Schizophrenia Flashcards

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1
Q

What is schizophrenia

A

A severe mental disorder characterised by disruption of cognitive and emotional functioning.

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2
Q

What does schizophrenia effect

A

Effects language, thoughts, perceptions, emotions and sense of self

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3
Q

What is Type 1: Acute onset

A

Obvious positive symptoms appear suddenly after stressful events

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4
Q

What is Type 2: chronic onset

A

Illness takes many years to develop, with gradual changes of increased disturbances and withdrawal occur. Characterised by negative symptoms

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5
Q

What are the 7 types of schizophrenia

A
  1. Disorganised - delusions, hallucinations and incoherent speech
  2. Catatonic - total immobility, or rocking back and forth or cataleptic stupor (adoption of strange body language)
  3. Paranoid - delusions of persecution
  4. Undifferentiated- patients are placed in this category if they don’t fit into any other ones
  5. Residual - patient has had schizophrenia in the past, but now doesn’t have enough symptoms to be classes as one. May have long term negative symptoms though
  6. Simple - no delusions/hallucinations present, but negative symptoms and psychosis may be present
  7. Post schizo-depression - they have had a schizophrenic episode and then followed by long term depressive episode
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6
Q

What does the DSM 5 say you must have to schizophrenia

A
  • 2 or more + (or one - and one +) symptoms like hallucinations for a period of one month and extreme social withdrawal for 6 months
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7
Q

What does the ICD 11 say you must have to schizophrenia

A
  • need to show one + positive and one - negative (or two -) for a least one month
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8
Q

What are 5 types of hallucinations symptoms of SZ

A
  1. Hallucinations - sensory experiences of stimuli that are distorted perceptions of things that are there
  2. Auditory hallucinations - hears voices making comments at them
  3. Visual hallucinations- seeing things which aren’t real
  4. Olfactory - smelling things which aren’t real
  5. Tactile - touching things which aren’t there
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9
Q

Positive symptoms of sz

A
  1. Hallucinations
  2. Disorganised speech
  3. Delusions
  4. Disorganised/catatonic behaviour
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10
Q

What are delusions (+ symptoms) and examples

A

Irrational, bizzare beliefs that seem real to that person.

Common delusions involve being an important historical, religious or political figure such as Jesus or Napoleon. Delusions also may involve being persecuted perhaps by government, aliens or even superpowers.

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11
Q

What is disorganised speech

A

Individual has problems organising thoughts and this shows up in their speech. May deviate from one topic to the next.

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12
Q

What is disorganised and catatonic behaviour

A

Inability or motivation to initiate or even complete a task Eg may lead to problems of personal hygiene or the person could be over active etc.

Catatonia refers to adopting rigid postures or aimless repetition of the same behaviour. (this symptom is diagnosed in the DSM but not ICD – extra symptom)

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13
Q

Negative Symptoms of Schizophrenia

A
  1. Speech poverty
  2. Abolition
  3. Affective flattening
  4. Anhedonia
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14
Q

What’s speech poverty

A

SZ is characterised by changes in patterns of speech – meaning the emphasis is on the reduction in the amount and quality of speech.

This is sometimes accompanied by a delay in the sufferer’s verbal responses during conversation.

May also be seen less complex syntax eg. Less clauses etc.

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15
Q

What is avolition

A

Described as finding it difficult to begin or keep up with goal-directed activity, i.e. actions performed in order to achieve a result.

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16
Q

What’s affective flattening

A

A reduction in the range and intensity of emotional expression, including facial expression, voice tone, eye contact and body language.

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17
Q

What is anhedonia

A

Loss of interest, or pleasure in most activities, or a lack of reactivity to normally pleasurable stimuli.

Physical anhedonia is inability to experience physical pleasures like bodily contact and social anadenia is ability to experience pleasure from interpersonal situations

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18
Q

What are 6 examples of issues associated with the classification and diagnosis of schizophrenia

A
  1. Reliability.
  2. Validity.
  3. Comorbidity.
  4. Symptom overlap.
  5. Gender bias
  6. Cultural bias
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19
Q

What is reliability, and inter rather reliability

A

It’s the consistency of a measuring instrument like the DSM.

Inter rather reliability is when 2 or more diagnosticians agree with the same diagnosis for the same individual – diagnosis would be done separately.

