Paper 3 - Schizophrenia Flashcards
What is schizophrenia?
A serious mental disorder suffered by about 1% of the population.
- more commonly diagnosed in men than women
- more commonly diagnosed amongst the working class
- sufferers may find their symptoms to dramatically interfere with everyday life
How does ICD-10 diagnose schizophrenia?
- requires two or more negative symptoms
- loss of usual abilities and experiences
- Avolition: decreased motivation, signs include poor hygiene, lack of persistence and energy
- Speech poverty: changed patterns of speech (delayed convo)
- recognises the subtypes of schizophrenia:
paranoid - delusions and hallucinations
hebephrenic - primarily negative symptoms
catonic disturbance in movement
How does the DSM-5 diagnose schizophrenia?
- believes it would be at least one positive symptom or one negative symptom (for over a month)
- Hallucinations: unusual sensory experiences where voices are heard (critical) or seen (senses)
- Delusions: paranoia and irrational beliefs; tend to involve religious, political figures (Jesus). May believe there is strong external control (government or aliens)
What is the difference between negative and positive symptoms?
Positive symptoms tend to be additional experiences beyond ordinary existence whereas negative involves the loss of usual abilities
Evaluate the methods of diagnosing schizophrenia
Poor reliability:
- Cheniaux had two psychiatrists independently diagnose 100 patients using both ICD-10 and DSM-5 crriterias
- poor inter-rater reliability; one said 26 (DSM) and 44 (ICD) and the other found 13 (DSM) and 24 (ICD)
- this poor reliability shows the methods of diagnosis are poor
Invalid:
- Chineaux’s study suggests that schizophrenia is more likely to be diagnosed with ICD than DSM
- the assessments do not arrive at the same diagnosis and therefore are not measuring what they are intending to; thus poor validity
Co-morbidity:
- two conditions occurring together; if this happens frequently, it questions validity of the diagnosis
- Buckley concluded that half of the patients with diagnosis of schizophrenia also had depression or substance abuse. PTSD also occurred in 29% of the cases
- difficult to tell the differences between conditions - or it could be a single condition
Culture bias:
- those with Afro-Caribbean origin are more likely to be diagnosed with schizophrenia that white people (but rates within Africa and West Indies are not that high; not genetic vulnerability)
- some positive symptoms (e.g. hearing voices) are more acceptable in African cultures (communication with ancestor) - these symptoms are often overlooked by white psychiatrists who tend to distrust black people (Escobar et al)
- forms of imposed etic
Describe schizophrenia running in families (genetic basis- bio)
- schizophrenia appears to run in families but it is difficult to determine as families tend to share aspects of the environment
- systematic investigations have suggested that the greater the genetic similarity between family, the greater the chance of both developing schizophrenia
- 100% genes shared between Mz twins but 50% with Dz twins - therefore Mz have greater genetic similarity and shared risk of schizophrenia
Gottesman’s family study= identical twins had 48% probability of sharing schizophrenia whereas first cousins is 2% - therefore supporting the assumption
Describe how candidate genes may cause schizophrenia (genetic basis - bio)
Candidate genes: individual genes are believed to be associated with risk of inheritance
- small number of genes appear to confer a small increased risk of schizophrenia: polygenic as it requires a number of factors to work in combination for it to manifest
- appears to be aetiologically heterogeneous - different combinations of factors = condition
- Ripke studied 37000 patients compared to 113000 controls and found there to be 108 separate genetic variations associated with the increases risk of schizophrenia (tended to code for neurotransmitters like dopamine)
Give strengths for the genetic explanation for schizophrenia (bio)
- strong evidence for genetic vulnerability to schizophrenia from different sources
- Gottesman’s study shows how genetic similarity and shared risks of schizophrenia are closely related
- Tienari’s adoption study showed that children of schizophrenia sufferers were still at a heightened risk of schizophrenia even when adopted into families with no history of the condition
- Ripke - molecular level - particular genetic variations significantly increase the risk
- parsimony ; isolation of one simplistic explanation - allows us to make treatments leading to positive applications for biological reductionism
Overwhelming support for the idea of genetics making an individual more vulnerable but does not mean it is entirely genetic as it could be the interaction with the environment causing the condition (diathesis-stress)
Describe the dopamine hypothesis (bio)
Dopamine is a neurotransmitter that is important in brain systems and may be implicated in the symptoms of the schizo
Hyperdopeminergia in subcortex: original hypothesis suggested that high levels of dopamine in the subcortex and in excess in the Broca’s area (speech production) are associated with negative symptoms (speech poverty) or auditory hallucinations
Hypodopaminergia in the cortex: recent hypothesis focuses on abnormal dopamine systems in the brain’s cortex: Goldman-Rakic identified the role of low levels in the prefrontal cortex are responsible for negative symptoms
Evaluate the dopamine hypothesis (bio)
Mixed evidence
