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Schizophrenia Flashcards

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1
Q

List the 5 schizophrenia symptoms

A 
Hallucinations
Delusions
Disorganised Thinking
Abnormal Motor Behaviour
Negative Symptoms
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2
Q

What are the 3 main symptoms of Schizophrenia?

A

Hallucinations
Delusions
Disorganised Thinking

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3
Q

Why might the diagnosis of a mental illness be problematic?

A
  • Stigma- Reliant on patients description of the symptoms
  • Subjective
  • Individual differences
  • Don’t want to be labelled or no realisation that ill
  • Misdiagnosis - stigma unnecessary medication or untreated
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4
Q

What are the advantages of having a diagnostic system for mental illness?

A
  • Standardised- more objective in a subjective area
  • Removes blurred boundaries when diagnosing
  • More accurate diagnosis
  • Treat patients
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5
Q

What are the names of the 2 classification symptoms used for defining and classifying mental disorders?

A

The international classification for disease (ICD)

The diagnostic and statistical manual of mental disorders (DSM)

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6
Q

What is the ICD?

A

The International classification for disease. Produced by World health Organisation, ICD 11 planned for 2018

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7
Q

What is the DSM?

A

DSM is produced by the American Psyciatric Association, DSM V released in 2013

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8
Q

Why has the DSM been continually revised?

A

Early version were no very reliable
More research gathered about new diseases
Differences in cultures
Changes in time (homosexuality)

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9
Q

Primary use of the DSM

A

Used by mental health professionals mainly to make diagnosis and research purposes

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10
Q

What is the main goals for DSM 5?

A

Improve quality of life for patients

Recognise and treat disorders

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11
Q

Define Delusions

A

Fixed beliefs that are not amenable to change in light of conflicting evidence.

May include a variety of themes such as Religious, persecutory, somatic, grandiose.

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12
Q

What is a persecutory delusion?

A

A belief that one is going to be harmed, harassed by an individual, organisation or other group. They are most common.

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13
Q

What is a referential delusion?

A

A belief that certain gestures, comments, environmental cues are directed at oneself. Also common.

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14
Q

What is a Grandiose delusion?

A

When an individual believes that he or she has exceptional abilities, wealth or fame.

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15
Q

What are erotomanic delusions?

A

When an individual believes falsely that another person is in love with him or her

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16
Q

What are Nihilistic delusions?

A

When an individual believes that a major catastrophe will occur

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17
Q

What is a somatic delusion?

A

When an individual focuses on preoccupations regarding health and organ function

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18
Q

Define Hallucinations

A

Hallucinations are perception like experiences that occur WITHOUT an external stimulus. They are vivd and clear and not under voluntary control.

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19
Q

What are auditory Hallucinations?

A

Auditory hallucinations are usually experienced as voices, familiar or unfamiliar that are perceives as distinct from the individuals own thoughts.

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20
Q

Define Disorganised thinking (speech)

A

Disorganised thinking int terms of speech is when an individual may switch from one topic to another. Or there answers to questioned may be unrelated and sometimes the speech may be nearly not understandable and resembles word salad.

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21
Q

Define Abnormal motor behaviour

A

It can range from childlike silliness to unpredictable agitation. It can lead to difficulties in performing activities of daily living.

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22
Q

What is catatonic behaviour ?

A

It is a marked decrease in reactivity to the environment. IT ranges from resisting instruction to having a complete lack of verbal or motor responses. Other features are repeated movements, staring and echoing of speech.

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23
Q

Define Negative Symptoms

A

Negative Symptoms are diminished emotional expression such as reduction in eye contact, facial expressions and hand movements.

-Avolition which is decrease in motivated self and purposeful activities.

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24
Q

What does Schizophrenia mean?

A

Severe disruption in psychological functioning

Psychotic

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25
Q

What is risk of developing Schizophrenia?

A

Lifetime risk of being diagnosed is 0.3-0.7% according to DSM 5

Equally common in males and females

Usually occurs in males 4-5 years earlier

Usually diagnosed between 15-25 yrs

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26
Q

To be diagnosed with schizophrenia what are the requirements?

A

Two or more of the symptoms for a 1 month period

One of the symptoms present has to be one of the main symptoms and has to be a common disturbance for at least 6 months

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27
Q

What are the “positive symptoms” of schizophrenia?

A

Delusions
Hallucinations
Disorganised Thinking
Abnormal motor behaviour

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28
Q

What do positive and negative symptoms mean in terms of mental illness?

A 
POSITIVE= Adding something to personality
NEGATIVE= Taking something away from personality
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29
Q

Who made the distinction between the two types of Schizophrenia?

A

Crow 1980

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30
Q

What did Crow do?

A

Made the distinction between the two types of schizophrenia

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31
Q

What is type 1 in terms of schizophrenia?

