Abnormal Psychology,
Thirteenth Edition
by
Ann M. Kring,
Sheri L. Johnson,
Gerald C. Davison,
& John M. Neale
© 2015 John Wiley & Sons, Inc. All rights reserved.
 Chapter
9: Schizophrenia
I. Clinical
Descriptions of Schizophrenia
II. Etiology of Schizophrenia
III. Treatment of Schizophrenia
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 Major
disturbances in thought, emotion, and
behavior
• Disordered thinking
 Ideas not logically related
 Faulty perception and attention
• Lack of emotional expressiveness
 Inappropriate or flat emotions
• Disturbances in movement or behavior
 Disheveled appearance
 Can
disrupt interpersonal relationships, diminish
capacity to work or live independently
 Significantly increased rates of suicide and death
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 Lifetime
prevalence ~1%
 Affects men slightly more often than
women
 Onset typically late adolescence or early
adulthood
• Men diagnosed at a slightly earlier age
 Diagnosed
Americans
more frequently in African
• May reflect diagnostic bias
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
Two or more of the following symptoms for at least 1
month; one symptom should be either 1, 2, or 3:
•
•
•
•
•
(1) delusions
(2) hallucinations
(3) disorganized speech
(4) disorganized (catatonic) behavior
(5) negative symptoms (diminished motivation or emotional
expression)
Functioning in work, relationships, or self-care has
declined since onset
 Signs of disorder for at least 6 months; if during a
prodromal or residual phase, negative symptoms or
two or more of symptoms 1-4 in less severe form

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 Three
major clusters of symptoms:
• Positive
• Negative
• Disorganized
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
Delusions

Hallucinations
• Sensory experiences in the
• Firmly held beliefs
• Contrary to reality
• Resistant to disconfirming
absence of sensory
stimulation
evidence

Types of delusions:
• Persecutory delusions
 “The CIA planted a listening
device in my head”
 65% have these
•
•
•
•
•
Thought insertion
Thought broadcasting
Outside control
Grandiose delusions
Ideas of reference

Types of hallucinations:
• Auditory
 74% have this symptom
• Visual
• Hearing voices
 Increased levels of activity in
Broca’s area during hallucinations
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
Avolition
• Lack of interest; apathy

Asociality
• Inability to form close personal
 Can
be grouped into
2 domains:
• Experience domain
 Motivation
 Emotional experience
 Sociality
relationships

Anhendonia
• Inability to experience
pleasure
 Consummatory pleasure
 Anticipatory pleasure

• Expression domain
Blunted affect
• Exhibits little or no affect in
face or voice

Alogia
• Reduction in speech
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 Outward expression of
emotion
 Vocalization
 Disorganized
speech (formal thought disorder)
• Incoherence
 Inability to organize ideas
• Loose associations (derailment)
 Rambles, difficulty sticking to one topic
 Disorganized
behavior
• Odd or peculiar behavior
 Silliness, agitation, unusual dress
 e.g., wearing several heavy coats in hot weather
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 Catatonia
• Motor abnormalities
• Repetitive, complex gestures
 Usually of the fingers or hands
• Excitable, wild flailing of limbs
 Catatonic
immobility
• Maintain unusual posture for long periods of
time
 e.g., stand on one leg
 Waxy
flexibility
• Limbs can be manipulated and posed by
another person
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
Schizophreniform Disorder
• Same symptoms as schizophrenia
• Symptom duration greater than 1 month but less than 6 months
• Symptoms must include either hallucinations, delusions, or
disorganized speech

Brief Psychotic Disorder
• Symptom duration of 1 day to 1 month
• Often triggered by extreme stress, such as bereavement
• Symptoms must include either hallucinations, delusions, or disorganized
speech
 Schizoaffective Disorder
• Symptoms of both schizophrenia and either a depressive or manic
episode
• Symptoms of a major mood episode are present for a majority of the duration
the illness
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 Delusional
Disorder
• Delusions may include:
 Persecution
 Jealousy
 Being followed
 Erotomania
 Loved by a famous person
 Somatic delusions
• No other symptoms of schizophrenia
© 2015 John Wiley & Sons, Inc. All rights reserved.
© 2015 John Wiley & Sons, Inc. All rights reserved.
© 2015 John Wiley & Sons, Inc. All rights reserved.

