Chapter15 Power Point Presentation


Published on

Published in: Health & Medicine, Education
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide
  • Chapter15 Power Point Presentation

    1. 1. Chapter 15 Psychological Disorders
    2. 2. Substance Abuse and Addictions <ul><li>Mental illness results from the combination of biological predisposition and experiences. </li></ul><ul><ul><li>Both play an important role. </li></ul></ul><ul><li>A solid understanding of both aspects is necessary for successful treatment. </li></ul>
    3. 3. Substance Abuse and Addictions <ul><li>Substance abuse is defined as a maladaptive pattern of substance use leading to clinically significant impairment or distress. (DSM IV) </li></ul><ul><li>Most recognize it as harmful but continue the pattern of addictive behavior. </li></ul><ul><li>Addictive substances increase dopamine activity in certain areas of the brain. </li></ul>
    4. 4. Substance Abuse and Addictions <ul><li>Olds and Milner (1954) placed rats in a Skinner box that allowed self-stimulation of the brain by the pressing of a lever. </li></ul><ul><li>Rats sometimes pressed the lever 2000 times per hour to stimulated the release of dopamine in the nucleus accumbens. </li></ul>
    5. 5. Fig. 15-1, p. 452
    6. 6. Substance Abuse and Addictions <ul><li>Other behaviors that release dopamine include sexual excitement, gambling, and video games. </li></ul><ul><li>fMRI research indicates dopamine is released during viewing of “attractive” people. </li></ul>
    7. 7. Fig. 15-2, p. 453
    8. 8. Substance Abuse and Addictions <ul><li>Berridge and Robinson (1998) suggest an important distinction be made between “liking” and “wanting” behaviors. </li></ul><ul><li>Activity in the nucleus accumbens seems to be related to “wanting”. </li></ul><ul><ul><li>Results in a monopolization of attention. </li></ul></ul>
    9. 9. Substance Abuse and Addictions <ul><li>Addiction results in the nucleus accumbens becoming sensitized and responding more strongly to the stimulus. </li></ul><ul><li>Repeated use of cocaine increases the ability of the nucleus accumbens to release dopamine and the ability to activate the prefrontal cortex. </li></ul><ul><li>Person increases tendency to seek the drug and responds less to other incentives. </li></ul>
    10. 10. Substance Abuse and Addictions <ul><li>Receiving a drug during a withdrawal period is a powerful experience that produces sensitization. </li></ul><ul><li>User learns that the drug relieves the distress caused by withdrawal and produces heightened effects. </li></ul><ul><li>Subjects that have abstained from a drug show heightened seeking of the drug upon any reminder of the drug. </li></ul>
    11. 11. Substance Abuse and Addictions <ul><li>Alcohol is a drug that has a long historical use and is used widely throughout the world. </li></ul><ul><li>In moderate amounts, alcohol is associated with relaxation. </li></ul><ul><li>In greater amounts it impairs judgment and damages the liver and other organs. </li></ul><ul><li>Alcoholism/alcohol dependence is the continued use of alcohol despite medical or social harm even after one has decided to quit or decrease drinking. </li></ul>
    12. 12. Substance Abuse and Addictions <ul><li>Alcohol has a number of diverse physiological effects including: </li></ul><ul><ul><li>Inhibition of sodium across the membrane. </li></ul></ul><ul><ul><li>Expansion of the surface of membranes. </li></ul></ul><ul><ul><li>Decreased serotonin activity. </li></ul></ul><ul><ul><li>Enhanced response by the GABA A receptor. </li></ul></ul><ul><ul><li>Blockage of glutamate receptors. </li></ul></ul><ul><ul><li>Increased dopamine activity. </li></ul></ul>
    13. 13. Substance Abuse and Addictions <ul><li>The genetic basis for early-onset alcoholism is stronger than for later-onset, especially in men. </li></ul><ul><li>Researchers distinguish between two types of alcoholism </li></ul><ul><ul><li>Type I/Type A </li></ul></ul><ul><ul><li>Type II/Type B </li></ul></ul>
