Schizophrenia Evaluation

+Positive contribuion: provides reasonable account for many positive sympoms e.g. hallucinations

+Support: McGuire et al (1996) found reduced activity in the parts of the brain involved in inner speech in schizophrenics who suffered hallucinations.

-Reductionist: It reduces a complex disorder to simply a cause of faulty cognitions, other factors have been found to have an influence, e.g. biological and so a combination explanation best

-The approach does not provide a full explanation only some symptoms, it can explain positive symptoms but not negative, only states they occur and so it can not be considered a completely valid explanation.

-Cause and effect?: The explanation only explains how information processing is affected but does not determine a cause of the faulty thinking. It may be that the faulty thinking is a symptom of the disorder as opposed to an explanation

Twin studies

-Twin studies are not representative of the wider population, identity confusion and upbringing may play an equal part in the findings.

Brain strucure

- We can not be certain that the differences in brain structure are the cause of schizophrenia or are caused due to sz.

-Enlarged ventricles may be due to medication: Ho (2010), study of 211 schizophrenics found that antipsychotic drugs have an influence on brain tissue loss over time.

+Support: Swayze reviewed 50 studies of schizophrenics, found many had abnormally large ventricles/liquid cavities in brain  

Dopamine Hyp

+Anti-psychotics (dopamine antagonists) block (or lower) dopamine activity and are often very successful in treating positive symptoms of sz e.g. chlorphromazine reduces the symptoms

+Parkinson’s sufferers have low levels of dopamine. L-dopa raises Dopamine activity People with Parkinson's develop schizophrenic symptoms if their L-dopa level is too high.

+Amphetamines such as LSD lead to increase in Dopamine levels, large doses lead to delusions and hallucinations in non schizphrenics and heighten symptoms in sufferers

-The theory cannot explain why sufferers only recover slowly when given neuroleptic drugs (often takes 4 weeks to see any sign they are working) – as the medication has an instant effect on dopamine levels.

- Leads to parents being blamed for their children’s problems, this theory led to many parents feeling guilty because of the implication of it being their fault, now recognised as unjust since it is accepted that biological problems probably influence the disorder.

-Data to support the explanation is retrospective,memories of people with SZ so may be distorted as a consequence of their illness.Research suggests most people with SZ don’t come from these types of family and particularly that mother’s personality is not a reliable indicator of schizophrenia.  Also some people with SZ will suffer a relapse even if they’ve been moved from their families entirely.

Inter rater reliablilty

+Soderberg et al. (2005)found 81% agreement using the DSM.

Test-retest

+Prescott et al. (1986) analysed test-retest reliability of several measures of attention and information processing in 14 chronic schizophrenics, performance was stable over 6 months.

- Read et al. (2004) reported test-retest reliability of only 37%.

General

-‘Schizophrenia’ is too broad a category for it to provide a reliable diagnosis.  Two patients could have completely different symptoms.

-Rosenhan 1972: recruited 8 people (he worked with them or knew him in some capacity). Each went to a psychiatric hospital and reported only 1 symptom. That a voice said only single words, like “thud”, “empty” or “hollow”. When admitted, they began to act “normally”. All were diagnosed with suffering from schizophrenia (apart from 1).

Rosenhan told the institutions about his results, and warned the hospital that they could expect other individuals to try & get themselves admitted. 41 patients were suspected of being fakes, and 19 of these individuals had been diagnosed by 2 members of staff. In fact, Rosenhan sent no-one at all! This demonstrates poor reliability and validity in diagnosis.

Comorbidity

Buckley et al. (2009) estimate comorbid depression occurs in 50% of sz patients

Symptom Overlap

Ellason and Ross (1995) found people with DID (dissociative identity disorder) have more first rank symptoms than schizophrenics

Conventionals and Atypicals

-Conventional SIde effects - tremors, muscle rigidity, blurred vision, tardive dyskinesa (involuntary sucking and chewing, jerky limb movements, writhing movements of moth or face)

-Atypical Side effects - weight gain, diabetes, n euroleptic malignant syndrome (life threatening neurological disorder – high fever, sweating, unstable blood pressure, muscular rigidity)

-If put on drugs, most likely will be for life.

CBT

-Classic model is over-simplistic, multiple genes affect vulnerability to sz and stress can come in many forms, not just dysfunctional parenting. Therefore vulnerability and stress do not have a single cause

+Useful approach – studies show the advantages of using combinations of treatments e.g. Tarrier (2004) found patients given bio and psy treatments showed lower symptom levels, though there was no difference in hospital readmission.

-We don’t know exactly the mechanisms by which vulnerability and stress interact