Chapter 15: Mood Disorders and Schizophrenia

Question 1

symptoms of depression and the evidence for a genetic contribution to depression

Answer 1

• intense and prolonged
• sad and helpless for weeks at a time, little energy, feel worthless, contemplate suicide, trouble sleeping, cannot concentrate, find little pleasure, find difficulty imagining ever being happy again
• absence of happiness
• moderate degree of heritability via twin and adopted children studies
• effect of gene varies with environment

Question 2

Forms of serotonin transporter genes and depression

Answer 2

• 2 short serotonin transporter genes=increase stressful experiences lead to big increase in probability of depression
• 2 long forms of gene=slight increase
• 1 long and 1 short gene=intermediate
• study could not be replicated

Question 3

possible roles of genetics, stress, hormones, abnormalities of hemispheric dominance, and viruses in the onset or worsening of depression

Answer 3

-partially explains why some people are more vulnerable to depression

Question 4

Viruses in onset or worsening of depression

Answer 4

• all people with this virus were suffering from major depression
• 5% of normal people, 1/3 of people with severe depression and schizophrenia

Question 5

Hormones and stress in the onset or worsening of depression

Answer 5

• stress releases cortisol
• declining testosterone associated with increased risk of depression
• few studies have been done that directly link hormones to depression therefore relationship=uncertain

Question 6

Post partum depression

Answer 6

-hormonal fluctuations

Question 7

Abnormalities of Hemispheric Dominance in the onset or worsening of depression

Answer 7

• strong relationship between happy mood and increased activity in left prefrontal cortex
• most people with depression have decreased activity in left and increased activity in right prefrontal cortex
• most people gaze to right during verbal tasks but most individuals with depression gaze to left suggesting right hemisphere dominance

Question 8

describe the short-term and long-term mechanisms of action of antidepressant drugs

Answer 8

• must take drug for 2+ weeks before experiencing mood elevation
• prolonged use increases BDNF production and improves learning and formation of new neurons
• only people with severe depression show significant difference when taking anti depressants

Question 9

Psychotherapy

Answer 9

• equally effective as antidepressants
• brief psychotherapy-ineffective for long term conditions
• adv.=more likely to have long term benefits reducing risk of relapse
• both therapy and drugs together increases slightly positive outcomes

Question 10

ECT

Answer 10

• quick most patients awaken calmly and do not remember the treatment
• relieved depression in many cases
• used today for severe depression when drugs do not work
• memory loss for a few months, high risk of relapse within a few months

Question 11

Altered Sleep patterns

Answer 11

• night of total sleep deprivation helps alleviate depression but increased sensitivity to pain
• go to bed earlier-> procedure often relieves depression for at least a week and often longer

Question 12

symptoms of bipolar disorder and the possible contributions of genetics

Answer 12

• increase glucose in brain during mania
• decrease glucose during depression
• mood swings, attention deficits, poor impulse control, verbal meaning impairment

Question 13

unipolar

Answer 13

-normal + depression

Question 14

bipolar

Answer 14

-mania + depression

Question 15

mania

Answer 15

-restless activity, excitement, laughter, self-confidence, laughter, rambling speech loss of inhibitions, danger to themselves and others

Question 16

bipolar I

Answer 16

full blown manic episodes

Question 17

bipolar II

Answer 17

hypomania (agitation/anxiety)

Question 18

bipolar disorder and the possible contributions of genetics

Answer 18

• genetic predisposition supported by twin/adoption studies
• 2 genes appear to increased probability of bipolar II
• just increase risk, none show strong relationship to the disorder

Question 19

mechanisms of action of drugs used to treat bipolar disorder

Answer 19

• lithium salts-> stabilizes mood, preventing relapse, must be regulated carefully as low dose=not effective and high dose=toxic
• > decrease # of AMPA type glutamate receptors in hippocampus (excessive glutamate=mania)
• > block synthesis of brain chemicals arachidonic acid produced during brain inflammation
• valoproate and carbamazepine

