Posted: Sat Mar 21, 2009 6:01 pm Post subject: eye blinking and parkinson's disease
I do not have eye blinking as I have dry eyes. This is the symptoms of Parkinson's. I feel tired easily as I use eye tears to moisten my eyes. I stop driving at night or rainy as I have poor vision. There are reasons: Is due to Parkinson's medication; Sinemet, Requip or Jumex that I am taking? Is my masked face (muscles stiffness) that affecting the rate of eyes automatic blinkinga? Is my T.I.A (Blood clot) recently that affecting my eyes automatic blinking as I do not have problem before?
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Dr. FernandezJoined: 20 Jan 2007Posts: 90
Posted: Tue Mar 24, 2009 10:37 pm Post subject:
Decreased blink rate is a very common finding in PD. It is probably not cause by any of the drug. Rather, it is intrinsic to the disease. There are some drugs however, such as anticholinergic drugs (trihexyphenydyl or benztropine) and amatadine that can occasionally cause dry eyes, which is not a good thing when one already has decreased blink rate. Usually though, it is not that bad. Natural/artificial tears often do the trick. But if the eyes are too dry, it could get irritated and there could be some scleral or corneal abrasion and this will need more aggressive treatment. See your ophthalmologist to make sure that your eyes don't need extra attention and simply needs lubricant. Yours,_________________Hubert H. Fernandez
Wednesday, March 25, 2009
movement and exercise
PD is a muscles movement disorders. It is a chronic neurogical illness i.e. not going away" PD patients are different from what we define themself as "patient" i.e only during acute, self-limited illness or injury that temporarily impact their lives as an inconvenience or comfort. The major functions of muscles are to produce movements of the body, to maintain the position of the body against the force of gravity,to produce movements of structures inside the body, and to alter pressures or tensions of structures in the body. The symptoms of muscles disorders are as follows: 1. Bradykinesia i.e. slowness of movement 2. Resting tremor i.e shaking,either one or both side 3. Rigidity i.e. marked stiffness 4.Decreased arm wing on one or both side 5. Problems with walking and balance i.e. freezing being unable to initiate a step forward 6. Small, cramped handwriting 7. Masked face ie. reduced facial expression 8. Low voice i.e not clear Therefore PD patients have to choose an exercises that gets their muscles moving i.e stretching, in order to overcome the muscles stiffness, rigidity and slow movement. A physiotherapy or doctor my be consulted as how to start on an exercise routine?
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Dr. FernandezJoined: 20 Jan 2007Posts: 90
Posted: Tue Mar 24, 2009 10:39 pm Post subject:
Yes, I am a strong believer and advocate of daily exercise for all PD patients! Yours,_________________Hubert H. Fernandez
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Dr. FernandezJoined: 20 Jan 2007Posts: 90
Posted: Tue Mar 24, 2009 10:39 pm Post subject:
Yes, I am a strong believer and advocate of daily exercise for all PD patients! Yours,_________________Hubert H. Fernandez
Are there any medicine that can slow progression of PD?
Posted: Sun Mar 22, 2009 5:54 pm Post subject: Are there any medicine that can slow progression of PD?
