Let's play.....EXPLAINNNN THIS!
 

I picture it as a game to play with my neuro next visit, but it is really intended to be a collection of observed symptoms, effects, etc that just don't fit the simplistic "dead cells, low dopamine, tough luck" theory. I'll start with one that got me thnking. If you have another, add it in.

When I am freezing and my feet are epoxied to the floor, I can break a foot loose by simply touching the top of my (bare) foot with the tip of a lightweight walking stick. I can achieve a similar effect by pivoting the foot to touch the heels together. Each "trick" is good for a single step and must be repeated.

As best I can tell, this has nothing to do with dopamine or the substantia nigra. My guess is that there is a sensory phenomenon involved, perhaps a result of neuropathy.

Anyone else have one?

Me 3
 

I have the same effect lifting my left arm(symptomatic side). I can put my right index finger on the back of my left hand and the arm lifts much easier and with far less cog wheeling. Just by touching it. :eek:

Arm Swing
 

I find a similar thing with arm swing but using mental prompts only

Reduced arm swing...

Think swing arm seems to cause confusion in the movement - works for a couple of cycles but seems to fail quickly.

Think pause at high point of forward swing and forget about the swing motion itself = seems to provide a more fluid movement that lasts a great deal longer before interruption.

Anyone else find the same or am I getting clogniton too?????

ken

All in good fun...
 

Ooooo, Rick, I bet your neuro just LOOOOOVES to see you coming. Twenty years of school and training would sure make anyone want to play games, LOL. Hey, they don't even really know how a normal brain works yet!

But seriously,

This is really why I responded. Why do you say this?/How do you know this?

Jaye

Get THIS!
 

I got one for you. Not all the time, but once in a while, when I am "off" I can concentrate really hard on a big step forward...and break out into a SPRINT!!! I can keep going as much as 1/2 a city block, maybe 20-30 seconds (?). When I stop running I slow down and within seconds (2-3) I am back to my "off" condition.

Try to explain THAT with a "lack of dopamine" theory.
Keith

techniques to fool our PD
 

whether its a foot to step accross, a laser beam or whatever, Anything that changes our motor responses works. I used to get yelled at work for running. I explained that I ran because I could not walk.

there are lots of things that work in this regard. You just need to try them til you find one that works for you.

Charlie

Explain this..
 

I am doing remarkable better in relation to all symptoms, even when I forget to take my meds..I have made 3 changes in the past 8 months, and they are..

Switch from 3x25/100 Sinemet daily to:..

2x50/200 Sinamet CR daily since around August

Ive taken 4 25/100 Sinemets daily before with nowhere near the results

1/2 Teaspoon of DM before bed since March

Seeing a Chiropractor once a month

I walk near normal now and the only new consequence being dystonia in my bad leg and foot

When I was at my AA meeting last night, I saw a friend who I havent seen for a few months, who used to work for the Chiropractor I used to see a few years ago, and she asked me what I did, because I am walking and moving so much better?

Keith yes!! I've had a similar experience.
Late to catch a flight in an off state and told "they're about to close the gate" I could suddenly run faster than the rest of my family and beat them all there. I then reverted to my off state.
Strange to say the least. It only happened to me the once but I remember reading of a similar encounter a PWP had in a burning house.
Lee

I do not do anything like you all describe
 

I decided along time ago to swing my arms anyway and to walk when my body said can't - I would walk backwards etc. the worst symptoms I have are caused by excessive worry which leads to stressing the adrenals,
my worst time of the month for PD crapola is the PMS timing...
otherwise, I was told the freezing is not the body but the eye gaze, so to stop look around the room and breathe some more, will unlock the entire freezing -my best scenario is if I freeze - I can run... so I will run to said spot ... but the weirdness of this scurge - I can only tell you is PD was mainly labled as a mental illness...
I do not have faith in illnesss.

I have been off meds in front of a world reknown neurosurgeon and many neurologist, and could show them -the running, it amazes the crapola out of all of them -more like scares them..
___________________

