A neurologist trained in movement disorders, Dr. Stamey has no relevant financial or nonfinancial relationships to disclose. His artistic rendering is by Emily Stamey.
Maine PD News receives no outside funding. www.mainepdnews.org
Levodopa, active ingredient of Sinemet, is the most effective drug we have for PD. The discovery of levodopa as a drug for use against parkinsonism in the late 1960s transformed life for people suffering with the disease. Prior to that time, the eventuality for many was to experience progressive stiffness and slowness until they became wheelchair- or bed-bound. I have heard of Parkinson wards in hospitals, where sufferers lingered until they died a premature death related to the complications of immobility. Levodopa liberated people with PD and brought lifespans to that of the general population. As happy as the patients were with this potent new drug, the exciting discoveries with levodopa also attracted bright minds to neurology and neuroscience, which led to a better understanding of the brain’s basal ganglia, which is affected in PD, and to related problems, such as dystonia, chorea, and tics.
The historical perspective
No history of levodopa can be complete. There were many contributors in science and medicine likely not given credit. I do not review the very interesting story in Oliver Sacks’ book Awakenings, though I recommend that related story regarding his work with parkinsonsim and levodopa. And, here I do not delve into Eastern medicine or the use of medicinal plants such as Mucuna pruriens, which was discussed in the article “PD and diet” (MPDN winter 2016/2017). Instead I will give a brief history of scientific discovery. What follows is a timeline as I understand it. It is also a window into how some of the most complex discoveries in science are made. It is a story of collaboration of sorts, the sharing of information and sometimes the reconsideration of some fact through the lens of another mind. It is amazing to me that so many labs from around the world were involved over such a long time. There is probably an earlier point of origin, but for the sake of starting, I will begin here with a timeline.
In 1895, visible lesions of the upper brainstem (a stalk-like structure connecting the brain and spinal cord) were described at autopsy of PD sufferers by Brissaud, who was a professor of pathology in Paris. Brissaud proposed these lesions were significant, but could not define precisely how. At the time, function of this structure was not known. Over the years, dopamine would be detected in the brain but it took time to determine the origin or function. Thus, it was an unconnected discovery when dopamine was synthesized in London by George Barger and James Ewens in 1910. At the same lab, Henry Dale discovered dopamine was chemically similar to epinephrine. There were limitations in biochemistry, and not until three decades later did Peter Holtz of Germany discover the enzyme which converts levodopa to dopamine (aromatic-L-amino-acid decarboxylase, a.k.a. dopa decarboxylase). This discovery would become very important because it gave researchers a mechanism to form dopamine in the brain, though at the time the meaning of this discovery, that it would help people with PD, was not yet understood. You and I can stand in the future and easily see why this discovery was important.
Dopamine, if given by mouth, cannot get from the bloodstream to the brain because it cannot cross the protective blood brain barrier, which shields the brain from many, but not all compounds in the blood.
On the contrary, levodopa is not blocked, and can cross the blood-brain barrier, after which it will be converted by this enzyme to dopamine. That is the basis of treatment with levodopa. However, that would take years to grasp. In fact, around that time Herman Blaschko in Cambridge hypothesized that levodopa and dopamine could be converted to epinephrine and norepinephrine (adrenaline), which was later proven, but again, missed the significance of dopamine in PD. In the next several years dopamine was found in other bodily organs such as the adrenal glands, the heart, and the kidneys, all interesting discoveries apart from the immediate significance in PD.
Redirection back to PD came in 1953 when Drs. Greenfield and Bosanquet of Queen’s Square, University of Oxford, reported the loss of pigment cells of the brainstem substantia nigra (which produce dopamine). In 1956, Oleh Hornykiewicz began working in Blaschko’s lab to clarify whether blood pressure was directly affected by dopamine, versus some breakdown product. He proved dopamine lowered blood pressure and that levodopa had a similar effect. In the 1950s and 60s American cardiac researcher Bernard Brodie showed that the drug reserpine lowered serotonin levels, which he proposed was responsible for controlling blood pressure and the heart rate. His postdoctoral fellow, Arvid Carlsson, was given the task of investigating how the drug reserpine does this. Carlsson argued that it was not serotonin, but a different related molecule responsible for lowering blood pressure. After returning to Sweden and starting his own research own laboratory he showed that an important side effect of reserpine could be reversed by levodopa and not serotonin. Reserpine depleted dopamine in the lab rabbits’ brains, resulting in a drug-induced parkinsonian syndrome, and in high enough doses, total unresponsiveness. Even in that state, when given levodopa, the rabbits’ ears would pop up and they would become alert. Kathleen Montagu, in London at around the same time, was the first to prove that dopamine was present in the brain. Carlsson developed a new technique to measure dopamine in tissue, and showed soon after that dopamine was present in the brain, but depleted with reserpine and restored with L-dopa. Two medical students in Carlsson’s lab, Ike Bertler and Evald Rosengren, mapped the distribution of dopamine in the dog’s brain, and showed concentrations in the basal ganglia. This work was repeated in humans by one of Carlsson’s collaborators, Isamu Sano in Japan.
These findings led Carlsson to speculate, at the 1959 International Pharmacology meeting, that Parkinson disease was related to dopamine.
Following this, in Vienna, Oleh Hornykiewicz began to measure dopamine both in people with Parkinson’s and with post-encephalitic parkinsonism, and in 1960 published a paper showing a marked depletion of dopamine in the basal ganglia (specifically the caudate and putamen) of patients with both of these conditions, but not in people with other brain disorders such as Huntington chorea.
How dopamine was formed in the brain was not known until the early 1960s, when Toshiharu Nagatsu, a postdoctoral fellow at the National Institutes of Health, discovered the enzyme tyrosine hydroxylase, which converts the amino acid tyrosine to levodopa. Thus, it was known that proteins break down to release amino acids such as tyrosine, which is converted to levodopa by tyrosine hydroxylase. Levodopa is then converted to dopamine.
In 1966, Oleh Hornykiewicz proposed that dopamine deficiency in the striatum of the basal ganglia is correlated with most of the motor symptoms of PD.
Over the next several years, using the new technique of histofluorescence, Swedish researchers Annica Dahlström, Kjell Fuxe, and Nils-Eric Andén mapped dopamine pathways in the brain and discovered the nigrostriatal pathway. Meanwhile, Ted Sourkes and Louis Poirier in Montreal demonstrated that, in animals, striatal dopamine levels fall when the nigra is injured. This connected the work of the two groups.
