SCHIZOPHRENIA Flashcards
limitations of diagnosis and classification of schizophrenia
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low reliability:
Cheniaux et al. had 2 psychiatrists independently diagnose 100 patients using both DSM and ICD crieria. inter-rater reliability was poor as one psychiatrist diagnosed 26 having Sz with DSM and 44 using ICD. the other diagnosed 13 wit DSM and 24 with ICD (also shows low diagnostic congruence). limitation of the diagnosis as inconsitiency between psychiatrists and manuals
low validitity:
assess validity of a diagnosis using criterion validity- do different assessment systems arrive at the same diagnosis for the same patient. Cheniaux’s study shows that Sz is much more likely to be diagnosed using ICD than DSM. Sz i either over-diagnosed in ICD or under-diagnosed in DSM so poor validity
co-morbidity:
when 2 or more conditions occur together and if they occur together a lot of the time it might call into question whether they are actually a single condition. Buckley et al. concluded taht around 1/2 patients with Sz also have diagnosis of depression or substance abuse. if very severe depression looks like Sz, it may be that they are a single condition
gender bias in diagnosis of Sz:
Longenecker et al. reviewed studies and concluded that since the 1980s, men have been diagnosed more often than women. Cotton et al. found female patients typically function better than men which may explain why some women escape diagnosis as their better interpersonal functioning may bias practitioners to under-diagnose. men and women with similar symptoms may experience differing diagnoses
strength for the genetic basis of sz as a biological explanaton
strong evidence for genetic vulnerability:
Gottesman twin study clearly shows how genetic similarity and shared risk of sz are closely related. adoption studies e.g Tienari et al. show children of people with sz are still at heightened risk of sz if adoped into families without a history of sz. sz may not be entirely genetic but overwhelming evidence that genetic factors make some poeple more vulnerable
limitation of the dopamine hypothesis of sz as a biological explanation
mixed support for dopamine hypothesis:
dopamine agonsists that increase dopamine can induce-schizophrenic like symptoms in people without sz. antipsychotic drugs that lower dopamine can be effective in reducing symptoms. however, some of the candidate genes identified code for the production of other neurotransmitters such as glutamate. dopamine cannot provide a complete explanation for sz and that t is just one important factor
limitation for neural correlates as a biological explanation of sz
correlation-causation problem:
question remains whether unusual activity in brain causes symptoms or whether there are other explanations for the correlation. negative correlation may suggest that low activity in the ventral striatum causes avolition but it could be that avolition means that less info passes through the striatum resulting in the low activity. although neural correlates exist, they tell us little about the causes of sz
limitation of genetic basis of sz as a biological explanation
clear the environment is involved:
probability of developing sz even if your identical twin has it is less than 50% (if it was purely caused by genetics would be 100%). evidece that environmental factors such as family dysfunction can also play a role in the development of sz. sz may be a result of the combination of bilogical and psycholigcal approaches (interactionist approach)
strengths of biological therapies for schizophrenia:
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evidence shows antipsychotics are moderately effective:
Thronley et al. reviewed data from 13 trials (over 1000 ppts) and found that chlorpromazine was associated with better functioning and reduced symtom severity compared with a placebo. further 3 trials found reduced relapse rate).
Meltzer et al. concluded that clozapine is more effective than typical antipsychotics and that it is 30-50% more effective in treatment-resistant cases. evidence therefore suggests they are reasonably effective
limitations of biological therapies for sz
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side effects:
typical antipsychotics are associated with dizziness, sleepiness and weight gain and long-term use can lead to lip-smacking and grimacing due to dopamine super-sensitivity. the most serious side effect is NMS which can be fatal and effects 0.1-2%. atypical antipsychotics were developed to reduce side effects but some still exist like agranulocytosis. serious limitation of antipsychotic drug therapies (could be 2 separate points) LIMIT COMPLIANCE
theoretical objection to use of antipsychotic drugs:
use of these drugs is strongly tied up with the dopamine hypothesis and the idea that there are higher than usual levels of dopamine in the subcortex of the brain. evidence that this may not be correct and that dopamine levels in other parts of the brain are too low rather than too high e.g in the prefrontal cortex and if so, antipsychotics shouldnt work. undermined the faith of some people that any positive effects are actually due to the pharacological effects of antipsychotics
strengths of psychological therapies or sz
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CBT provides coping mehcanisms for future:
they are taught how to challenge and rationalise beliefs by themselves by replicating their therapy. this means that reliance on medication decreases and if they come off it in future or symptoms increase then they have less chance of relapsing
strong support for effectiveness for family therapy:
Pharoah et al. did a meta-analyis of 53 studies on effectivesness of fmily therPY. he found the relative risk for hospital readmissions was 0.77, compliance with medication was 0.6 and relapse rate was 0.55