A

Type 1= more positive symptoms

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32
Q

What is type 2 in terms of schizophrenia?

A

Type 2= More negative symptoms

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33
Q

Why did DSM 5 and ICD 11 drop subtypes?

A

Trials showed that there is a lack of reliability in diagnosis of the sub types

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34
Q

Outline the clinical characteristics of Schizophrenia

A

Schizophrenia can involve positive symptoms (type 1) and negative symptoms (type 2). A positive symptom means that something is added to the patients personality. One positive symptom is a delusion. This is a false belief that is hard to change in the patient despite contrary evidence. One example is a delusion of persecution whereby the patient believes they are going to be harmed by either another person or organisation. A negative symptom infers something is taken away from the patients personality for example diminished emotional expression including a reduction in facial expression and hand movements. Diagnosis using the DSM requires two symptoms to be present during the 1 month period and one of these has to be a delusion, hallucination or disorganised thinking.

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35
Q

What is reliability?

A

Consistency

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36
Q

What is validity?

A

Truth/accuracy

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37
Q

What does reliability in diagnostic sense mean?

A

Reliability in the diagnostic sense means that the same diagnosis should be made by two or more clinicians (i.e. inter-rater reliability)

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38
Q

What are Kreitman’s 3 factors that affect reliability of diagnosis?

A

1) Differences in procedures e.g. use of classification systems
2) Differences between clinicians; subjective interpretation
3) Differences between patients; presentation

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39
Q

Research evidence for differences in procedures e.g. use of classification systems as a factor that can affect reliability

A

Doctors in different societies used very different diagnostic criteria.

Cooper:

  • American and British psychologists were shown the same videotaped clinical interviews and asked to make a diagnosis.
  • The psychiatrists from New York diagnoses schizophrenia twice as often and the London Psychiatrists diagnosed mania and depression twice as often

Cheniaux:
-found rates of diagnosis of schizophrenia using ICD were significantly higher than when using DSM-IV. Cheniaux was able to trace this directly to there being no need for symptoms in the last 6 months in ICD

40
Q

Differences between clinicians; subjective interpretation

A

Even if the same classification systems are being used, clinicians may interpret them differently. Many phrases in manuals are open to interpretation. For example, in DSM-5 delusions are defined as bizarre ‘if they are clearly implausible and not understandable to same-culture peers and do not derive from ordinary life experiences’.

41
Q

Research evidence for Differences between clinicians; subjective interpretation as a factor that can affect reliability

A

Mojtabi & Nicholson found weak inter-reliability (0.4) between clinicians in judgements of whether hallucinations were bizarre or not. This suggests that different doctors interpret the criteria differently.

42
Q

Differences in procedures e.g. use of classification systems

A
  • DSM dominant manual for diagnosis in US whilst a mixture is used int esc of world. DSM insists on some symptoms in the past 6 months
  • ICD allows diagnosis with symptoms only within last month
43
Q

Differences between patients; presentation

A

Patients may present differently on different days, depending on their mood and the variability of symptoms. A diagnosis on one day could be different from that on another day, depending on the symptoms and their severity. Patients may also react differently depending on the doctor.

44
Q

Improvements in reliability over time AO2

A

Early research on diagnosis showed worryingly low reliability

Beck:
- got 2 psychiatrists to diagnoses 154 patients
-Found inter-rater reliability was as low as 54% (diagnosis only agreed for 54%)
Coopers study also found poor agreement between US and UK psychiatrists

However these are all old pieces of research testing the reliability of DSM II. The first 2 editions of DSM were much weaker than subsequent editions illnesses were described in vague terms so low reliability was likely to result from their use.

Reliability improved with DSM III by removing vague descriptions and blurred boundaries between disorders and clarifying how many symptoms and of which types were needed.

Field studies for DSM III found high levels of reliability for diagnosis of schizophrenia. Across sample of patients consistent diagnosis in 81% of cases suggesting improvement.

Cheniaux found kappa statistics of 0.59 for DSM IV and 0.56 for ICD 10 The kappa between the two was 0.61

Field studies for DSM-5 found lower reliability by tougher trials were carried out: patients were assessed under really life conditions rather in idealised laboratory conditions.

The Kappa statistic for schizophrenia was 0.46

Reliability of sub-types of schizophrenia were low and have been dropped by DSM 5

45
Q

What is a kappa statistic?

A

A way of converting agreement between raters on nominal data onto a continuous scale that controls for chance.
k=1 there is perfect agreement k=0 no agreement 0.5-0.7 is good according to cheniaux

46
Q

What are the 2 main conditions that have to be satisfied for validity of diagnosis?

A
  • The illness has to be reliably defined/classified and diagnosed
  • The illness has to be validly defined or classified
47
Q

How does reliability affect validity of diagnosis?

A

Reliability of diagnosis is poor then so is the validity
If there is inconsistency in diagnosing schizophrenia across two or more clinicians then at least one must be an incorrect (invalid) diagnosis.

