Schizophrenia - A2

  • Created by: Simba2604
  • Created on: 23-09-17 12:30

Schizophrenia key terms

Schizophrenia = severe mental illness where contact with reality and insight, an example of psychosis

Classification = process of organising symptoms into categories based on which symptoms cluster together in sufferers

Positive symptoms (addition of) = atypical symptoms experienced in addition to normal experiences ---> hallucinations + delusions

1) Hallucinations = sensory experiences of stimuli that have no basis in reality or are distorted perceptions of things that are there

2) Delusions = involve beliefs that have no basis in reality ---> eg. belief that they are victim of a conspiracy

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Schizophrenia key terms continued

Negative symptoms = atypical experiences representing the loss of a usual experience

1) Alogia (speech poverty) = involves reduced frequency + quality of speech

2) Avolition = involves loss of motivation to carry out tasks and lowered activity levels

Co-morbidity = occurence of 2 or more illnesses or conditions together ---> eg. person has both Sz and DID

Symptom overlap = when 2 or more conditions share symptoms

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Schizo intro

  • Schizophrenia is one of the most chronic and disabling of the major mental illnesses affecting thoughts, emotions and behaviour
  • it involves a range of symptoms where the sufferer experiences a loss of contact with reality


  • unlike physical illnesses, there's no physical or medical test such as x rays, scans, blood/urine tests etc that can confirm the presence of a mental disorder like Sz
  • Classification symptoms have been developed to help clinicians make accurate and realible diagnoses of mental diorders

(2013) DSM-5 ----> used by USA + APA -----> based on american culture and norms

(1994) ICD-10 ----> used by UK + WHO -----> based on western culture

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Diagnostic criteria of Sz + types of symptoms

  • Generally, Sz patients lack insight into their condition ---> do not realise they are ill
  • Sz does not have a single defining characteristic but is a luster of symptoms
  • In order for a diagnosis to be made ---> 2 or more of the + symptoms must be present for more than month along with reduced social functioning
  • psychologists use DSM and ICD to diagnose a patient with Sz

The medical proffession makes a distinction between + and - symptoms of Sz


  • subjective ---> psychiatrist can't see patients hallucinations so patient must explain verbally
  • an excess or distortion of normal functions eg. hallucinations, delusions, passivity experiences and distorted thoughts


  • objective ---> psychiatrist can visually see avolition and alogia
  • involve a reduction or loss of normal functioning eg. no motivation and lack emo response
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  • Hallucinations involve disturbances in perception ---> false perceptions that have no basis in reality
  • usually auditory or visual perceptions of things that are not present but imagined stimuli can come from from any of senses (sensory modality)
  • Auditory = eg. running commentary, voices giving instructions
  • tactile somatory sensory ---> false perception of tactile sensory input that creates a a hallucinatory sensation of physical contact with an imaginary object ---> eg. feeling of imaginary insects/spiders on skin
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Delusions are false beliefs that are held very strongly

Examples of delusions:

1) grandeur ---> involve inflated beliefs about person's power and importance eg. Jesus, President, Queen

2) prosecution ---> may believ people are out to get them (paranoia)

3) Experiences of control ---> may believe they are under control of an external force thats using a special mechanism eg. insertion, withdrawal, broadcasting

4) Disordered thinking ---> feeling that thoughts have been inserted, withdrawn or broadcasted from the mind. Disorganised thinking cannot be directly observed but will manifest itself as disorganised speech (incoherent non-logical speech)

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Alogia (speech poverty)

Alogia is characterised by the lessening of speech, fluency and productivity

Speech has a 'loose correlation' ----> derailment from one topic to another

Said to reflect selective attention/attention deficit as filter mechanism doesn't work so Sz sufferers are bombarded with lost of info that they cannot analyse ---> thoughts become disorganised

Speech poverty manifests itself as short and empty responses to questions

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Avolition = kind of apathy ---> inability to generate goal driven behaviour


  • lack of attention + care to personal hygiene + appearance
  • lack of continued education or employment
  • lack of energy eg. no enthusiasm
  • extreme social withdrawal ---> isolation eg. no social media and don't see peers, often unbothered by it

Affective flattening ---> no range of emotion and show lack of emotional response to situations

