Schizophrenia v2 Flashcards
Define schizophrenia.
A severe mental psychotic disorder characterised by a profound disruption of cognition and emotion - insights and contact with reality is impaired.
Describe the two classification systems to diagnose schizophrenia and their differences.
DSM 5
- Devised by APA in 5th edition
- Two or more positive symptoms for one motnh
- Extreme social withdrawal for 6 months
ICD 11
- Devised by WHO in 11th edition
- One positive symptom and one negative symptom for at least a month (or two negatives)
Outline the two types of schizophrenia.
Type 1 = More positive symptoms
Type 2 = More negative symptoms
Describe three positive symptoms of schizophrenia
1. Hallucinations = sensory experiences of stimuli that have no basis in reality or are distorted perceptions of thing that are there e.g. auditory, tactile, olfactory, visual
2. Delusions = also known as paranoia - irrational or bizarre beliefs an individual believes to be real - typically involves historical, religious or political figures e.g. Jesus or Napolean; may involve them being persecuted by the government or aliens
3. Disorganised speech = result of abnormal thinking patterns; difficulties organising their thoughts and this appears in their speech - derailment is where they slip from one topic to another even mid-sentence; speech may be so incoherant, it sounds like gibberish - ‘word salad’ (only in DSM not ICD)
Describe four negative symptoms of schizophrenia.
1. Speech poverty (alogia) = changes to patterns of speech especially reduction in quality and amount of speech - delay in sufferer’s verbal responses; less complex syntax (fewer clauses, shorter utterances)
2. Avolition = difficulty starting or keeping up with goal-directed activity - they have a sharply reduced motivation to carry out range of tasks.
TRAITS = poor hygiene and grooming; lack of persistence in work or education; lack of energy
3. Affective flattening = reduction in the intensity and range of emotional expression including facial expressions, body language, voice tone and eye contact; deficit in prosody (intonation, tempo, loudness and pausing) which give cues to the emotional content of the conversation
3. Anhedonia = loss of interest and pleasure in most activities to normally pleasurable stimuli - physical anhedonia = inability to feel physical pleasures such as pleasure from food or bodily contact; social anhedonia = inability to feel social pleasures such as interacting with other people
Describe reliability as an issue with classification and diagnosis of schizophrenia.
- Reliability is the consistency of a measuring instrument
- Low inter-rater reliability (the extent to which two independent diagnosticians agree with the same diagnosis for the same individual)
- With DSM, inter-rater was as low as +0.11 in 2001
- Cheniaux (2009) had 2 psychologists diagnose 100 patients using both ICD and DSM
- One psychologist diagnosed 26 DSM and 44 ICD
- Other diagnosed 13 DSM and 24 ICD
- 2019 for DSM 5: inter-rater = +0.97 and test-retest reliability = +0.92
- Recent diagnosis with DSM 5 is reliable and good
Explain validity as an issue with classification and diagnosis of schizophrenia.
- Validity is the extent to which we are measuring what we intend to measure
- Criterion validity is when different assessments arrive at the same diagnosis for the same patient
- Cheniaux (2009) suggests that ICD is more likely to diagnose SZ than DSM so either under or over
- Rosenhan (1973) had 8 pseudo patients who were all able to get admitted into a hospital claiming they hear voices.
- All pseudo patients behaved normally in the hospital and all but one were discharged as ‘SZ in remission’ after 7-52 days
- However, this is an old study so diagnosis was much poorer in 1970s as DSM was not as reliable
How is co-morbidity an issue with classification and diagnosis of schizophrenia.
- Co-morbidity is the idea that two or more occur together at the same time within the same person
- Buckley et al (2009) found that 50% also have depression; 47% substance abuse; 29% PTSD; 23% OCD
- Classifications systems do not distinguish between disorders well which questions validity of diagnosis of SZ
Describe symptom overlap as an issue with classification and diagnosis of schizophrenia.
- Symptom overlap is where there is a considerable overlap between symptoms of SZ and other conditions
- People with DID actually have more schizophrenic symptoms than people diagnosed with SZ
- Questions validity of diagnosis and a patient may be diagnosed with SZ in ICD and with DID under DSM
Outline gender bias in classification and diagnosis of schizophrenia.
- Men are more likely to be diagnosed with SZ than women
- Women SEEM to function better than men by having good family relationships and more likely to work
- Women show better interpersonal function than men
Describe cultural bias in classification and diagnosis of schizophrenia.
