The New Yorker: The Lyme Wars

The Lyme-disease infection rate is growing. So is the battle over how to treat it.
by Michael Specter July 1, 2013

 tickKaleigh Ahern was twelve years old when a tick bit her. She noticed it “perched” on her shoulder when she was taking a shower one morning. “I thought it was your average, everyday bug,” Ahern told me recently. But, when she tried to brush it off, the tick wouldn’t budge. “The legs wiggled but it was embedded in my skin. I freaked out and started screaming.” Kaleigh’s mother, Holly Ahern, came running and removed it. “I took the kid and the tick to the doctor,” she said. “I told him, Here is my kid, here is the tick, and there is the place where it was attached to her.” That was in 2002. The Aherns live near Saratoga Springs, New York, where Lyme disease has been endemic for years. The infection is transmitted by tick bites, so Ahern assumed that the doctor would prescribe a prophylactic dose of antibiotics. But he said that he wasn’t going to treat it. “If a rash develops or she starts to have flulike symptoms, bring her back,” he told her. At the time, Ahern, an associate professor of microbiology at SUNY Adirondack, didn’t know much about tick-borne illnesses. She took Kaleigh home and watched for the signature symptom of Lyme disease: a rash that begins with a bright-red bull’s-eye around the tick bite.

No rash developed, and Kaleigh was fine—strong enough to become an all-American swimmer both in high school and at Union College. There were times during high school when she felt mentally hazy and not quite right physically, which she attributed to allergies or a teen-age bout of mononucleosis. But at the end of her freshman year in college she found herself crippled by anxiety, depression, and insomnia. She was beset by searing headaches, her muscles often felt as though they were on fire, and her brain seemed wrapped in a dense fog. Kaleigh tested positive for Lyme disease. Like most physicians, her doctor followed the standard medical practice, endorsed by public-health officials throughout the United States, and prescribed a three-week course of antibiotics. “I was so happy to know what was wrong with me,” Kaleigh said. “For a while, I didn’t mind the pain.”

The drugs didn’t work, though. At her mother’s insistence, the doctor extended the prescription three more weeks, but Kaleigh only got sicker. This brought the Aherns to a clinical impasse. The Centers for Disease Control and Prevention has established highly specific criteria for the diagnosis of Lyme disease: an acknowledged tick bite, the appearance of a bull’s-eye rash, and, for those who don’t live in a region where Lyme is common, laboratory evidence of infection. Most people who fit the profile respond well to antibiotics, even months or years after the initial infection. Many Lyme specialists, however, believe that short-term antibiotic therapy may suppress symptoms but rarely cures the disease. Kaleigh switched doctors and began a course of antibiotics that lasted eight more months.

lyme diseaseThere was no change. Furthermore, there is no evidence that prolonged antibiotic therapy helps patients with Lyme disease, so insurance companies almost never pay for it. “I realized that my parents were shoveling thousands of dollars into these antibiotics,” she said. “After the oral approach failed, I was recommended to go onto I.V. treatment, but I had had enough.” Kaleigh’s condition had become so grave that she withdrew from school. “I would have episodes where I would just lie on the ground writhing. And my parents could do nothing but watch. I wish they had taken videos and put them online, so people would know.”

Kaleigh turned to alternative treatments often recommended by Lyme patients with similar experiences. She took herbs—turmeric and ginger, which are thought by some to strengthen the immune system—and she gave up gluten, grains, refined foods, and sugar. The goal was to reduce inflammation caused by her body’s production of insulin and to inhibit the growth of the bacterium that causes Lyme. She also began treatments with a Rife machine, an electromagnetic device invented in the nineteen-twenties which emits radio signals that, some researchers suggest, can destroy harmful bacteria. Although thousands of people are convinced that Rife therapy has helped them with Lyme and other diseases, little empirical evidence exists to demonstrate that it works. Nonetheless, Kaleigh began to feel better. She still has headaches and severe muscular pain at times, but she returned to Union a year ago and graduated this spring. She knows that her approach to Lyme disease is controversial and acknowledges that the improvements might be due to her dietary regimen or to Rife treatments or to a placebo effect. She doesn’t mind; after enduring such pain, she has found that fine points don’t matter.

lyme disease rashLyme disease is the most commonly reported tick-borne illness in the United States, and the incidence is growing rapidly. In 2009, the C.D.C. reported thirty-eight thousand cases, three times more than in 1991. Most researchers agree that the true number of infections is five to ten times higher. Although some of that increase is due to heightened awareness, transmission is rising in areas, like New England, where the disease is well established, and is spreading to regions as far south as Florida, through changes in climate and the movements of infected animals.

The disease is caused by the bacterium Borrelia burgdorferi. In the Northeast and the Midwest, B. burgdorferi is transmitted by the bite of a black-legged tick, Ixodes scapularis. (In the Western United States, a related tick, Ixodes pacificus, prevails, and in Europe the main vector is Ixodes ricinus.) Lyme was all but unknown until 1977, when Allen Steere, a rheumatologist at Yale, produced the first definitive account of the infection. The condition was initially thought to have been an outbreak of juvenile rheumatoid arthritis in and around Lyme, Connecticut. In 1982, Willy Burgdorfer, a medical entomologist at the National Institutes of Health’s Rocky Mountain Laboratories, determined that the infection was caused by the previously unknown spirochete borrelia. As is common in scientific practice, the bacterium was named for him: Borrelia burgdorferi.

Those facts are undisputed. But nearly everything else about Lyme disease—the symptoms, the diagnosis, the prevalence, the behavior of the borrelia spirochete after it infects the body, and the correct approach to treatment—is contested bitterly and publicly. Even the definition of Lyme disease, and the terminology used to describe it, has fuelled years of acrimonious debate. The conventional medical assessment is straightforward: in most cases, the tick bite causes a skin rash, called erythema migrans, which is easily identified by its bull’s-eye. If left untreated, the bacteria can spread to muscles, joints, the heart, and even the brain. Public-health officials say that a few weeks of antibiotic treatment will almost always wipe out the infection, and that relapses are rare. In this view, put forth in guidelines issued by the Infectious Diseases Society of America, Lyme is normally easy to treat and easy to cure.

picture of lyme disease rashFor many people, though, the clinical situation is far more complicated. Some who have been infected with borrelia don’t notice the rash. Others—up to a quarter of those with Lyme, including Kaleigh Ahern—never even get one. Most troubling, some patients who are treated continue to suffer from a variety of symptoms long after their therapy has ended. Nobody really knows why they fail to get better. Infectious-disease experts refer to the phenomenon, which can affect up to twenty per cent of patients, as Post-Treatment Lyme Disease Syndrome. Researchers have attempted to resolve the mystery in experiments with monkeys, mice, and dogs; human studies are also under way. As the number of infections grows, so does the number of people struggling to figure out what is wrong with them.

Many of these patients say that medical officials pay little attention to their persisting symptoms, and that Lyme disease is anything but easy to treat or to cure. They believe that the bacteria can hide in the body for years, potentially causing harm long after treatment ends. This condition, they say, is pernicious, difficult to diagnose, rarely cured, and widely ignored. Moreover, at least four pathogens, in addition to the Lyme bacterium, can be transmitted by the black-legged tick: Anaplasma phagocytophilium, which causes anaplasmosis; Babesia microti, which causes babesiosis; Borrelia miyamotoi, a recently discovered genetic relative of the Lyme spirochete; and Powassan virus. Some of these infections are more dangerous than Lyme, and more than one can infect a person at the same time. Simultaneous infection, scientists suggest, may well enhance the strength of the assault on the immune system, while making the disease itself harder to treat or recognize.

“I am not sure why we act as if we know the answers,” Brian Fallon told me. Fallon, a psychiatrist who has studied the neurological impact of Lyme for years, is the director of the Lyme and Tick-Borne Diseases Research Center, at Columbia University. “The evidence that something more complex is going on is tantalizing and substantial.”

