Saturday, March 29, 2008

High Ferritin and Low TIBC

Posted: Fri Mar 28, 2008 4:56 am Post subject: High Ferritin and Low T.I.B.C.

I have a blood text recently as shown I have high of Ferritin 217 ug/L (10 -120) and low T.I.B.C 44.4 umol/L (45.0 - 70/0 ) I am worry of the increase/ reduce of my iron profile. Kindly elaborate the cause and the medication to minimize/ increase their level. Thanks
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Kathrynne Holden, MS, RDJoined: 22 Jan 2007Posts: 94Location:
Posted: Fri Mar 28, 2008 9:12 am Post subject:

Dear Friend, There are many, many possible reasons for such iron levels in your blood. It would be improper for me to speculate as to the cause. You must discuss this with your physician, who has access to your complete medical records. S/he can properly diagnose the cause and explain it to you. Write back and let us know the results._________________Best regards, Kathrynne Holden, MS, RD --

This is the reply from my doctor:-
Ferritin is a protein which is produced from the liver and use as a indicator of total body iron storage. High ferritin level can found in many conditions such as iron over load, liver disease, inflammatory disease, malignancy and aging.
TIBC have reflected iron status in the body and that low level can caused by iron over load, chronic disease and low protein diet.
According to your result : slightly high ferritin, slightly low TIBC, these might because of iron over load, aging and too low protein in diet ( so far from the health check up report did not find a chronic disease, malignancy and liver disease)
The way to improve this condition are exercising, increase protein in diet (but low red meat, organ meat
Kindly elaborate and advise

Joined: 22 Jan 2007Posts: 94Location:
Posted: Fri Mar 28, 2008 7:42 pm Post subject:

Dear Friend, Your doctor, having access to your medical history and records, has given you the best possible advice. Again I must say that it would be improper for me to elaborate on this report without complete information. Please follow your doctor's counsel, which is based on his/her examination of you and interpretation of your medical records._________________Best regards, Kathrynne Holden, MS, RD

Friday, March 21, 2008

message to PatientsLikeMe and Paulwick's Research Team

Recently diagnose ( 2 )

teokimhoeJoined: 03 Mar 2007Posts: 78Location: MalaysiaPosted: Wed Mar 19, 2008 9:37 pm Post subject:I was diagnosed at last as parkinson’s patient in the year 2005. It take me seven years to be diagnosed as Parkinson’s illness. I have seen three neurologlists for the past sven years in three different countries. The first neurologlist was told I am in the process of age ageing and am normal. I was also treated as a normal by the second neurologlist in another country. I am very fortunate I am in the early stage of Parkinson’s and slow in progression . Regular exercises and medications relieve me from body stiffness and mobility. I thank Dr. Chew Nee Kong. Kuala Lumpur, Malaysia for his execellent medications for treatment of my Parkinson’s disease. He is actively involved for awareness of Parkinson’s in Malaysia. I give him double bonus for his unselfish service for the care and welfare for Parkinson’s patients._________________to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
About 5% of Parkinson’s patients are young-onset PD ( symptoms starting before the age of 40). My youngest patient, a Chinese gentleman, was 23 when he was diagnosed to have PD. I have another Malay patient who started having PD when she was 26. Last year, I met another Indian gentleman who had his PD since age 32. Thus, PD deserves a lot of attention from our government because it does not spare any race or ethnic group, and even the young are also affected. This April - May, we are going on a massive publicity campaign for Malaysian Parkinson’s community, in conjunction with the World Parkinson’s Day (April 11). One of the important messages that we will highlight to the Malaysian government is the very fact that even the young, who are still in the productive period in their lioves, also suffer due to PD. Hopefully, five years from now, the Malaysian Parkinson’s community will no longer be neglected as they are today. Dr Chew Nee Kong, Kuala Lumpur, Malaysia.

Counteracting Parkinson's with Pilates

The reasons why I started my blog?

The reason I started my blog because I wanted to tell the world how I fight my Parkinson’s disease and hopefully send a message to the readers that there are people suffering from Parkinson disease (“PD”) who need public awareness of the existence of PD and the effects physically, emotionally and mentally. With this blog, I hope to help PD patients to understand the disease and let them know that they are not alone.PD sufferers have movement disorders which could be misdiagnosed or misunderstood as effects of ageing. This misdiagnosis or misunderstanding can be unfortunate for PD patients as PD is a progressive disease whereby early treatment would slowdown the progression of the disease.There are also patients who are reluctant to accept they have PD when they are diagnosed by doctors as they consider themselves suffering from the effect of ageing As far as I am aware, 2% of the world’s population above the age of 60 years are PD sufferers . There are also a small percentage of younger persons who also develop the disease.There are 3 out of 1000 people age 50 and above suffering from this disorder. This number is likely to increase as the population ages.Besides, PD does not have any social, ethnic, economic or geographic boundaries either.I hope that my blog would share my experience on how I cope with PD and to counter /slowdown the degenerative effects of the disease.There are effective medication for the symptoms and patients who seek earlier treatment can continue to lead independent and fruitful lives.Exercise is also essential to the PD sufferer because of the need to maintain good muscle tone, strength and posture. Exercise has important benefits for everyone regardless of age or physical condition. When your condition threatens to immobilize you, exercise keeps you moving to retain your mobility & function, use it or lose itEating a well-balanced nutritious diet can help prevent weight and muscles loss, minimize practical difficulties associated with eating or swallowing, reduce the risks of hospital admission due to falls and reduce drug-related side effects as dehydration and constipation.At the same time I want to express my gratitude and appreciation to Dr. NK Chew my Neurologist for encouraging me to start the blog and the National Parkinson Foundation (NPF) in USA for answering my questions and helping me whenever I do not understand the disease. Also, I want to thank my wife and family for their kind support and understanding.I feel proud that I am able to serve the community with this blog.My message is to help PD patients to be aware of the disease and to encourage the setting-up of support groups to educate PD patients and their immediate families.,the cause of the disease, signs and symptoms , aid to caregivers, and a well balance nutriti0nal diet to achieve the best quality of life.

In conclusion I wish to take this apportunity to thank the management of PatientsLikeMe website to help me to learn every medication, supplements or device to treat the disease. Knowing what treatment work for me but also having the ability to easily connect with other patients to share the treatments and the outcomes not just to help themselves , but to help others. Become part of making a difference for everyone with Parkinson’s today.TEOKIMHOO


His blog ( describes how he overcomes his illness with optimism and confidence. Despite not having any medical qualification, he discusses many medical issues which are considered to be difficult for the general public.

Dr. NK Chew

Thursday, March 20, 2008

Recently diagnose

Recently Diagonosed

I am 25 years old and the mother of an almost 3 year old and a 1 year old. I started getting hand tremors while pregnant with my oldest but assumed it was due to the medication I was on to stop pre-term labor because the tremors went away about 2 months after she was born. About 5 months ago the tremors started up again but seemed to be getting worse each week and the more tired I got. I was diagnosed about a month ago with YOPD and some of the other symptoms that I had just been dismissing as being an overtired mother were finally making sense (extreme fatigue, memory loss - couldn't remember what I had just asked someone 5 minutes prior, lack of balance, etc). I am currently on Azilect and it seems to be helping immensely but wearing off by the evening. I am a positive person and I have hope for my life and I try to just focus on my kids and husband and all the many other joys in the world so that the idea of having PD doesn't fully set in and send me into the world of "what if's". I would love to hear from others on their experiences not only with PD but how they have been able to continue to enjoy the world around them. I look forward to speaking with everyone as we all go through this journey together. Kim
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granniDJoined: 21 Oct 2007Posts: 84Location: Calgary Alberta Canada
Posted: Thu Mar 13, 2008 2:19 pm Post subject: Recently diagnosed

I really think you should see another Dr for a 2nd opinion a specialist in movement disorder ailments -a neurologist. It is vital that you get the proper treatment as soon as possible This is not going to go away. you need treatment ASAP grannid
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cfinlaysonJoined: 29 Jun 2007Posts: 62
Posted: Sat Mar 15, 2008 5:53 am Post subject:

Kim, I agree with GranniD about a second opinion. I am 36 and was diagnosed 3 years ago. I have been for a second opinion and I have 3 girls, not quite as young as yours, but still a hand full and they keep me busy. I would be more than happy to tell you my story, but it is rather boring. Don't ever be afraid to get a second opinion. My MDS agreed and supported my decision when I did. My best advice is to live each day one day at the time. Don't dwell on the past or the future. It is so easy to get stuck in "what if", but try so hard not to do that. I get my strength from my faith in God and prayer. I will be praying for you and your family, but please do inquire more about your condition. Again, you are in my thoughts and prayers. Candy
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jojobeanJoined: 03 Mar 2007Posts: 127Location: salt Lake city, Utah
Posted: Sun Mar 16, 2008 9:55 am Post subject: KIm and Candy yonger than springtime are you?

