Schizophrenia- P3 Flashcards
(18 cards)
Diagnosis and classification of schizophrenia AO1
- scz= a serious mental disorder experienced by 1% population
- characterised by disruption to the cognitions and emotions affecting language, thoughts, perceptions, many end up hospitalised/ homeless
- classification= organising symptoms that cluster together in sufferers and classifiying this as one disorder
- diagnosis= using classifications and someone’s symptoms to decide what disorder they have
- two major classification systems:
- ICD-10 and ICD-11: mainly used in UK/ Europe, scz= two or more negative symptoms or one positive symptom, range of subtypes e.g. paranoid scz
DSM-5: mainly used in the USA, scz= one positive symptom must be present, disturbance for at least 6 months, doesn’t recognise subtypes due to inconcsistency
positive symptoms
* additional, atypical experiences
* hallucinations= unusual sensory experiences, false perceptions that may be a distorted version of reality or have no basis in reality, these can be auditory (hearing voices) or visual (seeing things)
* delusions= irrational beliefs which have no basis in reality
1. delusions of persecution= belief that others want to harm you
2. delusions of granduer= belief that you are an important individual e.g. god/king
3. delusions of control= belief that someone is controlling you externally
4. delusion of reference= belief that events in the environment are directly related to you e.g. getting sent messages via TV characters
negative symptoms
- avolition= apathy, lack of goal-directed behaviour, reduced motivation, poor hygiene, lack of effort in work, catatonic behaviour (fronzen still)
- speech poverty= limited repetitive speeck, delayed responses, muddled speech (word salad)
Diagnosis and classification of schizophrenia AO3
- good reliability (agreement/consistency) in diagnosis: good inter-rater reliability and test-retest reliability, DSM-5 has improved reliability, Osario- reported excellent reliability in 180 diagnoses, pairs of psychologists score +0.97 inter-rater and +0.92 test retest reliability
- poor validity in diagnosis: the extent to which scz is a unique disorder with characteristics and symptoms, Cheniaux et al: two psychiatrists assessed the same 100 patients using the DSM-4 and ICD-10, 68 were diagnosed using ICD system vs 39 with the DSM= low criterion validity, HOWEVER: Osario reported that agreement was excellent when two measures both derived from the DMS-5 were used (criterion validity is good if both measures are derived from the same system)
- co-morbidity: the extent to which two disorders occur together (e.g. scz and depression)- this leads us to question the validity of diagnosis and classification as the two conditions may actually be one, Buckley: roughly half of those diagnosed with scz are also diagnosed with depression or substance abuse
- gender bias in diagnosis: since 1980’s men have been more commonly diagnosed (1.4 : 1)- this ratio may be because women are genetially less vulnerable, but more likely because women are more likely to seek support from friends/ family leading to over-functioning= women may not be recieving the same treatment as men
- symptom overlap: big overlap between scz symptoms and other disorders e.g. bipolar also involves avolition and delusions, this questions the classification- they may both be one disorder or variations of the same disorder
- culture bias in diagnosis: some symptoms (e.g. hearing voices) mean different things in different cultures (communication with ancestors), Escobar: British people of African descent are up to 9x more liekly to recieve a diagnosis than white British people= imposed etic of diagnostic methods
Biological explanations (genetic) AO1- half a page
family studies
* risk of scz increases in line with genetic similarity to a relative with the disorder
* Gottesman: demonstrated a positive correlation between increased genetic similarity and increased risk, siblings= 9% vs twins= 48% concordance, supports the idea that genes play a role in scz
candidate genes
* early research looked for one faulty gene but it is more likely to be polygenic (multiple genes involved), most likely to be genes involved with the coding for neurotransmitters including dopamine
* aetologically heterogenous= different combinations of genes can cause it, Ripke et al- found 108 genetic variations assoiated with increased risk
mutations
* some people may have scz even with no family history due to gene mutation
* parental DNA may mutate due to viral infections, radiation or poison
* evidence suggests a link between paternal age- older fathers= more likely scz due to sperm mutations
Biological explanations (genetic) AO3- half a page
- environmental factors: there is evidence to suggest that environmental factors increase risk of scz…
