What if PD doesn't really exist?
 

CTenaLouise raised a question in another thread that might be interesting. In part she said: "what if we really do not have Parkinson's Disease?
what if we have been categorized poorly, by doctors that never use their brains - they read the diagnosis right out of the book -and their technology is stagnant, they never let it grow into a different category, because
they are boxed in thinkers?

what if what we all have is a certain type of toxicity and the big pharmas
are encouraging the doctors not to think, by bribing their neurons to think
in terms of greed..."


Despite my thread title, I would ask "What if PD is something entirely different than we think?" I have a growing feeling that while there is a basic problem based in our physical self, there is also a major problem with our psyche, for want of a beyyer word.

Stress seems to be key to the latter part. Why are we so vulnerable to it? Is it possible that the basic problem induces a fragility in us? A breakdown similar to adrenal fatigue? Something so profound that allows the least little frustration to send us spiralling out of control?

Perhaps PD is some sort of hybrid disorder or something.

how do doctors diagnose individuals?
 

dear rev,

an article:from the National Geographic

it makes you think... ;)

http://news.nationalgeographic.com/n...ll_sounds.html

It would be a great thing!

What if?
 

This thread and the one started by ol'cs "Didn't know" which has diverted from the new patch drug to a general drug impact/side effect discussion raises some massive issues for us.

Firstly look at how many posts "Didn't know" has generated in less than 24 hours!

I am sure there is not one of us here who does not regularly mentally challenge his/her diagnosis.

We all have widely differing combinations of symptoms.
We all take widely differing combinations of PD drugs.
We all have widely differing responses to these drugs.
We all suffer widely differing drug side effects.
We all have widely varying rates and profiles of PD progression.

WHY???

The over simplistic answer is that PD is a complex illness.

Perhaps the more realistic answer is that PD is a generic term in the same way that the term "virus" is used.

There surely is not another disease like it:

Almost impossible to definately diagnose.
Relentless in it's progression.
Indescriminate in its selection of candidates.


It's a pity we all live so far apart and that many of us are so imobile because I am sure reverett123 has a good general point about what we all ought to be able to do together (despite what some of the posts to his thread have said). We are, as he often says, at the mercy of drug companies who primarily exist to generate a financial return for their investors and are also restrained by a mass of other outside factors.

Afterall we do all have one thing in common, we are desperate for a cure or even something to slow the disease progression!!

Not sure if any of that will be of any use to anyone but I feel better to getting it out .........

Chris

Do we really differ that much ...
 

"We all have widely differing combinations of symptoms"

How many of us don't suffer from tremor and/or rigidity and/or bradykinesia and/or impaired balance.

Remember pd is wrongly diagnosed many times.

"We all suffer widely differing drug side effects".

These are strong drugs taken by people of differing ages at different levels of health. My Neuro reckons Paracetemol with its side effects would be difficult to clear the authorities nowadays.

"We all have widely varying rates and profiles of PD progression".

What is new here, every disease does this, thats why we don't all die from Cancer. With pd we all end up pretty much the same.

Nice thoughts, nice thread, but I do believe in PD.

Neil.

yes we do!
 

after fifteen years with PD,
I can on very great days ---- run - can you?
I can jump up and down on a trampoline - can you?
I dare to live outside of what they say - "We can't do"
I can dance - can you?
I can sing?
On all days I try to have peace with all of those I know -do you? ;)
I try anyway - just to see if I can?

somedays - I wonder -if we are dealing with a disease that can be kept in slow mode of progression with certain vitamins and minerals and eating
healthier and not thinking in sick mode all the time?

maybe we are taking bad drugs because some greedy professional goes by the big pharma -book diagnosing rules...

PD does not define me - does it define you dear aftermathman???

Parkinson's Disease ? What Parkinson's Disease ?
 

25% of people "with" Parkinson's Disease are wrongly diagnosed, due either to having a Parkinsonism : , or toxicity :

Those people that are tremor dominant are frequently wrongly diagnosed. They often have Essential Tremor, which has many causes that are nothing to do with Parkinson's Disease.

Even those people that were correctly diagnosed with Parkinson's Disease would now not be considered as having Parkinson's Disease if it was not for the drugs that were prescribed when they were diagnosed as having Parkinson's Disease.

Parkinson's Disease is basically due to not forming sufficient dopamine. However, the amount of dopamine that somebody produces is changing all the time, which is why symptoms can fluctuate so much. Millions of people that are never diagnosed with Parkinson's Disease will have low dopamine levels at some time, but not for long enough in order to get a diagnosis.

