Specification Content

Clinical Characteristics of Schizophrenia

Issues surrounding the classification and diagnosis of schizophrenia, including reliability and validity.

Biological explanations of Schizophrenia, for example, genetics biochemistry.

Psychological explanations of Schizophrenia, for example behavioural, cognitive, Psychodynamic and socio-cultural

Biological therapies of Schizophrenia, including evaluation of the appropriateness and effectiveness

Psychological therapies of

CONTENTS

PSYA4: PSYCHOPATHOLOGY

Schizophrenia, for example, behavioural, Psychodynamic and cognitive-behavioural, including evaluation in terms of appropriateness and effectiveness.

Schizophrenia

This is a serious mental disorder characterised by severe disruptions in psychological functioning which affects thoughts, perception, language, emotion and a loss of contact with reality (psychotic symptoms).

Across the world there is a 1% chance of developing schizophrenia. Onset is between 15 – 45 years (usually about five years earlier for men than women but equally common for both genders).

Clinical characteristics

Positive Symptoms – those where there is an addition or an excess to cognitive functioning e.g. delusions or hallucinations

Negative symptoms – where there is something taken away or a diminishment of normal functioning e.g. affective flattening.

Positive SymptomsDefinition Picture

Delusions Bizarre beliefs Seem real Sometimes paranoid Grandiosity – e.g. I am God Reference – comments of

others e.g. on TV are about you

Experiences of control Individual believe they are under the control of someone else e.g. aliens

Auditory Hallucinations

Unreal perceptions of the environment, usually sound, may be visual, olfactory (smell) or tactile (feeling things crawl on you.

Disordered thinkingThoughts are being withdrawn or inserted into the mind. The individuals thoughts are being broadcast to everyone else

Negative symptomsDefinition Picture

Affective Flattening Emotional expression is reduced; facial, tome of voice, body language

Alogia Speech becomes less clear, less fluent this is probably because of slowing or blocked thoughts

Avolition Inability to take part in goal directed behaviour, appear to be disinterested

Catatonia This is where people stand in unusual positions, for very long period of time, completely still.

Activity – individual research. Using the A level textbooks, find out about the different types of schizophrenia. This could also be used in a question on clinical characteristics.

Diagnosing Schizophrenia

Diagnostic criteria (DSM IV) Two (or more) of the following (Criterion A symptoms), each present for a significant portion of time during a 1-month period (or less if successfully treated): • Delusions (beliefs that do not correspond to reality) • Hallucinations (sensory experiences that do not correspond to reality, usually

auditory – hearing voices – or somatosensory – strange sensations)

• Disorganized speech (e.g., frequent derailment – jumping from one conversations topic to another apparently at random - or incoherence)

• Grossly disorganized or catatonic behaviour (periods of waxy immobility) • Negative symptoms, i.e., affective flattening (apparent lack of emotion), alogia

(apparent inability or unwillingness to speak), or avolition (apparent inability or unwillingness to direct own activities)

Note: Only one Criterion A symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person's behaviour or thoughts, or two or more voices conversing with each other.

We will look at three biological explanations which have been shown to influence schizophrenia – 1. Genetic factors and 2. Brain biochemistry (dopamine) 3. Neurological (brain damage)

That schizophrenia runs in families is mainly investigated by twin studies. If schizophrenia is genetic we would expect to find a high concordance rate (the probability that the other twin is also schizophrenic)

Issues and problems surrounding the classification and diagnosis of schizophrenia

between known schizophrenics and their close relatives. Concordance is where both twins have schizophrenia.

TWIN STUDIES Gottesman summarised about 40 studies.

The concordance rate for schizophrenia is about 48% for monozygotic twins, but only 17% for dizygotic twins.

Some of the most striking support for genetic factors was reported by Rosenthal. He studied quadruplets, in which all four girls were identical to each other. Amazingly, all four of them developed schizophrenia, although they did differ somewhat in age of onset and the precise symptoms. They were known as the Genain (dreadful genes) quadruplets. It may be worth noting that they did also have a dreadful and aberrant childhood so, as with most evidence, the conclusion is not clear cut.

