AQA Psychology - Schitzophrenia

ICD-10 : international classifications of disease. DONT NEED TO KNOW

Symptoms should be present most of the time.

At least one :

hallucinations/voices

delusions

delusions of control/influence

thought echo

or at least two:

persistent hallucinations every day for at least one month

Neologisms, breaks.. in train of thought (result in incoherent speech)

'negative symptoms' (apathy, paucity of speech..)

DSM - 3 : diagnostic and statistical manual - american psychiatric. DONT NEED TO KNOW

experienced at least two of following :

delusions

halluciginations

disorganised speech

disorganized or catonic behaviour

negative symtoms

(at least one must be disorganised speech, halluciginations, delusions)

persist for at least 6 months

at least 1 month of active symptoms

social or occupations detoriation problems

Positive symptoms of SZ

Hallucinations:

Unusual sensory experiences

some related to events in environment, some have no relationship to what senses are picking up from environment

(eg : voices talking to sufferer, often criticising them)

can be experienced in relation to any sense - see distorted faces or animals not there eg.

Delusions:

Also known as paranoia - irrational beliefs.

common involve being an important historical political figure - eg Napoleon or Jesus.

Commonly involved being persecuted - government, aliens..

some delusions concern the body - they of part of them are under control.

can make people suffering behave in a way that makes sense to them but not to others.

vast majority not likely to be aggressive, more likely to be victims not perpetrators of violence, but delusions some can lead to aggression

disorganised thinking

catantonic behaviour

Negative symptoms of SZ

Avolition:

Losing the will to perform behaviour necessary to accomplish purposeful acts, such as activities of daily life, goals and desires.

finding it hard to keep up with goal-directed activity.

very reduced motivation to carry out range of tasks - lower activity levels - 'apathy'

signs : poor hygiene, lack of persistence in work/education, lack of energy.

Speech poverty:

Minimal verbal communication that lacks additional unprompted content characteristic of normal speech.

(ICD-10 recognises as negative symptom because emphasis is on reduction in amount and quality of speech)

sometimes accompanied by delay in sufferer's verbal responses during conversation.

characteristics : only speak when prompted

provide v limited answers

(eg : how did you feel when shouted at" "bad" - prompted to say more w follow up question but response still limited)

Reliability and validity in classification

R - consistency in classification system, counts for nothing unless systems and scales also valid.

V - extent to which diagnosis represents something real and distinct from other disorders.

diagnosis cannot be valid if not reliable.

Validity

extent to which we are measuring what we intend to measure - how accurate diagnosis is.

one standard way to assess validity of diagnosis is concurrent validity (amt of agreement between two different assessments.)

Cheniaux et all - evidence investigation validity

SZ more likely to be diagnosed using ICD than DSM. Either : SZ overdiagnosed using ICD/Underdiagnosed using DSM. Highlights issue with concurrent validity, different assessment systems not arrive at same diagnosis.

Reliability

consistency of symptom measurement - important measure inter-rater reliability.

(extent to which different clinicians agree to their assessments)

Extent to which two or more mental health professionals arrive at the same diagnosis for different patients.

Cheniaux et al - evidence investigating reliability

had 2 psychiatrists independently diagnose 100 patients using both DSM and ICD.

Inter rater - poor : one diagnosed 26 according to DSM and 44 according to ICD.

highlights weakness in classification systems to diagnose SZ. External reliabililty low, fail to diagnose patients consistently - issue for diagnosis of SZ

However : carried out using DSM-4 not DSM-5, reliability and validity improved as systems updated.

Jakobsen et al

tested reliability of ICD-10 classification system during diagnosis SZ.

100 Danish Patients - history of psychosis assessed using operational criteria, concordance between clinicians 98%.

high inter rater of clinical diagnosis using up to date classifications.

Classification systems

provide w common language - communication research ideas and findings

Symptom Overlap

symptoms of SZ also symptoms of other disorders.

despite claim + and - symptoms would lead to more valid diagnosis of SZ, many symptoms are often found w other disorders - difficult to decide which disorder patient suffering from.

issue w validity of classifying SZ as a patient may be diagnosed as SZ with ICD, but bipolar w DSM.

Consequence - misdiagnosis - lead to years of delay in recieving relevant treatment... suffering and further degeneration of symptoms may occur inbetween.

Read - Symptom overlap

argued people diagnosed with SZ have sufficient symptoms of other disorders that they could also recieve at least one other diagnosis.

EG - symptom overlap occurs especially w/bipolar disorder, negative symptoms (depression, avolition) also common symptoms as well as positive symptoms (halluciginations)

Co-Morbidity

phenomenon where 2 or more conditions occur together. (eg depression and bipolar)

SZ commonly diagnosed w other conditions

Buckley et al : around half patients with a diagnosis of SZ also have diagnosis of depression (50%) or substance abuse (47%). PTSD also occured in 29% and OCD in 23%.

