ABSTRACT
Additional intracellular Ca2+ may be released from the endoplasmic reticulum, due to partial damage to the cytoskeleton by the shearing forces. The rapid increase in cytosolic Ca2+ concentration is also capable of interfering with mitochondrial function, thus disturbing oxidative metabolism and leading to energy failure. An alternative way to produce ATP is by anaerobic glycolysis. Unfortunately, this pathway is far less effective than its aerobic counterpart and results in a massive accumulation of lactate and a consecutive decrease in brain pH. If the neuron is unable to produce enough ATP to maintain basal metabolism, cell death results.