Fallon is right, yet the medical issues have largely been eclipsed by the attention generated by another faction in the Lyme wars. These people—patients, advocates, politicians, and “Lyme literate” physicians, led by the International Lyme and Associated Diseases Society—refer to the illness as “chronic Lyme,” and argue that the traditional approach to diagnosis and treatment, put forth by most American physicians, all but guarantees failure. The Lyme Action Network, one of many political groups that have formed to increase awareness and raise funds, recently released a pamphlet called “It Might Be Lyme.” The group lists dozens of possible symptoms, including headache, joint pain, neck stiffness, chest pain, bladder dysfunction, hypersensitive skin, unexplained fevers, weight loss, sweats, chills, fatigue, blurry vision, heart murmurs, sleep disturbances (including too little or too much), difficulty with concentration, lightheadedness, and mood swings. Physicians associated with the network argue that a cure requires not weeks but months or years of strong antibiotics, and that relapses are common.

“There are two standards of care when it comes to Lyme,” Holly Ahern said. “One in which patients are diagnosed and treated until they get better, and the other where people are treated for three weeks with antibiotics—and, if you don’t get better, then there must be something else wrong with you, or perhaps you are making it up.” Ahern is a scientist, and hers is a measured critique. But emotion and despair are often the driving forces behind Lyme activism. The documentary “Under Our Skin: The Untold Story of Lyme Disease” essentially accused organized medicine of ignoring the illness. Scores of highly read blogs—Lyme Policy Wonk, Touched by Lyme, Living the Lyme Life—regularly overflow with fury.

picture of a tick Nobody disagrees that more research into the long-term effects of Lyme is needed. But most doctors reject the term “chronic Lyme,” in part because many people who say they have it are not infected with borrelia. Without biological proof—a positive blood test or the telltale skin rash—the symptoms are vague and varied and could apply to many conditions. Infectious-disease experts say that the lingering symptoms might be an autoimmune response to the original illness or residual damage to tissues caused by the infection. “There is no doubt that people can have symptoms after being treated for Lyme disease,” Roy Gulick told me when I visited him recently in his office at the Weill Cornell Medical College, where he is a professor of medicine and the chief of infectious diseases. “They can hang on for weeks or months. But you have to be specific about whether it’s plausibly related to Lyme.

“I am sympathetic to people who are suffering,” he continued. “And I have no doubt that they are. But if you have not been infected with borrelia you can’t have Lyme disease. We don’t have all the answers. We never do. These people are true believers. But I’m an infectious-disease doctor. I understand pathogens that cause disease and I understand the manifestations of those infections. Believing or not believing is not part of the process.”

I grew up in Connecticut, attended college in the Hudson Valley, and graduated in 1977, the year Lyme was first identified. I don’t recall hearing about the disease. I do remember going to a professor’s house for dinner one night that year and having him urge me to arrive before dusk, so that we might look for deer. We drove around for an hour without luck, and I wondered whether to believe him when he said he had seen one just the day before.

whitetail deerToday, deer are no longer exotic in the Hudson Valley, and the area has the highest rate of Lyme disease in the country. If you drive the back roads of Columbia County at dusk, deer are nearly impossible to avoid, and accidents are common. Ticks are constantly on residents’ minds, and watching children run barefoot to the edge of the bucolic woods is no longer a carefree delight. Deer are not Ixodes’s most important host, but they have come to symbolize the spread of Lyme, and represent an ecology that has changed dramatically in the past thirty-five years. “Once you have Lyme disease in the area, and once you start to carve up the forest into little bits, and especially when the fragmentation is done by suburban development, you get an increase in Lyme risk,” Richard Ostfeld told me recently when I met with him at the Cary Institute of Ecosystem Studies, in Millbrook, New York. Ostfeld, a senior scientist there, has studied Ixodes for more than a decade. “The best host for the tick and pathogens is not deer but white-footed mice,” he said. “And they do beautifully when you chop the forest into bits. They thrive. And competitors do not.”

Ixodes scapularis is surprisingly sophisticated for an organism that, until it is engorged with blood, is less than half the size of a pea. “These ticks are nimble, durable, and adaptable,” Ostfeld said. The black-legged tick passes through three distinct phases—larva, nymph, and adult—and females require a blood meal at each stage. They usually pick up the spirochete, which under the microscope looks like a spiral French fry, in their first meal, and pass the disease to the host—small mammals, birds, deer, and sometimes humans—during the second or the third. To insure that it becomes engorged, the tick can attach its barbed mouth to a host for up to a week. First, though, the tick releases a series of anti-inflammatory chemicals and antihistamines to numb the skin and make a bite difficult to notice. It then secretes a compound called cementum, a kind of glue that helps the tick adhere to its prey. With those tasks accomplished, the tick bores its mouthparts into its host. While it feeds, the tick can inject borrelia, and other pathogens, into the bloodstream.

Ostfeld is a thoughtful, soft-spoken man, not unduly excitable. But when he talks about the Lyme bacterium he sounds like a proud parent. “Borrelia is a remarkable creature,” he told me. “It has all my respect.” He went on to explain that the bacterium, after slipping through the tick’s mouthparts, can change its form, cloaking itself in the surface proteins of the tick’s saliva. Then, much like H.I.V., the bacterium hijacks the immune system. “It doesn’t stay in the bloodstream for long,” he said. “Instead, borrelia manages to insinuate itself into parts of the body that have fewer circulating antibodies, where it is harder for antibiotics to reach.”

The relationship between the tick and borrelia can be compared to the deadly, symbiotic partnership of Plasmodium falciparum parasites and the anopheles mosquitoes that transmit malaria, which have evolved together for thousands of years. Genetically, the bacteria are so adaptable that it is possible to find different strains of borrelia in the same tick. “Some of these infections are really very worrying,” Ostfeld said, as we sat, one sunny morning, in his green, airy office at the institute. “We can’t even know yet how big a problem a bacterium like miyamotoi will become. But it is possible that Lyme will turn out to be among the least threatening of the pathogens carried by Ixodes.”

Ostfeld, a field biologist, received his Ph.D. from the University of California at Berkeley, and studies the ecology of small mammals—skunks, possums, chipmunks, and white-footed mice—which are found in large numbers in the Hudson Valley. Soon after he arrived at the institute, in 1990, he noticed something striking about the thousands of mice he had trapped: their ears were often covered in ticks the size of poppy seeds. Those ticks, Ixodes nymphs and larvae, were feeding on the mice. “That was the beginning of my interest in Lyme disease,” he said. His 2010 book, “Lyme Disease: The Ecology of a Complex System,” describes the environmental relationship in detail. Before European colonists arrived in America, ninety per cent of New England and New York was covered in forest. Lyme was unknown. In the next century, forested areas were cut by half. “But it was a shitty life here,” Ostfeld said. “Colonists had a rough go of it. The rocky soil was infertile and difficult for agriculture.” In the eighteen-thirties, when the Erie Canal opened the Ohio Valley to agricultural development, the farms of the Northeast were abandoned. The forests returned, along with deer. Mice and other small mammals accompanied them.

Diagnostic failures cause much of the confusion associated with Lyme disease. It takes the tick at least thirty-six hours to transmit borrelia. If ticks are removed immediately, the threat of infection falls dramatically. But it takes weeks, and sometimes longer, for blood tests to detect antibodies; a test taken too soon will produce negative results. Even then, many people who become infected will test negative in error, while others who aren’t infected will test positive.

“You get people all the time who have Lyme but who do not know it,” Ostfeld said. “Their doctors don’t know it.” The basic blood tests look for antibodies but are not always sensitive enough to pick out the right ones. Another test for Lyme disease involves PCR, a technique that allows scientists to amplify the number of copies of a specific region of DNA. When done properly, that test can detect the Lyme spirochete directly. Yet it is prone to contamination, and it often produces positive results for people who are not infected. The situation is similar to one in India, where tens of millions of people test positive for tuberculosis. Few of them will actually get sick, but many are mistakenly treated with highly toxic drugs. A relatively new, but expensive, diagnostic machine can differentiate between latent and active t.b. infections. “We badly need that kind of diagnostic certainty with Lyme,” Ostfeld told me. “And we do not have it.”

