By Kory McHenry and Kenneth McHenry, M.D.

Illustration by Mark H. Adams

The late Dr. Patrick Wall found that about one in 15 SCI patients has central pain. The bizarre burning occurs only where the cord injury is incomplete. Electric shocks or muscle pain may also occur. The preservation of sensation may be very slight, but some nerve function is necessary to maintain central pain. Some relief may be found in opiates (opioids), tricyclic antidepressants, or anticonvulsants (see sidebar, p. 34). Most patients can still wear clothing and have only mild muscle pain.

Of people with SCI who experience central pain, about a quarter have more severe pain, which responds poorly to therapy, but they are clearly better off on medication than off. They tend to have more gut or bladder pain and function.

In the remainder, the pain may reach such severity that the touch of clothing is unbearable and no medication or therapy is of significant benefit. This last group is much more likely to have sought radical pain treatment. As might be expected, they are also the most depressed group (for more on central pain symptoms, visit or

Why Is Central Pain So Relentless?
Charged particles–ions–flow into nerve cells and cause a voltage spike (as many as 50 times per second). Frequency of spiking determines the strength of the signal. The main ion flowing in with an action potential is sodium. Sodium crosses the cell membrane through crooked tubes known as ion channels.

Tiny C fibers carry slow pain and big A-beta or A-delta fibers carry rapid pain. Both groups are subject to inhibitory messages from the brain which can lessen firing and diminish pain. Injured C fibers do not regrow well. So, powerful A-beta/delta fibers grow into the areas where C fibers used to be. These sprouts of new growth do not receive normal input from the brain to inhibit them.

Central pain causes a disastrous increase in ion channels. These are called Nav 1.3–normally found only in the fetus. They render nerves so sensitive that they cannot quit firing. The brain cannot contact these cells to tell them to shut off. The cells become pain puppets, not responding to injury, but continually firing automatically.

Also, injured neurons cannot make the protein that brings chloride to the cell membrane. The absence of chloride inverts any inhibition that does reach the cell into excitation. People affected by central pain catch it from both directions: First, greatly increased excitation; and second, absent or decreased inhibition.

More Research Needed
Neurotransmitters released in the gaps between nerves increase or decrease the strength of the pain signal. The main pain exciter is glutamate, which activates NMDA and AMPA receptors on the next nerve, going toward the brain. All NMDA can be blocked with MK-801, but glutamate is needed for all brain functions. Recently, it was learned that NR2B can selectively block only the chronic pain activity of NMDA. This gives hope for the future. Substance P also adds to pain by activating NK-1 receptors (slow pain). Rats can be given central pain by injuring their cords, but the naked mole rat, which lacks substance P genetically, cannot be made to acquire central pain.

If the person with central pain cannot bear the touch of clothing, the most that can currently be hoped for is sedation of some kind. Those with severe central pain should be treated by high-grade pain clinics (usually associated with university hospitals). A good clinician can thread out the various pains to know which are normal and which are neuropathic (due to nerve injury). Currently, work is also proceeding on controlling growth factors, released from glial cells along the neurons, which cause increased firing. The future is not bleak, but there is certainly a need for more research money. More money is spent on pain than any other medical problem, but the funds for basic research are sparse.

One final note: Psychiatric help can be very valuable, even lifesaving, so long as the therapist does not try to blame the patient or tell him or her that the pain is “all in your mind.”

Kory McHenry is a third-year dental student. Kenneth W. McHenry lives in Provo, Utah, and has written extensively on central pain. The Wall/McHenry criteria for central pain, published by the International Association for the Study of Pain, can be read online at



Tried (but not necessarily true) medications for central pain relief:

Tricyclic antidepressants. Amitryptiline has been proven of benefit and is inexpensive, but some patients have fewer side effects (blurred eyesight, dry mouth and constipation, rapid heart beat, drowsiness) on Nortryptiline. Benefit is probably related to the drowsiness-the CNS has been quieted. But drowsiness is not a cure.

Opiates. While central pain is primarily in the brain, opiates act primarily on the cord. Severe central pain may not yield to opiates, and where they do help, it may require very high doses, which should be administered by pain clinics. They are often reluctant to do this long-term, for fear of addiction.

Survey results at do not indicate that opiates are the answer for the vast majority. The fentanyl patch (known as Duragesic) is absorbed into the body, but is subject to the same concerns as intravenous morphine. Dextromethorphan, a type of cough syrup, gets some play in the literature, but has not appeared among the beneficial agents at Ketamine is an injectable anesthetic that does seem to stop some pain, but mental confusion and disorientation, even hallucinations, prevent much use of this drug.

Anticonvulsants. Notorious for containing medications which help peripheral nerve pain but not necessarily central pain. Carbamazepine and clonidine are the major players, but lately gabapentin and lamotrigine have gotten major positions. Lamotrigine is stronger for central pain in the literature, but so far the promised benefits have not been confirmed by surveys.

Membrane-active drugs. Mexilitine, related to local anesthetics, again helps peripheral nerve pain, but no randomized, double blind studies show benefit for central pain.

Agents acting on muscle. One might not expect muscle drugs to help central pain, but reports from Europe may provide a link. Drugs related to the benzodiazepines are commonly used. Clonazepam has gotten fairly good reports, but again, sedation seems part of the benefit-and oversedation can be a problem. Botulinum toxin, both A (known as Botox) and B (known as myobloc), may help through reducing glutamate release, but this remains to be proven and may not be suitable for use over wide areas of the body. Baclofen does seem to help the muscle cramping pain of central pain, but it is hard to talk about long-term use of a drug which is introduced into the spinal fluid.

Channel blockers. Neurotransmitter blockers will provide a treatment once developed. As of now, many agents have some effect on the channels, but are not specific enough to get the job done safely. Pregabalin and other drugs are now being tried, with help to some. Cone shell toxins (Ziconitide) are in clinical trials.

In summary, at present nothing seems completely satisfactory, and nothing may help really severe cases. However, since Nav 1.3 sodium channels seem to be causing most of the pain, and they do not appear to be necessary or even appropriate in adults, a place for research to begin would be to find an antibody to Nav 1.3 channels to try to blunt their effect.