Dopamine as a treatment
In 1960, Oleh Hornykiewicz had begun to consider levodopa as a possible treatment for PD. He and Walther Birkmayer, a Viennese neurologist, found that intravenous injections of levodopa produced dramatic, though short-lived benefits in PD patients. Investigators around the globe demonstrated sometimes positive and sometimes negative results with higher doses of levodopa. For example, Pat McGeer in Vancouver failed to benefit patients with 5 gram doses of the drug D, L-dopa. A major limiting factor was nausea (and perhaps medications used to prevent nausea, which we now know can block dopamine in the brain and cause parkinsonism).
In 1967, Greek researcher George Cotzias showed in a U.S. trial that if one starts with a low dose of levodopa and gradually increases, up to 16 grams daily, benefit can be found without nausea and vomiting. This was verified in several double-blind studies and was the birth of modern treatment.
Nausea was a factor because of the dopamine decarboxylase enzyme, which converts levodopa to dopamine in the body. As above, dopamine cannot cross the blood-brain barrier, and causes nausea. However, the addition of carbidopa to levodopa would increase the strength of levodopa about four-fold and allow most of the drug to reach the brain. This is because carbidopa blocks dopa decarboxylase. Thus, the drug Sinemet, a Latin derivation meaning “without vomit,” was made. Over time, researchers would show that lower doses were effective and perhaps less associated with complications, another complex history, for another time.
Different forms of levodopa
There have been multiple variations on carbidopa/levodopa, such as immediate release, controlled release, and the orally dissolving Parcopa formulation. We have also seen the addition of entacapone (a COMT enzyme inhibitor) in the drug Stalevo. In 2015, the FDA approved Rytary (a combination of long and short-acting carbidopa/levodopa) in a capsule of pellets, which are absorbed at different rates in the GI tract and allow a wider interval between doses in advanced disease than one would expect with the immediate or controlled release forms alone. The Duodopa dopamine pump was approved in Europe over a decade ago, and the Duopa dopamine pump was FDA approved in 2016. Duopa is a gel with a concentration of 20 mg levodopa per 5 mL infused continuously to the GI tract over the course of 16 hours per day. It requires a PEG-J tube (a tube from the small bowel sticking out of the body just below the rib cage) which is attached to the pump. It is typically used in patients who would not qualify for deep brain stimulation but suffer from uncontrolled motor fluctuations.
The levodopa drug development pipeline
The accordion pill, a novel gastro-retentive delivery system, is being developed by Intec Pharma. The pill expands like an accordion in the gut to keep it there while it slowly releases medication. The accordion pill has recently completed a phase II trial of 60 PD patients with doses of 250-500 mg levodopa over a 7-21 day period, given once or twice daily, and per the company’s website (unpublished data) there was a reduction in OFF time and dyskinesias. The baseline characteristics of the patients, including disease severity, were not apparent on the website. The drug will need to complete a phase III trial before FDA approval is sought.
Subcutaneous levodopa (a patch/pump system, clinical trials identifier ND0612), by Neuroderm, is a subcutaneous delivery system of up to 360 mg levodopa over a 24 hour continuous infusion of a patch/pump (a patch with a small needle placed under the skin). It is designed for moderate to severe PD as an alternative to the Duopa pump or deep brain stimulation. Two phase II studies have shown the drug is safe and tolerable. I understand the phase III studies will begin soon. At this point, Boston will probably be the closest option.
Inhaled levodopa, CVT-301, is a self-administered, inhaled form of levodopa by Acorda Pharmaceuticals which has recently completed a phase III trial with a new drug application submission. The idea with inhaled levodopa is to have rapidly effective levels of the drug in the blood, and subsequently, the brain. Thus, the drug would be ideal for rescue from unpredictable off times, such as at a restaurant or a movie.
More delivery systems are being investigated. Levodopa it seems, is going strong at 50.
It is a more common question than you might think. And, people are sometimes confused about what Lyme disease is. This is common with most medical conditions. Medicine is complicated. Without training and a lengthy, diligent effort, one can only have an incomplete understanding, and it will be easy to confuse the facts. Even with training we are left with many questions in science and medicine. That is probably true of any complex issue. This is where logic is needed and the scientific method is crucial. Science is still the best tool we have for trying to solve these difficult questions. When it comes to treating illness, one should learn about the disease in order “to know what you don’t know,” because the opposite situation is dangerous.
I will attempt to explain Lyme as we know it, and answer the question as to whether there is a connection with PD so that there is hopefully less confusion, and perhaps some clarity. This will be somewhat of long article for MPDN, in part because it is complicated, and in part because I am aware that even mentioning the topic of Lyme may upset some patients who have accepted a diagnosis or seem to believe that there is some effort to suppress information about Lyme disease. It is for some, a touchy subject. Still, because it keeps coming up, because it can be a very serious illness, and because the season for Lyme has come along, I want to try to address the issues that have been raised in my office. The best that I can offer is to carefully take points apart, and through this, I hope I can dispel false ideas and bring us closer to understanding this subject.
Why is Lyme a problem?
Lyme disease is on the rise in New England, and can cause serious illness, sometimes affecting the nervous system. The majority of infections are straightforward, and treatment is usually simple. However, diagnosis can sometimes be tricky, especially early after exposure, when the screening test is less accurate. There are, from time to time, complicated cases (such as when one has been untreated for a long duration), but antibiotics appear to be effective, even in that situation. As we will see below, most confusion arises around the post-treatment if patients have persistent symptoms. Some patients incorrectly interpret ongoing symptoms as an ongoing infection, and conclude that mainstream medicine is not the way to deal with diagnosis or treatment. That feeling is not limited to Lyme disease, as we live in a time of open anti-science sentiment and distrust of medicine, even in our elected officials. Out of this fringe, certain jargon has arisen around Lyme disease, reflecting confusion and misunderstanding. Examples include the terms “chronic Lyme,” “Lyme flare,” and “Lyme-literate doctor.” I will discuss the first two terms below. “Lyme-literate,” it is worth pointing out here, actually refers to a healthcare practitioner who accepts and uses alternative, unproven concepts and treatments. The terms listed above are not accepted by most neurologists, infectious disease doctors, or scientists who study Lyme. The language may still be spread by the occasional healthcare provider who does not accept or follow scientifically and evidence-based guidelines, or more commonly by patients who believe they are chronically infected by the organism that causes Lyme disease. Patient advocate groups have arisen and Lyme has become a political issue in New England. As we will see below, laws have been passed regarding Lyme which may be counter to medical guidelines. All of this may lead to confusion and distrust among patients who feel caught in the middle. So, what are the facts? How can we understand Lyme? Can we have some clarity about this disease?
