Clinical Characteristics of Schizophrenia

Schizophrenia is a severe psychotic disorder in which people have disturbances with the content of thought, perception and emotion

Positive Symptoms: something is added to the persons personality

  • Hallucinations: bizarre, unreal perceptions of the environment, they can be visual or auditory, e.g. seeing or hearing things that are not actually there
  • Delusions: bizarre beliefs that seem real to the individual

Negative symptoms: taking something away from a persons personality

  • Speech poverty: lessening od speech fluency and an inability to spontaneously produce words
  • Avoltion: lack of motivation and reduced interests


  • DSM-IV: They must have at least one positive symptom for a month
  • ICD-10: They must have at least 2 negative symptoms
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Evaluation of the Classification of Schizophrenia

Reliability: Inter-rater- This is whether different assessors agree on diagnosis. This is weak in terms of Schizophrenia. Rosenhan showed that even though the doctors were presented with 8 patients with exactly the same symptoms, 7 were diagnosed with shcizophrenis and 1 was diagnosed with manic depression. If there had been inter rater reliability, they all would have been diagnosed the same way. Test-retest- This refers to the idea that if we tested the same person again, we should get the same outcome. Rosenhan found that it took between 7-52 days for each patient to be released, even though all of them acted normal once inside the institution. If there had been this reliability, all the patients would have been released once they acted normal

Validity: Gender- Castle found that women were more likely to develop postive symptom, and men were more likely to possess negative symptoms. This means that since the ICD and DSM do not generalise for men and women, women are more likely to be diagnosed with the DSM, and men more with ICD. Culture- There is a tendency to overdiagnose other cultures, shown by Copeland who found that 69% of US and only 2% of UK diagnosed same patient with scz

Symptom Overlap: the symptoms of the disorder may overlap with others; Konstrantareas and Kewitt found that 7 autistic patients also had schizophrenia. This can lead to misdiagnosis

Comorbity: is the extent that two disorders occur at the same time; Buckley found that 50% of schizophrenics also had depression. This means the two conditions may be confused

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Biological explanations

Genetics: Gottesman found that in MZ twins, with whom you share 100% of DNA, the chance of developing scz is 48%. This shows that there is a genetic basis to schizophrenia as it runs in families. Although this can be considered weak as siblings and parents often share the same environment. However, in Tienari, it was found that even when a child was adopted into a conmpletely different environment, 6.7% developed schizophrenia when their biological mother also had it. Schizophrenia also appears to be polygenetic, meaning more than one gene is required to develop the condition. It is also aetiologically heterogenous, as different combinations of genes can lead to the condition. Ripke found that there were 108 genetic variations for scz

The Dopamine Hypothesis: The neurotransmitter Dopamine is associtated with scz. High levels of dopamine in the subcortex, also known as hyperdopaminergia are associated with positive symptoms such as auditory hallucinations. Low levels of dopamine in the cortex, known as hypodopaminergia result in negative symptoms. This was identified by Goldman-Rakic.

Neural Correlates: They are patterns of structure or activity in the brain that occur in conjunction with an experience and therefore may be implacated in the origins of that experience. In terms of negative symptoms, (Juckel) avolitions  is seen alongside lower levels of activity in the ventral striatum. Similarly,  (Allen) lower activity levels in the superior termporal gyrus and anterior cingulate gyrus were found in correlation with auditory hallucinations

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Evaluations of biological explanations

Research to support genetics from Gottesman and Tiernai, support neural correlates from Allen and Juckel and dopamine hypothesis from Goldman-Rakic

Biological treatments such as antipsycotics are effective. This shows that there is a biological basis for behaviour

The theory is extremely reductionist as it basis the disorder at a basic genetic and cellular level. This means wider factors such as the role of the environment is ignored.

There is a difficulty in establishing cause and effect as the neural correlates is based on correlational studies and we cannot know that just because the two things occur at the same time, whether one causes the other, or indeed which one came first. This is further implicated through the fact concordance rates are not 100% even in MZ twins

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Biological treatment for schizophrenia

Antipsychotics were established on the basis of the dopamine hypothesis. They generally aim to reduce dopamine activity. 

