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    Ppt Chap 15 Ppt Chap 15 Presentation Transcript

    • Chapter 15 Psychological Disorders
    • Mood Disorders
      • 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.
    • Mood Disorders
      • Major depression - feeling sad and helpless everyday for weeks and includes the following characteristics (DSM-IV):
        • Little energy.
        • Feelings of worthlessness.
        • Suicidal thoughts.
        • Feelings of hopelessness.
        • Difficulty sleeping.
        • Difficulty concentrating.
        • Little pleasure
    •  
    • Mood Disorders
      • Similar symptoms can result from hormonal problems, head injuries, brain tumors, substance abuse, or other illnesses.
      • Absence of happiness is more reliable symptom than increased sadness.
      • Occurs at any age, but uncommon in children
      • Twice as common in women
      • 10% lifetime prevalence.
    • 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).
    • Mood Disorders
      • Predisposition depends on a variety of genes.
      • Effects of these genes have varied between studies
    • Mood Disorders
      • One gene identified controls the serotonin transporter 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.
        • May alters people’s reactions to stressful events or make them more sensitive to environmental influences
    •  
    • Mood Disorders
      • A few cases of depression are linked to viral infections.
      • Borna disease is a viral infection which may predispose people to depression
      • Illustrates that many different causes can lead to similar behavioral results
    •  
    • Mood Disorders
      • Postpartum depression is depression after giving birth.
      • Affects about 20% of women and most recover quickly
      • More common among women who have suffered depression at other times.
      • May be associated with a drop in estradiol and progesterone levels .
      • Testosterone drop in men also associated with increased probability
    • Mood Disorders
      • Depression is also associated with the following brain activity:
        • Decreased activity in the left prefrontal cortex.
        • Increased activity in the right prefrontal cortex.
    • Mood Disorders
      • Many drugs used to treat psychiatric disorders discovered by accident
      • Categories of antidepressant drugs include:
        • Tricyclics.
        • Selective serotonin reuptake inhibitors.
        • MAOI’s.
        • Atypical antidepressants.
    •  
    • Mood Disorders
      • Tricylclics - operate by blocking transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release.
        • Examples: imipramine (Tofranil)
      • Also block histamine receptors, acetylcholine receptors, and certain sodium channels.
        • Creates side-effects (dry mouth, difficulty urinating, heart irregularities)
    • Mood Disorders
      • Selective serotonin reuptake inhibitors (SSRIs) - 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.
      • Milder side effects but same effectiveness
    • Mood Disorders
      • Monoamine oxidase inhibitors (MAOI’s) - blocks the enzyme monoamine oxidase that 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 if SSRI’s and tricyclics are not effective.
    • 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.
    •  
    • 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.
    • Mood Disorders
      • Studies indicate half of people show a good response within weeks after use of antidepressant drugs
      • About same percentage respond to therapy
      • 30% respond to a placebo
      • Combination of both benefits only a slightly higher percentage
      • Little difference regarding the various types of antidepressant drug
    •  
    • Mood Disorders
      • Benefits of antidepressant is greatest for people with severe depression.
      • Antidepressants are generally ineffective for people who suffered abuse, neglect, or other trauma during early childhood.
        • Usually respond better to psychotherapy
      • Use of antidepressants in children controversial
          • Most studies found ineffective and can sometimes increase suicidal thoughts
    •  
    • 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.
    • Mood Disorders
      • In some depressed people, neurons in the hippocampus and the cerebral cortex shrink.
      • Behavioral effects of antidepressant drugs often take longer than the effect on our neurochemisrty which happen within hours
      • One explanation is that antidepressant drugs increases the release of BDNF which promotes neuron growth and survival.
    • 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.
    •  
    • 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.
      • altering of the expression of genes in the hippocampus and frontal cortex is suggested.
    • 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.
    • 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.
    •  
    • Mood Disorders
      • A night of total sleep deprivation is the quickest method of relieving depression.
      • Increases proliferation of new neurons in the hippocampus
      • Half become depressed again after the next night’s sleep.
