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Schizophrenia:, Issues with reliability and validity:, Biological…
Schizophrenia:
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Symptoms:
Lifetime prevalence = 1% chance of developing
Approx 4 mil worldwide, men are more likely to suffer than women, onset = typically late adolescence and early adulthood
Prognosis:
- Approx rule of thirds, 1/3 recover, 1/3 episodic impairment and 1/3 chronic decline
- W/ treatment about 60% of patients manage a relatively normal life
:one:Type one: Onset can be sudden (acute) often precipitated by stress
:two:Type two: Sometimes more slowly (chronic)
- SZ often occurs with other conditions e.g. depression, co-morbidity, one individual diagnosed with 2 or more conditions.
Criterion validity: When 2 diagnostic systems (e.g. ICD and DSMV) come to the same conclusion in terms of diagnosis
Positive Symptoms: Those that appear to reflect an excess or distortion of normal functions - added to normal functions HDED
Negative Symptoms: Those that appear to reflect a reduction or loss of normal functions - taking away from normal functioning ADAP
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Treatments:
Biological:
Antipsychotics:
- Drugs which markedly reduced the symptoms in ppl who were severely ill
- Given to treat the most disturbing forms of psychotic illness e.g. Sz and bipolar disorder
- Two types:
-Typical: Combat positive symptoms, reduced amount dopamine
-Atypical: Combat positive and negative symptoms
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Appropriateness of drug therapy:
- Drugs treat the symptoms of the disorder, but not the cause
- An antipsychotic drug cannot seek out and kill/ change the cause of Sz
- We don't know what the cause of Sz is - so all drugs do is help reduce the effect of the illness
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- Diff to interpret the brain abnormalities associated w/ Sz, therefore researchers have suggested that the 2 types may reflect differences in aetiology
- Crow (1985) Sees the two types of Sz developing from diff underlying pathologies
Type Two:
- A neurodevelopmental disorder arising from prenatal or perinatal damage
- Characterised by negative symptoms
- Chronic in nature w/ poor pre-morbid functioning
- Marked by neurological deficits and doesn't respond to antipsychotic drugs well
Type One:
- A genetically inherited disorder associated w/ dopamine dysfunction
- Characterised by positive symptoms
- Acute in onset, it responds relatively well to antipsychotic medications
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SZ is characterised by a profound disruption of cognition and emotion, which affects lang, thought, perception and sense of self - distorted reality (DSMV sees as mental disorder, ICD as physical disorder
- Hallucinations: Can be visual, auditory or tactile (feeling something that is not there)
- Delusions:to do with belief system, believing despite their being evidence contrasting/against in e.g.
-Delusions of grandeur Believing they're someone significant
-Delusions of persecution Individual is on high alert as believe e.g. FBI is after them
- Experiences of control: Not in control of speech, actions and feelings, believe someone else is
- Disordered thinking:
-Insertion Believe someone is inserting thoughts into their head
-Withdrawal Believe someone is removing thoughts from their head
-Broadcasting Believe thoughts are being heard and read by others
- Avolition: Lack of goal oriented behaviour
- Disturbances of effect/affective flattening: Displaying inappropriate emotion to a situation =EF/showing no emotion to a situation = AF
- Alogia (speech poverty): Individual lacks fluency and coherency w/ speech
- Psychomotor disturbance: Actions repeated, ticks = not in control and exhibit repetitive uncontrolled behaviour
- Wing (1992) primary impariments are intrinsic to the disorder, whereas secondary result from the primary impairments
- Pre-frontal cortex and hippocampus correlated w/ symptoms of SZ
- Primary = hallucinations, delusions, disordered thoughts, apathy, emotional blunting
- Secondary
- Social: Unemployment, social drift, institutionalisation, rejection and prejudice
- Psychological: Low confidence, dependent, poor coping, no motivation
- Diagnostics must be repeatable (test-retest) the same conclusion must be possible even at 2 diff points in time
- Diagnostics must be agreed upon (Inter-rater reliability) 2 clinicians must reach the same concl. kappa score e.g. 1=perfect, 0.7 = good
- Regier et al (2013) showed DSM-V can only gain a 0.46 kappa score, however, Beck et al (1962) 54% concordance rate
- Soderberg et al (2005) 81% concordance rate
- Research has found the DSM to have a consistently higher concordance rates than the ICD
4 ways this can be assessed:
1) Through reliability (first step to establishing validity)
2) Predictive validity (successful treatment)
3) Descriptive validity (symptoms differ to other disorders)
4) Aetiological validity (same causes)
- Wanted to see if 'normal' ppl attempt admission, will they be detected. 8 sane ppl admitted
- 7-52 days for them to be released, all telephoned and reported same symptoms, a voice saying 'thud'
- None detected, 7/8 diagnosed, 35/118 patients were suspicious of PP
- All discharged with 'SZ in remission'
- Normal bhvr misinterpreted e.g. note taking recorded as pathological in 3 medical records + early queuing for lunch = oral acquisitive syndrome
- PP given 2,100 tablets, when some were flushed, PP spotted other real patients medications
- PPs approached staff w/ polite requests (also depersonalization)
-71% psychiatrists + 88% nurses ignored qs
- Rosenham claimed... "It is clear we cannot distinguish the sane from the insane in psychiatric hospitals
- Hospitals requested more patients to be sent, Rosenham agreed but didn't actually send any and hospitals were proved wrong
Ethical issues = no right to withdraw, not prevented from psychological/physical harm, tech no informed consent, deception of hospitals!!
