May 19 - Dr. Heidi Musgrave talks on Depression and Dementia.
Jun 16 - Disasters and Disabilities. This program is rescheduled from January. A panel from the Red Cross, Police, Fire, and other emergency agencies will present how PWP can handle emergencies.
March
A special “thanks” to Dr. Atiya Khan for her enlightening talk on sleep issues.
A brief synopsis follows:REM (Rapid Eye Movement) REM is identified by the acting out of your dreams and this “acting out” can predate your PD diagnosis. The only body parts moving during REM sleep are your eyes. The rest of your body is as if it were paralyzed. The paralysis leaves and there is sometimes violent acting out of your dreams. This acting out is called REM Behavior Disorder (RBD). It is treatable with clozapine.
Daytime Sleepiness- This could be caused by medications, and/or PD symptoms of stiffness and depression. Taking naps exacerbates your sleep cycle and you gradually alter your sleep habits from night to daytime. To help combat this problem keep your rooms brightly lit (including sunshine) up until about 9:30 p.m. or so. Use as much lighting as possible. Stay active. Activity wakes up the brain. Drink your caffeine in the morning. Drink little at night. If naps are a must, take short “power” naps, not long ones.
Sleep Apnea- Treat this problem with a CPAP (Controlled Positive Air Pressure) Machine. This helps keep normal air flow into your lungs and as long as your brain senses you are sleeping all is ok. Normally you take a breath every five seconds. It is usually ten or more seconds with sleep apnea. Some even take up to sixty seconds between breaths. When it takes longer than normal to breathe, your brain wakes you up to breathe. These repeated awakenings are the cause of loss of sleep.
Obstructive Sleep Apnea- This occurs as you tongue will fall back in your throat obstructing you trachea, and you feel like you are choking. This then can cause your brain to awaken thirty to fifty times per night, and you lose sleep,
Narcolepsy- This is the condition of dropping off to sleep very quickly. This is caused by a chemical imbalance in the hypothalamus. This is a dangerous condition when operating equipment, or driving.
Nightmares/Dreams/Hallucinations- Stopping or cutting back on nighttime med dosages can help alleviate these disorders. The use of the drug Seroquel can be helpful.
Restless Leg Syndrome- This manifests itself with the urge to move your legs in bed at night. Mirapex and methadone are possible meds for RLS.
Remember, the darker the room, the better the sleep. Clozapine can help you fall asleep; it just won’t keep you asleep.
For insomnia, cognitive behavior therapy nay is of help.
A NOTE FROM DAN SPANGLER
The February support group meeting was about “caring and sharing”. Sometimes it is difficult to share. Sometimes we are in denial, embarrassed, even angry. Others “can” learn from our experiences, especially if they are similar to ours. We can even be thankful that our symptoms are not as severe as someone else’s. Most importantly we can share, make others aware, and most of all encourage each other… One such encourager is Jim McKinnon. He had some enlightening words in our February “Caring and sharing” group. He has given us permission to share those words with you.Speech communications
“If you have Parkinson’s PLEASE investigate and sign up for the Lee Silverman speech class before you have any difficulty, or at least when you first suspect something is wrong. I first noticed a slight slur about ten years ago while giving a presentation at work. I have taken the course twice in the last year. Once at Parkview and once with Peg Maginn who really tried hard, but it was too late.”
Eyes/blindness
“Several times a day my eyes close and I can’t get them open for 5 to 45 minutes. The only way to open them is to take a dry wash cloth and rub it gently over the lids. That’s scary.”
Medication
“The medication has finally taken a toll on my teeth. During the last thirty years I have gone to the dentist every six months a checkup and cleaning which resulted in two cavities over that period. Now in the last three months I have had four extracted and another eight to go next month”
My present daily meds are:
- 6 Sinemet (Carbodopa) 25/100
- 3 Midotrine 10 mg hcl
- 1 Vit B
- 3 Amantadine 100 mg
- 1 Lanoxin 125 mg
- 1Docusate Sodium 10 mg
- 3 Mirapex .50 mg
- 1 Vitamin
- 1 Aspirin
“It’s been very difficult to drink or swallow. It takes 2-3 hours to eat dinner. I found the best way to drink and get fluids down is with a straw. That goes for taking pills especially.”
Feeding tube
“As a result of not being able to eat or drink properly I had to have a stomach feed tube installed. I lost so much weight. TAKE ARE OF YOURSELF Believe me you don’t want to have that done to you.”
Thanks, Jim. You’re a peach for sharing. We really appreciate your willingness to share.
