Abnormal Psychology in a
Changing World
SEVENTH EDITION
Jeffrey S. Nevid / Spencer A. Rathus / Beverly Greene
Chapter 12
(Pp 410-422)
Schizophrenia and
Other Psychotic
Disorders
Theoretical Perspectives
Psychodynamic Perspectives
Within the psychodynamic perspective, schizophrenia
represents the overwhelming of the ego by primitive sexual or
aggressive drives or impulses arising from the id.
These impulses threaten the ego and give rise to intense
intrapsychic conflict.
Under such a threat, the person regresses to an early period in
the oral stage, referred to as primary narcissism.
Learning Perspectives
Although learning theory does not offer a complete
explanation of schizophrenia, the development of some forms
of schizophrenic behavior can be understood in terms of the
principles of conditioning and observational learning.
From this perspective, people with schizophrenia learn to
exhibit certain bizarre behaviors when these are more likely
to be reinforced than normal behaviors.
Social-cognitive theorists suggest that modeling of
schizophrenic behavior can occur within the mental hospital,
where patients may begin to model themselves after fellow
patients who act strangely
Biological Perspectives
Although we still have much to learn about the
biological underpinnings of schizophrenia, most
investigators today recognize that biological
factors play a determining role through:
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Genetic Factors
Biochemical Factors
Viral Infections
Brain Abnormalities
TRUTH or FICTION
If you have two parents with schizophrenia,
it’s nearly certain that you will develop
schizophrenia yourself
Genetic Factors
The closer the genetic relationship between schizophrenia
patients and their family members, the greater the likelihood
(or concordance rate) that the relatives will also have
schizophrenia.
Overall, first-degree relatives of people with schizophrenia
(parents, children, or siblings) have about a tenfold greater
risk of developing schizophrenia than do members of the
general population.
The fact that families share common environments as well as
common genes requires that we dig deeper to examine the
genetic underpinnings of schizophrenia.
The familial risk of schizophrenia.
Generally speaking, the
more closely one is
related to people who
have developed
schizophrenia, the greater
the risk of developing
schizophrenia for oneself.
Monozygotic (MZ)
twins, whose genetic
heritages are identical,
are much more likely than
dizygotic (DZ) twins,
whose genes overlap by
50%, to be concordant for
schizophrenia.
Biochemical Factors
Contemporary biological investigations of schizophrenia have
focused on the role of the neurotransmitter dopamine.
The leading biochemical model of schizophrenia, the
dopamine hypothesis, posits that schizophrenia involves
an overreactivity of dopamine transmission in the brain.
Increasing evidence supports the view that schizophrenia
involves an irregularity in dopamine transmission in the brain
The imbalance seems to be related to D2 neurons in the
frontal lobe of the brain.
Biochemical factors seem to explain Type I or positive
symptoms of schizophrenia.
TRUTH or FICTION
Although schizophrenia is widely believed to
be a brain disease, evidence of
abnormalities in the brains of
schizophrenia patients remains lacking
Brain Abnormalities
We have compelling evidence of both structural changes (loss
of brain tissue) and functional disturbance (abnormalities of
functioning) in the brains of schizophrenia patients.
However, we have yet to discover any one source of pathology
in the brain that is specific to schizophrenia or present in all
cases of schizophrenia.
The most prominent finding of structural changes is the loss
of brain tissue (gray matter) of about 5% on the average in
schizophrenia patients as compared to normal controls.
These brain abnormalities are responsible for Type II
(negative) symptoms of schizophrenia.
Loss of brain tissue in adolescents with
early-onset schizophrenia
The brains of adolescents with early-onset schizophrenia (right image)
show a substantial loss of gray matter. Some shrinkage of gray matter
occurs normally during adolescence (left image), but the loss is more
pronounced in adolescents with schizophrenia.
Structural changes in the brain of a person with
schizophrenia as compared with that of a
normal subject
The magnetic resonance imaging (MRI) of the brain of a person with
schizophrenia (left) shows a relatively shrunken hippocampus (yellow)
and relatively enlarged, fluid-filled ventricles (white) when compared to
the structures of the normal subject (right).
PET scans of people with schizophrenia
versus normal's
Positron emission tomography (PET) scan evidence of the metabolic
processes of the brain shows relatively less metabolic activity (indicated
by less yellow and red) in the frontal lobes of the brains of people with
schizophrenia. PET scans of the brains of four normal people are shown
in the top row, and PET scans of the brains of four people with
schizophrenia are shown below.
Family Theories
An early, but since discredited theory, focused on the role of
the schizophrenogenic mother (Fromm-Reichmann, 1948,
1950).
In what some feminists view as historic psychiatric sexism,
the schizophrenogenic mother was described as cold,
aloof, overprotective, and domineering.
She was characterized as stripping her children of selfesteem, stifling their independence, and forcing them into
dependency on her.
Children reared by such mothers were believed to be at
special risk for developing schizophrenia if their fathers were
passive and failed to counteract the mother’s pathogenic
influences.
Today, investigators interested in family influences have
turned to consider the effects of:
• deviant patterns of communication within the family,
and
• intrusive, negative comments directed toward the
schizophrenic family member
Communication Deviance (CD)
A pattern of unclear, vague, disruptive, or fragmented
communication that is often found among parents and family
members of schizophrenia patients.
CD is speech that is hard to follow and from which it is
difficult to extract any shared meaning.
High CD parents often have difficulty focusing on what their
children are saying.
Expressed Emotion (EE)
Another form of disturbed family communication, EE is a
pattern of responding to the schizophrenic family member in
hostile, critical, and unsupportive ways.
Schizophrenia patients from high EE families stand a higher
risk of relapsing than those with low EE (more supportive)
families.
High EE relatives typically show less empathy, tolerance, and
flexibility than low EE relatives.
Relapse rates of people with
schizophrenia in high and low EE families
People with schizophrenia whose families are high in expressed emotion
(EE) are at greater risk of relapse than those whose families are low in
EE. Whereas low-EE families may help protect the family member with
schizophrenia from environmental stressors, high-EE families may
impose additional stress.
Family Factors in Schizophrenia:
Causes or Sources of Stress?
No evidence supports the belief that family factors, such as
negative family interactions, lead to schizophrenia in children
who do not have a genetic vulnerability.
Rather, a genetic vulnerability to schizophrenia renders
individuals more susceptible to troubled family and social
relationships.
Within the diathesis–stress model, disturbed patterns of
family interaction and communication represent sources of
life stress that increase the risks of developing schizophrenia
among people with a genetic predisposition for the disorder
The Diathesis–Stress Model
Note that the question of whether stress directly triggers the initial
onset of schizophrenia in genetically vulnerable individuals is still
open to debate (Walker & Diforio, 1997)
Endophenotypes?
To better understand how schizophrenia develops, we need to
dig under the surface to see how genes affect underlying
processes, and how these processes in turn contribute to the
development of the disorder.
Investigators are studying a number of possible
endophenotypes in schizophrenia- measurable processes
or mechanisms not apparent to the naked eye, which are the
means by which an organism’s genetic code comes to affect its
observable characteristics or phenotypes.
These phenotypes include disturbances in brain circuitry,
deficits in working memory and cognitive abilities, and
abnormalities of neurotransmitter functioning.
From genes to vulnerability
The End