Gottesman and Shields (1972) – looked at the history of 45 000 p’s between 1948 and 1964. They identified 57 schizophrenics with twins who could be located and agreed to be studied. They found:

MZ – identical 42% concordance DZ – non-identical 9% concordance This suggests that genetics may play a role as the identical twins have a

higher concordance rate.

Helson (1970) provides further support for genetics research and found a 90% concordance rate for MZ twins. Overall, studies on twins tend to show a concordance rate of 50% for identical and 15% for non identical twins.

Evaluation There is strong evidence of genetic factors in schizophrenia from the

studies of twins. It is worth noting that the concordance rates are not 100% and therefore even the data does not exclude environmental input.

The problem is that twins presumably share a very similar environment, more so for identical twins as people will respond to them in the same way. The cause could therefore be environmental.

Another problem of the research is that you might expect people with schizophrenia to be less likely to have children, yet the incidence rate is not vastly dropping.

First MZ twins elicit more similar treatment from their parents than do DZ twins (Lytton 77) this suggests that the greater genetic similarity of identical twins may be cause, rather than an effect, of their more similarity parental treatment.

Schizophrenia concordance rate for MZ twins bought up apart is presumably not due to a high level of environmental similarity, although critics have suggested that some of the reared apart twins in Shields

study had not always spent the whole of their childhood apart and some raised by relatives and even went to the same school.

ADOPTION STUDIES These studies can separate the effects of the environment and genetic factors. Researchers look at adopted children who later developed schizophrenia and compare them with their biological and adoptive parents.

Tiernari (91) did a study in Finland. He managed to find 155 schizophrenic mothers who had given up their children for adoption, and they were compared against 155 adopted children not having a schizophrenic parent. There was a large difference in the incidence of schizophrenia in these two groups when they were adults: 10.3% of those with schizophrenic mothers had developed schizophrenia compared with only 1.1% of those without schizophrenic mothers.

Kety et al (1988) (The Danish Adoption Study) Took a national sample from across Denmark. They looked at the relatives of adopted children who had developed schizophrenia. They found:

Biological relatives – had 14% occurrence of schizophrenia Adoptive parents – had 2% occurrence of schizophrenia

Evaluation This adoption study provides evidence of a genetic link for schizophrenia. A problem with the research is that these statistics were gathered from information over 70 years and the diagnostic criteria for schizophrenia are constantly being updated and changed. Earlier interpretations of symptoms were different from today, and probably less uniform.

Synoptic Evaluation for Twin studies

Synoptic Evaluation for Adoption Studies

FAMILY STUDIES Gottesman (91) reviewed other concordance rates. If both

your parents have schizophrenia, then you have a 46% chance of developing Schizophrenia as well. The concordance rate is 16% if one of your parents has schizophrenia, and it is 8% if a sibling has schizophrenia. These concordance rates should be compared against the 1% of someone selected at random suffering from schizophrenia.

Gottesman and Bertelsen (89) reported some convincing findings on the importance of genetic factors. One of their findings was that their parents had a 17% chance of being schizophrenic if they had a parent who was an identical twin and who has schizophrenia. This could be due to either heredity or environment. However, they also studied participants with a parent who was an identical twin and did not have schizophrenia, but whose identical twin did. These participants also had a 17% chance of being schizophrenic. In other words, what are of most importance are the genes that are handed on by the parents.

Commentary/ Conclusions The evidence seems to suggest the individuals may have a genetic predisposition to schizophrenia. However, it may be that other factors trigger the schizophrenia. This is the Diathesis – Stress model. Schizophrenia occurs because of a biological vulnerability (diathesis) to a disorder interacting with personally significant environmental stressor. The environment may ‘switch-on’ this gene or not.Synoptic Evaluation for Family Studies

Genetic Factors in schizophrenia Evidence for/ positive evaluations Evidence Against/ Negative

evaluations Twin studies provide strong

genetic evidence Focus on objective biological

evidence which is testable Reliability

There is not 100% concordance so genes can not tell us the whole story

Less than 50% of children where both parents have schizophrenia develop the disorder

Nature Vs nurture is difficult to separate. Higher concordance of identical twins may be because of a more similar environment

Methodology – family studies are retrospective

Small sample sizes Evidence on psychological

factors can be used against Reductionism focus on one

explanation (genetics) ignores the role of other factors such as environmental stress

Determinism- states that biology determines occurrence of schizophrenia. Some people can choose to over ride their biology with drug treatments.