the emotional component as the key to the cause and cure of genuine or idiopathic Parkinson's disease. I have come to the conclusion that the real underlying cause is an inappropriate response to panic situations. Instead of fighting or running away in a situation of extreme danger, the Parkinson personality will freeze up and 'play dead'. One may be born with this trait or it may be acquired in this lifetime.
If born with it, then in a frightening situation already as a baby or small child this personality type will freeze rather than scream and thresh about with arms and legs. There is a 'frozen panic' at the bottom of this personality, which causes them to move fearfully through life. However, the affected individual or friends and family members are usually not aware of this. Commonly it is covered by a rather rigid and inflexible personality that tries to control events and conditions in order not to be suddenly confronted by unexpected and potentially frightening situations.
The following case history may be typical for an acquired 'freeze-response'. This individual was a bomber pilot during the Second World War. Over the Strait of Dover his plane was hit and started burning. He was extremely frightened but remained outwardly calm at the controls. Several years later he started developing signs of Parkinson's disease.
In the case of an 'inherited' freeze-response regression therapy revealed an experience in which the patient was being burnt as a witch at the stake. Lately she had been so afraid of fire that she even froze when just watching a fire on television. After I suggested during regression that she mentally free herself of the ropes and run away, she was no longer afraid of fire and her Parkinson symptoms considerably improved.
My understanding of the connection between an inappropriate panic response and Parkinson's disease is about as follows. There is a two-way communication between the movement centres in the brain and related muscles. While dopamine dependent nerve impulses stimulate and control muscle action, there is also a communication from the muscles to the brain, relating the responsiveness or ability of the muscles to move. Muscles, like every other part of the body, retain a memory of past traumas. This can be shown with regression and similar therapies. However, in this case it is not just a mental memory, the real damage is done by 'frozen emotions'.
The emotions are the connecting link between the mental level and the bio-energy flows in the acupuncture meridians. The frozen emotional energy slows the meridian flows in the affected muscles and leads to increased rigidity and spasticity by affecting neuromuscular receptors and other biochemical parameters. This in turn leads to a reduced communication from the muscles to the brain, thus weakening the energetic as well as biochemical structures of the muscle control centres in the brain.
This makes these control centres susceptible to other harmful influences, be it emotional stress, vitamin-mineral deficiencies, endotoxins and microbes as well as chemical toxicity from the environment. I also noticed a connection with dislocations in the spine, which interfere with the movements of cerebrospinal fluid and energies within the spine. A combination of all of these factors may gradually lead to the degeneration of the substantia nigra and related structures.
Furthermore, it is known from Reichian or bio-energetic bodywork that the freezing of one important segment of the emotions leads to a general suppression or inappropriate response to all emotions. If the affected individual would start to feel strong negative emotions and especially anxiety, there would be an imminent danger that the memory of the frozen panic could awaken and emotionally overwhelm the mind and body. This must not happen and the only way the individual can keep suppressing any arising strong and potentially terrifying emotions is by tensing the affected muscles. While this gradually leads to more and more emotional and bodily rigidity and maintains the inappropriate body responses in the face of danger, this is the price that the individual subconsciously is willing to pay for keeping the panic memory from becoming conscious.
This basic underlying cause of P.D. needs to be removed if one wants to have any real chance of overcoming the disease. The key to removing the memory of the frozen panic from the body is to become conscious of it and emotionally relive it. This may be done with regression therapy, although one needs to be aware that there may be several incidents in different time frames. As the subconscious mind is very reluctant to revisit traumatic incidents, it needs to be firmly guided in the desired direction and many attempts may have to be made. Most promising is likely to be the exploration of the death experience in the previous incarnation. If successful, then initially the panic-causing incident will only be contacted at the mental or intellectual level. Repeated regressions need to lead deeper and deeper into the emotional aspects of it until the full emotional impact can be felt. This will be a terrifying experience with possibly strong bodily manifestations and requires the presence of a competent therapist, guide or helper.
Normally it will be necessary to get a professional therapist who is experienced with regression work. However, you may do some preliminary or additional work with the help of a reliable friend as described in Mind Tools. After a panic situation has been made conscious, it is equally important to relive it again during regression with the suggestion to act appropriately now and to use guided imagery for this purpose. In addition, use guided imagery during relaxation or meditation periods to imagine using the body appropriately in a variety of dangerous situations.
Until the individual becomes fully aware of the hidden panic, he or she will continue to prevent actually feeling anxiety and other negative emotions by increasing muscle tension which in turn reinforces the symptoms of Parkinson's disease. With this, the severity of Parkinson symptoms can fluctuate very much according to the momentary emotional condition. While good nutrition and supplements can more or less remove most of the symptoms of Parkinson's disease and improve the overall energy level, a real or complete cure should include both, emotional as well as nutritional therapy.
Mark Hurni made a great contribution to the understanding of the emotional component of Parkinson's disease by observing his bodily reactions to emotional challenges. He started developing symptoms of Parkinson's disease in 1990. Instead of using drugs, he decided to try body-based psychological therapies to heal his emotions.

More high weirdness
 

I, too, can run when I cannot walk. When I cannot turn I can hop up and down to pivot about, as well.

I don't like to call these "tricks" like the doctors do dismissively. These are observations they can't explain and should be of keen interest to them.

