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GA Review

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I have made some relatively minor contributions to this article, but I don't think they are extensive enough to disqualify me from reviewing it. I intend to be a bit more rigorous than usual for a GA review, since there is a plan to submit the article for FA in the near future. My own experience at FAC is that the process there tends to obscure content issues and focus more on details of form, so I am going to try to be especially careful about getting the content right. It will take me a while to make my way through the whole article -- I will add items as I go.

Reviewer: Looie496 (talk) 18:14, 23 November 2010 (UTC)[reply]

Hey Looie, many thanks for reviewing the article, specially if it is a FA directed review... I have to say that I first thought of you as a probable reviewer and it is good news that you have decided to do so. I will try to fix comments as fast as I can, although I am quite busy in real life..., anyway if the intention is to have an almost FA when the review ends neither of us should feel much time pressure.--Garrondo (talk) 21:04, 23 November 2010 (UTC)[reply]

The lead

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  • The first thing that occurs to me is that because this is a relatively common disease, it would be good to make clear right from the start that non-motor symptoms such as dementia do not become obvious until quite advanced stages of the disease.
Done.--Garrondo (talk) 21:11, 23 November 2010 (UTC)[reply]
  • The distinction between PD and parkinsonism is clearly defined, but I am afraid that readers may find it hard to understand. I think it would be preferable in the first paragraph to define PD without reference to parkinsonism, and then in the second paragraph introduce the term as a name for a broader range of conditions.
Done: I have simply eliminated mention of parkinsonism in the lead and left it for the classification section.--Garrondo (talk) 21:11, 23 November 2010 (UTC)[reply]

Continued

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After a delay I'm starting through. I'm actually not finding much wrong in terms of content, and mainly am doing copy-editing as I go. (If I seem to be introducing mistakes, please feel free to fix them.) Looie496 (talk) 19:19, 30 November 2010 (UTC)[reply]

Everything looks fine. Thanks for that.--Garrondo (talk) 19:28, 30 November 2010 (UTC)[reply]
  • Signs and symptoms: neuropsychiatric: I think the second paragraph could be expanded here. The list of symptoms is a bit too condensed to be easily grasped. In particular, I doubt most readers will know what "set shifting" is.
I will have to think out how to implement this. Sometimes it is hard to find balance between depth of content and summary and lay styles. I'll probably expand it without adding new info, so it is easier to understand.--Garrondo (talk) 19:28, 30 November 2010 (UTC)[reply]
That's basically what I had in mind. Looie496 (talk) 19:34, 30 November 2010 (UTC)[reply]
More or less done. I have mainly copied the definition from the executive function article and broken text into several sentences. What do you think? --Garrondo (talk) 21:01, 1 December 2010 (UTC)[reply]
  • Causes: I think this section and the following would be much easier for readers to understand it they began with some prefacing material. The thing that readers need to be told is that the form of neural damage responsible for PD is very clearly understood and has been known for decades -- it is caused by damage to a small midbrain area called the substantia nigra, specifically to cells there that synthesize the chemical dopamine. Anything that damages these cells can produce the set of symptoms known as parkinsonism. For example the drug MPTP, intended by its creators as a hallucinogen similar to LSD, turned out to be toxic to nigral dopamine cells and caused a number of people who took it to develop permanent parkinsonian symptoms. Or something along those lines.
I disagree this time: That is too similar to pathophisiology. In addition damage to midbrain is the cause of parkinsonism, but more a consequence of parkinson's disease, which in the classification section has already been defined as "idiopathic parkinsonims". It would be an incongruence to say that an idiopathic disease has a known cause. I feel I will leave it as it is.--Garrondo (talk) 20:44, 1 December 2010 (UTC)[reply]

Continued again

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  • Classification There is a point here that I think ought to be brought out, but I don't know the PD literature well enough to say whether it is sourceable. The point is that the definition of PD as "idiopathic parkinsonism" creates problems for researchers, because it means that as soon as you have identified the cause, what you are looking at is no longer Parkinson's disease. Looie496 (talk) 17:35, 14 December 2010 (UTC)[reply]
Yeap, but right now it is the definition, with the exception of genetic cause. It was defined so to eliminate all secondary parkinsonisms such as traumatic, epileptic, vascular... I suppose that if one day exact cause of primary parkinsonism is known definition will have to be changed.--Garrondo (talk) 21:27, 14 December 2010 (UTC)[reply]
With under-appreciated I meant that they received less attention than deserved. Nevertheless simply eliminated.
  • Neuropsychiatric I think it is important to emphasize that for most patients, cognitive symptoms do not become obvious until advanced stages, if at all. We need to keep in mind that many people will read this article because they have to interact with somebody with PD. If we give them the expectation that the person they are dealing with is probably mentally impaired, we are doing a disservice. Looie496 (talk) 17:43, 14 December 2010 (UTC)[reply]
Agreed. I have moved the possibility of having cognitive symptoms to later in the sentece to reduce their weight.
Agreed. Removed.
Mono-: prefix meaning only one. Monogenic: due to only one gene. Probably synonim of monogenetic. Reworded for clarity
  • Physiology I have made some adjustments in wording, but there are two points I will bring up here. First, the abbreviation GPe is used without being defined. Second, the explanation of direct and indirect pathways refers to the putamen. To my understanding this applies to the entire striatum, not just the putamen. Looie496 (talk) 18:06, 14 December 2010 (UTC)[reply]
I'll try to look at the references, but if I have to tell you the thruth phisiology is far from being my area of expertise and I am always unsure when editing these kind of sections. I do not know if it will be way too much to ask, but if you are interested you could try to check it out against the reviews provided as sources before taking it to FAC, and improve it at your will.
Fixed the first comment: GPe defined. Second will take me more time.
Done with the second comment. It has been some time, but I have been away during Christmas. I have been taking a look at several references and you are correct. References talk about striatum in general. Changed. Thanks for the catch.
Sure. Done
Longer explanation for clarity. I hope it helps.
Too tired to work on this today. I will look at it tomorrow.
Done: Changed to "while controlling fluctuations of the response to medication".

