Schizophrenia studies

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The international classification for disease (ICD)
Produced by the world health organisation. Next edition released 2015. Mental orders were not included until 6th edition in 1952.
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The diagnostic and statistical manual of mental disorders (DSM)
More common than ICD. Produced by American Psychiatric Association. Dominent manual in the US and is used elsewhere. Research in the US has to use DSM classifications and a DSM diagnosis for health insurance.
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Why is DSM always revised?
New disorders discovered, advanced science and understanding.
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Primary use of DSM by professionals?
To diagnose and compare symptoms and patients with reliability and consistency.
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What does schizophrenia mean?
Severe disruption in psychological functioning.
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Onset and prevalence of schizophrenia
Risk of diagnosis - 0.3-0.7% chance. Onset is usually between the ages of 15045. Equally common on males and females. Usually occurs earlier in males.
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Delusions
False beliefs resistant to change in the light of contrary evidence.
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Hallucinations
Perception-like experiences with no external stimulus. Usually auditory or visual.
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Disorganised thinking
Disorganised thought inferred from speech. 'Word salad'
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Grossly disorganised or catatonic behaviour
Disorganised - unpredictable agitation or silliness. Catatonic - decreased reactivity to the environment, rigid posture, lack of verbal/motor response.
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Negative symptoms
Reducation in eye contact, facial expression, hand movements. Level of functioning in major areas such as self care decreases.
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Crow (1980) - Type 1
Positive symptoms - Something is in some way added to the sufferer's personality.
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Crow (1980) - Type 2
Negative symptoms - Something is in some way taken away from the sufferer's personality.
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Changes in DSM 5
Dropped sub-types of schizophrenia, dropped GAF (Global Assessment of Functioning) Scale.
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Reliability/Validity
If disgnoses are inconsistent, they cannot all be correct (valid).
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Factors affecting reliability of diagnosis - Kleitman's 3 factors
1) differences in procedures eg: use of classification systems 2) differences between clinicians- subjective interpreation 3) Differences between patients and the presentation of their symptoms.
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Beck (1967)
Only found 54% inter-rater reliability between 2 psychiatrists' diagnosis of 154 patients. Example of problems with earlier DSMs.
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Improvments with DSM over time
removal of vague descriptions, blurred boundaries between disorders and clarifying how many symptoms/types of symptoms were needed.
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Kappa statistic (k)
A way of converting agreement between raters on nominal data. k=1 means perfect agreement. k=0 means no agreement.
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What is needed for a diagnosis to be correct/valid?
The illness must be reliably defined/classified and diagnosed. The illness has to be validly defined or classified.
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Relaibility vs. Validity of diagnosis
Poor reliability means poor validity. The more reliable the diagnosis the more likely the correct diagnosis is being made.
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Rosenhan (1973)
Patients reported that they were hearing a voice to doctors at psychiatric hospitals. All but one recieved a diagnosis of schizophrenia. The doctors were very reliable but were invalid as none of the patients had schizophrenia.
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Descriptive validity
Are the symptoms rights? It is usually possible to define medical illnesses by their symptoms
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Aetiological validity
Can we identify causes or mechanisms? It is possible to use evidence from causes or mechanisms to argue that an illness has been well-defined.
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Predictive validity
What is the prognosis/reaction to treatment? In a well-defined illness we are able to describe how the illness progresses over time and predict a reaction to treatments.
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What do you need to make a correct diagnosis?
Make sure: Psychiatrists are using a valid classification system, the same classification system and that the diagnosis are reliable.
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Consequences of lack of validity
Research into schizphrenia will be false/incorrect and there may be false postive/negative disnosing.
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Consequence of false positive - Perlman (2000)
Patients had been diagnosed with schizphrenia yet did not fit the criteria. Patients were administered with antipsychotic drugs that they did not need.
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Consequence of false postive - self-fulfilling prophecy
If a person is told they are a 'schizophrenic' then they are likely to adopt this identity. They may self-induce some symptoms. Doctors will simply interpret these symptoms as schizphrenic as that is what they presume the patient to be.
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Consequence of false negative
Untreated illness. The symptoms may worsen and the patients life will become increasingly harder.
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Two aspects of biological approach that I need to know
Genetic explanation and biochemical explanation
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Kendler et al (1985)
