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Psychopathology

Psychopathology. Rains Chapter 13. What is Psychopathology. Major psychiatric disorders can severely disrupt behavior and cause enormous suffering. Biological factors medical model illness lesion responsible for disorder psychosocial factors Problems in living. What is Psychopathology.

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Psychopathology

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  1. Psychopathology Rains Chapter 13

  2. What is Psychopathology • Major psychiatric disorders can severely disrupt behavior and cause enormous suffering. • Biological factors • medical model • illness • lesion responsible for disorder • psychosocial factors • Problems in living

  3. What is Psychopathology • Gleitman (1995) example • individual with no cognitive disability but has simply not been taught to read. • Someday may identify brain circuits for reading and be able reprogram them through microsurgery or gene therapy • Probably better to understand inability to read in terms of lack of training

  4. What is Psychopathology • General paresis as an example • syphilis caused by bacterial infection • in a few cases, symptoms seem to clear up then later general paresis appears • at first, thought general paresis was psychological disorder • progressive general decline of physical and psychological functioning culminating in personality changes, disturbed gait, delusions, dementia, and death

  5. The Schizophrenic Disorders • 1-1.5% of population • 400,000 persons hospitalized in US • about 30% of all hospital beds • Typically chronic • symptoms may be more or less intense but seldom recover completely • Onset in early 20’s

  6. Positive Symptoms • Delusions • Hallucinations • Bizarre behavior • Formal thought disorder • loose associations • word salad

  7. Negative Symptoms • Apparent absence of motivation (avolition) • social withdrawal • diminished emotional expression (blunted affect) • diminished verbal expression (alogia) • poor judgment • poor personal hygiene • decrease in level of attention • decrease in activity level • decrease in self direction

  8. The hypothesis of multiple etiologies of schizophrenia • May be a group of disorders • Perhaps with different underlying neurobiological abnormalities

  9. Genetic Factors • Twin studies • Concordance rate • 55% for monozygotic twins • 10% for dizygotic twins • Adoption studies • 15% of children of schizophrenic mothers become schizophrenic whether adopted by non schizophrenic mother or not

  10. Dopamine Hypothesis of Schizophrenia • Schizophrenia due to abnormally increased dopamine activity in the brain

  11. Evidence for Dopamine Hypothesis • Antipsychotic (neuroleptic) drugs such as chlorpromazine (Thorazine) or haloperidol (Haldol) control symptoms in many patients • neuroleptics block dopamine receptors • magnitude of therapeutic effect of different neuroleptics is proportional to the magnitude of dopamine blocking effect

  12. Neuroleptics as Anti-schizophrenic • not just anti-anxiety or sedative • If sedatives then barbiturates should work but they don’t • If anti-anxiety then neuroleptics should work with anxiety disorders but virtually ineffective • Neuroleptics calm hyperactive patients and make withdrawn patients more active • Anti-anxiety drugs are not effective with schizophrenia

  13. Amphetamine Psychosis • The only drug effect that is clinically indistinguishable from schizophrenia • True drug effect not a result of sleep loss or activation of latent schizophrenia • Phenothiazines are effective in treating amphetamine psychosis • Amphetamines in small doses activate schizophrenic symptoms

  14. Schizophrenia and Parkinson’s Disease • Parkinson’s disease is a degenerative (progressive and incurable) disease which results from a deficiency of dopamine or at least an insensitivity to dopamine. It is treated with L-dopa a precursor of dopamine which in some patients results in relief of the symptoms during the early stages.

