Talk:Paroxysmal exercise-induced dystonia

note

The first opening paragraph would be better written in the following way so that it is clearer for the reader: Paroxysmal exercise-induced dystonia is a rare neurological disorder characterized by sudden, transient, involuntary movements, often including repetitive twisting motions and painful posturing that is triggered by exercise or other physical exertion. It is in the class of paroxysmal dyskinesia, which is a group of rare movement disorders characterized by attacks of hyperkinesis with intact consciousness. The term paroxysmal indicates that the episodes are sudden and short lived and usually unpredicted, and the return to normal is also quick.[2] Episodes may last for several hours.

You say that episodes may last for several hours in the first paragraph, but under symptoms say they only last 5-30 minutes. This is a contradiction. Also, check for grammar mistakes within the entire article.

Is there any ongoing research for this condition? This would strengthen your article. The causes section for familial cases is complete, but you should add more for the sporadic causes. How do head injuries cause this? Is there a certain part of the brain that gets affected? Tothje (talk) 00:49, 30 November 2009 (UTC)

The opening paragraph might be better if a short definition is given for each term like it is for paroxysmal (like for dyskinesia and hyperkinesis). How do they all relate to dystonia? It’s just a little unclear. Also perhaps moyamoya could be discussed in the “Related Disorders” section or some other part of the article to include the findings of “Moyamoya disease presenting with paroxysmal exercise-induced dyskinesia” in Parkinsonism & Related Disorders. (Volume 13, Issue 7, Pages 446-448 C. Lyoo, D. Kim, H. Chang, M. Lee) (JLB1117 (talk) 03:36, 29 November 2009 (UTC))

There is a lot of good information packed into this article. In the Related Disorders section, it should be included that PED can be closely tied to Parkinson's disease. I have read that there are cases in which PED is the preceding symptom of familial Parkinson's disease. In rare cases, PED can also be the presenting symptom. You may also want to look into "epilepsy, rolandic with paroxysmal exercise-induced dystonia and writer's cramp". In the Treatments section, there needs to be some clarification as to why the limited benefits of levodopa on treating PED symptoms makes the disease a possible precursor to Parkinson's disease. CafeDelMar (talk) 01:49, 20 November 2009 (UTC)

You may want to mention the rarity of the disorder earlier on, or move up the Reported Cases section, because it would then make more sense reading about the causes of individual cases in the Causes section. In typical articles pertaining to diseases, you hear more about statistics than individual cases, so mentioning it sooner might make it clearer why you talk more about individual cases rather than statistics. “Paroxysmal exercise-induced dystonia: Eight new sporadic cases and a review of the literature,” Movement Disorders, Volume 12 Issue 6, Pages 1007 – 1012, Published Online: 4 Nov 2004. This is another paper by an author that you have used already, but it may be helpful to expanding your Sporadic Causes section which is only a couple of sentences right now. This should be enough information to find the article online. With such a rare disease, this paper should be helpful in expanding and analyzing other cases. Also, you make the point that there are only twenty cases reported worldwide of this disorder. I have not found anything to suggest that you are wrong, but since this paper talks about fifteen cases, you may just want to double check. Aaron.fishman (talk) —Preceding undated comment added 21:27, 22 November 2009 (UTC).

Is Paroxysmal Exercise-induced Dyskinesia the same as Paroxysmal Exercise-induced dystonia? If so this article may be of interest to you. You can find it at the following url: http://www.medscape.com/viewarticle/581684_5. The article can be used to greatly expand your wiki page with its analysis on the genetics behind the disorder. It explains how linkage studies on the pure disorder have been uneventful, but diseases,such as CSE, which include paroxysmal exercise-induced dystonia have been mapped to chromosome 1p among others. It also features a short segment on treatments that you may find useful. Giantsjs2000 (talk) 03:00, 24 November 2009 (UTC)

I found an article that suggests that paroxysmal exercise-induced dystonia, rolandic type epilepsy, and writer's cramp may be linked to the same gene and have autosomal recessive inheritance. The article is called "Autosomal Recessive Rolandic Epilepsy with Paroxysmal Exercise-Induced Dystonia and Writer's Cramp: Delineation of the Syndrome and Gene Mapping to Chromosome 16p12-11.2 and can be found here: [[1]]. You may want to include this information under the familial causes section to show the relationship between these three occurrences for additional information. There is also a typo in the related disorders section where you say, "PED is usually affects muscles...". Lastly, you can change the way you cite your information by assigning a "ref name" to a reference the first time you refer to it and then using this ref name to refer to the same reference further in your article. You can find out how to do this by going here: [[2]]. Farnhach (talk) 04:13, 29 November 2009 (UTC)

