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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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mood 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 disorders3
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 disorders5
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 disorders6
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 disorders7
Mood Disorders
  • Predisposition depends on a variety of genes.
  • Effects of these genes have varied between studies
mood disorders8
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 disorders10
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 disorders12
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 disorders13
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 disorders14
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 disorders16
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 disorders17
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 disorders18
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 disorders19
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 disorders21
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 disorders22
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 disorders24
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 disorders26
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 disorders27
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 disorders28
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 disorders30
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 disorders31
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 disorders32
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 disorders34
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 disorders35
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 disorders36
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 disorders37
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 disorders39
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 disorders40
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 disorders41
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 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)
  • 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.
  • Positive symptoms are behaviors that are present that should be absent
  • Two cluster of positive symptoms of schizophrenia include:
    • Psychotic
    • Disorganized
  • 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).
  • 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 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
  • 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.
  • 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.
  • 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)
  • 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.
  • 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.
  • 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
  • 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
  • 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
  • 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
  • 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.
  • 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.
  • 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 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.
  • 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.
  • Two chemical families of drugs used to treat schizophrenia include:
    • Phenothiazines - includes chlorpromazine
    • Butyrophenones - includes halperidol (Haldol)
  • Both drugs block dopamine synapses.
  • 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.
  • 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.
  • 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 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).
  • 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
  • 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.
  • 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.
  • 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.