How do DSM-5 and ICD-10 differ in the diagnosis of schizophrenia?
DSM-5 = one positive symptom must be present.
ICD-10 = two or more negative symptoms are sufficient.
What does positive symptoms of schizophrenia mean?
Additional experiences beyond those of ordinary existence.
Give 2 positive symptoms of schizophrenia
1) Hallucinations - sensory experiences with no basis in reality or distorted perceptions of real things e.g. hearing voices.
2) Delusions - beliefs that have no basis in reality; changing behaviour that may make sense to schizophrenic but isn’t in reality e.g. believing one’s the victim of a conspiracy.
What does negative symptoms of schizophrenia mean?
Loss of usual abilities and experiences.
Give 2 negative symptoms of schizophrenia
1) Avolition - severe loss of motivation to carry out everyday tasks e.g. work = lower activity and unwillingness to carry out goal-directed behaviours.
2) Speech poverty (Alogia) - a reduction in the amount and quality in speech
Give 4 issues in the diagnosis of schizophrenia
1) Reliability - consistency of diagnosis.
2) Validity - extent to which diagnosis and classification measure what they are designed to measure.
3) Co-morbidity - occurrence of two illnesses together confusing diagnosis and treatment.
4) Symptom overlap - two or more conditions sharing symptoms questions validity of classification.
What did Cheniaux et al. (2009) find with the diagnosis of schizophrenia?
- It had low reliability.
- Two psychiatrists independently diagnosed 100 patients using both ICD and DSM criteria.
- Low inter-reliability.
- (1) 26 diagnosed with DSM and 44 with ICD.
- (2) 13 diagnosed with DSM and 24 with ICD.
How is the diagnosis of schizophrenia questioned validity wise?
- Cheniaux showed that Sz is much more likely to be diagnosed with ICD than DSM.
- Over-diagnosed in ICD or under-diagnosed in DSM?
= poor criterion validity.
A part from low validity and reliability, give a further limitation of the diagnosis of schizophrenia
- two conditions = a single condition?
- Buckley et al. (2009) concluded half patients with Sz also have a diagnosis of depression (50%) or substance abuse (47%)
How is there gender bias in the diagnosis of schizophrenia
(i) Longenecker et al. (201) found that since the 1980s men have been diagnosed more often than women.
(ii) Cotton et al. (2009) - female patients typically function better than men = may escape diagnosis due to better interpersonal functioning.
What did Gottesman (1991) find the concordance rate of both schizophrenia was in MZ and DZ twins?
MZ = 48% DZ = 17%
How is schizophrenia polygenetic and aetiologically heterogeneous?
P = each gene confers a small increased risk of schizophrenia. AH = different combinations lead to schizophrenia
What did Ripke et al. (2014) find?
- 108 separate genetic variations associated with increased risk
How is dopamine (DA) involved with schizophrenia?
Featured in the functioning of brain systems related to the symptoms of schizophrenia
Hyperdopaminergia is linked with what areas of the brain which may lead to what symptoms?
- Hallucinations and speech poverty.
What is hyperdopaminergia?
High DA activity in the subcortex
What is hypodopaminergia?
Low levels of dopamine in the prefrontal cortex.
What can low levels of DA in the prefrontal cortex lead to?
Define neural correlates.
Measurements of the structure or function of the brain that correlate with the positive or negative symptoms of schizophrenia
How is avolition linked to the ventral striatum?
- VS involved in anticipation of reward (motivation)
= avolition explained by low levels here?
- Juckel et al. (2006) found a negative correlation beween VS activity and overall negative symptoms.
In terms of neural correlates, what would a negative correlation mean?
- There is a correlation between an area of the brain and the negative symptoms of schizophrenia
What part of the brain are hallucinations believed to be linked with?
- Superior temporal gyrus.
- Allen et al. (2007) - patients experiencing auditory hallucinations recorded lower activation levels in this area and anterior cingulate gyrus.
What strong evidence is there for genetic vulnerability of schizophrenia?
- Gottesman with his family study of schizophrenia.
- Tienari et al. (2004) did an adoption study.
- Showed children of people with Sz are still at heightened risk of Sz if adopted into families without history of Sz.
How is there mixed support for the dopamine hypothesis?
- Dopamine agonists, e.g. amphetamoines, that increase increase DA can induced schizophrenic-like symptoms in people without Sz.
- Anti-psychotics that lower DA can be effective in reducing symptoms
- Some candidate genes responsible for production of other genes
= DA inadequate.
A part from mixed support for the DA hypothesis, give 2 further limitations of the biological explanation of schizophrenia
1) Correlation-causation problem:
- is it unusual activity in the brain causing the symptoms?
e.g. it is assumed that low activity in VS caused avolition
= could be that less info passes through the VS resulting in low activity?
2) Clear that the environment is also involved:
- probability of developing Sz even if MZ twins is less than 50%
- suggests other factors like dysfunctional family
= interactionist approach more appropriate?
