New findings on troubling side effects of Parkinson’s medication

NewsPsychology (July 19, 2010) — One in every 100 elderly people suffers from Parkinson’s disease, a disease of the nervous system with symptoms including stiffness and shaking. The standard medication used to treat Parkinson’s is Levodopa, a drug that initially has major benefits but can later also produce serious side effects in the form of involuntary, jerky movements. A research group at Lund University has now found a way to study what it is in the brain that causes these side effects.

The jerky and unpredictable movements that form the side effects of the medication are known as dyskinesias. It is clear that dyskinesias are caused by long-term use of Levodopa, but researchers have been divided on the exact details of the mechanisms behind them and there has been no good way to study them in laboratory animals. This is what the Lund researchers have now developed.

“We use a harmless virus that introduces a small gene into the nerve cells. In a process involving several stages, the gene causes the nerve cells to stop producing dopamine, without destroying them,” explains Ayse Ulusoy. She has recently defended a thesis that includes these studies.

In a patient with Parkinson’s disease, the nerve cells that produce dopamine die. However, at the same time other cells in the brain also suffer changes. This makes it very difficult to find out which of these changes causes the dyskinesias. In the new model system that Ayse and her colleagues have developed, the laboratory rats’ nerve cells otherwise function normally. This is what makes it possible to see what causes the dyskinesias, the unpleasant side effect of the Parkinson’s medication.

“We have seen that they are linked to the ‘fibre terminals’ on the nerve cells that should release dopamine. These new findings open up great opportunities to improve the treatment of Parkinson’s disease in the long run,” says neurologist Gurdal Sahin.

Ayse Ulusoy and Gurdal Sahin are members of Professor Deniz Kirik’s research group at Lund University. The group has recently published its results in the journal PNAS (Proceedings of the National Academy of Sciences). Deniz Kirik believes that the study will be of great international interest, because Parkinson’s disease exists around the world and the side effects of the medication have long been seen as a very serious problem.

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The above story is reprinted (with editorial adaptations by newsPsychology staff) from materials provided by Lund University.

Journal Reference:

  1. A. Ulusoy, G. Sahin, D. Kirik. Presynaptic dopaminergic compartment determines the susceptibility to L-DOPA-induced dyskinesia in rats. Proceedings of the National Academy of Sciences, 2010; DOI: 10.1073/pnas.1003432107

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of NewsPsychology or its staff.

Parkinson’s patients more likely to stick with certain ‘add-on’ drugs

Of the three main types of oral drugs commonly added to levodopa therapy for patients with advanced Parkinson's disease, one might be the most effective, according to a new review.

People with Parkinson's disease often initially experience tremors, stiffness, slowed movement or difficulty with balance and coordination. These symptoms result from the destruction of brain cells that produce dopamine — an important chemical that transmits nerve impulses.

Many people with Parkinson's start treatment by taking levodopa, which the body converts to dopamine. After a time, however, levodopa alone is not always enough.

The three classes of drugs for add-on treatment are dopamine agonists, which stimulate dopamine receptors in the brain, drugs known as COMT inhibitors and MAOB inhibitors, which slow the breakdown of dopamine in the body.

Of these, dopamine agonists might be most effective, according to a new review.

The irony for patients and doctors alike is that while all of the add-on drugs help improve functional motor skills, they simultaneously might increase numerous other side effects such as dyskinesia, dizziness, sleep disturbances, nausea, constipation and even hallucinations.

Although the risk of side effects increased with all three types of add-on drugs, patients were most likely to continue treatment when they were taking dopamine agonists. This class includes medications such as pramipexole (Mirapex), ropinirole (Requip), cabergoline (Dostinex) and bromocriptine (Parlodel).

"There's a tendency to think that stronger drugs give more adverse effects, but we didn't find that with dopamine agonists," says review co-author Carl E. Clarke, M.D., a neurologist at the University of Birmingham in England. "They seem to be as well tolerated as the other classes, so the results are quite positive in terms of using the agonists ahead of the other two."

Parkinson's disease is a chronic, progressive disorder affecting more than 6 million people worldwide, making it the most common degenerative condition of the brain after Alzheimer's disease. Both illnesses are most common in the elderly, so with an aging U.S. population, their prevalence is likely to increase.

"No treatments have been proven to slow progression of the disease," said William J. Weiner, M.D., director of the Maryland Parkinson's Disease and Movement Disorders Center at the University of Maryland Medical Center. "Yet with treatment to alleviate motor symptoms, most patients can function extremely well for six to 10 years."