- People of Afro-carribean decent are 4.5 times more likely to be diagnosed with schizophrenia
- This is known as category failure
- Because in their culture, hallucinations are acceptable as communication with their ancestors
- Hence diagnosis rate of SZ in Africa are low and in the UK high
Outline family and twin studies as part of genetic explanations of SZ.
- Family studies - Gottesman (1991) found that if both parents had SZ, likelihood of offspring would be 46% - drops to 13% with one parent and 9% with a sibling
- More closer you are genetically related = more likely to develop SZ
- Twin studies - Joseph (2004) did a review of twin studies since 2001 and found overal concordance rate of MZ to be 40% and DZ as 7.4%
Outline candidate genes as part of genetic explanations of SZ.
- SZ is polygenic - combination of different genes implicated in SZ
- Family studies show that SZ is associated with 8p21-22 chromosome to identify a high-risk sample
- With gene mapping, PCM1 gene causes susceptibility
- Gene mapping showed NRG3 gene interacts with both NRG1 and ERBB4 gene variants to create susceptibility for SZ
Evaluate genetic basis of SZ.
ADV 1: Research evidence
- Wealth of research evidence to support genetic basis for SZ such as Gottesman, Joseph and Tienari
- Lots of support indicates strong link between genes and SZ
- High predictive value - if family member has SZ there is a chance you will have it too
DIS 1: Twin Studies issues
- Difficult to separate nature and nuture
- MZ twins are reared together, sent to same school, same clothes etc.
- Even in adoption studies, children tend to be adopted by relatives who may rear child similarly to parents
DIS 2: SZ without family history
- Mutation in parental DNA caused by radiation, poison or infection
- Brown et al (2002) found a positive correlation between paternal age and risk of schizophrenia - 0.7% with fathers under 25 increases to 2% in fathers over 50
- Although no direct genes are involved, age of father at fertilisation affects risk of SZ
- Role of nature and nuture both play a part
DIS 3: Biologically reductionist
- SZ is only caused by genes and ignoring other factors like psychological factors and family upbringing
- Certain parenting styles (schizophrenogenic mother) in an individual’s childhood can trigger SZ symptoms in adulthood
Define neural correlates.
Neural correlates are the measurements of the structure or function of the brain that have a relationship with SZ especially different regions of the brain
Outline the role of dopamine in the dopamine hypothesis in schizophrenia.
Dopamine is a chemical messenger responsible for:
- regulating movement
- attention
- learning
- emotional responses
Dopamine contributes to feelings of pleasure and satisfaction as part of a reward system, it also contributes to addiction.
- Excess dopamine in certain regions is associated with POSITIVE symptoms of SZ
- Neurons that transmit dopamine fire too easily, often leading to hallucinations and delusions
- They have high levels of D2 receptors on receiving neurons resulting in more dopamine binding and thus more dopamine firing
What are the two consequences of the dopamine hypothesis?
Hyperdopaminergia in subcortex
- High levels of dopamine in areas know as the subcortex
- e.g. excess in Broca’s area may be associated with problems in speech or auditory hallucinations
Hypodopaminergia in cortex
- Focused on low levels of dopamine
- Low levels in pre-frontal cortex (responsible for thinking and decision making) cause negative symptoms
Evaluate neural correlates explanation of SZ (dopamine hypothesis).
ADV 1: Drug research evidence
- Dopamine agonists like amphetamines work to increase levels of dopamine
- This makes schizophrenic symptoms worse in sufferers and induces SZ-like symptoms in non-sufferers
- This supports idea of hyperdopaminergia
- Anti-psychotic drugs act like dopamine antagonists and reduce levels of dopamine in SZ
- Chemicals to produce dopamine are taken up faster in SZ brains compared to controls
- Suggests SZs produce more dopamine
DIS 1: Biologically deterministic
- Individual has no control over onset of SZ
- There are other factors such as psychological factors or family upbringing or cognitive explanations - focus on impaired thinking
- Glutamate is another neurotransmitter than has been implicated in SZ so other neurotransmitters are involved other than dopamine
DIS 2: Correlation-causation issue
- Do high levels of dopamine cause SZ or are they caused by SZ?
- Many studies in biological approach are correlational not experimental so we cannot establish cause-effect relationship
Outline the schizophrenogenic mother in family dysfunction as a psychological explanation for schizophrenia.
