schizophrenia Flashcards

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1
Q

ICD

A

21 chapters, in which only one chapter is dedicated to mental health.

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2
Q

DSM

A

Produced by the American Psychiatric Association and is the dominant manual in the US (also used elsewhere). The DSM classifications have to be used in the US to make diagnosis. The most recent edition is the DSM 5 (2013).

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3
Q

The main goals of the DSM 5

A

assist clinicians
identify treatment
to provide better care for patients.

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4
Q

Why is the DSM revised

A

discovery of new disorders
improving consistency of diagnosis
for a greater understanding of already known disorders.

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5
Q

Why s the DSM 5 better than DSM 4

A

breaks downs into more specific categories so they can be better treated. It is more precise.

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6
Q

5 Diagnostic Criteria from DSM-5

A
dellusions
hallucinations 
disorganised thinking (speech)
grossly disorganised/catatonic behaviour
negative symptoms
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7
Q

describe delusions

A

fixed false beliefs resistant to change despite contrary evidence. May be thought withdrawal, thought insertion or delusions of control. (positive symptom)

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8
Q

describe hallucinations

A

Perception-like experiences with no external stimulus. Often auditory but could be other senses; smell or sight. (positive symptom)

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9
Q

describe disorganised thinking (speech)

A

Disorganised thought shown through speech. Involves switching topics illogically, irrelevance and incoherence. (positive symptom)

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10
Q

describe grossly disorganised/catatonic behaviour

A

Unpredictable behaviour. Catatonic refers to decrease in reactivity to the environment, i.e. rigid posture, lack of verbal or motor responses. (positive symptom)

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11
Q

describe negative symptoms

A

Reduced emotional expression- lack of eye contact, facial expressions, body language. Avolition: decrease in motivation and self-initiated purposeful actions. (Level of functioning in one or more major areas i.e. work, personal relations or self-care must have diminished for diagnosis)

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12
Q

type 1 schizophrenia

A

Positive symptoms

In some way adding to the sufferer’s personality

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13
Q

type 2 schizophrenia

A

Negative symptoms

Taking away from the sufferer’s personality

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14
Q

Reliability of Diagnosis (5 points)

A
  • How do clinicians diagnose patients with an illness?
  • Reliability is necessary but not sufficient for validity of diagnosis as consistent diagnoses may still all be incorrect.
  • Inconsistent classification systems could lead to unreliable diagnosis as they will create different diagnoses for the same patients.
  • Inter-rater reliability: Clinicians all reaching the same diagnosis- consistency of diagnoses.
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15
Q

Validity of Diagnosis

A

How is schizophrenia and its symptoms defined?
There is no physical sign characterises schizophrenia, diagnoses relies on observation of speech and behaviour.
The disorder has to be meaningfully classified - this is asses in three ways:
-descriptive validity
-aetiological validity
-predictive validity

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16
Q

descriptive validity

A

Are the symptoms right?
Defining medical illness through symptoms.
Patients with very different symptoms can all be diagnosed with schizophrenia i.g. type 1 and type 2 symptoms.
It may be better to treat all symptoms separately instead of the vague label of schizophrenia.

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17
Q

aetiological validity

A

Can mechanisms/causes be identified?

You can argue an illness is well defined if using evidence from causes and mechanisms.

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18
Q

predictive validity

A

What is the prognosis/reaction to treatment?

How the illness has progressed over time and predict how they react to treatments.

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19
Q

3 issues in classification of diagnosis

A
  • Reliability is necessary but not sufficient for a diagnosis to be valid – consistent diagnoses might all be consistently incorrect.
  • Inconsistent classification systems may lead to unreliable diagnosis as different classification may not give the same diagnosis – differences for the same people (not valid due to unreliability)
  • We gain reliable diagnoses when two or more clinicians give the same diagnosis (inter-rater reliability)
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20
Q

3 factors affecting reliability of diagnosis

A

Differences in procedures (e.g. use of classification systems)
Differences between clinicians; subjective interpretation
Difference between patients