Many medical practitioners propose exercise to slow progression of parkinson's disease as well as general health benefits. Unfortunaltely there are so far no answer on exercise how to slow progression of parkison's disease? Kindly elaborate Thanks
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Dr. FernandezJoined: 20 Jan 2007Posts: 90
Posted: Tue Mar 24, 2009 10:44 pm Post subject:
With or without Parkinson’s disease, the benefits of exercise have been consistently proven. Moderate to vigorous exercise is good for the heart, it helps control blood pressure, lowers the “bad cholesterol”, and lessens the likelihood of developing strokes and heart attacks! At least 30 to 45 minutes of aerobic exercise for most days of the week is recommended by the American Heart Association. If you have a pedometer, 10,000 steps per day is recommended for a healthy living! In Parkinson’s disease, the disease-modifying effect of exercise has been shown in animal models. Rats who were subjected to regular physical activity did better with their artificially-induced parkinsonism than those who were sedentary. In human epidemiological studies, Parkinson’s disease patients who exercise regularly did better than those who did not. Walking is the simplest form of exercise. Try to walk close to a mile each day (or more), if you can. We also encourage exercises that promote symmetry, such as swimming. Since Parkinson’s disease is often an asymmetrical illness affecting one side more than the other, swimming will force the arms in your ‘bad side’ to swing and propel as well as the arm on your good side. Any aerobic exercise seems to be beneficial. Other than consistency and symmetry, the most important thing to remember about exercise is safety. All the benefits are negated if one falls and sustains a hip fracture. Therefore, walking is only good if one has a reasonably low risk of tripping or falling. Biking is good if one can keep his or her balance, otherwise, a stationary bike will achieve the same effect (and many Parkinson’s disease patients choose stationary bikes with seats that have backs on them—to prevent falls). Yours,_________________Hubert H. Fernandez
Many medical practitioners propose exercise to slow progression of parkinson's disease as well as general health benefits. Unfortunaltely there are so far no answer on exercise how to slow progression of parkison's disease? Kindly elaborate Thanks
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Dr. FernandezJoined: 20 Jan 2007Posts: 90
Posted: Tue Mar 24, 2009 10:44 pm Post subject:
With or without Parkinson’s disease, the benefits of exercise have been consistently proven. Moderate to vigorous exercise is good for the heart, it helps control blood pressure, lowers the “bad cholesterol”, and lessens the likelihood of developing strokes and heart attacks! At least 30 to 45 minutes of aerobic exercise for most days of the week is recommended by the American Heart Association. If you have a pedometer, 10,000 steps per day is recommended for a healthy living! In Parkinson’s disease, the disease-modifying effect of exercise has been shown in animal models. Rats who were subjected to regular physical activity did better with their artificially-induced parkinsonism than those who were sedentary. In human epidemiological studies, Parkinson’s disease patients who exercise regularly did better than those who did not. Walking is the simplest form of exercise. Try to walk close to a mile each day (or more), if you can. We also encourage exercises that promote symmetry, such as swimming. Since Parkinson’s disease is often an asymmetrical illness affecting one side more than the other, swimming will force the arms in your ‘bad side’ to swing and propel as well as the arm on your good side. Any aerobic exercise seems to be beneficial. Other than consistency and symmetry, the most important thing to remember about exercise is safety. All the benefits are negated if one falls and sustains a hip fracture. Therefore, walking is only good if one has a reasonably low risk of tripping or falling. Biking is good if one can keep his or her balance, otherwise, a stationary bike will achieve the same effect (and many Parkinson’s disease patients choose stationary bikes with seats that have backs on them—to prevent falls). Yours,_________________Hubert H. Fernandez
how to stay positive when you have parkinson's?
1, Understand parkinson's, it cause,symptoms,treatment, and sideeffects
2. Find a good doctor you can trust and talk
3. Learn to manage and control your symptoms : exercise, physical therapies and proper diet
4. accept help when you need it
5. Keep doing things you enjoy
6.Remember you are not alone
7.Know and accept your limitation
8. Knowledge is power, educated your body, educating yourself
2. Find a good doctor you can trust and talk
3. Learn to manage and control your symptoms : exercise, physical therapies and proper diet
4. accept help when you need it
5. Keep doing things you enjoy
6.Remember you are not alone
7.Know and accept your limitation
8. Knowledge is power, educated your body, educating yourself
Tuesday, March 24, 2009
What are the risks factors of parkinson's?
What are the risk factors of Parkinson’s?
Posted on March 18th, 2009 by heroteo
Dear Dr. Chew,
The risks factors are yet to be identified and the cause of the disease so far are unknown.
The unknown risks factor as follows:
1.The advancing age.
Most people with Parkinson’s occur after at the age
50 years old.
2.A few of them have a family history.
3.Long-term exposure to certain environmental factors
such as pesticides, chemicals, or well water.
4. Regulation on safety users of pesticdes and
chemical
Kindly advise
TEOKIMHOE
Posted on March 18th, 2009 by heroteo
Dear Dr. Chew,
The risks factors are yet to be identified and the cause of the disease so far are unknown.
The unknown risks factor as follows:
1.The advancing age.
Most people with Parkinson’s occur after at the age
50 years old.
2.A few of them have a family history.
3.Long-term exposure to certain environmental factors
such as pesticides, chemicals, or well water.
