Schizophrenia Flashcards
Facts on SZ
(AO2)
- mostly for ages 15-35
- affects 1% population
- ppl with family x10 more likely
classification of SZ ?
(categorising)
- DSM - 5
- ICD - 11
diagnosis of SZ with
DSM-5 v ICD-11
- DSM - 5
- 2 positive symptom must be present for diagnosis of SZ
- No sub-types - ICD - 11
- 2 or more negative symptoms must be present for diagnosis of SZ
- 7 sub-types
positive symptoms of SZ?
EG?
+ symptoms = additional experiences that the general population don’t experience
- Hallucinations - unusual sensory experiences
- Delusions - irrational beliefs
- Jumbled speech
Negative symptoms of SZ
- = the loss of usual abilities + experiences
- abilities which have been removed due to SZ that the general population have
-
Speech poverty - changes in patterns in speech
reduction in quality + amount of speech - Avolition - reduced motivation to begin / keep up with goal-directed activity, becoming disinterested
- Anhedonia - loss of ability to feel pleasure
- lack of emotion
reliability AO3:
Validity AO3:
- low reliability of classification - DSM5 + ICD11 not consistent
- low reliability of diagnosis - low inter-rater reliability
- may be explained by low resources + time
. - low validity = high co-mobility overlap of symptoms
- culture bias
- gender bias
Issues with Reliability of CLASSIFICATION of SZ
- classification of SZ is not reliable as the classification in DSM-5 + ICD-11 are not consistent.
- This is because the DSM-5 diagnoses SZ if 2 positive symptom is present and has no sub-types
- whereas the ICD-11 diagnosis SZ if 2 or more negative symptoms are present and it also has 7 sub-types of SZ
- Showing there is no consistency in the classification in SZ
1
Issues with Reliability of DIAGNOSIS of SZ
- Evidence which shows that the diagnosis of SZ is not reliable.
- Cheniaux et al had 2 psychiatrists independently diagnose 100 ps using DSM + ICD
- one diagnosed 2ps according to DSM + 44 according to ICD
- the other diagnosed DSM: 13 + ICD: 24
- = more SZ likely to be diagnosed under ICD than DSM and SZ is either over diagnosed with ICD or under diagnosed with DSM.
- Beck et al looked at inter-rater reliability between 2 psychiatrists when considering 154 ps
- the reliability was only 54% = only agreed on a diagnosis for 54% of the 154 ps.
Low inter-rater reliability may be explained..
- Different hospital have different resources + demand for number of patients = time availability differs
= could explain low inter-rater reliability, as these factors could explain differences in diagnosis by different psychiatrists
- As diagnosis made may not reflect true diagnosis of symptoms but rather may be as a result of it being rushed due to high demand for professionals as they have less time available
2
symptom overlap
- validity
(comorbidity = 2 conditions present at same time)
- SZ + bipolar disorder both share positive symptoms (e.g. delusions) + negative symptoms (e.g. avolition) = there’s symptom overlap
- depression + schizophrenia both involve very low levels of motivation = creates problems of reliability = Does low motivation reflect depression or schizophrenia / both?
- Using ICD, 1 patient might be diagnosed with SCZ but using DSM, would receive diagnosis of bipolar disorder = questions the validity of the classification of SZ
- Lack of distinction questions the validity of both classification/diagnosis of SZ
- = difficult to choose suitable diagnosis + treatment
- misdiagnosis due to symptom overlap = years of delay in receiving relevant treatment= suffering + high suicide levels can occur
- Symptom overlap can have serious consequences - focusing on fixing this issue could save money/lives = focus should not heavily be about the name of the disorder but rather the success of the relevant treatment they should receive
3
Culture bias (validity)
-further limitation of schizophrenia diagnosis is the existence of culture bias.
- Some symptoms of schizophrenia (auditory hallucination - hearing voices) have different meanings in different cultures.
- For example in some cultures some people believe that voices actually are communications from ancestors.
- British people of African-Caribbean origin are 9x as likely to receive a diagnosis as white British people, although people living in African- Caribbean countries are not = ruling out a genetic vulnerability.
- The most likely explanation for this is culture bias in diagnosis of clients by psychiatrists from a different cultural background.
- This appears to lead to an over interpretation of symptoms in black British people = British African - Caribbean people may be discriminated against by a culturally-biased diagnostic system
= Diagnosis is taking an ethnocentric approach, lowering the validity of the diagnosis of SZ.
4
Gender bias (validity)
- further limitation of schizophrenia diagnosis is the existence of gender bias.
