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Abnormal Psychology, Twelfth Edition
by
Ann M. Kring,
Sheri L. Johnson,
Gerald C. Davison,
& John M. Neale
Copyright © 2012 John Wiley & Sons, Inc. All rights reserved.
Chapter
9: Schizophrenia
I. Clinical
Descriptions of Schizophrenia
II. Etiology of Schizophrenia
III. Treatment of Schizophrenia
© 2012 John Wiley & Sons, Inc. All rights reserved.
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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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
© 2012 John Wiley & Sons, Inc. All rights reserved.
Two or more symptoms lasting for at least 1 month;
one symptom should be 1, 2, or 3:
1)
2)
3)
4)
5)
Delusions
Hallucinations
Disorganized speech
Abnormal psychomotor behavior (catatonia)
Negative symptoms (blunted affect, avolition, asociality)
Functioning in work, relationships, or self-care have
declined since onset
Signs of disorder for at least 6 months; at least 1
month of the symptoms above; or, 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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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
© 2012 John Wiley & Sons, Inc. All rights reserved.
© 2012 John Wiley & Sons, Inc. All rights reserved.
Schizophreniform
Disorder
• Same symptoms as schizophrenia
• Symptom duration greater than 1 month but less than 6
months
Brief
Psychotic Disorder
• Symptom duration of 1 day to 1 month
• Often triggered by extreme stress, such as bereavement
Schizoaffective
Disorder
• Symptoms of both schizophrenia and mood disorder
DSM-5 likely to require appearance of major depressive or
manic episode
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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
Attenuated
Psychosis Syndrome
• Possible new category in DSM-5
© 2012 John Wiley & Sons, Inc. All rights reserved.
© 2012 John Wiley & Sons, Inc. All rights reserved.
© 2012 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
© 2012 John Wiley & Sons, Inc. All rights reserved.
© 2012 John Wiley & Sons, Inc. All rights reserved.
© 2012 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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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 activated related to negative
symptoms
• Disrupted communication among neurons due to
loss of dendritic spines
Disconnection Syndrome
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© 2012 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 evident
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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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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)
© 2012 John Wiley & Sons, Inc. All rights reserved.
© 2012 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
© 2012 John Wiley & Sons, Inc. All rights reserved.
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
© 2012 John Wiley & Sons, Inc. All rights reserved.
Copyright 2012 by John Wiley & Sons, Inc. All
rights reserved. No part of the material protected
by this copyright may be reproduced or utilized in
any form or by any means, electronic or
mechanical, including photocopying, recording
or by any information storage and retrieval
system, without written permission of the
copyright owner.
© 2012 John Wiley & Sons, Inc. All rights reserved.