Copeland (1971)
- Gave 134 US + 194 british psychiatrists a description of a patient
- 69% of US diagnosed Sz but only 2% of british
- One of the main characteristics of Sz "hearing voices" seems to be influenced by cultural environment
Luhrman et al (2015)
- Interviewed 60 adults diagnosed, 20 each in Ghana, India and US
- Each asked bout the voices they heard. Many African and Indian subjects reported positive experiences w/ their voices, describing them as playful whilst not one American did
- US subject more likey to report violent and hateful
- Suggests that violent voices in the west may not be an inveitable feature of Sz = Sz has a lack of consistent characteristics
Davison and Neale (1994)
- Explained in Asian cultures a person experiencing emotional turmail = praised and rewarded if no emotion displayed
- But in Arabic cultures outpouring of public emotion is encouraged
Braverman et al (1970)
- Gave a sex-role stereotype questionnaire consisting of 122 bipolar items + 79 actively functioning clinicians w/ 1/3 sets of instructions to describe a healthy, mature, socially competent...
a) adult, sex unspecified
b) men
c) a women
- Judgements differed according to sex
- Behaviours and characteristics of healthy judged for a), all behaviours judged healthy for men but not for women
- Result = women perceived as less mentally healthy
Schneider (1974)
- Proposed hallucinations, hearing voices and a feeling of being controlled = "First Rank Symptoms" (FRS)
- Being able to identify FRS means a valid diagnosis is possible and a dual-diagnosis
Nordgaard et al (2008)
- Concluded definitions of FRS were unclear and not operationalised = difficult for definitive diagnosis
- Therefore, validity and reliability of using FRS is questioned
Buckley et al (2009)
- Argue co-morbidity in Sz is poorly understood so making a dual diagnosis = difficult
- Prescribed treatment is not always appropriate
Konstantares and Hewitt (2001)
- Compared 14 autistic patients w/ 14 sufferes of Sz to find none of them had symptoms of autism, but 7 of the autistics had symptoms of Sz
Ellason and Ross (1995)
- Point out that ppl w/ dissociative identity disorder (DID) had more Sz symptoms than ppl diagnosed as being Sz = this affects the validity of the diagnosis
- Prevalence of Sz is the same all over the world (about 1%)
- Supports biological view as prevalence does not vary w/ environment
- However, there are variations w/in the broad geographical areas (e.g. southern ireland has 1 of the highest incidence of Sz - 4% followed by croatia
- Evidence Sz runs in families
- In the general pop. the risk is 1%, however, research has shown that the risk is proportional to the amount of genes people share
= the more closely related the more likely you are to have it
- Concordance refers to the fact that within families there is a greater prob. of developing if another mem of the fam has it
= 1st degree relatives share 50% of genes
= 2nd degree relatives share 25% of genes
- Spouse = 1%, child = 13, DZ twins = 17, MZ twins = 48
- Although there is strong evidence that SZ runs in fams. The problem w/ drawing conclusions about a genetic basis lies in the fact that people in fams don't share genes, they also share environment and experiences
= nature and nurture
- Adoption studies address the problem of twins sharing both their genes and their environment
- They can look at individuals who share their genes w/ one fam while sharing an environment with another
- Kety (1994) found that there was a higher concordance of SZ among biological relatives than adoptive relatives
- Tienari (1991) Studied 155 adopted children whose biological mothers had SZ and compared them w/ a control group of adopted children w/ no fam history of SZ
Findings: 10% of children of SZ mothers had the condition whereas 1% of the control group had the condition
- Has proven useful to study twins as they provide info relating to the number of shared genes
- Gottesman (1982) in a meta analysis found that there was a higher concordance rate for Sz w/in MZ's (46%) than DZ's (14%)
Genetics:
- :check: Substantial evidence for a genetic contribution
- :red_cross: Methodological problems: Fam, twin and adoption studies must be considered cautiously as they are retrospective and diagnosis may be biased by knowledge that other fam members may have been diagnosed = suggests a problem with demand characteristics
