Table 3.
Pharmacotherapy of acute spinal cord injury and mechanism(s) of action
| Methylprednisolone |
| Inhibition of lipid peroxidation/antioxidative/anti-inflammatory |
| Properties decrease ischemia, support energy metabolism, inhibit neurofilament degradation, decrease intracellular Ca, decrease PG F/ TxA, increase spinal neuron excitability, decrease cord edema |
| Ganglioside GM-1 |
| Stimulate neurite regrowth/regeneration |
| Opioid receptor antagonists |
| Antagonize the increase in endogenous opioid levels after SCI (opioid receptor activation can contribute to excitotoxicity) |
| TRH and its analogs |
| Antagonize endogenous opioids, platelet-activating factor, peptido- leukotrienes and excitatory amino acids |
| Nimodipine |
| Decrease intracellular Ca2+ accumulation, attenuate vasospasm |
| Gacyclidine (GK11) |
| Antagonism of glutamate receptors |
| Magnesium |
| Replace Mg2+ depletion that is common after SCI, diminish intracellular Ca2+ accumulation, block N-methyl-D-aspartate receptor ion channel, modulate binding of endogenous opioids |
| Hypothermia |
| Reduce extracellular glutamate, vasogenic edema, apoptosis, neutrophil and macrophage invasion and activation, and oxidative stress |
| Minocycline |
| Inhibition of microglial activation, inhibition of cytochrome c release |
| Erythropoietin |
| Reduced apoptosis and lipid peroxidation |
| Estrogen |
| Not clearly known |
| Progesterone |
| Reduce the production of inflammatory cytokines |
| Cyclooxygenase inhibitors |
| Prevents/antagonizes decreased blood flow/platelet aggregation from production of arachidonic acid metabolites |
| Riluzole |
| Blockade of voltage-sensitive sodium channels and antagonism of presynaptic calcium-dependent glutamate release |
| Atorvastatin |
| Prevents neuronal and oligodendrocytic apoptosis |
| Antioxidants |
| Antagonize deleterious effects of free radicals (lipid eroxidation, reperfusion injury, etc.) |
PG F: Prostaglandin F; SCI: Spinal cord injury.