Talk:Muscle relaxant

message: .:Wow... what a glaring error.  A muscle relaxant affects the gamma fibers on the alpha motor neuron which it turn decreases the tone of the muscle (the last theory that I recall since it still is likely unknown how it works).  What is described in this section are Paralytic agents!  As in prevent muscles from contracting completely:.
Example of relaxant:  flexeril, robaxin
Exapmle of paralytic: succinylcholine, rocuronium, pancuronium, vecuronium, etc..
I believe that cyclobenzeprine (flexeril), robaxin, etc. are relaxERS.  RelaxANTS are paralytics.  In any event, this article should NOT contain mention of spasticity-relieving drugs at all.  RelaxANTS are paralytics.      — Preceding unsigned comment added by Jsyzzle (talk • contribs) 21:58, 27 February 2012 (UTC)
thread_title: Relaxant

message: hmmm, gues I am too new to request a move, but the topic is completely wrong.  Its mixing paralytics and relaxants... two completely different drugs.  No wonder why I hate it when I hear patients state that they "read it on the internet."
:Given that you clearly know more, could you fix the errors? And why would a move be beneficial here? JFW | T@lk 20:24, 15 January 2006 (UTC)
thread_title:  Too many errors on this page 

message: While trying to get this page into some sort of clinically relevant form, and had my edits reverted because I removed paralytics from the discussion of muscle relaxants. As I said on Dr Cash's talk page "...Neuromuscular blockers are not muscle relaxants in any reasonable, clinical definition. Indeed, Rang Dale and Ritter specifically state that they should not be considered muscle relaxants because they have no clinical use. Furthermore according to the most recent Cochrane Review, there has never been a clinical trial investigating the use of paralytics in spacticity (apart from local injections of botox)."
As there are already two statements asserting this position, it seems that this consensus agrees, however does anyone think paralytics diserve to be discussed under muscle relaxants? (Apart from in the sense that "Paralytics are not muscle relaxants because they can not be used to clinically treat spasticity). Bilz0r 22:18, 19 September 2007 (UTC)
thread_title:  Paralytics are not muscle relaxants 

message: The "muscle relaxants" that are used in Irritable Bowel are smooth muscle relaxants, i.e. anti muscarinics like cimetropium. If they are considered muscle relaxants then so do all antihypertensives etc... Conclusion: Someoneone got confused, they are not muscle relaxants. Bilz0r 22:22, 19 September 2007 (UTC)
thread_title:  Muscle Relaxants are not used in IBS 

message: "gastrointestinal overactivity, such as in irritable bowel syndrome". While these drugs relax smooth muscle, they are antimuscarinics. Only the sloppiest users of the language would accept this(and yes I have seen in it peer-reviewed journals, but I don't think that is an excuse). If these drugs are considered muscle relaxants, then so do alpha-blockers, and any number of drugs. Even the article on Dicyclomine doesn't call it a muscle relaxantBilz0r 23:00, 20 September 2007 (UTC)
replies: text: I've been bold and removed it altogether. Fvasconcellos (t·c) 23:03, 20 September 2007 (UTC)
thread_title:  Again, muscle relaxants are not used in IBS. 

message: I made an image of the spinal cord showing the action of the muscle relaxants. Do you guys think adding another section to that image showing the neuromuscular junction would be called for, i.e. to replace the first image? Bilz0r 06:59, 23 September 2007 (UTC)
replies: text: Why not make this diagram the lead image? The article doesn't have one yet. Fvasconcellos (t·c) 16:00, 23 September 2007 (UTC)
replies: text: The image is excellent! Nice work! But I think the current placement of both images within their respective sections is adequate - moving either one to the top could be misleading. Not sure what to put as a lead image, though. Dr. Cash 21:46, 23 September 2007 (UTC)
replies: text: That's a tough one. I personally think Bilz0r's diagram in the lead would strengthen the article's focus on spasmolytics rather than neuromuscular blockers. Perhaps no lead image at all? I normally use structures of a representative compound (e.g. the structure of propranolol in beta blocker, and ondansetron in 5-HT3 antagonist), but the muscle relaxants are such a heterogeneous group. Fvasconcellos (t·c) 21:50, 23 September 2007 (UTC)

text: I'm all for keep all the information, I was just wondering if I could essentially make them one image, i.e. show a zoom in on Neuromuscular synapse, as well as the current, zoom in on the spinal synapse. i.e. two birds with one stone. Bilz0r 23:41, 23 September 2007 (UTC)
thread_title:  New Image 