- :red_cross: Nature v nurture: Difficult to separate out influence of nature v nurture. Concordance rates = not 100% = Sz cannot be explained wholly by genes and the individual may be predisposed to Sz and simply makes the individual more at risk of developing the disorder
- :red_cross: Biologically reductionist: The Genome project increases the understanding of the complexity of the gene. Given that, a much lower no of genes exist than anticipated. It's now recognised that genes have multiple functions. Sz is a multifactorial trait as it is the result of multiple genes and environmental factors
= suggests research into gene mapping is over simplistic as Sz is not due to a single gene, all evidence suggests environmental triggers
Twin Studies:
- :red_cross: MZs relatively rare in pop. and MZ's where one twin has SZ = even more rare therefore problems of sample size and twins share genes and environment
- :red_cross: Don't use all the same diagnostic criteria
- :red_cross: Hasn't always been easy to identify MZs and DZs = modern tech is better
- :red_cross: Concordance rate is not always calculated in a standardised way
- :red_cross: Concordance rates not always studied w/ scientific precision. Marshall (1990) suggests studies have become more rigorous, concordance rates have fallen
- :check: Studies have provided a great deal of evidence for a genetic component in the development of Sz
- :red_cross: However, ppl tend to share both genes and environment
- :check: Adoption studies provide strong evidence cos they look at patients who share genes w/ one fam whilst sharing environment with another fam
- :red_cross: However, adoption studies suffer from many of the methodological problems of twin studies in terms of the validity of findings
- Genetics are an obvious component but the pattern of inheritance is complex
A significant diff in Sz is hypofrontality in the frontal lobe (under activity) At rest! MRI scans show the cerebral blood flow in the cortex
- Sz is caused by excessive activity at the synapses that use dopamine as their primary NT
- Causes abnormal functioning of dopamine-dependent brain systems, resulting in many of Sz symptoms
- DBH (Dopamine Beta Hydroxylase) in low levels means NT dopamine cannot be broken down and reabsorbed.
Wise and Stein (1973)
- Reports abnormally low levels of DBH in post-mortem studies of Sz patients
- DBH = enzyme, would suggest abnormally high dopamine activity as a result
- Can't rule out cause of death/post-mortem changes as a source of error
Recent modifications:
- Post-mortem: studies have shown there to be many more dopamine D2 receptors in brain of ppl w/ Sz than in non-sufferers
- PET scans: Have showed greater no of D2 receptors in Sz
Agonist: increase amount of NT = speed up reaction
Antagonist: Decrease/inhibit NT = slow down reaction
- Sz symptoms can be treated w/ dopamine antagonists
- Effective in 60% of cases, w/ more improvement seen for positive symptoms
- Phenothiazines act by blocking dopamine at the synapse and are also effective in reducing some of the major symptoms of Sz
= Supports role of dopamine again but what about the other 40%
= Lack of impact on negative symptoms hints there may be 2 separate syndromes that we can treat in two diff ways
- Seeman et al (1993)
- PET scans showed 6x density of D4 receptors (similar to D2) in ppl suffering from Sz
- Iversen (1979)
- Reported that post-mortems on ppl who had Sz found excess dopamine in the limbic system
- Suggesting that the NT is involved in the disorder
- Kessler et al (2003)
- Used PET and MRI scans to compare with ppl w/ Sz and non-sufferers
- Sz's found to have elevated dopamine receptor levels in basal forebrain and substantia nigra/ventral tegmental brain areas
- Diff in cortical dopamine levels were found
- Suggesting dopamine is important in the onset of Sz
- :check: There has been consistent evidence for abnormal brain functioning in Sz patients
- :red_cross: No single factor identified, there could be 2 syndromes, one caused by dopamine activity and associated w/ positive symptoms, another caused by brain degeneration and associated w/ negative symptoms
- :red_cross: It's not clear whether increased dopamine levels cause Sz of if increased dopamine is the result of Sz. Therefore one needs to be careful when establishing cause and effect relationships in Sz patients