    14. 14. Substance Abuse and Addictions <ul><li>Type I/Type A characteristics include: </li></ul><ul><ul><li>Later onset. </li></ul></ul><ul><ul><li>Gradual onset. </li></ul></ul><ul><ul><li>Fewer genetic relatives with alcoholism. </li></ul></ul><ul><ul><li>Equal quantity between men and women. </li></ul></ul><ul><ul><li>Less severe. </li></ul></ul>
    15. 15. Substance Abuse and Addictions <ul><li>Type II/Type B characteristic include: </li></ul><ul><ul><li>Earlier onset (usually before 25). </li></ul></ul><ul><ul><li>More rapid onset. </li></ul></ul><ul><ul><li>More genetic relatives with alcoholism. </li></ul></ul><ul><ul><li>Men outnumber women. </li></ul></ul><ul><ul><li>Often severe. </li></ul></ul><ul><ul><li>Often associated with criminality. </li></ul></ul>
    16. 16. Substance Abuse and Addictions <ul><li>Twin studies and family studies suggest a genetic basis for Type II/Type B alcoholism. </li></ul><ul><li>Genes influence the likelihood of alcoholism in a variety of ways: </li></ul><ul><ul><li>Increase impulsive and risk-taking behaviors. </li></ul></ul><ul><ul><li>increase the stress response when trying to quit. </li></ul></ul><ul><li>Genes that increase adenosine, which has a calming effect, may decrease alcohol consumption. </li></ul>
    17. 17. Substance Abuse and Addictions <ul><li>Risk factors for alcoholism include children who are impulsive, risk-taking, easily bored, sensation-seeking, and out-going. </li></ul><ul><li>Studies of sons with alcoholic fathers indicates the following: </li></ul><ul><ul><li>Less intoxication after moderate drinking. </li></ul></ul><ul><ul><li>Greater than 60% probability of developing alcoholism. </li></ul></ul><ul><ul><li>Alcohol decreases stress response more. </li></ul></ul><ul><ul><li>Smaller amygdala in the right hemisphere. </li></ul></ul>
    18. 18. Fig. 15-3, p. 455
    19. 19. Substance Abuse and Addictions <ul><li>Medications used to combat alcoholism include: </li></ul><ul><ul><li>Antabuse. </li></ul></ul><ul><ul><li>Methadone. </li></ul></ul><ul><ul><li>Many do not respond to other treatments so medications have been used to reduce cravings. </li></ul></ul>
    20. 20. Substance Abuse and Addictions <ul><li>Antabuse (disulfiram) works by antagonizing the effects of acetaldehyde dehydrogenase. </li></ul><ul><li>After alcohol consumption, enzymes in the liver metabolize it into a poisonous substance called acetaldehyde . </li></ul><ul><li>Acetaldehyde is converted by the enzyme acetaldehyde dehydrogenase into acetic acid , a chemical that the body can use as a source of energy. </li></ul><ul><li>Accumulation of acetaldehyde results in sickness. </li></ul>
    21. 21. Substance Abuse and Addictions <ul><li>Most studies suggest that Antabuse has been only moderately effective. </li></ul><ul><li>When effective, it supplements the alcoholic’s own commitment to quit. </li></ul><ul><li>Daily routine of pill ingestion may reaffirm commitment not to drink. </li></ul><ul><li>Many quit taking the pill and continue to drink. </li></ul>
    22. 22. Substance Abuse and Addictions <ul><li>Methadone is an opiate similar to heroin and morphine but is absorbed and metabolized slowly. </li></ul><ul><li>Perceived to be less harmful than other drugs. </li></ul><ul><li>Assumed to satisfy the cravings associated with the previous drug use and allow the person to carry on with their life. </li></ul>
    23. 23. Mood Disorders <ul><li>Major depression - feeling sad and helpless everyday for weeks at a time and includes the following characteristics (DSM-IV): </li></ul><ul><ul><li>Little energy. </li></ul></ul><ul><ul><li>Feelings of worthlessness. </li></ul></ul><ul><ul><li>Suicidal thoughts. </li></ul></ul><ul><ul><li>Feelings of hopelessness. </li></ul></ul><ul><ul><li>Difficulty sleeping. </li></ul></ul><ul><ul><li>Difficulty concentrating. </li></ul></ul><ul><ul><li>Little pleasure from sex or food. </li></ul></ul>
