Psychological explanations of schizophrenia

The basic assumption is that adult characteristics are rooted in our childhood experiences, particularly, the quality of our early relationships and early traumatic experiences. 

Klein and Bion proposed that children go through a stage in the first few months characterised by feelings of persecution and omnipotence, they called this the 'paranoid-schizoid position'. A poor relationship with the primary care giver in the critical period can prevent the child from growing out of their sense of being omnipotent and persecuted. Bion (1967) describes such individuals as having a 'schizophrenic core or personality'. Those with a sz core are likely as adults to respond to stress by reverting to their early mental state, characterised by feelings of paranoia, omnipotence and classic symptoms of sz.

Fromm-Reichmann (1948) influential psychodynamic explanation for sz. 

Based on stories her patients told her about their childhoods, she suggested the existence of a particular type of parent, the schizophrenogenic mother. The word schizophrenogenic literally means 'generating schizophrenia'. The szg mother is cold and controlling, and creates a family climate characterised by tension and secrecy. 

+ Mothers with sz are more likely than fathers to have children who develop the condition themselves. 

There is ample evidence to suggest links between early experience and later development; remember, that even identical twins do not always share sz, so we would expect some element of the environment to be associated with the condition. 

Read et al 2005 - looked at studies linking childhood sexual and physical abuse and sz, and found sz was the most likely mental disorder to be associated with child abuse. 

Thus there is some evidence suggesting early family relations may be important in explaining some cases of sz (but restrictions with retrospective data)

These have focused on the impaired thought processes that characterise sz. 

Cognitive deficit theories explain sz in terms of attentional impairment; we are normally able to use selective attention mechanisms to filter incoming stimuli and extract meaning, but it is thought that these filters are defective in people with sz. They become overwhelmed with sensory info that they are unable to interpret. This is supported by people with sz performing poorly on various processing tasks i.e. reaction time, visual tracking, short term memory, size estimation and categorisation.

Cognitive theories of sz simply describe the symptoms in cognitive terms, rather than explaining how the symptoms originate.To explain the cause of these cognitive deficits, researchers integrate neurological and cognitive explanations, called neuropsychological models. The most notorious are proposed by Frith (1992) and Helmsley (1993)

He was interested in difficulties in 2 cognitive abilities:

• Metarepresentation - the ability to reflect on our own thoughts, behaviour and experience and allows us self-awareness of our own intentions and goals and to interpret the action of others. Problems with this would seriously disrupt our ability to recognise ones own actions and thoughts as being carried out by 'me' rather than someone else. 
• Central control - the ability to suppress our automatic responses to stimuli while we perform actions that reflect our wishes or intentions. 

He also distinguished between conscious and preconscious functioning: A) Conscious processing - highest level of cognitive functioning, takes place in full subjective awareness. Limited capacity to deal with more than one of these tasks at a time and B) Preconscious - operates without awareness, automatic and many tasks can be completed simultaneously. ////////// If the filter between the two break down, info could cross from the preconscious to conscious and is interpreted as important and needing to be acted upon. Frith believes this is how delusions are experienced. He also believes this faulty filter is underpinned by an irregularity of the neuronal pathways connecting the hippocampus to the prefrontal cortex which is linked to faulty regulation of dopamine, supported by his findings, demonstrating changes in cerebral blood flow in the brains of people with sz when engage in specific cognitive tasks. But there has not been universal support for this theory, it has been criticised for failing to take sufficient account of environmental factors. 

+ Bentall (1991) ps were asked either to read out category words (e.g. plants beginning with C) or think of category items themselves. These were subdivided into with sz or without sz. A week later, they were given a list of words and asked which words they had read, which were new and which they had thought of themselves. The sz group did significantly worse, suggesting they struggled to distinguish between words they had come up with themselves and those they had heard, supporting Frith's idea that people with sz have metarepresentation problems. 

+ Baker (2006) aimed to find out if patients with sz have more difficulty in a task of administering three drugs in a short period in virtual reality and found the sz group found the task harder than the control; they made more errors than the control in timing and dose of administration.  

He believes that some of the psychotic symptoms of sz arise from a disconnection between stored knowledge (i.e. schemas) and current sensory input. Because of our schemas, we know what information is new and needs to be paid attention to and which we take for granted. In people with sz, the differentiation between schemas and new situations does not occur and they do not know which information they need to attend to and which to ignore. Internal events are misinterpreted as sensations caused by external stimuli and can result in hallucinations, caused by, according to Helmsley, abnormalities in the hippocampus. 

- Again, there is no unequivocal evidence to support this theory. 