The more reliable the diagnosis the more likely the correct diagnosis is being made.

Some patients go to another doctor for a second opinion and if the 2 doctors agree then the diagnosis is reliable and patient more likely to believe it therefore valid.

Consistency is a precondition of validity.

Reliability can’t guarantee validity:

  • Illustrated by Rosenhans study where pseudo-patients reported that they were hearing a voice saying ‘thud’ to doctors at psychiatric hospitals. All but one received a diagnosis of schizophrenia.
  • In this case doctors were very reliable in their diagnoses but they were invalid as none of the pseudo-patients had schizophrenia.
48
Q

Major Problem with validity of diagnosis

A

What can be observed is an indirect of the illness. However usually some physiological marker that is accepted as showing the presence of the illness.

Medial researcher can test validity of their earlier diagnosis with reference to the later identification of the physiological marker

In schizophrenia there is no such indicator; there is no laboratory test that objectively settles whether someone has schizophrenia. All psychiatrists can do is observe behaviour and talk to patients. This makes genuine verification of the validity of a diagnosis very difficult.

49
Q

How validity of classification relates to validity of diagnosis?

A

Definition of disorder changed over time, disagreement over how to define the illness. The Lack of consistency in definition of the illness again shows there is a problem of validity.

In the absence of a definitive physiological marker for the illness we need to be confident that schizophrenia has been classified in a valid way

50
Q

How do you assess validity of classification?

A
  • Descriptive validity- are the symptoms right?
  • Aetiological validity- can we identify causes/mechanisms?
  • Predictive validity- what is the prognosis/reaction to treatment?
51
Q

AO1 for predictive validity of schizophrenia

A

A classification has predictive validity if prognosis is clear. But similar numbers of schizophrenics remain chronically ill, recover from initial onset or alternate between being ill and well. Response to treatment is somewhat unpredictable with 30% of patients failing to respond to typical anti-psychotics. Some drugs that have some success in treating schizophrenia target serotonin receptors in addition to dopamine receptors. It’s impossible to predict in advance which drugs will be successful for which patients.

52
Q

AO1 for descriptive validity of schizophrenia

A

Schizophrenia arguably lacks descriptive validity. Patients with very different symptoms can all be diagnosed with schizophrenia e.g. positive symptoms like delusions differ from negative ones like avolition. It could be argued that the diversity of symptoms in schizophrenia show that it is a vague label for a set of independent symptoms (Bengal) It might be better to explain and treat these independent symptoms rather than claim there is a single illness called schizophrenia. Schizophrenia symptoms can also overlap with other disorders e.g. the negative symptoms anhedonia is very similar to the core of depression.

53
Q

AO1 for aetiological validity of schizophrenia

A

Aetiological validity has also been questioned. There is no one cause of schizophrenia e.g. the dopamine hypothesis explains positive symptoms, but deterioration of brain tissue explain negative symptoms. Other explanations include stressful life events, dysfunctional family communication and defective cognitive processing.

54
Q

AO2 Evaluation for Validity

A

Explanations of causality- research shows that genetic vulnerability is involved in all types of schizophrenia. Significantly higher concordance in MZ than DZ tins has been reliably shown- answers criticisms over aetiological validity to some extent.

However type 1 schizophrenia characterised by positive symptoms of hallucinations appears to be caused by a dopamine imbalance. Suggests the classification of schizophrenia as a single illness is problematic. Lidless findings from cluster analysis could be case that distinctions within schizophrenia are needed. Type 1 and 22 may be separate disorders.

One way to investigate descriptive validity is to use cluster analysis. Little found 3 clusters of symptoms positive negative and symptoms of cognitive disorganisation. Suggests that the classification of schizophrenia as a single illness is problematic and that distinctions within it are needed.

Invalid diagnoses also have serious implications for treatment. Two errors can occur; a false positive (diagnosed with something they don’t have). and false negative( patient left undiagnosed no treatment)

Support for false negative by Swartz’s study of African American woman who was wrongly prescribed antipsychotics for 10 year to treat hallucinations and agitation. AN EEG later revealed evidence of epilepsy and when appropriate treatment given her symptoms disappeared.

False diagnosis may have negative effect on person- label schizophrenia might become part of persons identity. Might accept this label in a self-fulfilling prophecy and develop symptoms of illness or deteriorate in functioning. Might be difficult to escape from this as doctors may interpret behaviour consistently with the invalid diagnosis. Then will reinforce illness.

Supported by Rosenhan study where pseudo patients normal behaviour was interpreted in line with the diagnosis of schizophrenia- making notes while ton the ward was interrupted as writing behaviour as if it was abnormal and arriving early for lunch because there was nothing else to was interpreted as an oral-inquisitive symptom.