    24. 24. Mood Disorders <ul><li>Similar symptoms can result from hormonal problems, head injuries, brain tumors, or other illnesses. </li></ul><ul><li>Often comorbid with other disorders such as schizophrenia, substance abuse, anxiety or Parkinson’s. </li></ul><ul><li>Absence of happiness is more reliable symptom than increased sadness. </li></ul><ul><li>Occurs at any age. </li></ul><ul><li>Twice as common in women and rates suggest about 10% lifetime prevalence. </li></ul>
    25. 25. Mood Disorders <ul><li>Studies of twins and adopted children suggest a moderate degree of heritability. </li></ul><ul><li>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. </li></ul><ul><li>Risk is elevated among relatives of women with early-onset depression (before 30). </li></ul>
    26. 26. Mood Disorders <ul><li>Predisposition depends on a variety of genes. </li></ul><ul><li>One identified gene leads to an 80% decrease in the brain’s ability to produce serotonin. </li></ul><ul><ul><li>Most depressed people do not have this gene. </li></ul></ul><ul><ul><li>Those who have the gene have a higher predisposition. </li></ul></ul>
    27. 27. Mood Disorders <ul><li>Another gene identified controls the serotonin transporter protein. </li></ul><ul><ul><li>Protein controls the ability of the axon to reabsorb the neurotransmitter after its release. </li></ul></ul><ul><li>Two “short forms” of the gene are associated with an increased likelihood of depression after stressful events. </li></ul><ul><ul><li>Perhaps alters the way people react to stressful events. </li></ul></ul>
    28. 28. Mood Disorders <ul><li>Specific hormones are also involved with depression. </li></ul><ul><li>A likely trigger for an episode of depression is stress and the release of the hormone cortisol. </li></ul><ul><li>Prolonged elevated levels exhaust the body’s energies, impair sleep and the immune system. </li></ul><ul><ul><li>Set the stage for an episode of depression. </li></ul></ul>
    29. 29. Fig. 15-6, p. 460
    30. 30. Mood Disorders <ul><li>Postpartum depression is depression after giving birth. </li></ul><ul><li>Affects about 20% of women and most recover quickly. </li></ul><ul><li>.1% enter a serious, long-lasting depression. </li></ul><ul><li>More common among women who: </li></ul><ul><ul><li>have suffered depression at other times. </li></ul></ul><ul><ul><li>experience sever discomfort during the times around menstruation. </li></ul></ul><ul><li>May be associated with a drop in estradiol and progesterone levels . </li></ul>
    31. 31. Mood Disorders <ul><li>Childhood depression is equally common in both boys and girls. </li></ul><ul><li>After puberty, depression is twice as common in females. </li></ul><ul><li>The finding is consistent across cultures, suggesting a biological factor. </li></ul>
    32. 32. Mood Disorders <ul><li>Depression is associated with the following brain activity: </li></ul><ul><ul><li>Decreased activity in the left prefrontal cortex. </li></ul></ul><ul><ul><li>Increased activity in the right prefrontal cortex. </li></ul></ul><ul><li>Many people become seriously depressed after left-hemisphere damage. </li></ul><ul><li>Occasionally, people with right hemisphere damage become manic. </li></ul>
    33. 33. Mood Disorders <ul><li>Some cases of depression may be linked to viral infection. </li></ul><ul><li>Borna disease is an infection noted mostly by the behavioral effects of periods of frantic activity alternating with periods of inactivity. </li></ul><ul><li>Found in a variety of different species of animals. </li></ul><ul><li>Found more commonly in depressed people or people with bipolar. </li></ul><ul><li>Predisposes people to various psychiatric disorders. </li></ul>