Philharmonic Research Project data is now complete
A special "Thank You" to all who participated. And a special "Thank You" to IPFW, PHP, and the Philharmonic, for their sponsorship. Dr. Nancy Jackson, music therapy professor at IPFW, will be presenting the findings at a support group meeting later in the fall. ----
Turnstone's disABILIES Expo is scheduled for Saturday, May 6, 2011 from 10am until 4pm, at the Coliseum. The support group will again staff a booth to get the word out about Parkinson's. We need workers to volunteer for 90 minute shifts. If interested call Dan Spangler 260-486-4893. --
Chair Yo-lates is a new exercise program beginning at Turnstone April 12ththrough May 18. Participation is open to all Turnstone groups including members of the Parkinson’s support group and exercise class. Call Candace Risch, Fitness Specialist at Turnstone for times, dates, costs, and a program explanation. 260-483-2100 ext. 277 or 290.
CAREGIVERS' CORNER
by Ed Gatke
Coping With Stress and AnxietyHere are a few guidelines you can use now to help alleviate your anxiety.
1. Recognize and admit that you are feeling stressed and anxious.
2. Become aware of your body's symptoms. Don't let them scare you, let them talk to you.
3. Try to pinpoint what it is you are anxious about. What happened yesterday? What were you thinking about before you went to bed? If you can't pinpoint it, don't worry about it and move on.
4. Give yourself permission to feel anxious about whatever it is that is bothering you. "Of course, I feel anxious about this problem, anyone would. But how much anxiety is too much?"
If you do know what is bothering you, what can you do to eliminate or minimize the situation in someway so that it isn't so stressful? Most importantly, how can you react differently, so you won't be so affected by the situation? Here are some things to think about.
1. Listen to the dialog within yourself. Are you filling yourself with negative thoughts about a certain situation? What can you say to yourself that would feel more comforting?
2. Listen to the dialog of those around you. Is someone around you being negative and dragging you down with them? If so, how could you change your reaction to their negative attitude, so that you would be less affected by it?
3. Are you overwhelming yourself with "shouldas" and high expectations? If so, which ones could you eliminate?
4. Are you blaming someone else for your anxieties, unhappiness, poor health, lack of success, etc.?
How can you take responsibility for yourself and make some positive changes?
5. Give yourself positive reinforcement for even the smallest accomplishments.
No one lives a life without a certain amount of stress and anxiety. The key is to get the level of both down to a manageable level. Listening to your "inner voice" is a step in the right direction. You know best what you need.
TIPS TO MAKE YOUR LIFE BETTER
by Ed Gatke
The original article, written by Gary E. Cordingley, MD, PhD. lists ten points. We will cover the first five this month, and do the last five next month.Although PD is treatable, it can still interfere with one's quality of life. However, awareness of certain tricks of the trade and nuances of treatment can enable PD patients to maximize function and independence.
The doctor writes.....
Parkinson's disease is a condition for which available treatments are both wonderful and inadequate. They're inadequate because they don't stop the underlying disease from worsening over time and they don't address all the patient's needs. If you have PD, you need to grab every edge you can. Here are 5 tips your doctor probably agrees with, but doesn't have the time to emphasize at each visit.
These tips have to do with getting the most benefit from your medication.
1. Put your morning dose of medication and a glass of water on your nightstand.
Many PWP find that their ability to move around freely is worst in the morning. This might be because their last dose of medication, taken the previous evening, is already wearing off. By the time their morning dose has a chance to take effect, they have already been up and around for a while. The trick here is to plan ahead. Before retiring for the night, set tomorrow morning's first dose on the nightstand along with a glass of water. In the morning, take your dose as the first thing you do. Then the medication is already getting into your system while you're going through your morning routine. You can even set the alarm clock for an hour before you plan to awaken so you can take the dose and then roll over for another hour of sleep. By the time you get up for good, the morning dose has already gotten a head start.
2. Pay attention to whether you take your pills with food.
It is neither wrong nor right to take your pills with food, but there are consequences. In general, when you take your medication on an empty stomach, more of it is absorbed into your bloodstream. On the other hand, if your medication makes you queasy, then you can minimize this by taking it at mealtime.
3. Avoid most anti-nausea medications.
Most anti-nausea medications can worsen the symptoms of PD or interfere with the benefits of the PD medication. Some of the most common anti-nausea drugs, e.g. metoclopramide (Reglan), promethazine (Phenergan), and prochlorperazine (Compazine) block the body's chemical dopamine receptors. These are the very receptors that most PD medications seek to activate. Taking anti-nausea drugs while also taking PD medications means that you're taking a drug and its antidote at the same time, which means that they cancel each other out.
4. Be mindful of forgetfulness.
PWP may already be more prone to forgetfulness because of either their disease or their age. But certain medications used for PD ,e.g. tolerodine (Detrol) and oxybutynin (Ditropan), can worsen memory. So if you're having trouble remembering things, you should tell your doctor. A simple medication adjustment might solve the problem.
