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VNG videonystagmography interpretation BPPV positional nystagmus diagnosis criteria

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VNG interpretation BPPV positional nystagmus Dix-Hallpike McClure-Pagnini smooth pursuit saccades

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VideoNystagmography (VNG) Report — Detailed Analysis & Diagnosis

Patient: Savita Devi | Age: 63 | Gender: Female | ID: CCDA00291 Date: 19 May 2026 | Facility: Hear Clear India

1. SACCADES

ParameterRight EyeLeft EyeNormal Range
Horizontal Velocity355.13°/s561.32°/s>275°/s
Horizontal Precision99.38%92.53%80–134%
Horizontal Latency283.08 ms210.00 ms<260 ms
Vertical Velocity241.51°/s271.11°/s>275°/s
Vertical Precision91.67%98.13%80–134%
Vertical Latency403.64 ms410.91 ms<260 ms
Findings:
  • Right eye horizontal saccade velocity (355°/s) is within normal limits, but left eye velocity (561°/s) is hypermetric — possibly a data artifact or asymmetric pursuit disengagement.
  • Right eye horizontal latency (283 ms) is mildly prolonged (>260 ms); vertical latencies bilaterally (403–411 ms) are significantly prolonged.
  • Vertical velocities for both eyes (241–271°/s) are below the 275°/s threshold, indicating bilateral slowed vertical saccades.
  • Precision is normal bilaterally in all planes.
⚠️ Interpretation: Prolonged vertical saccade latencies and reduced vertical saccade velocities are a central nervous system (CNS) indicator. Isolated vertical saccade slowing can be seen in cerebellar, brainstem, or supranuclear pathologies.

2. SMOOTH PURSUIT

DirectionRight Eye GainLeft Eye GainNormal Range
Horizontal Rightward0.820.800.9–1.0
Horizontal Leftward0.740.770.9–1.0
Vertical Upward0.980.960.9–1.0
Vertical Downward0.640.630.9–1.0
Findings:
  • Horizontal smooth pursuit gain is reduced bilaterally (0.74–0.82 vs. normal ≥0.9) — consistent with bilateral symmetric smooth pursuit impairment.
  • Downward vertical pursuit is markedly reduced (0.63–0.64) — significant.
  • Upward vertical pursuit is normal (0.96–0.98).
⚠️ Interpretation: Bilateral horizontal smooth pursuit impairment with downward pursuit deficits suggests a central vestibular or cerebellar lesion (pursuit is mediated by the cerebellum and parieto-occipital cortex). Isolated downward pursuit deficits are classically associated with cerebellar or dorsal midbrain pathology.

3. OPTOKINETIC NYSTAGMUS (OKN)

DirectionRight Eye GainLeft Eye GainNormal
Left-to-Right0.970.96~1.0
Right-to-Left1.001.05~1.0
Top-to-Bottom0.170.27~1.0
Bottom-to-Top~1.0
Findings:
  • Horizontal OKN is symmetric and normal in both directions.
  • Vertical OKN (top-to-bottom) is severely reduced (0.17–0.27), and bottom-to-top OKN is absent/unmeasurable.
⚠️ Interpretation: A severe and asymmetric vertical OKN deficit with preserved horizontal OKN is highly suggestive of a central lesion (brainstem or cerebellar). Vertical OKN is particularly sensitive to dorsal midbrain and medullary pathology.

4. SPONTANEOUS NYSTAGMUS

ConditionFinding
In LightNo nystagmus (normal)
In Dark (Right Eye)SPV 1.53°/s, Amplitude 1.57°, Frequency 0.45 Hz
In Dark (Left Eye)No measurable nystagmus
Findings:
  • No spontaneous nystagmus in light (normal).
  • Mild spontaneous nystagmus in darkness in the right eye (SPV 1.53°/s) — borderline, as pathological threshold is typically ≥5°/s; however, even low-grade dark spontaneous nystagmus indicates possible peripheral or minor central asymmetry.
Interpretation: Mildly abnormal — suggests a subtle right-sided vestibular asymmetry or very early unilateral peripheral weakness.

