Talk:Parkinson's disease - Misplaced Pages

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Treatment

This is the next section in need of a major overhaul. Subsections probably need to be something like:

Pharmacotherapy
- Motor symptoms (including levodopa, dopamine agonists, amantadine, rasagiline, etc.)
- Non-motor symptoms (antidepressants, atypical antipsychotics)
Rehabilitation therapies
Surgical therapies

AFGriffithMD 07:40, 27 February 2006 (UTC)

There is also note of the following: Due to feedback inhibition, L-dopa causes a reduction in the body's own formation of L-dopa. So a point is reached where the drugs only work for periods of a few hours ("on" periods) which are sandwiched between longer interval during which the drugs are partially or completely ineffective ("off periods").

While I am familiar with feedback inhibition in situations such as steroids and testosterone, I have not seen a study that addresses nor suggests that there is feedback inhibition. It may be premature to suggest that feeback inhibition is a problem.

Carlwfbird 12:43, 7 March 2006 (EST)

Role of ND5 in pathophysiology of Parkinson disease

"microheteroplasmic mutations in one of the mitochondrial complex I genes, ND5, were found to be sufficient to diagnose sporadic PD correctly in 27 out of 28 cases. While additional studies are needed, mitochondrial microheteroplasmic mutations may be the cause of the majority of PD cases."

I believe this passage from the Toxins section strongly overstates the relative importance of ND5 mutations in particular, and microheteroplasmic mutations in general with respect to the pathophysiology of Parkinson disease. The only PubMed article I could find on ND5 mutations being used to classify PD cases versus controls is this one , and it mentioned correct classification of 15 of 16 samples, not the 27 out of 28 cited above. This means there were only 8 cases and 8 controls, which is a pretty small sample size, certainly not enough to make the sweeping statement, "mitochondrial microheteroplasmic mutations may be the cause of the majority of PD cases." AFGriffithMD 01:05, 16 February 2006 (UTC)

Awakenings

Awakenings deals with Parkinson's? I thought it was encephalitis. - Montréalais

The patients in Awakenings were suffering from post-encephalitic Parkinsonism. The encephalitis had occurred 50 years earlier and the infection was over. However it had left damage, causing their Parkinsonism. RTC 06:06 Nov 2, 2002 (UTC)

Amphetamines

I think it is more than worthwhile to mention amphetamines as a possible cause. (Minor comment reg. your last statement: the epidemic was in 1919-20 and the movie appears to play in the early fifties...which fits to the CV of Oliver Saks :-)

I'm sorry I edited the page. I was trying to prove to someone it doesn't actually edit it in real-time. Boy was I wrong. I did fix it though. Sorry again.

it's worth noting that ritalin is quite useful for the ADD like deficits in attention in PD.Bldavids 05:46, 10 January 2006 (UTC)

I think it is worthwhile to mention that the drug Selegiline (Eldepryl) which appears to inhibit disease progression is broken down into amphetamine and methamphetamine.

Ozzy?

Does Ozzy Ozbourne really have Parkinsons Disease? I know he has Parkinsonian symptoms, but I thought it was due to drug-induced damage to the dopaminergic system rather than actual PD. - Sayeth 22:24, Nov 18, 2004 (UTC

"Parkinson Disease" or "Parkinson's Disease"

The first name seems to be the more popular and proper one, being referenced more often in recent literature and on Google. taion 11:10, 23 Nov 2004 (UTC)

Disagree - Kittybrewster 22:28, 9 July 2006 (UTC)

"inclinations towards Catholicism"

Is this a bogus edit?

It's a jibe at John Paul II. JFW | T@lk 00:49, 18 August 2005 (UTC)

You don't have to be Catholic to have PD!

No, you can convert to Islam and get it too.

removed Katharine Hepburn

Katharine Hepburn did not have Parkinson's Disease. She had a condition called Essential tremor.

Hitler's Parkinson's Disease was not caused by a gas attack. He did not have even his first noticeable symptom of Parkinson's Disease until 15 years after the gas attack in 1918. At the time, in 1918, he exhbited no symptoms that were Parkinson's Disease. The gas used in the attack was not one of those known to cause Parkinson's Disease.

Hitler's PD is believed to have been consequential to encephalitis lethargica (a kind of sleeping sickness). There was an epidemic in the 1910's and a lot of people who suffered from the disease later developed PD. These are people Oliver Sacks wrote about in Awakenings. Balok 00:32, 10 July 2006 (UTC)

Micrographia

One of the symptoms mentioned is "micrographia (small handwriting)" — is this accurate? Is small handwriting symptomatic of disease? Either way, the link currently goes to an article about a popular science book, which I don't think was the author's intention. -- 213.122.16.164 20:04, 17 August 2005 (UTC)

Well, micrographia alone is not particularly indicative of PD. In the context of other symptoms, though, it is an informative symptom. JFW | T@lk 00:48, 18 August 2005 (UTC)

The statement is accurate; it's a classic symptom. So, its presence is definitely informative but not diagnostic. sensitive but not specific. Bldavids 05:48, 10 January 2006 (UTC)

Exercise neuroprotective

I am dubious about the alleged "neuroprotective effect" of exercise. I'd like to see a reference please. --Dubbin 23:23, 23 September 2005 (UTC)

See: “Parkinson's Disease” an on-line summary @http://www.bcm.edu/neurol/jankovic/educ_pd.htm, by Joseph Jankovic, M.D., an internationally recognized expert on Parkinson disease, and the medical director of the Udall Parkinson Disease Research and Treatment Center in Houston (Note: “Udall Center” is a federal designation denoting excellence in PD treatment and research):

“Recent animal research has provided strong evidence that exercise can increase brain levels of neurotrophic factors, increase resistance to brain insult or injury, and improve learning and mental as well as motor performance.” Dr. Jankovic is a highly credible sourcer.Bldavids 05:50, 10 January 2006 (UTC)

Here's a good place to start: PMID 15214505. (Then click on "Related Articles" and you'll see many studies on the topic.) --Arcadian 18:08, 3 January 2006 (UTC)

Terminology depends on which side of the Atlantic you are on

Parkinson disease is used in American scientific literature. There has been a move away from the apostrophe (e.g. Alzheimer disease vs. Alzheimer's disease). The British and the rest of the world use "Parkinson's disease" (preferred term).

219.95.213.43 00:40, 20 October 2005 (UTC)M K Lee

I see 22.7 million for "Parkinson Disease" and 23.3 million for "Parkinson's Disease". The apostrophes have it. --PaulWicks 21:32, 19 June 2006 (UTC)

neuropsychiatric aspects of parkinson's disease

Depression, anxiety, and executive dysfunction have been estimated to account for up to 70 percent of the disability associated with Parkinson disease. Dementia and psychosis may ultimately effect more than a third of all Parkinson patients. There is a movement among researchers and patients to weaken the emphasis on "movement disorder" and strengthen the emphasis on "neuropsychiatric disease".Bldavids 06:35, 16 January 2006 (UTC)

If you have documentary support for this shift in paradigm it would make a very important point in the article. JFW | T@lk 12:17, 16 January 2006 (UTC)

Gladly:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15043801&query_hl=3&itool=pubmed_docsum

Symptoms that cross over the physical into the cognitive and affective realms

The lists as constituted are poor vehicles for certain symptom sets: for example, speech-language problems. In PD, there are defects in articulation and breath support and voicing, but there are also problems with comprehension of complex syntax, with word finding, and with both expression and reception of prosody. Likewise vision and visual processing: the defects in vision are quite complex, seemingly a function of the combined effect of impaired attending, impaired gating of response, and slowed reaction time. The physical and cognitive and affective components of the disease are all snarled together, because the job of the pre-frontal cortex is precisely the integration of these kinds of inputs and outputs. The dysfunction observed in the prefrontal cortex when deprived of dopamine is subtle but radical: disconnects between physical stimulae and perception, between intention and action, between feelings and responses. At some point, these lists will not serve. Bldavids 23:18, 17 January 2006 (UTC)

