Talk:Benperidol

From WikiProjectMed
Jump to navigation Jump to search

Uses of benperidol.

"It is an antipsychotic, which can be used for the treatment of schizophrenia[2], but it is primarily used to control deviant, antisocial hypersexual behaviour[3], and is sometimes prescribed to sex offenders as a condition of their parole, as an alternative to anti-androgen drugs such as cyproterone.[4]"

In Germany, benperidol (Glianimon and generics) is used mainly as a highly potent antipsychotic in severely psychotic and manic (e.g. schizophrenia, almost exclusively in acute pharmacological intervention) patients, though not nearly as often as haloperidol and 2nd generation antipsychotics. No specific use in antisocial hypersexual behaviour (or, not more than other neuroleptics/antipsychotics) occurs; this drug is quite infamous among psychiatric patients and personal to be the ultimative, "superpotent" neuroleptic with massive EPMS side-effects.
Is it used in the UK really as the "antipsychotic of choice" for sexual deviants, as could be assumed from the publications quoted?
Also, the "dichotomisation of choice" of pharmacotherapy between an antiandrogen or an antipsychotic seems not really close to practical therapy routine; cyproterone treatment is quite often co-administred with psychopharmaceutical medication and non-pharmaceutical treatment options... But these are just my impressions and thoughts...--Spiperon 12:43, 1 May 2007 (UTC)[reply]

I doubt it even works in any sort of way that the person taking it finds helpful. On the other hand, its probably really easy to escape from a rapist doing the Thorazine Shuffle... Zaphraud (talk) 01:50, 7 February 2011 (UTC)[reply]

My Edit, would be cool If I get some answeres relatively soon

"Allthough benperidol is known for its highest exposure at dopamine d2, and d3 receptors therefore leading the typical neuroleptics potenz statistics, it differentiates itself from, for example, haloperidole by its behaving (haloperidole: inverse agonist, benperidol: Antagonist) and its elimination half-life. This could mean that benperidol does not have to also leading the statistics in epms-potential."

Can I post this? I don't have an explizit source but my facts stick to "already posted in Wikipedia Knowledge" 100%.

Please note that while this card is activated, no other summoning is allowed. After three complete rounds, including both your and your opponent's turns since activation, you have the opportunity to send thi Materie34 (talk) 22:19, 24 July 2023 (UTC)[reply]

ops the third Paragraph is from another Projekt sry Materie34 (talk) 23:00, 24 July 2023 (UTC)[reply]
Hi, @Materie34 - some questions & comments for you about this paragraph ...
What is the source of this information? I do not see this in anywhere in "already posted Wikipedia knowledge". We do not refer to drugs having "exposure" to a receptor - that is not a pharmacology term, and it is not clear what you mean. You seem to be suggesting that benperidol is greater in some sense than other neuroleptics, but it is not clear what characteristic you are measuring. If you are referring to greater "potency", note that there is no data in the current article for D3 receptors (a capital 'D' is used for dopamine receptor references, '3' should be a subscript).
It is incorrect to call haloperidol (note the correct spelling) an inverse agonist at all receptors. Do you mean only at D2 and D3 receptors?
The elimination half-life depends on the form of haloperidol used.
What do you mean by "epms-potential"? There is no such term in pharmacology. Do you mean the potential to cause extrapyramidal symptoms? If so, I must disagree with your source on this information ... there is NO reason to believe that differences in action at D2 and D3 receptors, or elimination half-life, determines differences in risk of extrapyramidal symptoms between benperidol and haloperidol - it just doesn't work that way.
Verytas (talk) 13:30, 26 July 2023 (UTC)[reply]
ok let me try to improve:
I tried to be pharmakological as korrekt as possible plus I did my best not to come up with wild theories, just mostly summarize the knowledge in case of epms-effects related to potency 😊
I also provide two sources this time (unfortunately one is in German)
So heres my new try for an edit:
" Since the first neuroleptical ever became popular, there is debate about how to measure and objektify the effective doses for schizophrenics. It started with a definition for an individual treshold for a patiened defined for the dose by which the patient develops a hyperkinese in his handwriting. Then due to improvements of measuring it became popular that the affinity to bind to dopamine receptors (mostly D2 receptors) was the new method to compare neuroleptics.
However since the new "atypicals" neuroleptics have reached the market, also the measurements according to the dopamine D2 affinity became outdated and even a new reference value for a comparison of potency between atypicals seems to be not desperatly needed since one can say that every atypical has its unique mechanism so instead of potency camparison its most of the time enough to work with Dose equivalents. Also the historically first measurement regarding the so called "neuroleptic treshold" (as above mentioned) isn't 100% akkurate as this side effects also depents on how every individual drug react with every individual brain, so with this technique, even then, one needed to operate with the so called "neuroleptic disposition" a factor used to compensate the individual response and reaction to epms-effects for a better regarding of the outcomes, plus for an easier integration in statistics. But also at the second "newer" potency measurement, you can see that epms-effects doesn't follow one strict rule, as for example despite perphenazines 2-3 fold less value in neuroleptical potency compared to haloperidole, it has, in same dosages circa the same severe epms-effects.[1]https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0028-1094207?device=mobile&innerWidth=412&offsetWidth=412</ref>[2] Materie34 (talk) 07:52, 29 July 2023 (UTC)[reply]
Materie34 - unfortunately, there are too many errors in the above paragraphs for me to correct. For example, we do not "measure and objektify" doses, that is not how the debate started, and Haase's graphometric method was never widely used to determine any kind of "threshold". I think a lot of the problems are simply language. We would never write "you can see" in this kind of article. As I mentioned before, there is no such thing as "epms-effects", I think you mean just EPS, which is an abbreviation for "extrapyramidal symptoms". However, another problem is that you are choosing to cite obscure papers, and obscure facts in those papers. A proper article requires reading many hundreds of articles, and years of experience, to make a coherent story from the countless papers that have been written.
If your primary language is German, why not just make edits to the German version of Wikipedia (or whatever your primary language is)? Please do not enter any of the above into the English version.
Verytas (talk) 06:38, 30 July 2023 (UTC)[reply]
don't worry Verytas, I don't have any Intentions to post, until you checked it.😊😊 Hmm it is somehow a Challenge for me to write in english, what doesn't mean I also have passion in writing german articles.
Hmm, when I have time and desire to make a new try regarding your critiques, I will post it here.
Have a nice day😊♥️ Materie34 (talk) 12:59, 2 August 2023 (UTC)[reply]

References