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20
Q

What is a study that showed how poor reliability is a weakness of the diagnosis of schizophrenia

A

Cheniaux et al (2009) showed low inter rater reliability amongst diagnosticians.

He had two psychiatrists independently diagnose 100 SZ patients using both ICD and DSM criteria.

Inter-rater reliability was poor with one psychiatrist diagnosing 26 with SZ according to DSM and 44 according to ICD, and the other psychiatrist diagnosing 13 according to DSM and 24 according to ICD

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21
Q

What is validity, and how do we assess things

A

Extent to which we are measuring what we intend to measure, for example, diagnosing SZ correctly based in the symptoms used in the manuals.

Asses them using criterion validity meaning dif assessment systems arrive at same diagnosis for the same patient (eg. Both using ICD and DSM)

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22
Q

Evaluation of validity and reliability of classification systems (3-)

A
  1. Rosenhan’s study (1973) supports the idea that the validity in the diagnosis of schizophrenia is low. Using a pseudo patients who were able to get themselves admitted in cycling hospitals by claiming they had auditory hallucinations. During their stay in the hospital, all patients behave normally and stayed for 7 to 52 days. But one patient was discharged with SZ in remission. But this was an old study meeting. The diagnosis was much poor in the 1970s, as the DSM was not as reliable at the time.
  2. Birchwood and Jackson (2001) found 20% of SZ patients show complete recovery and never have another schizophrenia episode, 10% show significant improvement, 30% show some improvement. 40% never really recover. Of the 40% that never recover, 10% are so affected that they commit suicide. This great variation in prognosis suggests very poor predictive validity.
  3. Another problem is that patients are more likely to be diagnosed when using ICD rather than DSM as shown in Cheniaux’s study. He used two diagnosticians to both diagnosed 100 SZ patient using ICD and DSM. Using the DSM, they classified 26 and 13 SZ patient, and and 44 and 24 SZ, patients using the ICD respectively. Thus, showing poor reliability.
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23
Q

What is comorbidity?

A

When two mental conditions occur at the same time

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24
Q

How is co morbidity a problem when classifying schizophrenia

A

Review Buckley et al. (2009) concluded that around half of the patients with SZ also have a diagnosis of depression (50%) or substance abuse (47%).

This gives a challenge for both classification and diagnosis of SZ. In terms of diagnosis, if half the patients are diagnosed with both SZ and depression, this suggests that we are not able to distinguish between both disorders very well.

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25
Q

What is symptom overlap?

A

Overlap between symptoms of schizophrenia and other conditions like bipolar disorders

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26
Q

How is symptom overlap a problem when classifying and diagnosing schizophrenia

A

Ellason and Ross (1995) show ppl with DID (Dissociative Identity Disorder) have more schizophrenic symptoms than people diagnosed with SZ. In fact, most people diagnosed with SZ have sufficient symptoms of other disorders that they could also receive at least one other diagnosis

Overlap would question validity of classification/diagnosis of SZ. For example, under the ICD, a patient may be diagnosed with SZ but under the DSM the same person will be diagnosed with bipolar disorder

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27
Q

Is there gender bias in classification and diagnosis of schizophrenia

A

Longenecker et al (2010) reviewed SS studies since 1980, and found men more likely to get it than women. They could be agenda in diagnosis as women seem to function better than men, having good family relationships and more likely to work, thus less likely to be diagnosed as said as women show better interpersonal function. So seems to be gender diagnosed with more males getting diagnosed than females.

28
Q

Is there cultural bias in the diagnosis of SZ?

A

Pinto and Jones (2008) African-American and English ppl of Caribbean origin, and nine times more likely to be diagnosed. Maybe as positive symptoms of acid like auditory hallucinations may be acceptable in Africa due to cultural beliefs which are acceptable and not warranted to a diagnosis in Africa (SZ rates low in Africa) but in UK, more likely to be seen as positive symptom of SZ.

29
Q

Evaluation: advantages of classification and diagnosis

A
  1. When a patient with a mental disorder that has numerous symptoms, it is simpler to incorporate the symptoms into a single diagnosis and makes communication better between mental health professionals
  2. Treatments are often specific to certain disorders, so a reliable diagnosis completed a therapy that will alleviate symptoms
  3. Although variation, there’s underlying biological abnormalities with SZ people. Hope that greater understanding of these abnormalities will lead to even more effective treatment.
30
Q

Gottesman (1991) family study

A

Gottesman (1991) found if both parents had SZ likely end of offspring having sz was 46%. if one parent had it likely had dropped the 13% thus showing the more closer you are genetically related, the more likely you are to get SZ

31
Q

Gottesman (1991) twin study

A

MZ, Twins share 100% of jeans, whereas DZ twins share, 50%. Thus, if schizophrenia is genetic, concordance rate should be much higher for MZ twins. Gottesman found 40% concordance rates for MZ and 17% concordance rates for DZ. Study shows that more genetically similar. You are more likely to get SZ.