In the beginning
Lyme disease in the U.S. is named for the small coastal Connecticut town where clusters of cases were first reported in 1975. The condition has spread over time, and in 2017 Lyme is found only rarely outside of the Northeast, mid-Atlantic, and
Adult deer tick, Ixodes scapularis, public domain, photo by Scott Bauer. (USDA ARS)
upper Midwest states. Lyme is caused by infection with Borrelia burgdorferi, a bacterium transmitted to humans though bite of an infected deer tick (Ixodes scapularis). Deer ticks are black-legged, and smaller than the more common dog ticks (1).
In Maine, deer ticks tend to cluster in southern and mid coastal regions, probably because of the warmer temperatures, the abundance of mice (which thrive near people and also host deer ticks), and the abundance of deer. It is still possible to catch Lyme disease in any part of the state, though cases are much rarer in western and northern regions where temperatures are lower and mice are probably less abundant (2).
Signs and symptoms of Lyme
Some patients with Lyme disease will have an expanding, and sometimes bullseye-shaped rash, called erythema migrans (EM),
erythema migrans (EM), public domain, photo by James Gathany
which may occur in about half of patients any time between 3 and 30 days after a tick bite. In 2003, when Lyme was not as common, or as well known, a study published in the New England Journal of Medicine (NEJM) (3) screened 10,936 people from 10 states where Lyme was endemic over a 20 month period in an attempt to identify all infections of Lyme, and to describe presenting symptoms. Ultimately, 201 confirmed cases were found. Frequent early symptoms of Lyme disease in the NEJM paper included EM, fever, headache, migratory joint pains, muscle pains, fatigue, and palpitations. The authors noted only 2 to 3 percent of the patients had later systemic involvement such as facial palsy, trigeminal neuropathy, or Lyme arthritis. These are issues that tend to arise only if treatment is delayed (though I would insert that I have seen facial palsy as the presenting symptom). Over time we have learned that another, albeit uncommon late sign of untreated Lyme is carditis (inflammation of the heart) causing AV block, which affects the rhythm of the heartbeat. Further, Lyme as a cause of meningitis (inflammation of the protective tissue covering the brain and spinal cord) is also rare in the U.S. Lyme is a reportable illness in Maine, meaning that doctors and labs are required to report cases to the Maine Centers for Disease Control (CDC). *see Footnote
Maine CDC investigates all reports of positive laboratory tests or clinical diagnoses of EM. Maine CDC also is compelled to produce a formal report for the State Legislature, who as shown below, has been interested in Lyme disease for several years (4).
From the report, we know that Lyme is on the rise, and in 2015 (the latest data publicly available at the time of this article) there were 1,171 “confirmed and probable” cases by federal CDC criteria (5). Among those cases, EM was present 51%, arthritis in 30%, Bell’s palsy or other peripheral cranial neuritis (infection of nerves of the face and head) in 10%. Hospitalization occurred in 3% of cases (38 total). There was no mention of meningitis or other neurologic illness in the report, except to say that these conditions are rare. There were no reports of parkinsonism.
So why do some people think PD is related to Lyme?
To be clear, most people don’t. Onset of PD during a Lyme infection is not common, and there is no evidence that Lyme will cause PD. Still, I am frequently asked by patients with new symptoms of parkinsonism to test for Lyme, if it could be Lyme, or some variation on that theme, and I am not sure why. Further, there are some patients who have been convinced that Lyme disease caused the parkinsonism they began to experience during or some time after a Lyme infection (whether or not they actually had an infection). It is often difficult to convince someone otherwise when the two conditions seemed to come together.
However, one should remember that correlation does not equal causation: two events may occur at the same time and have nothing to do with one another.
Alternatively, there may be a relationship of a sort, but it is not intuitive. Trauma or systemic illness may unmask early PD. Think of it like this: the brain will often compensate for neurologic disease and it may be some time before you know there is a problem as it is slowly smoldering along. Physicians refer to this as the “prodrome.” The progressive loss of dopamine people with PD experience usually takes a minimum of 6 to 7 years to become severe enough to cause visible signs of disease such as tremor, stiffness, or slowness. And, many conditions such as illnesses, surgeries, and traumas may stress the brain and body of a person on the verge of showing signs of PD. Perhaps that stress also uses up dopamine. Whatever the case, that person may then finally start to notice the early indications of parkinsonism that would have occurred in due time, but have become evident sooner. PD is not unique in this way. Several neurologic diseases become apparent a little sooner than they would have in the setting of some other illness. When this happens patients may incorrectly assume one problem caused the other. In fact, one author noted (5):
“Virtually every known neurologic disorder has been blamed on this infection. For most (multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer disease, Parkinson disease), evidence is scant, nonexistent, or coincidental.”
I can see why people might think there is a connection, and it is a very human trait to look for patterns and associations. We are essentially hard-wired that way. It is good idea for survival to remember dangerous correlations. The flaw is that they don’t always connect. We should reason through seemingly connected problems to see if there is a false lead.
The issue is further complicated as Lyme is a complex area in medicine. There is a great deal known about Lyme in science, but much of it is not straightforward, and requires some medical knowledge. There is ongoing research, and like any area of science, there is room for an elevated understanding. People outside of medicine who are trying to learn about Lyme should be careful what sources are used. There is unfortunately an excess amount of false and misleading information on the internet about Lyme. There are also legitimate sources, such as the CDC.
How do you test for Lyme?
The CDC recommends a two-step laboratory testing process. When Lyme is suspected, the first step is an enzyme-immunoassay (EIA). Physicians may also choose the less commonly used indirect immunofluorescence assay (IFA).
If the first step is negative, no additional step is recommended. However, the test checks for antibodies against Lyme which may not have developed in early disease, and may take as long as 8 weeks to develop. Therefore, the EIA test may be falsely negative about 32% of the time in early disease. Repeat testing is sometimes necessary, and often patients are treated empirically if clinical suspicion is high. Doctors should also consider alternative diagnoses, such as other tick-borne illnesses.
If the first step is positive or equivocal, this may mean that similar antibodies are detected, but not necessarily those against Lyme. Thus, the second step is an immunoblot test called a Western blot, a confirmatory test. Results are interpreted as positive only when both steps of the testing are positive. The CDC does not recommend skipping the first step.
There are other commercial lab tests available which are not approved by the FDA or the CDC, yet are still used by a minority of medical practitioners in Maine.
When unproven tests are used, the diagnosis is suspect at best, leaving the actual cause of suffering undiagnosed and untreated.
How is Lyme treated?
Treatment of Lyme disease in most cases is with the oral antibiotic doxycycline for 2 to 4 weeks. Antibiotics kill bacteria. The bacteria that causes Lyme disease is highly susceptible to the drug and a single round of antibiotics is curative in the majority of cases. Infrequently, IV antibiotics such as ceftriaxone are used, such as when a patient has been left untreated for some time and there is evidence of spread in the body.