Public-health officials stress that if doctors see a bull’s-eye rash they should assume that the patient has Lyme and prescribe antibiotics. The advice is often ignored. Nor do many doctors or patients consider the potential impact of simultaneous infection with several pathogens. “This is not resolved science,” Ostfeld said. “Clearly, not everyone claiming to have Lyme disease is sick, particularly those who have never tested positive for borrelia. But there are just too many questions we still have to answer about those who are infected: Does the bacterium persist after treatment? If so, is it capable of harm? What is the impact of co-infections, and what is really the best way to treat advanced stages of Lyme?

“The conventional view is that several studies have answered the most important questions about persistence and treatment,” Ostfeld went on. “But look at heart disease. How many thousands of studies were conducted on the relationship between cholesterol and heart disease? Over how many decades? And we still go back and forth. When it comes to Lyme, we have a long way to go.”

The controversy over Lyme disease is unlikely to diminish until scientists resolve at least two critical, but related, questions. Can the bacteria persist in the body, causing harm and illness months or even years after treatment has ended? And can prolonged antibiotic therapy destroy the remaining bacteria? Here, as with nearly every issue related to Lyme and its treatment, there is disagreement not only about the answers but also about the questions.

lyme diseaseDetermining whether Lyme spirochetes cause illness after treatment is difficult in part because the symptoms are so diverse. Moreover, it is nearly impossible, with current tests, to know whether the infection has been cured. Recent studies with mice and macaques provide interesting clues. In a study published last year in the online journal Plos One, a team of scientists led by Monica E. Embers, of the Tulane National Primate Research Center, and Stephen W. Barthold, the director of the Center of Comparative Medicine at the University of California at Davis, carried out two experiments on rhesus macaques to determine whether borrelia persists after antibiotic treatments.

First, twenty-four rhesus macaques were infected with the Lyme bacteria in the laboratory. After four to six months, half the macaques received aggressive antibiotic therapy, which, in theory, should have cured them, but the bacteria persisted in some of the animals. Then the scientists used a method called xenodiagnosis to determine if treatment worked in three other monkeys. They planted ticks that had been reared in the lab under sterile conditions on macaques that had received antibiotics, and let them feed for four days. When the ticks were removed and examined, the scientists found small numbers of intact, functioning spirochetes in two of them, which could have come only from the blood of the macaques. A team of scientists led by Adriana Marques, of the National Institute of Allergy and Infectious Diseases, and Linden Hu, of Tufts University School of Medicine, is conducting a similar study in humans. (The scientists have obtained permission from patients to permit ticks to feed on them.)

Other research, by Brian Fallon, the Columbia psychiatrist, found metabolic abnormalities in the brains of patients with confirmed cases of Lyme disease and chronic, post-treatment symptoms, when compared with the brains of healthy control subjects. That, too, suggests the bacterium continues to have an impact. None of these studies provide conclusive evidence, but together they strongly suggest that the infection can survive treatment in a primate. This finding raises the possibility that the bacteria could continue to cause illness long after a patient is supposedly cured. Similar research in mice, published last year in the Journal of Clinical Investigation by a team from Yale Medical School, found that while antibiotics stopped the infection, spirochete antigens persisted in areas adjacent to cartilage—a condition that could produce swelling.

None of these studies have swayed Gary Wormser, the chief of the division of infectious diseases at New York Medical College, and the lead author of the often criticized Infectious Diseases Society of America guidelines for Lyme. He says that, in the absence of new data, doctors should continue to treat Lyme with courses of oral antibiotics that generally take no more than thirty days.

“Right now, in the published literature, there is no evidence of persistence in humans, and if there were I would say, ‘So what?’ ” he told me recently. “You would have to show me that the spirochetes continue to produce disease and you would have to show me that they would respond to antibiotics.” Like most established scientists, Wormser maintains that one can rely only on the best current science-based evidence to practice medicine; otherwise, he may as well rely on voodoo. Furthermore, he stressed that it is dangerous to diagnose a disease based on symptoms alone. “There is a group of people with aches and pains and medically unexplained symptoms that are being treated for chronic Lyme.” He said these patients often go “from doctor to doctor” without a satisfactory diagnosis. “They are suffering and unhappy, and finally they go to a doctor who says, ‘I know what you have, it’s chronic Lyme.’ Then they get treated and treated and treated for chronic Lyme. And patients are happy because somebody has finally taken interest in them.”

Wormser continued, “If you had Lyme and nobody disputes it and you don’t feel back to normal, it’s logical to ask, ‘Does the antibiotic work?’ Or maybe the organism is still there. Those questions have been explored, and we continue to explore them.” Yet he added that the majority of people who are being treated as if they had post-Lyme symptoms have never had the disease. “Never had the test, the rash, swelling, not the slightest credible evidence of Lyme. If somebody walked into your office and said, ‘I have renal failure, I need dialysis,’ you would do a test. If it was negative, nobody in his right mind would give the patient dialysis.”

Wormser’s many critics regard his view of the disease as willfully limited. In response, he and others cite four double-blind, placebo-controlled trials funded by the N.I.H. over the past fifteen years. Each attempted to determine whether prolonged antibiotic treatment, given after the initial courses were completed, helps eliminate persistent symptoms of Lyme disease. The two largest studies reported no evidence of improvement; the results of the other two studies were equivocal. But none of the researchers concluded that the theoretical benefits outweighed the tangible risks of extended intravenous therapy, which included severe infections. In a separate case, a woman on intravenous antibiotics died after a blood clot.

Physicians who regularly see people with Lyme symptoms say that the conventional methods simply don’t work. “I think a lot of these people who are set in their ways need to see more patients,” Richard Horowitz told me when I called him at his office in Hyde Park, New York. Horowitz is one of the most prominent “Lyme literate” physicians: he is board certified in internal medicine and has practiced in the Hudson Valley for more than twenty-five years. Officials who endorse the Infectious Diseases Society of America’s approach to Lyme disease consider Horowitz a pariah, but patients wait for months to see him, and several told me that he had essentially cured them of a disease that nobody else seemed able to treat.

Horowitz told me that he has seen more than twelve thousand patients, all of whom have a tick-borne ailment. Whenever possible, he avoids antibiotics. “Most of my patients do not present simply with Lyme,” he told me. “They almost always have multiple co-infections. That means they have a suppressed immune system with complex symptomology. Thirty days of doxycycline”—the most common drug used to treat Lyme—“just isn’t going to cure this. Each of these pathogens requires different regimens.”

Horowitz offers a complex combination of dietary restrictions and supplements to help “detoxify” the body and starve the bacteria. He argues that organized medicine, by relying on a few double-blind trials, focusses only on borrelia and Lyme. “But we know the ticks can spread many pathogens. More than half of my patients present with babesiosis,” he told me. (It causes symptoms similar to those of Lyme, though it more frequently begins with fevers and chills.) The incidence of babesiosis, which is caused by microscopic parasites that infect red blood cells, has been increasing dramatically in the Hudson Valley, according to research done by Wormser. “That infection has to be treated in an entirely different way from Lyme, and together they cause far more harm than either one does alone,” Horowitz said. “I have never understood why that is a controversial assertion.”

David Roth is not a scientist, but he believes that only science can end the Lyme wars. I met with him one gray, cloudy day on the forty-third floor of the Blackstone Investment Group building in Manhattan, where he is a managing director. Roth was dressed in pinstripes, a crisp white shirt, a yellow tie, and spit-shined brogues. He has an air of distinguished nonchalance, and his brown hair is tousled in the manner of a Kennedy. Three years ago, Roth became very sick, and while it has been difficult for him, and for his family, his illness may be the best thing that has happened for people infected with tick-borne ailments.

