Stimulant psychosis, trying to understand what it really means.

[Mracid]

I was reading on ADHD meds and came across some reports of people talking about how they had to stop their ADHD med because of hallucinations and psychological issues. So I was thinking about what could be happening within the brain that could cause the symptomes and why does the psychosis happens.

I had an Idea, but I kinda need confirmation since I never experianced it. Here it is:

You know when people are OCD. They can't help themselves from finishing whatever process they have in their mind, this seems like an inability to stop focusing on something, the need to follow the idea until its done to be free from it. Well the first symptom that comes with stim psychosis is obsessive behavior. My first hypothesis is based on the theory that Dopamine is what helps centers the thoughts toward one goal (or at least it contributes to it).
It goes like this, since DA helps center the thoughts toward one only goal/Idea, then too much of it would lock the mind in a place where the goal has to be achieved to set the mind free, in this state the brain depletes its ressources to free himslef from the obsession by creating a pattern of thoughts and neurological triggers that will lead to the achievement of the goal.

Stopping here I'd have a possible reason why stims worsen OCD. But there's more.

Since stim psychosis happen more frequently after a period of sleep deprievation, there must be a correlation. Well sleep help restore the brain's ressources to make the cycles of neurotransmitters more stable. Altho when you deprieve a brain from sleep, it looses its ressources more quickly. So mixing this with the 1rst hypothesis;
A brain on stimulant will have the tendency to obsess on things and will spend more ressources on completing a task (like structuring thoughts and Ideas) making it more prone to instability, but when you add sleep deprievation to the equation, then the brain is in a state of no break, it uses its ressources on basically anything because of the stimulant and never gets to recover from it because of no sleep.

So my conclusion is that stimulant psychosis is the inability of the brain to provide the necessary ressources to litterally keep track of what happens in the real world, caused by an exaustion of the brain's ressources, and since the brain doesnt like blind spots it fills the holes with its best guess of what should actually be there.

Does that make any sense to any1?

Thanks for reading and possibly answering.

 

[kleinerkiffer]

I feel this is more suited for N&PD

 

[Mracid]

yeah I kinda hesitated, because in N&Ph there is a lower chance that some1 with experiance with stim psychosis respond, altho in other's the answers will be less precise. I even thought I could post in both but decided to let a moderator decide. Sometimes its harder than it seems to chose where to post.

 

[serotonin2A]

Although dopamine is commonly associated with reward, its major function is to indicate salience. In situations where there are very high levels of dopamine relase, abberant salience can be attributed to insignificant background stimuli. So people with stimulant psychosis will see random events like a helicopter flying overhead and misperceive it as being relevant to them. The sleep deprivation probably contributes to the sensory disturbances that some people also experience.

 

[JohnBoy2000]

Is it not as simple of an excess of DA in the mesolimbic DA pathway induces hallucinations?

Would that grandiose "salience" be more delusional - is that included in the definition of psychosis?
Delusion without hallucination?

I had delusions for years - much more profound that thinking a helicopter flying was related to my actions - but was never psychotic, and it certainly wasn't a product of an excess of limbic dopamine.

Stimulants raise DA levels - with time @ high doses, they're known to induce psychosis.
I don't know the exact mechanism but, desensitization of DA receptors to full agonist action, or perhaps that occurs in the ion channels - ultimately - too much dopamine, no?
Is it that straight forward?

 

[Cotcha Yankinov]

Is it not as simple of an excess of DA in the mesolimbic DA pathway induces hallucinations?

From the wiki on the dopamine hypothesis of schizophrenia - "Abnormal expression, thus distribution of the D₂ receptor between these areas and the rest of the brain may also be implicated in schizophrenia, specifically in the acute phase. A relative excess of these receptors within the limbic system means Broca's area which can produce illogical language, has an abnormal connection to Wernicke's area, which comprehends language, but does not create it. Note that variation in distribution is observed within individuals, so abnormalities of this characteristic likely play a significant role in all psychological illnesses. Individual alterations are produced by differences within glutamatergic pathways within the limbic system, which are also implicated in other psychotic syndromes. Among the alterations of both synaptic and global structure, the most significant abnormalities are observed in the uncinate fasciculus^[1] and the cingulate cortex.^[2]

The combination of these creates a profound dissymmetry of prefrontal inhibitory signaling, shifted positively towards the dominant side. Eventually, the cingulate gyrus becomes atrophied towards the anterior, due to long-Term Depression (LTD) and Long-Term Potentiation (LTP) from the abnormally strong signals transversely across the brain.^[3] This, combined with a relative deficit in GABAergic input to Wernicke's area, shifts the balance of bilateral communication across the corpus callosum posteriorly.^[4] Through this mechanism, hemispherical communication becomes highly shifted towards the left/dominant posterior. As such, spontaneous language from Broca's can propagate through the limbic system to the tertiary auditory cortex. This retrograde signaling to the temporal lobes, results in the parietal lobes not recognizing it as internal, resulting in the auditory hallucinations typical of chronic schizophrenia.