What is the story with “chronic Lyme?”
About 10% of patients treated for Lyme disease with a recommended course of antibiotics will report ongoing symptoms of fatigue, pain, or joint and muscle aches (6,7). This is unlikely to be an ongoing infection. Most of these residual symptoms resolve after six months, though an even smaller number of patients will report persistent symptoms. Patients, and some health care providers have occasionally referred to this syndrome as “chronic Lyme disease,” which is inaccurate, and the term has been rejected by experts (8).
This is not to say there is no condition. After bacteria are eradicated with antibiotics, if there is a residual condition as described here, it is known by the CDC as “Post-treatment Lyme Disease Syndrome” (PTLDS) (9).
Per the CDC many medical experts attribute lingering symptoms to tissue damage and probable activation of the immune system that occurred during the infection, producing what is called an autoimmune response, in which the immune system later attacks the body. This would not be a unique phenomenon. Examples of other infections that might cause persistent complications and autoimmune response include the bacteria Campylobacter jejuni, with resulting Guillain-Barre syndrome, or bacterial strep throat, resulting in Scarlet fever and later rheumatic heart disease. These are not chronic infections, but the result of the immune system being essentially confused by the original bacteria into attacking some part of the body, even long after the infection is gone. This is an area of medicine in which doctors of immunology and rheumatology are experts. They, along with the boards of neurology and infectious disease, do not recognize “chronic Lyme disease.”
Still, there do not seem to be satisfying treatments for many of the symptoms of PTLDS, and patients may understandably feel very frustrated and suspicious. Adding to the confusion, there are some health care providers who do not follow the guidelines and explain chronic symptoms as being due to chronic infection with Borreliaburgdorferi. I have heard from several Mainers over the last decade of how they have been given either very long, or repeated courses of antibiotics and other treatments (some of which are not FDA approved for any condition) to treat what they refer to as “Lyme flares.” Unless active infection is detected, antibiotics are not indicated, not helpful, and may be harmful to the patient and to others (10-15).
What’s the harm in taking extra antibiotics?
One way unnecessary antibiotics are harmful is through drug resistance. There are over 1,000 species of bacteria in the human gut, and many species in the upper respiratory system. We have more bacteria than you may think. There are more of them in us that there are cells in our own bodies. If that is hard to fathom, consider that their cells tend to be much smaller than ours.
Though most bacteria we possess are benign or even helpful to us, we may harbor bacteria that can turn against us if the conditions are right. And, if exposed to antibiotics, many species of bacteria are able develop drug resistance which may lead to infections that we cannot treat with medications that would have otherwise been curative (12).
Thus, a person may unwittingly develop drug resistant bacteria that may attack then, or lay in waiting for later. In either case, the results can be deadly. Drug-resistant bacteria, and there are some very scary ones, can directly affect the person taking the medication, and can also spread to others.
Antibiotics are not completely benign or risk-free. People may have side effects which can be serious, and death due to treatment for Lyme has been reported (15, 23). Between 2001 and 2014 the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), funded four placebo-controlled clinical studies evaluating whether or not giving prolonged courses of antibiotics to patients with persistent symptoms was helpful (16). The studies were well-designed, and published in peer-reviewed journals after rigorous statistical and scientific review (17-20). Specifically, studies evaluated:
whether B. burgdorferi was susceptible to the antibiotics used;
whether antibiotics remain at effective levels throughout the course of treatment;
whether antibiotics cross the blood-brain barrier to reach the brain and central nervous system;
whether the antibiotics kill bacteria living outside or inside cells of mammals;
safety and welfare of patients enrolled in the trials.
The bottom line was that prolonged antibiotic use was not recommended due to lack of efficacy and the risks of antibiotic therapy. Side effects were common and included intravenous line infections, blood clots, allergic reactions, and gall bladder removal.
Is there a link with Lyme and PD?
There is very little in medical literature linking Lyme to parkinsonism. In a review of the online NIH database Pubmed, which extends back decades and covers peer-reviewed medical journals in English and some foreign languages, there are very few reports of any possible association. In 1989, 12 cases of Lyme disease with neurologic complications were reported in a review of available data (21). Meningoradiculitis (infection of the protective covering of the brain and spinal cord) was seen in seven patients; facial palsy in two cases; infection of the end of the spinal cord, the cauda equina, was seen in one case; and inflammation of the spinal cord and its covering (meningomyelitis) was seen in two. Severe pain was a prominent feature in most cases, and this “consistently and rapidly” improved on high-dose intravenous penicillin, while paresthesias or fatigue often lasted several months, suggestive of the later-described post-treatment syndrome. In a patient who already had parkinsonism, the neurologic condition was not changed by the infection or the antibiotic.
A case which is sometimes cited was a 1997 report of a 78 year old man in Spain with sub-acute mental deterioration, and progressive supranuclear palsy (PSP) presentation (22). PSP is a form of atypical parkinsonism, which is not PD, and is caused by a completely different mechanism in the brain. While there may be some features that are similar to PD, PSP has distinct features: severe eye movement problems, very early falls, early and advanced stiffness of the spine, rather than the limbs. In this patient, Lyme tested positive in the blood and cerebrospinal fluid. The patient reportedly improved after treatment with ceftriaxone. However, this single case report is in question as no organism was found in the brain, and no later follow up as to whether the patient developed parkinsonism was given. Case reports in the medical literature are a description of an unusual situation. Many are written to simply call attention to a possible phenomenon. They are not proof of concept. If no more cases are reported, the association is either extremely rare, or nonexistent. As far as I can tell, no other compelling cases have been described in the literature. There is simply is not adequate evidence to suggest a link between PD and Lyme.
Is Lyme a political issue?
Though Lyme disease is complicated, there is a great deal more known than I have covered here. Obviously, keeping track of the intricate data is not simple. There are guidelines by the CDC, the American Academy of Neurology, and the Infectious Disease Society of America. And there are regulatory agencies in our state: the Maine CDC, the Maine Board of Licensure in Medicine, and the Maine Medical Association. Yet, the legislature of the State of Maine has weighed in contrary to guidelines on Lyme disease.
In 2013 “An Act to Inform Persons for the Options of Treating Lyme Disease” (23) recognized PTLDS, but confused the issue by stating “There are some doctors who believe that longer doses of antibiotics may sometimes be helpful.” One familiar with science will immediately recognize the problems with this statement. The first issue is that it promotes the idea of chronic infection, which is not supported by medical evidence. The second problem is in the terminology. Belief is not science. Belief is akin to faith, acceptance of an idea in the absence of evidence, or in spite of evidence disproving the idea. Doctors are not trained to follow belief. Doctors and other scientists are trained to use logic and the scientific method to question, test, and interpret nature. Through rigorous testing, studies, peer-reviewed publication, and the skills of critical analysis, doctors evaluate the available data to arrive at an understanding of disease. Guidelines are the product of consensus among a designated panel of experts in a field after very careful consideration of the data. Guidelines are meant to protect people and offer the best possible, and safest approach. When the Maine Board of Licensure takes action against a doctor who does not follow guidelines, it is to protect patients.