Boy, you're both just kids! Rotten deal! Well as much as the truth hurts, you and all the other 'youngsters' here got a great future possible- ahead of you. We oldsters have a lot of hope and faith as to a cure being found in time to help us too, but your future will surely include that and probably before too long, so buck up children, All is not lost after all. I am sorry that you or anyone else has to come to terms with this head knocker, believe me. But I know your's wlll be OK! God bless you and your families. I pray for us all. And Candy I don't believe anyone is at odds with anything you've said on this forum. I for one appreciate you spirit and spirituality. Keep singing your song. It surely is helping someone who needs you, even lurkers who don't speak up but appreciate your strength and faith. Thanks for being who you are. You're great! luv ya both, Jojobean (JoAnn)_________________jojobean (alias Jo, JoAnn, or The Good witch of the North,
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cfinlaysonJoined: 29 Jun 2007Posts: 62
Posted: Sun Mar 16, 2008 4:47 pm Post subject:

Thanks Jojo!!! You have a wonderful attitude and a great spirit. You have always put a smile on my face. God Bless You! Candy
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mdaxJoined: 04 Mar 2008Posts: 5
Posted: Mon Mar 17, 2008 10:56 pm Post subject:

HI - I'm so sorry about your dx. I am about to turn 40. I was dx on the week of my 38th bday. I have 2 sons ages 6 and 4. I had lots of symptoms that I attributed to pregnancy and to being tired after my second son was born. The pd meds have made a big difference. I find that a good nights sleep is the best medicine - which is hard to do with young children. I was really down for the first year, but it's a lot better now. I think I realized that I still have good years left :) . Anyway, I'd love to talk to you more. I can send you my email if you'd like. Michelle
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bratzskiJoined: 12 Mar 2008Posts: 3
Posted: Tue Mar 18, 2008 8:50 am Post subject:

Thank you for the support every one. I just started on the Sinemet and it is defininetly taking some getting used to however the two medications together seem to be working. I have been told by other doctors that the neurologist I'm going to is the best at the hospital and his specialty is movement disorders. I'm actually glad that the hospital he is associated with is a research hospital because I feel that there are more options available that way instead of seeing one of the doctors in the semi-rural area that I live. With God walking by my side and directing me where to go I have faith that everything will work out the way it is supposed to. Michelle, I would love to talk with you some more about what you are going through. You can e-mail me at
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sfraiseJoined: 15 Oct 2007Posts: 2
Posted: Tue Mar 18, 2008 6:41 pm Post subject:

Hi, I just turned 31 a few days ago and was diagnosed with early onset parkinson's a couple of months ago by a movement specialist who specializes in parkinsons. The thing that makes me kind of wonder though is that she told me that since the symptoms were mild and it was early enough that she didn't want to try and treat it. I understand I guess, but sometimes my muscles ache and are so stiff that they feel like they're going to snap. I basically just end up laying around the house all day when I'm like that and pretty much don't get any work done which effects us financially. In fact since I've been dealing with these symptoms for about 9 months now I'm pretty much broke and I think I just lost my health insurance on the 5th. They told me the last time that the funds weren't available for the auto withrawl that they would cancel me and that would be that. Does anyone know of any otc drugs that help with the stiffness and muscle aches? I eat ibuprofin by the handfull and it doesn't really seem to do much good.
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jojobeanJoined: 03 Mar 2007Posts: 127Location: salt Lake city, Utah
Posted: Wed Mar 19, 2008 4:05 am Post subject: Oh dear, Ibprofin by the handsful?

Dear one, I am sorry you have Parkinsons and still have a family of little ones to deal with. That would be doubly hard on all of you. But I would definately be worried about all that Ibprofin. That's gotta kill your tummy sometime soon. How about asking a natural food store for something to help? Save your tummy for when you get taking pD and arthritus meds. You'll need it. Tumysitus isn't fun either! God bless you, and all the young set. JOJo_________________jojobean (alias Jo, JoAnn, or The Good witch of the North,
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wheelersceJoined: 02 Mar 2007Posts: 387Location: MI
Posted: Wed Mar 19, 2008 5:36 am Post subject:

Sfraise, Does your doctor realize how much distress you're in? I know the docs on the Ask the Doctor forum are always suggesting we go ahead and take meds if we're as impaired in our daily lives as it sounds like you are. Missing income and losing health insurance are pretty serious. As for otc meds, before I was taking prescriptions, my neuro asked me if I had tried Benadryl. I really hope you will talk with your doctor, though. Sue W.
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teokimhoeJoined: 03 Mar 2007Posts: 78Location: Malaysia
Posted: Wed Mar 19, 2008 9:37 pm Post subject:

I was diagnosed at last as parkinson's patient in the year 2005. It take me seven years to be diagnosed as Parkinson's illness. I have seen three neurologlists for the past sven years in three different countries. The first neurologlist was told I am in the process of age ageing and am normal. I was also treated as a normal by the second neurologlist in another country. I am very fortunate I am in the early stage of Parkinson's and slow in progression . Regular exercises and medications relieve me from body stiffness and mobility. I thank Dr. Chew Nee Kong. Kuala Lumpur, Malaysia for his execellent medications for treatment of my Parkinson's disease. He is actively involved for awareness of Parkinson's in Malaysia. I give him double bonus for his unselfish service for the care and welfare for Parkinson's patients._________________to help the PD patients aware the diseases and encourage to set up support groups to educate the patients and their immediate families
Back to top

About 5% of Parkinson's patients are young-onset PD ( symptoms starting before the age of 40). My youngest patient, a Chinese gentleman, was 23 when he was diagnosed to have PD. I have another Malay patient who started having PD when she was 26. Last year, I met another Indian gentleman who had his PD since age 32. Thus, PD deserves a lot of attention from our government because it does not spare any race or ethnic group, and even the young are also affected. This April - May, we are going on a massive publicity campaign for Malaysian Parkinson's community, in conjunction with the World Parkinson's Day (April 11). One of the important messages that we will highlight to the Malaysian government is the very fact that even the young, who are still in the productive period in their lioves, also suffer due to PD. Hopefully, five years from now, the Malaysian Parkinson's community will no longer be neglected as they are today. Dr Chew Nee Kong, Kuala Lumpur, Malaysia.

Wednesday, March 19, 2008

Is exercise harmful for PD?

Early parkinson's patient

When do I tell and what do I say, whether to tell

Parkinson's Disease in ancient China

Do you agree this statement? Are diets delaying PD progression?

Sleep disorders

Is levodopa treated patients slowdown the progression of PD


Dry Mouth: Benzhexol

double vision and Parkinson's patient

what do you call your PD?

Are Fatigue the neurologocal diseases?

unhealthy food cause or worsen PD?

incoordination exercises

More young hit by parkinson's in Singapore

Tuesday, March 18, 2008

emotional and cognitive disorders in parkinson's disease

I have a stroke / brain attack

Water and dehydration by Dr.Chew

Blood Clot in the Brain

Vitamin supplements and Stroke

Remember the Three letters S.T.R

Medication and exercise

Diet reduces the risks of PD

Public awareness of PD in Malaysia

I have a stroke/brain attack?

Information to share about benzhrxol

To stay Single

Amantadine Side effects

Recording dosages of carbidopa/levodopa (Sinemet)

Monday, March 17, 2008

the side effect of Levodopa Therapy

The effects of Motor and non motor symptions of Parkinson's

Jan 18 Knowledge is the power battle with Parkinson's disease

Is exercise harmful?Can exercise worsen PD progression?

Quality Verus Quanity of life

Denial of Parkinson's disease at the early stage?

Is Parkinson an ageing disease

Cigarette smoking or caffeine intake reduce the risk of PD?

A Shame in the Medical World

Excess saliva and Dryness

New interest in an old disease?

Is PD a disease by itself, but rather a syndrome?

Controlled Release Sinemet

Parkinsons and the Bladder

Is it the cure of drug the beginning or the end of life?

Just a long sentence: a life - long sentence?

Urination and parkinson's

Sunday, March 16, 2008

What are the symptoms of your medicine wearing off until the next dosage

exercise and medicine to be optimized

Thirst signals leads to dehydration?

My profile

Amantadine Side effects

Sinemet/ Levodopa Medication

REQUIP (Ropinirole) and Complusive Behaviors

Water and dehydration by Dr.Chew

illness but not disease?

boxing-punching the heavy bag

Can Exercise do for Parkinson's Patients what medicine can't

Non motor or motor symptoms has great impact on PD

I have a stroke / brain attack

Blood Clot in the Brain

I have a stroke / brain attack

Do you challenge your doctor?

What do you call your PD?