But one negative is that if schizophrenia was based solely on genetics, concordance rate should be 100% , suggesting other factors also part in development

32
Q

Ripke et al. (2014) study on candidates genes

A

Compare genes of 37K SZ patients with 11 K control group. Found 108 separate genetic variations were associated with increased risk of SZ. These had connections to the functioning of session, transmitters like dopamine.

33
Q

Evaluation of genetic basis of SZ (1+ 3-)

A
  1. Large range of evidence to support genetic basis for SZ like findings from Gottesman and Ripke. For example, strength as it shows that if a child grows up in the family, we are both biological parents has SZ then chances of them getting it heighten compared to only if one parent has it, suggesting genes is important factor.
  2. However, the problem with twin and family studies is separating nature (genes) from nurture (the environment). For example, MZ twins are normally reared together and sent to the same school, then makes it difficult to separate upbringing from genes. If we look at adoption studies that attempt to separate genes from the environment, children tend to be adopted by relatives who may still rear child similarly to biological parents – thus adoption studies may not always be a good comparison for the effects of nature and nurture.
  3. SZ can take place in the absence of a family history. One explanation is that there may be a mutation in parental DNA, for example in paternal sperm cells. This can be caused by radiation, poison or infection. Brown et al’s. (2002) study showed a positive correlation between paternal age and increased risk of SZ increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50. Suggests although no direct genes are involved, a person can still get SZ if their father was older at the time of fertilisation. This suggests that the role of nature and nurture may both play a part rather than just genes.
  4. Genetic explanation of SZ is biologically reductionist as states one cause of SZ is simply your genes. Thus, insinuating if you possess the PCM1 gene then you will have SZ. This means that this explanation is ignoring other factors such as psychological factors and family upbringing which could be more important in explaining SZ – for example it has been found that certain parenting styles (e.g. the schizophrenogenic mother) in an individuals childhood could trigger symptoms of SZ in adulthood.
34
Q

What are neural correlates

A

Measurement of the structure or function of the brain that have a relationship with SZ especially different regions of the brain.

Also refers to how different neurotransmitters levels like dopamine, play part in SZ

35
Q

Evaluation of neural correlates (2+ 2-)

A
  1. Research to support structural changes in the brain between SZ and non-SZ. Torrey (2002) using brain-imaging techniques, discovered that many schizophrenics have enlarged ventricles, cavities in the brain that supply nutrients and remove waste – the ventricles of a person with SZ are on average about 15% bigger than normal.
  2. Research evidence can be validated through brain scanning, which is an objective method suggesting there is face validity to the neural correlates explanation as we can actually observe structural brain changes. This can also help tailor treatments that will reduce symptoms
  3. Problem with looking at different brain regions is the fact individual differences in SZ patients and not all have deficits in the functioning of different brain regions.
  4. Different brain regions involved in SZ, so maybe difficult to pinpoint which one is causing the symptoms. Plus maybe difficult to establish cause an effect in terms of neuroanatomy as evidence is correlational free example, did the suffer have abnormalities in a particular brain region and then get SZ what did the individual get SZ and then then show brain abnormalities.
36
Q

What is the dopamine hypothesis?

A

Claims excess of dopamine in certain regions of the brain is associated with positive symptoms of SZ. Thus messages from neurons that transmit dopamine fire, too easily and often leading to hallucinations..

Schizophrenics, I thought I have particularly high levels of D2 receptors on receiving neurons, resulting in more dopamine binding, and therefore more neurons firing .