5. GAZE TESTS

All gaze positions (Center, Left, Right, Up, Down) — no gaze-evoked nystagmus detected. This is normal. The absence of gaze-evoked nystagmus makes a gross cerebellar mass lesion or vestibulocerebellum lesion less likely, though does not exclude subtler pathology.

6. POSITIONAL TESTING — DIX-HALLPIKE

Right Side (Dix-Hallpike Right)

PositionSignificant Finding
Sit Head Right (pre)Left eye vertical SPV 1.76°/s, amplitude 2.35°, 0.36 Hz
Supine Head Ext. & RightHorizontal SPV: R −4.47°/s, L −5.05°/s; Vertical SPV: +4.33°/s (Right eye); Freq: 1.80 Hz (R), 0.99 Hz (L); Fast phase direction: 221.45°
Sit Head Right (post)No nystagmus
Positive Dix-Hallpike Right with combined horizontal and vertical nystagmus components. Fast phase at 221° (inferomedial direction) with frequency 1.80 Hz is consistent with right posterior semicircular canal (PSC) BPPV — though the torsional component confirmation requires visual trace review.

Left Side (Dix-Hallpike Left)

PositionSignificant Finding
Sit Head Left (pre)Horizontal nystagmus bilaterally (SPV 3.09–4.36°/s)
Supine Head Ext. & LeftHorizontal SPV: R +3.48°/s, L +4.00°/s; Vertical SPV: +3.09°/s (Right eye); Freq: 1.36 Hz (R), 0.56 Hz (L); Fast phase direction: 328.95°
Sit Head Left (post)Right eye horizontal nystagmus SPV 2.17°/s, Amp 3.50°, 0.45 Hz
Positive Dix-Hallpike Left as well. Bilateral Dix-Hallpike positivity with upward/torsional components and persistence of nystagmus across positions raises the possibility of bilateral BPPV or cupulolithiasis variant.

7. McCLURE-PAGNINI (HORIZONTAL CANAL) TESTING

This test specifically evaluates the horizontal (lateral) semicircular canals:
PositionKey Findings
Sit to SupineRight eye vertical SPV −5.00°/s, Amp −2.63°, 0.83 Hz
Right LateralHorizontal SPV: R +3.39°/s, L +3.65°/s; Vertical: +1.91°/s (R), +1.12°/s (L); Fast phase 22.59°/354.15°; Freq 1.87–2.43 Hz
Supine Head Neutral (1st)Horizontal SPV: R +6.29°/s, L +6.41°/s; Vertical: R −11.05°/s, L −13.68°/s; Freq 1.50–1.87 Hz — most active nystagmus in the test
Left LateralLeft eye horizontal SPV −8.01°/s, Amp −2.08°, 1.37 Hz
Supine Head Neutral (2nd)Horizontal SPV: R +3.45°/s, L +4.44°/s; Vertical −10.31°/s (R), −0.99°/s (L); Freq 1.45–1.46 Hz
Findings: Significant nystagmus is provoked in supine head-neutral position with both horizontal and downbeat vertical components. The strong geotropic horizontal nystagmus in supine neutral with direction change between right and left lateral positions suggests bilateral horizontal canal BPPV (canalolithiasis or cupulolithiasis variant).
The downbeat vertical nystagmus in supine neutral (SPV up to −13.68°/s) is particularly notable — downbeat nystagmus in supine is a key sign of anterior (superior) semicircular canal BPPV or central pathology (especially cerebellar, particularly floccular/parafloccular lesions).