"Catatonic" refers to an individuals movements, posture and responsiveness

  • Catatonic stupor = unresponsiveness, may stit/lie/stand for days and resists attempts to move
  • Catatonic aggitation = constantly moving, often repetetive eg. pacing/rocking
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Rank symptoms of Sz

Schneider's 1st rank:

= positive/type 1

  • auditory hallucinations
  • primary delusions of grandeur, persecution etc
  • thought disturbances
  • though insertion

Slater and Roth's 2nd rank:

= negative/type 2

  • Avolition
  • Alogia
  • Asociality
  • Affective flattening
  • Anhedonia (lack of pleasure in anything)
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Subtypes of Sz

Hebephrenic/disorganised Sz = 10% of sufferers

Paranoid Sz = 40% of sufferers

Catatonic Sz = 10% of sufferes


  • early age of onset (adolescence + young adults)
  • progrerssive + irreversible
  • behaviour has no purpose ----> no goal driven behaviour
  • disorganised throughts ---> leads to speech poverty + poor focus/attention
  • vivid auditory + visual hallucinations
  • some delusions
  • asociality
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Subtypes of Sz continued

Paranoid Sz:

  • later onset (late 20s+)
  • key = halluc + delusions
  • remain high functioning eg. organised, still in work etc
  • delusions of persecution

Catatonic Sz:

= physical/psychomotor disturbances

= refers to movements, posture + responsiveness

  • catatonic stupor ---> eg. hold posture for long periods eg. stand
  • catatonic aggitation ---> hyperactivity eg. constantly moving
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Functions of classification systems

The DSM-5 and ICD are classification systems and they serve 3 main functions:

1) provide an agreed set of criteria to be used by medical practioners to diagnose disorders in standardised, uniform way

2) to enable an understanding of the causes + development of different disorders

3) to provide a guide to ensure patients recieve most appropriate + effective treatment for a specific disorder

Issues with diagnosis:

  • reliability
  • validity
  • gender bias
  • cultural bias
  • co-morbility
  • symptom overlap
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Reliability in diagnosis of Sz


= reliability refers to consistency of a measurement

= reliability issue focuses on whether psychiatrists can agree on whether someone has Sz or not

= reliable disgnosis means that patients displaying the clinical characteristice that mee the disgnostic criteria for Sz should all recieve the same disgnosis

Inter-rater reliability ---> the extent/correlation to which assessors agree, involves 2 or more                                             ---> psychiatrists on the same case (same patient)

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Research evidence of inter-rater reliability

Researcher = Beck et al. (1962)

  • looked at inter-reliability of 2 psychiatrists
  • sample of 154 patients
  • only 54% agreement on diagnoses ----> not reliable

Researcher = Spitzer + Fleiss (1924)

  • meta-analysis of 6 studies
  • examined 18 disorders using DSM criteria
  • only 52% agreement on diagnoses ----> not reliable

= indicate lack of diagnostic reliability of Sz, however DSM + ICD changed so findings of that time may be different ---> time validity

- patient clinically interviewed for a diagnosis to me made = rely on retrospective verbal data --->  patient may exaggerate truth or not report all symptoms ---> subjective = not reliable

- neither DSM/ICD mention which degree of severity symptoms much reach to diagnosis

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Research evidence of inter-rater reliability2

However, diagnostic procedures developed greater rigour after thi sand subsequent studies found higher levels of diagnostic reliability

Eg. Soderberg (2005) reported a CR of 81% using the DSM

= suggests that classification systems have become more reliable over time

Eg. Jakobsen (2005) found CR of 98% in a study where 100 danish patients were assessed using ICD disagnostic criteria

= shows high reliability of clinical diagnosis

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Co-morbidity and Reliability


= describes people who suffer from 2 or more mental disorders ---> eg. Sz and depression are often found together ---> makes it more difficult to confidently diagnose Sz

Co-morbidity occurs because symptoms of different disoders overlap, eg. major depression and Sz involve very low levels of motivation (avolition)

= issue around the reliability of Sz diagnosis because does this avolition reflect depression or schizophrenia

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Issues with reliability + full evaluation

Lack of reliability is problematic because:

- patients may go for years without illness being correctly diagnosed ---> leads to patients not recieving most appropriate and effective treatments

- though classification systems have become more similar over time, still have different ideas about diagnostic criteria of Sz ---> diagnosed with Sz if subject to ICD but not DSM