“I started working on this problem because I was shocked by the approach of the medical community,” he told me. “I felt there was a real social injustice.” Roth’s story was similar to those of others I had heard. His illness began with flulike symptoms, enlarged lymph nodes, and insomnia. Doctors found no apparent cause. His symptoms worsened; full-body shakes, numbness in his feet and hands, pain in his tendons, and immense fatigue. “I went up and down this city seeing doctors,” he said. “I had CAT scans and PET scans and M.R.I.s.” Those tests also turned up nothing, but eventually—about four months after falling ill—he tested positive for both Lyme disease and babesiosis. He was treated with antibiotics as well as with malaria medication; they helped, but only for a while. “When I stopped, things got worse,” he told me.

The more he looked into the treatment of Lyme, the angrier he became. “Here is what I don’t understand,” he said. “Somebody can get ill and not know what it is and the symptoms get worse and worse. Two years or more later, they can learn that they have Lyme. They take antibiotics for a month. And then, according to their doctors and insurance companies, they are done. Cured. Sometimes that is enough. But many people continue to be sick, and the government’s position, in a world where there are ten times as many bacterial cells as human cells in our body, is that this particular bacteria has been removed forever and the problem must be due to something else.”

Roth is forty-six, goes to the gym several times a week, and looks robust. (“One of the problems with Lyme is that people tend to look better than they are,” he said.) He has received treatment—dietary supplements and dietary changes—from Horowitz, and his health has improved greatly. Like Kaleigh Ahern, he has difficult days, but they are less frequent. Recently, he was appointed to a federal advisory committee that is working on ways to improve Lyme diagnostics. He was one of the hosts of a gala, held by the Tick-Borne Disease Alliance, earlier this year, which raised eight hundred thousand dollars. “I try to act rationally and work with rational people,” he went on. “Sometimes that is hard to do.”

For Lyme activists to be taken seriously, they will have to be led more by people like Roth than by those who foster dark conspiracies. I was told by several Lyme activists that the government created the infection on Plum Island, that reporters at the Times have been “muzzled” and prevented from reporting honestly about Lyme, and that the N.I.H. has made a pact with pharmaceutical companies to ignore chronic Lyme. There is now a bill before the legislature in New York that would require insurance companies to reimburse long-term treatment with antibiotics—even though no study has proved their effectiveness, and treatment with I.V. antibiotics can cause serious, and sometimes fatal, complications.

Meanwhile, the scientists sometimes seem to respond more comfortably to data than to people. Researchers at the N.I.H. are pursing several lines of inquiry, including the possibility of bacterial persistence. The atmosphere resembles that of the early days of AIDS activism, when many of the individuals most at risk lost confidence in their doctors and sought their own medical answers. In the end, organizers of ACT UP and the Gay Men’s Health Crisis became well known for their public protests, but they succeeded for another reason: they did their homework. Nobody was more knowledgeable about the course of H.I.V. infection than the best-informed activists.

Lyme-advocacy organizations need to rely on similarly well-informed people. Kaleigh Ahern is one of them. She recently presented a paper on the behavior of black-legged ticks at the annual meeting of the Federation of American Societies for Experimental Biology. “It was my thesis at Union,” she explained. “I looked at the effects of soil pH on molting success. I wanted to know the ecological factors that make Lyme increase so steadily in this region.” She has applied to graduate school, where she hopes to help develop more useful diagnostics for Lyme.

I asked if her parents were surprised that she has chosen to work with Lyme ticks. “They are horrified,” she told me, laughing. “But, if I don’t do it, who will? ”

Chronic Inflammation – An Epidemic

Inflammation is an immune response; a response to an infection, an irritation, or an injury. Immune cells are called to the site through the blood stream. The blood vessels near the site become miraculously permeable and the site becomes warm and red due to the increased blood flow (warm, hence inflammation).

Neutrophils and macrophages engulf microorganisms and phagocytes are called in. Some immune cells try to “eat” the invaders; others excrete hydrogen peroxide (and other oxidative chemicals) trying to kill them so they can be cleaned up by the phagocytes and friends.

Inflammation is a part of the body’s natural defense system against injury and disease.

Chronic inflammation, on the other hand, is a disease. The system has gotten hung up, and instead of protecting the organism (our bodies) it starts to kill the organism, slowly but surely.

Today modern medicine is starting to admit that chronic inflammation is the main contributing factor to all chronic degenerative diseases, and the root cause of the two greatest killers in America: Cancer and Heart Disease. In deed, chronic inflammation might just be the root cause of all degenerative disease.

Accepting this would certainly simplify preventive medical practices (even as non existent as they presently are), but I find it interesting that once in our early history medicine tried to create a theory that reduced all disease into one or two categories. History does, it seems, repeat itself.

The Damage
Pro-inflammatory cytokines are the part of our immune systems that attack and kill cells with oxidative chemicals. If they don’t stop their attacks, they will start killing cells our bodies need. The inflammation in a joint can eat away at our cartilage and you’ve got a serious case of arthritis. Unchecked inflammation in an organ, say the pancreas, can cause diabetes. Unchecked inflammation is now thought to be responsible for cardiovascular disease and cancers. The elderly are especially vulnerable to this sort of unchecked inflammation since the body looses the ability to “down-regulate” inflammation with age.

You do not have to be old to have chronic inflammation. You can have it and not know it, until it is too late. Thus we are going to spotlight those tests for having chronic inflammation or being at risk for chronic inflammation.

After that, we will outline the therapies to bring down chronic inflammation and how to avoid it in the first place, for you will soon find that inflammation begins on the end of your fork.

Does anyone recall the headlines in the New York Times about blood vessels bursting like popcorn? The article told us that the latest theory on the cause of heart disease is inflammation. One of the doctors who made this discovery was Dr Paul Ridker. The results of his studies in the early 1900s landed on the front pages of the New York Times right around the turn of the century. We’ve covered this in our book, Bypassing Bypass, but we must tell you a little about it right now.

Microorganisms cause inflammation within our blood vessels, and the inflammation attacks the inside of the arteries. Besides immune cells being sent to the site to fight the inflammation, lipoprotein(a) is sent to form a sticky patch over the damaged area; a patch that that can grab onto cholesterol (supposedly bad cholesterol) and a cholesterol bandage is created over the site. However, the inflammation is inside now. The patch grows and bulges. The inflammation grows and bulges. Eventually, “blood vessels explode like popcorn.”

The reason I called the cholesterol “supposedly bad” is that it tried to save your life. If the inflammation continued without being patched by cholesterol, the artery would eventually open and you’d bleed out.

However, because the inflammation was not halted, the bandaged area has burst and the body must quickly respond because your artery is about to open wide. How is this patch formed? By a blood clot.

A clot is formed at the site to patch up the damage. Eventually, lipoprotein(a) will come along and form a sticky patch and attract cholesterol to form a better bandage, but there is a problem, and it has to do with our diet and lifestyle, our hypercoagulable lifestyles. Our blood tends to clot “too” much. The clot formed is usually bigger than it need be, and being such, the chances of it breaking loose increase. If it does break loose and it goes to your brain, you suffer a stroke. If it goes to your heart, you suffer a heart attack.

This sums up a good deal of what we have to say in Bypassing Bypass (which we are rewriting) but there is a lot more to learn (so if you want a copy, go get it here: Bypassing Bypass, and keep in mind that you are eligible to get the updated online version free when it is released).

Knowing you have a problem is the first step to fixing the problem.

The first test you should know about is called the C Reactive Protein test. If your CRP test is positive, you have are three times more likely to die of a heart attack, no matter how many cholesterol drugs you are on, or if your cholesterol is normal. [NEJM, 1997]

Please note that there are two CRP tests. The one that is needed MUST BE specified to the lab as H.S.C.R.P., which is high-sensitivity cardiac reactive protein test. This is crucial as it is measured in mg/L with a range of 3.0 mg/L being a high relative risk. Now, the regular test, CRP, is measured in ml’s. Thus if your results came back showing that your result is 3 you look great and are considered low risk. But, if the lab measured CRP and not hs-CRP than the number is actually 3.0 which is not good.

