Exam 4: Brain Disorders

Monday, April 23, 2012 7:41 AM

1. There's some genetic disorder to bipolar disorder. Identical twins share 50% concordance rate and the concordance rate goes lower and lower depending on your relationship. 2. Treatments a. Lithium works well to stabilize mood b. Anticonvulsant drugs that treat epilepsy can work well to stabilize, valproate (depakote) c. Decreasing overall glutamergic activity, dampening excitation d. Effect on synthesis of arachidonic acid (produced during brain inflammation). 3. Depression: Biological bases a. Constipation and decreased salivation & super sensitivity to cholinergic agonists b. Chronic pain c. High levels of plasma cortisol i. People who have depression have higher levels of cortisol compared to people who don't have depression or people who have a brain disorder other than depression d. A genetic component i. Concordance rate. Severe depression, concordance rate is up to 60%. 4. 5-HTT gene a. Controversial because some people claim that it cannot be reproduced b. Interaction of environment and gene. 5HTT (serotonin transporter gene)helps the reuptake of serotonin back into presynaptic terminal to recycle serotonin. The gene that controls serotonin transporter can come in the short form or the long form, can be two short, one short one long, two long in your genes. c. Graph: number of stressful life events vs probability of getting depressive episode. i. If you dont have a lot of stressful life situations the combination of short or long doesn't matter ii. More stressful life events, two short forms of 5HTT, higher risk of depression. iii. Two long forms, least likely to have depression. 5. Depression and sleep cycle a. No stage 3 or 4 b. Go into first REM sleep stage faster than people who don't have depression 6. Over activity in parts of the brain, orbitofrontal cortex (frontal cortex) and amygdala--> emotional control 7. Medications--all work through monoamine system a. Resperine: one of the first evidences that pointed to the relationship between monoamines and depression i. Was used as a treatment for High Blood Pressure and people found out that people who were on this medication became suicidal and depressed. Resperine depleted monamines (NE, DA, 5HT). People who did not have a history of depression showed depressive symptoms. Decreased MaO--depression b. MAO-I (Monoamine oxidase inhibitors) i. MaOIs-presynaptic level ii. Originally used to enhance effectiveness of TB treatment, but made some patients hyperactive/showed manic behavior. MAO-I inhibits breakdown of monoamine activity, enhances monoamine activity. Enhanced MaO--manic c. Tricyclic antidepressants (reuptake inhibitor) i. Synaptic level ii. Reuptake inhibitor of NE and 5HT. Effective at reducing depression but came with negative side effects, abnormal heart rhythms. Partially because it also targets NE system. iii. Prozac--SSRI, selective serotonin reuptake inhibitor
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iii. Prozac--SSRI, selective serotonin reuptake inhibitor d. Ketamine: people who got injections of ketamine, if they have depression, respond to it very well. Treatments for depression (see slide) Issues with Catecholamine/monoamine hypothesis a. Don't work for everyone b. Drug effect is immediate in the brain, but effect takes long to kick in. mismatch between what's happening in the brain and the way you feel. ECT (Electroconvulsive therapy) a. Main side effect is slight amnesia Sleep Deprivation therapy a. Total sleep deprivation i. Short lasting effect b. Selective rem sleep deprivation: takes several days to have an effect on depression

12. Seasonal affective disorder (SAD) a. Only occurs in certain season b. Exposing person to a very bright light can treat depressive episode. Just exposing that person to a very bright light can treat depressive episode somewhat. Maybe it's because of the light effects on serotonin and circadian rhythm but they really don't know. c. People who have SAD also have slightly different sleep cycle. People who have SAD are slightly delayed. 13. Post partum depression a. More common in women who have experienced depression prior to pregnancy b. Sometimes men also report post partum depression. A guy who just became a father. Men drop in testosterone level when they are about to become/become fathers. Adaptive so that they don't go out and do something stupid with high levels of testosterone. 14. Schizophrenia a. If your identical twin has schizophrenia, there's a 50% chance that you're going to have schizophrenia. b. Males tend to develop it earlier than females. More males who have schizophrenia. Over the course of the treatment, females tend to respond to treatments better and slightly more high functioning than males. c. Behavioral abnormalities--positive and negative symptoms i. Positive: symptoms that show up that do not usually show up in population that do not have schizophrenia. 1) Psychotic: hallucination and illusions 2) Disorganized: bizarre behavior, inappropriate emotional displays, thought disorders (using and understanding abstract concepts) ii. Negative: are symptoms that are lacking in schizophrenia that you would normally see in people who don't have schizophrenia. 1) Weak social interaction 2) Poverty of speech 3) Anhedonia (not taking pleasure in anything) 4) Social withdrawal 5) Poor working memory d. Neurodevelopmental hypothesis of Schizophrenia i. A lot of the disorders probably originate from neonatal time (when brain is developing) and are dormant as you go through childhood but come out as a manifestation of certain disorders as you hit teenage hood/ different environments that trigger this. ii. Neurodevelopmental hypothesis: something happened when your brain was developing. Very subtle changes that can happen when your brain is developing. Slight alteration in genes can lead to a multitude of consequences.
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alteration in genes can lead to a multitude of consequences. iii. There are some risk factors that can potentially lead to Schizophrenia : poor nutrition of mother during pregnancy, premature birth, low birth weight, complications during delivery, extreme stress of mother during pregnancy. iv. One effect that is consistent: season of birth, higher percentage of people with schizophrenia is they were born during winter times. If the mother had severe cold/ influenza during 2nd trimester, that can potentially lead to a higher percentage of kids with schizophrenia. v. More pronounced in areas with latitudes far from equator (colder). Biological evidence a. Increase in ventricular size b. Decrease in cortical volume c. Decrease in dendritic spines d. Hippocampus: less structured hippocampal cell layout. Aberrant layering of neurons. Hippocampus is unique in that it has an organized pyramidal cell layout. e. Frontal cortex i. Hypofrontality, even at rest, there's less activity going on with people who have schizophrenia. Excessive pruning of synaptic connections (less dendritic spines). Schizophrenia and dopamine a. Increased activity (esp. D2) i. Limitations 1) Disconnect between what dopamine does at the neural level and what it does behaviorally 2) Direct measurement Schizophrenia and glutamate a. Lower levels of glutamate and generally dopamine actually inhibits glutamate release. Higher levels of dopamine, more likely that it decreases glutamate activity. b. PCP is an antagonist/targets glutamate symptoms. Decreasing glutamate activity can potentially lead to schizophrenic like symptoms. Latest treatment methods a. Halperidol: popular choice of drug and maybe targeted on D2 receptors. Worked pretty well in targeting hyperdopamine activity. The brain lights up with serotonin binding in schizophrenia. Halperidol doesn't really do anything to serotonin. b. Clozapine & Risperidone: both work on serotonin and dopamine system and dampens them down. c. Improvement of symptoms: Halperidol was for positive symptoms and risperidone improved negative and positive symptoms. d. Decreasing NMDA activity is associated with schizophrenic like system. New drugs target glutamate system by increasing NMDA activity.

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