VNG Report Analysis — Mr. P N Sharma, 88M (Patient ID CCDA00426, dated 18‑Aug‑2026)

1. Ocular Motor Battery

2. Gaze Testing

• With visual fixation (center/left/right/up/down): No nystagmus in any position — normal.
• Without fixation:
  • Center: negligible vertical drift (1.6°/s) — not significant.
  • Left gaze: low-velocity horizontal nystagmus (~5.3–6.0°/s) with amplitude ~5°.
  • Up gaze: low-velocity vertical component (~4.2–5.4°/s).
  • Right and down gaze: no significant findings.

3. Positional Testing (BPPV battery)

• Dix-Hallpike Right: In the provoking (head-hanging right) position, low-to-moderate mixed horizontal-vertical nystagmus (~5°/s horizontal, ~6–6.5°/s vertical, ~1.5 Hz).
• Dix-Hallpike Left: In the provoking (head-hanging left) position, a purely vertical nystagmus of moderate velocity (10–12°/s, ~1.1 Hz) with no horizontal component recorded.
• Supine roll test (McClure-Pagnini): Low-grade nystagmus (3.4–4.7°/s) on both right and left lateral head turns.

4. Subjective Visual Vertical (Otolith/Utricular Function)

5. Notable Gap: No Caloric Test

6. Putting It Together in the Context of Recent Spine Surgery

1. Reduced smooth pursuit gain and poor saccadic accuracy — very commonly seen with residual anesthetic/analgesic agents (opioids, benzodiazepines, muscle relaxants), post-op fatigue/deconditioning, and simply advanced age (88 years). This pattern is non-focal and symmetric, which argues against an acute central lesion.
2. New/mild positional nystagmus (left Dix-Hallpike vertical component, mild roll-test findings) — BPPV is a well-recognized complication of surgery involving prolonged supine/prone positioning and head manipulation during intubation, because otoconia can become displaced from the utricle into a semicircular canal during positioning. Post-surgical BPPV (including after spine surgery) is a described entity and is the most likely single explanation if the patient is reporting positional vertigo since surgery.
3. Normal SVV, no spontaneous nystagmus, largely normal OKN — argue against an acute unilateral peripheral vestibular loss or significant central/brainstem process.
4. A less likely but important differential in an 88-year-old with recent major surgery and new dizziness is a perioperative posterior-circulation event (vertebrobasilar TIA/stroke), especially if prone positioning was prolonged. This VNG alone does not support that (no spontaneous or gaze-evoked nystagmus, symmetric OKN), but it should be actively excluded clinically if there are any additional neurological symptoms (diplopia, dysarthria, limb weakness, ataxia disproportionate to age).

Summary Impression (my read, pending clinician correlation)

• No spontaneous or fixation-suppressible gaze-evoked nystagmus — no evidence of an acute unilateral or destructive central vestibular lesion.
• Diffusely reduced smooth pursuit gain and saccadic dysmetria — most consistent with age/medication/fatigue effects in this immediate post-surgical elderly patient; central etiology cannot be fully excluded without clinical correlation.
• Positional testing raises possible left posterior canal BPPV (vertical-only nystagmus on left Dix-Hallpike, ~10–12°/s) — torsional confirmation was not possible with this VNG system; recommend targeted direct/Frenzel-lens re-examination of the Dix-Hallpike maneuvers, and if confirmed, an Epley/canalith repositioning maneuver, adapted as needed for spine-surgery precautions (may need modified/gentle positioning given recent surgery — discuss with the spine surgeon before any repositioning maneuver).
• Otolith function (SVV) and horizontal OKN normal — argues against significant unilateral peripheral vestibular pathology.
• Caloric testing is missing — should be completed when the patient can tolerate the required positioning, to fully exclude canal paresis.

Possible Diagnoses Based on the VNG Findings + Recent Spine Surgery

1. Benign Paroxysmal Positional Vertigo (BPPV) — most likely, probably left posterior canal

• Left Dix-Hallpike (head-hanging left) produced a distinct vertical nystagmus of 10–12°/s at ~1.1 Hz — a velocity/frequency well above the low-level "noise" seen elsewhere in the exam, and it appeared specifically in the provoking position, which is the hallmark of canalithiasis.
• Right Dix-Hallpike also showed a mixed horizontal-vertical response (lower amplitude), and the supine roll test showed low-grade nystagmus bilaterally on lateral turns — so a horizontal canal component or bilateral involvement can't be excluded either.
• Standard VNG (this device included) cannot record the torsional component that is the true confirmatory sign of posterior canal BPPV - Cummings Otolaryngology Head and Neck Surgery. So this remains a probable rather than a video-confirmed diagnosis until a clinician directly observes torsional nystagmus with Frenzel lenses or direct visualization during Dix-Hallpike.
• Mechanistically, this fits the recent spine surgery perfectly. Prolonged prone positioning, forced/sustained neck positions, and abrupt head movements during intubation, extubation, and transfers are recognized precipitants of otoconial displacement into a semicircular canal. This is a described phenomenon after spinal surgery specifically (case reports exist of BPPV secondary to spinal surgery from prolonged forced head positioning) and after prone/positioned procedures generally.
• Age is also a major independent risk factor — roughly a third of people over 70 will have had BPPV at least once, and otoconia degeneration accelerates with age, further raising probability in an 88-year-old.

2. Medication/anesthesia and deconditioning effect on ocular motor control (not a distinct "diagnosis" but explains the pursuit/saccade findings)

• The globally reduced smooth pursuit gains (0.14–0.33 versus a normal >0.6) and poor saccadic accuracy (44–65% versus normal >90%) are symmetric and non-focal. This pattern is classic for sedating/analgesic medication effect (opioids, benzodiazepines, muscle relaxants commonly used perioperatively), post-operative fatigue/deconditioning, or simply normal age-related decline in an 88-year-old, rather than a new structural brain lesion. Preserved, symmetric horizontal optokinetic gains argue against a destructive brainstem/cerebellar process.

3. Physiologic end-point nystagmus (benign)

• The mild nystagmus seen only in eccentric left and up gaze without fixation, absent with fixation and absent in primary position, is the textbook description of benign end-point nystagmus rather than pathological gaze-evoked nystagmus.

4. Less likely but worth actively excluding clinically

• Central (posterior circulation) cause of vertigo — e.g., a perioperative cerebellar/brainstem TIA or small infarct. This VNG does not support it (no spontaneous nystagmus, no fixation-resistant gaze-evoked nystagmus, symmetric OKN), but in an 88-year-old with recent major surgery and any of the following, this should be pursued with neuroimaging: truncal ataxia out of proportion to dizziness, dysarthria, diplopia, limb weakness/numbness, or a normal head-impulse test with directional-changing nystagmus (HINTS "central" pattern). Central causes are less common than peripheral overall, but red flags override the VNG reassurance.
• Cervicogenic dizziness — if the spine surgery involved the cervical spine, altered proprioceptive input from the neck is a recognized contributor to dizziness in older adults and can coexist with BPPV.
• Unilateral peripheral vestibular weakness (vestibular neuritis / labyrinthine injury) — cannot be fully assessed here because caloric testing is missing from this report. Normal SVV and absent spontaneous nystagmus make this less likely, but it isn't excluded without calorics or a video head-impulse test.
• Orthostatic/cardiovascular causes of postoperative dizziness (common after major surgery, bed rest, and blood loss) — not evaluated by VNG at all and should be checked with orthostatic vitals if the presenting complaint was generalized lightheadedness rather than true rotational vertigo.

Bottom line