message: Dr. Cash has nicely expanded the Spasmolytics section. May I suggest we make it into indented list format? It would look something like this:
*The benzodiazepines, such as diazepam...
*Baclofen is considered to be at least as effective...
*Clonidine and other imidazoline compounds...
*The hydantoin derivative dantrolene is a spasmolytic agent with a unique mechanism of action...
Thoughts? Fvasconcellos (t·c) 21:27, 23 September 2007 (UTC)
replies: text: Not real crazy about moving those items to a bulleted list. I generally favor using bulleted lists in very limited cases, and in this case, I think simple prose is adequate to get the point across. I also don't think that the bold text is necessary, either, and may go against the manual of style's excessive bold guidelines. Dr. Cash 21:36, 23 September 2007 (UTC)
replies: text: Well, it might indeed look too...busy. I'm guessing the text will expand further, so there would really be no point then. Fvasconcellos (t·c) 21:39, 23 September 2007 (UTC)
thread_title:  Spasmolytics 

message: Nice fleshing out of the spasmolytic section, I'm unsure of one bit thought. Quoting "Neurophysiologic studies also indicate that it reinforces both presynaptic and postsynaptic inhibition in the spinal cord, as well as inhibiting nociceptive transmission in the spinal dorsal horn". I can't comment on pain the the dorsal horn; and maybe I'm taking the rest of it too litterally (i.e. there is a difference between enhancing inhibition on a system level, and enhancing an inhibitory synapse), but it makes me a little uneasy. To quote from a 2003 Journal of Neuroscience paper (PMID: 12514232):
The investigated neurons included neurons of origin of the VSCTs [ventral spinocerebellar tract] (Jankowska et al., 1998; Hammar et al., 2002) and the two populations of inhibitory interneurons (Jankowska et al., 2000) further investigated in the present study, interneurons mediating reciprocal inhibition of motoneurons from group Ia afferents, and interneurons mediating nonreciprocal inhibition from group Ia and Ib afferents. The results reported in this study show that the previously described facilitatory actions of NA on these neurons are reproduced by ionophoretic application of the alpha 1-receptor agonist phenylephrine and, although to a lesser degree, by the beta -receptor agonist isoproterenol, but not by the alpha 2-receptor agonists clonidine and tizanidine. Clonidine, instead, has been found to depress activation of these interneurons (i.e., to have an effect opposite of that of NA), and tizanidine has been found to lack any effect.
These drugs also would weaken rather than enhance the inhibition of motoneurons by group I afferents (present study) and would not have any effect on the presynaptic inhibition of group I afferents (Anden et al., 1966). alpha 2-Receptor agonists, therefore, could not be expected to counteract spasticity by acting directly on motoneurons or by modulating input from group I afferents to these neurons.
That is to say alpha2 agonists either depress or have no effect on inhibitory interneurons of the spine.
Thankfully we find a paper My Jankowaska from 1990, in EJN (PMID: 12106064), showing the likely action.
Tizanidine depressed responses induced by stimulation of group II afferents in [excitatory] intermediate zone interneurons. [Conversley] injuries to the descending monoaminergic pathways might thus contribute to the development of exaggerated stretch reflexes, and spasticity, in at least two ways. One of these was discussed previously − by weakening tonic inhibition by NA, releasing neurons of transmission from group II afferents to intermediate zone interneurons which excite alpha- and gamma-motoneurons ( Eriksson et al. 1996; Jankowska et al. 1998).
That is to say alpha2 receptors depress the synapse between group II afferents (secondary spindle endings), and excitatory interneurons which then excite primary motor neurons.
So I'm changing that section to reflect those facts. (Primary research beats textbook) Bilz0r 23:37, 23 September 2007 (UTC)
thread_title:  Cellular Mechanism of Alpha2 Agonists. 

message: Would anyone mind if I created another version of :Image:Pancuronium.jpg highlighting its similarity with acetylcholine by using color instead of thicker bonds? I find the current diagram a little confusing—it's hard to parse thicker bonds as not indicative of stereochemistry at first glance. Fvasconcellos (t·c) 13:33, 29 September 2007 (UTC)
replies: text: Here it is. Fvasconcellos (t·c) 14:29, 29 September 2007 (UTC)
replies: text: I have fixed my image and replaced it already. Dr. Cash 19:42, 29 September 2007 (UTC)
replies: text: Thanks! Fvasconcellos (t·c) 19:49, 29 September 2007 (UTC)
thread_title:  Pancuronium 

message: I was shocked to view this page after having it listed in my talk section as a weekly cleanup topic. The most commonly used SMRs such as Cyclobenzaprine, Chlorzoxazone, Carisoprodol, Gabapentin (to a lesser extent), and many more are not mentioned at all for the entirety of this article, with exception to a note at the end for a few. These agents, however, make up the primary foundation of the overwhelming majority of commonly prescribed SMRs currently on the market and used today. I will begin working with this page by expanding the information available regarding the above mentioned agents (and their counterparts), but I have no clue how to go about getting rid of the large amount of garbage on this article that has almost nothing to do with the typical (or even atypical) SMRs. Any suggestions or comments for me? --Wikisystole 22:23, 29 September 2007 (UTC)
replies: text: If you can expand this article with relevant information, then please do. That's the purpose of a wiki. But I take offense to your comment regarding, "getting rid of the large amount of garbage on this article", as most of the information is well sourced with quite reliable academic publications and textbooks, and the overall quality has increased tremendously from what it used to be. Dr. Cash 07:01, 30 September 2007 (UTC)
thread_title:  Help - Centrally Acting Skeletal Muscle Relaxants 