55
Q

Biological explanations

A

The Dopamine hypothesis

Genetic approach

56
Q

The dopamine hypothesis AO1

A
  • Dopamine is a neurotransmitter which regulates movement and emotion in the limbic system and increased levels are said to contribute to symptoms of paranoia and hallucinations.
  • Excess in some parts of the brain linked to cause of Schizophrenia.
  • Dopamine found in basal ganglia
  • Psychotic symptoms could be result of: super sensitivity of dopamine receptors (D2), excess of dopamine, increased synthesis and release of dopamine from the pre-synaptic neuron.
57
Q

Evidence for Dopamine hypothesis

A

Supporting evidence is the use of some antipsychotics like phenothiazines which decrease dopamine levels in brain and are affective in treating schizophrenic symptoms. However not all patients respond to treatment and the drugs are only effective with positive symptoms (hallucinations and delusions).

L-dopa drugs increase the amount of dopamine in the brain and research shows that administering the drug to previously unaffected patients can induce symptoms of schizophrenia supporting hypothesis. Doesn’t worsen symptoms for currently diagnosed patients.

Seaman study : post examinations on schizophrenic patients show that there is an 60-110% increase in the dopamine receptor density compared to control groups.

58
Q

AO2 for dopamine hypothesis

A

Seeman:
Study may lack validity because patients who were in the study are on neuroleptic drugs for years and therefore it is difficult to determine whether the increase in dopamine levels were a result of the drugs rather the cause of the disorder.
Scans were also on dead brains which may be causing the dopamine receptor to be in excess.

Weakness of this study overcome by Wong et al study.
Ppts who were ton drugs had live scans show that it wasn’t the drugs causing the excess of dopamine. Found 2 fold increase in density of dopamine receptor sites in schizophrenic patients who had never been treated with drugs compared to those who had and control groups.

Inconsistent findings- not applying to all people with schiz
- drug treatments don’t help all patients
Not all users of amphetamines or L dopa develop schizophrenia type symptoms
Dopamine does seem to be involved in type 2 symptoms

59
Q

Genetic approach AO1

A

Genetic approach:

  • inherit 50% genes from parents
  • genes build bodies including brains
  • brain = source of all mental states
  • schizophrenia = disorder of mental state.
  • Genes determine brain structure/neurochemistry and these -determine our thoughts and behaviours
  • can inherit psychological traits including psychopathology.
  • risk of individual developing schizophrenia is proportional to the amount of genes they share with pro band

Liability threshold model- most behavioural geneticists believe that there are a number of genes that each have a small effect though some have more of an effect than others. More of these genes the higher risk of schizophrenia.

60
Q

Evidence for Genetic approach

A

Tienari adoption study showed concordance rates are higher for adopt children with biological mothers who had schizophrenia at a 7% chance compared to 1.5% for adopted children who’s mothers don’t have the disorder.

Liability threshold model- Meta analysis identifies an association between dopamine D2 receptor gene and schizophrenia (Glatt et al) Risk of developing schizophrenia was shown to increase by 30% in relation to a defect in the gene coding for the D2 receptor

Kety et al: Denmark, high rates of schiz found in adopted children whose biological parents were schizophrenic even though adopted by healthy parents.

Wahlberg et al: Re-examined TIenari data found strong effect of environmental factors where those at risk of developing schizophrenia were adopted into families with poor communication.

Gottesman review: twin 40 studies-
MZ twins reared together =48%
DZ twins rated together=17%
MZ twins reared apart= 58%

Gottesman and shields found 42% concordance for MZ twins reared together and 9% for DZ.

Carno found concordance rates 40% and 5.3% for DZ

61
Q

Genetic Approach AO2

A

Tienari: Supports genetic link because chance of developing schizophrenia was higher for those which has schizophrenic mothers even though they were in a adopted environment.

Gottesman + Shields and Carno Supports genetic link as MZ twins concordance is higher. HOWEVER as concordance rates aren’t 100% for MZ it shows it can’t be solely explained by genes and there must be contribution from environmental meaning an interaction between them.

Wahlberg shows that genes must be present but needs to a environmental trigger to cause the disorder. Genetic vulnerability + environment = disorder. Family upbringing could be a contributing facto

62
Q

Diathesis stress model AO1

A
  • Biological factors alone do not lead to schizophrenia and they are only one part of the picture.
  • Genes increase risk but needs to be an interaction with environmental factors.

Genes = diathesis (put someone at risk)
Environmental factors =stressor (determine who and when develops disorder)

63
Q

Evidence for diathesis stress model

A

Tienari study:
adoptees high risk (genetic vulnerability) + disturbed family =schizophrenia
Adoptees high risk (genetic vulnerability) + healthy family =schizophrenia well below general population rates
Adoptees low risk (no genetic vulnerability) + disturbed family = no schizophrenia

Shows how environmental factor of family contribute towards development of disorder

64
Q

Psychological explanations for schizophrenia

A

Cognitive deficit model
Expressed emotion
Family models

65
Q

Cognitive theories for schizophrenia AO1

A

Cognitive psychologists suggest that disturbed thinking processes are the cause not the consequence of schizophrenia.

