Schizophrenia autism etcl-1_sl


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Schizophrenia autism etcl-1_sl

  1. 1. Carlson (7e) Chapter 17: Schizophrenia and the Affective Disorders
  2. 2. Schizophrenia  Schizophrenia represents a disorder of thought and emotion but not a “split-personality” Thought disorder (e.g., loose associations)  Hallucinations (e.g., auditory)  Delusions (e.g., paranoia)  Bizarre behaviors   The incidence of schizophrenia is about 1-2%  No clear gender differences in incidence 17.2
  3. 3. Symptoms of Schizophrenia  Positive symptoms include delusions, hallucinations and thought disorder  Delusions are beliefs that are contrary to reality  Delusions can    involve control, grandeur, or persecution Hallucinations are perceptions that occur in the absence of stimuli (often auditory and/or olfactory) Thought disorder: disorganized and irrational Negative symptoms involve a loss of normal behaviors, such as    Poverty of speech and low initiative Social withdrawal and diminished affect Anhedonia 17.3
  4. 4. Heritability of Schizophrenia  The heritability of schizophrenia is a strong indicator of a biological basis for schizophrenia  Adoption studies  Adult schizophrenics that were adopted as children are likely to have schizophrenic biological relatives.  Twin studies  Concordance rates for schizophrenia are higher for identical than for fraternal twins:  No single gene has been identified for schizophrenia Genes may pass on a susceptibility to develop schizophrenia 17.4
  5. 5. The Dopamine Hypothesis of Schizophrenia  The “dopamine hypothesis” is that the positive symptoms of schizophrenia involve over activity of brain dopaminergic synapses  Chlorpromazine (CPZ) was identified as an effective antipsychotic (AP) agent CPZ was later found to block DA receptors (D2 receptors) D2 receptor blockade correlates with clinically effective dose of typical antipsychotic medications  Stimulants such as amphetamine that release DA can produce the positive symptoms of schizophrenia in “normals” and relapse in schizophrenics 17.5
  6. 6. DA Activity in Schizophrenia  PET studies indicate greater activity of dopamine in the striatum of schizophrenics to a test dose of amphetamine   Amount of dopamine activity was related to the increase in positive schizophrenia symptoms Studies of dopamine receptors in schizophrenic brain have provided mixed results (but generally supportive)  Postmortem studies suggest increased numbers of D2 receptors in striatum (but may be due to exposure to antipsychotic drugs) The striatum is a motor control region  Schizophrenia may be related to D4 or D3 receptors   Clozapine is an effective (atypical) antipsychotic drug that interacts with D4 and not D2 receptors strong effect on mesolimbic/mesocortical dopamine system (A10) 17.6  little effect on nigrostriatal dopamine system (A9) 
  7. 7. Dopamine Augmentation & Schizophrenia  Psychomotor stimulants (e.g., amphetamine) „normals‟ develop paranoid psychosis  schizophrenics release -- subjectively indistinguishable for worsening of endogenous illness (cf. LSD)   L-DOPA (precursor loading) little or no effect in „normals‟  worsening of psychotic symptoms in schizophrenics  schizophrenic symptoms in some Parkinson‟s patients   Stress (increased dopaminergic activity)  precipitate relapse & perhaps even initiate disorder
  8. 8. Dopamine Attenuation & Schizophrenia DA synthesis inhibitors (e.g., AMPT) abate schizophrenia  DA storage depleters (e.g., reserpine) abate schizophrenia  D2 receptor blockers (e.g., typical antipsychotics) abate schizophrenia  Even atypical antipsychotics (which do not effectively block D2 receptors) influence mesolimbic DA activity 
  9. 9. Antipsychotic Medications   Antipsychotic medications diminish the thought disorder & disruptive behavior evident in schizophrenia Side effects of antipsychotic medications include  Major  Extrapyramidal (Parkinsonism-like) side effects due to blockade of DA receptors  Tardive dyskinesia: facial tics and gestures due to an over stimulation of DA receptors (may be related to CNS sensitization and relapse)  Minor  Autonomic problems (dry mouth)  Skin-eye pigmentation  Breast development (increased prolactin release after blockade of 17.9 dopamine neurons)
  10. 10. Brain Damage and Schizophrenia  The negative symptoms of schizophrenia may be related to brain damage  The neurological signs evident in schizophrenia include Eye tracking problems  Catatonia  Problems with blinking, eye focusing, and visual pursuit    Schizophrenics exhibit enlarged brain ventricles, which suggests loss of brain cells Regions of schizophrenic brain that are abnormal include Prefrontal cortex  Medial temporal lobes  Medial diencephalon  17.10