    34. 34. Mood Disorders <ul><li>Categories of antidepressant drugs include: </li></ul><ul><ul><li>Tricyclics. </li></ul></ul><ul><ul><li>Selective serotonin reuptake inhibitors. </li></ul></ul><ul><ul><li>MAOI’s. </li></ul></ul><ul><ul><li>Atypical antidepressants. </li></ul></ul>
    35. 35. Fig. 15-9, p. 463
    36. 36. Mood Disorders <ul><li>Tricylclics - a category of antidepressant drugs that operate by preventing the presynaptic neuron from reabsorbing serotonin, dopamine, or norepinephrine after release. </li></ul><ul><ul><li>Examples: imipramine (Tofranil) </li></ul></ul><ul><li>Block histamine receptors, acetylcholine receptors, and certain sodium channels. </li></ul><ul><li>Side-effects include dry mouth, difficulty urinating, heart irregularities, and possible fatal overdose potential. </li></ul>
    37. 37. Mood Disorders <ul><li>Selective serotonin reuptake inhibitors (SSRIs) - a class of antidepressant drugs that works by blocking the reuptake of the neurotransmitter serotonin. </li></ul><ul><ul><li>Examples: Fluoxetine (Prozac), setraline (Zoloft), fluvoxamine (Luvox), citalopram (Celexa) and paroxetine (Paxil). </li></ul></ul><ul><li>Work in a similar fashion to tricyclics but are specific to the neurotransmitter serotonin. </li></ul><ul><li>Mild side effects include nausea, headache and occasional nervousness. </li></ul>
    38. 38. Mood Disorders <ul><li>Monoamine oxidase inhibitors (MAOI’s) - a class of antidepressant drugs that blocks the enzyme monoamine oxidase. </li></ul><ul><li>Monoamine oxidase metabolizes catecholimines and serotonin into inactive forms. </li></ul><ul><li>Blockage of the enzyme results in more of the transmitters in the presynaptic terminal available for release. </li></ul><ul><li>Usually prescribed after SSRI’s and tricyclics. </li></ul>
    39. 39. Mood Disorders <ul><li>Atypical antidepressants - a miscellaneous group of drugs with antidepressant effects and mild side effects. </li></ul><ul><ul><li>Example: bupropion (Wellbutrin) </li></ul></ul><ul><li>Works by inhibiting the reuptake of dopamine and to some extent, norepinephrine but not serotonin. </li></ul><ul><li>Nefazodone is an antidepressant drug which specifically blocks serotonin type 2A receptors and also weakly blocks reuptake of serotonin and norepinephrine. </li></ul>
    40. 40. Mood Disorders <ul><li>St. Johns’ wort is an herb that is often used as a treatment for depression by many. </li></ul><ul><li>Marketed as a nutritional supplement and not regulated by the FDA. </li></ul><ul><li>Believed to work in the same way as SSRI’s but effectiveness is controversial. </li></ul><ul><li>Increases the effectiveness of a liver enzyme that can decrease the effectiveness of other medications. </li></ul>
    41. 41. Mood Disorders <ul><li>Exactly how antidepressant drugs work is unclear. </li></ul><ul><li>Antidepressant alter synaptic activity quickly but the effects on behavior are not derived until weeks later. </li></ul><ul><li>Reveals depression is not directly and solely the result of low serotonin levels. </li></ul><ul><li>Blood samples show normal levels of serotonin turnover in depressed people. </li></ul>
    42. 42. Mood Disorders <ul><li>In some depressed people, neurons in the hippocampus and the cerebral cortex shrink. </li></ul><ul><li>Behavioral effects of antidepressant drugs most likely depend on two slow changes in the brain: </li></ul><ul><ul><li>Drug increases the release of BDNF which promotes neuron growth and survival. </li></ul></ul><ul><ul><li>Desensitize autoreceptors and thereby increase release of the neurotransmitter. </li></ul></ul>
    43. 43. Mood Disorders <ul><li>Electroconvulsive therapy (ECT) is an electrically induced seizure that is used for the treatment of severe depression. </li></ul><ul><li>Used with patients who have not responded to antidepressant medication or are suicidal. </li></ul><ul><li>Applied every other day for a period of two weeks. </li></ul><ul><li>Side effects include memory loss. </li></ul><ul><ul><li>Memory loss can be minimized if shock is localized to the right hemisphere. </li></ul></ul>