Psychological abnormalities lead to cognitive malfunctioning

Frith’s cognitive deficit model
-explains positive symptoms
-CMS voices etc
Faulty filtering of irrelevant thoughts

Shallice:

  • explains negative symptoms
  • 2 typed of actions self willed and environmental stimuli
  • deficit in supervisory attention system
  • self initiated actions like poverty of speech, social withdrawal and lack of volition affected
66
Q

Frith’s cognitive deficit model

A

deficit in CMS underlies positive symptoms. CMS labels thoughts and actions as ones own or done by me. Hallucination caused when inner speech are not recognised as self-generated patients may blame them on a external source and therefore experience the speech as voices belonging to others.

Faulty filtering process in brain of schiz patients. Failure to filter out irrelevant thoughts and information gained from the world around us. Lead to cognitive load and conscious mind overloaded and unable to block out some thoughts.

67
Q

Shallice

A

Shallice:

  • explains negative symptoms
  • 2 typed of actions self willed and environmental stimuli
  • deficit in supervisory attention system
  • self initiated actions like poverty of speech, social withdrawal and lack of volition affected
68
Q

Research evidence for Shallice

A

Frith & Done:

  • deficit in supervisory attention system is supported by evidence from experimental fluency tasks
  • Found that in a verbal fluency task schiz patients with negative symptoms produced very few words compared to control ppts.
  • Patients either did nothing, repeated previous response or responded to some irrelevant environmental stimuli
  • Shows that deficit in supervisory attention system is essential to self initiated actions.
69
Q

Research evidence for Frith

A

Bentall et al:

  • ppts asked to generate category items themselves
  • week later asked whether to decide whether the words were generated by them or if they were new
  • Results show that schizophrenic patients with hallucinations performed worse than those without
  • Shows how having a deficit makes it hard to distinguish between ones own thoughts and external influences as they couldn’t determine which words were new.
  • HOWEVER could be due to memory loss?
  • idea that hallucinations are a consequence of misattributing inner speech to external sources
70
Q

The cognitive explanation AO2

A

Bentall et al
-support for Frith’s deficit model
Shows how having a deficit makes it hard to distinguish between ones own thoughts and external influences as they couldn’t determine which words were new.
-HOWEVER could be due to memory loss?
-idea that hallucinations are a consequence of misattributing inner speech to external sources
-Schizophrenic patients had been taking medication for years- difficult to find a comparable control group of patients to use in experiments who been treated with medication. Hard to distinguish if cognitive deficit is reason for results or antipsychotics

Frith & Done:

  • supports shallice
  • Schizophrenic patients had been taking medication for years- difficult to find a comparable control group of patients to use in experiments who been treated with medication. Hard to distinguish if cognitive deficit is reason for results or antipsychotics
  • can’t be sure tasks results reflect cognitive deficit
  • artificial tasks

Diathesis stress model:
Shows cognitive explanation is not sufficient on its own
genetic vulnerability –> biochemical abonormality –> cognitive deficits + stressful life events = development if pstychotic symptoms.

Issues of causality:
Park et al identified working memory deficits in people with schiz and their first degree non-schizophrenic relatives.
Faraone found impairments in auditory attention claim that such memory and attention deficits are result of genetic predisposition to schizophrenia.

71
Q

3 parts of family models explanation

A

The schizophrenic family
Double blind
Express emotion

72
Q

The schizophrenic family AO1

A

Families with high emotional tension, secrets, close alliances and conspiracies.

Cold, domineering, manipulative and conflict causing mother might cause child to feel resentment and distrust which leads to psychotic symptoms of schizophrenia.

73
Q

The Double blind AO1

A

Bateson et al:
proposed that symptoms are expression of social interactions in which the individual is repeatedly exposed to conflicting messages

e.g.(mother saying love u then turning away in disgust)

one on verbal level and one of animosity on the nonverbal level.

One message invalidates the other.

Child not able to comment on the fact that they contradict (meta communicate)

Leads to any input from environment as conflicting information without being able to discriminate between.

The inability manifests itself as symptoms like hallucinations nd incoherent thinking and speaking.

74
Q

Family models AO2

A

Little empirical evidence in support of these early family models as explanations for schizophrenia.

Mischler: various observations and found mothers talking to daughters who had schizophrenia were rather aloof and unresponsive. However same mothers normal and responsive to healthy daughters

Berger: Research with white males aged 16-35. 4 conditions experimental and with patients with schiz symptoms and 3 controls. Found that those in experimental group had high recall of double blind statements by their mothers.

Liem: Measured patterns of parental communication in families with schizophrenic child and no difference when compared to controls.