- A psychodynamic explanation of SZ
- SZ causing mother - cold, rejecting and controlling
- Creates family climate full of secrecy and tension
- Leads to lack of trust in relationships
- Develops into paranoid delusions (belief that one is being persecuted by another) ultimately forming SZ
- Father is passive and doesn’t get involved in upbringing
Outline the double bind theory in family dysfunction as a psychological explanation for schizophrenia.
- Focused on family communication style
- When children frequently receive contradictory messages from their parents
- Child feels trapped where they feel they are doing the wrong thing but they get mixed messages about this (e.g. mother telling a child she loves her but showing disgust as she says this)
- Unable to comment on unfairness or to seek clarification
- Child may get it wrong (which happens often)
- They are punished by withdrawal of love
- Child feels confused about the world and sees it as a dangerous place
- Results in paranoid delusions
Outline expressed emotion in family dysfunction as a psychological explanation for schizophrenia.
Expressed emotion is the level of negative emotion expressed towards a patient by their carers. It involves:
- Verbal criticisms of the patient (sometimes violence)
- Hostility (including anger and rejection)
- Emotional over-involvement including needless self-sacrifice
High levels of EE causes serious levels of stress - can cause relapse in SZ patients or be an environmental trigger if they have a genetic vulnerability to SZ
Describe two advantages of family dysfunction explanation of SZ.
Research Support
- Tiernari et al (1994) adoption study
- Adopted children who had SZ biological parents were more likely to develop SZ than those with non-SZ parents
- This difference only occurred where the adopted family was rated disturbed or dysfunctional
- SZ only manifested itself under the appropriate environmental trigger
- Read et al (2005) found reviewed 46 studies of child abuse and SZ
- 69% of adult women diagnosed with SZ had history of physical, sexual or both in childhood
- 59% of men
Double Bind Theory support
- SZ patients reported higher recall of double-bind statements by their mothers than non-SZ
- May not be reliable as memory is not always accurate and can be flawed
- Recall affected by SZ due to hallucinations or delusions
Outline two drawbacks of family dysfunction.
EE and relapse
- Not all patients who experience high EE families relapse and not all who live in low EE avoid relapse
- One quarter of patients showed no physiological responses to stressful comments from their relatives
- Evidence for EE as factor of relapse is mixed
Environmentally reductionist
- Simplifying the cause of SZ to family upbringing and ignoring other factors
- Biological approach suggests that those with the PCM1 gene are more likely to become SZ
- Important to look at more holistic explanation
Describe the cognitive explanation for SZ.
Focus on role of mental processes. SZ is associated with several types of dysfunctional thought processing.
1. Metarepresentation:
- Cognitive ability to reflect on thoughts and behaviours which enables insight into our own intentions, goals and allowing interpretation of others
- Dysfunction disrupts ability to recognise our own thoughts as being our own rather than someone else
- This explains auditory hallucinations and delusions
2. Central Control:
- Cognitive ability to suppress automatic responses while we perform other actions instead
- Speech poverty could result from inability to ignore your own automatic thoughts
- They tend to experience derailment of their thoughts because there is too much going on in their thought processes so they lose control of their own thoughts
Give two strengths of cognitive explanation of SZ.
Strong research evidence
- Stirling et al (2006) compared 30 diagnosed schizo patients to 18 non-patient controls on a rnage of cognitive tasks
- Including the stroop effect (asking them to say the colour of a word that is written as a different colour)
- SZ took twice as long to answer compared to controls
- Displays dysfunctional thought processing
Supported by CBT
- As schizophrenia is a thought disorder, drugs cannot be solely used to treat it
- CBT will aim to question and challenge the hallucinations and delusions
- Through disputing and behavioural techniques (positive reinforcment)
- Proven as effective treatment of SZ.
Outline two disadvantages of cognitive explanations of SZ.
Cause or consequence?
- Did dysfunctional thought processing cause schizophrenia or is it a symptom of SZ instead?
Ignores biological factors
- Dysfunctional thought processing could be due to abnormal dopamine levels in the brain
- Reductionist explanation as you are simplifying SZ to basic elements
- no consideration of genes, neurotransmitters and stress which all have been shown to contribute to SZ.
Outline typical anti-psychotics as a biological therapy for schizophrenia.
SZ is treated through anti-psychotic drugs which have two types: typical and atypical
Typical anti-psychotics
- Dopamine antagonists and work by reducing the effects of dopamine
- They bind to but do not stimulate dopamine receptors thus blocking their action, reducing positive symptoms
- e.g. Chlorpromazine is an effective sedative & is faster absorbed as a syrup so it helps calm nerves
Describe atypical anti-psychotic drugs as a biological treatment for SZ.
