This is an interesting case with the differential being essentially that of bilateral middle cerebellar peduncle T2 signal abnormality. In the context of a prior pontine infarct the main differential consideration is that of bilateral AICA infarction and Wallerian degeneration.
Overall AICA infarction is favoured for the following reasons:
- The anatomy fits - the AICAs arise from the basilar at the same level in most people so it is not unreasonable that both be occluded along with at least part of the basilar simultaneously.
- Pontine infarction is common - why do we not see this proposed "wallerian degeneration" commonly if this is indeed the aetiology? Given we see it so rarely doesn’t a rare event like AICA occlusions which match in incidence therefore make more sense?
- Wallerian degeneration must by definition be in continuity with the primary process - these lesions do not show continuity.
- Wallerian degeneration should continue along the cerebellar white matter tracts - this is clearly not the case; the lesions are focal and limited (like a vascular territory with borders might….).
Acknowledgement: Prof Stephen Stuckey