Others- Taking my shoes off alters everything when freezing. Removing my socks does it again. A year ago I was seeing my GP and began freezing in the exam room. I told him that in all these years he was the only doctor to have had the opportunity to see me in that state. He is a good doctor and paid close attention as I demonstrated just what a pain in the butt PD can be. Then I told him "Watch this." and removed my shoes, picked them up, and walked completely normally out the door. He was suitably impressed. :D

Another bit of surreal PD lore- I find that talking to myself out loud explaining what I am about to do enables me to do it. "I am going to stand up and smoothly walk across the room and turn at the chair and sit down." And I do exactly that. If I had not done the vocal bit I would have frozen upon standing and struggled across the room. Now, that is weird.

not weird at all -rev -
 

you and I have brilliantly stumbled across the key -
if the synapses see :http://www.ericmcgehearty.com/synapse.html do not work correctly you are the ghost that runs the machine ie: the body...
the body is really trying its best to heal itself that is the way we were made.
the body is regenerative in cycles of 7 years in 7 years every cell in our body is made new again -the entire body is busy replacing old cells everyday.
you must tell your legs -now those of yoyu who think it stupid -please do not do this - however I do very well for a long time 15 years of watching this scurge.
okay
tell your body everyday -thank you for walking for me, I know you do the very best you can -and touch your legs and be nice to your legs -and tell them we are healing and say I love my legs anyway
say this to every part of your body: eyes -mouth and all things that will make your body feel self love
especially your heart and your mind aka
soul and brain areas -
the body is made from the same elements as the soil or mud - my mud body will heal, and then when my time is up on this earth my mud body with return to the earth as dust -dust to dust
in between we must take care and love ourselves -
none of us will ever really understand our illness, but the reason may be just to help us learn more about healing.
or perhaps not?
;)

There is truth here
 

I know some of the "hard science" crowd doth roll their eyes to the heavens, but there is, indeed, hard science to provide a rationale for talking to yourself.

The concept of our bodies being awash in informational chemicals is relatively new (about 20 years). Basically, there is a level of chatter going on that rivals the planetary grid. Every cell in the body has the ability to broadcast and receive and it is done by means of "messages in a bottle" such as neuropeptides, cytokines, hormones, etc. The primary difference in these chemicals is only what body system they originate from. Essentially, it is all one big network with all the cells talking to the whole and to each other.

It works something like this: a cell launches a bottle with a message into the liquids of the body. This bottle and message is a molecule of a precise structure and thus encodes information. That information may be simply "I feel good!" as in some cases of dopamine in the reward circuits. So thousands of little bottles go rushing out into the network bearing their message of joy. As they wash over other cells they are drawn to little receivers or "receptors" that are designed just for their type of bottle. A single cell may have hundreds of types of receptors just waiting for their type of bottle. In the case of our little message of joy, it locates its receptor and begins a sort of dance with it. The receptor is stimulated by this interaction and passes information through the cell membrane and triggers action within.

The action triggered will depend on the message received. The message will have been generated in response to a number of things such as input from the brain. Or the stomach. Or the vocal chords, Or your big toe. he point is that it is not a simple hierarchy of brain bossing everyone around. Instead, it is a network. Everyone chattering to everyone else.

This means feedback loops, one of the more amazingly simple concepts which yield a mind-boggling complexity when inserted into a network.

That is a really bad explanation of a really wonderful thing, but it is the best I can do. Bottom line is that we really do have a hand in creating our own state of being and something(s) listen when we say "I feel like crap!" or "I feel great!" and change their state and that changes ours.

One of the researchers at the NIH was a woman named Candace Pert who discovered the opiate receptor and touched off a boom in neuroscience we are still watching. (She also got fed up with the way Science is conducted and is somewhat controversial.) She made a statement that is quite true, that we are far more like a flickering flame than a hunk of meat.

Well, that is one of my more rambling posts but it is late and I didn't charge anything for it. :D:D:D

there is a study of words and effects
 

the man is a scientist from japan and he talks to water -because the body is more than 70 percent water...
basically he watches the water that he has spoken loving words to will make beautiful ice crystals and the water he has spoken negatively to -has alot of problems making ice crystals -they are damaged...
the words will effect your life - have you ever seen a dog that has been treated cruelly?
they cower -they are fearful -they do not relate well to life after being kicked
by their master...
and so is the tongue is the master of the body -as a man thinks -so is he...

thanks rick -excellent thought provoking post
:)

I, too, hate to be told symptoms are not related to PD or treatment.
 

