Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
In general Disorders are dealt with (biologically) on three levels PSY 210 Lecture 12: The Biological Basis of Mental Illness Genetic Contributions to Depression Depression Major depressive disorder (unipolar): Lengthy, uninterrupted periods of depressed mood Manic depressive disorder (bipolar): Cycling between periods of elevated mood (mania) and depression While sharing the common feature of depression, these are unique and separate disorders Brain Structure and Function in Depression Happy moods are associated with activity in the left frontal lobes Depression is correlated with increased right frontal lobe activity and decreased left frontal lobe activity Left hemisphere damage due to stroke and other medical causes is associated with depression Structural brain problems Chemical brain problems Genetic studies Concordance rate between identical twins is about 40 – 60% Adoption studies support a role for genetics in depression Families with depressed members also have very high rates of anxiety disorders Biochemistry of Depression Possibly due to problems in the HypothalamicPituitary-Adrenal Axis, depressed people show elevated: growth hormone levels thyroid hormone levels Stress hormone leves • cortisol levels • Glucocorticoid levels Depression Is Associated with Abnormal Sleep Patterns Neurotransmitters and Depression History: Depressed people: fall asleep faster enter REM earlier spend little time in Stage 3 or 4 awaken frequently Reserpine was found to deplete available monoamines and produces profound depression What is a monoamine? • Noradrenaline, dopamine, serotonin, etc…. What about “modern” antidepressants? How do antidepressants work? Antidepressant medications act on monoamines Monoamine Oxidase Inhibitors (MAOIs) • MAOIs suppress MAO, which breaks down monoamines • Bad side effects and dangerous dietary restrictions Selective serotonin reuptake inhibitors (SSRIs) inhibit the reuptake of serotonin Tricyclic antidepressants • Name comes from chemical structure- contains a 3 ring carbon chain • Inhibit the reuptake of serotonin and norepinephrine • Also acts on histamine and acetylcholine Leads to unwanted side effects Led to the desire to develop drugs that only worked in very specific ways Other drugs are currently under development Chemical Theories of Depression Monoamine theory of Depression First started as the catecholamine theory of depression • Noradrenaline and dopamine depletion led to depression (Reserpine) • Cocaine should help with this though, as it increases catecholamines Now it is generally called the monoamine theory • Depression is due to a deficiency in one or another of three monoamines: serotonin, noradrenaline, or dopamine Serotonin-noradrenaline reuptake inhibitors (SNRIs) Chemical Theories of Depression Receptor Sensitivity Theory of Depression Switches the focus from the neurotransmitters to the receptors Blocking of receptors with antidepressants takes place immediately • Leads to an immediate increase in monoamines • Patients don’t report benefits for weeks But it does not lessen depression • Minimizes the importance of serotonin Prozac, zoloft, lexapro These don’t work better than tricyclics, but are safer drugs Thus, it is not the immediate chemical changes that help the patient, but longer lasting (secondary) changes that may help the patient Schizophrenia Positive Symptoms Delusions Hallucinations Disorganized speech Disorganized behavior Negative © Najlah Feanny/CORBIS What about Schizophrenia? Symptoms Social withdrawal Mood disturbance John Nash Schizophrenia May Have Several Outcomes Prevalence of Schizophrenia Affects 0.5–1% of the world’s population 2.5 million Americans have schizophrenia Men and women are equally likely to be diagnosed to schizophrenia Current thought is that it is a group of related disorders and not just one disorder Age at diagnosis: Structural Brain Problems • Tissue loss • Frontal cortex, anterior temporal lobes, hypothalamus have all been found to be smaller as well Very rarely diagnosed in children as young as 6 years of age Mode: 18–25 Diagnoses may occur as late as a person’s 40s Structural Brain Problems • Enlarged ventricles • Shrunken Hippocampus Structural Brain Problems cell bodies in a control participant are arranged neatly Hippocampus cell bodies in a participant diagnosed with schizophrenia appear relatively disorganized Courtesy Arnold B Scheibel, University of California, Los Angeles Hippocampus A Comparison of Auditory Hallucinations and Listening to Real Voices Biochemical causes of Schizophrenia dopamine hypothesis • – overabundance of dopamine – Leads to overactivity – May be the basis for hallucinations and delusions Problems With a Dopamine Hypothesis 25% of patients do not respond to dopamine antagonists Atypical antipsychotic medications (clozapine) act primarily on neurotransmitters other than dopamine Drugs change dopamine activity immediately, but patient may not improve for weeks PCP produces symptoms similar to schizophrenia by blocking the NMDA glutamate receptor Prolactin levels in schizophrenics are normal Dopamine inhibits prolactin production Support for the Dopamine Hypothesis Drugs that increase Dopamine activity in Schizophrenics intensifies symptoms Drugs that block dopamine receptors lessen symptoms Seems to work for the hallucinations and delusions Does not help with social withdrawal symptoms Genetic Causes of Schizophrenia • Heritability Index of 40 60% • For fraternal twins only 10 - 20% chance • Children of a Schizophrenic patient: 1417% chance Psychological Causes of Schizophrenia early childhood experiences Neglect Physical abuse Sexual abuse Causes of Schizophrenia: Putting it all together Diathesis-Stress Model predisposition for schizophrenia triggers when person encounters great stresses Other Causes of Schizophrenia Sociocultural 8 times more schizophrenics among poor people poverty or social stress trigger schizophrenia or schizophrenics can't hold jobs which leads to poverty status Treatments for Schizophrenia In Insulin Coma Therapy Give patients Insulin Aids in the digestion of glucose (sugar) When enough insulin was given, patients went into a coma 1-10% mortality rate Main treatment used through the 60’s the past Most schizophrenics locked in asylums Given Sedatives Mid 1930’s: Insulin Coma Therapy Treatments for Schizophrenia Late 1950’s Started with antihistamines • Mainly sedated schizophrenics • Led to the discovery of thorazine Thorazine Calmed out How did it work? Clozapine Evidence from reserpine again… • Similarities between thorazine and reserpine Atypical Antipsychotics patients without knocking them Knew reserpine was linked to catecholamine depletion Both thorazine and reserpine led to Parkinsonian like symptoms – tardive dyskinesia • Once Parkinson’s was found to be linked to dopamine levels, it was assumed that thorazine worked on Dopamine Amphetamines led to schizophrenic like behaviors and work primarily on dopamine circuits Treatments for Schizophrenia Magnetic stimulation of the brain seems to reduce hallucinations Before Treatment After Treatment Works in 30-50% of the patients that did not respond to other antipsychotics Blocks dopamine receptors and serotonin receptors