Lecture 13
Schizophrenia: Etiology
Psychosocial Factors
Lecture Outline
I. Introduction
II. Vulnerability
A. Developmental Dysfunction
B. Social Factors
C. Summary
III.Psychosocial Stress Factors
A. Communication
1. Double Binds
2. General Communication Patterns
B. Expressed Emotion
IV. Conclusion
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I. Introduction
In today's lecture we will look at some of the psychosocial factors
that play important roles in the onset, course and treatment of
schizophrenia. Most researchers today see these factors as part of an
overarching diathesis-stress model - that is, there is an interaction
between genetic/biological predispositions and environmental stresses.
Today, we will focus on those psychological factors that have been
identified as important in the development of schizophrenia.
II. Vulnerability
To identify psycho-social vulnerability factors (ie: personal
attributes of the person and social/environmental conditions which
predispose the person to schizophrenia), it is necessary to examine the
person and his/her environment prior to the development of the disorder.
Typically, identification of such "high-risk" people is accomplished by
finding children with one or more schizophrenic blood relatives (usually
a parent). It is hypothesized that such individuals are at higher risk
than those without disturbed relatives (Goldstein, 1987). There is
evidence that indicates this is in fact the case (eg: Erlenmeyer-
Kimling, 1968):
Lifetime risk of developing Schizophrenia
Both parents normal: 1-2%
One parent Schizophrenic: 12%
Both parents Schizophrenic: 35-46%
(As we shall see next lecture, there is evidence of a genetic component
as well).
The lives of these high-risk children are then followed, and those
that go on to develop schizophrenia are compared to those who do not and
to those children who are not at risk.
Problems: Around 90% of schizophrenic persons do not have a
schizophrenic parent (Goldstein, 1987). In addition, only about 10 -
16% of the high risk children develop schizophrenia (Goldstein, 1987).
And finally, high risk children do not necessarily develop
schizophrenia, many children develop other types of psychological
disorders instead (Goldstein, 1987).
Questions (unanswered to date): To what extent can we actually
generalize from high risk studies to schizophrenia in general? To what
extent have we identified people at risk for schizophrenia as opposed to
people merely at risk for psychopathology in general? More research is
necessary before we can answer these questions.
A. Developmental Dysfunction
A number of cognitive and behavioral abnormalities have been
identified in children who later develop schizophrenia (Goldstein,
1987, for a review). These include:
-periods of disorganized or delayed motor, visual, physical
development
-impaired balance, motor coordination, perception, attention
-passive, unenergetic, short attention span
-cognitive impairment on complex tasks
These abnormalities, however, are not consistently found across
studies. Results are often contradictory. Currently, these
findings are suggestive at best.
B. Social Factors
Perhaps one of the most consistent social factors associated
with later onset of schizophrenia is marked social withdrawal and
generally poor interpersonal relationships (Goldstein, 1987,
Parnas, Schulsinger, Schulsinger, et al., 1982). These social
difficulties become particularly noticeable during later childhood
and adolescence.
Problem: Such social problems are seen with children who
develop other psychological disorders as well.
C. Summary
Only a subset of schizophrenic adults manifest these early
signs during their childhoods. Those children who do, however, may
be at the greatest risk for schizophrenia. Nevertheless, the
nonspecificity of these vulnerability factors (ie: schizophrenic
persons are not the only ones to experience them) makes it
impossible to use these factors to reliably identify those children
who are "at risk", at least at our present level of knowledge.
III. Psychosocial Stress Factors
The difficulties associated with identifying high risk individuals
and interpreting the findings of the vulnerability research apply here
as well. Thus, we should approach the following findings as suggestive:
as hypotheses regarding possible "provoking" or stress factors.
The family environment as a source of chronic stress has been
hypothesized to be a critical provoking factor in schizophrenic
disorders.
A. Communication
During the 1950's there was a growing interest in the role
disturbed family interactions might play in the development of
schizophrenia in a family member. Of particular interest were
disturbed patterns of communication.
1. Double binds: Bateson and his colleagues (eg: Bateson,
Jackson, Haley & Weakland, 1956) identified a particularly
insidious communication pattern that they hypothesized could
play a causal role in schizophrenia. They first noted that
communication occurs on multiple levels: verbal, facial, voice
tone, posture. In the double bind situation, a parent gives
the child simultaneous messages on more than one level which
contradict each other: he/she says one thing but acts
differently. For example:
A schizophrenic patient, glad to see his mother
"impulsively put his arm around her shoulders, whereupon
she stiffened. He withdrew his arm and she asked, "Don't
you love me anymore?" He blushed, and she said, "Dear,
you must not be so easily embarrassed and afraid of your
feelings." (Bateson, et al., 1956, p.251).
No matter what the child does, he/she loses. This "crazy"
type of communication, Bateson hypothesized, leads to "crazy"
behavior and thought processes.
Once a very popular theory of schizophrenia, there has not
been a lot of empirical support for the double bind
hypothesis. In addition, it has been difficult to explicitly
define double bind communication. Thus, even if it does
occur, it is difficult for researchers to agree on when it has
occurred (Ringuette & Kennedy, 1966).
