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VNG report interpretation saccade smooth pursuit gain normal values nystagmus vestibular
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I now have all the data needed to compile a comprehensive report. Let me synthesize everything from the VNG PDF (16 pages of objective data) and the handwritten clinical findings (images).
VideoNystagmography (VNG) Report — Detailed Interpretation
Patient: Gurdial Singh | Age: 81 years | Gender: Male
Patient ID: CCDA00283 | Date of Test: 02 May 2026
Clinic: Hear Clear India | Referred by: Dr. Amit Sharma
Clinical Findings (Bedside Examination — from handwritten notes)
| Test | Finding | Interpretation |
|---|---|---|
| Romberg Test | Sway to the Right | Positive — suggests peripheral vestibular hypofunction on the right side; proprioceptive/vestibular instability with eyes closed |
| Fukuda Stepping Test | Deviation to the Right > 30° | Positive (normal < 30°) — indicates unilateral vestibular weakness on the right side; the patient consistently steps toward the side of the lesion |
| Tandem Gait | Could not perform | Significant balance impairment; inability to walk heel-to-toe indicates substantial cerebellar or vestibular dysfunction with functional impact |
| Finger-to-Nose | Slow but accurate | Dysmetria absent; movement is cerebellar-adjacent but ultimately accurate — likely reflects psychomotor slowing of age rather than frank cerebellar pathology |
VNG Objective Test Results
1. Saccade Test (Oculomotor — Central Pathways)
| Parameter | Right Eye | Left Eye | Normal Range |
|---|---|---|---|
| Velocity (Horizontal) | 309.44°/s | 296.24°/s | ~300–700°/s |
| Precision (Horizontal) | 76.87 | 66.80 | ≥80% |
| Latency (Horizontal) | 363.64 ms | 334.55 ms | 150–250 ms |
| Velocity (Vertical) | 227.15°/s | 146.53°/s | ~150–500°/s |
| Precision (Vertical) | 95.07 | 43.76 | ≥80% |
| Latency (Vertical) | 280.00 ms | 250.91 ms | 150–250 ms |
Interpretation: Saccade latencies are prolonged bilaterally (horizontal: 364/335 ms vs. normal <250 ms), consistent with age-related slowing and possible central processing delay. Precision is reduced bilaterally — the left eye shows markedly poor horizontal precision (66.80) and vertical precision (43.76), suggesting saccadic dysmetria or an asymmetric ocular motor deficit. Vertical velocities are asymmetrically reduced in the left eye.
Significance: Saccade abnormalities, particularly prolonged latency and reduced precision, point to central (brainstem/cerebellum/frontal) involvement, not purely peripheral vestibular disease. — Cummings Otolaryngology, Quantitative Testing section
2. Smooth Pursuit Test
| Parameter | Right Eye | Left Eye | Normal Range |
|---|---|---|---|
| Rightward Gain (Horizontal) | 0.33 | 0.59 | ≥0.70 |
| Leftward Gain (Horizontal) | 0.32 | 0.53 | ≥0.70 |
| Upward Gain (Vertical) | 0.21 | 0.37 | ≥0.70 |
| Downward Gain (Vertical) | 0.18 | 0.31 | ≥0.70 |
Interpretation: Smooth pursuit gain is severely reduced in both eyes across all directions (all values well below the normal threshold of 0.70). The right eye is disproportionately worse. This pattern of bilateral pursuit degradation is the single most important central indicator in this study.
Lesions of the flocculus (cerebellum) impair smooth pursuit. The dorsal vermis and fastigial nuclei are critical for smooth pursuit; lesions produce saccadic inaccuracy and impaired pursuit. — Cummings Otolaryngology, p. 3178
Age note: Some pursuit gain reduction is expected in an 81-year-old, but values this low (0.18–0.37 range) significantly exceed age-expected decline and cannot be attributed to normal aging alone.