4. Regulation on safety users of pesticdes and
chemical
Kindly advise
TEOKIMHOE
Parkinson's disease by daniel tarsy
Parkinson's DiseaseBy Daniel Tarsy
I included below two excerpts from this article, too read a section of interest, click on the links below or to start at the top of the article, click this URL:
http://knol.google.com/k/daniel-tarsy/parkinsons-disease/AE5yaalj/iGg1CA#
Contents
Background
Epidemiology of Parkinson’s disease
Pathology of Parkinson’s disease
Clinical features of Parkinson’s disease
Differential diagnosis of Parkinson’s disease
Treatment of Parkinson’s disease
Education and support
Diet and lifestyle
Exercise and physical/speech therapy
Treatment with medications
Diet and lifestyle
Newly diagnosed patients often inquire about the amount of protein they should consume after reading that protein may interfere with gastrointestinal absorption of levodopa. This is actually more important in patients with advanced PD who experience motor fluctuations in response to levodopa. Certain large amino acids derived from protein may reduce levodopa absorption in the intestine and transport from the blood into the brain, thereby potentially interfering with its clinical efficacy. In such cases, levodopa should not be taken less than 30 minutes before or 60 minutes after meals. A protein redistribution diet which limits most protein intake to an evening meal is only necessary in occasional patients.
Nausea or vomiting after levodopa or dopamine agonists is alleviated by taking these medications during or following meals. In patients with early PD and a stable medication response this will not compromise therapeutic efficacy.
Large, high fat meals which slow gastric emptying may interfere with medication absorption and should be avoided.
Patients should consume sufficient fiber and fluid to prevent constipation, which is frequently associated with PD.
Weight loss is sometimes associated with PD or treatment with levodopa. Elderly patients are at greater risk for poor nutrition and weight loss. Recognition and management of this problem is important to avoid loss of bone and muscle mass. Dietary calorie and vitamin supplements may be indicated. In postmenopausal women, calcium supplements and medications to prevent osteoporosis are recommended.
Coenzyme Q10 enhances mitochondrial function. PD is associated with reduced platelet mitochondrial and serum coenzyme Q10 activity. In clinical trials in PD patients, coenzyme Q10 , 1200 mg/day has been proven safe and has been associated with slightly less progressive motor disability, compared with placebo.
Large doses of vitamin E do not slow progression of PD.
Large doses of vitamin B6 (pyridoxine) interfere with L-dopa metabolism and should be avoided in the currently very rare patient who takes L-dopa without carbidopa, a peripheral dopa decarboxylase inhibitor. This is not a practical concern when levodopa is combined with carbidopa.
Patients should be encouraged to assume a positive attitude, remain professionally and socially active, and assume a generally healthy lifestyle with emphasis on regular exercise and good general nutrition.
Exercise and physical/speech therapy
Regular exercise promotes a feeling of physical and mental well-being, important in the management of PD. Although exercise does not slow progression of PD symptoms it can prevent or alleviate orthopedic effects of akinesia, rigidity and flexed posture such as shoulder, hip, and back pain and has also been shown to improve some motor functions. Supervised training including cardiovascular fitness exercise, muscle stretching and strengthening, and balance training have been found to be useful in some short- and long-term studies. Occupational therapy to assess home safety, supervise use of walking aids, and provide instruction concerning sensory cuing plays a greater role in more advanced PD associated with gait and balance deficits. Tai Chi may be useful for balance training. Controlled trials have shown that acupuncture does not improve PD motor symptoms.
Loss of voice volume often becomes a significant problem in more advanced PD. Patients should be encouraged to be more consciously aware of their voice output and concentrate on projecting more loudly than they think is necessary. Lee Silverman voice therapy is a special technique which emphasizes increased volume production and has been demonstrated to be helpful in PD. More information regarding this may be obtained at www.lsvt.org
Treatment with medications
Treatment with medications is dictated by whether one is dealing with PD, atypical parkinsonism, or secondary parkinsonism. Antiparkinson medications are highly effective in PD but relatively ineffective in most patients with atypical parkinsonism. Secondary parkinsonism such as drug-induced parkinsonism, vascular parkinsonism, and normal pressure hydrocephalus are treated according to underlying causes. However, although there are established criteria for diagnosis of PD, they are not foolproof and a trial of antiparkinson medications is warranted in all patients with parkinsonism. However, patients with atypical parkinsonism are more liable to experience medication side effects.