- :red_cross: Fard et al (1990) found no diff btwn Sz's level of dopamine compared to non-sufferes and Noll (2009) argues 1/3 patients don't respond to drugs blocking dopamine = other NT's must be involved
- :red_cross: Biologically deterministic if the individual does have excessive amounts of dopamine it doesn't necessarily mean they will develop Sz = DH doesn't account for free will
- Comparing brains of patients of Sz to controls (non-sufferers) = originally only by post-mortems
- New brain scanning techniques allow living brains to be investigated
- Post-mortems cannot tell us whether there is a diff in the brain that is a cause of Sz or a result of Sz
- Ventricles: cavities in the brain containing cerebrospinal fluid that supply nutrients + remove waste
- Larger cavities means a reduction in overall brain volume = less activity in those parts
- Means the brains of Sz are lighter than normal
Flaum et al (1995)
- Found reduction in brain tissue = smaller thalamic, hippocampal and superior temporal vol.
Buchsbaum (1990)
- Abnormalities to frontal and prefrontal cortex
Brown et al (1986)
- Reduced brain weight and enlarged ventricles
- Abnormal early brain developments - research suggests abnormalities occur in the prenatal development of the cerebral cortex
- Asymmetry of the brain is much evident in the brains of Sz patients
Raz and Raz (1990) meta-analysis of studies of ventricular vol. in ppl w/ Sz compared w/ non-sufferer controls, the vol. was significantly large in Sz's
Johnstone et al (1976)
- Found Sz had enlarged ventricles, while non-sufferers did not = suggests Sz is related to a loss of brain tissue
Boos et al (2012)
- Performed MRI scans on 155 Sz, 186 of their non-Sz siblings + 122 non-related Sz, to find Sz participants had decreased grey matter density and cortical thinning compared w/ other participants
- Suggests brain tissue diffs in Sz are an effect of having the disorder rather than being due to genetic factors
- :check: Research has high reliability: Highly controlled environments w/ specialised, high tech equipment e.g. MRI and PET take accurate readings of brain regions such as frontal and prefrontal cortex, basal ganglia, hippocampus and amygdala = suggests that if the research was tested and retested, the same results would be achieved
- :check:Empirical support from Suddath et al (1990): Used MRI to obtain pics of brain structure in MZ twins in which one twin was Sz. The Sz twin generally had more enlarged ventricles and a reduced anterior hypothalamus. Diff so large that Sz twins could be easily identified from brain images in 12/15 pairs = Suggests there wider academic credibility for enlarged ventricles determining the likelihood of Sz developing
- :red_cross: Biologically deterministic: If the individual does have large ventricles then does it really mean they will develop Sz = suggests doesn't account for free will
- A parent verbally gives one message and non-verbally conveys the opposite e.g. a parent might ask for a hug and push the child away, telling them they are too old for cuddles
- This theory suggests that children will become confused and lose their grip on reality
- Negative symptoms of social withdrawal and flat affect may be an appropriate and logical response to double bind situations
- Bateson believed that Sz resulted from double-bind communication (causes stress and Sz develops as a way to deal with the stress)
- Parents who send out contradictory signals put their children in impossible situations where they cannot act w/out going against their parents wishes
= Sz symptoms are the result of an attempt to resolve the impossible situations
Supporting = Tienari (1987)
- Children w/ a biological mother w/ Sz adopted by non Sz fams
- However, the Sz gene only seemed to develop amongst those individuals whose adoptive fams was psychologically disturbed in some way
- Seems to suggest the individual may have a Sz gene but the fam that brings them up have an impact on whether or not that gene is activated
Criticisms = Mischler and Waxler (1968)
- Found significant differences in the way mothers spoke to their Sz daughters compared to their normal daughters
- Suggests that dysfunctional communication may be a result of living with the Sz rather than the cause of the disorders
- Research has found a link between expressed emotion and relapse rates
- Measured by:
- Expression of +ive and -ive emotion
- Hostility
- Critical comments through both tone and content
