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Tags >> Treatment

Peter A. LeWitt, MD

In March, the journal Lancet Neurology published the positive results of a study that investigated a new form of treatment for Parkinson's disease, gene therapy. Gene therapy refers to an experimental technique for transforming brain cells to follow new genetic instructions, such as producing an enzyme. In this case, a harmless virus was used as a transfer vehicle to bring a laboratory-engineered gene selectively into a brain region called the subthalamic nucleus. This location is also the target zone of the electrode in the Parkinson's disease therapy called deep brain stimulation. The goal of the gene therapy study was to learn if various problems of advanced Parkinson's disease could be helped, much as deep brain stimulation of the subthalamic nucleus can be effective for similar problems.

The study was carried out at 7 US Parkinson's disease research centers, led by Peter Le- Witt MD at Henry Ford Hospital in West Bloomfield. The gene therapy product, termed AAV2-GAD, was developed by Neurologix, Inc and underwent careful review by the Food and Drug Administration and institutional review boards before it was offered to the study participants. The experimental treatment plan, which involved a neurosurgical procedure to implant the engineered gene, resulted in clinically-meaningful improvements at 6 months for the group of subjects receiving AAV2-GAD as compared to other study participants who underwent a "sham" (placebo) treatment. The procedure proved to be safe and is now under review for its 12-month outcomes.

A follow-up study is planned to confirm the effectiveness and safety of treatment with AAV2-GAD. Other applications of this approach with different genes are also under investigation or in planning stages. The notion of modifying brain function, as an alternative to medications, provides an exciting alternative since it may lead to more permanent benefits without limitations that drugs can sometimes impose. It is also possible that gene therapy-based treatments that offer more than symptomatic therapies might be in the spectrum of future gene therapy for Parkinson's disease therapy.


Richard M.Merson, PhD, CCC-SLP
Kathleen Roeder, MA, CCC-SLP

Speech-Language Pathology Department William Beaumont Hospital, Royal Oak, Michigan

Dr. Richard Merson is Coordinator of Research, Speech and Language Pathology, William Beaumont Hospital and a Member of MPF's Professional Advisory Board. Kathleen Roeder is Supervisor, Acute Care Speech Pathology and William Beaumont Hospital.

  1. Persistent coughing after swallow

  2. Regular choking on liquids

  3. Difficulty maintaining your weight

  4. Increasing eating time

  5. Worsening tongue control

  6. Chronic slow or delayed food passage

  7. Significant loss of appetite

Swallowing problems in Parkinsonism are not unusual and rarely unmanageable. The typical muscle impairments of individuals with Parkinson's Disease ( i.e. weakness, slowness, delayed-initiation, freezing, or tremor) may cause significant difficulties in controlling food or liquids in the mouth, adequately chewing or masticating , quickly passing the food to the throat, , protecting the windpipe (i.e trachea) from food and liquid choking, and finally smoothly and firmly receiving the food into the esophagus for passage to the stomach. All of these actions require the coordinated work of more than two dozen muscle groups (i.e. lips, tongue, cheeks, palate, throat, voice box, and food tube) that must be performed hundreds of times each day in 4-8 seconds.

Breakdowns in this chewing-forming-pushing process can cause choking when the food particles or liquids pass into the windpipe (i.e aspiration). Further, individuals may find that eating is too time consuming, requires too much effort, or may frighten them when the food does not pass easily into the food tube. These problems may lead to weight loss or reduced calorie intake that is so critical in maintaining energy and general muscular activity. We cannot take swallowing difficulties for granted. Some swallowing difficulties may cause liquid , saliva or food to enter the lungs on a recurring basis and leave you vulnerable to a lung infection. If these symptoms are severe, unresponsive to treatment and insufficient calories are achieved daily then a medical procedure to place a tube inside the stomach (i.e. PEG tube: Percutaneous Endoscopic Gastrostomy) may be considered.

Dysphagia: Swallowing Disorders

In medical terminology a disorder of swallowing is identified as a "dys-phagia" (Latin for difficulty swallowing). Dysphagia symptoms may occur anywhere from the lips to the stomach. If swallowing difficulties occur in the esophagus (food tube) and down through the entryway into the stomach then an Esophagram (i.e. an xray to examine the swallow) may be ordered by your physician and a gastroenterologist ( G.I. physician specializing in the digestive system) may be consulted. Sometimes the G.I. specialist will perform a procedure to expand or open the esophagus by a procedure known as esophageal insufflation to improve the passage of food . The physician may also prescribe medications to assist in some esophageal swallowing disorders. If however, the swallowing difficulties occur in holding the food in the mouth, chewing the food, or safely passing the food to the esophagus then a speech-language pathologist may be consulted to identify the dysphagia and recommend some exercises or alter the diet to manage the problems.

Different types and severities of dysphagia may be present in patients after surgery, in association with chronic debilitating illness, from loss of dentition, loss of salivation or other conditions. Symptoms associated with aging, stroke, over-medication, traumatic brain injury, myasthenia gravis, muscular dystrophy, multiple sclerosis and Parkinson's disease can cause dysphagia symptoms. Individuals with chronic illness must develop a good daily nutritional program that provides adequate intake of calories, critical vitamin, protein and carbohydrates, and sufficient hydration (liquids). Patients should work closely with their physicians, nutritional experts and caregivers to maintain a daily healthy diet.

The Dysphagia Team

(Primary Care Physician, Gastroenterologist, Neurologist, Radiologist, Speech Pathologist and the Spouse/Caregiver)

The speech pathologist is often the rehabilitation professional who will assist you in maintaining good oral muscular control and prevent food from entering the windpipe through treatment techniques. If necessary a specialized xray procedure called a Modified Barium Swallow fluoroscopy will be completed. Your physician is always the first person to contact when you are experiencing difficulty swallowing. If you need some assistance or further treatment of how to improve your swallowing a consultation with a speech-language pathologist affiliated with a hospital, an outpatient rehabilitation program, a homecare service or a skilled nursing facility is available with a medical referral.

