Traumatic axonal injury – an update

Diffuse axonal injury (DAI) was originally described in patients with diffuse brain injury and coma without a mass lesion and damage to axons in the cerebral hemispheres, corpus callosum, brainstem and cerebellum. Silver stains demonstrated the axonal changes in the white matter in fatal head injuries that occurred at least 12 hours prior to death. DAI also occurred in vegetative or severely disabled patients. Three grades of DAI as determined by macroscopic and microscopic brain examination correlated with axonal changes and diffuse brain injury ranging from concussive syndromes to severe traumatic brain injury. Axonal damage could be identified in patients who did not conform to the concept of DAI. β-amyloid precursor protein is an early marker for axonal injury and the frequency of axonal damage had been underestimated using conventional silver stains. Axonal injury is now a non-specific term referring to axonal damage of any aetiology. Non-traumatic axonal damage occurs in infectious, demyelinating, metabolic and vascular conditions. Traumatic axonal injury (TAI) is damage to axons caused by trauma. In 2003, clincopathological categories were proposed for β-amyloid precursor protein staining patterns: 1 multifocal (mTAI), diffuse traumatic (dTAI), vascular (VAI), penumbra (PAI) and metabolic axonal injury (MAI). β-amyloid precursor protein immunohistochemistry has improved the understanding of axonal injury.