- men are diagnosed with SZ more than women (ratio of 1.4 : 1 Fischer + Buchanan)
- A possible explanation for this is that women are less vulnerable than men, perhaps because of genetic factors.
- some behavior which was regarded as psychotic in males was not regarded as psychotic in females
- However it seems more likely that women are under diagnosed because they have closer relationships + hence get support (Cotton et al ). = so better able to manage symptoms = less severe = less diagnosed
- This leads to women with SZ often functioning better than men.
-This under diagnosis is a gender bias = lower validity + means women may not therefore be receiving treatment + services that might benefit them.
symptoms easily fakes + no predictive validity
- no predictive validity as there are no pathognomic symptoms
Biological explanations for SZ ?
- Genetic hypothesis
- Dopamine hypothesis
- Neural correlates
Genetic hypothesis:
- There is no SZ gene
- candidate genes associated with risk of inheritance
- SZ is polygenic
= different combinations of genes make individuals more vulnerable to SZ
Twin studies:
Cardno et al:
- found 40% concordance rate in MZ twins
- 5.3% in DZ twins
Family studies:
- General population 1% risk
Gottesman :
- the more genetically related a person to someone who has SZ = the higher risk they have
1st degree relatives: 6-9%
2nd degree relatives: 2-4%
3rd degree relatives: 2%
Kendler et al: 1st degree relatives 18x more at risk than general population
Adoption studies:
Tienari et al :
- children of SZ parents have higher risk of developing SZ even if adopted family have no history of SZ
AO3 genetic hypothesis:
- supporting evidence
- Nurture elements ignored
- reductionism
- Supporting evidence
- Supporting evidence : Tienari et al (adoption studies) + Gottesman (family studies) + Cardno et al (Twin studies)
= these show that some people are more vulnerable to SZ due to genetic makeup.
- Nurture elements
- Nurture (Environmental) factors have not been considered.
- As MZ twins share 100% genes, it would be expected that concordance rate would also be 100% if it was purely genetic
- As it’s only 40% - it suggests other influences (environment) are playing a part
- Also limitation of Gottesman study, is that the high concordance rate may be due to increased chance of sharing the same environment.
- EG 1st degree relatives may share exact same environment, whereas 2nd degree would not
= cannot be concluded that genetic has caused SZ.
- Reductionist
- The genetic explanation for SZ is reductionist.
- It has reduced SZ, which is a complex + serious psychologoical disorder to genetics.
- This allows researchers to investigate the genetic link for SZ in great detail + makes it more scientific.
- However, reductionism is negative as it oversimplifies serious behaviour into small simple components, making SZ seem very simple whilst realistically it is very complex and large.
Dopamine hypothesis
Dopamine neurotransmitters linked with SZ
- Both hyper + hypo are involved in onset of SZ
- hyperdopaminergia in subcortex :
- excessive levels of dopamine in subcortex
= positive symptoms
(Jumbled speech + auditory hallucinations) - hypodopaminergia in pre-frontal cortex :
- Low levels of dopamine in pre-frontal cortex
= negative symptoms
(to do with thinking + decision making as pre-frontal cortex responsible for that)
AO3 Dopamine hypothesis:
- Use of anti psychotic drugs for treating SZ
- opposing evidence
- Supporting evidence from PET scans + post postmortems
- Supporting evidence : Drug therapy
use of anti psychotic drugs for treating SZ
- Barlow + Durand report that chlorpromazine is effective in reducing SZ symptoms in about 60% cases
= the effectiveness of drug therapy by recovering dopamine levels supports the dopamine hypothesis as it shows SZ was caused by the original excessive / limited amount of dopamine.
- opposing evidence
Kasper et al :
- found anti psychotic drugs effective only for positive symptoms = therefore excessive dopamine can at best explain only some types of SZ
- newer atypical anti psychotic drugs have proved more effective than traditional ones
- Supporting evidence from PET scans + post postmortems
Wise + Stein found that SZ pts who died in brain accidents showed abnormally low levels of dopamine hydroxylase (DBH) in brain fluid
(DBH is enzyme which breaks down dopamine after release)
- correlation not causation ?
neural correlates hypothesis
- certain structures + functions of the brain correlates with displaying symptoms of SZ
- positive symptoms: Allen et al found ps experiencing auditory hallucinations recorded lower activation levels in superior temporal gyrus + anterior cingulate gyrus, + made more errors, compared to a control group.
