Schizophrenia: AO3 Flashcards
Genetic Explanations AO3
- twin studies assumption environment is same: Joseph (2004) points out widely accepted MZ twins treated more similarly, encounter more similar environments, experience more ‘identity confusion’, reason to believe differences in concordance rates between MZ and DZ reflect environmental differences that distinguish two types, MZ always same sex whereas DZ twins can be combination, MZ share a more similar environment with each other than DZ
- environmental contribution: Tenari (1966) found that across both groups of adopted children level of symptoms was strongly correlated with level of disturbance in the adoptive family, Gottesman and Shields (1966) didn’t find a 100% concordance rate in MZ
- rooted in biological approach: humanistic argue biological ignores subjective experience of patient and first hand testimonies, Read et al (2006) found people with SZ symptoms and families attribute symptoms to psychosocial issues, big difference between scientists and doctors explanations and what sufferers say
- polygenic: means many genes at play, however a common feature of genes associated with SZ is code for dopamine, Ripke (2014) found looking at genetic makeup of 37,000 SZ patients compared to control group of 113,000, 108 separate genetic variations associated with increased risk and coded for functioning of dopamine
Dopamine Hypothesis AO3
+ animal experiment: Randrup and Monkvad (1966) dosed rats with amphetamines caused maladaptive behaviour interpreted similar to SZ in humans, then dosed with neuroleptics, these behaviours reduced suggesting dopamine causing these behaviours, many differences between SZ in humans and this behaviour in rats, didn’t have auditory or visual hallucinations
+ human research: Falkai et al (1988) post mortem studies brains of people with SZ, found increase of dopamine in the left amygdala, Owen et al (1978) did post mortem studies, found increase of density of dopamine receptors in caudate nucleus putamen, degrees of excess dopamine function positively correlated with severity of symptoms, correlational
- rooted in biological approach: humanistic argue biological ignores subjective experience of patient and first hand testimonies, Read et al (2006) found people with SZ symptoms and families attribute symptoms to psychosocial issues, big difference between scientists and doctors explanations and what sufferers say
- correlational research: correlation between increased dopamine function in brains and severity of symptoms, but just a correlation, cannot assume increased dopamine causes SZ, bidirectional ambiguity
Neural Correlates AO3
+ animal studies: Castner et al (1988) subjected monkeys to brain-damaging X-rays during foetal development, found showed no ill effects during childhood compared to control, in puberty developed symptoms characteristic of SZ, such as hallucinations, difficulties in memory and problem-solving tasks, supports brain damage hypothesis, relationship between brain damage when not born yet and later developing SZ, differences between monkeys and human beings, human brains more complex
+ historical evidence: Mednick et al (1988) reported increased risk for people who were foetuses during 1957 flu, researchers attempted to replicate finding, 50% achieved statistical significance, variety of other infections during pregnancy also increase risk, include maternal infections with other viruses (measles, rubella, varicella-zoster, polio), and bacterial infections.
