HeroTeo - The Parkinson’s FighterChronicles of A Parkinson’s Fighter |
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Your book is very well written and very inspiring to all of those who read it. I have enjoyed reading it if for only a brief time. My name is Douglas Dodson and you can find me on facebook at douglas.dodson@gmx.com. Please feel free to message me and let me know how your writing is coming.
Safe travels,
_Doug.
Posted: Wed Dec 16, 2009 2:34 pm Post subject: Posted: Wed Dec 16, 2009 2:34 pm Post subject: Mild shaking of right hand third finger
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Why Mild shaking of right hand third finger and still no difficulty doing weight lifting,Yoga and Muay Thai exercise daily?
Is it Parkinson’s Progression?
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
Posted: Thu Dec 17, 2009 11:09 pm Post subject:
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The general belief is that PD is a universally progressive illness….so, over time, patients typically get worse.
Having said that, the speed of progression varies widely between patients. in fact, just yesterday I saw a patient, who I still believe has PD, but has had minimal progression in the last 7 years. Now this is not typical and probably exceptional, but it does exists.
Your PD seems to be very slow and benign. In many ways, you should count your blessings! Happy holidays!
Yours,
_________________
Hubert H. Fernandez
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Why Mild shaking of right hand third finger and still no difficulty doing weight lifting,Yoga and Muay Thai exercise daily?
Is it Parkinson’s Progression?
Back to top
Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
Posted: Thu Dec 17, 2009 11:09 pm Post subject:
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The general belief is that PD is a universally progressive illness….so, over time, patients typically get worse.
Having said that, the speed of progression varies widely between patients. in fact, just yesterday I saw a patient, who I still believe has PD, but has had minimal progression in the last 7 years. Now this is not typical and probably exceptional, but it does exists.
Your PD seems to be very slow and benign. In many ways, you should count your blessings! Happy holidays!
Yours,
_________________
Hubert H. Fernandez
Anonymous
Posted: Sat Dec 05, 2009 9:44 am Post subject: sinemet and prevacid
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Dear Kathrynne,
Will taking Sinemet and Prevacid interfere with the absorption of the Sinemet?
If they are both supposed to be taken on an empty stomach, how does one do this?
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Sat Dec 05, 2009 11:46 am Post subject:
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Dear Friend,
If you are taking the prevacid once daily, try to schedule it in between Sinemet doses. For example, if you take Sinemet at 7:00 am, 11:00 am, 3:00 pm, and 7:00 pm, and have your meals at 8:00 am, 12:00 noon, and 5:00 pm, ask your prescribing doctor if you can take the Prevacid at 7:30 am. That will give the Sinemet 30 minutes to clear the stomach; then the Prevacid will have 30 minutes to clear; then at 8:00 you should be able to have your breakfast without concern.
Let me know if you have further questions, or if this did not help.
_________________
Best regards,
Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Thu Dec 03, 2009 5:05 pm Post subject: Parkinson’s, B6, B12, and Folate - What’s the Connection?
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Parkinson’s, B6, B12, and Folate - What’s the Connection?
Kathrynne Holden, MS, RD
Copyright 2008
Ms. Holden is a registered dietitian specializing in Parkinson’s
disease. She has published research, books, articles, and manuals on
nutrition and PD, including “Eat well, stay well with Parkinson’s
disease.”
In the past decade, there has been increasing interest among
researchers about the effects of three B vitamins - B6, B12, and folate.
We now know that deficiencies occur with greater frequency than ever
suspected previously, particularly in older adults. We also now know
that deficiencies, if not corrected, can result in irreversible damage
in some people. Some health professionals are beginning to suspect that
these three vitamins may be significant factors in Parkinson’s disease.
What are B6, B12, and folate, and what do they do?
These are essential nutrients, meaning that they are vital to life.
These three vitamins work both independently and together in many of the
body’s systems.
Vitamin B6 assists in making hormones, new proteins, and
neurotransmitters (”messengers” between nerve cells) for the body’s use.
