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