- rooted in biological approach: humanistic argue biological ignores subjective experience of patient and first hand testimonies, Read et al (2006) found people with SZ symptoms and families attribute symptoms to psychosocial issues, big difference between scientists and doctors explanations and what sufferers say
Family Dysfunction AO3
+ research support: Vaugh and Leff (1976) show people returning to high EE show much higher rate of relapse than people returning to low EE, found those returning home to high EE had 92% relapse rate compared to 15% relapse rate, when taking a placebo drug, Butzloff and Hooley (1998) meta-analysis found people with SZ twice as likely to relapse when going home to a high EE, causal direction isn’t clear, could be experience of living with person with SZ that causes EE instead of other way round due to high stress, not knowing best way to react and deal with situation
+ cross cultural: Kalafi and Torabi (1996) found high prevalence of EE in Iranian culture (overprotective mothers and rejecting fathers) one of main causes of SZ relapse, negative emotional climate of families arouses patient, leads to stress beyond coping mechanisms, triggering or exacerbating SZ episode
- ignores genetic evidence: family studies indicate closer related to someone with SZ have higher risk of developing, twin studies indicate strong genetic contribution, concordance rate for MZ twins 54%, genes play key role determining SZ, consider diathesis stress model
- socially sensitive: can lead to parent-blaming, for parents already having to watch child experience symptoms and take responsibility for care, to be blamed adds insult to injury
Cognitive Explanation AO3
+ slower on Stroop task: Stirling et al (2006) 30 SZ patients and 18 non patients complete Stroop test and an assessment of thought disorder, found mean time to complete higher for SZ patients (123.2) compared to the control group (58.12), higher levels of TD performed lower, correlational study, may not be a causational link, bidirectional ambiguity
+ poor performance on tasks predicts symptoms: Leeson et al (2010) 53 matched pairs one with SZ and one control carry out tests on perceptual organisation, verbal comprehension, processing speed and working memory, found significant difference between groups on memory and processing speed, those who performed worse presented worse symptoms when followed up after year
- addresses how rather than why: only explain positive symptoms experienced, offers no explanation for negative symptoms, Frith et al. (1992) cognitive deficits caused by abnormalities in areas of brain that use dopamine, especially prefrontal cortex, showed schizophrenics have reduced blood flow to these areas during certain cognitive tasks, could be problems caused by low neurotransmitters creates cognitive deficit, likely other factors that play role in causing SZ that account for presence of negative symptoms.
- correlational: may be third variable, such as genetics, which causes both cognitive impairment, and SZ symptoms, not clear whether cognitive dysfunction caused SZ or whether SZ caused cognitive dysfunction.
Drug Therapy AO3
+ effective: Vaughn and Leff found relapse rates decreased when on antipsychotics compared to placebo in high EE 92% to 53%, 15% to 12% in low EE, aren’t as effective for low EE, environments more supportive, emotionally calm, already help person to cope with symptoms, psychiatrists should understand patients home environment before prescribing, still experience side effects while drugs have little to no effect
- appropriateness: many pathways in brain and nervous system that work on dopamine, not just mesolimbic pathway, dopamine antagonists like antipsychotics reduce activity in all pathways leading to side effects, also interfere with functioning of extrapyramidal pathway, which is motor pathway, lead to side effects such as tardive dyskinesia.
- problems with supporting published research: publication bias, tendency to only publish findings that are statistically significant, most studies of drug therapy are of short-term effects and some data sets have been published several times, exaggerating size of evidence base (Healy, 2012), benefits seen after taking antipsychotics may be due to calming effects of drugs rather than real effects of symptoms.
CBT AO3
+ improves quality of life: address underlying cause of SZ more than drug therapy, tackle maladaptive thinking, more ethical, fewer side effects, often must be used in conjunction with drug therapy, expensive treatment, requires highly trained practitioners, patients must attend multiple sessions.
+ research support: Gould et al. (2001) found all seven studies in meta-analysis reported statistically significant decrease in positive symptoms of schizophrenia post-treatment, most studies of effectiveness of CBT have been conducted at same time with antipsychotic medication.
- subject attrition: problem of ps dropping out of research or refusing to cooperate with researcher partway through study, biased sample in research investigating effectiveness as could be researchers most likely to lose data from ps with most severe expression of schizophrenia, Wykes et al. (2008) found that more rigorous study, weaker effect of СВТ as treatment
- appropriateness: Kingdon and Kirschen (2006) studied 142 patients with sz, found many of them deemed unsuitable for CBT because psychiatrists believed they would not fully engage with therapy, found older patients were deemed less suitable for CBT than younger patients.