8. HEAD POSITION TESTS

PositionKey Findings
Yaw RightNo nystagmus
Yaw LeftVertical SPV: R +2.82°/s, L +3.69°/s; Amp 3.27°/3.09°; Freq 0.44–0.56 Hz
Pitch ForwardLeft eye horizontal SPV −3.29°/s; Vertical bilat +4.35–5.41°/s; Fast phase 211.65°; Freq 0.72–1.19 Hz
Pitch BackwardVertical SPV: R −6.06°/s, L −5.04°/s; Freq ~0.50 Hz — downbeat nystagmus
Roll RightNo nystagmus
Roll LeftRight eye horizontal SPV +2.43°/s, Freq 0.86 Hz
Findings:
  • Yaw Left provokes positional nystagmus — asymmetric compared to Yaw Right (which is clean), suggesting left labyrinthine or canal sensitivity.
  • Pitch Backward elicits downbeat nystagmus (SPV −5 to −6°/s) — this is a well-recognized sign of anterior canal BPPV or central downbeat nystagmus syndrome (cerebellar flocculus/paraflocculus pathology).
  • Roll Left provokes mild horizontal nystagmus in the right eye, consistent with lateral canal BPPV asymmetry.

SUMMARY & DIAGNOSIS

Primary Diagnosis

BPPV — Multiple Canal Involvement (Predominantly Right Posterior + Bilateral Horizontal Canal + Possible Anterior Canal Component)
The constellation of findings supports multi-canal BPPV as the primary vestibular diagnosis:
CanalEvidence
Right Posterior SCCPositive Dix-Hallpike Right with mixed horizontal-torsional nystagmus, fast phase 221°
Left Posterior SCCPositive Dix-Hallpike Left with similar features, fast phase 328°
Bilateral Horizontal SCCActive geotropic nystagmus on McClure-Pagnini Right Lateral (SPV 3.39–3.65°/s) and Left Lateral (SPV −8.01°/s), direction-changing in supine
Anterior SCC (possible)Downbeat nystagmus in supine neutral (SPV −11 to −13°/s) and Pitch Backward; provoked by McClure-Pagnini

Secondary/Concurrent Concern: Central Vestibular Features

Several findings cannot be attributed solely to BPPV and raise concern for a concurrent central vestibular disorder:
FindingImplication
Reduced bilateral horizontal smooth pursuit (gain 0.74–0.82)Cerebellar/cortical
Severely impaired downward smooth pursuit (0.63–0.64)Dorsal midbrain / cerebellar
Absent/severely reduced vertical OKN (especially bottom-to-top)Brainstem/midbrain
Prolonged bilateral vertical saccade latencies (403–411 ms)Supranuclear / brainstem
Reduced bilateral vertical saccade velocity (<275°/s)CNS involvement
Persistent downbeat nystagmus in supine-neutral & pitch backwardCerebellar flocculus/nodulus or anterior canal
⚠️ The combination of impaired smooth pursuit, vertical OKN deficits, prolonged vertical saccade latencies, and downbeat positional nystagmus in a 63-year-old woman warrants neuroimaging (MRI brain with posterior fossa/cerebellum protocol) to exclude central pathology — especially cerebellar degeneration, posterior fossa mass, or Arnold-Chiari malformation.

CLINICAL RECOMMENDATIONS

  1. Canalith Repositioning Maneuver (CRM):
    • Epley maneuver for right posterior canal BPPV
    • Modified Epley for left posterior canal BPPV
    • Barbeque roll (Lempert maneuver) for bilateral horizontal canal BPPV
    • Consider Semont liberatory maneuver if cupulolithiasis variant suspected
  2. MRI Brain (Posterior Fossa Protocol):
    • To evaluate for cerebellar atrophy, space-occupying lesion, demyelination, Chiari malformation, or brainstem pathology given the central features
  3. Neurology/Neuro-otology Referral:
    • Given the mixed central and peripheral findings and the patient's age (63)
  4. Follow-up VNG:
    • Repeat VNG after Epley maneuver to assess clearance of positional nystagmus and document whether central features persist in isolation
  5. Vestibular Rehabilitation Therapy (VRT):
    • Indicated regardless of central vs. peripheral final diagnosis to reduce fall risk and improve gaze stability

Overall VNG Impression: Abnormal — multi-canal BPPV (bilateral posterior + bilateral horizontal ± anterior canal) with superimposed central vestibular indicators necessitating neuroimaging. No caloric test data is present in this report; if not yet performed, bilateral caloric testing would further characterize peripheral vestibular function.
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