    • Typical antipsychotics: For example Chlorpromazine; these are antagonists as they bind onto dopamine receptor sites, especially the D2 receptor site. This blocks dopamine transmission and prevents stimulation of receptor at the post synaptic neuron. This reduces the level of dopamine and therefore reduces the positive symptoms of hallucinations. It has side effects of dizziness, weight gain and can also lead to tardive dyskinesia, causing involuntary facial moving. It was researched by Thornley, who found that the drug was associated with overall better function and reduced symptom severity.
    • Atypical antipsychotics: For example Clozapine or Risperidone. They bind to both dopamine and serotonin receptor sites. They temporarily lower levels of dopamine and serotonin, reducing negative symptoms and depressions and anxiety levels. Clozapine was found to cause a blood condition that can be fatal if not monitored. This severe side effects resulted in the development of Risperidone, which led to fewer side effects.
  • Bagnall found that typical antipsychotics were only effective in treating positive symptoms but were the cheaper option. On the other hand, atypical drugs were effective in treating both negative and positive symptoms, but were more expensive and generally had worse side effects.
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Evaluations of biological treatment

Research to support from Davis that found antipsychotics were 70% more effective than placebos in treating schizophrenia. This shows that typical treatments are effective in addressing schizophrenia

Drugs are a cheaper option compared to CBT and other therapies, and are easier to administer. This makes it easier on the patient, especiallf if their disorder is so severe they cannot leave the house

There are serious side effects associated with the drugs, such as tardive dyskinesia, which results in involuntary facial and other limb movements. Hill found that 30% of people taking the medication develop the disorder. The chance of developing the condition may deter people from taking the medication, making them ineffective.

The drugs are nomothetic, meaning they are not individually tailored. This can be seen with typical drugs, which do not treat negative symptoms.This means that they may not be as effective for everyone

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Psychological explanations: family dysfunction

Family dysfuction is defined as maladaptive relationships, including interpersonal conflict, difficulty communicating, and an environment that is critical and controlling. 

Schizophrenogenic mother: proposed by Reichmann, the mother is cold, rejecting and controlling, leading to an atmosphere of secrecy and tension, with the father often being passive. This leads to excessve stress and distrust. This triggers psychotic thinking and paranoid delusions, and ultimately schizophrenia. 

Double Bind theory: proposed by Bateson, who said that scz is developed when the child receives mixed messages, being unable to do the right things. When the get it wrong, they are punished with a withdrawal of love. This leads to a understanding of the world as confusing and dangerous. This triggers diorganised thinking patterns and unltimately schizophrenia

Expressed emotion: this is when the family or carer of the patient is overly involved in the life of the patient and vocalises their self sacrifice. There is control, verbal criticism and hostility towards the patient. This leads to excessive stress beyond what the patient can cope with, and this can trigger a relapse or an onset within those who are already vulnerable due to genetic make up.

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Psychological explanations: cognition

Refers to dysfunctional thought processing

Metarepresentation: when this is disrupted, the patient no longer has the ability to recognise their own thoughts and behaviour as their own. This means they are more likely to believe their hallucinations and delusions

Central Control: when this is disrupted, the patient cannot suppress their automatic thought processes, leading to failed speech processing

Joshua: found that schizophrenics had slower response times and slower suppression of inappropriate responses when asked to complete both sensible and nonsense sentences. This showed an impaired executive functioning control of thoughts, when compared to bipolar and control patients.

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Evaluations of psychological explanations

Research to support from Joshua (see previous), and Tienari, who found that adopted children whos mothers were schizophrenic, that went into dsyfunctional families had a 36.8% chance of developing schizophrenia, compared to 5.8% chance within healthy families.These studies suggest the role of congition in the onset of the disorder

Unlike biological explanations, the psychological explanations can account for both positive and negative symptoms

Cognitive Treatments are effective showing that there must be a psychological role

The approach is nomothetic as it suggests we all have the same resposes to hostile environments, meanig it also cannot explain why some people with dsyfunction families do not develop the disorder. It is also deterministic, as it states that those who have this kind of family will develop the disorder.

