Chapter 15 Psychological Disorders

1. Chapter 15Psychological Disorders

2. Substance Abuse and Addictions • Mental illness results from the combination of biological predisposition and experiences. • Both play an important role. • A solid understanding of both aspects is necessary for successful treatment.

3. Substance Abuse and Addictions • Substance abuse is defined as a maladaptive pattern of substance use leading to clinically significant impairment or distress. (DSM IV) • Most recognize it as harmful but continue the pattern of addictive behavior. • Addictive substances increase dopamine activity in certain areas of the brain.

4. Substance Abuse and Addictions • Olds and Milner (1954) placed rats in a Skinner box that allowed self-stimulation of the brain by the pressing of a lever. • Rats sometimes pressed the lever 2000 times per hour to stimulated the release of dopamine in the nucleus accumbens.

5. Fig. 15-1, p. 452

6. Substance Abuse and Addictions • Other behaviors that release dopamine include sexual excitement, gambling, and video games. • fMRI research indicates dopamine is released during viewing of “attractive” people.

7. Fig. 15-2, p. 453

8. Substance Abuse and Addictions • Berridge and Robinson (1998) suggest an important distinction be made between “liking” and “wanting” behaviors. • Activity in the nucleus accumbens seems to be related to “wanting”. • Results in a monopolization of attention.

9. Substance Abuse and Addictions • Addiction results in the nucleus accumbens becoming sensitized and responding more strongly to the stimulus. • Repeated use of cocaine increases the ability of the nucleus accumbens to release dopamine and the ability to activate the prefrontal cortex. • Person increases tendency to seek the drug and responds less to other incentives.

10. Substance Abuse and Addictions • Receiving a drug during a withdrawal period is a powerful experience that produces sensitization. • User learns that the drug relieves the distress caused by withdrawal and produces heightened effects. • Subjects that have abstained from a drug show heightened seeking of the drug upon any reminder of the drug.

11. Substance Abuse and Addictions • Alcohol is a drug that has a long historical use and is used widely throughout the world. • In moderate amounts, alcohol is associated with relaxation. • In greater amounts it impairs judgment and damages the liver and other organs. • Alcoholism/alcohol dependence is the continued use of alcohol despite medical or social harm even after one has decided to quit or decrease drinking.

12. Substance Abuse and Addictions • Alcohol has a number of diverse physiological effects including: • Inhibition of sodium across the membrane. • Expansion of the surface of membranes. • Decreased serotonin activity. • Enhanced response by the GABAA receptor. • Blockage of glutamate receptors. • Increased dopamine activity.

13. 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 • Type I/Type A • Type II/Type B

14. Substance Abuse and Addictions • Type I/Type A characteristics include: • Later onset. • Gradual onset. • Fewer genetic relatives with alcoholism. • Equal quantity between men and women. • Less severe.

15. Substance Abuse and Addictions • Type II/Type B characteristic include: • Earlier onset (usually before 25). • More rapid onset. • More genetic relatives with alcoholism. • Men outnumber women. • Often severe. • Often associated with criminality.

16. Substance Abuse and Addictions • Twin studies and family studies suggest a genetic basis for Type II/Type B alcoholism. • Genes influence the likelihood of alcoholism in a variety of ways: • Increase impulsive and risk-taking behaviors. • increase the stress response when trying to quit. • Genes that increase adenosine, which has a calming effect, may decrease alcohol consumption.

17. Substance Abuse and Addictions • Risk factors for alcoholism include children who are impulsive, risk-taking, easily bored, sensation-seeking, and out-going. • Studies of sons with alcoholic fathers indicates the following: • Less intoxication after moderate drinking. • Greater than 60% probability of developing alcoholism. • Alcohol decreases stress response more. • Smaller amygdala in the right hemisphere.

18. Fig. 15-3, p. 455

19. Substance Abuse and Addictions • Medications used to combat alcoholism include: • Antabuse. • Methadone. • Many do not respond to other treatments so medications have been used to reduce cravings.