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21
Q

Elaborate on Differences in procedures (e.g. use of classification systems) (4 points)

A
  • If different clinicians use different classification systems, they are likely to make different diagnoses.
  • Was a problem in the past because doctors used different diagnostic criteria in different parts of the world (DSM is dominant in US)
  • Cooper (1972) : American clinicians diagnosed SZ twice as often and British clinicians diagnosed mania and depression twice as often when shown the same video clip.
  • ICD allows diagnosis with symptoms within the last month, but DSM-5 insists on some symptoms being present for 6 months
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22
Q

Elaborate on Differences between clinicians; subjective interpretation (2 points)

A
  • Even if the same classification systems are being used, clinicians may interpret what they say differently.
  • example: DSM-5 states that delusions must be ‘bizarre’, which is a subjective phrase
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23
Q

Elaborate on Difference between patients (3 points)

A
  • Patients may act differently on different days, or differently to different doctors (empathy, warmth, friendliness, professionalism, gender, age, ethnicity)
  • It depends on their mood and the variability of their symptoms
  • This means a diagnosis could be different on different days
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24
Q

Improvements in reliability over time (2 studies)

A

Beck (1967) found that the inter-rater reliability between two psychiatrists diagnosing 154 patients was only 54%.
Cooper (1972) also found poor agreement between US and UK clinicians.
These two studies are dated and studied DSM-2, which was much weaker than subsequent editions – it was much vaguer and this meant that low reliability was likely.
Reliability improved with DSM-3 (1980) by removing the vague descriptions and clarifying how many and which symptoms were needed for a diagnosis.
Studies found that consistency for the diagnosis of SZ increased to 81%, which suggests an improved from DSM-2.

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25
Q

what makes a diagnosis valid

A
  1. Reliably defined/classified and diagnosed

2. Validly defined or classified

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26
Q

Brief outline of the genetic explanation

A

We inherit 50% of our genes from each parent. Genes are chemical ‘codes’ for construction of cells, including those in the brain.
The Brain is the source of all mental states therefore impacting disorders of mental state (schizophrenia).
If genes determine brain structure then we will inherit psychological traits- schizophrenia may be heritable.

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27
Q

liability threshold model

A

The idea that schizophrenia is not the result of a single gene or even that a combination of genes is the sole cause of schizophrenia. The more schizophrenia related genes you have the greater your chance of developing it.

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28
Q

molecular genetics

A

The link between specific genes and schizophrenia.

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29
Q

molecular genetics (Glatt et al)

A

association between the dopamine D2 receptor gene and schizophrenia. (30% increased chance)

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30
Q

Gottessman review

A

Based on 40 studies. Compared MZ twins reared together (concordance rate=48%), MZ twins reared apart (concordance rate= 58%), DZ twins reared together (concordance rate 17%).

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31
Q

Kendler

A

MZ twins reared together (concordance rate=53%), DZ twins reared together (concordance rate=15%)

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32
Q

Cardno

A

MZ twins reared together (concordance rate=50%), DZ twins reared together (concordance rate=4.1%)

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33
Q

Summary of twin studies

A

MZ twins have significantly higher concordance rates.

The more genes twins share the higher the concordance rate.

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34
Q

How does Gottessman support the genetic explanation

A

MZ twins separated at birth is higher than those reared in the same environment which provides strong evidence for the genetic explanation as it was not environmental factors that caused onset of schizophrenia.

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35
Q

Tienari

A

(Finland) Adopted children of schizophrenic mothers had a 7% chance of developing schizophrenia compared to a control group (adopted children with non-schizophrenic mothers) who had a 1.5% chance.

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36
Q

Wahlberg

A

Reevaluated Tienari, found environmental factors had significant impact in the development of schizophrenia (families with poor communication)

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37
Q

Kety

A

(Denmark) High rates of schizophrenia found in adopted children whose biological mothers had schizophrenia even if adopted by ‘healthy’ parents.

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38
Q

general trend in adoption studies

A

The general trend suggests that biological children of schizophrenic parents are at greater risk of developing the disorder. This suggests genetics have significant impact in development of schizophrenia.