  11. 11. Causes of Brain Damage in Schizophrenia  The neurological symptoms of schizophrenia may be caused by   Birth trauma (obstetrical issues) Viral infections that impair neural development during the second trimester  Seasonality   effects (schizophrenia is more likely for winter births) Nutritional issues (Hunger Winter: female offspring were more likely to exhibit schizophrenia than male offspring) Maternal stress may compromise the immune system of the mother and lead to a greater chance of contracting a viral infection 17.11
  12. 12. Seasonality and Schizophrenia  Children born during the late winter and early spring are more likely to develop schizophrenia   Seasonality effect occurs in cities but not the countryside Seasonality effect may be related to the mother contracting a viral infection during the second trimester of fetal development (or astrological sign?) 17.12
  13. 13. Hypofrontality and Schizophrenia  Hypofrontality refers to the decreased activity of the frontal lobe (dorsolateral prefrontal cortex).  Damage to the prefrontal cortex  impairs behavioral flexibility (card sorting task)  may disinhibit mesolimbic dopamine system   Schizophrenics show decreased activity in the prefrontal cortex Abuse of PCP produces positive and negative symptoms of schizophrenia    Positive: related to indirect actions of PCP on accumbens DA Negative: related to decreased DA utilization in prefrontal cortex following PCP treatment 17.13 Data are less compelling that dopamine-agonist effect
  14. 14. Major Affective Disorders  Affect refers to emotions, moods, and feelings Our affect is usually a reflection of our experiences  In the major affective disorders, our emotional reactions are at the extremes and may not be related to our actual experiences   The major affective disorders include  Bipolar disorder - alternating cycles of  Mania: euphoria, delusions  Depression: profound sadness, guilt, suicide risk  Unipolar depression: continuous, episodic 17.16
  15. 15. Biological Bases of Affective Disorder  Heritability of affective disorder (AD) has been established in twin studies and family studies   Bipolar disorder may be related to a single gene Depression is amenable to physical treatments including  Pharmacological treatments  MAO inhibitors (e.g. iproniazid)  Noradrenergic reuptake inhibitors (desmethylimipramine)  Serotonin reuptake inhibitors (e.g. Prozac) Electroconvulsive shock therapy (ECS)  Sleep deprivation  17.17
  16. 16. Monoamine Hypothesis of Depression  Depression results from reduced activity of brain monoamines Reserpine depletes monoamines--> depression  Suicidal depression is related to a low level of 5-HIAA (metabolite of serotonin)  Antidepressant medications increase either NE or 5-HT (serotonin)   Usually  via blockade of monoamine reuptake Tryptophan (precursor to 5-HT) deletion procedure:  Reduces brain 5-HT levels  Reinstates depression in former depressed patients 17.18
  17. 17. REM Sleep and Depression  Sleep pattern is disrupted in depressed persons Reduced REM latency (duration of sleep, from sleep onset to the onset of the first REM sleep period)  reduced stages 3 and 4 sleep  REM deprivation improves mood  Antidepressant drugs suppress REM sleep, and increase slow-wave sleep  Persons who have short REM sleep latency are more likely to develop depression  REM sleep deprivation is more effective than is total 17.19 sleep deprivation (effects last longer) 
  18. 18. Seasonal Affective Disorder SAD is a form of depression evident in winter months (short days/long nights)  SAD involves  Mood and sleep disturbances  Carbohydrate cravings and weight gain   Phototherapy for SAD: increased exposure to light improves mood in SAD (and also for unipolar depression) 17.20
  19. 19. Anxiety Disorders, Autistic Disorder, AttentionDeficit/Hyperactivity Disorder, and Stress Disorders Chapter 17
  20. 20. Lecture Preview     Anxiety Disorders Autistic Disorder Attention-Deficit/Hyperactivity Disorder Stress Disorders
  21. 21. Anxiety Disorders  Panic Disorder, Generalized Anxiety Disorder, and Social Anxiety Disorder  Description Disorder – a disorder characterized by episodic periods of symptoms such as shortness of breath, irregularities in heartbeat, and other autonomic symptoms, accompanied by intense fear. Anticipatory Anxiety – a fear of having a panic attack; may lead to the development of agoraphobia. Panic
  22. 22. Anxiety Disorders (Continued) Anxiety Disorder – characterized by excessive anxiety and worry serous enough to cause disruption to one’s life. Social Anxiety Disorder – characterized by excessive fear of being exposed to the scrutiny of other people that leads to avoidance of social situations in which the person is called on to perform. Generalized  Possible Causes May involved alleles of the 5-HTT.
