Mental Illness Chapter 22 PDF

Mental Illness Chapter 22   Understand the historical context behind the study of mental illnesses Learning  Learn about the three major types of psychiatric illnesses, their causes, and their current treatments: objectives  Anxiety disorder...

Mental Illness Chapter 22   Understand the historical context behind the study of mental illnesses Learning  Learn about the three major types of psychiatric illnesses, their causes, and their current treatments: objectives  Anxiety disorders  Affective (mood) disorders  Schizophrenia   Neurology  Branch of medicine concerned with the diagnosis and treatment of nervous system disorders  Neurological disorders  Ranging from multiple sclerosis to aphasia  Help illustrate the role of physiological processes in normal brain Neurology vs. function Psychiatry  Psychiatry  Branch of medicine concerned with the diagnosis and treatment of disorders that affect the mind or psyche  Psychiatric disorders  Anxiety disorders  Affective disorders  Schizophrenia   Human behavior  Can be thought of as the cumulative product of brain activity  Brain  Product of two mutually interacting factors  Heredity  Environment  DNA determines individualism. Mental illness  Health and illness along continuum of bodily function & the brain   Mental illness  Diagnosable disorder of thought, mood, or behavior that causes distress or impaired functioning Mental illness  Earlier belief  Disorders of the body (medical) & the brain  Disorders of the mind (spiritual)  Current belief  Most disorders of mood, thought, and behavior have biological explanations. The brain was linked to “craziness” since long before even the Middle Ages   Freud’s theory: mental illness: unconscious and conscious elements of psyche come into conflict  Treat by unearthing hidden secrets of unconscious Psychosocial  Skinner: Many behaviors are learned maladaptive responses to the approaches environment.  Treat by “unlearning” through behavior to mental modification illness  Psychosocial approaches to mental illness have sound neurobiological basis.  Psychotherapy  Verbal communication to help patients unravel psyche conflicts Good ol’ Sigmund Freud   Former major disorder: general paresis of the insane  Symptoms: mania, cognitive deterioration  Cause: infection with Treponema pallidum (syphilis)  Paul Ehrlich (1910) discovered treatment.  Penicillin (1928) treatment Biological  Other mental illnesses traced directly to biological causes.  Examples: vitamin deficiency, HIV in brain, autoimmune response approaches to mental illness Syphilis’ effects on the brain   Using genetic information to develop treatment  Discovery of pathophysiology—may suggest biological processes Molecular  Target with drug therapy medicine in  Unique challenges of brain diseases  Same diagnosis may arise from many psychiatry causes.  Genetic complexity  New approach: study the pathophysiology of neurons   Fear  Adaptive response to threatening situations  Many fears innate and species-specific.  Other fears learned  Anxiety disorders  Caused by inappropriate expression of fear Anxiety  Most common of psychiatric disorders disorders   Post-traumatic stress disorder (PTSD)  Symptoms Disorders  Increased anxiety  Intrusive memories, dreams, or characterized flashbacks  Irritability, emotional numbness by increased  Obsessive-compulsive disorder (OCD) anxiety  Obsessions: recurrent, intrusive thoughts, images, ideas, or impulses  Compulsions: repetitive behaviors to reduce anxiety   Genetic predisposition for many anxiety disorders  Fear evoked by threatening stimulus: stressor Biological  Manifested by stress response basis of  Stimulus–response relationship strengthened (or weakened) by anxiety experience  Stress response with the hypothalamic- disorders pituitary-adrenal axis  Humoral response: corticotropin- releasing hormone (CRH)  adrenocorticotropic hormone (ACTH)  cortisol HPA axis   Both amygdala & hippocampus regulate CRH neurons. Regulation of  Amygdala projects to bed nucleus of the stria terminalis, which activates the HPA the HPA axis axis. by the  Hippocampus deactivates the HPA axis.  