limitations of psychological therapies for sz:
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lack of effectiveness of CBT:
Jones et al. did a meta-analysis and found no difference in effectiveness between CBT and other and other psychological therapies
methodoloical issues in supporting study of family therapy:
in Pharoah’s meta-analysis, a sizeable proportion of studies were conducted in china. these studies lacked proper random allocation and blinding and therefore the results may overestimate the effectiveness of family therapy
ethical issues of token ecnomoy:
it has been argued that token economys could be used to manipulate the behaviour of already vulnerable patients. also, it discriminates against those with severe symptoms as they are less able to display behaviours that are rewarded
strengths of the interctionist approach to Sz
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support for the dual role of vulnerability and stress:
Tiernari et al. studied children adopted away from schizophrenic mothers. the adoptive parents’ parenting styles were assesseed and compared with a control group of adoptees with no genetic risk. a child-rearing style style with high levels of criticism and conflict and low levels of empathy was implicated in the development of schizophrenia but only for children with a high genetic risk. very strong support for approahc showing genetic vulnerability and family related stress combine in development of sz
useful in treatment:
Tarrier et al. randomly allocated 315 patients to 1. medication and CBT, 2. medication and supportive counselling or 3. control group medication only. pateints in the 2 combination groups showed lower symptom levels than the contol group. shows there is a clear practical advantage to adopting the interactionist approach
limitations of the interactionst approach to sz
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orignial diathesis-stress model is too simplistic:
multiple genes increase vulnerability, each with a small effect on its own: there is no schizogene and stress comes in many forms including dysfunctional parenting. researchers now believe stress can include biological factors e.g Houston et al. found childhood sexual trauma was a diathesis and cannabis use a trigger. shows that the old idea of diathesis as biological and stress as psychological has turned out to be too simple
treatment-causation fallacy:
Turkington et al. argue the fact that combined biological and psycholigcal therapies are more effective than either on their own doesn’t necessarily mean the interactionist approach to sz is correct. similarly the fact that drugs help schizophrenia does not mean it is biological in origin (error of this logic is called the treatment-causation fallacy). superior outcome of combined therapies shouldn’t be over-interpreted in terms of evidence in support of the interactionist approach
strength of neural correlates as a biological explanation of schizophrenia
Juckel found the ventral striatum was less active in schizophrenics with negative symptoms in a task involving anticipation of rewards and that there was a -0.66 correlation between activity in the ventral striatum and severity of negative symptoms
Strength of family dysfunction / expressed emotion as a psychological explanation for Sz
Support from family therapy studies:
Pharoah’s meta-analysis found family therapy to reduce relapse rate, hospital admissions and increased compliance with medication. Family therapy reduces levels of expressed emotion therefore suggesting it has a role to play in schizophrenia as therapy successful
Limitations of family dysfunction / expressed emotion as a psychological explanation of schizophrenia
X3
Methodological issues with supporting study:
A proportion of the studies included in the meta-analysis were conducted in China. Failed to use random allocation and blinding in their studies. Therefore methodological issues limits support and validity of results of meta-analysis
Supporting evidence is only correlational:
Family therapy might work without the theory being true as may not be reduction in expressed emotion which reduces relapse rate etc. Shown that therapy increases compliance with medication which may influence relapse rate etc
Contradicted by prospective study:
King interviewed 28 patients and their mothers 3 times at 9 month intervals to determine the direction of cause and effect between expressed emotion and relapse. Found verbal criticism and emotional over-involvement tended to be influenced by total symptom severity (mainly negative). Suggests expressed emotion is more of an effect of relapse than a cause
Strengths of cognitive explanations of schizophrenia
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Support for different info processing:
Stirling et al. Compared 30 patients with Sz to 18 non-patients in cognitive tasks like the Stroop Test. Found it took parsons twice as long to suppress the impulse to read the word and name the ink colour instead. Supports Frith’s theory of central control dysfunction
Cognitive explanation of positive symptoms supported:
Allen et al. Found patients with auditory hallucinations were worse than controls (including patients without auditory hallucinations) at identifying which voice was theirs or someone else’s in a voice recognition task. Shows that schizophrenics with auditory hallucinations make mistakes in processing auditory info and are poor at monitoring errors when they do make mistakes so dysfunction
Cognitive explanation of negative symptoms supported:
Juckel et al. Found schizophrenics with negative symptoms reacted more slowly to a task anticipating rewards and costs in a monetary reward situation than non-schizophrenics. Schizophrenics with negative symptoms display low responsiveness in a task requiring motivation which supports cognitive explanation of avolition
