Brainstem Lesion
Selective prolongation of central conduction with preserved peripheral input. MS and focal infarcts share a pattern but differ in tempo, laterality, and demographics.
Pattern
A central brainstem lesion that slows axonal or synaptic transmission produces selective IPL prolongation. Wave I and wave III may be preserved while wave V is delayed; IPL I–V is prolonged because of the central component1. The subdivision into IPL I–III (eighth nerve to lower pons) vs IPL III–V (lower pons to lateral lemniscus) localises further.Trainee
Multiple sclerosis
Bilateral and broadly symmetric IPL III–V prolongation with preserved I–III is the textbook MS pattern, reflecting demyelinating plaques in the lateral lemniscus2. The tempo is subacute; the demographics are young to middle-aged adults; concurrent or remote optic neuritis is common. ABR is one evoked-potential modality alongside visual and somatosensory evoked potentials, and complements rather than replaces MRI with gadolinium.
Pontomesencephalic infarct Clinician
Focal brainstem infarcts produce a unilateral pattern of similar magnitude — the affected side delayed, the other side normal. The clinical picture is acute, in older patients with vascular risk factors, often with concurrent cerebellar or cranial-nerve findings. The ABR pattern alone cannot make the MS-vs-infarct distinction; laterality, age, and tempo do.
Other central conduction failures
Leukodystrophies (adrenoleukodystrophy, metachromatic leukodystrophy), demyelinating variants in children, and post- radiation changes can all produce similar patterns. The ABR signal in each is "central conduction slowed, periphery intact"; the differential is clinical and radiological.
Stressing the response
High-rate stimulation (50–90/s) prolongs IPLs in normals slightly but disproportionately in early demyelinating disease. Rate stressing can unmask subclinical disease, though it has been largely supplanted by MRI in modern practice.