-biological risk factors= birth complications, smoking THC-rich cannabis in adolescence
-psychological risk factors= childhood trauma, Morkved found 67% of those with scz and related disoders reported at least one childhood trauma vs 38% of control group
-suggests that genetics can’t completely explain the disorder - research support : family studies such as Gottesman show that risk increases with genetic similarity to someone with the disorder
-Tienari: adoption studies, biological children of scz parents are at higher scz risk even if they grew up with an adoptive family
-Hilker et al: showed concordance rate of 33% for MZ twins vs 7% for DZ twins
-this evidence supports the idea that genes play a bigger role that the environment
Biological explanations (neural) AO1- half a page
original dopamine hypothesis:
* based on the idea that drugs used to treat scz reduced dopamine levels and also reduced similar symptoms in those with Parkinsons (associated with low dopamine)
* scz may be a result of high dopmaine levels= hyperdopaminergia in subcortical areas of the brain
* e.g. an excess of dopamine receptors in pathways from the subcortex to Broca’s area could explain speech poverty
updated/ revised dopamine hypothesis
* hypodopaminergia= low levels of dopamine
* e.g. low dopamine levels in the prefrontal cortex (responsible for thinking)- could explain the negative symptoms of the disorder
* also suggested that cortical hypodopaminergia leads to sub-cortical hyperdopaminergia
* abnormally high and low levels cause the disorder
Biological explanations (neural) AO3- half a page
- glutamate: neurotransmitter, central role in scz (not considered by the dopamine hypothesis), post-mortems show raised glutamate levels in several regions of scz patient’s brains
- research support:
-ampetamines increase dopamine- they increase symptoms in scz patients and induce symptoms in non-sufferers
-antipsychotic drugs- reduce dopamine levels and reduce symptoms
-some candidate genes act on the production of dopamine
Biological therapies AO1
typical antipsychotics
- 1950’s: first generation of drugs for psychotic disorders
- e.g. chloropromazine= tablets/ syrups/ injection, max dosage 1000mg, usually starts much smaller and builds up
- dopamine antagonists: links to dopamine hypothesis, typical antipsychotics like chloroproamazine work by acting as antagonists on the dopamine system- block dopamine receptors in the synapses, normalises neurotransmission, reduces symptoms like hallucinations
- sedation effect: chloropromazine is also a sedative due to it’s effect on histamine receptors, often used to calm people down especially when they are first admitted to hospital
atypical antipsychotics
- used since 1970’s
- developed to improve effectiveness and reduce side effects
- clozapine: more effective than typical antipsychotics, used when other treatments have failed, people taking it must have regular blood tests to ensure they aren’t developing agranulocytosis
- typical daily dosage of 300-450mg, acts on dopamine, serotonin and glutamate receptors- improves mood and reduces depression (often used for those with high suicide risk)
- risperidone: produced more recently to be as effective as clozapine with fewer side effects, typical dosage of 4-8mg, binds strongly to dopamine receptors so works at lower doses
Biological therapies AO3
- evidence of effectiveness for typical and atypical:
-Thornley et al: reviewed studies about chlorpromazine, used 13 trials and 1121 p’s, found the drug was associated with better functioning and reduced symptom severity compared to a placebo
-Meltzer: clozapine is more effective than typical and other atypical antipsychotics, effective in 30-50% of treatment resistant cases - HOWEVER: Healy suggested flaws in this evidence- most studies only look at short term effects, some succesful trials have their data published more than once (exaggerating their results), they also may just be calming rather than effective (sedation effect)
- mechanism unclear: we do not know why/how they work- usually linked to reducing dopamine levels but this is not a full explanation as often it is also caused by low levels of dopamine which should mean that the drugs don’t work
- serious side effects:
-typical- dizziness, agitation, sleepiness, stiff jaw, weight gain, itchy skin
-long term use can cause tardive dyskinesia (caused by dopamine supersensitivity, causes involuntary facial movements)
-most serious side effect= neuroleptic malignant syndrome (MNS) caused when the drug blocks dopamine action in the hypothalamus- results in high temp, delerium, coma and can be fatal
Psychological explanation (family dysfunction) AO1- half a page
scizophrenogenic mother
- Fromm-Reichmann: psychodynamic explanation
