1. Clinical Characteristics
1.1. Positive Symtoms
1.1.1. Addition to normal behaviour
1.1.2. e.g. hallucinations, delusions
1.2. Negative Symptoms
1.2.1. Loss of normal behaviour
1.2.2. e.g. social Withdrawal, apathy
1.3. It is the most common psychotic disorder, 1% of the population
1.4. Develops in early adult life
1.5. Peak age of onset in women is 5-10 years earlier than men
1.6. Depression is co-morbid with schizophrenia
2. Issues surrounding classificaiton and diagnosis of Schizophrenia
2.1. Prior to the 70's everyone had different diagnostic tools so the rates of schizophrenia were different to other countries.To eliminate these differences attempts were made to standardise the systems and now the ICD and DSM are very similar and so are more reliable as diagnostic tools
2.2. Other diagnostic tools have been developed specifically to diagnose schizophrenia. These help with the reliability of the diagnosis.
2.3. It is stigmatising to attach a "label" of schizophrenia. This is supported by Scheff who believed that people labelled with a diagnosis would conform to the label and it would become a self fulfilling prophecy.
2.4. It is difficult to define boundaries between schizophrenia and other disorders - depression is frequently co-morbid with schizophrenia. This is why the ICD and DSM proposed mixed disorder categories but the validity has been questioned.
2.5. Due to individual differences, there is a marked variability among schizophrenics in terms of symptoms, course, response to treatment and this has led to the suggestions that there are various sub-types of schizophrenia:
2.5.1. Paranoid
2.5.2. Catatonic
2.5.3. Disorganised
2.5.4. Undifferentiated
2.5.5. Residual
3. Therapies
3.1. Biological - Drug Therapy
3.1.1. Support for Therapy
3.1.1.1. Julien - drugs are effective in controlling positive symptoms and have allowed people with schizophrenia to live outside institutional care
3.1.2. Criticisms of Therapy
3.1.2.1. Majority of popular drugs are not effective against the negative symptoms
3.1.2.2. Rzewuska - symptoms often return if medication is stopped
3.1.2.3. Not effective against all schizophrenics, 30% of patients do not respond to drugs
3.1.2.4. Produce some distressing and irreversible side effects
3.1.2.5. Can lead to dependency which leads to revolving door syndrome
3.1.2.6. Regulation and monitoring is important, doses of medication are sometimes too high because they have not been reduced to a maintenance level after the acute stage is over, this leads to patients being exposes to an unnecessary risk of side effects. - INAPPROPRIATE
3.2. Psychological
3.2.1. Psychodynamic Therapy
3.2.1.1. Not effective as a therapy
3.2.1.2. Supported by Drake - patients exposed to psychoanalytic therapy may need longer hospitalisation
3.2.1.3. Less ethical as a therapy as more power is given to the psychologist
3.2.2. Social Interventions
3.2.2.1. Social factors affect the course of schizophrenia. This is supported by Wing who found women whose wards were stimulating had less negative symptoms compared to those who were from less stimulating wards.
3.2.2.1.1. Gender bias/ Ecological Validity - only looked at women
3.2.2.2. Milieu Therapy - used when patient is still in institutional care, aims to give patients more control in decision making and improving self-care routines, uses positive reinforcement etc
3.2.2.2.1. Ethical issues of essentially treating them like dogs
3.2.3. CBT
3.2.3.1. Tarrier - used detailed interviewing techniques, found schizophrenics can often identify triggers to the onset of their symptoms and helps them to develop strategies of coping
3.2.3.1.1. Effective because 70% of his sample reported that these strategies were successful in managing their symptoms
3.2.4. Family Interventions
3.2.4.1. Using research done on EE therapies have been developed such as family therapy sessions which aim to develop a trusting relationship and all the contributions of the family are valued. The therapist provides the family with information about the disorder and to provide the whole family with practical coping skills and to learn more constructive ways of communicating
3.2.4.2. Several studies in the UK as well as other countries have shown a reduction in the rate of relapse and a reduction in the ratings of EE within the family.
