symptoms of parkinsons disease : 7 Symptoms You Should Know

Parkinson's disease affects millions of people through out the world everyday. This affliction affects not only the people who are actually diagnosed with it, but also their family and friends. While research is being conducted everyday into a possible cure, it is important to understand Parkinson's disease symptoms and how they affect the daily life of the individuals who live with this illness everyday.

1- To understand Parkinson's disease, you must first have to have at least a minimal understanding of what the disease is and what it does to the human body. This is a chronic illness that takes place when the neurons or the brain cells begin to deteriorate. This results in an insufficient amount of dopamine to be produced. Dopamine controls muscle activity. The result is Parkinson's disease symptoms such as walking difficulties, coordination issues and uncontrollable shaking.

2- Generally, Parkinson's affects one-half of the body initially. The condition can then travel to the opposite side of the body. When this occurs, the patient essentially has no voluntary muscle control. The result is stiff muscles, poor balance and coordination along with the possibility of tremors.

3- The muscle issues that are associatated with Parkinson's disease symptoms can affect the face as well as the larger muscles of the body. As this disease progresses you may notice that a Parkinson's patient is not able to show the same signs of emotion that they used to. This is because the muscles of the face are not as easily controlled. This lack of muscle coordination will lead to not being able smile, swallow or speak as they used to.

4- Other tasks that may seem mundane and ordinary all of a sudden become very difficult. Parkinson's disease symptoms also include the loss of fine motor skills, writing, brushing teeth and buttoning a shirt become almost impossible as the fingers begin to lose their flexibility and control.

5- Walking is, of course another factor of daily life that can, and usually is, interrupted with the onset of Parkinson's disease. Because of the lack of muscle control, a foot may drag along as opposed to being raised during stepping. The ability to navigate through a narrow doorway or hallway because impaired as the lose of balance becomes an issue.

6- It is important to note that while these Parkinson's disease symptoms are common, not every patient will experience all of them. While some patients may only have an occasional balance issue, others will experience symptoms that run the gamut from the barely noticeable, to the absolutely debilitating.

7- If you are caring for someone who has this issue and is experiencing Parkinson's disease symptoms, it is important to accompany them to their doctor's appointments. Ask questions, read up on this condition. The best thing that you can do for them is to arm yourself with the knowledge of what they may be experiencing.

Visit http://about-parkinsons-disease.net or http://parkinsons-disease-online.info to learn more about chelation therapy for parkinsons disease and what is parkinsons disease.

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symptoms of parkinsons disease : The Progression of Parkinson's disease

One health problem that over 50,000 Americans are diagnosed with each year is Parkinson's disease.

While most people are diagnosed with this health issue after age sixty, some people can have an early onset of Parkinson's disease before the age of forty, roughly 5 - 10% of all diagnoses of the disease.

The health problems associated with the disease can be mild or severe, and men tend to get it more than women.

Parkinson's disease is a chronic progressive neurological disease.

It affects certain nerve cells in the brain, and these nerve cells die.

When this happens, body movements of every kind are affected, and it can cause other health issues as a result of the disease's progression.

The progression of Parkinson's disease as a health problem often begins gradually

The symptoms are usually mild to begin with, but progress as time goes on.

The first health symptoms to appear are often fatigue, slight tremors, forgetfulness, or changes in handwriting and speech.

It most cases, it is often family or friends who notice the changes in the person's health with Parkinson's disease first. They often see the gradual stiffening of muscles, and the continual lack of facial expressions.

It is important for people who notice that their health is not as good as it was to consult their doctor.

As the disease progresses, the health symptoms can get worse.

The tremors can become more pronounced. The patient's movements become slower, and muscles become more rigid.

As the Parkinson's progresses further, balance can become a problem, and walking, posture and the possibility of falls becomes more worrisome. Handwriting and speech can change a great deal, as well.

The good news is that for a lot of people with the health issue of Parkinson's disease, the symptoms are often mild to moderate and they can still lead productive lives.

They sometimes need to have treatment for the disease and modify their lifestyles, but it does not present a significant health issue.

Drug therapy is the most common way to slow down the progression of Parkinson's disease and keep the patient in good health.

While there is no cure for this health problem, a lot of research is currently being done in this field.

Sources:
http://www.pdtrials.org
http://www.webmd.com

Learn More About Parkinson's By Going to Symptoms and Signs of Parkinsons

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symptoms of parkinsons disease : Subarachnoid Hemorrhage: When a Brain Aneurysm Bleeds

Spontaneous subarachnoid (pronounced sub-uh-RACK-noid) hemorrhage is rightfully the most feared cause of sudden headache. Usually due to rupture of aneurysms (abnormal, balloon-like outpouchings of arteries) located near the base of the brain, subarachnoid hemorrhages involve bleeding into the space between the brain and its surrounding membrane, known as the meninges. A traumatic blow to the head can also cause subarachnoid hemorrhage, but this is a completely unrelated process and is not the subject of this essay.

About 10% of people with spontaneous subarachnoid hemorrhages die before they even get to a hospital and over a third die within the first four weeks following the bleed. Survivors can have significant impairments due to brain damage.

And while the effects of the initial bleed are bad enough, in the following few weeks individuals with subarachnoid hemorrhage can suffer additional, serious complications. One complication is that the aneurysm responsible for the initial hemorrhage can bleed a second time and cause even more damage. This occurs in 4% of cases within the first 24 hours and there is another 1.2% chance of re-bleeding each day thereafter for the first two weeks. Thus, without treatment 20% of cases have a second hemorrhage within the first two weeks.

The other serious complication is that the blood deposited in the subarachnoid space can cause otherwise healthy arteries passing through this space to go into spasm. The spasm decreases blood-flow to the parts of the brain ordinarily nourished by these arteries and thereby inflicts additional damage. Or, said another way, a blocked artery causes a new stroke, this time of the non-bleeding type. For reasons that are not entirely understood, these spasms of the arteries do not occur within the first few days after the initial hemorrhage. Instead, they typically develop after a delay of 4-9 days.

What can be done to reduce these complications? In the case of blood-vessel spasm, the best treatment is a preventive one. Administering a drug called nimodipine (prononounced nye-MO-dih-peen) intravenously makes spasming less likely to occur. But in order to prevent the other major complication, re-bleeding, the best treatments are those which physically stabilize the aneurysm. In one such procedure, a surgeon places a metal clip across the aneurysm where it joins the otherwise normal artery. An alternative surgery is to wrap the outside of the aneurysm with surgical gauze or plastic sheeting. A newer procedure involves filling the aneurysm with tiny metal coils inserted via a flexible catheter snaked through the arteries.

How can one tell if a particular headache is caused by a bleeding aneurysm? It can be a tough call, but certain features make a ruptured aneurysm more likely. First, a headache due to a ruptured aneurysm is typically of very abrupt onset (often described as a “thunderclap”) and is classically the worst headache of one’s life. In people who already have recurrent severe headaches from other causes, the headache due to a ruptured aneurysm might feel different from the more usual attacks.