Thanks a lot Looie for your useful comments. It is great to have a review such as this one. Bests.--Garrondo (talk) 21:27, 14 December 2010 (UTC)[reply]

Continued again, again

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Sorry for the long delay -- I am always a bit disfunctional in November and December, but I'll try to get through the rest of it quickly.

No problem... December is a horrible month in RL for everybody. :-)--Garrondo (talk) 09:50, 7 January 2011 (UTC)[reply]
  • Causes Shouldn't there be at least a short discussion of possible environmental causes? I know that none have been conclusively identified but many have been suggested. I have also heard some people say that they believe that dopamine cells tend to die naturally with age more rapidly than other neurons and therefore almost everybody who lives long enough will eventually become Parkinsonian, but I'm not aware of any literature relating to that idea. Looie496 (talk) 18:19, 6 January 2011 (UTC)[reply]
Well, I have given this a lot of thought and I still not decide myself. The thing is that I have tried to follow sources, and sources have two different approaches: since environmental factors are not proven as causes but only have appeared as risk factors in epidemiological studies, with no known mechanism for the risk-increasing; in many sources they talk about them in the epidemiology section as I have done, while others talk about them in the causes section. I prefer to leave them in epidemiology. Maybe I should add a sentence pointing from the causes section to the epidemiology section. What do you think?
  • Physiology I have taken the liberty of rewriting the second paragraph, which I thought included too much detail and was not understandable by a broad audience. This is the part of this topic that I understand best so I'm pretty sure I got it basically right, but feel free to edit, or to revert back to the other version if you think I'm completely off the mark. Looie496 (talk) 18:47, 6 January 2011 (UTC)[reply]
Sounds great... It is the part you know best, and the part I know less, so your help is great.
  • Pathology "affecting up to 70% of the cells" -- can you check on this? My understanding is that the level of dopamine cell loss can be much higher. In fact I thought that symptoms were minimal until dopamine loss exceeds 90%. Looie496 (talk) 18:51, 6 January 2011 (UTC)[reply]
I know. I have also read such numbers. The picture I made in my mind was that they are talking here about any kind of cells and not only dopaminergic. I am quite sure that the number is 70 in the source, but I will check it on monday (need access to journals at work)
  • Levodopa I think it would be good to explain that the concept underlying L-Dopa treatment is to compensate for the loss of dopamine cells by inducing the remaining cells to produce more dopamine. This approach works for a while but eventually fails when the few remaining cells reach the limits of their metabolic capabilities. Furthermore as this limit is approached, the behavior of the hyperstimulated cells becomes more and more erratic, causing uncontrollable fluctuations in the levels of dopamine in the system. Looie496 (talk) 19:10, 6 January 2011 (UTC)[reply]
Are you referring to the management section?
Yes.
Yes. Done. Good catch
  • Risk factors and protective factors The sentence reading "Toxins that have been consistently related to the disease are certain pesticides and herbicides, with exposure doubling the risk" is not good. It needs to make it clearly what sort of exposure it is talking about -- or else it could say something like with exposure increasing the risk by as much as a factor of two. Looie496 (talk) 22:36, 7 January 2011 (UTC)[reply]
Included your proposal.
  • Research directions I found this section quite difficult to understand, and in the process of copy-editing, have added some introductory statements that I hoped would make it clearer to non-experts. Please check that I haven't screwed up, and revise anything that seems incorrect or poorly stated. Looie496 (talk) 19:24, 11 January 2011 (UTC)[reply]
Sounds Ok, although it would be great to have a ref for the first paragraph. Also many thanks for the ce of the history section.--Garrondo (talk) 08:07, 12 January 2011 (UTC)[reply]
I can take a look into commons, although I believe I already did and found nothing.--Garrondo (talk) 19:01, 13 January 2011 (UTC)[reply]
While there is a specific symbol, in general red tulips are widely used as symbols. I have added a photo of a red tulip. Best I could found.--Garrondo (talk) 19:10, 13 January 2011 (UTC)[reply]

Passing

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At this point I am sufficiently satisfied to promote the article to GA. I wouldn't say that it is perfect, but I feel that it is an article that Wikipedia can be proud of and that somebody who wants to know about PD can read with great benefit. Thanks for putting up with the very lengthy review process. Looie496 (talk) 17:54, 15 January 2011 (UTC)[reply]