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Anatomy of an Illness as Perceived by the Patient Page 6
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The reason why aspirin is prescribed so widely for arthritic patients is that it has an antiinflammatory effect, apart from its pain-deadening characteristics. In recent years, however, medical researchers have suggested that the antiinflammatory value of aspirin may be offset by the harm it causes to the body’s vital chemistry. Doctors J. Hirsh, D. Street, J.F. Cade, and H. Amy, in the March 1973 issue of the professional journal Blood, showed that aspirin impedes the interaction between “platelet release” and connective tissue. In the Annals of Rheumatic Diseases, also in March 1973, Dr. P.N. Sperryn reported a significant blood loss in patients who were on heavy daily doses of aspirin. (It is not unusual for patients suffering from serious rheumatoid arthritis to take as many as twenty-four aspirin tablets a day.)
Again, I call attention to the article in the May 8, 1971, issue of Lancet, the English medical journal. Dr. M.A. Sahud and Dr. R.J. Cohen stated that the systematic use of aspirin by rheumatoid patients produces abnormally low plasma-ascorbic-acid levels. The authors reported that aspirin blocks the “uptake of ascorbic acid into the blood platelets.” Since vitamin C is essential in collagen formation, its depletion by aspirin would seem to run directly counter to the body’s need to combat connective tissue breakdown in arthritic conditions. The Lancet article concludes that, at the very least, ascorbic acid should be administered along with aspirin to counteract its harmful effects.
Aspirin is not the only pain-killing drug, of course, that is known to have dangerous side effects. Dr. Daphne A. Roe, of Cornell University, at a medical meeting in New York City in 1974, presented startling evidence of a wide range of hazards associated with sedatives and other pain suppressants. Some of these drugs seriously interfere with the ability of the body to metabolize food properly, producing malnutrition. In some instances, there is also the danger of bone-marrow depression, interfering with the ability of the body to replenish its blood supply.
Pain-killing drugs are among the greatest advances in the history of medicine. Properly used, they can be a boon in alleviating suffering and in treating disease. But their indiscriminate and promiscuous use is making psychological cripples and chronic ailers out of millions of people. The unremitting barrage of advertising for pain-killing drugs, especially over television, has set the stage for a mass anxiety neurosis. Almost from the moment children are old enough to sit upright in front of a television screen, they are being indoctrinated into the hypochondriac’s clamorous and morbid world. Little wonder so many people fear pain more than death itself.
It might be a good idea if concerned physicians and educators could get together to make knowledge about pain an important part of the regular school curriculum. As for the populace at large, perhaps some of the same techniques used by public-service agencies to make people cancer-conscious can be used to counteract the growing terror of pain and illness in general. People ought to know that nothing is more remarkable about the human body than its recuperative drive, given a modicum of respect. If our broadcasting stations cannot provide equal time for responses to the pain-killing advertisements, they might at least set aside a few minutes each day for common-sense remarks on the subject of pain. As for the Food and Drug Administration, it might be interesting to know why an agency that has so energetically warned the American people against taking vitamins without prescriptions is doing so little to control over-the-counter sales each year of billions of pain-killing pills, some of which can do more harm than the pain they are supposed to suppress.
If an account is ever written about the attempts of the medical profession to understand pain, the name of Paul Brand may have an honored place. Dr. Brand has worked with lepers for most of his medical career. He is an English orthopedic surgeon, recognized throughout world medical circles for his work in restoring crippled or paralyzed hands to productive use. His principal work at Medical College at Vellore, India, was as director of orthopedic surgery.
Paul Brand went to Vellore as a young man in 1947. His wife, also a surgeon, joined him at Vellore a year later. Together, they constituted one of the most remarkable husband-and-wife medical teams in the world. Paul Brand restored to thousands of lepers the use of their hands and arms. Margaret Brand saved thousands of lepers from blindness. Both of them taught at the medical college, undertook important research, and worked at the hospital and in field clinics.
Paul Brand’s main purpose in coming to the Christian Medical College and Hospital at Vellore was to see whether he might be able to apply his highly developed skills in reconstructive surgery to the special problems of lepers. Commonly, lepers’ fingers tend to “claw” or partially close up because of the paralysis of vital nerves controlling the muscles of the hand. Brand wanted to try to reactivate the fingers by connecting them to healthy nerve impulses in the leper’s forearm. This would require, of course, reeducating the patient so that his brain could transmit orders to the lower forearm instead of the hand for activating the fingers.
He wasn’t at Vellore very long, however, before he realized he couldn’t confine himself to problems caused by the clawish hands of lepers. He would have to deal with the total problem of leprosy—what it was, how it took hold in the human body, how it might be combated. He immersed himself in research. The more he learned, the greater was his awareness that most of the attitudes toward leprosy he had carried with him to Vellore were outmoded to the point of being medieval. He became determined to pit the scientific method against the old mysteries of leprosy.
He was to discover that the prevailing ideas about “leprous tissue” were mistaken. Wrong, too, was the notion that missing toes or fingers or atrophy of the nose were direct products or manifestations of the disease. Most significant of all perhaps was his awareness that leprosy was a disease of painlessness.
