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.

Somebody will usually get milder Parkinson's Disease if their dopamine formation is persistently down to less than 25%. In severe cases the dopamine levels can drop below 10%.

The average person without Parkinson's Disease does not have high levels of dopamine. I doubt if the average person is above 50%. There must also be tens or hundreds of millions of people that are borderline, with dopamine levels of 30% to 40%.

In the Rotterdam study, over 6000 people without Parkinson's Disease were assessed for Parkinson's Disease symptoms. Large numbers of them reported Parkinson's Disease symptoms (stiffness, tremors, and imbalance).

So these people's dopamine levels must have temporarily been going below the 25% level, but not persistently enough in order to be diagnosed as having Parkinson's Disease. Many never went on to develop Parkinson's Disease. It was a transient problem for them.

The formation of dopamine is dependent upon the activity of the enzymes involved in dopamine formation. Enzymes are substances that the body produces that enable chemical reactions to take place in the body. The activity of all enzymes is changing continuously according to need and capability. So nobody, not even somebody known to have Parkinson's Disease, will be producing the same amount of dopamine all the time. Levels can go down, but they can also go up.

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?

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.

"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.

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 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 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.

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.