Transcript Mood Disorders and Schizophrenia

Chapter Fifteen
Alcoholism, Mood Disorders, and Schizophrenia
Alcoholism
Defined-cannot stop drinking or control the amount you consume
Genetics
Two Types of Alcoholism
Type 1
Type II
Less genetic
Stronger genetic basis
Develops gradually
Rapid, early onset
Affects men and women equally
Overwhelmingly men
Concordance rates in twins is .55
Figure 15.3 Design for studies of predisposition to alcoholism
Sons of alcoholic fathers are compared to other young men of the same age and
same current drinking habits. Any behavior that is more common in the first group
is presumably a predictor of later alcoholism.
Alcohol Metabolism and Antabuse
Antabuse
Drug used to treat alcoholism
Mechanism-stops metabolism of alcohol
Results in nausea, headache and stomach pain when alcohol
is consumed
Only moderately effective
Risk Factors for Alcohol Abuse
Sons of alcoholics report low intoxication after drinking
Sons of alcoholics are more likely to report stress relief from
drinking
Depression
Major Depressive Disorder
Defined-long-term sadness and helplessness
Etiology
Observed more often in women than men
Peak frequency between 25 and 44
About 19% of all people suffer a bout of depression at least
once in their lives
Genetics
Depression does have a genetic link
Gene has not been located
Depression
Triggering Depressive Episodes
depression is episodic
Can be triggered by an event (ex: death of a loved one, birth of a
child, etc)
Potential Physiological Mechanisms
Abnormalities of Hemispheric Dominance
Depressed people have more activity in the right prefrontal cortex
than the left prefrontal cortex
Depression more commonly follows left-hemisphere damage
Viruses
Borna virus is found more commonly in depressed populations
than in non-depressed populations
Depression
Treatments
Antidepressants
Tricyclics-prevent reuptake of serotonin or
norepinephrine/epinephrine
MAO Inhibitors-block MAO from breaking down serotonin
and norepinephrine/epinephrine
SSRI’s-block reuptake of serotonin
Atypical antidepressants-miscellaneous group
ECT
Applied every other day for two weeks
Muscle relaxants and anesthetics minimize discomfort
Memory loss can be a side-effect (limited if shock is
given to right hemisphere only
Altered Sleep Patterns
Treat patient like someone with difficulty adjusting to
changing time zones
Figure 15.7 Routes of action of antidepressants
Tricyclics block the reuptake of dopamine, norepinephrine, or serotonin. SSRIs
specifically block the reuptake of serotonin. MAOIs block the enzyme MAO,
which converts dopamine, norepinephrine, or serotonin into inactive chemicals.
Atypical antidepressants have varying effects.
Depression
Physiology of Depression
Two Conclusions
Mood depends on the effects of a combination of
transmitters
Different depressed people have somewhat different
transmitter abnormalities
Video
Bipolar Disorder
Defined-alternate between mania and depression
Etiology
May last only days or for a year or more
1% of people have a mild case at some time in life
Average age of onset is early 20’s
Genetics
Concordance rate is .50
No specific gene has been identified
Bipolar Disorder
Treatments
Lithium
Stabilizes mood
Mechanism unknown but likely involves second messenger
systems
Anticonvulsant drugs
Mechanism of action is on second messenger systems
Seasonal Affective Disorder
Defined-depression that regularly recurs in a particular season
Usually treated by bright light therapy
Schizophrenia
Characteristics
Deteriorating ability to function
Accompanied by delusions, hallucinations, thought disorder,
movement disorder and inappropriate emotional expression
Behavioral Symptoms
Positive Symptoms-behavior that are present that should
be absent
Delusions, hallucinations, thought disorders
Negative Symptoms-behavior that is absent that should be
present
Weak social interactions, emotional expression,
speech, and working memory
Schizophrenia
Characteristics Cont’d
Acute-sudden onset with good prospects for recovery
Chronic-gradual onset and a long-term course of treatment and
resistance
Schizophrenia
Etiology
About 1.3% of people will suffer from schizophrenia at some
point in their lives
More common in developed countries
Equal occurrence for men and women
Onset is usually in the 20’s
Schizophrenia
Genetics
Concordance rate is 50%
However, genes are not the only influence
A gene has not been located for schizophrenia
Figure 15.15 Probabilities of developing schizophrenia
The closer the genetic relationship to someone with schizophrenia, the higher
the probability of developing it oneself.
Hypotheses of Causation in Schizophrenia
Neurodevelopmental
Either genes or difficulties early in life impair brain development in
ways that lead to schizophrenic-like symptoms in early adulthood
Dopamine Hypothesis-Excess dopamine activity causes behavioral
changes associated with schizophrenia
Supported by drug treatments that target dopamine
Glutamate Hypothesis-the problem is deficient glutamate activity
Phencyclidine-Inhibits glutamate type NMDA receptors and produces
both positive and negative symptoms of schizophrenia
Schizophrenia Treatment
Antipsychotic Drugs-All block postsynaptic dopamine receptors
Phenothiazines-chlorpromazine
Butyrophenones-haloperidol
Atypical Antipsychotics-clozapine (blocks D4 receptors but
not D2)