- cold, rejecting, controlling mother who causes a family characerised by tension
- leads to distrust= paranoid delusions
double-bind theory
- Bateson et al: emphasised role of communicatio style
- child themself in a situation where they fear doing wrong but recieved mixed messages about what this is
- when they inevitably do wrong, they are punished by withdrawal of love
- causes they to percieve the world as dangerous and confusing= delusions and disorganised thinking
expressed emotion
- high level of emotion (particularly negative) expressed towards someone with scz by family/ carers
- verbal criticsim
- hostility, anger and rejection
- emotional overinvolvement including needless self-sacrifice
- this may act as a trigger with someone who is already genetically vulnerable
Psychological explanation (family dysfunction) AO3- half a page
- research support
-indicators of family dysfunction include insecure attachment and childhood trauma
-Read et al: adults with scz are more likely to have insecure attachment, 69% of women and 59% of men with scz have a history of physical/ sexual abuse
-morkved also reported that 67% adults with scz also reported at least one childhood trauma - parent blaming- socially sensitive, places blame on parents who are already sufferring and often caring for their children
- explanations lack support: poor evidence base for all explanantions, little evidence for scz mother or bouble bind theory, these are based on clinical observations and informal assessments rather than systmeatic evidence
Psychological explanations (cognitive) AO1- half a page
- dysfunctional thinking: inapproperiately evaluate info, disruption to normal thought processing, Frith et al identified two types of dysfunctional thinking
1. metarepresentation: cognitive ability to reflect on your own thoughts and behaviour, allows us insight into our own behaviours
-if this is disrupted we may not be able to recognise our actions as our own- would explain auditory hallucinations and delusions like thought insertion
2. central control: speech poverty and thought disorder could be a result of an inability to suppress immediate thoughts and speech triggereed by other thoughts
-may experience derailment= each word triggers association which cannot be controlled
Psychological explanations (cognitive) AO1- half a page
- research support: Stirling et al- compared congitive performance on a range of tasks (30 scz patients and 30 controls) e.g. stroop task, people with scz took on average 2x longer to complete a task in which they had to name the font-colour of colour words
- proximinal explanation: only explains the proximinal origins of symptoms (what is happening now to produce symptoms) rather than what initially caused the disorder (a distal explanation)= partial explanation
Psychological therapies AO1
cognitive behavioural therapy
- aims to deal with cognitions and behaviours over 5-20 sessions
- helps them make sense of irrational cognitions (delusions and hallucinations)
- uses the ABCDE model to identify and gently dispute their irrational beliefs and restructure them, helps them to cope with and reduce the stress
- normalisation: therapist explains that other people experience similar symptoms to make them feel less alienated
family therapy
- patient encouraged to talk to their family, aims to improve communication and negotiate potential solutions together
- Pharoah: how it helps
-reduces stress and expressed emotion
-increases medication compliance, reducing relapse and hospital readmissions
-improves family’s balance of caring and also living their own life
- Burbach’s 7 phase model:
1. sharing basic info and providing emotional and practical support
2. identifying how the family can help
3. encourage mutual understanding
4. identifying unhelpful interactions
5. stress management
6. relapse prevention
7. maintenance for future
Psychological therapies AO3
CBT
- improved qualitt of life- allows them to make sense of and challenge their symptoms, may allow them to cope better and function more adequately
- HOWEVER: doesn’t cure the disorder as scz is largely biological, psycholgical therapies only help them to cope
- requires motivation: CBT requires patients to be motivated and committed to multiple sessions, also requires self-awareness and willingness to engage in the process… the positive symptoms lead to a lack of awareness and the negative symptoms lead to apathy and avolition= they may drop out, CBT may be inapproperiate for scz patients
family therapy
- benefits for whole family: helps the whole family which is important as they provide most of the care, strengthens the functioning of the whole family, lessens the negative impact of the disorder, strengthens family’s ability to support the patient