Since many MDs are still unsure of their positions on chronic inflammation, they often order the wrong test without realizing it. So, be on your toes and always try to know more than your doctor

If you have Vulnerable Plaque (the popcorn popping arteries described above) you have an 800% greater chance of a heart attack.

In July of 2001, JAMA published a study on chronic inflammation and the risk of diabetes. Another test they used, besides the CRP, was an inflammatory marker test, the IL-6. The study concluded that your chances of developing type two diabetes are easily predicted by the outcome of the CRP and IL-6 tests together. The ultimate test would be the Inflammatory Cytokine Profile consisting of the two mentioned plus TNF (tumor necrosis factor), interleukins -1 beta and 8.

What is at stake?
Depression, asthma, pancreatitis, Parkinson’s, lupus, anemia, kidney failure, psoriasis, and fibrosis might just be the start. All of these diseases have a suspected root cause of chronic inflammation.

Seemingly unrelated illnesses often exhibit excess levels of pro-inflammatory markers:

-Allergy — Inflammatory cytokines induce autoimmune reactions
-Alzheimer’s — Chronic inflammation destroys brain cells
-Anemia — Inflammatory cytokines attack erythropoietin production
-Aortic valve stenosis — Chronic inflammation damages heart valves
-Arthritis — Inflammatory cytokines destroy joint cartilage and synovial fluid
-Cancer — Chronic inflammation causes many cancers
-Congestive heart failure — Chronic inflammation contributes to heart muscle wasting
-Fibromyalgia — Inflammatory cytokines are elevated
-Fibrosis — Inflammatory cytokines attack traumatized tissue
-Heart attack — Chronic inflammation contributes to coronary atherosclerosis
-Kidney failure — Inflammatory cytokines restrict circulation and damage nephrons
-Lupus — Inflammatory cytokines induce an autoimmune attack
-Pancreatitis — Inflammatory cytokines induce pancreatic cell injury
-Psoriasis — Inflammatory cytokines induce dermatitis
-Stroke — Chronic inflammation promoted thromboembolic events
-Surgical complications — Inflammatory cytokines prevent healing

Lets take a closer look at some diseases and their inflammatory connection.

-Cancer: in an article entitled “Chronic Inflammation and Cancer,” by Emily Shacter, PhD published in Oncology, she sums up her findings thus:
A substantial body of evidence supports the conclusion that chronic inflammation can predispose an individual to cancer, as demonstrated by the association between chronic inflammatory bowel diseases and the increased risk of colon carcinoma. Chronic inflammation is caused by a variety of factors, including bacterial, viral, and parasitic infections, chemical irritants, and nondigestible particles. The longer the inflammation persists, the higher the risk of associated carcinogenesis. This review describes some of the underlying causes of the association between chronic inflammation and cancer. Inflammatory mediators contribute to neoplasia by inducing proneoplastic mutations, adaptive responses, resistance to apoptosis, and environmental changes such as stimulation of angiogenesis. All these changes confer a survival advantage to a susceptible cell. In this article, we discuss the contribution of reactive oxygen and nitrogen intermediates, prostaglandins, and inflammatory cytokines to carcinogenesis. A thorough understanding of the molecular basis of inflammation-associated neoplasia and progression can lead to novel approaches to the prevention and treatment of cancer. [ONCOLOGY 16:217-232, 2002]


Click on the picture to the right to view an interesting 10 minute video from the company that produces immune26 to help control inflammation and their recent pilot study on the reduction of C-Reactive Protein.


TMD Med-Legal

As trauma, especially the trauma of whiplash injury, has been identified as a precipitating factor for temporomandibular disorders, med-legal disputes frequently arise. This is specifically because casualty insurance, personal health insurance and dental insurance carriers do not want to be responsible for diagnostic and treatment costs. These companies then routinely deny coverage and compensation.

tmd legalThe general topic of temporomandibular disorders is a point of contention within the worlds of personal health and dental insurance because of the lack of specificity in identifying the signs and symptoms of TMD, a complete lack of standardization of protocol for diagnosing and treating them and the prevailing myth that TMD is a dental disorder. This allows any health insurance company to pass off diagnostic and treatment costs to the patients’ dental insurance. The dental insurance may well have a TMD exclusion (or not recognize TMD) and then the bills are then routinely denied.

The issue of traumatic causation is another issue. Casualty insurance carriers do not want to be responsible for TMD treatment delivered when causation is linked to trauma to persons insured by their companies. While coverage here is denied aggressively on the basis of causation, the same issues of diagnostic accuracy, need for treatment(s), acceptable treatment protocol(s) and prognosis are shared by all of these insurance entities.

Financial responsibility rests more heavily with the casualty insurance carriers however, as they do not have the same TMD exclusion clauses found in the health and dental insurance policies. Thus, for one reason or another, many TMD cases come to be litigated. This places a burden on all health professionals treating TMD and brings them into the world of lawyers and litigation. The good news is that examination, diagnosis and treatment of TMD is held to a higher standard. This is good for all concerned.

These issues will be addressed in detail on this blog.

TMD, Oral Orthotics and the Dental Role

I have spent well over 25 years helping to orchestrate co-operative and co-ordinated interdisciplinary diagnostic and treatment models for TMD. The examination, diagnosis and treatment guidelines I outline in work and can make a profound impact on this all too prevalent cause of chronic pain (ranked as second only to low back pain by the NIH in the US). I am hoping that this blog will generate interest and help develop effective treatment teams apart from the “Regional Expert” model. While we need these “TMD experts” and their input, there are far too many sufferers for that model to stand alone.

tmd splintThis is the first of a series of posts on the dental role in treatment of TMD. I’ll start with this; while it has become clear that “malocclusion” is not a cause of TMD and can not be used to predict the eventual onset of TMD, it can perpetuate a TMD once TMD symptoms arise. In that case a dentist can be an invaluable asset to the treatment team as some form of oral orthotic (case specific as to type) may well make all the difference in treatment outcome. PERMANENT CHANGES IN THE OCCLUSION SHOULD NEVER BE MADE WHILE THE PATIENT IS SYMPTOM EXPRESSIVE HOWEVER, AND PERMANENT OCCLUSAL CHANGES ARE RARELY NEEDED TO STABILIZE A SUCCESSFUL TREATMENT RESULT.

tmj splintThis section will be a work in progress and I would love to see a large volume of comments on this topic. It may seem odd that this information comes from a chiropractor but keep in mind that my seminars on this topic were approved for continuing education credits for dentists by the California Dental Board and the “Examination and Diagnosis” section of was reviewed and approved for publication by the University of Michigan School of Dentistry.

Here are three basic, but critically important guidelines… more detailed suggestions to follow:

tmjd splintFirst, and this is an absolute truth that is too often ignored: NO ORAL ORTHOTIC/BITE SPLINT WILL WORK IF THE PATIENT DOES NOT WEAR IT! You must have patient compliance to have any chance of success, no matter what technique or type of orthotic you use. This includes issues such as appearance, comfort, ease of swallowing, interference with speech patterns and more.

Second, when using an oral orthotic in treatment of a TMD you must make sure to avoid unwanted orthodontic movement of the teeth (e.g. extrusion, intrusion, etc.).

tmj splint fittingThird, outside of parafunctional activity (e.g. clenching and grinding), the maxillary teeth contact the mandibular teeth infrequently (about 5 minutes out of 24 hours when swallowing), however, initial occlusal contact influences head/neck posture and head/neck posture influences initial occlusal contact. These facts should be considered by anyone treating TMD patients.

The article below is interesting and I welcome comments:

Warning: “Diagnostic Tools” Proven to be Inaccurate
Scientists have studied the accuracy of electromyography (EMG) of jaw muscles and kinesiographic (KG) recordings that some dentists use to diagnose a TMJ problem. The findings of recent studies show these tools are inaccurate and can provide false positives (indicating that you have a TMD problem when you actually do not). Click here to read a summary of the research findings.

TMD Examination: The Importance of Palpation Findings

The importance of temporomandibular joint, oro-facial and cervical/trapezial palpation findings in the TMD exam (including screening for hypersensitivity, malingering and false complaint).