Genetically heterogeneous
• Not likely that disorder caused by single gene

Family studies
• Relatives at increased risk
• Negative symptoms have stronger genetic component

Twin studies
• 44% risk for MZ twins vs. 12% risk for DZ twins
• Children of non-schizophrenic MZ twin were more likely to
develop schizophrenia (9.4% vs. 1% in general population)

Adoption studies
• Increased likelihood of developing psychotic disorders

Familial high-risk studies
• Differing negative vs. positive symptomatology
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 Association
studies
• Two genes associated with schizophrenia
 DTNGP1
 NGR1
• Two genes associated with cognitive deficits
 COMT
 BDNF
 Genome-wide
scans
• Identification of gene mutations
• Several identified but results need to be replicated
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 Dopamine Theory
• Disorder due to excess levels of dopamine
 Drugs that alleviate symptoms reduce dopamine activity
 Amphetamines, which increase dopamine levels, can induce a
psychosis
 Theory
revised
• Excess numbers of dopamine receptors or
oversensitive dopamine receptors
• Localized mainly in the mesolimbic pathway
 Mesolimbic dopamine abnormalities mainly related to positive
symptoms
• Underactive dopamine activity in the mesocortical
pathway mainly related to negative symptoms
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© 2015 John Wiley & Sons, Inc. All rights reserved.
© 2015 John Wiley & Sons, Inc. All rights reserved.
 Dopamine
theory doesn’t completely explain
disorder
• Antipsychotics block dopamine rapidly but symptom
relief takes several weeks
• To be effective, antipsychotics must reduce dopamine
activity to below normal levels
 Other
neurotransmitters involved:
• Serotonin
• GABA
• Glutamate
 Medication that targets glutamate shows promise
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 Enlarged
ventricles
• Implies loss of brain cells
• Correlate with
 Poor performance on cognitive tests
 Poor premorbid adjustment
 Poor response to treatment
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 Prefrontal Cortex
• Many behaviors disrupted by schizophrenia (e.g.,
speech, decision making) are governed by prefrontal
cortex
• Individuals with schizophrenia show impairments
on neuropsychological tests of prefrontal cortex
(e.g., memory)
• Individuals with schizophrenia show low metabolic
rates in prefrontal cortex
 Failure to show frontal activaty related to negative
symptoms
• Disrupted communication among neurons due to
loss of dendritic spines
 Disconnection Syndrome
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© 2015 John Wiley & Sons, Inc. All rights reserved.
 Structural
and functional abnormalities in
temporal cortex
•
•
•
•
Temporal gyrus
Hippocampus
Amygdala
Anterior cingulate
 Reduced gray matter and volume
• Disrupted connectivity in the brain
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evident
 Environmental Factors
• Damage during gestation or birth
 Obstetrical complications rates high in patients with
schizophrenia
 Reduced supply of oxygen during delivery may result in loss of
cortical matter
• Viral damage to fetal brain
 Presence of parasite, toxoplasma gondii, associated with
2.5x greater risk of developing schizophrenia
 In Finnish study, schizophrenia rates higher when mother
had flu in second trimester of pregnancy
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 Developmental
factors
• Prefrontal cortex matures in adolescence or early
adulthood
• Dopamine activity also peaks in adolescence
• Stress activates HPA system, which triggers cortisol
secretion
 Cortisol increases dopamine activity
• Excessive pruning of synaptic connections
• Use of cannabis during adolescence associated with
increased risk
 May
explain why symptoms appear in late
adolescence but brain damage occurs early in life
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 Reaction
to stress
• Individuals with schizophrenia and their first-degree
relatives more reactive to stress
 Greater decreases in positive mood and increases in negative
mood
 Socioeconomic
status
• Highest rates of schizophrenia among urban poor
 Sociogenic hypothesis
 Stress of poverty causes disorder
 Social selection theory
 Downward drift in socioeconomic status