5. Know the difference between tremors and dyskinesias.
PD often causes tremors, which are rhythmic oscillations of hands or other parts of the body. However, many Parkinson medications, when dosed high enough, can produce another kind of excessive, involuntary movements called dyskinesias. These might involve muscles of the face, neck, trunk, arms, or legs and have the appearance of wiggles and fidgets rather than a rhythmic oscillation. Distinguishing between these different movement disorders is important because the presence of one might mean that the dose of medication should be increased, while the presence of the other might mean that the dose should be decreased.
Part two of Dr. C's report will continue next month.
Are We There Yet?
There was an elderly couple sitting on the bar stools at the counter in the drugstore. The man says, “Honey, do you think that we will look like the couple sitting at the end of the bar in another 10 years?” The wife looks his way and mutters, “Dear, that is a mirror at the end of the counter.”What Causes Brain Cell Death in Parkinson's Patients?
Science Daily (Jan. 11, 2011) — Just 5 percent of Parkinson's disease cases can be explained by genetic mutation, while the rest have no known cause. But a new discovery by researchers at The University of Texas Health Science Center may begin to explain why the vast majority of Parkinson's patients develop the progressive neurodegenerative disease.This week in The Journal of Neuroscience, the researchers demystified a process that leads to the death of brain cells -- or neurons -- in Parkinson's patients. When researchers blocked the process, the neurons survived.
The findings could lead to an effective treatment to slow the progression of Parkinson's disease, rather than simply address symptoms that include tremors, slowed movement, muscle stiffness and impaired balance. Further studies could lead to a diagnostic test that could screen for Parkinson's years before symptoms develop, said Syed Z. Imam, Ph.D., adjunct assistant professor at the UT Health Science Center.
Parkinson's disease, which usually is not diagnosed until age 60 or later, affects an estimated half-million people in the United States.
Dr. Imam joined the U.S. Food and Drug Administration (FDA) after the research was conducted. Co-authors are from the Health Science Center's Barshop Institute for Longevity and Aging Studies; the South Texas Veterans Health Care System; and the Hertie Institute for Clinical Brain Research in Tübingen, Germany.
The mechanism
After analyzing cells and post-mortem brain tissue from animals and humans, researchers noted that oxidative stress -- a known culprit in neuron death -- activated a protein called tyrosine kinase c-Abl in the nigra-striatum area of the brain. Neurons in this part of the brain are particularly vulnerable to Parkinson's injury.
Activation of this protein led to changes in another protein called parkin, which is known to be mutated in hereditary Parkinson's. The altered parkin lacked the capacity to break down other proteins, leading to harmful clumps of unprocessed protein in the neuron. The scientists believe this accumulation leads to progressive neuron death, resulting in Parkinson's symptoms that worsen over time.
Implications
"When we blocked tyrosine kinase c-Abl activation, parkin function was preserved and neurons were spared," Dr. Imam said. "We believe these studies provide sound rationale for moving forward with a preclinical trial of tyrosine kinase c-Abl inhibitors, with the goal of developing a potent therapeutic drug for slowing the progression of Parkinson's."
If preclinical trials in animal models of Parkinson's disease yield positive results, the next step would be clinical trials in human patients, Dr. Imam said.
Tyrosine kinase c-Abl inhibitors are approved by the FDA for treating myeloid leukemia and gastrointestinal tumors. This could speed approval of the drug for Parkinson's and its translation from bench research to clinical practice.
"The race is on to understand the mechanism of the 95 percent of Parkinson's cases with no known cause, and our finding certainly is a building block," Dr. Imam said. "We have found a specific signaling mechanism that is only turned on by oxidative stress and is selective only to Parkinson's-affected neurons of the nigra-striatum, which is the area that sends signals for balance to the cerebellum."
Taken from www. science daily.com
Stress Takes Its Toll in Parkinson's Disease
Science Daily (Nov. 11, 2010) — We all know that living a stressful lifestyle can take its toll, making us age faster and making us more susceptible to the cold going around the office.The same appears to be true of neurons in the brain. According to a new Northwestern Medicine study published Nov. 10 in the journal Nature, dopamine-releasing neurons in a region of the brain called the substantia nigra lead a lifestyle that requires lots of energy, creating stress that could lead to the neurons' premature death. Their death causes Parkinson's disease.
"Why this small group of neurons dies in Parkinson's disease is the core question we struggled with," says lead author D. James Surmeier, the Nathan Smith Davis Professor and chair of physiology at Northwestern University Feinberg School of Medicine. "Our research provides a potential answer by showing this small group of neurons uses a metabolically expensive strategy to do its job. This 'lifestyle' choice stresses the neurons' mitochondria and elevates the production of superoxide and free radicals -- molecules closely linked to aging, cellular dysfunction and death."