20. Substance Abuse and Addictions • Antabuse (disulfiram) works by antagonizing the effects of acetaldehyde dehydrogenase. • After alcohol consumption, enzymes in the liver metabolize it into a poisonous substance called acetaldehyde. • Acetaldehyde is converted by the enzyme acetaldehyde dehydrogenase into acetic acid, a chemical that the body can use as a source of energy. • Accumulation of acetaldehyde results in sickness.

21. Substance Abuse and Addictions • Most studies suggest that Antabuse has been only moderately effective. • When effective, it supplements the alcoholic’s own commitment to quit. • Daily routine of pill ingestion may reaffirm commitment not to drink. • Many quit taking the pill and continue to drink.

22. Substance Abuse and Addictions • Methadone is an opiate similar to heroin and morphine but is absorbed and metabolized slowly. • Perceived to be less harmful than other drugs. • Assumed to satisfy the cravings associated with the previous drug use and allow the person to carry on with their life.

23. Mood Disorders • Major depression - feeling sad and helpless everyday for weeks at a time and includes the following characteristics (DSM-IV): • Little energy. • Feelings of worthlessness. • Suicidal thoughts. • Feelings of hopelessness. • Difficulty sleeping. • Difficulty concentrating. • Little pleasure from sex or food.

24. Mood Disorders • Similar symptoms can result from hormonal problems, head injuries, brain tumors, or other illnesses. • Often comorbid with other disorders such as schizophrenia, substance abuse, anxiety or Parkinson’s. • Absence of happiness is more reliable symptom than increased sadness. • Occurs at any age. • Twice as common in women and rates suggest about 10% lifetime prevalence.

25. Mood Disorders • Studies of twins and adopted children suggest a moderate degree of heritability. • Some of the genes associated with depression are also associated with anxiety disorders, ADD, OCD, substance-abuse disorders, bulimia, migraine headaches, irritable bowel syndrome, and several other conditions. • Risk is elevated among relatives of women with early-onset depression (before 30).

26. 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.

27. 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.

28. Mood Disorders • Specific hormones are also involved with depression. • A likely trigger for an episode of depression is stress and the release of the hormone cortisol. • Prolonged elevated levels exhaust the body’s energies, impair sleep and the immune system. • Set the stage for an episode of depression.

29. Fig. 15-6, p. 460

30. Mood Disorders • Postpartum depression is depression after giving birth. • Affects about 20% of women and most recover quickly. • .1% enter a serious, long-lasting depression. • More common among women who: • have suffered depression at other times. • experience sever discomfort during the times around menstruation. • May be associated with a drop in estradiol and progesterone levels.

31. 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.

32. Mood Disorders • Depression is associated with the following brain activity: • Decreased activity in the left prefrontal cortex. • Increased activity in the right prefrontal cortex. • Many people become seriously depressed after left-hemisphere damage. • Occasionally, people with right hemisphere damage become manic.

33. Mood Disorders • Some cases of depression may be linked to viral infection. • Borna disease is an infection noted mostly by the behavioral effects of periods of frantic activity alternating with periods of inactivity. • Found in a variety of different species of animals. • Found more commonly in depressed people or people with bipolar. • Predisposes people to various psychiatric disorders.

34. Mood Disorders • Categories of antidepressant drugs include: • Tricyclics. • Selective serotonin reuptake inhibitors. • MAOI’s. • Atypical antidepressants.

35. Fig. 15-9, p. 463

36. Mood Disorders • Tricylclics - a category of antidepressant drugs that operate by preventing the presynaptic neuron from reabsorbing serotonin, dopamine, or norepinephrine after release. • Examples: imipramine (Tofranil) • Block histamine receptors, acetylcholine receptors, and certain sodium channels. • Side-effects include dry mouth, difficulty urinating, heart irregularities, and possible fatal overdose potential.

37. Mood Disorders • Selective serotonin reuptake inhibitors (SSRIs) - a class of antidepressant drugs that works by blocking the reuptake of the neurotransmitter serotonin. • Examples: Fluoxetine (Prozac), setraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa) and paroxetine (Paxil). • Work in a similar fashion to tricyclics but are specific to the neurotransmitter serotonin. • Mild side effects include nausea, headache and occasional nervousness.