I agree, the symptom section needs to be reorganized. I did a bit of minor cleanup in one section, but it should be something like:

Symptoms:

Cardinal Symptoms
Other Motor Symptoms
Non-Motor Symptoms
- Sensory
- Visual
- Neuropsychiatric
- Cognitive

AFGriffithMD 23:31, 14 February 2006 (UTC)

dear afgriffith; you really did a super job. it's much clearer, more logical, and internally consistent. it also reads better. i appreciate that you left the language about patient rights and relationships, as that section above all others that i've contributed matters to me. i would like to ask you a question re: pd data, since i looked up your professional affiliation, and am very pleased to have someone with a connection to booth gardner contributing as you are: what is your best sense of both incidence and prevalence of dementia, by subpopulations, and also across the broadest historical study that you're aware of? i have found radically divergent estimations--30%, 40%, 40-80%. it strikes me that there mu[st be some real bias in the data, because people who are doing badly are more frequently lost to follow-up than are indvidiausl who are doing well. barb

Thanks, Barb. I'm working on this article section by section, mostly trying to reorganize without completely overwriting what has gone before, unless it's inaccurate or outdated. With respect to your question about dementia, I think Heiko Braak's work on Parkinson disease pathology is most illuminating. He published an article in Neurology linking incidence of dementia to severity of pathology. I'm going to be working on the pathology/pathophysiology section next, and will have more to say on that subject. AFGriffithMD 19:26, 20 February 2006 (UTC)

Dear A: I'd like to use your first name some variant of it, but don't wish to be presumtuous. may i use your your/ first initial? i'd also ask if you'd take a look at both this article and the wikipedia dementia article, in light of a citation i just came across: (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12567332&query_hl=21&itool=pubmed_docsum) "making it the most common cause of degenerative dementia after AD" and also: (http://jnnp.bmjjournals.com/cgi/content/extract/76/7/903) Patients with Parkinson’s disease (PD) have a significant risk of developing dementia in the course of their illness. Cross sectional studies suggest a dementia prevalence rate of 30% to 40%.1 Longitudinal studies indicate that the cumulative frequency of dementia in patients with PD is 60% to 80%.1 The risk of dementia for individuals with PD is approximately six fold greater than that of age matched controls.

80 percent is a looooong ways from 30 percent.

thanks for your thoughts.

I assume you know bill bell?

barb

To current editors - I think both Griffith & Davids are no longer editting this, however they raise an interesting point. Coupla years ago I did a bit of research & susbequently submitted a grant ptoposal (turned down, sob!) with a friend who's a psychometrician because we found that the accounts of dementia in PD were simply clinical observation, no comparisons. We thought, well for heavens sake!, people that age tend to get demented anyway. The question was (and still is) do people with PD get dementia at a different rate and in a different fashion than other people their age. We don't know, unless someone has answered the question since I last looked. --Dan 15:20, 15 July 2006 (UTC)

Parkinson's speech

I didn't see anything about Parkinson's speech in this article. That isn't my speciality but I regularly get calls from PD patients whose speech has been affected. Judging from these individuals, speech symptoms are one of the most devastating effects of PD, so this article should say something about Parkinson's speech. I've written a short article about Parkinson's speech in WikiBooks. What I wrote is too short to be a WikiBook, but the subject is too big for a Misplaced Pages article. I'm hoping that someone with more expertise will expand my WikiBook article. I also added a link at the bottom of the Misplaced Pages article to my WikiBooks article, and a link to LSVT.Tdkehoe 18:11, 1 March 2006 (UTC)

Pathology section

I'm going to add to the mix my (probably) unwanted request to have in the pathology section something about the physiology of the diseas e.g. how the degenration of dopaminergic neurons causes the motor disorders. (Basal ganglia, anyone?). Yeah, and to ensure the universal hatred of me, four times the exact same link about the already well (perhaps even too) detailed biochemistry is definitely an overkill... --80.221.29.185 17:08, 10 May 2006 (UTC)

Understood the idea and actually fixed the links to point straight to the correspondings posts rather than the first one. Maybe that way it does not seem so repetitive. Still think it's overkill though.--80.221.29.185 18:07, 10 May 2006 (UTC)

Please refer to the Misplaced Pages help page on links. The only aspect that this doesn't fully give the "how to" for is that the part of the URL after the # is the bookmark in the HTML code of the target page. The "clever" changes made by user:80.221.29.185 are just implementations of this general wiki format for external links. In his/her wisdom, he/she obviously grasped that in their original format, because all your citations looked identical, they gave an appearance of being something you had not intended, and which I had the temerity to question. Now that he/she has amended these citations such that they now all appear as different "link names", this has had the benefit of being an incremental improvement to the pathology section. To obtain each #bookmark simply required him/her to follow the original links, find the part of the page you were referring to, examine the HTML code, and constuct the external link complete with the bookmark accordingly. One might almost say that this could have been done without more than a rudimentary knowledge of biochemistry, as long as each bookmark name matched the topic you had described. DFH 19:36, 13 May 2006 (UTC)

Toxins

You know just reading this page again, I think it's insane that there's a whole page about these utterly unfounded theories about "toxins" before you get to a brief mention of the frontline, highly effective treatment for PD, being the Dopamine agonists! I might even go so far as to suggest there is a new page called "hypotheses for the pathogenesis of Parkinson's Disease" in which these theories can be vaguely alluded to, but for now I think there is far too much emphasis placed on these scatty paragraphs. If the majority of other editors are in agreement I will begin the pruning. --PaulWicks 18:09, 19 June 2006 (UTC)

Agreed. Go. Good luck not getting reverted. --Dan 18:19, 19 June 2006 (UTC)

Major revision

This article is currently too long. There is some very useful stuff in here but it's not the sort of thing that's directly relevant to someone looking it up for the first time. There are also glaring omissions such as the diagnostic process. I am trying my best to chunk off new articles in as rational a fashion as possible in accordance with these two guidelines:

Misplaced Pages:Article size Misplaced Pages:Summary style

I am acting in good faith to make this a better article to read as I worry that a newly diagnosed patient would come across this and be utterly flummoxed!

I would appreciate the input of ALL the other editors on this article to help improve this article. --PaulWicks 14:53, 20 June 2006 (UTC)

And why take down the picture of Michael J Fox?

--PaulWicks 20:26, 20 June 2006 (UTC)

Major Revision - Principles

I'm going to try to outline my rationale for a major revision of the article Parkinson's disease.

1. The article is too long. (Misplaced Pages:Article size).

2. The article goes in to too much detail about the biochemistry of Parkinson's, which whilst informative and valid is too complex for the vast majority of readers. In particular please consider this from Misplaced Pages:Summary style: "Since Misplaced Pages is not divided into a macropaedia, micropaedia, and concise versions like Encyclopaedia Britannica is, we must serve all three user types in the same encyclopedia. Summary style is based on the premise that information about a topic should not all be contained in a single article since different readers have different needs;

many readers need just a quick summary of the topic's most important points (lead section),
others need a moderate amount of info on the topic's more important points (a set of multi-paragraph sections), and
some readers need a lot of detail on one or more aspects of the topic (links to full-sized separate articles)."

3. There are other articles about neurological disease which are better. IMHO these include:

I don't see any reason why we can't make PD as good if not better and make it a featured article.

4. There are several people working on the article that are expert in various fields. For instance it would seem Profsnow is an epidemiologist, General Tojo is a biochemist, I'm a neuropsychologist. Therefore I would suggest that for now we stick firmly within our areas of expertise. We should find a neurologist to take an overview of the introduction, diagnosis, prognosis sections.

