1. Chapter 15 Psychological Disorders

2. Substance Abuse and Addictions Mental illness

3. Substance Abuse and Addictions Substance abuse

4. Substance Abuse and Addictions Olds and Milner (1954)

5. Fig. 15-1, p. 452

6. Substance Abuse and Addictions Other behaviors that release dopamine

7. Substance Abuse and Addictions Berridge and Robinson (1998) –Nucleus accombans

8. Substance Abuse and Addictions Addiction

9. Substance Abuse and Addictions Withdrawal

10. Substance Abuse and Addictions Alcohol

11. Substance Abuse and Addictions The genetic basis for early-onset alcoholism is stronger than for later-onset, especially in men. Researchers distinguish between two types of alcoholism 1.Type I/Type A 2.Type II/Type B

12. Substance Abuse and Addictions Type I/Type A characteristics

13. Substance Abuse and Addictions Type II/Type B characteristic

14. Substance Abuse and Addictions Twin studies and family studies suggest a genetic basis for Type II/Type B alcoholism.

15. Substance Abuse and Addictions Risk factors for alcoholism

16. Substance Abuse and Addictions Medications used to combat alcoholism

17. Mood Disorders Major depression - feeling sad and helpless everyday for weeks at a time

18. Mood Disorders Similar symptoms can result from hormonal problems, head injuries, brain tumors, or other illnesses. Often comorbid with other disorders

19. Mood Disorders Studies of twins and adopted children suggest a moderate degree of heritability.

20. Mood Disorders Predisposition depends on a variety of genes. One identified gene leads to an 80% decrease in the brain’s ability to produce serotonin. –Most depressed people do not have this gene. –Those who have the gene have a higher predisposition.

21. Mood Disorders Another gene identified controls the serotonin transporter protein. –Protein controls the ability of the axon to reabsorb the neurotransmitter after its release. Two “short forms” of the gene are associated with an increased likelihood of depression after stressful events. –Perhaps alters the way people react to stressful events.

22. Mood Disorders Specific hormones are also involved with depression.

23. Mood Disorders Postpartum depression

24. Mood Disorders Childhood depression is equally common in both boys and girls. After puberty, depression is twice as common in females. The finding is consistent across cultures, suggesting a biological factor.

25. Mood Disorders Depression is associated with the specific brain activity

26. Mood Disorders Some cases of depression may be linked to viral infection. –Borna disease

27. Mood Disorders Categories of antidepressant drugs include: 1.Tricyclics. 2.Selective serotonin reuptake inhibitors. 3.MAOI’s. 4.Atypical antidepressants.

28. Fig. 15-9, p. 463

29. Mood Disorders Tricylclics (imipramine -Tofranil)

30. Mood Disorders Selective serotonin reuptake inhibitors (SSRIs) – Examples: Fluoxetine (Prozac), setraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa) and paroxetine (Paxil).

31. Mood Disorders Monoamine oxidase inhibitors (MAOI’s)

32. Mood Disorders Atypical antidepressants - Example: bupropion (Wellbutrin)

33. Mood Disorders Exactly how antidepressant drugs work is unclear.

34. Mood Disorders In some depressed people, neurons in the hippocampus and the cerebral cortex shrink.

35. Mood Disorders Electroconvulsive therapy (ECT)

36. Mood Disorders Drawbacks

37. Mood Disorders “Receptive transcranial magnetic stimulation”

38. Mood Disorders 1.Unipolar disorder 2.Bipolar disorder (manic-depressive disorder)

39. Mood Disorders Bipolar disorder I – Bipolar disorder II -

40. Mood Disorders Research suggests a heritability basis for bipolar disorder (Craddock & Jones, 1999).

41. Mood Disorders Treatments for bipolar –brain chemical arachidonic acid.

42. Schizophrenia

43. Causes are not well understood but include a large biological component.

44. Schizophrenia Two cluster of positive symptoms of schizophrenia include: 1.Psychotic 2.Disorganized

45. Schizophrenia 1.Psychotic - consists of delusions and hallucinations. –Delusions –Hallucinations 2.Disorganized

46. Schizophrenia Negative symptoms

47. Schizophrenia Twin studies suggest a genetic component.

48. Schizophrenia Prenatal environment

49. Schizophrenia One study identified a gene linked to high levels of negative symptoms (Fanous et al., 2005).

50. Schizophrenia The neurodevelopmental hypothesis

51. Schizophrenia Supporting evidence for the neurodevelopmental hypothesis

52. Schizophrenia Prenatal risk factors increasing the likelihood of schizophrenia include: –Poor nutrition of the mother during pregnancy. –Premature birth. –Low birth weight. –Complications during delivery. Head injuries in early childhood are also linked to increased incidence of schizophrenia.

53. Schizophrenia Schizophrenia is associated with mild brain abnormalities

54. Schizophrenia Schizophrenia typically develops after the age of 20 but many show sign at an earlier age.

55. Fig. 15-17, p. 476

56. Schizophrenia Antipsychotic/neuroleptic drugs Chlorpromazine

57. Schizophrenia Two chemical families of drugs used to treat schizophrenia include: 1.Phenothiazines - includes chlorpromazine 2.Butyrophenones - includes halperidol (Haldol) Both drugs block dopamine synapses.

58. Schizophrenia Second-generation antipsychotics

59. Schizophrenia The dopamine hypothesis of schizophrenia –Substance-induced psychotic disorder

60. Schizophrenia Research indicates increased activity specifically at the D 2 receptor. Limitations of the dopamine hypothesis

61. Schizophrenia The glutamate hypothesis of schizophrenia

62. Schizophrenia Schizophrenia cannot be explained by a single gene or single transmitter. Dopamine and glutamate may play important roles in schizophrenia to different degrees in different people. Schizophrenia involves multiple genes and abnormalities in dopamine, glutamate, serotonin and GABA.