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39
Q

methodological issues in adoption studies (2)

A
  • Adoptive parents likely to be aware of mental illness in biological parents. This means these children are at greater risk of being in psychologically harmful environments as better informed parents may not adopt these children.
  • Therefore similarities between biological mothers and their children is better explained by environment.
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40
Q

summary of the dopamine hypothesis

A

Biochemical abnormalities causing schizophrenia-a result of over-activity in parts of the brain controlled by dopamine.

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41
Q

limbic system summary

A

limbic system –> dopamine (neurotransmitter) –> regulates emotion

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42
Q

How would disturbances in the limbic system contribute to schizophrenia?

A

Disturbances/irregularities in this system may lead to abnormalities. As dopamine regulates emotion it may contribute to paranoia and hallucinations notable in schizophrenia.

43
Q

3 ways in which dopamine activity would contribute to schizophrenia

A
  1. Supersensitivity of dopamine receptors
  2. Excess of dopamine receptors
  3. Increased synthesis and release of dopamine from pre-synaptic neuron.
44
Q

4 evaluative points of dopamine as a cause of schizophrenia

A
  1. Antipsychotics: symptoms stopped by drugs that block dopamine at the synapse. HOWEVER they do not work on everyone.
  2. Recreational use of amphetamines: Increased availability of dopamine and noradrenaline caused by use can induce symptoms of schizophrenia. HOWEVER this does not worsen symptoms in everyone.
  3. Postmortem evidence: Seeman found increased levels of dopamine in parts of the brain in schizophrenics. HOWEVER cannot identify causality, dopamine levels may be a result of drug therapy.
  4. Dopamine is unlikely to be the only factor in schizophrenia because it is implicated in a number of mental disorders.
45
Q

Diathesis Stress Mode (evaluation of biological explanation)

A

Biological factors alone do not lead to schizophrenia. Genes increase risk but will not schizophrenia will not develop without environmental factors. The genes are the diathesis as they put someone at risk, stressors are the environmental factors that determine who develops the disorder and when.

46
Q

evaluate both genetic and biochemical factors

A

when an individual is placed into a disturbed family environment they are much more likely to develop schizophrenia. Those who have a genetic vulnerability but were placed in an equally disturbed family unit did not develop schizophrenia.

47
Q

outline the cognitive explanation

A

Schizophrenia is characterised by thought disturbance. It can be suggested that disturbed thinking is the cause not consequence of schizophrenia. Mechanisms that function in a normal brain to filter out certain info are somehow inactive in schizophrenics. Thus too much irrelevant material is let in. This results in an overwhelming amount of info coming from external stimuli.

48
Q

Park et al : issues of causality

A

Working memory deficits identified in schizophrenics andf their first-degree relatives. This means they are present before the disorder develops. The cognitive impairment cannot cause schizophrenia alone, it must be a combination of factors. (diathesis-stress model).

49
Q

physiological malfunction

A

Physiological malfunction as a result of abnormalities.

A result of biological impairment.

50
Q

basic explnaation of Frith’s Cognitive Deficit Model

A

Deficit in central monitoring system → mistaking inner speech as hallucinations → positive symptoms

51
Q

Frith’s Cognitive Deficit Model: explanation of hallucinations and delusions and disorganised speech

A

A deficit in the Central Monitoring System results in hallucinations and delusions. The CMS identifies actions and thoughts as ‘done by me’. Frith claims that hallucinations occur when inner thoughts are not recognised as self-generated.
In addition Frith claimed that a faulty filtering process can be found in schizophrenic patients: an inability to filter out irrelevant thoughts and info.
This accounts for delusions, hallucinations and disorganised speech.

52
Q

Research evidence for Frith’s Cognitive Deficit Model

A

Frith and Drone: Conducted experimental fluency tasks. Compared with a control group schizophrenics with negative symptoms had great difficulty producing spontaneous responses. This supports as t shows an inibility to produce self-initiated response when negative symptoms are present.

