PSYCHOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA

To read up on biological explanations of schizophrenia, refer to pages

397408 of Eysencks A2 Level Psychology.

Ask yourself
How would the psychodynamic approach explain schizophrenia?
How would the behavioural approach explain schizophrenia?
How would the cognitive approach explain schizophrenia?

What you need to know

PSYCHODYNAMIC COGNITIVE SOCIO-CULTURAL
EXPLANATION EXPLANATIONS EXPLANATIONS
Freuds Based on the Life events
explanation of assumption that Interpersonal
the factors cognitive communication
involved in the impairments within families
development of play a role in the Social causation
schizophrenia development hypothesis
and
maintenance of
schizophrenia

Psychodynamic explanation

According to the psychodynamic approach, abnormality is caused

when trauma from unresolved conflict between the id, ego, and
superego is repressed into the unconscious and this causes regression
to an earlier stage of psychosexual development. (see A2 Level
Psychology pages 397399 for a more detailed review of the
psychosexual stages and fixation and regression).

Fixation and regression mean that the ego is not fully developed and so
the individual may be dominated by the id or the superego, and
because the ego is weak the individual will lack a sound basis in reality.
The psychodynamic explanation suggests most schizophrenics
experienced very harsh childhood environments, often because their
parents were very cold and unsupportive. This leads to fixation or
regression to early stages of psychosexual development. In particular,
schizophrenia is linked to an early part of the oral stage called primary
narcissism during which the ego has not separated from the id. The
ego is the rational part of the mind and so the person ceases to
operate on the basis of the reality principle, therefore losing touch with
reality. This explains some of the symptoms of schizophrenia.
Evaluation of the psychodynamic explanation
Accounts for loss of contact with reality. Freuds theory
accounts for this with the assumption that people with
schizophrenia regress to a period of early childhood during which
infants have no proper notion of reality.
Accounts for some symptoms. For example, delusions of
grandeur, neologisms.
Cant be tested. The theory is speculative because it is
impossible to test empirically concepts such as the unconscious,
ego, regression, etc., and so there is lack of research evidence.
Whist there is some face validity in assuming that the
schizophrenic experiences inner turmoil, this may not necessarily
be due to primary narcissism or strong sexual impulses. The fact
the theory cannot be tested means it cannot be falsified and so it
lacks scientific validity.
Sample bias. Freud used his own patients, upper-class Viennese
hysterical women, as the sample and so population validity may
be low.
Ignores current problems. The psychodynamic emphasis on
the past means current problems are often neglected.
Schizophrenics do not resemble young children. The
comparison between schizophrenics and children is unfair on
children. The lack of motivation and emotional blunting bear no
resemblance to childrens natural enthusiasm and motivation.
Mothers of schizophrenics. Waring and Ricks (1965, see A2
Level Psychology page 399) contradict the account of the
mothers of schizophrenics as harsh and withholding. Instead they
found they tended to be anxious, shy, withdrawn, and
incoherent. It can also be argued that there is no difference
between parents of schizophrenics and those of non-
schizophrenics and that any differences in family interactions are
an effect of having a relative with schizophrenia rather than a
cause.
Doesnt explain onset of schizophrenia. The theory suggests
the problems begin in childhood, which doesnt explain why
schizophrenia does not develop until late adolescence or early
adulthood.
Psychodynamic therapy. Has generally proved to be
unsuccessful (Comer, 2001, see A2 Level Psychology page 399).

Cognitive explanations
According to this approach, the cognitive impairments shown by
people with schizophrenia (e.g. poor attentional control; language
deficits; disorganised thinking) play an important role in the
development and maintenance of schizophrenia. McKenna (1996, see
A2 Level Psychology page 399) suggests schizophrenia may be due to
a defect in selective attention and so the symptoms depend in part on
the poor ability of a person with schizophrenia to concentrate.

Recent research suggests that schizophrenic symptoms may be due to

a lack of self-monitoring, and consequently thoughts and ideas are
attributed to external sources such as hallucinations, or result in
delusions because the individual does not realise that they are self-
generated. As a result, they mistakenly regard their own thoughts as
alien and as having come from someone else. This explains symptoms
such as disorganised speech, delusions, and hallucinations. Frith (1992,
see A2 Level Psychology pages 399400) speculated the cognitive
deficits were linked to an irregularity in the neuronal pathways running
between the septo-hippocampal system and the prefrontal cortex.