What 2 types of drug treatments are there for schizophrenia?
- Typical antipsychotics
- Atypical antipsychotics.
Describe typical antipsychotic drugs.
- E.g. Chlorpromazine, first introduced in the 1950s.
- Aim to reduce the action of dopamine; acting as antagonists.
- Work by blocking dopamine receptors in the synapses in the brain.
- C’mazine normalises neurotranismission.
- C’mazine also has effect on histamine receptors, leading to sedation effect.
How do typical and atypical antipsychotics differ in what they target?
Typical = dopamine
Atypical = dopamine and serotonin.
Describe atypical antipsychotic drugs
- E.g. Clozapine, first introduced in the 1970s.
- Aimed to improve effectiveness and suppress psychoses and also minimising side effects.
- Bind to serotonin and dopamine receptor sites.
- Also reduces depression and anxiety, improving cognitive functioning.
Why is clozapine lowering mood significant?
- Up to 50% of people suffering from schizophrenia attempt suicide.
Why was risperidone developed after clozapine?
- Clozapine involved in deaths because of a blood condition.
- It binds more strongly to DA receptors so is more effective in smaller doses and has fewer side effects.
What evidence is there for the effectiveness of drug therapy for schizophrenia?
- Thornley et al. (2003) - data from 13 trials found that chlopromazine was associated with better functioning and reduced symptom severity compared with placebo.
- Meltzer et al. (2012) - clozapine more effective than typical drugs, 30-50% more effective in treatment-resistant cases
Give 3 evaluative limitations of drug therapy as a treatment for schizophrenia
1) Side effects:
- typical drugs associated with dizziness, agitation - long term may lead to lip smacking due to DA super-sensitivity.
- Most serious is neuroleptic malignant syndrome (NMS)
= Rate of attrition? Mistrust?
2) Doubts about true effectiveness of antipsychotics:
- Healy (2002) - data from successful trials have been published multiple times, exaggerating positive effects.
- Also mostly short-term effects.
- As they calming effect = easy to demonstrate they have a positive effect.
3) Antipsychotics drugs may be a ‘chemical cosh’:
- may be used in hospital to calm patients and make them easier for staff to work with, not benefit patients directly.
- Human rights’ abuse? Ethics?
In terms of psychological explanations for schizophrenia, how many family dysfunction explanations are there? Name them.
1) Schizophrenogenic mothers.
2) Double-bind theory.
3) Expressed emotion.
Describe schizophrenogenic mothers
- Fromm-Reichmann (1948) psychodynamic explanation based on early experiences.
- Cold, rejecting, creating a family climate of tension and secrecy.
- Leading to distrust, paranoid delusions and Sz.
Describe the double-bind theory.
- Bateson et al. (1972) - child regularly trapped in situations where they fear doing the wrong thing; receiving conflicting messages about what counts as wrong.
- Cannot express feelings about unfairness of situation.
- When they ‘get it wrong’ - child is punished by withdrawal of love.
= World is confusing and dangerous –> disorganised thinking and delusions.
How’s expressed emotion different from schizophrenogenic mother and double-bind theory?
- It’s to do with what can cause relapse, not the cause.
Describe expressed emotion
- EE is the level of emotion, mainly negative, expressed towards the Sz patient.
- Verbal criticism of them, hostility, over-involvement in their life.
- High levels of EE cause stress in the Sz patient = relapse.
In terms of the psychological explanation for schizophrenia, what is the cognitive explanation?
- Dysfunctional thought processing, low levels of it suggest impairment
e. g. VS with negative symptoms
- Dysfunction of metarepresentation disrupts our ability to recognise our thoughts as our own, leading to sensation of hearing voices (hallucinations) and having thoughts placed in minds by others (delusions).
What is metarepresentation?
- The cognitive ability to reflect on thoughts and behaviour (Frith et al. 1992)
How did Frith et al. (1992) say dysfunction of central control can lead to speech poverty?
- Central control = cognitive ability to suppress automatic responses while performing deliberate actions.
- People with Sz experience derailment of thoughts and spoke sentences because each word triggers automatic assocations they can’t suppress.
What support is there for different information processing?
- Stirling et al. (2006) compared 30 Sz patients with 18 patients on cognitive tests, e.g. Stroop Test.
- Patients 2x longer than control group = had to suppress impulse to read word, supports Frith’s theory.
= cause of symptoms or cause of disorder?
How is evidence for family relationships a weakness?
- Often retrospective.
- Read et al. (2005) - 42 studies, 69% of all adult female patients with Sz had a history of abuse (as well as 59% of men).
- Most info gathered after diagnosis.
- Symptoms distorting patients’ recall?
A part from family relationship evidence being retrospective, give 2 more evaluative limitations of psychological explanations of schizophrenia
1) Evidence for family-based explanations is weak:
- poor childhood experiences may be associated with Sz, but little evidence for family dysfunction.
- theories based on clinical observation.
- blame game on parents too.