Medical evaluation of patients with ruptured aneurysms can turn up additional clues, like a stiffened neck or changes in the backs of the eyes made visible through an ophthalmoscope. Of course, if the patient is drowsy or confused, this might suggest that something serious is going on, as would any new impairment in the ability to move the eyes, an arm or a leg. A computed tomographic (CT) scan of the head performed within the first 24 hours is very sensitive in detecting a hemorrhage, but if the scan is delayed it is less able to detect the bleed. A lumbar puncture (also known as a spinal tap) always detects subarachnoid hemorrhage even when it is a few days old, but if the needle causes bleeding by piercing a blood-vessel on its way to the subarachnoid space, the test might give the false impression that a subarachnoid hemorrhage occurred when it hadn’t.

After discovery of subarachnoid hemorrhage, the next round of testing focuses on where exactly the bleeding occurred. While in over two-thirds of the cases it originates from ruptured aneurysms, other potential sources include tangles of abnormal blood-vessels known as arteriovenous malformations or from bleeds within the brain tissue that secondarily leak into the subarachnoid space. The managing physician can order any of three tests to image the blood vessels themselves and pinpoint the source of bleeding.

The oldest test--still considered the gold-standard--is known as an arteriogram or, alternatively, an angiogram. An arteriogram is considered an “invasive” test because the doctor must slide a long, flexible catheter through the arterial system (which is under much higher pressure than the veins) so that dye infused through the catheter will enter the arteries in question. Two newer tests are “non-invasive,” though, in truth, they often involve an infusion into a vein. One is magnetic resonance arteriography (MRA) which is performed with the help of an MRI-scanner. The other is computed tomographic arteriography (CT-A) which is performed with the help of a CT-scanner. While the non-invasive tests are getting better all the time, they still occasionally miss aneurysms otherwise visible on arteriograms.

Apart from identifying the bleeding aneurysms, these tests can detect additional aneurysms, when present. About 20% of people experiencing a ruptured aneurysm have one or more co-existing, unruptured aneurysms.

Subarachnoid hemorrhages occur annually in about 10 people out of 100,000. This computes to a 0.01% rate of annual occurrence. Contrast this figure with the 12% of the adult population who have migraine (most of whom have at least one severe headache per year) and it is apparent that the vast majority of severe headaches are not due to ruptured aneurysms. But the concern about missing a ruptured aneurysm means that many people without subarachnoid hemorrhage must receive tests in order to diagnose the few who have it.

What causes aneurysms in the first place? More than one factor is involved. First, there can be an inborn weakening of the artery’s wall. When the wall subsequently deteriorates in ways that can be accelerated by hypertension and smoking, an aneurysm can form.

Actually, aneurysms affecting the brain’s arteries are fairly common. Autopsy and arteriogram studies indicate that about 1-4% of the general population have them. This is many more people than have subarachnoid hemorrhages, so a logical conclusion is that most people with aneurysms go through their entire lifetimes without having symptoms. Studies show that aneurysms less than 5 millimeters (0.2 inches) in diameter have a very low rate of rupture, while aneurysms greater than 10 millimeters (0.4 inches) in diameter have a significant risk of bleeding.

Do ruptured aneurysms run in families? A 2005 report from the Scottish Aneurysm Study Group showed a slight tendency for this trait to be shared by close relatives. The 10-year risk for subarachnoid hemorrhage in first-degree relatives (parents, siblings and children) was 1.2%. The risk was even lower in more distant relatives. In families with two affected first-degree relatives there was a trend toward higher risk. The authors felt that most relatives of patients suffering subarachnoid hemorrhages have low risk of future hemorrhages, and that routine screening of family members is inappropriate unless there are multiple affected individuals in the same family.
symptoms of parkinsons disease
(C) 2005 by Gary Cordingley

Gary Cordingley, MD, PhD, is a clinical neurologist, teacher and researcher who works in Athens, Ohio. For more health-related articles see his websites: http://www.cordingleyneurology.com and http://www.neurologyarticles.com

Article Source: http://EzineArticles.com/?expert=Gary_Cordingley

symptoms of parkinsons disease : Blepharospasm: That Blinkety-Blink Movement Disorder

The range of ailments falling under the umbrella-term of "abnormal involuntary movement disorders" is diverse and includes conditions as different from each other as Parkinson's disease, restless legs syndrome and blepharospasm. Cases of blepharospasm, like those of other movement disorders, often go unrecognized or are blamed on other causes.

The term "blepharospasm" is the sum of its parts. "Blepharon" is Greek for eyelid and "spasm" means excessive muscular contractions. In blepharospasm the eyes blink excessively. The blinking can be too frequent, too sustained, or both. The distinction between normal blinking and excessive blinking is not exact. A practical method for sorting out cases relies on the answers to two questions:

Does the blinking cause distress?
Does the blinking interfere with usual activities?

Blepharospasm can occur alone or in combination with other involuntary movements. When paired with involuntary movements of the lower face -- like puckering of the lips or grimacing expressions -- the problem is collectively known as Meige syndrome, named for Dr. Henri Meige who described the condition in 1904. Blepharospasm and Meige syndrome are forms of dystonia, a sub-grouping within the overall range of involuntary movement disorders. Another example of dystonia is torticollis, in which there is sustained involuntary twisting or cocking of the neck.

Blepharospasm, like any other condition, can be mild, moderate or severe. It is not necessarily disabling, but if the blinking is so frequent or sustained that it interferes with vision, then it can impact activities like driving. Blepharospasm does not appear to be an insurmountable barrier for people whose job is to appear in public, as a well-known television personality with blepharospasm seems to be doing just fine.

How common is this condition? Not very. Researchers at Mayo Clinic tracked cases of blepharospasm in Olmsted County, Minnesota, between 1976 and 1995. They calculated just 1.2 new cases per year per population of 100,000, although this might be an underestimate of the true incidence because it doesn't include undiagnosed cases. The diagnosed patients were equally divided between the sexes and half of the people had Meige syndrome, meaning that the blepharospasm was accompanied by dystonia of the lower face. One in four cases resolved on their own.

The diagnosis of blepharospasm is based mainly on its appearance. This condition is sometimes misidentified as a reaction to (or "secondary" to) an irritation of the eyes, and is treated with eyedrops. However, in true cases of blepharospasm (designated as "primary" or "essential" blepharospasm) the excessive blinking is not driven by irritation of the eyes. Instead, the eyelids are just following orders from overactive brain-circuits, though in fairness, those brain-circuits might be misinterpreting non-irritated eyes as being irritated. Eyedrops are not helpful for primary blepharospasm.

Another condition which is similar in appearance is hemifacial spasm in which there is excessive blinking of just one eye, often accompanied by excessive twitching of the lower face on the same side. But hemifacial spasm is not a form of primary blepharospasm. In hemifacial spasm the affected muscles are driven by an overactive nerve rather than an overactive brain-circuit. That's why just one side of the face is affected. There is another, unaffected nerve controlling the opposite side of the face.

Although the source of excessive blinking in blepharospasm is undoubtedly the brain, the disorder does not show up on usual, brain-oriented tests like computed tomographic (CT) scans, magnetic resonance imaging (MRI) scans or electroencephalograms (EEGs).

How about treatment? There is no curative treatment available. Existing treatments can relieve symptoms, but don't affect the course of the underlying disorder which usually continues long-term. Thus, the state of a person's blepharospasm in five or ten years will be the same whether or not symptom-relieving treatment is used in the meantime.

