schizophrenia essay plans Flashcards
Diagnosis AO1
Classification of mental disorder - CD10 and DSM5 cluster symptoms together to identify disorders and distinguish them from eachother
Positive symptoms - atypical symptoms in addition to normal experiences
Hallucinations - unreal or distorted sensory experiences eg auditory and visual
Delusions - beliefs with no basis in reality eg believing someone is persecuting you
Negative symptoms - atypical experiences through loss of usual experience
Speech poverty - reduced frequency or quality of speech
Avolition - loss of motivation, low activity levels
Co-morbidity - two disorders or conditions occur together - frequently diagnosed together - questions validity of classifying two separately
Symptom overlap - when two or more conditions share symptoms - question validity of classifying the two disorders separately
Diagnosis AO3
Good reliability
P – strength as high reliability
E – psychiatric diagnosis said to be reliable when different diagnosing clinicians have same diagnosis (inter-rater reliability)
E - DSM-5 reliability has improved – inter-rater reliability = +.97 and test-retest reliability = +.92 - Osorio et al
L – we can be reasonably sure that the diagnosis of schizophrenia is consistently applied
Low validity
P – limitation is diagnosis has low validity
E – validity over concerns whether we assess what we are trying to assess
E - 100 clients assessed, 68 diagnosed with schizophrenia using ICD-10 and 39 with DSM-4 – low criterion validity - Cheniaux et al
L – schizphrenia is either over- or under-diagnosed according to the diagnostic system so criterion validity is low
Counterpoint
P – excellent agreement between clinicians when used two measures
E - alternative diagnostic procedures within DSM-5 show good agreement - Osorio et al
L – criterion validity is good provided it takes place within a single diagnostic system
Co-morbidity
P – limitation due to co-morbidity with other conditions
E – calls into question validity of diagnosis
E - Around half of clients also have another diagnosis eg depression, substance abuse - Buckley et al
L – problem as schizophrenia may not exist as distinct condition – problem with diagnosis
Gender bias
P – limitation due to gender bias existing in diagnosis
E – Since 1980s more men than women have received a diagnosis – maybe less vulnerable or genetic factors
E – however more likely under diagnosed as have closer relationships and support so better functioning than men
L – alpha bias – women may not therefore be receiving treatment and services that might benefit them
Culture bias
P – cultural bias existing in diagnosis
E - African-Caribbean British – 9 times more likely to be diagnosed than white British
E - Maybe because norms in African-Caribbean communities misinterpreted by white clinicians
L - British African-Caribbean people may be discriminated against by a culturally-biased diagnostic system
Symptom overlap
P – symptoms overlap with other conditions
E - Symptoms of schizophrenia and eg bipolar disorder overlap, both conditions involve delusions and avolition
E - Makes diagnosis and classification difficult as suggests variations of single condition
L – schizophrenia may not exist as a distinct condition so classification and diagnosis are flawed
Biological explanation AO1
Genetics - DNA impacting psychological features - transmitted from parents
Neural correlates - patterns of structure of activity in the brain that occur in conjunction with an experience and may be implicated in the origins of that experience
Dopamine - neurotransmitter - high levels associated with schizophrenia - generally has an excitatory effect and linked with sensations of pleasure
Family studies - MZ 48% DZ 17% general population 1%
Candidate genes - individual genes may be associated with increased risk eg dopamine coding genes
Role of mutation - parental DNA may mutate (radiation, virus) - explains schizophrenia when no family history
Neural correlates - research identified some neural correlates ie brain structure or function - best known of schizophrenia is is dopamine
Original dopamine hypothesis - high levels in subcortical brain areas - hyperdopaminergia - based on discovery that drugs used to treat schizophrenia caused symptoms similar to those with parkinson’s
Updated version - abnormally low levels - hypodopaminergia - Davis et al - cortical hypodopaminergia - in brain’x cortex can lead to hyperdopaminergia in subcortical areas
Biological explanation AO3
Research support
P - strength as strong evidence base
E - family studies show risk increases with genetic similarity, adoption studies who biological children with parents with schizophrenia are heightened risk even if they grow up in an adoptive family
E - recent twin study by Rikke Hilker et al showed a concordance rate of 33% of identical twins and 7% for non-identical twins
L - shows people are more vulnerable to schizophrenia as a result of their genetic make-up
Environmental factors
P - limitation of genetic explanation is clear evidence of environmental influence
E - include both biological and psychological influences - biological risk factors include birth complications and smoking THC-rich cannabis in teenage years - psychological risk factors eg childhood trauma leaves people more vulnerable
E - 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of matched group with non-psychotic mental health issues
L - genetic factors alone cannot provide a complete explanation for schizophrenia
Genetic counselling
P - application of understanding is genetic counselling