It also helps release stored sugar when we need it for fuel. It works
together with B12 and folate to remove homocysteine from the blood.
Homocysteine is a substance increasingly associated with a number of
diseases; more about this later.
Vitamin B12 plays a role in the synthesis of DNA, needed for formation
of new red blood cells. It takes part in the manufacture of the myelin
sheath - the protective coating that surrounds nerve cells. With B6 and
folate it removes homocysteine from the blood.
Folate, also called folacin or folic acid, is a partner with B12 in DNA
synthesis and in removal of homocysteine, and is required in many other
vital processes. Without folate, B12 would be unable to complete many of
its functions, and vice versa. Folate is the form found in foods, folic
acid is the form in dietary supplements.
How much do we need of these vitamins?
Nutrient needs are broken down by gender, age group, pregnancy, and
lactation. New guidelines have also established a Tolerable Upper Intake
Level. So, for example, while the RDA for vitamin B6 for males and
females age 19-30 years is 1.3 mg/day, the Tolerable Upper Intake Level
for both is 100 mg/day, making it easier to provide recommended amounts.
RDA* Tolerable Upper Intake Level ** +
Vitamin B6*** + 1.7 mg/day 100 mg/day (age 19 and older)
Vitamin B12 + 2.4 mcg/day Not Determined
Folate + 400 mcg/day 1000 mcg/day
* Recommended Dietary Allowance
** The Tolerable Upper Intake Level is the maximum level of daily
nutrient intake that is likely to pose no risk of adverse effects, and
represents the total intake from food, water, and supplements.
*** Adults age 51 and older
+ not applicable if pregnant or lactating
Why do deficiencies occur, and what are signs of deficiencies?
Vitamin B6. Mild deficiencies of B6 are fairly common in the U.S.,
mostly because of dietary deficiencies, but sometimes due to use of
certain medications which interfere with B6, including hydralazine,
isoniazid, MAO inhibitors, penicillamine, and theophylline. (Conversely,
large amounts of B6 can interfere with the absorption of levodopa, an
important medication for Parkinson’s disease. Current use of the
combinations of carbidopa-levodopa or benserazide-levodopa offset this
interaction for the most part; but use of supplements containing more
than 15 mg of B6 can overwhelm the protective effects of the carbidopa
and benserazide.)
Good food sources of B6 include chicken, fish, eggs, nuts and seeds,
dried beans and peas, soybeans, wheat germ, bananas, avocados, and
brewer’s yeast. Also, some foods, including a number of breakfast
cereals, are fortified with B6.
Signs of B6 deficiency include irritability, depression, and confusion;
sore tongue, sores or ulcers of the mouth, and ulcers of the skin at the
corners of the mouth.
Vitamin B12. The human body stores this vitamin so well that it can
take a long time to deplete, sometimes several years. Nevertheless,
there are several reasons why people sometimes do experience deficiency.
Animal foods are the only source of B12, therefore people who eat few or
no animal products (meat, fish, poultry, eggs, milk) are at risk unless
they use vitamin supplements.
Another problem is that B12 in foods cannot be absorbed by the body
until it is freed from the proteins in the food; the stomach produces an
acid that removes this protein. However, with age, we produce less and
less of this stomach acid. Many older adults don’t produce enough acid
to allow them to absorb B12. Further, people who have acid reflux often
use medications that reduce stomach acid, which unfortunately also
decreases absorption of B12. Vitamin B12 is one of the few nutrients
that is better absorbed in pill form than from dietary sources.
Signs of B12 deficiency include numbness or a tingling “pins and
needles” sensation, or a burning feeling; a red, sore, or burning
tongue; loss of appetite; gait abnormalities, personality changes, an
Alzheimer-like dementia, psychosis, depression, and agitation,
particularly in older adults. Other signs are megaloblastic anemia, and
elevated serum homocysteine, in people of all ages. Researchers believe
that as many as 42% of people aged 65 and older may have some degree of
B12 deficiency. Many people with PD are age 65 or older, and should be
considered at risk and tested for B12 deficiency.
