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 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)