• Research supports social selection
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 Schizophrenogenic mother
• Cold, domineering, conflict-inducing
• No support for this theory
 Communication deviance (CD)
• Hostility and poor communication
• Inconclusive at this time
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 Family
environment impacts relapse
 Expressed Emotion (EE)
• Hostility, critical comments, emotional overinvolvement
 Bidirectional
association
• Unusual patient thoughts → increased critical comments
• Increased critical comments → unusual patient thoughts
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 Use
of retrospective or “follow-back” studies
 Developmental histories of children who
later developed schizophrenia
• Lower IQ
• More often delinquent (boys) and withdrawn (girls)
 Coding
of home movies
• Poorer motor skills
• More expression of negative emotion
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 New
Zealand study
• Cognitive deficits evident at early age
 Australian
study
• Reduced gray matter volume predicted later development of
psychotic disorder
 North
American Prodrome Longitudinal Study
• Identified factors associated with development of psychosis
 Having a biological relative with schizophrenia
 Recent decline in functioning
 High levels of pos
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 First-generation
antipsychotic medications
(neuroleptics; 1950s)
• Phenothiazines (Thorazine), butyrophenones
(Haldol), thioxanthenes (Navane)
 Reduce agitation, violent behavior
 Block dopamine receptors
 Little effect on negative symptoms
 Extrapyramidal side effects
• Tardive dyskinesia
• Neuroleptic malignant syndrome
 Maintenance dosages to prevent
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relapse
 Second-generation antipsychotics
• Clozapine (Clozaril)
 Impacts serotonin receptors
• Fewer motor side effects
• Less treatment noncompliance
• Reduces relapse
 Side effects
• Can impair immune symptom functioning
• Seizures, dizziness, fatigue, drooling, weight gain
 Newer medications may improve cognitive
function:
• Olanzapine (Zyprexa)
• Risperidone (Risperdal)
© 2015 John Wiley & Sons, Inc. All rights reserved.
© 2015 John Wiley & Sons, Inc. All rights reserved.
 Clinical
Antipsychotic Trials of Intervention
Effectiveness (CATIE) study
• Second-generation drugs were not more effective
than the older, first-generation drug
• Second-generation drugs did not produce fewer
unpleasant side effects
• Nearly three-quarters stopped taking the
medications before study ended
 Second-generation
antipsychotics have
serious side effects
• Weight gain, diabetes, pancreatitis
 Disturbing trend for people of color:
• Not prescribed second-generation antipsychotics
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 Patient
Outcomes Research Team (PORT)
treatment recommendation:
• Medication PLUS psychosocial intervention
 Social
skills training
• Teach skills for managing interpersonal situations
 Completing a job application
 Reading bus schedules
 Make appointments
• Involves role-playing and other practice exercises,
both in group and in vivo
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 Family
therapy to reduce expressed emotion
• Educate family about causes, symptoms, and signs of
•
•
•
•
•
relapse
Stress importance of medication
Help family to avoid blaming patient
Improve family communication and problem-solving
Encourage expanded support networks
Instill hope
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 Cognitive
behavioral therapy
• Recognize and challenge delusional beliefs
• Recognize and challenge expectations associated with
negative symptoms
 e.g., “Nothing will make me feel better so why bother?”
 Cognitive
remediation training or cognitive
enhancement therapy (CET)
• Improve attention, memory, problem solving and other
cognitive-based symptoms
 Case management
• Multidisciplinary team to provide comprehensive services
 Residential treatment
• Vocational rehabilitation
© 2015 John Wiley & Sons, Inc. All rights reserved.
Copyright 2015 by John Wiley & Sons, Inc. All
rights reserved. No part of the material protected
by this copyright may be reproduced or utilized in
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