message: Semi Auto Peer Review has been done of this article Muscle_relaxant.  It can be perused at the above link to allow for changes and improvements to help Muscle_relaxant achieve GA status.  SriMesh | talk 01:46, 8 October 2007 (UTC)
replies: text: I personally don't find these automated per reviews helpful in any way. Most times in the past, the automated scripts suggest things to improve the article that just aren't issues, because the scripts lack the "intelligence" of a real human reviewer. It should also be pointed out (a) the review you're referring to is not "semi-automated" - it's "full automated" (you didn't post any of your own comments or assessment there, and just let the script's answers stand on their own), and (b) none of the comments that are suggested on the page relate to the actual Good Article criteria. As an experienced GA reviewer myself, I should also point out that the use of automated reviewing scripts in the GA process is strongly discouraged, and should generally not be done. Dr. Cash 18:56, 8 October 2007 (UTC)
thread_title: [[Wikipedia:Peer_review/Automated/October_2007#Muscle_relaxant|Semi Auto Peer Review]]

message: This article failed good article nomination. This is how the article, as of  , , compares against the  six good article criteria:
:1. Well written?: Fair
:#Lead is confused, uses are not grouped together and the explanation that the term is used for two main groups of drugs appears twice.
:#"enzymatically destructed by acetylcholinesterase" - this is not a good way of putting this - what about "broken down into choline and acetate by acetylcholinesterase"
:2. Factually accurate?: Not wholly
:#"The combination of two acetylcholine molecules results in the opening of the sodium-potassium channel of the nicotinic receptor" - two molecules of acetylcholine do not combine at receptors, this is a binding reaction, not a chemical reaction.
:#"All neuromuscular blocking drugs are structurally similar to acetylcholine" - might be true for agonists/antagonists but certainly not for AchE inhibitors.
:3. Broad in coverage?: No
:*The major problem. The article covers how these drugs act very thoroughly, however what they are used for is only briefly touched on in the lead. There needs to be an "Applications" section that explains why they are used in surgery and what other major uses the drugs have.
:4. Neutral point of view?: Yes
:5. Article stability? Yes
:6. Images?: 
:Could use an image of acetycholine next to the picture of pancuronium to allow easy comparison with the highlighted parts of the structure.
When these issues are addressed, the article can be renominated.  If you feel that this review is in error, feel free to take it to a Good article reassessment.  Thank you for your work so far. Tim Vickers 02:15, 13 October 2007 (UTC)
thread_title: Failed "good article" nomination

message: Been taking these as my doc prescribed, and seem to be able to handle less weight during a workout after taking it. That's to be expected, right?  —Preceding unsigned comment added by Aadieu (talk • contribs) 20:22, 15 January 2010 (UTC)
thread_title:  Lowered strength while under its effects, right? 

message: http://www.foxnews.com/slideshow/entertainment/2010/06/10/vintage-ads-thinking/#slide=25 natural belladonna alkaloids with phenobarbital Sounds like some great stuff... Bizzybody (talk) 07:26, 17 November 2010 (UTC)
thread_title:  Vintage advertisement for muscle relaxers 

message: Seems Wikipedia once had a page for hydroquinine, then someone deleted it because "it's not hydroquinOne".  Well duh,  but what kind of reason is that???  Anyway, why isn't it on this page?  It's prescribed for stopping cramps, specifically night cramps of the calf, under the name "Inhibin" in the Netherlands.  Is the Netherlands the only country that does??  From http://www.fk.cvz.nl/Preparaatteksten/H/hydrokinine.asp?blPrint=True  
"It's a cinchona alkaloid like quinine and quinidine which strengthens muscle contractions. It lengthens the refactory period of the muscle which lessens the response to tetanic stimulation.  Quinine lowers the irritability of the motor endplate so reactions to repeated nerve stimlutations and acetylcholine lessen. Clinical relevance is unknown at this time. ... contraindications: Myasthenia gravis. High sensitivity to cinchona-alkaloids. Tinnitus. Optic neuritis." (also no recommended during pregnancy and breast-feeding).
Apparently this started being given by doctors after this study: http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2897%2980085-2/abstract
What is given out is usually (for adults): 100mg hydroquinine hydrobromide dihydrate.
Is this used in the States, UK, Canada or Aus/NZ?  Gaviidae (talk) 08:51, 7 January 2011 (UTC)
thread_title:  Hydroquinine 

message: Why this aspect has been removed?  — Preceding unsigned comment added by 62.176.24.68 (talk) 09:09, 31 August 2017 (UTC)
thread_title:  Inhumane euthanasia of animals