37
Q

Evaluation of dopamine hypothesis (2+ 2-)

A
  1. Evidence from drug research to support the hypothesis. This neural correlate explanation is supported through research as dopamine agonist like amphetamines tend increase dopamine levels and make SZ symptoms worse and produce similar symptoms in non-suffers.
  2. Antipsychotic drugs which reduce the levels of dopamine support the idea that dopamine levels are high and SZ and can be reduced through drugs. Lindstroem et al. (1999) found chemicals needed to produce dopamine taken up faster in the brains of schizophrenics suggesting they produce more.
  3. This could be criticised to be biologically, determined meaning individual has no control over this. Hypothesis cannot be seen as a cause of SZ as there are other biological/psychological factors that contribute like upbringing in terms of family dysfunction. Recent research has focused on attention of glutamate another neurotransmitter that has been implicated in SZ suggesting don’t mean might not be only neurotransmitter responsible for SZ.
  4. Number of neuro correlates of brain structure in your transmitters, but still number of questions are left unanswered. For example, does high or low levels of dopamine called SZ. There is a correlation between high levels of dopamine and experiencing symptoms, but did the individual start having excess levels of dopamine in the brain region and start experiencing symptoms or did the individual first experience symptoms and then have high levels of dopamine. Thus neuro correlates explanation doesn’t really explain the cause an effect.
38
Q

What is family dysfunction? What are the three ways to explain it?

A

Psychologist have attempted to link as to childhood and adult experiences of living in dysfunctional families.

  1. The schizophrenogenic mother
  2. Double bind theory
  3. Expressed emotion.
39
Q

What is schizophrenogenic mother

A

Reichmann (1948) proposed a psychodynamic explanation for schizophrenia based on accounts, heard from patients childhood. Not many patients spoke about particular type of parent. The term schizophrenogenic means schizophrenia, causing characteristics of this type of mother are cold and controlling leaves. The child having lack of trust in relationships are develop into paranoid delusions, then developing SZ. When the mother is schizophrengenic, father is often passive and doesn’t get involved in child upbringing.

40
Q

What is the double bind theory by Bateson et al (1972)

A

Stated family climate is important in development in SZ focused more actual family communication. Suggested children who frequently receive contradictory messages from parents, If the child finds itself trapped in situations where they feared doing the wrong thing, but received mixed messages. as a result, child is unable to comment about fairness of the situation or see clarity so child may get it wrong and then punished by withdrawal of love. They feel confused about the world and see it as a dangerous place, reflected in that symptoms like paranoid delusions.

41
Q

What are expressed emotions?

A

The level of emotion in particular negative emotion expressed towards a patient by their carers.

EE includes verbal criticism of the patient , hostility, emotional of involvement in the life of the patient, needless self sacrifice

42
Q

What does high levels of expressed emotion cause?

A

High levels by the carers of the patients create serious stress, which may be a reason for the patient relapse. Express emotion can also be triggered for the onset SZ, especially if personal has genetic vulnerability to disorder

43
Q

Evaluation of family dysfunction as a risk factor (3+, 3-)

A
  1. Tienari et al (1994) study shows adopted children who had SZ biological parents are more likely to have it themselves than those without them. But this only emerge in situations where the adopted family was rated as disturbed/dysfunctional. Does illness only manifest itself under appropriate environmental conditions and genetic vulnerability alone wasn’t sufficient family dysfunction is a contributing factor to SZ
  2. Read et al. (2005)< reviewed 46 case, studies of child abuse, and SZ, found that 69% of adult women in patients with a diagnosed of said, had history of physical abuse, sexual abuse, or both in childhood. Men figure was 59%.
  3. Evidence to support double bind theory. Berger (1965) found SZ’s reported, high Riccall of double buying statements by mothers. But this evidence may be reliable as patients recall may be affected by the SZ. In other words because they have suffered from hallucinations and delusions they may just be assuming their mothers use more double by statements and we don’t know if their memory has been affected
  4. Evidence for family dysfunction for contributing factor isn’t very strong. Double theory, Liem (1974) measured pattern of parental communication and families with child, and found no difference when compared to normal families
  5. Altorfer at all (1998) suggested not all patients who live in high expressed emotion, families relapse and not all patients who live in low ones, avoid relapse. 1/4 of patient studied so no physiological response to stressful comments from their relatives showing evidence for EE as contributing factor is mixed
  6. Family dysfunction explanation is environmental reductionist as it simplifies cause of SZ to family upbringing and ignores other factors.
44
Q

What are the two types of dysfunctional thought processing

A

Meta representation

Central control

45
Q

What is meta representation, and what happens if there’s dysfunction in it

A

Cognitive ability to reflect on thoughts and behaviour, enabling insight into our own intentions and goals, allowing us to interpret the actions of others.

