PSYCHOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA
To read up on biological explanations of schizophrenia, refer to pages 397–408 of
Eysenck’s 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
EXPLANATION

Freud’s explanation
of the factors
involved in the
development of
schizophrenia
COGNITIVE
EXPLANATIONS
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Based on the
assumption that
cognitive
impairments play a
role in the
development and
maintenance of
schizophrenia
SOCIO-CULTURAL
EXPLANATIONS
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Life events
Interpersonal
communication
within families
Social causation
hypothesis
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 397–399 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. Freud’s 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.
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Accounts for some symptoms. For example, delusions of grandeur,
neologisms.
Can’t 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 children’s 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 nonschizophrenics and that any differences in family interactions are an effect of
having a relative with schizophrenia rather than a cause.
Doesn’t explain onset of schizophrenia. The theory suggests the problems
begin in childhood, which doesn’t 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 selfmonitoring, 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 399–400) 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.
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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 Birley’s (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 individual’s personal
circumstances to take into account context. They also considered whether the life
event was independent of the patient’s 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.
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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 Birley’s research didn’t 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
According to some research, schizophrenia is a consequence of maladaptive behaviour and poor
communication within the family.
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 can’t explain why some develop schizophrenia and
others develop different disorders.
 Expressed emotion refers to the criticism, hostility, and emotional overinvolvement 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 nonschizophrenics.
 Mischler and Waxler (1968, see A2 Level Psychology pages 403–404) found
significant differences in the way mothers spoke to their schizophrenic
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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
power—they don’t 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 crosscultural 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.
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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 African–Caribbean 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 African–Caribbean 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 African–Caribbean people in
the UK is higher than that of first-generation African–Caribbean people. This
supports social causation as many African–Caribbean 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 diathesis–stress 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 doesn’t. The diathesis–stress
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)