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Lecture

PSYB65_Lecture_6.docx

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Department
Psychology
Course
PSYB65H3
Professor
Ted Petit
Semester
Fall

Description
PSYB65 Human Brain and Behaviour Lecture 6: Psychiatric and degenerative disorders (Chapter 2, 14) Monday, October 29, 2012 Psychiatric Disorders  Generally not found in neuropsychological textbooks  Chemical problems in the brain Schizophrenia What does it look like with the behavioural symptoms?  Hallucinations o Commonly verbal o They hear people talking to them when nobody is there  Delusions o Just thinking that people are plotting against you.  For example: his sister thinks aliens will attack  Can phenomenal or paranoid in nature o Can rarely lead to violentbehaviour o Extreme delusional ideas come to mind The History  Earlier: Freud assumed schizophrenia was due to absent mother or fathers, etc., but are NOT true o Was the theory of cause for a long time for psychoanalyst  Lots of research has been done on the classic neuropsychology of schizophrenia on parts of the brain that don’t work well  Classic neuropsychological approach, you can actually see that you do a bunch of tests to assess different functions of the each lobe; schizophrenics do show o Poor performance on tests on frontal lobe function o Reduced ability in terms of verbal and nonverbal memory o Most of these people have enlarged ventricles and lighter brain weight  Problem: with this is that these studies that were done were taken on schizophrenics that have been this way for a long time and have been on medications o Not clear whether it was because of drugs they took or is it because the disorder itself  Real issue here is the transmitter not neuropsychological  Other tests show that their brain is normal  Age of onset: 30 years old, the first 30 years if don’t have schizophrenia, then you’ll be fine o You usually become schizophrenia by 20s Genetic Studies  Before neuroscience became a sophisticated as it is, has a long way to go for humans due to ethical issues  About 1% of the population (1 out of 100 people) gets schizophrenia  If you look at people’s direct family (parents, children or siblings), the rate of schizophrenia is about 10-15% o Basically, 10-15% of people’s family can have this disorder Twin Studies  Non-identical twins (dizygotic): if one twin is schizophrenics, the other one is 10-15% likely to be one as well  Identical twins (monozygotic): if one twin is schizophrenics, the other one is 40-75% likely to be one as well o Suggests a genetic component here  Study: 12 sets of identical twins, have to be separated for the first year of life, and one of them is schizophrenia o Results: 9/12 were also schizophrenic o So you can’t really blame the parenting, so the genetics is a pretty large part of this o Interesting that they have the same DNA and it’s not 100% likely the other identical twin will have the disorder  this means other factors play a part in this Psychopharmacology of Schizophrenia  Historical point of view: o Antihistamines (what you take when you have a cold) caused people to calm down o Used it on schizophrenics and it worked a bit o Used different classification of drugs o Anti psychotic drugs  most effectives one were all dopamine and antagonists  Best blockers for dopamine o The most famous ones were phenotahiazines and chlorpromazine (most commonly prescribed)  Blocked the site for the biogenic amines (monoamines)  As they worked with these drugs, they found the effectiveness was directly related to their ability to block dopamine receptors o Specifically dopamine receptor blockers were the most effective in treating schizophrenia  This clearly suggested that dopamine was a problem and it appeared to be the problem with something about the receptors o Because the receptor blockers were the most effective, they reduce the symptoms of schizophrenia  Then what they noticed is that dopamine stimulant (such as amphetamines) did two things: o If you were schizophrenics, if you had the disease, but weren’t haven’t any symptoms, you immediately became psychotic/schizophrenic and go nuts o Even in normal individuals, if you give them high level dopamine stimulants, they begin to show schizophrenic types of behaviour  Now, to do that, you haveto give the stimulant 24 hours straight to produce the symptoms of schizophrenia within a normal person  So it become very clear that over stimulation of dopaminergic receptors caused schizophrenic symptoms and if they were reducedthen schizophrenic patients were better  They looked at the brains of schizophrenics: o Too many dopamine receptors  Two subsets of receptors: D2 and D4 o If you look at the number of dopamine receptors they have 6 time the numbers of D2 and D4 receptors o Therefore some gene is obviously coding for dopamine receptors and something is wrong with this gene and this causes schizophrenia  If you reduce/suppress the dopaminergic receptors too much it can increase Parkinson like symptoms in patients  Problem with taking drugs: o Side effects of drugs cause compliance with patients who don’t want to take drugs to stop this disorder Affective disorders: problems in their emotions  Depression and mania= bipolar disorder (manic to depression to manic, unending cycle) o Bipolar disorder go from manic to depression, vice versa  Cyclic changes in mood Depression  Feeling of being very sad, Psychiatric  sleeping problems, food intake issues, suicidal feelings Mania  People are super excited about life, it can be delusional/unrealistic  Don’t like to take their medications, but they are more compliant History  Giving out blood pressuremedication o High blood pressure can lead to a stroke  Regularly used Reserpine –caused people to get depressed because they had those symptoms of depression  Reserpine causes the transmitters, particularly the monoamines to leak from the presynaptic vesicle o Caused fewer monoamines to be around can cause depression o If any transmitter is not stored in the synaptic vesicle, there’s chemicals that go around and destroy them when they are floating around  Came out with another drug: Aldomet o Lowers blood pressure o Blocked the synthesis of norepinephrine, which also caused depression  Suggested that out of the 3 biogenic amines, norepinephrine was the one involved, not clear about the other 2 (serotonin and dopamine) Brains of Depressed Patients  They looked at autopsy of depressed people who commit suicide  Depression was a neurological disorder  20-25% have a reduction in 5HIAA (serotonin metabolite) o Reduction in serotonin  Reason to believe that both norepinephrine and serotonin caused depression, but clear enough Treatment to increase the activity of biogenic amines  Most effective: o Tricyclic antidepressants: have little effect on dopamine , so dopamine is not involved in depression o Tetracyclis antidepressants o
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