- diff classifications made for diff cultures/countries ---> diagnosed with Sz but not in europe

+ one valuable contribution of such evidence is that in later versions, DSM-3 improved the criteria so become less vague by adding standardised clinical interview scchedules eg. SAD ('78)

+ research evidence suggests that reliability of Sz diagnoses have significantly improved with revisions of diagnostic criteria + proceudres eg. SCID-5 (2016)

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Validity in diagnosis of Sz


  • validity refers to accuracy of a measurement

Depression + Bi-polar support alliance (2002) found 70% of bipolars reported that their illness had been misdiagnosed at least once, usually with Sz or depression

= suggests the diagnosis of disorders like Sz is not consistent + reliable ---> therefore not accurate

Issue of validity is whether Sz can be accurately diagnosed as a seperate disorder, with specific set of symptoms ---> because there is substantial heterogeneity (variation) in symptoms across patients diagnosed with Sz

= eg. approx. 70% patients have halluc + delusions but 30% don't

- Sz does not have any pathognomic symptoms eg. characteristics unique to Sz ---> ao cannot diagnose Sz on the basis of these symptoms only

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Sane in insane places

Researcher = Rosenhan (1973)

  • aimed to test validity of Sz diagnosis
  • placed 8 pseudo (sane) people in 12 diff hospitals across 5 states in USA
  • 3 women + 5 men
  • all pps told their psychiatrists that they heard voices ---> auditory hallucinations (only 1 symptom)
  • this was chosen due to no mention of existential psychosis in the DSM at the time
  • once inside pps were instructed to stop simulating any symptoms of abnormality
  • pps could only get out by convincing staff that they were now sane
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Rosenhan conclusion + evaluation

= took up to 52 days for all pps to be released, despite no real evidence they were schizophrenic

= pps diary writing was seen as an aspect of pathological behaviour ---> normal behaviour viewed as abnormal ---> even mood swings

= pps deprived of many human rights such as privacy --->  eg. toilets with no doors, all staff could access any medical records

= staff were credible witnesses but patients were not ---> dehumanisation

= actual medical staff only came into ward for 7 minutes or less per day

= in a follow up study thy rejected genuine patients whom they assumed were part of the deception

- patients were not actually schizophrenic ---> lacks validity as the symptoms were simulated

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Explanations of Schizophrenia

Biological explanations:

  • genetics
  • dopamine hypothesis
  • neural correlates ---> structural + functional abnormalities in specific beain regions
  • neurodevelopment

Psychological explanations:

  • family dysfunction
  • cognitive explanations
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Bio explana of Sz - Genetics


  • it is a well-documented fact that Sz runs in families
  • this explanation views Sz as hereditary
  • research has involved investigations to assess the extent to which Sz may be genetically influenced
  • fortunately, all genetic researchers aggree that a number of genes must be involved, rather than one single gene (POLYGENIC)
  • research evidence comes from: family studies + twin studies + adoption studies
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Genetics - Family studies

Family studies: - compared rates of Sz in relatives of diagnosed ppl, and made comparison with rates of diagnosis in control family relatives

Gottesman (1991) - large-scale family study, found % risk for diff relatives of diagnosed Szc

  • MZ twins = 48%
  • DZ twins = 17%

= suggests that more genetically related 2 ppl are higher CR for Sz

= However, MZ CR was significantly lower than 100%, means that, despite shared genotype, MZ twins do not always share schizophrenic symptoms ---> suggests that genetics is not the only cause of schizophrenia.

= genes may predispose a person towards Sz, but needs to be environmental trigger, this is called diathesis stress model and considers nature/nurture debate

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Genetics - twin + adoption studies

Twin studies:

  • research has compared CR for Sz between MZ and DZ twins
  • the evidence demonstrates that the CR for MZ twins is significantly higher

Researcher = Gottesman + Shields (1976) - meta-analysis of 5 twinstudies, found                  CR for MZ Sz varied around 75%-91%

= evidence suggests that genetics play a significant role in such serious cases

Researcher = Janicak (2004) found MZ ---> 48%, found DZ ---> 17%

Adoption studies:

Researcher = Kety + Ingraham (1992) - found prevalence rates of Sz

  • 10x higher among genetic relatives compared to adopted relatives of schizophrenics
  • means that environmental factors must be less significant than genes in Sz development
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Genetics - candidate genes