Folate. Folate is available in many foods: lima beans, brewer’s yeast,
orange juice, dried beans, green peas, asparagus, beets, Brussels
sprouts, broccoli, corn, spinach and other dark green leafy vegetables,
soybeans, nuts and seeds. Further, the U.S. government requires that
food manufacturers fortify processed grain products with folic acid.
Yet, deficiencies of folate are not uncommon. This could be in part
because folate is another of the few nutrients in which the synthetic
form is absorbed much better (about 40 percent better) than the natural
form.
Because of the possibility of deficiency, women, including women with
PD, who are pregnant or wish to become pregnant are advised to take
supplements of folic acid; deficiencies can result in neural tube
defects in the unborn child.
Deficiencies of folate are also being increasingly studied for a
possible role in other diseases:
. A low intake of folic acid is associated with risk for colon cancer.
Chronic constipation, experienced by many people with PD, also increases
risk for colon cancer; it is prudent for those with PD to control
constipation and to be sure the diet is adequate in folate.
. A low level of folic acid in the blood is associated with higher
levels of serum homocysteine, a substance in the blood that may
contribute to heart disease, stroke, and dementias.
. Animal studies point to a link between low levels of folic acid and
Alzheimer’s disease; and people with Alzheimer’s are often found to have
low levels of folic acid. Some people with PD develop an Alzheimer-type
dementia. Again, prudence dictates consumption of adequate folate.
. Another study using mice found that folic acid deficiency led to
increased levels of homocysteine and symptoms of Parkinson’s disease.
Researchers speculate that homocysteine may damage DNA in the substantia
nigra, the area of the brain affected in Parkinson’s disease.
. There are reports of improvement in restless leg syndrome (RLS) with
use of folate supplements; this has not as yet been studied thoroughly,
so it is too early to say whether there is a definite link. However,
people with PD often complain of RLS, and physicians should rule out the
possibility of folic acid deficiency.
Signs of folic acid deficiency include appetite loss, weight loss,
burning tongue, fatigue, weakness, shortness of breach, memory loss,
irritability, megaloblastic anemia, and increased levels of serum
homocysteine.
Should people with PD be concerned about these vitamins?
Although there are concerns, as mentioned above, that deserve further
study, it’s too early to say definitely that these three vitamins are of
significance to people with PD. However, if you are over age 50 these
vitamins are of importance independently of PD. Furthermore, studies
have demonstrated that some people who use levodopa, considered the best
medication for PD, develop elevated levels of serum homocysteine, due to
the way in which the medication is metabolized. It is certainly a good
idea to ask your doctor to test levels of serum homocysteine annually,
and to check for signs of B vitamin deficiencies.
Should you take supplements?
There is growing agreement that older adults are at risk for nutrient
deficiency, whether PD is present or not, and that supplements can help.
. One study of older adults found that a multivitamin containing 100% of
the Daily Value improved low levels of several nutrients, including
vitamins B6, B12, and folate.
. A recent study in the United Kingdom suggests that folic acid intake
should be about three times that of the current recommendation for
elderly people.
. Other studies indicate that up to 10% of older adults with low-normal
levels of B12 are actually deficient and could benefit from supplements.
Because folate supplements can mask a B12 deficiency, it becomes extra
important to get enough B12 daily.
. The American Heart Association recommends a folate-rich diet to lower
homocysteine levels, and supplements of 2 mg B6, 400 mcg folic acid, and
6 mcg of B12 if dietary means are not sufficient to lower the
homocysteine.
For people with PD who use a medication that contains levodopa (such as
Sinemet, Madopar, Syndopa, Larodopa, etc.), you should be aware that
large amounts of vitamin B6 (more than 15 mg) can affect the absorption
of levodopa, by converting levodopa to dopamine in the stomach and
bloodstream. Dopamine cannot cross the blood-brain barrier, so it is
effectively blocked from its purpose.