The Modified Barium Swallow Procedure is the most common medical procedure jointly conducted by a speech-language pathologist specializing in swallowing disorders and a physician-radiologist to evaluate dysphagia. This xray procedure is not a complicated or lengthy diagnostic procedure. The patient sits comfortably erect in a special chair. The speech-language pathologist prepares and feeds the patient liquids, applesauce or crackers mixed with a Barium material for brief videofluouroscopic filming of the mouth, pharyngeal and esophageal swallowing events. This usually requires 15-20 minutes. The physician identifies any anatomic or physiologic disorders as he observes the swallowing tasks and the speech-language pathologist identifies any swallowing difficulties that can be treated. There are many other medical procedures that your physician may choose to diagnose your dysphagia and recommend treatment. They may include a Radiologic Imaging, Barium Esophagram, Manometry, Bolus Scintigraphy, Flexible Endoscopic Evaluation, or Ultrasound. Your physician will decide, based on examination, what dysphagia medical procedure(s) is most appropriate.

Swallowing Rehabilitation

Speech-Language pathologists usually provide the behavioral treatment for individuals with dysphagia. Treatment may focus on one or more of the following dysphagia symptoms: (1) improving or compensating for the individual's difficulty in chewing or managing food in the mouth; (2) preventing food or liquid from entering the windpipe ( i.e. the trachea); (3) reducing delays in transit of food by adjusting the textures, timing or preparation of food to be swallowed; (4) managing the schedule of eating to reduce fatigue and muscle weakness. The speech-language pathologist or physician may recommend a consultation with a dietitian to train caregivers to provide instruction or food preparations for some patients.

When the Dysphagia Team decides that an individual's diet should be changed to make swallowing healthier and safer, they may suggest a PUREED DIET or a MECHANICAL SOFT DIET. Usually, when swallowing liquids is difficult with persistent cough on thin liquids ( i.e. water leaking into the windpipe), a PUREED DIET with THICKENED LIQUIDS may be recommended. When liquid swallowing is safe but muscular weakness persists (slow eating, food gets stuck, food is poorly chewed), then a MECHANICAL SOFT DIET may be recommended. Some individuals have difficulty chewing, but can manage thin liquids. Special adjustments can be made to suit individual needs.

Dietary Suggestions for Dysphagia

Tips & Precautions

  • Don't eat when fatigued

  • Sit erect

  • Emphasize soft , moist foods

  • Don't talk while eating

  • Take smaller bites

Example of a PUREED DIET

  • *Thicken liquids to honey consistency

  • Cooked cereals, whipped- potatoes & squash

  • Strained fruits, applesauce, mashed banana

  • Strained meat, soft scrambled egg

  • Strained & whipped vegetables Thickening material available at drugstores include Thick-it, Nutra Thickt, ThickenUp

Example of a MECHANICAL SOFT DIET

  • Thickened liquids if necessary

  • Cooked or ready-to-eat cereal, soft bread

  • Well cooked vegetables

  • Cut-up canned fruit without tough membrane

  • Tender cuts of meat extra sauce or gravy

  • Eggs, cheese, macaroni, moist casserole

Summary

Swallowing problems or Dysphagia are not uncommon in patients with Parkinson disease symptoms. You should consult your primary care physician if you have persistent difficulty choking on liquids or eating comfortably on a regular basis. Most of the swallowing problems can be managed by a few individualized exercises, swallowing techniques or modifications in your diet. Good health is dependent on a well rounded diet, the use of plenty of liquids and an enjoyable eating experience.

Website References

American Speech-Language-Hearing Association, Dysphagia Research. http://search.asha.org (Conduct a search for the keyword Dysphagia.)

Dysphagia Resource Center: www.dysphagia.com

National Institute on Deafness and other Communication Disorders [NIDCD]: http://www.nidcd.nih.gov/health/voice/Pages/dysph.aspx

 

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By Amer G. Aboukasm

Although the daytime clinical manifestation of Parkinson's disease have been well recognized for almost two centuries, the nocturnal (nighttime) symptoms, which occur in as many as 75% of patients and the associated sleep disorders were not studied until the 1960s. A variety of psychological and physiological processes can lead to disruption of the normal rhythm of the sleep-wake cycle in patients with Parkinsonism. First, the degenerative process in Parkinson's disease affects the neurophysiological and neurochemical systems responsible for sleep organization, thus results in disruption of sleep. Second, the motor, respiratory and behavioral phenomena accompanying the disease may produce nocturnal symptoms. Third, the medication used in its treatment may induce new symptoms, such as nightmares or nocturnal movements. All these effects on sleep have implications for treatment planning.

Clinical features:

Insomnia with difficulty falling asleep and remaining asleep are the most common sleep-related complaints. Nocturnal vocalization and daytime dozing are also common. The inability to turn over in bed and to get out of bed to go to the bathroom, are especially bothersome complaints.

Sleep disturbances including daytime sleepiness tend to increase with disease progression. Patients with on-off phenomena and hallucinations are particularly likely to have severe sleep disruption. Depression and dementia, which commonly affect late-stage Parkinson's disease, are usually associated with increased severity of sleep disturbances, including nocturnal hallucinations and vocalization, and sometimes the REM sleep behavior disorder (which consists of violent movements related to the patient acting his/her dreams; this is due to lack of the physiologic paralysis of the skeletal muscles during Rapid Eye Movement stage of sleep).

The Sleep-Wake Organization Disturbances, mostly consist of sleep fragmentation. The time to fall asleep and the number of awakenings tend to increase in proportion to the severity of the parkinsonian symptoms. The proportions of lighter stages of sleep are increased and REM sleep is remarkably reduced.

The Motor Activity during sleep: tremors are generally suppressed, although they may appear during stages 1 and 2 of sleep, with awakenings, body movements or during bursts of rapid eye movements or after an REM period. Simple and complex movements are common during sleep in patients with parkinsonism. These include blinking, blepharospasms (spasms of the eyelids), persistent contraction of the muscles in Non-REM and in REM sleep, vocalization, periodic limb movements (resulting in extension of the big toe, foot or fingers) and REM sleep behavior. Furthermore, REM sleep behavior may appear years before the onset of daytime symptoms of Parkinson's disease or other related degenerative disorders. -Sleep-Related Respiratory Disturbances include irregular breathing due to central apnea from lack of the respiratory drive or obstructive sleep apnea due to upper airway closure.