38. Mood Disorders • Monoamine oxidase inhibitors (MAOI’s) - a class of antidepressant drugs that blocks the enzyme monoamine oxidase. • Monoamine oxidase metabolizes catecholimines and serotonin into inactive forms. • Blockage of the enzyme results in more of the transmitters in the presynaptic terminal available for release. • Usually prescribed after SSRI’s and tricyclics.

39. Mood Disorders • Atypical antidepressants - a miscellaneous group of drugs with antidepressant effects and mild side effects. • Example: bupropion (Wellbutrin) • Works by inhibiting the reuptake of dopamine and to some extent, norepinephrine but not serotonin. • Nefazodone is an antidepressant drug which specifically blocks serotonin type 2A receptors and also weakly blocks reuptake of serotonin and norepinephrine.

40. Mood Disorders • St. Johns’ wort is an herb that is often used as a treatment for depression by many. • Marketed as a nutritional supplement and not regulated by the FDA. • Believed to work in the same way as SSRI’s but effectiveness is controversial. • Increases the effectiveness of a liver enzyme that can decrease the effectiveness of other medications.

41. Mood Disorders • Exactly how antidepressant drugs work is unclear. • Antidepressant alter synaptic activity quickly but the effects on behavior are not derived until weeks later. • Reveals depression is not directly and solely the result of low serotonin levels. • Blood samples show normal levels of serotonin turnover in depressed people.

42. Mood Disorders • In some depressed people, neurons in the hippocampus and the cerebral cortex shrink. • Behavioral effects of antidepressant drugs most likely depend on two slow changes in the brain: • Drug increases the release of BDNF which promotes neuron growth and survival. • Desensitize autoreceptors and thereby increase release of the neurotransmitter.

43. Mood Disorders • Electroconvulsive therapy (ECT) is an electrically induced seizure that is used for the treatment of severe depression. • Used with patients who have not responded to antidepressant medication or are suicidal. • Applied every other day for a period of two weeks. • Side effects include memory loss. • Memory loss can be minimized if shock is localized to the right hemisphere.

44. Mood Disorders • A drawback of ECT is the high risk of relapse. • Usually accompanied with drug treatment, psychotherapy and periodic ECT after initial treatment. • How exactly ECT relieves depression is unknown. • Animal studies suggest an altering of the expression of genes in the hippocampus and frontal cortex.

45. Mood Disorders • “Receptive transcranial magnetic stimulation” is another treatment for depression in which an intense magnetic field is applied to the scalp, to stimulate the neurons. • Like ECT in its level of effectiveness. • Exact mechanisms of its effects are also unknown.

46. Mood Disorders • Disruption of sleep patterns is common in depression. • Typically fall asleep but awaken early and are unable to get back to sleep. • Enter REM sleep within 45 minutes and have an increased average number of eye movements during REM sleep. • Sleep pattern disruption also increases the likelihood of depression and is a lifelong trait of people that are depressed.

47. Fig. 15-11, p. 466

48. Mood Disorders • A night of total sleep deprivation is the quickest known method of relieving depression. • Half who experience relief become depressed again after the next night’s sleep. • Extended benefits can be derived from altering sleep schedule on subsequent days. • Combining sleep alteration with drug therapies can provide long-lasting benefits. • Exact mechanism of how sleep disruption relieves depression is unknown.

49. Mood Disorders • Unipolar disorder is characterized by an alternating states of normality and depression. • Bipolar disorder (manic-depressive disorder) is characterized by the alternating states of depression and mania. • Mania - restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibition.

50. Mood Disorders • Bipolar disorder I -characterized by full blown episodes of mania. • Bipolar disorder II - characterized by much milder manic phases, called hypomania, of which anxiety and agitation are the primary symptoms. • Affects approximately 1% of people. • Average age of onset is in the early 20’s. • Brain’s use of glucose increases during periods of mania and decreases during periods of depression.