Shell Shock: An Old Injury with New Weapons

Table 1.

Novel or Experimental Interventions Targeting Traumatic Brian Injury (TBI)

Classification	Mechanism/Rationale
Cell cycle inhibitors (e.g., flavopiridol) (58, 64)	Reduces neuronal cell death, reduces astroglial scar formation, decreases lesion volume, improves experimental motor and cognitive performance
Magnesium salts (49, 52, 58)	Blocks calcium entry, potentiates adenosine action, attenuates brain edema, cerebral vasospasms, glutamate excitotoxicity, calcium-mediated events, lipid peroxidation, mitochondrial permeability transition, and apoptosis
Cyclosporin A (49, 52)	Inhibits opening of the mitochondrial permeability transition pore, attenuates post-traumatic cytoskeletal changes and axonal injury, decreases lesion volume, improves brain oxygen consumption, blocks free radical production, and inhibits traumatic axonal injury
Substance P (neurokinin 1) receptor inhibitor (52, 58)	Reduces neurogenic inflammation, blood-brain barrier permeability, edema, lesion volume
Progesterone (32, 49, 52, 58)	Modulates neuronal excitability, reduces membrane lipid peroxidation, and inhibits caspase-3 activation
Cannabinoids (49, 58)	Reduces glutamate excitotoxicity, free radical production, and inflammatory response
Cyclic dipeptides (58)	Attenuates apoptotic and necrotic cell death, reduces intracellular calcium, stabilizes mitochondrial membrane potential, and decreases cytochrome c release