Diagnostic Evaluation:

Clinical history, examination and sleep studies are used to determine the most important factor in the patient sleep disorder. The description from the bedpartner is essential to determine the presence of movements or awakenings and daytime sleepiness. The medication schedule is important. If dopamnergic drugs medication are not taken in the evening, nocturnal rigidity may contribute to sleep disruption; on the other hand the same drugs taken excessively or late may induce sleep-onset insomnia.

Sleep studies are useful when sleep apnea is suspected based on history of snoring, witnessed respiratory difficulties during sleep, or excessive daytime sleepiness. Sleep studies are helpful in documenting abnormal limbs movements or REM sleep behavior disorder.

Treatment:

The treatment of sleep disturbances in patients with parkinsonism is rarely straightforward because treatment of the disease may impact on or result in sleep disorders. The dual action of the dopaminergic drugs must be kept in mind: low doses of these medications may promote sleep, whereas high evening doses may result in sleep disruption in the first half of the night and improve sleep in the second half of the night. When managing the sleep disturbances of parkinsonism, the physician must balance the effects on sleep of changes in medication dosage with the effects of such changes on daytime parkinsonian symptoms.

Improvement of sleep hygiene in addition to simple measures such as placing a portable commode at the bedside may lead to substantial improvements. Concurrent psychiatric disorders should be addressed. In advanced stages of the disease, the patient's spouse should be advised to sleep in a different bed or room; inadequate rest for the spouse or other caregiver may make the patient's sleep disturbances intolerable leading to institutionalization.

For patient with insomnia without nocturnal hallucinations or vocalizations, a small dose of a dopaminergic drug, such as Sinemet 25/100, at bed time with a second similar dose at 2 or 3 AM if needed may be considered. In that regard, Sinemet CR 50/200 is particularly useful. Unfortunately these drugs may results in new sleep problems including vivid dreams, nightmares and night terrors. These occur in up to 30% of patients especially those with dementia. Small dose of short-acting sleep medication (Ambien, Sonata ), for few days or weeks may help normalize the sleep-wake schedule. Antidepressants with sedating properties such as amitriptyline are frequently helpful for sleep-onset insomnia.

Nocturnal vocalization and REM sleep behavior disorder respond to clonazepam (Klonopin). Nocturnal hallucination may require reduction in the dopminergic drugs dosages or the use of antipsychotic drugs such Seroquel or Clozaril.

The treatment of sleep apnea in parkinson's patients is similar to the treatment of such problems in other patients. In patients with sleep apnea, Continuous Positive Airway Pressure is the most effective treatment. Upper airway surgery may help some patients. For patient's with severe vocal cord dysfunction tracheostomy often is necessary.

Tips for Dealing with Sleep Problems

By Linda Mondoux

  • Sleepiness during the day or frequently waking up during the night are signs that you should evaluate your sleep pattern.

  • It would be helpful if you had a diary to share with the physician. You could include the following items:

    1. When do you go to bed and how long you sleep? Is this a consistent pattern?

    2. How long it typically take you to fall asleep?

    3. Describe any rituals that help you to fall asleep or anything that helps if you are awakened during the night.

    4. Do you take any medications routinely that are for sleeping or that you think keep you awake.

    5. Do you worry about things before you fall asleep or if you wake up during the night?

    6. Do you exercise and, if so, when do you exercise?

    7. Do you eat or drink anything just before you go to bed?

    8. Do you feel rested during the day or are you usually tired feeling all day?

  • There are sleep clinics with specialist who can evaluate your sleep pattern and develop specialized plans for you to achieve more restful nights.

  • Psychological and mental health problems like depression, anxiety and stress are often associated with sleeping difficulty. In many cases, difficulty staying asleep may be the only presenting sign of depression. A physician should be consulted about these issues to help determine the problem and the best treatment

  • Work with your physician and pharmacist to determine if any medications can cause insomnia. Both prescription and over-the-counter medications can have side effect of sleeplessness. Check with your doctor to question if any of the medications that you re taking could be potential culprits.

  • Choose a consistent time to go to bed and to wake up. This is important even if you do not have schedules to follow during the day. Your body recognizes that it is time to go to sleep if you can develop a regular time to go to bed. Your "biological clock" gets set with a regular sleep pattern.

  • Try to avoid thinking about troubling thoughts or trying to solve problems after you lie down to go to sleep. Set aside a time earlier in the night to deal with "heavy thinking."

  • Most people function best with 7 ½ -8 hours of sleep a night. If you go to bed after midnight, it is generally harder to get to sleep, as many people start to feel more awake after midnight.

  • Use the bedroom only for sleeping and sex to minimize the association with other activities that do not equate to sleep.

  • If you try to fall asleep and are unsuccessful after 15-20 minutes, then get up and go into another room and read or relax by listening to soothing music or reading light material. You should, however, not expose yourself to extremely bright light, as that gives a message to your body that you are to wake up. Tranquil music with sounds of nature, such as waterfalls and ocean waves, can aide in falling asleep. Don't watch television or engage in any challenging activity or strenuous exercise.

  • Evaluate your bedding to make sure that is comfortable and make changes as you identify areas for improvement. There are many specially contoured pillows to provide neck support depending on whether you are a "side sleeper" or an "on the back" sleeper. There are also pillows that allow you to have your head more elevated if you have any respiratory distress at night or if you have acid reflux (GERD).

  • Be sure that the bedroom's temperature is comfortable for you. Sometimes people sleep better in a cooler room.

  • Eliminate any noises and lights that might cause distractions. Earplugs that can comfortably mold to the ears are sometimes beneficial. Some people find "white noise" machines or a blowing fan noise to be conducive to sleep.

  • Naps are not recommended during the day. If you do take a nap, take it before 3 PM and don't sleep longer than an hour.

  • Rituals that signal that it is soon time to go to sleep have proven helpful. Sometimes a bath just before going to bed can help you to relax and fall asleep more easily. Some people listen to soothing music or drink decaffeinated tea, such as chamomile tea. Before using any herbal teas, you should check with your physician.

  • Getting outdoors daily to be exposed to natural light can help to establish a circadian rhythm.

  • Coffee, colas, and chocolate have caffeine and this can be a stimulant, causing you to stay awake at night. Smoking before bedtime is also detrimental, as nicotine is a stimulant.