The first consideration is when to initiate medication. Currently available medications are given to improve symptoms; they have no proven ability to slow progression of the underlying disease. Therefore, drug treatment should be initiated only when symptoms begin to interfere with routine activities of daily living, employment, lifestyle, or physical appearance. Patient age and level of physical and professional productivity are also important considerations. The decision on when to begin treatment and which medications to use should be considered jointly by the physician, patient, and patient’s family. Active research is ongoing to identify disease modifying or neuroprotective drugs to slow disease progression. To date no proven agents have emerged from the many medications which have been screened. The following groups of medications are for treatment of only the motor symptoms of PD, which are tremor, bradykinesia (slowness), and rigidity and are listed in the table. They are listed approximately in the order in which they are often introduced into treatment but it should be realized that different patients may require different medications and that there is no firm or absolute rule for the order of using these medications.
Treatment of non-motor PD symptoms In addition to the well known motor symptoms of PD, non-motor symptoms are currently attracting increased interest and concern.
Sleep disorders are extremely common in PD; they affect 90% of patients. Poor night-time sleep and excessive daytime drowsiness are common. Possible causes include sedative effects of some antiparkinson medications such as the dopamine agonists, poor sleep hygiene, and poor sleep at night due to obstructive sleep apnea, restless legs syndrome, REM sleep behavior disorder, depression, anxiety, nocturnal stiffness, and fragmented sleep of unknown cause. Proper treatment relies on identifying the cause in a particular patient. REM sleep behavior disorder commonly precedes the onset of motor symptoms and is relieved by clonazepam taken before sleep. Sudden onset of sleep while driving (“sleep attacks”) have also been described, particularly in patients taking dopamine agonists although this is not necessarily associated with specific antiparkinson drugs.
Fatigue is a related problem but more common in advanced PD. Treatable causes include poor sleep, depression, and bradykinesia but it may also be an independent symptom. Empiric treatment with methylphenidate, modafinil, or selegiline may be considered but the response to these is usually disappointing.
Depression and anxiety often appear for the first time in early PD and may even be presenting symptoms. Treatment of these is important and will help patients to tolerate otherwise relatively mild motor symptoms. SSRI antidepressants are effective for both depression and anxiety and are usually well tolerated in patients with PD. Patients with PD may also exhibit apathy, with lack of motivation and emotional reactivity, in the absence of true depression. When severe enough to warrant pharmacologic intervention, this complaint may be responsive to methylphenidate.
Psychosis and visual hallucinations occur in more advanced PD where they are usually side effects of antiparkinson drugs. They are managed by adjustment of medications or introduction of antipsychotic medications that do not exacerbate motor symptoms of PD, such as clozapine or quetiapine. Other antipsychotic drugs, all of which interfere with dopamine transmission, should be avoided in PD. This does not include antidepressants and anti-anxiety medications which may be safely used in PD and do not exacerbate parkinsonism. Cognitive impairment of varying severity occurs in up to one-third of patients with PD. More severe cognitive impairment or dementia must be distinguished from other causes of dementia in older patients such as Alzheimer’s disease, cerebrovascular disease, normal pressure hydrocephalus, hypothyroidism, and vitamin deficiency. When due to PD the pattern of deficits differs from Alzheimer’s disease in that frontal lobe functions such as multitasking, judgement, and personality are affected more than recent memory, language function, and spatial orientation. Treatment with cholinesterase inhibitors such as donepezil, galantamine, rivastigmine, or memantine is recommended, and are often more effective in PD than in Alzheimer’s disease. The presence of psychosis, visual hallucinations, or dementia in early PD raises the possibility of dementia with Lewy bodies.Autonomic symptoms are not usually present in early PD, by contrast with multiple system atrophy, where they often appear before or together with onset of motor symptoms and are a major cause of difficulty. Nonetheless, proper attention should be paid to management of constipation, low blood pressure with standing (orthostatic hypotension), urinary frequency, and impotence. Constipation is managed with high fiber diet, stool softeners, and laxatives. Bladder symptoms usually require consultation with a urologist to identify the specific pattern of bladder dysfunction, to guide medication treatment, and to exclude other causes.
2 Mark this post as helpful
I included below two excerpts from this article, too read a section of interest, click on the links below or to start at the top of the article, click this URL:
http://knol.google.com/k/daniel-tarsy/parkinsons-disease/AE5yaalj/iGg1CA#
Contents
Background
Epidemiology of Parkinson’s disease
Pathology of Parkinson’s disease
Clinical features of Parkinson’s disease
Differential diagnosis of Parkinson’s disease
Treatment of Parkinson’s disease
Education and support
Diet and lifestyle
Exercise and physical/speech therapy
Treatment with medications
Diet and lifestyle
Newly diagnosed patients often inquire about the amount of protein they should consume after reading that protein may interfere with gastrointestinal absorption of levodopa. This is actually more important in patients with advanced PD who experience motor fluctuations in response to levodopa. Certain large amino acids derived from protein may reduce levodopa absorption in the intestine and transport from the blood into the brain, thereby potentially interfering with its clinical efficacy. In such cases, levodopa should not be taken less than 30 minutes before or 60 minutes after meals. A protein redistribution diet which limits most protein intake to an evening meal is only necessary in occasional patients.