Dysfunction would disrupt ability to recognise our own actions as our own rather than someone else’s. maybe explaining auditory hallucinations and delusions like thought insertions (Believing someone is putting thoughts into your head.)

46
Q

What is central control?

A

Call Mathi ability to suppress automatic responses while we perform other actions. Speech, poverty and disorder may result from inability to ignore your own automatic dots. SZ experience, derailment of thoughts, and what they say as as too much going on in the thought processes, so they lose control.

47
Q

Evaluation of cognitive explanations for schizophrenia (2+ 2-)

A
  1. Sterling et al. (2006) compared 30 SZ patients with 18 non-patient controls on range of cognitive tasks, the Stroop effect. This is when the colour word is written in a different colour and you have to say the actual colour of the word. Found S said patient took twice as long to say the colour of the word and the controls showing dysfunctional thought processing since they were struggling with separating the colour word from the actual word.
  2. Another strength is success of cognitive behaviour therapy used alongside drugs to treat SZ. As it’s a thought disorder, drugs cannot completely treat disorder, so CBT will aim to question and challenge hallucinations.
  3. It’s difficult to establish whether dysfunctional processing is a cause, or consequence of SZ. E.g. did the dysfunctional processing begin, and then the symptoms of SZ or vice versa
  4. Cognitive explanations is problematic and that it fails to take into account. Biological factors and doesn’t acknowledge dysfunctional. Thought processing could also be due to abnormal dopamine levels. Explanation is therefore reductionist as it simplifies as SZ to being very basic.
48
Q

What are the two main types of antipsychotic drugs?

A
  1. Typical.
  2. Atypical.
49
Q

What are typical antipsychotics

A

Dopamine antagonist that work by reducing effects of dopamine and thus SZ symptoms. Drugs bind to, but don’t stimulate receptors, specifically, D2 receptors, thus blocking their action in reducing the positive symptoms of SZ.

50
Q

What is chlorpromazine?

A

It’s a typical antipsychotic, that’s been used around 1950. When first taken dome levels would build up, but then the production of dopamine reduce so, with reference to the dopamine hypothesis, this drug would normalise the dopamine production and transmission.

51
Q

What are atypical antipsychotics?

A

Emerging later, in the 1970s, they were used to improve upon effectiveness of typical ones and minimise side-effects. Have beneficial effects on negative symptoms.

They blocked D2 receptors like typical antipsychotics, but they only temporarily occupy the data receptors and then rapidly dissociate to allow normal dopamine and transmission. This rapid dissociation is thought to be responsible for the lower levels of side-effects.

52
Q

What is risperidone

A

Was invented in the 1990s, and is taken as tablets or an injection.

It binds receptors works better in binding to them to drugs, like clozapine. so much smaller dose required and evidence suggested lead a few side-effects, the most other antipsychotics

53
Q

Evaluation of drug therapy (3+ 2-)N

A
  1. Thornley (2003) compare use of chlorpromazine with a placebo. Data from 13 trials showed it was associated with red reduce symptoms and better overall functioning plus data from three trials with over 500 people should relapse rate was low when chromosome was taken
  2. Research evidence to support appropriate of atypical antipsychotics. Meltzer (2012) concluded, clozapine is more effective than typical antipsychotics and other atypical ones in treating SZ. Seen as effective in 30 to 50% of cases were typical antipsychotics had failed.
  3. Evidence to support. The fact relapse rate are much lower when patients take antipsychotic drugs as opposed to placebos. Leucht et al (2012) carried meta analysis of 65 studies involving 6000 patients. Some were taken off antipsychotic medication and given placebo instead and within 12 months 64% of those patients have been given placebo relapsed, whereas only 27% relapse on the drugs.
  4. Biggest weakness of drug therapy and treating acid is the side-effects. typical antipsychotic side-effects include dizziness, agitation weight gain an itchy skin. Side-effect of typical antipsychotics neuro malignant syndrome which could be a high temperatures and cause of death. Atypical drugs developed to overcome the side effects, but side effects still do exist.
  5. Ethical issues related to use of drug therapy. Most profound ethical issue would be consent as many schizophrenic patients might not be in right frame of mind to give fully informed consent and as drugs do have severe side-effects, one could question the extent of the harm, and whether effects the drugs were reversible.
54
Q

What are the three main psychological therapies for schizophrenia?

A
  1. CBT
  2. Token economy.
  3. Family therapy.
55
Q

What is CBTp and what are the 6 stages?