53
Q

basic explanation of Shallice on negative symptoms

A

Defecit in the supervisory attention system → Lack of initiation of action → negative symptoms

54
Q

How does Shallice explain negative symptoms

A

Two types of action;
Self-willed- driven by ourself
Environmental stimuli driven actions
Shallice states that patients with negative symptoms have a deficit in the ‘supervisory attention system’. The supervisory attention system is the cognitive process responsible for self-initiated actions.
This deficit can be seen as the cause for negative symptoms such as lack of volition, poverty of speech, social withdrawal.

55
Q

research evidence for Shallice

A

Bentall et al: When asked to generate category items/read out category items schizophrenic patients with symptoms performed worse than patients without hallucinations. Overall, all schizophrenic patients performed worse than the control group. The fault in the CMS that results in hallucinations indicates hallucinating patients have issues with memory.

56
Q

evaluation of Shallice

A

A laboratory experiment was used; the results will lack ecological validity as the study produces simplistic results which do not represent complex schizophrenic symptoms in real life.

57
Q

diathesis stress model and cognitive deficit

A

genetic vulnerability→biochemical abnormality→cognitive deficit + stressful life events
= development of psychotic symptoms

58
Q

the schizophrenogenic family

A

Fromm-Reichmann
Describes families with high emotional tension, secrets, close alliances and conspiracies. Often a cold, domineering mother who is manipulative and conflict causing, may cause the child to feel resentment and distrust. This could lead to the psychotic symptoms of schizophrenia.

59
Q

the double-bind (6 points)

A

-Bateson et al
-Double-bind = emotionally distressing situation in which an individual receives conflicting messages. i.e. mother tells child she loves him whilst looking away in disgust.
-Creates a situation where the individual’s response is never correct.
-This is two conflicting messages- affection on the verbal level and hostility on a nonverbal level.
-As the child is dependent on the mother the child is unable to comment on the occurrence of contradiction.
This happens when they cannot comment on occurring contradiction nor escape it.

60
Q

how does the double-bind theory cause schizophrenic symptoms? (3)

A
  1. Individual learns to perceive everything in contradictory ways.
  2. Any environmental input is seen as conflicting information where they are unable to discriminate between different communicative levels.
  3. This inability embodies itself in symptoms such as delusions and hallucinations, incoherent thinking and speaking.
61
Q

overall trend for research support for the double-bind theory

A

no strong evidence

62
Q

studies in support of double-bind theory (+ evaluation)

A

Mischeler: Observed daughters with schizophrenia and their mothers. Mothers tended to be cold and unresponsive. Same mothers were normal & responsive whilst talking to healthy daughters. HOWEVER, this study is weak as the schizophrenic patient can cause poor communication.
Berger: The schizophrenic sample (¼ of participants) reported higher levels of double-bind statements by their mothers than the non-schizophrenic control groups. HOWEVER, this relied on retrospective info which may be inaccurately reported - retrospective interference. In addition schizophrenic reports may be impacted by delusions.

63
Q

theories not in support of double-bind theory

A

Liem: Found no difference in patterns of parental communication between families of a schizophrenic child and control groups.

64
Q

define expressed emotion (EE)

4 points

A
  • Qualitative measure of ‘amount’ of emotion displayed in families.
  • Measures the family environment: how the relatives of a psychiatric patient spontaneously talk about the patient
  • High levels of EE may worsen the onset of schizophrenia/ act as a potential risk for onset.
  • EE is often identified using The Camberwell Family Interview (CFI).
65
Q

summary of Camberwell Family Interview and how it identifies EE
(3 points)

A
  • Answers to questions and non-verbal cues determine if someone has high expressed emotion.
  • The patient’s perception of how the family feels about them and the disorder is also rated (i.e they are not caring enough or too protective)
  • This attitude may cause the patient to relapse.
66
Q

3 dimensions of EE

A
  1. Hostility
  2. Critical comments
  3. Emotional over involvement
67
Q

Hostility (EE)

A

A negative attitude directed at patient as family blame them for not getting better. Patient is scapegoated as cause of family issues.

