schizophrenia onset - late adolescent and early adulthood symptoms - delusions - inappropriate...
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Schizophrenia
Onset - late adolescent and early adulthood
Symptoms- delusions - inappropriate affect- hallucinations- incoherent thought- odd behavior (extreme - catatonia)
Causes
Genetic - some roleconcordance in identical twins - 45%
Suceptibility idea- environment plays some role- flu (or related virus) in 2nd trimester?- the latitude effect- the seasonality effect (born in feb to may - slight increase)
Dopamine hypothesis
Chlorpromazine - surgical antihistamine
- blocks DA receptors- neuroleptics
Refinement - D2 receptors most important
too much dopamine - schizophrenic behaviorBlock dopamine - schizophrenia gets better
Too much dopamine? - no evidencetoo many receptors - some evidence
(but changes due to treatment?)- more sensitive to dopamine
- ventral tegmental area - just above S.N. (mesocortical - mesolimbic system)- nucleus accumbens - receives dopamine from VTA
- perhaps screwed up systems rewards bad thoughts and behaviors- process gets worse and worse
- or VTA -> prefrontal area -> Limbic system- damage to prefrontal cortex (which INHIBITS Limbic system)- hypoactivity of prefrontal cortex (PET Studies)- hyperactivity in limibc system (goes wild - no inhibition)
- amygdala - emotion - increased activity of dopamine system in temporal lobe
** positive symptoms & negative mental symptoms
** negative physical symptoms - the other dopamine system - basal ganglia- brain damage - enlarged ventricles
Affective Disorders
Depression-Reactive-endogenous (unipolar) - 6%
-- twice as high in women (?)-- 10% suicide
Mania (bipolar disorder)- about 1%- no sex difference
Causal Factors
Genetic- concordance in identical twins - 60%
(origin - organic vs experience?)
- why gender difference?- genetic? (X chromosome?)- experience/behavioral?
Experience- stress
- acute (precipitating factor/ trigger)- sustained (?)
Brain changes- lower volume of prefrontal cortex- fewer glial cells
- fewer and smaller neurons- enlarged ventricles (means?)
- cerebellum & basal ganglia?
- due to depression or the drug treatment
Amygdala involvement?- too active?- involved in negative emotion
Treatment- monoamine oxidase inhibitors (MAOI)
- agonist effect
- problem - tyramine (cheese, wine)- usually metabolized by MAO- if not, raises blood pressure - stroke
- tricyclics- block reuptake
- serotonin- norepinephrine
Lithium- bipolar disorder- much faster, but low compliance- effects serotonin system? - receptors
SSRI’s- here and anxiety disorders- effective on lots of things (previously psychther)- few side effects??
ECT - Shock therapy- still used- also magnetic stimulation
Anxiety disorders- generalized- phobic- panic- obsessive compusive
Cause- genetic component- experience - more individual/more closely linked
Treatment
Benzodiazepines- 10% of adults taking them??- GABA agonist (increase binding)
Serotonin agonists- MAOI, TriC, SSRIs- anxiolytic
Tourette’s Syndrome
Tics - motor, vocal, simple, complex
Treatment - dopamine receptor blockers (neuroleptic)
-suggests basal ganglia is involved (motivation for action)-- also limbic cortex (emotional/control)
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