Insight - Pain

Chronic pain is the universal constant with arthritis,its a hallmark. To some extent,everyone with arthritis is going to suffer pain. There's no getting around it,but you can learn to cope with it. How you meet "the challenge of pain" will in large part determine not only how well you cope with your illness but how much pain you experience. It's a matter of pain management ,says a pain specialist in Montreal,Dr. Warner. He teaches patients to regain measure of control over their bodies so that they can achieve some mastery of their medical condition,and thus don't feel so much that the pain is controlling them.

"Different people react differently to pain and illness," he says. "Some become paralyzed. They sit at home,don't go out,become more and more alienated, depressed. Other people say,"I can't let this pain get to me,"and they go out and do all kinds of things,trying to prove to themselves that they can do it,and finally they crash. We try to bring everybody toward the miccle,and utilize their good strategies and minimize their maladaptive strategies."

The first step,,is the tough one: learning to understand and accept the pain. Only then can you begin to deal withit,establishing priorities and setting goals-taking resposibility for yourself. There are skills you can learn that will help you to maximize your level of everyday functioning,but you have to help yourself first. You have to take a close look at yourself and your lifestyle and learn to accept your own limitations.

In other words,you're going to learn to accept that there are certain things you can't do any longer. Activities that increase your pain will have to be mocified or eleminated,and you may have to adopt practices that will maximize your ability to do the everyday things you have to do to maintain your ability to do the everday things you have to do to maintain your altered self-image and self-respect. Painkillers are a partial answer at best: they only mask the pain,and they can cause real harm by allowing you to do things that cause damage to arthritic joints,activities that would "tell" you to avoid. No one expects someone in chronic pain to stop taking medication, to drug therapy that help people take repossession of their lives.

One of the simplest isn't always easy,but it is effective: Relax. Pain,it should come as no surprise,causes stress and tention,and not only psychological tension. Taking a relaxation training session teaches you to enter a relaxed more physical state that lowers blood pressure,repiratory rate,and adrenalin flow.

You'll be taught to lie down and find a comfortable breathing rhythm. Close your eyes,focus on your body.s different muscle groups,starting with your calf muscles. Slowly relax your muscles,moving progressively up your body to your neck and shoulders. As the muscles relax,there's a concomitant release of the body's natural opiates,called endorphins,pain-relieving hormones that are related to synthetic opiates like morphine.

Pain is one of the simplest and and most elementary sensations we can experience, yet it represents a physiological mechanism of considerable subtlety and complexity. Scientists are still struggling to understand many aspects of this biochemical system, which includes a vast network of nerves conducting signals from across the skin's surface, through the conduit of the spinal cord and into the brain. These signals consist of pain information packages passed along with the help of materials contained within the body's nerve cells. As researchers continue to explore precisely how and why such transmissions take place, the behaviour of a component known as Substance P (SP) is providing new insights into this often paradoxical process.

Stub your toe or burn your finger, and you know it immediately. The formal scientific name for this awareness is nociception, but most people think of it simply as pain. At a microscopic level, the perception of pain starts with the injury-sensitive receptors in the skin. When these receptors encounter potentially harmful mechanical, thermal or chemical conditions, their findings travel along a specific set of neural pathways. While that description sounds transparently mechanistic, pain remains ahighly subjective phenomenon: It's hard to explain why similar injuries seem more painful to one person than another, or why the same person might regard an injury differently under different circumstances. A widely accepted pain theory suggests that a biochemical 'gate' exists near the base of the spinal column, where peripheral pain impulses are assessed and modulated before reaching the brain.

This gate would enable other factors to assign pain a specific priority. For example, our attitude toward an injury, based on previous experience with similar injuries, can make it seem minor or drastic. A shaving nick may draw more blood than a gash from a carving knife, but the latter may be more alarming because it's less expected. Such psychological influences can apparently swing the gate open or shut, determining how we experience the severity of pain.

At the heart of the system is Substance P, a neuropeptide transmitter that plays a key role in stimulating neurons to convey the urgent news of aninjury along intricate links called synapses. As a peptide, SP belongs to a group of organic chemicals more sophisticated than simple amino acids (the so-called 'building blocks of life') but less complex than the large proteins that make up living organisms. Produced by the neurons themselves, SP spreads through rope-like nerve fibres that reach from the base of the spine in two directions: to the pain centre at the brain stem and to the pain receptors found under the skin.