We've got a neurologist on board already, user AFGriffithMD. He's in on discussions further up the page. --Dan 16:04, 27 June 2006 (UTC)

5. Until these principles are agreed I don't think anyone should make anymore changes to the page. --PaulWicks 10:13, 21 June 2006 (UTC)

I support a revision, but please start by reducing unsourced nonsense. At the moment whole sections are unreferenced or use the p4.forumforfree.com site as sources. This is not acceptable. Scientific review articles are the ideal source, not primary studies (the impact of which cannot be judged). Please use your judgement in moving unsupported material to the talkpage, always leaving clear and polite edit summaries.

At present we have no Misplaced Pages neurologist, so unless one of you can recruit one we'll have to make do without.

I would like to propose that blind reverts are not performed on this article. Rather, a contentious edit can be discussed on this very talkpage, and reverted if other editors agree it was not appropriate.

All editors please familiarise yourself with cite.php and make it a habit to cite peer-reviewed academic studies rather than URLs on potentially unreliable websites. JFW | T@lk 10:43, 21 June 2006 (UTC)

Prognosis This section has litle to do with the realities of what occurs in most people with Parkinson's Disease. The first section claims increased mortality, but even the second section nullifies it. It then misrepresents what usually occurs by implying that most people with PD die of pneumonia. Very few do, and the biochemistry of pneumonia has nothing to do with PD biochemistry. In disorders such as HIV it is reelvant to describe what usually eventually occurs. However, in PD there is no usual. The prognosis section is misleading, and of no practical use to anyone with PD.

General Tojo from what I understand you are a biochemist. Not a patient. Not an advocate. Not a clinican. Therefore on what basis can you put yourself forward as a representative of "anyone with PD"?. Frankly I'm not finding your edits to be helpful. --PaulWicks 17:49, 21 June 2006 (UTC)

It is obvious that we're talking here about dementia as part of Parkinson's. Also, they are both fairly common and it's quite possible that someone with Parkinson's will also develop dementia (James + Alois). All this is not reason to remove the whole paragraph. I'm pleased to see that General Tojo has now agreed to only remove part of the "prognosis" section. However, I would still like to see some data on the actual odds of death for PD patients. The argument that PD does not directly cause death is quite irrelevant: it predisposes for lethal conditions. Heart attacks do not cause death - only cardiac arrest does. JFW | T@lk 19:56, 21 June 2006 (UTC)

Once more unto the breach...

Right, that's better. OK what do you say we take up JFDWolff's suggestion about evidence? We could for instance start with adding and updating lines with the best evidence e.g. Cochrane reviews, then lit reviews, then big studies (esp RCTs), then small studies, then case series and then case reports.

Everyone might find it useful to read this section if they haven't already: WP:REF http://en.wikipedia.org/Wikipedia:Reliable_sources#Finding_a_good_source_may_require_some_effort

What do you reckon?

--PaulWicks 08:22, 23 June 2006 (UTC)

http://search.cochrane.org/search?q=parkinson%27s+disease&restrict=cochrane_org&scso_cochrane_org=this+site&scso_review_abstracts=reviews+only&scso_evidence_aid=evidence+aid&scso_colloquia_abstracts=colloquia+abstracts&scso_newsletters=newsletters&ie=&site=my_collection&output=xml_no_dtd&client=my_collection&lr=&proxystylesheet=http%3A%2F%2Fwww.cochrane.org%2Fsearch%2Fgoogle_mini_xsl%2Fcochrane_org.xsl&oe=&filter=0&sub_site_name=Cochrane.org+search

I would propose we try and get together a brief table of meds that patients might find useful, like a cutdown version of this: http://wiki.iop.kcl.ac.uk/default.aspx/Neurodegeneration/Drugs%20used%20in%20the%20treatment%20of%20PD.html

Treatment	Method of Action	Result	Side effects
Levodopa	Chemical precusor of dopamine	Improves stiffness, bradykinesia	"Wearing off" over time, tardive dyskinesia
Pergolide	Dopamine agonist	Treats symptoms of PD. May be more suitable for younger patients.	Associated with fibrotic heart disease, may increase risk of psychosis
Entacapone	COMT inhibitor, Increases half-life of doapmine	Reduces "wearing off". When used with L-Dopa reduces the amount of the latter required, thereby reducing liklihood of tardive dyskinesia.	May increase heart rate
Amantadine	NMDA agonist, blocks reuptake of dopamine	May help with tremor, may be particularly useful for young-onset PD	May worsen non-motor symptoms
Selegiline	MAOB inhibitor, decreases metabolism of dopamine thereby increasing half-life	Add-on therapy, may improve "wearing off" effects of dopamine replacement	May worsen non-motor symptoms
Entacapone	COMT inhibitor, decreases metabolism of dopamine thereby increasing half-life	Add-on therapy, may reduce the dose of dopamine replacement needed	May cause cardiac and gastrointestinal side effects

Sorry gotta go, back Monday. References would be nice! --PaulWicks 09:00, 23 June 2006 (UTC)

This is a useful way of presenting this information, especially if reliable sources are brought. Alternatively, we can start by simply presenting basic treatment algorhythms and leave in-depth comparison between the drugs for a separate page, such as antiparkinsonistic drug (compare anti-diabetic drug). JFW | T@lk 10:58, 23 June 2006 (UTC)

I really like teh succinctness of this table, teh article can discuss at greater length each treatment group, but as a quick aid this is well thoughtout. The risk is that too much info gets inserted over time - shorter is better. Also standardise/shorten method descriptions as 'COMT inhibitor: decreases dopamine metabolism' & 'MAOB inhibitor: decreases dopamine metabolism' and reverse word-order Levodopa method of action to 'Dpopamine precursor'. David Ruben 18:27, 15 July 2006 (UTC)

Cardinal symptoms

Paul, - first, because PD is a disease with a long latency and development, with patients able to ignore symptoms or ascribe them to old age, presentation is highly variable and the collection of symptoms people will have through the course of their disease is likewise variable. Second, in nosology in western medicine we define diseases by three main ways: by the cause (eg. Tuberculosis or asbestosis), by the anatomic site affected (almost any cancer, or by the symptoms (Parkinson's, Depression, and tuberculosis before we knew about the bug). People can be sickened by a rhinovirus, and have differing constellations of symptoms - it does not negate the concept of 'common cold'. Just so, varying symptoms of Parkinson's patients does not negate that disease concept. One could argue that more successfully with something like "fibromyalgia" or "chronic fatigue syndrome", though. --Dan 19:42, 30 June 2006 (UTC)

Non-motor symptoms

I've made a first early attempts to start citing material from Pubmed. I've also paved the way for the non-motor symptoms of Parkinson's disease article as I think this could turn into a disproportinately large part of the article.

Sorry I wasn't logged in, I'm away from home and clearly failing to have my wikibreak --PaulWicks 15:48, 23 June 2006 (UTC)

Pathophysiology and epidemiology sections

a) Terminology

When people refer to Parkinson's disease, it seems they are usually referring to the idiopathic disease first described by Dr. Parkinson. There are other less common diseases that are symptomatically similar to idiopathic Parkinson's, but either present with a few different symptoms, or have a known cause (that means they're not really idiopathic anymore, right?).

I think it's confusing to refer to these Parkinson's-like diseases as Parkinson's.

I have heard various researchers propose using the term "parkinsonism" when referring to diseases similar, but not identical, to idiopathic Parkinson's. (The "Related Diseases" section seems to allude to that.)

Perhaps this article could do something similar with the terminology?

A terminology clarification would mostly help the pathophysiology section. As currently written, I think it is hard to tell which of the various listed genotypes, toxins, traumas, or drugs are causes of idiopathic Parkinson's, and which are causes of different diseases that present with symptoms of parkinsonism.

b) Unilateral Causes vs. Part of Multifactorial Disease

Which of the aforementioned mentioned causes will induce parkinsonism all by themselves, and which are associated with the disease without causing it singlehandedly? (see Sir Austin Bradford Hill's criteria for causation).

