Delusions: Working Model of Neuroendocrinology of Delusions in Psychosis

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Model of the development of delusions.

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  • This model of delusions includes some novel concepts like the way that dopamine enhances salience and leads to a cognitive interpretation (application of meaning based on affective tone) that attempts to 'explain' the salience based affective experience. It also incorporates the understanding of the fast limbic circuit in its role of fast but error prone perception (perception the combination of sensation and meaning context). It also looks at the way that the rate of cognitions change under elevated fight/flight states as well as the way that hypoactivation of the frontal lobe can lead to error prone cognitions not being fully assessed for accuracy. Also the way that dopamine along with salience increases the rate of stable neuroplastic changes via long-term potentiation. These lead to inaccurate fast perceptions, being interpretated as highly salient, a cognitive explanation of the felt-experience of salience that is encoded in a upregulated rate of neuroplasticity and the low level of frontal lobe activity reduces the ability to change or challenge cognitive frame based on difficulty holding multiple cognitions in working memory to evaluate them together. Also the fuzzy appraisal of limbic circuit grabs other memories encoded with the same tone and makes 'cognitive slippage' possible by creating more loose associations that are retained through upregulation of neuroplasticity. Notable that this model would have specific treatment predictions and some testable biological markers implied...
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