3.2.4.2.1. Effective as a treatment
4. Explanations
4.1. Biological
4.1.1. Genetic Hypothesis
4.1.1.1. The risk for an individual developing schizophrenia is proportional to the amount of genes they share
4.1.1.2. This is supported by controlled genetic studies such as the ones carried out by Gottesman
4.1.1.3. Even for a genetically identical relative, the chances are well below 100% this suggests that there are other factors that cause schizophrenia
4.1.2. Twin Studies
4.1.2.1. Genetically identical (monozygotic) twins have a higher concordance rate than dizygotic twins
4.1.2.2. This is supported by Gottesman and Cardno et al's research and implies that there is a genetic component involved
4.1.2.3. Evaluation
4.1.2.3.1. MZ twins are relatively rare so sample sizes are usually small
4.1.2.3.2. Twin studies don't always use the same diagnostic criteria and so comparisons cannot always be made
4.1.2.3.3. Although we have the technology now, earlier research used different criteria to distinguish between DZ and MZ twins and so the earlier research may not be valid
4.1.2.3.4. Concordance rates can be calculated in different ways and vary depending on the method used, they also do not establish a causal relationship
4.1.3. Adoption Studies
4.1.3.1. Adoption studies try to separate genetics and environment, if genetics are the cause of schizophrenia, then an adopted child with a biological schizophrenic parent will develop schizophrenia
4.1.3.2. Supported by Kety who found high rates of schizophrenia in individuals whose biological parents had the disorder but who had been adopted by psychologically healthy parents
4.1.4. Dopamine Hypothesis
4.1.4.1. Schizophrenia results from an excess of dopamine receptors or over-sensitivity of dopamine receptors
4.1.4.2. Supporting evidence
4.1.4.2.1. Davidson - the drug L Dopa increases dopamine levels and can produce many symptoms of schizophrenia in previously unaffected individuals
4.1.4.2.2. Phenothiazines (drugs which act by blocking dopamine at the synapse) are effective in alleviating some of the major symptoms of schizophrenia
4.1.4.2.3. Seeman - post mortems of schizophrenic's brains have found higher levels of dopamine
4.1.4.3. Criticisms
4.1.4.3.1. Phenothiazines do not work for everyone diagnosed with schizophrenia. They alleviate the positive symptoms not the negative ones
4.1.4.3.2. Post mortems are usually carried out on people who have been taking neuroleptic drugs for years and so it is hard to tell if the increase in dopamine levels is due to the disorder or the drug therapy
4.1.5. Neuroanatomical Factors
4.1.5.1. Jernigan - found abornomalities in the limbic system of schizophrenics which has a role in the regulation of emotions
4.1.5.2. Evaluation: although abnormalities have been found in the brain much of the research is difficult to interpret and there have been contradictory findings
4.2. Psychological
4.2.1. Psychodynamic
4.2.1.1. Schizophrenia arises from the inability to test reality
4.2.1.2. The root of difficulties is traced back to childhood experiences
4.2.1.3. Evaluation: little evidence to support psychodynamic view
4.2.2. Behavioural
4.2.2.1. Children learn to behave in odd, bizarre ways and repeat these behaviours because they are rewarded by attention
4.2.2.2. Evaluation: this explanation doesn't account for the extraordinary range of behaviours characteristic of schizophrenia
4.2.3. Cognitive
4.2.3.1. Focuses on impaired thought processes that characterise schizophrenia. Frith's Model: Delusions are simply a misinterpretation of information Helmsley's Model: Events are misinterpreted and can result in hallucinations
4.2.3.2. Evaluation: very little to no evidence to support both models
4.2.4. Family Models
4.2.4.1. Expressed Emotion (EE) is refering to behaviour such as hostility, criticism and over concern Suggestion that people with schizophrenia are more likely to relapse if returning to a home with high EE.
4.2.4.2. This is supported by Tarier et al who found a strong relationship between relapse and living with a high EE relative
4.2.4.3. Studies of EE are correlational and so no causal relationship can be established. Kavanagh found high EE patterns in families of patients with depression and eating disorders to EE is not a defining characteristic of families with a schizophrenic member
4.2.4.4. Several prospective studies have shown high-risk children who go on to develop schizophrenia are more likely to come from families characterised by negative relationships. i.e. schizophrenia is caused by bad parenting
4.2.4.5. This is supported by the Israeli study of which found that children who had "good parenting" did not develop schizophrenia. NOT ECOLOGICALLY VALID