The law further required the Maine CDC website to list “different alternatives for treatment” instead of simply stating that the evidence-based, expert consensus-driven, peer-reviewed CDC guidelines should be followed. The federal CDC has described some alternatives to therapy (24) as a caution, and noted that none of these are proven helpful, and some are dangerous:
“Patients given a diagnosis of chronic Lyme disease have been prescribed various treatments for which there is often no evidence of effectiveness, including extended courses of antibiotics (lasting months to years), IV infusions of hydrogen peroxide, immunoglobulin therapy, hyperbaric oxygen therapy, electromagnetic frequency treatments, garlic supplements, colloidal silver, and stem cell transplants.”
The state was not finished with Lyme however. In 2015 “An Act to Improve Treatments for Lyme Disease” (25) was passed in Maine, indicating that physicians may prescribe long-term antibiotic therapy against Lyme, thus blocking the Maine Board of Licensure in Medicine from taking action against doctors who treat patients outside of the guidelines for this condition. In June 2015, the Portland Press Herald ran an article about the law, “Maine Legislature clears way for long-term Lyme disease treatment,” (26), in which patients who believed they had chronic Lyme disease gave positive statements in support of the new legislation. However, Dr. Phillip Baker, executive director of the American Lyme Disease Foundation, was quoted to say the law was counterproductive, and it was “sad and most unfortunate that this bill was passed.” He cited the above four NIH studies proving extended antibiotic therapy was not beneficial to patients and may instead be harmful. He noted:
“To ignore such evidence to promote an unproven, unsafe therapeutic approach cannot be in the best interests of the public health and the citizens of Maine.”
Less restraint was voiced by an online blogger for the Society for Science-Based Medicine (27), who reacted to the 2015 Maine law and noted regarding chronic Lyme:
“A whole health care cottage industry has grown up around this fictitious diagnosis, which includes, in addition to physicians, various alternative medicine practitioners, and labs which use unconventional tests to sell the patient on the diagnosis. Having dispensed with the need for objective testing and firm diagnostic criteria, a capacious range of symptoms is a ready rationale for all manner of CAM treatments, such as herbs, supplements, homeopathy, cranial sacral therapy, and such. The favored medical treatment for “chronic” Lyme is long-term antibiotic therapy, an odd choice in the normally pharmaceutically adverse pseudoscience universe.”
Finally, June 16, 2017 the CDC Morbidity and Mortality Weekly Report (MMWR) “Serious Bacterial Infections Acquired During Treatment of Patients Given a Diagnosis of Chronic Lyme Disease — United States” described five patients, one of whom died from the treatment, and others who experienced serious infections after unnecessary treatment with antibiotics. In one case a fatal neurologic diagnosis unrelated to Lyme was missed.
Summary
Lyme disease can be a serious illness.
Proper diagnosis and treatment should be sought (following guidelines).
There is no known connection between Lyme disease and PD.
Chronic Lyme disease is a term that is not accepted by the CDC, which has instead noted that after bacteria are eradicated with antibiotics, if there is a residual condition as described above, it is known as “Post-treatment Lyme Disease Syndrome” (PTLDS).
*Footnote:
Federal CDC defines cases for reporting as “confirmed,” “probable,” or “suspect,” (5) when a person has certain of the following:
1) EM or
2) at least one disseminated manifestation and laboratory confirmation of one of the following:
Positive culture for B. burgdorferi
IgG positive Western blot
Positive ELISA test and an IgM positive Western blot within 30 days of onset (and confirmed by IgG Western blot)
CSF antibody positive by EIA or IFA, when the titer is higher than in serum
Probable cases must meet one of the laboratory criteria mentioned above and be physician diagnosed.
De Wild, et al., Ceftriaxone-induced immune hemolytic anemia as a life-threatening complication of antibiotic treatment of ‘chronic Lyme disease’. Acta Clin Belg. 2016 May 12:1-5. [Epub ahead of print]
Ettestad, et al, Biliary complications in the treatment of unsubstantiated Lyme disease. J Infect Dis. 1995;171:356–361.
Holzbauer, et al. Death due to community-associated Clostridium difficile in a woman receiving prolonged antibiotic therapy for suspected Lyme disease. ClinInfect Dis. 2010;51:369–370.
Lantos, et al. Unorthodox alternative therapies marketed to treat Lyme disease. Clin Infect Dis. 2015 Jun 15;60(12):1776-82.
Marks, et al. Antibiotic treatment for chronic Lyme disease-Say no to the DRESS. JAMA Intern Med. 2016 Dec 1;176(12):1745-1746.
Patel, et al., Death from inappropriate therapy for Lyme disease. Clin Infect Dis. 2000;31(4):1107-9.
Berende et al., Persistent Lyme empiric antibiotic study Europe (PLEASE)–design of a randomized controlled trial of prolonged antibiotic treatment in patients with persistent symptoms attributed to Lyme borreliosis. BMC Infect Dis. 2014 Oct 16;14:543
Klempner, et al., Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. New Eng. J. Med.2001;(345):85-92
Krupp, et al, Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial. Neurology. 2003 Jun 24;60(12):1923-30.
Fallon, et al. A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy. Neurology. 2008 Mar 25;70(13):992-1003.
21..Viader et al, Neurologic forms of Lyme disease. 12 cases. Rev Neurol.1989;145(5):362-8.
Garcia-Moreno, et al. Neuroborreliosis in a patient with progressive supranuclear paralysis. An association or the cause?. Rev Neurol. 1997 Dec;25(148):1919-
CDC Morbidity and Mortality Weekly Report (MMWR) “Serious Bacterial Infections Acquired During Treatment of Patients Given a Diagnosis of Chronic Lyme Disease — United States” online at https://www.cdc.gov/mmwr/volumes/66/wr/mm6623a3.htm
Randall Curtis is in a community of Parkinson Disease (PD) patients who have been through the LSVT BIG program, and have been meeting for a graduate class in Belfast over the last year and half. Mr. Curtis estimates about 30 have been through the class, and many continue to meet. “It is twice a month and doing the class is really good for reinforcing the BIG exercises. We add new moves we don’t do at home. These are extensions of the program. The occupational therapy part is always good, working on core and some pretty interesting things. They added music to try to get us to work with rhythm. It’s a really great workout.” He notes that his daughter, Amanda Curtis, PT, is an instructor, along with Patrice Fox, OT. “They give up their lunch hour for the sessions,” says the proud father and student.