Issue for diagnosis and classification. Different diagnoses can be given to the same person (diagnosed w SZ in one condition, Bipolar in other and then both in another)

Can lead to inconsistencies in diagnosis between clinicians in relation to what disorder is diagnosed.

issues w reliability.

simulatenous disorders suggests that SZ may not be a separate disorder - lowers descriptive validity of SZ - make effective treatment difficult to achieve.

Culture bias - diagnosis

tendency to over-diagnose members of other cultures as suffering from SZ.

affects validity.

Cross-cultural research suggests a similar prevalence across races, however, despite culturally formulated updates to diagnostic manuals, SZ is repeatedly diagnosed at a higher rate in African American population.

Cochrane - research - culture bias

incidence of SZ in West Indies and Britain similar : 1%.

People of Afro-Carribean orgin are 7x more likely to be diagnosed when living in Britain.

because incidence in both cultures is very simular - suggests higher diagnosis rates are not due to genetic vulnerability, but instead cultural bias.

Reasons why African Americans may be over represented

clinician bias - unconscious processes stemming from stereotypes and biases - result in misdiagnosis.

Under diagnosis of other disorders (depression/bipolar) in African Americans may contribute to over diagnosis of SZ.

Gara et al - cultural bias

African American men w severe depression tend to be misdiagnosed w SZ in comparison to other racial groups.

Findings - suggest clinicians put more emphasis on psychotic than depressive symptoms in AA, scews diagnosies towards SZ when show simular depressive and manic symptoms as white patients.

Lack validity in diagnosing AA orgin - differences in symptom expression overlooked or misinterpreted by clinicians.

prevents from receiving optimal treatment - risk of side effects from medication (diabetes and weight gain)

Gender Bias in diagnosing SZ

tendency for diagnostic criteria to be applied differently to male and females - differences in classification of disorder.

Critics of DSM diagnostic categories - biased towards pathologising one gender rather than the other.

Broverman et al

clinicians in the US eqauted mentally healthy 'adult' behaviour, with mentally healthy 'male' behaviour - form of androcentrism.

Tendency for women to be perceived as less mentally healthy when they do not show 'male' behaviour.

Loring and Powell

research has indicated a psychiatrists gender might affect their ability to diagnose.

Randomly selected 290 male and female psychiatrists to read case studies of patients behaviour and make judgement using standardised diagnostic criteria - eg DSM.

when patient described as 'male' or no info about gender - 56% gave SZ diagnosis.

when described as female - 20%.

gender bias was not evident amongst female psychiatrists, however - not only induced by gender of clinician but also patient.

gender bias sz

further -

clinicians also fail to consider that males tend to suffer more negative symptoms than women (Galderisi et al)

Women typically function better than men, able to go to work and have good family relationships (Cotton et al)

high functioning may explain why women have not been diagnosed whereas men with simular symtpoms are.

better interpersonal functioning may bias clinicians to underdiagnose disorder - either because symptoms masl together by good interpersonal functioning or because quality of interpersonal functioning makes case seem too mild to warrant diagnosis.

affect validity.

Predispositional factors :

first onset - male : 18-25, Female : 25-30.

different types of stressors, experience at different ages, menstraul cycle, etc.

Biological explanations for SZ

See the disorder caused by physiological means.

Genetics, abnormal dopamine functioning and neural correlates.

General genetic link theory

SZ transmitted through genes passed on to individuals from their families.

Share % of genetics with relatives depending on how genetically simular we are to them (eg 50% with 1st degree).

Investigations into genetic link and Gottesman

good evidence for understanding influence genes play - have to be careful, family tend to share environment and genes etc.

Conducted a large scale family study and found a strong relationship between the degree of genetic simularlity and shared risk of sz.

eg : 48% concordance rate in MZ twins and 17% in DZ.

General population : 1%

Parents: 6%

Siblings: 9%

DZ: 17%

MZ : 48%

More specific genetic

not believed there is a single 'sz gene' - several genes involved increasing an individuals overall vulnerability to developing sz.

Polygenetic - number of factors work in combination.

different studies have identified different candidate genes, aetiologically heterogeneous - different combinations can lead to disorder.

Ripke et al

huge study combining all previous data from genome wide studies - looking at whole genome not just particular genes) of SZ. Genetic makeup of 37k patients compared to 113k controls - 108 seperate genetic variations were assosiated w risk of SZ.

genes assosiated w increased risk : brain and tissues with an important role in immunity, as well as those coding for functioning of a number of neurotransmitters including dopamine - overall support for biological causation

Genetic explanations : evaluation - supporting evidence

overwhelming evidence for idea genetic factors make some people more vulnerable to developing SZ

Kety and Ingraham - prevalence rates were 10x higher among genetic than adoptive relatives of schitzophrenics - genetics play greater role than environment.

role of environment eliminated by looking at individuals who grew up away from biological parents.

if individual still develops SZ it must be due to genetics and not to living with parents whose behaviour might have had an impact on development of the disorder.