There is a lot of great information in this article, but I think you could benefit from the above suggestions in terms of re-organization to make sure the information flows logically from section to the others. Also, in your introduction I would change the sentence "and return to normal is also quick" to something that sounds a bit more clinically sound. In terms of adding more information to enhance the "Causes" section of the article, I would go into greater detail as to how paroxysmal exercise-induced dystonia is related to epilepsy and Parkinson's Disease. Even though you mention that the relationship is unknown, there is literature on PubMed that discusses how in some cases, PED can rarely be the first and only feature of PD (http://www.ncbi.nlm.nih.gov/pubmed/14673897?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=9. There was also another article that examined a case study involving post-traumatic paroxysmal exercise-induced dystonia, found at http://www.ncbi.nlm.nih.gov/pubmed/12853238?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=10. I think this would be a good addition to the article to elaborate on potential causes, especially due to the condition's rarity and the lack of current information. The article also discusses treatment with baclofen, which I think could enhance your "treatment" section. Additionally, I found an article that discusses the specific sections of the brain that the disorder affects, which I feel would justify the addition of a "pathophysiology" section. The article is called "Changes in perfusion pattern using ECD-SPECT indicate frontal lobe and cerebellar involvement in exercise-induced paroxysmal dystonia" and can be accessed through PubMed, http://www.ncbi.nlm.nih.gov/pubmed/9452337?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=21. Naweston (talk) 17:29, 29 November 2009 (UTC)

Hey, great article, especially since it’s such a rare disease, it must have been hard to find literature. I noticed that the link between Parkinson’s and PED may not be that strong. In one of the articles mentioned above (http://www.ncbi.nlm.nih.gov/pubmed/14673897?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=9) the researchers note that only two cases were observed, and that PED it is likely neither the first nor the only presenting feature of Parkinson’s Disease, as well as the fact that it is only related to young-onset Parkinson’s. Additionally in this article (http://www.ncbi.nlm.nih.gov/pubmed/14978684?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=12) researchers note that the set of cousins showing both PED and early onset Parkinson’s, lack the parkin mutation associated with early onset Parkinson’s. They claim that the family may in fact show a genetic variant of PD. Again, good job, and good luck! Philipthegreat88 (talk) 00:10, 30 November 2009 (UTC)

This is a well-written article with a good amount of information. The only suggestion I have is that you maybe add more to the Treatments section. You discussed that a possible contributor to PED may be mutations in SLC2A1, so you may want to include this as a potential new treatment option. I found that autosomal dominant heterozygous SLC2A1 mutations are currently undergoing research as a possible source of treatment for this syndrome. You may want to look into this further and include some data supporting this method of treatment. Hope you find this useful! bartond (talk) 00:43, 30 November 2009 (UTC)

As stated above, you might rethink your location of the Related Disorders entry to be either integrated into or following the topic introduction. It would make it a much easier read if it was stated how rare this disorder is worldwide. The section discussing the causes of paroxysmal exercise-induced dystonia is well done, but I would have liked more information on sporatic exercise induced-dystonia with regard to how the trauma alters the brain to cause these neurological problems or whether the symptoms are progressive with the onset of the trauma. Bhattacharyya KB, et al. describes the case of a patient demonstrating sproatic exercise induced dystonia in the article, "Sporadic paroxysmal exercise induced dystonia : report of a case and review of the literature" which may be helpful in expanding this section.

The treatment section should also clarify that while paroxysmal exercise induced dystonia can occur with Parkinson’s disease, it is in rare cases that it is a presenting symptom. You might also think of including the case discussed by Michiko K Bruno, MD, et al., which describes the curling up of the toes in two patients as presenting symptoms for Parkinson’s disease, which both patients developed later. An example of a preceding symptom might be interesting in this section. Additionally, possible expansion of which symptoms are reduced with treatment or what the drugs actually do in relation to reducing symptoms would be helpful in reading the article and understanding the mechanisms of the disorder. Good luck! Daigleal (talk) 02:11, 30 November 2009 (UTC)

Great article about a very interesting condition. In the introduction you say that episodes can last a few hours, but under symptoms you say they can last between 5-30 minutes. One statistic I saw said the average range was about 5 minutes-2hours so you may just want to expand 30 minutes to 2 hours. Here is the source for that http://www3.interscience.wiley.com/cgi-bin/fulltext/109747681/PDFSTART. That article also mentions a few more drugs which can be used for PED. You can add these to your treatments section. You may want to mention something about hemidystonic attacks, in which only one leg for example may be affected. Also, you may want to get into the specifics of muscle contractions and stimuli which trigger PED. Here is a link to a controlled experiment investigating the specific stimuli which seem to cause PED http://jnnp.bmj.com/content/70/2/247.full.Sunderv (talk) 01:41, 30 November 2009 (UTC)