If somebody has low dopamine for just a few months they can be diagnosed with Parkinson's Disease. They will usually end up on L-dopa or a dopamine agonist at some point. However, due to a process called feedback inhibition, no common substance actually lowers somebodys own L-dopa formation than L-dopa itself. Although dopamine agonists initially stimulate dopamine receptors, their long term effect is to make the dopamine receptors progressively less receptive. This is why people tend to need higher and higher dosages, and more and more drugs, until they end up having hardly any effect.

So if somebody has low dopamine for a few months they will get a diagnosis and then be put on drugs which themselves will end up causing Parkinson's Disease, due to how the body reacts against them. Their problem ends up not being Parkinson's Disease at all, but the drugs that they have been given to relieve the Parkinson's Disease.

That's no problem for the pharmaceutical companies. At over a billion dollars a year, a downward spiral in symptoms, due to the drugs that they themselves have produced means that they have customers for years or decades that have ever increasing need for their products.

Daffy ...
 

I read that we need to cut dopa production by 80% to display symptoms of PD. Have you seen such a reduction expressed as a temporary condition from which the patient recovered naturally ??? (the pope's miracle doesn't count :) ).

If so over what timeframe did this occur ?

Neil.

p.s. Tena, you really don't want to see my dancing.

Dopamine levels
 

Some further thoughts on PD as a "hybrid" condition
 

Thinking out loud...

Some aspects of PD are a common element amongst ourselves and even with "normal" folks. The damage to the SN is an example. The conventional wisdom is that we all have it. The CW also is that a normal who develops such damage will develop PD.

Some aspects are a common element with other conditions. There is an element of neuropathy, for example, that we share with diabetics. This neuropathy and other problems worsen with time, as does the movement element. So PD is an ongoing process. It doesn't seem to stop.

When does it begin? There are reports of children with PD. Polls on this forum have shown that half of us remember constipation - a PD related factor - as being a big deal in our childhood.

Our reaction to stress, however, is near unique. Is there any other disease where the simplest of stressors quickly renders one helpless? If this response is indeed unique, isn't it sensible to think there may be a key there?

I like your thinking, Tena.
 

I don't think Parkinson's is a disease at all.

My best guess is that it's essentially a structural problem (musculoskeletal, soft tissue - fascia?) that creates an over the top demand for dopamine - and we just can't keep up with the demand.

Along that line, I'd like to ask how many of us experienced Frozen Shoulder prior to PD symptoms? I did - and evidently so have many others. http://jnnp.bmj.com/cgi/content/abstract/52/1/63 Mine seemed to gradually resolve....but what if there are still problems originating in that area?

Last summer I was doing quite well and then a minor (?) slip-bump threw me WAY back to the worst symptom days. Overnight I almost couldn't walk...and continue to decline. I feel it in my left -once frozen - shoulder. Maybe there is scar tissue in there that's disturbing, interrupting, blocking something?

Scoliosis also seems to be a PD feature. HOw many of us have that? I do...just slightly - but I can tell it's worsening. Supposedly it's due to an unstable pelvis.

Maybe this should be a new thread...?:wink:

Ibby

Wyoming doesn't exist
 

My Opinion:
 

The brain model that is used to explain movement is in serious need of updating. To view the brain as being housed only in the head confines us to an illogical acceptance of the presentation of Parkinson's disease as well as other neurological diseases. In order for the Parkinson's model to work and make any sense, it would mean that the brain MUST be present throughout the entire body. If that is not the case, then Parkinson's disease is NOT a brain disease at all. That is not to say that the "brain" is not affected, but it is to say that the "brain" is but one area that is affected by a much more widespread intruder.

What is affected? Our ability to move, smell, speak, hear correctly, breathe correctly, peristalsis and proper bowel function, etc. are among the affecterd areas. The only neurological entity that I can find that is proximal to and influences the functioning of all these areas of the body is the Vagus Nerve. When this nerve becomes inflamed acetylcholine production is overstimulated which creates a problem in afferent and efferent nerve impulses that allow proper extension and contraction in muscle tissue. Attempting to explain all of these varied symptoms by using our current brain model just does not work.

michael b.

I'm on the
 

"What the heck is this anyway" team....Parkinson's the name is just that, -someones last name. Everything about is highly subjective, and the mental processes (our thoughts) have a huge effect on our day (and night). If there is an actual Parkinson's disease it is located right where our thoughts walk out of the gate of our cerebral abstracts factory and into the grey matter of our actual brain. That's one reason we all wonder if we are just losing our minds. The drugs we take mess with everything about us and can contribute as much as they can confuse and betray. I've said this before...but it has always been notable to me that the two "types" of PD manifest themselves in two common expressions we use to describe fear: shaking in our boots or scared stiff. Fear is certainly one of the underpinings of PD.

