1. Chapter 14 Psychological Disorders

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

3. Figure 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. Prevalence, Causes, and Course n Epidemiology n Prevalence n Lifetime prevalence n Diagnosis n Etiology n Prognosis

5. n American Psychiatric Association n Diagnostic and Statistical Manual of Mental Disorders – 4th ed. (DSM - 4) n Multiaxial system n 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 Psychodiagnosis: The Classification of Disorders

6. n Anxiety Disorders n Somatoform Disorders n Dissociative Disorders n Mood Disorders n Schizophrenic Disorders Axis I: Clinical Syndromes

7. n Generalized anxiety disorder  “Free-floating anxiety” n Phobic disorder  Specific focus of fear n Panic disorder and agoraphobia  Physical symptoms of anxiety/leading to agoraphobia n Obsessive compulsive disorder  Obsessions  Compulsions Clinical Syndromes: Anxiety Disorders

8. Figure 14.6 Common phobias. The most frequently reported phobias in a large-scale survey of mental health (Eaton, Dryman, & Weissman, 1991) are listed here. The percentages reflect the portion of respondents who reported each type of phobia. Although the data show that phobias are quite common, people are said to have full-fledged phobic disorders only when their phobias seriously interfere with their activities. Overall, about 40% of the subjects who reported each fear qualified as having a phobic disorder.

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

11. Figure 14.7 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)

12. Figure 14.8 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.

13. Figure 14.9 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.

14. n Somatization Disorder  Conversion Disorder  Hypochondriasis n Etiology  Reactive autonomic nervous system  Personality factors  Cognitive factors  The sick role Clinical Syndromes: Somatoform Disorders

15. n Dissociative amnesia n Dissociative fugue n Dissociative identity disorder  Etiology severe emotional trauma during childhood n Controversy  Media creation? Clinical Syndromes: Dissociative Disorders

16. n Major depressive disorder  Dysthymic disorder n Bipolar disorder (manic-depressive disorder)  Cyclothymic disorder n Etiology  Genetic vulnerability  Neurochemical factors  Cognitive factors  Interpersonal roots  Precipitating stress Clinical Syndromes: Mood Disorders Launch Video

17. Figure 14.13 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. Figure 14.13 Age of onset for bipolar mood disorder. The onset of bipolar disorder typically occurs in adolescence or early adulthood. The data graphed here, which were combined from 10 studies, show the distribution of age of onset for 1304 bipolar patients. As you can see, bipolar disorder emerges most frequently during the 20s decade. (Data from Goodwin & Jamison, 1990)

20. Figure 14.17 Interpersonal factors in depression. Behavioral theories about the etiology of depression emphasize how inadequate social skills may contribute to the development of the disorder.

21. Figure 14.15 Interpreting the correlation between negative thinking and depression. Cognitive theories of depression assume that consistent patterns of negative thinking cause depression. Although these theories are highly plausible, depression could cause negative thoughts, or both could be caused by a third factor, such as neurochemical changes in the brain.

22. Figure 14.14 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 or schizophrenic disorders which suggests that genetic factors may be particularly important in mood disorders. (Data from Gershon, Berrettini, & Goldin, 1989)

24. Figure 14.16 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)

25. n General symptoms  Delusions and irrational thought  Deterioration of adaptive behavior  Hallucinations  Disturbed emotions Clinical Syndromes: Schizophrenia

26. Figure 14.18 Gender differences in age of onset for schizophrenia. The onset of schizophrenia typically occurs in adolescence or early adulthood, as these data show. Although the relation of age to onset is reasonably similar for both sexes, males are somewhat more likely to manifest the disorder at younger ages. (Data from Loranger, 1984)

27. n 4 subtypes  Paranoid type  Catatonic type  Disorganized type  Undifferentiated type  New model for classification n Positive vs. negative symptoms Subtyping of Schizophrenia

28. n Genetic vulnerability n Neurochemical factors n Structural abnormalities of the brain n The neurodevelopmental hypothesis n Expressed emotion n Precipitating stress Etiology of Schizophrenia

29. Figure 14.17 Genetic vulnerability to schizophrenic disorders. Relatives of schizophrenic patients have an elevated risk for schizophrenia. This risk is greater among closer relatives. Although environment also plays a role in the etiology of schizophrenia, the concordance rates shown here suggest that there must be a genetic vulnerability to the disorder. These concordance estimates are based on pooled data from 40 studies conducted between 1920 and 1987. (Data from Gottesman, 1991)

32. Figure 14.20 Schizophrenia and the ventricles of the brain. Cerebrospinal fluid (CSF) circulates around the brain and spinal cord. The hollow cavities in the brain filled with CSF are called ventricles. The four ventricles in the human brain are depicted here. Recent studies with new brain imaging techniques suggest that an association exists between enlarged ventricles in the brain and the occurrence of schizophrenic disturbance.

33. Figure 4.21 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 youngsters develop. This neurological damage is believed to increase both vulnerability to schizophrenia and the incidence of minor physical anomalies.

34. Figure 14.23 The stress-vulnerability model of schizophrenia. Multifactorial causation is readily apparent in current theories about the etiology of schizophrenic disorders. A variety of biological factors and personal history factors influence one’s vulnerability to the disorder, which interacts with the amount of stress one experiences. Schizophrenic disorders appear to result from an intersection of high stress and high vulnerability.

35. n Anxious-fearful cluster  Avoidant, dependent, obsessive-compulsive n Dramatic-impulsive cluster  Histrionic, narcissistic, borderline, antisocial n Odd-eccentric cluster  Schizoid, schizotypal, paranoid n Etiology  Genetic predispositions, inadequate socialization in dysfunctional families Personality Disorders

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

37. n Cultural variations n Culture bound disorders  Koro  Windigo  Anorexia nervosa Culture and Pathology

38. Figure 14.24 Age of onset for anorexia nervosa. Eating disorders emerge primarily during adolescence, as these data for anorexia nervosa show. This graph shows how age of onset was distributed in a sample of 166 female patients from Minnesota. As you can see, over half the patients experienced the onset of their illness before the age of 20, with vulnerability clearly peaking between the ages of 15 and 19. (Data adapted from Lucas et al., 1991)