Sinemet and Madopar contain either carbidopa or benserazide, which
“protect” the levodopa from B6; so ordinary supplements of B6 should not
be a problem for most people. However, very large amounts of B6, greater
than 15 mg (and in sensitive persons, possibly as low as 10 mg), could
overwhelm the protective effects of the carbidopa or benserazide. Such a
supplement should be taken at bedtime with a light snack, or with meals
at least two hours separately from levodopa.
In summary, older adults are acknowledged to be at increased risk for B
vitamin deficiencies. People with PD who are age 50 and over, therefore,
are at increased risk also. Whether younger people with PD should be
concerned about such deficiencies remains to be seen. A prudent and
rational approach for all those with PD is to:
. Discuss the possibility with their physicians, and to request tests
for B vitamin deficiencies
. Be aware of the signs of B vitamin deficiency
. Take a multivitamin/mineral supplement daily. Unless anemic, choose a
supplement that does not contain iron
. Take a B complex supplement if deficiencies occur; and take the
supplement separately from levodopa by at least two hours, preferably
with meals or a snack.
Knowledge is strength; awareness of dietary needs can prevent illness,
malnutrition, suffering, and hospitalization. If you have questions
about B vitamins or other nutrition or dietary needs, please visit the
National Parkinson Foundation website:
The above article may not be reproduced in any form except with
permission from the author.
References
Giovannucci, E. et al. Alcohol, low-methionine-low-folate diets, and
risk of colon cancer in men. Journal of the National Cancer Institute.
1995; volume 87: pages 265-273.
Kruman II, Kumaravel TS, Lohani A, Pedersen WA, Cutler RG, Kruman Y,
Haughey N, Lee J, Evans M, Mattson MP. Folic Acid deficiency and
homocysteine impair DNA repair in hippocampal neurons and sensitize them
to amyloid toxicity in experimental models of Alzheimer’s disease. J
Neurosci 2002 Mar 1;22(5):1752-62.
Lobo A, Naso A, Arheart K, Kruger WD, Abou-Ghazala T, Alsous F, Nahlawi
M, Gupta A, Moustapha A, van Lente F, Jacobsen DW, Robinson K. Reduction
of homocysteine levels in coronary artery disease by low-dose folic acid
combined with vitamins B6 and B12. Am J Cardiol 1999 Mar 15;83(6):821-5.
Malinow, M.R. et al. Homocyst(e)ine, diet, and cardiovascular diseases:
a statement for healthcare professionals from the nutrition committee,
American Heart Association. Circulation. 1999; volume 99: pages 178-182.
Muller T, Werne B, Fowler B, Kuhn W. Nigral endothelial dysfunction,
homocysteine, and Parkinson’s disease. Lancet. 1999 Jul
10;354(9173):126-7.
Muller T, Woitalla D, Hauptmann B, Fowler B, Kuhn W. Decrease of
methionine and S-adenosylmethionine and increase of homocysteine in
treated patients with Parkinson’s disease.
Neurosci Lett. 2001 Jul 27;308(1):54-6.
Naurath HJ, Joosten E, Riezler R, Stabler SP, Allen RH, Lindenbaum J.
Effects of vitamin B12, folate, and vitamin B6 supplements in elderly
people with normal serum vitamin concentrations. Lancet 1995; 346:85-89.
O’Keeffe ST. Restless legs syndrome. A review. Arch Intern Med.
1996;156:243-248.
_________________
Best regards,
Kathrynne Holden, MS
–
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
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Anonymous
Posted: Thu Dec 03, 2009 7:49 pm Post subject:
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Nuts and seeds cure all ills … ;o)
Nice detailed recap of the B Vitamins
Rich
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Fri Dec 04, 2009 8:51 am Post subject:
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.
Tut, Rich, you did not read the part about B12: “Animal foods are the only source of B12…..meat, fish, poultry, eggs, milk…”
See? dietitians aren’t just about nuts and seeds.
