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    • 1. Chapter 15 Psychological 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 GABA A 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.
    • 51. Mood Disorders
      • Research suggests a heritability basis for bipolar disorder (Craddock & Jones, 1999).
      • Twin studies suggest monozygotic twins share a 50% concordance rate.
      • Dizygotic twins, brothers, sisters or children share a concordance rate of 5-10%.
      • Comparison of chromosomes have identified several genes that are somewhat more common in people with the disorder.
      • Genes simply increase the risk but do not cause the disorder.
    • 52. Mood Disorders
      • Treatments for bipolar include:
        • Lithium - a salt that stabilizes mood and prevents relapse in mania or depression
        • Drugs - anticonvulsant drugs such as valproate (depakote) and carbamazepine
          • Usually prescribed for bipolar II.
      • All three drugs work by blocking the synthesis of the brain chemical arachidonic acid, which is produced during brain inflammation.
    • 53. Mood Disorders
      • Seasonal affective disorder (SAD) is a form of depression that regularly occurs during a particular season.
      • Patients with SAD have phase-delayed sleep and temperature rhythms; most depressed people have phase-advanced patterns.
      • Treatment often includes the use of very bright lights.
      • Most likely explanation is that the light affects serotonin synapses and alters circadian rhythms.
    • 54. Fig. 15-13, p. 468
    • 55. Schizophrenia
      • Schizophrenia is a disorder characterized by deteriorating ability to function in every day life and some combination of the following:
        • Hallucinations.
        • Delusions.
        • Thought disorder.
        • Movement disorder.
        • Inappropriate emotional expression.
          • (DSM IV)
    • 56. Schizophrenia
      • Causes are not well understood but include a large biological component.
      • Symptoms of the disorder can vary greatly.
      • Can be either acute or chronic:
        • Acute - condition has a sudden onset and good prospect for recovery.
        • Chronic - condition has a gradual onset and a long-term course.
    • 57. Schizophrenia
      • Two cluster of positive symptoms of schizophrenia include:
        • Psychotic
        • Disorganized
    • 58. Schizophrenia
      • Psychotic - consists of delusions and hallucinations.
        • Delusions: unfounded beliefs
        • Hallucinations: abnormal sensory experiences associated with increased activity in the hypothalamus, hippocampus and cortex
      • Disorganized - inappropriate emotional displays, bizarre behaviors and thought disorders (difficulty using and understanding abstract concepts).
    • 59. Schizophrenia
      • Negative symptoms are behaviors that are absent that should be present.
        • Weak social interaction.
        • Emotional expression.
        • Speech.
        • Working memory.
      • Negative symptoms are usually stable over time and difficult to treat.
    • 60. Schizophrenia
      • Schizophrenia affects about 1% of the population and range in severity.
      • Occurs in all parts of the world, but is 10 to 100 times more common in the United States and Europe than in third-world countries.
      • More common in men than in women by a ration of about 7 to 5.
      • More severe and earlier age of onset for men (early 20’s versus late 20).
      • Likelihood increases as the age of the father increases.
    • 61. Schizophrenia
      • Twin studies suggest a genetic component.
      • Monozygotic twins have a much higher concordance rate (agreement) than dizygotic twins.
      • But monozygotic twins only have a 50% concordance rate.
        • Other factors may explain the difference.
      • Greater similarity between dizygotic twins than siblings suggests a prenatal/postnatal environmental effect.
    • 62. Fig. 15-14, p. 472
    • 63. Schizophrenia
      • Adopted children studies suggest a genetic role, but prenatal environment of the biological mother can not be discounted.
      • Attempt to link adult-onset schizophrenia to an identified gene have provided inconsistent results.
      • Research has identified a gene for child-onset schizophrenia but cases are rare.
      • Schizophrenia most likely depends on a combination of genes or different genes in different families.
    • 64. Schizophrenia
      • One study identified a gene linked to high levels of negative symptoms (Fanous et al., 2005).
      • Perhaps geenetic research should focus on specific aspects of schizophrenia rather than schizophrenia in general.
      • Schizophrenia most likely results from environmental factors in addition to biological factors.
    • 65. Schizophrenia
      • The neurodevelopmental hypothesis suggests abnormalities in the prenatal or neonatal development of the nervous system.
      • Leads to subtle abnormalities of brain anatomy and major abnormalities in behavior.
      • Abnormalities could result from genetics, difficulty during birth, or a combination of both.
    • 66. Schizophrenia
      • Supporting evidence for the neurodevelopmental hypothesis includes:
        • Several kinds of prenatal or neonatal difficulties are linked to later schizophrenia.
        • People with schizophrenia have minor brain abnormalities that originate early in life.
      • Abnormalities of early development could impair behavior in adulthood.
    • 67. 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.
    • 68. Schizophrenia
      • Mother/child blood type differences increase the likelihood of schizophrenia.
