Transverse Myelitis Association
Volume 4 Issue 1
March 2001

Page 4
Chronic Pain in TM Patients
Douglas Kerr, MD PhD

 

Dr. Kerr is an Assistant Professor in the Departments of Neurology and Molecular Microbiology and Immunology, Johns Hopkins Hospital. He is also the Co-director of the Johns Hopkins Transverse Myelopathy Center. Dr. Kerr serves on The Transverse Myelitis Association Medical Advisory Board.

Many patients with TM report symptoms of chronic pain. In our experience at the Johns Hopkins Transverse Myelopathy Center, approximately 2/3 of patients report severe pain at some time in the acute or convalescent stage. In approximately 40% of patients, pain continues as a major feature in the convalescent stage. Each patient describes the pain differently, but many phrases are commonly used to describe chronic pain from TM: "burning", "shooting", "aching", or "pins and needles". Other patients report an ill?defined uncomfortable sensation that cannot otherwise be characterized.

What are the reasons for this pain and what can we do about it? I am not a pain specialist, but I will try to illustrate some of the basic principles in neuropathic pain and its treatment. Subsequent articles will explore additional treatment options. For this article, I will excerpt generously from an article by Dr. Peter Staats, my colleague at Johns Hopkins and a member of the JHTMC (Ashburn and Staats, The Lancet 252, May 1999, p. 1865-1869).

Hundreds of millions of people worldwide suffer from chronic pain. Neuropathic pain is a subset of chronic pain due to irritation or damage to peripheral or central nervous system cells. The end result is conduction of impulses to the brain that convey the sensation of pain. In TM patients, chronic pain may be due to one or several mechanisms. There may be damage to sensory nerves outside the spinal cord (nerve root damage), or demyelination or neuronal injury to the region of the spinal cord that mediates sensory input to the brain (the dorsal column). Other mechanisms may include aberrant regeneration of nerves following the acute injury. This mechanism, termed collateral sprouting, has been demonstrated following peripheral nerve injury and may account for the fact that many TM patients report pain only after the acute injury. One final possible mechanism for chronic pain is called disinhibition: removal of tonic descending input from the brain that normally serves to inhibit pain due to the TM. I should mention that not all chronic pain in TM patients is neuropathic pain. Following the acute stage, patients perform even the (previously) simple tasks differently. Without knowing it, your body invokes new strategies to carry out a task, whether that task is walking or urinating or having sex. This creates a new burden on the musculoskeletal system. Muscles that previously were not important in this task are called into action; ligaments that were previously "quiet" now become stretched in unusual ways; and joints experience pressures that are new, often leading to arthritic pain. This mechanism for chronic pain illustrates the need for continuous and aggressive physical therapy to strengthen and adapt the musculoskeletal system to the new stressors (see below).

We know that damaged neurons conduct impulses differently, often leading to a perception of pain (or other uncomfortable sensations). A variety of neurochemical changes occur to propagate the pain impulses: inflammatory mediators (such as prostaglandins) are released in the peripheral nervous system and spinal cord that make the pain conducting nerves more irritable, neurotransmitters (such as substance P, bradykinins and endorphins) are differentially produced and secreted, and sodium channels that are responsible for the ability of nerves to conduct impulses are differentially produced and localized. The end result of these changes is that nerves that normally conduct pain impulses do so at a lower threshold, and nerves that normally don't conduct pain impulses now do so. Though these changes are complex and are not understood well even by experts, I include this information to convey the message that the pain you are experiencing is real, not imagined.
 
I quote directly from Dr. Staats' article to illustrate the central principle of treating chronic pain:
         
Whatever the cause, the effect of chronic pain on the patient tends to be more pervasive than that of acute pain: it often profoundly affects the patient's mood, personality, and social relationships. People with chronic pain typically experience concomitant depression, sleep disturbance, fatigue and decreased overall physical functioning. As a result, pain is only one of many issues that must be addressed in the management of patients with chronic pain. Single modalities of treatment are rarely sufficient to treat chronic pain. Indeed, pain therapy that addresses only one component of the pain experience is destined to fail.Thus, the goal of therapy is to control pain and to rehabilitate the patient so that they can function as well as possible.In the interdisciplinary management of chronic pain, the core team typically comprises a pain management physician, a psychologist, a nurse specialist, a physical therapist, a vocational counselor, and the pharmacist.In many cases, the most realistic treatment goals for patients are: the reduction, but not elimination, of pain; improvement in physical functioning, mood and associated symptoms such as sleep; the development of active coping skills and a return to work.