_________________
Best regards,
Kathrynne Holden, MS
–
For a Parkinson Tip of the Day visit:
http://www.nutritionucanlivewith.com/
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June 15, 2009 (Paris, France) - Patients with Parkinson’s disease (PD) who exercise on a stationary tandem bicycle with a healthy partner during a single 40-minute session experience a 35% improvement in motor function and increased brain activation similar to that found with levodopa treatment, new research shows.
The study, by researchers at the Cleveland Clinic in Ohio, found that maintaining a steady rate of 80 to 90 revolutions per minute (rpm) on the bicycle not only improved function in lower extremities but also in upper extremities.
The improvement was dramatic and similar to that achieved by levodopa therapy, said 1 of the researchers, Jay L. Alberts, PhD, from the Center for Neurological Restoration at the Lerner Research Institute, in Cleveland.
“It looks like there are global effects in terms of the improvement in motor function,” he told Medscape Neurology. “It suggests to us that maybe we’re changing central motor function or maybe we’re actually changing brain function through something very noninvasive.”
The study was presented during the Movement Disorder Society’s 13th International Congress of Parkinson’s Disease and Movement Disorders.
A previous published study by this Cleveland research group found that the same forced exercise intervention administered 3 times a week for 8 weeks provided a similar 35% improvement in motor function.
“Couple these new findings with our longer-term data, and for us it’s very encouraging,” said Dr. Alberts. “Maybe if we can alter brain function, we can potentially alter the course and potentially slow the progression of this disease.”
Tandem Exercise
For the study, researchers selected 11 male and female patients ranging in age from mid 50s to early 70s who had mild to moderate PD but no cardiac concerns. They tested these patients under 3 random conditions: not on medication, on medication (levodopa), and not on medication but completion of the forced-exercise intervention.
When on a stationary bicycle, PD patients normally pedal at a sustained rate of about 40 to 60 rpm. In this intervention, however, the patients sat on the back of a tandem bicycle while a healthy young adult trainer occupied the front seat and regulated the pedaling rate, ensuring that it remained between 80 to 90 rpm for 40 minutes.
Researchers monitored each patient’s heart rate and made sure it stayed within 60% to 80% of his or her age-determined target range.
Patients also performed a force-tracking task and a bilateral finger-tapping task to demonstrate their level of control and coordination. Similar grasping tasks are necessary to perform daily activities such as buttoning a shirt or tying shoe laces, said Dr. Alberts.
The researchers found that the forced exercise and the levodopa produced similar significant reductions in Unified Parkinson’s Disease Rating Scale (UPDRS III) motor scores, 35% with exercise and 38% with levodopa. Data from functional magnetic resonance imaging (fMRI) showed increased activation in the supplementary motor area (SMA) and primary motor cortex (M1) regions of the brain in response to both interventions.
“In terms of the fMRI data, we found that there was an increase in the level of cortical activation in the 2 motor areas - the SMA and the primary motor cortex - and this increase in activation looks very similar to the increase you see when you administer L-dopa,” said Dr. Alberts.
For the force-tracking task and bilateral finger tapping, motor performance was 35% better following forced exercise compared with no exercise.
“Overdriving” Central Nervous System
These findings suggest that the exercise and the drug treatment elicit the same underlying mechanisms that provide similar symptomatic relief from PD symptoms, said Dr. Alberts.
The researchers surmise that the exercise may facilitate central motor control processes in Parkinson’s patients. “For lack of a better word, we may be ‘overdriving’ the central nervous system by providing an increase in the quantity and quality of sensory information provided to the patient,” said Dr. Alberts.
He added that this type of intervention could also be carried out on a treadmill, but it may be riskier and less practical than on a tandem bike. “We can’t increase someone’s walking rate 30% without having them in a harness and even then, I think you’ll find that their feet would be dragging.”
The next step in this line of research, he said, is to develop a motor-assisted cycle that will allow patients to do this type of exercise at home.
