Transcript Chapter 15 – psychological disorders

Chapter 15
Psychological Disorders
Substance Abuse and Addictions
• Mental illness
Substance Abuse and Addictions
• Substance abuse
Substance Abuse and Addictions
• Olds and Milner (1954)
Fig. 15-1, p. 452
Substance Abuse and Addictions
• Other behaviors that release dopamine
Substance Abuse and Addictions
• Berridge and Robinson (1998)
– Nucleus accombans
Substance Abuse and Addictions
• Addiction
Substance Abuse and Addictions
• Withdrawal
Substance Abuse and Addictions
• Alcohol
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
Substance Abuse and Addictions
• Type II/Type B characteristic
Substance Abuse and Addictions
• Twin studies and family studies suggest a
genetic basis for Type II/Type B alcoholism.
Substance Abuse and Addictions
• Risk factors for alcoholism
Substance Abuse and Addictions
• Medications used to combat alcoholism
Mood Disorders
• Major depression - feeling sad and helpless
everyday for weeks at a time
Mood Disorders
• Similar symptoms can result from hormonal
problems, head injuries, brain tumors, or
other illnesses.
• Often comorbid with other disorders
Mood Disorders
• Studies of twins and adopted children
suggest a moderate degree of heritability.
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.
Mood Disorders
• Postpartum depression
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 specific
brain activity
Mood Disorders
• Some cases of depression may be linked to
viral infection.
– Borna disease
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 (imipramine -Tofranil)
Mood Disorders
• Selective serotonin reuptake inhibitors
(SSRIs) –
• Examples: Fluoxetine (Prozac), setraline
(Zoloft), fluvoxamine (Luvox), citalopram
(Celexa) and paroxetine (Paxil).
Mood Disorders
• Monoamine oxidase inhibitors (MAOI’s)
Mood Disorders
• Atypical antidepressants - Example:
bupropion (Wellbutrin)
Mood Disorders
• Exactly how antidepressant drugs work is
unclear.
Mood Disorders
•
In some depressed people, neurons in the
hippocampus and the cerebral cortex shrink.
Mood Disorders
• Electroconvulsive therapy (ECT)
Mood Disorders
• Drawbacks
Mood Disorders
• “Receptive transcranial magnetic stimulation”
Mood Disorders
1. Unipolar disorder
2. Bipolar disorder (manic-depressive disorder)
Mood Disorders
• Bipolar disorder I –
• Bipolar disorder II -
Mood Disorders
• Research suggests a heritability basis for
bipolar disorder (Craddock & Jones, 1999).
Mood Disorders
•
Treatments for bipolar
– brain chemical arachidonic acid.
Schizophrenia
• Schizophrenia
Schizophrenia
• Causes are not well understood but include a
large biological component.
Schizophrenia
•
Two cluster of positive symptoms of
schizophrenia include:
1. Psychotic
2. Disorganized
Schizophrenia
1. Psychotic - consists of delusions and
hallucinations.
– Delusions
– Hallucinations
2. Disorganized
Schizophrenia
• Negative symptoms
Schizophrenia
• Twin studies suggest a genetic component.
Schizophrenia
• Prenatal environment
Schizophrenia
• One study identified a gene linked to high
levels of negative symptoms (Fanous et al.,
2005).
Schizophrenia
• The neurodevelopmental hypothesis
Schizophrenia
• Supporting evidence for the
neurodevelopmental hypothesis
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
• Schizophrenia is associated with mild brain
abnormalities
Schizophrenia
• Schizophrenia typically develops after the
age of 20 but many show sign at an earlier
age.
Fig. 15-17, p. 476
Schizophrenia
• Antipsychotic/neuroleptic drugs
• Chlorpromazine
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.
Schizophrenia
• Second-generation antipsychotics
Schizophrenia
• The dopamine hypothesis of schizophrenia
– Substance-induced psychotic disorder
Schizophrenia
• Research indicates increased activity
specifically at the D2 receptor.
• Limitations of the dopamine hypothesis
Schizophrenia
• The glutamate hypothesis of schizophrenia
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.