As head of the research section, Paul Brand first needed to find out as much as he could about tissue from the affected parts of lepers. Medicine had long known that leprosy was produced by a bacillus somewhat similar to the organism that causes tuberculosis. This discovery had been made by Gerhard Henrik Hansen almost a century and a half ago; the term “Hansen’s disease” became synonymous with leprosy. As in the case of tuberculosis, the bacillus leprae produced tubercles. The leprosy tubercles varied in size from a small pea to a large olive. They appeared on the face, ears, and bodily extremities. It was commonly thought that the bacillus was responsible in some way for the sloughing-off of fingers and toes, and even of hands and feet. Yet very little had been done in actual tissue research. Was there anything in the flesh of finger stumps or toes that differentiated this tissue from healthy cells? Was the bacillus leprae an active agent in the atrophy? Dr. Brand put the pathologists to work. Through research, they came up with the startling finding that there was no difference between healthy tissue and the tissue of a leper’s fingers or toes.
One point, however, was scientifically certain: the bacillus leprae killed nerve endings. This meant that the delicate sense of touch was missing or seriously injured. But the flesh itself, Dr. Brand ascertained, was otherwise indistinguishable from normal tissue.
As is often the case in medical research, some of Paul Brand’s most important discoveries about leprosy came about not as the result of systematic pursuit but through accident. Soon after arriving in Vellore he observed the prodigious strength in lepers’ hands. Even a casual handshake with a leper was like putting one’s fingers in a vise. Was this because something in the disease released manual strength not known to healthy people?
The answer came one day when Paul Brand was unable to turn a key in a large rusty lock. A leprous boy of twelve observed Dr. Brand’s difficulty and asked to help. Dr. Brand was astonished at the ease with which the youngster turned the key. He examined the boy’s thumb and forefinger of the right hand. The key had cut the flesh to the bone. The boy had been completely unaware of what was happening to his fingers while turning the key.
Dr. Brand had his answer at once. The desensitized nerve endings had made it possible
for the child to keep turning the key long past the point where a healthy person would have found it painful to continue. Healthy people possess strength they never use precisely because resistant pressure causes pain. A leper’s hands are not more powerful, he reasoned; they just lack the mechanism of pain to tell them when to stop applying pressure. In this way serious damage could be done to flesh and bone.
Was it possible, Dr. Brand asked himself, that the reason lepers lost fingers and toes was not because of leprosy itself but because they were insensitive to injury? In short, could a person be unaware that, in the ordinary course of a day’s activity, he might be subjecting his body to serious physical damage? Paul Brand analyzed all the things he himself did in the course of a day—turning faucets and doorknobs, operating levers, dislodging or pulling or pushing things, using utensils of all kinds. In most of these actions, pressure was required. And the amount of pressure was determined both by the resistance of the object and the ability of his fingers and hands to tolerate stress. Lacking the sensitivity, he knew, he would continue to exert pressure even though damage to his hands might be incurred in the process.
He observed lepers as they went about their daily tasks and was convinced he was correct. He began to educate lepers in stress tolerance; he designed special gloves to protect their hands; and he set up daily examinations so that injuries would not lead to ulceration and to disfigurement, as had previously occurred. Almost miraculously, the incidence of new injuries was sharply reduced. Lepers became more productive. Paul Brand began to feel he was making basic progress.
Some mysteries, however, persisted. How to account for the continuing disappearance of fingers, in part or whole? Why was it that parts of fingers would vanish from one day to the next? Were they knocked off? There was nothing to indicate that bones of lepers were any more brittle than the bones of normal people. If a leper cut off a finger while using a saw, or if a finger were somehow broken off, it should be possible to produce the missing digit. But no one ever found a finger after it had been lost. Why?
Paul Brand thought about the problem. Then, suddenly, the answer flashed through his mind. It had to be rats. And it would happen at night, while the lepers were asleep. Since the hands of lepers were desensitized, they wouldn’t know they were being attacked and so would put up no resistance.
Paul Brand set up observation posts at night in the huts and wards. It was just as he had thought. The rats climbed the beds of lepers, sniffed carefully, and, when they encountered no resistance, went to work on fingers and toes. The fingers hadn’t been dropping off; they were being eaten. This didn’t mean that all “lost” fingers had disappeared in this way. They could be knocked off through accidents and then carried away by rats or other animals before the loss would be observed. But a major cause of the disappearance had now been identified.
Paul Brand and his staff went to work, mounting a double-pronged attack against the invaders. The program for rodent control was stepped up many times. Barriers were built around the legs of beds. The beds themselves were raised. The results were immediately apparent. There was a sharp drop in the disappearance of fingers and toes.
All this time, Paul Brand kept up his main work—reconstructing hands, rerouting muscles, straightening out fingers. Where fingers were shortened or absent, the remaining digits had to be made fully operative. Thousands of lepers were restored to manual productivity.