- Fams who persistently exhibit criticisms and hostility exert a - influence esp. upon recovering Szs who when returning to their fam's react to expressed emotion by relapsing to an active phase of the disorder and experience severe +ive symptoms of hallucinations and delusions of persecution
- Sociocultural explanations look at the person's environment to explain Sz
- Fams can influence both the onset (through socialisation and double binds) and the maintenance (through high EE) of Sz
- Diathesis stress model = may be triggered by fam dysfunction and EE
Schizophrenogenic mother:
- Someone who is cold, dominant and creates conflict
- These mothers are rejecting, overprotective, self-sacrificing, moralistic about sex and fearful of intimacy
- Sz emerges in child as a result
- Many diff cognitive explanations for the development of Sz have been suggested
- They all share same assumption that the various cognitive impairments shown by ppl w/ Sz
-e.g. poor attentional control, lang deficits, disorganised thinking, play an important role in the development and maintenance of the disorder
- It is believed that symptoms such as disorganised speech, delusions and hallucinations may all depend at least in part on the poor ability of a person w/ Sz to concentrate
- Hemsley (1993) suggests there is a substantial breakdown in the relationship btwn memory and perception in ppl w/ Sz
- As a result they are often unable to activate schemas which would allow them to predict what will happen next, their conc is poor they focus on unimportant or irrelevant aspects of the environment
- Their poor integration of mem and perception leads to disorganised thinking and behaviour
- Hemsley believes these deficits can be attributed to abnormalities in the hippocampus
- Frith (1992) suggested that +ive symptoms of Sz can be explained by an ability to filter out irrelevant info from the environment
- Individuals w/ Sz have problems w/ self-monitoring, and so fail to keep track of their own intentions (meta cognitions)
- As a result, they mistakenly regard their own thoughts as having come from someone else
= thus explaining auditory hallucinations
- Similarly, they may attribute some of their thoughts and movements to others
= explaining symptoms such as delusions of control
- He believes this 'faulty filter' is caused by abnormalities in the pathway connecting the hippocampus to the prefrontal cortex
:book: McGuigan (1966)
- Found the larynx of patients w/ Sz was often active during the time they claimed to be experiencing auditory hallucinations
= suggests they mistook their own inner speech for that of someone else
:book: McGuire et al (1966)
- Found patients w/ Sz to have reduced activity on those parts of the brain involved in monitoring inner speech
:book: PET scans
- Show under activity in the frontal lobe of the brain, which is linked to self-monitoring and so provides bio support for this explanation
- :check: Practical applications: Yellowless et al (2002) dvlpd a machine that produces virtual hallucinations intentions were to show Sz that thier hallucinations aren't real
= suggests understanding the effects of cognitive deficits allow psychologists to improve quality of life for Sz's
- :check: Nurture approach: For example, suggests Sz behaviour is the cause of environmental factors e.g. cognitive
- :red_cross: Problems w/ cause and effect: Do not explain causes of cognitive deficits and where they come from e.g. chicken and egg
- :red_cross: Reductionist: Doesn't consider other factors e.g. genes. Could be problems caused by low NT creates cognitive deficits
= suggests that the cognitive approach = over simplistic when considering explanations
- Although research shows the importance of biological factors in Sz, it also highlights the significance of environmental factors
- An explanation that links biological vulnerability to environmental stressors in the diathesis-stress model
- Explains that individuals will develop Sz if they have a biological predisposition and if they are exposed to stressful situation - nature and nurture
- Carried out a prospective study of 19000 Finnish children adopted away from biological fams w/ Sz mothers
- Also assessed the rearing style of the adoptive fam
- After 21 yrs = adoptive fam w/ a higher level of criticism and conflict was a significant predictor of Sz
- suggests that either factor on it's own doesn't cause Sz but when combined they increase risk of developing disorder.
