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Ketamine and Antiphsycotics

HighRolls

Greenlighter
Joined
Feb 8, 2016
Messages
1
Hi,

Just wanted to find out some information about the connection and effects with Ketamine and Antiphyscotics.

I'm currently on 50mg a day of 'Solian' which is primarily used to treat Schitsophrenia in high doses. I am using it to treat Anxiety.

I plan on doing Ketamine in the near future.

Does anyone have any information about the interaction, dangers, side effects etc?

Would be greatly appreciated. Cheers.
 
Anti-psychotics generally don't interact much with NMDA antagonists like ketamine but NMDA antagonists are used in the laboratory to induce schizophrenia in animals so just be aware that ketamine is kinda opposite to what your medicine is trying to accomplish: sanity.
 
How do you theorize that?

Ketamine does not seem to have any pharmacological action that would seem to contribute to the syndrome, in fact it has some things in common with amantadine which is one of the possible treatments.

To be sure, I would always go very slow with a combo like this and I am not saying I recommend or reassure people doing this... also I would look out for what is also an observation noted for MXE (ab)use: cerebellar intoxication. This is shrugged off as just a way of describing the impairment from a dissociative on proprioception / movement and also to be reversible but I would worry about eventually affecting the lower brain or brainstem too much and nasty synergy with neuroleptics.
 
The symptoms I have noticed in reports of adverse reactions with the disassociative phencyclidine have similarities with Neuroleptic Malignant Syndrome. In instances this group of symptoms originates from illegal drug overdose they name the group of symptoms Excited Delirium and in instances with antipsychotics they name the the group of symptoms Neuroleptic Malignant Syndrome. Perhaps ketamine has the same potential as phencyclidine in causing those symptoms. Hence, I say avoid the combination.
 
I think the thing to consider is that a similar set of symptoms might have 2 very different possible causes as far as pathophysiology goes. Extreme dopamine antagonists and NMDA antagonists do have sympathetic hyperactivity in common regarding high high dosages and this is thought to be a key part in neuroleptic malignant syndrome but they go about achieving sympathetic hyperactivity in fairly opposite ways, so I don't think the two will synergize to cause that big of a risk of neuroleptic malignant syndrome, and I think OP will be okay as long as he takes things slow.

I'd be much more worried about a psychotic break and such though.
 
@blackpirate:
Could you be more specific? Do you mean the rhabdo, changes in consciousness, changes in movement?

I realize that syndromes may be brought on by different causes, but the underlying mechanisms here are not shared or similar but even contradictory.

What may be similar is partially a general dysfunction in the CNS / autonomic dysregulation, other symptoms that may remind you of PCP seem to be coincidences since they are explained quite differently. (As cotcha seems to suggest as well) For example the dissociative anaesthesia is not considered to be a consequence by removing disinhibition via the dopaminergic system.

From PCP to ketamine is even a further leap considering how ketamine is relatively safe to use (even at narcosis doses for children) while PCP may indeed be much more problematic and psychotomimetic (>> dopaminergic agonism NOT antagonism).

NMS seems to be a result of unusual sensitivity, apparently from predisposition to dopaminergic antagonism having adverse effects on particular brain functions.

Solian / amisulpride is a dopamine antagonist, including of D2 .. so generally the risk exists.

Ketamine could perhaps potentiate it by competing for the CYP enzyme, I have not checked.

If there is an interaction between them, it's not one that I can easily predict - but if you don't wish to run risks do not use other drugs while on it.
And yes, using psychedelics and dissociatives with an existing mental problem can be asking for more problems ^ maybe not psychosis if it's used for anxiety like OP says but still.
 
I theorize Neuroleptic Malignant Syndrome and Excited Delirium are possibly different manifestations of the same underlying problem. Oddly these symptoms also manifest in people with no known drug usage. Extreme physical exertion and drug usage both cause this group of symptoms. Rhabdomyolysis is involved in almost every presentation of these symptoms. I can't say why seemingly different causes have the same breakdown of symptoms and require the same supportive care. I can't comment much further without more research done.

I should add, after your comment I researched this topic and learned others have also theorized similarly in medical journals.

journal of Neuropsychiatric Disease and Treatment said:
Neuroleptic malignant syndrome is manifested in severe muscle rigidity, fever, cognitive confusion, elevated creatinine phosphokinase and/or white blood count levels allegedly related to the administration of neuroleptic medications.4,32 A 1991 study found that cocaine abusers treated with neuroleptics developed NMS whereas nonabusers did not.33 Khaldarov34 successfully treated a patient, with a history of cocaine abuse and recent treatment with fluphenazine, with lorazepam on the basis of the assumption that cocaine-associated rhabdomyolysis with hyperthermia and NMS are the same condition.

Lopez-Canino and Francis,35 in their review of the literature on drug-induced catatonia from the study of phencyclidine intoxication by McCarron and colleagues,36 also noted an association between rhabdomyolysis and catatonia. Other studies have reported an association between psychosis (eg, mania and schizophrenia) involving overactivity, catatonia and rhabdomyolysis.37–39 In sum, the literature appears to suggest some association between the state of excited delirium, rhabdomyolysis, NMS and even catatonia. Studies have also noted that NMS and catatonia seem to be different aspects of the same syndrome (cf, Fink;40 Carroll;41 Koch and colleagues42). Petrides and colleagues43 propose that NMS itself is a form of catatonia whose features are similar to those of malignant catatonia and that they may both benefit from similar treatment.

The association researchers have established between excited delirium and the potentially life-threatening syndromes of rhabdomyolysis, NMS, and catatonia give impetus to the need for critical emergency medical interventions when encountering a person thought to be in a state of excited delirium.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695211/

In the end my objective was saying "avoid the combination".
 
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I don't think excited delirium (say from amphetamines) and NMS have much in common as far as the source of the pathophysiology goes - I think the reason why previous cocaine abusers that were administered neuroleptics were more vulnerable to NMS than non abusers is because their dopamine was down regulated and hence they were more vulnerable to dopamine deficits.

Hyper-sympathetic activity and excess muscle tone might be caused by either cocaine/amphetamines or dopamine blockade but the routes by which either one leads to hyper sympathetic tone and rhabdomyolysis are essentially opposite of each other, one does it by means of excess dopamine/adrenaline, another by lack of dopamine, so I don't think there is as much risk of the two effects synergizing and leading to rhabdomyolysis compared to combining two substances that lead to NMS or excited delirium by the same route. If anything, I would wager that NMDA antagonism will increase dopamine.
 
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