|
Obtained from the ASAMS WEBSITE This document was reproduced by ASAMS on its website with permission of its original Author. The Author has made this document available for public access on the strict understanding that the Author holds all Copyrights over this document and only under certain conditions. This document may be stored electronically and/or printed out for personal research and reference purposes ONLY. Any retransmission and/or reproduction for any other reason, whether in part or in whole, by any means, is prohibited unless permission is obtained by the Author. |
Understanding Pain
Excerpt from: Briefing on the Brain-Body Connection
Subcommittee on Labor-DHHS, Education and Related Agencies
Committee on Appropriations
U.S. House of Representatives
More than just another form of "touch" sensation, pain demands our attention. When serious, it may stop us in our tracks, and it carries intense negative emotions. Pain is a great teacher, altering our behavior in the service of survival: to put it simply, a child does not put a hand in the fire twice. Pain is a protector: an injured person is forcibly reminded to protect an injury until it heals. But there is also a terrible price to pay for possessing such an effective survival system. When pain becomes chronic it may disrupt and even destroy lives. Worse yet, chronic pain often persists long after the source of tissue damage is gone, and thus conveys no benefit at all, but only suffering. The most common cause of serious chronic pain, whether caused by injury, cancer, or a herniated disc, is damage to the nervous system itself, leading to persistent false alarms to the brain. Pain that is caused by an injury to the nervous system itself is called neuropathic pain. Basic and clinical neuroscience have, over the last decade, made remarkable advances in understanding pain, but as anyone with chronic neuropathic pain knows all too well, much remains to be discovered.
Why is pain such an insistent form of sensation? Why does it keep coming into the foreground of thoughts and feelings, when the sufferer would rather tune it out and return to work? Incoming pain messages from skin, muscle, bone, or internal organs are relayed to higher centers in the brain via two largely segregated pathways beginning in the spinal cord. The smaller of these pathways is more recent in evolution, and therefore sometimes is called the neospinothalamic tract. It relays information about the precise localization and nature of the pain to those brain regions that analyze bodily sensations. It permits us to point to an area of our bodies in the doctor's office and to describe the sensations, for example, as pricking or burning.
The older and larger tract conveying pain information is called the paleospinothalamic tract. It does not relay specific sensory information at all, but rather communicates with brain regions that produce arousal, that increase the heart rate and blood pressure, and most importantly, that process emotion. Via this tract, pain messages are hardwired into emotional centers that ensure that pain has an intense, aversive quality. The nervous system must be set up this way if pain is to protect even the stoics among us from damaging themselves, but this emotional hard wiring means that chronic pain brings with it chronic suffering.
Many individuals with chronic pain become depressed, not because they are weak, but because of the direct relentless stimulation of brain regions that produce negative emotion. Depression in chronic pain often responds to antidepressant treatments, even when the pain itself cannot be fully relieved, but depression in the chronic pain patient too often goes untreated, due to a misplaced sense that it is somehow appropriate that the pain sufferer be depressed. Depression and pain lead to a vicious cycle, however; pain can cause depression, and depression turns up the gain on pain, making the pain less tolerable and moving it front and center in the sufferer's life.
I have been speaking of the relentless quality of chronic pain, but one of the most remarkable observations about acute pain, is that it can be suppressed, at least transiently, depending upon the context in which it occurs. The great anesthesiologist, Beecher, noted with surprise, as he examined men with serious shrapnel wounds at Anzio beach, that many of them refused morphine, something that he almost never saw in Boston, when he tended to patients with the far less serious wounds produced by controlled surgery. How could such a phenomenon be explained? Under conditions that produce extreme stress or fear, higher emotional centers in the brain can activate a descending system that suppresses incoming pain signals. This descending analgesic system utilizes the body's own endogenous opiate-like neurotransmitters, the endorphins. The threshold for activation of descending analgesia by stress is high; otherwise pain would lose its survival value, but the nervous system appears to be organized such that in circumstances which produce the greatest stress or fear, for example, pursuit by a predator, or mortal combat, circumstances in which the survival value of running or fighting far outweighs the risk of using already damaged limbs, pain can be completely suppressed.
Opiate drugs are analgesic because they mimic the body's endorphins. Unlike stress, however, opiate drugs are extremely reliable in their ability to suppress pain ( they work even when one is not fleeing for one's life. Unfortunately, opiate drugs act not only on pain pathways, but elsewhere in the brain and peripheral organs with the result that unwanted side effects markedly limit their use.
Of particular interest in the context of today's hearing, there has been research as to whether acupuncture and also the much misunderstood placebo response might act via descending analgesic pathways (but this research has been hard to perform for many reasons, including the fact that acupuncture, while effective for some people in some circumstances, is not as potent or reliable as pharmacologic analgesics). You can see now, parenthetically, that placebos do not separate malingerers from those with real pain ( indeed a "placebo" injection might work very well, if only for a very limited time, on someone suffering severe pain and stress, by serving as a trigger for descending analgesic pathways).
What can we take away from this discussion? First we need research not only on pharmacologic alternatives to opiates, and an understanding of how to deliver and use opiates better, but also on better nonpharmacologic strategies to deal with chronic pain ( perhaps there are ways of tapping into the descending pain suppression systems within us that are more robust than the approaches we now have, which include transcutaneous electrical nerve stimulation, or its acronym TENS, and acupuncture). Second, when patients with chronic pain become depressed, it is important not to write it off as expectable, but to treat it vigorously. Third, for many there can be a vicious cyclic of depression and disability if people disengage from their normal work and family lives. People with chronic pain should be encouraged to work and to retain responsibility at home at the level their pain and underlying medical conditions allow. I should add that I have not discussed in this testimony the issue of the all too common phenomenon of undertreatment of acute pain. This is a separate but important issue that has been addressed in many other forums.