That said, many patients benefit from symptom-relieving treatment which nowadays usually takes the form of periodic injections of botulinum toxin (e.g. brand name Botox) beneath the skin, overlying the affected muscles. This weakens or relaxes the muscles involved in the excessive blinking to an extent that relieves the symptom without interfering with normal eye closure. Typical treatment cycles are no more often than every three months. Prior to the development of botulinum treatment for blepharospasm it was often treated with orally administered medications, though usually with a lower success rate.

As an example of clinical experience in treating blepharospasm, we can look at the results obtained by neurologists at the Sao Paulo School of Medicine in Brazil. Over the ten-year span from 1993 to 2003 they administered a total of 379 botulinum toxin treatments to 30 patients with blepharospasm. Sixty-six percent of the patients had previously tried oral medications for their condition and just 15% considered them satisfactory. (Of course, patients who were totally satisfied with oral medications were unlikely to seek treatment with botulinum toxin, so this figure probably underestimates the success rate with oral medication.)

So how did they do? Ninety-three percent of the patients showed significant improvement after their first injections with botulinum toxin and there was no loss of effectiveness when the first and last treatments were compared. Adverse effects -- "mostly minor" -- developed at least once in 53% of the patients. Six patients (20%) discontinued the treatment.

(C) 2006 by Gary Cordingley

Gary Cordingley, MD, PhD, is a clinical neurologist, teacher and researcher who works in Athens, Ohio. For more health-related articles see his websites at: http://www.cordingleyneurology.com and http://www.neurologyarticles.com

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symptoms of parkinsons disease : A Brief Look At Parkinson's Disease

The primary cause for developing the Parkinson's disease is the widespread damage of the dopamine-producing cells in a person's brain. Once the rate of damage rise up to 80% the risk against Parkinson's disease is inescapable.

This condition is a brain disease. Once the nerve cells in the substantia nigra, a part of the middle brain, die or become impaired, the production of the dopamine will diminish. Dopamine maintains the coordination and the smooth functioning of the body movements. If this condition occurs, other brain movement control centers become unchecked. This is the major reason why people affected with Parkinson's disease are experiencing shaking or tremor, slowness of movements, stiffness or rigidity and incapability of maintaining body balance. Other symptoms may include:

- Firm facial expression
- Small handwriting or micrographia
- Depression
- Muffled speech
- Irregular walks
- Reduced automatic movements

The initial symptoms of the disease are mild and may not even need to be attended medically. The most common sign of the disease is the rest tremor, but not all patients develop tremor. Unlike other symptoms, tremor does not seriously disable a person's usual activities but it is the most damaging if viewed on the psychological interpretation. a patient needs to hold onto something to gain control over the trembling hand or to put them in a secured place, like the pocket of the pants.

Symptoms are normally restricted on a single limb in the first phases of the disease. But they eventually affect the other half of the body. Most patients are aware of this nature of the disease, and this knowledge makes the condition even more unbearable (both physically and psychologically) which often leads to over-monitoring of their cases.

Women and men are at equal standing against the risks of developing the disease. In America, the present number of Parkinson's disease victims is near to 2 million. This makes it the second most prevalent neurodegenerative disease after the Alzheimer's disease.

Though the disease is more prevalent during the later years of a person's life, specifically age 65, individuals aged 50 comprises 15% of people diagnosed of the disease. And one in a group of 100 people is potential of developing the disease.

The diagnosis of the Parkinson's disease is complex. There are no ways that a person may be identified as a patient with blood tests and x-rays and other conventional methods of diagnosis. Often, a neurologist may only arrive at a result once a thorough MRI or Magnetic Resonance Imaging is complete. However, MRI is helpful only in separating the symptoms of Parkinson's disease with other neurological and brain disorders.

A number of medicines may be taken to diminish the occurrence of the symptoms of the disease. Most of these are aimed at replacing or copying the effects dopamine have over the abnormalities associated with the dopamine insufficiency in the brain such as rigidity, slowness and tremor. Newer researches are focused on finding the solution to control the progress of the disease and many are promising to bring new improvements to patients inflicted with Parkinson's disease.

Surgery is one solution that experts consider in Parkinson's disease treatment. However, it is not the answer to cure the disease. Because brain surgery is risky, it is usually placed at the bottom priority unless all necessary medications taken failed. It is important that both a brain surgeon and a neurologist are first consulted for the pre-treatment procedures.

Modern-day medicine has not yet found ways to cure the Parkinson's disease. Diagnosis would only identify if the person has it and how to minimize and control the symptoms. It is not aimed at banishing the disease itself.

Robert Thatcher is a freelance publisher based in Cupertino, California. He publishes articles and reports in various ezines and provides Parkinson's disease resources on http://www.about-parkinson-disease.info

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symptoms of parkinsons disease : Signs of Parkinson's Disease

Parkinson's disease tends to be a very frightening disease to be diagnosed with. Knowing what it is and what the symptoms are will help you to catch it in the early stages and begin treatment right away.

What is Parkinson's Disease?

When brain cells (neurons) deteriorate, Parkinson's disease is the result. It is considered a chronic condition, as opposed to acute, because it has no cure and doesn't go away by itself. It is also a degenerative disease, meaning that it breaks down the body of the person it attacks. Muscle control is lost due to a lack of dopamine in the brain and, because of this, a difficulty in walking, coordination, and severe shaking develop.

Characteristics and Signs of Parkinson's

Some of the signs of Parkinson's to look out for include:

• Tremors or Trembling: for nearly three quarters of patients diagnosed with Parkinson’s disease, the appearance of tremors or trembling is the first noticeable symptom.

• Muscle stiffness -Parkinson’s patients experiencing stiffness or rigidity may not notice any other symptoms of this characteristic. In fact, the person may not even notice the signs of rigidity unless a physician notes it during a physical examination.

The presence of physical rigidity, such as decreased arm swing, is especially useful in helping medical personnel establish a diagnosis of Parkinson’s disease.

This may also include 'Freezing' which is the sudden inability to move when you want to , a foot on one side starts to drag, and difficulty walking through doorways and hallways.

• Lacking coordination

• Difficulty maintaining balance

• Difficulty controlling facial muscles - Akinesia and bradykinesia - these characteristics may manifest themselves in the face, for example, as reduced facial expression, infrequent blinking, and slow swallowing resulting in increased saliva secretion, and occasionally, drooling.

A person with Parkinson’s disease may also notice a change in his or her voice: it may become low and monotone, with little or no inflection. Akinesia and bradykinesia may also appear as trouble executing certain movements, and increased slowness when movements are attempted or executed.

• Talking more quietly

• Raspy voice

• Difficulty with motor skills - The result is lessened in fine motor skills dexterity and may mean the person with Parkinson’s may require help with everyday tasks such as shaving, tying laces, fastening buttons, and handwriting.

• Oily skin and dandruff - Seborrheic dermatitis: Parkinson’s patients may notice that they have developed greasier skin, especially around the nose and eyebrows, and a greasier scalp. This symptom is usually accompanied by increased sweating.

• Non-specific sensory symptoms - Unusual sensory feelings such as numbness, pain, burning sensation, restlessness and fatigue can also be indicators of Parkinson’s disease.

• Depression and senility, as well as dementia, are secondary symptoms of Parkinson's.

