VNG Report Interpretation — Munni Devi, 73F (ID: CCDA00272) | 20 May 2026

Summary of Findings

Overall impression: Significant oculomotor dysfunction consistent with a central (cerebellar/brainstem) vestibular lesion, with no evidence of peripheral vestibular weakness or BPPV.

1. Saccades — Abnormal

2. Smooth Pursuit — Markedly Abnormal

3. Optokinetic (OKN) Testing — Mildly Abnormal

4. Spontaneous Nystagmus (Light & Dark) — Absent

5. Gaze Testing — No Gaze-Evoked Nystagmus

6. Head-Shake Test & Hyperventilation — No Post-Shake Nystagmus

7. Positional Testing (Dix-Hallpike & McClure-Pagnini) — No Positional Nystagmus

8. Subjective Visual Vertical (SVV) — Within Normal Limits

Clinical Interpretation & Recommendations

Pattern Recognition:

Conclusion:

• Severely impaired smooth pursuit (gain 0.04–0.22, all directions)
• Markedly prolonged saccade latency (342–608 ms)
• Reduced saccade precision

1. Cerebellar atrophy / degenerative cerebellar disease (most likely given bilateral symmetric smooth pursuit failure)
2. Small vessel cerebrovascular disease affecting brainstem/cerebellar white matter
3. Medication effect (sedatives, anticonvulsants, antihypertensives — should be reviewed)
4. Less likely: cerebellar neoplasm, paraneoplastic cerebellar degeneration, MSA-C

Recommended Next Steps:

• MRI brain with cerebellum/posterior fossa protocol (with and without contrast) — to look for cerebellar/brainstem atrophy, infarcts, or mass lesions
• Review medications for CNS-sedating agents (benzodiazepines, carbamazepine, phenytoin, gabapentin, etc.)
• Neurological consultation (movement disorder / cerebellar subspecialty)
• Caloric testing (bithermal) was not included in this report — if dizziness is ongoing, caloric irrigation should be performed to evaluate peripheral labyrinthine function directly
• Consider vestibular rehabilitation referral regardless of etiology for functional improvement

• All nystagmus parameters: dashed (absent)

• All nystagmus parameters: dashed (absent)

• All nystagmus parameters: dashed (absent)

Regarding "Supine to Sit" in the Left DHT Sequence

Clinical Significance

• In posterior canal BPPV (pc-BPPV), the return to sitting from the Hallpike position typically produces a brief reversal nystagmus (opposite direction to the provoked nystagmus) as the displaced otoconia shift back toward the ampulla
• Its presence would confirm canalith-dependent geotropic/apogeotropic mechanics
• Its absence, as seen here, is consistent with:
  • No posterior canal BPPV on the left (supports the earlier conclusion)
  • A cupulolith mechanism (less mobile debris — though usually still produces some reversal)
  • Central positional nystagmus (which typically does not fatigue or reverse)
  • Adequate compensation / no active canalith displacement

Bottom Line

Central Causes of Positional Dizziness

How Central Lesions Produce Position-Dependent Symptoms

Specific Central Mechanisms Causing Positional Dizziness

• The nodulus and uvula of the cerebellum are the primary central processors of otolith-canal integration
• Lesions here produce central positional nystagmus (CPN) — which can mimic BPPV in timing and provocation but differs in character (direction-changing, non-fatiguing, persistent, vertical/torsional without clear canal plane alignment)
• Importantly, CPN from nodular lesions is often direction-changing with head position

• As the cerebellum degenerates, its ability to suppress and modulate vestibulo-ocular reflex (VOR) signals during position changes is lost
• The patient experiences dizziness with any head movement — turning in bed, bending forward, looking up — because the cerebellum can no longer dampen the vestibular mismatch signal
• This is not BPPV, but the patient's subjective experience of positional triggering is identical
• VNG in these patients often shows: abnormal smooth pursuit + prolonged saccade latency (exactly as in this case) but negative DHT/positional nystagmus — because the problem is in gain modulation, not canalith displacement

• Lesions of the medial vestibular nucleus, nucleus prepositus hypoglossi, or paramedian tract neurons disrupt the neural integrator
• This produces gaze-evoked nystagmus and position-dependent instability
• Small vessel ischemic disease in the brainstem is common in elderly patients with vascular risk factors

• The velocity storage mechanism (mediated by the vestibular commissure and nodulus) prolongs and modulates VOR responses
• Central dysfunction here causes abnormal decay of vestibular signals — patients feel prolonged dizziness after positional changes even without nystagmus being recordable

Why This Patient's VNG Fits This Pattern

A patient with central oculomotor disease can complain of positional dizziness and have a negative DHT — not because BPPV was missed, but because the central system can no longer handle the vestibular demands of position change.