Family Therapy AO3
+ effectiveness research support: Leff et al. (1985) worked with families of people with sz rated as having high EE based on Camberwell Family Interview, provide intervention aimed at providing education, reducing EE, and increasing patient’s independence from high EE relatives, during first 9 months, 50% of ps who received routine care relapsed, compared to 8% of ps whose family’s received intervention, after 2 yrs 78% relapse rate for treatment as usual group compared to 20% for group receiving family intervention, concluded family therapy effective in reducing symptoms, expensive and time consuming treatment, often not complete solution, aetiologically heterogeneity of sz means multiple treatments needed which increases cost
+ appropriateness other benefits: increases medication compliance, main benefit is makes people more likely to comply with medication regime, leads to improvements in mental state and reduces relapse rate, economic benefits, NICE review of family therapy studies (NCCMH, 2009) demonstrated family therapy and standard treatment had relapse rate of 26% compared to 50% from stand-alone standard treatment condition, found family therapy associated with significant cost savings when offered to people with sz as extra cost offset by reduction in costs of hospitalisation because of lower relapse rates
- effectiveness refuting research: Garety et al. (2008) failed to show better outcomes for ps given sessions of family therapy compared to those who had carers but no family therapy, both groups found to have unexpectedly low rates of relapse, contrasting markedly with rates found in no carer group, concluded for many family intervention may not improve outcomes further than good standard of treatment as usual, Pharoah et al. (2010) reviewed 53 studies to investigate effectiveness, found overall results for mental state mixed, some reported improvement overall mental state of ps compared to receiving standard care whereas others didn’t, did appear to show some improvement on general functioning, family intervention didn’t appear to have much of effect on more concrete outcomes of social functioning such as living independently or employment.
Token Economies AO3
+ effectiveness research support: Ayllon and Azrin (1968) examined use of token economies in 45 female schizophrenic ps institutionalised in hospital in Illinois, foraverage of 16 yrs, before token economies behaviours such as screaming, not using cutlery while eating, and wearing undergarments over clothing common, ps given tokens for tasks such as brushing hair or making bed, exchanged for being allowed to listen to music, viewing film, or visiting canteen, found average number of daily chores completed increased from 5 to 42 within few weeks, Cromer (2013) suggests major problem in assessing effectiveness of token economies is that use is uncontrolled, all ps are in program rather than having token economy group and control group
+ appropriateness: make wards calmer and more manageable: major review of treatment recommendations by Lehman (2004) advocated token economy system as being useful for promoting changes in behaviour in institutional care settings, by extension, positive behaviours encouraged when displayed meaning wards calmer and more manageable for staff, promoting positive interactions between staff and inps and more positive environment for ps, issue of appropriateness is ethical concerns, give clinicians power to control people, if target behaviours are not identified sensitively, may mean people have privileges taken aware unfairly.
- appropriateness not useful for ps not in institution: Corrigan (1991) argues problems administering token economy method with outps who live in community, in psychiatric ward, inps receive 24-hour care so better control for staff to monitor and reward ps appropriately, once ps released token economies not appropriate as ps not able to receive tokens for all behaviours, vulnerable to extinction, problem in real world because goal is to get patients to function independently.
- effectiveness research yet to provide evidence on if they work: few published randomised trials that have been carried out to support token economies as being effective in managing symptoms, file drawer problem, leads to bias towards positive published findings because undesirable results have been ‘filed away’, era of evidence-based medicine, lack of support considered unacceptable, token economies fallen out of use in many institutional care settings for people with scz in developed world.
Interactionist Explanation AO3
+ research support: Tienari’s (1985) Finnish Adoption Study found 29% of children with bio mothers with SZ went on to develop SZ compared to 16% of control, found 6/7 severe cases had bio mother with SZ, found across both groups of adopted children level of symptoms strongly correlated with level of disturbance in adoptive family
- original model oversimplified: Meehl’s original diathesis-stress model proposed in 1962 suggested ‘diathesis’ entirely genetic, result of schizogene and ‘stress’ always disturbance in family dynamic such as schizophrenogenic mother, Houston (2008) found childhood sexual trauma emerged as vulnerability factor whilst cannabis use was trigger showing older explanation too simplistic.
- refuting research for urban environment theory: Vassos at al. (2012) suggests densely populated urban environments significant stress factor, Romans-Clarkson (1990) found no urban-rural differences in mental health among women in NZ, Paykel et al. (2000) found that while there were some urban-rural differences, disappeared after adjusting for socio-economic differences for two groups.
