Kindly give detailed report. Patient feels vertigo during waling and sit to supine

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BPPV diagnosis VNG videonystagmography

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VideoNystagmography (VNG) Detailed Interpretation Report

Patient: Gurdial Singh | Age: 81 years | Gender: Male Patient ID: CCDA00283 | Date: 02-May-2026 Clinic: Hear Clear India | Referred by: Dr. Amit Sharma Chief Complaint: Vertigo during walking and during sit-to-supine transition

I. CLINICAL HISTORY & CONTEXT

An 81-year-old male presents with positional vertigo provoked by ambulation and by the sit-to-supine transition. These are characteristic trigger patterns of Benign Paroxysmal Positional Vertigo (BPPV), particularly involving the horizontal (lateral) semicircular canal. The VNG battery was performed to objectively characterize the vestibulo-ocular reflex, oculomotor pathways, and to identify the specific canal(s) involved.

II. TEST-BY-TEST FINDINGS

1. Saccade Testing

ParameterRight EyeLeft EyeNormal Range
Horizontal Velocity309 °/s296 °/s300–700 °/s
Horizontal Precision76.8766.80>80
Horizontal Latency363 ms334 ms150–250 ms
Vertical Velocity227 °/s147 °/s250–550 °/s
Vertical Precision95.0743.76>80
Vertical Latency280 ms251 ms150–250 ms
Interpretation:
  • Latency prolonged bilaterally (>250 ms in both eyes, both planes). Prolonged saccadic latency is a non-specific finding but is commonly seen in elderly patients and can reflect slowed central processing, mild cerebellar or cortical involvement, or reduced attention.
  • Reduced horizontal velocity (below 300 °/s in the left eye) and reduced vertical velocity bilaterally. Hypometric slow saccades may suggest cerebellar or brainstem pathway involvement.
  • Reduced horizontal precision (both eyes <80) with markedly asymmetric vertical precision (Right 95, Left 43). Left eye vertical precision is significantly reduced, suggesting asymmetric vertical gaze control.
  • Overall: Saccadic abnormalities are present — particularly slowed vertical velocities and reduced accuracy — warranting central pathway evaluation.

2. Smooth Pursuit Testing

ParameterRight EyeLeft EyeNormal (age-adjusted >65 yrs)
Horizontal Rightward Gain0.330.59≥0.55
Horizontal Leftward Gain0.320.53≥0.55
Vertical Upward Gain0.210.37≥0.50
Vertical Downward Gain0.180.31≥0.50
Interpretation:
  • Smooth pursuit gain is severely reduced bilaterally in all directions, more so in the right eye than the left.
  • Horizontal gains of 0.32–0.59 (normal ≥0.55–0.7 for younger adults, age-adjusted ~≥0.5 for elderly) are markedly depressed, especially in the right eye.
  • Vertical gains (0.18–0.37) are very significantly reduced bilaterally, indicating impaired vertical smooth pursuit.
  • Severely reduced smooth pursuit gain, particularly in the vertical plane and asymmetrically between the two eyes, is a central sign pointing to involvement of the cerebellum, brainstem, or cortical pursuit pathways (parieto-occipital cortex).
  • While mild pursuit degradation is expected at age 81, the degree seen here — especially vertical — exceeds age-expected norms.

3. Optokinetic Testing (OKN)

Stimulus DirectionRight Eye GainLeft Eye GainNormal
Left-to-Right0.580.53≥0.70
Right-to-Left0.630.62≥0.70
Top-to-Bottom0.15≥0.50
Bottom-to-Top0.13≥0.50
Interpretation:
  • Horizontal OKN gains are mildly reduced (~0.58–0.63), with reasonable symmetry between leftward and rightward stimulation — no significant directional asymmetry horizontally, which argues against a unilateral peripheral deficit as the primary mechanism.
  • Vertical OKN is severely impaired (gains 0.13–0.15), with the right eye not generating a measurable response and only the left eye responding weakly.
  • Severe vertical OKN depression, consistent with the vertical smooth pursuit reduction, further supports central (cerebellar/brainstem) pathway involvement affecting vertical gaze control.
  • The relative preservation of horizontal OKN symmetry (vs. vertical) is characteristic of anterior or flocculonodular cerebellar or midbrain/pontine dysfunction.