- Negative symptoms: loss of motivation (Avolition)
- ventral striatum is involved in this
- abnormality in this area may be involved in development of Avolition
- Juckel et al measured activity of ventral stratum in SZ ps
= found lower activity levels than control
Neural correlates AO3
- supporting evidence: Suddath et al
- Methodological strength of supporting evidence
- Correlation / causation issue
- supporting evidence
- Evidence which supports the neural correlates hypothesis comes from Suddath et al.
- Suddath et al used MRI on MZ twins where one was SZ and found large differences:
- the SZ twin had more enlarged ventricles and reduced anterior hypothalamus.
= supporting the hypothesis that there’s a correlation between brain structures and the display of SZ symptoms.
= therefore validating the neural correlates hypothesis
- Methodological strength of supporting evidence
- Research is carried out in highly controlled environments, with specialist high tech equipment such as MRI (Suddath et al)
- MRI take accurate readings on the different regions of the brain such as the hippocampus
- If this research was replicates and re-tested, the same results would be achieved due to its scientific nature.
- This increases the validity of the findings from the supporting evidence and in return adds credibility to the neural correlates hypothesis
3
causation / correlation
- difficult to establish cause + effect
- Do abnormalities in the brain cause SZ symptoms, or are the SZ symptoms affecting brain structures after SZ is developed
- Therefore neural correlates limited explanation as does not tell us much more / further our understanding as we are unable to accurately conclude that brain structures are the onset of SZ
Essay on biological explanations of SZ:
AO1 + AO2
AO1: Genetic hypothesis: SZ is polygenic as different combinations of genes make individuals more vulnerable to SZ.
AO2: Family studies such as Gottesman found the more genetically related a person to someone who has SZ = the greater the risk
AO2: Twin studies (Cardno et al) found that MZ twins are more concordant than DZ = suggests the greater similarity is due to genetic factors.
AO2: Tienari et al: children of SZ parents have higher risk of developing SZ even if adopted family have no history of SZ
AO1: Dopamine hypothesis: Dopamine neurotransmitters linked with SZ.
- Hyperdopaminergia - excessive levels of dopamine in subcortex = positive symptoms
- hypodopaminergia - Low levels of dopamine in pre-frontal cortex = negative symptoms
AO1: neural correlates: certain structures + functions of the brain correlates with displaying symptoms of SZ
AO2: Allen et al found ps experiencing auditory hallucinations recorded lower activation levels in certain parts of their gyrus brain region
AO3 Evaluation for biological explanations of SZ:
- supporting evidence
- causation - correlation problem
- biologically reductionist
- supporting evidence
(or SE from genetic hypothesis)
Support for the dopamine hypothesis comes from drug therapy for SZ.
The mechanism of antipsychotic drugs is to reduce the effects of dopamine = reduce the symptoms of SZ.
- Barlow + Durand report that chlorpromazine is effective in reducing SZ symptoms in about 60% cases
= This therefore, shows that the use of antipsychotic drugs is proven to be more effective in the treatment of positive + negative symptoms which is achieved through the normalisation of dopamine
= The effectiveness of drug therapy by recovering dopamine levels supports the dopamine hypothesis as it shows SZ was caused by the original excessive / limited amount of dopamine.
- causation - correlation problem
- There’s a causation-correlation
- Does the unusual activity in the brain cause the symptoms or are other possible explanations for the correlation.
-Neural correlates hypothesis may suggest that low activity in the striatum causes avolition,
but it could be that avolition means that less information passes through the striatum resulting in the low activity
= Therefore, although neural correlates exist, its limited as it does not further out understanding on the onset of SZ, but instead leaves us confused on whether its correlation or causation.
- Biological reductionist
-Biological for explanations for SZ or biologically reductionist.
- This is scientific as by breaking complex behaviours such as SZ into smaller parts
= makes it easier to investigate
= allowing researchers to focus on specific causes of SZ in more detail
= giving more valid in depth findings
- Biological reductionist can be criticised as it oversimplifies SZ to just genes + neurotransmitters, + the social context which it develops in is not considered.
- It’s said that although biological factors predispose someone to SZ, this has to be triggered by some sort of experience / stressor for symptoms to be displayed.
= Therefore in order to explain SZ effectively, it would be better to take an interactionist approach such as the diaphrases stress model.
Biological therapies for SZ : drug therapies
What are the 2 types of antipsychotic drugs?
- Typical antipsychotic (1st generation) drugs
- Atypical antipsychotic (2nd generation) drugs
Typical antipsychotic drugs
(1st generation drug)
- work as dopamine antagonist
- block dopamine receptors in the synapses of the brain = reducing the action of dopamine.
- also an effective sedative due to its effect on histamine receptors (reduces anxiety + calms down)
- have more side effects