Levodopa typically controls symptoms very well for up to five years, but eventually a patient's symptoms start to reappear each day before the next dose is due — or symptoms might reappear and disappear unpredictably. Patients might also develop dyskinesia, which results in uncontrollable jerking and writhing movements.

Doctors can then add another medication to the levodopa therapy.

"The greater efficacy and reduced likelihood of patient withdrawal with dopamine agonist therapy possibly outweighs the disadvantage of increased side effects," concludes the review. This finding matches Weiner's clinical experience gained from decades of treating people with the disease.

"Most [Parkinson's] patients prefer to have these dyskinesias and other moderate side effects than to have more disabling motor complications like being unable to walk," he says. "Hallucinations may be troublesome and frightening initially, but they are typically benign — a patient might think he sees a dog — and people can get used to them."

The review appears in the current issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates research in all aspects of health care. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing trials on a topic.

This review assessed data from 44 randomized trials involving 8,436 participants. The authors caution, however, that the studies compared each class of drugs against placebo, rather than conducting "head-to-head" comparisons of each class against the others.

This leaves open the possibility that the findings arose not from actual differences in the treatments, but rather from other factors such as differences in the types of people included in the various trials. A large trial featuring direct comparisons of the three drug classes currently is underway in the United Kingdom, Clarke said.

Of the drugs in the COMT inhibitor class, the review suggests that tolcapone (Tasmar) is as effective as the dopamine agonists. However, tolcapone has been linked to a few cases of fatal liver toxicity and can now only be prescribed in the United States with intense monitoring.

"Tolcapone is worth using in patients where [the alternative] is not working well, and we mustn't discount it," Clarke said. "This evidence clearly states that."

The review disclosed that Clarke has received payments for consulting, lectures and travel from Boehringer-Ingelheim, GlaxoSmithKline, Lundbeck, Orion, Teva, UCB, and Valeant.


Journal Reference:

  1. Stowe et al. Evaluation of the efficacy and safety of adjuvant treatment to levodopa therapy in Parkinson´s disease patients with motor complications. Cochrane Database of Systematic Reviews Reviews, 2010; DOI: 10.1002/14651858.CD007166.pub2

Skin cells could help discover cause of Parkinson's disease

Researchers are applying new stem cell technology to use skin samples to grow the brain cells thought to be responsible for the onset of Parkinson's disease, according to a presentation at the UK National Stem Cell Network (UKNSCN) annual science meeting.

Dr Richard Wade-Martins, head of the Oxford Parkinson's Disease Centre, explained how he and his team will be gathering data from over 1,000 patients with early stage Parkinson's disease and taking small samples of skin tissue to grow special stem cells — induced pluripotent stem cells (iPS cells). iPS cells can be generated from accessible tissue such as the skin and then used to generate specific types of cell.

The researchers will use the iPS cells to grow dopamine neurons — the brain cells responsible for the production of dopamine, as it is these cells which die in patients with Parkinson's, leading to the onset of the disease.

Dr Wade-Martins explains: "Parkinson's disease is the second most common neurodegenerative disease in the UK and is set to become increasingly common as we live longer. iPS cells provide new and exciting opportunities to grow and study dopamine neurons from patients for the first time. This technology will prove to be extremely important in diseases which affect the brain because of its relative inaccessibility — it's far easier to get a skin sample than a brain biopsy. Once we have neurons from patients we can compare the functioning of cells taken from patients with the disease and those without to better understand why dopamine neurons die in patients with Parkinson's."

Over the next five years, the researchers funded by the charity Parkinson's UK, will combine their stem cell work with the latest techniques in molecular genetics, protein science and brain imaging to develop ways of detecting the early development of Parkinson's disease in individuals before symptoms arrive.

The £5 million Monument Discovery Award given to Dr Wade-Martins and his team is the largest grant ever awarded by Parkinson's UK.

Dr Kieran Breen, Parkinson's UK Director of Research said: "We are passionate about finding a cure for Parkinson's. This is vital research that will help us better understand the causes of this devastating condition and how it develops and progresses. We hope the work will pave the way for new and better treatments for people with Parkinson's in the future."

High vitamin D levels associated with reduced Parkinson's disease risk

Individuals with higher levels of vitamin D appear to have a reduced risk of developing Parkinson's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.