According to McGill University physiologist Dr. James Henry, SP's exact function in the transmission of pain signals is still being evaluated: 'Perhaps surprisingly, 90 per cent of the Substance P that's produced is transported to the periphery. While we are looking at a role for Substance P in nociception and a role for Substance P in regulating synaptic transmission at the central terminal, it must play a very important role at the periphery. 'Henry has found that SP levels vary with particular types of pain, such as the contrast between short, sharp episodes and more lingering sensations. These different forms of nociception travel along different nerve path-ways: fast, bright pain utilizes nociceptors called A-delta, while diffuse, persistent and generally more unpleasant pain employs smaller diameter nociceptors called C fibres. The C fibres are particularly relevant when considering the pain caused by a chronic and/or systemic disease like arthritis.

'Substance P doesn't necessarily participate in brief, acute types of painful input,' says Henry. 'It participates more in the longer term activation of C fibres. A brief painful stimulus is usually not sufficient to release enough Substance P for it to have a physiological effect. Yet apply the stimulus for a longer time, and enough is released. It seems to be triggered into the system once the input has been coming for a longtime.'

Such observations have led researchers to take a fresh look at the relation between SP and the painful symptoms of such conditions as rheumatoid arthritis (RA), osteoarthritis (OA), diabetes and herpes zoster (shingles). Any compound that could interfere with SP would also effectively and directly relieve the associated pain. One place researchers have sought such compounds is within a class of agents known as counter irritants. Counter irritants are usually applied to a painful region of the body, producing a temporary local reaction. The result may be skin irritation, mild swelling or a temperature change-warmer or cooler. In each case, the counterirritant takes advantage of the 'pain paradox,' a corollary of the gate theory, which is based on the fact that a new pain appears to reduce existing pain by distracting the brain. Theoretically this new input excites the neurons controlling the gate to the spinal cord and the brain, which attempts to moderate the flow of impulses by closing the gate. Whatever their precise means of action, counterirritants occupy a traditional place in pain treatment. Basic liniments and poultices have laid the foundation for a more extensive pharmacopoeia ranging from camphor, menthol, turpentine and eucalyptus oil to a host of more elaborate recipes that can be found in any drug store. In each case, the underlying goal is much the same: confront one pain with another, and so convince thebody to lower its sensitivity.

A compound that affects SP addresses the problem of pain in a much more fundamental way. Rather than trying to head off signals by closing theirpath to the brain, an SP 'antagonist' would reduce the ability of neurons to send those signals in the first place. And beyond mere signals, SP mayturn out to be the culprit behind certain aspects of the condition causing the pain.'Substance P has been implicated in inflammatory responses in the knee,'says Henry. 'It's been found at higher levels in the knees of arthritic animals, and Substance P antagonists seem to reduce that response in these animals. It's quite possible that, although we've been looking at the roleof Substance P in nociception-in arthritis or toothache and other kinds of pain-these antagonists will not only relieve pain but they may also reduce the inflammatory response.'

At least one clinically appropriate SP antagonist has been recruited fromthe counterirritants: capsaicin, the alkaloid providing chili peppers with their fire. This chemical's qualifications as a counterirritant are obvious to anyone who's ever felt the numbing effects of a spicy pepper on bare skin. Ointments consisting of 0.025 to 0.25 per cent capsaicin (a tube ofcream may contain as much pure capsaicin as hundreds of chili peppers) can generate a feeling of warmth on the skin, although the effect is muted enough for patients to apply the treatment several times a day. Moreover, capsaicin appears capable of reaching well beyond the surface level of pain to the molecular level of neurons and SP.

'Capsaicin works a little differently from other counterirritants,' saysDr. Ira Lawrence, vice-president of clinical research for the Chicago-based GenDerm Corporation, which manufactures a capsaicin-based topical creamcalled Zostrix®. 'Capsaicin specifically affects the chemical that transmits the pain impulses into the central nervous system.'Several multicentre clinical trials of topically applied capsaicin have shown it to be an effective therapy for people suffering from the pain of arthritis, diabetes and herpes. According to this research, capsaicin first stimulates neurons to release SP, then prevents the neurons from producing more. Once depleted of their essential transmitter, the neurons can nolonger relay pain signals.

'We believe capsaicin inhibits the secretion of Substance P and, more importantly, its synthesis,' says Lawrence. 'That critical combination of getting rid of what you have and not letting you make any more is a simple but clear way of explaining how it works.'To a patient, the pain relief can be comparable with that achieved bynon steroidal anti-inflammatory drugs (NSAIDs). Yet the therapy calls for nothing more than rubbing cream on an affected area, which causes a brief burning sensation but none of the significant side effects that often accompany NSAID use, such as gastric upset (or, worse, ulcers and gastric bleeding) and rashes. Capsaicin, which only temporarily inhibits the ability of neurons to produce SP, can also be used as an adjunct to ongoing NSAID treatment.