Glucocorticoid receptors amygdala &  Feedback loop hippocampus  Push–pull regulation  Decrease in hippocampal volume in chronically anxious subjects   Psychotherapy  Anxiolytic medications  Role of GABA Treatments  Benzodiazepines for anxiety  Makes cells much more sensitive to GABA disorders  Serotonin-selective reuptake inhibitors (SSRIs)  Target for new drugs: CRH receptors Effects of benzos on GABA receptors   Recurrent depression  Major depression  Dysthymia  Bipolar disorder, or manic-depressive disorder  Recurrent, repeated episodes  Type I: mania  Type II: hypomania Affective (mood) disorders   Incidence of affective disorders is higher in prolific creative people / accomplished artists  10x higher incidence of major depressive disorder  30x higher incidence of bipolar disorder  Artistic output often cycles with mood states especially with mania/hypomania  Hypomanic states may improve some cognitive processes / reduce inhibitions Affective (mood) disorders   The monoamine hypothesis  Deficit in central diffuse modulatory systems  Studied by effects of drugs  Reserpine  Monoamine oxidase (MAO) inhibitors  Imipramine Biological  Monoamine hypothesis of mood disorders  Treatment focus on central serotonergic and/or noradrenergic basis of synapses affective disorders   The diathesis-stress hypothesis  Genetic predisposition (diathesis), other stress factors  Role of HPA axis – strong comorbidity with anxiety disorders  Impact of CRH  HPA function becomes hyperactive. Biological  Glucocorticoid receptor gene expression regulated by early experience. basis of  Anterior cingulate cortex dysfunction  Resting-state metabolic activity in anterior cingulate cortex increased in affective depression. disorders   Electroconvulsive therapy (ECT): localized electrical stimulation  Unknown mechanism in relieving depression  Affects temporal lobe  Advantage: quick relief of depression, mania  Adverse effect: loss of prior memories, impaired storage of new information  Psychotherapy: Help patients overcome negative views. Treatments  Effective for mild to moderate depression for affective  Antidepressants: MAO inhibitors, tricyclics, and SSRIs disorders   Lithium treatment for bipolar disorder  Discovered by accident, as with many other psychiatric disorder treatments  Mechanism for stabilizing mood completely unknown, but interferes with many 2nd messenger chemical cascades Treatments for affective disorders Effects of lithium on 5 patients’ moods   Deep brain stimulation  When severe depression fails to respond to other treatment  Electrode implanted deep in the brain  Region of anterior cingulate cortex (Brodmann’s area 25)  Electrical stimulation  decrease activity in brain circuits that are chronically overactive Treatments  Immediate relief from depression  Preliminary findings, brain surgery a treatment of last resort for affective disorders   The most severe mental disorder—loss of contact with reality  Positive symptoms  Delusions, hallucinations  Disorganized speech  Grossly disorganized or catatonic behavior  Negative symptoms  Reduced expression of emotion, poverty of speech  Difficulty initiating goal-directed behavior Schizophrenia  Memory impairment Artwork from schizophrenic individual – look closely   Primarily a genetic disorder  Faulty genes  vulnerability to environmental factors  Associated with physical changes in the brain  Larger ventricle-to-brain size ratio  Other important physical changes in brain  The dopamine hypothesis: psychotic episodes triggered by activation of dopamine receptors Biological  Neuroleptic drugs—potent blockers of dopamine receptors basis of schizophrenia   The glutamate hypothesis  Observed behavioral effects of phencyclidine (PCP) and ketamine  Neither affects dopaminergic transmission.  Both affect synapses that use glutamate as a neurotransmitter.  Inhibit NMDA receptors  Hypothesis: Schizophrenia reflects diminished activation of NMDA Biological receptors in the brain basis of schizophrenia   Drug therapy combined with psychosocial support  Conventional neuroleptics, such as chlorpromazine and haloperidol, act at D2 Treatments receptors  Reduce the positive symptoms of for schizophrenia schizophrenia  Numerous side effects  Like symptoms of Parkinson’s disease  Tardive dyskinesia  Newest focus of drug research  NMDA receptor   Impact of neuroscience on psychiatry  Mental illness recognized as pathologic modifications of the brain  Genes and environment play an important role, causes not fully Summary understood.  Chemical synaptic transmission is affected by drugs.  Unclear why therapeutic drug effects take weeks.  Less known about how psychosocial treatments act on the brain.   Areas of focus for each chapter:  Brain regions / circuits involved in certain behaviors Exam #3  Important neurochemicals & hormones that affect behavioral change advice  Where they are released as well, if they are released in the brain  Effects of damage to brain regions involved in behaviors  You may bring 1 index card of notes Questions?