The cause and effect is not clear, as faulty thinking may be a consequence of schizophrenia, or it could be a cause

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Token Economies

The token economy is based on learning theory principles. The patient must be in an instituation for this to work, as it is a controlled environment. The patient is given tokens alongside cooperating with a primary reinforcer such as food or hygiene. This reward for doing simple things such as getting dressed or combing their hair can be exchanged for a pleasure such as watching TV or playing sports. This is an example of conditioning; classical because the patient asscociates the primary reinforcer with the token, operant because they then link it to the reward they can obtain at the end. Modyfying these behaviours does not cure schizohphrenia but it improves a patients quality of life and brings them one step closer to being able to live outside the hospital.

There is research to support from Dickerson who found that 11/13 studies based on the effects of token economies showed benefits for the patients

The treatment is ideographic and tailored to the needs of the patient meaning they are more likely to respond well to it

Kazdin and Bootzin showed refuting evidence that the token economy only leads to temporary change as once the reinforcement is removed, the undesirable behaviour returns

The treatment only works in a controlled community meaning it may lead to institutionalisation

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Cognitive behavioural therapy

Aims to change maladaptive thinking and distorted perceptions, using Ellis's ABC model

  • 1. (A) activating agent is identified: thinking about what caused the onset of the symptoms. 
  • 2. (B) Beliefs are explored about a particular topic
  • 3. (C) The ability to recognise consequences: the content of their delusions is evaluated
  • 4. (D) Irrational beliefs are disputed in order to test the validity of these beliefs, e.g. logical disputing where the beliefs are questioned on how reasonable they are, or empirical disputing where beliefs are questioned for how much evidence there is for them being real
  • 5. (E) Reconstructed beliefs: alternatives are offered and the patient vocalises how that makes them feel

Tarrier compared CBT alone, to CBT and drugs together, and drugs alone. They found that in the combination group, 15% of patients were free of all positive symptoms, and in the CBT alone group, 7% were free of all positive symtoms. This was compared to the drugs alone group which saw no patients being symptom free. This research shows that CBT has a significant impact but has improved impact with drugs

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Evaluation of CBT

There is research to support from Tarrier, showing that CBT has a significant impact in the reduction of symptoms of schizophrenia

CBT is a ideographic treatment, meaning it is tailored to the needs of the patient. This makes it more likely that the patient with respond well to it and it will work

Many patients may not be suitable for CBT because they will not engage with it, particularly as it requires a lot of effort from the patient to go to the sessions, especially if their disorder is severe

CBT is normally used in conjunction with drugs, meaning it is difficult to work out whether the CBT has an much of an impact alone

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Family Intervention

Family intervention aims to reduce hostility and expressed emotion in the home by:

  • reducing the emotional climate and burden of care
  • enhancing carers ability to anticipate episodes and how to solve them
  • reduction in expression of guilt or anger
  • enforce reasonable expectations with family members
  • encourage some separation with limits

Pharoah compared standard care to family intervention, They found that there was a mixed option on the difference it caused in mental state; there was an increased compliance with medication with family intervention; there was no significant impact on independent living or employment; overall, family intervention reduced relapse rate

There is research to support from Pharoah to show the effectiveness of family intervention

Economically, it is cheaper than standard care. This means treatment is more accessible

It is palliative as it only improves a patients quality of life rather than curing the disorder

Its main impact may be increased medication use rather than actually contributing itself

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Interactionist approach

The interactionist approach proposes that the cause of schizophrenia is a combination of psychological and biological factors, through the diathesis stress model


  • Diathesis: Gottesman has shown that there is an genetic variable in schizophrenia. The closer the schizophrenic relation, the higher the genetic chance of inheriting the disorder. This genetic susceptibility relates to the disthesis aspect of the model
  • Stress: everyday stresses like harsh parenting and expressed emotion can cause the onset of the disorder. This refers to the remaining vulnerability within the environment. Significant life changes and events combined with genetic vulnerabilty can cause the onset. Urban environments also have been known to increase the chance of development


  • interactionism believes in a combination of biological treatments and psychological ones.

Tarrier found that there were lower levels of symptom severity when treatments were combined, compared to just a singular treatment. However, there was no difference in the rate of hospital readmission

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Evaluation of interactionist approach

There is research to support from Tarrier who exhibited the effectiveness of combining treatments 

This is a holistic approach as it combines more than one explanation. This means it will be more widely applicable

Tarrier's research also refutes the approach as there was no difference in hospital readmission between single treatments and combining them. This means that the combination of treatment may only be treating the symptoms and not the cause

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