I could be mistaken, but except possibly for acute PD and MPTP, I don't think there are any unilateral causes. Here's a worthwhile article on causation . I adhere mostly to the Rothman model of causation, with a little Popper thrown in (we were all mad for Popper about 20 years ago). --Dan 15:43, 26 June 2006 (UTC)

That's what I thought ... I think this should be discussed in the pathophysiology section, because it doesn't really read that way now. I actually rather agree with PaulWicks's earlier opinion on that matter (see the Toxins discussion ...) --GeekPhilosopher 17:42, 26 June 2006 (UTC)

c) More Epidemiology

Speaking of these causes, I've heard of several twins studies and of a career study, the results of which would enhance the epidemiology section. Is there an epidemiology-saavy person out there?

GeekPhilosopher 09:04, 25 June 2006 (UTC)

Hi GeekPhilospher, my understanding is this: If it looks like Parkinson's but it's not idiopathic (e.g. resulting for neuroleptics, MPTP exposure, brain damage) then it is parkinsonism. If it's MSA or PSP then it's a Parkinson's plus syndrome. I agree that things have got a bit confusing. There is a parkinsonism article, I don't know if you'd like to weave those together.

And we do have an epidemiologist knocking around, ProfSnow, who should be back from holiday tomorrow. Twin studies are important, as are the suggestions of a premorbid low-sensation-seeking personality. Cheers, --PaulWicks 09:17, 25 June 2006 (UTC)

sounds good ... I will see what I can do incorporating that into the pathophysiology section. Speaking of, is "pathophysiology" the best name for that section? --GeekPhilosopher 12:27, 25 June 2006 (UTC)

And I am back from the Society for Epidemiologic Research meeting in Seattle - and it was a very nice holiday, thank you. Twin studies and career studies I'm not sure on but can find out. Off the top of my head I'd bet Carlie Tanner did any twin studies. As far as careers go, we're all pretty tightly focused on farming & have been ever since Bill Langston found the MPTP outbreak, and even before - maybe since Barbeau? I will put my descriptive epidemiology, including incidence, section back as soon as things are open again, or in an appropriate sub-article. I'd frankly rather have epidemiology separate from pathophys, if you all don't mind. --Dan 15:35, 26 June 2006 (UTC)

Images

from my talk page, massive thanks to Chris_73, all round legend:

On a side note, Image:Parkinson surgery.jpg may be interesting to you -- Chris 73 | Talk 09:49, 25 June 2006 (UTC)

Just uploaded Image:PET scan Parkinson's Disease.jpg from a NASA (and hence free) site. CHeck also commons:Category:Parkinson's disease -- Chris 73 | Talk 09:56, 25 June 2006 (UTC)

One more: uploaded Image:Sir William Richard Gowers Parkinson Disease sketch 1886.jpg. Also Picture of Parkinson is here, which is PD due to its age. The image is not very good, however, and I do not know the painter or other source. Ok, hope this helps, best wishes, -- Chris 73 | Talk 10:08, 25 June 2006 (UTC)

Can someone more talented than me integrate these images? --PaulWicks 10:26, 25 June 2006 (UTC)

Sure can. See Misplaced Pages:Picture tutorial on how to do it yourself, and Misplaced Pages:Finding images tutorial for image needs -- Chris 73 | Talk 10:41, 25 June 2006 (UTC)

Related disease section

Essential tremor and Wilson's disease have been included as part of the Parkinson-plus diseases. However, while they may be associated with parkinsonism, my (naive) sense is that these are distinct clinical entities and would not be considered a Parkinson-plus disease like Shy-Drager syndrome. Andrew73 12:16, 27 June 2006 (UTC)

I think we're on the same page. These disorders which have similar symptoms like Wilson's disease, etc. would probably be better off included under parkinsonism rather than under Parkinson's disease. Or alternatively, perhaps a section about differential diagnosis, so that the distinction can be more explicit. Andrew73 13:02, 27 June 2006 (UTC)

I like the differential diagnosis section with pointers very much, Andrew. Familial tremor is, of course, far and away the most common miss, probably simply because it's common. So perhaps we should think in terms of rate of misdiagnosis for a given disease, thereby correcting for the rarity. When you have diseases such as PD that are defined and diagnosed solely by symptoms that vary from person to person and even for hour to hour, both clinical diagnosis and research can be tricky. --Dan 15:24, 27 June 2006 (UTC)

I like the idea of a "differential diagnosis" section too. The "diagnosis" section does need plumping up too, maybe on average time to diagnosis or average symptom duration? Other things to include or link off to new articles might be dopamine challenge, DAT-scan, and of course progression. i.e. Although many people may be misdiagnosed at any one particular timepoint, diagnoses can be revised if a period of time has past in which progression is at an unusual rate (either too fast or too slow). --PaulWicks 16:42, 27 June 2006 (UTC)

The time to diagnosis question is a good one. I've done some work on that and on time from initial diagnosis to final, correct diagnosis assuming the initial dx wasn't right. PD patients typically do not attach much significance to their initial symptoms at the time, but once diagnosed they realize that that symptom on that day was the (clinical) start. I don't recall details, but the work I did showed that time to dx was shorter for women, of course. --Dan 19:49, 30 June 2006 (UTC)

Toxins

An RCT is a Randomized Clinical Trial. A comprehensive summary of current knowledge would be here: or here: and a website indicating current questions is here: . --Dan 17:51, 28 June 2006 (UTC)

American Academy of Neurology

Recently a colleague coincidentally emailed me an article from Neurology about PD. It was one of four reports on Parkinson's disease this year by the Quality Standards Subcommittee of the American Academy of Neurology. They were made through systematic review of the current literature by a committee of movement disorder specialists and general neurologists.

See Neurology 66(7):966-1002 ... it's free to download at http://www.neurology.org/content/vol66/issue7/

Anyway, I think the 4 articles outline quite well the important questions and the answers currently known regarding diagnosis and treatment of PD, so I'm copying the conclusions from their abstracts:

"Diagnosis and prognosis of new onset Parkinson disease" (Neurology 66:968-975)

1. Early falls, poor response to levodopa, symmetry of motor manifestations, lack of tremor, and early autonomic dysfunction are probably useful in distinguishing other parkinsonian syndromes from Parkinson disease (PD).

2. Levodopa or apomorphine challenge and olfactory testing are probably useful in distinguishing PD from other parkinsonian syndromes.

3. Predictive factors for faster disease progression (more rapid motor progression, nursing home placement, and shorter survival time) include older age at onset of PD, associated comorbidities, presentation with rigidity and bradykinesia, and decreased dopamine responsiveness.

"Neuroprotective strategies and alternative therapies for Parkinson disease" (Neurology 66:976-982)

1. Levodopa does not appear to accelerate disease progression.

2. No treatment has been shown to be neuroprotective.

3. There is no evidence that vitamin or food additives can improve motor function in PD.

4. Exercise may be helpful in improving motor function.

5. Speech therapy may be helpful in improving speech volume.

6. No manual therapy has been shown to be helpful in the treatment of motor symptoms, although studies in this area are limited.

"Treatment of Parkinson disease with motor fluctuations and dyskinesia" (Neurology 66:983-995)

1. Entacapone and rasagiline should be offered to reduce off time (Level A). Pergolide, pramipexole, ropinirole, and tolcapone should be considered to reduce off time (Level B). Apomorphine, cabergoline, and selegiline may be considered to reduce off time (Level C).

2. The available evidence does not establish superiority of one medicine over another in reducing off time (Level B). Sustained release carbidopa/levodopa and bromocriptine may be disregarded to reduce off time (Level C).