  15. Schizophrenia and Parkinson’s Disease • In many ways schizophrenia is the opposite of Parkinson’s disease. Schizophrenics act as if they have too much dopamine. • Parkinson’s patients act as though they have a deficiency of dopamine

  16. Schizophrenia and Parkinson’s Disease • Never been a case on record of a Parkinson’s patient developing schizophrenia although if Parkinson’s patients are overmedicated they show temporary schizophrenic symptoms

  17. Schizophrenia and Parkinson’s Disease • The anti-schizophrenic drugs produce Parkinson like symptoms as a side effect, presumably because they block dopamine and cause the individuals brain to resemble a Parkinson’s patient

  18. Evidence for Dopamine Hypothesis • Dopamine enhancing drugs (eg: amphetamines and L-dopa) may produce transient psychotic states indistinguishable from schizophrenia • autopsy evidence suggests overabundance of dopamine receptors rather than too much dopamine (studies include individuals who have never been on neuroleptics)

  19. Problems with Dopamine Hypothesis • Blockade effect on dopamine occurs in hours, symptoms don’t start to effect symptoms for weeks • Some patients respond to dopamine blockers, others don’t • Positive symptoms seem to be more related to dopamine abnormality • Negative symptoms seem more related to structural abnormalities

  20. Refinement of Dopamine Hypothesis • Recent development of atypical antipsychotics such as clozapine (Clozaril), risperidone (Risperdal), and olanzapine (Zyprea) • These block both dopamine and serotonin and are more effective (particularly with schizophrenics with mainly negative symptoms) • led to dopamine-serotonin interaction hypothesis

  21. Gross Structural Abnormalities • Enlarged Ventricles • correlational • not all schizophrenics show it • Cortical Atrophy • generalized atrophy not in particular regions

  22. Two-Syndrome Hypothesis • Type I • normal ventricle size and no atrophy • predominantly positive symptoms • Type II • enlarged ventricles and cortical atrophy • predominantly negative symptoms

  23. Microstructural Abnormalities • Pyramidal cells show disorganized orientation • Disrupted connections in hippocampus • Also reports of problems in a number of other areas

  24. Abnormalities from Functional Imaging • Hypofrontality • decreased frontal activity in schizophrenia • decreased activation of frontal and prefrontal areas in tasks that normally activate these areas

  25. Neuropsychological Functioning • Attentional Impairment • poor performance on Continuous Performance Test (vigilance type task) • Temporal Lobe and Prefrontal dysfunction • tests of verbal and non-verbal memory, working memory, flexibility, and planning • Left Hemisphere Hypothesis • schizophrenia -- abnormality in left hemisphere • overactivity may produce positive symptoms • mood disorders -- abnormality in right hemisphere

  26. Prefrontal Dysfunction Hypothesis • Positive symptoms result from excessive dopamine activity in limbic system • Negative symptoms result in decrease in dopamine activity in prefrontal cortex • working memory impaired

  27. Pharmacological Treatment of Schizophrenia • Psychotherapy is virtually ineffective with the schizophrenic symptoms • Drugs are somewhat effective for about 60% • Once the drugs have taken effect patient is in need of therapy, rehabilitation, social skills training, and help getting re-integrated into society

  28. Extrapyramidal Side Effects • Caused by blocking the dopamine in the basal ganglia and not blocking the cholinergic input from the cortex • Produces an inballance • Can use anticholinergic drugs such as Artane and Cogentin to bring the Acetylcholine levels in line with dopamine and stop the Parkinson like or extrapyramidal side effects • Anticholinergic psychosis can occur from overdose (dry mouth, dilated pupils, psychosis)

  29. Side Effects • Dystonia: tonic movements, twist of body, looks like a seisure • Acute dyskinesia: ticks and smacking • Acathesia: motor restlessness, can’t sit still, pace floor • Psychic restlessness • Tardive dyskinesia • Fly catchers tongue • Smacking • Foot tapping • Irreversible particularly after a long time on high doses • Need to give drug holidays

  30. Side Effects • Retinal Pigmentation • Jaundice • Leuconemia • Cardiac arythmia • Sexual difficulties

  31. Mood Disorders • Affective disorders • Disorders that have a long-term disturbance of mood as predominant feature. • Major depressive disorder • Seasonal affective disorder • Bipolar disorder

  32. Major Depressive Disorder • Also called unipolar depression • Lifetime risk – 12% • Prevalence – 5% of population at any given time • Suicide risk – 15%

