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Schizophrenia autism etcl-1_sl

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Physiological Psychology

Physiological Psychology

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  • 1. Carlson (7e) Chapter 17: Schizophrenia and the Affective Disorders
  • 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Anxiety Disorders, Autistic Disorder, AttentionDeficit/Hyperactivity Disorder, and Stress Disorders Chapter 17
  • 20. Lecture Preview     Anxiety Disorders Autistic Disorder Attention-Deficit/Hyperactivity Disorder Stress Disorders
  • 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. 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. 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. 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. 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. 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. 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. Figure 17.9 Delay of Reinforcement Gradients in ADHD
  • 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. 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. 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. 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. 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. Figure 17.12 Control of Secretion of Stress Hormones
  • 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Stress Disorders (Continued)  Stress, Health, and Disease Stress decreases immune function.  Stress increases the susceptibility to infection. 

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