Feeling anxious, angry, discouraged or downright depressed is common as the brain is undergoing a number of chemical changes. Approximately 40-70 percent of Parkinson’s sufferers experience depression at times, while 20 percent of these are considered a major depressive disorder.

Anxiety or panic attacks are common psychological elements of the disease as well. An average of 70 percent of people who have pre-existing depression also develop anxiety whereas 90 percent who first experience anxiety fall victim to depression.

Dementia is evidenced in 20-30 percent of sufferers and this gradual decline first starts with slowness in thought and advances to a difficulty in properly organizing thoughts.

In Closing

In most cases, only one side of the body will be affected in the early stages of the disease, and the hands and feet are the most likely area where tremors will first be noticed.

One symptom does not mean that you have Parkinson's. It usually arrives in the form of a combination of symptoms over a prolonged period.

If you have concerns, consult your doctor.

Get The Information About Parkinson's By Going to Symptoms and Signs of Parkinsons.

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symptoms of parkinsons disease : The Facts About Glutathione and Parkinson's Disease

Parkinson's Disease (PD), a devastating illness, occurs in one of every 100 people over 65.

It is a slowly progressing disease of the nervous system that results in progressive destruction of brain cells (neurons) in an area of the brain called the substantia nigra. Death occurs usually as a result of secondary complications such as infection.

One of the mechanisms known to destroy neurons is damage by free radicals or reactive oxygen species - destructive molecules produced by oxidation of the neurotransmitter dopamine.

The Role of Dopamine

The cells of the substantia nigra use dopamine - a chemical messenger between brain or nerve cells - to communicate with cells in another region of the brain called the striatum.

When nigral cells are lost, nigral dopamine levels fall, resulting in a decrease in striatal dopamine.

The typical symptoms of PD - motor function deficiencies characterized by muscle rigidity, jerky movements, rhythmic resting tremors - are the result of low levels of striatal dopamine.

Most dopaminergic drugs used to treat PD, are aimed at temporarily replenishing or mimicking dopamine. They improve some symptoms, but do not restore normal brain function nor halt brain cell destruction.

Dopaminergic drugs are generally effective at first in reducing many PD symptoms, but over time they lose their effect.

They also cause severe side effects because they overstimulate nerve cells elsewhere in the body and cause confusion, hallucinations, nausea and fluctuations in the movement of limbs.

The Role of Antioxidants

When dopaminergic neurons are lost in the course of Parkinson's disease, the metabolism of dopamine is increased - which in turn increases the formation of highly neurotoxic hydroxyl radicals.

The most important free radical scavenger in the cells of the substantia nigra is the powerful brain antioxidant, glutathione. Glutathione levels in PD patients are low.

And as we age, levels of glutathione in the dopaminergic neurons of the substantia nigra decreases. This appears to hasten cell death and advance the progression of PD.

At least 80 percent of the substantia nigra cells are lost before symptoms of Parkinson's disease become apparent. This is why it becomes essential to protect or maintain these cells under oxidative stress.

How does Glutathione help in Parkinson's Disease?

Several factors explain why glutathione is so beneficial in Parkinson’s disease.

1. Glutathione increases the sensitivity of the brain to dopamine. So although glutathione doesn't raise dopamine levels, it allows the dopamine in the brain to be more effective.

2. Glutathione's powerful antioxidant activity protects the brain from free radical damage.

3. An even more intriguing benefit of glutathione lies in its powerful detoxification ability.

Its a well known fact that most Parkinson’s patients are deficient in their ability to detoxify chemicals to which they are exposed.

The unfortunate few who harbor an inherited flaw in their detoxification pathways are at far greater risk to the brain damaging effects of a wide variety of toxins.

Glutathione is one of the most important components of the liver’s detoxification system. Glutathione therapy is one of the most effective techniques for enhancing liver and brain detoxification.

Glutathione treatments considerably improve some of the symptoms of Parkinson's disease including difficulties with rigidity, walking, movement, coordination and speech. A marked reduction of tremor has been observed as well as a decrease in depression.

Glutathione and N-acetyl-L-cysteine (a glutathione precursor) have been shown to be very effective in protecting the nerves in the substantia nigra from being destroyed by oxidative stress.

Glutathione Therapy in Parkinson's Disease

The practical problem in increasing glutathione levels is that taking glutathione itself as a supplement does not boost cellular glutathione levels, since glutathione breaks down in the digestive tract before it reaches the cells.

However, intravenous glutathione therapy and taking glutathione precursors are both effective in boosting intracellular levels of glutathione.

Intravenous Glutathione Therapy:

Intravenous glutathione injections have been shown to have amazing and quick results.

Dr. David Perlmutter, a pioneer in this therapy, has developed a protocol utilized at the Perlmutter Health Center for administering intravenous glutathione to Parkinson's patients.

Following even a single dosage of intravenous glutathione - often in as little as 15 minutes - the ability to walk, turn around and move their arms is almost completely restored.

Glutathione Precursors:

Dietary antioxidants and supplements that increase cellular glutathione, such as alpha lipoic acid, NAC, pycnogenol, the herb silymarin (milk thistle), are effective in restoring normal function.

N-acetyl-cysteine (NAC) and un-denatured, whey protein both supply glutathione precursors intracellularly, enhance the body’s production of glutathione and aid the detoxification process.

Other nutritional supplements which aid the detoxification process include selenium, vitamins E and C.

Read the detailed report with references on Parkinson's Disease and Glutathione

Copyright © 2004 Priya Shah


About the author: Priya Shah is the Editor of The Glutathione Report, a newsletter featuring regular updates on the health benefits of glutathione. Get a Free report on Glutathione in Health and Disease

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symptoms of parkinsons disease : Who Gets Parkinson's Disease?

Parkinson's Disease affects generally elder adults, among about 90% of the known cases are diagnosed in people over the age of 60. Within that population, there is a small amount of variance, with the danger increasing from age 60 through age 75, and then going down sharply. Currently, Parkinson's Disease is known to affect about 3% of the population over the age of 65. With present statistics and the probable aging of the population, authorities think that that percentage will double in the next 40 years.

When those with mild symptoms of Parkinsons (symptoms of Parkinson's Disease that may be caused by other things, or could develop into Parkinson's Disease), those numbers increase dramatically. 15% of those between the ages of 60 and 74 have been diagnosed with Parkinson's Disease. Between the ages of 75 and 84, that percentage rises to almost 30%.

However, when you look at it in terms of inception of symptoms, the picture changes. Fewer than 10% of new cases of Parkinson's disease are diagnosed in younger adults - under age 40. The majority of new diagnoses of Parkinson's disease are made between the ages of 60 and 75. After age 85, the danger of developing Parkinson's Disease then seems to fall off dramatically.

What are the factors that effect diagnoses?

Gender

Men appear to be at greater risk of developing Parkinson's Disease than women. Men have to deal with about double the risk of developing Parkinson's Disease as women in any age group. Scientists think that estrogens may play a function in protecting the body from the chemical changes that occur in Parkinson's Disease. This is further borne out by two facts - women who've had hysterectomies have a somewhat higher rate of Parkinson's Disease, and women who've had estrogen replacement therapy have a lower rate of Parkinson's Disease than other women their age.

