1. Chapter 14 Psychological Disorders

2. Table of Contents Abnormal Behavior The medical model What is abnormal behavior? –3 criteria Deviant Maladaptive Causing personal distress A continuum of normal/abnormal

3. Table of Contents Fig 14.2 – Normality and abnormality as a continuum. There isn’t a sharp boundary between normal and abnormal behavior. Behavior is normal or abnormal in degree, depending on the extent to which one’s behavior is deviant, personally distressing, or maladaptive.

4. Table of Contents Prevalence, Causes, and Course Epidemiology Prevalence Lifetime prevalence Diagnosis Etiology Prognosis

5. Table of Contents Fig 14.5 – Lifetime prevalence of psychological disorders. The estimated percentage of people who have, at any time in their life, suffered from one of four types of psychological disorders or from a disorder of any kind (top bar) is shown here. Prevalence estimates vary somewhat from one study to the next, depending on the exact methods used in sampling and assessment. The estimates shown here are based on pooling data from Wave 1 and 2 of the Epidemiological Catchment Area studies and the National Comorbidity Study, as summarized by Regier and Burke (2000) and Dew, Bromet, and Switzer (2000). These studies, which collectively evaluated over 28,000 subjects, provide the best data to date on the prevalence of mental illness in the United States.

6. Table of Contents Psychodiagnosis: The Classification of Disorders American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders – 4th ed. (DSM - 4) Multiaxial system 5 axes or dimensions –Axis I – Clinical Syndromes –Axis II – Personality Disorders or Mental Retardation –Axis III – General Medical Conditions –Axis IV – Psychosocial and Environmental Problems –Axis V – Global Assessment of Functioning

7. Table of Contents Axis I Clinical Syndromes Discussed in Text Anxiety Disorders Somatoform Disorders Dissociative Disorders Mood Disorders Schizophrenic Disorders

8. Table of Contents Clinical Syndromes: Anxiety Disorders Generalized anxiety disorder –“free-floating anxiety” Phobic disorder –Specific focus of fear Panic disorder and agoraphobia –Physical symptoms of anxiety/leading to agoraphobia Obsessive compulsive disorder –Obsessions –Compulsions

9. Table of Contents Etiology of Anxiety Disorders Biological factors –Genetic predisposition, anxiety sensitivity –GABA circuits in the brain Conditioning and learning –Acquired through classical conditioning or observational learning –Maintained through operant conditioning Cognitive factors –Judgments of perceived threat Personality –Neuroticism Stress –A precipitator

10. Table of Contents Fig 14.6 - Twin studies of anxiety disorders. The concordance rate for anxiety disorders in identical twins is higher than that for fraternal twins, who share less genetic overlap. These results suggest that there is a genetic predisposition to anxiety disorders. (Data based on Noyes et al., 1987; Slater & Shields, 1969; Torgersen, 1979, 1983)

11. Table of Contents Fig 14.7 - Conditioning as an explanation for phobias. (a) Many phobias appear to be acquired through classical conditioning when a neutral stimulus is paired with an anxiety- arousing stimulus. (b) Once acquired, a phobia may be maintained through operant conditioning. Avoidance of the phobic stimulus reduces anxiety, resulting in negative reinforcement.

12. Table of Contents Fig 14.8 - Cognitive factors in anxiety disorders. Eysenck and his colleagues (1991) compared how subjects with anxiety problems and nonanxious subjects tended to interpret sentences that could be viewed as threatening or nonthreatening. Consistent with cognitive models of anxiety disorders, anxious subjects were more likely to interpret the sentences in a threatening light.

13. Table of Contents Clinical Syndromes: Somatoform Disorders Somatization Disorder Conversion Disorder Hypochondriasis –Etiology Reactive autonomic nervous system Personality factors Cognitive factors The sick role

14. Table of Contents Fig 14.10 - Glove anesthesia. In conversion disorders, the physical complaints are sometimes inconsistent with the known facts of physiology. For instance, given the patterns of nerve distribution in the arm shown in (a), it is impossible that a loss of feeling in the hand exclusively, as shown in (b), has a physical cause, indicating that the patient’s problem is psychological in origin.

15. Table of Contents Clinical Syndromes: Dissociative Disorders Dissociative amnesia Dissociative fugue Dissociative identity disorder –Etiology severe emotional trauma during childhood –Controversy Media creation?

16. Table of Contents Clinical Syndromes: Mood Disorders Major depressive disorder –Dysthymic disorder Bipolar disorder (manic-depressive disorder) –Cyclothymic disorder Etiology –Genetic vulnerability –Neurochemical factors –Cognitive factors –Interpersonal roots –Precipitating stress

17. Table of Contents Fig 14.11 - Episodic patterns in mood disorders. Time-limited episodes of emotional disturbance come and go unpredictably in mood disorders. People with unipolar disorders suffer from bouts of depression only, whereas people with bipolar disorders experience both manic and depressive episodes. The time between episodes of disturbance varies greatly with the individual and the type of disorder.