Genetic explanations : evaluation - issues with research investigating biological explanations

research conducted to assess relative contribution of genetics to development of SZ can be criticised for many reasons.

EG - crucial assumption underlying all twin studies - environment of MZ and DZ twins is equivelent.

Assumption - greater concordance rates for SZ between MZ twins is a product of greater genetic simularity than greater environmental simularity.

Joseph- widely accepted MZ twins treated more simularly than DZ twins, encounter more simular environments and experience more 'identity confusion'. - reason to believe difference in concordance rates between MZ and DZ twins reflects nothing more than the environmental differences that distinguish the two types of twin.

issues encountered - contribution of genes to SZ can never truly be established.

Genetic explanations : evaluation - nature/nurture

Nature/Nurture debate highly relevant in discussion of causes of SZ.

Genetic explanation - falls under nature side of debate, implying SZ is solely caused by genes inherited from parents. Fails to consider involvement of environmental factors - eg family disfunction.

The argument may be fault as SZ development cannot be entirely genetic in basis. demonstrated by fact concordance rates between MZ would be 100% if purely genetic.

Diathesis stress model - individuals may inherit different levels of genetic predispostion but ultimately environmental triggers determine whether an individual will go on to develop SZ.

The dopamine hypothesis

dopamine - a neurotransmitter involved in initiating movement and has a major role in reward motivated behaviour.

Widely believed to work different in brain of someone with SZ, may result in symptoms observed in sufferers.

probable genetic factors are linked to faulty dopaminergic systems.

Orginal dopamine hypothesis

High levels of dopamine (hyperdopaminergic activity) - Found mesolimbic pathway and subcortex (certain areas of brain eg Brocas) - may be assosiated w positive symptoms of SZ (pov speech, halluginations) - why?

Perhaps because person has an increased amount of D2 receptors in the brain or because messages from neurons that transmit dopamine either fire too readily or often leading to the cha

revised dopamine hypothesis

low levels of neurotransmitter dopamine (hypodopaminergic activity) - found Mesocortical pathway particularly the frontal lobes (pre frontal cortex) - may be associated with the negative symptoms.

Evaluation: dopamine hypothesis - supporting evidence

support from a number of sources for abnormal dopamine functioning in SZ

Curren et al - when amphetamines, which activate dopamine production) are given to non-sufferers, it can produce SZ like symptoms and make symptoms worse in those already suffering from SZ.

Kessler et al - used PET and MRI scans to compare people with and without SZ, finding that schizophrenics had elevated dopamine receptor levels in certain brain areas and differences in levels of dopamine in the cortex were also found.

suggest an important role for dopamine in the onset of SZ.

Evaluation: dopamine hypothesis - issues w causation

evidence for dopamine hypothesis remains inconclusive and there are issues with establishing causation.

differences in biochemistry in schitzophrenics and non sufferers could ust be an effect of the disorder.

Lloyd et al - believe if dopamine is a causative factor, it may be an indirect factor mediated through environmental factors, because abnormal family circumstances can lead to high levels of dopamine, which in turn trigger SZ symptoms.

Illustrates we should be cautious in drawing firm conclusions about direct role of dopamine in development of SZ.

Evaluation: dopamine hypothesis - biological reductionism

can be criticised for being biologically reductionist.

simplifies the complex development of SZ to a single biological component - the neurotransmitter dopamine in this case

could be the case that many other neurotransmitters are involved in the development of the disorder, eg - much of the attention in current research has shifted to role of a transmitter called glutamate, as well as newer antipsychotic drugs that also implicate serotonins involvement too.

this reductionist approach can be problematic because a variety of factors that may be involved in the development of SZ are being overlooked by isolating a single biological cause.

however - can also be beneficial taking a reductionist approach as it has helped to inform the development of drug therapies and treatments to treat SZ.

EG - anti-psychotic drugs that affect dopamine levels are the principle treatment offered to patients experiencing a SZ episode and have been shown to be effective in reducing severity of symptoms.

shows usefulnes of explanation despite reductionist nature.

Neural correlates of SZ

suggests abnormalities within specific brain areas may not be associated with the development of SZ.

research uses non-invasive scanning techniques, eg fMRI, to compare brain functioning of SZ to non suffers, to identify brain areas that may be linked to the disorder.

P's often given task assosiated with types of functioning known to be abnormal in sufferers, eg social cognition, thought processing...

Negative symptoms - Johnstone et al

focussed on SZ having enlarged ventricles - these are especially associated with damage to central brain areas and pre-frontal cortex, which more recent scanning studies have also linked to the disorder.

Tomoyuki

conducted a 10 year longitudinal MRI study on 15 patients and 12 controls (matched closely age, education etc) and found progressive ventricular enlargements in patients with SZ, but not controls.

