VNG Interpretation Report - Kamal Sachdeva

SECTION 1 - SACCADE TEST

Norms for reference (adult, 57 years):

• Latency: 180-250 ms (upper limit ~260 ms; values >260 ms = abnormal per StatPearls/NIH)
• Velocity: >275 °/s (pathological below this)
• Precision/Accuracy: 80-134%

Horizontal Saccades (0.3 Hz & 0.45 Hz) - Data & Interpretation:

Vertical Saccades (0.3 Hz & 0.45 Hz):

• Upward latency of 330 ms bilaterally - this is significantly prolonged and is the most notable saccade abnormality in this test.
• Precision for left eye downward movements is slightly reduced, approaching the lower limit of normal.
• Prolonged vertical (especially upward) saccade latency is a central sign. It is a characteristic feature of supranuclear gaze palsy (e.g., Progressive Supranuclear Palsy - PSP) and cerebellar disorders affecting the dorsal vermis/fastigial nucleus. However, given the patient's age and overall mild changes, early central oculomotor involvement or age-related central slowing should be considered.

SECTION 2 - SMOOTH PURSUIT TRACKING

Norms: Gain = 0.9-1.0 for target velocities <20°/s; gain decreases physiologically with age and frequency. At 0.4 Hz for a 57-year-old, gain >0.6 is broadly expected; significant asymmetry >30% is abnormal.

Horizontal Pursuit:

Vertical Pursuit:

• Posterior fossa lesions (dorsal midbrain, periaqueductal gray area)
• Rostral interstitial nucleus of MLF (riMLF) dysfunction
• Dorsal midbrain syndrome (Parinaud syndrome) in its subtler forms
• Cerebellar degeneration, particularly involving the flocculus and nodulus

SECTION 3 - OPTOKINETIC TEST

SECTION 4 - GAZE TEST

• Absence of spontaneous nystagmus in light with fixation is the expected normal finding.
• Left-beating nystagmus in left gaze without fixation is a direction-appropriate gaze-evoked nystagmus (Alexander's Law compliance). This is characteristic of a left-sided peripheral vestibular lesion but can also occur with contralateral (right-sided) central lesions - the interpretation depends heavily on the caloric and positional findings. Given the overall central picture, this finding may reflect a central gaze-holding defect (e.g., neural integrator dysfunction in the nucleus prepositus hypoglossi or flocculus).

SECTION 5 - SPONTANEOUS NYSTAGMUS

• In light: No nystagmus (NORMAL - fixation suppresses peripheral vestibular nystagmus)
• In dark: Slight left-beating nystagmus observed (noted in DOCX report; waveform data shown as "-" in raw PDF tables, implying mild/borderline amplitude not automatically quantified)

• A compensating asymmetry from a prior peripheral insult (old unilateral vestibular lesion, right-sided) that is now revealing itself without fixation
• A mild central spontaneous nystagmus (especially if slow phase velocity is <3-4°/s, which cannot be confirmed from the "-" entries)

SECTION 6 - HEAD-SHAKE TEST

SECTION 7 - POSITIONAL TESTS

Head Position Test:

Supine Roll Test (McClure-Pagnini):

• Supine position (roll): Leftward beats observed in supine third position
• Sit upright: Rightward beats observed

• In geotropic variant (cupulolithiasis or canalolithiasis): leftward roll provokes geotropic (toward-the-ground) nystagmus on the involved side
• Leftward beats in supine + rightward beats on sitting upright is consistent with a pattern of horizontal (lateral) canal BPPV. The direction reversal on sitting up is typical of canalolithiasis of the horizontal canal.
• The involved side determination requires knowing which roll position (left-roll vs. right-roll) was more intense, which is not fully quantified from the raw data. The overall pattern suggests involvement of the left horizontal semicircular canal (leftward beats in supine suggest the otoconia are generating a larger response toward the left).

Dix-Hallpike Tests:

• Slight left-beating nystagmus in "sit head right" position
• No reported dizziness

• Slight left-beating nystagmus in "supine head extension and left" position
• No reported dizziness

• Normal posterior canal BPPV would produce: upbeat-torsional nystagmus (beating toward the undermost ear) with latency of 1-5 seconds, duration <60 seconds, and associated intense vertigo. This is NOT what is found here.
• The absence of subjective dizziness and presence of horizontal left-beating (not torsional-upbeat) nystagmus bilaterally during both Dix-Hallpike maneuvers is atypical for classic posterior canal BPPV.
• Horizontal nystagmus without vertigo during Dix-Hallpike is a recognized finding in:
  • Central positional nystagmus (posterior fossa lesion - vermis, flocculus, nodulus)
  • Light cupula variant of horizontal canal BPPV
  • Cervical origin (cervicogenic vertigo)
• The lack of fatigability (both sides showing similar nystagmus) further supports a central mechanism.