- Work like typical anti-psychotics by binding to D2 receptors but then they rapidly dissociate to allow normal dopamine transmission
- This minimises the side effects and has a beneficial effect on negative symptoms & cognitive impairment
- e.g. Clozapine binds to dopamine receptors but also acts on serotonin and glutamate receptors
- Helps reduce depression and anxiety + improve cognitive functioning
- It generally improves mood - for high suicide risk patients (30-50% of SZ patients are likely to attempt)
- Risk of agranulocytosis - fatal blood condition
- e.g. Risperidone works better in binding to the dopamine receptors so less side effects - less dosage
Evaluate Drug therapy.
ADV 1: Thornley et al (2003)
- Comparing chlorpromazine with placebo
- 13 trials and 1100 pps showed reduced symptoms and better overall functioning
- 3 trials and 500 pps showed lower relapse rates
- Typical anti-psychotics are effective against placebo
ADV 2: Leucht et al (2012)
- Meta-analysis of 65 studies + 6000 patients
- Some pps taken off their anti-psychotic medication and given placebo instead
- In 12 months, 64% placebo pps relapsed and 27% relapsed on anti-psychotics
DIS 1: Extreme side-effects
- Typical: dizziness, agitation, weight gain, itchy skin
- Also tardive dyskinesia caused by dopamine supersensitivity: involuntary facial movements
- Neuro malignant syndrome (NMS) leads to high temp, derilium, coma and can cause death (0.1-2%)
- Clozapine: agranulocytosis (stops production of white blood cells leads to immunity issues so blood tests are required regularly)
DIS 2: Ethical Issues
- SZ is a psychotic disorder so patients may not be in the right frame of mind to give fully informed consent
- Severe side effects would question extent of the harm (physical and mental) and whether effects are reversible e.g. NMS and tardive dyskinesia
Describe CBTp and its phases as a psychological treatment of SZ.
NICE recommends at least 16 sessions of CBTp for SZ
1. Assessment = realistic goals are discussed using patient’s distress as motivation for change
2. Engagement = therapist empathises with patient perspective and feelings of distress and stresses
3. ABC model = gives explanation of activating event that induces their irrational beliefs that cause emotional and behavioural consequences. Irrational beliefs are rationalised, disputed and changed
4. Normalisation = explaining that their unusual experiences e.g. hallucinations reduce anxiety and sense of isolation - patients feel less alienated and stigmatised
5. Critical collaborative analysis = gentle questioning to help them understand illogical deductions and conclusions (must be trust, empathy and non-judgemental environment)
6. Developing alternative explanations = patient develops own alt explanations for previously unhealthy assumptions
Evaluate CBTp as a treatment of SZ.
ADV 1: NICE (2014) Review
- Compared to standard care (anti-psychotics alone)
- CBTp effective in reducing rehospitalisation rates up to 18 months following treatment
- Reduces severity of symptoms
- Improves social functioning
- However, difficult to assess CBTp alone as patients were treated alongside medication
DIS 1: Lack of Availability
- In UK, only 1 in 10 pp with SZ have access to CBTp
- In NW England, only 7% offered CBTp
- Many who are offered refuse or fail to attend, limiting the effectiveness further
DIS 2: Issues with meta-analysis of CBTp
- Fails to account for quality of studies e.g. no random allocation or control conditions
- Some fail to assess subsequent assessment of symptoms or general functioning after CBTp
- Wykes et al (2008) - the more rigorous the study, the weaker the effect of CBTp
Describe family therapy as a treatment of SZ.
- Family therapy is the range of interventions aimed at the family of someone with SZ
- Its main aim is to provide support for carers to make family life less stressful + reduce rehospitalisation
- Reduces levels of expressed emotion by increasing capacity of relatives to solved related problems
- Involves psychoeducation, reducing emotional climate and burden of care for family members, reduces expression of anger and guilt by relatives
Outline Pharoah (2010) study of family therapy.
- Review of 53 studies investigating family intervention
- Compared outcomes of family therapy to standard care (anti-psychotic medication alone)
Results:
- Some studies reported improvement in overall mental state (mixed impressions)
- Family therapy increased compliance with medication
- Improvement in general functioning but no concrete outcomes like employment or independent living
- Reduction in relapse and readmission up to 24 months
Evaluate family therapy as a treatment of SZ.