- :check: Can explain why concordance rate for MZ twins is always below 100% for mental disorders incl. Sz e.g. if one twin is bullied at school, they will have a higher stress level than the other and more likely to develop Sz
- :red_cross: Treatments based on the diathesis stress model = more expensive than bio treatments alone but their greater effectiveness may make them cheaper in LT by making hospitalisation less likely
- :red_cross: Appears to be more holistic and complete, but what isn't explained is how stress acts on the NS to trigger the development of the disorder = this model could be used to prevent the development of mental disorders like Sz as if know an individual has a bio vulnerability to a mental disorder they could be educated on avoiding stress and potential triggers
Lobotomy anatomy: Nerve fibres are cut in the brain often leaving a patient apathetic and childlike
Electroconvulsive Therapy (ECT) Involves electrocution
- Work by binding to dopamine hypothesis and thus blocking their action, not stiumlating them
- By reducing stimulation of the dopamine system in the brain, antipsychotic drugs can eliminate the hallucinations and delusions experienced by patients w/ Sz
- Effectiveness of these dopamine antagonists in reducing the symptoms of Sz is what led to the development of the dopamine hypothesis
- Kapur et al (2000) approx 60-75% of D2 receptors needed to be blocked in the mesolimbic pathway for drugs to be effective
- This also means the D2 receptors in the rest of the brain are blocked too, leading to side effects
Side effects:
- E.g. where the extrapyramidal network in the cerebral cortex is impacted = area concerned w/ movements and motor activity
- Prolonged use of typical antipsychotics (neuroleptic) = side effect of involuntary movements of tongue, face, jaw (Tardive Dyskinesia)
- Examples of this drug include clozapine, these newer types of drugs (founded in 1990s) are said to combat the positive and negative symptoms of Sz
- This is because, as well as acting on the dopamine system, they are also thought to be serotonin receptors
- They also bind to D2 receptors but...
= Rather than permanently block the dopamine action, they temporarily bind to the receptors and then rapidly dissociate to allow normal dopamine transmission.
Leucht (2012) meta-analysis:
- Included nearly 6000 patients, 3000 in each condition
- 64% of placebo group relapsed within 12 months
- 27% of drug group relapsed within 12 months
- :check: Since mid-1950s antipsychotic medications have greatly improved treatment. Medications reduce (+) symptoms esp. hallucinations and delusions and allow the patient to function more effectively
- :check: Highly effective and relatively cheap to produce and easy to administer and have a positive effect on many sufferers = However, don't cure Sz, rather dampen symptoms so sufferers can live a relatively normal life
- :red_cross: Clozapine targets many NTs and shown to be more effective but severe side effects = loss of white blood cells. Newer drugs e.g. risperidone are safer and may be better tolerated, but not treat illness as well as clozapine
- :red_cross: Ethics = antipsychotics used in hospitals to calm patients for the staff's benefit = abuse of human rights as subjecting them to degrading treatment and lack of consent
- The CBT approach to treatment differs slightly from conventional CBT methods
- The aims of this therapy are:
1) To challenge and modify delusory beliefs
2) To help the patient to identify delusions
3) To challenge those delusions by looking at evidence
4) To help the patients to begin to test the reality of the evidence
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- Client expressed their experiences and symptoms to the therapist
- Goals and expectations of therapy can be established here
- Rapport and baseline established
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- Therapist provides a therapeutic environment for the patient where they can engage in therapy
- Includes the therapist emphasising w/ the patient's perspective, feelings of distress ect...
- The therapist must also stress that explanations for the patient's distress can be dvlpd together
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- Patient describes (A)ctivating event that is causing their irrational (B)eliefs, as well as the (C)onsequences
- Beliefs can then be challenged or disputed and changed
- Knowing there are other people who experience the same things as you can help to greatly reduce feelings of isolation and anxiety
- Placing psychotic experiences on a continuum of 'normal' experiences can help patients feel less stigmatized
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- Gentle questioning is used by the therapist to help the patient understand their illogical thought processes
= "if ur voices are real, why can't anyone else hear them?"
- The therapeutic relationship is essential here so q can be used in a non-threatening way
- Means there needs to be trust btwn therapist and patient
= core conditions of empathy and UPR must be present
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- Very CBT technique of discussing alternative explanations for unhealthy assumptions
- This can be done in collab. w/ therapist
- From therapy seeks to treat members of the same fam as well as the patient w/ Sz
- The hope is to hopefully reduce the high level of EE w/in the household which is causing the relapse
- Usually takes place at the home w/ typically two therapists
- Lasts between 3-12 months w/ sessions 2-4 weeks.