'Older patients, the principal sufferers from arthritis, generally have other diseases and frequently require one or more systemic medications unrelated to their arthritis management,' concluded a 1991 paper on treatment with capsaicin. 'Consequently, a topical treatment, devoid of the potential of drug interactions or serious systemic side effects, may be of benefit for these older patients.''There's no question some patients find this helpful, and there's a very good physiological rationale for its use,' says Dr. W. John Reynolds, a rheumatologist at the Toronto Hospital-Western Division. 'I'd expect that in most clinical settings of appropriate use it would be beneficial as a pain medication. The only thing that bothers patients is that sometimes there's a local burning, but that should disappear after a couple of days. 'Reynolds points out that the diet of people in many tropical countries includes food laced with significant amounts of capsaicin. While these foods can cause serious pain to the tongue and throughout the mouth, the pain receptors adapt and don't react as violently after a while. Similarly, concludes Reynolds, the painful response of skin to capsaicin-based creams also diminishes.

Yet while topical capsaicin cream has been marketed for more than 10 years,the full ex-tent of its clinical implications is still being weighed byresearchers. Reynolds cites a relatively small American research project that examined the cream's effectiveness for OA affecting the hands. Although only 21 patients were involved in the study, which was published in The Journal of Rheumatology in 1992, he finds the associated interpretation convincing.

In the treatment of RA and OA, for example, increasing amounts of SP appear to lead a cascade of biochemical events producing inflammation and joint deterioration. SP incites the reproduction of synoviocytes, the cells occupying the protective and lubricating membrane surrounding a joint. Besides leading to the thickening of this membrane, these cells release chemicals such as prosta-glandins, which can produce inflammation, and collagenase, which can degrade the structure of the joint's cartilage. Recent research has shown capsaicin's ability to inhibit SP also inhibits these arth-ritic processes. Findings from a small pilot study conducted in California, due to be published this summer, show that decreased SP levels corresponded with decreased levels of agents such as prostaglandins. Lawrence sees the need for more comprehensive research to reinforce these observations, but he finds them exciting because they point to a potentially trouble-free means of resolving a complicated biochemical problem.

'It's the first evidence we have that using a topical agent can affect intra-articular inflammatory media,' he says. 'Where you target it is at the periphery-that's the beauty of it. 'Nevertheless, researchers such as Henry confess they still see the interaction of capsaicin and SP as something of a black box whose inner workings are largely unknown. He notes that if topical capsaicin does indeed yield a massive release of SP in neurons, there should be acorresponding massive influx of pain when the pain is initially applied. Yet most patients report only a mild irritation or limited reddening of the skin.

Meanwhile, a competing theory suggests that capsaicin performs in an entirely different way, affecting the electrochemical properties of C fibres so they can no longer conduct SP. 'I really don't see how either of these proposed mechanisms of action could be useful,' says Henry. 'On the other hand, if it's working for some patients, it must be working for a reason.'

In the case of a local nerve block, any one of a number of local anesthetics may be used; the names of these compounds, such as lidocaine or Novocaine, usually have an aine ending. Regional blocks affect a larger area of the body. Nerve blocks may also take the form of what is commonly called an epidural, in which a drug is administered into the space between the spine's protective covering (the dura) and the spinal column. This procedure is most well known for its use during childbirth. Methadone and morphine and are opioid narcotics (such drugs end in ine or one) that are sometimes used for regional analgesia and are administered as an injection.

Neurolytic blocks employ injection of chemical agents such as, phenol,alcohol or glycerol to block pain messages and are most often used to treat cancer pain or to block pain in the cranial nerves. In some cases, a drug called guanethidine is administered intravenously in order to accomplish the block.

Surgical blocks are performed on cranial, peripheral, or sympathetic nerves. They are most often done to relieve the pain of cancer and extreme facial pain, such as that experienced with trigeminal neuralgia. There are several different types of surgical nerve blocks and they are not without problems and complications. Nerve blocks can cause muscle paralysis and, in many cases, result in at least partial numbness. For that reason, the procedure should be reserved for a select group of patients and should only be performed by skilled surgeons. Types of surgical nerve blocks include:

Neurectomy (including peripheral neurectomy) in which a damaged peripheral nerve is destroyed.
Spinal dorsal rhizotomy in which the surgeon cuts the root or rootlets of one or more of the nerves radiating from the spine. Other rhizotomy procedures include cranial rhizotomy and trigeminal rhizotomy, performed as a treatment for extreme facial pain or for the pain of cancer.
Sympathectomy, also called sympathetic blockade, in which a drug or an agent such as guanethidine is used to eliminate pain in a specific area (a limb, for example). The procedure is also done for cardiac pain, vascular disease pain, the pain of reflex sympathetic dystrophy syndrome, and other conditions. It may involve,e.g.,cutting a nerve,e.g.,cutting a nerve that controls contraction of one or more arteries