Hemsley (1993, 2005, see A2 Level Psychology page 400) suggests

there is a substantial breakdown in the relationship between memory
and perception in schizophrenics. As a result, people with
schizophrenia are often unable to predict what will happen next, their
concentration is poor, and they attend to unimportant or irrelevant
aspects of the environment. Their poor integration of memory and
perception leads to disorganised thinking and behaviour.

RESEARCH EVIDENCE FOR COGNITIVE FACTORS

McGuigan (1966, see A2 Level Psychology page 400) found that
the larynx of patients with schizophrenia was often active during
the time they claimed to be experiencing auditory hallucinations.
This suggests that they mistook their own inner speech for that
of someone else.
McGuire et al. (1996, see A2 Level Psychology page 400) found
schizophrenics to have reduced activity in those parts of the
brain involved in monitoring inner speech.
Drury, Robinson, and Birchwood (1998, see A2 Level Psychology
page 401) found schizophrenics performed very poorly on
measures designed to assess Theory of Mind when tested during
a schizophrenic episode.
PET scans show under-activity in the frontal lobe of the brain,
which is linked to self-monitoring and so provides biological
support for this explanation.

RESEARCH EVIDENCE AGAINST COGNITIVE FACTORS

The research into brain structural abnormality did not identify
such dysfunctions and so there is a need for further research to
link together the cognitive and biological explanations.
Schizophrenics poor performance on Theory of Mind tasks may
have occurred simply because they experience information-
processing overload when faced with complex tasks.
EVALUATION OF RESEARCH ON COGNITIVE FACTORS
Accounts for positive symptoms. The cognitive approach
provides a reasonable account of many of the positive symptoms
of schizophrenia.
Generalisability. The self-monitoring explanation accounts for
the positive symptoms but not the negative symptoms.
Scientific validity. Research on self-monitoring employs the
experimental method and so has scientific validity.
Artificiality. The research, being experimental, lacks mundane
realism and so may lack generalisability to the schizophrenic
symptoms.
Cause or effect? It is not clear whether the cognitive
dysfunction is a cause or effect of the disorder. Prospective and
longitudinal research with children at risk for schizophrenia being
assessed over time or with self-monitoring is necessary to
establish the direction of the effect.
Brain-damaged patients. Many brain-damaged patients have
problems with attention or with the relationship between
memory and perception. Despite having these cognitive deficits,
however, they fail to develop the symptoms of schizophrenia and
so this challenges the cognitive explanations.
Other factors. Other factors with little relevance to cognitive
deficits have been found to influence the development of
schizophrenia. It is not clear how or if genetic factors, stressful
life events, and various social factors inter-link with cognitive
factors.

Socio-cultural explanations
Life events
Stressful life events may trigger schizophrenia, as supported by Brown
and Birley (1968, see A2 Level Psychology page 402) who found that
50% of patients with schizophrenia had experienced at least one major
life event in the 3 weeks beforehand; only 12% had experienced a life
event in the preceding 9 weeks; very few healthy controls reported any
life events over the same 12-week period.

Hirsch et al. (1996, see A2 Level Psychology page 402) carried out a
study dealing with the limitations of Brown and Birleys (1968) study
(see evaluation below). It was a prospective study in which they
checked on life events experienced in a year period. They used the Life
Events and Difficulties Scale, where independent raters assessed how
severe a life event was accounting for the individuals personal
circumstances to take into account context. They also considered
whether the life event was independent of the patients illness. They
found a 23% risk of patients having a relapse during the 1-year period
due to life events. Second, the risk was 41% for patients who had twice
the average number of life events. The findings contradict Brown and
Birley (1968) as they did not find that the life events needed to
immediately precede the schizophrenic episode.

Myin-Germeys et al. (2003, see A2 Level Psychology page 403) found

patients with schizophrenia showed more intense negative emotional
reactions to daily hassles. This suggests that these emotional reactions
make patients with recent major life events more vulnerable to relapse.

EVALUATION OF LIFE EVENTS

Life events do not always precede schizophrenia. Many
patients illnesses do follow a major life event but this is not a
clear-cut relationship because life events are not a prerequisite of
schizophrenia; some develop schizophrenia without any recent
life events.
Relapse rather than onset. Life events are more strongly
linked to relapse than onset.
Retrospective. Patients recall of life events is retrospective and
so may be biased by reconstructive memory and the fact they
had experienced a schizophrenic episode. They may have their
experience of life events to explain their schizophrenic episode.
Cause and effect. The data is correlational and so we cannot
conclude that life events cause schizophrenia, we can only
conclude that they are associated.
Direction of effect. Brown and Birleys research didnt
distinguish between whether the life events preceded the
schizophrenia or whether they were a result of the disorder and
so prospective research is needed to better understand the
direction of effect.
Need to consider context. The wider context of the life event
needs to be considered as some may cope with marital
separation with a good network of friends or if they have a new
partner. This was considered in the Hirsch et al. (1996) study and
so this offers better insight into the impact of life events.
Individual differences. Not all schizophrenics experience an
episode in response to life events and so this shows we need to
understand the impact of individual vulnerability factors not just
the life events.
Different types of life events. Are some more likely to trigger
an episode than others?