Sex and PD

Thursday, March 13, 2008

Parkinson's Disease and Acid reflux Kathrynne Holden, MS, RD
Copyright 1999

Disclaimer: Information obtained at this online site is not exhaustive and does not cover all diseases, ailments, physical conditions or their treatment. The information contained here should not be considered complete, nor should it be used in place of a visit, call, consultation or advice of your physician or other health care provider. Self-management of health problems is not recommended. You should never ignore medical advice or postpone seeking it because of something you have read here.
Many people have heartburn, or its more severe condition called gastroesophageal reflux (acid reflux). People with Parkinson's disease, however, are especially prone to acid reflux. Why? To understand its cause, we need to know a little about the gastrointestinal tract (GI tract).
When food is swallowed, it moves down the throat until it reaches a valve called the esophageal sphincter. This valve remains tightly closed, only opening up to allow food to pass through into the stomach. Its job is to keep food down in the stomach where it can be prepared for digestion.
Once food arrives in the stomach, special muscles begin grinding it into a paste. This paste of tiny food particles is then mixed with acids and other chemicals before moving on to the small intestine.
A strong Lower Esophageal Sphincter acts as a one-way valve at the top of the stomach to keep food and fluids down.
How does Parkinson's disease change the action of the GI tract?
Parkinson's disease can change these processes. The nerves that guide the muscles of the GI tract may be slowed, and this slows the muscle action as well. The stomach takes longer to grind and mix the food. When food and stomach acid sit in the stomach for too long, the acid acts on the food to form gas, which can distend the stomach, causing burping, and sometimes severe bloating and painful cramping.
Also, the esophageal sphincter may be weakened, so that it's harder for it to stay closed properly. This means that stomach acids, gas, and food may be pushed upward against the sphincter, causing a feeling of "fullness." If the sphincter becomes too weak, it can be pushed open, allowing acids to come up into the throat, and producing a burning feeling. This is acid reflux.
Why is acid reflux a problem?
· The throat and esophageal sphincter have a delicate lining. The powerful stomach acids can eventually lead to permanent scarring. The sphincter may become deformed and unable to close.
· The throat scarring can lead to a precancerous condition. The individual will have increasing difficulty with swallowing, more frequent reflux, and may even develop cancer.
· Stomach acids and/or food may be aspirated (inhaled) into the lungs. The lungs provide a warm, moist environment. Food particles, warmth and moisture provide perfect conditions for bacteria to breed. This leads to infection and pneumonia. Hospitalization for pneumonia is not uncommon in people with PD.
Controlling bloating and acid reflux
To avoid these problems, it's best to control bloating and acid reflux before they can cause damage. Certain foods are more likely to trigger reflux; avoiding these foods can help. Foods that can trigger reflux include alcohol, tomatoes, citrus fruits, caffeine, chocolate, and peppermint. Other foods may be trigger foods for you, though -- different people are affected by different foods. Keeping a record of foods eaten can help you detect which foods are a problem for you.
Large meals can also lead to bloating and reflux, because the stomach needs more time to process a lot of food. The large meal will stay in the stomach longer, and increase the likelihood that gas will form, and produce upward pressure against the esophageal sphincter.
A meal high in fat will also stay in the stomach longer, because fat takes more time to empty from the stomach than carbohydrate or protein. It's usually fine to eat fatty foods; however, portions should be small so that they can clear the stomach quickly.
If you're troubled with reflux, pay close attention to your personal "trigger foods" ­ those that trigger an attack. Avoid those foods whenever possible. For both bloating and reflux, try to eat smaller meals and eat more frequently. Instead of three large meals daily, aim for five or more smaller meals and nutritious snacks. Or, you can eat half your meal, wait an hour or so, then eat the other half.
Example: If your usual breakfast is juice, cereal with milk, and toast, eat the cereal, wait at least an hour, then have the toast and juice.
For difficulty with bloating and acid reflux, ask your physician for a referral to a registered dietitian who specializes in diet for Parkinson's disease. Dealing early with acid reflux can help you prevent such problems as pneumonia, scarring, and hospitalizations later on.

