Carlson 7e chapter 17 schizophrenia and the affective disorders
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Carlson (7e) Chapter 17: Schizophrenia and the Affective Disorders. Schizophrenia. Schizophrenia represents a disorder of thought and emotion but not a “split-personality” Thought disorder (e.g., loose associations) Hallucinations (e.g., auditory) Delusions (e.g., paranoia)

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Carlson (7e)Chapter 17: Schizophrenia and the Affective Disorders

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  • Schizophrenia represents a disorder of thought and emotion but not a “split-personality”

    • Thought disorder (e.g., loose associations)

    • Hallucinations (e.g., auditory)

    • Delusions (e.g., paranoia)

    • Bizarre behaviors

  • The incidence of schizophrenia is about 1-2%

    • No clear gender differences in incidence


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Symptoms of Schizophrenia

  • Positive symptoms include delusions, hallucinations and thought disorder

    • Delusions are beliefs that are contrary to reality

      • Delusions can involve control, grandeur, or persecution

    • Hallucinations are perceptions that occur in the absence of stimuli (often auditory and/or olfactory)

    • Thought disorder: disorganized and irrational

  • Negative symptoms involve a loss of normal behaviors, such as

    • Poverty of speech and low initiative

    • Social withdrawal and diminished affect

    • Anhedonia


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Heritability of Schizophrenia

  • The heritability of schizophrenia is a strong indicator of a biological basis for schizophrenia

    • Adoption studies

      • Adult schizophrenics that were adopted as children are likely to have schizophrenic biological relatives.

    • Twin studies

      • Concordance rates for schizophrenia are higher for identical than for fraternal twins:

    • No single gene has been identified for schizophrenia

      • Genes may pass on a susceptibility to develop schizophrenia


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The Dopamine Hypothesis of Schizophrenia

  • The “dopamine hypothesis” is that the positive symptoms of schizophrenia involve over activity of brain dopaminergic synapses

    • Chlorpromazine (CPZ) was identified as an effective antipsychotic (AP) agent

      • CPZ was later found to block DA receptors (D2 receptors)

      • D2 receptor blockade correlates with clinically effective dose of typical antipsychotic medications

    • Stimulants such as amphetamine that release DA can produce the positive symptoms of schizophrenia in “normals” and relapse in schizophrenics


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DA Activity in Schizophrenia Disorders

  • PET studies indicate greater activity of dopamine in the striatum of schizophrenics to a test dose of amphetamine

    • Amount of dopamine activity was related to the increase in positive schizophrenia symptoms

  • Studies of dopamine receptors in schizophrenic brain have provided mixed results (but generally supportive)

    • Postmortem studies suggest increased numbers of D2 receptors in striatum (but may be due to exposure to antipsychotic drugs)

      • The striatum is a motor control region: may be the wrong site

      • Schizophrenia may be related to D4 or D3 receptors

    • Clozapine is an effective (atypical) antipsychotic drug that interacts with D4 and not D2 receptors

      • strong effect on mesolimbic/mesocortical dopamine system (A10)

      • little effect on nigrostriatal dopamine system (A9)


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Dopamine Augmentation & Schizophrenia Disorders

  • Psychomotor stimulants (e.g., amphetamine)

    • ‘normals’ develop paranoid psychosis

    • schizophrenics release -- subjectively indistinguishable for worsening of endogenous illness (cf. LSD)

  • L-DOPA (precursor loading)

    • little or no effect in ‘normals’

    • worsening of psychotic symptoms in schizophrenics

    • schizophrenic symptoms in some Parkinson’s patients

  • Stress (increased dopaminergic activity)

    • precipitate relapse & perhaps even initiate disorder

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Dopamine Attenuation & Schizophrenia Disorders

  • DA synthesis inhibitors (e.g., AMPT) abate schizophrenia

  • DA storage depleters (e.g., reserpine) abate schizophrenia

  • D2 receptor blockers (e.g., typical antipsychotics) abate schizophrenia

  • Even atypical antipsychotics (which do not effectively block D2 receptors) influence mesolimbic DA activity

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Antipsychotic Medications Disorders

  • Antipsychotic medications diminish the thought disorder & disruptive behavior evident in schizophrenia

  • Side effects of antipsychotic medications include

    • Major

      • Extrapyramidal (Parkinsonism-like) side effects due to blockade of DA receptors

