Download 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
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- Treatment

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
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

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
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
Genetics
– Concordance rate is 50%
– However, genes are not the only influence
– A gene has not been located for schizophrenia
Probabilities of
developing
schizophreniaThe 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)