2. General Communication Patterns: Other lines of research
have looked at general patterns of communication within the
family as a whole. Families of schizophrenics tend to have
deviant communication patterns. For example, parents are
unable to establish a focus of attention and instead
communicate with each other and other family members in an
incoherent manner (Wynne, Singer, Bartko & Toohey, 1975).
Verbal exchanges are often confused, vague, or incomplete.
For example (Wynne & Singer, 1963, quoted in Neale & Oltmanns,
1980, p.315):
Daughter (presenting patient), complainingly: Nobody
will listen to me. Everybody is trying to
still me.
Mother: Nobody wants to kill you.
Father: If you're going to associate with intellectual
people, you're going to have to remember that
still is a noun and not a verb.
One hypothesis is that such communication patterns teach the
child the disturbed thinking associated with schizophrenia.
In addition, these communication disturbances are often
occurring in the context of marital conflicts, thus making the
home environment even more stressful for the child. The child
is caught between his parents (Neale & Oltmanns, 1980), in a
situation that makes very little sense.
It seems clear that deviant communication occurs in these
families, but such deviance may not be causally related to
schizophrenia. For instance, both the schizophrenia disorder
and the deviant communication patterns may be due to some
third variable, such as a family genetic defect (Reis, 1974,
Goldstein, 1987). Alternatively, we may just have our causal
arrows pointing the wrong way: the presence of a
schizophrenic person in the family may give rise to the
disturbed communication. Perhaps such communication is how
the family learned to cope with the schizophrenic child. For
example, in one study (Liem, 1974), 11 families with
schizophrenic sons were compared with 11 families with normal
sons. Results:
disorder was not observed in the communications of
parents of schizophrenic sons - there was no
significant difference between the two sets of
parents
normal and schizophrenic sons were not
differentially affected by the communications of
normal and schizophrenic parents
both sets of parents were adversely affected by the
communications of schizophrenic sons
Finally, we must ask: Why do not all the children in the
family develop schizophrenia?
In any event, the communication variables that are
hypothesized to be stressful and thus provoke a schizophrenic
episode also appear to contribute to its exacerbation.
Interventions that teach family members more adaptive
communication methods have lead to substantial reductions in
relapse rates. Indeed, family based communication skills
training appears more effective than individual psychotherapy
or drug treatment in reducing relapse rates over a 1 year
period (Goldstein, 1987).
B. Expressed Emotion
Another family variable associated with schizophrenia is a
negative emotional climate, or more generally, a high degree of
expressed emotion (EE). Of particular interest are things like
critical comments, hostility and emotional overinvolvement (high
levels of tension and emotion).
It has been claimed by some that families with high EE seem
more likely to have a member who develops a schizophrenic disorder
(Goldstein, 1987). Nevertheless, the problems with interpreting
communication deviance discussed above, apply here as well.
The most consistent evidence is that EE modulates relapse
(Falloon, 1988): A patient returned to a family with high EE is
much more likely (eg: 76%) to relapse, than a patient whose family
is low in EE (eg: 28%) (Brown, Monck, Carstairs & Wing, 1962; see
also Brown, Birley & Wing, 1972). What seems to then happen is
that the negative emotional climate (eg: hostility and criticism)
in these families raises the patient's arousal and stress beyond
his or her already impaired coping mechanisms.
An alternative explanation: patients in high EE families are
initially more disturbed than patients in low EE families - ie:
severe pathology is the key variable for both the negative
emotional climate and the increased relapse rate. The data, do not
support this, however: neither relapse rate nor level of EE is
related to the degree of disturbance.
Indeed, relapse rates have been found to be related to the
extent to which the patient is actually exposed to the EE climate:
In one study (see Neale & Oltmanns, 1980), relapse rates were
examined not only for low EE and high EE groups, but also within
the high EE groups based on the amount of time the patient spent in
face-to-face contact with family members. The results (N=128):
Relapse rates
Low EE 13% (n=71)
High EE 51% (n=57)
a)with less than 35 hours per week contact: 28%
b)with more than 35 hours per week contact: 69%
Family based therapies, already shown to be particularly
effective in reducing relapse rates, also typically decrease
(Doane, Goldstein, Miklowitz & Falloon, 1986). In fact, whatever
the therapy method (family based, individual...), when family
members shift to low EE patterns, relapse rates are as low as 0%;
if EE stays high, relapse rates stay high (Hogarty, Anderson,
Reiss, et al., 1986).
IV. Conclusion
Today we have looked at a few of the psychosocial factors
identified as important in the etiology of schizophrenia: developmental
dysfunctions, social factors, communication deviance, and expressed
emotion. The picture is still far from complete, of course. It is
difficult to specify the direction of causality in these findings.
Nevertheless, family factors appear to play some important role in the
course of schizophrenic disorders. [Note: "Cause" vs "Course" - as we
saw with Expressed Emotion, a variable can have importance in the course
of a disorder (its duration, severity, prognosis, etc), if not in its
initial cause].
The deviant communication patterns and high EE undoubtedly have
complex origins. We are talking about individuals, within a family
context, who are attempting to cope with the many overwhelming demands
of a relative with schizophrenia (Goldstein, 1987).
A purely psychosocial explanation of schizophrenia, however, is
probably unlikely. In our next lecture we shall examine some of the
biological factors that are associated with the development and course
of schizophrenia.