A little off topic but I had a moment of revelation yesterday when I was talking to my Neurologist. We were discussing some changes to my med routine and I referred to the regular sinemet as "the yellow pills". He paused for a moment and said "what do you mean 'yellow pills'?" I said "you know, the regular sinemet...the pills are yellow..." It occurred to me later that he did not know they are yellow because he never sees them, just writes the prescriptions! (just had to share:eek: )

This thread could give someone a headache ( a neurological problem also). But the short of it is, I'm with Rick on this one.

Some "inconvenient truths"
 

According to the work of German researcher Braak, the holy substantia nigra is the LAST part of the CNS to be affected. The first is the olfactory bulb closely followed by the myenteric plexus in the wall of the stomach. One of our first losses is our sense of smell. The usual dopamine explanation does not account for this.

The GI tract has a prominent role in PD. Everything from gastric emptying to constipation and some of it shows up before anything else. According to Michael Gershon, MD, author of "The Second Brain" the enteric nervous system rivals the spinal cord in complexity, operates independently of the brain, is connected to the brain by only a few thousand fibers of the vagus nerve, functions quite well if the vagus is severed, overrules the brain when appropriate, and produces a huge amount of neurotransmitters. Among other things.

Finally, it is interesting to contemplate the historical role of PD. We are all the time reading that forensic historians have determined that Flavius Floovius had an infected roobius leading to deadly impetion deficiency. Given the distinctive symptoms of PD, doesn't it seem odd that there is so little historical evidence for it? The first written description in the West was James Parkinson's in 1817. JP was a London physician for 40 to 50 years. He wrote many works besides "The Shaking Palsy" and was a keen observer. Yet he was only able to draw on SIX cases of PD for his paper and three of those were people he passed on the street and never saw again! Think about that. He lived in the crowded city of London for decades, was keenly watching people he passed, and felt that PD was interesting enough to write about. Yet he could only come up with three cases. Folks, PD didn't really exist before then.

In 1817, London was not a nice place to live. The Industrial Revolution was in full swing. Coal fired it and London's air reflected that. Killer smogs and so on. Soot in the air. Interesting stuff, soot and similar particulate matter. You breath it in. It sticks to your sinus mucosa and finds its way into your GI tract. What does it do there? Among other things, it not only easily penetrates the wall of the GI tract, it acts like a tiny sponge and carries toxins such as LPS into the body.

There are two non-western mentions of PD-like symptoms prior to 1817. One is the ancient Indus Valley works handed down in India and the other is China about 500 BC. What do they have in common with London 1817? The Indus Valley had an advanced copper smelting industry and we still admire the great bronzes of that Chinese period.

Coal fires
 

Parkinson's Disease has always existed. Besides being known in Ancient China and India, Parkinson's Disease was also known in Ancient Greece. Virtually all civilisations have practiced smelting for for thousands of years. These civilisations were not exceptional in this respect. The observance and treatment of Parkinson's Disease also took place in parts of these civilisations that did not practice smelting. Smelting would not explain its occurence there.

History of Parkinsons's Disease :

At the time of James Parkinson in 1817, London was a small city. His observations of six cases took place only in Shoreditch, which is only a very small part of London. So to come up with six cases in Shoreditch alone is actually quite a lot rather than evidence than so few people in London at the time had Parkinson's Disease.

The use of coal fires in London continued from his time until the 1960's, with all the accompanying dense fogs and smogs. In the 1970's there was a massive and rapid reduction in the use of coal fires in London. The use of coal fires went from the norm to being virtually eliminated. If the effects of coal fires were the cause of Parkinson's Disease in London, the prevalence of Parkinson's Disease amongst Londoners would have massively reduced in the 1970's. However, the prevalence of Parkinson's Disease hasn't stopped increasing since the use of coal fires was virtaully eliminated.

dear neil ~
 

dear neil,
:Funny-Post:
wanna bet! love to see you dance! :)

all of us oldies like ole cs, and paula, and peggy, and me and gregw and his wife annw - we promised one another long ago that we are going to meet at the Parkie Dance, when we are well - so we extend the invitations out to you all!!
*smile

thank you!!
 

12.18.2006
Can Coal Come Clean?
How to survive the return of the world's dirtiest fossil fuel.
by Tim Folger


On a steamy, torpid summer morning in Florida, the Polk power plant is performing a small feat of modern alchemy. Every hour it converts 100 tons of the dirtiest fuel on the planet—coal—into 250 million watts of power for about 56,000 homes and businesses around Tampa. The alchemy part? Vernon Shorter, a tall, bluff consultant for the Tampa Electric Company (TECO), points to a looming smokestack. "Look at the top of that stack," he shouts over the cacophony of generators and coal-grinding machines. "That is the main emissions source. You can't see anything. You don't even see a heat plume."