      • Extended benefits derived from altering sleep schedule on subsequent days and combining sleep alteration with drug therapies
      • Exact mechanism are not unknown.
    • Mood Disorders
      • Hormone leptin has shown some promise as an alternative treatment.
      • Regular exercise is also effective.
      • Increases blood flow to the brain.
      • Reduces the effects of stress.
      • Can be combined with other treatments to magnify benefits.
    • 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.
    • 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.
      • Each 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.
    •  
    • 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.
    • 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
      • Drugs work by:
      • decreasing glutamate activity
      • blocking the synthesis of the brain chemical arachidonic acid, which is produced during brain inflammation.
    • 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.
    •  
    • 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)
    • 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.
    • Schizophrenia
      • Positive symptoms are behaviors that are present that should be absent
      • Two cluster of positive symptoms of schizophrenia include:
        • Psychotic
        • Disorganized
    • Schizophrenia
      • Psychotic - consists of delusions and hallucinations.
        • Delusions: unfounded beliefs
        • Hallucinations: abnormal sensory experiences associated with increased activity in the thalamus, hippocampus and cortex
      • Disorganized - inappropriate emotional displays, bizarre behaviors and thought disorders (difficulty using and understanding abstract concepts).
    • 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.
    • 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 ratio of about 7 to 5.
      • More severe and earlier age of onset for men (early 20’s versus late 20).
        • May be related to release of dopamine
    • Schizophrenia
      • Twin studies suggest a genetic component, but does not depend on a single gene.
      • 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.
    •  
    • Schizophrenia
      • Adopted children studies suggest a genetic role, but prenatal environment of the biological mother can not be discounted.
      • Attempt to 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.
    • Schizophrenia
      • Researchers have identified more than a dozen genes that appear to be more common in people with schizophrenia.
      • DISC1 (disrupted in schizophrenia 1) gene controls the rate of generation of new neurons in the hippocampus.
      • Another gene important for brain plasticity and development.
      • New gene mutations are also an explanation. (microdeletions and microduplications more common)
    • 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, trouble during prenatal development, birth, or early postnatal development.
      • Environmental influences later in life aggravate the symptoms.
    • 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.
    • Schizophrenia
      • Risk factors increasing the likelihood include:
        • Poor nutrition of the mother during pregnancy.
        • Premature birth.
        • Low birth weight.
        • Complications during delivery.
        • Head injuries in early
        • Extreme stress of mother during pregnancy
    • 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.
        • Response weak in first child but stronger in later pregnancies
    • Schizophrenia
      • 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.
        • More pronounced in latitudes far from the equator.
        • Might be explained by complications of delivery, nutritional factors, or increased likelihood of viral infection in mother
    • Schizophrenia
      • Viral infections in mother can:
      • Increase cytokines in mother that impair brain development of fetus
      • Cause fever which damages the fetal brain
      • Other infections during childhood can also increase risk
        • Taxoplasma gondii
    • Schizophrenia
      • Associated with mild brain abnormalities:
        • Strongest deficits found in the left temporal and frontal lobe of the cortex.
        • Thalamus smaller than average
        • Larger than normal ventricles (especially common in those with complications during birth)
        • dorsolateral prefrontal cortex (areas that mature slowly)
          • Schizophrenics have deficits in working memory and attention.
    •  
    •  
    • 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.
    • 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.
      • No sign of neuron death
    • 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.
    •  
    • 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.
    • Schizophrenia
      • Two chemical families of drugs used to treat schizophrenia include:
        • Phenothiazines - includes chlorpromazine
        • Butyrophenones - includes halperidol (Haldol)
      • Both drugs block dopamine synapses.
    • 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.
    • 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.
    • 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.
    •  
    • 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).
    • Schizophrenia
      • Effects of phencyclidine (PCP) support glutamate hypothesis.
      • Low doses produce intoxication and slurred speech
      • Larger doses produce positve and negative symptoms
      • Produce little psychotic responses in preadolescents
      • produces relapse in people with prior schizophrenia
      • Glycine increases effectiveness of glutamate
    • 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.
    •  
    • 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.
    •  
    • 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.