#neuroleptics

[dorianbrightmusic]

New Antipsychotic FDA Approval – Cobenfy

Cobenfy (xanomeline/trospium chloride) has just been approved for schizophrenia treatment in the US. This is huge. It's the first antipsychotic in decades to not target dopamine directly. It's got a much, much better side-effect profile, and it might work for negative and cognitive symptoms.

FOR MORE READING – news report/patient-centred plain language overview: See here.

FOR MORE READING – scientific evidence report: See here (note: the drug is referred to as 'KarXT' in this report).

I couldn't be happier right now. People with psychosis go through so, so much trying to find medications that are both useful and tolerable, and psychiatry has historically neglected psychotic people's needs so, so awfully. (Not to mention how little there is that actually helps with anything other than positive symptoms.) So I'm really, really hoping that with the proof that we can, in fact, make antipsychotics that aren't based on the same old pharmacological things we've tried before. Cobenfy is a muscarinic agonist/antagonist in fixed combination – and it also indirectly regulates dopamine and glutamate. And given that we know both dopamine and NMDA are probably involved in schizophrenia somehow – AND that treating things to do with either is hard – this is so, so, so exciting.

This isn't to say Cobenfy doesn't have side-effects (the most common ones being nausea, constipation, dyspepsia, vomiting, hypertension, dry mouth, and tachycardia. We also know that there is a small risk of extrapyramidal symptoms, and that prolactin-related side-effects do happen, unfortunately). We don't know much about how it affects folks in the long-term, or much about the long-term tardive dyskinesia risk. But even so, it's progress compared to some of the worse antipsychotic side-effects.

Moreover, there is a possibility it might be useful for negative and cognitive symptoms. Holy crap.

I'm really really really excited. I hope this is the start of a shift in psychiatry towards better standards of patient-centred care for psychosis. Y'all have deserved better for far too long – here's hoping this is the start of more ethical, effective treatment.

[neuroticboyfriend]

patient education about psychiatric medications is abysmal. seroquel in many ways is harming my health and can potentially be deadly. it makes my sleep apnea worse. it makes my dysautonomia worse, mainly temperature dysregulation (which makes me sometimes housebound in summer due to heat illness). it puts me at risk of stroke and diabetes, when i already have a family history of. it may be harming my cognition. it can leave me with a permanent movement disorder or one of multiple potentially fatal conditions (long QT, NMS), which the likelihood of getting increases the longer im on it (5 years now). it might be part of why i have a fatty liver.

and the withdrawal sets in really fast. after about 24 hrs without it, i get histamine rush because seroquel is also an anithistamine and NO ONE TOLD ME. withdrawal also makes my insomnia 10x worse, i cant sleep *at all.* my body is extremely dependent on this medication. and they intend to keep me on it for the rest of my life. instead of actually getting me the help i need, they leave me to rot in an abusive home and further traumatize me in the psych ward, and put me on a medication that can KILL ME. without ever telling me it could do that. all to make me sane.

it's just so fucked up. psychotic patients deserve better.

[arnold-layne]

pov you forgot to take corrective meds for fluanxol

[eligalilei]

More Extensive Redditversations on Psychtogenesis:

Person A:

Truthfully, APs are really only effective in treating hallucinations. They don’t treat much else. No pill is going to stop you from holding a fixed false belief in the face of all contrary evidence.

My psychiatrist won’t even prescribe APs if you don’t hallucinate. Maybe a low dose of seroquel Person B:

Idk about that, maybe to some degree but I was out here thinking skin walkers were real, in an alternate reality, while they showed up as anything here, there they looked like shadow creatures that took control of people’s bodies. I was the prophet of that reality who couldn’t be touched by them, while I could telepathically speak with anyone and any living organism. Including god, zeus, animals, etc.

It wasn’t until I was on my way to my PO’s office, I was talking to all of them, but specifically one, he was the devil, I was Jesus, came to an agreement to work together, only for me to betray him by speaking with the others and discovering we were just schizophrenics that need meds, and as the realization came, all the people in my head left, leaving just me and “the devil”, who turned out to be my brother. Then it was a matter of getting him help, him being a long term user of fentanyl and others, was in rehab. He didn’t want to get help, we were in a shared psychosis. Only to finally discover after several weeks of investigating when it was only him and I in my head, that it was actually me who was the voice in my head, and it had begun to just say what I was already thinking but before I would. Eventually getting to the point where it just makes comments about what’s going on, sometimes it’s nice other times it’s an asshole, all depends.

