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Lecture 16

PSYO 2470 Lecture 16: Mental Illness II
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Department
Psychology
Course
PSYO 2470
Professor
Stamp Jennifer
Semester
Winter

Description
Mental Illness II BDZs and anxiety - Induces physiological stress response when asking people to introduce themselves for a job interview or doing math problems o Not a huge change in heart rate compared to placebo - Sometimes a separation between physiology and behavioural state - BDZs have a reinforcement property o People who take these drugs, especially those with addictive personalities, will self- administer the drug ▪ Barbituates used to be used for anxiety – BDZs replaced due to less chronic damage to the body ▪ Mice previously exposed to cocaine – treated with barb, BDZ, and ethanol • All have reinforcement properties • Heavily self-administer the drugs – history of the person taking the treatment drugs can effect usage and effectiveness • BDZ used in acute situations for short term – most effective Treatments for anxiety cont. - Psychotherapy - Anxiolytics o BZDs o GABA agonists o Commonly used in conjunction with SSRIs - SSRIs o Increase levels of serotonin in synaptic cleft ▪ Release of 5-HT into the synapse – increase accumulation in synapse using MAO inhibitors • Inhibits the breakdown of MAO ▪ Also increase using SSRIs o Usually used in conjunction with BZDs o Tricyclics ▪ Block reuptake of serotonin Affective disorders - DSM5 – diagnosis o Depressive disorders ▪ Disruptive mood dysregulation ▪ Major depressive disorders ▪ Single and recurrent depressive episodes ▪ Persistent depressive disorder o Bipolar related disorders ▪ Bipolar I disorder ▪ Bipolar II disorder - Symptoms of depression o o Many drugs used to treat are working on multiple channels o Somatic symptoms ▪ More to do with behaviour o decreases in dopamine leads to lack of motivation o decreases in serotonin leads to lowered mood - Monoamine hypothesis o Serotonin systems ▪ ▪ Raphe nuclei – important nuclei • Target nuclei for drugs o Norepinephrine thalamus ▪ ▪ Locus coeruleus • Target nuclei for drugs o Very extensive pathways ▪ Widespread projections to brain, spinal cord, and cerebellum ▪ Deficit in central diffuse systems o Drugs used to lower blood pressure affects norepinephrine system ▪ Depletes catecholamines ▪ Can result in depressive mood o MOA inhibitors ▪ Enhance mood and treat other depressive symptoms • Inhibit breakdown of dopamine and other catecholamines – keeps levels high in synaptic cleft o Reuptake blockers – eniporine ▪ Tricyclic ▪ Improve symptoms of depressive behaviour o Treatment focuses on central serotonergic systems and centreal norepinephrine system - Diathesis-stress hypothesis o Relationships between certain copies of genes and the emergence of depressive phenotype o Different forms of serotonin transporter ▪ Target for anti-depressants • Regulates serotonin depletion ▪ Isoforms of genes important for transporter expression • Have short or long copies of genes o Number of stressful events and long/short genotype important in emergence of depressive episode ▪ ▪ Which two copies of genes had increases or decreases risk of major depressive episode • With increasing stress, with short-short genotype, have higher risk of major depressive episode o Have long-long genotype, have some resilience to developing major depressive - Stress, cortisol, and vulnerability to risk of mental disorders o o What is the increased probability that an episode will occur when given certain stimuli ▪ Provoking events – most poignant are exit events • Exit events show highest odds ration – increase probability of an episode • Exit events – death, divorce, etc. ▪ Vulnerability o Odds ratio tells us the probability of an outcome given a certain stimulus ▪ Exit events show highest odds ratio • Increase probability of an outcome occurring compared to absence of an exit event - Anterior cingulate cortex o o ACG resting activity increases with depression ▪ Increased neural activity during depressive episodes o Important for where depression effects o Resting activity increases with depression o Induce an electrical current into it to interrupt neuron activity to lower depressive episode ▪ Neural activity heightened in those with depressive episodes ▪ Deep brain stimulation used to interrupt neural communication • Not for stimulation - Untreated depression o Hippocampal volume decreases with longer depressive episodes o Reduction in hippocampal size associated with depression ▪ Longer episodes of depression cause decreases in hippocampal activity - Treatments o Electroconvulsive therapy ▪ Similar to deep brain stimulation ▪ Used to disrupt or reset electrical communication in brain ▪ Last resort technique for severe depression ▪ Produces a brief seizure • Exciting multiple neurons simultaneously ▪ Can have some permanent damage • Memory loss o Psychotherapy ▪ Cognitive behavioural therapy • Expand on self appraisal as well as modifying behaviour o Also looking at effects of drugs within this ▪ Drugs usually used in conjunction with CBT • Best remission rates o Teach someone how to reappraise life they learn it and don’t lose it ▪ Whereas treatments with drugs are transient • Things we learn are more persistent • Remove drug, remove activation of reception o With teaching/learning, more permanent results • Can be done with and without drug intervention ▪ Learned behavioural intervention o Antidepressants o MAOIs ▪ Issues – have bad side effects ▪ Lots of drugs have bad food and drug interactions o TCAs ▪ Blocking reputable of catecholamine’s and 5-HT ▪ Some are also used for neuropathic pain relief o SSRIs ▪ A lot of metabolites from our foods are used to build serotonin • Food can effect ability for drug to work o Foods high in serotonin metabolites can effect ability for drug to work o Drug treatments have multiple side effects ▪ Drugs can have effect
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