Our differential diagnosis included central pontine myelinolysis (CPM) because of the patient's recent alcoholic binge. There was no history of rapid correction of the patient's serum sodium. CPM can also result in Wallerian degeneration of the middle cerebellar peduncles. The CT angio therefore allowed us to confirm the diagnosis of an infarct.

The middle cerebellar peduncle carries afferent fibers from the contralateral pons to the cerebellar cortex, therefore these middle cerebellar peduncular lesions are regarded as Wallerian degeneration. This secondary degeneration should not be misinterpreted as a newly developed infarction or other diseases.

Diffusion tensor imaging may also help to diagnose Wallerian degeneration.

Wallerian degeneration develops through different stages:

1st stage: No signal intensity abnormalities are recognisable and is characterized by physical disintegration of the axons and myelin sheaths with little chemical changes.

2nd stage: from 20 days to 2-4 months after the stroke, is characterized by hypointense T2-signal and the tissue becomes more hydrophobic because of myelin-protein breakdown.

3rd stage: Myelin lipid breakdown, gliosis and changes in water content. Tissue becomes hydrophillic and there is hyperintense signal on T2WI and FLAIR and hypointense signal on T1WI.

4th stage: after several years, characterized by volume loss from atrophy.

There may be great variability in the temporal relationships between the imaging findings and the stages of wallerian degeneration but our case more or less fits in with stage 2.