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.