- Support: dopmaine agonists like amphetamines increase levels of dopamine and make schizophrenia worse and may produce schizophrenia-like symptoms in non-sufferers
- furthermore, antipsychotic drugs work to reduce dopamine activity
- radioactive labelling studies found that the chemicals needed to produce dopamine are taken up faster in the brains of schizphrenics than controls
- both suggest the importance of dopamine in schizophrenia
Weakness: REDUCTIONIST
Some of the genes in Ripke’s study code for the production of other neurotransmitters so suggests dopamine is not the only factor (e.g. glutmate appears to hold a more significant effect in more recent research)
Describe how neural correlates affect schizophrenia (bio)
- neural correlates measure structure or function of the brain that correlate with experience - positive/negative symptoms have neural correlates
Negative symptoms: avolition involves loss of motivation which involves the ventral striatum which is believed to be involved in anticipation for rewards
- therefore abnormality in the ventral striatum = negative symptoms
- Jucket et al = low levels of activity in ventral striatum in schizophrenics rather than controls (observed negative correlation between ventral striatum and severity of negative symptoms)
Positive symptoms: Allen et al scanned the brains of patients experiencing hallucinations and compared to control group whilst they identified recorded speech
- lower activity in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group - and they also made more errors
Evaluate research in neural correlates
correlation-causation
- does the unusual activity cause the symptom?
- it could be other factors influencing the ventral striatum
- or it could be that the negative symptoms cause less info to pass through the striatum resulting in less activity
Evaluate biological explanations for schizophrenia as a whole
- ignores nurture and psychological explanations
- could be effected by social/ environmental factors ]
- therefore the approach needs to be more holistic and inclusive of other theories
How are antipsychotics involved in treating schizophrenia (bio treatments)?
- taken as tablets or in syrup form or may be injections
- required in the short or the long term
- typical and atypical
Describe typical antipsychotics (bio treatments)
- around since the 1950’s and include chlorpromazine (syrup, tablet, injection) - small doses gradually increase (max 1000mg)
- associated with the dopamine hypothesis and work as dopamine antagonists as they block dopamine receptors in the synapses, reducing the action)
- initially, may cause build up but will eventually reduce
- reduces symptoms and is also an effective sedative as relates to histamine receptors
Describe atypical antipsychotics (bio treatments)
- around since 1970’s and the aim was to reduce side effects and improve effectiveness
- Clozapine was introduced but withdrawn after deaths linked to agranulocytosis (blood condition)
- however was reintroduced for schizophrenia treatment as a last resort and the patient will need regular blood tests
- binds to dopamine, serotonin and glutamate receptors and improves mood as well as reducing depression - improves cog function
- only prescribed at high risk (suicide attempts)
Risperidone: 1990’s to produce more effective and less serious side effects
- max 12 mg
- binds more strongly to receptors and leads to fewer side effects
Difference between atypical and typical antipsychotics
typical - first formed and tend to be dopamine antagonists
atypical - developed afterwards and target a range of different neurotransmitters
Give a strength for biological treatments to schizophrenia
Thornley: reviewed studies comparing the effects of chlorpromazine to controls with placebos
- data from 13 trials suggests that chlorpromazine was associated with better overall functioning and reduced symptom severity - in 3 of these trials, there was a lower relapse rate
Meltzer et al - found clozapine to be more effective than typical antipsychotics - effective in 30-50% of treatment-resistant cases where the typical had failed
- however, in some studies, the differences between some drugs appeared to be inconclusive due to individual differences - drugs effect different people in different ways
Give weaknesses for biological treatments in schizophrenia
Problems
- Healy suggested that there was severe publication bias as only successful trials have been published/ exaggerated
- furthermore, the effectiveness from calming does not mean it reduces the severity of psychosis
- only publishing short term effects
Severe side effects:
- serious and potentially fatal effects
- long term use of typical antipsychotics may cause tardive dyskensia which is caused by dopamine super sensitivity - causes involuntary facial movements
- most serious side effect of typical = neuroleptic malignant syndrome - the drug blocks dopamine sction in the hypothalamus which regulates many systems - NMS = coma, death
- in atypical = aimed to reduce side effects and succeeded but they do still exist and clozapine may cause a blood condition
Reductionist:
- ignores nurture so the therapies are limited
- need to be holistic and include both drug therapy and psychological therapy - which research shows lower relapse rate and improvement in both positive and negative symptoms
Dependence on the dopamine hypothesis
- furthermore, drugs tend to focus on the dopamine hypothesis - antipsychotics reduce levels of dopamine
- the theory suggests both too high or too low levels of dopamine can cause schizophrenia but it is an incomplete explanation