4. Spontaneous Nystagmus

ConditionFindings
In LightNo spontaneous nystagmus (all parameters absent)
In DarkRight eye vertical: SPV 6.54 °/s, amplitude 7.89°, frequency 0.49 Hz
Interpretation:
  • No spontaneous nystagmus in light — fixation is successfully suppressing any underlying vestibular imbalance (fixation suppression intact, a peripheral sign).
  • Spontaneous vertical nystagmus in darkness in the right eye (SPV 6.54 °/s): this is a significant finding. Spontaneous vertical nystagmus — especially in darkness — is unusual for isolated peripheral BPPV and suggests a central vestibular component. Vertical spontaneous nystagmus is often associated with cerebellar or brainstem pathology.
  • The nystagmus appears exclusively in the right eye's vertical channel, suggesting an asymmetric, possibly central mechanism.

5. Gaze Testing

PositionRight EyeLeft EyeFinding
CenterNo nystagmusNo nystagmusNormal
Left GazeSPV 3.11 °/s, Amp 2.37°, Freq 0.71 Hz (horizontal)NoneLeft gaze-evoked nystagmus (right eye)
Up GazeVertical SPV −3.06 °/s, Amp −2.05°, Freq 0.53 HzNoneUp gaze nystagmus (right eye)
Right GazeNo nystagmusNo nystagmusNormal
Down GazeNo nystagmusNo nystagmusNormal
Interpretation:
  • Gaze-evoked nystagmus (GEN) is present at left and upward gaze positions, exclusively detected in the right eye.
  • Gaze-evoked nystagmus indicates failure of the neural integrator — the brainstem/cerebellar mechanism that maintains eccentric gaze. This is a central sign, classically seen with cerebellar (flocculus/paraflocculus) or brainstem lesions.
  • The asymmetry (right eye only, left and up directions) may indicate directional preference of residual vestibular imbalance or asymmetric cerebellar involvement.
  • The absence of gaze-evoked nystagmus at right or down gaze makes this a partial/directional neural integrator deficit.

6. Positional Testing — Dix-Hallpike (Right Ear)

a) Sit with Head Right (Phase 1)

  • Left eye horizontal: SPV −3.40 °/s, Amp −3.86°
  • Right eye vertical: SPV 8.62 °/s, Amp 3.62°, Freq 0.96 Hz
  • Left eye: Freq 1.63 Hz, Fast Phase Direction 177.52°

b) Supine Head Extended & Right (Classic Dix-Hallpike position)

  • Right eye horizontal: SPV −2.41 °/s, Amplitude −1.66°
  • Right eye vertical: SPV 4.82 °/s, Amp 2.34°, Freq 2.26 Hz, Fast Phase Direction 234.61°

c) Return Sit with Head Right

  • Left eye horizontal: SPV −2.98 °/s, Amp −2.74°, Freq 0.72 Hz
Interpretation:
  • Nystagmus is provoked in both the head-right sitting and supine-right extended positions, indicating genuine positional sensitivity of the right posterior/superior canal system.
  • The fast phase direction of 234.61° in the supine-right position is consistent with geotropic (toward the ground) torsional-vertical nystagmus of posterior canal BPPV affecting the right ear.
  • The right eye shows a predominantly vertical nystagmus component (SPV 4.82–8.62 °/s), consistent with posterior canal involvement. The amplitude and velocity are moderate, typical for canalith repositioning.
  • A return nystagmus on coming back to sitting (SPV −2.98 °/s in left eye) is expected and supports the BPPV diagnosis.
  • Conclusion: Positive Dix-Hallpike for RIGHT posterior canal BPPV.

7. Positional Testing — Dix-Hallpike (Left Ear)

a) Sit with Head Left (Phase 1) — No nystagmus

b) Supine Head Extended & Left

  • Left eye horizontal: SPV −2.30 °/s, Amp −1.85°, Freq 0.78 Hz
  • No vertical component
Interpretation:
  • The left Dix-Hallpike is essentially negative — no significant vertical nystagmus provoked. The mild horizontal nystagmus in the left eye is sub-threshold (SPV < 3 °/s) and does not fulfil criteria for posterior canal BPPV.
  • Left Dix-Hallpike: Negative (no significant left posterior canal BPPV).

