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...?

Ibby

The primary symptoms of Parkinson's Disease are due to excessive muscle contraction.

Acetylcholine increases muscle contraction

Dopamine reduces muscle contraction

Stress increases the formation of adrenaline. Adrenaline increases the formation of acetylcholine. Acetylcholine increases muscle contraction :

Stress >>> adrenaline >>> acetylcholine >>> increased muscle contraction

So it is to be expected that stress can exacerbate Parkinson's Disease.

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.

"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 )

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

The primary fault in Parkinson's Disease is in the dopaminergic neurons in the brain. Nerves connect the brain to muscles all over the body. Muscles are involved in a wide variety of bodily functions, such as respiration and digestion - not just movement.

The dopaminergic neurons are also connected to other parts of the brain such as those affecting the emotions and smell. This is why the symptoms of Parkinson's Disease can be so widespread.

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.

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,

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

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...

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