Compression of the cauda equina by spinal stenosis is a major clinical problem associated with intermittent claudication. A large number of experimental studies have shown that compression of the cauda equina may induce neurophysiologic dysfunction and reduce blood flow in compressed nerve roots. 1–4
Reduction of blood flow in the peripheral nerve leads to demyelination or axonal degeneration, depending on the magnitude of the ischemic injury. 5–7 In peripheral nerve, injuries that cause axonal degeneration also cause neuropathic pain, whereas mild degrees of ischemia producing demyelination do not produce hyperalgesia. 8–10 Likewise, endoneurial expression of tumor necrosis factor-[alpha] (TNF-[alpha]) in Schwann cells produces primary demyelination, whereas its expression by macrophages in more severe injuries produces axonal degeneration and pain. 11,12 TNF-[alpha] is also related to apoptosis of DRG cell bodies, although this is quite a complicated relationship with respect to its effect on pain. 13 In this study, we undertook to explore these relationships in more detail by using a variable compression model of rat cauda equina to simulate the clinical condition of spinal stenosis