    44. 44. Mood Disorders <ul><li>A drawback of ECT is the high risk of relapse. </li></ul><ul><li>Usually accompanied with drug treatment, psychotherapy and periodic ECT after initial treatment. </li></ul><ul><li>How exactly ECT relieves depression is unknown. </li></ul><ul><li>Animal studies suggest an altering of the expression of genes in the hippocampus and frontal cortex. </li></ul>
    45. 45. Mood Disorders <ul><li>“Receptive transcranial magnetic stimulation” is another treatment for depression in which an intense magnetic field is applied to the scalp, to stimulate the neurons. </li></ul><ul><li>Like ECT in its level of effectiveness. </li></ul><ul><li>Exact mechanisms of its effects are also unknown. </li></ul>
    46. 46. Mood Disorders <ul><li>Disruption of sleep patterns is common in depression. </li></ul><ul><ul><li>Typically fall asleep but awaken early and are unable to get back to sleep. </li></ul></ul><ul><ul><li>Enter REM sleep within 45 minutes and have an increased average number of eye movements during REM sleep. </li></ul></ul><ul><li>Sleep pattern disruption also increases the likelihood of depression and is a lifelong trait of people that are depressed. </li></ul>
    47. 47. Fig. 15-11, p. 466
    48. 48. Mood Disorders <ul><li>A night of total sleep deprivation is the quickest known method of relieving depression. </li></ul><ul><li>Half who experience relief become depressed again after the next night’s sleep. </li></ul><ul><li>Extended benefits can be derived from altering sleep schedule on subsequent days. </li></ul><ul><li>Combining sleep alteration with drug therapies can provide long-lasting benefits. </li></ul><ul><li>Exact mechanism of how sleep disruption relieves depression is unknown . </li></ul>
    49. 49. Mood Disorders <ul><li>Unipolar disorder is characterized by an alternating states of normality and depression. </li></ul><ul><li>Bipolar disorder (manic-depressive disorder) is characterized by the alternating states of depression and mania. </li></ul><ul><ul><li>Mania - restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibition. </li></ul></ul>
    50. 50. Mood Disorders <ul><li>Bipolar disorder I - characterized by full blown episodes of mania. </li></ul><ul><li>Bipolar disorder II - characterized by much milder manic phases, called hypomania, of which anxiety and agitation are the primary symptoms. </li></ul><ul><li>Affects approximately 1% of people. </li></ul><ul><li>Average age of onset is in the early 20’s. </li></ul><ul><li>Brain’s use of glucose increases during periods of mania and decreases during periods of depression. </li></ul>
    51. 51. Mood Disorders <ul><li>Research suggests a heritability basis for bipolar disorder (Craddock & Jones, 1999). </li></ul><ul><li>Twin studies suggest monozygotic twins share a 50% concordance rate. </li></ul><ul><li>Dizygotic twins, brothers, sisters or children share a concordance rate of 5-10%. </li></ul><ul><li>Comparison of chromosomes have identified several genes that are somewhat more common in people with the disorder. </li></ul><ul><li>Genes simply increase the risk but do not cause the disorder. </li></ul>
    52. 52. Mood Disorders <ul><li>Treatments for bipolar include: </li></ul><ul><ul><li>Lithium - a salt that stabilizes mood and prevents relapse in mania or depression </li></ul></ul><ul><ul><li>Drugs - anticonvulsant drugs such as valproate (depakote) and carbamazepine </li></ul></ul><ul><ul><ul><li>Usually prescribed for bipolar II. </li></ul></ul></ul><ul><li>All three drugs work by blocking the synthesis of the brain chemical arachidonic acid, which is produced during brain inflammation. </li></ul>
    53. 53. Mood Disorders <ul><li>Seasonal affective disorder (SAD) is a form of depression that regularly occurs during a particular season. </li></ul><ul><li>Patients with SAD have phase-delayed sleep and temperature rhythms; most depressed people have phase-advanced patterns. </li></ul><ul><li>Treatment often includes the use of very bright lights. </li></ul><ul><li>Most likely explanation is that the light affects serotonin synapses and alters circadian rhythms. </li></ul>
    54. 54. Fig. 15-13, p. 468
    55. 55. Schizophrenia <ul><li>Schizophrenia is a disorder characterized by deteriorating ability to function in every day life and some combination of the following: </li></ul><ul><ul><li>Hallucinations. </li></ul></ul><ul><ul><li>Delusions. </li></ul></ul><ul><ul><li>Thought disorder. </li></ul></ul><ul><ul><li>Movement disorder. </li></ul></ul><ul><ul><li>Inappropriate emotional expression. </li></ul></ul><ul><ul><ul><li>(DSM IV) </li></ul></ul></ul>
    56. 56. Schizophrenia <ul><li>Causes are not well understood but include a large biological component. </li></ul><ul><li>Symptoms of the disorder can vary greatly. </li></ul><ul><li>Can be either acute or chronic: </li></ul><ul><ul><li>Acute - condition has a sudden onset and good prospect for recovery. </li></ul></ul><ul><ul><li>Chronic - condition has a gradual onset and a long-term course. </li></ul></ul>
    57. 57. Schizophrenia <ul><li>Two cluster of positive symptoms of schizophrenia include: </li></ul><ul><ul><li>Psychotic </li></ul></ul><ul><ul><li>Disorganized </li></ul></ul>
    58. 58. Schizophrenia <ul><li>Psychotic - consists of delusions and hallucinations. </li></ul><ul><ul><li>Delusions: unfounded beliefs </li></ul></ul><ul><ul><li>Hallucinations: abnormal sensory experiences associated with increased activity in the hypothalamus, hippocampus and cortex </li></ul></ul><ul><li>Disorganized - inappropriate emotional displays, bizarre behaviors and thought disorders (difficulty using and understanding abstract concepts). </li></ul>
    59. 59. Schizophrenia <ul><li>Negative symptoms are behaviors that are absent that should be present. </li></ul><ul><ul><li>Weak social interaction. </li></ul></ul><ul><ul><li>Emotional expression. </li></ul></ul><ul><ul><li>Speech. </li></ul></ul><ul><ul><li>Working memory. </li></ul></ul><ul><li>Negative symptoms are usually stable over time and difficult to treat. </li></ul>
    60. 60. Schizophrenia <ul><li>Schizophrenia affects about 1% of the population and range in severity. </li></ul><ul><li>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. </li></ul><ul><li>More common in men than in women by a ration of about 7 to 5. </li></ul><ul><li>More severe and earlier age of onset for men (early 20’s versus late 20). </li></ul><ul><li>Likelihood increases as the age of the father increases. </li></ul>
    61. 61. Schizophrenia <ul><li>Twin studies suggest a genetic component. </li></ul><ul><li>Monozygotic twins have a much higher concordance rate (agreement) than dizygotic twins. </li></ul><ul><li>But monozygotic twins only have a 50% concordance rate. </li></ul><ul><ul><li>Other factors may explain the difference. </li></ul></ul><ul><li>Greater similarity between dizygotic twins than siblings suggests a prenatal/postnatal environmental effect. </li></ul>
    62. 62. Fig. 15-14, p. 472
    63. 63. Schizophrenia <ul><li>Adopted children studies suggest a genetic role, but prenatal environment of the biological mother can not be discounted. </li></ul><ul><li>Attempt to link adult-onset schizophrenia to an identified gene have provided inconsistent results. </li></ul><ul><li>Research has identified a gene for child-onset schizophrenia but cases are rare. </li></ul><ul><li>Schizophrenia most likely depends on a combination of genes or different genes in different families. </li></ul>
    64. 64. Schizophrenia <ul><li>One study identified a gene linked to high levels of negative symptoms (Fanous et al., 2005). </li></ul><ul><li>Perhaps geenetic research should focus on specific aspects of schizophrenia rather than schizophrenia in general. </li></ul><ul><li>Schizophrenia most likely results from environmental factors in addition to biological factors. </li></ul>