      • If the mother has a Rh-negative blood type and the baby is Rh-positive, the child has about twice the probability of developing schizophrenia.
    • 69. Schizophrenia
      • Certain viral infections may be an alternative or supplement genetic influences.
      • The seasoned-of-birth effect refers to the tendency for people born in winter to have a slightly (5% to 8%) greater probability of developing schizophrenia.
        • More pronounced in latitudes far from the equator.
        • Might be explained by complications of delivery, nutritional factors, or increased likelihood of viral infections
    • 70. Schizophrenia
      • Schizophrenia is associated with mild brain abnormalities:
        • Strongest deficits found in the left temporal and frontal lobe of the cortex.
        • Larger than normal ventricles.
          • Especially common in those with complications during birth.
      • Areas that mature slowly such as the dorsolateral prefrontal cortex.
        • Schizophrenics have deficits in working memory.
    • 71. Fig. 15-15, p. 474
    • 72. Schizophrenia
      • At a microscopic levels, smaller cell bodies than usual, especially in the hippocampus and prefrontal cortex.
      • Differences in lateralization include the right planum temporale of the temporal lobe being the same size or larger than the left.
        • Usually the right side is larger.
      • Also lower than normal overall activity in the left hemisphere, suggesting subtle changes in early development.
    • 73. Schizophrenia
      • Overall, abnormalities are small and vary from person to person.
      • Reasons behinds brain abnormalities are not certain.
        • May be due to substance abuse.
      • Results are inconclusive if brain damage associated with schizophrenia is progressive.
    • 74. Schizophrenia
      • Schizophrenia typically develops after the age of 20 but many show sign at an earlier age.
        • Deficits in attention, memory and impulse control.
      • Prefrontal cortex damage may not show signs of damage until later.
        • Structure matures slowly and does not do much at an earlier age.
        • Neurodevelopmental hypothesis is thus plausible but not firmly established.
    • 75. Fig. 15-17, p. 476
    • 76. Schizophrenia
      • Antipsychotic/neuroleptic drugs are drugs that tend to relieve schizophrenia and similar conditions.
      • Chlorpromazine (thorazine) is a drug used to treat schizophrenia that relieves the positve symptoms of schizophrenia.
        • Relief usually experienced 2-3 weeks after taking the drug, which must be taken indefinitely.
    • 77. Schizophrenia
      • Two chemical families of drugs used to treat schizophrenia include:
        • Phenothiazines - includes chlorpromazine
        • Butyrophenones - includes halperidol (Haldol)
      • Both drugs block dopamine synapses.
    • 78. Fig. 15-18, p. 477
    • 79. Schizophrenia
      • The dopamine hypothesis of schizophrenia suggests that schizophrenia results from excess activity at dopamine synapses in certain areas of the brain.
      • Substance-induced psychotic disorder is characterized by hallucinations and delusions resulting from repeated large doses of amphetamines, methamphetamines, or cocaine.
        • Each prolongs activity of dopamine at the synapse, providing further evidence for dopamine hypothesis.
    • 80. Schizophrenia
      • Research indicates increased activity specifically at the D 2 receptor.
      • Limitations of the dopamine hypothesis include the following:
        • Direct measurement of dopamine and its metabolites indicate generally normal levels in people with schizophrenia.
        • Antipsychotic drugs block dopamine within minutes but effects on behavior gradually build over 2 to 3 weeks.
    • 81. Schizophrenia
      • The glutamate hypothesis of schizophrenia suggests the problem relates partially to deficient activity at glutamate receptors.
        • Especially in the prefrontal cortex.
      • In many brain areas, dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release.
      • Increased dopamine thus produces the same effects as decreased glutamate.
    • 82. Fig. 15-19, p. 479
    • 83. Schizophrenia
      • Schizophrenia is associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex and hippocampus.
      • Further support comes from the effects of phencyclidine (PCP/angel dust).
        • Inhibits the NMDA glutamate receptors.
        • Produces positve and negative symptoms at high doses.
    • 84. Schizophrenia
      • The mesolimbocortical system is a set of neurons that project from the midbrain tegmentum to the limbic system.
        • Site where drugs that block dopamine synapses produce their benefits.
      • Drugs also block dopamine in the mesostriatal system, which project to the basal ganglia.
        • Result is tardive dyskinesia, characterized by tremors and other involuntary movements.
    • 85. Fig. 15-20, p. 479
    • 86. Schizophrenia
      • Second-generation antipsychotics (atypical antipsychotics) are a class of drugs used to treat schizophrenia but seldom produce movement problems.
        • Examples: clozapine, amisulpride, risperidone, olanzapine, aripiprazole.
      • More effective at treating the negative symptoms and are now more widely used.
      • Have less effect on dopamine D 2 receptors and more strongly antagonize serotonin type 5-HT 2 receptors.
    • 87. 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.