Chapter Fifteen Alcoholism Mood Disorders and Schizophrenia Alcoholism

Chapter Fifteen Alcoholism, Mood Disorders, and Schizophrenia

Alcoholism n n 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 n 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 n 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 n 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 n n 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 n 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 n 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 n n n 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 of onset is early 20’s Genetics – Concordance rate is. 50 – No specific gene has been identified

Bipolar Disorder-Treatments n 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 n n Defined-depression that regularly recurs in a particular season Usually treated by bright light therapy

Schizophrenia n 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 n n n 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 schizophrenia. The closer the genetic relationship to someone with schizophrenia, the higher the probability of developing it oneself.

Hypotheses of Causation in Schizophrenia n Neurodevelopmental – Either genes or difficulties early in life impair brain development in ways that lead to schizophrenic-like symptoms in early adulthood n Dopamine Hypothesis-Excess dopamine activity causes behavioral changes associated with schizophrenia – Supported by drug treatments that target dopamine n 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 n Antipsychotic Drugs-All block postsynaptic dopamine receptors – Phenothiazines-chlorpromazine – Butyrophenones-haloperidol – Atypical Antipsychotics-clozapine (blocks D 4 receptors but – not D 2)