A

Cognitive behavioural therapy for psychosis.

  1. Assessment - patient expresses thoughts, the therapist, and real estate goals are discussed
  2. Engagement - therapist emphasises patient perspective and feelings of distress and stresses explanations for their distress can be developed.
  3. ABC model - patient gives explanation of their activating event (A) that appear to cause emotional and behavioural (B) consequences (C). These beliefs can be rationalise and changed.
  4. Normalisation - conveyor. Many people have unusual experiences like hallucinations, which reduces an anxiety and sense of isolation. Patient feels less alienated and stigmatised and recovery seems more likely.
  5. Critical collaborative analysis - therapist uses gentle questioning to help patient understand, illogical, deductions and conclusions. E.g. ‘ if your voice is real, why can’t hear them.’
  6. Developing alternative explanations - patient develops alternative explanations for previously unhealthy assumptions. if they aren’t forthcoming with healthy alternatives, new ideas can be constructed in cooperation with the therapist eg. positive self talk
56
Q

Evaluation of CBT (2+ 2-)

A
  1. CBTp motivated in treating acid compared to antipsychotic medication alone. The NICE review of treatments found consistent evidence that CBTp was more effective in reducing rehospitalisation rate up to 18 months, following treatments ending. Also showing to be effective in reducing severity of symptoms as well as social function improvement.
  2. Addington (2005) claims initial in acute phase of SZ, self reflection isn’t appropriate. But following stabilisation of psychotic symptoms patients can benefit from group base CBTp which can normalise experience by meeting similar individuals. Thus reach out shows individuals and more experience of SZ and greater realisations of their problems are most likely to benefit.
  3. There is a lack of availability and patience refused to attend sessions. Estimated in the UK 1/10 with S actually have access to CBTp. Survey found that in north-west of England out of 187 SZ patients, only 7% were offered it, and those who were offered significant number failed or refused to attend therapy sessions, so limiting its effectiveness
  4. There are problems with meta analysis of CBTp. Problems in this area which can reach unreliable conclusions about it is the failure it’s taken into account the quality of the studies. Free example, some failed to randomly allocate participants to CBTp or control conditions, while others fail to assess patient subsequent assessment of symptoms. Juni et al (2001) found clear evidence that problems associated with methodologically weak trials, translated into bias findings about the effectiveness of CBTp.
57
Q

What is the main name of family therapy?

A

Provide support for carers in attempt to make family life, less stressful and reduce rehospitalisation

58
Q

How does family therapy work? What strategies may they use?

A

Reduces level of expressed emotion and increases capacity for relatives to solve related problems

A. Psychoeducation meaning, helping the person and the terrorist to understand and be better able to deal with illness.

B. Forming alliance with relatives with care for person with SZ

C. Reducing emotional climate within family and burden.

D. Increasing relatives ability to solve anticipate problems.

E. Reducing expressions of anger/guilt by family member.

F. Maintain reasonable expectations among family members.

G. Encourage relatives to set appropriate limits, but maintain degree of separation when needed.

59
Q

Evaluation of family therapy (2+ 2-)

A
  1. Economical benefits. e.g. the NICE review demonstrated family therapy is associated with significant cost savings when offered to people with SZ in addition to standard care. Or family therapy is offset by reduction in cost of hospitalisation due to lower relapse rates. Also evidence that family therapy reduces relapse rates for significant period of intervention, meaning the cost saving associated with family therapy would be even higher
  2. Impact on family members is also advantageous. Logan et al (2013) analysed 50 family therapy studies that included intervention to support relatives. 60% reported significant positive impact on intervention on at least one outcome category for relatives like problem-solving skills. But methodological quality of many of these studies, poor making it difficult to distinguish effective from ineffective intervention.
  3. Pharaoh’s study questions family therapy, effectiveness. States family therapy increasing patient compliance with medication which can lead to improvement and mental state and social functioning suggesting it’s effective as it teaches family mental about important taking medication but does this mean medication or the family therapy improve patient symptoms, so evidence family therapy is mixed
  4. Problems with the lack of blinding in family therapy studies. E.g. in pharaoh study 10/53 studies reported in the matter analysis didn’t use any form of blinding meaning the raters were not blinded to the condition to which participants have been allocated. This meant they knew where the participants were attached to experimental/control conditions, creating rater bias. So they may reproduce allocated to the family therapy conditions are showing an improvement in symptoms rather than participants allocated to control conditions, so not telling us if family therapy is actually effective
60
Q

What is token economy?

