Schizophrenia Symptoms, Causes & Treatment

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

 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

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 more frequently in African
Americans
• May reflect diagnostic bias

 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

Three major clusters of symptoms:
• Positive
• Negative
• Disorganized

 Delusions
• Firmly held beliefs
• Contrary to reality
• Resistant to disconfirming
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
 Hallucinations
• Sensory experiences in the
absence of sensory
stimulation
 Types of hallucinations:
• Auditory
 74% have this symptom
• Visual
• Hearing voices
 Increased levels of activity in
Broca’s area during hallucinations

 Avolition
• Lack of interest; apathy
 Asociality
• Inability to form close personal
relationships
 Anhendonia
• Inability to experience pleasure
 Consummatory pleasure
 Anticipatory pleasure
 Blunted affect
• Exhibits little or no affect in face
or voice
 Alogia
• Reduction in speech
 Can be grouped into
2 domains:
• Experience domain
 Motivation
 Emotional experience
 Sociality
• Expression domain
 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

 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

 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

Delusional Disorder
• Delusions may include:
 Persecution
 Jealousy
 Being followed
 Erotomania
 Loved by a famous person
 Somatic delusions
• No other symptoms of schizophrenia

 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

 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

 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

 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

 Enlarged ventricles
• Implies loss of brain cells
• Correlate with
 Poor performance on cognitive tests
 Poor premorbid adjustment
 Poor response to treatment

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

Structural and functional abnormalities in
temporal cortex
• Temporal gyrus
• Hippocampus
• Amygdala
• Anterior cingulate
Reduced gray matter and volume evident
• Disrupted connectivity in the brain

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

 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

 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

Schizophrenogenic mother
• Cold, domineering, conflict-inducing
• No support for this theory
Communication deviance (CD)
• Hostility and poor communication
• Inconclusive at this time

 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

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

 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

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 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)

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

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

 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

 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

Copyright 2015 by John Wiley & Sons, Inc. All
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by this copyright may be reproduced or utilized in
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