carlson 7e chapter 17 schizophrenia and the affective disorders l.
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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


symptoms of schizophrenia
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


heritability of schizophrenia
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


the dopamine hypothesis of schizophrenia
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


da activity in schizophrenia
DA Activity in Schizophrenia
  • 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)


dopamine augmentation schizophrenia
Dopamine Augmentation & Schizophrenia
  • 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
dopamine attenuation schizophrenia
Dopamine Attenuation & Schizophrenia
  • 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
antipsychotic medications
Antipsychotic Medications
  • 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)


brain damage and schizophrenia
Brain Damage and Schizophrenia
  • 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


causes of brain damage in schizophrenia
Causes of Brain Damage in Schizophrenia
  • 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


seasonality and schizophrenia
Seasonality and Schizophrenia
  • 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?)


hypofrontality and schizophrenia
Hypofrontality and Schizophrenia
  • 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


major affective disorders
Major Affective 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


biological bases of affective disorder
Biological Bases of Affective 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


monoamine hypothesis of depression
Monoamine Hypothesis of Depression
  • 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


rem sleep and depression
REM Sleep and Depression
  • 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)


seasonal affective disorder
Seasonal Affective Disorder
  • 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)