Psychological explanations of schizophrenia

Overview:

According to Freud the Pleasure Principle means that as children develop in stages from birth onwards, the ID is dominant. This means they become focussed on gratification from certain erogenous zones. If a child is under/over gratified at any of these stages then they may become fixated at this stage and suffer abnormal behaviour in adult life. Later in life, adults who suffer stressful conditions may suffer regression. This means their behaviour becomes less mature and they behave in a similar way to the stage they were fixated at.

There are a number of psychoanalytic explanations for SZ including:

• parental upbringing causing fixation
• unresolved conflicts

Freud suggests that most adults suffering from SZ suffered harsh upbringings.

Cold and unsupportive parents meant the child became fixated at early stages of development. This means adult SZPhrenic suffers regress to a stage before the ego has developed.

The sufferer .:. ceases to operate on the "reality principal" (which develops with the superego in stage 3), so the ego looses touch with reality. It .:. cannot distinguish between the self and the external world.

Rather than resolving the conflict, the individual retreats to a pre-ego state of primary-narcissism, where only its own needs are felt. The regression to an early childhood stage leads to "childhood" behaviour such as:

• delusions of grandeur
• gibberish/disorganised speech
• neologisms
• other symptoms, such as hallucinations, may be the unconscious mind attempting to regain contact with reality.

Between the ID and the guilt of the Superego.

.:. they regress to a childlike state as a defence mechanism to escape the conflict.

This then results in the SZ symptoms and behaviours.

EVALUATIONS

SZphrenic behaviour isn't that similar to infantile behaviour

Infants have a varied interest in the world around them - not really similar to catatonic and emotionally flattened SZphrenics.

.:. the theory may not be valid and it seems to describe other disorders.

The Psychodynamic Model cannot predict SZphrenic outcome.

• Not all individuals who have harsh childhoods turn out to be SZphrenic - no cause and effect.
• .:. there must be other factors (genetics or neurotransmitters) that influence the onset of SZ.

Most parents of SZphrenics aren't harsh and unloving

• Waring and Ricks (1965) found parents tended to be shy and withdrawn. .:. they may be inadequate but not in the way Freud was suggesting.
• Also no cause & effect - maybe social desirability.

Freuds explanations of SZ:

• has very little scientific support for his assumptions - lack of empirical support
• isn't falsifiable - cannot be proven to be right or wrong
• it would be vey difficult to cnduct studies to prove the experiences of the first 2 years of life cause SZ 20 years later.
• it doesn't explain why SZ has a sudden onset in late teens/ early 20's
• as a result it provides a quite limited explanations of the disorder.

IDA's

• Bias in Psychological research
• Ethical issues
• Nature vs Nurture
• Free will vs Determinism
• Reductionism

SZ is characterised by severe thought disturbance. Therefore there must be some cognitive aspect. Disturbed thought processes could be the cause rather than a symptom of SZ.

There are 3 main areas of this theory:

1. The role of attention

2. Physiological abnormality and cognitive malfunction

3. Genetics links

In all our brains there are mechanisms which filter and process incoming information.

This is to allow us to pay attention to important things and to filter out less useful information.

If we couldn't do this the world would be a maddening, crazy place and we wouldn't be able to deal adequately with all the information.

People with SZ cannot filter incoming infomation.

The "let in" too much irrelevant information and are .:. bombarded with stimuli.

They're unable to process all this information properly .:. experience the world in a very different way.

AO2: This is supported by the fact that SZphrenics typically do badly on lab tests that require attention to certain tasks. 

Hemsley (1993) suggests that a main cause of SZ may be the failure of schemas to function normally.

The relationships between new incoming stimuli and existing stimuli is interrupted.

Processing normally occurs quickly and subconsciously - but in the case of SZ this doesn't occur correctly.

AO2: There is no evidence to support Helmsley's model. Cognitive theories simply explain symptoms in terms of cognitive deficits they don't explain where the deficts come from so there isn't yet a complete theory. The diathesis-stress model (Zubin & Spring, 1977)

Hemsley also suggests that the break down in Schema means that:

• internal thoughts aren't recognised as coming from memory.
• they are seen as being from outside the body and .:. experienced as hallucinations.

