino ✓

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6. SUBJECTIVE VISUAL VERTICAL

• Results largely normal (±1-3°)
• Marginal left tilt (-3°) on anti-clockwise trial - suggests subtle left otolith asymmetry, not diagnostically definitive in isolation

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REVISED DIAGNOSIS

Primary Diagnosis:

CENTRAL VESTIBULAR DYSFUNCTION

Most likely: Vestibulo-Cerebellar Pathway Disorder (Central Positional Nystagmus pattern)

1. Globally severely reduced smooth pursuit (bilateral, all frequencies, H+V)
2. Selective downward OKN failure
3. Gaze-evoked nystagmus (right gaze, without fixation)
4. Vertical spontaneous nystagmus in darkness
5. Central positional nystagmus - pure vertical, bilateral, non-fatigable, direction-changing, present in supine neutral
6. Downbeat positional nystagmus on Yacovino

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Differential Diagnoses (Ranked):

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WHAT IS NOT PRESENT (Important Negatives)

• No caloric test results in this VNG - this is a significant limitation; caloric results would clarify peripheral vs. central distinction further
• No unilateral canal paresis pattern suggested
• No head impulse test result documented
• No direction-fixed unidirectional horizontal nystagmus - ruling against acute unilateral peripheral vestibulopathy (vestibular neuritis)
• No tinnitus/hearing loss data - Meniere's disease cannot be excluded or confirmed from VNG alone

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Recommendations (Revised)

1. Contrast-Enhanced MRI Brain + Posterior Fossa (with CISS/FIESTA sequences and sagittal views of foramen magnum) - mandatory to exclude demyelinating plaques, cerebellar lesions, Chiari malformation, neurovascular compression of CN VIII
2. Bithermal Caloric Testing - not performed in this VNG; essential to determine whether there is unilateral or bilateral peripheral vestibular hypofunction
3. Neurology/Neurotology Consultation - central vestibular findings in a 35-year-old woman require specialist evaluation
4. Medication History Review - exclude all CNS-acting drugs that could suppress smooth pursuit and generate GEN
5. Migraine history assessment - if there is a history of migraine with vestibular symptoms, vestibular migraine (most common central vestibular disorder in young women) becomes the leading diagnosis
6. Audiological Assessment - pure tone audiogram and tympanometry
7. Scalp lesion (MRI finding) - clinically unrelated to vestibular symptoms; Doppler ultrasound for elective characterization

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Summary in plain terms: The VNG does not show the pattern of benign positional vertigo. Instead, it shows a pattern of central vestibular dysfunction - the eye movement control pathways in the cerebellum and brainstem are not working normally. The brain MRI (plain, without contrast) is normal, but this does not rule out the causes listed above. A contrast MRI and specialist neurology/neurotology opinion are the priority next steps.

This analysis is intended to assist clinical interpretation and must be correlated with the patient's full clinical history, examination findings, and treating physician's judgment.