He's right. No smoke mars the lazy blue Florida sky. The Polk plant captures all its fly ash, 98 percent of its sulfur—which causes acid rain—and nearly all its nitrogen oxides, the main component of the brown haze that hangs over many cities. Built to demonstrate the feasibility of a new way to wring economical power from coal without belching assorted toxins into the air, the $600 million plant has been running steadily since 1996. "It makes the lowest-cost electricity on TECO's grid," Shorter says. "It also has very, very low emissions. Particulate matter is almost undetectable."

What is both distressing and remarkable about the Polk plant is that it could do much more. "There's no requirement for mercury capture, but 95 percent of it could be captured very easily," Shorter adds. More important, the plant could also capture nearly all of coal's most elusive and potentially disastrous emissions: carbon dioxide, the main gas that drives global warming.

That capability could prove vital. With oil and natural gas prices rising rapidly and nuclear power stuck in political limbo, the world's appetite for coal is soaring. In the United States, the Department of Energy estimates that 153 new coal-fired power plants will be built by 2025. Meanwhile, China and India, the world's second and third largest coal producers, are embarking on a coal power plant building spree. China alone is expected to construct 562 new coal-fired plants over the next eight years. Since the life span of a typical coal-fired plant is 50 years, coal's share of the world's energy production will rival oil's for most of the century.

http://discovermagazine.com/2006/dec...oal-technology

PS: I live about an hour from one of these coal /electricity plants... hmmm... :D

more damage is done to the brain than substantia nigra
 

I was told by a famous neurosurgeon more damage is done to the brain than just the substantia nigra...

I was told as people aged - it was fairly normal for the black matter -aka substantia nigra to loose pigmantation?

what about the
Neuropsychological correlates of amygdala activity
Early research on primates provided explanations as to the functions of the amygdala, as well as a basis for further research. As early as 1888, rhesus monkeys with a lesioned temporal cortex (including the amygdala) were observed to have significant social and emotional deficits.[4] Heinrich Klüver and Paul Bucy later expanded upon this same observation by showing that large lesions to the anterior temporal lobe produced noticable changes, including overreaction to all objects, hypoemotionality, loss of fear, hypersexuality, hyperorality. Some monkeys also displayed an inability to recognize familiar objects and would approach animate and inanimate objects indiscriminately, exhibiting a loss of fear towards the experimenters. This behavior disorder was later named Klüver-Bucy syndrome accordingly.[5] Later studies served to focus on the amygdala specifically, as the temporal cortex encompasses a broad set of brain structures, making it difficult to find which ones specifically may have correlated with certain symptoms. Monkey mothers who had amygdala damage showed a reduction in maternal behaviors towards their infants, oftentimes physically abusing or neglecting them.[6] In 1981, researchers found that selective radio frequency lesions of the whole amygdala caused Klüver-Bucy Syndrome.[7]

Studies on the amygdala in the human brain have produced similar findings. In 2006, researchers observed hyperactivity in the amygdala when patients were shown threatening faces or confronted with frightening situations, and that patients with more severe social phobia showed a correlation with the increased response in the amygdala. Recently, researchers have paid close attention to the amygdala, as its hyperactivity has been shown to have a role in certain anxiety disorders.[8]

Two preliminary small-scale studies also have linked lower neuron density in the amygdala with autism, though it's unclear whether this is a cause or an effect of the condition. [9]

look up amygdala at www.answers.com

For a parkie who has devoted his entire life with PD to studying the connection between stress or childhood trauma and PD: (he even just completed a Ph.D. on such a thesis):
Psychological aspects of Parkinson's disease

http://www.parkinsonforum.com/enterforum.htm

I know for sure I have Parkin Disease
 

I have had an FDOPA PET scan in New York Mount Zion hospital, considered along with UCLA as haveing the most releable results. Mine came back as moderately advanced.

Not enough to convince you? I have also had a commercial company check my Parkin2 gene for mutations. I have two. I also have a sister diagnosed with PD.

In Europe I would be diagnosed as having Parkin disease because of my genetic mutations. I agree that their are several different reasons we have all been diagnosed with Parkinson's. Although all of you may have idiopathic Parkinson's disease, you still have PD. Somewhere along the line you and I were exposed to something that caused the dopamine neurons to stop producing, or to overproduce causing them to self destruct because protein chain tangles (alpha-synuclein) have blocked the dopamine from traveling down the delivery system. Few of us were exposed at exactly the same time or even by the exact reason for the protein tangles. We are all in different stages of the illness, and may have been exposed to a toxin in different amounts, explaining the rapid or slow growth of symptoms.