  • Alcohol can cause you to feel sleepy; however, during your sleep it might cause you to have a sleepless night.

  • Strenuous exercise less than 3-4 hours before bedtime can cause you to have difficulty falling asleep; however, yoga or relaxation exercises can aid in falling asleep.

  • When the sun goes down, the pineal gland is stimulated and produces a natural chemical called melatonin. Your body needs melatonin to feel sleepy. Melatonin can be found in oats, rice, ginger, tomatoes, bananas, barley and sweet corn. You can also eat foods that help to stimulate the production of melatonin in your body. Such foods include soy nuts, cottage cheese, chicken, pumpkin, and turkey.

  • Small snacks before bed, particularly foods high in the amino acid tryptophan, such as peanut butter and dairy products, can cause sleepiness and help you to fall asleep.

  • For individuals that have allergies to dust or dust mites, paying attention to decreasing allergens by dusting frequently, using vacuum cleaners with HEPA filters, using air conditioners, and replacing old pillows and carpeting. Pets can also interfere with sleep with their dander, but also with their movements on the bed.

  • There are some herbal scents that can induce relaxation and sleep, such as lavender and vanilla.

 

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The 2009 Gorell Memorial Lecture, "Behavioral Aspects of Parkinson's Disease," was presented by Dr. Joseph Friedman of Brown University, Rhode Island. Dr. Friedman is a practicing clinical neurologist, a clinical professor, a scientist and the author of "Brain and Behavior." The fourth annual Gorell Lecture was held at the Farmington Hills Library and was simultaneously webcast to nine different locations in Michigan: Adrian, Alpena, Battle Creek, Bay City, Gaylord, Gladwin, Lansing, Scottville and St. Joseph. Ms. Robyn Gorell, a member of the Michigan Parkinson Foundation Board of Directors, welcomed Dr. Friedman in honor of her late husband and thanked the audience for attending.

Dr. Friedman outlined the important non-motor symptoms of Parkinson's Disease that are often overlooked or considered less important than the familiar cardinal motor symptoms. The classic motor symptoms of tremor, rigidity and slowness of movement usually receive the primary attention and focus of medical management. Friedman emphasized that, very often, the non-motor symptoms of anxiety, depression, hallucinations, apathy, cognitive slowing and memory difficulties are more problematic and directly affect "quality of life" issues. Dr. Friedman highlighted a number of somatic complaints of PD patients that require medical attention, such as frequent sweating, chronic pain, rhinorrhea (runny nose), poor taste or smell and frequent stomach ailments. Further, he defined a number of behavioral disorders common to PD patients, including anxiety episodes, crippling depression, easily triggered anger, tendency for compulsivity (gambling, repetitive activities, hypersexuality) and increasing cognitive loss consistent with dementia. He identified these non-motor disorders as either iatrogenic, caused by the use of PD medications, hallucinations, psychotic episodes, sleep disorders and obsessive compulsive behaviors; or intrinsic to dopamine loss in PD, as in persistent depression, apathy, dementia, fatigue and akathisia.

Immediately following Dr. Friedman's lecture, a panel of four physicians from the Michigan Parkinson Foundation's Professional Advisory Board, moderated by Dr. Kelvin Chou, directed questions to Dr. Friedman and answered others from members of the audience and participants from the webcast audience. More than 200 patients, spouses, caregivers and rehabilitation professionals attended or observed via webcast this highly successful event.

DVDs will be available for viewing through Michigan Parkinson Foundation support groups, or by contacting the MPF office.


Excerpts reprinted with permission from the APDA Saint Louis Parkinson Newsletter, #1, 2006

The first-ever World Parkinson Congress (WPC, February 22-26, 2006) provided a unique international forum for sharing the latest scientific findings, medical practices and caregiver initiatives related to Parkinson's disease (PD). There were over 3000 participants who filled the new Washington D.C. Convention Center each day for this historic event. By bringing together Parkinson's researchers, health professionals, patients and caregivers, and some of the world's leading neuroscientists, a multi-layered dialogue was sparked between participants contributing their collective knowledge of PD.

Parallel sessions were divided into: a) Science sessions focusing on specific cutting-edge research; b) community sessions focusing on care delivery and quality of life topics; c) interactive sessions focusing on multidisciplinary approaches to care, advocacy and public policy issues. Each day was divided into a theme with an emphasis on how can knowledge be used to improve care delivery. Themes included: What causes PD?; How do brain cells lose their vitality in PD?; How can PD be identified before clinical onset? The final day was devoted to the needs of PD patients and families be met in relieving symptoms, improving quality of life and slowing progression.

Highlights for the Community and Integrative Sessions

Contributed by Deborah Dahlin Guyer, Speech and Language Pathologist

I tended to gravitate to the community sessions and interactive workshops. Here are some of the items that "stuck in my mind."

• A diminished sense of smell can be a precursor to PD.

• Gait problems arising from dysfunction of axial (midline) muscles and cognitive impairment are more likely to cause complications (morbidity) for patients with PD. These features are more common in older-onset patients and do not appear to be related to the overall duration of the illness.

• Non-motor features of PD include cognitive issues, visual hallucinations and depressed mood. These are under-reported, under-recognized (75% miss the diagnosis) and under- treated (94% not treated), yet they have a significant impact on the quality of life.

• Non-motor symptoms that are resistant to L-dopa can include cognitive decline, dementia, hallucinations, depression, choking, urinary incontinence, and hypotension. All add to the burden of disability.

• Apathy develops in 16-42% of persons with PD and contributes significantly to caregiver burden. This apathy is not just a simple reaction to disability. Its features include reduced emotion, diminished motivation, lack of initiative, difficulty sustaining activity, a seeming lack of concern and indifference. These individuals may stop reading the newspaper, no longer take part in family conversations, have difficulty articulating thoughts and prefer to sit around the house and take frequent naps. Apathy often co-exists with depression but can occur independently. Apathy is difficulty to differentiate from depression, but it is important to do so in terms of treatment. Apathy does not correlate with dementia. It is associated with impaired executive function (planning). It can co-exist with anxiety. It also fluctuates with motor function. Apathy is diminished when medication is working.