3. Amantadine may be considered to reduce dyskinesia (Level C).

4. Deep brain stimulation of the subthalamic nucleus (STN) may be considered to improve motor function and reduce off time, dyskinesia, and medication usage (Level C). There is insufficient evidence to support or refute the efficacy of deep brain stimulation (DBS) of the globus pallidus interna (GPi) or ventral intermediate (VIM) nucleus of the thalamus in reducing off time, dyskinesia, or medication usage, or to improve motor function.

5. Preoperative response to levodopa predicts better outcome after DBS of the STN (Level B).

"Evaluation and treatment of depression, psychosis, and dementia in Parkinson disease" (Neurology 66:996-1002)

Screening tools are available for depression and dementia in patients with PD, but more specific validated tools are needed. There are no widely used, validated tools for psychosis screening in Parkinson disease (PD).

The Beck Depression Inventory-I, Hamilton Depression Rating Scale, and Montgomery Asberg Depression Rating Scale should be considered to screen for depression in PD (Level B). The Mini-Mental State Examination and the Cambridge Cognitive Examination should be considered to screen for dementia in PD (Level B).

Amitriptyline may be considered to treat depression in PD without dementia (Level C).

Cholinesterase inhibitors are effective treatments for dementia in PD, but improvement is modest and motor side effects may occur.

For psychosis in PD, clozapine should be considered (Level B), quetiapine may be considered (Level C), but olanzapine should not be considered (Level B).

Hope that's of interest (despite the length). I think it may help with cleaning up the PD article. --GeekPhilosopher 03:09, 29 June 2006 (UTC)

Very nice; thank you. To my mind, we need a good study of the incidence of dementia in PD patients compared with general population of that age. I put in a proposal to the feds a coupla years back to do that, and included stuff about developing a dementia instrument specific to PD. The reviewers thought we were biting off too much. I should go back in on that, though - I think it still hasn't been done, and I have the credibility in the field. What do you guys think? The underlying alternate hypothesis is that dementia is diagnosed more often in PD patients because they're seen more often by docs and because docs are keyed to look for it. --Dan 04:31, 29 June 2006 (UTC)

People?

Some of the other common disease have lists of afflicted famous people, such as List_of_people_with_multiple_sclerosis. Would it be worth consideration for this page set as well? Bdelisle 00:38, 4 July 2006 (UTC)

While we're at it, I also restored the "see also" section. This one, however, may need some population. -- Chris 73 | Talk 16:27, 5 July 2006 (UTC)

They are now at Category:Parkinson's disease sufferers which incorporates people said to have died from it, or complications around it- Kittybrewster 22:33, 9 July 2006 (UTC)

Toxins

Just to clarify, my understanding is that reactions to toxins like cyanide produce an acute onset syndrome resembling Parkinson's disease. But they do not produce Parkinson's. Is that correct? So should these toxins be listed under Parkinsonism rather than Parkinson's disease? --PaulWicks 17:31, 10 July 2006 (UTC) http://www.postgradmed.com/issues/1999/07_99/conley.htm

Agreed. I tried clarifying that with a sentence in the beginning, but perhaps this needs to be stated more explicitly. Andrew73 17:40, 10 July 2006 (UTC)

The distinction I've seen made clinically is this;

Parkinsonism is a syndrome of symptoms resembling idiopathic PD which usually does not usually respond to DA treatment such as sinemet or DA agonists. It can be caused by brain damage, vascular infarcts, and toxins. Sometimes it is progressive, sometimes not. In the case of toxicity, it may be reversible following removal of the toxin. The most obvious case I have heard of is poisoning by antipsychotic medication leading to an acute but reversible parkinsonism. Other toxic causes may be irreversible.
Parkinson's disease is progressive and responds to dopamine therapy and is the main clinical syndrome we all know and love.
Parkinson's Plus refers to PSP and MSA which are important to identify for the reason that they can be more aggressive and in the case of PSP have greater ocular and cognitive involvement. --PaulWicks 19:04, 10 July 2006 (UTC)

Parkinson Plus is clinically highly relevant, e.g. when there is a need to treat autonomic phenomena in MSA with autonomic features (formerly Shy-Drager). Toxins are certainly relevant, and if there has been rapid clinical deterioration a clinician may suspect carbon monoxide poisoning. Other toxicities are not generally suspected unless there are obvious clues (e.g. plethora and/or polycythemia in chronic HbCO). This is one of the reasons why in the UK the diagnosis of PD is now left to neurologists rather than general physicians. JFW | T@lk 20:38, 10 July 2006 (UTC)

Some ideas for parts that could be split off into new pages

Just ideas to cut down on article size and varying levels of detail, let's discuss before doing anything.

http://en.wikipedia.org/Parkinson%27s_disease#Symptoms - These could be summarised more briefly on the PD page with the main articles being Motor symptoms of Parkinson's disease and Non-motor symptoms of Parkinson's disease which would allow more space for explanation

http://en.wikipedia.org/Parkinson%27s_disease#Pathology - The level of detail here might be too much for the overview article. Suggest creating new article for full biochemistry.

http://en.wikipedia.org/Parkinson%27s_disease#Toxins - A version of this that cited original references could be useful.

Interested in views. --PaulWicks 17:01, 11 July 2006 (UTC)

p.s. Updated the drugs table above. We could if we wanted to split off another page for that as suggested a while back by JFDWolff, copied below. --PaulWicks 17:15, 11 July 2006 (UTC)

Rotenone

I wasn't sure why the link to the experimental model of rotenone toxicity was deleted, so I restored the text. The speculation here is grounded in a published article, so I think it's worthwhile including the reference. Andrew73 02:50, 12 July 2006 (UTC)

On the subject, I noticed there is a mistake in spelling in a sentance in that part of the article. Rotenone is an insecticide that has the (poptential)... --Sonicos 20:47, 28 July 2006 (UTC)

External links

Is there a guideline on what order to put external links in? It's a bit higgledypiggledy. First it's GT's forum, then one for Europe, then Canada... Alphabetical? By size of organisation? --PaulWicks 07:27, 12 July 2006 (UTC)

You mean order at the bottom of the article? I think it simply goes by order of citation in the article; I could be mistaken...--Dan 15:25, 15 July 2006 (UTC)

Differential

I removed this list of differential diagnoses:

Diseases that are in the differential for Parkinson's disease include:

Cerebellar thoracic outlet syndrome
Antiphospholipid syndrome
Vascular parkinsonism
Encephalitis lethargica
Hydrocephalus
Essential tremor
Wilson's disease

It is unreferenced, it has come from nowhere, and doesn't explain the relationship. Antiphospholipid syndrome is not associated with any extrapyramidal phenomena in the vast majority of cases. Essential tremor is usually ruled out early-on on clinical grounds. Wilson's disease should be mentioned, but not in such a random fashion (young PD patients should have copper studies, though).

Can we get a list from a reliable medical textbook, instead of someone's personal preferences? JFW | T@lk 07:33, 12 July 2006 (UTC)

All of the above are well known to cause symptoms some of which can coincide with those of Parkinson's Disease. A link was previously provided to the Parkinsonism page of the The Parkinson's Disease Forum. They are also linked to pages on Misplaced Pages where more information is given. So if somebody wants to expand on this section with additional brief inormation for each disorder the links and information are available for them to do this.

