Talk:Ketamine

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2-Cl-2’-oxo-PCM

Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about Ketamine. PubMed provides review articles from the past five years (limit to free review articles) The TRIP database provides clinical publications about evidence-based medicine. Other potential sources include: Centre for Reviews and Dissemination and CDC

The contents of the Recreational use of ketamine page were merged into Ketamine. For the contribution history and old versions of the redirected page, please see its history; for the discussion at that location, see its talk page.

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There is much evidence out there that the long term effects of ketamine may cause fear based pathways to develop in people's brains, and cause trauma due its effects. It is a hallucinogenic drug, it induces a catatonic state at anesthesia levels, causes blindness, acute speech and motor pathway impairments, intellectual impairments and effects that are akin to a locked in syndrome where the patient may be in distress but may not even be able to tell you while being wide awake. I wouldn't call the psychological effects of ketamine at doses producing anesthesia to be safe at all. Who writes this article? I assume medical professionals who have no knowledge of what it's like to be sedated with ketamine? It is also directly associated with the death of Death of Elijah McClain and the Killing of Tony Timpa in relation to the controversial condition Excited delirium which by all sensible medical accounts from coroners reports shows that there has never been a death as a result of excited delirium without a doctor, paramedic, or police officer involved.

It's highly controversial as to whether it's safe at all and only entered into the predilections of being "safe" as accounted for by medical scientists due to its profile of not causing respiratory failures while not accounting for the other dangers involved in its administration vs. other sedating agents that were previously typically used such as midazolam. As a person with a lived experience of being anesthatised with both ketamine and midazolam any "science" that says its safer in the sense of causing fewer deaths hasn't accounted for the fact that the primary modality of anesthesia with ketamine is disasociation, and the main paralytic is an induced state of catatonia and therefore it is quizzical to a person like me who also has enough medical and scientific knowledge as to how anyone who has been directly stupefied with ketamine could indeed call it safe. In fact it may well induce psychological trauma as a well known side effect.

I suggest any clinician who considers ketamine "safe" goes and injects them self with it at a full adult dose for sedation just to feel how "safe" you don't feel under the effects of it.

This article is quizzical and needs to represent these facts. Ketamine has come back into vogue after basically being a drug of last resort listed by the WHO for use in field hospitals. In the sense that a person can self respirate on ketamine so you can perform operations basically in war zones, yeah maybe. But it has been adopted as a sedative/paralytic agent and has been implicated in many similar deaths such as the people above. Further to the point, the fact that a person breathes themselves under the effects of ketamine is entirely not guaranteed introudcing the facts that the person may well indeed need to be respirated or bagged for oxygen in the case they do indeed stop breathing.

The actual effects of this drug are far more controversial than what this article suggests and should reflect that. At present this article is poor and largely represents a clinical perspective taken by clinicians who have never felt the actual effects of the drug or been stuck in the metaphorical "K Hole."

The safety rates are generally hyperbole as they don't include the likelihood of prolonged psychological distress from the effects of the drug especially when injected for psychiatric uses as a tranquilizer which may indeed feel like a trip into some kind of oblivion as an experience at the doses they use for rapid sedation. As a clinician or scientist involved in this hyperbole please feel free to take a dose of ketamine required for rapid sedation yourself and then come back and tell me how "safe" you felt. The safety of ketamine needs to be highly qualified by patient experience, as likewise being sedated with a large dose of midazolam. For such an equivalency test though its already abundantly obvious midazolam sedation feels like nothing more than going into a deep peaceful sleep, and when the patient emerges from sedation it will be like nothing ever happened to them. A comparative test for patient experience would almost certainly highlight the nightmarish amount of side effects that are necessary to achieve anesthesia and paralytic effects.

The notion that ketamine is "safe" in that sense is highly quizzical and full of large academic potholes that don't account for the sensation of patient safety and look at it purely from a clinical perspective without the knowledge of dissociative from an actual lived experience to qualify patient "safety" while under the influence of said drug. I can assure you if you had been injected with a large dose of ketamine you may not feel safe at all.

