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Top DAMAGE to the peripheral and central nervous system can lead to the development of neuropathic pain in which patients often experience a combination of sensory deficits with spontaneous and stimulus-evoked pain allodynia and hyperalgesia.


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Because of the multiplicity of causes of neuropathy, ranging from trauma to viral infections to diabetes, and the number of possible resultant symptoms, the underlying dysfunctional mechanisms are likely to be diverse.


The resultant neuronal hyperpolarization leads to a decrease in the opening of voltage-dependent calcium channels, and at presynaptic locations, a reduction in the release of neurotransmitter from the afferent nerve ensues.

This presynaptic action is common to all opioid-mediated inhibitory effects at other sites, the net result being a reduction in neuronal excitability.

This study uses the spinal nerve ligation model, confirmed by behavioral testing, to induce a neuropathic state.

Selective tight ligation of spinal nerves L 5 and L 6 and a sham procedure were performed as first described by Kim and Chung 1992.

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Part of the L 6 transverse process was removed to expose the L 4 and L 5 spinal nerves, and L 6 was identified lying just under the sacrum. Using 6-0 silk thread, the left spinal nerves L 5 and L 6 were tightly ligated distal to their dorsal root ganglion and proximal to their conjunction to form the sciatic nerve.

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