ADV 1: Economical benefits
- NICE review demonstrated that family therapy is associated with significant cost savings compared to standard care
- Reduction in costs of rehospitalisation (lower relapse rates for a sig. period after intervention)
ADV 2: Lobban et al. (2013)
- Analysed results of 50 studies involving family therapy
- 60% of studies reported significant positive outcomes for at least one category for relatives
- Coping and problem solving; family functioning; relationship quality (including EE)
- But methodological quality was poor for most of 50 studies
DIS 1: Lack of blinding
- In Pharoah’s meta-analysis, 10 out of 53 studies did not use blinding so raters are aware of the conditions allocated to each pp in the study
- This creates rater bias and reduces validity of studies
Outline token economies as a way to manage SZ.
- Reward systems used to manage the behaviour of SZ patients in a hospital setting
- Institutionalisation may have led to maladaptive behaviours due to spending too long with other catatonic patients and leads to bad hygiene and habits
- Improves patient’s quality of life so they can live outside a hospital setting
- Based on operant conditioning
- Tokens (secondary reinforcers) are given immediately so patient can associate the positive behaviour with a rewards rather than delayed rewards
Evaluate token economies as a method to manage SZ.
ADV 1: Dickerson et al (2005)
- Reviewed 13 studies using token economies
- 11 reported beneficial effects directly attributed to the use of token economies to manage SZ
- Provide evidence of TE to increase adaptive behaviours
- However, many studies have methodological issues which could’ve affected the impact of TEs
DIS 1: Ethical concerns
- To make reinforcement effective, clinicians may exercise control over resources like food, privacy or access to activities that stop boredom
- However, all human beings should have basic rights that shouldn’t be violated regardless of the positive consequences through TE programmes
DIS 2: Lack ecological validity
- Only works in hospital setting not real life
- Issues with administration to outpatients in the community as hospitals have 24 hour care and tokens are given immediately
- In real life, not all behaviours are rewarded or rewarded immediately so reinforcement goes extinct
- Lacks ecological validity as it cannot be applied in real world
Breifly outline the interactionist approach to SZ.
Interactionist approach is an approach that acknowledges that there are biological, psychological and societal factors in the development of SZ.
Biological factors include genes and neurotransmitters while psychological factors include upbringing, stress and family environment.
Describe how interactionist approach explains the onset of SZ.
- Diathesis-stress model
- Diathesis means vulnerability - genetic component
- Stress is a negative psychological experience
- Both a genetic vulnerability and stress trigger are necessary to develop SZ
- Modern view of diathesis also includes psychological trauma as well as genes
- Modern understanding of stress is anything that can risk triggering SZ e.g. cannabis use makes it 7 times more likely to develop SZ symptoms
- Cannabis interferes with the dopamine system
Describe how interactionist approach treats SZ.
- Associated with combining anti-psychotic medication and psychological therapies like CBTp
- Unusual to treat with CBTp alone as it is a complex psychotic disorder and drug therapy is required to control the patient’s symptoms first
- Drug therapy is used in hospital setting with token economies to manage behaviour
Evaluate the interactionist approach to SZ.
ADV 1: Evidence for diathesis-stress model
- Tiernari et al (2004) adoption study of SZ
- Adoptive parents parenting style was assessed for children with SZ mothers and compared to a control group of children with no SZ risk
- Child-rearing style with high criticism and conflict and low levels of empathy implicated in development of SZ but only with high genetic risk
- Genetic vulnerability and family-related stress combine in the development of SZ
ADV 2: Tarrier et al (2004)
- Randomly allocated 300 patients to medication + CBT group; medication + counselling group; control group (medication oly)
- Patients in the combination groups showed lower symptom levels than those in control
- But no difference in hospital readmission
- Clear practical advantage to adopting interactionist approach to treatment
DIS 1: Too simplistic diathesis stress model
- Multiple genes increase vulnerability not one schizogene
- Stress comes in many forms including dysfunctional parenting not just genes
- Childhood sexual trauma can be a diathesis and cannabis as a trigger - Houston et al (2008)
DIS 2: Incomplete understanding
- There is strong evidence of some sort of underlying vulnerability coupled with stress
- We don’t understand mechanisms by which SZ symptoms appear and how vulnerability and stress produce them
- Doesn’t undermine support but explanation is incomplete