  23. 23. Anxiety Disorders (Continued)  Obsessive-Compulsive Disorder  Description A mental disorder characterized by obsessions and compulsions. Obsessions – unwanted thought or idea with which a person is preoccupied. Compulsion – feel that one is obliged to perform a behavior, even if one prefers not to do so.  Possible Causes Tourette’s Syndrome Streptococcal Hemolytic Infection
  24. 24. Autism  Autism: impairments of Social relations with others  Ability to communicate  Imaginative ability   Incidence of autism is 4/10,000  Males are 3 times more likely to develop autism
  25. 25. Autistic Disorder  Description   A chronic disorder whose symptoms include failure to develop normal social relations with other people, impaired development of communicative ability, lack of imaginative ability, and repetitive, stereotyped movements. Possible Causes Heritability  Brain Pathology 
  26. 26. Biological Bases of Autism   Heritability: MZ twins exhibit a 96% concordance rate for autism Autism is associated with neurological disorders:  Phenylketonuria (PKU)  Tourette‟s syndrome  Fragile  X syndrome (mental retardation) Factors that impair development lead to autism:  Rubella, hydroencephalus  Drugs such as Thalidomide
  27. 27. Attention-Deficit/Hyperactivity Disorder  Description   A disorder characterized by uninhibited responses, lack of sustained attention, and hyperactivity. Possible Causes  Delays in reinforcement render reinforcement relatively ineffective, but immediate reinforcement is highly effective.
  28. 28. Figure 17.9 Delay of Reinforcement Gradients in ADHD
  29. 29. Stress  Stress – a general, imprecise term that can refer either to a stress response or to a situation that elicits a stress response.
  30. 30. Stress  Aversive stimuli can elicit emotional responses: Behavioral component: Fight or Flight response Autonomic component: Sympathetic activation Endocrine: secretion of epinephrine, NE  Physiological reactions to chronic aversive stimuli/situations can be damaging Stressors: the aversive stimuli  Stress Response: our reaction to stressors 
  31. 31. Hormone Secretion during Stress   Stressors evoke activity in sympathetic N.S. Adrenal glands release  Epinephrine: biases energy flow to muscles, increases blood pressure and blood flow to heart  Norepinephrine: increases blood flow and pressure  Glucocorticoids: break down protein and fats to glucose
  32. 32. Physiology of the Stress Response  Glucocorticoid – one of a group of hormones of the adrenal cortex that are important in protein and carbohydrate metabolism, secreted especially in times of stress.
  33. 33. Physiology of the Stress Response (Continued) The process involved in the production of glucocorticoids:  Corticotropin-Releasing Hormone (CRH) – hypothalamic hormone that stimulates the anterior pituitary gland to secrete ACTH.  Adrenocorticotropic Hormone (ACTH) – hormone released by the anterior pituitary gland in response to CRH; stimulates the adrenal cortex to produce glucocorticoids.
