I want to share something which I feel is a really important idea that I wish I could pin to the top of this thread
Related to this video
Follow on in this paper
and the function of dopamine.
This basically says that organisms act as structure systems to maintain a state of aliveness by minimising surprise. Taking a path of least resistance by minimising danger and increasing survival. Suprise happens as a result of a prediction error between the internal representation of the world and expectations of what is happening. Schizophrenia can then be seen as a problem of predicting what is happening. Dopamine aberrant/hyperfunction changes affect entire brain pathways that create prediction errors and the flow-on effect being you change your internal state to match the number of surprising prediction errors you see. Medication, dopamine antagonists then act in a way that minimises prediction errors. Basically, they modulate neurotransmission acting as dampeners and tranquilisers to remove errors. Which is also how antidepressants work for depression.
Basically that antipsychotics act in an analogous way to for prediction errors as SSRIs do for depression by acting as numbing agents to fine-tune the number of prediction errors into a lower symptom range.
How antidepressants work
The key learning is that more anything that modulates neurotransmission to remove errors will fix the issue. Namely, anything which has dampening or tranquilising effects. This is how NDMA agents, TAAR1 Agonists, CBD ect work even though they work via different pathways. As long as you modulated neurotransmission to remove prediction errors then you’re going to treat symptoms regardless of if you change dopamine. This is also kind of self-evident if you think about it because antipsychotics aren’t anti-schizophrenics since they only treat symptoms and not cure the disorder. Further, the whole dopamine hypothesis is built around the idea that it’s dopamine which is the issue when it’s really not it’s just that aberrant dopamine is encoding prediction errors and that modulating smooths some of these errors.
The key learning is that anything that modulates neurotransmission to remove errors will fix the issue. Particularly stuff which has dampening or tranquilising effects. Not the entire picture since this doesn’t hold true for GABA, Anti-convulsants, SSRIs for positive symptoms, but the brain isn’t that simple. Basically, the idea is simply the reformulation of the dopamine hypothesis in Bayesian brain terms where medication works by treating the symptom of prediction errors. Not an entirely wild idea but regardless this has important implications as the proposed mechanism for the above stack which works via other mechanisms than dopamine alone.
Secondly, I learnt that ipseity disturbance explains schizophrenia prodrome.
These involve the person feeling as if they lack an identity, as if they are not really existing, that the sense of their experiences being their own (the “mine-ness” of their experiential world) is failing or diminishing, as if their inner experiences are no longer private, and that they don’t really understand the world. These experiences lead to the person engaging in hyper-reflectivity , or abnormally prolonged and intense self-reflection, to attempt to gain a grasp on these experiences, but such intense reflection may further exacerbate the self-disorders. Self-disorders tend to be chronic, becoming incorporated into the person’s way of being and affecting “how” they experience the world and not necessarily “what” they experience. This instability of the minimal self may provoke the onset of psychosis.