  33. Major Depressive Disorder • Older classification • Endogenous depression – biological component • Reactive depression – external (interpersonal and social) factors • Now realize most disorders are result of both • Vegitative symptoms: loss of appetite, diurnal mood variation, decreased sex drive, sleep disturbance

  34. Monoamine Hypothesis of Depression • Monoamines • Catecholamines • Dopamine • Norepinephrine • Indolamine • Serotonin

  35. Monoamine Hypothesis of Depression • Drugs that increase brain monoamine levels alleviate depression • Tricyclic antidepressants • Monoamine oxidase inhibitors • Drugs that decrease monoamine levels induce depression • Reserpine • Hypothesize that abnormally low levels of monoamines play role in depression

  36. Major Depressive Disorder • Dopamine agonists don’t help major depression • So conclude it is serotonin and norepinephrine • Many depressives have low levels of serotonin metabolite • Selective serotonin reuptake inhibitors (SSRI’s) work on serotonin alone • Fluoxetine (Prozac) • Paroxetine (Paxil) • Sertaline (Zoloft)

  37. Possible Endocrine Dysfunction in Depression • Some depressed patients release too much cortisol in response to stress • Don’t know what this means

  38. Abnormalities Revealed by Functional Imaging • Hypofrontality similar to that found in schizophrenia but • Do not show absence of activation on specific tasks and • Do not show cognitive impairments associated with specific brain areas • Don’t know what this means

  39. Genetic Factors in Depression • Concordance rate for major depression for monozygotic twins is four times higher than for dizygotic twins

  40. Pharmacological Treatment of Depression • Tricyclic Antidepressants • Tofranil • Elavil • Sinequan • Side Effects • Dry mouth • Dizziness • Cardiovascular

  41. Pharmacological Treatment of Depression • MAO Inhibitors • Phenelzine (Nardil) • Isocarboxazid (Marplan) • Tranylcypromine (Parnate) • Beer-Cheese reaction • Foods containing tryptamine • Nose spray

  42. Pharmacological Treatment of Depression • SSRI’s • Prozac • Paxil • Zoloft • Dual Action Antidepressants • Nefazodone (Serzone) • Mirtazapine (Remeron)

  43. Seasonal Affective Disorder • Some people become depressed during the winter when days are short and nights are long. • Treated with exposure to bright lights for several hours a day • Don’t know much about biological basis of this but data doesn’t seem to relate to cycling of hypothalamus

  44. Bipolar Disorder • Manic-depressive disorder • 0.5-1% of population • Mania • Few hours to several months • Elevated, expansive, irritable mood • Inflated self-esteem, decreased need for sleep • Hypersexuality, flight of ideas, high risk taking

  45. Bipolar Disorder • Neurochemical factors • Lithium carbonate (Eskalith) • Anti-convulsant drugs • Carbamazepine (Tegretol) • Sodium valproate (Depakote) • These drugs are highly effective, but • Don’t know how they work so doesn’t lead to a theory

  46. Genetic Factors in Bipolar Disorder • Specific genetic links have been identified • No single mechanism accounts for all cases • We are a long way from understanding bipolar disorder

  47. Anxiety Disorders • Phobic disorders • Specific (snake or spider) • Social phobia • Agoraphobia • Generalized Anxiety Disorder • Panic Disorder • Obsessive-Compulsive Disorder

  48. Neurochemical Factors in Anxiety Disorders • Anxiolytics bind to benzodiazapine receptors that are part of the benxodiazepine-GABA complex • Serotonin agonists (Proxac) are effective also • Don’t know how this fits together

  49. Simple Phobias • Preparedness theory of phobias • Phobias develop for snakes, spiders, and heights which people in modern civilization are rarely threatened by • Don’t develop to electric sockets and automobiles that are real threats • People are genetically programmed to rapidly learn to fear certain stimuli • Most people with phobias have never actually been harmed by the object they fear.

  50. Dementing Diseases • Alzheimer’s Disease • Huntington’s Chorea • Parkinson’s Disease

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