I too get very frustrated when my neurologist blows off some symptom as being unrelated to PD. But neurologists are not receiving the best training. Since drug companies offer "credit classes" for free for physicians to take to keep their continiuing credits education up to date, they may be missing out on courses which would be of more value when working with patients. I refer you to the following research study:

SAN FRANCISCO— Nearly 90% of psychiatrists recognize that atypical antipsychotic drugs differ significantly regarding their association with metabolic dysfunction. However, although a majority acknowledges that diabetes and weight gain may result from these drugs, many more are unaware of other serious metabolic disorders that can occur. These were among the key findings of a survey that evaluated physicians’ management of metabolic complications in patients taking atypical antipsychotics.

“[Psychiatrists] do recognize that select atypicals pose a greater risk for metabolic disorders, and that these are sometimes unrecognized because monitoring is not being done sufficiently,” said Henry Nasrallah, MD. “Atypical antipsychotics are not all the same. This is one of the key issues in psychiatric practice.” Dr. Nasrallah is a Professor of Psychiatry, Neurology, and Neuroscience and Associate Dean of the University of Cincinnati College of Medicine.

“I think the real issue for the field is that people are waiting for some kind of a consensus, evidence-based guideline that helps psychiatrists judge the different risks and benefits of the various drugs,” added P. Murali Doraiswamy, MD. Dr. Doraiswamy is Chief of the Division of Biological Psychiatry in the Department of Psychiatry at Duke University Medical Center in Durham, North Carolina. Both physicians made their presentations at the 156th Annual Meeting of the American Psychiatric Association.

ATYPICAL ANTIPSYCHOTIC AWARENESS

The survey included 300 randomly selected US physicians who treated at least eight patients with schizophrenia and related disorders per month. The goal was to assess the extent of physician awareness as to the adverse effects of antipsychotic drugs, the physician’s perception of metabolic disorders, and the extent to which their clinical practice was affected by these problems.

Dr. Doraiswamy addressed a number of questions from the survey, beginning with whether physicians found the body of evidence for a diabetes–atypical antipsychotics association to be compelling. “An overwhelming majority of psychiatrists (84%) either agreed or strongly agreed that this was the case,” he said. “There have been good data suggesting that schizophrenia itself may be associated with a number of risk factors for diabetes. Schizophrenics get poor medical care. Many of them don’t routinely get preventive health care, so they may have preexisting risk factors. What doctors are saying is that in addition to those risk factors, they believe there is also a link between some atypical antipsychotic agents and diabetes.”

Physicians were also asked if they viewed current reports of diabetes and other metabolic changes resulting from some atypical antipsychotics as not clinically significant. Dr. Doraiswamy said that about 76% of psychiatrists disagreed or strongly disagreed. “In other words, most doctors viewed these reports as clinically significant, because they are aware of the implications that diabetes and metabolic complications confer on the overall health risks for the patient.”

About 71% of psychiatrists either agreed or strongly agreed that the development of metabolic issues associated with some atypical antipsychotics makes it much more difficult to manage schizophrenia. “Patients with schizophrenia are already having a hard time dealing with their mental illness, and if you have a second metabolic complication on top of that, it makes it much more difficult,” Dr. Doraiswamy commented. Approximately 91% of psychiatrists believed that the development of metabolic issues had a negative impact on patient compliance. “If they have side effects with these medications, then patients may stop taking these medications without even informing their health care practitioner,” he said.

On another topic, 62% of practitioners either agreed or strongly agreed that metabolic issues would negatively affect the efficacy of antipsychotic therapy. “When we think about efficacy, we are really looking at short-term clinical trials, and in short-term clinical trials there is really no difference as far as the efficacy of most antipsychotic drugs,” said Dr. Doraiswamy. “Clearly, we need long-term studies to tease out this particular issue.”

Asked if they believed that atypical antipsychotic agents differed significantly in their likeliness to cause metabolic dysfunction, 87% of psychiatrists either agreed or strongly agreed. “Even though they may still think that all these drugs can sometimes cause some of these effects, they believe there is a difference in risk,” said Dr. Doraiswamy. “They believe that not all atypical drugs are the same as far as their ability to cause metabolic illness. And this also, I think, tells us that they believe that all these effects are not entirely due to the disease itself.”

RISK PREVENTION

Dr. Nasrallah also addressed the issue of risk prevention and antipsychotic medication. “In medicine, one of the key principles or guidelines for physicians is ‘Above all, do no harm.’ We recognize that all medications have side effects, but one can adopt a policy in managing patients in which you get the maximum possible efficacy with the least amount of harm.” He noted that approximately 72% of psychiatrists agreed or strongly agreed that first-line agents associated with significant weight gain or other metabolic risks should not be considered for initial therapy.