Great article. One thing that I was a little confused about was the movements that occur sound like a seizure but other literature makes it seem more like a writer’s cramp. Maybe in the article you could clarify the severity of the movements (or use a picture) so that someone that is looking this up quickly could better understand it. If there is literature, I might also include the mechanism by which homovanillic acid and 5-hydroxyindoleacetic acid could potentially contribute to PED. It was also stated that concussions and head injuries could lead to PED, but does not specifically mention which parts of the brain are affected. Finally, A Munchau et al performed a study and concluded that PED is not linked to the PNKD, FHM, or ICCA loci, indicating that can be shown to be different from the other disorders by the position of its locus. They go on to state that the gene could code for an ion channel which could be the likely underlying cause of the disease.lavallco (talk) 20:23, 29 November 2009 (UTC)

Good job, I researched and had a hard time finding specific information about this. A few grammatical errors need to be addressed. Under the “Symptoms” heading, a sentence is written not very clearly. “Cerebral spinal fluid (CSF) analysis before and after exercise showed a two-fold increase of homovanillic acid and 5-hydroxyindoleacetic acid in the CSF was observed after exercise” is confusing because two components present in the CSF are addressed, but it should read something clearer, like: …analysis before and after exercise showed a two-fold increase of homovanillic acid, and (either increase or decrease, and to what extent, two-fold, etc. here, because it is unclear if you mean a two-fold increase in both components, or if there was simply an observed increase in 5-hydroxyindoleacetic acid) . Also, the phrase “was observed after exercise”, sounds awkward, so you can also restructure the sentence to read like the following (these are just suggestions, because it was just confusing to me when I read it): Analysis of cerebral spinal fluid (CSF) before exercise versus after exercise shows a two-fold increase of homovanillic acid and a ______ increase of 5-hydroxyindoleacetic. This way, you can avoic repeating “was observed after exercise”. Also, I believe that under the heading “Causes/Familial” you probably meant to say autosomal-dominant, not “autosomal-dominate”.

Additionally, since so many hits on the internet for this disorder also bring up epilepsy, I think it would be great to research a bit more on how these two things are related. I found an article on PubMed which looks potentially useful in discussing current research about the correlation between the two. The abstract includes a hypothesis that perhaps a common pathophysiological process exists underlying both a type of epilepsy called “childhood absence epilepsy” and later on in life, the development of paroxysmal dystonia. http://www.ncbi.nlm.nih.gov/pubmed/16244563?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3 aryberg89 (aryberg89) 23:58, 30 November 2009

Potential Revisions

Great start guys. I have a general idea of what PED is, which is definitely a start. I do have a few questions and suggestions though.

• I would put PED after you introduce the term in the introduction and possible in the page title because I inferred that that meant Paroxysmal exercise-induced dystonia in the subsequent sections, but it is possible that some people will be confused.
• Does it only last for 5-30 minutes or can it last for hours? You contradict yourself. In the first part you say it can last hours and then in the symptoms section you say it only lasts 5-30 min
• Also in the symptoms section the first sentence of the second paragraph is a bit confusing if you read it out loud. You will see that you said it showed ____ and that ____ was observed. I would just cut out the "was observed" and you should be all set
• Can you explain the physical symptoms a bit more in the symptoms section. You give an overview of what happens in the introduction, but I think you need to include a little more about it in the symptoms section.
• You mention it is related to epilepsy. Do you know how?
  • Same question for Parkinson's. You explain this slightly in the treatments section but is that the only way they think they are connected? check out this site it may have a bit of information on that: http://www.ncbi.nlm.nih.gov/pubmed/14978684

• You might want to mention something about the male to female ratio (3:1) http://www.ionchannels.org/showabstract.php?pmid=10766892
  • Do they know why that is?

• You mention that insulinomers, do they occur only in the sporadic cases or have there been any in the familial cases
  • I know you said there were only 2 cases that had them but that is 1 in 10 which is a somewhat significant percentage

• Do they know which chromosomes are involved in familial PED?
• You should probably link Xenopus oocytes and cerebral perfusion
  • And re-link the Parkinson's Disease and insulinomers in the treatment section
• Do they know why Acetazolamide was helpful in some cases and harmful in others?

