Schizophrenia

From the biological approach.

The more closely related we are the more genetics we share. There may be a genetic componenet to schizophrenia as those more closely related to schizophrenics seem more likely to have it too.

Gottesman & Shields found a concordance rate of 48% for monozygotic twins and 17% for dizygotic twins. Suggests a genetic factor to schizophrenia. However it wasn't 100% concordance in identical twins, suggesting other factors.

Kety et al found that for adopted children, there was a 13% prevelance of schizophrenia among biological parents but only 2% among adoptive parents. Suggests that genetics are a more influential factor than environment.

Tienari et al found a 30% prevelance of all severe psychological disorders among bio parents vs a 15% prevelance among adoptive parents.

Psychological disorders including schizophrenia may have a genetic factor. However research doesn't show a clear causal link, therefore there may be other factors like environment or brain structure.

Post-mortems and PET scans of schizophrenics have shown over activity in the dopamine receptors. Suggests schizophrenia may be caused by the production of too much dopamine.

This is further supported by the fact that anti-psychotic drugs reduce the symptoms of schizophrenia by blocking dopamine receptors and therefore decreasing production. This does reduce psychotic symptoms.
Also drugs like amphetamines that increase dopamine activity cause psychotic symptoms that are found in schizophrenics. 

However anti-psychotics only work in reducing positive symptoms of schiophrenia. This suggests that there must be other functions at work causing the other symptoms.
Also the dopamine link is correlational and doesn't show cause and effect, therefore the hypothesis can't be proved.
Serotonin reducing drugs are found to reduce negative symptoms, so serotonin may play a part in the development of schizophrenia. 

Schizophrenics have been found to have abnormal brain structure.

Johnstone et al found that people with schizophrenia have unusually large ventricles. This suggests that schizophrenia may be caused by a loss of brain tissue.

MRI scans and post mortems of schizophrenics have found other brain abnormalities like changes in blood flow, too much fluid in cavaties and unusually large corpus collosums. These all may lead to schizophrenia.

An overactive hippocampus may be what causes the delusions.

However non-schizophrenics have also been found with large ventricles.
these findings are correlational so do not show cause and effect. We therefore cannot prove thay are causing schizophrenia. 

Behaviourists argue that schizophrenia is learnt through operant conditioning. This suggests that when schizophrenics are rewarded for the behaviour, they will repeat it.

For example token economies use positive reinforcement to encourage normal behaviour in schizophrenics. Someone may learn to be schizophrenic to gain these rewards.

However biological research suggests there are other causes.
Also there is little evidence to back up the behaviourist theory. 

The social causation hypothesis suggests that schizophrenia is caused by the stress of having a low social status and being part of a minority.

Harrison et al found that people from deprived areas are more likely to develop schizophrenia. This suggests a cause from factors like unemployment and poverty.
However the low social status may be an effect of having schizophrenia, not the cause, as people with scizophrenia tend to drift from society. 

The psychodynamic theory suggests that schizophrenia is caused by anxiety and the wish to regress back to an early stage of development. Hallucinations may be the ego's attempt to restore contact with reality.

There is no research evidence to support this. Also psychoanalysis is a largely unaffective treatment, suggesting it doesn't explain schizophrenia.

Cognitive theory suggests the symptoms are caused by faulty cognitions and information processing.

Schizophrenics take longer to encode stimuli and have short term meory problems, suggesting faulty thought and processing.

However it is suggested that faulty cognitions are caused by dopamine over activity, so it may be a biochemical cause after all.

Advantages

• Effective for reducing positive symptoms (typical) and some negative symptoms (atypical)
• Successful for many patients meaning more can live in the general community
• Most widely used and effective treatment
• Used alongside almost all other treatments.

Disadvantages

• Treats the symptoms but not the cause, leading to relapse when it is stopped
• Some say it is unethical as it doesn't help the patient, just controls their behaviour
• Most experience short term side effects like blurred vision and weight gain
• Some experience long term side effects like increased risk of heart disease and diabetes, and tardive dyskinesia
• 2/3 of patients stop taking drugs because of side effects

Advantages

• Token economies produce significant improvements in self care and desirable behaviour
• Study found that patients went from performing 5 to 40 chores a day

Disadvantages

• Low ecological validity as it doesn't transfer to the real world
• Behaviour may be superficial during therapy (only doing it to get reward)
• Argued that it doesn't really help the patient, just makes their behaviour more acceptable

Advantages

• Effective for those who don't respond to drug treatment
• Helps both positive and negative symptoms
• Patients continue improvement for 9 months
• Since the patient is in charge of their own recovery and it tackles causes it is more ethical

Disadvantages

• Relies on self-report so it is difficult to measure effectiveness
• Less objective than some therapies
• Patients can become dependent on the therapist

Advantages

• Aims to treat underlying cause not just symptoms
• Patients have control over treatment

Disadvantages

• Not found to be effective
• Difficult to prove effectiveness as it involves the unconcsious and subjective data
• Patients may formulate false memories

Two types: Type 1 = Positive symptoms, Type 2 = Negative symptoms

Perceptual symptoms: Auditory and sensory hallucinations 

Social symptoms: Social withdrawal, lack of eye contact

Cognitive symptoms: Delusions, thought control, language impairment

Emotional symptoms: Depression, lack of emotion, inappropriate emotions

Behavioural symptoms: Stereotyped behaviours, psychomotor disturbance, catatonia

DSM IV: Two or more of following present for a significant period of time during a 1 month period

-Delusions, hallucinations, disorganised speech, catatonia, gross disorganisation. 

Reliability
How far does the classification produce the same diagnosis for a particular set of symptoms? If it is reliable the same diagnosis should be made each time it is used, however this is not always the case, as different clinicians interpet the information differently.

May be affected by cultural bias. Harrison et al shows an over-diagnosis of West Indian psychiatric patients in Bristol. Suggests symptoms of ethnic minorities are misinterpreted.

Validity
Does the classification system measure what it intends to? If it was valid then the causes and symptoms would be consistent for all patients, but it isn't, suggesting seperate disorders.

Rosenhan got people to pretend they had been hearing voices so they would be admitted. After that they acted normally, but clinicians interpreted their behaviour as symptoms. Suggests that once someone is labelled people may misinterpret their behaviours as one thing.

Should it be one disorder or a spectrum like autism?