Figure 2.

Neurometabolic cascade following traumatic injury. (1) Nonspecific depolarization and initiation of action potentials. (2) Release of excitatory neurotransmitters (EAAs). (3) Massive efflux of potassium. (4) Increased activity of membrane ionic pumps to restore homeostasis. (5) Hyperglycolysis to generate more adenosine triphosphate (ATP). (6) Lactate accumulation. (7) Calcium influx and sequestration in mitochondria leading to impaired oxidative metabolism. (8) Decreased energy (ATP) production. (9) Calpain activation and initiation of apoptosis. A, Axolemmal disruption and calcium influx. B, Neurofilament compaction via phosphorylation or sidearm cleavage. C, Microtubule disassembly and accumulation of axonally transported organelles. D, Axonal swelling and eventual axotomy. K⁺, potassium; Na⁺, sodium; Glut, glutamate; Mg²⁺, magnesium; Ca²⁺, calcium; NMDA, N-methyl-D-aspartate; AMPA, d-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid.