Ppt Chap 15


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Ppt Chap 15

  1. 1. Chapter 15 Psychological Disorders
  2. 2. Mood Disorders <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. Mood Disorders <ul><li>Major depression - feeling sad and helpless everyday for weeks 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 </li></ul></ul>
  4. 5. Mood Disorders <ul><li>Similar symptoms can result from hormonal problems, head injuries, brain tumors, substance abuse, or other illnesses. </li></ul><ul><li>Absence of happiness is more reliable symptom than increased sadness. </li></ul><ul><li>Occurs at any age, but uncommon in children </li></ul><ul><li>Twice as common in women </li></ul><ul><li>10% lifetime prevalence. </li></ul>
  5. 6. 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>
  6. 7. Mood Disorders <ul><li>Predisposition depends on a variety of genes. </li></ul><ul><li>Effects of these genes have varied between studies </li></ul>
  7. 8. Mood Disorders <ul><li>One gene identified controls the serotonin transporter protein. </li></ul><ul><ul><li>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>May alters people’s reactions to stressful events or make them more sensitive to environmental influences </li></ul></ul>
  8. 10. Mood Disorders <ul><li>A few cases of depression are linked to viral infections. </li></ul><ul><li>Borna disease is a viral infection which may predispose people to depression </li></ul><ul><li>Illustrates that many different causes can lead to similar behavioral results </li></ul>
  9. 12. 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>More common among women who have suffered depression at other times. </li></ul><ul><li>May be associated with a drop in estradiol and progesterone levels . </li></ul><ul><li>Testosterone drop in men also associated with increased probability </li></ul>
  10. 13. Mood Disorders <ul><li>Depression is also 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>
  11. 14. Mood Disorders <ul><li>Many drugs used to treat psychiatric disorders discovered by accident </li></ul><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>
  12. 16. Mood Disorders <ul><li>Tricylclics - operate by blocking transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release. </li></ul><ul><ul><li>Examples: imipramine (Tofranil) </li></ul></ul><ul><li>Also block histamine receptors, acetylcholine receptors, and certain sodium channels. </li></ul><ul><ul><li>Creates side-effects (dry mouth, difficulty urinating, heart irregularities) </li></ul></ul>
  13. 17. Mood Disorders <ul><li>Selective serotonin reuptake inhibitors (SSRIs) - 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>Milder side effects but same effectiveness </li></ul>
  14. 18. Mood Disorders <ul><li>Monoamine oxidase inhibitors (MAOI’s) - blocks the enzyme monoamine oxidase that 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 if SSRI’s and tricyclics are not effective. </li></ul>
  15. 19. 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><ul><li>Works by inhibiting the reuptake of dopamine and to some extent, norepinephrine but not serotonin. </li></ul></ul>
  16. 21. 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>
  17. 22. Mood Disorders <ul><li>Studies indicate half of people show a good response within weeks after use of antidepressant drugs </li></ul><ul><li>About same percentage respond to therapy </li></ul><ul><li>30% respond to a placebo </li></ul><ul><li>Combination of both benefits only a slightly higher percentage </li></ul><ul><li>Little difference regarding the various types of antidepressant drug </li></ul>
  18. 24. Mood Disorders <ul><li>Benefits of antidepressant is greatest for people with severe depression. </li></ul><ul><li>Antidepressants are generally ineffective for people who suffered abuse, neglect, or other trauma during early childhood. </li></ul><ul><ul><li>Usually respond better to psychotherapy </li></ul></ul><ul><li>Use of antidepressants in children controversial </li></ul><ul><ul><ul><li>Most studies found ineffective and can sometimes increase suicidal thoughts </li></ul></ul></ul>
  19. 26. 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>
  20. 27. 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 often take longer than the effect on our neurochemisrty which happen within hours </li></ul><ul><li>One explanation is that antidepressant drugs increases the release of BDNF which promotes neuron growth and survival. </li></ul>
  21. 28. 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>
  22. 30. 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>altering of the expression of genes in the hippocampus and frontal cortex is suggested. </li></ul>
  23. 31. 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>
  24. 32. 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>
  25. 34. Mood Disorders <ul><li>A night of total sleep deprivation is the quickest method of relieving depression. </li></ul><ul><li>Increases proliferation of new neurons in the hippocampus </li></ul><ul><li>Half become depressed again after the next night’s sleep. </li></ul><ul><li>Extended benefits derived from altering sleep schedule on subsequent days and combining sleep alteration with drug therapies </li></ul><ul><li>Exact mechanism are not unknown. </li></ul>