Quality of Life

Parkinson's Disease
Quality of Life Issues
Barbara Fitzsimmons, RN, MS
Lisette K. Bunting, RN, MScN
Individuals who develop Parkinson's disease (PD) are confronted not only
with the physical manifestations of the disorder but with the psychosocial issues
that impact on quality of life. Psychosocial aspects of PD may present as subtle
changes with progression of the disease. Many patients with PD are reluctant to
discuss these concerns with health care providers, however. Unfortunately, these
unvoiced concerns have a negative effect on acceptance of the disease state, corn-
phance with treatment, and response to therapy, and they can significantly affect
quality of life.
Current nursing literature has focused on management of mobility in PD, and
little attention has been devoted to psychosocial issues. This paucity of literature is
attributed to the belief that if motor symptoms are treated, psychosocial aspects of
the disease will spontaneously improve. Quality of life has been reported to be the
primary concern of patients with PD and their famidy members.(12) Medicine is
learning to recognize and accept quality of life as a major criterion in evaluation of
health interventions. "The concept of quality of life then goes beyond the dimen-
sions of health functioning to performance of social roles, mental acuity, emotional
states, subjective well-being, and interrelationships."(5) Life satisfaction, self-esteem,
and physical health have also been identified as key elements of quality of fife.
This article briefly reviews salient points regarding PD as a degenerative
neurologic process and focuses primarily on the motor and nonmotor features that
impact on quality of life. In addition, nursing care is presented and reviewed to
assist the reader in facilitating the development of goals with the patient and family
that are congruent with achieving maximum quality of life (Table 1).
James Parkinson, a London general practitioner, first described Parkinson's
disease in a monograph entitled "An Essay on the Shaking Palsy" in 1817. It was
Nursing Diagnosis Expected Outcomes Nursing Interventions
Impaired physical mobility Patient will demonstrate Consult with physical
related to rigidity, maximal independence therapy for exercises and
bradykinesia, and/or with performing activities assistive devices to
postural instability of daily living. maximize independence
with self-care activities.
Plan for patient to
participate in care when
medications are at peak
Provide for safety in
Impaired verbal Patient will communicate Facilitate consultation with
communication related to effectively with others. speech therapy.
softening of voice Provide opportunities for
patient to practice speech
Encourage patient not to
hurry to complete speech.
Refrain from completing
sentences for patient.
Altered self-esteem related Patient will actively Incorporate patient into
to dependency on participate in decisions decision-making process
spouse/significant other related to care prior to about taking medication,
discharge, participating in diversional
activities, and so on.
Offer suggestions for
patient to have
opportunities to socialize
in the community.
Altered thought processes Patient will state that Provide reality orientation to
related to hallucinations hallucinations are not real patient as needed.
and confusion prior to discharge. Be calm and offer
reassurance if patient
becomes fearful.
Umit environmental stimuli.
Promote restful sleep-wake
here that Dr. Parkinson described the classic parkinsonian symptoms of resting
tremor, propulsion, and stooped posture. Parkinson wrote that he found that
11 senses and intellect" were "uninjured;" however, he went on to describe patients
as "unhappy," "dejected," and "melancholic."(2)
PD is a chronic, progressive disease of the central nervous system. The classi(-
triad of symptoms is resting tremor, rigidity, and bradykinesia. PD has been de-
scribed as a collection of symptoms rather than one distinct clinical picture. Thus,
diagnosis can be difficult in the early stages of the disease. Typically tremor or
rigidity are noted on one side of the body, although they may progress to bilateral
involvement. (13)
Physicians often refer to PD as the "waiting room diagnosis." This refers to the
classic signs of pill-rolling tremor, stooped posture, bradykinesia, and masked face
that are easily observed in the clinical setting. Patients typically seek consultation
with a neurologist to confirm or rule out a diagnosis of PD. Frequently patients will
request testing to substantiate the diagnosis. No such test exists, however. PD is a
diagnosis made by history and physical. In today's technologic health care environ-
ment, patients are often frustrated with the fact that PD is a clinical diagnoSis.13
Approximately 1 million Americans are currently diagnosed with PD. Men
have a slightly higher incidence of the disease, and whites are disproportionately
affected when compared with other races. PD is typically considered to be a disease
of the aged. The mean age of onset is 60 years of age, although cases have been
identified in individuals as early as 30 years of age.
With increased incidence of PD in young patients, that is, in those diagnosed
before the age of 50, a new set of quality-of-life issues has emerged.(6,8) For example,
an older patient, a more "traditional Parkinson's patient," has probably planned
for retirement. Facing a degenerative disease in what had been hoped to be the
"golden years," elderly couples are often confronted with not being able to travel
and thus change their focus to planning for long-term care. On the other hand, the
concerns of the younger patient with PD focus on raising children, managing a
career, and maintaining a home. These two age groups have distinct differences in
issues affecting their quality of life.
The cause of PD is unknown. However, the following theories are the focus of
current research: genetic, viral, and environmental toxins. Genetic research is fo-
cusing on mitochondrial defects and family linage.'-' Twin studies have failed to
demonstrate any clear inherited trait, however. The viral theory was first suggested
with the outbreak of encephalitis lethargica, which occurred worldwide from 1918
to 1926. This viral epidemic resulted in postencephalitic parkinsonism killing more
than 2000 Americans. The mortality rate approached 40%, and only 15% of
patients fully recovered. As survivors of this viral epidemic die, fewer individuals
with this form of PD are seen. Environmental toxin theories have continued to be a
focus of epidemiologic studies. (13)
The hallmark pathologic feature of PD is the degeneration of the dopaminergic
nigrostriatal pathway. It has been shown that 80% of the dopan-dne-producing
cells must be lost before manifestations of the disease can be seen. The severity of
PD is associated with the degree of neuronal loss in the midbrain at the level of the
substantia nigra.11
Dopamine, a neurotransn-titter, is the primary neurocheniical responsible for
the signs and symptoms of PD. The balance of dopamine and acetylcholine are
responsible for normal motor function. The development of symptoms is explained
by an imbalance of dopaminergic (inhibitory) and chohnergic (excitatory) activity in
the caudate and putamen of the basal ganglia. When degeneration of the dopamin-
ergic nigrostriatal pathway occurs, there is depletion of dopan-dne and relative
excess of cholinergic activity in the feedback circuit involving the cerebral cortex,
basal ganglia, and thalamus. This change in neuronal activity is responsible for the
classic manifestations seen in PD.(9)
The Motor features of PD include the classic triad of tremor, rigidity, and
bradykinesia. In addition, there is postural instability and disordered gait as well as
disorders in fine motor movement. A brief description of each motor feature
Resting tremor is the most classic and visible sign of PD. Seventy percent of
patients present with resting tremor as their chief complaint for seeking diagnosis
and treatment. Parkinsonian tremor has been described as having a pfll-rolling
quality and can affect all four limbs and the head.(13)
Many patients express feelings of embarrassment related to their tremor.
Tremor is the most difficult symptom to treat but the least disabling. It subsides
with action and is thus described as a resting tremor. The resting quality of the
Parkinson tremor allows patients to maintain activities of daily living within some
lin-titations. Unfortunately, patients will restrict social activities due to fear of social
stigma and being labeled as ill. In addition, stress can intensify tremor, which
further restricts the patient's willingness to participate in social life,
Rigidity is often described as a plastic resistance to passive movement. Patients
often describe this characteristic as stiffness. On examination, rigidity can be de-
tected as a coglike release of muscle resistance in the wrist, elbows, neck, and knees
as the limb is moved through passive range of motion.(13)
Rigidity can cause the face of the patient with PD to take on a masklike quality.
The face appears fixed and rigid, and previously recognizable nonverbal messages
are misinterpreted or lost in communication. Fanifly members find this change to
be most disturbing because the patient no longer has a change of facial expression.
Bradykinesia refers to difficulty with initiating and continuing movement.
Movements are slowed and are performed with conscious effort. Patients have
described bradykinesia as feeling as if "My brain is sending the message to the
body, but the body won't listen."(7)
Postural Instability and Gait Disorders
As PD progresses, patients may demonstrate difficulty maintaining erect pos-
ture. Typically, there is forward flexion of the neck, hips, knees, and elbows.
Postural abnormalities greatly reduce the patients' ability to be ambulatory and
places them at high risk for injury.(7) This may also lead to reliance on assistive
Because of rigidity and postural changes, patients also develop a shuffling
quality to their gait and use small steps. Another abnormal gait characteristic is
propulsion, a disturbance in which the patient goes from a slow walking pace to
runnin with an inability to stop. Patients are only able to stop themselves by
grabbing stationary objects such as a door frame. It is important to note that
patients who develop an unsteady festinating gait may appear to be under the
influence of drugs or alcohol.
The inability to be freely ambulatory restricts the independence of the patient
with PD. The use of a cane, walker, or wheelchair gives the patient a message that
the disease is progressing. Resistance to the use of assistive devices is often an
attempt to maintain self-esteem as the patient is dealing with declining health.
Limitations of mobility further restrict social fife, and many patients express an
inability to maintain pace with friends or family members. Often patients will
express embarrassment due to their gait disturbance and verbalize a realistic fear
that others will assume they have a substance abuse problem.
On-Off Phenomenon
As the disease advances, patients enter a narrow therapeutic window. Re-
sponse to treatment is less predictable, resulting in what is termed the "on-off"
phenomenon. This phenomenon refers to a syndrome in which patients are freely
ambulatory one n-tinute and then find they are "frozen" and unable to move the
next. Patients also describe "off" periods as if someone has turned off the switch
and their feet have sprouted roots. The cause of the on-off phenomenon is un-
known but may be associated with years of therapy compounded with continued
loss of dopan-tine-producing cells.(13)
Because the on-off phenomenon is unpredictable, it can play a major role in
family dynan-dcs. The concept of a person exhibiting a behavior that is severely
disabling, sudden in onset, and resolving without intervention is a difficult concept
for patients and health professionals to grasp. Understanding that on-off phenom-
enon behavior is not intentional and is not psychogenic in origin is essential.
Patients and farnfly members need education about this feature of the disease
process to assist the patient with PD to maintain a sense of control.
Swallowing and Speech Defects
Dysphagia is a common disorder that affects patients with PD and was first
recognized by James Parkinson. He described patients as having significant weight
loss with complaints of difficulty swallowing solid foods as compared to liquids. As
the disease progresses, patients report difficulty with chewing or moving food to
the back of the mouth. This may lead to choking episodes and places the patient at
high risk for aspiration. Management of dysphagia in PD may be difficult. Consul-
tation with a dietitian and swallowing therapist may be beneficial in providing
optimal nutrition. In addition, meals should be eaten when levodopa dosages are
reaching maximum effectiveness. (10,16)
The motor disturbances responsible for swallowing deficits can also lead to
disorders of speech in the patient with PD. Dysarthria, a form of speech distur-
bance, is characterized by deviations in phonation, prosidic disturbances in which
speech may be slow or extremely fast, and an articulatory disorder in which vocal
sounds are distorted. Dysarthria is a common problem for patients with PD and can
have a dramatic and devastating effect in a patient's interpersonal communication
and self-image. Management of dysarthria involves the use of medication and
speech therapy. Levodopa has been shown to improve speech intelligibility, and
speech therapy can assist the patient in using techniques to enhance projection. To
gain maximum benefit from speech therapy, the patient must be invested in
practicing the exercises assigned by the speech therapist. (10)
Difficulty with handwriting can be an early sign of PD. Patients with PD
typically will initiate handwriting with normal-sized penmanship and trail off
words and sentences with smaller illegible handwriting. This small writing is
referred to as "n-dcrographia." Patients with micrographia can have difficulty sign-
ing checks, and banks frequently request patients to sign a new bank card because
of the dramatic change in signature. The inability of patients to spontaneously
write can also inhibit communication. (14)
Depression in PD has been the focus of numerous studies. Research indicates
that 20% to 90% of patients with PD will experience a major depressive episode as
compared to 7% of the general population. Depression accounts for the majority of
psychiatric referrals in patients with PD and can be the initial feature of PD. It has
been hypothesized that the shared neurochemistry of these two disorders accounts
for the high incidence of depression in PD.(2)
Depression can be viewed in two ways. Some patients may become demora-
lized with the diagnosis of PD and experience a "reactive depression." Reactive
depressions are linked to external events and are short in duration. Typically the
patient experiencing a reactive depression is able to resolve the issue and accept the
diagnosis. Individuals experiencing a reactive depression may benefit from sup-
portive psychotherapy, however.(2)
The most typical depression experienced by the patient with PD is endogenous
depression. Endogenous depression is caused by a biochemical imbalance in the
brain and can be life-threatening if not treated. The difficulty in diagnosing depres-
sion in patients with PD lies in the shared clinical features of the two disorders
(Table 2).
Dementia is also a common feature of PD. It is estimated that 20% of patients
with PD will become demented.(11,14) Dementia can be defined as an acquired,
Features Parkinson's Disease Depression
Motor manifestations Stooped posture, bradykinesia, Slumped posture, psychomotor
masked face retardation, diminished facial
Sleep disturbances Insomnia, sleep fragmentation Insomnia, early morning
Gastrointestinal Constipation, weight loss Constipation, weight loss
Concentration Bradyphrenia Poor concentration
Hallucinations Visual, usually nonthreatening Visual, auditory, olfactory and
Adapted from Bunting LB, Fitzsimmons, B: Depression in Parkinson's disease. J Neurosci Nurs
23(3):160, 1991; wwith permission.
persistent impairment of intellectual function with compron-dse in at least three of
the following areas of mental activity: language, memory, visuospatial skills, emo-
tionality and personality and cognition in the presence of clear consciousnesS.3,4
