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VNG Diagnostic Report — Nishi Kathuria

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I. TEST-BY-TEST DATA SUMMARY

A. Saccades

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B. Smooth Pursuit

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C. Optokinetic Test (OKN)

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D. Spontaneous Nystagmus

• No spontaneous nystagmus in light (normal).
• Spontaneous nystagmus in darkness: A low-amplitude, predominantly downward-oblique nystagmus (fast phase at ~67–68°, predominantly upward-vertical component). The horizontal component is minimal (2.25 °/s in the left eye only). The dominant vertical slow-phase velocity is −5 °/s bilaterally — present only in darkness (disappears with visual fixation).

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E. Head-Shake Nystagmus (High-Frequency)

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F. Hyperventilation-Induced Nystagmus

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G. Gaze Tests

1. All gaze positions with fixation: normal — no gaze-evoked nystagmus.
2. Without fixation (eyes open in dark): Nystagmus is revealed in all gaze positions with a predominantly downward slow-phase velocity (fast phase upward-oblique, ~50–140°). The nystagmus is consistently suppressed by visual fixation, indicating good central fixation suppression mechanism is partly intact.
3. Horizontal components emerge in left and down gaze without fixation, suggesting a slightly oblique (downbeat + horizontal) vector rather than pure downbeat. This could represent a down-beating + torsional component typical of posterior canal/floccular pathology.

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H. Positional Tests — Dix-Hallpike (DH)

DH Right

DH Left

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I. Yacovino Maneuver (Central Positional Test for Anterior Canal / Cupulolithiasis)

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J. McClure-Pagnini Test (Horizontal Canal BPPV)

• Nystagmus is present in all positions of the roll test, including the neutral supine head position (which should be absent or minimal in peripheral HC-BPPV).
• Left lateral roll produces the most intense response: H SPV −30–35 °/s, V SPV −43 °/s, frequency 2.55 Hz — extremely vigorous.
• The fast phase directions are consistently ~120–140° across all positions (oblique upward-left/torsional fast phases) — this is a non-direction-changing pattern relative to head position, which is atypical for horizontal canal BPPV (which should produce direction-changing geotropic or direction-fixed apogeotropic nystagmus that reverses with head roll to the opposite side).
• The persistence in neutral supine and the consistent fast phase direction regardless of roll direction is more consistent with central persistent positional nystagmus.

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K. Subjective Visual Vertical (SVV)

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II. INTEGRATED DIAGNOSTIC INTERPRETATION

Pattern Recognition

1. Persistent downbeat-predominant nystagmus — present in darkness, without fixation, in all gaze positions, in supine, and provoked in all positional maneuvers. Suppressed (but not abolished) by fixation.
2. Positional nystagmus present in ALL positions of ALL maneuvers — including positions that should be null/resting (supine neutral, sitting upright) — indicating the nystagmus is gravity-dependent and persistent, not paroxysmal.
3. Non-fatiguing, non-fatigable pattern — BPPV characteristically produces fatigable, short-lived paroxysmal nystagmus (<1 min). Here, nystagmus is present across extended recordings.
4. Extremely high SPV during left Dix-Hallpike supine (V SPV up to −47 °/s) and left lateral roll (H SPV −35 °/s, V SPV −43 °/s) — amplitudes this high in a 61-year-old woman are unusual for uncomplicated peripheral BPPV.
5. Smooth pursuit: diffusely impaired bilaterally — central pattern.
6. Saccades: normal — brainstem saccadic generator intact.
7. OKN: normal and symmetric — no hemispheric lesion.
8. Head-shake nystagmus: vertical (downbeat), no horizontal — no asymmetric peripheral loss.
9. SVV deviated left — left utricular involvement.
10. Hyperventilation-induced nystagmus (downbeat) — raises concern for demyelinating or compressive posterior fossa pathology.

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III. DIAGNOSIS

Primary Diagnosis:

Most consistent with dysfunction of the cerebellar flocculus/nodulus or anterior canal/posterior fossa pathology, producing gravity-dependent persistent downbeat nystagmus that is not position-specific, is present in supine and all provocative positions, is not fatigable, and is accompanied by diffuse smooth pursuit impairment.

Secondary / Co-existing Finding:

The left Dix-Hallpike provoked the highest-amplitude positional nystagmus in the study. While the background persistent downbeat nystagmus complicates interpretation, the directionality and peak amplitude during left DH supine (fast phase 110–121°, upbeat-torsional) is consistent with a concurrent left posterior semicircular canal canalithiasis component, superimposed on the central baseline nystagmus.

Supporting Diagnosis:

Based on SVV deviation of up to −6° leftward on anti-clockwise trial, indicating left utricular/saccular otolithic imbalance.

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IV. DIFFERENTIAL DIAGNOSES TO EXCLUDE

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V. CRITICAL RECOMMENDATIONS

1. MRI Brain with contrast (including high-resolution posterior fossa protocol, CISS/FIESTA sequences for IAC): To exclude cerebellar/brainstem lesion, Arnold-Chiari malformation, MS plaques, or posterior fossa tumor. This is the highest priority investigation given the persistent downbeat nystagmus pattern.
2. Neurology / Neuro-otology referral: Persistent downbeat nystagmus with smooth pursuit impairment requires formal neurological evaluation.
3. Left Epley Maneuver: If the co-existing left posterior canal BPPV component is confirmed clinically (onset latency, fatigability on repeat DH), a left Epley canalith repositioning maneuver can be attempted. However, clinician should be aware the baseline downbeat nystagmus will complicate assessment of success.
4. Medication review: Check for aminoglycosides, anticonvulsants (phenytoin, carbamazepine), lithium, alcohol, or benzodiazepines — all known causes of cerebellar downbeat nystagmus.
5. Serum B12, folate, magnesium, thiamine: Metabolic screen for reversible causes of cerebellar nystagmus.
6. 4-Aminopyridine (4-AP) consideration: Evidence supports 4-AP (fampridine) as a pharmacotherapy for downbeat nystagmus of cerebellar origin — neurologist should assess.

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VI. REPORT SUMMARY TABLE

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