Disease Patterns
Central Vestibular Disorders
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Signature on CDP
The figure below shows the archetypal Central pattern across the six SOT conditions, MCT response, and ADT adaptation, compared against an age-matched normal reference.
In this module
- Central vestibular disordersFoundation · Trainee · Clinician
- Cerebellar signs on CDPTrainee · Clinician
- Brainstem involvementTrainee · Clinician
- Differentiating central from peripheralFoundation · Trainee · Clinician
Central vestibular disorders
Central vestibular disorders include strokes affecting the brainstem or cerebellum, demyelinating disease, cerebellar degeneration, brainstem tumours, and a long tail of less common pathologies. The common thread on CDP is that they affect the long-loop pathway, the adaptive machinery, or both.
Typical CDP findings in central disease are not subtle. The pattern is usually a combination of across-the-board SOT reduction (no specific input-isolated pattern), prolonged MCT latency, and impaired ADT adaptation. Any two of these three is highly suggestive; all three is essentially diagnostic of central involvement.
What CDP doesn't do is localise the central lesion. The same triad can arise from a cerebellar haemorrhage, a brainstem demyelinating plaque, or a chronic neurodegenerative process. Imaging and the rest of the neurological exam carry the localising work.
Cerebellar signs on CDP
Cerebellar disease most often produces non-adapting ADT, sometimes with relatively preserved SOT and MCT. The ADT signature — sway energy on trial five roughly equal to trial one — reflects the cerebellum's role in motor learning.
Truncal ataxia from anterior-vermis lesions can produce broad-based SOT abnormality even on relatively easy conditions, sometimes with characteristically large mediolateral sway. Limb ataxia alone (interposed nuclei) is less likely to produce overt SOT abnormality.
Spinocerebellar degenerations follow this pattern with variable temporal evolution. SCA-3 (Machado-Joseph), SCA-6, and Friedreich ataxia all show progressive non-adapting ADT with gradually-evolving SOT abnormality; serial CDP can document the disease course objectively.
Brainstem involvement
Brainstem lesions affecting the descending vestibulospinal or reticulospinal tracts most often produce prolonged MCT latencies. The latency prolongation can be dramatic — 30–50 ms above normal in moderate-sized lesions.
Multiple sclerosis with brainstem demyelination is the most common cause of substantial MCT latency prolongation in younger patients. Lateral medullary (Wallenberg) stroke can produce striking CDP abnormalities ipsilesional to the stroke on some metrics.
Brainstem tumours producing CDP findings are usually large enough to be obvious on imaging by the time the CDP is abnormal. Subtle brainstem CDP findings without imaging correlates are uncommon and should prompt repeat imaging or a longer interval before diagnostic conclusions.
Differentiating central from peripheral
The cleanest CDP discriminator between central and peripheral causes is the combination of SOT pattern and the other two protocols. A pure C5/C6 vestibular pattern with normal MCT and normal ADT adaptation is overwhelmingly peripheral. The same SOT pattern accompanied by prolonged MCT latency and non-adapting ADT is central until proven otherwise.
A few caveats. A normal head impulse test in a patient with abnormal CDP is a useful central pattern flag — peripheral lesions producing CDP findings usually have HIT abnormalities. Conversely, a positive HIT to one side with CDP findings matches the peripheral picture.
When the picture is mixed — for example, a peripheral SOT pattern with isolated ADT non-adaptation — the safest interpretation is 'mixed central-peripheral pathology' rather than pure either, with imaging to clarify the central component.