One of the grim but familiar marks of many lepers is the apparent decay of their noses. What caused the shrinkage? It was highly unlikely that the nose suffered from the kind of persistent injury that frequently affected the desensitized hands and feet. What about rats? This, too, seemed unlikely. Enough sensitivity existed in a leper’s face, especially around the mouth, to argue strongly against the notion of rodent assault.
As Paul Brand pursued the riddle, he became convinced that neither injuries nor rats were involved. Finally, he found his answer in his research on the effect of bacillus leprae on the delicate membranes inside the nose. These membranes would contract severely in lepers. This meant that the connecting cartilage would be yanked inward. What was happening, therefore, was not decay or loss of nasal structure through injury. The nose was being drawn into the head.
It was a startling discovery, running counter to medical ideas that had lasted for centuries. Could Brand prove it? The best way of proceeding, he felt, was by surgery that would push the nose back into the face. He therefore reconstructed the nose from the inside. It was a revolutionary approach.
He knew that the operation couldn’t work in all cases. Where the leprosy was so far advanced that membrane shrinkage left little to work with, it was doubtful that the operation would be successful. But there was a good chance that, in those cases where the disease could be arrested and where the shrinkage was not extreme, noses could be pushed back into place.
The theory worked. As a result, the nose restorative operation developed at Vellore has been used for the benefit of large numbers of lepers at hospitals throughout the world.
Next, blindness. Of all the afflictions of leprosy, perhaps none is more serious or characteristic than blindness. Here, too, it had been assumed for many centuries that loss of sight was a specific manifestation of advanced leprosy. At Vellore, this assumption was severely questioned. Intensive study of the disease convinced Paul Brand and his fellow researchers that blindness was not a direct product of leprosy but a by-product. A serious vitamin A deficiency, for example, could be a major contributing cause of cataracts and consequent blindness. Where cataracts were already formed, it was possible to remove them by surgery.
It was in this field that Dr. Margaret Brand became especially active and effective. On some days she would perform as many as a hundred cataract operations. This number would seem high to the point of absurdity to many European and American eye surgeons for whom twelve such operations in a single day would be considered formidable. But the eye surgeons at Vellore have to contend with literally thousands of people waiting in line to be saved from blindness. They often work fourteen to sixteen hours a day, using techniques that facilitate rapid surgery.
Dr. Margaret Brand was part of a medical and surgical field team that would make regular rounds among villages far removed from the hospital. Surgical tents would be set up. Electricity would be supplied by power take-off devices from the jeep motors.
Cataracts, however, were not the whole story in blindness among lepers. Many lepers at Vellore didn’t suffer from cataracts, yet were losing their sight from eye ulcerations. Did the bacillus leprae produce the infection and the resultant ulcerations and blindness? Or, as in the case of fingers and toes, was the loss of function a byproduct in which other causes had to be identified and eliminated?
The latter line of reasoning proved to be fruitful. Human eyes are constantly exposed to all sorts of irritations from dust and dirt in the air. The eyes deal with these invasions almost without a person being aware of the process. Thousands of times a day the eyelids close and open, washing the surface of the eye with soothing saline fluid released by the tear ducts.
Paul Brand and his colleagues believed this washing process didn’t take place in lepers because there was a loss of sensation on the eye surface caused by the atrophy of nerve endings. This hypothesis was easily and readily confirmed. They observed the eyes of lepers when subjected to ordinary irritations. There was, as they had suspected, no batting of the eyelids; therefore, there could be no washing process. The big problem, then, was to get the eyelids working again.
Why not educate lepers to make a conscious effort to bat their eyes? There being no impairment of a leper’s ability to close his eyes at will, it ought to be possible to train lepers to be diligent in this respect. But experiments quickly demonstrated the disadvantages of this approach. Unless a leper concentrated on the matter constantly, it wouldn’t work. And if he did concentrate, he could think of almost nothing else. No; what was needed was a way of causing eyelid action that would clean the
eyes automatically.
In the case of fingers or toes, it was possible to educate lepers in stress tolerances and to give them protective gloves or shoes. How to keep dirt and foreign objects from getting into the eye? Eye goggles might be one answer but they were not airtight, were cumbersome, would fog up because of the high humidity, and were too easily lost. Something more basic would have to be found.
The answer, again, was found in reconstructive surgery. Paul Brand and his team devised a way of hooking up the muscles of the jaw to the eyelid. Every time a leper opened his mouth the new facial muscles would pull the eyelids and cause them to close, thus washing the eyeball. In this way, a leper could literally talk, and eat his way out of oncoming blindness. Countless numbers of lepers have their sight today because of this ingenious use of surgery in facilitating the use of nature’s mechanism to get rid of dirt and dust in the eyes.
Gradually, as the result of research at Vellore and other leper centers throughout the world, the terrible black superstition about leprosy is receding. Contrary to popular impressions, it is not highly contagious. In fact, it is virtually impossible to transmit leprosy to a healthy person. As with tuberculosis, of course, persons in weakened conditions are vulnerable in varying degrees. The disease is not hereditary; again, however, as with other diseases, increased susceptibility can be passed along from parent to child.