The retention of long-term memory permits the patient to maintain aspects of
normal social behavior early in the disease. The severe loss of ability to learn new
material and the limitations of short-term memory result in episodes of frustration
that can escalate into agitation, however. In addition, individuals with dementing
illnesses may have enough insight to experience a clear sense of loss, thus leaving
patients and families demoralized and dispirited.(4) Nursing management of demen-
tia care should encompass the principles of preservation of dignity and provision of
Sleep Disturbances
Sleep disorders are a frequent complaint in patients with PD. Disorders of
sleep initiation, sleep fragmentation, early morning awakening, excessive daytime
somnolence, and parasomnias represent the disorders of sleep seen in PD. A
detailed history of the sleep complaint, validated by a bedpartner, is the best
method of establishing the cause of sleep disturbances.(11)
Patients may complain of initiation insomnia as, "I can't get to sleep." C)nce
asleep they are able to sleep soundly through the night, however. Researchers have
concluded that sleep initiation insomnia in PD is related to anxiety, agitated de-
pression, or levodopa therapy.
The more typical sleep disorders seen in PD are sleep fragmentation and early
morning awakening." Sleep fragmentation can be related to the inability to turn
over in bed. Rigidity compounded by the wearing off of medication reduces pa-
tients' ability to reposition themselves in bed. Patients state that they must wake up
to change sleeping positions and then are unable to return to sleep. One solution to
this problem is the use of satin sheets to decrease friction and facilitate turning.
Early morning awakening typically represents onset of a depressive episode, and
the nurse should evaluate the patient for other vegetative symptoms such as
decreased appetite, psychomotor retardation, and constipation. Early morning
awakening may be related to focal dystonic cramping in the calf and feet, however.
Focal dystonia is related to diminished levels of levodopa.(11)
Excessive daytime somnolence is the most frequent sleep complaint made by
family members of PD patients. In some individuals, daytime somnolence is related
to a disturbance in the circadian control of sleep. These patients are up at night and
take multiple naps throughout the day. Families report that daytime sonuiolence is
disruptive to normal family life. Families should discourage day time napping in an
attempt to correct the circadian clock. Patients who are described as sleeping all
day, however, should be screened for metabolic abnormalities that may cause
disturbances in the sleep-wake cycle.
Parasomnias are the most debilitating and difficult of the sleep disorders to
manage. Sleep talking, sleep walking, vivid dreams, and nightmares are the most
frequently reported parasomnias experienced by patients with PD. Most typically,
these occur as a side effect of levodopa therapy. Unfortunately, treatment for
parasomnias is limited.(11)
Sexual Dysfunction
Sexual functioning in patients with PD has received inadequate attention. The
paucity of literature can be attributed to the assumption that patients with PD are
elderly and therefore have a diminished interest in sex. Research indicates that
frequency of sexual intercourse decreases with age; however, sexuality continues to
play a role in the lives of the elderly. Sexual dysfunction has a significant impact on
patients who are diagnosed with PD in their midadult years when an active sex life
is the norm.(1)
Dysfunction of the autonomic nervous system, depression, medications, and
interpersonal issues all play a role in sexual dysfunction in PD. Autonomic dys-
function in the urogenital system resulting in impotence is the primary reason for
sexual dysfunction in male patients with PD. Secondary issues affecting sexual
function include motor fluctuations, fatigue, medications, sleep disorders, depres-
sion, and interpersonal issues.(1)
The motor fluctuations and fatigue can be related to antiparkinsonian drugs,
primarily levodopa. Patients with PD find that they are better able to function in
the morning, after their initial dose of medication, and become more fatigued with
greater motor fluctuations as the day progresses. Numerous reports document
hypersexuality with the use of levodopa. This may result in a problem when one
partner has heightened sexual interest that is not shared by the other partner. To
adapt to these changes in their sexual life, couples may need to change their daily
routine to accommodate morning sexual activity and take advantage of optimum
energy levels and motor functioning. Unfortunately, sleep disorders experienced in
patients with PD may result in bedpartners sleeping in separate beds, which
diminishes opportunity for spontaneous sexual activity.(1)
Depression can also have a significant impact on sexual activity in patients
with PD. As discussed earlier, depression is common in patients with PD and can
produce a markedly decreased libido. Sexual partners may also experience depres-
sion and fatigue as they struggle with the caregiving role in the relationship; thus,
they also may not have the energy or interest to engage in sexual activity. In
addition, autonon-dc dysfunctions that result in droohn& diaphoresis, and excessive
facial oiliness may interfere with perceived attractiveness of the patient by the
sexual partner.(1)
The issues surrounding sexuality in PD are complex. Patients should be rou-
tinely questioned regarding satisfaction of their sexual life. A referral to a urologist
or sex therapist can assist in identifying issues affecting sexuality. Open conununi-
cafion regarding sexual issues can be limited by the patient's reduced facial expres-
sion and altered speech pattern. The ability of the couple to communicate their
sexual needs within the liniitafions of the disease state can have a significant impact
on the couple's marriage and sexual life.(1)
Driving Performance
When a patient is seen for the management of PD, no discussion would be
complete without addressing driving. Motor manifestations of the disease as well as
a decline in cognition may impair the pafient's ability to function safely behind the
wheel. Some patients may willingly retire their driver's license, whereas others may
view this as giving up valued independence. Evaluation of driving skills by a
professional driving instructor may provide a nonthreatening avenue to assess auto
safety. Family members should be involved in the evaluation of driving to arrange
alternate transportation if the patient's driving is found to be unsafe.
PD can be a disability and liability in the work place. Many patients ask,
"Should I tell my boss?" There is no clear answer to this question because each
situation is different. Patients should be encouraged to have a frank and open
discussion with their health professionals regarding the limitations imposed by
their symptoms and the effect of these lin-dtations on their job responsibilities. This
discussion should include the benefits and potential disadvantages of revealing this
information to their supervisor. Frequently, coworkers have suspected that a prob-
lem exists. By sharing the diagnosis, an empathefic supervisor may facilitate a
pafient's medical appointments and make environmental adjustments to expedite
an optimum working relationship. Unfortunately, the risk of sharing the diagnosis
of PD can have a negative impact on job security. It has been the experience of
these authors that patients have been reassigned to other job responsibilities or
pressured into early retirement. Physicians and nurses should strive to provide
strategies and guidance for handling this difficult situation.
Drug therapy is the mainstay of management of PD. The primary medications
used in PD are classified as anticholinergics, antihistamines, dopaminergics, and
dopamine agonists (Table 3). (17) Unfortunately, all drugs used in the treatment of PD
have potential for side effects that impact on quality of life. Indication for medica-
tion is determined when the patient develops deficits in activities of daily living or
is expressing embarrassment from tremor or gait disturbances. The approach to
drug therapy is to maintain the patient on conservative levels of medication while
maintaining mobility. As the disease progresses, patients become less responsive to
medications and experience end of dose failure, peak dose dyskinesias, and painful
dystonic cramps. They are also more prone to developing de@um and hal-
Levodopo Therapy
Levodopa is the drug of choice for treatment of PD. It is marketed as a
combination drug called Sinemet and is composed of carbidopa and levodopa. The
Type Drug Name Indications Side Effects
Anticholinergics Tdhexyphenidyl Tremor, rigidity, Dry mouth,
(Artane), drooling constipaflon,
benztropine blurred vision,
(Cogentin) confusion, visual
Antihistamine Diphenhydramine Tremor, rigidity, Dry mouth, lethargy,
(Benadryl) insomnia confusion
Dopaminergics Amantadine Rigidity, Leg edema, livedo
(Symmetrel), bradykinesia, reticularls,
carbidopa/ tremor hallucinations,
levodopa orthostatic
(sinemet) hypotension,
nausea, confusion
Dopamine agonists Bromocriptine Motor fluctuations in Hallucinations,
(Parb"), Parkinson's mental cloudiness
pergolide (Permax) disease orthostatic
action of carbidopa is to block the breakdown of levodopa in the peripheral organs
and allows more levodopa to cross the blood-brain barrier. Levodopa is converted
to dopamine. in the brain through a series of enzymatic reactions.(13)
Levodopa therapy is responsible for promoting quality of life for the vast
majority of patients with PD. Levodopa therapy has lin-dtations, however. Early in
treatment, patients are maintained on low doses of levodopa to preserve the
therapeutic window for the future. Typically patients respond well to levodopa and
only experience mild side effects such as nausea and orthostatic hypotension. As
the illness progresses, patients require higher levels of levodopa, a@d'response to
therapy is less predictable.(13)
Levodopa has a relatively short half-life. It has a rapid onset of actions and
patients report getting a surge of energy with each dose. Similarly, patients com-
plain of "wearing off" symptoms as levodopa is metabolized and PD features
return. When levodopa is at therapeutic levels, the patient's functioning may
appear quite normal. As the medication "wears off," however, patients may be-
come akinetic and rigid. Like the on-off phenomenon, wearing off can be frustrat-
ing for the patient and family. In contrast to the on-off phenomenon, however, the
wearing-off symptoms are predictable and are associated with declining levodopa
levels. When levodopa alone is not maintaining symptomatic control, the physician
may add a dopamine agonist such as bromocriptine (Parlodel) or pergofide (Per-
max). There agents act to smooth out levodopa levels and help to control the rapid
rise and fall of levodopa levels.(13,14)
With progression of symptoms, patients with PD may experience peak-dose
dyskinesias. The term "dyskinesia" describes the development of extra movements
of the head, neck, trunk, and extremities as levodopa doses rise and peak rapidly.
Most patients find that these extraneous movements limit social activities. Al-
though dyskinesias can be devastating, patients can function within the limitation
of the movement disorders.(13)
Compliance in taking prescribed drugs is essential to successful management
of PD. Patients with PD often verbalize feelings of being chained to the clock
because they require levodopa to maintain mobility. Levodopa dosage schedules
can be prescribed as frequently as every 2 hours during the waking day. The need
for levodopa can overshadow all other aspects of the patients life because he or she
is unable to function without it. If medications are late or missed, the patient can
experience dystonic pain, increased tremor, rigidity, and personality changes. Com-
pliance can also be an issue when patients with PD take extra doses of levodopa to
boost their levels of energy and function. This behavior should be discouraged, and
any change in treatment plan should be discussed with the physician. Alarm clocks
or pill boxes with alarms can assist the patient with remembering to take the
medication on time.
Cost of medication can also affect compliance. It is not uncommon for patients
to spend approximately $300 per month on medications for PD. The financial
impact of medications can preclude physicians from ordering additional therapy.
Nurses can assist in deterring the cost of therapy by investigating drug-cost-
sharing programs sponsored by drug companies or pricing mafl-order pharmacies
to find lower Cost medications.
Side Effects of Delirium and Hallucinations
Medications used in the management of PD often need to be titrated. Usually,
the higher the dose of drug, the more frequently side effects are encountered. (13) The
side effect of delirium is a constant danger with all medications usld in PD. The
probability of delirium is determined by each patient's tolerance to the medication
and predisposing factors such as age and general health. Living with a drug-
induced delirium is a difficult issue for many patients and families. Families are
often asked to make a choice between clear mentation and motor functioning. It
may be easier for a family to care for a mobile patient with PD who is cognitively
The occurrence of hallucinations is well documented in the management of
patients with PD. Amantadine, a dopaminergic medication, is notorious for causing
visual hallucinations. Other medications in which hallucinations have been docu-
mented as a side effect include anficholinergic medications such as trihexyphenidyl
(Artane) and benztropine (Cogentin), levodopa in the form of carbidopa/levodopa,
and dopan-dne agonists such as bromoctiptine and pergolide. All of these drugs act
to increase the levels of dopamine in the brain through different mechanisms of
action. (13)
Patients frequently are able to tolerate continued use of medications knowing
that hallucinations are a side effect of therapy. Typical treatment-induced halluci-
nations in PD are visual and may consist of seeing small children or animals. These
hallucinations are seldom threatening. If hallucinations become auditory or threat-
ening in content, patients should be evaluated for depression or dementia by a
qualified psychiatrist.
PD affects many dimensions of quality of life. This article has identified motor
and nonmotor features of PD that are directly related to a patient's quality of life.
Medication therapy can help to ameliorate some of the symptoms, yet side effects
can be as disabling as the symptoms of PD. Nursing care should include assess-
ment, intervention, and evaluation of both physical and psychosocial aspects of
care for patients with PD to assist them in achieving maximum functioning,
1. Brown RG, Jahanshahi M, Quinn N, et al: Sexual function in patients with Parkinson's
disease and their partners. J Neurol Neurosurg Psychiatry 53:480-486, 1990
2. Bunting LK, Fitzsimmons B: Depression in Parkinson's disease. J Neurosci Nurs 23(3):
158-164, 1991
3. Cummings JL, Benson DF: Dementia: Definition, prevalence, classification, and approach
to diagnosis. In Dementia: A Clinical Approach. Massachusetts, Butterworth, 1992, p 1
4. Folstein MF, Ross C: Cognitive impairment in the elderly. In Kelly WN led); Textbook of
Internal Medicine. JB Lippincott, 1992, p 2408
5. Gentile KM: A review of the literature on interventions and quality of fife in the frad
elderly. In Birren JE, Lubben JE, Rowe JC, et a] (eds): The Concept and Measurement of
Quality of Life in the Frafl Elderly. San Diego, Academia Press, 1991, p 74
6. Giovannini P, Piccolo 1, et al: Early onset Parkinson's disease. Movement Disorders
6(l):36-42, 1991
7. Hickey J: Nervous system degenerative diseases. In The Clinical Practice of Neurological
and NeUTOSurgical Nursing. Philadelphia, JB Lippincott, 1992, p 651
8. Marttila Rj: Epidemiology. In Koller WC led): Handbook of Parkinson's Disease. New
York, Marcel Dekker, 1987, p 35
9. McCance KL, Huether, SE: Alterations in neurologic function. In Pathophysiology: The
biologic basis for disease in adults and children. St. Louis, CV Mosby, 1990, p 509
10. Micoch AG: Diagnosis and treatment of patkinsonian dysarthria. In Koller WC (ed):
Handbook of Parkinson's Disease. New York, Marcel Decker, 1987, p 181