Vitamin D is known to play a role in bone health and may also be linked to cancer, heart disease and type 2 diabetes, according to background information in the article. "Recently, chronically inadequate vitamin D intake was proposed to play a significant role in the pathogenesis of Parkinson's disease," the authors write. "According to the suggested biological mechanism, Parkinson's disease may be caused by a continuously inadequate vitamin D status leading to a chronic loss of dopaminergic neurons in the brain."

Paul Knekt, D.P.H., and colleagues at the National Institute for Health and Welfare, Helsinki, Finland, studied 3,173 Finnish men and women age 50 to 79 who did not have Parkinson's disease at the beginning of the study, in 1978 to 1980. Participants completed questionnaires and interviews about socioeconomic and health background, underwent baseline examinations and provided blood samples for vitamin D analysis.

Over a 29-year follow-up, through 2007, 50 of the participants developed Parkinson's disease. After adjusting for potentially related factors, including physical activity and body mass index, individuals in the highest quartile (one-fourth of the study population) of serum vitamin D levels had a 67 percent lower risk of developing Parkinson's disease than those in the lowest quartile of vitamin D levels.

"Despite the overall low vitamin D levels in the study population, a dose-response relationship was found," the authors write. "This study was carried out in Finland, an area with restricted sunlight exposure, and is thus based on a population with a continuously low vitamin D status. Accordingly, the mean [average] serum vitamin D level in the present population was about 50 percent of the suggested optimal level (75 to 80 nanomoles per liter). Our findings are thus consistent with the hypothesis that chronic inadequacy of vitamin D is a risk factor for Parkinson's disease."

The exact mechanisms by which vitamin D levels may affect Parkinson's disease risk are unknown, but the nutrient has been shown to exert a protective effect on the brain through antioxidant activities, regulation of calcium levels, detoxification, modulation of the immune system and enhanced conduction of electricity through neurons, the authors note.

"In intervention trials focusing on effects of vitamin D supplements, the incidence of Parkinson disease merits follow up," they conclude.

Editorial: Findings Add to Research on Neurological Effects of Vitamin D

"The study by Knekt et al in this issue of the Archives is the first longitudinal analysis of vitamin D status as a risk of incident Parkinson's disease and examines a cohort of more than 3,000 participants from the Mini-Finland Health Survey," writes Marian Leslie Evatt, M.D., M.S., of Emory University, Atlanta, in an accompanying editorial.

"A growing body of basic research lends plausibility to a role for adequate vitamin D status protecting against development of Parkinson's disease," Dr. Evatt writes. "Knekt and colleagues' study provides the first promising human data to suggest that inadequate vitamin D status is associated with the risk of developing Parkinson's disease, but further work is needed in both basic and clinical arenas to elucidate the exact role, mechanisms and optimum concentration of vitamin D in Parkinson's disease."

"With the animal data showing a U-shaped curve for neuroprotective effects of vitamin D, it seems prudent to confirm the findings presented in this issue and investigate whether the apparent dose-response relationship observed in the current study maintains its slope, levels off or becomes negative with higher 25-hydroxyvitamin D concentrations. In the interim, data from interventional studies of fractures and falls appear to justify optimizing vitamin D levels to greater than 30 to 40 nanograms per milliliter."


Journal References:

  1. Paul Knekt; Annamari Kilkkinen; Harri Rissanen; Jukka Marniemi; Katri Saaksjarvi; Markku Heliovaara. Serum Vitamin D and the Risk of Parkinson Disease. Arch Neurol, 2010; 67 (7): 808-811 [link]
  2. Marian Leslie Evatt. Beyond Vitamin Status: Is There a Role for Vitamin D in Parkinson Disease?Arch Neurol, 2010; 67 (7): 795-797 [link]

Parkinson's: New clues to alleviating gait disorders and falls

Many of the symptoms of Parkinson disease can be alleviated with drugs that target dompamine, a chemical in the brain that is involved in nerve cell communication and therefore known as a neurotransmitter. However, such drugs do not improve the gait disorders and falls that commonly affect individuals with severe and advanced forms of Parkinson disease.

Understanding which nerve cells in the brain are involved in these symptoms of Parkinson disease might provide researchers with new therapeutic targets. In this context, a team of researchers, led by Chantal François and Etienne Hirsch, at Université Pierre et Marie Curie — Paris 6, France, has now determined that the presence of gait disorders in patients with Parkinson disease and in aged monkeys with Parkinson-like disease was associated with loss of nerve cells that produce the neurotransmitter acetylcholine in a region of the brain known as the pedunculopontine nucleus (PPN).