Nausea or vomiting after levodopa or dopamine agonists is alleviated by taking these medications during or following meals. In patients with early PD and a stable medication response this will not compromise therapeutic efficacy.
Large, high fat meals which slow gastric emptying may interfere with medication absorption and should be avoided.
Patients should consume sufficient fiber and fluid to prevent constipation, which is frequently associated with PD.
Weight loss is sometimes associated with PD or treatment with levodopa. Elderly patients are at greater risk for poor nutrition and weight loss. Recognition and management of this problem is important to avoid loss of bone and muscle mass. Dietary calorie and vitamin supplements may be indicated. In postmenopausal women, calcium supplements and medications to prevent osteoporosis are recommended.
Coenzyme Q10 enhances mitochondrial function. PD is associated with reduced platelet mitochondrial and serum coenzyme Q10 activity. In clinical trials in PD patients, coenzyme Q10 , 1200 mg/day has been proven safe and has been associated with slightly less progressive motor disability, compared with placebo.
Large doses of vitamin E do not slow progression of PD.
Large doses of vitamin B6 (pyridoxine) interfere with L-dopa metabolism and should be avoided in the currently very rare patient who takes L-dopa without carbidopa, a peripheral dopa decarboxylase inhibitor. This is not a practical concern when levodopa is combined with carbidopa.
Patients should be encouraged to assume a positive attitude, remain professionally and socially active, and assume a generally healthy lifestyle with emphasis on regular exercise and good general nutrition.
Exercise and physical/speech therapy
Regular exercise promotes a feeling of physical and mental well-being, important in the management of PD. Although exercise does not slow progression of PD symptoms it can prevent or alleviate orthopedic effects of akinesia, rigidity and flexed posture such as shoulder, hip, and back pain and has also been shown to improve some motor functions. Supervised training including cardiovascular fitness exercise, muscle stretching and strengthening, and balance training have been found to be useful in some short- and long-term studies. Occupational therapy to assess home safety, supervise use of walking aids, and provide instruction concerning sensory cuing plays a greater role in more advanced PD associated with gait and balance deficits. Tai Chi may be useful for balance training. Controlled trials have shown that acupuncture does not improve PD motor symptoms.
Loss of voice volume often becomes a significant problem in more advanced PD. Patients should be encouraged to be more consciously aware of their voice output and concentrate on projecting more loudly than they think is necessary. Lee Silverman voice therapy is a special technique which emphasizes increased volume production and has been demonstrated to be helpful in PD. More information regarding this may be obtained at www.lsvt.org
Treatment with medications
Treatment with medications is dictated by whether one is dealing with PD, atypical parkinsonism, or secondary parkinsonism. Antiparkinson medications are highly effective in PD but relatively ineffective in most patients with atypical parkinsonism. Secondary parkinsonism such as drug-induced parkinsonism, vascular parkinsonism, and normal pressure hydrocephalus are treated according to underlying causes. However, although there are established criteria for diagnosis of PD, they are not foolproof and a trial of antiparkinson medications is warranted in all patients with parkinsonism. However, patients with atypical parkinsonism are more liable to experience medication side effects.
The first consideration is when to initiate medication. Currently available medications are given to improve symptoms; they have no proven ability to slow progression of the underlying disease. Therefore, drug treatment should be initiated only when symptoms begin to interfere with routine activities of daily living, employment, lifestyle, or physical appearance. Patient age and level of physical and professional productivity are also important considerations. The decision on when to begin treatment and which medications to use should be considered jointly by the physician, patient, and patient’s family. Active research is ongoing to identify disease modifying or neuroprotective drugs to slow disease progression. To date no proven agents have emerged from the many medications which have been screened. The following groups of medications are for treatment of only the motor symptoms of PD, which are tremor, bradykinesia (slowness), and rigidity and are listed in the table. They are listed approximately in the order in which they are often introduced into treatment but it should be realized that different patients may require different medications and that there is no firm or absolute rule for the order of using these medications.