This model suggests a biological predisposition to an illness, but it only triggered by environmental stressors, The predisposition may be due to either genetics and/or illness or damage in early life (e.g. prenatallty). Environmental stressors include life events, traumatic experiences or dysfunctional families, that may act as a 'trigger' in a high-risk individual. 

• + Support from prospective longitudinal studies. Even though such studies showed the compelling support for the importance of genetic factors, but not all people with a genetic disposition developed sz, which led researchers back to the environmental factors. 
• + The Finnish Adoption Study by Tienari (1987) investigated environmental factors by assessing the quality of parenting through a series of tests and interviews. All of the cases of sz occurred in families rates 'disturbed'. Furthermore, when the rearing environment was rated as 'healthy', the occurence of sz was well below general population rates. BUT this can't be seen as purely environmental as 'low-risk' children from 'disturbed' families did not develop sz. 
• + The Israeli High Risk Study (Marcus 1987) environmental factors - assessed parents on hostility, inconsistency and over-involvement. All reported cases of sz had poor ratings. However, all cases showed signs of neuropsychological abnormalities at initial assessment, which could have affected parent-child interactions. Ongoing studies, but strongly support diathesis-stress. 

• Socio-economic status - One consistent finding is that sz occurs more in lower socio-economic (S-E) groups. This could be explained in two ways: either low S-E status is itself a risk factor or people with sz can no longer cope adequately with jobs or relationships and so 'drift' down the S-E heirarchy, BUT Fox (1990) found no evidence for the social drift hypothesis. It seems more likely that factors associated with poorer living conditions e.g. high levels of stress may trigger the onset of sz. 
• Migrant Populations - Finding that sz occurs more frequently in migrant populations, controversially, particularly Afro-Caribbeans in the UK. It is not exactly clear why, but might reflect racial bias in diagnosis or factors associated with other migrant populations e.g. psychosocial adversity or stress of living with racial discrimination.
• Evaluation - There is certainly evidence that acute life stressors can precipitate sz, but it is unlikely that social class or economic status can be anything other than a contributory factor. 

• Fromm-Reichmann (1948) suggested the idea that disturbed patterns of communication within families might be a factor in the development of sz. The term 'schizophrenic families' was used to describe families with high emotional tension, many secrets, close alliances and conspiracies.
• Bateson (1956) suggested the 'double blind hypothesis' where children are given conflicting messages from parents who express care, but at the same time appear critical, leading to confusion, self-doubt and eventual withdrawal. 
• Lidz (1965) 'Marital Schism' - discord between parents was associated with sz in offspring.

Evaluation

• - Theory was based on methodologically flawed studies: - Didn't include control groups - Used poorly operationalised definitions of schizophrenia
• - Families were studied retrospectively, long after the person's mental disorder may have affected the family system. Living with someone with sz can be difficult and distressing, routines are disrupted and often one parent has to give up paid work. To suggest the family has caused the disorder is unhelpful and highly destructive. 

By the mid 1970s, psychologists were interested in the part the family played in the course, rather than the cause, of sz. Unfortunately, there is high risk that someone who has had one episode of sz will experience another one, but this gives researchers the ability to set up prospective studies to investigate the degree of relapse in people who have already been diagnosed. Most research into EE suggests families maintain sz rather than cause it.

Vaughn and Leff (1976) suggested the extent of EE within a family was a strong predictor of relapse rates among discharged patients.

Their study was informed by Brown's (1972) study showing that patients with sz who returned to homes where there was a high level of EE (hostility, criticism, over-involvement and over-concern) showed a greater tendency to relapse than those returning to a low EE home.

Vaughn and Leff found similar results: 51% relapse rates in high EE homes, 13% in low EE homes.

They also looked at the amount of time spent in face-to-face contact with relatives after discharge and found relapse rates increased as face-to-face contact increased with high EE relatives. 

Individuals who went to work or attended a day center (so spent less than 35 hours/week exposed to negative home environment) were significantly less likely to relapse. 

• + EE is now a well established 'maintenance' model of sz, thanks to the support of many prospective studies, so that treatment programmes for sz now include education and training for family members in controlling levels of EE. Interestingly, lower relapse rates have been found in places like Nigeria and India, possibly because there is less stigma attached to a diagnosis of sz and extended families provide strong support for the individual and consequently exhibit lower levels of negative EE. 
• - The theory is not without its critics; many patients with sz are estranged from their families or have minimal contact with them so they do not experience high levels of EE, yet there is no evidence such people less are prone to relapse. HOWEVER, it does not negate the model as social involvement with anyone (not just family members) could be regarded as low or high EE. Research focuses on families more because often they are the first and most frequent point of contact. 
• - Miklowitz (2004) said that high EE is less common in families of first-episode patients than those in frequent re-admissions, suggesting that high EE may well develop as a response to the burdens of living with someone suffering from sz.