2) Biological factors sometimes overlooked:
- can’t explain it psychologically with biological explanation too.
- can both separately produce same symptoms?
- diathesis-stress model instead?
Give the 3 psychological therapies for schizophrenia
2) Family therapy
3) Token economies.
In terms of psychological therapy for schizophrenia, describe CBT.
- Aims to help patients identity irrational thoughts and try to change them,
- Discussion of how true they are, considering less threatening possibilities.
- Helps patients understand their symptoms, and how they impact on their feelings and behaviour
= realise their beliefs are not based on reality-> reduced anxiety.
In terms of psychological therapy for schizophrenia, describe family therapy
- Improve communication and interaction in the family.
- Reduce stress in the family that may contribute to relapse; reduced EE.
What do Pharoah et al. (2010) propose to improve family functioning?
- To reduce likelihood of relapse and readmission.
1) Reduce stress of caring for a relative with Sz.
2) Improve ability to anticipate and solve problems.
3) Reduce guilt and anger in family members.
4) Improve beliefs about and behaviour towards Sz.
In terms of psychological therapy for schizophrenia, describe token economies
- Reward systems (tokens) for desirable behaviours, by operant conditioning e.g. getting dressed.
- The reward reinforces desirable behaviour, reward given immediately preventing delay discounting.
- Tokens have no value in themselves, but are swapped for rewards e.g. cigarettes
- Tokens = secondary reinforcers as value is learned by association (classical conditioning) with innate primary reinforcers.
How does evidence for psychological therapies show limited evidence?
- Jauhar et al. (2014) CBT significant but small effect on positive and negative symptoms.
- McMonagle + Sultana (2009) - 1 of 3 studies of token economies that used random allocation showed improvement.
- Pharoah et al. reviewed his proposal and found moderate evidence for reduction in relapse over one year = evidence inconsistent.
How might the therapies help but not be a cure?
- CBT = make sense of symptoms.
- Family therapy = reduce stress.
- TE = behaviour socially acceptable.
= do not cure.
A part from limited benefits of psychological therapies and therapies helping but not being a cure, give 2 limitations of psychological therapies for schizophrenia.
1) Ethical usses:
- severely ill patients cannot get privileges b/c they are less able to comply with desirable behaviours than moderately ill patients.
- Also, CBT challenges paranoia but what about freedom of thought? Some may believe in a controlling Gov?
= challenging this may be modifying people’s political beliefs.
2) Quality of evidence:
- positive results found for therapies
- but these studies may lack a control group or random allocation
- overestimation of evidence?
What does diathesis and stress also mean?
What is the diathesis-stress model?
- Vulnerability and trigger.
- Vulnerability (to Sz), stress in this context refers to negative psychological experiences.
; vulnerability and stress both needed to develop Sz.
Describe Meehl’s model of schizophrenia?
- Gene + stess = schizophrenia.
- Someone without a ‘schizogene’ should never develop schizophrenia, no matter the exposed stress.
- Those with the gene are vulnerable to the effects of chronic stress.
- Gene not sufficient, just necessary for development of schizophrenia.
What is the modern understanding of diathesis?
- Diathesis not due to one schizogene, instead its many genes increasing vulnerability.
- Diathesis not necessarily genetic, may be early psyhological trauma affecting brain development e.g. child abuse affects HPA, making vulnerability to stress.
What is the modern understanding of stress?
- Anything that risks triggering Sz, including psychological stress.
- E.g. cannabis use can increase the risk of Sz 7x as it interferes with DA system.
What is the treatment for schizophrenia according to the interactionist approach?
- Combine antipsychotic medication and CBT.
- Turkington et al. (2006) - possible to believe in biological causes and still practice CBT to relieve psychological syptoms.
- One should not adopt solely one approach.
How is the interactionist approach useful in treatment of schizophrenia?
(i) Tarrier et al. (2004)
- randomly allocated 315 patients to;
(1) medication + CBT
(2) medication + supportive counselling.
(3) control group
= patients in combo groups showed lower symptom levels than medication only.
= no difference in readmission though.
How is the original diathesis-stress model too simplistic?
- No sole ‘schizogene’
- Stress also comes in ma forms.
- Stress can also include biological factors.
- Houston et al. (2008) - childhood sexual trauma was a diathesis and cannabis was the trigger.
A part from simplicity of the diathesis-stress model, give 2 further limitations of the interactionsist approach to schizophrenia.
1) Don’t know exactly diathesis and stress work;
- evidence to suggest underlying vulnerability coupled with stress can lead to Sz.
- do not understand mechanisms by which Sz symptoms work, and how vulnerability and stress produce them.
= incomplete understanding.
2) Treatment-causation fallacy:
- Turkington et al. (2006) arguing that an interactionist approach is more effective does not mean it is simply correct.
- Drugs helping does not mean its biological in origin = treatment-causation fallacy.
- Superior outcomes of combined therapies should not be over-intererpreted in terms of evidence in support.