68
Q

Critical Comments (EE)

A

Relatives feel the patients is wholly/partly responsible for the disorder.

69
Q

Emotional Over Involvement (EE)

A

Family member blames themselves for the disorder. They show great concern/pity for the patient. The pity may cause stress for patient, resulting in relapse to cope with the pity.

70
Q

Research evidence in support of EE (2)

A

Brown: Patients with schizophrenia returning to high EE homes showed greater tendency to relapse than those returning to low EE homes.
Vaughn and Leff: (supports Browns) 51% relapse in high EE homes. 13% relapse in low EE homes. Relapse rate increased when greater face-to-face time was spent with high EE relatives.

71
Q

Evaluation of EE

A

Correlational research: High EE may reflect consequences of living with severely disturbed individual rather than having any causal significance. For example; high EE is less common in families of first-episode patients. This suggests high EE develops in response to burdens of living with a sufferer of schizophrenia.
-This does not rule out the idea that high levels of EE results in re-admission.

72
Q

practical applications of EE

A

EE is an established maintenance model of schizophrenia. It educates family members in controlling levels of EE to reduce chances of relapse in the patient, aiding treatment.

73
Q

diathesis stress model on EE

A

EE as an explanation on its own is not sufficient. Integrated with genetic factors, biological vulnerability, a biochemical abnormality and cognitive deficit.
High EE acts as a trigger in the individual as they are left vulnerable by other factors.

genetic vulnerability→biochemical abnormality→cognitive deficit + high EE
= development of psychotic symptoms

74
Q

Examples of typical anti-psychotics

A

Chlorpromazine (low potency), Haloperidol (high potency)

75
Q

URAP (typical anti-psychotics)

A

USE: Reduce positive symptoms.
RATIONALE: Based on the idea schizophrenia is caused by excess dopamine activity at certain synaptic sites.
AIM:Chlorpromazine reduces dopamine activity at receptor sites.
PROCESS: Blocking D2 dopamine receptors, reduces ability of dopamine to bind to post synaptic receptor, lessening the response.

76
Q

Examples of a-typical

A

Clozapine, Resperidone

Newer drug therapies that reduce side effects but are equally effective.

77
Q

URAP (atypical anti-psychotics)

A

USE: Reduce both positive and negative symptoms with fewer side-effects.
RATIONALE: Based on the idea schizophrenia is caused by excess dopamine activity at certain synaptic sites. Also re-balance other neurotransmitters associated with schizophrenia i.e. serotonin. Target serotonin and dopamine receptors in the brain.
AIM: Target serotonin and dopamine receptors in the brain. Precise biochemical mechanisms are unknown but they appear to impact serotonin receptors by blocking them.
PROCESS: Precise biochemical mechanisms are unknown but they appear to impact serotonin receptors by blocking them.

78
Q

FOR drug therapies (2)

A
  • patients do not have to spend long in psychiatric wards

- reduction in positive (and negative symptoms)

79
Q

AGAINST drug therapies (6)

A
  • Do not cure, simply put off symptoms
  • 30% of patients do not respond to medication
  • 40% relapse rate
  • Minor and extreme side effects
  • About ½ of patients taking antipsychotics stop after a year as side effects are too severe.
  • Clozapine can reduce white blood count, this weakens immune system.
80
Q

APPROPRIATENESS of drug therapy (how suitable)
Side Effects
(3)

A
  • Clozapine reduces white blood cell count which weakens the immune system, rarely, but can result in death.
  • Dry mouth, dizziness, blurred vision, low blood pressure.
  • Dysfunction of nerve tracts = side effects that mimic symptoms of parkinson’s disease i.e. involuntary muscle contraction.
81
Q

APPROPRIATENESS of drug therapy (how suitable)

Compliance

A

Some patients have trouble remembering to take medication .This can be helped with depot injections every few weeks. This creates a depot that slowly releases medication into the body.