Parkinson's Disease seems to growth more quickly in men than women according to one study, and another found a difference in the way that symptoms present. Men are more prone to rigidity and tremor, and women more at danger from gait disturbance and shuffling.

Ethnicity

Caucasians have a higher danger of developing Parkinson's Disease than either African Americans or Asian Americans. People of European descent appear most prone to usual Parkinson's Disease, but some studies hint at that non-Caucasians may be more at risk for a particular type of non-typical Parkinsonis that causes a disturbance in judgment.

Heredity

In a small percentage of cases, family history may play a part in the inception of Parkinson's Disease. People who have parents or brothers and sisters who had young-onset Parkinson's Disease, in which symptoms develop before the age of 40, are more probable to develop Parkinson's Disease than others their age. When Parkinson's Disease was diagnosed at older ages, family history looks like it's to play no part.

Cigarette Smokers

Oddly, cigarette smokers appear to have a diminished incidence of Parkinson's Disease, which has led researchers to explore the probability that nicotine may give some protection from the fluctuations caused by Parkinson's Disease. They are quick to point out that the other health problems associated with cigarette smoking are far too significant to think cigarette smoking as a way to avoid getting Parkinson's Disease.

Coffee Drinkers

Caffeine also seems to have a protective result against Parkinson's Disease. A study of Japanese-American men suggested that those who commonly drank coffee ran a lesser risk of developing Parkinson's Disease than other men their age. The more coffee they consumed, the lower the risk.

To find a host of tips and information on all aspects of Parkinsons Disease visit http://www.parkinsonsdiseaseadvisor.com

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symptoms of parkinsons disease : Neurologists Can Improve 'Deep Brain' Therapy for Parkinson's

WEDNESDAY, July 12 (HealthDay News) -- Neurologists with expertise in a therapy called deep brain stimulation can help improve outcomes for Parkinson's disease patients undergoing the treatment, a Canadian study finds.

Deep brain stimulation is a surgical procedure in which electrodes are implanted into the brain to electronically stimulate neurological areas controlling movement. The procedure is used to treat Parkinson's symptoms such as tremors, stiffness and difficulty walking, and is the most effective surgical treatment for advanced Parkinson's, according to background information in the study.

The treatment requires intensive patient management, such as adjustment of electrical currents and patient medication dosages. However, at many medical centers in North America, these duties are assigned to health workers -- such as surgical nurses, fellows or neurophysiologists -- who do not have extensive experience in caring for Parkinson's patients, the study authors explained.

In their study, the team from the University of Toronto followed outcomes in 44 Parkinson's patients treated with deep brain stimulation to see whether treatment could be improved through the direct involvement of a neurologist.

The patients in the study had already undergone deep brain stimulation treatment for an average of 3.5 years. For this study, the neurologist became directly involved in the treatment -- for example, making adjustments to electrical currents during the procedure and to the doses of medication received by patients after the procedure.

Patients' Parkinson's disease symptoms were assessed before and after (an average of five months, with a range of one hour to 14 months) they began this reprogrammed treatment.

The study found that 54.6 percent (24) of the patients showed additional improvement in their Parkinson's symptoms, while 36.4 percent (16) remained unchanged, and 9.1 percent (4) experienced worsened symptoms. Those who showed improvement had fewer tremors, less rigidity and slowness of movement (bradykinesia), and reductions in their medication dosages.

The four patients with worsened symptoms suffered more speech and gait problems. They were put back on their original treatment settings.

The findings were published in the July 11 online issue of the Archives of Neurology, and are expected to be in the September print issue of the journal.


HealthDay

Copyright (c) 2006 ScoutNews LLC. All rights reserved.

symptoms of parkinsons disease : Diagnosing Parkinson's Disease

There are no laboratory tests currently available that can identify Parkinson's disease. Because it usually affects people over fifty, it is important to see a doctor if you begin experiencing mild tremors, shakiness, or any of the above-mentioned symptoms. Other diseases cause similar symptoms; your doctor can determine if what you are suffering from is, indeed, Parkinson's disease.

Young-onset Parkinson's disease, though rare, occurs in those younger than forty. The disease follows a smoother course. Those with young-onset Parkinson's typically have fewer problems with balance and memory loss. They can, however, have more problems with movement because of some of the medications.

Prognosis

Parkinson's disease is chronic and progressive, meaning it gets worse with time. Different people are affected by different symptoms; there is no way to predict the degree to which a person will be affected. Some people may become incapable of functioning normally, but others may experience only minor symptoms.

Treatment

Currently there is no cure for Parkinson's disease. There are, however, medications that can dramatically reduce the symptoms. The most common is levodopa combined with carbidopa. Nerve cells use this to replace the diminishing supply of dopamine in the brain. If used in young-onset Parkinson's, however, this can cause movement problems. Not all patients respond equally to the drug, but it helps at least 75 percent of cases. It does not affect all of the symptoms, either, helping most with bradykinesia and rigidity. It may only slightly affect tremors, and may not reduce other symptoms at all. Other drugs are available that mimic the role of dopamine in the brain; talk to your doctor about treatment options. Proper treatment and planning for the future are essential to living with Parkinson's disease.

Progress

Research is being done on all aspects of the disease, studying new drugs to reverse, delay, or prevent the disease, and trying to pinpoint the cause of the disease with the hope of prevention.

By Julia Countryman

symptoms of parkinsons disease : Parkinson Patients Can Be Apathetic without Depression

ST. PAUL, Minn. – People with Parkinson disease can be apathetic without being depressed, and apathy may be a core feature of the disease, according to a study published in the July 11, 2006, issue of Neurology, the scientific journal of the American Academy of Neurology.

Apathy is a mental state characterized by a loss of motivation, loss of interest, and loss of effortful behavior. In apathy, the mood is neutral and there is a sense of indifference. In depression, the mood is negative and there is emotional suffering. Because apathy and depression share some of the same symptoms, the disorders can be misdiagnosed.

“This study shows that it’s important to screen for both apathy and depression so patients can be treated appropriately,” said study author Lindsey Kirsch-Darrow, MS, of the University of Florida in Gainesville. “It will also be important to educate family members and caregivers about apathy to help them understand that it is a characteristic of Parkinson disease. Apathetic behavior is not something the patient can voluntarily control, and it is not laziness or the patient trying to be difficult – it is a symptom of Parkinson disease.”

The study compared 80 people with Parkinson disease to 20 people with dystonia, another movement disorder. The researchers hypothesized that apathy would occur more often in people with Parkinson disease, because the disease affects areas of the brain in the frontal cortex that are involved in non-motor activities, whereas dystonia affects areas mainly involved with movement.

Of those with Parkinson disease, 51 percent had apathy, compared to 20 percent of those with dystonia. Apathy with no depression occurred in 29 percent of those with Parkinson disease and none of those with dystonia. The rate of depression was the same in both groups.

Treatments for depression and apathy in people with Parkinson disease are still being evaluated.

The current criteria for diagnosing depression may not be appropriate for people with Parkinson disease, according to neurologist Irene Richard, MD, of the University of Rochester in New York, who wrote an editorial accompanying the study.

“A person with Parkinson disease might be diagnosed with minor depression based solely on the presence of apathy,” she said. “The recognition that apathy can be present without depression is important so that we do not inappropriately diagnose and treat a depressive disorder that is not present.”