    65. 65. Schizophrenia <ul><li>The neurodevelopmental hypothesis suggests abnormalities in the prenatal or neonatal development of the nervous system. </li></ul><ul><li>Leads to subtle abnormalities of brain anatomy and major abnormalities in behavior. </li></ul><ul><li>Abnormalities could result from genetics, difficulty during birth, or a combination of both. </li></ul>
    66. 66. Schizophrenia <ul><li>Supporting evidence for the neurodevelopmental hypothesis includes: </li></ul><ul><ul><li>Several kinds of prenatal or neonatal difficulties are linked to later schizophrenia. </li></ul></ul><ul><ul><li>People with schizophrenia have minor brain abnormalities that originate early in life. </li></ul></ul><ul><li>Abnormalities of early development could impair behavior in adulthood. </li></ul>
    67. 67. Schizophrenia <ul><li>Prenatal risk factors increasing the likelihood of schizophrenia include: </li></ul><ul><ul><li>Poor nutrition of the mother during pregnancy. </li></ul></ul><ul><ul><li>Premature birth. </li></ul></ul><ul><ul><li>Low birth weight. </li></ul></ul><ul><ul><li>Complications during delivery. </li></ul></ul><ul><li>Head injuries in early childhood are also linked to increased incidence of schizophrenia. </li></ul>
    68. 68. Schizophrenia <ul><li>Mother/child blood type differences increase the likelihood of schizophrenia. </li></ul><ul><li>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. </li></ul>
    69. 69. Schizophrenia <ul><li>Certain viral infections may be an alternative or supplement genetic influences. </li></ul><ul><li>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. </li></ul><ul><ul><li>More pronounced in latitudes far from the equator. </li></ul></ul><ul><ul><li>Might be explained by complications of delivery, nutritional factors, or increased likelihood of viral infections </li></ul></ul>
    70. 70. Schizophrenia <ul><li>Schizophrenia is associated with mild brain abnormalities: </li></ul><ul><ul><li>Strongest deficits found in the left temporal and frontal lobe of the cortex. </li></ul></ul><ul><ul><li>Larger than normal ventricles. </li></ul></ul><ul><ul><ul><li>Especially common in those with complications during birth. </li></ul></ul></ul><ul><li>Areas that mature slowly such as the dorsolateral prefrontal cortex. </li></ul><ul><ul><li>Schizophrenics have deficits in working memory. </li></ul></ul>
    71. 71. Fig. 15-15, p. 474
    72. 72. Schizophrenia <ul><li>At a microscopic levels, smaller cell bodies than usual, especially in the hippocampus and prefrontal cortex. </li></ul><ul><li>Differences in lateralization include the right planum temporale of the temporal lobe being the same size or larger than the left. </li></ul><ul><ul><li>Usually the right side is larger. </li></ul></ul><ul><li>Also lower than normal overall activity in the left hemisphere, suggesting subtle changes in early development. </li></ul>
    73. 73. Schizophrenia <ul><li>Overall, abnormalities are small and vary from person to person. </li></ul><ul><li>Reasons behinds brain abnormalities are not certain. </li></ul><ul><ul><li>May be due to substance abuse. </li></ul></ul><ul><li>Results are inconclusive if brain damage associated with schizophrenia is progressive. </li></ul>
    74. 74. Schizophrenia <ul><li>Schizophrenia typically develops after the age of 20 but many show sign at an earlier age. </li></ul><ul><ul><li>Deficits in attention, memory and impulse control. </li></ul></ul><ul><li>Prefrontal cortex damage may not show signs of damage until later. </li></ul><ul><ul><li>Structure matures slowly and does not do much at an earlier age. </li></ul></ul><ul><ul><li>Neurodevelopmental hypothesis is thus plausible but not firmly established. </li></ul></ul>
    75. 75. Fig. 15-17, p. 476