The symptoms of Parkinson's patients

Parkinson’s disease (also known as Parkinson disease or PD) is a degenerative disorder of the central nervous system, that affects the control of muscles, and so may affect movement, speech and posture. Parkinson’s disease belongs to a group of conditions called movement disorders. It is often characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia), and in extreme cases, a loss of physical movement (akinesia).The primary symptoms are due to excessive muscle contraction, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain.PD is both chronic, meaning it persists over a long period of time, and progressive. PD is the most common cause of parkinsonism, a group of similar symptoms. PD is also called “primary parkinsonism” or “idiopathic PD” (”idiopathic” meaning of no known cause). While most forms of parkinsonism are idiopathic, there are some cases where the symptoms may result from toxicity, drugs, genetic mutation, head trauma, or other medical disorders.
Symptoms of Parkinson’s disease have been known and treated since ancient times. However, it was not formally recognised and its symptoms documented until 1817 in An Essay on the Shaking Palsy by the British physician Dr. James Parkinson. Parkinson’s disease was then known as paralysis agitans. The underlying biochemical changes in the brain were identified in the 1950s, due largely to the work of Swedish scientist Arvid Carlsson who later went on to win a Nobel prize. L-dopa entered clinical practice in 1967[1], and the first study reporting improvements in patients with Parkinson’s disease resulting from treatment with L-dopa was published in 1968.Parkinson disease affects movement (motor symptoms). Typical other symptoms include disorders of mood, behavior, thinking, and sensation (non-motor symptoms). Individual patients’ symptoms may be quite dissimilar; progression is also distinctly individual. The disease can be difficult to diagnose accurately. Indeed, only 75% of clinical diagnoses of PD are confirmed at autopsy. Early signs and symptoms of PD may sometimes be dismissed as the effects of normal aging. The physician may need to observe the person for some time until it is apparent that the symptoms are consistently present.Usually Doctors look for shuffling of feet and lack of swing in the arms. Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. However, CT and MRI brain scans of people with PD usually appear normal.
The worldwide prevalence of Parkinson’s disease is estimated to be 4 to 6 million people. There are over 1.7 million in China alone. The disease usually has a long, subtle onset, so diagnosis occurs most often after many years of subclinical disease. Prevalence estimates range from a low of 7 per 100,000 in Ethiopia to a high of 329.3 per 100,000 in Nebraska, U.S.A. (although that figure was arrived at using capture-recapture estimates), and 328.3 cases per 100,000 in the Parsi community in Bombay, India. The greatest prevalence of any country is the U.S.A., with between 100 and 250 cases per 100,000. In countries where Parkinson’s Disease is common, the average age at which symptoms begin is 55-60. Symptoms can occur at any age. In 1875, Henri Huchard (1844-1911) described the first case of juvenile Parkinson’s disease, who was a 3-year-old child who had all the clinical features of Parkinson’s disease. However, it is highly unusual for people under 30 to develop Parkinson’s Disease.It occurs in all parts of the world, but appears to be more common in people of European ancestry than in those of African ancestry. Those of East Asian ancestry have an intermediate risk. It is more common in rural than urban areas in developed countries, but the converse is true in poorer countries, leading Tanner to speculate about environmental causes .Men are more commonly affected than women. However, in many countries, especially Japan, women are affected far more commonly than men. There is a suggestion of increased prevalence in the California Hispanic population. About 2% of the population develops the disease some time during life.