In addition, significant cortical grey matter volume reductions are observed in this disorder. Specifically, the right hemisphere atrophies more, while both sides show a marked decrease in frontal and posterior volume.^[6] This indicates abnormal synaptic plasticity occurs, where certain feedback loops become so potentiated, others receive little glutaminergic transmission. This is a direct result of the abnormal dopaminergic input to the striatum, thus (indirectly) disinhibition of thalamic activity. The excitatory nature of dopaminergic transmission means the glutamate hypothesis of schizophrenia is inextricably intertwined with this altered functioning.

5-HT also regulates monoamine neurotransmitters, including dopaminergic transmission. Specifically, the 5-HT2A receptor regulates cortical input to the basal ganglia and many typical and atypical antipsychotics are antagonists at this receptor. Several antipsychotics are also antagonists at the 5-HT2C receptor, leading to dopamine release in the structures where 5-HT2C is expressed; striatum, prefrontal cortex, nucleus accumbens, amygdala, hippocampus (all structures indicated in this disease), and currently thought to be a reason why antipsychotics with 5HT2C antagonistic properties improves negative symptoms. More research is needed to explain the exact nature of the altered chemical transmission in this disorder."

So dopamine is really just one piece of the puzzle.

 

[serotonin2A]

Is it not as simple of an excess of DA in the mesolimbic DA pathway induces hallucinations?

Would that grandiose "salience" be more delusional - is that included in the definition of psychosis?
Delusion without hallucination?

I had delusions for years - much more profound that thinking a helicopter flying was related to my actions - but was never psychotic, and it certainly wasn't a product of an excess of limbic dopamine.

Stimulants raise DA levels - with time @ high doses, they're known to induce psychosis.
I don't know the exact mechanism but, desensitization of DA receptors to full agonist action, or perhaps that occurs in the ion channels - ultimately - too much dopamine, no?
Is it that straight forward?

It can't be as simple as just increasing DA because if it was then amphetamine and cocaine would cause the effect acutely. There has to be some type of change that occurs regarding how the system functions. It might be sensitization to dopamine effects. Alternatively, the dopaminergic circuits ultimately control activity flowing back to cortex, so there could be a change in how information is processed in cortex and from cortex to the limbic system. The explaination I gave is overly simplistic with regard to the specific events that magnify the effect of dopamine, but my general point is that we at least have a pretty good idea why people suffering from the disorder become very ego-centric.

Schizophrenia is thought to be a disorder of aberrant salience. That usually isn't the only symptom that schizophrenia patients exhibit of course. But you could argue tht abberant salience is a much bigger component of stimulant psychosis than it is of schizophrenia.

From the wiki on the dopamine hypothesis of schizophrenia - "Abnormal expression, thus distribution of the D₂ receptor between these areas and the rest of the brain may also be implicated in schizophrenia, specifically in the acute phase. A relative excess of these receptors within the limbic system means Broca's area which can produce illogical language, has an abnormal connection to Wernicke's area, which comprehends language, but does not create it. Note that variation in distribution is observed within individuals, so abnormalities of this characteristic likely play a significant role in all psychological illnesses. Individual alterations are produced by differences within glutamatergic pathways within the limbic system, which are also implicated in other psychotic syndromes. Among the alterations of both synaptic and global structure, the most significant abnormalities are observed in the uncinate fasciculus^[1] and the cingulate cortex.^[2]

The combination of these creates a profound dissymmetry of prefrontal inhibitory signaling, shifted positively towards the dominant side. Eventually, the cingulate gyrus becomes atrophied towards the anterior, due to long-Term Depression (LTD) and Long-Term Potentiation (LTP) from the abnormally strong signals transversely across the brain.^[3] This, combined with a relative deficit in GABAergic input to Wernicke's area, shifts the balance of bilateral communication across the corpus callosum posteriorly.^[4] Through this mechanism, hemispherical communication becomes highly shifted towards the left/dominant posterior. As such, spontaneous language from Broca's can propagate through the limbic system to the tertiary auditory cortex. This retrograde signaling to the temporal lobes, results in the parietal lobes not recognizing it as internal, resulting in the auditory hallucinations typical of chronic schizophrenia.