SECTION 8 - SUBJECTIVE TESTS (from DOCX report)

CORRECTED OVERALL INTERPRETATION

Summary of Abnormal Findings:

DIFFERENTIAL DIAGNOSIS

PRIMARY (Most Likely): Central Vestibulopathy

• Flocculus/paraflocculus dysfunction: causes pursuit impairment, gaze-holding nystagmus, fixation suppression failure
• Nodulus/uvula dysfunction: causes positional nystagmus of central type, atypical BPPV-like positional nystagmus
• Dorsal vermis: saccade dysmetria and pursuit degradation
• Specific diagnoses to exclude: posterior circulation TIA/ischemia (PICA, AICA territory), cerebellar degeneration, multiple sclerosis, posterior fossa tumor

• Upward pursuit and upward OKN reduction with preservation of downward components is a hallmark of dorsal midbrain dysfunction
• Diagnoses: Parinaud syndrome (dorsal midbrain syndrome), midbrain infarction, pineal region lesion, MS plaque

• Horizontal gaze asymmetry (rightward pursuit deficit) can arise from right pontine PPRF involvement
• Diagnoses: Pontine glioma, infarct, demyelination

SECONDARY (Coexisting): Peripheral Component

• Positive Unterberger's test rotating left (right-sided weakness)
• Left-beating spontaneous nystagmus in dark (slow phase toward right)
• Absent head-shake nystagmus suggests this is a compensated/chronic lesion
• Diagnoses: Old right vestibular neuritis, right labyrinthine hydrops (Meniere's disease), right labyrinthine ischemia

• McClure-Pagnini test pattern (leftward beats supine, rightward beats sitting) consistent with left horizontal canal BPPV (canalolithiasis)
• However, this may be a component of or confused with central positional nystagmus given the overall central picture

LESS LIKELY (to exclude):

• Symptoms provoked by head turning, history consistent
• However, VNG findings of pursuit and saccade abnormalities would not be explained by cervicogenic cause alone; cervicogenic does not produce central oculomotor signs

• Certain antihypertensives (calcium channel blockers, beta-blockers) can mildly reduce pursuit gain
• Hypothyroidism (if undertreated) can cause vestibular symptoms
• These would not fully explain the bilateral severe pursuit asymmetry or vertical latency prolongation

RECOMMENDATIONS (Corrected Report):

1. MRI Brain with contrast - posterior fossa protocol (FLAIR + DWI + T2 + gadolinium enhancement) to exclude cerebellar/brainstem infarct, demyelination, tumor, or degeneration - HIGH PRIORITY given central signs on VNG
2. Neurology/Neuro-otology referral for evaluation of central oculomotor abnormalities - rule out PSP, cerebellar degeneration, multiple sclerosis
3. Thyroid function tests (TSH, FT4) - ensure euthyroid state; hypothyroidism can worsen vestibular function
4. Medication review - check if antihypertensive class could be contributing to pursuit degradation
5. Canalith Repositioning for horizontal canal: If horizontal canal BPPV is confirmed clinically, Barbecue Roll maneuver (Lempert 360°) or Gufoni maneuver toward the left
6. Vestibular Rehabilitation - customized program focusing on gaze stabilization exercises (VOR adaptation), dynamic balance training; habituation exercises alone may be insufficient given the central component
7. Follow-up VNG in 3-6 months after neuroimaging and treatment

CORRECTED IMPRESSION:

Mixed Vestibulopathy - Central Predominant

VNG demonstrates multiple central oculomotor abnormalities: severely reduced smooth pursuit in both horizontal (rightward predominant) and vertical (upward predominant) planes with marked gain asymmetry, mildly prolonged saccade latency predominantly for vertical upward and leftward horizontal directions, reduced vertical optokinetic gain (upward), and atypical positional nystagmus (horizontal, bilateral, without subjective dizziness) on Dix-Hallpike. These collectively indicate central vestibular pathway dysfunction, most likely involving the cerebellum (flocculus-nodulus complex) and/or dorsal brainstem (midbrain-pontine junction).

A coexisting right peripheral vestibular hypofunction (likely chronic/compensated) is supported by Unterberger's test deviation and left-beating spontaneous dark nystagmus. A horizontal canal BPPV component (left side) is suggested by McClure-Pagnini findings.

MRI brain (posterior fossa protocol) is urgently recommended before attributing these findings to a benign peripheral cause.

• Cummings Otolaryngology Head and Neck Surgery, Quantitative Testing section (VNG/ENG methodology and norms)
• VNG/ENG Testing - StatPearls (NIH) - saccade/pursuit normal ranges
• Recording and interpretation of ocular movements (ACN 2023) - saccade latency norms, vertical pursuit