The instructors and I spoke about the program. Amanda Curtis reports that the class takes place at the Waldo County Hospital rehab facility on the second and fourth Wednesday of each month, and lasts about an hour. They tend to split into two groups and break the session into 15-minute segments. They may run through LSVT, then do circuit training on balance, fine motor skills, core strengthening, and boxing. “We’re pretty proud of it up here, because patients have been able to maintain what they have learned in BIG.”
She reports that the high intensity exercise takes a lot of effort, especially given the number repetitions. “We really push people, but it pays off.” In fact, she and Patrice Fox have recently traveled to St. Paul, Minnesota to become PWR! (Power) certified and to expand their PD workout repertoire. “I love this population, obviously, and I have a special place in my heart because of my father. They tell me it is really hard but they want to keep coming back because it works. And they do, they come early and stay late. For me there is something really rewarding about that.”
Patrice Fox noted, “One thing I really love about the group, aside from the physical gains they are making, is that this has become more of a support system. When people exercise together it gets them talking about what they are doing, about medications, and about other issues that they have in common. I think it makes them realize they are not alone on this journey, and there are other people here to support them.” She finds that the camaraderie is important and that “they encourage one another without realizing it. It’s wonderful to watch it happen.” It goes the other way too. She feels supported by the all the positive feedback, and was very touched when a man in the class had a revelation of sorts with her when he realized it was not just him. “It opened up his world to see that there are others with PD.”
Summer is here, time for more Maine PD News. We first launched the site in April, 2016 and since then we have experienced about 7500 visits. And, the number of subscribers is growing rapidly. We are happy to see it. For both methods, we have tried to keep the interaction as uncomplicated as possible, and have had a lot of good feedback from readers. Though this talk we have also come to realize the layout of the website may still not be as user-friendly as it could be.
Changes to the Website
We are looking into making some changes to the way the website is navigated and organized. Whatever changes there are, most visitors seem to find using the search tool to be helpful. If you want to find information on a specific topic, then please try a search. We also try to post upcoming events in the PD community of Maine. If you have an event, please let us know via the Contact Us button. We have additionally found that very few people download a .pdf of the entire issue and we stopped producing that format after the winter issue. We will probably take down the Facebook site as it is not apparently useful to the PD community (and frankly, since it comes down to me, I am not good at setting up articles on FB). Finally, we would like to use this space as a table of contents for the summer issue, and a place to discuss current events.
In This Issue
We will try to tackle the question of whether there is any link between Lyme disease and PD. This is actually a fairly common topic in the office, and apparently for some it is a contentious subject. Reviewing this area raises several points about how we investigate issues and evaluate information in science.
We will discuss the important points and laws around driving, a daily conversation in the neurology office.
We review the history of levodopa as a treatment over the last 50 years. That article concludes with new formulations on the horizon.
We will learn about PD exercise intervention in the Belfast area.
Current Events/In the News
This June Drs. Sarah Dodwell, Markos Poulopoulos, Michael Kleinman, and I met in Vancouver, BC for the annual International Parkinson Disease and Movement Disorders Society Meeting. The event was attended by 4200 registrants from 90 countries and featured a week-long packed schedule of basic science lectures, research presentations, and discussion of other advances. There were 1000s of abstracts presented as well as thought-provoking unusual case presentations. I think we all took away a lot of new information and felt inspired by the conference and the staggering amount of research going on worldwide. However, progress is under threat in this country. In fact, among other groups, the American Academy of Neurology (AAN) has opposed the White House position onfunding of research noting, “The Trump administration released its FY2018 budget proposal which calls for drastic cuts to the National Institutes of Health (NIH), the Center for Disease Control and Prevention, and other federal agencies tasked with health care research and safety.” Likewise, the BRAIN Initiative sent a letter to the Senate Appropriations Committee to request increased funding. The letter was also signed by ten senators, one of whom was Susan Collins. To learn more visit https://www.aan.com/public-policy/capitol-hill-report/june-12-2017/
The AAN was joined by multiple other medical associations across the country, including the largest, the American Medical Association (AMA), whose CEO James Madara has written that the legislation violates the precept of “first do no harm” on many levels. He was quoted on CNN to say “We believe that Congress should be working to increase the number of Americans with access to quality, affordable health insurance instead of pursuing policies that have the opposite effect...” Dr. David Barbe, the president of the AMA was quoted on NPR to say “… does it improve coverage? No. Does it improve affordability? No. Does it stabilize the safety net? Medicaid? No.” Some other organizations opposing the bill include: American Hospital Association, AARP, American Heart Association, American Association of Medical Colleges, American College of Physicians, American Academy of Family Physicians, American Academy of Pediatrics, National Association of Medicaid Doctors, American Psychiatric Association, Federation of American Hospitals, American Lung Association, The National Center on Addiction and Substance Abuse, American Cancer Society Cancer Action Network. The Michael J Fox Foundation issued a “FoxFlash” email the final week of June calling for “Urgent Action Needed: Tell the Senate to Vote ‘No’ on the Health Care Bill.” The notice states that the bill would “seriously negatively impact countless Americans living with Parkinson’s disease (PD), especially older individuals and those who rely on Medicaid.” Lastly, June 22 when the bill was revealed, Senator Angus King went to Facebook with a video statement that the new healthcare bill “… basically increases the cost of health care, particularly for seniors, massively cuts Medicaid, which supports people in nursing homes, disabled people, children, it is a really cruel bill…and it’s going to have a devastating effect economically in Maine on our hospitals and our rural healthcare system…”
Friday, June 23 • 1 p.m.
Smith Auditorium at Sills Hall
Bowdoin College • Brunswick, Maine
This FREE talk–sponsored by Mid Coast Hospital Parkinson’s Disease Support Group will include information on factors important for maintaining brain health and cognitive functioning.
The presentation will review the latest studies on behaviors,
lifestyle choices, and activities for brain health, as well as models of care
that can help patients and caregivers optimize daily functioning.
Dr. Wong is a clinical neuropsychologist with Massachusetts General Hospital/Harvard Medical School. She was previously on staff at Beth Israel Deaconess Medical Center for more than a decade, where she provided neurodiagnostic assessments for patients with neurologic, developmental, and psychiatric disorders.
For more information, or to register,call (207) 373-6585
For parking information and a map of the Bowdoin campus, please download the attached file.
Tuesday May 2nd, 2017 at the Boothbay Region YMCA in support the Maine Parkinson Society. Hunter de Garmo will be running an ultra distance of 50K from 8am – 4pm.
