Psychological Disorders - Download as PowerPoint

							Psychological Disorders
   Substance Abuse and Addictions


• 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.
   Substance Abuse and Addictions


• Substance abuse is defined as a maladaptive
  pattern of substance use leading to clinically
  significant impairment or distress. (DSM IV)
• Most recognize it as harmful but continue the
  pattern of addictive behavior.
• Addictive substances increase dopamine
  activity in certain areas of the brain.
   Substance Abuse and Addictions


• Olds and Milner (1954) placed rats in a
  Skinner box that allowed self-stimulation of
  the brain by the pressing of a lever.
• Rats sometimes pressed the lever 2000 times
  per hour to stimulated the release of
  dopamine in the nucleus accumbens.
Fig. 15-1, p. 452
   Substance Abuse and Addictions


• Other behaviors that release dopamine
  include sexual excitement, gambling, and
  video games.
• fMRI research indicates dopamine is released
  during viewing of “attractive” people.
Fig. 15-2, p. 453
   Substance Abuse and Addictions


• Berridge and Robinson (1998) suggest an
  important distinction be made between
  “liking” and “wanting” behaviors.
• Activity in the nucleus accumbens seems to
  be related to “wanting”.
   – Results in a monopolization of attention.
   Substance Abuse and Addictions


• Addiction results in the nucleus accumbens
  becoming sensitized and responding more
  strongly to the stimulus.
• Repeated use of cocaine increases the ability
  of the nucleus accumbens to release
  dopamine and the ability to activate the
  prefrontal cortex.
• Person increases tendency to seek the drug
  and responds less to other incentives.
   Substance Abuse and Addictions


• Receiving a drug during a withdrawal period
  is a powerful experience that produces
  sensitization.
• User learns that the drug relieves the distress
  caused by withdrawal and produces
  heightened effects.
• Subjects that have abstained from a drug
  show heightened seeking of the drug upon
  any reminder of the drug.
   Substance Abuse and Addictions


• Alcohol is a drug that has a long historical
  use and is used widely throughout the world.
• In moderate amounts, alcohol is associated
  with relaxation.
• In greater amounts it impairs judgment and
  damages the liver and other organs.
• Alcoholism/alcohol dependence is the
  continued use of alcohol despite medical or
  social harm even after one has decided to
  quit or decrease drinking.
   Substance Abuse and Addictions


• Alcohol has a number of diverse physiological
  effects including:
   – Inhibition of sodium across the membrane.
   – Expansion of the surface of membranes.
   – Decreased serotonin activity.
   – Enhanced response by the GABAA
     receptor.
   – Blockage of glutamate receptors.
   – Increased dopamine activity.
    Substance Abuse and Addictions


• The genetic basis for early-onset alcoholism
  is stronger than for later-onset, especially in
  men.
• Researchers distinguish between two types
  of alcoholism
  1. Type I/Type A
  2. Type II/Type B
   Substance Abuse and Addictions


• Type I/Type A characteristics include:
   – Later onset.
   – Gradual onset.
   – Fewer genetic relatives with alcoholism.
   – Equal quantity between men and women.
   – Less severe.
   Substance Abuse and Addictions


• Type II/Type B characteristic include:
   – Earlier onset (usually before 25).
   – More rapid onset.
   – More genetic relatives with alcoholism.
   – Men outnumber women.
   – Often severe.
   – Often associated with criminality.
   Substance Abuse and Addictions


• Twin studies and family studies suggest a
  genetic basis for Type II/Type B alcoholism.
• Genes influence the likelihood of alcoholism
  in a variety of ways:
   – Increase impulsive and risk-taking
     behaviors.
   – increase the stress response when trying
     to quit.
• Genes that increase adenosine, which has a
  calming effect, may decrease alcohol
  consumption.
   Substance Abuse and Addictions


• Risk factors for alcoholism include children
  who are impulsive, risk-taking, easily bored,
  sensation-seeking, and out-going.
• Studies of sons with alcoholic fathers
  indicates the following:
   – Less intoxication after moderate drinking.
   – Greater than 60% probability of developing
     alcoholism.
   – Alcohol decreases stress response more.
   – Smaller amygdala in the right hemisphere.
Fig. 15-3, p. 455
   Substance Abuse and Addictions


• Medications used to combat alcoholism
  include:
   – Antabuse.
   – Methadone.
   – Many do not respond to other treatments
     so medications have been used to reduce
     cravings.
   Substance Abuse and Addictions