How to Distinguish Central Positional Dizziness from BPPV

Clinical Recommendation for This Patient

1. Do not treat empirically with Epley — there is no canalith to reposition
2. MRI posterior fossa is mandatory to characterize the central lesion
3. Cerebellar-specific vestibular rehabilitation (gaze stabilization exercises, balance retraining) can reduce positional dizziness by enhancing compensatory mechanisms
4. Address vascular risk factors if small vessel disease is found on imaging
5. Review all medications — especially in a 73-year-old, polypharmacy is a common contributor to cerebellar/central vestibular dysfunction

Recent Research: Cerebellar Dysfunction → Oculomotor Abnormalities

1. Oculomotor Endpoints as the Most Sensitive Biomarker of Cerebellar Disease

• Quantitative oculomotor assessment is the most sensitive and reliable method to capture disease severity and progression in cerebellar disease — more sensitive than clinical scales
• The specific parameters that best discriminate cerebellar patients from controls and correlate with disease severity are: smooth pursuit gain, saccade velocity, saccade accuracy, and VOR gain — precisely the measures that are severely abnormal in your patient
• The working group recommends harmonized VNG/eye-tracking protocols as primary endpoints for future trials — underlining that oculomotor dysfunction is the cardinal measurable feature of cerebellar degeneration
• Relevance to your patient: The profoundly reduced smooth pursuit gains (0.04–0.22) and prolonged saccade latencies seen in Munni Devi fall squarely within the oculomotor fingerprint of cerebellar degeneration described across all studied ataxia subtypes

2. Central Positional Nystagmus: Cerebellar Origin

• Central positional nystagmus (CPN) accounts for up to 12% of all patients presenting with positional nystagmus — a significant proportion that is frequently misdiagnosed as BPPV
• CPN is most commonly caused by cerebellar/brainstem structural lesions (stroke, tumour, demyelination) or diffuse degenerative involvement (cerebellar atrophy, paraneoplastic, autoimmune)
• Pathomechanism: Abnormal integration of semicircular canal signals by the cerebellar nodulus, uvula and tonsil, producing an erroneous estimation of head tilt — the patient experiences positional dizziness without any displaced otoconia
• CPN is almost always associated with other cerebellar oculomotor signs (impaired pursuit, dysmetric saccades) — which is exactly the pattern in this VNG
• Crucially: CPN does not respond to Epley or liberatory manoeuvres — treating it as BPPV will fail
• Pharmacotherapy with 4-aminopyridine (4-AP) is the current recommended symptomatic treatment

3. Positional Downbeat Nystagmus: Cerebellar Differential Diagnosis

• Positional downbeat nystagmus (pDBN) is a common finding in dizzy elderly patients, with etiologies spanning from BPPV variants to central vestibular lesions
• The vestibulocerebellum (nodulus and uvula) is the most commonly implicated structure in central pDBN — lesion models confirm that nodular dysfunction removes the inhibitory control over otolith-canal integration, producing position-triggered symptoms
• Central causes include: vascular events, tumours, immune-mediated, toxicity, demyelinating disease — but also degenerative cerebellar atrophy, which is the most common cause in elderly patients
• Important clinical warning: Clinicians should remain vigilant for central vestibular dysfunction in cases of apparently refractory BPPV — if Epley fails repeatedly, a central cause must be reconsidered
• Posterior fossa MRI is mandatory when central positional dizziness is suspected

4. Cerebellar Oculomotor Signs as Diagnostic Discriminators

• In late-onset cerebellar ataxia (the category most relevant to a 73-year-old), cerebellar oculomotor signs — impaired smooth pursuit, saccade dysmetria, gaze-evoked nystagmus — were among the top 3 clinical features that most reliably discriminate different etiological subtypes
• SCA27B (spinocerebellar ataxia 27B, caused by FGF14 GAA expansion) is now recognised as the most common genetic late-onset cerebellar ataxia — it presents with episodic dizziness, cerebellar oculomotor signs, and ataxia, often in patients aged 60–80
• The study obtained an AUC of 0.87 using only three clinical features — episodic symptoms, cerebellar oculomotor signs, and dysdiadochokinesia — to classify patients, reinforcing that VNG oculomotor findings carry major diagnostic weight
• MSA-C (cerebellar multiple system atrophy) must also be considered; it is distinguished from pure cerebellar atrophy by the presence of autonomic features and the "hot cross bun" sign on brainstem MRI

5. VR-Based Oculomotor Analysis Correlated to Regional Brain Atrophy

• In 100 MSA patients, smooth pursuit and voluntary saccade dysfunction were the most discriminating oculomotor findings, separating MSA patients from healthy controls with high accuracy
• Eye movement abnormalities directly correlated with the degree of cerebellar and frontal lobe atrophy on volumetric MRI — the worse the atrophy, the worse the oculomotor parameters
• VR-based eye tracking is proposed as a portable, objective biomarker for cerebellar atrophy severity — the same parameters your patient's VNG is already measuring

6. Treatment: 4-AP + Physical Therapy for Cerebellar Oculomotor Disease

• A 70-year-old man with downbeat nystagmus syndrome (cerebellar basis) showed clinically meaningful improvements in gait, balance, and fall frequency with combined 4-aminopyridine pharmacotherapy + vestibular physical therapy over 6 months
• 4-AP (a potassium channel blocker) improves Purkinje cell firing regularity, thereby restoring some cerebellar inhibitory control over eye movements
• The authors call for controlled trials combining pharmacotherapy + physiotherapy, as neither alone appears optimal
• Direct relevance: This treatment combination should be considered for your patient if cerebellar atrophy is confirmed on MRI

Clinical Takeaway for This Patient