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Author Topic: Antipsychotic issues such as induced sensitization, tolerance and more  (Read 41 times)

Offline Chip (OP)

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source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4944179/

I am on a court ordered monthyly depot of Olanzapine but i only feel it on the day they IM my butt. So I did a little ressearch on the fact that I also now have to use an oral prep to feel it and I use it to bring me down off meth, mainly.

Antipsychotic-induced sensitization and tolerance: Behavioral characteristics, developmental impacts, and neurobiological mechanisms

Abstract

Antipsychotic sensitization and tolerance refer to the increased and decreased drug effects due to past drug use, respectively. Both effects reflect the long-term impacts of antipsychotic treatment on the brain and result from the brain’s adaptive response to the foreign property of the drug.

In this review, clinical evidence of the behavioral aspect of antipsychotic sensitization and tolerance is selectively reviewed, followed by an overview of preclinical literature that examines these behavioral characteristics and the related pharmacological and nonpharmacological factors.

Next, recent work on the developmental impacts of adolescent antipsychotic sensitization and tolerance is presented and recent research that delineates the neurobiological mechanisms of antipsychotic sensitization and tolerance is summarized. A theoretical framework based on “drug learning and memory” principles is proposed to account for the phenomena of antipsychotic sensitization and tolerance.

It is maintained that antipsychotic sensitization and tolerance follow basic principles of learning or acquisition (“induction”) and memory (“expression”).

The induction and expression of both effects reflect the consequences of associative and nonassociative processing and are strongly influenced by various pharmacological, environmental, and behavioral factors.

Drug-induced neuroplasticity, such as functional changes of striatal dopamine D2 and prefrontal serotonin (5-HT)2A receptors and their mediated signaling pathways, in principle, is responsible for antipsychotic sensitization and tolerance.

Understanding the behavioral characteristics and neurobiological underpinnings of antipsychotic sensitization and tolerance has greatly enhanced our understanding of mechanisms of antipsychotic action, and may have important implications for future drug discovery and clinical practice.



Click here for Facts about Antipsychotic Medications



source: https://www.aafp.org/afp/2010/0301/p617.html

an introduction only:

Adverse Effects of Antipsychotic Medications

The use of antipsychotic medications entails a difficult trade-off between the benefit of alleviating psychotic symptoms and the risk of troubling, sometimes life-shortening adverse effects.

There is more variability among specific antipsychotic medications than there is between the first- and second-generation antipsychotic classes.

The newer second-generation antipsychotics, especially clozapine and olanzapine, generally tend to cause more problems relating to metabolic syndrome, such as obesity and type 2 diabetes mellitus. Also, as a class, the older first-generation antipsychotics are more likely to be associated with movement disorders, but this is primarily true of medications that bind tightly to dopaminergic neuroreceptors, such as haloperidol, and less true of medications that bind weakly, such as chlorpromazine.

Anticholinergic effects are especially prominent with weaker-binding first-generation antipsychotics, as well as with the second-generation antipsychotic clozapine. All antipsychotic medications are associated with an increased likelihood of sedation, sexual dysfunction, postural hypotension, cardiac arrhythmia, and sudden cardiac death.

Primary care physicians should understand the individual adverse effect profiles of these medications. They should be vigilant for the occurrence of adverse effects, be willing to adjust or change medications as needed (or work with psychiatric colleagues to do so), and be prepared to treat any resulting medical sequelae.

View/Print Table

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

FGAs with lower potency dopamine D2 neuroreceptor blockade (Table 1) are no more likely than most SGAs to cause extrapyramidal symptoms.

A

4, 5, 9

FGAs and the SGA risperidone (Risperdal) commonly cause hyperprolactinemia. Physicians should be vigilant for signs and symptoms of hyperprolactinemia in patients taking these medications.

C

6, 19

Patients taking SGAs, especially clozapine (Clozaril) and olanzapine (Zyprexa), should be monitored closely for weight gain and other metabolic syndrome–related adverse effects (Table 4).

C

39

Antipsychotic medications should be used with caution in older adults because of the risk of increased mortality from sudden cardiac death and cerebrovascular accidents.

A

40–42


FGAs = first-generation antipsychotics; SGAs = second-generation antipsychotics.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to https://www.aafp.org/afpsort.xml.


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I do not condone or support any illegal activities. All information is for theoretical discussion and wonder.
All activities discussed are considered fictional and hypothetical. Information of all discussion has been derived from online research and in the spirit of personal Freedom.

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