Occurs as a result of shearing forces at the moment of injry and cause particular damage of the axons of neurons at the junction between grey and white matter (differing density causes fragility). DAI can often be very serious and cause coma, vegetative states and death. It is characterised by an initial accumulation of beta-amyloid-precursor protein (beta-APP) in the first 2-4hrs, followed by axonal varicosity, swelling glial reaction and neuronal degeneration which could manifest over months-years. It can be graded as follows
- Axonal injury mainly in parasagittal white matter of the cerebral hemispheres
- Plus lesions in the corpus callosum
- Plus a focal lesion in the cerebral peducle
Molecular mechanisms
In a normal brain, sodium channels are distributed nodally to maximise the conduction of the action potential. In injured brain, these nodes are redistributed to partially restore conduction.
Unfortunately, in injured brain, there is also blockade of some of the sodium channels, further impairing reduction.
There are also a number of factors that increase the demand on mitochondria. This eventually leads to an influx of Calcium which causes damage to the cell and cell death.
Notes on Medicine/Surgery 