Chapter 15 psychological disorders
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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.

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Chapter 15 psychological disorders l.jpg

Chapter 15Psychological Disorders

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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.

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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

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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.

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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).

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Mood Disorders

  • Predisposition depends on a variety of genes.

  • Effects of these genes have varied between studies

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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

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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

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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

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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.

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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.

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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)

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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

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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.

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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.

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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.

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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

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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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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  • 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)

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  • 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.

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  • Positive symptoms are behaviors that are present that should be absent

  • Two cluster of positive symptoms of schizophrenia include:

    • Psychotic

    • Disorganized

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  • 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).

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  • 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.

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  • 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

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  • 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.

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  • 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.

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  • 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)

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  • 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.

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  • 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.

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  • 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

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  • 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

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  • 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

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  • 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

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  • 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.

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  • 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.

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  • 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

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  • 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.

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  • 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.

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  • Two chemical families of drugs used to treat schizophrenia include:

    • Phenothiazines - includes chlorpromazine

    • Butyrophenones - includes halperidol (Haldol)

  • Both drugs block dopamine synapses.

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  • 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.

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  • Research indicates increased activity specifically at the D2 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.

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  • 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.

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  • 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).

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  • 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

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  • 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.

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  • 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 D2 receptors and more strongly antagonize serotonin type 5-HT2 receptors.

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  • 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.