75
Q

Expressed emotion AO1

A

Qualitative measure of amount of emotion displayed typically in the family setting but family or caregivers.

High level of EE in home = worsen prognosis or act as risk for development of schizophrenia.

Determined whether a person or family has high EE through a taped interview known as the Camberwell family interview.

3 Dimensions:
Hostility- negative attitude towards patient, blame on them
Critical Comments- patient responsible for disorder
Emotional over involvement- family member blames themselves shows concerns and pity

EE can be seen as a maintenance model for schiz as it serves to maintain disorder rather than being cause of it.
High EE in fav may be predictor of relapse rates in discharged patients.

76
Q

What is the Camberwell Family interview?

A

Interview to determine whether a person or family has high express emotion and may be a risk for an individuals development of schizophrenia

  • Conducted with key carers of patient
  • Interviewer tries to create a picture of how things have been in household in moths leading up to onset of schiz
  • Interview is recorded and transcript rated
  • Objective information about events in home and subjective information concerning relatives feelings towards patient when discussing disorder.
  • Interview rated by number of statements of resentment, over involvement, critical comments towards patient.
77
Q

Expressed emotion AO2

A

Brown: showed patients who returned to high EE homes more likely to relapse than those returning to low EE homes

Vaughn and Leff: Found similar results with 51% relapse in those in high EE homes and only 13% relapse in those in Low EE homes. relapse rates increased as face to face contact increased with high EE relatives

Correlational research- family relationships work both ways High EE might reflect the consequences of living with a severely disturbed individual rather than having any causal significance. First episode patient families high EE less common. Suggests high EE may well develop as a response to the borders of living with a person suffering from disorder. Doesn’t rule out that High EE results in the re admissions.

PA- well established maintenance model- treatment programmes include education and training fro family members in controlling levels of EE.

Diathesis-stress model:

Genetic factors might lead to biological vulnerability which might take form of biochemical abnormality and therefore manifest itself as an inability to process cognitive information (cognitive deficit). The deficit can lead to distortion and if individual is exposed to stressful life events or a family environment with high EE these cognitive difficulties might manifest as symptoms for schizophrenia (hallucinations)

The diathesis stress model shows that the role of EE on its own is not sufficient in establishing the cause of schizophrenia. It must be considered in combination with other factors. The israeli high risk project found that among the high risk group those who experienced negative family environments were mor likely to develop schizophrenia. Among the high risk group none of those who received good parenting went on to develop schizophrenia. Shows how there needs to be a combination of high risk (genetically vulnerable) and a trigger of negative family environment to develop disorder.

78
Q

Biological Therapies for schizophrenia

A

Drug treatment

ECT

79
Q

Drug treatment for schizophrenia AO1

A

Conventional/typical antipsychotics:

  • Chlorpromazine (low potency)
  • Linked to reduction of positive symptoms
  • side effects

Unconventional/atypical antipsychotics:

  • Clozapine
  • Newer antipsychotics
  • shown to be as effective as chlorpromazine
  • fewer side effects
  • Controls positive symptoms in those resistant to neuroleptics
  • Advantage of reducing negative symptoms
  • If prescribed need to undergo regular blood tests to check its not reducing white blood cells

Potency of drugs depends on how it binds to receptor. Chlorpromazine binds more weakly to D2 receptor than does haloperidol

Antipsychotics usually take orally- absorbed from digestive tract, pass blood/brain barrier and then go to synapses where they bind to post-synaptic receptors. Can be injected- depot injections in bum slowly released and useful for those who forget to take medication. Interval is 2-4 weeks

Patients who benefit from antipsychotics need to continue taking them to prevent symptoms returning. (Maintenance treatment)

80
Q

URAP for chlorpromazine

A

U- reduce positive symptoms of schizophrenia
R- based on theory that schizophrenia results from an excess of dopamine activity at certain synaptic sites
A- Aim of chlorpromazine is to reduce dopamine activity at receptor sites
P- Works by blocking D2 receptors reducing ability of dopamine to bind on post-synaptic receptor, lessening the response

81
Q

URAP for Clozapine

A

U- treat schizophrenia without the previous problems of side effects
R- Based on theory that schizophrenia results from excess of dopamine at certain synaptic sites. And based on that an imbalance in other neurotransmitters such as serotonin are linked.
A- aim of clozapine is to target serotonin and dopamine receptors in brain
P- Precise biochemical mechanisms unknown they do appear to have a major impact on serotonin receptors, blocking these receptors.