18. Table of Contents

19. Fig 14.13 - Twin studies of mood disorders. The concordance rate for mood disorders in identical twins is much higher than that for fraternal twins, who share less genetic overlap. These results suggest that there must be a genetic predisposition to mood disorders. The disparity in concordance between the two types of twins is greater for mood disorders than for either anxiety disorders (see Figure 14.7) or schizophrenic disorders (see Figure 14.19), which suggests that genetic factors may be particularly important in mood disorders. (Data from Gershon, Berrettini, & Goldin, 1989)

20. Table of Contents Fig 14.15 - Negative thinking and prediction of depression. Alloy and colleagues (1999) measured the explanatory style of first-year college students and characterized them as high risk or low risk for depression. This graph shows the percentage of these students who experienced major or minor episodes of depression over the next 2.5 years. As you can see, the high-risk students who exhibited a negative thinking style proved to be much more vulnerable to depression. (Data from Alloy et al., 1999)

21. Table of Contents Fig 14.16 - Interpersonal factors in depression. Behavioral theories about the etiology of depression emphasize how inadequate social skills may contribute to the development of the disorder.

22. Table of Contents Clinical Syndromes: Schizophrenia General symptoms –Delusions and irrational thought –Deterioration of adaptive behavior –Hallucinations –Disturbed emotions Prognostic factors

23. Table of Contents Subtyping of Schizophrenia 4 subtypes –Paranoid type –Catatonic type –Disorganized type –Undifferentiated type New model for classification –Positive vs. negative symptoms

24. Table of Contents Etiology of Schizophrenia Genetic vulnerability Neurochemical factors Structural abnormalities of the brain The neurodevelopmental hypothesis Expressed emotion Precipitating stress

25. Table of Contents Fig 14.18 – The dopamine hypothesis as an explanation for schizophrenia. Decades of research have implicated over-activity at dopamine synapses as a key cause of schizophrenic disorders. However, the evidence on the exact mechanisms underlying this over-activity, which is summarized in the graphic, is complex and open to debate. Recent hypotheses about the neurochemical bases of schizophrenia go beyond the simple assumption that dopamine activity is increased. For example, one theory posits that schizophrenia may be accompanied b decreased dopamine activity in one area of the brain (the prefrontal cortex) and increased activity or dysregulation in other areas of the brain (Egan & Hyde, 2000). Moreover, abnormalities in other neurotransmitter systems may also contribute to schizophrenia.

26. Table of Contents Fig 14.20 – The neurodevelopmental hypothesis of schizophrenia. Recent findings have suggested that insults to the brain sustained during prenatal development or at birth may disrupt crucial maturational processes in the brain, resulting in subtle neurological damage that gradually becomes apparent as a youngsters develop. This neurological damage is believed to increase both vulnerability to schizophrenia and the incidence of minor physical anomalies (slight anatomical defects of the head, face, hands and feet).

27. Table of Contents Personality Disorders Anxious-fearful cluster –Avoidant, dependent, obsessive-compulsive Dramatic-impulsive cluster –Histrionic, narcissistic, borderline, antisocial Odd-eccentric cluster –Schizoid, schizotypal, paranoid Etiology –Genetic predispositions, inadequate socialization in dysfunctional families

28. Table of Contents

29. Psychological Disorders and the Law Insanity –M’naghten rule Involuntary commitment –danger to self –danger to others –in need of treatment

30. Table of Contents Fig 14.22 – The insanity defense: Public perceptions and actual realities. Silver, Cirincione, and Steadman (1994) collected data on the general public’s beliefs about the insanity defense and the realities of how often it is used and how often it is successful (based on a large-scale survey of insanity pleas in either states). Because of highly selective media coverage, there are dramatic disparities between public perceptions and actual realities, as the insanity defense is used less frequently and less successfully than widely assumed.

31. Table of Contents Culture and Pathology Cultural variations Culture bound disorders –Koro –Windigo –Anorexia nervosa

32. Table of Contents Fig 14.25 - Weight trends among Playboy centerfolds and Miss America contestants. This graph charts how the average weight of Playboy centerfolds and Miss America contestants changed over the course of 30 years (from 1959 to 1989). To control for age and height, each woman’s weight was compared to the average weight for a woman of that age and height and expressed as a percentage of the expected weight. Given the small samples, the figures are a little erratic, but overall, the data show a clear downward trend. (Data from Garner et al., 1980; Wiseman et al., 1992; graphic from Barlow & Durand, 1999)