The survey also found that the majority of physicians believe that patients with schizophrenia generally already have a higher risk for metabolic complications than does the general population. “Patients with psychosis—schizophrenia, especially—tend to be overweight, have a very poor lifestyle and poor nutritional habits, and they rarely exercise,” noted Dr. Nasrallah. “They have multiple risk factors, and on top of that they also have diabetes.” Furthermore, a “vast majority” of psychiatrists believe that weight gain contributes to the development of metabolic issues or disorders in patients with schizophrenia. “It is a no-brainer that weight gain is one of the most important initial foundations of metabolic disorders,” he said.

As to what metabolic adverse effects, if any, were associated with some atypical antipsychotic drugs, two thirds of psychiatrists were concerned about diabetes and the majority were concerned about weight gain in their patients. However, metabolic complications such as change in lipids, hyperglycemia, obesity, and increased glucose were noted far less frequently. For most patients, weight gain is an acceptable risk in return for other benefits of antipsychotics, Dr. Nasrallah said. “About 43% [of psychiatrists] agree that diabetes is an acceptable risk factor in return for the other benefits of atypical antipsychotics. When you compare that with 67% who acknowledge that diabetes is a serious side effect, what this tells you is that some psychiatrists are so eager to get rid of the hallucinations of the patients that they would allow the patient to have diabetes in return for that. I personally don’t believe that is a good risk to take.”

STRIVING FOR BETTER CARE

Dr. Nasrallah pointed out that 35% to 40% of patients are switched within a year from one antipsychotic drug to another, because either the drug is not working or the drug is causing a lot of adverse effects. “You cannot tell if your patient is developing a serious medical problem unless you look,” said Dr. Nasrallah. “There has been no consistent national guideline for monitoring these serious metabolic side effects, despite the fact that they are the hottest topic in the country. [Rates of] diabetes are increasing, weight gain is increasing, high lipids and cholesterol are increasing. Are you looking for it? Are you measuring them at baseline and following up the patient?” When asked if first-line agents associated with significant weight gain or other metabolic risks should not be considered for initial therapy, however, only 28% of psychiatrists surveyed agreed or strongly agreed. “Certain atypicals are guaranteed to give you more than 20 pounds of weight gain within a year; others, zero weight gain in a year.”

Physicians were asked how many patients with schizophrenia and related disorders were routinely monitored for various health concerns. One third said that they monitored all their patients for blood pressure. “That’s such an important public health screening for hypertension, which again is one of the metabolic disorders,” said Dr. Nasrallah. About 63% measured or were cognizant of the weight of their patients; 29% measured lipid levels; and 43% screened for blood glucose. “Despite the fact that they’re aware of the seriousness of the problems, there’s still not sufficient monitoring going on,” said Dr. Nasrallah.

Dr. Nasrallah emphasized that psychiatrists who prescribe antipsychotics need to consider all metabolic consequences before selecting the first-line drug. Furthermore, he said, “Ongoing education is important to minimize risk. I’m a strong believer in patient education, parent education, and, of course, physician education.”

—Colby Stong

From current issue of "Neurology Today."

Although the article refers to schizophrenia, it applys to PD patients. PD is the counterpart illness to schizophrenia; I.E., schizophrenia is too much dopamine; PD is not enough.

Vicky

Part of the answer
 

Been experimenting a little with "talking to my Self" and have come to see a little more about what is going on.

If I have the INTENT to walk from "A" to "B", I can approach the task a couple of different ways. I can see it as a series of discrete steps, each being an obstacle to overcome. In fact, the very first one can be the most difficult.

Or, I can see it as a whole and leave the subroutines of the individual steps to my unconscious mind which hasn't suffered the same damage as the conscious.

So, oddly enough, taking a "wholistic" approach works better than a "Cartesian" one of breaking the task into bits.

The lengths to which I can run the "program" probably varies depending on a number of conditions such as how tired I am. As to why it has to be audible rather than silent, I can only assume that the subconscious part is not privy to the silent track but is to the audible.

If this is true of anyone else, we may have a whole new type of "talk therapy/" :D

Rick, I saw a study on tv which reminded me of something I read awhile ago. It was a functional MRI study of a person in a minimally conscious state (not quite vegetative). When they asked the person to think about playing tennis, or some other motor activity, the area in their brain that controls movement lit up just like in a healthy person.

I think that's why our tricks work. I think that PLANNING or REHEARSING stimulates that area of the brain and then we're actually able to perform the activity better. It's like priming the pump, that part of our brain, or those circuits involved.

Without my tricks, I'd be in awful shape. They help me constantly. I think I'm planning because my automatic planning is out to lunch.

~Zucchini

quote -
 

Wouldja look at this
 

I ask a question and I get an education! Do ya love this place or what?