This is the idea that schizophrenics have abnormally high levels of the neurotransmitter dopamine in their brains. A slightly different view is that neurons in the brains of schizophrenic patients are over sensitive to dopamine. There are four pieces of evidence to support this:

1) Post mortems of schizophrenics consistently show above normal levels of dopamine. However Haracz (1982) found that those who had received treatment had high levels of dopamine whilst those who had not received treatment showed normal levels of dopamine.

2) Drugs that individuals take for schizophrenia are believed to work because they block dopamine activity in the brain. Antagonists (e.g. chlorpromazine) are effective in 60% of cases with more impact on positive symptoms.

3) Parkinson’s disease Ps (impaired motor functioning) is believed to have abnormally low levels of dopamine. They are treated by being given L Dopa, a drug to increase dopamine levels. Often a side effect of this is schizophrenic like symptoms. At the same time, schizophrenic Ps can develop Parkinsonian like symptoms as a side effect of their drugs.

4) Neuroleptic drugs (Phenothiazines) that block dopamine seem to reduce the symptoms of schizophrenia; this mainly has the most effect on positive symptoms.

Further evidence is from individuals who take hallucogenic drugs, as the experience is similar to the positive symptoms of schizophrenia. Cocaine and amphetamines stimulate the receptors for dopamine and users report delusions of persecutions and hallucinations. Davies (1974) found that if you give p’s cocaine or amphetamines it exaggerates their symptoms.

Evidence Against This doesn’t tell us why dopamine levels are high and it is not

possible to establish cause and effect. Maybe the schizophrenia comes before the change in dopamine levels.

Drugs such as cocaine increase levels of other neurotransmitters too.

Anti-psychotic drugs block dopamine receptors very quickly, yet it can take days to change the behaviour of people with schizophrenia.

Barlow and Durand (1995) believe that neuroleptic drugs block dopamine fairly rapidly, but generally fail to reduce the symptoms of schizophrenia for days or weeks thereafter. These puzzling high levels of dopamine are responsible for maintaining the symptoms. What is also puzzling from the perspective of the dopamine hypothesis is that the fairly new drug Clozapine is frequently more effective than that of the neuroleptics in reducing schizophrenic symptoms. Clozapine blocks dopamine activity less than the neuroleptics, and so it should be less effective, according to the dopamine hypothesis.

How can we explain the effectiveness of Clozapine? According to Barlow and Durand (95), there is growing support for the view that the 2 neurotransmitters, dopamine and serotonin, both play a role in producing the symptoms of schizophrenia. Clozapine blocks both of these neurotransmitters, which is not the case with neuroleptics.

The evidence on the relationship between schizophrenia and dopamine levels is mostly correlation in nature. As a result, we do not know whether the changed dopamine activity in schizophrenics occurs before or after onset of the disorder. If it occurs after, then clearly dopamine plays a part in causing schizophrenic symptoms.

Synoptic Evaluation for the Dopamine Hypothesis

Recent advances in brain scanning have shown that the brains of schizophrenics appear to be different to those of healthy people. In particular many of the ventricles (fluid filled cavities) in the brain seem enlarged.Two explanations:

1) Damage at birth – children in a difficult labour are more likely than babies born without complications to develop schizophrenia

2) Damage to the unborn foetus – research has shown that pregnant mothers who contract flu during the middle of their pregnancy are more likely to produce children who will develop schizophrenia. However there is contradictory evidence e.g. they found this to be true in Finland, England and Wales, but not in Scotland.

Stevens (1982) said individuals with schizophrenia tend to show indications of neurological disease e.g. eye blinks/ stares.