• Antabuse (disulfiram) works by antagonizing
  the effects of acetaldehyde dehydrogenase.
• After alcohol consumption, enzymes in the
  liver metabolize it into a poisonous substance
  called acetaldehyde.
• Acetaldehyde is converted by the enzyme
  acetaldehyde dehydrogenase into acetic acid,
  a chemical that the body can use as a source
  of energy.
• Accumulation of acetaldehyde results in
  sickness.
   Substance Abuse and Addictions


• Most studies suggest that Antabuse has been
  only moderately effective.
• When effective, it supplements the alcoholic’s
  own commitment to quit.
• Daily routine of pill ingestion may reaffirm
  commitment not to drink.
• Many quit taking the pill and continue to drink.
   Substance Abuse and Addictions


• Methadone is an opiate similar to heroin and
  morphine but is absorbed and metabolized
  slowly.
• Perceived to be less harmful than other
  drugs.
• Assumed to satisfy the cravings associated
  with the previous drug use and allow the
  person to carry on with their life.
             Mood Disorders


• Major depression - feeling sad and helpless
  everyday for weeks at a time and includes the
  following characteristics (DSM-IV):
   – Little energy.
   – Feelings of worthlessness.
   – Suicidal thoughts.
   – Feelings of hopelessness.
   – Difficulty sleeping.
   – Difficulty concentrating.
   – Little pleasure from sex or food.
             Mood Disorders


• Similar symptoms can result from hormonal
  problems, head injuries, brain tumors, or
  other illnesses.
• Often comorbid with other disorders such as
  schizophrenia, substance abuse, anxiety or
  Parkinson’s.
• Absence of happiness is more reliable
  symptom than increased sadness.
• Occurs at any age.
• Twice as common in women and rates
  suggest about 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.
• One identified gene leads to an 80%
  decrease in the brain’s ability to produce
  serotonin.
   – Most depressed people do not have this
     gene.
   – Those who have the gene have a higher
     predisposition.
              Mood Disorders


• Another gene identified controls the serotonin
  transporter protein.
   – 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.
   – Perhaps alters the way people react to
     stressful events.
              Mood Disorders


• Specific hormones are also involved with
  depression.
• A likely trigger for an episode of depression is
  stress and the release of the hormone
  cortisol.
• Prolonged elevated levels exhaust the body’s
  energies, impair sleep and the immune
  system.
   – Set the stage for an episode of depression.
Fig. 15-6, p. 460
              Mood Disorders


• Postpartum depression is depression after
  giving birth.
• Affects about 20% of women and most
  recover quickly.
• .1% enter a serious, long-lasting depression.
• More common among women who:
   – have suffered depression at other times.
   – experience sever discomfort during the
     times around menstruation.
• May be associated with a drop in estradiol
  and progesterone levels.
             Mood Disorders


• Childhood depression is equally common in
  both boys and girls.
• After puberty, depression is twice as common
  in females.
• The finding is consistent across cultures,
  suggesting a biological factor.
              Mood Disorders


• Depression is associated with the following
  brain activity:
   – Decreased activity in the left prefrontal
     cortex.
   – Increased activity in the right prefrontal
     cortex.
• Many people become seriously depressed
  after left-hemisphere damage.
• Occasionally, people with right hemisphere
  damage become manic.
               Mood Disorders


• Some cases of depression may be linked to
  viral infection.
• Borna disease is an infection noted mostly by
  the behavioral effects of periods of frantic
  activity alternating with periods of inactivity.
• Found in a variety of different species of
  animals.
• Found more commonly in depressed people
  or people with bipolar.
• Predisposes people to various psychiatric
  disorders.
               Mood Disorders


•   Categories of antidepressant drugs include:
    1. Tricyclics.
    2. Selective serotonin reuptake inhibitors.
    3. MAOI’s.
    4. Atypical antidepressants.
Fig. 15-9, p. 463
              Mood Disorders


• Tricylclics - a category of antidepressant
  drugs that operate by preventing the
  presynaptic neuron from reabsorbing
  serotonin, dopamine, or norepinephrine after
  release.
   – Examples: imipramine (Tofranil)
• Block histamine receptors, acetylcholine
  receptors, and certain sodium channels.
• Side-effects include dry mouth, difficulty
  urinating, heart irregularities, and possible
  fatal overdose potential.
              Mood Disorders


