Kindly provide detailed report of VNG WITH INTERPREATION
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VNG videonystagmography normal values interpretation saccades pursuit optokinetic caloric
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VNG interpretation saccades smooth pursuit optokinetic positional gaze nystagmus normal values abnormal
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I now have all the data needed to write a comprehensive VNG interpretation report. Let me compile this into a detailed clinical report.
Cranio-Oculography (Extended Videonystagmography) - Detailed Report with Interpretation
Patient: Suraj Mehra | Age: 60 years | Gender: Male
Patient ID: Q0266A00016 | Date: 18-Jun-2026
TEST 1: SACCADE TESTING
A. Horizontal Saccades
0.3 Hz Bidirectional Horizontal
| Parameter | RE Rightward | RE Leftward | LE Rightward | LE Leftward |
|---|---|---|---|---|
| Avg. Velocity | 233.27 °/s | 191.46 °/s | 224.61 °/s | 198.80 °/s |
| Peak Velocity | 297.47 °/s | 305.38 °/s | 301.20 °/s | 301.20 °/s |
| Precision | 27.85 | 19.41 | 26.20 | 24.70 |
| Latency | 280 ms | 270 ms | 290 ms | 310 ms |
| Peak to Avg Ratio | 1.28 | 1.31 | 1.32 | 1.27 |
0.45 Hz Bidirectional Horizontal
| Parameter | RE Rightward | RE Leftward | LE Rightward | LE Leftward |
|---|---|---|---|---|
| Avg. Velocity | 212.93 °/s | 158.23 °/s | 215.36 °/s | 214.86 °/s |
| Peak Velocity | 303.80 °/s | 316.46 °/s | 301.20 °/s | 277.11 °/s |
| Precision | 24.84 | 24.95 | 20.48 | 21.69 |
| Latency | 260 ms | 280 ms | 240 ms | 280 ms |
| Peak to Avg Ratio | 1.32 | 1.38 | 1.33 | 1.29 |
B. Vertical Saccades
0.3 Hz Bidirectional Vertical
| Parameter | RE Upward | RE Downward | LE Upward | LE Downward |
|---|---|---|---|---|
| Avg. Velocity | 184.62 °/s | 169.23 °/s | 164.09 °/s | 163.19 °/s |
| Peak Velocity | 215.38 °/s | 246.15 °/s | 209.88 °/s | 206.79 °/s |
| Precision | 16.35 | 24.81 | 12.31 | 16.32 |
| Latency | 290 ms | 260 ms | 250 ms | 260 ms |
0.45 Hz Bidirectional Vertical
| Parameter | RE Upward | RE Downward | LE Upward | LE Downward |
|---|---|---|---|---|
| Avg. Velocity | 161.54 °/s | 158.97 °/s | - | 155.86 °/s |
| Peak Velocity | 226.92 °/s | 234.62 °/s | - | 203.70 °/s |
| Latency | 220 ms | 890 ms | - | 280 ms |
Saccade Interpretation
Velocity: Peak horizontal velocities range from 277-316 °/s, generally at or near the lower boundary of normal (normal threshold: >275 °/s). Vertical peak velocities are lower (206-246 °/s), which is physiologically expected, as vertical saccades are inherently slower than horizontal.
Latency: Several latency values exceed the normal upper limit of 260 ms - notably LE Leftward at 310 ms (0.3 Hz), RE Downward at 890 ms (0.45 Hz vertical - this is markedly prolonged and likely represents a patient attentional lapse or artifact, but should be noted), and multiple values at 280-290 ms range.
Precision: Values range from 12 to 28. Normal precision (accuracy) should fall between 80-134% in standard scoring, but raw precision scores in this format suggest dysmetria is present. Relatively low precision values indicate mild hypometric saccades (undershooting).
Summary - Saccades: Mildly reduced average velocities bilaterally, with multiple latency values at or above the upper limit of normal. Mild hypometric (undershooting) saccades noted in all directions. This pattern is non-localizing but warrants attention; saccadic abnormalities with central features (bilateral involvement, both horizontal and vertical) raise the possibility of cerebellar or brainstem pathway involvement.
TEST 2: SMOOTH PURSUIT (TRACKING)
| Condition | Parameter | Right Eye | Left Eye |
|---|---|---|---|
| 0.2 Hz Horizontal | Rightward Gain | 0.20 | - |
| 0.2 Hz Horizontal | Leftward Gain | 0.06 | - |
| 0.2 Hz Horizontal | Gain Asymmetry | 70.00% (R) | - |
| 0.4 Hz Horizontal | Rightward Gain | 0.10 | 0.07 |
| 0.4 Hz Horizontal | Leftward Gain | 0.02 | 0.01 |
| 0.4 Hz Horizontal | Gain Asymmetry | 80.00% (R) | 85.71% (R) |
| 0.2 Hz Vertical | Upward/Downward Gain | - | - |
| 0.4 Hz Vertical | Upward/Downward Gain | - | - |
Smooth Pursuit Interpretation
This is markedly abnormal. Normal smooth pursuit gain should be 0.9-1.0 for low-frequency targets (<20 °/s). The gains recorded here are severely reduced - 0.20 at 0.2 Hz and 0.10 at 0.4 Hz for the right eye, with even lower values for the left eye. A gain of 0.02-0.20 represents an 80-98% reduction from normal.