Such damage has often been associated with the worsenning of negative symptoms - avolition.. cannot explain all symptoms and incidences of SZ.

positive symptoms - allen et al

found positive symptoms also have neural correlates.

Scanned brains of patients experiencing auditory hallucinations and compared them to a control group whilst they identified ore-recorded speech as theirs or others.

Lower activation levels - superior temporal gyrus and anterior cingulate gyrus were found in hallucination group who made more errors in the control group.

reduced activity in these 2 areas of the brain is a neural correlate of auditory hallucination.

Evaluation : neural correlates - supporting evidence

there are a number of neural correlates of SZ symptoms including both positive and negative. the research helps to identitfy particular brain systems that may not be working normally.

Tito - used fMRI scans to investigate the level of activity in the Wernicke brain area, when SZ and non SZ were asked to talk about a Rorschach ink-blot.

they found that in SZ patients , the severity of their disorder was negatively correlated with the level of activity in their Wernickes area.

Supports idea abnormal functioning in specific brain areas being related to SZ symptoms - eg speech disorganisation

Evaluation : neural correlates - issue w causation

cannot establish causation - major limitation

does the unusual activity in that region cause SZ or does the disorder itself cause these brain differences.

EG - appears to be people w severe symptoms of SZ and who do not respond to medication are the ones who suffered the enlarged ventricles.

this could mean the physical brain damage might be an effect from suffering SZ over a long period rather than brain damage leading to SZ in the first place.

existance of neural correlates in SZ therefore tell us little in itself

Evaluation : neural correlates -challenging evidence

there is scientific evidence to support the issue of causation

Ho et al - performed MRI scans on recent-onset SZ and re-scanned them 3 years later. They found evidence of brain damage in the recent onset patients which worsened over time, especially in the frontal lobes, which correlated with an increase in the severity of their symptoms.

Suggests brain damage does increase in SZ over time and may not be the initial cause of the disorder.

consideration - possible role of a third variable impacting on the relationships we see between brain abnormalities and the development of SZ.

EG - environmental factors, substance abuse, stress levels may have damaging influence on brain tissue.

more longitudinal research is needed - assess whether damage progressively worsens.

Biological therapies - antipsychotic drug treatment

most common treatment for SZ

can be taken in tablets, syrup or injection

may be required short term or long term

some can take a short course and then stop them without return of symptoms,

some may be required to take them for life or risk recurrence of symptoms.

Typical antipsychotics - around since 1950s

eg chlopromazine

work by acting as antagonists in the dopamine system, in other words, reduce the action of the neurotransmitter.

dopamine antagonists block D2 receptors in the synpases of the brain that absorb dopamine thus reducing positive symptoms.

chlorpromazine - effective sedative and is often used to calm patients when they are very anxious, may be because it effects histamine receptors.

tend to block all types of dopamine activity which can be harmful.

Atypical antipsychotics - used since 1970s

made/purpose was to improve upon the effectiveness of drugs in suppressing symptoms and also to minimise extrapyramidal side effects (drug-induced movement disorders).

large range which work in different ways.

Clozapine and atypical antipsychotics also act on dopamine receptors, reducing positive symptoms.

In addition, it acts as an antagonist for serotonin and an agonist (increase release of) for glutamate receptors - improve mood and reduce negative symptoms in patients - avolition. May also improve cog functioning by reducing disorganised thinking.

sometimes prescribed when patient as high risk of suicide.

Risperiodone - believed to bind to dopamine receptors more strongly than clozapine and therefore more effective in smaller doses and can lead to fewer side effects.

evaluation : drug therapy - supporting evidence for typical anti-psychotics

Thornley et al - reviewed studies comparing the effect of chlorpromazine to control conditions in which patients received a placebo, so their experiences were identical except for the presence of chlorpromazine in meds.

data from 13 trials with a total of 1121 ps showed that CP was assosiated w better overal functioning and reduced symptom severity.

also evidence of relapse rates being lower from 3 trials when chlorpromazine was taken

support use

evaluation : drug therapy - effectiveness and appropriateness

also support for benefits of atypical antipsychotics, particularly clozapine.

Meltzer - concluded it was more effective than typical and other atypical anti-psys and that it was effective in 30-50% of treatment resistant cases where typical antipsychotics had failed.

suggests atypical could be seen as a more effective drug therapy in comparison to typical antipsychotics as well as being a more appropriate drug treatment for certain individuals who do not respond well to other types of anti-psychotics.

evaluation : drug therapy - economic implications

drug therapies can have positive economic implications

people suffering prevented from going to work

sometimes have to be hospitalised - significant effects on economy.

if anti-psychotic lead to symptom reduction , they could enable individuals to return to work or prevent hospitalisation - reducing negative impact on economy.

evaluation : drug therapy - appropriateness

an issue with antipsychotic drug treatments is the likelihood of side effects, ranging from mild to serious,

typical - assosiated w a number of side effects such as dry mouth, constipation, legarthy and confusion, long term can involve involuntary muscle movements... tardive dykinesia - caused by dopamine oversensitivity.

