Calcium influx

While sometimes only the cytoskeleton is disturbed, frequently disruption of the axolemma occurs as well, causing the influx of Ca2+ into the cell and unleashing a variety of degrading processes (Povlishock and Pettus, 1996; Lopachin and Lehning, 1997). An increase in Ca2+ and Na+ levels and a drop in K+ levels is found within the axon directly after injury (Lopachin and Lehning, 1997; Wolf et al., 2001). Possible routes of Ca2+ entry include sodium channels, pores torn in the membrane during stretch, and failure of ATP-dependent transporters due to mechanical blockage or lack of energy (Wolf et al., 2001). High levels of intracellular Ca2+, the major cause of post-injury cell damage (Zhou et al., 2001), destroy mitochondria (Smith and Meaney, 2000), contribute to the generation of reactive oxygen species (Arundine et al., 2004) and trigger phospholipases and proteolytic enzymes that damage Na+ channels and degrade or alter the cytoskeleton and the axoplasm (Lopachin and Lehning, 1997; Castillo and Babson, 1998). Excess Ca2+ can also lead to damage to the blood brain barrier and swelling of the brain (Zhou et al., 2001).

Source: http://en.wikipedia.org/wiki/Diffuse_axonal_injury