Here is the rephrased version of the VNG report analysis, written in clear, clinical language:
VNG Report Interpretation
Patient: Yash Pal Singh | Female, 59 years | Date: 02 June 2026
Saccades
Saccade testing showed abnormal results. The left eye was significantly faster than the right eye, and the precision values for the left eye were nearly double those of the right - indicating the left eye is overshooting the target (hypermetric saccades). Response latencies were prolonged in both eyes. These findings point toward a cerebellar dysfunction, as overshooting saccades are not seen in peripheral (inner ear) problems.
Smooth Pursuit
Pursuit gains were mildly reduced, especially at higher frequencies (0.4 Hz vertical: ~0.5-0.6 in both eyes). Normal gain should be above 0.7. The symmetric reduction across both eyes and both directions suggests a central (cerebellar or brainstem) cause rather than a peripheral one.
Optokinetic Testing
All optokinetic gains were within normal limits (0.86-1.10), and no abnormal fast phases were recorded. This part of the test was normal.
Spontaneous Nystagmus
No spontaneous nystagmus was seen in light or darkness. Head-shake, hyperventilation, and Valsalva tests were also negative. This is normal and rules out active peripheral vestibular decompensation.
Gaze Testing - Important Finding
When the patient looked to the right without fixation, a low-level nystagmus was recorded (SPV -2.43°/s, frequency 0.98 Hz in the right eye). Large waveform movements were also seen in the left without-fixation and vertical without-fixation positions. Gaze-evoked nystagmus is a central sign and is not produced by inner ear disorders.
Positional Testing - The Key Section
Dix-Hallpike Right:
- No nystagmus was triggered during the actual head-hanging (supine) position.
- Nystagmus appeared only when the patient sat back up (SPV 8.23°/s, Freq 0.91 Hz in right eye).
- In classic BPPV, nystagmus is provoked during the Hallpike position itself - not on return to sitting. This is an atypical and suspicious finding.
Dix-Hallpike Left:
- Clear nystagmus was triggered in the supine head-extended-left position (R eye SPV -10.84°/s, L eye SPV -10.11°/s).
- Importantly, both eyes were involved simultaneously with comparable velocities and frequencies.
- In typical BPPV, nystagmus follows a canal-specific pattern (torsional + upbeat). Bilateral symmetric eye involvement does not fit this picture.
Static Head Position Tests:
- Pitch Backward (head tilted back): Nystagmus in both eyes (SPV -5.68°/s right, -8.40°/s left) - this is a downbeat pattern in a static position, which is a recognized sign of central (nodular/uvular cerebellar) pathology.
- Yaw Right (head turned right): Nystagmus in both eyes (SPV ~2°/s bilaterally).
- Pitch Forward, Yaw Left, Roll Right and Left: No nystagmus.
Nystagmus was provoked in multiple, unrelated head positions. In BPPV, nystagmus is triggered by specific positioning that stresses one particular semicircular canal. Multi-positional nystagmus that does not follow a single canal plane strongly suggests a central origin.
Subjective Visual Vertical (SVV)
Small deviations of 1-2 degrees were noted across trials. These minor deviations are within or close to normal limits (±2°) and do not add strong lateralizing information on their own.
BPPV vs. CPPV - Comparison Table
| Feature | Classic BPPV | This Patient's Findings | Interpretation |
|---|
| Saccades | Normal | Dysmetric (hypermetric left eye) | Central sign |
| Smooth pursuit | Normal | Mildly reduced at 0.4 Hz | Central sign |
| Gaze nystagmus | Absent | Present (right gaze, no fixation) | Central sign |
| Nystagmus timing | During Hallpike position | On sitting back up (DH-Right) | Atypical |
| Nystagmus direction | Torsional + upbeat (posterior canal) | Downbeat / bilateral | Central sign |
| Eyes involved | Predominantly one eye pattern | Both eyes simultaneously | Central sign |
| Number of positions positive | One specific position | Multiple planes (DH-L, Pitch back, Yaw R) | Central sign |
| Epley response | Resolves symptoms | No clear resolution data | Inconclusive |
Overall Impression
This VNG report does not support a straightforward diagnosis of BPPV. The pattern of findings - dysmetric saccades, reduced smooth pursuit, gaze-evoked nystagmus, multi-positional nystagmus with bilateral eye involvement, and a downbeat component in pitch-backward position - is far more consistent with Central Paroxysmal Positional Vertigo (CPPV).
The most likely anatomical site of involvement is the cerebellar nodulus or uvula, or the dorsal brainstem/fourth ventricular region. This pattern has been described with cerebellar infarction, demyelination (MS), and drug toxicity (e.g., amiodarone).
Recommended Next Steps
- MRI brain - posterior fossa protocol (not CT - small lesions in the cerebellum and brainstem are frequently missed on CT).
- Urgent neurology referral - this should not be managed as routine BPPV.
- Do not rely on Epley maneuver as the sole treatment without first ruling out central pathology.
- Consider workup for: posterior circulation stroke/TIA, multiple sclerosis, cerebellar atrophy, or drug-induced cerebellar toxicity.
Bottom line: The Epley maneuver and a BPPV label are not appropriate for this patient until MRI of the posterior fossa has been reviewed by a neurologist or neurotologist.