Wallerian degeneration is the process of antegrade degeneration of the axons and their accompanying myelin sheaths following proximal axonal or neuronal cell body lesions. It may result following neuronal loss due to cerebral infarction, trauma, necrosis, focal demyelination, or hemorrhage.
In cases of cerebral infarction, Wallerian degeneration appears in the chronic phase (>30 days).
It is usually classified into four stages:
- degeneration of the axons and myelin sheaths with mild chemical changes (0-4 weeks)
- rapid destruction of myelin protein fragments that were already degenerated, lipids remain intact (4-14 weeks)
- gliosis replaces the degenerated axons and myelin sheaths, myelin lipid breakdown (>14 weeks)
- atrophy of the white matter tracts (months to years)
CT is not as sensitive as MRI, and Wallerian degeneration is generally observed only in its chronic stage. It is seen as a contiguous tract of gliosis leading from a region of cortical or subcortical neuronal injury towards the deep cerebral structures, along the expected topographical course of the involved white matter tract.
Corresponding stages have been described on MRI.
- no changes
- T1 hyperintense
- T1 hypointense
- brainstem atrophy with or without hypointensity
- no changes
- T2 hypointense
- T2 hyperintense
- brainstem atrophy
History and etymology
It is named after the English neurophysiologist Augustis Volney Waller (1816-1870), who described the process in 1850 6.
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- 6. Waller A. "Experiments on the section of the glossopharyngeal and hypoglossal nerves of the frog, and observations of the alterations produced thereby in the structure of their primitive fibres." Philos. Trans. R. Soc. London 1850, 140:423–29
- 7. Musson R, Romanowski C. Restricted diffusion in Wallerian degeneration of the middle cerebellar peduncles following pontine infarction. (2010) Polish journal of radiology. 75 (4): 38-43