Question 20

mechanisms of action of drugs used to treat bipolar disorder

Answer 20

• lithium salts-> stabilizes mood, preventing relapse, must be regulated carefully as low dose=not effective and high dose=toxic
• > decrease # of AMPA type glutamate receptors in hippocampus (excessive glutamate=mania)
• > block synthesis of brain chemicals arachidonic acid produced during brain inflammation
• valoproate and carbamazepine

Question 21

describe seasonal affective disorder and a treatment for it

Answer 21

-depression that recurs during a particular season (winter)
-most common near poles
-not as severe as major depression
-sleepy and wakeful later than normal
-most people with SAD have mutation in gene responsible for circadian rhythm
TREATMENT- very bright lights for 1hr each day

Question 22

positive symptoms of schizophrenia

Answer 22

• delusions
• hallucinations
• disorganized speech
• disorganized behaviour
• present but should be absent

Question 23

negative symptoms of schizphrenia

Answer 23

• weak or absent emotions, speech, disorganized behaviour
• stable over time
• difficult to treat
• absent that should be present
• difficult to treat

Question 24

conditions resembling schizophrenia, with which it may be confused

Answer 24

• mood disorder with psychotic features
• substance abuse
• brain damage
• undetected hearing deficits
• Huntington’s disease
• Nutritional abnormalities

Question 25

demographic factors related to schizophrenia

Answer 25

• 1% of people worldwide suffer from schizophrenia at some point in their life
• occurs in all ethnic groups and all parts of world
• 10 to 100x more common in US and Europe than developing countries
• more common in men than women 7:5 ratio

Question 26

describe the evidence for a genetic contribution to schizophrenia

Answer 26

• has genetic basis but does not depend on any single gene
• related to someone with schizophrenia=increased likelihood
• monozygotic twins have much higher concordance than dizygotic twins for schizophrenia (50% concordance)
• researchers have identified 12+ genes that seem to be more common in people with schizophrenia ex) DISc1 (disrupted in schizophrenia 1) controls production of dendritic spines and generation of new neurons in hippocampus
• hypothesis: many cases of schizophrenia arise from new mutations

Question 27

neurodevelopmental hypothesis

Answer 27

• schizophrenia begins with abnormalities in prenatal or neonatal development of nervous system based on genetics or other influences
• early problems leave brain vulnerable to disturbances later in life

Question 28

Supporting evidence for neurodevelopmental hypothesis

Answer 28

1) several kinds of pre and neo natal difficulties are later linked to schizophrenia:l poor nutrition, low birth weight complications during delivery, extreme stress, head injuries in childhood, Rh-ve mom with Rh+ve baby could trigger immunological rejection by mother
2) people with schizophrenia have minor brain abnormalities that seem to originate early in life; less than average gray and white matter, increase size of ventricles, thalamus smaller
3) plausible abnormalities from early life could impair behaviour in adulthood

Question 29

evidence for and against the dopamine hypothesis of schizophrenia

Answer 29

• schizophrenia results from excess activity at dopamine synapses in certain areas of brain
• dopamine concentration is not higher than normal, turnover is elevated neurons release dopamine at faster than average rate and synthesize more to replace molecules they do not absorb
• drugs most effective block dopamine receptors
• use of meth etc. induces substance induced psychotic disorder (symptoms=hallucinations and delusions) increase or prolongs dopamine activity at synapses

Question 30

describe the evidence for the glutamate hypothesis of schizophrenia and the potential role for glycine and for metabotropic glutamate receptors in treating it

Answer 30

• problem=deficient activity @ glutamate synapse (especially in prefrontal cortex)
• lower than normal release of glutamate and fewer receptors in prefrontal cortex and hippocampus
• support from drug PCP that inhibits NMDA glutamate receptors
• low dose=intoxication and slurred speech
• high dose=+ve and -ve symptoms of schizophrenia
• drugs that stimulate kind of metabotropic glutamate receptors show promise in treating schizophrenia

Question 31

one undesired effect of antipsychotic drugs and the mechanisms of action of the newer drugs that minimize these effects

Answer 31

• undesired effect=tardive dyskinesia (tremors and other involuntary movements)
• 2nd generation antipsychotics alleviate without movement problems
• less effects on dopamine D2 receptors and more strongly antagonize serotonin type 5-HT receptors, also increase release of glutamate