Is there a disease called Parkinson's disease? Absolutely. Do we know the etiology of the disease, absolutely not. But if research starts focising on the etiology of the disease we have a positive change of finding the cure. When we stop chasing unproven theories, and stabs in the dark in an attempt to accidentally happen upon the cure the chances are slight and the expence is not worth it. Research requires a clear understanding of what causes a disease to find a cure. The chances of accidentally finding the cure is remote.

Vicky

A scholarly disagreement
 

Daffy-

As to whether or not PD has always existed, we come back to the question of what is PD and what is its prevalence. If we slice the definition too finely, then everyone on here who has PD has different disease. If we slice it too broadly then everyone, including yourself, has it. That lends itself to a view of PD as a spectrum disorder with symptoms varying within the group.

That is the situation James Parkinson faced. A cloud of symptoms broadly labeled "Palsy". He defined the specific collection he was discussing as follows:

"Involuntary tremulous motion, with lessened
muscular power, in parts not in action and even
when supported; with a propensity to bend the
trunk forwards, and to pass from a walking to a
running pace: the senses and intellects being un-
injured."

He then went on to point out that tremor per se had been discussed by others such as Galen. He did not feel that Galen was discussing PD but rather that he was one of several who had discussed tremor.

"The term Shaking Palsy has been vaguely employed
by medical writers in general. By some it has been used
to designate ordinary cases of Palsy, in which some
slight tremblings have occurred; whilst by others it has
been applied to certain anomalous affections, not be-
longing to Palsy.

The shaking of the limbs belonging to this disease was
particularly noticed, as will be seen when treating of the
symptoms, by Galen, who marked its peculiar character
by an appropriate term. The same symptom, it will also
be seen, was accurately treated of by Sylvius de la Boe¨.

Parkinson's whole point was that while others had written about similar conditions, he had noted something a little different. In a scholarly fashion he goes on to mention others in a similar context, but he still felt that his observations were worth writing a pamphlet and not a historical tract.

As for the smelting reference, the two cultures mentioned stand out in this regard and are noted by scholars as something special about each. If soot in the air is important in PD, then the lowly peasent fire would have indeed been a source but that would have gone up a magnitude in the charcoal maker's life and again at the smlter. As for the lessening of coal fires, the relevant point here is particulate matter from a number of sources- auto exhaust and diesel in particular but even house dust has a role.

As for London's population at the time, it was 1,000,000 strong according to http://www.londononline.co.uk/factfile/historical/
and growing rapidly, hardly "a small city."

The original tract can be read at http://neuro.psychiatryonline.org/cg.../full/14/2/222
and in the intro, the authors add the following:

"James Parkinson (1755–1824) is considered the father of modern paleontology and a pioneer in geology, pediatrics, child welfare, and physical chemistry.1 However, in our field, he is best known for the disorder that bears his name. Parkinson's disease is a prototypical neuropsychiatric disorder that affects multiple systems regulating motor function, mood, perception, and cognition.2 Parkinson's original description of the disorder, reprinted here, was published in 1817 as a short monograph in London.3

Parkinson was an astute observer whose report contains observations from three patients he saw in his clinic as well as three individuals he observed on city streets. Much of the description of the longitudinal course of the illness was derived from his observations of a single case (Case I). His original report has clear descriptions of resting tremor, rigidity, and disturbances in gait and posture. He speculated that the pathology of the disorder would be localized to the medulla. He appealed for future anatomic studies to examine the neural substrate of the disorder.

For fifty years after publication, there was little attention paid to this report.4 In 1861, Charcot and colleagues at the Salpêtrière further distinguished the disorder from other neurologic disorders and were first to use the term "Parkinson's disease."5"

So, after 60 years in a city of a million, he is moved to write. The malady is so rare as to not attract attention again for forty more years. Like all things about this damned beast, it isn't a simple matter.

Is George W.Bush really Bulgarian ?
 

London was only 8% of its present size in James Parkinson's time. James Parkinson didn't carry out his assessment in the whole of London either. He did it solely in Shoreditch. Shoreditch is the size of a village. I've walked through Shoreditch in less than ten minutes. So six people, not in Shoreditch, but just from his window in Shoreditch is quite a lot of people with Parkinson's Disease.

The continuous increase in the prevalence of Parkinson's Disease despite the sudden ridding of coal fires in London in the 1970's is completely inconsistent with the claim that, pollution, smog and coal fires caused Parkinson's Disease. Up until that time, respiratory disorders were rampant, but Parkinson's Disease wasn't.

As to what is Parkinson's Disease is, is a simple question. It is a dopaminergic deficiency (or more precisely when dopaminergic activity is less than cholinergic activity).

There is not one group of people with Parkinson's Disease and those without. Due to how dopaminergic activity fluctuates so much, they all merge together, with somebody "with" Parkinson's Disease at times having lesser symptoms, and those people supposedly "without" Parkinson's Disease having symptoms that are no different from those of Parkinson's Disease.