This explanation does suggest reasons why individuals who have no family history of schizophrenia may develop the disorder. However, large ventricles have been found in non-schizophrenics. Cause and effect con not be established as only associations have been identified. Brain dysfunction is linked to negative symptoms only

Evaluation of biological explanations

Positive Negative Maybe the different

explanations explain different types of schizophrenia. For example, anti psychotic drugs mainly relieve positive symptoms and so a biochemical explanation may be appropriate for Type 1. Brain dysfunction is linked to negative symptoms and so may be linked with type ii schizophrenia.

Saying that there is one biological cause is reductionist as there are many different types of schizophrenia e.g. Type 1 – display mainly positive symptoms and Type 2 display mainly negative symptoms

We will look at 4 psychological explanations of schizophrenia: 1. Family Relationships 2. Cognitive Explanation 3. Psychoanalytic Explanation 4. Expressed Emotion.

Dysfunctional Families/ Family relationships

This theory states that abnormal family interactions may be the cause of schizophrenia. Most of the theories start off with a psychoanalytical origin. The following were big in the 1960s and 1970s. These theories by Laing and Lidz are known as schizophrenogenic family theories.

Laing and Esterson – ‘Sanity, Madness and the Family’ are a number of case studies of young schizophrenic women. Laing found clear and consistent abnormal patterns of parenting across the families:

Mystification-

Double Bind -

Research support Bateson et al suggest that the child’s inability to respond to the mother is

incapacitated by these contradictions, because one message effectively invalidates the other. If there is a combination of these in parenting there will be disorders of thinking in the child, which is one of the major symptoms of schizophrenia. These processes tend to occur in secretive and overprotective families. Often the parents themselves are psychologically unstable. Laing therefore suggests that schizophrenia is the sane response to a dysfunctional family.

Berger found schizophrenics reported a higher recall of double bind statements by their mothers then non-schizophrenics. However, p’s recall may not be reliable.

Lidz TheoryHe thought that two types of family could lead to children developing schizophrenia:

1) The Schizmatic family – both parents have major private personal problems usually the marital relationship is poor. The child ends up being used as a pawn, with each parent competing for the child’s affection and often being openly hostile about the other parent. Lidz believed that the combination of emotional trauma and confusion could spark schizophrenia in their children.

2) Skewed family – one parent is very dominant, the other is passive. The dominant parent is deeply disturbed. They impose their strange views on the entire family ignoring the needs of the children and intruding in their lives. The passive parent accepts this behaviour to help keep the family in tact. This reinforces it in the children’s eyes and the whole family starts to think and act in the same strange way.

StressLife events may cause so much emotional trauma that this is a cause. High levels of physiological arousal associated with major neurotransmitters may occur. Brown et al (1968) found 50% of people experienced a major life event in the 3 weeks before a schizophrenic episode. A problem is this study is retrospective. Van Os et al found no link between life events and schizophrenia. Cause and effect cannot be established. The start of the disorder could cause a major life event such as job loss/ divorce.

Synoptic Evaluation for Family Relationships as an explanation

Schizophrenia is characterised by disordered thinking patterns. Cognitive psychologists see this as the cause rather than a consequence of schizophrenia.

The role of attention. Most people are able to filter and process incoming stimuli, yet it is thought that schizophrenics cannot focus attention selectively. They let in too much irrelevant information, they are inundated with inappropriate stimuli and so they experience the world very differently.

Frith (1992) says that positive symptoms are a result of inability to monitor own cognition and behaviour. They cannot differentiate between actions that are brought about by external forces and those that are generated internally. We need to be aware of our own goals and intentions and understand the beliefs and intentions of others .Faults in this area are due to a functional disconnection between the frontal area of the brain concerned with action and more posterior areas that control perception.

Evidence. Frith has produced some evidence for his ideas by detecting changes in cerebral blood flow in the brains of schizophrenic patients engaged in specific cognitive tasks.

Hemsley (1993)

What did Hemsley believe about schemas??