• Many PD patients suffer mild cognitive impairment, but this often does not clearly interfere with activities of daily living. Cognitive impairment increases with disease duration and in later stages. Current anti-PD medications have little effect on cognitive function. Rivastigmine (Exelon) may help mild cognitive impairment.

• Dementia occurs in 20-40% of PD patients. Associated features include visual hallucinations, confusion and daytime somnolence. The risk factor grows as the patient ages.

• Exercise promotes brain changes and is a legitimate therapeutic option. It slows the progression of the disease. It is a physiological tool to promote neuroplasticity. Use it or lose it! Use it and improve it! The BIG and LOUD approach combines physical exercise and speech exercises with great results and is being researched as a viable option for therapy.

• We must treat the patient, NOT the disease (patient-centered care vs. disease-centered model). One size does not fit all!

• An interdisciplinary team approach is needed. Interdisciplinary care favors quality of life issues. It is patient-centered and deals with symptom management, activity and functional improvement, education, patient and clinician adherence, awareness, prevention and risk reduction. Caregiver, community, society and the patient all take an active role. A wellness focus is not the same as focus on the disease.

Scientific Program Highlights

Contributed by: Dr. John L. Goudreau

The contributions of environmental and genetic causative factors in PD were vigorously discussed. While epidemiological studies on large populations cannot prove a cause-effect relationship, some occupations increase the risk of developing PD (e.g., farmers, teachers and health care workers), perhaps because and environmental exposure. Cigarette smoking and increased caffeine consumption has inverse associations with the developing PD; i.e., both significantly reduce the risk of developing PD. Genetic studies have identified 12 genes that are clearly involved with the development of familial PD. Both environmental factors make an important contributions to the cause of PD, aptly captured by the phrase "Genetics load the gun but environment pulls the trigger."

Some of the difficulty in identifying causes of PD stems from how one defines the disease; i.e., by brain pathology or by responsiveness to dopaminergic medication. Accuracy of the clinical diagnosis of PD was reviewed: about 10% of rigorously classified PD are not found to be PD when examined pathologically. When pathological diagnosis is used, about 6% of autopsy proven cases of PD have atypical symptoms. Up to 5% of patients in a movement disorders subspecialty clinic are incorrectly classified. There may be clinical subtypes of PD that include a tremor-dominant, postural instability gait difficulty (PIGD), akinetic/rigid and mixed forms of PD. The etiology, pathology and evolution of these subtypes may be distinct.

"Evil proteins and their mischief " were explored as underlying features of PD pathogenesis. Modifications in a-synuclein that promote protein aggregation contribute to disease pathogenesis and are targets for neuroprotective therapies. A new protein, LRRK 2 or dardarin, has been identified through genetic studies and may explain a significant portion of cases as inherited PD. The function of this protein is currently unknown, but discovering the normal and pathological function of LRRK-2 has great promise for providing new targets for PD therapies. Inflammation following initial injury appears to be an important mechanism in sustaining neurodegeneration in PD and anti-inflammatory medications can slow this process. Finally, proteosomal proteins involved in removing "mischievous" proteins may be dysfunctional in PD and this pathway also provides a compelling target for therapy development.

Neuroimaging studies are being refined for use as biomarker of PD and progression. For example, "PD related pattern" of changes on PET scanning may provide a method for confirming the diagnosis of PD and following the course of the disease, both essential to accelerate the development of new therapies. Neuroimaging may be effectively combined with other approaches such as smell testing to identify early PD. A "bionomics" approach to identifying important core biochemical features of PD was proposed that included a global evaluation of all genes and how they are translated into cell proteins in patients with Parkinson disease. Cutting edge tools are rapidly being developed to accomplish this goal.

Advanced approaches to patient care were reviewed. While dopaminergic treatments liberate patients from the grasp of rigidity and bradykinesia, they can cause involuntary movements (dyskinesias) and fluctuating responses to dopaminergic medications (short duration reponses). Dyskinesias developed in 13%, 35-40% and 100% of patients having PD for 0-5, 6-9 and >10 yrs, respectively. The frequency of dyskinesias may be declining as treatment strategies have changed over the last decade and dyskinesias appear to have little impact on quality of life. The classification and treatment of dyskinesias were reviewed; they all may be a form of stereotypic movement. Adjustments in dopaminergic drugs and amantadine are the current treatments; sarizotan and NR2b glutamate and A2A adenosine blockers are future treatments being developed. New treatments under development by pharmaceutical companies are: sublingual selegiline, new MAO-B inhibitors (rasagiline), istradephylline and other adenosine blockers, dopamine agonist patch (rotigitine). Cutting-edge therapies on the horizon were discussed including: manipulating synuclein expression, modification or removal; gene therapies to deliver or nerve growth factors enzymes that produce dopamine or GABA; transplanting stem cells or encapsulated cells producing growth factors. Early clinical (Phase I) studies are beginning with some of these new and exciting approaches and provide a ray of hope for those living with PD. A unique component of the WPC was the emphasis on Creativity. The following is an excerpt from the newly developed website,wwwcreativity.pdf.org, where you can also view the web gallery, featuring works displayed during the Congress. A Committee has been created to further study the phenomenon that many people with PD develop creative abilities. Many people living with Parkinson's disease have found ways to rise above its impact to produce truly beautiful works of art, including visual arts, music, writing, drama, dance, craft, and web design. The therapeutic value of creativity was evident throughout the program. A component of the WPC, Creativity & Parkinson's - an exhibition of artwork made solely by people diagnosed with Parkinson's - provided a rich, comprehensive and inspirational message to the participants and gave tangible evidence that creativity can have an impact on one's quality of life. "The impact of the artwork and the artists' statements will hopefully fuel further study on the creative process and the therapeutic value of creativity."

 

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By: David Bartczak, Member, MPF Board of Directors, Michigan Parkinson Foundation and Support Group Facilitator, Royal Oak Support Group; with Dr. Kelvin Chou, MD, Member MPF Professional Advisory Board and Assistant Professor, University of Michigan Medical Center and Richard Trosch, MD, Member, MPF Professional Advisory Board, and Director, Parkinson's and Movement Disorders Center, Southfield, MI

Deep Brain Stimulation (DBS) is not a cure, but rather an option to be considered when conventional pharmaceutical approaches no longer provide the quality of life the patient desires. Often, a patient is referred for DBS because he experiences wearing-off or dyskinesias that cannot be controlled with further medication adjustments. Patients with severe tremor may also qualify for DBS. Unfortunately, not every Parkinson's patient is a suitable candidate for DBS.