Exercise for the Parkinson Patient

Exercises For The Parkinson Patient
Just as running water does not freeze, so moving muscles do not freeze.
Know the facts. The maintenance of normal muscle tone and function is an important aspect of the treatment of parkinsonism. In part, medication administered for your illness achieves this goal. However, to realize the full benefit of the medication daily exercise and activity are essential. This booklet outlines some of the exercises capable of maintaining muscle power and tone and preventing deformities of the limbs and spine. Their daily performance has proved most beneficial to patients with this illness.
TEN BASIC EXERCISES FOR THE PARKINSON PATIENT1. Bring the toes up with every step you take. In Parkinson's disease, "you never make a move", without lifting the toes.
2. Spread the legs (10 inches) when walking or turning, to provide a wide base, a better stance, and to prevent falling. It may not look "beautiful," but neither does falling.
3. For greater safety in turning, use small steps, with feet widely separated. Never cross one leg over the other when turning. Practice walking a few yards and turn. Walk in the opposite direction and turn. Do so fifteen minutes a day.
4. Practice walking into tight corners of a room, to overcome fear of close places.
5. To insure good body balance, practice rapid excursions of the body. Backward, forward and to the right and left, five minutes, several times a day. Don't look for a wall when you think you are falling. It may not be there. Your body will always be there to protect you, if you will practice balance daily.
6. When the legs feel frozen or "glued" to the floor, a lift of the toes eliminates muscle spasm and the fear of falling. You are free to walk again.
7. Swing the arms freely when walking. It helps to take body weight off the legs, lessens fatigue, and loosens the arms and shoulders.
8. If getting out of a chair is difficult, rise with "lightning speed," to overcome the "pull of gravity." Sitting down should be done slow, with body bent sharply forward, until one touches the seat. Practice this at least a dozen times a day.
9. If the body lists to one side, carry a shopping bag loaded with books or other weights in the opposite hand to decrease the bend.
10. Any task that is difficult, such as buttoning a shirt. or getting out of bed, if practiced 20 times it day, becomes easier the 21st time.
STANDING1. Stand ln front of a wall, facing it about 8" away. Raise arms and reach as high as possible toward the top of the wall. Lean toward the wall and stretch.
2. With your back to the wall, alternate raising legs as high as possible by bending the knee as if marching in place.
3. Holding on to something secure, squat down as far as possible, bending knees; then come up.
SITTING1. Sitting in straight-back chair, place your arms behind the chair and bring your shoulders back as far as possible; raise your head up and look at the ceiling.
2. Sitting In the same chair, grip the ends of a broom or mop stick with both hands, try to raise it over your head until you get it behind your head. Keep head and shoulders as erect as possible.
3. Sitting in same chair, place one leg at a time on another chair and press the knee straight. Keep it there 15 minutes. Try both legs together.
4. Sitting in a chair, raise legs up from the knee alternately, as if stamping your feet.
LYING ON A FIRM BED OR FLOOR1. Lie on the floor or bed, flat on your back; try to press your body to the floor as flat as possible. Move your head from right to left as far as possible. Make sure your head, shoulders, back, and knees touch the surface.
2. Lie on the floor or bed on your abdomen. Do the following one by one:
Put your hands behind back and look up to ceiling, trying to raise your chest off the floor.
Kick your legs alternately, as if swimming.
Turn your head from right to left.
FOR BETTER BALANCE1. Stand with hands on hips, feet spread apart:
Practice marching in place
Practice raising leg straight out to the rear.
Practice raising leg out to the side.
Practice drawing a circle with the leg.
2. Standing with hands at side, feet spread apart:
Lean forward and back
Lean to both sides
Lean in a circular motion and reverse the motion
Take as large a step as possible
Raise your toes as you step forward, hitting ground with your heels
Keep legs apart and posture straight
Swing arms and look straight ahead - your feet know where the floor is located.
2. Collect a dozen magazines; lay them out in a straight line. Space them so that you can take as long a step as possible. Practice walking over these magazines without stepping on them.
3. For a better swing to arms, walk holding a rolled magazine in each hand; keep elbows straight.
4. Practice walking sideways, backwards, and take big steps.
FOR TURNING1. When practicing turning:
Keep feet spread-apart and head high
Use small steps; rock front side to side
Raise legs from the knees
2. If you feel glued to the floor:
Raise your head, relax back on your heels and raise your toes
Rock from side to side, bend knees slightly and straighten up and lift your toes
It sometimes helps if the arms are raised in a sudden short motion
FOR GETTING IN AND OUT OF A CHAIR1. If you become glued a few steps before you reach the chair, try this: Don't aim for the chair but some object past it. Pass the chair as closely as possible and as you go by it sit down.
2. To sit down, bend forward as far as possible and sit down slowly. Get close to the chair. Do not fall into the chair.
3. To get up, move to the edge of the chair, bend forward and push up vigorously using your arms; try to count 1 2 3 GO! If you have a favorite armchair, raise the back legs with 4" blocks. This will help you to get up easily. Don't let people drag you up by your arms, but help you by pulling you under your arms, or with a slight push on your back.
FOR GETTING OUT OF BED1. Place blocks under the legs of the head of the bed. This will elevate the head of the bed, & make it easier for you to sit up and swing the legs off the bed.
2. A knotted rope tied to the foot of the bed can help you to pull yourself up.
3. To get to a sitting position, shift the body down and rock yourself by vigorously, throwing your arms and legs toward the side of the bed.
FOR USING YOUR ARMS AND HANDS1. Practice buttoning and unbuttoning your clothes; practice cutting food and writing. Squeeze a ball or work with "Silly Putty." Keep your fingers busy many times a day. Tear paper; take coins out of the pocket; play the piano.
2. Always try to dress yourself completely. Use shoehorns, elastic laces, or extra-long shoelaces to get a better grip. Dress in the most relaxed and comfortable position, sitting or standing, but make sure you are in a safe position.
3. To keep elbows straight and shoulders loose, install a pulley in doorway, place a chair under it or slightly in front. Stretch your arms and shoulders in all directions. By working the pulley when seated, you can get a more vigorous pull.
FOR GREATER SAFETY IN BATHTUB AND TOILETIf it is difficult to sit down in a bathtub, try the following:
1. Place a bench, stool or chair inside the tub; have the legs sawed off to tub height. Sit on the chair and soap yourself. Use shower to rinse, or rubber shower extension.
2. Bathtub grab bars are available. Purchase only those that attach securely.
3. Raised toilet seats are commercially available.
4. Toilet armrest for getting on and off the toilet are available.
FOR SPEECH, FACE AND CHEWING DIFFICULTIES1. Practice singing and reading aloud with forceful lip movements. Talk into a tape recorder, if one is available.
2. Practice making faces in front of a mirror. Recite the alphabet and count numbers with exaggerated facial motions. Massage your face with vigor when washing and bathing.
3. When chewing food, chew hard and move the food around; avoid swallowing large lumps.
The previously outlined general exercises and suggestions are designed to help you. They are ancillary to medical treatment which should be carried out in consultation with your physician. In special instances where other diseases are associated with parkinsonism, your physician may wish to limit the intensity of your physical activity. Conversely, more intensive physical therapy may be indicated and in some instances should be done under the direction of a physical therapist.
All activities possible should be engaged in: work, walking, shopping, house chores, gardening, visiting, senior clubs, church organizatiotheater, swimming, sports, gymnasium, health clubs, "Y" activities, etc.

Wednesday, March 12, 2008

Medication and exercise

Both medications and regular physical exercise are helpful - they complement each other in the treatment of PD. Exercise helps to maintain body fitness. For the purpose of carrying out regular exercise, the PD patient should be taking adequate dose of medications (obviously). A common observation in Malaysia is that there are many PD patients who do not carry out physical exercise simply because they are under-medicated. In our country, the treatment of PD is rather conservative - the total daily dose of medications is relatively low compared with other countries. This is a pity because without adequate dose of medications, many of our PD patients are deprived of activities such as physical exercise, driving, etc. Dr Chew Nee Kong, Kuala Lumpur.

I agree exercise is very important and find it really helps me. I go Nordic Walking (with two poles) twice a week. The class are all younger than me and it is at a fast pace. I struggle to keep going but after I have had my post walk shower I feel great. Am going to join a gym (local authority grant) to do even more

I worked for 7 years after my first sympton, 6 years after diagnosis. My 3 girls were ages 2-12 years. After working and going home to another job, I had no time nor energy to exercise. I was married but my husband was not suppportive. As my girls grew, I have always been too tired and with the symptons I experienced, there was no way I was going to a gym. Now is the first time I feel like doing something. I want to start walking. Walking was one of the things I enjoyed and had to give up. No one mentioned exercise to me at the beginning. But then I didi not try to educate my self

See that breaks my heart that with all the money & relief help going on that people have to suffer.DR.have you tried reaching drug companies in U.S.Alot of them do humanitary work[even if for tax exemption].Please let me know maybe we can light a fire under them.With your data there and our efforts here Contact me so we could brain storm.Tom

I never ever would have believed that exercise was SOOO IMPORTANT in fighting my PD symptoms...but it is...I have less pain and I do move better now for the most part. I think one of the best decisions I have made since being dx was requesting physical therapy. I now have many different stretches and see the benefits of exercise.

Tuesday, March 11, 2008

vitamin supplements and Parkinson's Disease

Posted: Mon Mar 10, 2008 1:05 am Post subject: Vitamin supplements and Parkinson Disease


Dear Doctor,

There are some vitamin supplements not suitable for people who have a stroke to take:-

Boron, Chromium, Copper, Magnesium,Manganese,Molybdenum,,Selenium, and Zinic
Please kindly enlighten the matter soonest.


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Dr. Fernandez

Joined: 20 Jan 2007
Posts: 90

Posted: Mon Mar 10, 2008 11:50 pm Post subject:


None of these are contraindicated in PD.

If manganese is injested in high quanitities, however, it is known to cause parkinsonism.

High copper content in the liver and brain (but usually due to an enzyme abnormality, not due to heavy injestion) can be the result of an rare inherited parkinson-like disorder (Wilson's disease).