I agree with JFW that a laundry list of diseases that may resemble Parkinson's disease is not necessarily that useful (e.g. echoing again antiphospholipid antibody syndrome, which is quite distinct diagnostically and clinically). Andrew73 12:13, 12 July 2006 (UTC)

I just read the article describing three patients with movement disorders. All of these patients underwent intensive investigation, since their symptoms were more than just parkinsonism (apraxia, etc.). It doesn't seem like these patients were given a primary diagnosis of Parkinson's disease, the concern that you raised. It seems a bit of an overcall then to include APA in the differential. Andrew73 12:58, 12 July 2006 (UTC)

A cure for Parkinson's disease

1. Everyone who has a PhD has expertise in that subject ??? Be serious. He never said that - you're setting up a strawman. --Dan 22:25, 12 July 2006 (UTC)

Well then it's not a personal attack as you claimed when I point out that PhD's mean nothing. I assume you don't have one? The bare minimum qualification as a scientist? --PaulWicks 07:20, 13 July 2006 (UTC)

2. None of those people he referred to have ever cured anyone of Parkinson's Disease is a very relevant fact.

Have you ever cured anyone of PD? Last I heard it was an incurable disease. --Dan 22:25, 12 July 2006 (UTC)

I'd like to know of the cure for Parkinson's too! Andrew73 00:33, 13 July 2006 (UTC)

I have seen some people rid their symptoms altogether, and have seen many more continuously reduce their symptoms. That is why one of the largest and most prestigious hospitals in Britain is very enthusiastically arranging a full scale clinical trial to prove this formally and on a large scale. The methods Wimpys so called experts support could never cure anyone because they are so scientifically unsound from the outset.

Could you provide additional detail about this trial? Andrew73 00:33, 13 July 2006 (UTC)

Just because a trial is being discussed it doesn't mean it will happen. Even if it does it does not mean it will work. I've seen major hospitals do trials of quack substances before just out of curiosity. Also if there's money involved they'll do quite a lot of things.

I'm interested in the fact that when I use an appeal to authority (working at a large and prestigious hospital) you denigrate it, whereas when you're trying to persuade us, you want us to know that the trial is going on at another "of the largest and most prestigious hospitals in Britain". Or is it only institutions which you deem to be large and prestigious? --PaulWicks 07:20, 13 July 2006 (UTC)

3. Neurologists do not study biochemitsry. It is simply not part of a medical degree courses.

Actually, they do and it is. and in any case, so what? Biochemists don't study neurophysiology, so shouldn't be expounding on neurologic diseases. --Dan 22:25, 12 July 2006 (UTC)

Yup, all the neurologists I know are quite handy with their biochemistry actually. It sort of helps when you're prescribing drugs, but you've never done that.--PaulWicks 07:20, 13 July 2006 (UTC)

Actually, the formation of dopamine is studied in medical school, at least in the U.S. Andrew73 00:33, 13 July 2006 (UTC)

Likewise in UK David Ruben 00:37, 13 July 2006 (UTC)

I know it is at GKT. --PaulWicks 07:20, 13 July 2006 (UTC)

Thanks for the information. I'm not familiar with how clinical trials are done in the UK, but in the U.S. they're generally registered at http://clinicaltrials.gov/. Is there a similar reporting mechanism for this trial? I'm surprised that the full formulation has not yet been disclosed if it's already undergoing a clinical trial. Andrew73 12:15, 13 July 2006 (UTC)

Sorry Keith, I do apologise. I can see now where this has all sprung up from, it's a great misunderstanding.

I had incorrectly assumed that because you used the language of a scientist and spoke with such authority that you might actually be one. But if you don't have a PhD (even though I have three) then no wonder you're unable to work within the field (although I have all my adult life), publish peer-reviewed articles (although I've been published in seven languages in over 150 countries), obtain grant funding (even though I have), or collaborate with others (even though I am doing so continuously, and have done so for many years). We've all been addressing you as a fellow scientist (even though you're not one yourself) when in reality you are a layman (even though I'm not). I'm very sorry for the confusion this must have caused you, we will all endeavour to explain the way of the world in simpler terms from here on. --PaulWicks 14:02, 13 July 2006 (UTC)

So let me summarise then - there is no current available cure for Parkinson’s, but you are involved in a study that hopes to change this. Whilst I wish the study luck, there is therefore, as yet, no published peer-reviewed paper (WP:Reliable sources) to back up the current accepted wisdom that Parkinson’s is incurable - assertions to the contrary is, for now, just personal opinion/speculation and not acceptable under WP:NOR policy. If and when the study you are involved with is published, then medical knowledge will have advanced and wikipedia will I am sure reflect this (with suitable citations provided to verify).

Tyramine containing foods

I've included the comment about tyramine-containing foods being okay with MAO-B inhibitors in order to distinguish it from other MAO inhibitors that are used for depression, e.g. phenelzine. I imagine this is practically relevant information that should be kept in the article. (I'm not saying that tyramine-containing foods are a treatment for Parkinson's disease!) Andrew73 12:17, 13 July 2006 (UTC)

Incidence rates

True Parkinson's disease is global and Misplaced Pages is global. However, I think it's worthwhile to include the incidence rates, even if it's specific to one area. The information is factual and referenced. Instead of not including it at all, why not add information about incidence rates globally? Andrew73 18:33, 13 July 2006 (UTC)

Incidence and prevalence vary globally for many reasons, primary among them being diagnostic and ascertainment differences, with risk factor and true rate differences adding to that variation. Incidence rates are ascertained by counting all cases of disease arising in a defined population over a defined period of time. There are very few places in the world where that sort of study is practical Notice that I did include European studies. There are very few Asian PD epidemiologists, and those are mostly focused on risk factor epidemiology rather than descriptive epidemiology, although I have reviewed a prevalence study from Korea. The rates from northern California are solid because they come from a closed, well-defined population (Kaiser Permanente) with systematic surveillance mechanisms and excellent diagnostic standards (Dr. Caroline Tanner). --Dan 19:24, 13 July 2006 (UTC)

Incidence of 13.4 per 100,000 per year in California

Incidence of 186.8per 100,000 per year in Spain

Limited quoting of incidence rates is useful - either it highlights a need for the WP article to have a more rounded review of reported results added, or if there is a paucity of studies from which cite then that in itself is notable and should be commented upon. Likewise if there is great discrepency of reported incidence rates, this may indicate poor studies, different criteria for the studies (either diagnositic or inclusion criteria eg prospective or retrospective) or truely indicate that there might be genetic or environment variability. None of these suggest removing data just for being incomplete - WP after all specifically allows incomplete articles, namely stubs, which are tagged as such until they can be expanded into a full articles - no one goes about deleting stubs just for being incomplete. David Ruben 00:00, 14 July 2006 (UTC)

See, David, here's the thing. What you're really after with descriptive epi is etiological hypotheses. As you know, prevalence studies are limited in their value for that because they're too prone to bias. Incidence studies are sounder methodologically, but tougher to do (ie expensive) because you have to count all new cases in a defined population over time. And after you've done the study, what do you have? Well, some interesting rates and maybe some ideas on who gets more/less of the diease. But with Parkinson's, we think we've already got some pretty good ideas and what might be causing it, i.e. the farming chemicals, so why bother with the incidence studies - makes much more sense (and more likely to be funded) to jump right into the hypothesis testing studies, case-control design (if you're Karen Semchuk or Walter Rocca) or even cohort studies (if you're Alberto Ascherio and have access to the Nurses' Health Study). Which means the next section I oughta write up is the risk factor epidemiology section. I'm not convinced farming chemicals are going to be the big payoff everyone thought after Bill Langston found that MPTP outbreak back in what, 1986? I think there might be something else about farming. But we shall see. --Dan 14:44, 14 July 2006 (UTC)

Thanks for the points raised. My posting was mainly counter-arguement to DiamondPlus objecting to any such incidence info, if not a complete world-picture. You make some good points, but if "I'm not convinced farming chemicals are going to be the big payoff everyone thought " then perhaps "we think we've already got some pretty good ideas and what might be causing it" is not the case (hence a need appropriate studies). Even if hypothesis testing studies prove the cause, the cause might not be eliminatable: if it proved (for sake of discussion) due to nitrogenous toxins from meat-eating, then are people really going to fully stop eating meat (issues also of risks iron deficiency) - and I still would like to know the incidence rates (clearly 100% of meat eaters do not go on to get PD, if 10% risk it might affect my dietary habits, but at 0.1% I might decide to ignore the risk). Similarly incidence rates are useful in health planning. Leaving aside reduced incidence rates if the causative factors are identified and eliminated, if 2% of the current population have already been exposed to a causative factor and will inevitably now get PD at some point, then this will be a major health care service requirement, yet if incidence rates are just 0.1% then provision needs are relatively small compared to other diseases. Even if cause of PD is found and 100% prevention ensues, I would still like to know how much of a historical imposition this was to healthcare/social-services/individuals (in increasing importance) :-) David Ruben 15:39, 14 July 2006 (UTC)

