Reducing sympathetic activity within somatic nerves by direct injection of the sympathetic ganglia in affected regions of the body (stellate ganglion for arm pain and lumbar ganglia for leg pain) has met with mixed success in neuropathic pain, including that of causalgia and reflex sympathetic dystrophy. A variant of this technique uses regional intravenous infusion of a sympathetic-blocking drug (bretylium, guanethidine, reserpine) into a limb that is isolated from the systemic circulation by the use of a tourniquet. This is known as a “Bier block,” after the developer of regional anesthesia for single-limb surgery. These techniques, as well as the administration of clonidine by several routes and the intravenous infusion of the adrenergic blocker phentolamine, is predicated on the concept of “sympathetically sustained pain,” meaning pain that is mediated by the interaction of sympathetic and pain nerve fibers or by the sprouting of adrenergic axons in partially damaged nerves. These forms of treatment have been under study for many decades and have given variable results but the most consistent responses to regional sympathetic blockade are obtained in cases of causalgia resulting from partial injury of a single nerve (CRPS I).
A number of other treatments have proven successful in some patients with reflex sympathetic dystrophy and other neuropathic pains but the clinician should be cautious about their chances of success over the long run. One of these has been bisphosphonates (pamidronate, alendronate), which have been beneficial in painful disorders of bone, such as Paget disease and metastatic bone lesions. It is theorized that this class of drug reverses the bone loss consequent to reflex sympathetic dystrophy but how this relates to pain control is unclear (Schott, 1997). Electrical stimulation of the posterior columns of the spinal cord by an implanted device, as discussed below, has become popular. Another treatment of last resort is the intravenous or epidural infusion of drugs such as ketamine; sometimes this has a lasting effect on causalgic pain.
The approaches enumerated here are usually undertaken in sequence; a combination of drugs—such as antiepileptics, narcotics, and clonidine—in addition to anesthetic techniques—is usually required. The ongoing attention and support of the neurologist is often a cornerstone of a successful treatment plan. Further references can be found in the thorough review by Katz.
Ablative Surgery in the Control of Pain
Only when a variety of analgesic medications (including opioids) and other practical measures, such as regional analgesia or anesthesia, have completely failed, should one turn to neurosurgical procedures. Also, one should be very cautious in suggesting a procedure of last resort for pain that has no established cause as, for example, limb pain that has been incorrectly identified as causalgic because of a burning component but where there has been no nerve injury.
The least-destructive procedure consists of surgical exploration for a neuroma if a prior injury or operation may have partially sectioned a peripheral nerve. Magnetic resonance imaging of the region should be performed first and will demonstrate most such lesions, but we are uncertain if all small neuromas are visualized, and it is this ambiguity that justifies exploration. Another nondestructive procedure is implantation of a spinal electrical stimulator, usually adjacent to the posterior columns.
This procedure, in which there is now a resurgence of interest, has afforded only incomplete relief in our patients and may be difficult to maintain in place. However Kemler (2004) and colleagues found a sustained reduction in pain intensity and an improved quality of life in patients with intractable reflex sympathetic dystrophy, even after 2 years in a randomized trial. Others have found it less durable. It is clear that careful selection of patients, including a test trial of an externalized device, is partial assurance of a good outcome.