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. An increase in Ca2+ and Na+ levels and a drop in K+ levels is found within the axon directly after injury. 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. High levels of intracellular Ca2+, the major cause of post-injury cell damage, destroy mitochondria, and trigger phospholipases and proteolytic enzymes that damage Na+ channels and degrade or alter the cytoskeleton and the axoplasm. Excess Ca2+ can also lead to damage to the blood brain barrier and swelling of the brain.