Yup, good counter-points. Being an etiologic epidemiologist, the health services/public health impact tends to be something that occurs to me later rather than earlier, but of course for someplace like Nebraska, with a proportinally large old population, it's a serious matter. The town of Grand Island, for instance, in the late 90s underwent a boom in old people because some very nice supported living and nursing homes were built, drawing lots of people from the surrounding counties (nobody lives in those counties anyway), so of course the Nebrasks Parkinson's registry observed a rise in prevalence in Grand Island. At the same time, however, an obnoxious neurologist in north-eastern Nebraska steadfastly refuses to report his PD patients to the registry, so of course prevalence seems low there. --Dan 16:01, 14 July 2006 (UTC)

Risk Factor Epidemiology

A new section for the page, to go below "Descriptive Epidemiology". It would, I hope, help to answer some of the questions raised above, eg. "why aren't more descriptive studies being done?". One should perhaps call it "Analytic Epidemiology Studies", but that's a little too epidemiology-nerdy. So, try this for starters:

Introduction

Perception of a risk of Parkinson’s disease with rural exposures was not considered until the finding of acute Parkinson’s disease produced by a garage lab-made street narcotic in the early 80’s . Since MPTP resembles certain common herbicides (viz. paraquat), investigations of “rural” exposure or “well-water” use are a proxy for toxic chemicals. Since those initial descriptive studies we have moved from using the proxy exposure to see if the association exists to looking directly at the specific farm chemicals. Even more recently, lack of clear results from studies of pesticide exposure has led the PD research community to an interest in pesticide-gene interactions. There really is comparatively little work on rural exposures other than pesticides. Some of the other possibilities include diet; occupational chemicals other than pesticides - such things as heavy metals, sawdust, engine fumes, paints, and so on; zoonotic infectious agent exposures from farm animals. Farmers often have ample opportunity for exposure to all of these, and given that many farmers find it financially necessary to take supplementary jobs in the local area, they also have opportunity for more exposure to the types of industry, often quite dirty, commonly seen in rural areas. Tojo raised the question about sawdust, how could that be a risk factor - it seems unilkely, but of course farmers do their share of carpentry, and the sawdust generated includes not only wood components, but the chemicals the wood is often treated with for preservative and other reasons. Carpenters have been shown to have high rates of certain cancers, so sawing wood does pose health hazards.

and a bit of history

Early Observations

It's interesting that while PD in its later stages is readily noticeable and distinct, it was first described in detail by James Parkinson in 1817 , as the Industrial Revolution was gathering speed. A number of other neurologic conditions had been well described before that time. Therefore it might be that until Parkinson’s day the disease was very rare. Parkinson indeed noted conspicuous symptoms such as a gentleman who found it necessary to have a servant walk backwards in front of him to keep him from falling forward. It was not long following Parkinson that PD was noted to be among the more common illnesses seen in neurologic practice . Possibly some environmental exposure added significantly to the population risk of Parkinson’s Disease in the cities of the European Industrial Revolution. These may have now shifted to the rural areas as cities have become cleaner. This doesn't mean necessarily that the rural exposures are agriculturally related, but could be a result of some of the dirtier industries preferentially locating in more remote areas, whether to be near natural resources needed in that industry or to avoid the more restrictive regulatory environment of major cities.

Here's the early risk factor epidemiology, which was heavily influenced by Langston's findings, although at that time no animal model for PD existed.

Preliminary Descriptive and Ecologic Studies

Before the MPTP studies, a study in Finland relied upon the traditional two stage prevalence study design to examine descriptive epidemiology issues, but did not find a significant rural/urban difference, something they do not remark upon. While they did not regard this as a major concern, slightly later workers, in particular Ali Rajput cite the Langston work as a rationale for believing rural living to be a concern. Later workers followed Rajput’s lead in this.

Numerous case-control studies (Need a definition here?) report elevation of risk in rural areas , a few report elevated risk in urban areas , and there are reports of no association . Part of these differences are likely a result of geographic differences (comparing China versus Kansas, for instance), part due to methodologic problems, but part remains unexplained. Carlie Tanner suggests risk is associated with rural living in developed countries and city living in poorer countries.

A question not fully addressed by the early studies is precisely what is meant by “rural living”. Does it refer to farming, cattle ranching, living in the deep woods? Barbeau and Zayed both differentiated rural areas into farming and areas of rural industries, but ranches have not to this writer's knowledge been examined for association with PD, and the size of a community before it is termed ‘rural’ has had only cursory examination. Most of the arly studies focused upon proxies for chemical exposure such as use of well water or length of time spent in farming regions or occupations.

Literature Cited

1. Langston J.W., Ballaro P. and Tetrud J.W., Chronic Parkinsonism in humans due to a product of mepridine-analog synthesis, Science, 219, 979, 1983.

2. Langston J.W. and Irwin I., MPTP: current concepts and controversies, Clin. Neuropharmacol., 9, 485, 1986.

3. Ross G.W. et al., Association of coffee and caffeine intake with the risk of Parkinson disease, JAMA, 283(20), 2674, 2000.

4. Parkinson J., An Essay On The Shaking Palsy, London: Sherwood, Neely and Jones, 1817.

5. Charcot J.M., Lectures On The Diseases Of The Nervous System, Vol 1, Sigerson G., trans. London: The New Sydenham Society, 1878.

6. Gowers W.R., Diseases Of The Nervous System, American ed. Philadelphia: P Blakiston, Son and Co, 1888.

7. Barbeau A. and Roy M., Uneven prevalence of Parkinson’s disease in the province of Quebec, Can. J. Neurol. Sci., 12,169,1985b.

8. Aquilonius S.M. and Hartvig P., A Swedish county with unexpectedly high utilization of anti-Parkinsonian drugs, Acta. Neurol. Scand., 74, 379, 1986.

9. Rybicki B.A. et al., Parkinson’s disease mortality and the industrial use of heavy metals in Michigan, Mov. Disord., 8, 87, 1993.

10. Granieri E. et al. Parkinson’s disease in Ferrara, Italy, 1967 through 1987, Arch.. Neurol., 48, 854, 1991.

11. Svenson L.W., Platt G.H. and Woodhead S.E., Geographic variations in the prevalence rates of Parkinson's disease in Alberta, Can. J. Neurol. Sci., 20, 307, 1993.

12. Barbeau A. et al., Environmental and genetic factors in the etiology of Parkinson's Disease, Adv. Neurol., 45, 299, 1985a.

13. Tanner C.M. and Langston J.W., Do environmental toxins cause Parkinson's disease? A critical review, Neurology, 40(supp 3), 17, 1990.

14. Marttila R.J. and Rinne U.K., Epidemiology of Parkinson’s Disease in Finland, Acta. Neurol. Scandinav., 53, 81, 1976.

15. Bermejo F. et al., Problems and issues with door-to-door, two-phase surveys: An illustration from central Spain, Neuroepidemiology 20, 225, 2001.

16. Rajput A.H. et al., Etiology of Parkinson’s disease: environmental factor(s), Neurology, 34 (Supp I, 1), 207, 1984.

17. Rajput A.H. et al., Early onset Parkinson's disease and childhood environment, Adv. Neurol., 45, 295, 1986.

18. Rajput A.H. et al., Geography, drinking water chemistry, pesticides and herbicides and the etiology of Parkinson's Disease, Can. J. Neurol. Sci., 14, 414, 1987.