As to what causes Parkinson's Disease is not really in doubt either. Virtually all medical disorders can be caused by either toxicity, infection (viral, bacterial, fungal), drugs, genetics, physical injury, or insufficent function - not one or the other, but by potentialy all of them.

Causes of Parkinson's Disease :What people get wrong is what proportion of cases are caused by each. Many people stress toxicity as THE cause of Parkinson's Disease. For some people it is, but there is no evidence that any more than a small proportion of people with PD have PD due to toxicity.

I must hand it to you, ...
 

...you don't give up.
First, to argue that London was "only 8% of its present size" is silly. A million people is a million people.

Second, I will assume that you have some source as to how Parkinson limited his search to this village. That is rather irrelevant since it lies almost in the center of London today and at the time involved was a major industrial center for textiles and furniture. In short, a large part of London would have come to Parkinson.

Third, your statement "As to what is Parkinson's Disease is, is a simple question." Please see the Lanston post that follows in this thread.


Finally, the role of particulate matter is perhaps outside your area of study. One suggested report:
1: Inhal Toxicol. 2005 Apr;17(4-5):235-41.

Effects of subchronic exposures to concentrated ambient particles. VII.
Degeneration of dopaminergic neurons in Apo E-/- mice.

Veronesi B, Makwana O, Pooler M, Chen LC.

National Health and Environmental Effects Research Laboratory, Neurotoxicology
Division, U.S. Environmental Protection Agency, Research Triangle Park, North
Carolina 27711, USA. veronesi.bellina@epamail.epa.gov

This study reports that subchronic exposure of Tuxedo, NY concentrated ambient
particulates (CAPs) produces neuropathological damage in the brains of Apo
E-deficient mice (Apo E-/-). These genetically modified mice are characterized
by elevated levels of oxidative stress (OS) in the brain. Microscopic
examination of coronal sections of the brain, immunocytochemically stained for
dopamineric neurons, indicated that neurons from the substantia nigral nucleus
compacta were significantly reduced by 29% in CAPs-exposed Apo E-/- mice
relative to air-exposed Apo E-/- controls. In addition, statistically
significant increases (p < .05) in immunocytochemically stained astrocytes were
noted. The dopaminergic neurons of the nucleus compact are specifically targeted
in Parkinson's disease. The present study expands the systems affected by
particulate matter to include the brain, and supports an environmental role for
the development of neurodegeneration in OS-susceptible individuals.

PMID: 15804941 [PubMed - indexed for MEDLINE]

one very important paper
 

Fall 2006 Newsletter of NPF

PD: More than a Movement Disorder
J. William Langston, M.D.

What exactly is Parkinson's disease?

How we answer this question is not just a game of definitions, nor is it getting easier. But finding the answer is important because how we define Parkinson's is likely to be the difference between success and failure as we look for clues to the cause(s) and for ways to combat it.

James Parkinson, the English physician who first defined the condition clinically almost two centuries ago, called it the "shaking palsy." More than a century and a half later, neurologists began to define it as one of several "movement disorders," characterized by the classic triad of rigidity and slowness of movement, as well as the "shaking," or tremor, that had long been associated with Parkinson's.

The focus on these motor symptoms and signs was dramatically sharpened in the 1960s by the discovery that they were due to a loss of dopamine-producing cells in the brain that make up an area known as the "nigrostriatal system" and that these motor symptoms could be improved by administration of the dopamine precursor L-dopa. Yet even at the time of this breakthrough, doctors were becoming increasingly aware that their Parkinson's patients were showing up in their offices with other symptoms - among them, such diverse complaints as fatigue, constipation, depression and even diminished ability to smell - that seemed to be as different from one another as they all were from the physical-movement symptoms that had served for so long as the defining characteristics of PD. Indeed, these motor symptoms have become so ingrained in the medical lexicon that we now call them "parkinsonism."

What does this mean for our understanding and management of Parkinson's? I believe it means that we have been defining Parkinson's too narrowly, and by so doing, have been restricting our investigations too much upon one part of the brain - the dopamine-producing nigrostriatal system - at the expense of other crucial areas of investigation. Put bluntly, it is increasingly clear that "parkinsonism" - the motor aspects of Parkinson's - is only one characteristic of what is increasingly becoming seen as a multifaceted and complex disorder. No person who lives with Parkinson's (PWP) needs to be told this. It is their reports as much as anything else that have been prodding Parkinson's specialists and researchers to look beyond their natural "turf" - the dopamine-producing nigrostriatal system - to examine other areas of the brain and body.