Many Beneficial Effects
Asked for a comment, Kapil D Sethi, MD, professor of neurology and director of the movement disorders program at the Medical College of Georgia, in Augusta, said the research highlights additional benefits of exercise. “Exercise has many beneficial effects both physical and psychological,” he told Medscape Neurology. “There is evidence in the animal models and now in humans that exercise may have beneficial effects in PD. The exact mechanism is unclear, and the exact paradigm is unknown.”
Mark Hallett, MD, from the National Institute of Neurological Disorders and Stroke, in Bethesda, Maryland, added in a press release that the finding of similarities between exercise and drug treatment “is certainly interesting and may indicate that exercise, in the short term, causes dopa release.”
Dr. Alberts has no disclosures. Dr. Sethi is a member of the editorial advisory board for Medscape Neurology. He has disclosed he has served as an advisor or consultant to and received grants for clinical research from Boehringer Ingelheim Pharmaceuticals, Schering-Plough, GlaxoSmithKline, Allergan, Novartis Pharmaceuticals, and Solvay. He owns stock, stock options, or bonds in and has received grants for educational activities from Pfizer and Elan Pharmaceuticals.
Movement Disorder Society’s 13th International Congress of Parkinson’s Disease and Movement Disorders: Abstract LB-13. Presented June 10, 2009.
Dear Doctor,
I have different low blood pressure at time either sit and stand.
I feel slightly dizziness and nearly losing my balance.
My Blood test:
*RBC* 4.3 X10 12/L (below normal level Male 4.5-
Haemoglobin 13.7 g/dL,PCV 40 %
MCVC 32 pg,MCH 91 fl,MCHC 35 g/dL,
*Platelets* 141 X10 9/L, (below normal 150-400 ),
WBC 6.2 X10/9L,Neutrophils 70 %,
Lymphocytes 28 %, Monocytes 1,below normal 2-10
Eosinophils 1 ,Baspphils 0
My medication:
Sinemet regular 1, Sinemet CR 3, Requip 6 mg,Jumex 10mg Plavix 75mg, Zantac 300 mg daily
Xatral XL 10mg, Stilnox 5 mg, Xanax 0.25 mg,Seroquel 12.5 mg
Lexapro 5mg *nightly*
I had T.I.A 2008, gastrointestinal disorder and insomina, bladder dysfunction.
Kindly advise
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Kathrynne Holden, MS
Joined: 22 Jan 2007
Posts: 94
Location: www.nutritionucanlivewith.com
Posted: Fri Dec 04, 2009 9:03 am Post subject:
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.
Dear Friend,
I am not a doctor, rather a nutritionist, and I recommend you address your question to “Ask the Doctor” on the Discussion Corner. However, I can make some comments:
Certainly your lab tests are somewhat low with regard to iron, and anemia can cause dizziness, and lightheadedness.
However, Requip can also cause dizziness as a side effect; Jumex (selegiline) can cause both dizziness and hypotension (low blood pressure, especially when changing position, such as rising, or lying down).
Further, PD itself can, in some people, cause hypotension.
If the dizziness is due to hypotension, one possible course of action is to add salt to the diet and drink plenty of water. This increases blood volume and helps to correct the blood pressure. However, this must only be done under the care of your doctor, because the dizziness might be due to some other cause. And the addition of salt is potentially harmful in some cases, such as for persons with congestive heart failure.
I believe the doctors on “Ask the Doctor” can provide much better help than I, and I would also discuss this with your own neurologist and/or primary care physician. You might need an adjustment in your medication regime.
_________________
Best regards,
Kathrynne Holden, MS
PostPosted: Fri Dec 04, 2009 10:09 am Post subject: Low blood pressure Reply with quote
Dear Doctor,
My low blood pressure measurement varies from each time either sitting and standing
I feel slightly dizziness and nearly losing my balance.
