Well, it just keeps getting more and more interesting...

I seem to recall several people posting here whose tremor was not alleviated by PD drugs. Could it be in essence because all of the research is based on a premise that PD is due to mass death of dopamine neurons? Tossing l-dopa at our brain sure does help alleviate a lot of our symptoms but really it has taken
over 50 years to get here to proving that our little localized brain lesion is so much more?

Although it is very widely claimed that there is a massive loss of the brain cells involved in Parkinson's Disease, not a single piece of research has ever shown this. from that (******* site on all things PD)

Evidence that PD tremor did not stem from loss of dopamine was first published in the 60's by one person, then resurrected in the 80's by two intrepid researchers and now over 20 years later we have a replicating experiment that confirms "ta da" there is no correlation between loss of dopamine upon PET scan and presence of tremor. Absolutely no evidence that tremor is caused by dopamine loss. Along come these guys in 2012:

A role for locus coeruleus in Parkinson tremor

However, researchers studied the the Locus Coereleus (home of Norepinephrine) during an activity and found that intensity of tremor varied by task but frequency remained constant. The LC is where we process stress and where adrenalin is released. This all makes a lot of sense because my tremor has always and still does respond to a beta-blocker. Note: I initially had a diagnosis of ET that lasted five years.

Authors conclude:

The introduction of the LC in the neural network dynamics of parkinsonian tremor might well explain many of its remarkable features. In particular, (1) tremor would appear only in PD subject with no functional damages of the LC; (2) eventually, along with PD progression and a consequent degeneration of LC-NA system, tremor will diminish; (3) tremor will appear during maneuvers that trigger LC activity, above all stress; and (4) PD patients do not manifest tremor during sleep being the LC silent. Finally, given a putative neuroprotective and compensatory activity of LC-NA on its target cells (including the substantia nigra and the striatum), it is tempting to speculate that an intact, or hyperactive, LC-NA system might be responsible for a more benign progression of PD in patients with tremor.

All these pending questions obviously require further studies in the future both by imaging and laboratory techniques. On this track, we hypothesize that parkinsonian tremor might represent the clinical sign of an enhanced LC activity as possible compensatory process over dopaminergic loss.

Everyone that I've ever tested (PD or not) has a tremor. Sometimes it is so mild as to be nearly invisible but it is still there.

A very easy test is to hold a laser pointer in your hand as you would a pencil and aim the beam at a corner of the ceiling. This will allow the adjoining walls and the ceiling to act as a kind of XYZ graphical axis.

I've found that it comes in really handy if I want to quickly see how well my PD meds are working.

Thanks for your post!

Steve

Thanks for a great post.
My experience is the following. In the first 3 years after PD diagnosis I had very mild tremor which did not seem to respond to Sinemet. Later on, tremor increased and remained the main symptom. About 7 years after my diagnosis tremor was responding to sinemet but unfortunately dyskinesia developed as well. So here I am squeezed between the stone and hard thing, with no good options
I can only hope that the present amazing research can lead to more effective drugs.

My most dominant symptom is tremor, which responds to amantadine. I have other characteristic PD symptoms as well, such as slowness of movement and no arm swing, but I have yet to exhibit balance or gait problems. This is 14 years after diagnosis.

I didn't take sinemet for 6 years post dx; only agonists. After they had completely screwed up my life, I started on both sinemet and amantadine. So, now 8 years on sinemet, I for the first time, am experiencing significant "off" times, feeling as if my body is drained of oil until I can pop that c/l pill. Regardless of increasing physical disability, I am loathe to increase dosage of any of my medications (they are minimal) because I fear the (unknown) consequences and damages that might do to my body. I have so far been able to avoid dyskinesia.

This fear stems from the fact that no one can yet tell me, definitively (even though my PD diagnosis came easily and appears to be text book idiomatic tremor dominant PD) that I actually have Parkinson's or that they know what Parkinson's is. All they can say is, "take this pill and you will feel better, but we don't know why." Nor am I about to let anyone drill into my brain to make my hands stop shaking.

That's why I have put my faith in MJFF because they are the only ones who can look me in the face and say, without snicker or smile, "We don't know. But we are looking everywhere." The one statement, made last year by MJFF CEO Todd Sherer, that makes me hopeful is "What we do know, is that it is much more than dopamine." It almost made me cry with relief - no snark or irony, and there wasn't any from Todd, either.

It's taken me a decade's worth of harassing scientists and organizations to find this level of honesty. If anyone of us on this board, writers and readers, had the resources of Michael J Fox we would have done exactly the same thing he has done with his - marshal the best team and tell them to get it done fast - without skipping the details, like maybe we need to find out just what it is we are dealing with before we can cure it. Thus a 50 million dollar investment in the PPMI or biomarkers study.

I think we tend to view MJFF with some suspicion. We shouldn't. We should all be supporting them as much as we can by participating in clinical trials and raising money. We should go to their research round tables, participate in their phone calls on research topics, -- do anything we can to make them think even harder by asking the right questions. Never stop questioning.

Their motive is as pure as ours. Instead of trying to come up with a new way to a cure, we should be funneling our efforts into theirs. It is the only way to make the science faster and smarter. We don't have to be sycophants to do this, we just have to be partners, and remain as smart and independent-thinking as always. And not be foolish enough to look a gift horse in the mouth.

I'm not sure this post belongs entirely in this thread, but I've been stewing on it for awhile, and it emerged here. Hard to type because my tremors are much worse with stress (back to the topic).

What puzzels me is that tremor is reduced dramatically with pumpkin seeds and penut butter and fava sprouts for some people (even just eating the bean for some....there is something else in the makeup of the bean that contributes to it's effectiveness.)Those of you that cannot try favas...try eating a handful of raw unsalted pumpkin seeds a couple times a day and see if it helps your tremor. Aunt Bean

http://www.hindawi.com/journals/pd/2012/370190/

IMark, I love the info in the rest of the thread that discusses tremors and.....Maybe I am missing something, but what does this article you quote have to do with tremor dominant parkinsonism. It appears to me to be discussing (to the extent I can peel through all the jargon) dyskinesia.... About the only two words I could understand in this piece is "poorly understood." .... I'm just sayin'......

After using Klonopin as a sleep aid for a few weeks I no longer require PD. My symptoms have always been aggravated by stress.

Hi Arsippe,
I am sorry that you don't see the relevance of the article to the thread which is entitled (PD Tremor is not result of dopamine loss). Tremor and dyskinesia are the most difficult symptoms to treat presently and both seem to be caused by similar dynamics. New research discussed by Laura reveals A role for locus coeruleus (which controls Adrenaline) in Parkinson's tremor and interestingly, a healthy locus coeruleus will cause more severe tremor while a degenerated LC would result in attenuation of tremor (according to the research).
The paper that I presented suggests that serotonin system as a "key player in the appearance of L-DOPA-induced dyskinesia (LID)". More over it suggests that " the 5-HT1A receptor agonist buspirone has been shown to suppress GID in these patients, suggesting that serotonin neurons might be involved in the etiology of GID as for LID".
I hope this helps.

Cheers.

Thanks for the clarification. This is the first I've heard about similarities between the tremor that tremor dominant folks suffer and the kind of movement folks with dyskinesia suffer. If a healthy LCD means strong tremors, my LCD must be a very healthy critter indeed! The only thing that completely shuts it down is sleep, though during the past year, I've been learning how to attenuate it a bit thru certain supplements and very modest exercise. Thanks again for the info.