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Lecture 6

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Lecture 6 - Psychiatric Disorders Schizophrenia - most patients have auditory hallucinations – ppl talking to them, and delusions – ppl plotting against them - recent findings show that sch and affective (emotional) disorder like depression share the same genes - age of onset prior to 30, usually early adulthood Neuropsychological: - poor performance in frontal lobe tasks; tests of frontal lobe function => issues in the frontal lobes, studies aren’t 100% conclusive - poor performance on tests of verbal and nonverbal memory - most other neuropsych tests show completely normal - most patients have enlarged ventricles and lighter brains => may be due to the prescribed tranquilizers that patients have to take for many years - hard to determine what effects are caused by the actual disease, and what effects are caused due to side effects of the medication Genetic: - 1% of population develops sch, in immediate family 10-15% will develop if a relative has it (parents, children, siblings) => suggests genetic basis - twin studies show di-zygotic (non-identical) ratio is about 10-15% (same as other family members); monozygotic (identical) prevalence goes up 40-75% => something else at play, since identical twins have identical DNA, should be 100% prevalence => other factors alter the prevalence - twins separated at birth 9 out of 12 cases had sch in both twins => predominantly genetic Psychopharmacology: - early work done w anti-histamines – makes ppl drowsy => tried w sch patients – first pharmacological tool, in order to attempt to calm patients down - it was found that drugs that were most effective were all dopamine antagonists => most used were phenothiazines, most common being chlorpromazine (most effective) => block biogenic amines/monoamines receptor site, effectiveness of the drug were selective dopamine antagonists – blocking the dopamine receptor - stimulating dopaminergic system, eg by using amphetamine (ecstasy) resulted in sch symptoms reappearing - ppl who take amphetamines in high doses over long time show sch symptoms (psychiatrists cant tell them from real sch patients) => have hallucinations and delusions *blocking receptors makes ppl better, stimulating receptors makes ppl worse/makes normal ppl appear like sch - brain tissue showed normal dopamine levels, but # of dopamine receptors (D4 receptor) is 6 times more abundant => certain ppl born w more dopamine receptors - need to be careful w blocking too many receptors => too little dopamine can result in Parkinson’s symptoms - continuum between Parkinson’s and Schizophrenia Affective Disorders 1. Depression: => used chemicals to reduce blood pressure, eg rhezorpine – causes reduction in monoamines (leak from synaptic vesicles) => patients taking the drug got an induced depression – monoamines related to depression 1 - aldomet which lowers bp blocks the synthesis of norepinephrine => also causes depression => led to basis for depression as a neurological disorder - not situational/environmental - brains of depressed patients (suicidal victims) were used to measure levels of monoamines => 20-25% had a reduction in 5HIAA (metabolite – byproduct of serotonin) - serotonin itself was reduced in depressed patients - treatments was tried by increasing levels of biogenic amines => most effective were tricyclic antidepressants – block serotonin and norepinephrine re-uptake resulting in increased activity due to them remaining in the synaptic cleft => very little effect on dopamine – dopamine not involved in depression - tried increasing serotonin by increasing the precursor (tryptophan) – very effective at treating depression Monoamine oxidases: enzymes that break down the transmitters that aren’t packaged effectively Monoamine oxidase inhibitors: inhibit monoamine oxidase activity, allows for monoamine availability; increased monoamines resulted
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