1. Chapter 14 Psychological Disorders
Module 14.2
Mood Disorders
Module 14.3
Schizophrenia
Module 14.4
Autism Spectrum Disorders

2. Mood Disorders

3. Mood Disorders
Unipolar disorder is characterized by alternating states of normality and depression.
Symptoms include:

4. Depression Similar symptoms can result from: hormonal problems
head injuries
brain tumors
other illnesses
Often comorbid with other disorders such as:
schizophrenia
substance abuse
anxiety
Parkinson’s disease
Occurs at any age
10% lifetime prevalence

5. Depression
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.

6. Genetics of Depression
Studies of twins and adopted children suggest a moderate degree of heritability.
Risk is elevated if one has a relative with early-onset depression (before age 30).

7. Genetics of Depression
One gene has been identified that 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.

8. Depression and Hormones
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.

9. Postpartum Depression
Occurs after giving birth.
Affects about 20% of women and most recover quickly.
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.

10. Depression and Brain Activity
Depression is associated with:
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.

11. Treatment of Depression: Antidepressant Drugs
Categories of antidepressant drugs include:
Tricyclics prevent the presynaptic neuron from reabsorbing serotonin, dopamine, or norepinephrine
Selective Serotonin Reuptake Inhibitors (SSRI’s) block the reuptake of the neurotransmitter serotonin

12. Treatment of Depression: Antidepressant Drugs
Monoamine Oxidase Inhibitors (MAOI’s) block the enzyme monoamine oxidase that metabolizes serotonin into an inactive form
Atypical antidepressants work by inhibiting the reuptake of dopamine and to some extent, norepinephrine but not serotonin.

13. Treatment of Depression: Electroconvulsive Therapy (ECT)
electrically induced seizure used for the treatment of severe depression
used with patients who have not responded to antidepressant medication or who are suicidal
fast-acting, but effects diminish rapidly
best used in conjunction with other forms of therapy

14. Treatment of Depression: Electroconvulsive Therapy (ECT)
Side effects include memory loss.
Memory loss can be minimized if shock is localized to the right hemisphere.
increases the proliferation of new neurons in the hippocampus
alters expression of at least 120 genes in the hippocampus and frontal cortex

15. Treatment of Depression: Transcranial Magnetic Stimulation
an intense magnetic field is applied to the scalp, to stimulate the neurons
moderately effective

16. Treatment of Depression: Disruption of Sleep Patterns
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.

17. Treatment of Depression: Disruption of Sleep Patterns
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.
Therefore, often best used in conjunction with other therapies

18. Bipolar Disorder
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.

19. Bipolar Disorder
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.

20. Genetics of Bipolar Disorder
Twin studies suggest monozygotic twins share a 50% concordance rate.
Dizygotic twins, brothers, sisters or children share a concordance rate of 5-10%.
Several genes are somewhat more common in people with the disorder.
Genes simply increase the risk but do not cause the disorder.

21. Treatments for Bipolar Disorder
These chemicals/drugs are used to stabilize mood:
Lithium - a salt that prevents relapse in mania or depression
Anticonvulsant drugs such as valproate (depakote) and carbamazepine
Usually prescribed for bipolar II.

22. Seasonal Affective Disorder (SAD)
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.

23. Schizophrenia
Schizophrenia is a disorder characterized by deteriorating ability to function in every day life and some combination of the following symptoms:
Hallucinations: abnormal sensory experiences
Delusions: unfounded beliefs
Disorganized speech: rambling
or incoherent
Grossly disorganized behavior
Weak or absent signs of emotion,
speech, and socialization
Inappropriate emotional
expression
Thought disorder: difficulty
using and understanding
abstract concepts

24. Schizophrenia: Inappropriate Emotional Expression
Positive symptoms are behaviors that are present that should not be present.
hallucinations
delusions
disorganized speech

25. Schizophrenia: Inappropriate Emotional Expression
Negative symptoms are behaviors that are absent that should be present, including:
weak social interaction
lack of emotional expression
speech deficit
working memory deficit
Negative symptoms are usually stable over time and difficult to treat.

26. Schizophrenia: Incidence Rates
Schizophrenia affects about 1% of the population and ranges in severity.
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.

27. Schizophrenia: Incidence Rates
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’s).
Likelihood increases as the age of the father increases.

28. Schizophrenia: Genetics
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.
Greater similarity between dizygotic twins than siblings suggests a prenatal/postnatal environmental effect.

29. Schizophrenia: Genetics
Attempt to link adult-onset schizophrenia to an identified gene have provided inconsistent results.
Schizophrenia most likely results from environmental factors in addition to biological factors.

30. Schizophrenia: 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.

31. Schizophrenia: Neurodevelopmental Hypothesis
Supporting evidence 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.

32. Schizophrenia: Neurodevelopmental Hypothesis
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.

33. Schizophrenia: Neurodevelopmental Hypothesis
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.

34. Schizophrenia: Neurodevelopmental Hypothesis
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 infections

35. Schizophrenia: Brain Abnormalities
Schizophrenia is associated with mild brain abnormalities:
Less than average gray and white matter
Strongest deficits found in the left temporal and frontal lobe of the cortex
Larger than normal ventricles
Smaller than normal hippocampus
Schizophrenics have deficits in working memory.

36. Schizophrenia: Development
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.

37. Schizophrenia: Treatment
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 positive symptoms of schizophrenia.
Relief usually experienced 2-3 weeks after taking the drug, which must be taken indefinitely.

38. Schizophrenia: Treatment
Two chemical families of drugs used to treat schizophrenia include:
Phenothiazines - includes chlorpromazine
Butyrophenones - includes halperidol (Haldol)
Both drugs block dopamine synapses.

39. 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.

40. Glutamate Hypothesis of Schizophrenia
suggests the problem relates partially to deficient activity at glutamate receptors
especially in the prefrontal cortex
Schizophrenia is associated with lower than normal release of glutamate and fewer receptors in the prefrontal cortex and hippocampus.
Support comes from the effects of phencyclidine (PCP/angel dust).
Inhibits the NMDA glutamate receptors.
Produces positive and negative symptoms at high doses.

41. Schizophrenia: Treatment
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.

42. Schizophrenia: Treatment
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.

43. 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.

44. Autism Spectrum Disorders
Primary characteristics:
Deficits in social and emotional exchange
Deficits in gestures, facial expression and other nonverbal communication
Repetitive behaviors
Resistance to change in routine
Unusually weak or strong emotional reactions

45. Autism Spectrum Disorders
Worldwide prevalence estimated at 1 in 160 people
More common in boys than girls

46. Autism Spectrum Disorders
Often comorbid with Attention Deficit Disorder (ADD)
Can involve cerebellum, resulting in movement deficit

47. Autism Spectrum Disorders
Many genes have been linked to autism, but no single gene is found in a high percentage of people with autism
Most cases probably result from new mutations or microdeletions in multiple genes.