Interactionist Treatment AO3
+ research support for effectiveness: Tarrier et al (2004) randomly allocated 315 ps to: medication and counselling group, medication and CBT group or control group (medication only), ps in 2 combination groups showed lower symptom levels than in control, CBTp usually offered alongside drug treatment, family therapy requires ps to take antipsychotics and token economies are used to encourage patients to comply with drug regimes
+ research support for effectiveness and appropriateness: Vaugn and Leff (1976) studied relapse rates of people returning home after undergoing stay in institutional setting with SZ, found relapse rates lowest (12%) when people returned to families with low EE and taking drugs, important to note those going back to low EE family and not taking antipsychotics only had marginally higher relapse rate of 15%
- treatment-causation fallacy: argued good logical fit between interactionist approach and using combination treatments, fact that both biological and psychological therapies combined more effective than either on own doesn’t mean that approach itself correct in explaining or treating, fact that drugs reduce symptoms doesn’t mean that biological in origin, same way that having headache doesn’t mean have deficit in paracetamol
Co-Morbidity and Symptom Overlap AO3
- not valid: US/UK diagnostic project videotaped interviews with ps and showed to psychiatrists based in London and New York, found most fell between two extremes of SZ and BPD and had mixture of symptoms from both, high symptom overlap and co-morbidity shown means dimensional diagnostic model more appropriate than categorical model as ps are on distribution rather than in categories
- c-m leads to inappropriate treatments: Buckley et al (2009) concluded around half of ps with diagnosis of SZ also have diagnosis of depression (50%) or substance abuse (47%), found PTSD occurred in 29% of cases and OCD in 23%, shows SZ co-morbid, can lead to polypharmacy as multiple different drugs are prescribed to target all different disorders one person presents.
Culture and Gender Bias AO3
- real world application black people over diagnosed and over medicated: Rack (1982) pointed out in many cultures normal to see and hear recently deceased loved ones as part of normal grieving process, symptoms such as hearing voices more acceptable in some cultures, people from these cultures more ready to acknowledge and express these experiences, reported to psychologist from different cultural tradition these experiences may be diagnosed as bizarre and irrational.
- refuting research hypothesis of biological differences: WHO (200) found prevalence of SZ roughly similar around world, ranging from 343 per 100,000 in Africa to 544 in Japan and Oceania for men and from 378 in Africa to 527 in SE Europe for women, shows racial differences in diagnosis aren’t biological and cultural differences are within not between countries.
- real world consequence leads to inappropriate treatment: men may be overdiagnosed due to suggestion by Goldstein (1993) that men perceived as more socially deviant and so committed involuntarily even when only have mild symptoms, women may be underdiagnosed as suggested by Goldstein (1993) more likely to seek help and perceived as less likely to exhibit socially deviant behaviour, men given treatments don’t need and women miss out on treatments do need, women’s superior social support networks, Cotten et al (2009) suggest women’s superior interpersonal functioning may convince psychiatrists to under-diagnose sz, women’s symptoms may be less strongly expressed because of better social support
Reliability and Validity AO3
- low validity gender bias inappropriate treatments: men may be overdiagnosed due to suggestion by Goldstein (1993) that men perceived as more socially deviant and so committed involuntarily even when only have mild symptoms, women may be underdiagnosed as suggested by Goldstein (1993) more likely to seek help and perceived as less likely to exhibit socially deviant behaviour, men given treatments don’t need and women miss out on treatments do need, women’s superior social support networks, Cotten et al (2009) suggest women’s superior interpersonal functioning may convince psychiatrists to under-diagnose sz, women’s symptoms may be less strongly expressed because of better social support
- low reliability symptom overlap and co-morbidity: US/UK diagnostic project videotaped interviews with ps and showed to psychiatrists based in London and New York, found most fell between two extremes of SZ and BPD and had mixture of symptoms from both, high symptom overlap and co-morbidity shown means dimensional diagnostic model more appropriate than categorical model as ps are on distribution rather than in categories
- low validity co-morbidity inappropriate treatments: Buckley et al (2009) concluded around half of ps with diagnosis of SZ also have diagnosis of depression (50%) or substance abuse (47%), found PTSD occurred in 29% of cases and OCD in 23%, shows SZ co-morbid, can lead to polypharmacy as multiple different drugs are prescribed to target all different disorders one person presents.