Jaye

Sorry, Jaye, didn't mean to ignore your question
 

Looked back and saw that I had. Apologies. Yes, my neuro loves me. :D

As for the other, I see no link between the sensory input and the question of dopamine levels, at least if it is confined to a matter of initiating motor action. It seems more like a breakdown in the feedback loop that enables one to track position in space - something the banding experiments also seemed to do. But it isn't simple neuropathy - or at least there is no numbness nor pain. Maybe it is more central than peripheral, after all. Ideas?

emotional cause and cure of PD etc link
 

http://users.mrbean.net.au/~wlast/parkinsons.html

this is the link you requested dear friends

Brain, Vol. 117, No. 4, 877-897, 1994

The functions of the basal ganglia and the paradox of stereotaxic surgery in Parkinson's disease
C. D. Marsden1,0 and J. A. Obeso2


The basal ganglia play a role in controlling movement. The motor circuits within the striato-pallidal complex are thought to facilitate desired movement and inhibit unwanted movement through their influence via thalamus, mainly on precentral motor cortical regions. Lesions in the motor thalamus, or in the globus pallidus, therefore might be expected to impair voluntary movement.

But stereotaxic lesions in patients with Parkinson's disease directed at the motor thalamus verified at autopsy, and lesions in the globus pallidus, which improve rigidity and tremor, apparently do not worsen parkinsonian hypokinesia and bradykinesia; nor do they regularly cause dyskinesias. Reasons for this discrepancy are reviewed.

It is concluded that the motor circuits of the basal ganglia are part of a distributed motor system which can operate, albeit imperfectly, in the absence of striato-pallido-thalamo-cortical feedback.

There may, however, be subtle defects in motor performance after thalamic and pallidal lesions which have escaped attention. Further consideration leads to two hypotheses concerning normal basal ganglia motor function. First, it seems most likely that it is a pause in firing of medial pallidal and substantia nigra reticulata neurons that, by disinhibition of thalamic targets, permits movements generated by cortical motor areas.
\
An increase in firing of medial pallidal neurons, which so far has been the major focus of attention, may be more concerned with inhibition of unwanted movement. Secondly, we suggest that the basal ganglia play a particular role in motor control. A change in firing of medial pallidal neurons appears to occur too late to initiate a new movement. However, the motor circuit within the striato-pallidal system routinely receives a continuous delayed read-out of cortical motor activity and issues an output directed via thalamus mainly to premotor cortical regions. This may permit the routine automatic execution of sequences of movements generated in cortical motor areas.

There is evidence that other regions of the striatum respond to significant external or internal cues as dictated by their cortical inputs, the significance being determined by memory, novelty, emotional and other contexts. We suggest that such events capture the attention of the non-motor striatum, which then interrupts the routine operation of the motor circuit, perhaps at the level of the medial pallidum and substantia nigra pars reticulata, to permit new cortical motor action.


Received February 15, 1993.

http://brain.oxfordjournals.org/cgi/...ract/117/4/877

Stages in the development of Parkinson’s disease-related pathology

Journal Cell and Tissue Research
Publisher Springer Berlin / Heidelberg
ISSN 0302-766X (Print) 1432-0878 (Online)
Issue Volume 318, Number 1 / October, 2004

Abstract The synucleinopathy, idiopathic Parkinsonrsquos disease, is a multisystem disorder that involves only a few predisposed nerve cell types in specific regions of the human nervous system. The intracerebral formation of abnormal proteinaceous Lewy bodies and Lewy neurites begins at defined induction sites and advances in a topographically predictable sequence. As the disease progresses, components of the autonomic, limbic, and somatomotor systems become particularly badly damaged.

During presymptomatic stages 1–2, inclusion body pathology is confined to the medulla oblongata/pontine tegmentum and olfactory bulb/anterior olfactory nucleus.

In stages 3–4, the substantia nigra and other nuclear grays of the midbrain and forebrain become the focus of initially slight and, then, severe pathological changes.

At this point, most individuals probably cross the threshold to the symptomatic phase of the illness. In the end-stages 5–6, the process enters the mature neocortex, and the disease manifests itself in all of its clinical dimensions.

Distribution and roles of metabotropic glutamate receptors in the basal ganglia motor circuit: implications for treatment of Parkinson's Disease and related disorders

Susan T. Rouse, Michael J. Marino, Stefania R. Bradley, Hazar Awad,

Available online 30 April 2001.

Abstract

The basal ganglia (BG) are a set of interconnected subcortical structures that play a critical role in motor control. The BG are thought to control movements by a delicate balance of transmission through two BG circuits that connect the input and output nuclei: the direct and the indirect pathways. The BG are also involved in a number of movement disorders. Most notably, the primary pathophysiological change that gives rise to the motor symptoms of Parkinson's Disease (PD) is the loss of dopaminergic neurons of the substantia nigra pars compacta (SNc) that are involved in modulating function of the striatum and other BG structures.