82
Q

APPROPRIATENESS of drug therapy (how suitable)

Ethics

A

People may not want their lives dominated by drugs.
They are able to chose whether or not they wish to continue with their course of medication if side effects have too much of a negative impact.

83
Q

EFFECTIVENESS of drug therapy

Research Findings

A

Cochrane Review 1: Effectiveness of chlorpromazine is short to medium term. Improves symptoms.
Cochrane Review 2: Lower relapse rate with clozapine than typical antipsychotics. Fewer motor effects with clozapine. Better long term.

84
Q

EFFECTIVENESS of drug therapy

Reduction in Symptoms

A

Rapid reduction in symptoms

Decreased stay in hospital

85
Q

EFFECTIVENESS of drug therapy

Relapse

A

Chlorpromazine reduces only positive symptoms
Clozapine also reduces negative symptoms
30% of patients don’t respond to drugs
Relapse almost certain if patients stops taking medication

86
Q

Cochrane - Review of Chlorpromazine

method, results, evaluation

A

Method:
-Meta-analysis of 302 studies in the effectiveness of chlorpromazine
-All used placebo
-All used random allocation to conditions
Results:
Chlorpromazine reduces relapse in short and medium term, but less so for long term.
-Improves symptoms, functioning and probability of leaving treatment.
-Most common side effects: movement disorders, sedation and lower blood pressure.
Evaluation:
-Meta-analysis = reliable as results are less likely to be a fluke.
-Only used studies that used control groups and random allocation (well-designed)
-Placebos means results are not caused by participant reactivity.
-Random allocation = not selecting participants who are more likely to react well to medication.

87
Q

Cochrane - Clozapine vs Atypical Antipsychotics

9method, results, evaluation)

A

Method:
-Meta-analysis of 52 randomised control trials.
-44 were less than 13 weeks in duration.
Results:
-No difference between clozapine and typical drugs when comparing broad outcomes. (ability to work suitability for discharge at end of study)
-Symptom reduction was more frequent as well as fewer relapses in those taking clozapine.
-Clozapine was more effective as a long term treatment.
-For patients resistant to typical antipsychotics clozapine was more effective (34% of treatment resistant patients have clinical improvements)
Evaluation:
-More blood problems in those taking clozapine.
-Clozapine patients experiences more drowsiness, hypersalivation but less motor effects.
-The data is weak as conducting and reporting of trials that are prone to bias favouring clozapine.
-Clozapine is of higher potency that other drugs such as Haloperidol.

88
Q

URAP (electro convulsive therapy)

A

Use: To treat schizophrenia but now more common in treating depression.
Rationale: Schizophrenia is caused by abnormal activity of neurotransmitters/hormones.
Aim: The applied shock corrects abnormal activity of neurotransmitters/hormones.
Process:
1.Anaesthetic/muscle relaxants are administered.
2.Electric current applied through electrodes placed on either 1 or both sides of the head for 0.5 - 5 seconds
3.Takes place over several sessions across a number of weeks.

89
Q

research evidence for ECT

A

Tharyan and Adams - Cochrane Review:

Method: Meta-analysis of 26 studies.
Results:
ECT compared with sham ECT - more patients improved with real ECT (therefore not placebo effect)
ECT resulted in less relapse in short term than sham ECT
No evidence for medium/long term advantage
When compared with drug treatment results favoured drugs
Limited evidence showing ECT combined with drug therapy was more effective than drugs alone.
Conclusions:
For some schizophrenic patients ECT can act as a short term treatment.
When rapid reduction in symptoms is needed ECT combined with drug therapy may be beneficial to some.

90
Q

effectiveness of ECT

A

Use of sham ECT in studies shows its effectiveness. Real ECT resulted in decreased symptoms and reduced relapse rate.
The benefits are not long term
Drug treatment tends to be more effective
Can be effective for those who do not respond to drugs
A quick way to reduce severe symptoms i.e. psychotic episode

91
Q

appropriateness of ECT

Side Effects

A

Cognitive deficits

Memory loss that can last up to 6 months

92
Q

appropriateness of ECT

Ethical Issues

A

Memory loss can be upsetting, confusing and disruptive to patients lives
Can be given without consent - on agreement of 2 doctors and a social worker when patient is at serious risk to their own health.