Evidence for/ positive evaluations Evidence Against/ negative evaluations

There is a lot of evidence for a physical basis for cognitive deficits

PET scans show under activity in the frontal lobe of the brain which is linked to self monitoring

The research being experimental, lacks mundane realism and so may lack generalisabilty to schizophrenic symptoms

Cause or effect?

add more to the evaluation table - discuss in pairs

Freud: It is a result of two related processes:

1) Regression to a pre-ego state2) Attempts to regain ego control

If the world is a harsh place (cold and uncaring parents) a child may regress to a stage of development before the ego was properly formed and the child had developed a realistic awareness of the external world. So schizophrenia is an infantile state.

The ego may be upset by the demands of the id, or upset by the guilt placed by the superego. The ego may have returned to the oral state and this is why they experience hallucinations and delusions as fantasies get confused with reality.

Evidence for/ positive evaluations Evidence Against/ negative evaluations

May gain support by linking to the family relationships

Very little research support. It is impossible to test

explanations concepts of the unconscious mind id, ego and superego

Dated – the research may be era dependant and context bound

Schizophrenia is not that similar to child like behaviour

Expressed EmotionThe idea that a negative climate is responsible. EE is associated with hostility, criticism and emotional over-involvement.

A Patient returning to a home with high EE is 4 times as likely to suffer relapse. Kalafi et al (1996) found that high prevalence of EE in Iranian culture was one of the main causes of relapse. EE has more empirical studies in support than other family relationship ideas.

Research Support Vaughn and Leff they believed that expressed emotion was a strong

predator of relapse rates among discharged patients. This was stimulated by an earlier study by Brown showing that patients

with schizophrenia who returned to homes where a high level of emotion was expressed such as hostility, criticism, over involvement and over concern – showed a greater tendency to relapse than those returning to low expressed emotion homes.

Vaughn and Leff found similar results, with 51% relapse in those in high expressed emotion homes and only 13% relapse in those in low-expressed emotion homes.

Face-to –face contact increased with high expressed emotion

Evidence for/ positive evaluations Evidence against/ negative evaluations

Adoption studies show the importance of family relationships. Tienari et al (1984) found that adopted children with schizophrenic biological parents were more likely to become ill themselves than children with non – schizophrenic parent – this seems to support genetics. However, this difference only emerged when the adopted family was rated as disturbed i.e. the illness only manifested itself in appropriate environmental conditions. Genetic vulnerability alone was not sufficient.

It is difficult to accurately test these theories – lack of evidence

They add guilt to an already distressed family

Schizophrenics have often been brought up along side healthy siblings; it seems unlikely that parenting patterns should be consistently different across different children.

Many children experience the schismatic family that Lidz describes yet do not develop schizophrenia.

Klebanoff (1959) says a family of a schizophrenic shows these abnormal parenting patterns because of the behaviour of an unusual child, this reaction to the child’s first sign of symptoms may in turn also have an influence on the illness. Doane found that recurrence of schizophrenia was reduced when parents reduced hostility towards the children.

Biological explanations

AQA Specimen Paper Questions

1. Outline and evaluate one or more biological explanations for schizophrenia. In your evaluation you must refer to research evidence. (25 marks)

2. (a) Outline the clinical characteristics of schizophrenia (5 marks)

(b) Explain issues associated with the classification and diagnosis of schizophrenia. (10 marks)

(c) Outline and evaluate one or more explanations of schizophrenia. Refer to research evidence in your answer. (10 marks)

3. (a) Explain the use of one psychological therapy as applied to the treatment of schizophrenia. (10 marks)

(b) Outline and evaluate biological therapies in the treatment of schizophrenia.(10 marks)

Extend yourself!

Find resources for all AQA topics on ‘Psychlotron’http://www.psychlotron.org.uk/newResources/indDisordersSchiz.html

Revise the topic at s-coolhttp://www.s-cool.co.uk/alevel/psychology/psychopathology/explanations-of-schizophrenia.html

Watch the film ‘A Beautiful Mind’ which is based on John Nash’s life with schizophrenia.