Without the meds though I don’t think my beliefs would have changed, or that any of the revelations would have come. I easily could have been the guy sitting on a corner talking to myself for days, but thanks to the meds, I’m back to pretty much how I was. No more delusions, and I’m back in this reality. Able to decipher what’s real and what’s not, it’s nice.

If I stop taking them though, would I create another alternate reality for myself? Fixed beliefs, that I can’t change on my own? Me: That's a delusional complex with hallucinatory elements. They're talking about delusion by itself, which maybe APs will help somewhat, but basically only at the point where thought has been eliminated. Person B:

I like that explanation. I don’t understand the last sentence in the sense of, do you mean all thoughts are eliminated, or certain thoughts in particular.

I have thoughts that are almost impulsively thought that are delusional, but am able to blow the thought off as quickly as it came. When I was delusional, all those thoughts were put on the table as a possibility.

Would it be the meds that are helping me block the delusions, or is it me just becoming better at differentiating? Genuine question btw, you seem nice and knowledgeable.

extra banter I’ve only been back to “normal” for a few months and don’t know anything about SZA other than there’s delusions, hallucinations are involved (sometimes?), and my psychiatrist thinks I have it (although hasn’t diagnosed). I guess there’s a sort of test or something that they perform to determine if you have it or not? Idk.

extra extra banter Never really talked to anyone about it, was just forced to take meds(if I didn’t take them they brought a needle out and it was either I was going to take them or I was getting it injected forcibly lol)

Any insight would be nice when you’ve got the time and if you’d like to give some, I’d like to learn more about it rather than just the the things I mentioned above. I’d really like to stop meds because of side effects, but am worried I’d slip back into a psychosis. Me:

I was being cynical, tbh, and suggesting that, and experiences tend to bear this out, neuroleptics work by reducing thoughts... which is kind of true, but it's both the same and different as another way in which AP action is explained: via the dampening of one's experience of, and procedure for assigning, valence. What this means, basically, is that they make things seem less significant or urgent. This fits with your experience of having odd thoughts, but being able to dismiss them.

One way to fit these two ideas together, is to consider how 'valence', or significance ('salience' is another word that's often used), operates on conscious and unconscious levels. The suppression of conscious valence is experienced as having a, possibly 'psychotic', thought, and just not investigating it or investing in it to produce a series of spinoffs and sequels, as might happen in psychosis.

But valence/significance/importance/energy/salience is a property of, or at least is a concept which can be expanded upon and used to describe by analogy, all manner of mental phenomena. There's presumably a constant murmur of unconscious 'maybe' thoughts clamoring for the ear of the conscious mind, which is itself not fully situated in it (Freud call this domain the 'preconscious', and others have called it 'subconscious' in contrast with the 'unconscious.' In other contexts it is referred to as or related to the function of the 'censor', which selects and edits information on its way to the conscious/ego). The greater the volume of any of these unconscious voices, and/or the more 'interested' the conscious mind is, the more likely it becomes that it produces, or is encoded in, a thought that is experienced.

Of course, what occurs in the domain of consciousness is fed back into the unconscious, and is amplified and split into more more murmurs, which may or may not make their way into awareness. We could think about psychosis as a runaway feedback loop rapidly accelerating and expanding in content due to the volume and quantity of unconscious murmurs-become-shouts, the relaxed indiscretion of the preconscious censor (that usually rejects or suppresses potentially problematic tangents), to whom everything suddenly feels important, and the excitation of the conscious ego under the sway of this rapidly proceeding tempest of exciting mental happenings.

On some level, at least in some kinds of psychosis, what we're experiencing is a very unstable and disordered excitement due to everything seeming just so damn important or significant. And if something feels significant (though actually for no good reason besides brain stuff), other parts of the brain will run off and figure out 'why' it is significant, based on nothing but the all-too-enthusiastic assumption that it is.

Instead of evaluating phenomena, and the assignation of importance being largely under the power of the conscious or processes with which consciousness and society are largely comfortable, it's like importance sneaks in at an odd intermediary step, and things, due to one's being complacently accustomed to shit making sense, start to run backwards in an attempt to maintain a feeling of coherence.

Seen thusly, the delusions, or rather the rejection of, or failure to attain, 'insight', are, in fact, a way to maintain sanity: the fundamental delusion underpinning all particular delusions is the idea that the mind (or in traumagenic psychoses, the world) is still working correctly. This is why the 'insight criterion' (of delusion, or, for some people, psychosis itself, though I see that as being a bit heavy handed) developed: it's only a delusion if you believe it. That is, in fact, only part of the picture, the entirety of which you might be able to guess from here, and that I won't begin to render, since this is already getting a bit long, and I may still have to add more without even going on that tangent.