Candidate genes:

  • likely that Sz is polygenic ---> inheritance of traits that are determined by more tha one gene
  • but these genetic factors can be influenced by environmental factors

Researcher = Ripke et al (2014) ---> large-scale study that combined all data from genome-wide reserarch of Sz

  • genetic make-up of 37,000 Sz patients was compared to 113,000 controls
  • 108 seperate genetic variations found to be associated with increased risk for Sz
  • some of genes identified coded for the functioning of several neurotransmitters (eg. dopamine)
  • suggests there are a number of genes that are responsible for onset of Sz
  • findings are supported by Gurling (2006) - where gene-mapping was used that found PCM1 gene was implicated in vulnerability to Sz
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Neural correlates

Neural correlates:

  • NC argues abnormalities in certain brain structures and functions may contribute to onset of Sz and may explain +/- symptoms experienced

Brain areas associated with + symptoms:

  • superior temporal gyrus (STG)
  • anterior cingulate gyrus (ACG)

Brain areas associated with - symptoms:

  • enlarged ventricles (EVs)
  • vental striatum (VS)
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Neural correlates of + symptoms

Superior temporal gyrus (STG):

  • contains primary auditary cortex, used for processing of sounds + verbal communication

Anterior cingulate gyrus (ACG)

  • area is implicated in broad range of behaviours and cognitive processes
  • sub-region plays crucial in processing social info

Research evidence:

  • Researcher = Allen et al. (2007)
  • examined brains of Sz patients experiencing auditory halluc and controls using scans
  • pps asked to identify whether pre-recorded voice was own or not

= reduced neural activity in both areas of Sz patients

= Sz patients made more voice identification errors

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Neural correlates of - symptoms

Enlarged ventricles:

  • ventricles = internal brain cavities that contain + produce CSF
  • cerebro-spinal fluid = provides cushioning to revent brain
  • MRI scans have shown differences in ventricular size of Sz and non Sz

Research support:

  • Researcher = Ho et al (2004)
  • investigated relationship between size of Vs and developing Sz
  • larger Vs and brains made more CSF in Sz

= bigger Vs ---> worse symptoms

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Evaluation of Neural correlates

+ research into enlarged Vs + brain structures has high reliability as reearch was carried out in highly controlled environments with specialist and scientific equipment such as MRI scans, which are widely used because of their accuracy

- enlarged Vs are not found in all Sz ---> challenges claims made

- correlational results so hard to identify whether enlarged Vs are result or cause of Sz

- no set criteria to preciseely define "enlargement" ---> lack of consistency means we cannot develop fim conclusions about ventricle size and Sz

- biologically deterministic as abnormalities in brain structures and their functions doesn't always lead to Sz 

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Dopamine hypothesis

Dopamine hypothesis:

  • argues that a dopamine imbalance/dysfunction in certain areas of the brain may be involved in the onset of Sz

Snyder (1976)

  • created original theory that says excessive amount of dopamine (DA) at synapses in the subcortex can lead to the of Sz ---> aka hyperdopaminergia
  • eg, excess of DA receptors in Broca's area known to contribute to alogia + hallucinations

Davis (1991)

  • updated theory and suggested that DA levels in mesolimbic DA pathway causes neural hyperactivity and is associated with pos symptoms ---> hyperdopaminergia
  • in contrast, high DA levels in the mesocortical DA pathway can cause neural hyperactivity and  associated with neg symptoms ----> aka hypodopaminergia
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Dopamine hypothesis2 and conclusion

Goldman-Rakic (2004)

  • supporst hypodopaminergic explanation
  • found reduced DA levels in the PFC (used in thinking/decision making)
  • therefore, could explain neg symptoms such as avolition

Overall conclusion:

  • it is probable that both hyper + hypo dopaminergia are both correct explanations for Sz ie. both high and low levels
  • however, other research suggests that it may be the hypersensivity of dopamine receptors that contributes to Sz rather than abnormal levels of dopamine
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Evaluation of Dopamine hypothesis

+ evidence supporting hyperdopaminergic explanation comes from substantial research confriming the effectiveness of anti-psychotic medication

+  theory supports Ripke's view that dopamine dysfunction might be affected by gene variants that code for production of DA