3. Optokinetic Test (OKN)
| Direction | Right Eye Gain | Left Eye Gain | Normal |
|---|---|---|---|
| Left → Right | 0.58 | 0.53 | ≥0.70 |
| Right → Left | 0.63 | 0.62 | ≥0.70 |
| Top → Bottom | — | 0.15 | ≥0.70 |
| Bottom → Top | — | 0.13 | ≥0.70 |
Interpretation: Optokinetic gains are reduced bilaterally in horizontal directions (0.53–0.63 vs. normal ≥0.70). Vertical OKN is markedly impaired. As optokinetic responses parallel smooth-pursuit pathways, these findings corroborate the central (cerebellar/brainstem) pattern seen on smooth pursuit. The absence of right eye data for vertical OKN is notable.
4. Spontaneous Nystagmus
| Condition | Finding |
|---|---|
| In Light | Absent (no nystagmus) — Normal |
| In Dark (Right Eye) | SPV: 6.54°/s, Amplitude: 7.89°, Frequency: 0.49 Hz |
| In Dark (Left Eye) | Absent |
Interpretation: The presence of spontaneous nystagmus in darkness only in the right eye, with SPV of 6.54°/s (abnormal threshold: >5°/s), represents spontaneous vestibular nystagmus suppressed by visual fixation. This is a classic feature of peripheral vestibular hypofunction — the nystagmus beats away from the lesion side. Its suppression with fixation points to a peripheral (labyrinthine/vestibular nerve) origin, consistent with right-sided vestibular weakness seen on the Fukuda and Romberg tests.
5. Gaze Test (Fixation Nystagmus)
| Gaze Direction | Finding |
|---|---|
| Center | Normal — no nystagmus |
| Left | Right eye: SPV 3.11°/s, Amplitude 2.37°, Frequency 0.71 Hz |
| Up | Right eye: SPV −3.06°/s, Amplitude −2.05°, Frequency 0.53 Hz |
| Right | Normal |
| Down | Normal |
Interpretation: Low-amplitude gaze-evoked nystagmus is present on leftward and upward gaze. This type of direction-changing gaze nystagmus (present in eccentric gaze positions) is a central sign and may indicate cerebellar (floccular) dysfunction or failure of the neural integrator to maintain eccentric eye position. — Cummings Otolaryngology, p. 3178
6. Positional Tests (Dix-Hallpike)
Right Dix-Hallpike
| Position | Key Findings |
|---|---|
| Sit Head Right | Right eye vertical SPV 8.62°/s; Left eye horizontal SPV −3.40°/s |
| Supine Head Extended & Right | Right eye vertical SPV 4.82°/s, horizontal −2.41°/s; Fast phase 234.61° |
| Return to Sit | Left eye residual SPV −2.98°/s |
Interpretation: The right Dix-Hallpike elicits upbeat-torsional nystagmus in the right eye with SPV 8.62°/s — this is the characteristic pattern for right posterior canal BPPV. The fast phase direction of 234.61° (toward the affected ear) during the extended position is consistent with this diagnosis.
Left Dix-Hallpike
| Position | Key Findings |
|---|---|
| Sit Head Left | No nystagmus |
| Supine Head Extended & Left | Left eye horizontal SPV −2.30°/s, Frequency 0.78 Hz |
| Return to Sit | No nystagmus |
Interpretation: Left Dix-Hallpike is essentially negative. Minimal residual low-SPV activity is not diagnostic. Left posterior canal BPPV is not present.
7. Positional Tests (McClure-Pagnini — Horizontal Canal)
| Position | Findings |
|---|---|
| Sit to Supine | Negative |
| Right Lateral | Right eye vertical SPV +4.45°/s; Left eye horizontal SPV −4.03°/s |
| Supine Head Neutral | Negative |
| Left Lateral | Right eye minimal (SPV 0.39°/s) |
| Supine Head Neutral (after left lateral) | Left eye horizontal SPV −9.15°/s, Amplitude −4.07°, Frequency 0.92 Hz |
Interpretation: Activity in the right lateral position with horizontal components, and significant left eye horizontal nystagmus (SPV −9.15°/s) in the supine neutral position following left lateral roll, suggests possible horizontal canal (cupulolithiasis) component, though findings are not definitively diagnostic. This pattern warrants clinical correlation.