There are tons of more biochemically oriented theories of antipsychotic action, though none of them are really very totally confirmed. Most of them, though, relate to a reduction of some kind of activity, and comport pretty well with the ideas in the above sketch. While this is kind of my own spin, the general idea is referred to in psychology as the 'aberrant salience' theory of psychosis.

As far as what's happening in your mind goes, I think we can look at it both ways and a sort of third halfway one based on the above (we can call one the 'unconscious' understanding of cause, one the 'conscious learning' model, and the third a kind of 'cybernetic' or 'pseduo-psychoanalytic one):

Salience is being suppressed on multiple levels, which leads to fewer and less intense thoughts,

and now, knowing that you've been through psychosis, you no longer uncautiously receive the phenomena issuing from your unconscious mind with open arms and a set of keys to your car.

In a sort of hybrid of the two, we might say that decreased salience allows you to re-establish a 'normal' relationship between conscious and unconscious mind by reinstalling brakes on the feed-forward process of salience-driven, backwardsly-working, enthusiasm which uncritically meets the demands for extraordinary causes made by your extraordinary feelings. As salience ceases to be injected in large doses at an 'unnatural' stage of thought production (or noögenesis; isn't that a cool word?), though the thoughts you once thunk remain, they become compared with those constructed under 'normal' conditions, and may eventually be seen as the grotesqueries they may be.

That said, once a thought has been established as true, a drug is not going to make you not believe it, especially if it's one that has become especially important to you. They aren't going to just make you think different things. I am of the unpopular conviction that another person can often stand in for one's own ego in the journey back to sanity. ....but if you're seeing fucking dragons all the fuck over and feel like your limbs are about to fall off? Well, uh, it's just kind of hard to argue with that. Probably maybe take a pill and see if you'll make better decisions when not besieged by a menagerie of mythical monsters.

So, I mean, I was being a little overcynical about APs not helping delusions. They can re-establish a neurological environment that can make it easier for you to soberly reflect on them, and they can prevent the production of new ones, but often at the cost of mostly just getting rid of everything interesting in your brain. Sometimes that's a cost worth paying, or it need only be a temporary sacrifice.

Plus, therapy and hand-holding is financially and emotionally expensive. Pills and padded rooms are cheap low maintenance 'solutions' to the problem, though they only sometimes succeed in so being. Pills do have a place, plus, they may sometimes prevent the further propagation of actually toxic pathological perniciousness, though that hasn't been established to be universally true. In my (actually only somewhat) humble opinion, one of the best ways to establish whether this is true in any given case, is that of determining whether the pills seem to be necessary, and whether you actually feel better taking them. Some do, and some don't, find either or both true.

There's still more I could say on the last point, but I'm trying not to pontificate excessively, and this has already become rather an epistle. If you want more such nonsense, feel free to ask.

[skowcia]

Quetiapine is all i need

[caramelcactus]

I mean that’s pretty accurate tho

[blood-orange-juice]

Science time in this mostly-fandom blog.

Ritalin cures or improves some cases of stuttering (Trenque et al. 2019, SheikhBahaei et al. 2022). That's huge. That's the first time meds work for this particular condition.

It seems to work for a subgroup of stutterers who have a misbalance between activation of D1 and D2 receptors (rather than the usual excessive dopaminergic activity+disregulation of pretty much everything).

So if you stutter, especially if you also have any kind of ADHD traits, go poke your doctor. It's new so they probably don't know even if they are a good doctor.

(be sure to show them the papers I linked, stimulants usually have the opposite effect, so it will take some convincing to even try)

[alexalblondo]

Oh, why does my brain feel like that™️???

[xylophonetangerine]

The 6AM nightcap aka the gentleman's Ambien

[disc0-hospital]

Running low on meds

Kinda wanna die c:

(lol it's like i swallowed shampoo song hghfbbvghggghhhhhhhh fuck it all)

[stroyent]

Absolutely hate mental illnesses. Why are you making my friends suffer. Fuck off

[arnold-layne]

oh the sweet taste of a videogame binge

[taimoorkhan]

Neuroleptic malignant syndrome (NMS) is a rare, but potentially life-threatening condition that can occur as a side effect of certain medications known as neuroleptics or antipsychotics. These medications are often used to treat psychiatric disorders such as schizophrenia, bipolar disorder, and major depression, but they can also be used for other conditions such as nausea and vomiting, or as a sedative.

Symptoms of NMS may include fever, muscle rigidity, altered mental status, and abnormal movements. These symptoms can progress quickly and may lead to organ failure and death if not treated promptly.

