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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.
It is usually classified into four stages 2,3:
stage 1 (0-4 weeks): degeneration of the axons and myelin sheaths with mild chemical changes
stage 2 (4-14 weeks): rapid destruction of myelin protein fragments that were already degenerated, lipids remain intact
stage 3 (>14 weeks): gliosis replaces the degenerated axons and myelin sheaths, myelin lipid breakdown
stage 4 (months to years): atrophy of the white matter tracts
The distribution of Wallerian degeneration depends on the region of injury and how it relates to white matter tracts that originate there. The most commonly observed pattern is an injury to the precentral gyrus (such as may be seen in an MCA infarct) with resultant degeneration of the corticospinal tracts.
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 2,3.
stage 1: no changes
stage 2: T1 hyperintense
stage 3: T1 hypointense
stage 4: brainstem atrophy with or without hypointensity
stage 1: no changes
stage 2: T2 hypointense
stage 3: T2 hyperintense
stage 4: brainstem atrophy
DWI: high signal on DWI and low signal on ADC have been demonstrated along the affected white matter tracts, from the first days after insult until 8 months after 7.
History and etymology
It is named after the English neurophysiologist Augustis Volney Waller (1816-1870), who described the process in 1850 6.