E - if one or more potential parents have a relative with schizophrenia, they risk having a child who would go on to develop the condition
E - however the risk estimate provided by genetic counselling is just an average figure
L - it will not really reflect the probability of a particular child going on to develop schizophrenia because they will experience a particular environment which also has risk factors
Evidence for dopamine
P - strength as support for idea
E - amphetamines increase DA and worsen symptoms in people with schizophrenia and induce symptoms in people without
E - antipsychotic drugs reduce DA activity and reduce the intensity of symptoms - some candidate genes act on the production of DA or DA receptors
L - strongly suggests that dopamine involved in the symptoms of schizophrenia
Glutamate
P - limitation as evidence for central role of glutamate
E - post-mortem and live scanning studies have consistently found raise levels of neurotransmitter glutamate in several brain regions of people with schizophrenia
E - several candidate genes for schizophrenia are believed to be involved in glutamate production or processing
L - equally strong case can be made for role of other neurotransmitters
Amphetamine psychosis
P - Catherine Tenn et al - induced schizophrenia-like symptoms in rats using amphetamines
E - Relieved symptoms using drugs that reduce DA action - this supports the dopamine hypothesis
E - however, other drugs that also increase DA levels do not cause schizophrenia-like symptoms
L - Garson has challenged the idea that amphetamine psychosis closely mimics schizophrenia
Psychological explanation AO1
Family dysfunction - poor family communication, cold parenting and high levels of expressed emotion - risk factors for the development and maintenance of schizophrenia
Schizophrenogenic mother - Fromm-Reichmann - psychodynamic explanation - mother is cold, rejecting and controlling, family climate of tension and distrust - leads to paranoid delusions - leads to distrust to develop into paranoid delusions
Double-blind theory - Bateson et al - child confused by mixed messages in communications and punished by withdrawal of love - risk factor rather than cause
Expressed emotion - high levels of verbal criticism, hostility, emotional over-involvement (needless self-sacrifice) - stress can trigger diathesis-stress model
Cognitive explanations - explanations that focus on mental processes such as thinking, language and attention
Dysfunctional thinking - disrupted through processing in ventral striatum (negative symptoms) and temporal gyri associated with hallucinations (pos)
Metarepresentation dysfunction - Frith et al - disruption of ability to reflect on own thoughts and behaviour leads to thinking that own actions and thoughts are being carried out by someone else - explains some hallucinations and delusions
Central control dysfunction - Frith et al - people with schizophrenia tend to have derailment of thoughts because a word triggers an association and cannot suppress automatic central response
Psychological explanation AO3
Research support
P - strength as evidence linking family dysfunction to schizophrenia
E - indicators include insecure attachment and childhood trauma
E - Read at al - disproportionately likely to have insecure attachment (type C or D) - 69% of women and 59% of men have history with abuse - Morkved et al - adults with schizophrenia reported at least one childhood trauma
L - suggests family dysfunction makes people more vulnerable to schizophrenia
Explanations lack support
P - limited as poor evidence base for any of the explanations
E - none to support the importance of traditional family-based theories such as schizophrenogenic mother and double blind
E - both theories based on clinical observation and information assessment of mother’s personalities not systematic evidence
Parent-blaming
P - useful even though no research support
E - as shows insecure attachment and experience of childhood trauma affect individual vulnerability to schizophrenia
E - high socially sensitive as parent-blaming, especially the mother
L - for people already having to watch their chilled experience schizophrenia and care for them, blame adds insult to injury
Research support
P - strength as evidence for dysfunctional thought processing
E - Stirling et al - compared performance of range of cognitive tasks in 30 people with schizophrenia and a control group of 30 without
E - Frith et al’s central control theory supported - people with schizophrenia took longer - over twice as long on average - to complete task
L - cognitive processes of people with schizophrenia are impaired
A proximal explanation
P - limited as only explain the proximal origins of symptoms
E - they explain what is happening now to produce symptoms - as distinct from distal explanations with focus on what initially caused the condition
E - possible distal explanations are genetic and family dysfunction explanations - unclear how geentic variation or childhood trauma can lead to problems with metarepresentation or central control
L - cognitive theories on their own only provide partial explanations for schizophrenia
Psychological or biological
P - cognitive approach provides an excellent explanation for symptoms of schizophrenia
E - argument for seeing schizophrenia primarily as a psychological condition
E - appears that the abnormal cognitive associated with schizophrenia in partly genetic in origin and the result of abnormal brain development - Toulopoulo et al
L - suggests that schizophrenia is a biological explanation
Biological therapies AO1
