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36.Schizophrenia 4. Antipsychotic Drugs, An Overview.doc

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University of Toronto St. George
Mac Burnham

SCHIZOPHRENIA 4: THERAPY FOR SCHIZOPRENIA TYPES Physical: • Lobotomy (outdated) • ECT (outdated) o Recall forced-normalization – it was the motivation for ECT Talking: • Analysis, cognitive behavior therapy (adjunct; not in isolation) Drugs: derived from antihistamines (that target the H1 receptor) • First called “major tranquilizers” • Then called “neuroleptics” • Now called “anti-psychotics” USES OF ANTIPSYCHOTICS  Anti-schizophrenia Also:Anti-emetic [vomiting/nausea – area postrema/chemo trigger zone [CTZ] is very sensitive to dopamine agonists – they make you throw up – antagonists are anti-emetic)], anesthesia and other psychotic disorders (i.e., Alzeimers patients presenting with psychotic symptoms) Do they work? Yes, 95% improvement in acutely ill (positive symptoms) • Seeman: Help positive symptoms: 95% (Carlson: only 65%) But absolute normality? Normal enough to live at home and work Relapse? Don’t like the drugs and many go off them - need family support At what cost? • relief is symptomatic – need to take them for the rest of your life • drugs are often perceived as unpleasant • there is risk of serious side effects (e.g. 10 -20% tardive dyskinesia) o Tardive dyskinesia develops months after use and is irreversible movement disorder. Funny facial/mouth/tongue movements. TRADITIONAL DRUGS: “TYPICALS” TYPES : Phenothiazines -  Slight change = thioxanthines o e.g. thiothixene  Antipsychotic effects + motor side effects + sedation + hypotension o These early drugs bound to many receptors (dirty drugs)  E.g.: chlorpromazine, fluphenazine, fluphenazine decanoate o Fluphenzine decanoate is fluphenazine modified to have a high partition coefficient. When injected intramuscularly, this high P.C. will enable it to aggregate into globules and become slow release  good for relapse Butyrophenones  Antipsychotic effects + motor side effects o Went from dirty drugs to drugs that only blocked D receptor 2 o Recall: D 2eceptors are represented not only in the nucleus accumbens, but also in the striatum (putamen and caudate nucleus)  Correcting over activity in n. acc. leads to hypofunction in the striatum, leading to motor side effects!  E.g.: haloperidol Oddities:  Droperidol o Sedation and immobile o + fentanyl (synthetic opiod) leads to “neuroleptnalgesia”. This is the combination used to perform open brain surgeries etc.  Domperidone o D b2ocker only in the pheriphery (does not cross BBB). Therefore used as an antiemetic o Recall chemical trigger zone (CTZ)/area postrema does not have a BBB, so domperidone will get into it and block D receptors and provide its 2 antiemtic function SIDE EFFECTS: • Parkinsonism and Dystonia o Strange changes in voluntary behavior system – became Parkinson-like (immobile, quiet etc.) o Dystonia is twisting out of shape • Akathisia o Can’t sit still • Sedation • Orthostatic Hypotension o Blocking noradrenergic receptors throughout the body • Dry Mouth, etc. o Muscarinic cholinergic blocking (atropine-like effects). Parasympathetic muscarinic activation keeps you secreting(?) not sure • Pseudopregnancy (prolactin elevation) o System in hypothalamus that’s dopaminergic that inhibits the release of prolactin. Blocking dopamine disinhibits prolactin release and leads to pseudopregnancy. • Lowered Seizure Threshold • Jaundice (rare) • Dermatitis and Photosensitivity (rare) • Tardive Dyskinesia Moving on to the butryophenones from phenothiazines got rid of many of these side effects except: Parkinsonism, dystonia, akathisia or pseudopregnancy. Carlson: discusses tardive dyskinesia (~10% have it)  Using D fa2ily blockers to block D 2like receptors in the mesolimbic system (VTA  nucleus accumben
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