Participants can make a $10 donation and walk, jog or run any distance they choose.
There will be food, music, vendors & activities in the Coastal Club Room from 9am – 12 Noon.
We have long known that constipation is a common non-motor feature of Parkinson disease (PD) (1). One study of 7000 men over a period of 24 years showed that those with initial constipation (less than one bowel movement per day) had a three-fold risk of PD after an average of 10 years (2). Thus, unexplained and persistent constipation in adults is associated with an increased risk of PD: 1/3 will have constipation a year prior to PD diagnosis, and 2/3 will have constipation after diagnosis (3,4). Ultimately, greater than 80% of PD patients will have GI dysfunction of some type early in disease. Investigators have tried to explain this for many years. In the 1970s, one idea was the “slow transit hypothesis,” the idea that slowing down of the gut allowed the absorption of toxins which might trigger PD (5). Though this fell out of mainstream discussion, and may have seemed an oversimplification, the idea is not so far from current thought.
To understand what we now call the gut-brain axis, it helps first to know that your gut, or your digestive tract, contains a lot of bacteria, tens of trillions of them. Largely because of the population in the gut, there are more bacteria than human cells in our bodies. One way they get away with this is that they tend to be much smaller than our cells. Bacteria tend to be about 0.1-5 micrometers in size (millionths of a meter). Human cells range from about 10 to 100 micrometers, so our cells tend to be many times bigger than bacteria. And, as long as they stay in specific locations, bacteria work with, not against us; but when they go to the wrong place, illness occurs: think diarrhea, nausea, vomiting, etc. Under ideal circumstances, among several jobs, many gut bacteria help us to digest food and collect certain nutrients we otherwise would not be able to extract or produce. In exchange for this, they are given food, shelter, and a chance to move along to some other environment – a great reason why we should all wash our hands when leaving a restroom. Half of the dry weight of our stool is bacteria, and if it winds up travelling the fecal-oral route, e.g., hand to doorknob to someone else’s hand to mouth, the consequences can be bad. A few minutes spent in a busy public restroom will alert you that hand washing is not a universal practice.
A healthy gut requires a healthy population of bacteria. To understand this a little better, let’s define a few terms. A single bacterial cell is a microbe. The terms microbiome and microbiota are used a lot when discussing this topic, and for our purposes, they are the collection of bacteria in the gut. There is a group of over a thousand different species of microbes in the gut. Their library of unique genes is over 100 times larger than the number of genes in a person’s DNA library. That is a considerable genetic power. The balance among types of organisms present in the gut is important as well. When there is too much or too little of one type or another, this is imbalance, which we call dysbiosis. Dysbiosis has been linked to inflammation, metabolic disease, certain cancers, and neurologic disease.
Dysbiosis can cause disease because one of the roles of a healthy microbiome is to regulate gut and bodily inflammation. They do this by the release of tiny chemical messengers. In PD, delayed gastric emptying and slow transit of stool may increase the over-production of some types of bacteria, which not only upsets the local balance, but creates the symptoms of gas, colic, and inflammation (6,7). This makes it even easier to get their messengers into the bloodstream. Further, as if pretending to be nerve cells, bacteria can produce neurotransmitters and neuromodulators such as GABA, serotonin, dopamine, or short-chain fatty acids (8). This may allow bacteria to communicate with our nervous system (9).
It also goes the other way. The drugs PD patients take may influence the microbiome (10). One study evaluated 197 PD patients and 130 controls without PD. They were able to identify the types and numbers of microbes taken from stool of each person. Investigators took into account 39 potential confounders such as medications, diet, GI symptoms, and demographics. The gut microbiome was different in PD, and multiple families of bacteria were much more robust. In the PD patients there were also different balances corresponding to different drugs, such as COMTs and anticholinergics. In the study, the effect of L-dopa could not be separated out as 90% of PD patients were taking the drug.
Another reason dysbiosis may be a risk factor for disease is that our gut bacteria protect us by breaking down xenobiotics (herbicides, flame retardants, insect repellents we encounter in the environment). Living in agricultural settings is a known risk factor for PD and this may explain why. In the lab we know that xenobiotics can cause the death of dopamine-producing cells and motor abnormalities in animal models of PD. Therefore, dysbiosis might expose humans to toxins which would otherwise have been broken down. The toxins may trigger disease. The evidence that this may be happening is supported by the observation that the pathologic hallmark of PD, the Lewy body, may be seen in neurons of the gut years prior to the development of motor symptoms of PD, and may be seen in the gut of lab animals given xenobiotics. These observations helped lead to the hypothesis that PD starts in the gut (11).
The most common protein in Lewy bodies is called alpha-synuclein (aSyn). This little protein is found at the point of communication between neurons called the synapse. The job of aSyn is to stabilize little bags of dopamine (vesicles), and to help control synaptic plasticity (the formation of new neural pathways in the brain involved with learning). This protein, like all others, has a very specific three-dimensional shape which it must maintain in order to work. This is similar to a key, which must be shaped a certain way to fit into a lock and turn the tumblers. If the key is bent, it will not work. If aSyn is misfolded, it does not work, dopamine is not released, and new pathways are not made. It may be that exposure to certain toxins triggers the misfolding of aSyn, or there may be other factors such as gene mutations. Whatever the cause, misfolded aSyn may behave very much like a prion, where one bad protein warps others of the same class (think one bad apple spoils the whole bunch).
Testing this idea, researchers exposed lab mice to the pesticide rotenone, which has long been associated with risk of PD in humans (12). The mice developed misfolded aSyn in the gut. Abnormal aSyn in the gut activates immune cells in the brain known as microglia (13). These microglia are then primed to destroy neurons containing abnormal aSyn. This is one of the ways PD patients lose neurons. If present long enough, misfolded aSyn will also travel up the long vagus nerve to the brainstem, where it will spread upwards in the same way the protein spreads in humans with PD. Of note, mice and men with a severed vagus nerve have a lower risk of PD.
In order to test the effects of microbes and molecules on animals, researchers relied on the first gene abnormality identified in PD, the PARK1 gene (14). The PARK1 gene causes the overproduction of aSyn. When the gene is present in mice, they manifest a form of parkinsonism very early in life. However, if the mice are treated with antibiotics to kill the microbiome, motor symptoms of disease become minimal, and there is reduced activation of microglia (15). This led the investigators to raise PARK1 mice in a sterile environment with no microbiome. These mice too, had minimal motor issues. When colonized with a microbiome (transplanted feces) from humans without PD, the mice were unchanged. When given the microbiome from PD patients, the mice developed impaired motor function. This supports the “two-hit” hypothesis, that PD is likely caused by genes and environment. In other words, if someone is predisposed to develop PD because of genes, they may not do so until exposed to some trigger such as a toxin. Researchers were also able to normalize the affected mice by adding normal chemical messages such as short chain fatty acids that a normal microbiome would produce.