First degree relatives of those with schizophrenia are 18x more at risk of developing schizphrenia than the general population.
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A01 Genetics
Schizophrenia appears to run in families, gene coding for schizophrenia may be passed down
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A02 Genetics
Twin studies and seperated twin studies and adoption studies can allow further insight into the genetics approach
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Family study - Gottesman (1991)
Review of 40 major European family and twin studies. MZ twin 48% of developing schizo. Child w/ 2 schizo parents 46% chance. Spouse of schizo 2% chance
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Despite the fact that evidence shows the close the bio relationship the greater risk of developing schizo, why may this be inconclusive?
Gottesman ('91) showed high concordance rates in spouses than the general public. This suggest environmental factors.
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Twin study - Gottesman Review (1991)
MZ twins reared togehter 48% chance, DZ twins reared together 17% chance, MZ twins reared apart 58% chance
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Twin study - Gottesman & Shields (1972)
MZ twins reared togehter 42% concordance and DZ twins reared together 9% concordance
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Twin study - Cardno et al (1999)
MZ twins reared together 40% concordance, DZ twins reared together 5.3% concordance
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3 methodological flaws with twin studies
Generalised with specific cases not always acccounted for, age of seperation is important and not always accounted for, in early days of adoption and twin research there was no way of being certain if twins were MZ/DZ
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Adoption study - Tienari's Finnish adoption study
Children adopted-away from schizo mothers(index) compared with children adopted-away from 'healthy' mothers (control). 7% of index got schizo, 1.5% controls got schizo. Supports genetics.
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Adoption study - Kety et al (1994)
Studied Denmark's national sample and found that there were high rates of schizophrenia in adoptees whose biological parents shared the same diagnosis, even though they were adopted-away to healthy parents. Shows genetics>environment
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Critisicm of Tienari - Wahlberg
Strong interaction between genetic and environmental factors. Only children who were adopted into families with poor communication were at increased risk. Also, longitudinal study is bad as diagnositic criteria constantly changes.
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General criticism of adoption studies
Keiman (1977) Twins reared apart may share very similar environments as adoption agencies adopt out to families with very similar backgrounds and lives.
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Biochem Explanation - Dopamine Hypothesis A01
Focuses on neurotransmitters. Dopamine is a neurotransmitter found in the limbic system. This is involved in regulating emotion. Is also found in basal ganglia - regulates movement and emotion. All of these are linked with schizo.
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Biochem Explanation - Dopamine Hypothesis A01
Some symptoms of schizphrenia are the result of excess dopamine, super-sensitiivity of dopamine receptors, excess dopamine receptors
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Biochem Explanation - Dopamine Hypothesis A02
Supporting: antipsychotics work and dopamine receptor density in the causate nuclei is greater in schizos. However -they do not work for everybody
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Biochem Explanation - Dopamine Hypothesis A02
L-dopa produces symptoms of schizo (parkinsonian patients). However - does not always worsen symptoms of all people diagnosed with schizo.
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Biochem Explanation - Dopamine Hypothesis A02
Seeman - post mortem evidence Increased dopamine receptor density between 60-110% in schizos. However - most have been treated for years
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Type 1 and Type 2 A02 commentary of biochemical explanation
This distinction explains why not all patients respond to antipsychotics in the same way. Type 1 schizo is mostly causes by genetics linked with dopamine dysfunction and type 2 is usuallt caused by brain structural abnormalities.
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Diathesis stress model
Links biological vulnerability to environmental stressors. Some people may have a genetic/injury-caused vulnerability to the disorder but will only develop it if exposed to stressful situations.
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Support for diathesis stress model - Tienari's Finnish adoption study
Assessed quality of parenting through interviews and tests. All cases of schizo came from 'disturbed' families. The 'healthy families' of the high risk sample had lower schizo rates than general population. Shows importance of environment.
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Evaluation of Finnish adoption study
Low-risk children from 'disturbed' families did not develop the disorder. Shows genetics are still important.
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Practical applications of biological approach
Powerful drugs have been created to help with mental illness. Awareness of risk within families eg: twins or adopting.
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Cognitive Explanation
Disturbed thinking processes are the cause not the consequence of schizophrenia. People with schizo cannot filter information.
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Frith's Cognitive deficit model (explains positive symptoms)
Deficit in central monitoring system. This labels thoughts and actions as ones own thoughts or actions. Hallucinations are caused when inner speech is not recognised as self-generated. Patients think inner sppech is an external source.
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Frith's Cognitive deficit model (explains positive symptoms)