- the currently established relationship between dopamine and psychosis would suggest that antipsychotics will not work
Describe family dysfunction as a cause for schizophrenia (psych explanations)
Schizophrenogenic mother:
- Fromm-Reichmann et al proposed the psychodymaic explanation for schizophrenia based on accounts of patients childhood
- noted consistency in descriptions of their mother: tended to be cold, controlling and rejecting
- created a family climate characterised by tension, secrecy which leads to distrust which may later become paranoid delusions - schizophrenia
Double-bind theory:
- Bateson et al agreed that the family climate may pose vulnerability to the development in schizophrenia
- developing child is often in fear of doing the wrong thing but may receive mixed messages and feel unable to seek clarification
- the child may be punished by withdrawal of love which may leave them to think the world is confusing and dangerous - disorganised thinking, paranoid delusions
- this was suggested to be a risk factor, not the main type of communication
Expressed emotion:
- EE is the level of negative emotion expressed towards a patient by their carers
- verbal criticism (often accompanied by violence), hostility towards (anger) and emotional over-involvement in their life
- this may be a source of stress for the patient and is primarily the explanation for relapse in patients
- assumed that these could act as environmental triggers for genetically vulnerable individuals
What is the main assumption of the psychological explanation of schizophrenia?
- assumes that psychological environment may make individuals particularly vulnerable to schizophrenia
Evaluate family dysfunction as an explanation for schizophrenia
Evidence:
- evidence suggesting that difficult family relationships in childhood are associated with increased risk of schizophrenia
- Read et al reviewed 46 studies of child abuse and schizophrenia and concluded that 69% of adult women with diagnosis of schizophrenia had a history of physical/sexual abuse
- was 59% in men
- Berry found those with insecure attachments were also more likely to have schizophrenia
HOWEVER… information about childhood was gathered after the development of symptoms which may have distorted their perception of childhood
- poses serious validity problems - there is only some prospective evidence linking the two
Weak evidence:
- little support for the importance of the schizophrenogenic mother or double-bind - both are based on clinical observations and assessed mother’s personality
- Furthermore, led to parent-blaming who will then bear lifelong responsibility even after seeing their child descent into schizophrenia - further trauma
Describe cognitive explanations of schizophrenia
Schizophrenia is characterised by disruption to normal thought processing
- reduced processing in ventral striatum (negative symptoms) and temporal and cingulate gyri (positive)
- Frith suggested two kinds of dysfunctional thought processing that could underlie some symptoms
Metarepresentation: cognitive ability to reflect on own thoughts and behaviour to allow us insight into our own intentions and goals - allows us to also interpret other
- dysfunction in metarepresentation would disrupt our ability to recognise our own actions - would explain hallucinations of voices and delusions
Central control: cognitive ability to suppress automatic responses while able to perform deliberate actions
- disorganised speech and thought= inability to suppress automatic thoughts and speech
- schizophrenia sufferers tend to have dysfunction central control meaning they cannot suppress automatic responses which may be triggered by words
- cog biases and selective attention
Evaluate cognitive explanations of schizophrenia
Strong evidence:
- support for the idea of information being processed differently in the mind of a schizophrenic - Stirling et al compared 30 patients with 18 non-patient controls on tasks like the Stroop Test (name ink colours of colour word, suppressing the impulse to read the word) - patients took twice as long to name the ink colours as the control group due to central control dysfunction = supports Frith’s assumption
Practical application
- Yellowless developed a hallucination stimulator in order to show patients their hallucinations were not real. Helping schizophrenics understand their cog defects promotes psychological initiatives to improve
However, links between symptoms and faulty cognition do not tell us about the origin of the faulty cognition despite being clear
- lacking cause and effect
Describe CBT as a treatment of schizophrenia (psychological therapy)
- commonoly used to treat sufferers
- 5-20 sessions
- generally involves trying to help patients identify irrational thoughts and trying to change them - this may involve arguments or discussions about patient beliefs and urging consideration of less threatening possibilities
- helps patients make sense of their delusions and hallucinations which may impact their feelings/behaviour - offering psychological explanations for unusual symptoms (hallucinations/hearing voices) may reduce anxiety due to challenging
Describe family therapy as a treatment of schizophrenia (psychological therapy)
- takes place with families rather than individual patients in hopes to improve the quality of communication and interaction between family members
- before, therapists may have seen family to be the root cause of the condition but now it will reduce family stress (which could lead to a patients relapse) - reduces levels of EE
Pharoah et al identified different strategies by family therapists to aim to improve the functioning of a family with a schizophrenia sufferer:
- therapeutic alliance
- reducing stress
- improving ability of the family to solve problems
- helping family achieve balance
- improve family beliefs
These strategies may also increase patient’s compliance with medicine and reduce likelihood of relapse and readmission
Describe how token economies may treat schizophrenia
- rewards are used to manage behaviour of patients who have developed patterns of maladaptive behaviour (from institutionalisation)
- this may modify bad habits to improve patients quality of life - not to treat schizophrenia
Tokens: reinforcement mechanisms to encourage repetition of desirable behaviour - the immediacy of this reward is important to prevent ‘delay discounting’ - act as secondary reinforcers
Rewards: tokens have no value but may be traded for tangible rewards - based on the idea of operant conditioning - could be goods or services
Evaluate psychological treatments for schizophrenia
Evidence for effectiveness
- Jauhar reviewed 34 studies of CBT and found there was a significant but fairly small effect on positive and negative symptoms
- Pharoah found that family therapy significantly reduces hospital readmission and improves a patients quality of life
Problems with research
- some research suggested that token economies only showed improvement in 1/3 studies (Sultana)
- Different studies were inconsistent - making it unreliable
Do not cure:
- these treatments make life more manageable (making sense of issues, reducing stress of families, making behaviour more socially acceptable)
- these, like the biological treatments, do not cure schizophrenia therefore a weakness
- biological reduces severity of symptoms more
Ethical issues:
- token economies have been proven to be controversial: patients with mild symptoms may become more available to privileges or services but those with severe may have certain symptoms preventing them from carrying out desirable behaviours (discrimination)
- CBT interferes with a patients freedom of thought (e.g. patient is concerned with government control.. may lead to political arguments)
Alternate
- focuses too much on nurture but ignores nature
- may be best to do a combo of the two as it can reduce symptoms
- biological treatments require less motivation which may be better for schizophrenia sufferers who tend to have avolition
What is the assumption of the interactionist approach?
- acknowledges biological, psychological, societal factors in the development of schizophrenia
- suggests biological factors interact with psychological
Explain the original diathesis stress model to schizophrenia (interactionist)
suggests that vulnerability (diathesis) may be paired with a trigger in order to develop the condition
Meehl’s model:
- original model - suggested the diathesis was entirely genetic and the result of a single ‘schizogene’
- this explanation led to the development of ‘schizotypic personality’ which involves sensitivity to stress
- if a person does not have the schizogene, then no amount of stress would lead to schizophrenia however, carriers of the gene may develop schizophrenia if exposed to chronic stress and presence of schizophrenogenic model
Explain the modern understanding for diathesis (interactionist for schizophrenia)
Ripke suggested there was no schizogene but the diathesis was a range of factors beyond genetics (including psychological trauma) - trauma may be seen as the vulnerability rather than stressor
- Read et al proposed the neurodevelopmental model in child abuse which may affect aspects of brain development - HPA system may be overactive making someone vulnerable
Explain the modern understanding for stress (interactionist for schizophrenia)
modern definition of stress: anything which risks triggering schizophrenia (Houston)
- recent research suggest cannabis is a stressor because it increases the risk of schizophrenia by seven times according to the dose
- this is because cannabis interferes with the dopamine system
- however most people do not develop it so must be multiple vulnerability factors
Describe the treatment for schizophrenia according to the interactionist model
- believes in combining psychological therapies with antipsychotic drugs
- Turkington found that it is possible to believe in biological causes and practise CBT - however, you must adopt the interactionist approach
- more common in Britain as history of conflict in the USA
Give a strength for interactionist treatments
- TTarrier had 315 patients who were randomly allocated to medication + CBT or medication + counselling
- both groups showed lower symptom levels than those in the control (with just medicine) - however difference in hospital readmission rates
- clear practical advantage
Evaluate the interactionist approach in explaining
Evidence for the role of vulnerability and trigger:
- Tienari et al - investigated children adopted from 19000 Finnish mothers with schizophrenia
- their adoptive parents were assessed for child-rearing style and the rates of schizophrenia were compared to those in a control group of adoptees (without genetic risk); child rearing with criticism and low empathy was implicated in the development of schizophrenia only with children with high genetic vulnerability
- genetically vulnerable children are more sensitive to parental styles
- strong support
Original is over simple:
- No single schizogene
- theory believes that schizophrenogenic mother is most significant source of stress but there are many forms of stress
- newer models have showed vulnerability may even root from trauma as well as genetic makeup
- old model is too simple