  26. 35. Mood Disorders <ul><li>Hormone leptin has shown some promise as an alternative treatment. </li></ul><ul><li>Regular exercise is also effective. </li></ul><ul><li>Increases blood flow to the brain. </li></ul><ul><li>Reduces the effects of stress. </li></ul><ul><li>Can be combined with other treatments to magnify benefits. </li></ul>
  27. 36. 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>
  28. 37. 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>Each 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>
  29. 39. 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>
  30. 40. 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><li>Drugs work by: </li></ul><ul><li>decreasing glutamate activity </li></ul><ul><li>blocking the synthesis of the brain chemical arachidonic acid, which is produced during brain inflammation. </li></ul>
  31. 41. 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>
  32. 43. 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>
  33. 44. 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>
  34. 45. Schizophrenia <ul><li>Positive symptoms are behaviors that are present that should be absent </li></ul><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>
  35. 46. 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 thalamus, 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>
  36. 47. 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>
  37. 48. 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 ratio 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><ul><li>May be related to release of dopamine </li></ul></ul>
  38. 49. Schizophrenia <ul><li>Twin studies suggest a genetic component, but does not depend on a single gene. </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>
  39. 51. 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 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>
  40. 52. Schizophrenia <ul><li>Researchers have identified more than a dozen genes that appear to be more common in people with schizophrenia. </li></ul><ul><li>DISC1 (disrupted in schizophrenia 1) gene controls the rate of generation of new neurons in the hippocampus. </li></ul><ul><li>Another gene important for brain plasticity and development. </li></ul><ul><li>New gene mutations are also an explanation. (microdeletions and microduplications more common) </li></ul>
  41. 53. 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, trouble during prenatal development, birth, or early postnatal development. </li></ul><ul><li>Environmental influences later in life aggravate the symptoms. </li></ul>
  42. 54. 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><ul><li>Abnormalities of early development could impair behavior in adulthood. </li></ul></ul>
  43. 55. Schizophrenia <ul><li>Risk factors increasing the likelihood 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><ul><li>Head injuries in early </li></ul></ul><ul><ul><li>Extreme stress of mother during pregnancy </li></ul></ul>
  44. 56. 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><ul><ul><li>Response weak in first child but stronger in later pregnancies </li></ul></ul>
  45. 57. Schizophrenia <ul><li>The season-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 infection in mother </li></ul></ul>
  46. 58. Schizophrenia <ul><li>Viral infections in mother can: </li></ul><ul><li>Increase cytokines in mother that impair brain development of fetus </li></ul><ul><li>Cause fever which damages the fetal brain </li></ul><ul><li>Other infections during childhood can also increase risk </li></ul><ul><ul><li>Taxoplasma gondii </li></ul></ul>
  47. 59. Schizophrenia <ul><li>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>Thalamus smaller than average </li></ul></ul><ul><ul><li>Larger than normal ventricles (especially common in those with complications during birth) </li></ul></ul><ul><ul><li>dorsolateral prefrontal cortex (areas that mature slowly) </li></ul></ul><ul><ul><ul><li>Schizophrenics have deficits in working memory and attention. </li></ul></ul></ul>
  48. 62. 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>
  49. 63. 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><ul><li>No sign of neuron death </li></ul>
  50. 64. 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>
  51. 66. 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>
  52. 67. 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>
  53. 68. 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>
  54. 69. 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>
  55. 70. 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>
  56. 72. 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>
  57. 73. Schizophrenia <ul><li>Effects of phencyclidine (PCP) support glutamate hypothesis. </li></ul><ul><li>Low doses produce intoxication and slurred speech </li></ul><ul><li>Larger doses produce positve and negative symptoms </li></ul><ul><li>Produce little psychotic responses in preadolescents </li></ul><ul><li>produces relapse in people with prior schizophrenia </li></ul><ul><li>Glycine increases effectiveness of glutamate </li></ul>
  58. 74. 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>
  59. 76. 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>
  60. 78. 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>