The good news is preclinical research shows this stress can be controlled with a drug already approved for human use. By preventing calcium entry, the drug isradipine reduced the mitochondrial stress in dopamine-releasing neurons to the levels seen in neurons not affected by the disease.
Northwestern Medicine scientists currently are conducting a clinical trial to find out if isradipine can be used safely and is tolerated by patients with Parkinson's. Isradipine is already approved by the Food and Drug Administration for treatment of high blood pressure.
Parkinson's disease is the second most common neurodegenerative disease in the United States, second only to Alzheimer's disease. The average age of diagnosis is near 60. More than 1 million Americans currently have Parkinson's disease, and this number is rising as the population ages. The symptoms of Parkinson's disease include rigidity, slowness of movement and tremors. No treatment currently is known to prevent or slow the progression of Parkinson's disease.
Although most cases of Parkinson's disease have no known genetic link, Surmeier's study in mice showed that the mitochondrial stress in dopamine-releasing neurons was worsened in a genetic model of early-onset Parkinson's disease, suggesting a similar mechanism in rare familial forms of the disease and the more common forms.
Everyone loses dopamine-releasing neurons with age, Surmeier noted. "By lowering their metabolic stress level, we should be able to make dopamine-releasing neurons live longer and delay the onset of Parkinson's disease," he said. "For individuals diagnosed with Parkinson's disease, the hope is that this drug can slow disease progression, giving symptomatic therapies a broader window in which to work."
The study was supported by the National Institutes of Health, United States Department of Defense, Thomas Hartman Foundation For Parkinson's Research, Inc., The Picower Foundation and Dr. Ralph and Marian Falk Medical Research Trust.
Taken from www.sciencedaily.com
Natural Toxin Implicated as Triggering Parkinson's Disease
Science Daily (Feb. 11, 2011) — n new research from Saint Louis University, investigators have found evidence that a toxin produced by the brain is responsible for the series of cellular events that lead to Parkinson's disease. The study, published in PLoS One, found that the brain toxin DOPAL plays a key role in killing the dopamine neurons which trigger the illness.In earlier research, Saint Louis University investigators found that DOPAL seemed to be responsible for killing healthy dopamine cells, which in turn causes Parkinson disease to develop. Now, research in an animal model gives them further reason to suspect the chemical as the culprit.
Parkinson's disease is a debilitating neurodegenerative movement disorder, affecting 2 percent of individuals older than age 65 and 4 to 5 percent older than 85 years. The disorder is due to a loss of dopamine neurons and is characterized by bradykinesia and tremors while at rest.
Dopamine, a vital chemical that allows for coordinated function of neurons controlling the body's muscles and movements, is produced by nerve cells in the substantial nigra. When 80 percent of these cells die or become damaged, symptoms of Parkinson's disease begin to appear, including tremors, slowness of movement, rigidity and stiffness, and difficulty with balance.
Lead researcher, W. Michael Panneton, Ph.D., professor of pharmacological and physiological science at Saint Louis University School of Medicine, says the research offers a big step forward in the understanding of Parkinson's disease.
"In Parkinson disease, we knew that the death of dopamine cells is responsible for patients' symptoms," said Panneton. "But no one knew why the cells are dying."
From a cellular perspective, doctors know some pieces of the puzzle. They know that Parkinson patients have a loss of dopamine neurons in a part of the brain called the substantia nigra, leading to severe dopamine loss in another part of the brain called the striatum, and the aggregation of a protein called alpha-synuclein.
Alpha-synuclein is found throughout the brain. In some people, the protein clumps together. We found that it is DOPAL that causes alpha-synuclein protein in the brain to aggregate. This induces further increases of DOPAL leading to the death of the dopamine-producing cells, which in turn causes Parkinson's symptoms to develop.
Currently, the main approach to Parkinson's disease is to treat symptoms by replacing dopamine that's lost when the cells die. This approach however does not prevent the loss of dopamine neurons causing Parkinson's disease.
These findings open up promising new research avenues to prevent dopamine neuron loss and the progression of Parkinson's disease.
The research was funded by Saint Louis University School of Me
Taken from www.sciencedaily.com
COGNITIVE COMMUNICATION CLASS
There are two sessions per week. ($6.00 for one session or $10 for both) Mondays and Wednesdays from 9:30 to10:15 a.m. at theTurnstone Auditorium, 3320 N Clinton in Ft Wayne.Peg Maginn, Speech Pathologist, is instructor. (260-483-2100)(260-483-2100, Ex.229) The class addresses speech, voice, swallowing, and cognitive thinking.
