Schizophrenia

• (R&V) Inter rater- Beck et al found 54% CR when assessing 153 patients. TS Inter rater reliability is limited.  
• (R&V) Predictive validity- Birchwood and Jackson- 20% of schizophrenics recover and never have another episode whereas 10% are so affected they commit suicide. TS too much disparity for high predictive validity.
• (R&V) Has been argued the ICD is more reliable than the DSM. TIABP the DSM is considered more reliable due to increased specificity e.g., DSM 5 specifies symptoms like hallucinations and delusions compared to ICD 11 which specifies symptoms as either positive or negative. Supported by READ ET AL 69% of Americans diagnosed with schizophrenia compared to 2% of British when given a case description. TS DSM most reliable to use.
• (R&V) Issue- the problems associated with an invalid diagnosis. Label of schizophrenia has long standing consequences e.g. social relationships, work prospects, self-esteem. Supported by ROSENHAM whose research demonstrated how his 8 pseudo-patients were all released from psychiatric institutions with a label of ‘schizophrenic in remission’. TS careful diagnostic procedure needed. 
• (C&G bias) Culture bias - Cochrane found people of afro-Caribbean origin are 7x more likely to be diagnosed with schizophrenia in Britain. TS more stressors or invalid diagnosis.
• (C&G bias) Gender bias - Reichleir-Rossler and Hafner - males have more severe negative symptoms than women which was reinforced by GALDERISI ET AL who found that males scored higher for negative symptoms. TS a prevalent gender bias leading to question the reliability and validity
• (G&C bias) Influence of psychosocial issues on reliability and validity of diagnosis. TIAPB factors such as racism and deprivation of immigrants are bound to impact mental health. This has been supported by Cochrane. TS behaviour is attributed to ethnicity rather than considering all psychosocial factors which could impact diagnosis.
• (C&G bias) Different causes between the genders. TIAPB females tend to develop schizophrenia 4-10 years later than males and women can also develop later post-menopausal forms of schizophrenia. This has been supported by KULKARNI ET AL who found that estradiol (female sex hormone) was effective in treating schizophrenia in women when added to antipsychotic therapy. TS different predisposing factors which are not recognised in diagnosis or classification of the disorder.
• (CM&SO) Co-morbidity - Goldman reported that 50% of schizophrenics had co-morbid medical conditions such as substance abuse or polydipsia (excessive thirst). Therefore suggesting problems for reliability and validity in diagnosis of comorbid conditions.
• (CM&SO) Symptom overlap - Ophoff et al assessed genetic material from 50,000 patients to find that of 7 gene locations associated with schizophrenia, 3 were implicated with bipolar disorder. TS genetic overlap supporting symptom overlap.
• (CM&SO) Co-morbidity - Difficulty of generalisation in research studies. Co-morbid patients have often been excluded from research despite forming the majority of schizophrenics. Supported by Jeste et al who found co-morbid patients cannot be generalised to this research, all of which can impact the treatment the patient receives highlights importance in validity and reliability.
• (CM&SO) Symptom overlap - potential practical application - TIGB genetic overlap for mental disorders suggests gene therapies could be developed which target more than one condition simultaneously. This has been supported by Ophoff et al. TS suggesting benefits for research into symptom overlap.
• (genetic) Torrey et al - reviewed evidence from twin studies, found if one MZ twin developed schizophrenia, 28% chance other twin will do as well. TS - genetic explanation has high validity and reliability when explaining onset of schizophrenia.
• (genetic) Tienari et al - Of 112 adopted children whose mothers had schizophrenia, 7% developed the disorder compared to 1.5% of a matched low risk adopted control group. TS genetic influence.
• (genetic) NvN - explanation suggests onset due to individual's biology and denies environmental influence in causing the disorder, adopting nativist stance. Supported by Gottesman and Shields. TD how explanation adopts nature side of the debate. HE as CR is not 100%, indicates other factors may be involved such as faulty cognition. TS - the diathesis stress model could be the best approach to take when assessing the genetic influence of schizophrenia due to acceptance of negative stressors implicating the disorder.