Drug therapy - most common treatment - involves the use of antipsychotic drugs
Antipsychotics - reduce intensity of schizophrenia symptoms, especially positive ones eg hallucinations
Typical antipsychotics - the first generation of drugs for schizophrenia and other psychotic disorders, having been used since 1950s - chlorpromazine
Dopamine antagonists - acting as antagonists for dopamine - reduce action of neurotransmitter, block dopamine receptors in synapses of brain - dopamine levels increase but then production is reduced - reduces hallucinations
Sedation effect - effective sedative - effect on histamine receptors - often used to calm down individuals with other conditions - syrup is absorbed faster than tablets so tends to be given when chlorpromazine used for sedative properties
Atypical antipsychotics - drugs for schizophrenia - developed after typical antipsychotics - typically target a range of neurotransmitters such as dopamine and serotonin
Clozapine - developed in 1960s - withdrawn 1970s - caused blood condition called agranulocytosis - 1980s - more effective than typical antipsychotics however regular blood tests and not available as an injection - works by binding to dopamine receptors can acts on serotonin and glutamate receptors to improve move and reduce depression and anxiety - prevents suicide
Risperidone - more recent - 1990s - tablets, syrup or injection - bind to dopamine and serotonin receptors - binds stronger than clozapine - fewer side effects cause smaller dosage
Biological therapies AO3
Evidence for effectiveness
P - strength as evidence to support effectiveness
E - Thornley et al - studies comparing effects of chlorpromazine to control conditions - data from 13 trials with a total of 1121 participants showed that chlorpromazine associated with better functioning and reduced symptoms between than placebo
E - Melter - clozapine more effective than typical antipsychotics and other atypical antipsychotics - effective in 30-50% of treatment-resistant cases where typical antipsychotics have failed
L - shows that they are effective treatments
P - However, Healy argues theres a serious flaw with evidence for effectiveness
E - most studies are of short-term effects only and some successful trials have had data published multiple times, exaggerating the size of the evidence base for positive effects
E - because antipsychotics have calming effects - positive effect on people experiencing the symptoms of schizophrenia - not same as saying they reduce severity of psychosis
L - evidence base for antipsychotic effectiveness is less impressive than it first appears
Serious side effects
P - limitation as high likelihood of side effect
E - typical antipsychotics associated with side effects eg dizziness, agitation, sleepiness, stiff jaw, weight gain. Long-term can result in tardive dyskinesia - caused by dopamine supersensitivity - involuntary facial movements - can also cause neuroleptic malignant syndrome
E - NMS - caused when drug blocks dopamine action in hypothalamus - associated with regulation of number of body systems - high temperature, delirium, coma and can be fatal - 0.1% to 2%
L - antipsychotics can do harm as well as good and individuals who experience these may avoid such treatments which makes the treatment ineffective
Mechanism unclear
P - limitation of antipsychotics is that we do not know how they work
E - understanding of mechanism by which antipsychotic drugs work strongly tried to original dopamine hypothesis
E - original dopamine hypothesis is not complete - dopamine levels are instead too low - antipsychotics should not work - questioning effectiveness so argued to be ineffective
L - at least some of antipsychotics may not be the best treatment to opt for - perhaps some other factors involved in success
The chemical cosh
P - widely believes antipsychotics used in hospital situations to calm people with schizophrenia
E - allows them to be easier for staff to work with rather than benefiting the people themselves - Moncrieff
E - however, calming people distressed by hallucinations and delusions almost certainly makes them feel better
L - allowing them to engage in other treatments such as CBT and other services
Psychological therapies AO1
What is CBT - method for treating mental disorders - based on cognitive and behavioural approach
Aim of CBT - deal with thinking of the patient - such as challenging negative thoughts - identify and challenge irrational thinking
Coping strategy enhancement - initial assessment (behaviour analysis and assessment of coping strategies), help with dysfunctional metarepresentation, education and rapport training (coping strategies enhanced), symptom targeting
How does CBT help - helps with dysfunction in central control as they learn to block out their automatic negative thoughts through copying strategies - shows clients how delusions and hallucinations affect their feelings and behaviour - reality testing
Case study - Turkington et al - thinks mafia observing how to kill and asks if the therapist thinks its mafia - therapists says possible but introduces other explanations eg how do you know it’s the mafia
Family therapy - a form of psychological therapy - involves all or some members of a family
Aim of family therapy - improving the communications within the family and reducing the stress of living as a family
How does family therapy help - Pharoah et al - identify a range of strategories that family therapists use to try to improve the functioning of a family such as reducing negative emotions and improving family’s ability to help
