Chapter 15: Mood Disorders and Schizophrenia Flashcards
symptoms of depression and the evidence for a genetic contribution to depression
- 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
Forms of serotonin transporter genes and depression
- 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
possible roles of genetics, stress, hormones, abnormalities of hemispheric dominance, and viruses in the onset or worsening of depression
-partially explains why some people are more vulnerable to depression
Viruses in onset or worsening of depression
- all people with this virus were suffering from major depression
- 5% of normal people, 1/3 of people with severe depression and schizophrenia
Hormones and stress in the onset or worsening of depression
- 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
Post partum depression
-hormonal fluctuations
Abnormalities of Hemispheric Dominance in the onset or worsening of depression
- 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
describe the short-term and long-term mechanisms of action of antidepressant drugs
- 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
Psychotherapy
- 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
ECT
- 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
Altered Sleep patterns
- 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
symptoms of bipolar disorder and the possible contributions of genetics
- increase glucose in brain during mania
- decrease glucose during depression
- mood swings, attention deficits, poor impulse control, verbal meaning impairment
unipolar
-normal + depression
bipolar
-mania + depression
mania
-restless activity, excitement, laughter, self-confidence, laughter, rambling speech loss of inhibitions, danger to themselves and others
bipolar I
full blown manic episodes
bipolar II
hypomania (agitation/anxiety)
bipolar disorder and the possible contributions of genetics
- 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
mechanisms of action of drugs used to treat bipolar disorder
- 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
mechanisms of action of drugs used to treat bipolar disorder
- 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
describe seasonal affective disorder and a treatment for it
-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
positive symptoms of schizophrenia
- delusions
- hallucinations
- disorganized speech
- disorganized behaviour
- present but should be absent
negative symptoms of schizphrenia
- weak or absent emotions, speech, disorganized behaviour
- stable over time
- difficult to treat
- absent that should be present
- difficult to treat
conditions resembling schizophrenia, with which it may be confused
- mood disorder with psychotic features
- substance abuse
- brain damage
- undetected hearing deficits
- Huntington’s disease
- Nutritional abnormalities
demographic factors related to schizophrenia
- 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
describe the evidence for a genetic contribution to schizophrenia
- 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
neurodevelopmental hypothesis
- 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
Supporting evidence for neurodevelopmental hypothesis
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
evidence for and against the dopamine hypothesis of schizophrenia
- 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
describe the evidence for the glutamate hypothesis of schizophrenia and the potential role for glycine and for metabotropic glutamate receptors in treating it
- 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
one undesired effect of antipsychotic drugs and the mechanisms of action of the newer drugs that minimize these effects
- 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