The very high gain asymmetry (70-86% rightward) indicates that rightward pursuit is relatively better preserved than leftward, though both are severely impaired.
Vertical pursuit is unmeasurable/unrecordable in all conditions.
Clinical significance: Severely degraded smooth pursuit bilaterally (both horizontal and vertical) is a strong indicator of central nervous system (CNS) dysfunction, specifically involving the cerebellum (flocculus/paraflocculus), brainstem pursuit pathways (PPRF, nucleus prepositus hypoglossi), or diffuse cerebral hemisphere disease. This is NOT consistent with an isolated peripheral vestibular disorder.
TEST 3: OPTOKINETIC NYSTAGMUS (OKN)
| Direction | RE Gain | LE Gain |
|---|---|---|
| Left to Right | 0.38 | 0.33 |
| Right to Left | 0.44 | 0.37 |
| Top to Bottom | - | - |
| Bottom to Top | - | - |
OKN Interpretation
Reduced and abnormal. Normal OKN gain at 10 °/s should be approximately 0.52-1.15 (mean ~0.84). The recorded gains of 0.33-0.44 are below the normal range. There is a mild left-right asymmetry (rightward slightly lower than leftward), suggesting relatively greater impairment of leftward-directing OKN.
Vertical OKN is absent/not recordable.
Clinical significance: Reduced OKN gain, especially with bilateral involvement and vertical absence, further supports central pathway dysfunction. Asymmetric OKN suggests possible unilateral hemispheric or parieto-occipital cortex involvement (the slow phase of OKN is driven by pursuit pathways; impaired OKN in the direction of the lesion indicates an ipsilateral hemisphere lesion).
TEST 4: GAZE TESTING
| Gaze Position | With Fixation | Without Fixation |
|---|---|---|
| Center | No nystagmus | No nystagmus |
| Left | No nystagmus | No nystagmus |
| Right | No nystagmus | No nystagmus |
| Up | No nystagmus | No nystagmus |
| Down | No nystagmus | No nystagmus |
Gaze Interpretation
All gaze positions: No nystagmus detected in any direction, with or without fixation. This is a normal finding. Gaze-evoked nystagmus (direction changing with gaze) would suggest cerebellar dysfunction; its absence is reassuring but does not exclude central pathology given the pursuit and OKN findings above.
TEST 5: SPONTANEOUS NYSTAGMUS
| Condition | RE H | RE V | LE H | LE V |
|---|---|---|---|---|
| In Light (with fixation) | Absent | Absent | Absent | Absent |
| In Dark (without fixation) | Absent | Absent | Absent | Absent |
Interpretation
No spontaneous nystagmus in light or dark. This is normal. Absence of spontaneous nystagmus rules out an acute active unilateral peripheral vestibular imbalance (such as acute vestibular neuritis or ongoing Meniere's disease). If this test had shown nystagmus that disappeared with fixation (fixation suppression intact), it would have pointed to a peripheral vestibular lesion.
TEST 6: HIGH FREQUENCY HEAD SHAKING NYSTAGMUS (HSN)
No nystagmus parameters recorded - all fields show no measurable slow phase velocity, frequency, amplitude, or direction.
Interpretation
No post-head-shaking nystagmus. A normal finding. Head-shaking nystagmus, when present, typically beats away from the side of a peripheral vestibular weakness. Its absence makes a significant acute unilateral peripheral hypofunction less likely, though chronic compensated unilateral weakness can also give a negative result.
TEST 7: POSITIONAL TESTING
Bow and Lean Test
No nystagmus parameters recorded (all values absent/dashes).
Interpretation: No nystagmus with bow (chin down) or lean (chin up) positioning. A normal finding. Bow and lean nystagmus would suggest a horizontal canal cupulolithiasis (HC-BPPV in the cupular variant).
Supine Roll Test (McClure-Pagnini Test for HC-BPPV)
No nystagmus parameters recorded.
Interpretation: Negative for horizontal canal BPPV (both canalolithiasis and cupulolithiasis variants). No geotropic or apogeotropic horizontal nystagmus was elicited with head roll to either side.
Dix-Hallpike Right
No nystagmus parameters recorded in the parameter table. The waveform tracings show variable eye movements but no structured nystagmus.
Interpretation: Negative Dix-Hallpike on the right. No upbeat-torsional geotropic nystagmus was evoked, which would have been expected in right posterior canal BPPV.
Dix-Hallpike Left
No nystagmus parameters recorded.
Interpretation: Negative Dix-Hallpike on the left. No posterior canal BPPV on the left side.