A

A reward system used to manage behaviour of patients with SZ in hospital settings. It’s common for patients who are institutionalised to develop bad hygiene. For example, so changing these bad habits doesn’t kill as said, but improve the patient’s quality of life makes it more likely they can live outside the hospital setting.

Patient is given a token for carrying out good behaviour (positive reinforcement) which should encourage them to repeat behaviour.

61
Q

Evaluation of token economy (1+ 3-)

A
  1. Dickerson et al. (2005) gives research support. Reviewed 13 studies using it and 11 reported beneficial effects that were directly attributable to use of token economy. He concluded the studies, provide evidence of its effectiveness in increasing adaptive behaviour of patients.
  2. Ethical concerns were using it in psychiatric settings. e.g. to make reinforcement, effective clinicians may exercise control of important primary reinforces like food. Patient may exchange tokens if they display the target behaviour, but it’s generally accepted that all human beings have certain basic rights. They shouldn’t be violated regardless of positive consequences that might be gained through token economy
  3. The program lacks ecological validity. Reducing negative symptoms has only been shown to work in hospital settings. In the real world, when people with schizophrenia are living in a community, who will give them token straight away to exchange for a tangible item, thus they cannot cannot be used in a real world community.
  4. No real conclusive evidence for the programs working. Economy programs are not really used in the developed world. Critics would argue economies were only use hospitals to manage manage and control patience rather than treat their symptoms
62
Q

What is the interactionist approach

A

Approach that acknowledges there’s bio, psychological and society factors in SZ development.

Bio factors - genetic vuln, neurological abnormalities

Pysch factors - stress from life events, poor quality family interactions

63
Q

How does the diathesis explain the onset of SZ

A

Model states that both vulnerability to SZ and an stress-trigger are necessary to develop the condition.

One or more underlying factors make a person particularly vulnerable to developing SZ but the onset of the condition is triggered by stress.

64
Q

What is one exmaple off a stress trigger for SZ

A

Use of cannabis use makes it 7 times more likely for a person to develop schizophrenic symptoms, because cannabis interferes with the dopamine system.

Although most people don’t develop SZ through cannabis use most people don’t take cannabis but will develop SZ – this suggests that there are clearly other stressors which contribute to the development of SZ.

65
Q

what is treatment of SZ according to the interactionist approach

A

Model is associated with combining antipsychotic medication and psychological therapies such as CBT.

It is unusual to treat SZ using psychological therapies alone as SZ is a complex psychotic disorder.

So drug therapy will be first given to control the symptoms of SZ with token economy to manage the behaviour of patients with SZ. Then CBT and family therapy will precede this.

66
Q

Evaluation of interactionist approach (2+ 3-)

A
  1. Tienari et al. (2004) studied children adopted away from schizophrenic mothers. The adoptive parents’ parenting styles were assessed and compared with a control group of adoptees with no genetic risk. A child-rearing style with high levels of criticism and conflict, and low levels of empathy was implicated in development of SZ but only for children with a high genetic risk.
  2. usefulness of the interactionist approach in treatment of SZ. Tarrier et al. (2004) random 315 ppl to (1) medication and CBT group, or (2) medication and supportive counselling, or (3) control group. Ppl in groups 1 and 2 showed lower symptoms of those medication only.
  3. Original diathesis stress model is simple. Multiple genes inc. vulnerability. There’s no schizogene. Researchers think stress can also include biological factors. Houston et al. (2008) found childhood sexual trauma was a diathesis and cannabis was a trigger. Shows old ideas of diathesis as biological and stress as psychological has turned out to be overly simple.
  4. don’t know exactly how diathesis stress work. Evidence to suggest underlying vulnerability coupled with stress lead to schizophrenia. But we don’t understand the mechanisms by which symptoms of schizophrenia appear and how both vulnerability and stress produce them. This does not undermine support for the approach, but it does mean we have an incomplete understanding of the actual medication.
  5. Turkington et al. (2006) argued fact that bio and pysch therapies r more effective than either on their own does not necessarily mean the interactionist approach to schizophrenia is correct. Similarly as drugs help doesn’t mean that SZ is biological in origin. This error of logic is called the treatment-causation fallacy. It means that the superior outcomes of combined therapies should not be over-interpreted.