Current and future medical therapeutic strategies for the functional repair of spinal cord injury

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.