chapter15 power point presentation

Chapter 15Psychological 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 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.


• 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


• 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


• 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.


• 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.


• 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.


• 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.


• 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.


• 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


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


• 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.


• 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.


• 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


• Medications used to combat alcoholism include:– Antabuse.– Methadone.– Many do not respond to other treatments

so medications have been used to reduce cravings.


• 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.


• 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.


• 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.

chapter15 power point presentation

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