• (genetics) FWvD - genetics play a role in the incidence of the disorder due to running in the family. This has been supported by Gottesman who found for a child with one schizophrenic parent the risk was 7% and increased to 46% when both had disorder. This could be argued to be socially sensitive as the blame is being placed onto the parents, potentially causing distress within the family. TS careful consideration is needed.
• (Biochem) Iversen - excess dopamine found in the limbic systems of schizophrenics when carrying out postmortems. TS support for the biochemical explanation and the dopamine hypothesis
• (Biochem) Kessler et al - used Pet scans to compare schizophrenics and non, finding schizophrenics have elevated dopamine receptor levels in the basal forebrain. Differences in cortical dopamine levels also found, suggesting dopamine is important in onset of schizophrenia.
• (Biochem) NvN - supports nature stance as sees excessive levels of dopamine as causing possible schizophrenia symptoms. Supported by Kessler et al. TD how this explanation adopts nature stance. However, there is a suggestion environmental factors may be linked to disorder. Supported by family dysfunction explanation and research by Kavanagh who reviewed 26 studies of EE, finding more relapse rates for those returning to high EE environments (46% compared to 21%). TS interactionist approach using diathesis stress model is more appropriate.
• (Biochem) difficulty establishing cause and effect - correlational research makes it difficult to determine whether high dopamine causes schizophrenia or schizophrenia causes high dopamine, this is furthered as drugs do not always reduce symptoms but do reduce dopamine. This would suggest other factors such as serotonin may be involved. TS biochemical explanation can be criticised for overall validity when using to explain schizophrenia, highlighting need for more detailed account to fully understand disorder
• (neural) Boos et al - schizophrenics had decreased grey matter density and cortical thinking compared to healthy siblings when using MRI scans. TS brain tissue differences cause schizophrenia.
• (neural) Johnstone et al - schizophrenics had enlarged ventricles, while non sufferers did not. TS physiological brain differences implicate the disorder.
• (neural) NvN - strong nature side of the debate. Other factors have been implicated e.g., family dysfunction. This has been supported by research. BUTZLAFF AND HOOLEY, they found 70% of schizophrenics within high EE families, compared with 30% in low EE families when reviewing 20 cases. As well as IVERSEN who found high levels of dopamine in the limbic system. TS, other factors need to be considered.
• (neural) Cause and effect difficult to establish - schizophrenics with enlarged ventricles often don’t respond well to medication and so brain changes could be due to schizophrenia rather than a cause of it. Highlights the need for early intervention programmes which could prevent later development. Supported by ADDINGTON ET AL who suggested by using lots of assessments including neuroimaging to see who was likely to develop psychosis treatment as prevention could be introduced.
• (fam dys) Kavanagh - reviewed 26 studies of EE, finding mean relapse rate for schizophrenics who returned to live with high EE families 48% compared to 21% who went to low EE families. Supporting idea EE includes risk of relapse, maintains schizophrenia, supporting family dysfunction theory.
• (fam dys) Berger - found schizophrenics reported higher recall of double-bind statements by mothers than non. However, other studies less supportive, found by Liem who measured patterns of parental communication in families with schizophrenic child, found no difference than normal families. TS inconsistencies in research to support DB and family dysfunction, making it difficult to establish reliability of theory when using to explain the significance of family variables in development of schizophrenia.
• (fam dys) NvN - supports nurture side, argues dysfunctional characteristics being cause/maintenance of disorder, supported by Kavanagh, providing reliable evidence for EE contributing to relapse, demonstrating empiricist stance. However can be criticised for failure to acknowledge nativism when assessing debate. Biological factors implicated, especially genetic vulnerability. Due to this, could be argued that to fully understand schizophrenia, interactionist approach should be taken, such as diathesis stress model, recognising genetic vulnerability and environmental stressors.
• (fam dys) Socially sensitive - absolves blame and blames family members, specifically parents for maintaining and causing the disorder. This could lead to more stressful environments and conflict and potential worse health so careful consideration is needed.