The study is consistent with guidelines issued recently by the American Academy of Neurology recommending that all people with Parkinson disease be screened for and treated for depression, which can affect their quality of life and how well they function.

Media Contact: Robin Stinnett, (651) 695-2763, rstinnett@aan.com

symptoms of parkinsons disease : Apathy often a part of Parkinson's disease

NEW YORK (Reuters Health) - Patients with Parkinson's disease may exhibit apathetic behavior without being depressed, a group of clinicians report. They suggest in the medical journal Neurology that apathy may therefore be a "core" feature of the disease.

"It's important to screen for both apathy and depression so patients can be treated appropriately," noted Dr. Lindsey Kirsch-Darrow in an American Academy of Neurology statement.

"It will also be important to educate family members and caregivers about apathy to help them understand that it is a characteristic of Parkinson's disease," she continued. "Apathetic behavior is not something the patient can voluntarily control, and it is not laziness or the patient trying to be difficult -- it is a symptom of Parkinson's disease."

Kirsch-Darrow, of the University of Florida in Gainesville and colleagues compared 80 patients with Parkinson's disease to 20 patients with dystonia, or impaired muscle control.

The team found observed a "significantly higher severity and frequency of apathy" in the Parkinson's disease patients compared to the dystonia patients. Fifty-one percent of Parkinson's disease patients exhibited apathy compared with 20 percent of those with dystonia.

Apathy in the absence of depression was common in Parkinson's disease patients (29 percent but was not seen in any of the dystonia patients. "This was the most dramatic and potentially important finding of the study," the researchers write.

In an editorial, Dr. Irene Hegeman Richard from the University of Rochester in New York notes that the "recognition that apathy can be present without depression is important so that we do not inappropriately diagnose and treat a depressive disorder that is not present."

For patients with apathy, stimulant-type drugs have been suggested as a possible treatment. "However, it is important to stop and ask ourselves who we are treating," Richard writes. "With apathy, it is generally the spouse, family or friends and not the patient who complain because the patient requires constant prompting to do anything and does not want to go anywhere."

SOURCE: Neurology, July 11, 2006.

Copyright © 2006 Reuters Limited. All rights reserved.

symptoms of parkinsons disease : Complementary Treatments

A number of modalities and nutritional supplements can help relieve symptoms and improve quality of life. It is imperative that patients inform their physician of any over-the-counter medications, herbs, or other supplements that they use on a regular basis, because they may interact with medication and because drug dosages may need to be adjusted.

Physical therapy can help strengthen and tone underused muscles, and give rigid muscles a better range of motion. The goal is to help build body strength, improve balance, overcome gait problems, and improve speaking and swallowing.

Simple physical activity such as walking, gardening, and swimming can improves one's sense of well-being.

Gentle, soothing massage techniques may provide relief from muscle rigidity and may have some neuromuscular benefit as well.

The slow flowing movements of Tai Chi help maintain flexibility, balance, and relaxation. The Struthers Parkinson's Center in Minneapolis, which teaches a modified form of Tai Chi, consistently reports benefits achieved by patients in all stages of Parkinson's.

Support groups provide a caring supportive environment in which patients and their loved ones can ask questions about Parkinson's, expressing their frustrations, and obtain advice about coping with and treating symptoms from people who share the same problem.

Parkinson's appears to progress more slowly in those who remain involved in activities that they enjoyed before the onset of symptoms and in those who engage in new interests.

by Healthcommunities.com, Inc. All rights reserved.

symptoms of parkinsons disease : Surgery

Surgery is another method of controlling symptoms and improving quality of life when medication ceases to be effective or when medication side effects, such as jerking and dyskinesias, become intolerable.
Not everyone is a good candidate for surgery. For example, if a patient never responded to, or responded poorly to levodopa/carbidopa, surgery may not be of any help. Only about 10% of Parkinson's patients are estimated to be suitable candidates.

Those who are suitable but forgo surgery may feel the risk outweighs the benefit. Every surgical procedure carries inherent risk. Additionally, there is the risk that symptoms will not improve or will worsen following the operation.

There are three surgical procedures for treating Parkinson's disease: ablative surgery, stimulation surgery or deep brain stimulation (DBS), and transplantation or restorative surgery.

Ablative Surgery
This procedure locates, targets, and then destroys (ablates) a clearly defined area of the brain affected by Parkinson's. The object is to destroy tissue that produces abnormal chemical or electrical impulses that produce tremors and dyskinesias.

A heated probe or electrode is inserted into the targeted area. It is often difficult to estimate how much tissue to destroy and the amount of heat to use. It is always safer to burn a small area and risk the tremor returning or not being eliminated, rather than burning a larger region and risking serious complications such as paralysis or stroke.

The patient remains awake during this procedure to determinine if the tremor or dyskinesia has been eliminated. A local anesthetic is used to dull the outer part of the brain and skull. The brain is insensitive to pain, so it can be manipulated and probed without the patient feeling it.

This type of surgery involves either pallidotomy or thalamotomy. Pallidotomy—ablation in the part of the brain called the globus pallidus—involves putting a hole (i.e., otomy) in the globus pallidus, the globe-shaped structure located deep inside the brain. This procedure is performed to eliminate uncontrolled dyskinesias.

Thalamotomy—ablation of brain tissue in the thalamus—involves creating an otomy in the thalamus. This structure is located below the globus pallidus. The procedure is performed to eliminate tremors.

A related procedure, cryothalamotomy, uses a supercooled probe that is inserted into the thalamus to freeze and destroy areas that produce tremors.

Deep Brain Stimulation (DBS)
DBS targets the subthalamic nucleus, which is located below the thalamus and is difficult to reach, the globus pallidus, or the thalamus. In DBS, the targeted region is inactivated, not destroyed, by an implanted electrode.

The electrode is connected via a wire running beneath the skin to a stimulator and battery pack in the patient's chest. It is reversible—just turn off the current—and allows for precise calibrated symptom control.

The risk for hemorrhage or stroke is reduced, but the electrode can become infected, the simulator may have to be periodically programmed, and the battery must be replaced every 5 years. Battery replacement involves minor surgery.

Transplantation or Restorative Surgery
In transplantation, or restorative, surgery dopamine-producing cells are implanted into the striatum. The cells used for transplantation may come from one of several sources: the patient's body, human embryos, pig embryos.

Using cells from the patient's body has been unsuccessful because of an insufficient supply of dopamine cells and the inability of the implanted cells to survive.

To use fetal cells, between three and eight embryos are needed per procedure, and even under the most favorable conditions, 90% of transplanted cells do not survive. This procedure is only moderately effective in some patients and usually in those younger than age 60.

Preliminary studies have shown that pig embryo cells do survive transplantation and have an effect on symptoms.

Stem cells, primitive cells that can grow into nerve cells, are able to survive and reproduce. Once they grow as nerve cells, they can be transformed into dopamine-producing cells.

Stem cells are obtained from discarded blood in a newborn's umbilical cord, the bone marrow of an adult, or an aborted embryo.

by Healthcommunities.com, Inc. All rights reserved.

symptoms of parkinsons disease : What Is It?

Parkinson's disease is one of a larger group of neurological conditions called motor system disorders. Historians have found evidence of the disease as far back as 5000 B.C. It was first described as "the shaking palsy" in 1817 by British doctor James Parkinson. Because of Parkinson's early work in identifying symptoms, the disease came to bear his name.