The safety aspect needs a high degree of discretion with many qualifications as to how it is considered "safe" v. other sedatives and paralytics. Of course in a modern hospital the safety aspect v. propofol is negated by having the necessary equipment should something go wrong. I have been anesthetized with propofol when I broke my arm also, and all it caused was a sense of emergence amnesia that the operation to put my arm back into place ever happened. 120.22.119.22 (talk) 11:59, 25 December 2022 (UTC)[reply]

Evidently, you know nothing about ketamine and are a deranged fear mongering fool. 172.117.119.78 (talk) 08:56, 30 April 2024 (UTC)[reply]

I agree. Daimontoppi (talk) 18:14, 5 November 2024 (UTC)[reply]

There's evidence of addiction and toxic effects from telemedicine prescriptions of ketamine in the US. [1]https://www.nytimes.com/2023/02/20/us/ketamine-telemedicine.html?smid=url-share Neiabr (talk) 18:32, 25 February 2023 (UTC)[reply]

Currently, under the "Mechanism of action," the article states: "In any case, it has been elucidated that acute blockade of NMDA receptors in the brain results in an activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPA receptors), which in turn modulate a variety of downstream signaling pathways to influence neurotransmission in the limbic system and mediate antidepressant effects of NMDA receptor antagonists like ketamine." The article does not address why the acute blockade of NMDA receptors in the brain results in an activation of AMPA receptors, which is very important to the explanation. The most accepted explanation of this appears to be due to a "glutamate surge".

This except explains it well: "Subanesthetic-dose ketamine administration leads to immediate presynaptic disinhibition of glutamatergic neurons, producing a glutamate surge (Moghaddam et al., 1997). This surge is thought to result from the blockade of NMDA receptors targeting γ-aminobutyric acid-ergic interneurons, leading to local inhibition of interneuron tonic firing and subsequent disinhibition of glutamate transmission (Homayoun and Moghaddam, 2007). Due to a blockade of NMDA receptors on postsynaptic excitatory neurons, excess synaptic glutamate is primarily taken up by AMPA receptors, thereby activating neuroplasticity-related signaling pathways (including mammalian target of rapamycin complex 1 (Li et al., 2010; Li et al., 2011) and brain-derived neurotrophic factor (Liu et al., 2012), both of which result in increased synaptogenesis and synaptic potentiation)." Gilbert JR, Yarrington JS, Wills KE, Nugent AC, Zarate CA (August 2018). "Glutamatergic Signaling Drives Ketamine-Mediated Response in Depression: Evidence from Dynamic Causal Modeling". The International Journal of Neuropsychopharmacology. 21 (8): 740–747. doi:10.1093/ijnp/pyy041. PMC 6070027. PMID 29668918.

I am thinking that the sentence should be changed to something to the effect of: "In any case, it has been elucidated that acute blockade of NMDA receptors in the brain results in an increase in glutamate production, which leads to an activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPA receptors), which in turn modulate a variety of downstream signaling pathways to influence neurotransmission in the limbic system and mediate antidepressant effects of NMDA receptor antagonists like ketamine." Wikipedialuva (talk) 08:31, 11 October 2023 (UTC)[reply]

Agreed, please change. 2001:9E8:4629:A400:F5BF:1E33:500D:E6E2 (talk) 21:02, 17 December 2023 (UTC)[reply]

mechanism of action and pharmacokinetics 2409:40F4:2045:27D4:8000:0:0:0 (talk) 13:39, 9 July 2024 (UTC)[reply]

I think the long form chemical name of Ketamine (2-Cl-2’-oxo-PCM) should be added to the article. Who else has been looking for this information but can not find it? Daimontoppi (talk) 15:44, 5 November 2024 (UTC)[reply]

Do you have a reliable source the indicates that is another name for ketamine? OhNoitsJamie ^Talk 15:58, 5 November 2024 (UTC)[reply]