• (cog) O’CARROLL - cognitive impairment is found in 75% of schizophrenics, particularly in memory, attention, motor skills, executive functioning, and intelligence. TS support for Beck and Rector’s cognitive model.
• (cog) Knoblich et al - got schizophrenics and non to draw circles on writing pad connected to PC monitor, asked to continuously monitor relationship between hand movements and visual consequences. Found schizophrenics impaired in ability to detect mismatch between self generated movement and consequences. TS - schizophrenics suffer with cognitive inability to self monitor leading to core symptoms of disorder.
• (cog) HvR - holistic stance in comparison to other explanations like genetic, as it looks at higher levels of explanation such as cognitive levels, as Beck and Rector proposed. Supported by O'Carroll. TD how this explanation can be regarded as holistic in the HvR debate, demonstrating its appropriateness.
• (cog) PA - foundations of cognitive explanation has led to the development and use of CBT to treat schizophrenia, which is proved as a successful treatment for society. Supported by Torrier who reviewed controlled trials of CBT using 739 patients, finding persistent evidence of reduced symptoms, especially possibility of low relapse and speedier recovery rate of acutely ill patients. TD how this explanation has led to PA which are beneficial for society.
• (drugs) Davis et al - meta-analysis of 100 studies comparing antipsychotics and placebos and found 70% of sufferers improved with the drugs compared to 25% of the placebo group. TS effective treatment.
• (drugs) Marder - atypical drug clozapine is effective at reducing positive symptoms and is effective in 30-61% patients who do not respond to typical drugs. TS effective for treating schizophrenia.
• (drugs) Undesirable side effects - tardive dyskinesia is very common in about 30% of people taking antipsychotic medication and in 75% of cases, irreversible. Supported by Lieberman et al who found 74% of 1,432 patients had to discontinue treatment within 18 months due to intolerable side effects. TIAPB treatments are causing harm to patients. TS when it comes to treatments, may not be most appropriate.
• (drugs) Only treat symptoms, not cause - Taking drugs reinforces that there is something wrong with them which could lead to the ‘self-fulfilling prophecy’ where patients live up to their label. Dependency on drugs could lead to complacency to not try other methods of treatment which could potentially be more beneficial. Supported by HOGARTY who found 0% relapse rate for family therapy plus social support and antipsychotic medication. TS that combination therapy may be most appropriate and effective.
• (psych therapies) Tarrier et al - found schizophrenics receiving 20 psychotherapy sessions coupled with drug therapy did better than those receiving drug therapy alone. 1/3 patients receiving psychotherapy achieved 20% reduction in psychotic episodes, 15% symptom free. TS psychotherapy is an effective psychological treatment for schizophrenia. However does question how effective it is as a sole treatment.
• (psych therapies) Anderson et al - found relapse rate almost 40% when patients had drugs only, compared to 20% when family therapy or social skills training were used. Relapse was <5% when both used with medication. TS family therapy is an effective psychological treatment for patients with schizophrenia but both can be used to maximise effective treatment.
• (psych therapies) considerable evidence to suggest CBT plus drugs are most effective form of treatment for schizophrenia. However, difficult to determine how effective CBT is as single treatment, as a lot of the time patients also using biological treatments. Supported by Tarrier et al. TIAPB makes it difficult to determine the effect of CBT as a sole treatment, but highlights effectiveness of combined therapies. TS - to fully help schizophrenics, should use combined therapy.
• (psych therapies) FT is cost effective - FT can educate family members to help manage patient's medication routine, decreasing need for clinicians to do this, making treatment cost effective. Supported by schizophrenia commission who said FT cheaper than standard care by £1004 a patient over 3 years, suggest it is cost effective. Further economic benefits as it reduces relapse rates, so patient less likely to take up hospital beds and resources. The NICE review of FT studied demonstrated significant cost savings when offered alongside standard care. TS - FT highly appropriate as reduces costs.