Treatment of non-motor PD symptoms In addition to the well known motor symptoms of PD, non-motor symptoms are currently attracting increased interest and concern.
Sleep disorders are extremely common in PD; they affect 90% of patients. Poor night-time sleep and excessive daytime drowsiness are common. Possible causes include sedative effects of some antiparkinson medications such as the dopamine agonists, poor sleep hygiene, and poor sleep at night due to obstructive sleep apnea, restless legs syndrome, REM sleep behavior disorder, depression, anxiety, nocturnal stiffness, and fragmented sleep of unknown cause. Proper treatment relies on identifying the cause in a particular patient. REM sleep behavior disorder commonly precedes the onset of motor symptoms and is relieved by clonazepam taken before sleep. Sudden onset of sleep while driving (“sleep attacks”) have also been described, particularly in patients taking dopamine agonists although this is not necessarily associated with specific antiparkinson drugs.
Fatigue is a related problem but more common in advanced PD. Treatable causes include poor sleep, depression, and bradykinesia but it may also be an independent symptom. Empiric treatment with methylphenidate, modafinil, or selegiline may be considered but the response to these is usually disappointing.
Depression and anxiety often appear for the first time in early PD and may even be presenting symptoms. Treatment of these is important and will help patients to tolerate otherwise relatively mild motor symptoms. SSRI antidepressants are effective for both depression and anxiety and are usually well tolerated in patients with PD. Patients with PD may also exhibit apathy, with lack of motivation and emotional reactivity, in the absence of true depression. When severe enough to warrant pharmacologic intervention, this complaint may be responsive to methylphenidate.
Psychosis and visual hallucinations occur in more advanced PD where they are usually side effects of antiparkinson drugs. They are managed by adjustment of medications or introduction of antipsychotic medications that do not exacerbate motor symptoms of PD, such as clozapine or quetiapine. Other antipsychotic drugs, all of which interfere with dopamine transmission, should be avoided in PD. This does not include antidepressants and anti-anxiety medications which may be safely used in PD and do not exacerbate parkinsonism. Cognitive impairment of varying severity occurs in up to one-third of patients with PD. More severe cognitive impairment or dementia must be distinguished from other causes of dementia in older patients such as Alzheimer’s disease, cerebrovascular disease, normal pressure hydrocephalus, hypothyroidism, and vitamin deficiency. When due to PD the pattern of deficits differs from Alzheimer’s disease in that frontal lobe functions such as multitasking, judgement, and personality are affected more than recent memory, language function, and spatial orientation. Treatment with cholinesterase inhibitors such as donepezil, galantamine, rivastigmine, or memantine is recommended, and are often more effective in PD than in Alzheimer’s disease. The presence of psychosis, visual hallucinations, or dementia in early PD raises the possibility of dementia with Lewy bodies.Autonomic symptoms are not usually present in early PD, by contrast with multiple system atrophy, where they often appear before or together with onset of motor symptoms and are a major cause of difficulty. Nonetheless, proper attention should be paid to management of constipation, low blood pressure with standing (orthostatic hypotension), urinary frequency, and impotence. Constipation is managed with high fiber diet, stool softeners, and laxatives. Bladder symptoms usually require consultation with a urologist to identify the specific pattern of bladder dysfunction, to guide medication treatment, and to exclude other causes.
2 Mark this post as helpful
Are there any medicine that can slow progression of PD?
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teokimhoeJoined: 03 Mar 2007Posts: 125Location: Malaysia
Posted: Sun Mar 22, 2009 4:00 am Post subject: Are there any medicine that can slow progression of PD?
Many patients and physicians believe exercise, physical therapy and a proper diet may slow the progression of parkinson's. There is not a clear answer to that question yet._________________to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
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inspectorJoined: 29 Jan 2009Posts: 23Location: Stockton, CA.
Posted: Mon Mar 23, 2009 11:16 am Post subject:
There has been some discussion regarding COQ10 that may have the ability to slow the progression of PD. There are several clinical trials in progress to hopefully shed light on this particular supplement. The dosage is fairly high, around 1000-1500mg/day.