19. Ho S.C., Woo J. and Lee C.M., Epidemiologic study of Parkinson's disease in Hong Kong, Neurology, 39, 1314, 1989.

20. Koller W. et al., Environmental risk factors in Parkinson's disease, Neurology, 40, 1218, 1990.

21. Tanner C.M., Influence of environmental factors on the onset of Parkinson's disease, Neurology, 36(suppl), 215, 1986.

22. Tanner C.M., et al., Dietary antioxidant vitamins and the risk of developing Parkinson’s disease, Neurology 39(suppl), 181, 1989.

23. Zayed J. et al., Facteurs environnementaux dans l'étiologie de la maladie de Parkinson, Can. J. Neurol. Sci., 17, 286, 1990.

24. Butterfield P.G. et al., Environmental antecedents of young-onset Parkinson's disease, Neurology, 43,1150, 1993.

25. Stern M. et al., The epidemiology of Parkinson's disease: a case-control study of young-onset and old-onset patients, Arch. Neurol., 48, 903, 1991.

26. Semchuk K.M., Love E.J. and Lee R.G., Parkinson's disease and exposure to rural environmental factors: A population based case-control study, Can. J. Neurol. Sci., 18, 279, 1991.

27. Barbeau A. et al., Ecogenetics of Parkinson's Disease: Prevalence and environmental aspects in rural areas, Can. J. Neurol. Sci.,14, 36, 1987.

28. Sethi K. et al., Neuroepidemiology of Parkinson's disease: Analysis of mortality data for the U.S.A. and Georgia, Intern. J. Neuroscience, 46, 87, 1989.

29. Tanner C.M. et al., Environmental factors and Parkinson's disease: A case-control study in China, Neurology, 39, 660, 1989.

30. Sasco A.J. and Paffenbarger R.S. Jr., Measles infection and Parkinson's disease, Am. J. Epidemiol., 122(6), 1017, 1985.

Protection?

While the article is protected (which is likely to last a few weeks), we should discuss which sections of this important article need improvements, and in what way. I think the "toxins" section, despite General Tojo's insistence, occupies way too much space and should be reduced to the most established toxic causes (e.g. MTPT, HbCO). There may be room for a subarticle if all material is found to be highly-relevant (toxic causes of Parkinson's disease). JFW | T@lk 09:50, 14 July 2006 (UTC)

Agree, it needs to be debulked or spun off into a subarticle. Right now, it reads like a laundry list. I'm surprised that H₂O or O₂ aren't listed. Andrew73 12:27, 14 July 2006 (UTC)

You know what? I was looking through the older versions of the article, and up till Feb 2006 or so, as Barb Davids finished up her contributions, this was a pretty darn good page. Needed some epidemiology, of course, but it was pretty good. --Dan 19:00, 14 July 2006 (UTC)

Agreed. Please note that I created two other subpages, Motor symptoms of Parkinson's disease and Non-motor symptoms of Parkinson's disease that we can use to go into more detail. A postdoc just started in our team who specialises in hallucinations and I'd really like her to add more on non-motor symptoms. There simply isn't need for such detail on the main page though. If everyone's happy with the drug table I've put on the talk page (or would like to add to it) then I think we should have a drugs used in the treatment of parkinson's disease as Jfdwolff has suggested in the past. --PaulWicks 21:18, 14 July 2006 (UTC)

I reduced to semi-protection, as Tojo uses newer socks Jaranda 23:26, 15 July 2006 (UTC)

Re-protection please. --PaulWicks 11:54, 16 July 2006 (UTC)

(Personal attack) --Porcupine 99 11:58, 16 July 2006 (UTC)

Removed --GW_Simulations_{|User Page | Talk | Contribs | E-mail} 12:13, 16 July 2006 (UTC)

Possible forks created

I have noticed two new articles that are possible forks of this article have recently been created by a new user: The symptoms of Parkinson's Disease and Biochemistry of Parkinson's Disease. As I am not familiar enough with the topic to determine if these are valid content spin-offs or POV forks, and given the current protection status of the main article, I am bringing attention to the articles here so that appropriate actions may be taken by others if needed. --Allen3 21:10, 18 July 2006 (UTC)

Looking the material over, those are almost certainly posted by Bridgeman, aka General Tojo and over 150 sockpuppets. --Dan 21:22, 18 July 2006 (UTC)

Certainly look that way to me. Admins can you nominate for deletion please? --PaulWicks 21:46, 18 July 2006 (UTC)

The AfD for both articles is at Misplaced Pages:Articles for deletion/The symptoms of Parkinson's Disease. --Allen3 22:13, 18 July 2006 (UTC)

I've blocked Dundee Cake as tojo. If there's no use in having these pages, I could just delete them; or I (or anyone else) could remove all the content and redirect them here; or if anyone wants it to, the AfD discussion can continue: that's the default action unless there's a near-universal consensus to do something else. Tom Harrison 22:59, 18 July 2006 (UTC)

I'm inclined to think with what we've got from the pre-Bridgeman days (before Feb 2006) and what the rest of can contribute, we have plenty of solid, accurate material. --Dan 23:03, 18 July 2006 (UTC)

IMHO there should be a link under Notable Parkinson's sufferers to Category: Parkinson's disease sufferers - Kittybrewster 09:01, 29 July 2006 (UTC)

Archive?

I'd like to archive the older parts of this talk page. Is there a date before which the discussions are no longer active? Tom Harrison 18:06, 14 July 2006 (UTC)

Is the size a problem? I think most stuff before Jan 2006 is no longer active, since those earlier contributors - like BLDavids - aren't around anymore. A shame, but part of the size problem is Bridgeman's proliferative posting. --Dan 18:35, 14 July 2006 (UTC)

It's not so long as to be a problem, if it's useful to keep it. I'll leave it alone for now. Tom Harrison 19:52, 14 July 2006 (UTC)

Why not just archive all that is GT-related and leave the actual discussions up? Also please leave my drug table there! --PaulWicks 21:20, 14 July 2006 (UTC)

If you want I'll try to refactor the page, removing GT's remarks and all the replies to them. They'll still be in the history if anyone wants to refer to them. I'll be sure and leave the drug table. I'll try to do it tomorrow if no one objects. Tom Harrison 21:29, 14 July 2006 (UTC)

I wouldn't mind. --Dan 21:30, 14 July 2006 (UTC)

Some form of archiving is required - this page takes ages to load on my slow dial-up connection (almost makes me dread the boredom of waiting to view the latest postings here)- I agree in first instance archive off GTs trolling and then lets see if/where we wish to archive older historical discussion threads. David Ruben 23:47, 14 July 2006 (UTC)

I have finished refactoring the page. I tried to remove all the extraneous conversations, and in a few cases summarized people's words. Please correct any mistakes I made. The un-refactored version will of course be available in the history. Tom Harrison 13:14, 15 July 2006 (UTC)

Thanks, Tom - good work. Hope this helps you, David. Alternatively I hope Santa Claus (or maybe your Hallowe'en bag) brings you a fast connection. --Dan 15:31, 15 July 2006 (UTC)

Talk page now a pleasure to visit it loads so fast :-) Suspect will need wish hard, as would need faster computer to cope with broadband... David Ruben 13:34, 16 July 2006 (UTC)

Reprotected

King of Hearts (talk · contribs) unprotected the page, and within hours Tojo is all over it again. I see no other option but to protect it again. JFW | T@lk 22:31, 2 August 2006 (UTC)

Copyright vios

I'd like to thank DocRogers for removing a lot of the irrelevant info that has been clogging up that article for a while. Please don't anybody revert his improvements. --PaulWicks 12:51, 4 August 2006 (UTC)

Not to mention he directed us yet again to his private PD pages. And reminded us that there was some sort of copyright violation somewhere. Maybe we copied his copies. --Dan 16:09, 4 August 2006 (UTC)