Frith (1992) suggests SZphrenics cannot distinguish between:

• actions brought about from external forces
• actions generated internally

SZ can be explained in terms of deficits in:

• inability to generate willed action
• inability to monitor willed action
• inability to monitor/understand the beliefs and intentions of others

AO2: not all SZphrenics experience this

.:. positive symptoms occur as sufferers fail to keep track of their own intentions.

They may regard their own thoughts as "Alien to them" - possibly "beamed into their head"

They might even attribute their own movements as being from outside influences.

They may also lack the ability to realise other people's intensions - Theory of Mind.

An explanations for this could be irregularities in the neural pathways that run from the hippocampus to the prefrontal cortex.

AO2: it has provided a comprehensive framework for explaining many positive symptoms.

Research support is far from conclusive and the theory is still regarded as speculative.

Reductionist, fails to take into account the role of environmental and biological factors

Cognitive psychologists merge their theories with biological explanations - Neuropsychological theories

Park et al. (1995) have identified working memory deficits in SZ sufferers and their 1st degree relatives.

Faraone et al. (1999) suggests memory and attention impairments are a manifestion of the genetic predisposition towards SZ.

They recognise that this doesn't explain why some relatives of SZ sufferers don't develop it even though they have the predisposing genes.

AO2: if it's genetics it should be 100%

Reductionist

• Cognitive theories don't really explain the cause of SZ.
• they really only describe the symptoms in cognitive terms
• they may .:. be limited in providing a holistic explanation
• they need to be combined with biological and genetic explanations.

Useful applications

• the approach provides reasonable explanations for the positive symptoms of SZ.
• hallucinations, delusions, disorganised thoughts are all clearly explained through impaired awareness of their own internal thoughts.
• the findings that SZ sufferers have deficits in Theory of Mind is also of potential significance.

Lack of Empirical evidence

• Hemsley's work has little clear cut evidence, but there has been some promising work with animals
• Frith's work also has little research evidence despite being a comprehensive framework for explaining the symptoms,
• It has also been accused of being reductinist as it ignores the environmental influences that can cause SZ.

Doesn't explain negative symptoms

• it fails to give a clear account for symptoms such as catatonia, flattened emotions, lack of motivation etc.
• 

Causality

• direction of causality isn't clear
• cognitive problems may trigger the onset of SZ, but it's also possible that having SZ in the 1st place produces cognitive defects
• many brain damaged patients have cognitive defects but these don't cause the onset of SZ.

Various S-C explanations may play a role in the onset of SZ.

It's reasonable to assume that environmental factors must have an impact, even if it's to trigger off the onset of SZ from those who are biologically or genetically predisposed.

• Major Life Events
• Interpersonal communication in the family
• Socio-economic/cultural explanations

Brown & Birley (1968) found that at 50% of patients who had recently had a SZphrenic episode had experienced at least 1 major life event in the previous 3 weeks.

Only 12% had experienced a major life event in the previous 9 weeks.

Very few healthy controls reported any major life events.

AO2: The data was obtained by self-reports retrospectively

What matters is the significance of the life event to the individual not the fact that it's simply a life event.

We need to distinguish between life events that: occurred as a consequences of being SZphrenic and occured independently of the disorder.

Only life events  that are independent of the disorder can play a role in the development of SZ.

Hirsch et al. (1996) - a prospective study which gathered info on life events across the course of 1 year. They used the LED scale which allows P's to rate who severe the life event is for them. They also took into account the extent to which each life event was independent of the disorder.

Findings - 23% of SZphrenic episodes were a result of independent life events. Patients who had twice the average number of life events were at 41% risk of having an episode. However, no evidence found that life events were likely immediately before an episode. Instead they found the risk of having an episode increased as life events increased over time. Those with recent life events also reacted more negatively to daily hassles - which also increases the chances of relapse.

AO2: The onset of SZ doesn't depend only on life events.

If this were true everyone who suffered a sever life event would be SZphrenic. .:. the start of SZ must depend on both life events and a specific vulnerability in the patient. Biological and genetic factors must help detetermine the impact of life events on S suffers, but this approach doesn't consider this.

Some theorists suggests that abnormal and inadequate communication between parents and children can cause SZ.

There are 2 main theories here:

Schizophrenogenic families

Expressed emotions within families (EE)

The idea that families with high emotional tension, secrets, close alliances and conspiracies can lead to SZ in children.