Consistent with this, disrupting these nerve cells induced gait and postural deficits in monkeys. The authors therefore suggest that targeting acetylcholine-producing nerve cells in the PPN might provide a way to alleviate the gait disorders and falls experienced by individuals with Parkinson disease.


Journal Reference:

  1. Carine Karachi et al. Cholinergic mesencephalic neurons are involved in gait and postural disorders in Parkinson disease. Journal of Clinical Investigation, DOI: 10.1172/JCI42642

Link between brain activity and Parkinson's disease symptoms: New strategy for treating movement disorders identified

 Scientists at the Gladstone Institute of Neurological Disease (GIND) and Stanford University have shown how key circuits in the brain control movement. The research, published in the journal Nature, not only establishes the function of these circuits, but offers promise for treating movement related disorders, such as Parkinson's disease.

The research team was led by GIND investigator Anatol Kreitzer, PhD, who collaborated with Stanford's Karl Deisseroth, MD PhD, creator of a light activation technology that enabled scientists to activate specific circuits in the motor regions of brain.

"Scientists had identified and diagrammed these circuits in the late 80s and early 1990s, but there had been no way to test their function in animal models," explained Dr. Kreitzer. "This research used genetic methods to allow mice to produce a light-sensitive protein in very select group of cells in the brain."

For decades, a leading theory predicted that our movements are controlled by "go" and "stop" circuits, or pathways, that exert a sort of push-pull control over motor function. Signals are sent to the motor control center in the brain cortex to say, "Yes, go ahead and do this," or "No, stop. Don't do this." In Parkinson's disease, these pathways were thought to go out of balance, causing "stop" signals to dominate. But the function of these pathways had never been experimentally tested.

The researchers used a molecular "switch" from green algae called channelrhodopsin-2 (ChR2), which is turned on by blue light. Scientists genetically engineered ChR2 specifically into cells of either the stop or go pathways in a mouse.

A fiber optic the width of a human hair was then inserted into the brain. When a laser connected to the fiber optics was illuminated, the light in the brain caused the ChR2 to turn on, and this action stimulated only the stop cells or only the go cells. When the light was off, the cells were quiet. As soon as the light was turned on, they became active. When the light was turned off, the activity stopped.

"The theory about Parkinson's is that the 'stop' pathway becomes more active," Kreitzer said. "We wanted to see if we could mimic a Parkinson-like state simply by activating the stop pathway in a mouse."

Researchers found that the mouse with the fiber optics implanted in the brain moved normally with the laser turned off and froze when the laser was turned on. With the laser off, and the mouse's movement was restored. "It's not something we can do for just a second," Kreitzer said. "We can do this for as long as the laser is on."

The fundamental nature of movement makes diseases of the motor system, such as Parkinson's disease, particularly devastating. After Alzheimer's disease, Parkinson's is the second most common neurodegenerative disease. It is caused by a loss of the brain chemical dopamine, and it affects 1-3% of those over 65, or about one million Americans. Its major symptoms are resting tremor, rigidity (an increase in muscle tone), slowed movements, problems with posture, and difficulty walking.

"We found that by activating the 'stop' pathway we could mimic Parkinson's disease. But what we really wanted was a strategy to treat the disease symptoms." For this, Dr. Kreitzer and colleagues turned to the "go" pathway. "We thought that by activating the 'go' pathway, we could re-balance these brain pathways and directly restore movement, even in the absence of dopamine." The strategy worked even better than expected. "We generated mice that lacked dopamine, and these mice showed many of the same symptoms found in humans with Parkinson's disease. But when we activated the 'go' pathway in these mice, they began to move around normally again. We restored all of their motor deficits with this treatment, even though the mice still lacked dopamine."

He added that selective stimulation of the motor planning circuitry might be important for treating Parkinson's and also other disorders involving these circuits, such as Huntington's disease, Tourette's syndrome, obsessive-compulsive disorder, and addiction. Finally, by using these methods to identify the important circuits, new drugs can be developed to home in on these specific circuits now that their function is known.

Other contributors to this work are Lex Kravitz, Benjamin Freeze, Philip Parker, Kenneth Kay, and Myo Thwin.

The research was funded by the Gladstone Institutes, the W.M. Keck Foundation, the Pew Scholars Program in the Biomedical Sciences, the McKnight Foundation, and the NIH.

