Many theories have been proposed for explaining the pathophysiology of chronic pain after injury to peripheral nerves, dorsal roots, or dorsal root ganglia. The various proposed mechanisms of chronic pain production remain controversial, but it is generally accepted that hyperactivity in noci-ceptive pathway neurons as well as neuronal hypersensitivity to abnormal discharges from injured peripheral ganglia or neurons are involved in the pathophysiology of chronic neuropathic pain.
When a patient sustains a traumatic plexus avulsion, as in the case of a motorcyclist striking a tree impacting mainly over the lateral chest and shoulder, the sudden and forceful impact avulses some of the nerve roots directly from their attachments at the posterolateral spinal cord. The second order neuronal cell bodies in the posterior horn of the spinal cord are thus ''deafferented,'' removing their normal input. In many cases, these deaffer-ented cell bodies progress, over a variable period, to spontaneously fire impulses along their axons toward the third order neurons in the thalamus. A similar situation occurs after traumatic hemipelvectomy with resultant lum-bosacral plexus avulsion.
The DREZ lesion was designed to coagulate and destroy these second order neuronal cell bodies in the substantia gelatinosa of the posterior horn. It, eliminates the firing of pain impulses along the spinothalamic axons and often rids the patient of pain. One typically generates a zone of hypalgesia into the previously painful region, but this is rarely cause for complaint. The exact mechanisms by which chronic pain is produced have yet to be elucidated and remain somewhat controversial; the phenomenon, however, is real and DREZ lesioning has provided effective results in eliminating chronic pain of various etiologies.
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