- fails to offer a complete explanation for Sz as it fails to consider psychological factors

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Psycho explanations for Sz

= arise from major psychological persepectives, or thought socio -cultural factors, in that they stress the rols of social and family relatioships in development of Sz

Consists of:

  • family dysfunction
  • cognitive explanations - eg. dysfunctional thought processing
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Family dysfunction - schizo mother

Family dysfunction:

  • idea suggests that maladaptive relationships + disturbed patterns of communication within families are viewed as acting as environmental stressors that contribute to onset of Sz

Schizophragenic mother:

= introduced by Fromm-Reichman (1948) ---> describes a type of parenting that appears to cause a child to develop Sz

  • Sz mother is cold, rejecting, controlling
  • tends to be dominant power, ruling family in an atmosphere of secrecy, collusions, and tension
  • family climate creates distrust and can result in paranoid delusions such as persecution which may develop into Sz

- she was only researcher ---> results were subject to her own view (researcher bias)

- retrospective accounts were taken from patients, verbal reports may not be accurate

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Family dysfunction - double bind

Double bind:

  • Researcher = Bateson (1956)
  • emphasised role of communication patterns within families as a risk factor for Sz
  • younch child experiences contradictory messages which leaves them in a "no win" situation       aka double bind

1) primary communication eg. "we never cuddle"

2) meta communication eg. refucing cuddles when given

  • when child "gets it wrong" they are punished with withdrawal of love
  • child is left confused, anxious, believing their actions are wrong, not knowing how to respond     ---> may lead to withdrawal + disorganised/delusional thinking
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Family dysfunction - expressed emotion (EE)

Expressed emotion:

  • refers to level of emotion, usually negative/hostile, thats directed towards patient from family 
  • serious source of stress that acts as a trigger for onset in vulnerable individuals

EE characterised by:

  • verbal critisism
  • hostility eg. anger/rejection
  • emotional over-involvement in patient's life eg. self sacrifice

Kavanagh (1992)

  • reviewed 26 studies of EE and examined relapse rates
  • High EE families = 48% RR
  • Low EE families = 21% RR

= supports idea that EE increases relapse risk for recovering Sz

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Family dysfunction - evaluation

+ evidence shows that therapies that reduce family levels of EE, also reduce RR

+ family dysfunction and EE are now established maintenance model of Sz

- EE may be a result of Sz, rather than a cause --> issue of cauality

- majority of research blames the onset of Sz on parents, particularly the mother (unethical + gender bias)

- env reductionist as it doesn't consider other factors such as biology that may also have an influence on the development of Sz

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Cognitive explan of Sz

Cog explanation:

  • believes Sz is characterised by disruptions to normal though processing
  • eg. reduced activity in ventral stiatum is associated with neg symptoms
  • eg. reduced activity in temporal and cingulate gyri are associated with pos symptoms
  • cog model proposes that such cognitive dysfunctions are a cause of Sz rather than a consequence

Frith (1992)

= identified 2 types of dysfunctional thought processes that could be related to Sz

  • metarepresentation
  • central control
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Cog explan for Sz - metarepresentation


= the cog ability to reflect on our own throughts and behaviours

  • also enables us to interpret the actions of others + to distinguish between real and imagines
  • disruption of metarepresentation disrups our ability to recognise which thoughts/behaviours are performed by ourself and others

Bentall (1991)

  • found Sz patients struggled to distinguish between words that previously read or generated themselves
  • this supports Frith's model becauseit shows that brain cannot distinguish who's voice it is
  • dysfunction would explain pos symptoms of Sz such s hallucinations (auditory)
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Cog explan for Sz - central control

Central control:

= cog ability to suppress automatic responses and perform more deliberate, intentional actions instead

= eg. derailment where any word just spoken might trigger tanfentiality ---> speech poverty

  • cog process of selective attention filters out irrelevant info and enables us to focus our attention on relevant information
  • Hemsley suggests that main cog dysfunction is a breakdown of selective attention mechanism
  • this means there is a breakdown between information already stored as schemas, and new, incoming info so that schemas are not activated ---> results in sensory overload
  • therefore, trivial events in the background are interpreted as being highly significant
  • this coud explain symptoms of Sz such as delusions
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Research evidence for central control

Stirling (2005):

