Chapter FifteenAlcoholism, 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 alcoholismSons 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 DisorderDefined-long-term sadness and helplessnessEtiology

Observed more often in women than menPeak frequency between 25 and 44About 19% of all people suffer a bout of depression at least

once in their livesGenetics

Depression does have a genetic linkGene has not been located

Depression

Triggering Depressive Episodesdepression is episodicCan be triggered by an event (ex: death of a loved one, birth of a

child, etc)Potential Physiological Mechanisms

Abnormalities of Hemispheric DominanceDepressed people have more activity in the right prefrontal cortex

than the left prefrontal cortexDepression more commonly follows left-hemisphere damage

VirusesBorna virus is found more commonly in depressed populations

than in non-depressed populations

Depression

TreatmentsAntidepressants

Tricyclics-prevent reuptake of serotonin or norepinephrine/epinephrine

MAO Inhibitors-block MAO from breaking down serotonin and norepinephrine/epinephrine

SSRI’s-block reuptake of serotoninAtypical antidepressants-miscellaneous groupECT

Applied every other day for two weeksMuscle relaxants and anesthetics minimize discomfortMemory loss can be a side-effect (limited if shock is

given to right hemisphere onlyAltered Sleep Patterns

Treat patient like someone with difficulty adjusting to changing time zones

Figure 15.7  Routes of action of antidepressantsTricyclics 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 depressionEtiology

May last only days or for a year or more1% of people have a mild case at some time in lifeAverage age of onset is early 20’s

GeneticsConcordance rate is .50No 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 schizophreniaThe closer the genetic relationship to someone with schizophrenia, the higher

the probability of developing it oneself.

Hypotheses of Causation in Schizophrenia

NeurodevelopmentalEither genes or difficulties early in life impair brain development in

ways that lead to schizophrenic-like symptoms in early adulthoodDopamine Hypothesis-Excess dopamine activity causes behavioral

changes associated with schizophreniaSupported by drug treatments that target dopamine

Glutamate Hypothesis-the problem is deficient glutamate activityPhencyclidine-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)