Reducing negative emotions - eg anger and guilt which create stress - reduces likelihood of relapse
Improving the family’s ability to help - form therapeutic alliances, improving beliefs towards schizophrenia, achieving balance between caring for individual and maintaining their own lives
Model of practice -
Burbach - seven phases
1. Share basic information and provide emotional and practical support
2. Identifying resources including what different family members can and cannot offer
3. Aims to encourage mutual understanding - safe space
4. Involves identifying unhelpful patterns
5. Skill training
6. Relapse prevention training
7. Maintenance for future
Psychological therapies AO3
Evidence for effectiveness
P - strength as research to show effectiveness
E - Jauhar et al - analysis of 34 studies of CBT with schizophrenia, clinical advice from NICE
E - clear evidence for small but significant effects on both positive and negative symptoms, reductions in frequency and severity of auditory hallucinations, NICE recommends CBT for schizophrenia
L - both research and clinical experience support the benefits of CBT for schizophrenia
Quality of evidence
P - limited as there is a wide range of techniques and symptoms included in the studies
E - Thomas - different studies involved different CBT techniques - people with different combinations of positive and negative symptoms
E - individual differences - CBT techniques and symptoms vary widely - overall modest benefits of CBT for schizophrenia probably conceal a wide variety of effects of different CBT techniques on different symptoms
L - effectiveness is different for different people - hard to say how effective CBT will be for a particular person with schizophrenia
Does CBT cure
P - CBT is associated with the improvement of the quality of life for those with schizophrenia
E - limited by the fact that CBT does not provide a cure - due to biological links with the condition such as dopamine hypothesis - psychological therapy just benefits people by improving their ability to live with schizophrenia
E - however, studies report significant reductions in severity of symptoms (negative and positive)
L - CBT is able to aid in symptoms showing it does more than simply enhancing coping strategies
Evidence of effectiveness
P - strength as there is evidence that shows it’s effectiveness
E - Review of studies from McFarlance, NICE
E - family therapy - one of most consistently effective treatments - relapse rate reduced (usually 50-60%) - NICE recommends family therapy for everyone with a schizophrenia diagnosis
L - family therapy is likely to be of benefit to people with both early and full-blown schizophrenia
Benefit to whole family
P - strength as benefits all family members
E - Lobban and Barrowclough - effects are important because families provide the bulk of care for people with schizophrenia
E - strengthens functioning of whole family - lessens negative impact of schizophrenia on other family members and strengthens the ability of family to support the person with schizophrenia
L - means family therapy - wider benefits
Which matters most
P - argued to be cost-effective - economic benefits
E - this is due to family therapy reduces relapse rates and makes families better able to provide the bulk of care it has huge economic benefits - the state does not need to pay so much
E - however, not just economic benefits - family therapy also has very significant therapeutic benefits for people with schizophrenia and families
L - family therapy has both economic and therapeutic benefits - but which is primary use
Token economies AO1
What is a token economy - form of behavioural modification - desirable behaviours encouraged through operant conditioning
Reinforcers - tokens are secondary reinforcers and exchanged for primary reinforcers such as food or privileges
Development of token economies -
Ayllon and Azrin
- Women on ward with schizophrenia
- Plastic tokens for tasks eg making bed
- Exchanged for privileges eg watching film
- Found tasks increased significantly
- Popular in 1960s and 1970s - declining now
Why is it now declining - growth of community based care and closure of psychiatric hospitals - ethical issues raised by restricting rewards to people with mental disorders
Rational for token economies - Matson et al - three categories - personal care, condition-related behaviours and social behaviours - improves quality of life and normalises behaviour - adapt back into community
What is involved - Cooper et al - target behaviours decided on individual basis and token swapped out for tangible items
Theoretical understanding - operant conditioning - tokens are secondary reinforcers, gain value link with primary reinforcers (meaningful rewards)
Token economies AO3
Evidence of effectiveness
P - strength is evidence that it’s effective
E - Glowacki et al - seven high quality studied published between 1999 and 2013 - examined effectiveness of token economics for chronic mental health issues in hospital living
E - all studies showed reduction in negative symptoms and a decline in the frequency of unwanted behaviours
L - supports the value
P - small evidence base to support the effectiveness of a technique
E - issue with a small number of studies is the file drawer problem
E - this phenomenon leads to a bias towards positive published findings because undesirable results have been filed away - only included small numbers of studies
L - serious question over evidence for the effectiveness of token economies
Ethical issues
P - limited as ethical issues have been raised
