Pontine infarction and secondary Wallerian degeneration of the middle cerebellar peduncles
Presentation
Patient presented with features of "locked-in syndrome". He had recently been binge-drinking.
Patient Data
CT scan reveals a hypodensity of the ventral and central portions of the pons. This is suggestive of a brainstem (pontine) infarct most commonly caused by thrombosis of the basilar artery.
CT 4 days later
This has become more obvious on the CT scan done four days after the patient was admitted.
MRI done 3 wk after initial CT
Increased T2- signal is evident in the ventral and central portions of the pons. These areas also demonstrate rim- enhancement post-contrast as well as restricted diffusion on DWI and ADC. These characteristics are suggestive of an acute pontine infarct.
There is also increased T2- signal evident in the middle cerebellar peduncles and these areas also demonstrate restricted diffusion.
A small caliber basilar artery-tip flow void is evident on the T2- axial sequence and there is absence of a basilar artery flow- void at the level of the cerebellopontine angles. There is also absence of a right vertebral artery flow void.
There are no bleeds and only a small ovoid area of "blooming" is evident in the right parietal lobe at the grey/white matter interface which is not seen on the CTs.
CTA done 4 wk after initial CT
CT angiography confirms a cut-off of the basilar artery due to thrombosis. It also confirms that the thrombus extends to involve the distal aspect of the right vertebral artery.
Case Discussion
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.
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