Hubert H. Fernandez

Dear Mr. Teo,

Sorry about your illness.
Stroke is shares risk factors with coronary disease such as dyslipidemias, hypertension, diabetes, obesity, nutritional deficiency and high homocysteine, etc. These risk factors can be prevented and modified by dietary intervention (sodium restriction), supplement (especially vitamin B group ,folic acid ,vitamin E, magnesium , calcium and fish oil), life style modification such as exercise regularly, stop smoking which is you already done. Chromium is function as an insulin cofactor, mean help to reduce diabetes risk. About Selenium, low selenium intake is suspected to increase the risk of coronary heart disease. The other mineral that you have mentioned : Boron, Molybdenum, Manganese, Copper and Zinc have controlled blood levels and so far do not have any medical report about these mineral are increasing the risk of stroke but if you have that report please send them to me.
Best Regards and Please take care,
Kridakorn Watcharachotpimai M.D., ABAAM.

From: teo teo [mailto: ] Sent: Monday, March 10, 2008 11:22 AMTo: Kridakorn WatcharachotpimaiSubject: Re: hormone report

Dear Dr. Kridakorn,

Just to inform you that I had a minor stroke last week and now recovery to normal..
I was told that some of my add-life prescription are not suitable for stroke patient.

They are Boron, Chromium, Copper, Magnesium,Manganese,Molybdenum,,Selenium, and Zinic
Please kindly enlighten the matter soonest.

Best regards

Yours faithfully,
Back to top

Dear Mr. Teo,

This is a journal about Manganese and Parkinson disease. Usually we get high exposure if we work in some industry such as steel industry not from a diet or supplements.
Willson’s disease is an abnormallity in copper metabolism which is a rare genetic disease . Your copper level in blood is in low –normal.

Best Regards and Take care,

Kridakorn Watcharachotpimai M.D., ABAAM

J Neuropathol Exp Neurol. 2007 Aug;66(8):675-82. Links
The neuropathology of manganese-induced Parkinsonism.
Perl DP, Olanow CW.
Department of Pathology, Mount Sinai School of Medicine, New York , NY 10029-6574 , USA .
Manganese is an essential trace metal that is widely used in industry, particularly in the manufacture of steel. Exposure to high levels of manganese can cause neurotoxicity with the development of a form of parkinsonism known as manganism. It has recently been hypothesized that manganese exposure might also cause or accelerate the development of Parkinson disease (PD). This article is a review of the pathologic studies that have been reported in patients with manganism and in primates experimentally intoxicated with manganese. They demonstrate a consistent pattern characterized by damage to the globus pallidus (particularly the internal segment) with sparing of the substantia nigra pars compacta and the absence of Lewy bodies. This finding contrasts with what is seen in PD, in which there is preferential degeneration of dopamine neurons in the substantia nigra pars compacta coupled with Lewy bodies and preservation of the pallidum. These pathologic findings do not support the notion that manganese causes PD but rather argues that manganese-induced parkinsonism and PD are distinct and separate disease entities.

One of the causes of Parkinson’s disease is over in oxidative damage and low in antioxidant. Some mineral such as Copper, Selenium and manganese are an important part in antioxidant enzyme production ( SOD or superoxide dismutase) which is a protective mechanism. Our brain is very sensitive to free radicals especially you need to take sinemet that help increase energy production for brain cell which mean these will increase free radical production as well. So we need to balance your antioxidant and control oxidative stress. Next visit for antiaging program, I would suggest you to do a comprehensive anti-aging programe which included the tests for oxidative damage, total antioxidant capacity ( not only the levels in the blood) and risks of health disease. Other mineral such as Boron is importance for bone mineral density. Nutrients in supplement have a more benefit than i have told you here, included energy production, memory, immunity etc.
Best Regards,
Kridakorn Watcharachotpimai M.D.,ABAAM.
Nutr Neurosci. 2002 Dec;5(6):363-74. Links
Selenium intake, mood and other aspects of psychological functioning.
Benton D.
Department of Psychology, University of Wales Swansea , Swansea SA2 8PP, Wales , UK .
Selenium is an essential trace element although the level of selenium in food items reflects the soil in which they were grown and thus varies markedly between different parts of the world. The metabolism of selenium by the brain differs from other organs in that at times of deficiency the brain retains selenium to a greater extent. The preferential retention of selenium in the brain suggests that it plays important functions. To date mood is the clearest example of an aspect of psychological functioning that is modified by selenium intake. Five studies have reported that a low selenium intake was associated with poorer mood. The underlying mechanism is unclear although a response to supplementation was found with doses greater than those needed to produce maximal activity of the selenoprotein glutathione peroxidase. Although the functions of many selenoproteins are unknown some play important roles in anti-oxidant mechanisms. As there are suggestions that oxidative injury plays a role in normal aging, schizophrenia, Parkinson's and Alzheimer's disease, the possible role of selenium is considered. Although there is evidence that supplementation with anti-oxidant vitamins shown some promise with Alzheimer's patients, and in preventing the development of tardive dyskinesia in schizophrenics taking neuroleptics
Nutr Neurosci. 2002 Oct;5(5):291-309. Links
Role of oxidative stress and antioxidants in neurodegenerative diseases.
Rao AV, Balachandran B.
Department of Nutritional Sciences, University of Toronto , Ont. , Canada .
Neurodegenerative diseases (NDD) are a group of illness with diverse clinical importance and etiologies. NDD include motor neuron disease such as amyotrophic lateral sclerosis (ALS), cerebellar disorders, Parkinson's disease (PD), Huntington's disease (HD), cortical destructive Alzheimer's disease (AD) and Schizophrenia. Numerous epidemiological and experimental studies provide many risk factors such as advanced age, genetic defects, abnormalities of antioxidant enzymes, excitotoxicity, cytoskeletal abnormalities, autoimmunity, mineral deficiencies, oxidative stress, metabolic toxicity, hypertension and other vascular disorders. Growing body of evidence implicates free radical toxicity, radical induced mutations and oxidative enzyme impairment and mitochondrial dysfunction due to congenital genetic defects in clinical manifestations of NDD. Accumulation of oxidative damage in neurons either primarily or secondarily may account for the increased incidence of NDD such as AD, ALS and stroke in aged populations. The molecular mechanisms of neuronal degeneration remain largely unknown and effective therapies are not currently available. Recent interest has focused on antioxidants such as carotenoids and in particular lycopene, a potent antioxidant in tomatoes and tomato products, flavonoids and vitamins as potentially useful agents in the management of human NDD. The pathobiology of neurodegenerative disorders with emphasis on genetic origin and its correlation with oxidative stress of neurodegenerative disorders will be reviewed and the reasons as to why brain constitutes a vulnerable site of oxidative damage will be discussed. The article will also discuss the potential free radical scavenger, mechanism of antioxidant action of lycopene and the need for the use of antioxidants in the prevention of NDD.
J Physiol Anthropol. 2008 Jan;27(1):7-10. Links
The relationship between bone density and the physical performance of ambulatory patients with Parkinson's disease.
Kamide N, Fukuda M, Miura H.
School of Allied Health Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara , Kanagawa , Japan .,jp
Compared to the general population, Parkinson's disease (PD) patients have a higher risk of hip fracture and secondary osteoporosis. In the general population, it is known that physical performance is related to bone density. However, the relationship between bone density and physical performance in ambulatory PD patients has not been studied. This study investigated the relationship between bone density and physical performance in ambulatory PD patients. Fourteen ambulatory PD patients (9 men and 5 women; mean age, 67.3+/-7.7 years; Hoehn & Yahr stages 1-3) were enrolled. Bone density of the right calcaneus was assessed using a speed of sound (SOS) ultrasound measurement device. Disease severity was categorized using the Japanese Unified Parkinson Disease Rating Scale (UPDRS). Furthermore, to assess physical performance, lower extremity strength, 10 m gait time, and body sway were measured. Since SOS is strongly affected by age and gender, it was standardized by the patient's age and gender, and the t-score was calculated with the use of SOS. Significant correlations were found between the t-score and UPDRS,lower extremity strength, and 10 m gait time. When the 4 parts of the UPDRS were analyzed separately, only the correlation between part IV and the t-score was not significant. The findings of this study suggest that higher disease severity and weaker lower extremity physical performance decreased bone density in ambulatory PD patients. Therefore, in order to prevent hip fractures in ambulatory PD patients, assessing the UPDRS and lower extremity physical performance may be clinically useful.

Dr. OkunJoined: 19 Jan 2007Posts: 251Location: University of Florida
Posted: Thu Mar 13, 2008 8:24 pm Post subject:

None of these vitamins have an evidence based record in PD so I cannot advise you. I have not seen a tremendous improvement with these sorts of regimens in my patients. I recommend a multivitamin for patients who are interested._________________Michael S. Okun, M.D.

Dear Mr Teo I do not routinely recommend vitamins and other chemical substances (such as selenium, copper, etc) to my patients as there is no direct evidence that they help in PD. Dr Chew Nee Kong, Kuala Lumpur