Atypical - developed to reduce the frequency of side effects and this has generally succeeded., however they do still exist - likely include weight gain, cardiovascular problems, developing diabetes.

problems -

lead to reduction in quality of life

lead to sufferers stopping treatment and experiencing relapse.

Psychological explanations for SZ

Family dysfunction and cognitive explanations

Family dysfunction

much evidence has now accumulated to suggest that like other mental health problems, SZ can be a reaction to stressful events and life circumstances.

Family dysfunction explanation identifies sources of stress within families which can cause the development of SZ.

- maladaptive patterns of communication

- experience of conflict

- high levels of critisism

- controlling behaviours

Double Bind theory - Bateson et al

believes family climate is important in development of SZ and emphasises role of communication style within a family.

Developing child regularly finds themselves trapped in situations where they fear doing the wrong thing, but receive mixed messages about what this is, and feel unable to comment on the unfairness of the situation/seek clarification.

message (words spoken)

Meta message (way in which message transmitted through tone and body) can have different meanings. - parent who says they love their child but constantly are critical of them. false sense of reality.

double bind - 'no win', when they 'get it wrong' (often) child punished y withdrawal of love.

Prolonged exposure to such interactions may leave an individual with an understanding of the world as confusing and dangerous.

individual loses touch with reality, reflected in SZ symptomd like disorganised speaking and thinking and paranoid delusions.

some may hear voices telling them they are worthless.

disorganised speech - attempt to not communicate - keep social world at bay.

High expressed emotion

families may exhibit criticism, hostility, exaggerated involvement and/or control and exert a negative influence on the sufferer.

primarily an explanation for relapse. Also may be a source of stress and trigger onset of SZ in an individual vulnerable due to genetic predisposition (diathesis stress model)

can lead to child experiencing overwhelming emotion that can effect how an individual may respond to future stress and interpret new challenging experiences - paranoid thinking.

individuals may dissosiate or 'mentally leave' as a result of high stress and trauma which can explain negative symptoms such as speech poverty and avolition.

An unhealthy level of involvement and control could explain why the sufferer experiences paranoia around the world.

Vaughn and Leff

showed that relapse rates were higher amongst patients who had been discharged into home environments which were higher in expressed emotion.

high EE families - 51%

low EE families - 13%

in high EE families, relapse rates correlated with amount of time spent w family members.

Evaluation: family dysfunction - research support

evidence to support role of family dysfunction in childhood and increased risk of developing SZ in adulthood.

Tienari et al - found level of SZ diagnosed in adopted children of SZ mothers was 5.8% higher than those adopted into healthy family environments.

36.8% for children raised in dysfunctional families.

Supports not only the family dysfunction explanation, but also the idea individuals with high genetic vulnerability to SZ are more affected by environmental stressors.

Butzlaff and Hooley - performed a meta analysis of 26 studies to find that SZ returning to a family environment experienced more than 2x the average relapse rate of symptoms.

provides valuable support for the role of family dysfunction in the onset and relapse of those suffering w / SZ.

Evaluation: family dysfunction - useful contribution

the family dysfunction explanation highlights the importance of considering how social and environmental factors may contribute to the onset of the condition.

emphasises the role families play in the onset and relapse of SZ which other explanations fail to consider.

contributed to the interactionalist approach to explaining the cause of the disorder - adopts a more holistic approach highlighting the complexity of the onset of symptoms, providing an explanation for high relapse rates.

useful applications - confirms peoples friends and families can be very important in helping loved ones recover and has informed methods of family therapy which has been found to be successful in preventing relapse - people in a calm supportive home atmosphere tend to do better.

Demonstrates theories value and the useful contributions the explanation has made to understanding.

Evaluation: family dysfunction - issues w causation

criticised due to correlational nature and inability to establish cause of SZ

very difficult to establish direction of the relationship between environment and behaviour.

family dysfunction including maladaptive communication may be the result of the childs symptomatic behaviour rather than the cause of the illness.

furhter - there is ample theory and evidence to suggest there is a genetic and or neural cause - family dysfunction may act as a contributing factor or trigger for the condition - not be at root cause.

challenges support and ability to explain cause.

Evaluation: family dysfunction - social sensitivity

adopting family disfunction explanation may have negative implications.

blaming parents of sufferers for their childs disorder

the theory suggests SZ is caused by families maladaptive communication and the home environment. result - parents may feel responsible for their childs illness.

further, responsibility being placed on parents for their childs illness can cause greater levels of stress anf anxiety in the family which may then trigger or exacerbate the illness.

potential negative implications , social sensitivity - not widely researched or accepted by society.

Family therapy

form of psychotherapy that involved the whole family, including the member w sz if it is practical.