Thus, the gut-brain axis raises several interesting questions:
Would a simple stool test reveal risk to PD and other diseases?
Would understanding the microbiome help physicians in selecting the appropriate drugs for people with PD, or lead to the formation of new treatments?
Would changing the microbiome improve disease for people with PD?
If you know, tell me. Otherwise, stay tuned. This is a big topic in PD.
Stylistic and copy editing of this article, as well as helpful insights, by Sarah Savard, RN, and Liz Stamey, RN.
Mulak A, Bonaz B. Brain-gut-microbiota axis in Parkinson’s disease. World Journal of Gastroenterology. 2015;21(37): 10609-10620.
Singharam. Lancet 1995; 346: 861–64.
Hasegawa, et al. Intestinal dysbiosis and lowered serum lipopolysaccharide-binding protein in Parkinson’s disease. PLoS ONE 2015;10, e0142164.
Keshavarzian, et al. Colonic bacterial composition in Parkinson’s disease. Mov. Disord. 2015; 30: 1351–1360.
Lyte M. Microbial endocrinology: Host-microbiota neuroendocrine interactions influencing brain and behavior. Gut Microbes 2014; 5:381-389.
Mayer , et al. Gut/brain axis and the microbiota. J Clin Invest 2015; 125: 926-938.
Hill-Burns et al. Parkinson’s Disease and Parkinson’s Disease Medications have Distinct Signatures of the Gut Microbiome. Movement Disorders. 2017:00: (00)epub online Feb, 2017.
Braak H. Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiology of Aging, 2003 24: 197.
Pan-Montojo, et al. Progression of Parkinson’s disease pathology is reproduced by intragastric administration of rotenone in mice. PloS One 2010;5:e8762.
Erny, et al. Host microbiota constantly control maturation and function of microglia in theNS. Nat. Neurosci. 2015; 18: 965–977.
Polymeropoulus, et al. Mutation in the α-Synuclein Gene Identified in Families with Parkinson’s Disease. Science 1997: 276 (5321);2045-2047.
Sampson et al. Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease. Cell 167, 1469–1480, December 1, 2016.
In the Summer 2016 issue of MPDN we included an article titled Balance in Parkinson Disease (1) which noted that among various interventions, boxing training may be useful in PD. The article summarized a boxing trial published in the journal NeuroRehabilitation (2) which described patients working with certified trainers at the University of Indiana who focused the participants on a circuit of stretching, punching bags, resistance exercises, and aerobic exercise training. Before and after completion at many weeks, those involved demonstrated significant improvements in gait velocity, endurance, balance, mobility, and quality of life. The investigators were building upon an earlier boxing intervention trial published in the journal Physical Therapy (3). Boxing and exercise at large are part of an ongoing effort over the last few decades to identify physical approaches that will not only improve mobility and dexterity, but decrease fall risk, and possibly slow down disease. More on various exercise approaches may be found in the Fall 2016 article by Dr. Kleinman (4).
Building in this direction, in 2016 Cate Parker, MS, RN, CEP, Director of Mid Coast Center for Community Health & Wellness, formed a team of specialists and began a series of ongoing exercise programs at the Landing YMCA in Brunswick (5). There are three classes: a general exercise class for people with PD, a class for graduates of the LSVT program, and Rock Steady Boxing (RSB). I can say anecdotally that feedback from those taking RSB has been very positive.
Cate Parker is happy these programs are taking off, and would stress that physical activity has many potential benefits in PD, including improved strength, mobility, flexibility and balance. “To obtain the greatest benefits, patients must commit to daily exercise for life, just like medicine. Many of our support group participants commented on how difficult it was to exercise on their own or how they were challenged to maintain any improvements they achieved during the LSVT program. The group asked for help. As a result we investigated the best exercise options and decided to collaborate with the YMCA to develop a multi-option approach. Exercise is only helpful if you ‘do it,’ so we decided to provide different options for different people. Our programs include LSVT, dance, yoga and boxing. Almost any exercise is good medicine for someone with Parkinson’s disease.”
Boxing coaches from right to left are Zach Hartman, Kristy Rose Follmar, and Jennifer Anderson.
RSB trainers Zachary Hartman, EP, and Jennifer Anderson, PT, MPT, flew to Indianapolis to learn the technique and become certified instructors. In a written response to questions about the programs, they note that “Parkinson’s specific programs at the YMCA Brunswick Landing offer a range of activities for those of all ability levels. The staff emphasizes safety of each of the participants, while pushing each individual to their intensity threshold in order to help them reach their full potential. After the Rock Steady Boxing class, participating athletes have reported immediate improvements in symptoms such as bradykinesia, posture, and fine motor skills. One boxer reported that he was able to type for the first time in a few years. Other boxers have been able to learn to transfer off the floor independently. A few participants have been quick to report that the high intensity exercise has improved their ability to sleep at night. Participants not only report improvements in physical strength, balance, and range of motion; but they also appreciate improvements in mental and emotional health. The exercise programs allow for great comradery, and they truly feel like they are members of a team working together in order to improve quality of life. The group members are quick to encourage one another. Staff members have heard them commenting to each other on the improvements they can see from one week to the next. Individuals may have good or bad days but as a whole the group is always improving and having fun while doing it. These exercise groups are intentionally not focused on what the athletes cannot do, but instead on what they can do. That positive atmosphere is therapeutic in itself.” Boxing classes for PD take place from 1:30 to 3:30pm, Tuesdays and Thursdays (6).
To learn more about boxing in Brunswick, see the online articles and videos that have been produced lately (7,8,9,10).
footnote: None of the participants were punched in the making of this article.
Combs et al., Community-based group exercise for persons with Parkinson disease: a randomized controlled trial. NeuroRehabilitation. 2013;32(1):117-24.
Combs, et al, Boxing Training for Patients WithParkinson Disease: A Case Series Physical Therapy. 2011;91(1):132-142.
Patrice Fox noted, “One thing I really love about the group, aside from the physical gains they are making, is that this has become more of a support system. When people exercise together it gets them talking about what they are doing, about medications, and about other issues that they have in common. I think it makes them realize they are not alone on this journey, and there are other people here to support them.” She finds that the camaraderie is important and that “they encourage one another without realizing it. It’s wonderful to watch it happen.” It goes the other way too. She feels supported by the all the positive feedback, and was very touched when a man in the class had a revelation of sorts with her when he realized it was not just him. “It opened up his world to see that there are others with PD.”