In addition, significant cortical grey matter volume reductions are observed in this disorder. Specifically, the right hemisphere atrophies more, while both sides show a marked decrease in frontal and posterior volume.^[6] This indicates abnormal synaptic plasticity occurs, where certain feedback loops become so potentiated, others receive little glutaminergic transmission. This is a direct result of the abnormal dopaminergic input to the striatum, thus (indirectly) disinhibition of thalamic activity. The excitatory nature of dopaminergic transmission means the glutamate hypothesis of schizophrenia is inextricably intertwined with this altered functioning.

5-HT also regulates monoamine neurotransmitters, including dopaminergic transmission. Specifically, the 5-HT2A receptor regulates cortical input to the basal ganglia and many typical and atypical antipsychotics are antagonists at this receptor. Several antipsychotics are also antagonists at the 5-HT2C receptor, leading to dopamine release in the structures where 5-HT2C is expressed; striatum, prefrontal cortex, nucleus accumbens, amygdala, hippocampus (all structures indicated in this disease), and currently thought to be a reason why antipsychotics with 5HT2C antagonistic properties improves negative symptoms. More research is needed to explain the exact nature of the altered chemical transmission in this disorder."

So dopamine is really just one piece of the puzzle.

My impression of the OP's question is that it relates to stimulant psychosis specificilly and not to schizophrenia. I don't think most of what is known about schizophrenia would necessarily apply.

 

[Cotcha Yankinov]

Sorry I kind of posted a novel because Johnnyboy was asking about other things a while ago (and everybody seems to tunnel-vision on receptors rather than the brain as a network, so I thought it might be better to see a bigger picture example), but the bit I thought may be relevant to stimulant psychosis hallucinations was "Through this mechanism, hemispherical communication becomes highly shifted towards the left/dominant posterior. As such, spontaneous language from Broca's can propagate through the limbic system to the tertiary auditory cortex. This retrograde signaling to the temporal lobes, results in the parietal lobes not recognizing it as internal, resulting in the auditory hallucinations typical of chronic schizophrenia."

From my experience with auditory hallucinations from amphetamines and sleep deprivation I really connected with the bit about language not being recognized as internal, and I assume with "word salad" type auditory hallucinations from stimulant psychosis other people have a similar experience. Could the mechanism quoted occur in some manner with dopaminergic use over a couple of days with sleep deprivation, or is that something specific to schizophrenia? Are there any alternatives proposed, perhaps a different mechanism by which illogical language could be created and propagate, and then not be recognized as internally generated?

I assume that people with stimulant psychosis still can't tickle themselves like schizophrenics, but I have seen a study on efference copies/collorary discharges playing a role in audio in the instance of crickets. They essentially use efference copies to ignore the sound of their own wings. Maybe not too relevant, just thought it was interesting

 

[Mracid]

Thanks your answer was very helpful.

 

[d1nach]

Idk if this helps but whenever I start to feel like I am having that psychosis from stimulants where sounds make you jump and sound abnormally loud or people seem threatening or I start having anxious paranoid thoughts I use a ton of tobaccco because for me it feels like it turns down the intensity dial of my emotions and turns up my ability to control my thoughuts and rational cognition

 

[Nagelfar]

Psychoanalyticially it can best be described (n.b. on the *psychological*, not 'neurological', that is: the albeit off-topic for this section spectrum of categorizing symptom and function for rationale (i.e. "qualia", non-inductive); an unofficial but quite fitting DSMesque nomenclature: which I think explains the psychosis better than physiological contingencies do when approached by way of neurology instead; it is abstract, not concrete, to the subject meaning to grasp the tautology) as confirmation bias:

Which is the short circuited (quite literally) quick firing overzealous/tightly-wound hair-trigger for your subconscious to render an affirmative response to any sensory inquiry as to what pertains to whatever you are experiencing as to whether novelty is involved or what requires more of your brains resources; fight/flight/fun/f**k: confirmation bias exposition examples: "is that a man, or a shrub in that dark park? Yes! I *know* it's someone watching me (walk right up to it) huh, must've run off... but they were in this bush, I saw 'em"... also: "Did you hear that (other person at same level of altered state says)- "Yes I heard that too! Same thing, am sure I did!"...

This confirmation-bias is also the mechanism by which such dopaminergic stimulants are an aphrodisiac; exponential exaggeration of incentive salience via *confirmation bias", whereas just specifically this latter term (and not the commonly used "incentive salience" term et al) is the logically-consequent meeting point where the type of euphoria gained along also with the paranoia / psychosis can be explained by one a and the same methodology of our psyche and what in the pathways affected are distorted to skew our view of reality in a detrimental way for some things but is what is sought as the altered state for other situational instances.