8. Head Position Tests
| Position | Key Findings |
|---|---|
| Pitch Forward | Bilateral vertical nystagmus: R 18.60°/s, L 12.77°/s — Abnormal |
| Pitch Backward | Negative |
| Roll Right | Right eye vertical SPV 9.03°/s |
| Roll Left | Left eye vertical SPV 4.84°/s |
Interpretation: Pitch-forward position elicits prominent upbeat nystagmus bilaterally (SPV 18.60°/s and 12.77°/s) — this is significantly abnormal and raises the possibility of anterior canal BPPV or, importantly, a central lesion (e.g., cerebellar pathology). Roll-position nystagmus in both directions suggests positional vestibular sensitivity that is not clearly localised to one canal.
Summary and Overall Impression
| Domain | Finding | Localisation |
|---|---|---|
| Saccades | Prolonged latency bilaterally; reduced precision (left > right) | Central (frontal/brainstem) |
| Smooth Pursuit | Severely reduced gain bilaterally (0.18–0.59) | Central — cerebellar (flocculus/vermis) |
| OKN | Reduced horizontal gain; markedly abnormal vertical OKN | Central |
| Spontaneous Nystagmus | Present in darkness, right eye only, SPV 6.54°/s | Peripheral — right vestibular hypofunction |
| Gaze Nystagmus | Left and upward gaze nystagmus | Central |
| Dix-Hallpike Right | Upbeat-torsional nystagmus, SPV 8.62°/s | Right posterior canal BPPV |
| Dix-Hallpike Left | Negative | No left BPPV |
| Romberg Test | Sway to right | Right vestibular hypofunction |
| Fukuda Test | Deviation right >30° | Right vestibular hypofunction |
| Tandem Gait | Could not perform | Significant balance/cerebellar impairment |
| Finger-to-Nose | Slow but accurate | Age-related, no frank dysmetria |
Clinical Interpretation
This 81-year-old male presents with a mixed peripheral and central vestibular disorder:
-
Right Posterior Canal BPPV — The right Dix-Hallpike is positive with characteristic upbeat-torsional nystagmus (SPV 8.62°/s). This is the most treatable finding. Epley canalith repositioning maneuver (right-sided) is indicated.
-
Right Peripheral Vestibular Hypofunction — Spontaneous dark nystagmus (SPV 6.54°/s) suppressed by fixation, Romberg sway right, and Fukuda deviation right >30° all consistently indicate reduced right labyrinthine/vestibular nerve function. Differential includes: vestibular neuritis sequelae, labyrinthitis, or early vestibular schwannoma. Audiological evaluation is recommended.
-
Central Vestibular/Cerebellar Dysfunction — The significantly reduced smooth pursuit gain (bilaterally, ~0.18–0.59), bilateral OKN reduction, gaze-evoked nystagmus (left and upward), prolonged saccade latencies, and markedly abnormal pitch-forward positional nystagmus (SPV 18.60°/s) all point to central pathway involvement. At age 81, this pattern is concerning for cerebellar or brainstem pathology, and may include cerebrovascular disease (small vessel ischemia), cerebellar atrophy, or a mass lesion. MRI brain (with and without contrast, including posterior fossa sequences) is strongly recommended.
-
Functional Impact — Inability to perform tandem gait and bilateral balance deficits place this patient at high fall risk. Vestibular rehabilitation therapy (VRT) is recommended alongside BPPV treatment.
Recommendations
- Immediate: Epley canalith repositioning procedure for right posterior canal BPPV
- Audiology: Pure tone audiometry and speech discrimination testing (rule out sensorineural hearing loss / vestibular schwannoma)
- Imaging: MRI brain with posterior fossa protocol (rule out central lesion — cerebrovascular disease, cerebellar atrophy, schwannoma)
- Neurology/Neurotology referral: Given combined peripheral and central findings in an elderly patient
- Falls prevention: Vestibular rehabilitation therapy, mobility aids assessment, home safety evaluation
- Follow-up VNG: Post-Epley to document BPPV resolution; reassess after treatment
Report based on VNG data from Hear Clear India (02 May 2026) and bedside clinical examination findings. All measurements interpreted in the clinical context of an 81-year-old male with multifactorial vestibulopathy. Final clinical diagnosis should be made by the treating physician.
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