Bateson et al. (1956) suggests the Double-Bind hypothesis where children are given conflicting messages from parents. These contradictory verbal and non-verbal messages can confuse children. It leads tothem to confusion, self doubt and withdrawal from relationships.

Lidz (1965) used the term "Marital Schism" to describe an abnormal family pattern that can lead to SZ in offspring.

AO2: flawed methodology - often no control groups used, poorly operationalised definitions of SZ and families were studied retrospectively where it could have been the disorder in the child that caused the poor family relationships.

This theory suggests that some families help to maintain SZ in children, rather than causing it.

Expressed emotions refers to parents and family members who show:

• too much criticism
• hostility
• emotional over-protectiveness towards children

Kavanagh (1962) suggests sufferes living in families with EE are 4 times more likely to relapse.

Butzlaff & Hooley (1998) carried out a meta-anaysis and found EE was a good predictor of relapse in chronic suffers.

Vaughn & Leff (1976) found: 51% relapse in high EE families and only 13% in low EE families.Chance of relapse increased as amount of time soent in contact with high EE relative increased (positive correlation)

Paterson et al. (2000) suggests that EE could be due to interactions within the family with SZ patients, not the direct fault of family members. They suggest that EE in families can develop due to the presence of a SZ sufferer, which is then in turn made worse by the high EE. High EE develops in 3 stages:

• family members experience "loss" over the person they once knew
• family members engage in emotional over-involvement with the sufferer to resolve the "new" problems the family faces
• when the emotional over-involvement fails to help the sufferer it's replaced by anger and criticism which helps to maintain the SZ.

Most studies on EE have failed to determine direction of causality

EE is important in understanding relapse in SZ sufferers, but doesn't show a distinct cause of the disorder

It has however become an accepted model which has influenced treatment programs for sufferers to include training for family members as to how to cope with the disorder.

Biological, life events and cognitive issues are ignored by this theory - reductionist

Many sufferes of SZ are estranged from their families or have minimal contact

• .:. they don't suffer high EE
• however it may not just be the family unit that could show high EE towards sufferers
• other caregivers, psychiatric intuitions etc. could also provide high EE.

1 constant findinf in research on Sz is that it occurs in:

• lower social classess
• ethnic minorities

why?

• Bias form clinicians
• socail causation
• social drift

Bias from clinicians - Doctors might be more willing to diagnose SZ on patientss from a lower social class/ ethnic minority.

Johnstone (1989) claims WC patients are more likely to receive a diagnosis of SZ compared to MC patients even when there were few (if any) differences in symptoms

Social causation - This hypothesis suggests that lower social classes:

• experiences more stressful lives
• have poorer health/poverty
• suffer discrimination

This could lead to them being more vulnerable to SZ

Social drift - individuals who develop SZ are likely to lose their jobs. This means their social status may be reduced. Thus reduced Social Status rather than Low Social Status causing SZ.

Dohrenwend et al. (1992) - tested both SC and SD by comparing 2 groups in Israel:

• European Jews who had been seettle for sometime
• More recent immigrants from Africa and Middle East

The 2nd group were of a lower class, suffered more poverty and discrimination. So according to the Sc hypothesis group 2 should suffer from more SZ. The findings actually showed that the 1st group had more Szphrenics. This would seem to contradict the SC hypothesis.

Cooper (2005) found stronger support for the SC hypothesis in the UK:

• SZ is found more in inner city areas than in rural areas, suggesting being raised in a poor inner city environment is a big risk factor in developing SZ.
• SZ is now 7 times more common in Afrcan-Caribbean people than White people in the UK

• The level of SZ on the Caribbean is similar to that of White people in the UK
• Level od SZ in 2nd generation African/Caribbean people in the UK is higher than that of 1st generation.
• This suggests there must be a social aspect to the development of SZ.

AO2:

• Little evidence of bias, radical or otherwise, in diagnosis of WC/ ethnic minority patients.
• There is evidence both for and against the SC and SD hypothesis, which makes drawing conclusions difficult.
• Factors associated with poorer living conditions and low social class may help trigger the onset of SZ, but are unlikely to be a root cause.
• Any work studying different ethinc groups has the risk of ethnocentrisim - and the possible portrayal of that group as inferior.
• We must not over-exaggerate the effects of socail deprivation in causing SZ. Most people who live in poor conditions don't develop SZ.
• Social explanations tend to ignore biological/genetic and cognitive explanations.