Unable to filter out irrelevant information gained form the world around them which leads to a cognitive overload which makes it hard to focus as random thoughts may be interpretted as more important than they actually are.
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Support for Frith - Bentall et al (1991)
Ppts asked to either generate items themselves eg: food beginning with B or to read out a list. A week later, asked if they had thought of or read the words. Schizophrenics - no recall if had thought of or read the words.Espesh. hallucinaters.
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Shallice (1988) (explains negative symptoms)
2 types of actions; self willed and environmentally driven. Patients with negative symptoms have a deficit in the supervisory attention system'. This cog. process generates self-initiated actions. Deficit can lead to lack of volition etc.
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Support for Shallice - Frith & Done (1986)
Experimental fluency task. Patients asked to generate self-initiated actions and responses were measured. eg: name as many fruits as you can. In comparrison, schizos named very few fruits. Either said nothing, repeated words or spoke irrelevently.
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Criticism of frith and done and bentall
Patients have usually taken medication therefore it is hard to find a comparable control group. This makes it almost impossible to distinguish between whether results are due to cognition or medication. Reduces validity.
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Park and Faraone
Cognitive impairment has some causal role because there are cognitive deficits in non-schizphrenic relatives. (the disorder cannot cause the cognitive impairment) but the cognitive deficit cannot cause schizo by itself or all relatives would have it
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Cognitive approach - link to other approaches
Need to combine cog. approach with bio. approach for a more complete explanation. Genes cause cog. deficit, deficit brings vulnerability to certain symptoms.
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Family Models
Key concepts: schizophrenogenic families (including double-bind and marital schism) and expressed emotion.
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Schizophrenogenic families (Fromm-Reichmann 1948)
disturbed patterns of communication within families, families with high emotional tension, families with secrets or close alliances.
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Bateson (1956) Double blind hypothesis
Constant exposure to conflicting injunctions. Where one message invalidates the other. ie: saying i love you to your son with a disgusted face. Child looses ability to discriminate between difference communcation levels.
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Lidz - Marital Skew
One parent dominates the other
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Lidz - Marital Schism
Parents have contrary views
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Expressed Emotion
Hostility, critical comments and emotional over involvement. Can be assessed through camberwll family interview.
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Brown (1972) Evaluation of Expressed Emotion
Patients more likely to relapse if they returned to their homes if they were characterised by high levels of espressed emotions than low levels.
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Evaluation of Schizophrenogenic Families
Mainly based on case studies - discuss methodological issues with these
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Diathesis stress model eval of family model
The Israli High Risk Study (1987) Envronmental factors assessed through assessing parents. All cases of schizo had poor parenting. However, all cases showed neuropsychological abnormalities. Their influence is questionable but supports dia.stress mod
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Practical applications of family model
Treatment of schizo now usually includes education and training for family members in controll EE levels. Supported by less relapse rates in countries where schiz has less stigma.
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Drug treatment - conventional/typical antipsychotics
eg: chlorpromazine. Aim to reduce positive symptoms. Based on idea that schizo is excess of dopamine activity. Reduces dopamine activity at certain receptor sites. Blocks D2 receptors, lessening their response.
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Drug treatment - atypical antipsychotics
eg: clozpine. Much newer drugs. Shown to be as effective as typical drugs but with less side effect. Reduces both neg & pos symptoms. Based on dopamine & seretonin problems. Works by blocking receptors.
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Antipsychotic drugs - general
Usually taken orally, absorbed from the digestive tract, pass the blood/brain barrier ad then go to the synapses and bind to post-synaptic recepts. Drugs can also be injected, especially for those who forget to take them orally.
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A02 Drugs - positive of traditional drugs
Drugs are much more human than previous methods of controlling patients such as straitjackets, drugs have rapidly reduced the average length of time in hospital, those who respond positively to drugs are kept on maintenance doses
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A02 Drugs - limitations of traditional drugs
Traditional drugs cause severe side effects such as dizziness, parkinsonian symptoms, dry mouth, constipations, muscular rigidity etc. Traditional drugs delay rather than prevent symptoms. Many relapse within a year.
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A02 Drugs - newer atypical drugs
targets both positive and negative symptoms, patients are less likely to drop out of treatment programme, less side effects generally but motor side effects are more serious
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A02 Drugs - cochrane- review of chlorpromazine
Meta-analysis of 302 studies. All used placebo + random allocation. Found that chlorpromazine reduces relapse, improves symptoms, leads to various side effects