Many DBS centers employ a team approach, in which a movement disorders neurologist, a neurosurgeon and other staff screen potential patients in order to select candidates most likely to benefit from the surgery. The purpose of this article is to inform you of the evaluation criteria for a DBS candidate. The main criteria can be broken down into the four "D"s.

Diagnosis: The patient must have a diagnosis of Parkinson 's Disease. Many other neurological disorders may mimic the symptoms of PD, including Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP) and Dementia with Lewy bodies (DLB). Some physicians will also use the term "parkinsonism" when they are unsure if a patient truly has PD. The diagnosis is important because patients with these other disorders do not benefit from DBS. An essential part of the DBS evaluation is a consultation with a neurologist specializing in PD to ensure the correct diagnosis.

Dopaminergic response: Patients should respond to dopaminergic medications. PD patients initially show a stable response to medications in the first few years of the disease. However, as their disease severity progresses, the medication's benefit duration may shorten and the Parkinson's symptoms return before the time for the next dose. This phenomenon, called wearing-off, can sometimes be corrected with medication adjustments. Patients may also develop dyskinesias over time. These involuntary, fidgety-type body movements can be severe. When patients begin to experience disabling wearing-off or dyskinesias not correctable with changes to medication, it is time to consider DBS. It is important to remember that, in general, DBS only makes patients as good as their best medication "on" state, but it also helps decrease the severity of the "off" times, allowing patients to feel as if they are "on" throughout the day. The exception to this rule is tremor. Parkinsonian tremor can be treated with DBS even if it does not respond to medications. Some DBS centers may test dopaminergic response with an off-on evaluation, in which patients are examined 12 hours after stopping their PD medication and then an hour or two after taking it. To be a suitable candidate for DBS surgery, a patient should have at least a 30-point improvement between the non-medicated/"off" state and the medicated /"on" state on a Parkinson's disease rating scale score.

No Dementia: Patients who have evidence of dementia or significant problems with thinking and memory are not candidates for DBS. That is because patients with significant cognitive problems may have difficulty fully understanding all the risks and benefits of surgery. There are cases in the medical literature where patients with borderline dementia progress to full-blown dementia after DBS surgery. As a result, part of the DBS evaluation may include neuropsychological testing to be certain that patients do not have severe problems in this area.

No uncontrolled Depression: Some patients have been reported to be suicidal after DBS surgery for PD. While it is not exactly clear why this happens, it is reasonable to make sure patients do not have significant depression before undergoing surgery.

Other factors that may impact whether someone is offered surgery include age and medical history. While there is no absolute cutoff for age, younger patients tend to do better. The preferred age is younger than 70, since the surgery and recovery times become longer for more elderly patients, but many DBS centers have operated on patients older than 70 with good results. Multiple medical problems may also make the surgery more challenging. For example, a history of brittle diabetes can affect healing of the incisions. Presence of a pacemaker may also make the surgery more difficult, because MRI is often used to visualize the area where the electrode will be placed. These are issues to discussed with the neurologist and neurosurgeon during the evaluation process.

Selection of the proper candidates is one of the keys to success for DBS surgery. However, a patient's expectations must also be realistic for the surgery to be successful. DBS will only be as good as the best medicated state prior to surgery. PD symptoms that do not respond to medications, such as gait or balance, also will not benefit from DBS. DBS can be a life-changing procedure, but only for the right patients.

 

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by Dr. John Goudreau, DO, Ph.D.,

Are you considering traveling overseas for a medical procedure to treat Parkinson Disease (PD)? Medical tourism for "restorative" stem cell therapy to treat PD is the rapidly growing practice of traveling across international borders for health care. More than 50 countries identify medical tourism as a national industry.

Medical tourism is marketed by dozens of private for-profit clinics from Guatemala to China, mainly through internet and patient-to-patient communications. These companies claim to help patients with a variety of illnesses, especially incurable conditions such as PD, while offering little or no scientific evidence.

For decades, doctors have been using adult stem cells from blood, bone marrow and umbilical cord blood to treat cancers of the blood like leukemia and lymphoma. Unlike mature nerve cells, stem cells can replicate, making them potentially powerful weapons against many neurological diseases, including PD. Adult stem cells can be harvested from numerous sources - including one's own bone marrow or from umbilical cord blood. Subsets of cells collected this way are considered "pluripotent" - the cells can mature into any type of cell in the body. Once multiplied and conditioned, the pluripotent stem cells can be injected into the blood stream, spinal fluid via a lumbar puncture, or directly into the brain. Adult stem-cell treatments, often arranged by American-based intermediaries, run between $10,000 and $35,000, depending on the treatment (other travel costs are extra).

Adult stem cell therapy for PD carries a significant risk of complications. Pluripotent stem cells can form cancerous tumors. Stem cells harvested from other people can carry infectious disease and usually require anti-rejection medications for the foreign cells to survive. The only published series on patients receiving adult stem cell therapy for spinal cord injury in China showed a majority of patients suffered complications, while none appeared to benefit. Finally, the pursuit of unproven alternative therapies abroad can be an obstacle for the use of proven effective therapies or clinical trials available in the United States.

Medical tourism for stem cell therapy is often a journey of hope for people struggling with the accumulating ravages of PD. The proper way of establishing that a new treatment is safe and effective through the Food and Drug Administration (FDA) may seem to slow for some. People hope the pluripotent stem cells, like magic bullets, will provide immediate benefit by finding their way to correct targets and developing into the appropriate cell types to repair PD-damaged brain regions.

Medical tourists for stem cell therapy often claim some success when they return home. Peer-reviewed documentation of these claims is conspicuously absent. While there may indeed be a therapeutic benefit to peripherally delivered stem cells in PD, anectdotal statements of improvement are no substitute for clinical proof of effectiveness. Some reports of improvement may be a placebo response, or a desire to believe that the money spent had to have been effective.