      • Tardive dyskinesia: facial tics and gestures due to an over stimulation of DA receptors (may be related to CNS sensitization and relapse)

    • Minor

      • Autonomic problems (dry mouth)

      • Skin-eye pigmentation

      • Breast development (increased prolactin release after blockade of dopamine neurons)


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Brain Damage and DisordersSchizophrenia

  • The negative symptoms of schizophrenia may be related to brain damage

    • The neurological signs evident in schizophrenia include

      • Eye tracking problems

      • Catatonia

      • Problems with blinking, eye focusing, and visual pursuit

    • Schizophrenics exhibit enlarged brain ventricles, which suggests loss of brain cells

    • Regions of schizophrenic brain that are abnormal include

      • Prefrontal cortex

      • Medial temporal lobes

      • Medial diencephalon


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Causes of Brain Damage in Schizophrenia Disorders

  • The neurological symptoms of schizophrenia may be caused by

    • Birth trauma (obstetrical issues)

    • Viral infections that impair neural development during the second trimester

      • Seasonality effects (schizophrenia is more likely for winter births)

    • Nutritional issues (Hunger Winter: female offspring were more likely to exhibit schizophrenia than male offspring)

    • Maternal stress may compromise the immune system of the mother and lead to a greater chance of contracting a viral infection


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Seasonality and Schizophrenia Disorders

  • Children born during the late winter and early spring are more likely to develop schizophrenia

    • Seasonality effect occurs in cities but not the countryside

  • Seasonality effect may be related to the mother contracting a viral infection during the second trimester of fetal development (or astrological sign?)


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Hypofrontality and Schizophrenia Disorders

  • Hypofrontality refers to the decreased activity of the dorsolateral prefrontal cortex

    • Damage to the prefrontal cortex

      • impairs behavioral flexibility (card sorting task)

      • may disinhibit mesolimbic dopamine system

    • Schizophrenics show decreased activity in the prefrontal cortex

  • Abuse of PCP produces positive and negative symptoms of schizophrenia

    • Positive: related to indirect actions of PCP on accumbens DA

    • Negative: related to decreased DA utilization in prefrontal cortex following PCP treatment

    • Data are less compelling that dopamine-agonist effect


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Major Affective Disorders Disorders

  • Affect refers to emotions, moods, and feelings

    • Our affect is usually a reflection of our experiences

    • In the major affective disorders, our emotional reactions are at the extremes and may not be related to our actual experiences

  • The major affective disorders include

    • Bipolar disorder - alternating cycles of

      • Mania: euphoria, delusions

      • Depression: profound sadness, guilt, suicide risk

    • Unipolar depression: continuous, episodic


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Biological Bases of DisordersAffective Disorder

  • Heritability of affective disorder (AD) has been established in twin studies and family studies

    • Bipolar disorder may be related to a single gene

  • Depression is amenable to physical treatments including

    • Pharmacological treatments

      • MAO inhibitors (e.g. iproniazid)

      • Noradrenergic reuptake inhibitors (desmethylimipramine)

      • Serotonin reuptake inhibitors (e.g. Prozac)

    • Electroconvulsive shock therapy (ECS)

    • Sleep deprivation


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Monoamine Hypothesis of Depression Disorders

  • Depression results from reduced activity of brain monoamines

    • Reserpine depletes monoamines--> depression

    • Suicidal depression is related to a low level of 5-HIAA

    • Antidepressant medications increase either NE or 5-HT

      • Usually via blockade of monoamine reuptake

    • Tryptophan deletion procedure:

      • Reduces brain 5-HT levels

      • Reinstates depression in former depressed patients


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REM Sleep and Depression Disorders

  • Sleep pattern is disrupted in depressed persons

    • Reduced REM latency, reduced stages 3 and 4 sleep

  • REM deprivation improves mood

  • Antidepressant drugs suppress REM sleep, and increase slow-wave sleep

  • Persons who have short REM sleep latency are more likely to develop depression

  • REM sleep deprivation is more effective than is total sleep deprivation (effects last longer)


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Seasonal Affective Disorder Disorders

  • SAD is a form of depression evident in winter months (short days/long nights)

  • SAD involves

    • Mood and sleep disturbances

    • Carbohydrate cravings and weight gain

  • Phototherapy for SAD: increased exposure to light improves mood in SAD (and also for unipolar depression)