I really liked the Related Disease section, especially the way you pointed out the distinctions between the 3 diseases. I also thought the Causes section was written quite well. You guys have a really good start here and I am sure the final product will be great! Good Luck Finishing this up. (Liskak (talk) 22:31, 29 November 2009 (UTC)

Potential Revision A description of the neuroanatomy of the brain, which this disorder specifically targets, would inform viewers know which parts of the brain are being altered or damage or what motor neuron is being affected to cause the jerks. You mentioned in your reported cases section of your article that a MRI analysis of a patient showed “increase cerebral perfusion in the primary somatosensory cortex area, and a mild increase in the region of the primary motor cortex and cerebellum.” Is there any other cases which support this finding? I think it would be helpful to put more of the reported cases in the reported cases section especially since the disorder is so rare. There was one website: (http://www3.interscience.wiley.com/journal/109747681/abstract) which discussed eight new sporadic cases. In the related disorder section, there was also another related disease, which I found would made sense with this disorder, Parkinson disorder or migraine disorder http://www3.interscience.wiley.com/journal/105559565/abstract; http://www.ncbi.nlm.nih.gov/pubmed/14978684; http://www.ionchannels.org/showabstract.php?pmid=10766892 There is also a recently new article concerning pediatric movement disorders. which might be help and Paroxysmal exercise-induced dystonia was mentioned in this article so it might be helpful to look it up and see if any new conclusions or research has been made about this disorder.

	A social/psychological section on your page would also help people understand how this disorder affects people on an emotional level because it is so rare. Here is a website: http://www.experienceproject.com/groups/Have-Epilepsy-Rolandic-With-Paroxysmal-Exercise-induced-Dystonia-And-Writers-Cramp/95462

(Jesspf (talk) 11:49, 29 November 2009 (UTC)

Good job, I researched and had a hard time finding specific information about this. A few grammatical errors need to be addressed. Under the “Symptoms” heading, a sentence is written not very clearly. “Cerebral spinal fluid (CSF) analysis before and after exercise showed a two-fold increase of homovanillic acid and 5-hydroxyindoleacetic acid in the CSF was observed after exercise” is confusing because two components present in the CSF are addressed, but it should read something clearer, like: …analysis before and after exercise showed a two-fold increase of homovanillic acid, and (either increase or decrease, and to what extent, two-fold, etc. here, because it is unclear if you mean a two-fold increase in both components, or if there was simply an observed increase in 5-hydroxyindoleacetic acid) . Also, the phrase “was observed after exercise”, sounds awkward, so you can also restructure the sentence to read like the following (these are just suggestions, because it was just confusing to me when I read it): Analysis of cerebral spinal fluid (CSF) before exercise versus after exercise shows a two-fold increase of homovanillic acid and a ______ increase of 5-hydroxyindoleacetic. This way, you can avoic repeating “was observed after exercise”.

Also, I  believe that under the heading “Causes/Familial” you probably meant to say autosomal-dominant, not “autosomal-dominate” which is there currently.  Additionally, since so many hits on the internet for this disorder also bring up epilepsy, I think it would be great to research a bit more on how these two things are related.  I found an article on PubMed which looks potentially useful in discussing current research about the correlation between the two.  The abstract includes a hypothesis that perhaps a common pathophysiological process exists underlying both a type of epilepsy called “childhood absence epilepsy” and later on in life, the development of paroxysmal dystonia. http://www.ncbi.nlm.nih.gov/pubmed/16244563?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=3 aryberg89 (aryberg89) 23:58, 30 November 2009

It's a good start, but overall I think more detail is needed in your article. In your intro I would include a short definition of hyperkinesis so that the reader can be informed right from the start. I think you should discuss the CSF analysis in more depth. Exactly how does it indicate increased dopaminergic transmission? And what does this mean for PED? How does dopaminergic transmission relate to PED? You talk about the GLUT1 gene and how a mutation in the gene leads to reduced GLUT1 transporter activity, but what role does the GLUT1 trasporter play in PED mechanistically? When you talk about the sporadic cases of PED, you mention one case of PED after a concussion? Is this the only case of sporadic PED known? If that is the case, is it enough to cite and refer to? I think your article is very interesting, but you should consider adding more detail about the mechanisms and pathophysiology behind the disorder. (Brikathleen (talk) —Preceding unsigned comment added by 136.167.247.48 (talk) 05:05, 30 November 2009 (UTC)

Overall, the article is pretty good, but could use more specificity. There are also some grammatical errors. I noticed that there is a discrepancy in the noted duration of of episodes between the introduction and the symptoms section. In the sporadic section, only the experience of one person is noted-- more information could be used. In the treatment section, several treatments are listed, but not HOW or WHY they work. The reported cases section is a little confusing. There is an explanation of what happens in the brain, but not how that relates to symptoms. Finally, it would be interesting (if possible) to discuss why this disorder is so rare and why, even though it tends to be hereditary, it can be induced by trauma. (alexbodo (talk) 7:14, 30 November 2009 (UTC)