In the normal brain, some nerve cells produce the chemical dopamine, which transmits signals within the brain to produce smooth movement of muscles. In Parkinson's patients, 80 percent or more of these dopamine-producing cells are damaged, dead, or otherwise degenerated. This causes the nerve cells to fire wildly, leaving patients unable to control their movements. Symptoms usually show up in one or more of four ways:

tremor, or trembling in hands, arms, legs, jaw, and face
rigidity, or stiffness of limbs and trunk
bradykinesia, or slowness of movement
postural instability or impaired balance and coordination.
This diagram of the brain shows several structures related to Parkinson's disease. Basal ganglia affect normal movement and walking; substantia nigra are types of basal ganglia that produce the neurotransmitter dopamine, which sends messages that control muscles. The globus pallidus is part of a larger structure connected to the substantia nigra affecting movement, balance and walking. The thalamus serves as a relay station for brain impulses, and the cerebellum affects muscle coordination.
Though full-blown Parkinson's can be crippling or disabling, experts say early symptoms of the disease may be so subtle and gradual that patients sometimes ignore them or attribute them to the effects of aging. At first, patients may feel overly tired, "down in the dumps," or a little shaky. Their speech may become soft and they may become irritable for no reason. Movements may be stiff, unsteady, or unusually slow.

Joe Dulaney says he was in "perfect health" nine years ago when his wife noticed that he had stopped swinging his right arm when he walked. Soon, simple tasks such as brushing his teeth and combing his hair became major ordeals. His right hand was always ice cold and he produced small, jerky letters when he wrote.

Dulaney's doctor diagnosed the problem as arthritis and prescribed drugs to treat it. But symptoms worsened. Dulaney's voice dwindled to a slight whisper. Leg cramps, dry mouth, severe constipation, itchy eyes, and trouble turning over in bed tormented him. "My wrists were rigid and my fingers were not flexible, so I couldn't even button my shirt," he says. Still, another doctor seconded the arthritis diagnosis and prescribed different drugs.

Finally fed up because his deteriorating condition prevented him from doing simple tasks such as turning newspaper pages, putting money in his wallet, and replacing a light bulb, Dulaney checked himself into a local hospital, arriving in such a weakened state he couldn't walk.

Though a Parkinson's diagnosis rarely comes quickly, the three doctors who examined Dulaney at the hospital agreed within minutes that his classic symptoms indicated Parkinson's. The doctors gave him the Parkinson's drug levodopa, marketed as Larodopa and in generic forms, and the effect was nearly immediate.

"In one hour or so I was walking the halls. I took a shower by myself and did one push-up to show off," says Dulaney. It was, for the moment, as if the disease had somehow vanished. But Dulaney says he soon became "fully aware" that because Parkinson's is progressive, he could manage some symptoms with drugs, but the disease wasn't about to go away.

by John Henkel

symptoms of parkinsons disease : New Treatments Slow Onslaught of Symptoms

Joe Dulaney calls himself the Backward Man.

Although the tag is lighthearted, the awkward and dangerous dilemma he often faces as his lower limbs simply lock in mid-stride is not. At these moments, his body halts abruptly like a movie freeze-frame, and the only way he can walk is to step backward.

"I've gotten to where I can move pretty fast in reverse," says Illinois resident Dulaney, 65, whose finessed footwork helps him cope with one of many symptoms of Parkinson's disease.

Nationwide, as many as 1.5 million people suffer from Parkinson's, according to the Parkinson's Disease Foundation. A chronic and progressive disorder, Parkinson's strikes slightly more men than women and more whites than blacks in the United States. Though the disease is found most often in patients over 50, as many as 10 percent of patients--afflicted with the so-called "young-onset" Parkinson's--are under 40. About 50,000 Americans are diagnosed with Parkinson's yearly, according to the National Institute of Neurological Disorders and Stroke, which estimates that the total cost of health care for Parkinson's patients will exceed $5.6 billion this year.

The Food and Drug Administration has approved nearly a dozen drugs for treating Parkinson's, three of which have been put on the market just in the past year. Also approved in 1997 was a device that is surgically implanted in the brain to lessen the violent shaking experienced by some Parkinson's patients. The 1996 discovery of a gene believed responsible for a form of Parkinson's may result in future innovative treatments. Despite the range of therapies available to ease the disease's debilitating symptoms, however, treatments now on the market can neither replace the faulty nerve cells that cause the disease nor stop Parkinson's from progressing.

Numerous public figures have acknowledged their battle with Parkinson's. Attorney General Janet Reno, evangelist Billy Graham, former boxer Muhammad Ali, and former Alabama governor George Wallace all are fighting the disease. Chinese leader Deng Xiaoping was in the late stages of Parkinson's when he died last year at age 92.

Parkinson's also gained attention last year with passage of the Morris K. Udall Parkinson's Research Act, which authorized $100 million for Parkinson's research. At press time, the funds had not yet been appropriated. Udall, who has Parkinson's, served in the House of Representatives for 30 years.

by John Henkel

symptoms of parkinsons disease : HOW IS PARKINSON'S DISEASE DIAGNOSED?

Parkinson's disease is usually diagnosed by a neurologist who can evaluate symptoms and their severity. There is no test that can clearly identify the disease. Sometimes people with suspected Parkinson's disease are given anti-Parkinson's drugs to see if they respond. Other tests, such as brain scans, can help doctors decide if a patient has true Parkinson's disease or some other disorder that resembles it. Microscopic brain structures called Lewy bodies, which can be seen only during an autopsy, are regarded as a hallmark of classical Parkinson's. Autopsies have uncovered Lewy bodies in a surprising number of older persons without diagnosed Parkinson's -- 8% of people over 50, almost 13% of people over 70, and almost 16% of those over 80, according to one study. As a result, some experts believe Parkinson's disease is something of an "iceberg; phenomenon," lurking undetected in as many as 20 people for each known Parkinson's patient. A few researchers contend that almost everyone would develop Parkinson's eventually if they lived long enough.

WHAT TREATMENTS ARE AVAILABLE?

There is no cure for Parkinson's disease. Many patients are only mildly affected and need no treatment for several years after the initial diagnosis. When symptoms grow severe, doctors usually prescribe levodopa (L-dopa), which helps replace the brain's dopamine. Sometimes doctors prescribe other drugs that affect dopamine levels in the brain. In patients who are very severely affected, a kind of brain surgery known as pallidotomy has reportedly been effective in reducing symptoms. Another kind of brain surgery, in which healthy dopamine-producing tissue is transplanted into the brain, is also being tested. Finally, researchers are trying to identify substances that will prevent dopamine-producing brain cells from dying.


NINDS health-related material is provided for information purposes only and does not necessarily represent endorsement by or an official position of the National Institute of Neurological Disorders and Stroke or any other Federal agency. Advice on the treatment or care of an individual patient should be obtained through consultation with a physician who has examined that patient or is familiar with that patient's medical history.

All NINDS-prepared information is in the public domain and may be freely copied. Credit to the NINDS or the NIH is appreciated.