My Blood test:
*RBC* 4.3 X10 12/L (below normal Male 4.5-6.5)
Haemoglobin 13.7 g/dL,PCV 40 %
MCVC 32 pg,MCH 91 fl,MCHC 35 g/dL,
*Platelets* 141 X10 9/L, (below normal 150-400 ),
WBC 6.2 X10/9L,Neutrophils 70 %,
Lymphocytes 28 %, Monocytes 1,below normal 2-10
Eosinophils 1 ,Baspphils 0
My medication:
Sinemet regular 1, Sinemet CR 3, Requip 6 mg,Jumex 10mg Plavix 75mg, Zantac 300 mg daily
Xatral XL 10mg, Stilnox 5 mg, Xanax 0.25 mg,Seroquel 12.5 mg
Lexapro 5mg *nightly*
I had T.I.A 2008, gastrointestinal disorder and insomina, bladder dysfunction.
Kindly advise
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Dr. Okun
Joined: 19 Jan 2007
Posts: 251
Location: University of Florida
PostPosted: Fri Dec 04, 2009 3:56 pm Post subject: Reply with quote
If it is low blood pressure and dizziness:
Ask your doc about getting rid of dopamine agonists, hydrating (6-8 glasses of water a day), stiockings, and in some cases midodrine or florinef.
_________________
Michael S. Okun, M.D.
Singing is the therapy that help your swallowing.
Speaking and swallowing use many muscles and nerves in common, much as those of the lower
face, lips, tongue, voice box, and throat. The nerves and muscles of these structures are often
affected by the Parkinson’s disease process. The speech and swallowing problems of Parkinson’s
mirror other movement problems associated with the disease.
http://www.npfocc.org/uploads/swallowingproblems.pdf
2 people marked this post as helpful.
I am newly diagnosed with Parkinson’s disease, what factors are considered by my doctor when starting me on a medication?
You ask a very important question. Several factors require consideration when initiating symptomatic drug therapy in Parkinson’s disease. The choice of pharmacotherapy depends on the patient’s age, degree of disability, and cognitive status, as well as the impact of dosing, possible impact on the patient’s employment, domestic responsibilities, and lifestyle. Potential drug side effects must also be considered. Thus there are a lot of factors to consider!
The patient’s age is an important factor in predicting how well certain medications might be tolerated, as the risk of developing dyskinesia and motor fluctuations, especially with levodopa use, increases with earlier/younger onset Parkinson’s disease (most especially those who get it before 50 to 60 years old). Dopamine agonists, which delay the risk of dyskinesia and end-of-dose wearing off, may be offered as a first-line treatment option for younger patients. However, in older patients (which in our field means greater than 70 years old), the dopamine agonists have a higher risk for producing psychiatric and cognitive side effects. In addition, dopamine agonists have a complicated initial titration schedule before a therapeutic dose can be achieved. They require multiple dosing throughout the day, making the use of these agents challenging for many patients but especially so for patients 70 and older, who may be on several therapies for other conditions. Morover, the elderly patient is less likely to develop motor fluctuations and dyskinesias compared to the younger patient. Thus, in the currently published treatment algorithm, it is suggested that for the older patient, levodopa may be a better choice as initial first-line therapy compared to dopamine agonists.
The good news is that recent data suggest that an alternative option for initial monotherapy for early PD patients is rasagiline, a selective monoamine oxidase type B (MAO-B) inhibitor that offers effective control of symptoms and appears to be have a much lower incidence of the dopaminergic side effects seen with dopamine agonists and levodopa.
In one large placebo-controlled, multi-center clinical trial, after 5 years of levodopa use and as Parkinson’s disease progressed, about 50% of patients who were given levodopa from the onset developed motor complications compared to only 20% of patients who were first started on dopamine agonists for their early symptoms. However, the traditional view that treatment of Parkinson’s disease should begin only when symptoms become functionally significant has been challenged by some recent studies suggesting that initiation of treatment at the time of diagnosis results in better clinical outcome later in the course of the disease.