This is very important information for any practitioner who is examining, referring and/or treating patients who present with headache, neck pain, dizziness, tinnitus, primary ear symptoms and/or TMJ/orofacial pain. If you are curious about why I list these particular symptoms (and you should be) you might want to read through the this research paper.

More detailed information can be found in the “Examination & Diagnosis” link on my website I have bolded the key points in this blog version. All reference numbers found here correspond to references found in the website version. The palpation portion of the examination is demonstrated at 29 minutes 51 seconds on my TMD Training DVD.

All your comments are welcome on this blog!

The six parts of the standard TMD office examination should include at least:

1. Case history
2. TMJ Range of motion
3. Mandibular tracking
4. Palpation
5. TMJ auscultation
6. TMJoint/masticatory muscle challenges (provocations)

This list does not include radiology and special tests which may need to be ordered pending review of the findings documented during the exam above.

Of particular interest is that the most telling findings may well come from the palpation exam when the findings are reviewed in light of the case history and symptom report.

palpation: the act of feeling with the hands or fingers – a phase of the examination procedure in which the sense of touch is used to gather information essential for diagnosis.
palpation, bilateral: a method of examination in which both hands are used to simultaneously examine and compare symmetrical body structures on opposite sides of the body.

Palpation is perhaps the most undervalued and misunderstood of the TMD exam procedures. Palpation findings for muscles, joints, ligaments and tendons are often considered equally reliable or unreliable and lumped under the heading of “subjective” data. In fact, with regards to muscles and joints, inter-examiner and serial intra-examiner reliability is different for each tissue. This includes studies of the cervical, lumbar and masticatory regions (19, 44, 60,90).

The effectiveness of palpation for differentiating patients from non-patients has not been thoroughly validated, however palpation findings have proven very valuable in developing an accurate diagnostic impression when examining a symptomatic patient. 

Interpreting palpation findings:

1. Cervical and/or masticatory muscle tenderness is not a reliable indicator of local muscle pathology as tenderness may represent the affect of a CNS process stimulated by peripheral pathology (90, 105, 115).

2. Identification of trigger points by palpation is reliable (111). Just keep in mind that while trigger points are a source of pain that is expressed elsewhere, they themselves may exist because a neural trigger is stimulating abnormal and perpetuated muscle contraction. This is what drives the peripheral symptom expression of temporomandibular joint specific disorders and why so many TMD cases are misdiagnosed as myogenous when, in fact, they are arthrogenous.

3. In a TMD patient population tenderness over the lateral poles of the temporomandibular joint condyles identifies capsular inflammation accurately especially if the tenderness is equal to or greater than 2 on a 0 to 3 scale and the condyles are as tender or more tender than the ipsilateral masseter and temporalis musculature (105).

4. Palpation of the lateral and posterior capsule of the temporomandibular joint with an algometer shows acceptable inter and intra-examiner reliability and can identify patients from non-patients (13).

5. Females report temporomandibular joint capsule pain at a lower pain pressure threshold than males when tested by algometer (13).

Many difficult questions are now being asked which challenge our ideas about myofascial disorders. In the field of TMD this is very troublesome as a “myofascial” diagnosis is one of the most commonly assigned in clinical practice. Results from four surgical studies and two temporomandibular joint anesthetic injection studies challenge the idea that we can identify myogenous disorders exclusively by the presence of muscular tenderness to palpation. These studies have demonstrated remission of both masticatory and cervical myofascial tenderness when the temporomandibular joints are injected with an anesthetic and/or operated (17, 68, 70, 105, 113). This is not to say that all myofascial presentations are driven by joint inflammation, but rather that muscle tenderness alone cannot rule in a true primary myogenous disorder, cannot rule out an arthrogenous disorder and cannot rule in a mixed arthrogenous/ myogenous disorder as the arthrogenous disorder is capable of driving the entire muscular component (105). Joint tenderness as an isolated finding may not be an accurate inclusionary factor for symptomatic capsulitis as it has been noted that joint receptor discharge increases with muscle activity (66). In fact, comparing locations, patterns and relative degrees of tenderness in the muscles and joints of the head and neck may give us the most useful diagnostic impression (105). It should be noted that the presence of cervical muscle tenderness in patients expressing symptoms in the head and neck has been identified as indicating a high probability of TMD (40, 109, 115).

Palpation of the masticatory and cervical/upper shoulder regions is necessary and important in the TMD examination. These tests are necessary to satisfy the demands of standard of care and can provide useful information in the following ways. First, identification of trigger points and muscle hypertonicity provides targets for treatment in true non-arthrogenous myofascial conditions (112). Second, certain patterns of muscle tenderness and hypertonicity can be informative diagnostically when temporomandibular joint tenderness is present concurrently (105). Third, when temporomandibular joint pathology is suspected of being the driving force behind the symptoms, specific areas of muscle tenderness and hypertonicity can serve as target areas for anesthetic temporomandibular joint injections and/or joint-specific treatment trials (17, 105, 107).

To palpate the temporomandibular joints most effectively have the patient move the chin to the side opposite the joint palpated. When the joint is palpated with the teeth together or the mandible at rest there is approximately 5-10 min of tissue between your finger and the joint capsule. Having the patient maneuver the chin to the opposite side will surface the condyle for more accurate palpation findings.

Palpate the condyle with three to five pounds of pressure with the pad of the index finger.

Palpate the entire condyle accessible to you as the lateral capsule is complex and certain areas may be tender while others remain nontender. Any tender areas of the capsule should be recorded.


1. Condyle tenderness which is equal to or greater than 2 on a 0 to 3 scale and which is more pronounced than ipsilateral anterior temporalis and superficial masseter tenderness indicates temporomandibular joint capsulitis. Patients with this finding are very likely to express TMD symptoms which are driven by temporomandibular joint-specific inflammation and/or mechanical deformation.

2. Tenderness of the belly of the sternocleidomastoideus and/or upper trapezius may be produced by inflammation of the temporomandibular joints. This can be unilateral, bilateral or ipsilateral to the involved joint. These muscles are almost always hypertonic as well as tender if temporomandibular joint inflammation is the driving force behind this finding. This indicates that this is not just referred pain, but a muscular reaction to heightened neurologic activity produced by joint inflammation. This has been confirmed by retrospective surgical testing (70,105) and anesthetic injection studies (17, 105).

3. Temporomandibular joint inflammation produces substantial hypertonicity and tenderness of the paracervical musculature especially in the suboccipital region. It may also cause hyper-contraction and tenderness of the scalene muscles with associated pain and paresthesia in the upper extremities.

4. Temporomandibular joint inflammation does not usually cause isolated tenderness of the spinous processes and interspinous spaces in the cervical region. This helps to differentiate primary cervical injury/pathology from temporomandibular joint-cervical affect.

5. The stylomandibular ligaments and the temporal tendons at their coronoid attachments should also be palpated. Referred pain from the coronoid attachment includes the eye, bridge of the nose, temporomandibular joint and ear (101). Stylomandibular ligament inflammation refers pain to the preauricular region, ear, neck and head (101).

6. The mastoid processes are useful control areas for palpation. Except for mastoiditis or a direct blow to the area, this region is nontender in most all patients (severe temporomandibular joint inflammation may produce slight tenderness in a few patients). This area is above the sternocleidomastoideus insertion and lateral to the upper trapezial insertion. This is an area of thinly covered bone and, while not identical to the temporomandibular joint condyle, is similar. It thus provides an ideal area for comparison of palpation responses. The area should be palpated two to three times during the examination with the same pressure (3-5 pounds of pressure applied with the pad of the pad of the index finger). This allows the doctor to check for consistency of response. This is a valuable screening test for hypersensitivity, false complaint and malingering.