A characteristic of SZ is that individuals are often suspicious about their treatment and so involving them more actively helps overcome this and symptoms of paranoia.

family therapy - aims

main : reduce stress levels in families to aid recoverey for SZ sufferers therapists meet regularly w the paitient and family members between 9 months and a year.

- decrease negative forms of communication

- decrease stress of caring for a relative

- increase skill development for use after therapy has ended

- decrease criticism levels

- increase tolerance levels

- decrease expressions of anger / guilt

- increase ability to anticipate and solve problems

- decrease feeling of responsibility for causing illness (family)

direct links to symptoms

- altering relationships and communication patterns within dysfunctional families can help to reduce instances of double bind and its accompanying stress - reduction of symptoms

- lowering levels of expressed emotion - reduce relapse rates

eg asked to set reasonable expectations for individual w SZ, set appropriate levels of involvement by the family - decreases stress for sufferer and reduces symptoms like paranoid thinking.

- reduction in stress levels within the family - increase chances of patient complying w medication.

combination of benefits result in unlikelihood of relapse.

Evaluation: Family therapy - effectiveness

reliable support from research into the effectiveness of using family therapy to help reduce symptoms and prevent relapse in sufferers of SZ.

McFarlane et al - reviewed available evidence to find family therapy improved family relationships resulting in symptom reduction and reduced relapse rates among family members - increased wellbeing for patients.

family therapy - effective treatment with an indication better family relationships play a role in symptom reduction.

Pharoah et al - moderate evidence to show family therapy significantly reduces hospital readmission over the course of a year and improves quality of life for patients and their families.

further demonstrates therapies effectiveness in not only symptom reduction but reducing likelihood of relapse and improving quality of life.

Evaluation of family therapy - appropriateness

can be more appropriate for some suffers than others.

family interventions in early psychosis have been found to significantly reduce relapse and readmission rates.

particularly useful for younger patients who still live at home with their families and who are also undergoing medical treatment and require support and. for patients who lack insight into their illness and cannot speak coherently about it as family members may be able to assist and act as an advocate.

may not always be appropriate.

attending a family program conveys a series of demands to the sufferer and caregivers, such as transportation, time, motivation and energy.

Stigma can sometimes cause relatives to quit.

severity of symptoms may also prevent some sufferers from participating in family therapy and lead to high dropout rates

should be carefully considered in relation to appropriateness for each individual and their family

Evaluation: Family therapy - economic implications

economic benefits

family therapy is often not widely available due to its time consuming and costly nature, however the NICE review of family studies demonstrated that when implemented, it was assosiated with significant cost savings when offered to service users in combination with other treatments like drug therapy.

extra cost of the recourse required for family therapy is offset by a reduction in cost through preventing the need for further and longer lasting treatment.

Has been found to reduce relapse rates and therefore prevent the cost for further care which may recquire (eg hospitalisation)

Cognitive explanations

focusses on role of mental processes. Cognitive impairments shown by people w SZ play an important role in the development and maintenance of SZ.

Attentional bias - Bentall

suggested people w SZ have deficits and biases in the way they process info. Unusual attentional bias to stimuli of a threatening and/or emotional nature.

eg content of hallucinations and delusions regarding their orgin may be understood in terms of biased info processing.

paranoid delusions may be a result of an individual misinterpreting an event as threatening due to an exaggerated amount of processing surrounding that experience or specific stimuli

eg person cutting cake, knife too much focus, fear going to be used as weapon.

Dysfunctional thought processing - frith et al

identified 2 types of dysfunctional thought processing that could underlie some symptoms of SZ.

Metarepresentation

cognitive ability to identify and reflect on our own thoughts, behaviours, emotions and experiences.

A lack or dysfunction in this monitoring tool - disrupt ability to recognise own thoughts and actions and distinguish them from thoughts and actions being carried out by others - own thoughts and ideas may be attributed to external sources.

can explain the experience of auditory hallucinations.

commonly experienced delusions such as being controlled or persecuted can be explained by failures in metarepresentation and the inhability to make judgements about people's intentions.

thought insertion - a common delusion experienced by sufferers which can also be explained through faulty meta-representation.

central control

the ability to suppress or override automatic thoughts/actions in response to a stimuli.

cog ability to suppress undesired automatic responses while we perform deliberate actions that reflect our wishes and intentions.

enables us to suppress stimulus-driven behaviour and activate willed behaviour and a dysfunction in central control may result in the display of behaviour seen as abnormal.

if an individual has an impaired central control , then they are unable to control their automatic response to any stimuli.

specific language communicated to sufferers through convo can trigger assosiations and memories that they would be unable to suppress their automatic responses to - disorganised speech, derailment of thought may be a result.

Inability to suppress automatic thoughts and speech can be triggered by other thoughts - explains experience of paranoia and delusions.

EG - live w symptoms of SZ, in a convo about what you did at the weekend - suddenly had thought of forgetting to buy sausages - say out loud because cannot supress thought.

