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 | COGNITIVE EXPLANATIONS | SOCIO-CULTURAL EXPLANATIONS | * Freud’s explanation of the factors involved in the development of schizophrenia | * Based on the assumption that cognitive impairments play a role in the development and maintenance of schizophrenia | * 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. * 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 non-schizophrenics 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 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 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. * 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. * 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 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 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 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 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)