Management of NMS in the emergency department (ED) is crucial to prevent complications and ensure the best possible outcome for the patient. The first step in the management of NMS is to immediately stop the neuroleptic medication that may be causing the syndrome. The patient should also be closely monitored for changes in vital signs, mental status, and any other symptoms that may occur.

Intravenous fluids, electrolytes, and medications such as dantrolene and bromocriptine may be used to help control the symptoms of NMS. Dantrolene helps to relax the muscles and reduce muscle rigidity, while bromocriptine can help to reduce fever and improve mental status. In severe cases, mechanical ventilation may be necessary to assist with breathing.

It is important to closely monitor the patient for any changes in their condition and to promptly address any complications that may arise. Close communication with the patient's healthcare team, including their primary care provider and a psychiatrist, is also essential in the management of NMS.

In addition to the steps mentioned above, it is important for the healthcare team to be aware of any potential risk factors for NMS. These may include:

• Use of high doses of neuroleptic medications

• Rapid escalation of neuroleptic dosage

• Use of multiple neuroleptic medications

• Previous history of NMS

• Older age

• Alcohol or substance abuse

• Dehydration

• Electrolyte imbalances

It is also important for the healthcare team to be aware of the potential for NMS to occur in patients who are taking other medications that may increase the risk of NMS. These may include:

• Lithium

• Tricyclic antidepressants

• Monoamine oxidase inhibitors (MAOIs)

• Selective serotonin reuptake inhibitors (SSRIs)

In order to prevent NMS, it is important to carefully monitor patients who are taking neuroleptic medications and to use the lowest effective dosage. Regular monitoring of vital signs and mental status, as well as monitoring for any adverse reactions or side effects, is also important.

If NMS is suspected, it is important to immediately stop the neuroleptic medication and to seek medical attention. Early recognition and treatment of NMS can significantly improve the outcome for the patient.

There are several medications that may be used in the treatment of NMS. These include:

• Dantrolene: This medication helps to relax the muscles and reduce muscle rigidity, which is a common symptom of NMS. It is typically given intravenously, and may be used in combination with other medications. The recommended starting dose of dantrolene is 2.5 mg/kg intravenously, followed by 1.25-2.5 mg/kg every six hours as needed. The maximum daily dose is typically 20-30 mg/kg.

• Bromocriptine: This medication can help to reduce fever and improve mental status in patients with NMS. It is typically given orally or intravenously. The usual starting dose of bromocriptine is 2.5-5 mg orally or intravenously, followed by 1.25-5 mg every six hours as needed. The maximum daily dose is typically 20-30 mg.

• Levodopa: This medication is a precursor to dopamine, a neurotransmitter that is involved in the regulation of muscle movement and other functions. It may be used in combination with a decarboxylase inhibitor to help reduce muscle rigidity and other symptoms of NMS. The usual starting dose of levodopa is 250-500 mg orally, followed by 250-500 mg every four hours as needed. The maximum daily dose is typically 3-4 grams.

• Benzodiazepines: These medications are commonly used to treat anxiety and sleep disorders, but they can also be used to help control muscle rigidity and other symptoms of NMS. Common benzodiazepines include lorazepam and diazepam. The usual starting dose of lorazepam is 2-4 mg orally or intravenously, followed by 1-2 mg every six hours as needed. The maximum daily dose is typically 10-20 mg. The usual starting dose of diazepam is 2-10 mg orally or intravenously, followed by 2-10 mg every six hours as needed. The maximum daily dose is typically 40 mg.

It is important to note that the specific treatment plan for NMS will depend on the severity of the condition and the individual needs of the patient. Close monitoring and communication with the healthcare team is essential to ensure that the appropriate treatment is provided.

In conclusion, the management of NMS in the ED is crucial to prevent complications and ensure the best possible outcome for the patient. Prompt recognition and treatment of NMS is essential, and close communication with the patient's healthcare team is key to ensuring a successful outcome. Careful monitoring of patients taking neuroleptic medications and the use of the lowest effective dosage can help to prevent the development of NMS. If NMS is suspected, it is important to immediately stop the neuroleptic medication and seek medical attention. Early recognition and treatment of NMS can significantly improve the outcome for the patient.

[a-mossy-opossum]

old workspace and autoportrait

[dorianbrightmusic]

having a special interest in the neuroleptics is actually a really good asset in behaviour and cognitive neuroscience class. the lecture mentions the effects of basal ganglia damage, complete with graphs of agonist and antagonist muscle activation during a movement, and i'm like finally, that explains cogwheel rigidity

[beastblade69]

the best feeling after drinking a little is feeling your muscles soften. such a sudden relief because before this you don't even realise how strained they are all the time