'had a nice time with harry, i forgot to buy sausages, we had beers, theres a fly on the wall..'

Evaluation: Cognitive Explanations - research support

strong support information is processed differently in the mind of a sufferer of SZ (both + and - symptoms)

Stirling et al - compared 30 patients w SZ and 18 non on a range of cog tasks - including the STROOP TEST, had to name the ink colours of colour workds, supressing the impulse to read the words..

sufferers took over 2x as long as the control group to name the ink colour - sufferers therefore suffering w central control dysfunction.

supports Friths theory that dysfunctional thought processes have a role in cause of SZ - support

Evaluation: Cognitive Explanations - issues w causation

despite long body of research between symptoms and faulty cognition, cog theories do not tell us about orgins of faulty conditions.

structual brain abnormalities may lead to differences in thought processes seen in symptoms of the disorder - Eg research has found some SZ have enlarged ventricles int he prefrontal cortex and also that sufferers experiencing hallucinations have lower activation levelsnin their superior temporal gyrus.

suggest neural basis to cog symptoms. such as derailment of thought and language.

cog approach may be criticised for not providing us with underlying causes of dysfunctional cognitive processing and the symptoms experienced by sufferers.

suggest interactionalist explanations using theories of cog neuroscience would be more effective in explaining onset.

cog explanation alone - limited - inability to provide complete explanation.

Evaluation: Cognitive Explanations - predictive validity positive contribution to effective treatment.

cog treatments found to be effective - further support validity of explanation

CBT has a significant effect in reducing both + and - symptoms of SZ through brief intervention programmes.

eg - CBT can help develop the functioning of meta representation through the sufferer challenging the origin of delusions and recognising the course of hallucinations.

strategies therefore adopted in the therapy have been found to improve symptoms - suggests cog dysfunction is the cause of such symptons.

effectiveness - demonstrates predicitive validity of cog explanation.

Cognitive Behavioural Therapy - Schitzophrenia

structured talking therapy. NICE (national institute for health and care excellence) currently recommends CBT for everyone with psychosis. It usually takes place for 5-20 sessions, either in groups or individually.

Basic assumption - people have distorted beliefs which influence beh and feelings in maladaptive ways,

eg - may believe behaviour is being controlled by someone else.

Delusions - thought to result from faulty interpretations of events. CBt help correct and identify faulty interpretations.

AIM - help patient make links between cognition, emotions and behaviours of their symptoms.

Monitoring - able to consider alternative ways of explaining why they feel and behave the way they do - reduces distress and improves functioning (how a traumatic event has contributed to their paranoid delusions.)

CBTp strategies - ABCDE framework

- initial ASSESSMENT of patients experiences

- ENGAGEMENT of patients experiences

- ABC model

(patient gives explanation of activating events (A) that appear to cause emotions, behaviours and beliefs (B)

Their beliefs which are usually causes of the consequences (C) can then be rationalised, disputed and changed)

EG - through reality testsed, patient is encouraged to evaluate the content of their delusions and voices and consider ways to test their validity.

therapist challenge delusions so they can come to learn their beliefs are not based on reality.

- believe being watched, individual can identify internal belief and realise there is no evidence of this and control the way they respond to this future.

reduce negative symptoms like avolition - less likely to demonstrate avoidant behaviour.

normalisation

placing psychotic experiences on a continuum with normal experiences to reduce alienation and stigma

critical collaborative analysis

gentle questioning to help patient understand illogical deductions and conclusions. - goal of helping patient develop alternative explanations for previously unhealthy assumptions.

Evaluation: CBT - effectiveness - supporting evidence

evidence for effectiveness of using CBT to treat SZ

Tarrier - reviewed 20 controlled trials of CBT using 739 patients, showing consistent evidence that CBT reduces persistent positive symptoms in chronic patients and may have modest effects in speeding recovery in acutely ill patients.

Suggests CBT is viable treatment for SZ, particulalry for reducing positive symptoms like delusions and hallucinations.

Evaluation: CBT - effectiveness - evidence could highlight need for combination treatments

Jauher et al - performed a meta-analysis of 34 studies of CBT for SZ.

Concluded CBT has a significant, but fairly small effect on positive and negative symptoms.

Potential reason for small effect - CBT investigated as a lone treatment? - tarrier et al suggests CBT plus antipsychotics is effective in treating SZ, and more effective than drugs or CBT alone.

May be more beneficial for CBT to be used in combination w drug therapy.

Evaluation: CBT - appropriateness - sufferers may not be able to engage w therapy

May not be appropriate for all sufferers.

Relies on individual having to engage w the therapy and the therapist, which may be difficult for those experiencing paranoia, or who are too disorientated or agitated to form trusting alliances w practitioners.

Important to consider the individual sufferer when suggesting CBt as a treatment option, as it may only be appropriate when the sufferer is in the position to engage in the process of CBT.