Why Chiropractors do not get TMD referrals, and why they should

chiropractorsTemporomandibular disorders (TMD) have been treated for over a century while practitioners and researchers still struggle with the questions of TMD symptom profile, causation and pathogenesis (1). In the same vein, practitioners in virtually every health care profession treat TMD patients despite the lack of a standardized examination protocol and diagnostic language. As a result, treatments are generally grounded solely in the training and educational perspective of the specific discipline handling the case (e.g. dentistry, maxillo-facial surgery, medicine, chiropractic, physical therapy, psychology, etc.), and if there is more than one practitioner treating the patient, they may never communicate with one another. This is clearly a formula for failure.

Despite the fact that I focused my chiropractic practice on TMD for over 20 years (, and realize how prevalent TMD is, I was recently shocked to find out that more than four billion dollars are spent every year in the United States on the diagnosis and treatment of TMD (NIH). I find it particularly ironic that the bulk of this money is spent on examinations and treatments provided by dentists, despite the fact there is little to support the concept that TMD is caused by malocclusion (2), or effectively treated by occlusal alterations.

In fact, a review of TMD research would lead one to conclude that doctors of chiropractic should be an integral part of any TMD treatment model. This treatment model would certainly include dentists, maxillo-facial surgeons, medical physicians and other health care providers trained to recognize, diagnose, refer and/or treat TMD. Unfortunately, as it exists today, a technique and discipline intensive approach to TMD care funnels this four billion dollars into a chronic pain producing nightmare for many TMD patients, despite the fact that much is known about TMD and chiropractic has much to offer these patients. The following information would suggest that an interdisciplinary TMD treatment model, including doctors of chiropractic, would better serve these patients.

Temporomandibular disorders are a subclassification of musculoskeletal disorders (3,4). Symptoms of TMD are associated with dysfunction of the craniomandibular region and TMD only exists when symptoms are present. There are, in fact, no signs which predict the eventual onset of TMD, e.g. malocclusion (2,5) and bruxism (6). Tumors, vascular disorders, primary neurologic disorders and odontogenic pains are not included under the heading of TMD. Rheumatologic disorders which affect the temporomandibular joints include rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and psoriatic arthritis (3).

tmd headacheLocal TMD symptoms include jaw pain, painful clicking in the temporomandibular joints and limited capacity for mandibular function such as chewing and mouth opening (non-painful clicking in the temporomandibular joint (TMJ) is not considered a symptom, and is not predictive of the development of TMD). While limitation of the capacity for full mandibular movement is usually pain-mediated, mechanical limitations which the patient perceives as dysfunctional are also considered local TMD symptoms. Chronic pain has been associated with TMD, although a clear etiologic relationship between psychological profile and TMD has not been established (7).

Dysfunctional craniomandibular tissues can actually produce symptoms at some distance from themselves, including certain symptoms which appear quite general in nature (8,9,10). It has been demonstrated, for example, that headache, neck pain, upper shoulder muscle pain, dizziness and tinnitus can be direct manifestations of the pathophysiology/pathomechanics of the temporomandibular joints specifically (11,12). These findings may be explained by the impact of the trigeminal-cervical complex on other cranial nuclei (e.g. cranial XI), the cervical dorsal horn, the thalamus and higher order brain centers (13,14). The fact that these symptoms may also be cervicogenic in origin (15) can, and does, cause confusion as to the source of symptoms and may lead to mis-directed treatment. This should interest any practitioner treating head and neck symptoms. This is especially problematic when examining and/or treating a patient who has sustained a whiplash type injury, as whiplash is a known cause of both cervical and TMJ injuries (16,17,18,19,20,21,22). The need for interdisiplinary co-operation becomes even more apparent in these cases, especially between chiropractic and dentistry, when you consider that head/neck posture affects initial occlusal contact and that habitual mandibular posture affects tonicity of the sternocleidomastoid and upper trapezial musculature (23).

neck painIn any case, as headache, neck pain, ear symptoms, upper shoulder muscle pain, dizziness and tinnitus may be produced by any number of disorders, an effective interdisciplinary model is clearly called for. This model should be based on standardized language and examination procedures, source of symptoms diagnoses, time referenced treatment goals and interdisciplinary co-operation. In this vein, a referral for chiropractic care should spring to mind for any practitioner diagnosing TMD and, by the same token, a standardized TMD exam should be performed by any chiropractor examining a patient with head and neck symptomatology.

In that spirit, all examinations of the head and neck region should include the following tests for TMD (1,9,19,24): 1-TMJ range of motion 2-mandibular tracking 3-TMJ auscultation 4-TMJ/oro-facial palpation. Other examination options include TMJ joint and masticatory muscle challenges. It’s interesting to note that this exam parallels the chiropractic musculoskeletal spinal exam in that it seeks to separate arthrogenous from myogenous disorders and access the impact of each on neural function ( This TMJ examination takes only 3-5 minutes and will help identify the source of symptoms. The net result will be timely application of effective treatment and improved treatment outcome.

This a great service that doctors of chiropractic can easily provide their patients and it can lead to substantial practice growth by generating both patient and professional referrals. Once again, four billion dollars per year is spent in the U.S. on TMD with little of that being spent on the benefits of chiropractic care. This does not serve the patients, and limits the growth of chiropractic. With a little effort on our part we can easily make a timely and much needed change for the better on both accounts.

1 Bell,W. Clinical Management of Temporomandibular Disorders. Year Book Medical Publishers, Chicago, 1984.

2- Pullinger AG, Seligman DA. The role of intercuspal relationships in TMD, a review. J Craniomand Dis; Facial and Oral Pain. 199 1; 5:96-105.

3-McNeill C: Temporomandibular disorders; guidelines for classification, assessment, and management. Quintessence Publishing Company, Inc., London.

4- Storey AT; neurophysiology. In: The temporomandibular joint, a biological basis for clinical practice; Sarnat BG, Laskin DM (eds.). WB Saunders Company Publishing, Philadelphia, Pennsylvania 1992:109, 114, 120.

5- DeLaat A, Van Steenberghe D, Lesafre E: Occlusal relationships and TMJ dysfunction. Part II. Correlation between occlusal and articular parameters and symptoms of TMJ dysfunction by Means of Stepwise Logistic Regression. J. Prosthet Dent 1986;55:116-121.

6- Pullinger AG, Seligman DA. The degree to which attrition characterizes differentiated patient groups of temporomandibular disorders. J Orofacial Pain 1993; 7:196-208.

7- King S. Psychologic aspects. In: Temporomandibular disorders, diagnosis and treatment. WB Saunders Publishing, Philadelphia, 1991.

8- Ciancaglini R, Loreti P and Radelli G. Ear, nose, and throat symptoms in patients with TMD: the association of symptoms according to severity of arthropathy. J Orofac Pain 1994; 8(3):293-297.

9-Gelb H. Effective management and treatment of the craniomandibular syndrome. In: Clinical management of head, neck and TMJ pain and dysfunction – a multi-disciplinary approach to diagnosis and treatment. Gelb H. ed. Philadelphia: WB Saunders Company 1977:292-369.

10–Hanson T, Nilner M. A study of the occurrence of symptoms of diseases of the temporomandibular joint, masticatory muscles and related structures. J Oral Rehab. 1975; 2:313-324.

11-Steigerwald DP, Verne S, Young D. A retrospective evaluation of the impact of temporomandibular joint arthroscopy on the symptoms of headache, neck pain, shoulder pain, dizziness and tinnitus. J Craniomand Prac. 1996; 14(l):46-54.

12- Vallerand WP, Hall NIB. Improvement in myofascial pain and headaches following TMJ surgery. J Craniomand Disord 1991; 5 (3): 197-204.

13- Griffin CJ, Harris R. Innervation of the temporomandibular joint. Aust Dent J. 1975; 20:78-85.

14- Bronton JG, Hu JW, Sessle BJ. Effects of temporomandibular joint stimulation on nociceptive and nonnociceptive neurons of the cat’s trigeminal subnucleus caudalis (medullary dorsal horn). J Neurophysiol. 1988;59:1575-1589.

15- Bogduk N. Innervation and pain patterns of the cervical spine. In: Physical therapy of the cervical and thoracic spine. Grant D (ed). Churchill Livingstone, New York 1994:69.