8. Positional Testing — McClure-Pagnini Roll Test (Horizontal Canal)

PositionRight EyeLeft EyeFast Phase
Sit to SupineNo nystagmusNo nystagmus
Right Lateral RollRight Vertical SPV 4.45°/s, Amp 4.04°, Freq 0.52 HzLeft Horizontal SPV −4.03°/s, Amp −4.52°, Freq 0.39 Hz
Supine Head NeutralNo nystagmusNo nystagmus
Left Lateral RollRight Vertical SPV 0.39°/s, Amp −0.28°, Freq 1.46 HzNo nystagmus
Supine Head Neutral (after left roll)No nystagmusLeft Horizontal SPV −9.15°/s, Amp −4.07°, Freq 0.92 Hz
Interpretation:
  • Right Lateral Roll: Horizontal nystagmus is triggered in the left eye (−4.03 °/s) with a vertical component in the right eye. This is direction-fixed geotropic nystagmus (beating toward the ground when rolling right), indicating horizontal canal canalith repositioning (canalolithiasis) affecting the right horizontal canal.
  • Supine Neutral after Left Roll: A significant horizontal nystagmus emerges in the left eye (SPV −9.15 °/s, well above the 3 °/s threshold). This is a notable finding suggesting apogeotropic or transitional nystagmus — consistent with cupulolithiasis or canalith movement in the horizontal canal.
  • The sit-to-supine (McClure) transition shows no nystagmus at rest but provokes symptoms during the rolling phase — clinically correlating with the patient's complaint of vertigo during sit-to-supine movement.
  • Conclusion: Horizontal Canal BPPV (right HC) — canalolithiasis pattern, likely combined with posterior canal involvement.

9. Positional Head Position Testing

PositionRight EyeLeft Eye
Pitch Forward (chin down)Vertical SPV 18.60°/s, Amp 12.53°, Freq 0.86 HzVertical SPV 12.77°/s, Amp 9.60°, Freq 0.80 Hz
Pitch Backward (head extension)No nystagmusNo nystagmus
Roll RightRight Vertical SPV 9.03°/s, Amp 6.38°, Freq 0.67 HzNo nystagmus
Roll LeftNo right eye nystagmusLeft Vertical SPV 4.84°/s, Amp 3.16°, Freq 0.82 Hz
Interpretation:
  • Pitch Forward (chin down) provokes strong bilateral vertical nystagmus (SPV 12.77–18.60 °/s, amplitudes 9.6°–12.53°). This is a highly significant finding. Chin-down position loading the anterior/superior canals or stimulating the horizontal canal cupula produces this response. SPV >10 °/s is clearly pathological and is the strongest positional finding in this battery.
  • This bilaterally symmetric high-SPV vertical nystagmus on forward pitch is consistent with anterior canal BPPV or cupular involvement of the horizontal canal (cupulolithiasis), and may also be seen in central positional nystagmus.
  • Head Roll Right produces vertical nystagmus in the right eye only (9.03 °/s) — reinforcing right-sided vestibular asymmetry.
  • Head Roll Left produces left eye vertical nystagmus (4.84 °/s) — lower magnitude, suggesting mild bilateral positional sensitivity.
  • The pitch backward position shows no response — arguing against isolated anterior canal canalolithiasis and more toward cupulolithiasis of the horizontal canal or anterior canal variant.

III. OVERALL INTERPRETATION & DIAGNOSIS

Primary Diagnosis

1. Benign Paroxysmal Positional Vertigo (BPPV) — Multi-Canal, Right-Sided Predominance
  • Right Posterior Canal BPPV (Canalolithiasis): Positive Dix-Hallpike right with transient upbeat-torsional nystagmus (SPV up to 8.62 °/s, fast phase ~234°), consistent with free-floating otoconia in the right posterior semicircular canal.
  • Right Horizontal Canal BPPV: Geotropic horizontal nystagmus on right lateral roll (SPV 4.03–9.15 °/s) consistent with canalolithiasis of the right horizontal canal. This directly explains the patient's vertigo during sit-to-supine transition and walking, as horizontal canal BPPV is exquisitely sensitive to head pitch and roll movements encountered in everyday activities such as turning in bed and ambulating.