Evaluation: CBT - appropriateness - reduces distress

Psychological therapies like CBT do not help everyone, for others they can make a huge difference in their lives.

Even when they do not reduce the frequency or intensity of their experiences of delusions and hallucinations, they often help reduce distress.

Help people find ways of achieving their goals and getting on with their lives, even if their experiences continue.

Important to consider CBT as a treatment option for SZ.

Token Economics - Schitzophrenia

behaviourist approach to the management of SZ, where tokens are rewarded for demonstrations of desired behavioural change.

mainly used with long term hospitalised patients to enable them to leave hospital and live relatively independently within the community.

similar programs have also been used in outpatient facilities.

particularly aimed at changing negative symptoms such as low motivation, poor attention and social withdrawal.

uses operant conditioning, where patients recieve reinforcement in the form of tokens immeditely after producing a desired behaviour - eg making the bed.

Tokens can be exchanged for goods or privalleges - sweers, a walk.

Reward acts as primary reinforcer and token secondary reinforcer.

Evaluation : token economics - effectiveness limited evidence

some evidence to support the effectiveness of token economics within a care setting.

Eg - one small study looking at token economy being used in a psychiatric hospital favoured the token economy approach with improvement in negative symptoms in 3 months.

partially supports token economy as a way of managing SZ and its ability to reduce symptoms.

However, overall there is limited evidence to support the effectiveness of token economy at treating symptoms long term.

Evaluation : token economics - effectiveness

Problem w token economics, the effects may not be maintained beyond care setting.

desirable behaviour becomes dependant on being reinforced which means these rewards stop when individuals w SZ are no longer under the care of the provision.

Can lead to relapse of symptoms eg - sufferer may lose motivation which could lead to avolition reoccurring and might lead to high re-admittance rates.

Evaluation : token economics - ethical concerns

Raises ethical concerns in psychiatric institutions.

token economies work on principles of rewarding patients with everyday pleasures, such as watching TV. Could be seen as unethical as they are denying people w SZ access to these pleasurable activities until they behave in a way the institution finds desirable, whereas these activities are freely available outside the institution.

raises serious ethical and moral questions as to whether token economy should be used as a managing symptoms of SZ within a hospital setting.

interactionalist approach in explaining and treating SZ - diathesis-stress model

biological, psychological and societal factors in the development of SZ.

Biological factors include genetic vulnerability, neurochemical and neurological abnormality.

Psych factors include stress, eg, resulting from life events and daily hassles, including poor quality interactions in the family

diathesis stress model

diathesis - vulnerability

stress - negative psychological experience

Both the vulnerability to SZ and stress trigger are necessary in order to develop the condition.

One or more underlying factorr make a person particularly vulnerable to developing the disorder, onset of condition triggered by stress.

Early DSM, diathesis was seen as entirely genetuc and reslt of single 'schziogene'. Howver - clear now many genes appear to increase genetic vulnerability slightly.

Modern views on diathesis include a range of factors beyond genetic, including psychological trauma, so trauma becomes the diathesis rather than the stressor.

In OG model, stress was seen as psychological in nature, particularly related to parenting. Eg - family dysfunction of high expressed emotion where families exhibit criticism and hostility - can trigger onset of SZ for someone already vulnerable.

Modern definitions - stress anything that is a risk for triggering SZ - Drug abuse...

combination treatments most effective - reflect interactionist model of using biological and psychological treatments.

Read et al

early trauma alters developing brain. Early and severe trauma such as child abuse can severely affect aspects of brain development - eg HPA system can become overactive - person more vulnerable to stress later in life.

Evaluation: Interactionist DSM - appropriate

Tienari et al - level of SZ diagnosed in adopted children of SZ mothers was 5.8% when adopted into healthy family environments. this rose to 36.8% when raised in dysfunctional families.

suggests individuals with high genetic vulnerability to SZ are more affected by environmental stressors - supporting importance of using an interactionist approach to explain SZ.

Evaluation: Interactionist DSM - necessity for combination treatments

Tarrier et al - randomly allocated 315 patients to a medication and CBT group, medication and supportive councelling group or a control group (meds only).

Patients in combination groups showed lower symptoms than those in control groups after 18 months, although there was no difference in rates of hospital readmissions.

suggests using just biological treatments alone will lead to less successful treatment outcomes compared to combination treatments.

demonstrates importance of interactionist approach - superior long term treatment outcomes.

Evaluation: Interactionist DSM - too simplistic?

focussed only on a single gene (schizogene) as the diathesis and dysfunctional parents as major source of stress.

however, multiple genes can increase genetic vulnerability to SZ rather than just a single 'schizogene' and research suggests psychological trauma can also make some vulnerable to stress triggers.

stress can come in may forms - parenting, family dysfunction, substance misuse....

suggests number of vulnerabilities and stressors that could be involved in onset of SZ and therefore its important to adopt an interactionalist approach that considers complexity of diathesis stress.