Dr. Kreitzer's primary affiliation is with the Gladstone Institute of Neurological Disease where his laboratory is located and his research is conducted. Dr. Kreitzer is also Assistant Professor of Physiology and Neurology at the University of California, San Francisco.

Tests help predict falls in Parkinson's disease

A group of tests may help predict which people with Parkinson's disease are more likely to fall, according to a study published in the June 23, 2010, online issue of Neurology®, the medical journal of the American Academy of Neurology.

"Falls are a major problem for people with Parkinson's disease and can lead to injuries and reduced mobility, which can result in increasing weakness, loss of independence and increased use of nursing homes," said study author Graham K. Kerr, PhD, of Queensland University of Technology in Brisbane, Australia. "Despite these issues and their impact on the health care system and society, little research has been done to help predict which people with Parkinson's disease are more likely to fall so we can try to prevent these falls."

For the study, 101 people with Parkinson's disease who were able to walk without any aids took a variety of tests evaluating their Parkinson's symptoms, balance and mobility. The participants then reported any falls that occurred over a six-month period.

Most participants were in the early stage of the disease, with an average of six years since the disease was diagnosed. The majority of the participants (77 percent) had the type of Parkinson's that is mainly affected by difficulty with voluntary movements, while 20 percent had tremors as the central symptom of the disease.

A total of 48 percent of the participants had a fall during the study and 24 percent had more than one fall. A total of 42 percent reported that they had fallen in the year before the study started.

The tests that were the best predictors of whether a person was likely to fall included a test of overall Parkinson's symptoms, a questionnaire on how often people tended to "freeze" while walking, and a test of balance. When these tests were combined, the results produced a sensitivity of 78 percent and a specificity of 84 percent for predicting falls. Sensitivity is the percentage of actual positives that are correctly identified as positive, and specificity is the percentage of negatives that are correctly identified.

"These tests are easy to implement and take only a short time to complete," Kerr said. "Once we can identify those at risk of falling, we can take steps to try to prevent these falls." In the United States, it is estimated that about one million people have Parkinson's disease.

The study was supported by Parkinson's Queensland Inc., the Queensland University of Technology, and the Australian National Health and Medical Research Council.

The American Academy of Neurology, an association of more than 22,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease, and multiple sclerosis.

Parkinson's patients' 'risky behavior' explained

Scientists at UCL (University College London) have explained Parkinson's patients' risky behaviour, a rare side effect of standard treatments for the disease. The finding has implications for future medication of patients.

The standard treatments for Parkinson's disease, which work by increasing dopamine signalling in the brain, can trigger highly risky behaviours, known as 'impulsive-compulsive spectrum behaviours' (ICBs) in approximately 5-10% of patients.

New results, published June 23 in the journal Neuropsychopharmacology, uncover a possible explanation for this behaviour — impaired self-control combined with surprisingly normal motivation. Researchers have shown that Parkinson's patients with ICBs are much more willing to take immediate but smaller benefits rather than waiting for larger ones in the future.

"Some patients end up gambling away their life savings while others run up huge credit card debts. This work sheds light on the reasons behind such behaviours, and may help to treat sufferers of Parkinson's disease in the future," said Charlotte Housden who carried out the work at UCL's Institute of Cognitive Neuroscience, and is now at the University of Cambridge.

Researchers studied a group of 36 Parkinson's disease patients, half of whom had ICBs, and compared them to a group of 20 elderly volunteers without Parkinson's disease. All the participants completed two tests: a computer game that measured motivation, on which the participants attempted to win cash by responding quickly and learning associations between pictures and money; and a questionnaire about financial decisions.

This questionnaire measured a form of impulsivity called "delay discounting," by asking whether someone would prefer receiving a smaller payment quickly, as opposed to waiting for a larger payment. For example, would you prefer to receive £50 today or £80 in a month's time?

The data revealed a clear pattern of results. Against the researchers' expectations, the Parkinson's patients who suffered from ICBs were not more motivated to win money on the computer game than the control volunteers. They were also no better at learning about which stimuli predicted money. On the other hand, they were considerably more likely to choose smaller immediate payments over larger but delayed ones on the questionnaire.

Dr Jonathan Roiser, from the UCL Institute for Cognitive Neuroscience, and supervisor of the study said: "The pattern of more impulsive choices together with intact motivation and learning suggests that ICBs may be mediated by impaired self-control, and not excessive motivation for rewards."

The researchers hope that this study might help in the identification and treatment of ICBs in the future.