Stem cell clinic Web sites and brochures highlight stories of success, often including scientific articles from animal studies to give the appearance of effective treatments. They over-promise their treatments' benefits, while grossly downplaying or ignoring risks. Some sites even cite the few clinical trials using fetal brain cell transplants, instead of the adult stem cell therapy they actually are offering.

Not surprisingly, "magic cure by stem cell" medical tourism has been criticized for consumer fraud, blatant lack of scientific justification and disregard for patient safety. There is potential physical, psychological and financial harm to patients, as well as the general lack of scientific transparency and professional accountability of those profiting from these clinics. If patients undergoing unproven and unregulated stem cell therapies abroad develop serious complications, then the progress of legitimate clinical research could be undermined.

Let's not demonize all innovative stem cell therapeutic approaches, including those delivered outside the United States. PD patients have legitimate and ethical motivation to pursue all avenues of treatment available, particularly given the shortcomings of current proven therapies in some cases. Nevertheless, there is a clear distinction between the commercial purveyance of unproven interventions and legitimate attempts at medical innovation outside of traditional medical research. While medical breakthroughs have evolved from medical innovation, novel medical approaches to treatment must undergo rigorous scientific and ethical review, as well as have appropriate measures for patient protection.

Fortunately, there are steps to avoid falling into a medical "tourist trap." Here are a few examples of key questions and potential "red flags." This list is not comprehensive and additional information, including what to ask before agreeing to undergo an unproven therapy, can also be found at the International Society for Stem Cell Research Web site: www.isscr.org/clinical_trans/pdfs/ISSCRPatientHandbook.pdf.

Some key questions to ask about unproven therapies being offered abroad

Have pre-clinical studies been published, peer-reviewed and repeated by other experts?
Do the providers have independent committee approval, e.g., Institutional or Ethics Review Board, to ensure risks are as low and worth any potential benefits, and that patient rights are being protected?
Do the providers have approval for the safe conduct of clinical trials or medical use of a product for PD from a national or regional regulatory agency, e.g., FDA or the European Medicines Agency?
What are the alternative treatment options for my condition?
If I have this treatment, can I participate in otherclinical trials or have other interventional treatment options?
What compensation am I entitled to if I am injured as a result of participating in this therapy?
What are the total costs of the treatment and what does this include?
What would be the costs of emergency treatment, if needed, should a complication arise?

Red Flags raising concerns about a medical tourism facility

Claims of efficacy only based on patient testimonials
Claims of multiple diseases being treated with the same type of stem cell
Unclear documentation of the source of the cells or how the treatment will be done
Claims of little or no risk
High cost of treatment or hidden costs
Suggestions that repeat treatments may be needed if not initially successful

 

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Peter A. LeWitt, MD
Henry Ford Health System, Michigan

Readers may be surprised to learn that a placebo - a "sugar pill" containing no drug content can teach us a lot about Parkinson's disease (PD). Placebos mainly are used in medical research, commonly serving as tools for sorting out what a drug does and what its human recipient might expect it to accomplish. Their intent is not to be deceptive but, rather, to control for an inevitable part of the human experience: feeling better by taking a pill, no matter what its contents are. The placebo effect is a very real perception that a medication is helping, whether or not that pill actually has any pharmacological activity.

What are we learning about the Placebo Effect?

As recent science has shown, the placebo effect can be more than just an ill person's wishful thinking or positive attitude. Studies carried out in Parkinson's disease (PD) have provided fascinating insights into the placebo effect and has emphasized this phenomenon's importance in clinical research. There's experimental evidence that taking a placebo leads to changes in the brain, not unlike taking a dose of levodopa (the active ingredient of Sinemet). These investigations have used a research tool called positron emission tomography, which images the chemistry of the brain. Scientists at the University of British Columbia have shown that a placebo can enhance the signaling between nerve cells with dopamine, the brain chemical specifically deficient in PD. How is somewhat of a mystery, but the implication is clear - expecting an improvement from taking a pill thought to be therapeutic can exert a very real effect on the brain and PD symptoms. In some clinical trials, the degree of improvement on standard PD rating scales can be 20 percent or more. Any medication that has real promise needs to do much better.

Placebo effects are well-known to be active in other realms of brain function. For example, research into mechanisms of pain control also has emphasized that relief of 20 percent or more can occur just on the basis of expectation. Studies of depression, cognitive impairment, and of sleeping pills and many other medications, have also shown that, in proven therapies, there also may be some placebo effect. Many investigations of placebo effect have charted it as a changing response over time. In some clinical studies, the effect is most robust in the first few weeks after starting an experimental medication and gradually wanes thereafter. It has been demonstrable for three months or longer in some studies. Curiously, studies have detailed different magnitude and time course of placebo effects when examined in diverse populations participating in the same clinical trial. It should be obvious why using placebos in clinical research is so important. Any study judging the effectiveness of a new medication could yield misleading information if comparison to a placebo is not available.

Evaluating the Impact on Treatment

While modern medicines offer far more than placebo effect, both physician and patient should keep this in mind when evaluating the impact of treatments. Is that new (and expensive) medication really helping, or is just providing the perception of benefit? How long should a drug trial continue before reaching a conclusion as to whether it should be continued? Are there more objective ways to gauge the usefulness of a drug than just a "gut impression"? These questions can be challenging in everyday experiences of using PD medications. Fortunately, it is always possible to start and stop (and re-start) medications to discover what really works. As PD patients commonly experience fluctuations from dose to dose of medications with "good days and bad days," recognizing placebo effects may not be easy. Factors such as mood, anxiety, a restful night's sleep and distractions of a busy day al may modulate the perception of medication effect. So, the often-disparaged placebo effect may be just part of the bargain for the complexity of a human mind. Al¬though it can be confusing and adds to the cost of drug research for better PD drugs, the placebo effect is here to stay.

 

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Don Hitko, Facilitator of the Greater Lansing Area Parkinson's Support Group, is a very positive individual who is an inspiration to many. He has been creatively working to "make sense" out of Parkinson's disease from a person with PD and family point of view. This article is intended to persuade others to look beyond the obvious when you are with someone who has....THE PARKINSON MASK

(Permission to reproduce by author)

In this age of computers, any subject of choice usually can get more than enough coverage. This is a blessing for those of us who have Parkinson's disease. As we prompt and poke at our computers, an avalanche of descriptions, advice, reports, treatment trends, testimony, and inspirational offerings becomes available. Never in short supply are accounts of courage, sacrifice, and determination as we attempt to cope with our disorder.