E - power control and professionals have considerably more power to control behaviour - problematic if target behaviours not identified sensitively
E - restricting availability of pleasures - seriously ill people have a worse time - legal action by families who see their relative in this position has been major factor in decline of use
L - benefits of token economies may outweigh impact on personal freedom and short-term reduction in quality of life
Alternative approaches
P - limited as existence of more pleasant and ethical alternatives
E - other approaches with a comparable evidence base that do not raise same ethical issues - Chiang et al - art therapy
E - art therapy - high-gain low-risk approach to managing schizophrenia - even if benefits are modest - generally true for all approaches to treatment and is a pleasant experience without major risks of side effects or ethical abuse - NICE guidelines recommend art therapy
L - art therapy might be a better alternative
Benefits
P - they are difficult to continue once the person has left a hospital setting
E - due to target behaviours being unable to be monitored closely so the tokens that they would have received cannot be administered immediately
E - however, some people with schizophrenia may only get the chance to live outside a hospital if their personal care and social interaction can improve
L - using token economy can grant these people with the freedom of being able to leave the hospital and may be the best way to achieve this during hospital care
Interactionist approach AO1
What is the interactionist approach - there are a range of factors that can influence the development of schizophrenia - biological, psychological ect - combine in a way that cant be predicted by each one separately eg interact
What is the diathesis-stress model - schizophrenia is result of both diathesis (vulnerability) and a stressor (trigger) - one or more underlying factors make a person particular vulnerable to developing schizophrenia but onset is triggered by stress
Original diathesis stress -
Meehl’s model
- Diathesis is genetic - schizogene - led to schizotypic personality
- This personality is sensitive to stress
- Chronic stress eg schizophrenic mother - development of disorder
- Without schizogene, cannot develop schizophrenia no matter stress levels
Modern view of diathesis -
Ripke et al - many genes - no single schizogene
Ingram and Luxton - Range of factors beyond genes are influential including psychological trauma
Read et al - proposed a neurodevelopmental model - early trauma alters the developing brain eg the hypothalamic-pituitary-adrenal system can become overactive - more vulnerable to stress
Modern view of stress -
Also includes anything that risks triggering schizophrenia eg cannabis use
Cannabis - stressor - increase up to seven times according to dose - interferes with dopamine system
- People may lack the requisite vulnerability factors so do not develop schizophrenia
Treatment -
Combination of antipsychotics and psychological therapies such as CBT
- Interactionist model
- Increasing practice in the UK
- Medication without accompanying psychological treatment more common in the US
Interactionist approach AO3
Support for vulnerability and triggers
P - strength of interactionist approach to schizophrenia is evidence supporting role of both vulnerability and triggers
E - Tienari et al - impact of genetic vulnerability and psychological triggers - 19000 Finnish children whose biological bothers diagnosed - high genetic risk group compared to control of adoptees without family history in adult hood
E - adoptive child-rearing style - assessed - high levels of criticism, hostility and low levels of empathy associated but only in high genetic risk group
L - combination of genetic vulnerability and family stress can lead to increased risk
Diathesis and stress are complex
P - original model limited as argued to be oversimplified
E - multiple genes in multiple combinations influence diathesis - stress comes in many forms such as dysfunctional parenting - diathesis can also be influenced by psychological factors and stress biological factors
E - Housten et al - childhood sexual abuse - vulnerability, cannabis - trigger
L - multiple factors, both biological and psychological - supporting modern understanding of both diathesis and stress
Real-world application
P - strength is the combination of biological and psychological treatments
E - practical application - combining treatments enhances their effectiveness
E - Tarrier et al - 315 randomally allocated - (medication and CBT), (medication and counselling), (medication - control) - two combination groups showed lower symptoms following trial - no different in hospital readmission
L - clear practical advantage in interactionist approach for treatment outcomes
P - limited as one successful treatment cannot argue explanation is correct
E - Jarvis and Okami - saying that treatment for mental disorder justifies explanation - like saying alcohol reduces shyness so shyness is caused by lack of alcohol
E - this logical error is called the treatment-causation fallacy
L - cannot assume success of combined therapies means that the interactionist explanations for schizophrenia are correct
Urbanisation
- Schizophrenia - more commonly diagnosed in urban areas
E - justifies interactionist position as urban areas argued to be more stressful so city living acts as a trigger
E - however, more likely to be diagnosed in cities or people with diathesis for schizophrenia tend to migrate to cities
L - greater frequency in area cannot act as full explanation