Secondary / Co-Existing Finding

2. Central Vestibular / Cerebellar Pathway Dysfunction (cannot be excluded)
The following constellation of findings exceeds what is expected from isolated peripheral BPPV and raises concern for a co-existing central component:
Central SignFinding
Spontaneous vertical nystagmus in darknessRight eye, SPV 6.54 °/s
Gaze-evoked nystagmusLeft and upward gaze (neural integrator failure)
Severely reduced smooth pursuit gainAll directions, bilaterally, right > left
Severely reduced vertical OKNGains 0.13–0.15 (markedly abnormal)
Prolonged saccade latency + asymmetric precisionBoth eyes
High-SPV bilateral nystagmus on pitch forward12.77–18.60 °/s
These findings collectively suggest involvement of the flocculus/paraflocculus of the cerebellum or vestibulocerebellar tracts, which are responsible for smooth pursuit, gaze holding, fixation suppression, and OKN. At age 81, cerebellar atrophy, lacunar infarct in the brainstem, or vertebrobasilar insufficiency must be considered.
⚠️ The combination of positive positional tests (peripheral BPPV) with central oculomotor signs (gaze-evoked nystagmus, severely impaired smooth pursuit/OKN, spontaneous vertical nystagmus) warrants neuroimaging (MRI brain with posterior fossa protocol) to rule out structural central pathology before attributing all symptoms to BPPV alone.

IV. CLINICAL CORRELATION

Why does this patient feel vertigo while walking? Walking involves rhythmic head pitch and roll movements, precisely the directions that provoke nystagmus in this patient (pitch forward: strongest response 18.6 °/s; roll right: 9.03 °/s). The right horizontal canal BPPV is particularly motion-sensitive during ambulation.
Why does sitting to supine provoke vertigo? The McClure-Pagnini test directly replicates this movement. The absence of nystagmus at the initial supine-neutral position but emergence after rolling (SPV −9.15 °/s in left eye post-left roll) confirms that the horizontal canal BPPV is the primary driver of sit-to-supine vertigo.

V. RECOMMENDATIONS

  1. Canalith Repositioning Maneuvers:
    • For right posterior canal BPPV: Modified Epley Maneuver (right side).
    • For right horizontal canal BPPV: Lempert/Barbecue Roll Maneuver (rotating 360° toward the unaffected/left side in supine).
    • Perform under supervision given age 81 and gait instability.
  2. Neuroimaging: MRI brain with dedicated posterior fossa/cerebellum protocol to evaluate for cerebellar atrophy, lacunar disease, or vertebrobasilar ischemia given the constellation of central oculomotor signs.
  3. Vestibular Rehabilitation Therapy (VRT): Given the central oculomotor deficits (reduced pursuit, OKN), formal VRT with a trained physiotherapist is recommended to improve gaze stabilization and reduce fall risk.
  4. Fall Prevention: At age 81 with significant positional vertigo and central oculomotor dysfunction, fall risk is high. Assistive devices and home safety modifications are warranted.
  5. Pharmacotherapy: Acute vestibular suppressants (e.g., betahistine) may provide symptomatic relief. Avoid long-term use of antihistamines/benzodiazepines in an 81-year-old due to fall and cognitive risks.
  6. Cardiovascular Assessment: Orthostatic hypotension and cardiovascular contributors to dizziness should be excluded given the patient's age.
  7. Caloric Testing: This VNG battery did not include caloric irrigation. Bithermal caloric testing would further characterize the extent of peripheral labyrinthine function and detect unilateral canal paresis.

VI. SUMMARY

This 81-year-old male demonstrates multi-canal BPPV predominantly affecting the right ear (positive right Dix-Hallpike for posterior canal; positive right lateral roll for horizontal canal), directly explaining his symptoms of vertigo during walking and sit-to-supine transitions. Superimposed on this peripheral finding is a pattern of central oculomotor dysfunction — including gaze-evoked nystagmus, severely reduced bilateral smooth pursuit and vertical OKN, and spontaneous vertical nystagmus in darkness — which cannot be attributed to BPPV alone and warrants neuroimaging to exclude posterior fossa pathology.
Primary Impression: Multi-canal BPPV (Right posterior + Right horizontal canal), with co-existing central oculomotor signs requiring further evaluation.

Report based on VNG data from Cyclops VNG system, Hear Clear India. Interpreted per standard criteria. — K.J. Lee's Essential Otolaryngology, pp. 350–351; Roberts & Hedges' Clinical Procedures in Emergency Medicine, pp. 1458–1461.
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