TEST 8: SUPINE STRAIGHT HEAD EXTENSION
| Parameter | RE Horizontal | RE Vertical | LE Horizontal | LE Vertical |
|---|---|---|---|---|
| Slow Phase Velocity | - | 10.58 °/s | - | - |
| Frequency | - | 4 BPM | - | - |
| Amplitude | - | -0.27 | - | - |
| Direction | - | -90.00° | - | - |
Interpretation
This is a positive finding. A vertical slow phase velocity of 10.58 °/s at 4 beats per minute was detected in the RE vertical channel during supine head extension. The direction of -90.00° indicates downward nystagmus (downbeating nystagmus in the straight head-hanging position).
Clinical significance: Downbeat nystagmus elicited or enhanced in the supine head-extended (Hallpike) or straight-back position is a well-recognized sign of central vestibular pathology, most commonly involving the cervicomedullary junction, the vestibulocerebellum (flocculus/nodulus), or the craniovertebral junction. It is classically associated with:
- Cerebellar degeneration
- Arnold-Chiari malformation
- Multiple sclerosis plaques in the brainstem/cerebellum
- Foramen magnum lesions
- Wernicke's encephalopathy
- Drug toxicity (lithium, anticonvulsants)
OVERALL IMPRESSION AND INTERPRETATION
Summary of Findings
| Test Component | Finding | Normal/Abnormal |
|---|---|---|
| Saccades (horizontal) | Borderline peak velocity; latency mildly prolonged; mild hypometria | Mildly abnormal |
| Saccades (vertical) | Reduced velocity bilaterally; one markedly prolonged latency (890 ms) | Mildly abnormal |
| Smooth Pursuit | Severely reduced gain (0.02-0.20); marked gain asymmetry rightward | Markedly Abnormal |
| Optokinetic | Reduced gain bilaterally (0.33-0.44); vertical absent | Abnormal |
| Gaze Nystagmus | Absent in all positions | Normal |
| Spontaneous Nystagmus | Absent in light and dark | Normal |
| Head Shaking Nystagmus | Absent | Normal |
| Bow and Lean Positional | No nystagmus | Normal |
| Supine Roll (HC-BPPV) | No nystagmus | Normal |
| Dix-Hallpike Right | No nystagmus | Normal |
| Dix-Hallpike Left | No nystagmus | Normal |
| Supine Head Extension | Vertical downbeat nystagmus (SPV 10.58°/s, 4 BPM) | Abnormal - Significant |
Clinical Interpretation
1. BPPV is excluded. All positional tests (Dix-Hallpike bilateral, Supine Roll, Bow and Lean) are negative. There is no evidence of posterior canal, horizontal canal, or anterior canal BPPV.
2. No acute peripheral vestibular lesion. The absence of spontaneous nystagmus (in light and dark), absent head-shaking nystagmus, and normal gaze testing argue against an active peripheral vestibular lesion such as vestibular neuritis, labyrinthitis, or uncompensated unilateral labyrinthine hypofunction. Note: bithermal caloric testing was not performed in this study and would be needed to formally assess peripheral canal paresis.
3. Central vestibular/oculomotor dysfunction is strongly indicated. The combination of:
- Severely impaired smooth pursuit bilaterally (gains 0.02-0.20, well below normal 0.9-1.0)
- Reduced optokinetic gain bilaterally
- Abnormal saccadic metrics (velocity and latency)
- Downbeat nystagmus on supine head extension
...constitutes a central pattern. This dissociation - abnormal central oculomotor tests with normal gaze and no spontaneous nystagmus - is a classic pattern for cerebellar or brainstem involvement.
4. Downbeat nystagmus in the supine head-extended position is the most diagnostically specific finding here. This localizes to the vestibulocerebellum (predominantly flocculus/paraflocculus) or the cervicomedullary/craniocervical junction. Combined with the severely degraded smooth pursuit and reduced OKN, this clinical picture points toward a cerebellar or central oculomotor pathway process.
Recommendations
- MRI Brain with contrast including posterior fossa protocol - to evaluate the cerebellum (flocculus, nodulus, vermis), brainstem, and cervicomedullary junction for structural lesions, demyelination, or atrophy.
- Neurological/neuro-otological consultation - given the central oculomotor pattern.
- Bithermal caloric testing (if not previously performed) - to formally assess horizontal semicircular canal function and determine if a peripheral component is superimposed.
- Consider rotary chair testing - for a more complete assessment of the VOR.
- Medication review - exclude drug-induced downbeat nystagmus (lithium, carbamazepine, phenytoin, alcohol, amiodarone).
- Serum electrolytes and B1 (thiamine) - to exclude metabolic causes.
Report prepared based on Cranio-Oculography (Extended VNG) data recorded on 18-Jun-2026. Interpretation based on established normative values: saccade velocity >275 °/s, latency <260 ms, accuracy 80-134%; smooth pursuit gain 0.9-1.0; OKN gain 0.52-1.15 (StatPearls - VNG/ENG Testing, NCBI; K.J. Lee's Essential Otolaryngology; Normal VNG Values - PMC 2024).
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