16- Croft AC. Cervical acceleration/deceleration trauma: a reappraisal of physical and biomechanical events. J Neuromusculoskeletal System 1993; 1(2):45-51.

17- 3-Braun BL, DiGiovanna A, Schiffman E, Bonnema J, Fricton J. A cross-sectional study of temporomandibular joint dysfunction in post-cervical trauma patients. J Craniomand Disord 1992; 6 (1): 24-31.

18- Garcia RG, Arrington JA. TMJs evaluated in patients with cervical whiplash injury; News Journal of the American Academy of Head, Neck, Facial Pain and TMJ Orthopedics. Vol.4 No. 1, March, 1992.

19- Goldman JR. Soft tissue trauma. In: Temporomandibular disorders: diagnosis and treatment. Kaplan AS, Assael LA, eds. Philadelphia: WB Saunders Company, 1991:190-223.

20- Kronn E. The incidence of TMJ dysfunction in patients who have suffered a cervical whiplash injury following a traffic accicent. J Orofac Pain 1993; 7(2):209-213.

21- Lader E. Cervical trauma as a factor in the development of TMJ dysfunction and facial pain. Craniomand Pract 1983; 1:86-90.

22- Pullinger AG, Monteiro AA. History factors associated with symptoms of temporomandibular disorders. J Oral Rehab 1988; 16:117-124.

23- Zuniga C, Miralles R, Mena B, Montt R, Moran D, Santander H, Moya H. Influence of variation in jaw posture on sternocleidomastoid and trapezius electromyographic activity. J Craniomand Pract 1995; 13(3): 157-162.

24- Steigerwald DP, Croft A. Whiplash and temporomandibular disorders; an interdisciplinary approach to case management. Keiser Publishing, San Diego, 1992.

TMJ Manipulation

TMJ Manipulation
I’ll do my best here to describe the TMJ manipulation/mobilization technique I have used to treat thousands of TMD patients in both conservative and surgical cases however the technique is best learned by observation. As I can’t actively lecture anymore I have recorded it on the TMD Training DVD along with all of the examination procedures necessary for an accurate diagnosis.

Manipulation of the temporomandibular joints should be a gentle, painless, simultaneous distraction of both joints with guided translatory movements. Manipulative thrusts onto the mandible, especially A-P or lateral thrusts should be avoided at all times and the temporomanidublar joints should not be manipulated in any fashion if the joints demonstrate signs of substantial acute inflammation.

Manipulation Technique
Temporomandibular joint distraction manipulation should be performed with the patient supine to eliminate the effects of gravity on the neuromuscular tone of the elevator muscles of the temporomandibular joints. This is a bimanual, bilateral distraction to avoid distracting one joint only to overload the contralateral joint. The temporomandibular joints should, in fact, be viewed as two halves of one joint and incapable of independent movement.

The objectives of temporomandibular joint manipulation include:
1. Cavitate the joints
2. Adhesion release
3. Capsular stretch and capsular adhesion release
4. Disc “recapture”, that is, allowing the anterior displaced disc to re-seat itself on top of the mandibular condyle.

When distractive temporomandibular joint manipulation is combined with guided translatory movement and proprioceptive neuromuscular facilitation techniques for the external ptyerygoid musculature, it can:
1. Reestablish pterygoid synergy
2. Strengthen and stretch pterygoid musculature
3. Help guide connective tissue matrix formation

The patient is instructed to lie supine with a cervical support pillow placed under the head and cervical spine. The patient’s head is placed in a neutral or slightly flexed posture. The patient is instructed to open the mouth just enough to allow the practitioner to place the thumb pads over the first and second mandibular molars bilaterally. If these teeth are missing, an oral orthotic, dentures, or bridge needs to be in place for support/leverage. The practitioner then flexes the thumbs approximately 5 to 10 degrees forming a slight fulcrum and places the remaining fingers of each hand under the bottom of the mandible with the fifth digits under the chin. The patient is the instructed to slowly bite down. This biting action will initiate distraction of the joints. The practitioner immediately begins to apply gradual distractive pressure by pressing down on the molars while pulling up under the chin with the second through fifth digits of each hand. This rotates the joint, effectively distracting it without trauma. The patient is then instructed to relax the bite while the practitioner maintains and slightly increases the distractive pressure. The practitioner then moves the condyles in a slow, gentle figure-8 movement within the confines of the joint capsule for approximately 5 seconds. While continuing to maintain distraction, the practitioner then instructs the patient to allow the mandible to drop back (retrusion) and then subsequently the patient is instructed to protrude the mandible. Distractive force is maintained during these movements while the practitioner guides parallel joint movement. The patient is then instructed to move the mandible to one side and then the other (laterotrusive movement) while the practitioner increases distraction the contralateral side while maintaining distraction on the ipsilateral side. Distraction is maintained while the patient allows the mandible to fall back into a neutral position. This completes the manipulation/mobilization procedure. This entire process should take less than 30 seconds and need not be repeated more than two times per session. This manipulative procedure is best applied in the subacute and chronic stages of temporomanidular dysfunction and is essential for the effective management of post surgical cases. In the post whiplash scenario, manipulation should enter the treatment protocol as signs of acute joint inflammation begin to subside and continued throughout the protocol until acceptable range of motion is achieved and maintained, adhesion formation is no longer considered an active process and optimum external pterygoid function is restored. In a variation on this maneuver the inferior heads of the external pterygoids can be treated with properioceptive neuromuscular techniques. To accomplish this, have the patient protrude the mandible while you resist mandibular movement for two or three seconds. Then instruct the patient to allow the mandible to passively drop back (retrusion). Repeat this procedure one more time. Follow this immediately with guided protrusion preventing deviation or deflection.

TMD Self Help & Home Care

Patient compliance and self-help initiative can make all the difference when a person suffers from TMD and a treatment plan is developed and initiated. This requires action and compliance by the patient and understanding by the health professionals co-ordinating and delivering the necessary therapies. The world’s best at TMJ manipulation, state of the art physiotherapy, oral orthotic support, TMJ surgery and more will FAIL if home care education is not delivered to the patient and/or the patient does not comply and does not actively participate in the program. In some cases, especially when TMD is accurately diagnosed early on in its pathogenesis, patient self-help and home care may in fact serve to turn the tide toward a spontaneous resolution. This is specifically why all trauma patients reporting head and neck symptoms (with or without local TMJ complaints) should be examined for signs of TMD and placed on a TMD self-help and home care program if there is ANY possibility that one or both of the TMJ’s may have been injured (e.g. there are over 4 million whiplash injuries reported to the police every year in the US alone!).

This page is a work in progress and will grow in content and specificity but the following are the ABSOLUTE MINIMUM instructions to be given to and complied with by the patients:

1. Follow a soft food/no-chew diet for approximately one month. This will include avoidance of foods of various textures including:
– Chewy foods, e.g. sourdough bread crust, pizza and steak.
– Hard foods, e.g. carrots and hard candy.
– Sticky foods, e.g. gum or caramel.

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2. Use a soft, cold compress over the inflamed temporomandibular joint 10-15 minutes per application, 3-4 times per day.

3. Avoid wide mouth opening, especially of a prolonged nature. Suppress yawning and avoid dental visits other than those which are deemed to be medically necessary. (Suppressing yawning can be achieved by either putting your hand under your chin when yawning or lower your head toward your chest when yawning. While both techniques work, a whiplash patient may best be served by using the hand under their chin so they don’t strain their neck.)

4. Avoid repetitive and/or expressive speech. (In severe cases you may have to be placed on temporary disability depending upon your job description.)

5. Avoid clenching. Patients are frequently unaware of any tendency to clench their teeth and, in fact, may only develop this tendency secondary to a whiplash injury or other traumatic event. Avoiding clenching in the early phases of the disorder may well serve to modify this perpetuating influence. One simple suggestion is to focus on keeping the lips together with the teeth apart and having the tongue rest on the roof of the mouth.