So how, in light of this broader and more complex clinical evidence, do we go about re-examining the scientific theory of Parkinson's? One good place to start is with the German scientist F.H. Lewy, who identified a distinctive type of matter in the brains of people who die with Parkinson's called the Lewy body. The presence of Lewy bodies in the brain has long been considered the pathological hallmark of Parkinson's disease.

What is less widely recognized is that Lewy described these bodies not in the nigrostriatal dopamine system, but in other areas of the brain. Also, they have since been found in other parts of the body, including collections of nerve cells that lie just outside the spinal cord (known as sympathetic ganglia) and the wall of the gut. In fact, it seems increasingly likely that Parkinson's does not begin in the nigrostriatal system, but possibly in the lower brainstem and the olfactory bulb (the part that controls ability to smell) or even the nerves in the heart and intestinal tract ... and that only at a later stage of the disease does it begin to affect the nigrostriatal system.

It is also becoming apparent that many of these changes outside the nigrostriatal system cause non-motor clinical symptoms that often predate the motor symptoms of Parkinson's. These are therefore often considered "predictors," or "biomarkers," of Parkinson's. I would argue that calling them "predictors" misses the point. The evidence is increasing that they are not just advance warnings of Parkinson's but are actually part of the condition itself.

Take, for example, rapid-eye-movement sleep behavioral disorder (RBD) which is characterized by agitation and physical activity during sleep. It turns out that nearly 40 percent of men diagnosed with RBD develop Parkinson's later in life - on average, 13 years later. In these cases, RBD is almost certainly Parkinson's disease in the lower brainstem, before it has affected the nigrostriatal system and caused parkinsonism. Among people who already have been diagnosed with PD, 50 to 60 percent exhibit physiological evidence of the disorder, indicating that RBD is a common (though not universal) clinical sign of people with diagnosed Parkinson's.

Or take the issue of olfactory function (sense of smell). There is now literature suggesting loss of smell as an early sign of Parkinson's, with some studies showing olfactory abnormalities in up to 100 percent of people with Parkinson's. The German neuroanatomist H. Braak has observed that the olfactory sense is one of the first areas of the central nervous system to be affected by Parkinson's and should therefore be a part of a multifaceted diagnostic battery to detect "pre-parkinsonian" PD.

Another area of scientific interest is autonomic dysfunction - that is, problems with bodily functions over which we have no conscious control, such as the beating of the heart, sweating or bowel function. Several studies have shown that most, if not all, people with Parkinson's experience a loss of one component of the autonomic innervation of the heart (this phenomenon is known as sympathetic cardiac denervation). One could speculate indeed that fatigue, one of the most common complaints among people with Parkinson's, might be traced to diminished heart function.

Then there is the matter of constipation, another very frequent complaint among people with Parkinson's. First noticed by the eagle-eyed Dr. Parkinson, this problem was traditionally attributed to lack of activity, or inadequate hydration, or both. Then, in the late 1980s, scientists noticed the presence of Lewy bodies in the autonomic nervous system of the lower bowel, as well as in the esophagus. This suggests that swallowing, lower bowel and even bladder dysfunction are direct manifestations of the pathological process that underlies Parkinson's, and in fact may be one of the earliest features.

Lending support to this hypothesis is a surprising finding from the famous Honolulu Heart Program, a long-term study of 8,000 Japanese-American men born in the early years of the last century, and who have been followed medically since the 1960s. Unexpectedly, the study showed that men who reported less than one bowel movement per day in midlife were more than four times as likely to develop Parkinson's than men who reported two or more movements per day.

How do we connect the dots among these wide-ranging observations? Increasingly, scientists are looking to do just this. One group has recently explored the link between the RBD syndrome and loss of the sense of smell. Their finding: an astonishing 97 percent of the RBD patients had also experienced loss of olfactory function.

How precisely we proceed from here - what new studies are needed, what symptoms we should be studying, how we can connect the dots among them, whether in fact we need to rename Parkinson's to redirect attention beyond its exclusively motor symptoms - is far from clear, and will require the attention of scientists from a variety of specialties and viewpoints. What is clear is that our concept of Parkinson's must change, perhaps radically.

We need, among other things, to broaden the clinical definition of Parkinson's to include all of the syndromes described in this article along with depression, anxiety and other problems that are commonly reported among people with the condition. This will serve as a constant reminder that we need to look at our patients as more than just victims of a failing nigrostriatal system, and look at a variety of other symptoms and signs - many of which do not traditionally fall within the purview of the neurologist. (This last point, incidentally, suggests that we either need to develop multi-disciplinary teams to treat these patients, or find some way to ensure that the neurologists who care for them seek much more diverse training.)