    76. 76. Schizophrenia <ul><li>Antipsychotic/neuroleptic drugs are drugs that tend to relieve schizophrenia and similar conditions. </li></ul><ul><li>Chlorpromazine (thorazine) is a drug used to treat schizophrenia that relieves the positve symptoms of schizophrenia. </li></ul><ul><ul><li>Relief usually experienced 2-3 weeks after taking the drug, which must be taken indefinitely. </li></ul></ul>
    77. 77. Schizophrenia <ul><li>Two chemical families of drugs used to treat schizophrenia include: </li></ul><ul><ul><li>Phenothiazines - includes chlorpromazine </li></ul></ul><ul><ul><li>Butyrophenones - includes halperidol (Haldol) </li></ul></ul><ul><li>Both drugs block dopamine synapses. </li></ul>
    78. 78. Fig. 15-18, p. 477
    79. 79. Schizophrenia <ul><li>The dopamine hypothesis of schizophrenia suggests that schizophrenia results from excess activity at dopamine synapses in certain areas of the brain. </li></ul><ul><li>Substance-induced psychotic disorder is characterized by hallucinations and delusions resulting from repeated large doses of amphetamines, methamphetamines, or cocaine. </li></ul><ul><ul><li>Each prolongs activity of dopamine at the synapse, providing further evidence for dopamine hypothesis. </li></ul></ul>
    80. 80. Schizophrenia <ul><li>Research indicates increased activity specifically at the D 2 receptor. </li></ul><ul><li>Limitations of the dopamine hypothesis include the following: </li></ul><ul><ul><li>Direct measurement of dopamine and its metabolites indicate generally normal levels in people with schizophrenia. </li></ul></ul><ul><ul><li>Antipsychotic drugs block dopamine within minutes but effects on behavior gradually build over 2 to 3 weeks. </li></ul></ul>
    81. 81. Schizophrenia <ul><li>The glutamate hypothesis of schizophrenia suggests the problem relates partially to deficient activity at glutamate receptors. </li></ul><ul><ul><li>Especially in the prefrontal cortex. </li></ul></ul><ul><li>In many brain areas, dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release. </li></ul><ul><li>Increased dopamine thus produces the same effects as decreased glutamate. </li></ul>
    82. 82. Fig. 15-19, p. 479
    83. 83. Schizophrenia <ul><li>Schizophrenia is associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex and hippocampus. </li></ul><ul><li>Further support comes from the effects of phencyclidine (PCP/angel dust). </li></ul><ul><ul><li>Inhibits the NMDA glutamate receptors. </li></ul></ul><ul><ul><li>Produces positve and negative symptoms at high doses. </li></ul></ul>
    84. 84. Schizophrenia <ul><li>The mesolimbocortical system is a set of neurons that project from the midbrain tegmentum to the limbic system. </li></ul><ul><ul><li>Site where drugs that block dopamine synapses produce their benefits. </li></ul></ul><ul><li>Drugs also block dopamine in the mesostriatal system, which project to the basal ganglia. </li></ul><ul><ul><li>Result is tardive dyskinesia, characterized by tremors and other involuntary movements. </li></ul></ul>
    85. 85. Fig. 15-20, p. 479
    86. 86. Schizophrenia <ul><li>Second-generation antipsychotics (atypical antipsychotics) are a class of drugs used to treat schizophrenia but seldom produce movement problems. </li></ul><ul><ul><li>Examples: clozapine, amisulpride, risperidone, olanzapine, aripiprazole. </li></ul></ul><ul><li>More effective at treating the negative symptoms and are now more widely used. </li></ul><ul><li>Have less effect on dopamine D 2 receptors and more strongly antagonize serotonin type 5-HT 2 receptors. </li></ul>
    87. 87. Schizophrenia <ul><li>Schizophrenia cannot be explained by a single gene or single transmitter. </li></ul><ul><li>Dopamine and glutamate may play important roles in schizophrenia to different degrees in different people. </li></ul><ul><li>Schizophrenia involves multiple genes and abnormalities in dopamine, glutamate, serotonin and GABA. </li></ul>