  34. 34. Figure 17.12 Control of Secretion of Stress Hormones
  35. 35. Stress Disorders (Continued)  Effects of Stress on the Brain Elevates glucocorticoid levels.  Impairs development of primed-burst potentiation.  Disrupts learning.  Prenatal Stress:  Increases size of the lateral nucleus of the amygdala. Elevates glucocorticoid response to stress.  Hippocampal Damage
  36. 36. Chronic Exposure to Stressors  Chronic stress is damaging to health  Air traffic controllers: more likely to develop    High blood pressure Ulcers and diabetes Chronic secretion of glucocorticoids leads to: Increased blood pressure (--> stroke, heart attacks) Loss of neurons in brain (e.g. hippocampal field CA1) Suppression of the immune system (--> illness) Suppression of the inflammatory system (delays healing)
  37. 37. Stress Disorders (Continued)  Health Effects of Long-Term Stress Hypertension – stress causes an increase in hypertension.  Wound Healing – stress causes an increase in the time to heal wounds. 
  38. 38. Posttraumatic Stress Disorder  Posttraumatic Stress Disorder (PTSD):  Acute exposure to intense stressors can have delayed effects (Air disasters, war, assault) Dreams, recall of trauma event Flashback episodes of event Intense distress
  39. 39. Stress Disorders (Continued)  Posttraumatic Stress Disorder A psychological disorder caused by exposure to a situation of extreme danger and stress; symptoms include recurrent dreams or recollections; can interfere with social activities and cause a feeling of hopelessness.  Involves many brain regions, including the amygdala and prefrontal cortex. 
  40. 40. Predisposing Factors for PTSD  Personality variables that predispose to PTSD:   Tendency to brood about feelings Vietnam Veterans study:      Family financial difficulty History of drug abuse/dependence History of affective disorders History of childhood behavior problems Genetic factors for PTSD:  Vietnam PTSD soldiers were more likely to possess an allele of the dopamine D2 receptor
  41. 41. Coping Responses and Stress   Stress reflects our reaction to stressors Coping implies modifying our responses:  Exerting control over aversive stimuli can reduce stress responses  Weiss study: rats that avoid shock show fewer ulcers  Coping may involve an increase in the level of benzodiazepines in brain (would act via GABA sites to reduce anxiety)
  42. 42. Psychoneuroimmunology  Psychoneuroimmunology: Study of the interactions between the immune system and behavior. The branch of neuroscience involved with interactions between environmental stimuli, the nervous system, and the immune system.  Stress responses can impair the immune system  Leading to illness and potential death
  43. 43. Psychoneuroimmunology  Antigen – protein present on a microorganism that permits the immune system to recognize the microorganism as an invader.  Antibody – protein produced by a cell of the immune system that recognizes antigens present on invading microorganisms
  44. 44. Stress Disorders (Continued) B-Lymphocyte – a white blood cell that originates in the bone marrow.  Immunoglobulin – an antibody released by Blymphocytes that bind with antigens and help destroy invading microorganisms.  T-Lymphocyte – a white blood cell that originates in the thymus gland. 
  45. 45. Overview of the Immune System  Immune system destroys foreign organisms (viruses, bacteria, fungi)  Nonspecific reaction: act to destroy organisms or infected cells  Inflammatory reaction: damaged cells leak substances that increase blood flow  Phagocytotic white blood cells: destroy damaged cells  Cell infection --> interferon secretion (reduces viral replication  Natural killer cells: detect and destroy infected cells
  46. 46. Immune System Overview, continued  Specific Immune reactions:  Chemically-mediated: immune system produces antibodies that recognize the antigens present on surface of a foreign cell  B-lymphocytes: produce immunoglobulin antibodies that destroy foreign cells  Cell-mediated: antibodies on exterior of T-lymphocytes detect foreign antigens (viruses)
  47. 47. Stress and the Immune Response  Stress increases likelihood of infectious disease   Students are more likely to be ill during exam times Death of a spouse leads to illness of survivor  Explanation: stress releases glucocorticoids that in turn impair the immune system  Supporting Evidence:    Bereavement leads to reduced immune response Alzheimer‟s caregivers have impaired immune response Inescapable shock in rats reduces T-cells, B-cells and natural killer cells
  48. 48. Stress Disorders (Continued)  Stress, Health, and Disease Stress decreases immune function.  Stress increases the susceptibility to infection. 
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