• Selective serotonin reuptake inhibitors
  (SSRIs) - a class of antidepressant drugs that
  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.
• Mild side effects include nausea, headache
  and occasional nervousness.
              Mood Disorders


• Monoamine oxidase inhibitors (MAOI’s) - a
  class of antidepressant drugs that blocks the
  enzyme monoamine oxidase.
• Monoamine oxidase 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 after SSRI’s and tricyclics.
             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.
• Nefazodone is an antidepressant drug which
  specifically blocks serotonin type 2A
  receptors and also weakly blocks reuptake of
  serotonin and norepinephrine.
              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


• 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
  most likely depend on two slow changes in
  the brain:
  1. Drug increases the release of BDNF
     which promotes neuron growth and
     survival.
  2. Desensitize autoreceptors and thereby
     increase release of the neurotransmitter.
              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.
• Animal studies suggest an altering of the
  expression of genes in the hippocampus and
  frontal cortex.
              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.
Fig. 15-11, p. 466
             Mood Disorders


• A night of total sleep deprivation is the
  quickest known method of relieving
  depression.
• Half who experience relief become depressed
  again after the next night’s sleep.
• Extended benefits can be derived from
  altering sleep schedule on subsequent days.
• Combining sleep alteration with drug
  therapies can provide long-lasting benefits.
• Exact mechanism of how sleep disruption
  relieves depression is unknown.
              Mood Disorders


1. Unipolar disorder is characterized by an
   alternating states of normality and
   depression.
2. 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.
• Affects 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:
  1. Lithium - a salt that stabilizes mood and
      prevents relapse in mania or depression
  2. Drugs - anticonvulsant drugs such as
      valproate (depakote) and carbamazepine
      Usually prescribed for bipolar II.
• All three drugs work by 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.
Fig. 15-13, p. 468
               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


•   Two cluster of positive symptoms of
    schizophrenia include:
    1. Psychotic
    2. Disorganized
               Schizophrenia


1. Psychotic - consists of delusions and
   hallucinations.
   – Delusions: unfounded beliefs
   – Hallucinations: abnormal sensory
      experiences associated with increased
      activity in the hypothalamus,
      hippocampus and cortex
2. 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
  ration of about 7 to 5.
• More severe and earlier age of onset for men
  (early 20’s versus late 20).
• Likelihood increases as the age of the father
  increases.
              Schizophrenia


• Twin studies suggest a genetic component.
• 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.
Fig. 15-14, p. 472
               Schizophrenia


• Adopted children studies suggest a genetic
  role, but prenatal environment of the
  biological mother can not be discounted.
• Attempt to link adult-onset 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


• One study identified a gene linked to high
  levels of negative symptoms (Fanous et al.,
  2005).
• Perhaps geenetic research should focus on
  specific aspects of schizophrenia rather than
  schizophrenia in general.
• Schizophrenia most likely results from
  environmental factors in addition to biological
  factors.
              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,
  difficulty during birth, or a combination of
  both.
                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


• Prenatal risk factors increasing the likelihood
  of schizophrenia include:
   – Poor nutrition of the mother during
     pregnancy.
   – Premature birth.
   – Low birth weight.
   – Complications during delivery.
• Head injuries in early childhood are also
  linked to increased incidence of
  schizophrenia.
               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.
               Schizophrenia


• Certain viral infections may be an alternative
  or supplement genetic influences.
• 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.
   – More pronounced in latitudes far from the
     equator.
   – Might be explained by complications of
     delivery, nutritional factors, or increased
     likelihood of viral infections
                Schizophrenia


• Schizophrenia is associated with mild brain
  abnormalities:
   – Strongest deficits found in the left temporal
     and frontal lobe of the cortex.
   – Larger than normal ventricles.
       Especially common in those with
        complications during birth.
• Areas that mature slowly such as the
  dorsolateral prefrontal cortex.
   – Schizophrenics have deficits in working
     memory.
Fig. 15-15, p. 474
               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.
              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.
Fig. 15-17, p. 476
               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:
  1. Phenothiazines - includes chlorpromazine
  2. Butyrophenones - includes halperidol
     (Haldol)
• Both drugs block dopamine synapses.
Fig. 15-18, p. 477
               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 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.
              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.
Fig. 15-19, p. 479
              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).
   – Inhibits the NMDA glutamate receptors.
   – Produces positve and negative symptoms
     at high doses.
               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.
Fig. 15-20, p. 479
               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 D2 receptors
  and more strongly antagonize serotonin type
  5-HT2 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.