This ultimately results in an increase in activity of the indirect pathway relative to the direct pathway and the hallmark PD symptoms of rigidity, bradykinesia, and akinesia.

A great deal of effort has been dedicated to finding treatments for this disease. The current pharmacotherapies are aimed at replacing the missing dopamine, while the current surgical treatments are aimed at reducing transmission through the indirect pathway. Dopamine replacement therapy has proven to be helpful, but is associated with severe side effects that limit treatment and a loss of efficacy with progression of the disease. Recently developed surgical therapies have been highly effective, but are highly invasive, expensive, and assessable to a small minority of patients.

For these reasons, new effort has been dedicated to finding pharmacological treatment options that will be effective in reducing transmission through the indirect pathway. Members of the metabotropic glutamate receptor (mGluR) family have emerged as interesting and promising targets for such a treatment.

This review will explore the most recent advances in the understanding of mGluR localization and function in the BG motor circuit and the implications of those findings for the potential therapeutic role of mGluR-targeted compounds for PD.

FULL ARTICLE:

http://www.sciencedirect.com/science...aa7f454ba3dda8

"The direct and indirect pathways of the BG act as a fine-tuning mechanism in movement control (Alexander et al., 1986). The balance of transmission through the direct and indirect pathways is tightly regulated by a major modulatory projection from dopaminergic neurons in the substantia nigra pars compacta (SNc). This dopamine input to the striatum regulates the direct and indirect pathways differentially, due to the presence of different postsynaptic dopamine receptors on the two populations of medium spiny neurons. D1 receptors are primarily expressed on medium spiny neurons that project directly to SNr, while D2 receptors are primarily expressed on the medium spiny neurons that constitute the indirect pathway (Gerfen et al., 1990). Because of this differential expression, the release of dopamine in the striatum has a net excitatory effect on the direct pathway, and an inhibitory influence on the indirect pathway."

...the primary pathological change giving rise to the motor symptoms of PD is the selective death of dopaminergic neurons in the SNc. The loss of this important modulatory input results in a decrease in activity through the direct pathway and an increase in activity through the indirect pathway (Albin and Wichmann). These changes lead to increased inhibition of thalamocortical neurons, which is believed to underlie the hallmark symptoms of the disease: rigidity, bradykinesia, and akinesia. The right panel of Fig. 1 schematically illustrates the activity changes in BG-thalamocortical circuitry that are thought to occur in PD.....

....there has been a major focus on developing novel treatment strategies that are aimed at acting downstream of the lost dopaminergic neurons to restore balance to the direct and indirect pathways. This effort has led to development of highly effective surgical treatments, such as pallidotomy (Baron and Laitinen) or high-frequency stimulation of the SNT (Limousin et al., 1995), that are aimed at reducing activity through the indirect pathway. .....

Metabotropic glutamate receptors provide novel therapeutic targets for treatment of movement disorders

That part is complicated!

We compensate!

Cortical motor reorganization in akinetic patients with Parkinson's disease
A functional MRI study
U. Sabatini1,5, K. Boulanouar1, N. Fabre1,2, F. Martin1, C. Carel1,2, C. Colonnese5, L. Bozzao5, I. Berry1,3, J. L. Montastruc4, F. Chollet1,2 and O. Rascol1,4


Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies.

Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex.

These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex.

These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.

Brain, Vol. 123, No. 2, 394-403, February 2000

http://brain.oxfordjournals.org/cgi/...full/123/2/394

TRY THIS!

Motor task
The activation paradigm consisted of a sequential movement performed with the right hand. This sequential task had been chosen among several others, according to preliminary fMRI data from our laboratory, because it induces a clear activation signal in areas known to be involved in both motor programming and motor execution. To perform this task, the subjects had to (i) make finger-to-thumb opposition movements in the specified order of the index, middle, ring and little finger; (ii) open and clench the fist twice; (iii) complete finger-to-thumb oppositions in the opposite order (i.e. little, ring, middle and index finger); (iv) open and clench the fist twice again; and finally (v) repeat the same series of movements during the 30 s of data acquisition. This was intentionally a more complex and cognitively demanding task than generally used in previously published SPECT and PET studies performed in patients with Parkinson's disease.


Conclusions
The present fMRI neuroimaging study shows that the subcortical putaminal dopamine deficit which characterizes Parkinson's disease disorganizes the cortical motor pathways in a complex way.

It induces a focal `underactivation' restricted to the rostral SMA and DLPC, possibly responsible for the patients' akinesia. It also induces an abnormal pattern of `overactivation' in most of the other known motor cortical areas, including the caudal SMA, the anterior cingulate cortex, the lateral premotor, the primary sensorimotor and the parietal cortices.