  • compared 30 patients with diagnosis of Sz with 18 controls on a cog task requirin the suppression of an automatic response
  • Sz took 2x as long as controls to complete task

= indicates that cog processes work differently in brains of Sz and supports Frith's concept of central control dysfunction

Takahaski (2013)

  • found that ability to identify changes in auditory tones was severely limited in schizophrenics
  • Sz = 410, compared to controls = 247

= supports idea of dysfunctional thought processing in Sz as it shows that Sz experience cog deficits such as inability to rapidly encode new info to understand it

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Evaluation of Cognitive explanations

+ cog explanation can offer a comprehensive explanation for Sz because it explains both pos and neg symptoms

+ bridges a gap between biological and psychological explanations, so is less reductionist than better theories

- cog theories are challenged for being descriptive, rather than explanatory ie. describes links between symptoms and syfunctional thoughts but does not fully explain the origins ---> explains proximal causes of Sz rather than ultimate ones

- cog processes are difficult to test experimentally, therefore, difficult to verify its validity

- some brain traumas can result in cog dysfunction, but rarely leads to Sz

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Biological treatments of Sz - drug therapy

Typical antipsychotic drugs:

  • Neuroleptics introduced in early 1950s
  • Phenothiazines most commonly prescribed neuroleptic
  • Chlorpromazine ---> a phenothiazine first used for Sz in 1954 in USA

= can be taken as tablets/syrup (orally) or injected (intravenous)

= was found to have a calming effect in patients and became preferred treatment

Chlorpormazine - mechanism of action:

  • act as D2 antagonists ---> work by blocking D2 dopamine receptors in synapse therefore, dopamine is released by pre SN at the synapse then prevented from binding to the D2 receptors on the post SN
  • reduces neural hyperactivity along dopaminergic pathways
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Evaluation of typical antipsychotic drugs

- wide range of individual differences in response to the drugs, eg. approximately 40% of patients do not respond to the drugs ---> often have to be used in conjunction with psychological treatments

- does not address the root cause of Sz and so we cannot say it is curative

- patients may be able to live in community but they may not be able to maintain a job, relationships etc

- high relapse rates: typically 40% in first year of treatment but 15% after that

- severe side effects with 50% of patients stop taking medication after 1 year

+ drug therapy has reduces the economic burden of patients being hospitalised ---> eliminated patient warehousing

+ drug therapy has revolutionised patient care and management

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Bio treatments of Sz - drug therapy2

Atypical antipsychotic drugs:

  • introduced in 1990s ---> eg. clozapine
  • produce therapeutic benefits for Sz patients who don't respond favourable to traditional neuroleptics

Clozapine - mechanism of action:

  • have similar, though weaker, D2 blocking effects
  • also act on serotonin and glutamate receptors with antagonistic effects
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Evaluation of atypical antipsycho drugs

+ more effctive in reducing po symptoms than traditional drugs

+ may improve impaired cog function ---> higher rates of participation in social skills training programmes

+ Kane (2001) reported that patients were less likely to drop out of treatment due to fewer side effects

+ discharged patients maintain medication and so, RR reduced

- 1-2% are affected by agranulocytosis ---> immune system impairment/lowered white blood cell count

- precise biochemical mechanisms of clozapine's therapeutic effects are not fully understood and therefore there are ethical issues about its use

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Psycho treatments of Sz - Token economy

Token economy systems:

  • based on behavioural approach, so assumes abnormality is due to maladaptive learning
  • so treatment focuses on helping patient to unlearn maladaptive responses
  • they can then learn new, more desireable adaptive behaviour using selective positive reinforcement or reward

= basic principle is that a person earns a certain number of token by engaging in desired behaviours (target behaviours eg. getting out of bed to shower)

  • tokens have no intrinsic value, and act as secondary reinforcers
  • but instead, tokens acn be exchanged for various goods or priviledges - primary reinforcers
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Research evidence for Token economy

Allyon + Azrin (1975):

  • studied sample of female Sz patients who'd been hospitalised for avg. 16 years
  • patients were rewarded with plastic tokens for actions such as self-care behaviours eg. making their beds, showering, combing hair etc
  • tokens were then exchanged for activities that the patients desired

= number of self-care activities performed increased from 5 to 42

= tokens are successful in socialisng patients into taking more responsibility for themselves and their care ---> can be viewed as an effective behavioural management programme