Pharmacological Therapies There are several pharmacological therapies that have been employed for patients with intractable neuropathic pain. None of them works for every patient, and unfortunately a "trial and error" approach is usually required since there are no known features that predict responses to particular approaches. Non-steroidal anti-inflammatory agents (NSAIDS) including medicines such as ibuprofen, indomethacin, naprosyn and the newer COX-2 inhibitors Vioxx and Celebryx have a role in some patients with chronic pain from TM. These medicines are often more effective for the musculoskeletal pain triggers described above. The use of opioid analgesics such as Demerol, Percocet, and Morphine is controversial because of the risk for addiction and common adverse side effects: constipation, sedation, rebound pain and impaired cognition. Tricyclic antidepressants, such as imipramine, nortriptyline and amitriptyline, have a benefit in chronic pain that is independent of their anti-depressant activity, and can be very beneficial in TM patients with chronic pain. However, because of the anti-depressant effect and the beneficial effect on sleep, these drugs may "get two or three birds with one stone." Patients on these drugs need to be aware of the important side effects including urinary retention, constipation, dry mouth and sedation. Anti-convulsants such as carbamazepine (Tegetol) and gabapentin (Neurontin) function by stabilizing sodium channels thus decreasing firing of irritable nerves. This mechanism explains the manner in which they protect patients from seizures and probably underlies the ability to decrease neuropathic pain (especially burning or shooting pain). Several other medicines such as Ultram, clonidine, baclofen and dextromethorphan (the last of which is an inhibitor of glutamate receptors on neurons) have been tried in patients with neuropathic pain and have been successful in some.

Behavioral/Cognitive Therapies Behavioral approaches have been used with success in patients with neuropathic pain with some successes. "Cognitive-behavioral therapy is a psychological method that attempts to change patterns of negative thoughts and dysfunctional attitudes to foster more healthy and adaptive thoughts, emotions and actions in the patient. Relaxation and hypnotic techniques utilize imagery, distraction or directed relaxation to obtain attention focusing" (Ashburn and Staats).

Interventional Methods Nerve blocks can be performed to modulate pain perception and can be performed in multiple areas of the body. Unfortunately, these blocks are rarely helpful in TM patients unless the primary pain generator exists outside of the spinal cord (in the pelvis, for example). Epidural steroid injections are more likely to be helpful and involve the use of a needle to inject steroids into the space just outside of the spinal cord. This approach results in decreased edema in the area and decreased synthesis of pain mediators and can be beneficial in pain that is in a localized area of the back with or without radiation to the front of the body or buttocks.

Implantable methods Two implantable methods of pain therapy are often employed in patients with TM: pump delivery of medicine to the epidural or subarachnoid space in the base of the spine, or spinal cord stimulation. Each of these approaches is invasive and presents a risk of surgical complication or infection. However, for intractable pain, these can be procedures that allow restoration of function in some TM patients.

An important predictor in whether or not chronic pain can be controlled in a given patient is the undertaking of an aggressive multidisciplinary approach. In many cases, patients have to be the aggressor with their health care teams. Many physicians are uncomfortable treating patients with pain. If this is the case with your physician, fire him or her. Or at least, get a referral to see a pain specialist. Ask your physicians about the modalities described here. Each may or may not be appropriate for a given patient. I would even suggest reading the article that I have referenced here and any others that discuss neuropathic or chronic pain. Family and caregiver support is critical. And most importantly, once you have received input from the health care team, sit down with your family or close friends and decide on how YOU will beat this and begin to function better. Taking control and setting goals are critical!

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