This reorganization, which involves parallel-acting multiple motor areas, can be seen as an attempt at motor recovery.

The general aspect of this reorganization resembles what has been described previously with PET in other motor diseases, such as paresis induced by acute stroke (Chollet et al., 1991Go; Weiller, 1995Go; Chollet and Weiller, 1997). It is also interesting to compare the present results with those reported in patients with cerebellar degeneration (Wessel et al., 1995Go). The pattern of motor activation in this last condition appeared to be the opposite to what we observed in Parkinson's disease: several areas of the lateral motor circuit, including the lateral premotor cortex and the lobus parietalis inferior, were less activated in the cerebellar patients than in the normal controls, probably as a result of defective cerebellar inputs, while, in contrast, other premotor systems, including the SMA, were used more heavily in the cerebellar patients than in the controls. It is thus tempting to speculate that these phenomena illustrate the capacity of the adult human brain for functional plasticity in compensating for one motor circuit deficit by recruiting another parallel one. The exact mechanisms of these phenomena remain to be understood.

ANOTHER ARTICLE:

http://www3.interscience.wiley.com/c...405/HTMLSTARTW

Plasticity of the nigropallidal pathway in Parkinson's disease

From another article:

It is hypothesised that bradykinesia is not simply a compensation for defective preparatory processes, but may reflect a defective internal cue in PD which disrupts and impairs the outflow of motor responses.

http://www.springerlink.com/content/l1wkju7393q363tn/

It seems to me that researchers should consult with knowledgeable patients who can describe how PD really feels, and who can show how their tricks work.

That data is important and is missing from most of the research going on.

When I sit on the train for awhile, when I stand up, it's hard to straighten my legs and takes great effort. Then it's difficult to get my legs moving. It actually feels as if there is some unseen force pulling my legs downward. What IS that?

Then, with great effort my legs move slowly, and I stomp like Frankenstein. I get going with a slow gait, but after a while I can walk faster and my legs don't feel as if they're being pulled downward.

But I must focus on a physical thing on the floor ahead of me. As I approach it, I automatically focus on the next thing on the ground ahead of me. I need to be reaching for something with my feet!

I rely on visual cues. I can't walk in the dark, or with my eyes closed. Well, I can, but it's so slow and tentative it's ridiculous. I can't find one study with PD patients walking with eyes closed. I can't walk backwards, probably because I can't see behind myself!

Hello - you whrithe very good about PD, I will print this , my family needs this explaining, it will make them understand the way I behave.
Let me know if it is o.k.

Annelise

This is a very common practice amongst musicians. It is called mental practicing instead of physical practicing, and it is found to be just important. The performer will go through the movements, and music in their head so that the music is well rehearsed mentally so when they have to play in public, the music is second nature.

Who would've thought about using this for every day living! :)

In regards to getting the movements going after sitting for awhile, I feel the same thing too. It's as though there is glue or suction cups on my shoes, and I can't get moving, but once I do move I'm okay.

I too wish that the researchers and doctors would consult us more because we really kinow what it's like to live with this. All of the theories in the world don't cover the bases like the real thing.

John

One of the reasons for this thread
 

Was the hope of generating data such as this. It is almost insulting that these observations are dismissed as "tricks." It would be different if it was simply our ignorance, but the researchers are the same for much of this.

And, while many of us lack the vocabulary of academia, a good researcher could overcome that with the right questions. Any lurkers out there want to explore this? Not holding my breath, of course.

It is not entirely off the wall to suggest that ldopa's success at the symptomatic level has led to the wrong conclusions. Maybe it is more a matter of data processing of stimuli than we think. There are some interesting similarities between schizophrenia, autism, and PD for example. Sensory overload is a problem in all three as well as stress response.

John, when I played the piano and memorized a piece, I played automatically without thinking at all, as if my hands knew what to do all by themselves, as a result of all the practicing.

Problem was, if I had a glitch and stopped, I had to restart from the beginning!

Maybe if we rehearse enough, some of our movements can become more automatic like they used to be, when our internal cues worked by themselves.

Now we have to develop new loops, that may in time become automatic, if we rehearse long enough.

Rick, a study I read yesterday mentioned the disorders you mentioned, and said that they actually worked in an opposite way than PD. I can't recall the details! I don't have time to find it.

I agree with what you said!

I'm unable (over time limit) to post this is my earlier post, so here it is:

I forgot to say that after I stand up, I rehearse walking in my mind. Thinking of walking side to side helps. I also count, so I have a rhythm...1,2.....1,2.....I still have trouble getting going, but practice and an inner metronome make it easier.