Interpersonal communication within families

Accordingtosomeresearch,schizophreniaisaconsequenceofmaladaptivebehaviourandpoor
communicationwithinthefamily.
RESEARCH EVIDENCE FOR INTERPERSONAL COMMUNICATION
Double-bind communication is destructive and ambiguous
interpersonal communication in which the parent sends the child
mixed messages and places them in a no-win situation. For
example, assurances of love in a tone of voice that suggests the
opposite. It is suggested that this explains the confused thinking
of the schizophrenic (Bateson et al., 1956, see A2 Level
Psychology page 403).

RESEARCH EVIDENCE AGAINST INTERPERSONAL COMMUNICATION

Ringuette and Kennedy (1966, see A2 Level Psychology page
403) asked clinicians to analyse letters written by parents to
their hospitalised children. They found no difference in the
amount of double-bind communication in the letters to children
with schizophrenia than to those with other disorders. Therefore
double bind cant explain why some develop schizophrenia and
others develop different disorders.
Expressed emotion refers to the criticism, hostility, and
emotional over-involvement directed at the schizophrenic by
family members. High expressed emotion has been well
supported as a factor in relapse (i.e. a factor in maintenance
rather than cause) as individuals are four times more likely to
relapse if expressed emotion is high (Kavanagh, 1992, see A2
Level Psychology page 404).
Patterns of communication are no different from those of parents
of non-schizophrenics.
Mischler and Waxler (1968, see A2 Level Psychology pages 403
404) found significant differences in the way mothers spoke to
their schizophrenic daughters compared to their normal
daughters, which suggests that dysfunctional communication
may be a result of living with the schizophrenic rather than the
cause of the disorder.
The biological explanations challenge environmental causes.

EVALUATION OF RESEARCH INTO INTERPERSONAL COMMUNICATION

Ethical implications. There are serious ethical concerns in
blaming the family, particularly as there is little evidence upon
which to base this. Gender bias is also an issue as the mother
tends to be blamed the most, which means such research is
highly socially sensitive. It is questionable whether the ends
justify the means.
Lack of evidence. There is little research evidence that
schizophrenic families are different and there is research
evidence that dysfunctional communication characterises all
family interactions to some extent. See if you can think of a time
when you experienced a double-bind.
 Lack of explanatory power. Given that communication may be
similar in schizophrenic and non-schizophrenic families, the
theories lack explanatory powerthey dont account for the
varied expression and severity of the disorder.
Explains maintenance rather than cause. The research on
expressed emotion provides compelling evidence that family
dynamics influence the maintenance rather than cause
schizophrenia.
Expressed emotion may be more relevant to other
disorders. Research has shown that the impact of expressed
emotion on relapse was greater for depression and for eating
disorders than for schizophrenia, so expressed emotion has
negative effects on several mental disorders.
Cross-cultural differences. Expressed emotion can account for
cross-cultural differences such as the finding that those who
have experienced one schizophrenic episode are much less likely
to relapse in developing countries than in developed countries.
This is explained by the fact that Leff et al. (1990, see A2 Level
Psychology page 404) found much lower levels of expressed
emotion in the families in developing countries than in developed
ones.
Cause and effect. It is too simplistic to say that expressed
emotion causes relapse. At best, research has identified
differences between families high and low in expressed emotion.
Such natural experimental research (the level of expressed
emotion being a naturally occurring IV) allows associations only
to be concluded, and so cause and effect cannot be concluded. It
is also worth noting that such interactions are most likely to
develop over the course of the illness rather than have preceded
the original onset of the disorder.
Direction of effect. The direction of effect is also an issue as it
is not clear if high expressed emotion exacerbates the
schizophrenia episode or if the increasing severity of the
schizophrenia episode provokes more negative expressed
emotion.
Multi-dimensional approach. Not all siblings develop
schizophrenia, which challenges family interaction as a cause,
although different family members will have their own micro-
environment. But it is more likely that this can be explained by
differences in genetic vulnerability, cognition, and unconscious
motivations, so a multi-dimensional approach is needed.