- many studies of effectiveness of TES lack randomly allocated matched treatment and control groups eg. study above only used females

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Research evidence for Token economy2

Silverstein et al. (2009):

  • found that people with Sz in community would really participate in activities where they were rewarded frequently
  • but same patients struggled performing activities where they were rewarded on a more long term basis eg. monthly ---> "delay discounting" stopped the effect of the reward

= evidence suggests that token economy methods are only effective when the target behaviours are rewarded immidiately

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Evaluation of token economy

+ system helps patients modify their behaviour to make it more socially acceptable ---> supports the patient in becoming more independant and have more successful intergration to society

- this can also be viewed as an issue because it means that behaviour can be managed but the root cause of the disorder is not addressed ---> not curative

- some patients seem to experience discrimination in the way tokens are awarded eg. patients with milder symptoms of Sz may be able to perform self-care activities better than petients with more severe symptoms

- in addiction, such treatments are critisized for being demeaning and dehumanising because they treat vulnerable people as little more than circus animals performing for treats

- desireable behaviour can become dependant on the provision of rewards and so patients may struggle to replicate the same behaviour in the real world ---> may lead to high RR

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Psychological treatments of Sz - CBT

Cognitive behavioural therapy:

  • assumes cognitions affect behaviour
  • primary aim is to modify effects of dysfunctional thought processing
  • usually takes place every 10 days, for about 8-20 sessions (time bound therapy)

Typical CBT stages:

  • antipsychotic medication given prior to CBT to reduce psychotic thought processing
  • therapist uses normalising strategies to help client understand nature of illness so they know their symptoms are "normal"
  • client to identifies delusions/hallucinations/neg thoughts so client can recognise when they occur ---> client becomes aware of how beliefs contribute to dysfunctional behaviour and anxiety
  • therapist uses reality testing to challenge irrational thoughts/delusions with direct questionning
  • coping strategies examined to help client develop alternative explan of unhelpful thinking
  • role-play + homework set to improve general levels of fucntioning (behav assignments)
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Research evidence for CBT

Tarrier et al. (2000) - 3 groups of Sz patients

  • A) - personal therapy of 20 sessions over 10 weeks, coupled with drug therapy
  • B) - drug therapy alone
  • C) - supportive counselling

group A = 50% reduction + 15% free of all positive symptoms

group B = no patient was symptom-free

group C = 15% reduction

= suggests that CBT is a more useful in reducing positive symptoms and a more appropriate treatment overall however, a combination of drug therapy and CBT together is the most effective method of treating Sz

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Research evidence for CBT2

Jauhar et al. (2014) - conducted meta-analysis of 34 studies of CBT for Sz

  • found that CBT has a high significant, but small, therapeutic effect on + and - symptoms
  • however, the effect was not found when only "blind testing" studies were analysed

= this means that the use of CBT as a treatment for Sz is still debateable

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CBT for Sz evaluation

+ evidence suggests CBT + drug therapy is effective in treating Sz as either method alone has shown to be ineffective ---> supports case for combined treatments

+ effective at reducing positive symptoms, RR, and for enhancing recovery when Sz is diagnosed early

+ empowers client to take control of their symptoms through development of coping strategies, this enables individual to acquire life-long skills in dealing with disturbances eg. thoughts/feelings

+ it is evidence-based, making it recommended therapeutic treatment by NICE guidelines

+ CBT presumes that ppl have free will and can change their behaviour, this is humane and optimistic view of the disorder

- however, means that ppl can be blamed for not changing, they are held responsible for their symptoms

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CBT for Sz evaluation2

- CBT only treats the symptoms; isn't a cure as it doesn't address the root cause of the disorder

- difficult to assess effectiveness of CBT because it relies on patient self-report and therapist assessments, this doesn't follow the scientific method and is open to subjective interpretation rather than objective measurement

- patients may become over-dependent on the therapist

- not suitable for all patients eg. disoriented, agitated, paranoid

- has fewer side effects  than medication but is more expensive in terms of clinical time: consider in relation reduced healthcare budgets and reuced avilibility of CBT

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Psycho treatments of Sz - Family therapy

Family therapy:

  • based on family dysfunction model
  • assumes that disturbed relationships and patterns of communication play a role in the onset + maintenance of Sz
  • and so approach focuses on "treating" or working with whole family as opposed to one family member to help and support the patient
  • this reduces potential environmental stressors that could increase a patient's risk of relapse eg. high levels of EE
  • therapist+family meet regularly and everyone is given opportunity to discuss how the illness affects them such as the patient's symptoms,behaviour or progress
  • family members are also encouraged to find strategies to support each other by increasing tolerance levels and decreasing criticism/neg communications
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Research evidence for family therapy

Pharoah (2010) - conducted research review

  • concluded that there is moderate evidence to show that family therapy does improve quality of life for patients and their famillies, as well as significantly reducing relapse and hospital admissions

- however, they did note that findings from different studies showed inconsistencies due to poor methodologies ---> therefore, evidence base for this treatment is reatively weak

Falloon et al. (1985):

  • devised a form of family management that teaches family members to be constructive, undemanding and empathic in their dealings with each other + sz relative for 9-12 months
  • found that RR was markedly lower amongst patients recieving family therapy (11%) than those recieving individual therapy (50%)
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Evaluation of Family therapy

+ patients more likely to be cared for at home ---> reduces long term patient warehousing in hospitalised which often expensive

+ large amount of evidence for EE and reduced RR suggesting that the therapy is useful to the majority of Sz patients

+ patients tend to lack social skills eg. symptoms such as alogia have a tendency to isolate Sz patients socially so therapy may aid in social functioning which is a highly important life skill

- effectiveness is limited as the therapy is not curative; it improves social functioning however, it does not provide a cure for Sz and even so, the social functioning of schizophrenics is unlikely to reach the level of healthy controls

- unikely to work on its own, FT is more useful when used in conjunction with drug therapy (supports interactionist approach)

- every member has to engage and be fully active therefore a lack of motivation and effort will reduce the overall effectiveness of FT

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Interactionist approach

Interactionist approach:

  • recognises that there are multiple factors that play a role in the development of Sz
  • accepts that there is an underlying vulnerability eg. genetic predisposition
  • but also negative psychological experiences that act as a trigger such as high EE

Meehl (1962):

  • developed original model
  • thought that Sz was entirely genetic, the result of a single "schizogene"
  • according to Meehl, if person does not have schizogene, then no amount of stress would lead to Sz, however, in carriers of the gene, chronic stress through childhood and solescence in particular the Sz mother could result in the development of the condition

over time, many genes have appeared to increase genetic vulnerability to Sz (Ripke et al 2014) and so may psychologists believe the disorder is beyond simply genetic factors but also a range of factors, including psycho trauma - so trauma becomes the diasthesis rather than the stressor

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Research evidence for Interactionist approach

There's evidence to support the dual role of vulnerability and stress in the development of Sz

Pekka Tienari et al (2004) - investigated combo of gen vulnerability + parenting style (trigger)

  • 19,000 children adopted from Finnish mothers with Sz between 1960-79
  • adoptive parents were assessed for their child-rearing style and rates of Sz were compared to those in a control group of adoptees withoth any genetic vulnerabiity
  • high levels of critisicm + conflict + low empathy was implicated in development of Sz but only for children wih genetic risk not control group

= suggests that both gen vulnerability and family related stress are important in onset of Sz

+ very strong direct support for importance of adopting interactionist approach to Sz

+ identifies poor parenting as a possible stress therefore, may help parents to assess their own child-reearing style

+ large sample size and so the results are more representative of the entire population (validity)

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Evaluation of interactionist approach

+ studies show advantage of using combinations of treatments for Sz eg. Nicholas Tarrier et al (2004) - 315 patients RA to a medication and CBT group, medication and supportive counselling or medication only (control group)

= patients in the 2 combat groups showed lower symptom levels than those in the control group, although no diff in rates of hospital readmission

= show there is a clear practical advantage to adopting interactionist approach in the form of superior treatment outcomes, and therefore, highlight the importance of taking this approach

- OG model of single schizogene known to be very over-simple instead, multiple genes increase vulnerability, each having small effect on its own, there is no single schizogene

- and schizophragenic parenting style as the single stressor has been critisized as stress can come in many forms and is not limited to dysfnctional parenting

- Douglas Turkington et al (2006) believes its perfectyly possible to believe that Sz has a bio cause and still practice CBT to relieve patient of psycho symptoms (contrasting views)

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