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A02 Drugs - cochraine - review of clozapine vs. typical antipsychotics
Meta-analysis of 52 controlled trials, no significant difference to typical drugs in terms of broad outcome, fewer relapses, more acceptable as long term treatment than traditional drugs.
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ECT - electroconvulsive therapy
Originally used to treat schizophrenia but now usually used for depression. The shock of the convulsions disrupts/corrects the abnormal neurotransmitter activity.
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ECT process
muscle relaxant & anaestetic, electric current applied via electrodes on either one or both sides of bread. Small current is passed for 0.5-5 seconds. Several sessions over a number of weeks.
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Evaluation of ECT - Tharyan et al
Meta analysis of 26 studies. ECT can be a short term improvement for some people with schizo. ECT combined with drug treatment may be considered for a more long term solution.
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Evaluation of ECT
Drugs are more evasive than ECT as they enter the blood stream. A combination of the 2 does not hold much improvement.
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Evaluation of ECT
A good option for someone that has become a danger to themselve or others or is suicidal. Also for people who are pregnant or old and cannot take antipsychotics.
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Evaluation of ECT - side effects
Memory less may occur of recent events, names and dates but is usually forgotten tememorarily. ECT has no impact on intelligence. As long as muscle relaxant is used, no bones should be injured.
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Evaluation of ECT
The argument that ECT disturbed the memory so that all disordered thinking can be restructured is not legit as unilateral ECT causes minimal memory loss and still works.
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Evaluation of ECT
The idea that schizo and depression can be treated in the same way is illogical as they have different symptoms. This suggests that one of the disorders that is being treated through ECT is being treated incorrectly.
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Cognitive Behavioural Therapy
A treatment designed for those who are capable of gaining insight into their problems. The aim is so adjust people's way of thinking and alter inapproprite beliefs.
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One type of CBT - belief modification
Cognitvely challenges beliefs ie: hallucinations/dellusions. Patients learn to challenge initial interpretations and see them as hypothesis instead of reality.
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One type of CBT - RET/REBT
1) patient pinpoints activating event and consequence eg: voices and subsequent behaviour. They discuss the belief about the event that caused the behaviour. Therpist shows that belief is illogical by providing counter evidence.
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Evaluation of CBT - Jones et al (2000)
meta analysis on trials of belief modification and found it reduced both the frequency and intensity of hallucinations
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Evaluation of CBT - Drury et al (2000)
Followed a treatment programme, found that short term gains were positive but after a 5 year follow up the treatment group showed no advantage over control group.
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Evaluation of CBT - Bradshaw (1998)
Followed the case study of an american woman who did not respond to drug treatment and who often went to hospital, after 3 years of regular CBT she showed positive improvements and maintained the benefits after a year.
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Evaluation of CBT - appropriateness
Does not cure the patient of their symptoms but normalizes/reduces them. Is ethically sound as it is a collaborative therpay, patient does not become passive. If patients do not realise that they have a prob, they gain more insight through CBT
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Family Intervention
To reduce the chance of relapse in a schizphrenic patient. Provide coping skills. Create a trusting environment. Family members as will as patient are educated on this disorder and ways of managing it.
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Family Intervention
Process: 1) family gets info on the disorder, each member discusses their feelings on the patient and the disorder, contructive ways of communication are taught, taught how to express anger, training on early signs of relapse.
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A02 Family Intervention - Research - Cochrane Review
Meta analysis of studies focusing on families of people with schizo, comparing family based intervention with standard care. Found that familie intervention may reduce relapse risk, encourage compliance with meds. Data not sound, can't be confident
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A02 Family Intervention - Research - Leff et al (1982)
Programme created, educational sessions, group family meetings with other well coping families, social workers discussed fam's concerns. 2 year programme. 78% of control group readmitted to hosp, 14% of treatment group. Treat. gr. showed less EE.
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Negative of Family Intervention and CBT
Both very time consuming. Particularly with CBT, can be expensive.
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Card 2

Front

More common than ICD. Produced by American Psychiatric Association. Dominent manual in the US and is used elsewhere. Research in the US has to use DSM classifications and a DSM diagnosis for health insurance.

Back

The diagnostic and statistical manual of mental disorders (DSM)

Card 3

Front

New disorders discovered, advanced science and understanding.

Back

Preview of the back of card 3

Card 4

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To diagnose and compare symptoms and patients with reliability and consistency.

Back

Preview of the back of card 4

Card 5

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Severe disruption in psychological functioning.

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