We also need to recognize that the observations reported in this article have profound implications for the investigation of the causes of PD, suggesting the need for studying mechanisms of neurodegeneration that underlie the entirety of the condition, not just the part that leads to problems with movement. Knowing how the disease evolves from its inception could be hugely important in suggesting clues to its cause. The process will also have implications for efforts to modify and slow disease progression before motor symptoms have emerged. Waiting until motor symptoms are clinically manifest, as we do today, forces us to confine our therapeutic efforts to the advanced stages of PD, when its burden may be too heavy and the options too limited.

I close by noting that none of the new dimensions of PD I have discussed here will be news to Parkinson's scientists. What may be new is that they are coming together in compelling ways and this process in turn is generating a growing interest in addressing them as a group. This will be important for the wellbeing of patients, for the understanding of doctors and for the potential of science to solve the Parkinson's mystery.

Dr. J. William Langston is the founder, CEO and Scientific Director of The Parkinson's Institute in Sunnyvale, CA.

too many words, guys...
 

what about frozen shoulder? did anyone listening in have that before pd set in?

:eek:

Ibken
 

I had frozen shoulder BAD 10 years before I became symptomatic and 12 before I was actually diagnosed. Also, I have developed scoliosis just prior to becoming symptomatic.........and it is getting progressively worse and very painful as time goes on. It is funny that you have brought these two things up. I asked the original neuro I went to about the shoulder and back issues and if they had any relation to PD and he said NO ! I am now under the care of an MDS but have not really discussed these with him. Believe I will next time I have an appointment with him. Thanks for your input here.

Caya

Frozen schoulder
 

Hi Caya & Ibkin,

I have had a frozen left schoulder for 2 years. How do you treat it? The pain is excruciating. Heat, cold and exercise are useless. Help!!

Vicky

Rick, the highest prevalence of Parkinson's Disease in Europe is in the unindustrialised and largely pollution free Faeroe Islands and San Marino.

Prevalence of Parkinson's Disease :They have prevalence rates that are about ten times those of the heavily industrialised and heaviliy polluted South Korea, where Parkinson's Disease is hardly known.

If your theory was correct the exact opposite would be true.

"Who will rid me of this..."
 

1- As to the portrayal of James Parkinson as a simple isolated soul with a small pool of patients:
http://pds.live.poptech.coop/Templat...p?NodeID=98698

2- As to the portrayal of Shoreditch as a suburb of Oz:
http://en.wikipedia.org/wiki/Shoreditch

3- As to the refusal to talk about particulates as a whole and the attempt to limit the discussion to coal alone, those are the tactics of one who has no argument to offer/

With that, I leave this particular stage to the noble *******.:D

Quack Quack
 

Please take it off line
 

Everett123 and Daffyduck,

Please take your argument and put it into private messaging. I really am hoping that someone on this forum can give me help with how to treat frozen shoulder.

IT IS MAKING ME VERY, VERY, CRABBY!!!!!!!!!

My intent is not to create censoring of a lively discussion, only to put the focus back on helping others. Lord knows I have done a fair amount of arguing that has bored members of this forum to tears.

Vicky

Vicky
 

I had frozen shoulder some years back before I was even dx with PD. After ruling out torn rotator cuff and several other things, they did major physical therapy. Took close to 8 months of this therapy to get it somewhat workable again and probably close to 2 years to get it really back to normal. Matter of fact, about twice a year even now, I get the feeling it is trying to get bad on me again at which point I get out the small rubber bands and pole and the exercize diagrams and start doing them all over again for a week or two and that then usually does it for a while. I was told inactivity makes frozen shoulder worse.

Caya

Caya
 

I went through the same thing with a frozen shoulder a year before my dx. It was a mystery - mri showed nothing - then a year of painful physical therapy to 'fix' it.

FROZEN SHOULD...see new thread

debates are very helpful
 

Good idea to move the shoulder posts Carolyn. I need to make one comment and then I'm out of this.

Now it's my turn to say sorry Vicky but I don't agree about taking their argument off the forum. As long as there are no personal attacks or upsetting language, they should have the right to debate till the cows come home.

Wouldn't it be more fair to just not read posts we are not interested in, rather than try to criticize or censor other posters?

respectfully,
paula

Aluminum
 

I don't know if this is relevant but I worked in a plant that coated aluminum coils that were later produced for building materials, eavestrough, siding, etc. for 11 years.

Mind you I worked in the office, but the smell of the paint being baked onto the aluminum was over-powering some days. My eyes would actually water. I was diagnosed with Parkinson's some 14 years after I left.

I then worked for a school board where I was in constant touch with kids, new Canadians, etc. etc.

I moved the post in the best interest of those who suffer from Frozen Shoulders.

I considered the topic important and didn't want it to get lost within this heavy discussion.

p.s. Don't ask Paula what she does in the morning to unlock hers...:eek:...what a site to see :p