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Chapter 22: Mental Illness

Neuroscience: Exploring the Brain, 4e. Chapter 22: Mental Illness. Introduction. Neurology Branch of medicine concerned with the diagnosis and treatment of nervous system disorders Neurological disorders Ranging from multiple sclerosis to aphasia

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Chapter 22: Mental Illness

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  1. Neuroscience: Exploring the Brain, 4e Chapter 22: Mental Illness ..

  2. Introduction • 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 function

  3. Introduction—(cont.) • 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

  4. Mental Illness and the Brain • Human behavior • Product of brain activity • Brain • Product of two mutually interacting factors • Heredity • Environment • DNA determines individualism. • Health and illness along continuum of bodily function

  5. Mental Illness and the Brain—(cont.) • Mental illness • Diagnosable disorder of thought, mood, or behavior that causes distress or impaired functioning • Earlier belief • Disorders of the body • Disorders of the mind • Current belief • Most disorders of mood, thought, and behavior have biological explanations.

  6. Psychosocial Approaches to Mental Illness • Freud’s theory: mental illness: unconscious and conscious elements of psyche come into conflict • Treat by unearthing hidden secrets of unconscious • Skinner: Many behaviors are learned maladaptive responses to the environment. • Treat by “unlearning” through behavior modification • Psychosocial approaches to mental illness have sound neurobiological basis. • Psychotherapy

  7. Biological Approaches to Mental Illness • 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 • Other mental illnesses traced directly to biological causes. • Examples: vitamin deficiency, HIV in brain, autoimmune response

  8. Molecular Medicine in Psychiatry • Using genetic information to develop treatment • Discovery of pathophysiology—may suggest biological processes • Target with drug therapy • Unique challenges of brain diseases • Same diagnosis may arise from many causes. • Genetic complexity • New approach: study the pathophysiology of neurons

  9. Molecular Medicine

  10. Anxiety Disorders • Fear • Adaptive response to threatening situations • Many fears innate and species-specific. • Other fears learned • Anxiety disorders • Caused by inappropriate expression of fear • Most common of psychiatric disorders

  11. Common Anxiety Disorders • Panic disorder • Agoraphobia • Generalized anxiety disorder; severe anxiety >6 months • Specific phobias • Social phobia

  12. Other Disorders Characterized by Increased Anxiety • Post-traumatic stress disorder • Symptoms • Increased anxiety • Intrusive memories, dreams, or flashbacks • Irritability, emotional numbness • Obsessive-compulsive disorder • Obsessions: recurrent, intrusive thoughts, images, ideas, or impulses • Compulsions: repetitive behaviors to reduce anxiety • Equally affects males and females unlike other emotional disorders

  13. Biological Bases of Anxiety Disorders • Genetic predisposition for many anxiety disorders • Fear evoked by threatening stimulus: stressor • Manifested by stress response • Stimulus–response relationship strengthened (or weakened) by experience • Stress response • Humoral response: corticotropin-releasing hormone (CRH)  adrenocorticotropic hormone (ACTH)  cortisol

  14. Hypothalamic-Pituitary-Adrenal Axis

  15. Regulation of the HPA Axis by the Amygdala and Hippocampus • Both regulate CRH neurons. • Amygdala projects to bed nucleus of the stria terminalis, which activates the HPA axis. • Hippocampus deactivates the HPA axis. • Glucocorticoid receptors • Feedback loop • Push–pull regulation

  16. Location of Amygdala and Hippocampus

  17. Push–Pull Regulation of the HPA Axis

  18. Treatments for Anxiety Disorders • Psychotherapy • Anxiolytic medications • Role of GABA • Benzodiazepines • Serotonin-selective reuptake inhibitors (SSRIs); via chronic and adaptive changes • Target for new drugs: CRH receptors

  19. The Action of Benzodiazepine

  20. Diminished binding of BDZ in a patient with panic disorder (PET)

  21. Affective Disorders • “Mood” disorders • Recurrent depression • Major depression • Dysthymia (Persistent depressive disorder (PDD); less severe but long-lasting) • Bipolar disorder, or manic-depressive disorder • Recurrent, repeated episodes • Type I: mania • Type II: hypomania

  22. Biological Bases of Affective Disorders • The monoamine hypothesis • Deficit in central diffuse modulatory systems • Studied by effects of drugs • Reserpine (inhibit VMAT2; ves MA [5-HT/NE/DA..] transporter) • Monoamine oxidase (MAO) inhibitors • Imipramine (inhibit reuptake of 5-HT and NE) • Monoamine hypothesis of mood disorders • Treatment focus on central serotonergic and/or noradrenergic synapses

  23. Diffuse Modulatory Systems Implicated in Affective Disorders

  24. Biological Bases of Affective Disorders—(cont.) • The diathesis-stress hypothesis • Genetic predisposition (diathesis), other stress factors • Role of HPA axis • Impact of CRH • HPA function becomes hyperactive. • Glucocorticoid receptor gene expression regulated by early experience.

  25. Anterior Cingulate Cortex Dysfunction • Resting-state metabolic activity in anterior cingulate cortex increased in depression.

  26. Treatments for Affective 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. • Effective for mild to moderate depression

  27. Treatments for Affective Disorders—(cont.) • Antidepressants: MAO inhibitors, tricyclics, and SSRIs

  28. Treatments for Affective Disorders—(cont.) • Lithium treatment for bipolar disorder • Lithium Blocks turnover of PIP2, inhibits AC and GSK

  29. Deep Brain Stimulation • When severe depression fails to respond to other treatment (severe treatment-resistant depression [TRD] and OCD) • 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 • Immediate relief from depression • Preliminary findings, brain surgery a treatment of last resort

  30. Schizophrenia • 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 • Memory impairment

  31. Biological Bases of Schizophrenia • 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 • Neuroleptic drugs—potent blockers of dopamine receptors

  32. Familial nature of Schizophrenia

  33. Enlarged lateral ventricles in Schizophrenia

  34. Loss of cortical gray matter in Schizophrenia

  35. Dopaminergic Diffuse Modulatory Systems of the Brain

  36. Neuroleptics and D2 receptors

  37. Biological Bases of Schizophrenia—(cont.) • 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 receptors in the brain.

  38. Blocking of the NMDA Receptor by PCP

  39. Social withdrawal in NMDAR/GluN1 mutant mice

  40. Treatments for Schizophrenia • Drug therapy combined with psychosocial support • Conventional neuroleptics, such as chlorpromazine and haloperidol, act at D2 receptors • Reduce the positive symptoms of schizophrenia • Numerous side effects • Like symptoms of Parkinson’s disease • Tardive dyskinesia (involuntary, repetitive body movements) • Newest focus of drug research  NMDA receptor

  41. Concluding Remarks • Impact of neuroscience on psychiatry • Mental illness recognized as pathologic modifications of the brain • Genes and environment play an important role, causes not fully 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.

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