- A minimum of 10 sessions recommended
- Leads to a more supportive and warm atmosphere = helps patients to make better progress and relatives feel more positive about, and more effective in, their supporting roles
- Relatives made more aware of the info regarding psychosis and the particular diagnosis their relatives have been given. Therapists encourages qs
- Fam members learn more constructive ways of communicating and focusing on the good
- Find ways of coping w/ feelings w/out resorting back to high EE patterns of behaviour
- Fam and patient trained to recognise early signs of relapse so they can respond rapidly to reduce severity
- Garety (2008) Relapse rates reduced to 25% following fam therapy as opposed to 50% for those receiving standard care alone (neuroleptics)
- Involves a system of rewards being set up for desired behaviour (sometimes punishments for undesirable)
- Rewards are usually tokens or points, and these can be periodically exchanged for something the individual wants
- Tokens have no intrinsic value and so are called secondary reinforcers
- They can however be exchanged for primary reinforcers which are things wanted by the person
Must be clear definitions of:
- What is desired bhvr
- What is a token
- How tokens are allocated and how many of each reward
- What is a reward
- How there'll be a gradual changing of the giving of tokens to control behaviour
- How token will be removed when bhvr achieved
- :book: Ayllon and Arzin (1968)
- Used token economy in women's ward in a mental institution in the US
- Rewarded w/ tokens for self-care, exchanged for privileges e.g. watching films
- 'Desirable' behaviour increase significantly but decrease significantly when system was withdrawn
- :book: Ayllon and Milan (1979)
- Reviewed no of programs and found it worked for certain behaviours e.g. general keeping of rules and control over interpersonal aggression
- :book: Milby (1975)
- Found they were successful in psychiatric hospitals and helped in preparing someone to leave hospital but we do not know long term
- :check: Economic benefits: Fam therapy is highly cost effective because it reduces relapse rates, so the patients are less likely to take up hospital beds and resources
NICE review of family therapy studies demonstrated that it was associated with significant cost savings when offered to patients alongside standard care = relapse rates are also lower suggesting the savings could be even higher
- :check: Pharaoh et al. (2003) meta - analysis found family interventions help the patient to understand their illness and to live with it, developing emotional strength and coping skills, thus reducing rates of relapse.
identified examples of how family therapy works: It helps family members achieve a balance between caring for the individual and maintaining their own lives, it reduces anger and guilt, it improves their ability to anticipate and solve problems and forms a therapeutic alliance.
- :check: Anderson et al. (1991) found a relapse rate of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy or Social Skills training were used and the relapse rate was less than 5% when both were used together with the medication.
- :red_cross: Lengthy It takes months compared to drug therapy that takes weeks which leads to disengaged treatment as they don't see immediate effects - a patient who is very distressed and perhaps suicidal may benefit better in the short term from antipsychotics
- :red_cross: Addington and Addington (2005) claim that CBT is of little use in the early stages of an acute schizophrenic episode, but perhaps more useful when the patient is more calm and beginning to worry about how life will be after they recover. In other words, it doesn’t cure schizophrenia, it just helps people get over it.
- :red_cross: Kingdon and Kirschen (2006) found that CBT is not suitable for all patients, especially those who are too thought disorientated or agitated, who refuse medication, or who are too paranoid to form trusting alliances with practitioners.
- :check: Paul and Lentz (1977) Token economy led to better overall patient functioning and less behavioral disturbance, More cost effective (lower hospital costs)
- :red_cross: Ethical issues: Severely ill patients can't get privileges because they are less able to comply with desirable behaviours than moderately ill patients = may suffer from discrimination. And dehumanisation: subjecting the patient to a regime which takes away their right to make choices. In the 1950s and 60s nurses often “rewarded” patients with cigarettes. Due to the pivotal role of dopamine in schizophrenia this led to a culture of heavy smoking in psychiatric hospitals
- :red_cross: It is difficult to keep this treatment going once the patients are back at home in the community. Kazdin et al. Found that changes in behavior achieved through token economies do not remain when tokens are with¬drawn, suggesting that such treatments address effects of schizophrenia rather than causes. It is not a cure
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