As we access the multitude of resources for our information, a realization can form from the sense that with all this knowledge, inspiration, and support that we are fondling, something is still not on target. What seems to be beckoning is the need for expression of the turmoil that churns in our bodies, minds, and souls. Knowing is not enough! We can feel from one moment to the next that we are trapped in a body and mind that is becoming increasing hard to manage. This moment to moment awareness is fueled by a blunt sense of isolation and alienation.

Contributing to this dilemma is the unfortunate way that Parkinson's sculptures our minds and bodies. It is how this chronic ailment affects our inner and outer selves as we try to interact with our families, friends, any other good folk. This has its beginning with the conditioning we all have to each other's body language, and to the abilities needed to connect and communicate.

The person with Parkinson's disease doesn't project an approachable persona. The loss of some of the control of the face and head muscles creates a stare-like feature that is referred to as the "Parkinson Mask." The eyes don't blink as much; the smile, if there is one, appears forced or is of a short duration. The stiff neck and shoulders remind us of Frankenstein. There may be uncontrolled movements that vary from excessive to a Zombie-like absence. The hunched back is a reminder ofthe bell ringer from Notre Dame. There can be a funny gait, drooling, an unkempt appearance, and - heaven forbid - a body odor! This all adds up to an approachability that is uncomfortable, if not repelling.

If contact is eventually made, further dissonance is encountered. The voice of a Parkinson Person is often raspy and lacks volume that is not perceived by its owner. Any exchange of conversation is followed by a request to repeat what he has just spoken. Sometimes, no attempt to hear is resorted to. As the Parkinson one speaks, there is a tendency to run the words together, especially in a telephone conversation.

If a request is made to help communication by writing down the message or idea, then another Parkinson hardship is on tap: the lack of coordination causes handwriting that is barely legible.

Difficulty with memory is another burden a PD person can experience. The slow responses, the mixed up details, further make the situation uneasy.

Low libido due to the disease or the medicine taken, puts into hibernation the masculine and feminine interplay that can add radiance to any interaction. Balance problems plus muscle weakness and stiffness result in a reluctance to move about, which leads to judgments that you want to be left alone.

Parkinson People are too often slow and fumbling. This does not go well with our hurry hurry lifestyles. The whining response from the PD person is "I am doingit as fast as I possibly can. Please be patient!

Sleep disturbance is more than occasional for the one with the masked face. Yawning and loss of attention help to pile on the discord.

Fluctuation of moods can add to disruptions. Within the short span of time that medication wears down, a swing in feelings or any sense of well being can change into a "joyless cranky wanting to withdraw" mood. This inconsistency adds a wariness to the relationship.

The focus in this presentation is not meant to detract from the lofty qualities that are companion to warm hearted people and their care givers. It is meant to raise the curtain on the predominant struggle that too often is buried under the "chin-up" rallying cry that can misdirect some well-intended cheerfulness.

Suppression of the powerful torment that can encompass this chronic condition can lead to an unwillingness to engage the despair and inaction that can bring life to a creep!

The Parkinson mask can hide the face from the reality that exists in a warm and tender heart that may be in disguise.

 

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By Susan R. Vergilio, OTR

It has been said that the "horse symbolizes the drive for freedom shared by people of all nations" (author unknown) and that "in riding a horse, we borrow freedom" (Pam Brown). All who come in contact with these beautiful animals, especially those patients receiving hippotherapy, can confirm these quotes. Hippotherapy is a treatment tool used by a specially trained occupational, physical, or speech therapist to treat patients with neurological problems. By using the specific movement of the horse, the therapist can influence the patient's nervous system and ability to plan their movement. Why the horse? The horse's movement is rhythmic and repetitive, and with the right horse, it is symmetrical. The horse's stride also simulates human walking in terms of the influence of movement on the hips of its rider. It also encourages motor learning, a treatment principle that therapists use in treatment, so the movement of the horse creates responses that are essential for walking and other activities, which can be carried over off of the horse. The horse acts as a three-dimensional mobile mat from which therapy can occur. As therapists, we are continuously trying to teach "normal" movement to our clients with neurological problems, and the horse can naturally assist us with this. The movement of the horse can improve balance, strength, tone, timing, coordination, and postural control, which can all lead to improved functional ability of the person with Parkinson's disease. In addition to the natural influence of the horse's movement, there is added benefit from the natural animal-human bond that occurs throughout the sessions. Animals are extremely motivating and can inspire us and touch us in ways that the traditional setting for therapy cannot. This is especially important because therapy is a participatory program. Your therapist can't just do therapy to you; you have to participate and be engaged in the activities in order for them to be effective. Let's face it, when you have been involved in the same traditional treatment activities for a long time, they become a bit repetitious. This leads to decreased patient motivation and participation and therefore decreased improvements in treatment. This is why hippotherapy opens up a whole new opportunity for patients.

Tim is a 47 year old man with Parkinson's. He receives hippotherapy treatments once a week. Tim was in his 30's when diagnosed with Parkinson's disease. In the past, he has been involved in traditional therapy and recently started hippotherapy. He, as well as his family, feel that the hippotherapy has improved his function at home as well as improved his mobility overall. He had developed the very classic signs associated with Parkinson's disease, including a flexed posture, decreased coordination, increased rigidity, as well as "scissoring" in both of his legs. He was wheelchair-dependent prior to starting his hippotherapy sessions. He is now able to walk short distances, with improved control and coordination. He is noted to have a visible change in control over his legs, with less "scissoring" immediately following his session. Tim says he feels he hasgreater self- esteem, and feels the sessions are "good for the soul," not to mention feeling less rigidity through out his body following his hippotherapy sessions.

Hippotherapy is not for everyone. All patients must be carefully screened. Typical hippotherapy sessions are 1-2x/week, 30-60 minutes in duration, and are used in addition to traditional therapy techniques. Treatment can only be effective if the therapist has been specially trained to utilize the proper movements of the horse from an accredited program. For more information regarding hippotherapy or if you interested in receiving hippotherapy services please contact Sue Vergilio, OTR at Stable Possibilities LLC, at 586-292-8472.

 

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