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Teddy Graham3Joined: 23 Oct 2008Posts: 1
Posted: Mon Mar 23, 2009 9:41 pm Post subject: Living w/Parkinson's Symptoms
I'm new to this forum and I hope to have some positive feedback after I hit send. I live in the nation's capital and I would like to find out if there any meeting places in and around the DC, MD & VA area. I still drive somewhat and I take Water Aerobics I am very active in my church and I take this disease one day at a time. I try to maintain positive thoughts and I try not to dwell on the progressiveness of the disease. If it had not been this it could have been something worse. I'd like to hear from some of you regarding Toe curling, I had a torn ligament last year and though the ligament is healed the alignment of the Big Toe is not straight and my Big Toe overlaps the toe beside it. I read a comment the other night from someone who mentioned it but I can not find that particular person's name and e-mail address. I am not prejudice but I would like to know if there are any African Americans in this area who are suffering w/this disease also. It would be nice to know your thoughts and help on dealing w/Spasms. I welcome and look forward to hearing comments from all persons, races, creed or color. We are after all in this together and we have to accept and play the Hand the Lord has allowed us to be dealt. I also believe there is a cure in the near future!
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johnball20Joined: 09 Mar 2007Posts: 198Location: Whittier, California
Posted: Thu Mar 26, 2009 9:28 pm Post subject: Toe curling
Teddy, I suffered from what I called cramps or spasms in my left foot for 12 years before it was finally diagnosed as PD. My toes would curl under my foot so hard that I ripped off a couple of toenails on one episode. Now I know it is officially called dystonia and it is a common feature of a sub-group of young on-set PD patients. I was diagnosed with PD at 39 and the dystonia still is my primary indicator that I've let my medication levels get too low. It is controllable when I'm properly medicated. The primary relief comes from carbidopa/levodopa. Dopamine agonists help a little, and the COMT and MAO-B inhibitors slow down the loss of dopamine but without my l-dopa, I couldn't function. I've been taking it for 25 years now, and it still works just fine so don't be afraid of it. When I say it still works, I mean that it really is a miracle drug...I just ran my 20th mararthon and finished in under 5 hours. By the way, we do know that this diasease is non-discriminatory. I have friends with PD in every category imaginable...in fact, I just met my first Hopi Indian with PD a month ago. I wish we could encourage more diversity among our advocacy group (PAN) and our support groups. It does seem hard to engage many people from our diverse communities here in LA. I don't know why that is, because we all suffer from PD whether black, white, asian or native American. John_________________We are working to raise awareness and find a cure.
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rittersJoined: 24 Dec 2008Posts: 77Location: Minnesota
Posted: Mon Mar 23, 2009 10:10 pm Post subject:
Welcome Teddy, I don't know of the problems with toe curling, however others here might. Also, posting to Ask the Doctors can be very informative. As far as I'm concerned, my computer does not see the color of skin, so know that you are welcome. I have one grandaughter that is half Native American and another that is half African American and they are as precious as they can be. I am a Sweedish, Norwegion, English mix. I wish you the best. It's sounds like you have a great attitude and please feel free to post whenever you can. Steve
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rittersJoined: 24 Dec 2008Posts: 77Location: Minnesota
Posted: Mon Mar 23, 2009 10:13 pm Post subject:
Teddy, Forgot to mention German.
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johnball20Joined: 09 Mar 2007Posts: 198Location: Whittier, California
Posted: Thu Mar 26, 2009 9:28 pm Post subject: Toe curling
Teddy, I suffered from what I called cramps or spasms in my left foot for 12 years before it was finally diagnosed as PD. My toes would curl under my foot so hard that I ripped off a couple of toenails on one episode. Now I know it is officially called dystonia and it is a common feature of a sub-group of young on-set PD patients. I was diagnosed with PD at 39 and the dystonia still is my primary indicator that I've let my medication levels get too low. It is controllable when I'm properly medicated. The primary relief comes from carbidopa/levodopa. Dopamine agonists help a little, and the COMT and MAO-B inhibitors slow down the loss of dopamine but without my l-dopa, I couldn't function. I've been taking it for 25 years now, and it still works just fine so don't be afraid of it. When I say it still works, I mean that it really is a miracle drug...I just ran my 20th mararthon and finished in under 5 hours. By the way, we do know that this diasease is non-discriminatory. I have friends with PD in every category imaginable...in fact, I just met my first Hopi Indian with PD a month ago. I wish we could encourage more diversity among our advocacy group (PAN) and our support groups. It does seem hard to engage many people from our diverse communities here in LA. I don't know why that is, because we all suffer from PD whether black, white, asian or native American. John_________________We are working to raise awareness and find a cure.
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