Charlotte Housden explained: "Often, when neurologists identify these risky behaviours, their only option is to reduce the dose of drugs which treat the primary symptoms of Parkinson's disease, such as tremor and stiffness. However, this is far from ideal, since an inevitable consequence of this strategy is that these primary symptoms get worse. Our results suggest that treating impulsivity in Parkinson's disease patients with ICBs, for example with drugs used to treat other types of impulsive behaviours, might reduce their risky behaviours without worsening their primary symptoms."


Journal Reference:

  1. Charlotte Housden et al. Intact Reward Learning but Elevated Delay Discounting in Parkinson's Disease Patients With Impulsive-Compulsive Spectrum Behaviors. Neuropsychopharmacology, (in press)

Genes and pesticide exposure interact to increase men's risk for Parkinson's disease

Genetic mutations and workplace exposure to some insecticides together appear to be associated with an increased risk for Parkinson's disease among men, according to a report in the June issue of Archives of Neurology, one of the JAMA/Archives journals.

"In most cases, the etiology of Parkinson's disease is likely to be multifactorial, and environmental factors as well as their interaction with susceptibility genes are considered to contribute to the disease," the authors write as background information in the article. Humans exposed to certain pesticides, including organochlorines such as DDT, have been shown to develop Parkinson's disease through damage to neurons that produce the neurotransmitter dopamine.

"If environmental chemicals can increase Parkinson's disease risk, host factors that contribute to variability in their uptake, metabolism and distribution in the body may modulate individual risk," the authors write. "Genetic polymorphisms of xenobiotic [compounds not naturally found in the body] metabolizing enzymes may act as susceptibility factors." The gene ABCB1 may encode the production of compounds essential to this process.

Fabien Dutheil, Ph.D., of Université Paris Descartes, Assistance-Publique Hôpitaux de Paris, and colleagues studied 207 individuals with Parkinson's disease and 482 matched controls. Participants were assessed to detect two known ABCB1 polymorphisms and classified as never users, users for gardening and professional users of pesticides. For professional users, detailed information on lifelong pesticide use was gathered.

Overall, ABCB1 polymorphisms were not associated with Parkinson's disease risk. However, among 101 men with Parkinson's disease and 234 matched controls, the relationship between organochlorine insecticide exposure and Parkinson's disease was approximately 3.5 times stronger in men who carried two variant alleles (gene copies) compared with those who were not carriers.

"Based on a biological hypothesis, we show that organochlorine insecticides may interact with ABCB1 in determining the risk of Parkinson's disease," the authors conclude. "These findings support the hypothesis of gene x pesticide interactions in Parkinson's disease."


Journal Reference:

  1. Fabien Dutheil; Philippe Beaune; Christophe Tzourio; Marie-Anne Loriot; Alexis Elbaz. Interaction Between ABCB1 and Professional Exposure to Organochlorine Insecticides in Parkinson Disease. Arch Neurol, 2010; 67 (6): 739-745 [link]

Spinal cord stimulation may benefit Parkinson's patients

A new study from Rhode Island Hospital indicates that spinal cord stimulation may be able to modulate Parkinson's disease symptoms.

The lead author will present the findings at the 2010 American Society for Stereotactical and Functional Neurosurgery (ASSFN) Biennial Meeting, June 14-16 in New York City.

Ming Cheng, MD, is a neurosurgeon at Rhode Island Hospital and the lead author on an abstract called "Outcome of Spinal Cord Stimulation." Other studies previously found motor function improvement with spinal cord stimulation (SCS) in an animal model of Parkinson's disease (PD). The findings from these studies prompted the researchers to test SCS on a single 82-year-old male with PD.

Cheng, who is also an assistant professor of neurosurgery at The Warren Alpert Medical School of Brown University, worked with colleagues at Brown to implant the SCS system and then test the effects at multiple frequencies while the patient was off medication.

"Our study shows no changes in pain assessment to control for reduction in pain as the reason for motor improvement," says Cheng. "What we did find is that low-frequency SCS produced a readily apparent and statistically significant worsening of Parkinson's disease symptoms." Cheng, who is also a physician with the Neurosurgery Foundation, Inc., continues, "These findings and locomotion 'walking time' were reversed at high stimulation frequencies."

This work has been replicated in a second patient, with similar results. Cheng notes that the results of the study are extremely limited as it was performed in only one patient; however, he believes that further studies are in order to determine the possible benefits of this approach for PD patients.