- economic benefits: reduces the cost of hospitalisation as it is associated with reduced relapse rates (significatnly reduces relapse for a long period after therapy), also may allow them to lead a more normal lifestyle e.g. going to work= economic benefits for society and NHS
token economies
Management of schizophrenia AO1
- token economies= reward systems used to manage behaviour especially in hospitals
- based on operant conditioning, tokens= secondary reinforcers, primary reinforcers= the tangiable rewards that they can be exchanged for e.g. sweets
rationale for token economies
- institutionalisation can develop through prolonged hospital stays= may lead to bad habits like poor hygiene
- Mateson identified 3 categories commonly tackled by token economies
1. personal care
2. condition related behaviours (apathy)
3. social behaviours
- two major benefits: improves quality of life within the hospital setting, and normalises behaviours and good habits making it easier for them to adjust into society
how they work:
- token (e.g. coloured disks) are given when the patient displays a target behaviour e.g. they make their bed
- these can then be swapped for tangiable rewards
Management of schizophrenia AO3
- ethical issues: gives professionals power over patients, inevitably involves imposing one person’s norms onto someone else- target behaviours must be identified sensitively e.g. someone who likes to look scruffy may have this personal choice taken away from them
-restricting the pleasures (e.g. sweets and films) of someone already experiencing the condition= ethical issues and legal action has been taken- reduces use - alternative approaches: more pleasant, ethical alternatives like art therapy exist, evidence base is limited but appears to show that art therapy is low risk high reward, even if benefits are limited, this is the case for most scz treatments, it is more ethical and pleasant so may be prefferrable
- evidence of effectiveness: Glowaki reviewed 7 high quality studies into the effectiveness of token economies in hospital settings, found that all studies showed a reduction in negative symptoms and unwanted behaviours
- HOWEVER: file drawer problem- 7 studies is uite a small evidence base, may have been a bias towards positive published findings as undesirable results have been ‘filed away’ so are ignored
Interactionist approach AO1
- attempts to explain the disorder as a combination of nature (biological) and nurture (environment), biological factors predispose someone to the disorder and the psychological element refers to external stressors which trigger it
early diathesis-stress model- Meehl
* the diathesis (vulnerability) is entirely genetic and the result of a “schizogene”, without which someone cannot develop the disorder
* if someone with this gene experiences chronic stress in childhoos/ adolescence, this may trigger the disorder
modern understanding of diathesis
* Ripke et al: many genes involved rather than just one schizogene
* diathesis also includes factors beyond genetics such as trauma
* Read et al: trauma can alter the developing brain if it is early and severe, the HPA system can become overactive making them more sensitive to later stress= trauma can become the diathesis as well as the stress
modern understanding of stress
* anything that can trigger scz
* e.g. cannabis can become a stressor as it can increase scz risk by up to 7x possibly because it interferes with the dopamine system, however many of those who smoke cannabis never develop the disorder- presumably because the lack genetic factors
treatments
* tend to combine antipsychotics with therapies like CBT
* antipsychotics treat the biological cause whilst CBT helps to relieve symptoms
* standard treatment in UK but not in US
Interactionist approach AO3
- original diathesis model is oversimplified: idea of a single ‘schizogene is too simple- many genes and combinations contribute to scz, stress comes in mnay forms not just trauma and can also be biological
- support for genetic vulnerability and environmental triggers: Tienari studied 19000 Finnish children whose biological mothers had scz, in adulthood this high genetic vulnerability group were compared with a low genetic vulnerability control group and found that highly critical, hostile and unempathetic parenting was associated with scz but only in the high genetic risk group
- real-world application- this approach has lead to the combination of biological and psychological treatments, studies show that combining treatments makes them more effective
- HOWEVER: treatment causation fallacy: saying that a successful treatment justifies a particular explanation is illogical- direction of causation is confused, we cannot assume that the explanation is correct because the treatments work