National Institute of Neurological Disorders and Stroke

symptoms of parkinsons disease : Study Shows Impact of Parkinson's Gene

Researchers report that inheriting even one copy of a mutated gene known to cause Parkinson's disease might trigger early symptoms.

The parkin gene -- already known to hasten the age at which Parkinson's symptoms appear -- was previously linked to early-onset Parkinson's when two copies of the mutant gene were copied. This new study, conducted by a research team at Massachusetts General Hospital, shows that the risk increases with even one copy of the aberrant gene.

"This is the first time anyone has shown that a single parkin mutation can lower the age of onset," study author James Gusella, director of the MGH Center for Human Genetic Research, said in a prepared statement. "We don't know if that would be sufficient to cause the disease. It's more likely that these mutations increase susceptibility to other factors underlying the development of Parkinson's. The result also lets us know that future researchers shouldn't just study the effects of completely knocking out the parkin gene -- we'll need to examine knocking out a single copy as well."

The finding appears in the June issue of the Archives of Neurology.

The research team wanted to evaluate which genes are responsible for the hereditary forms of Parkinson's disease. To do so, they studied 329 families with at least two cases of Parkinson's per family from across North America, Europe and Australia.

Two types of families were studied from this group: those with siblings who have the same versions of the chromosome 6 region (where the parkin gene is found); and those with one family member whose symptoms appeared before age 54. Early onset for Parkinson's is defined as symptoms before age 50.

Patients in each family with the earliest symptoms underwent genetic screening to search for parkin mutations. If the screen was positive, the other family members with Parkinson's were also screened. Of the 183 families in this section of the study, 23 families had parkin mutations, 13 of which had at least one family member who had two mutated copies of the gene. Ten of the families had only one mutated copy of the parkin gene.

Of the population of families with parkin mutations, 43 was the average age at which symptoms began to appear. Onset began at an average age of 61 in families with identical chromosomal markers and no mutations, and about age 50 in families with one parkin gene mutation. Patients with two mutated copies of the parkin gene experienced onset at an average age of 36.

"This study reinforces the fact that there are multiple mechanisms behind Parkinson's disease, and will lead us to examine other pathways with which parkin interacts," Gusella said.


By Diana Kohnle

symptoms of parkinsons disease : Pesticides Could Raise Parkinson's Risk

Exposure to pesticides, but not other environmental contaminants, may boost the long-term risk for developing Parkinson's disease by 70 percent, a new study suggests.

The researchers did not assess the length, frequency, or strength of pesticide exposure, and they stressed that the absolute risk of developing Parkinson's remains relatively small.

However, their finding does back up earlier animal studies linking pesticide exposure to motor function abnormalities and lower levels of the brain neurotransmitter dopamine. Declines in dopamine have long been associated with Parkinson's.

"This is the first large human study that shows that exposure to pesticide is associated with a higher incidence of Parkinson's," said study lead author Dr. Alberto Ascherio, associate professor of nutrition and epidemiology at the Harvard School of Public Health in Boston.

"It is, of course, a relative increase," emphasized Ascherio. "So, whereas normally the lifetime risk for developing Parkinson's is three percent, pesticide exposure will bring the risk to five percent."

Ascherio and his colleagues discussed their work in the July issue of the Annals of Neurology.

The authors reviewed lifestyle surveys completed in both 1982 and in 2001 by over 143,000 participants in the U.S. "Cancer Prevention Study II Nutrition Cohort," launched in 1982.

In addition to pesticide exposure, participants were asked about exposure to a host of chemicals and dusts, such as: asbestos, acids, solvents, coal and stone dust, coal tar, asphalt, diesel engine exhaust, dyes, formaldehyde, gasoline exhaust, herbicides, textile fibers, wood dust, and x-ray or radioactive materials. Nearly all the patients were white, with an average age just of over 60.

The researchers studied 413 participants who were diagnosed with Parkinson's disease.

The surveys revealed that just over eight percent of the men and just over three percent of the women reported exposure to pesticides.

Exposed patients were twice as likely to be blue-collar workers and 14 times more likely to work as either a farmer, rancher, or fisherman.

However, no differences were found in terms of risk increase between patients who experienced exposure because of their work, such as farmers, and those who came into contact with the chemicals because of home or garden use.

The Harvard team found that, regardless of occupation, pesticide exposure boosted long-term Parkinson's risk by 70 percent over the long-term.

Ascherio stressed that although the association found in his study was stronger than any previously documented, more work is needed to pinpoint what exactly it is about pesticides that may help spur Parkinson's.

"The key point would be to identify which chemicals cause Parkinson's," he said. "It's not very practical to tell people to avoid pesticides, because many people find it very useful. So this will require more detailed study," he added.

Robin Elliot, executive director for the Parkinson's Disease Foundation in New York City, described the findings as "important and solid."

"This is certainly the biggest and most serious populations study on people, and it appears to be the best proof today that there is a general association between pesticide and Parkinson's among people," said Elliot. "It merits further investigation," he said.

In a separate smaller study, published in the June issue of Movement Disorders, a team of researchers from the Mayo Clinic in Olmsted County, Minn., found that pesticide exposure seemed to increase Parkinson's risk for men, but not women.

Telephone interviews were conducted with 149 men and women, all local-area Parkinson's patients who developed the illness between 1976 and 1995. The Mayo team also interviewed 129 healthy individuals.

They found that male patients were 2.4 times more likely than healthy individuals to have been exposed to pesticides. No such increased risk was evident among the female patients.

Copyright (c) 2006 ScoutNews LLC. All rights reserved.

symptoms of parkinsons disease : FDA Approves the First Treatment for Dementia of Parkinson’s Disease

The Food and Drug Administration (FDA) today approved Exelon (rivastigmine tartrate) for the treatment of mild to moderate dementia (chronic loss or impairment of intellectual capacity) associated with Parkinson's disease, a disorder of the central nervous system. Exelon was previously approved for the treatment of mild to moderate dementia of the Alzheimer's type.

"It's been recognized for almost a decade that the dementia of patients with Parkinson's disease differs from the dementia of patients with Alzheimer's," said Dr. Steven Galson, Director of FDA's Center for Drug Evaluation and Research, "but until now, there has been no treatment that has been shown to be effective specifically for the dementia associated with Parkinson's Disease. Today's approval of Exelon helps to fill this medical need."

It is estimated that about 0.2 percent to 0.5 percent of people over 65 years of age are affected by Parkinson's dementia and experience such symptoms as impairments in executive function, memory and attention. The approval of Exelon for the treatment of Parkinson's dementia is based on the results of a randomized, placebo-controlled clinical study with 541 patients who showed symptoms of mild to moderate dementia two years or later after their diagnosis for Parkinson's disease. At the end of the 24-week trial, the condition of the Exelon-treated patients, as shown on a scale that measures mental processes, was significantly better than the condition of the patients on placebo.

The use of Exelon has been associated with significant gastrointestinal adverse reactions. In clinical trials, 47 percent of the patients treated with the drug developed nausea, and 26 percent of women and 18 percent of men on high doses of Exelon experienced significant weight loss. Other common adverse events reported by patients on Exelon include vomiting, anorexia, dyspepsia and asthenia (loss of strength). In some patients with Parkinson's disease, treatment with Exelon was associated with a worsening of tremor.

by Novartis Pharmaceutical Corp. in East Hanover, NY.