Psychological explanations of schizophrenia

 Freud (1924) suggested that Schizophrenia is a result of two related processes.

1. Regression to a pre-ego stage                                   2. Attempts to re-establish ego control

He suggested that the disorder is seen as an infant style stage by symptoms such as delusions to reflect a primitive condition. He said that regression to the oral stage could result in a self centered disorder as the person lives their life in a state of self-absorption.

Evaluation

It is reductionist as it doesn't take on the role of genetics/biological factors and is also deterministic as it states we have no control over our behaviour as its all down to childhood experiences. The research he did was very specific to the cases he looked at so would find it difficult to generalise to others. There is no other research to suppotrt freud's ideas.

studies have shown that parents of SZ's do behave differently from parents of other kinds of patients, particularly in the presence of their disturbed offspring. (Oltmanns et al, 1999) but this is likely to be a consequence of their childrens problems as a cause.

This explanation aknowledges the role of biological factors causing initial sensory symptoms / experiences of schizophrenia. It also claims that other symptoms are a result of the individual attempting to rationalise / understand the symptoms.

when a schizophrenic experiences a scary sensory experience like a hallucination, they will turn to others to confirm the validity of what they are experiencing. some fail to confirm and the people they turn to cant validate it, they assume people are trying to hide the truth from them. They may then reject feedback and develop delusional beliefs that they are being persecuted by others around them.

Evaluation

There is lots of research to support the initial sensory experiences caused by biology e.g the excess Dopamine D2 Receptors and over activity of dopamine in the brain. (Meyer - Lindenberg et al, 2002)

Stressful life events such as the death of close relatives or the breakdown of established relationships have been linked to there being higher risk of the onset of schizophrenia 

• Supported by (Brown and Birley 1968)  who found that schizophrenia sufferers reported having twice as many stressful life events prior to an episode of schizophrenia than a healthy control group
• mechanisms which trigger SZ factors, are not known, however high levels of psychological arousal associated with neurotransmitter changes are thought to be involved. (Falloon et al, 1996)

EVALUATION

• It is alsio suggested that the onset of schizophrenia may be the cause of some stressful life events rather than the other way round, eg losing a job due to schizophrenic characteristics.
• (Vanos et al, 1994)   suggests that there are no links between life events and schizophrenia onset.

Double-Bind Theory:

Bateson et al (1956) suggested that children are likely to develop schizophrenia if they frequently recieved contradictory messages from their parents. For example if a mother tells her son she loves him but turns her head away in disgust at the same time, both these messages conflict.

These conflicting messages then lead to the child development of a internally coherent construction of reality which over the long term can lead to schizophrenia.

Evaluation:

Berger et al (1965) supported the link by finding that schizophrenia patients reported a much higher level of double-bind statements by their mothers then non-schizophrenics.

Adoption study by (Tienari et al, 1994) found children who had SZ biological parents = more likely to be ill themselves. however only occured if the situation in the adopted family was rated as disturbed.

genetic vulnerability alone was not sufficient.

Expressed Emotions (EE):

EE is a famiy communication, which involves criticism, hostility, and emotional over - involvement.

High levels of EE are more likely to influence relapse rates. a patients who returns to a family with high EE is 4x more likely to relapse than a patient returning to a family with low EE (Linszen et al, 1997).

evaluation:

Issues as to whether EE is a cause or an effect of schizophrenia. Either way it has led to an effective form of therapy where high EE relatives are shown how to reduce levels of EE.

(Hogarty et al, (1991) therapy can reduce relapse rates, howeveer, as with all therapies, it is not clear whether the EE intervention was the key of the therapy or whether other aspects of family intervention may have helped.

popularised by (Scheff 1999) states social groups construct rules for members of the group to follow.

symptoms of SZ are seen as deviant from the rules we ascribe to 'normal' experience. those considered to show these unusual behaviours are considered to be deviant, and the label of 'schizophrenic' may be applied.

once the label is applied it becomes a self - fulfilling prophecy that promotes the development of other symptoms of schizophrenia. (Comer,2003)

Evaluation:

Rosenhan, 1973 - once 'labeled' as SZ the 'diagnosis' influenced behaviour.

(Scheff 1974) evaluated 18 studies. He judged 13 to be consistent with the theory and 5 to be inconsistent, concluding the theory was supported by evidence.