Social causation hypothesis

According to the social causation hypothesis, social class and
deprivation might be important factors in causing schizophrenia. This is
based on the fact that individuals belonging to the lower social classes,
and AfricanCaribbean people, are much more likely than whites
belonging to the middle class to be diagnosed with schizophrenia. It is
hypothesised that members of the lower classes experience more
stressful lives than other people because of poverty, poorer physical
health, and so on. Stress is also more likely to arise through
discrimination, because ethnic and racial minorities in many cultures
often belong to the lower social classes. The high level of stress makes
people more vulnerable than members of the middle class to
schizophrenia.

RESEARCH EVIDENCE FOR THE SOCIAL CAUSATION HYPOTHESIS

Cooper (2005, see A2 Level Psychology page 405) reviewed a
number of studies and found that schizophrenia is much more
often found in decaying inner-city areas than in poor rural areas.
Schizophrenia and other psychoses are almost seven times more
common in AfricanCaribbean people than in white people who
have emigrated, whereas the incidence of schizophrenia in
Caribbean countries is similar to that of white people in the UK.
Also, the incidence of schizophrenia in second-generation
AfricanCaribbean people in the UK is higher than that of first-
generation AfricanCaribbean people. This supports social
causation as many AfricanCaribbean people in the UK live in
more stressful and deprived conditions than in the countries from
which they came.

RESEARCH EVIDENCE AGAINST THE SOCIAL CAUSATION HYPOTHESIS

Dohrenwend et al. (1992, see A2 Level Psychology page 405)
tested the social causation and social drift hypotheses. They
compared two immigrant groups in Israel: (1) European Jews who
had been settled in Israel for some time; and (2) more recent
immigrants from North Africa and the Middle East. Group 2
experienced much prejudice, discrimination, and poverty, and so
should have had higher rates of schizophrenia if the social
causation hypothesis is correct. In fact, group 1 had higher rates
of schizophrenia, especially among those in the lower social
class. This supports the social drift hypothesis because it seems
the members of the advantaged group are more likely to find
themselves in the lowest social class because they have
developed schizophrenia.

EVALUATION OF THE SOCIAL CAUSATION HYPOTHESIS

Bias in diagnosis. Any differences in incidence of schizophrenia
across social class and ethnic groups may be better explained by
bias in diagnosis than social causation. However, it should be
noted that there is no conclusive evidence for bias in diagnosis,
as in retrospect it is impossible to know if the patients diagnosis
 was due to their social or ethnic group or because they
presented with clear symptoms of the disorder.
The social drift hypothesis. According to this, schizophrenia
causes a lower social status because the person is unable to hold
a job and so will drift down the class structure.
Reductionism. Both the social causation and the social drift
hypotheses are too reductionist (simplistic) on their own. It is
much more likely that an interaction of both accounts for
schizophrenia.
Difficult to interpret. A number of factors in the social
causation hypothesis are identified (social deprivation, poverty,
poor housing, poor education) and it is difficult to know which, if
any, is more linked to schizophrenia, and so interpretations of the
data are limited.
Generalisability. The explanation lacks generalisability because
many experience deprivation without developing schizophrenia.
Ignores biological factors. The social explanation can be
criticised for putting too much emphasis on social factors and
ignoring biological factors, when there is strong evidence that
the latter do have a significant effect.

So what does this mean?

Now that we have covered psychological factors it is no doubt clear
there are numerous possible contributing factors to schizophrenia,
which of course makes it all the more difficult to explain the disorder.
However, it is fair to say that psychological factors offer less of a full
explanation of schizophrenia than possibly any other disorder because
there is such strong evidence for the role of biological factors and so
these must not be ignored.

The diathesisstress model offers a more comprehensive account

because it considers the interaction of nature and nurture. This better
accounts for individual differences, particularly in those who share
genes in common such as identical twins where one develops
schizophrenia and the other doesnt. The diathesisstress model can
explain this because, whilst both twins will have inherited the genetic
component, they may experience different interactions within the
family, stressful life events, or a different pre-natal environment in
terms of placenta size and nutrition. Consequently, the predisposition
may be triggered in one twin but not the other. Genetic predispositions
may interact with the psychological explanations as faulty cognitions
and negative family interactions may be linked to genetics.

A multi-dimensional approach is needed to explain schizophrenia as

clearly multiple factors interact to explain the disorder. It is also worth
noting that an idiographic (individually-specific) rather than a
nomothetic (universal) approach is needed as the factors will interact
in different ways for different cases of schizophrenia.

Over to you
1. Outline and evaluate one or more psychological explanation(s) of
schizophrenia. (25 marks)