82
Q

AO2 for Chlorpromazine

A

Effectiveness:

Conventional/typical antipsychotics:
Cochrane review of chlorpromazine- meta analysis of 302 studies of effectiveness. All used placebo and random allocation.
-Found reduces relapse rates in short and medium term but less in long term
-Reduces symptoms, improving functioning and probability of leaving treatment
-Meta analysis more reliable that individual study as no fluke.
Well designed chosen studies with appropriate control groups
All used placebos so effects are not a result of participant reactivity
Random allocation- so no bias

Appropriateness:
- leads to various side effects; movement disorders, sedation and lower blood pressure.
-Some suggest that given this side effect,
administration of these drugs is unethical, and defies articles regarding harmless treatment in the
Human Right Acts 1988. Therefore, physicians prescribe conventional antipsychotics less frequently
than they used to because of the potential for serious side effects. Instead, physicians often
preferentially prescribe a newer family of antipsychotic medications, known as atypical
antipsychotics.
-30% don’t respond favourably
-maintenace dose- can’t hold down a job as revolving door effect
+Davison et al tried to educate patients and family about relapses and how to monitor signs and support

83
Q

AO2 for Clozapine

A

Effectiveness:
Meta analysis of 52 randomised controlled trials
44 less than 13 weeks in duration

  • Found no significant difference in effects of clozapine and typical antipsychotic in terms of brand outcomes including ability to work and suitability for discharge at end of study (short term effects)
  • Symptom reduction seen more frequently
  • Fewer relapses
  • More acceptable in long term treatment than conventional treatment
  • Clinical effect more pronounced in patients resistant to typical antipsychotics. 34% of treatment resistant patients had improvement with clozapine.

Appropriateness:

  • Blood problems occurred more frequently whereas none experienced this with typical antipsychotics
  • Clozapine patients experienced more drowsiness, hyper salivation
  • but Fewer adverse motor effects
  • Weak data conducting and reporting of trials prone to bias to favour clozapine
  • chemical straightjacket (depot injections)
84
Q

General AO2 for drug treatment

A

General AO2 for drug treatment

Maybe older atypical antipsychotics but at lower potency may be more favourable outcome

+ Biological
+Objective
+real life application

  • Deterministic- placebo of taking drugs
  • Reductionist: Individual differences.
85
Q

ECT AO1

A

U- Developed to treat schizophrenia but now used to treat depression. For treatment resistant patients, acute onset
R-Based on theory that abnormal activity of NT/hormones causing schizophrenia
A- Shock disrupts/corrects this abnormal NT activity in brain
P- Anaesthetic and muscle relaxants, electrodes on head electrical current (70-130mv) for 0.5-5 seconds. Induces mini seizure by producing electrical convulsion in brain. Current given bilaterally or unilaterally. Several session over number of weeks, quick fix not long term. Reduces positive symptoms rapidly

86
Q

ECT AO2

A

Cochrane review- Tharyan & Adams

  • to determine whether variations in the administration of ECT influences outcome.
  • Meta analysis -26 studies
  • Randomised controlled clinical trials comparing ECT with sham ECT, non pharmacological interventions and antipsychotics.
  • Found more patients improved in real ECT group
  • Real ECT had less relapses in short term
  • No evidence that this relapses rate is maintained
  • Drugs favoured in comparison
  • Limited evidence that ECT and drug treatment resulted in greater improvement that drugs alone

ECT can in short term result in increase in global improvement for some but COMBINED with drug treatment may be considered an option especially when rapid global improvement and reduction of symptoms required.

87
Q

What is appropriateness in terms of treatment?

A

1) Side effects
2) Ethics
3) Compliance

88
Q

What is Effectiveness in terms of treatment?

A

1) Research findings
2) Methodological evaluation
3) Reduction of symptoms
4) Relapse

89
Q

Psychological therapies

A

Cognitive behavioural therapy

Family intervention

90
Q

Cognitive Behavioural therapy AO1

A

U- to treat schizophrenia

R- Based upon the idea that schizophrenia is caused or maintained by irrational beliefs that patients have about their experiences

A- To address and change the patients believes and though processes which contribute to their symptoms

P- Agendas set between the therapist and patient are generally more flexible than traditional CBT. Patient generally has between 12 and 20 sessions

Cognitive element- make patient aware of their cognitions and how they impact on functioning;question,challenge and try to change the patients beliefs.

Behavioural element- Reality testing, role-play, homework.

Example: Rational emotive behavioural therapy

91
Q

Rational Emotive behavioural therapy (REBT)

A

Ellis: to challenge irrational beliefs used in CBT sessions.
Would start by asking patient to express thoughts and feelings about experience. ABC model allows patient to organise confusing experiences

92
Q

ABC model

A

A =activating event

B = Beliefs

C= Consequences

Example:
A = voices
B= Voices are driving me mad, they control me
C = Emotions- sorrow lonely depressed Behaviour =isolation

Step 1 Patient pinpoint activating event
Step 2: Patients beliefs which is cause of C is discussed
Step 3 Therapist tries to get patient to understand that beliefs have are illogical by testing evidence for and against maladaptive beliefs

Techniques to challenge beliefs:

Goal setting- measurable, realistic and achievable
Normalisation- give examples and see from different viewpoint
Decastrophising techniques- place on continue with normal experiences point of recovery seems less distant
Developing trust- no judgement, gentle questioning

93
Q

Research evidence for CBT

A

Effectiveness:
Startup et al- 90 patients admitted to hospital suffering from an acute episode of psychosis. 43 given standard drugs and nursing care vs 47 given in addition to drugs up to 25 90 minute sessions of CBT with 1 of 3 psychologists. Assessed for symptoms and social functioning on admission then 6 months on and 1 year after

-60% showed reliable change vs 40% control with fewer positive and negative symptoms and no signs of long term deterioration whereas 17% of controls did

Jones- Cochrane review 2012 Randomised controlled trials of CBT for people with schizophrenia-like illnesses. 31 papers described 20 trials they were often small and of limited quality.

  • found no difference in effectiveness between CBT and talking therapy. CBT better at improving mental state but not better at managing symptoms.
  • Few people left study compared to drug trials meaning that CBT + other therapies may be better at retaining and keeping people in treatment. Review suggests that might be long term advantage in CB! for dealing with emotions and distressing feelings.
94
Q

AO2 for CBT

A

Research evidence:
Startup et al- can’t establish effectiveness as single treatment for schizophrenia as no individual CBT trial, all with drugs.
Supports CBT as 60% of patients in CBT and drugs condition showed reliable change and fewer symptoms

Jones- found CBT not more effective single treatment but positive long term

Drugs + CBT = better alternaitve for treatment

Appropriateness:

  • Not a cure- can improve certain symptoms but no cure just a way of normalising symptoms
  • Ethics: collaborative therapy and involves active cooperation of client- avoids criticisms of drug patients becoming passive recipients of treatment
  • Lack of insight: Can’t understand schizophrenic patients thoughts.
95
Q

Family Intervention AO1

A

U- To treat schizophrenia

R- Based on idea that Schizophrenic patients with families who have high levels of Expressed emotion have more frequent relapses

A- To develop cooperative and trusting relationships within the family to help patient - Family intervention programme.

P- 1) Family members learn constructive ways of interaction and communication.

2) Family + patient trained to recognise early signs of relapse
3) Used in conjunction with routine drug treatment
4) Teach family about cause,course and symptoms
5) Lower the levels of expressed emotion in the family environment by discussing feeling and how to express anger regarding family member with disorder.

96
Q

Research evidence for Family intervention

A

Leff et al:
Programme developed which involved:
- Educational sessions- nature of schiz and symptoms and dealing with behaviour
-group meetings: with families who coped well with patient
-Family sessions: social workers met family to discuss concerns

Effects of intervention evaluated following 2 years. Families who didnt take part in programme were control. Patients in both groups took antipsychotic medication
-Found families who had been through programmed showed significant decrease in number of critical comments made about the patient and in emotional over-involvement both major characteristics of high EE.
78% of patients in control readmitted to hospital at least once but only true for 14% of programme group

Meta analysis NCCMH:
-32 studies , approx 2500 ppts
Significant evidence for effectiveness of family intervention
Compared to patients receiving standard care there was reduction in hospital admissions during treatment and less severe symptoms for 2 years following
Relapse rate for FI patients was 26% vs control 50%

Pharaoh et al meta analysis
-Review of 53 studies
Studies were conducted in Europe, Asia and North America
-FI may reduce risk of relapse
FI patients compliance with medication
Improvement in mental state and general social functioning but no effect on things like independence and employment.

97
Q

AO2 for Family intervention

A

Leff et al:
supports and suggests good long term treatment when combined with drugs.

Meta Analysis NCCMH + Pharaoh support

Methodological limitations of studies:

  • randomisation claim but large number of studies were from peoples republic of China where its emerged that random allocation was stated as having been used when it wasn’t- Wu

Lack of blinding- possibility of observer bias where raters were not blinded to condition FI vs standard care . 10 studies reported that no form of blinding was used and further 16 didnt mention whether it had.

Appropriateness:
McCreadie et al- 63 relatives of 52 schizophrenics living at home offered a package of treatment by professionals who worked in NHS. These were educational seminars, relatives groups and family meetings. 32 relatives refused intervention 14/31 that aggress didnt attended the educational seminars nor relative groups. Shows ppts dropping out and shows family intervention may not be an effective treatment as it may be too much effort for families or difficult for them to open up.

Family intervention also doesn’t consider adults who are not living at home and orphans.

Economic benefits:
Family intervention makes patient more compliant to drugs as it costs the NHS. Means less money spent on drugs and less admission to hospitals which will reduce costs for NHS in future as less wastage on drugs that cause relapses.

FAMILY INTERVENTION IS NOT A SUBSTITUTE TREATMENT

Psychology A2 (6 decks)

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