The patient’s perception of their level of disability and its impact on their lifestyle is also a driver of initial choice of therapy. Patients at the early stage whose major presenting symptom is tremor and who have minimal slowness or stiffness may respond to drugs such as anticholinergic agents or amantadine before their symptoms worsen. Rasagiline, selegiline, dopamine agonists or levodopa may be added as the disease progresses.
The potential of therapies to produce untoward side effects based upon the patient age and comorbid conditions is another important factor in choosing initial Parkinson’s disease therapy. As mentioned, dopamine agonists are not a good first choice in older patients due to concerns of leg swelling, cognitive impairment, and hallucinations. In patients in whom excessive sleepiness and drowsiness may affect daily activities, dopamine agonist use may also not be appropriate.
Yours,
_________________
Hubert H. Fernandez
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Anonymous
PostPosted: Tue Nov 17, 2009 8:43 am Post subject: Reply with quote
Good recap … thanks!
Rich
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
PostPosted: Thu Nov 19, 2009 7:37 pm Post subject: Reply with quote
You are welcome!
_________________
Hubert H. Fernandez
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Anonymous
PostPosted: Sat Nov 21, 2009 11:01 am Post subject: Reply with quote
Let me pull out a small portion of your post that is very important - the fact that motor complications occurred more often with the patients on sinemet than on the dopamine agonists after five years.
For those just beginning therapy you must realize that many of these motor complications can be very very minimal. I for example will have movement of my feet first thing in the morning when my sinemet hits my brain. The movement is minimal and causes no problems. No the dopamine agonists did not cause a problem like this but they caused me to faint at least 15 times a day. I did not change because I was afraid to take dopamine.
My point is - don’t be afraid to try sinemet (dopamine). It really does work amazingly well (it stopped ALL my PD problems from drooling to freezing to tremor) and the side effects can be controlled one way or another by adjusting dosage and adding or subtracting other things. If the dopamine agonists work for you - GREAT. But if they don’t - DON’T WAIT. Get on sinemet. I lost three years of my life because I waited too long to get on dopamine because of the older articles that said that taking it caused the disease to progress faster. From what I understand this is no longer thought to be true.
Good luck all!
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Dr. Fernandez
Joined: 20 Jan 2007
Posts: 90
PostPosted: Sat Nov 21, 2009 5:46 pm Post subject: Reply with quote
Thank you for your comments!
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Hubert H. Fernandez
Amanatadine initially was an antiviral medication against influenza, but its main use now is as a type of pain reliever as it inhibits something called an NMDA receptor.
The NMDA receptor is a nervous system receptor that can bind to aspartate (or more specifically to N-methyl-D-aspartate) or glutamate to create chronic pain. Even worse, when glutamate or aspartate binds to this receptor, a stimulus that is normally not painful actually becomes painful.
By coincidence it was found to help the symptoms of Parkinson’s disease. It may be used alone or in combination with levodopa or dopamine agonists. Amantadine reduces symptoms of fatigue, tremor and bradykinesia.
I was taking 2 Sinemet CR and 1 Sinemet 25/100, 12 Requip (2 mg) daily in the year of 2006 and to my surprise when added 3 Amantadine (100mg ) it caused reddish mottling on few part of my body and legs which was sideeffect of Amantadine and I apply Antiseptic cream to stop itchiness. I had stopped the medicine.
In general sideeffects of this medication may cause stomach upset, nausea, drowsiness, constipation, headache, dizziness, anxiety, or purplish-red blotchy spots on the skin during the first few days as your body adjusts to the medication. If these symptoms persist or become severe, inform your doctor promptly. Notify your doctor if you develop: slurred speech, shortness of breath, swelling of the ankles/feet, unusual fatigue, vision disturbances, difficulty urinating, skin rash, mental/mood changes (sometimes severe, including rare thoughts of suicide), muscle stiffness, uncontrolled muscle movements, unusual sweating, fast heartbeat, unexplained fever. If you notice other effects not listed above, contact your doctor or pharmacist.