93
Q

URAP (cognitive behavioural therapy)

A

Use: Treat schizophrenia.
Rationale: Based on the idea schizophrenia is caused, or maintained by the patient’s irrational thoughts.
Aim: Address and change the patient’s beliefs and thoughts that contribute to symptoms.
Process:
1. 12-20 sessions with patient and therapist.
2. COGNITIVE ELEMENT- make patient aware of cognitions and how they impact functioning. Trying to challenge and question irrational beliefs.
3. BEHAVIOURAL ELEMENT - reality testing, role-play, homework.
This may be done with Ellis’ ABC model to organise patient’s confusing experiences.

94
Q

Ellis’ ABC model

A

A- Activating Event (example - voices)
B- Beliefs (example - ‘’voices are controlling my life’’)
C- Consequences (example - sorrow, loneliness)
The therapist challenges beliefs by testing evidence for and against.
GOAL SETTING - Using consequences of ABC model to encourage change. Goals must be realistic and achievable, revisited during at end of therapy.
NORMALISATION TECHNIQUE - Understanding the patients delusions. Discussing beliefs in a form that it could occur. Clarify the belief is not unfounded but also not specific to the person - i.e. an irrational fear.
The therapist must gain trust by being non-judgemental.

95
Q

research support for CBT

A

Startup et al:
Method: Random allocation of 90 patients with schizophrenia suffering from acute episodes to either standard care (nursing and drug therapy) or standard care + CBT. Symptoms and social were assed upon arrival, 6 months later and 1 year later.
Results: Control group showed 40% significant improvement and 17% showed deterioration from admission assessment.
CBT group showed 60% significant improvement, fewer negative and positive symptoms. 0% showed deterioration from admission assessment.
Evaluation: Random allocation strengthens the study.

96
Q

research support against CBT

A

Jones et al (Cochrane review)
Findings:
No overall difference between CBT and other talking therapies.
Relapses and re-hospitalisation were not reduced.
Fewer people left CBT trials early compared to drug trials - suggests CBT may be a more effective way of maintaining treatment for people schizophrenia.
CBT may however, have long term advantages for dealing with emotions and stress.

97
Q

effectiveness of CBT

A

Symptom reduction/relapse prevention:
Startup et al: ECT (w. nursing and drugs) was more effective than nursing and drugs alone.
Jones et al: Symptom reduction no different from other talking therapies.
Overall effectiveness:
Could aid compliance with treatments.

98
Q

appropriateness of CBT

A

Not a cure:
Normalises symptoms, does not cure them.
Ethics:
More ethical than treatments like ECT and drugs. It requires active cooperation from patient.
Overall appropriateness:
Most appropriate in collaboration alongside other therapies such a drug therapy.

99
Q

URAP (family intervention)

A

Use: To treat schizophrenia.
Rationale: High levels of EE in the patient’s family home leads to more frequent relapse.
Aim: Reduce levels of EE in the home and help develop cooperating and trusting relationships within families.
Process:
1.Therapist provides info on cause, course and symptoms of schizophrenia.
2.Family members discuss experiences of living with the disorder.
3.Family learn constructive means of communication and interaction to reduce emotional climate.
4.Discussion of how to deal with emotions such as anger and impatience without high EE.
5.Family and individual trained to recognise early signs of relapse so they can respond rapidly to reduce severity.

100
Q

research support for effectiveness of family intervention

A

Pharoah et al (EFFECTIVENESS)
Method:
Meta-analysis of 53 studies looking at effectiveness of family intervention.
Studies from; Europe, Asia and North America.
Compared outcomes of standard care and family intervention.
Results:
FI reduce risk of relapse compared to standard care.
Fi increases compliance with medication.
Some improvement in general functioning but no significant impact i.e. ability to live independently or employment.

101
Q

Evaluating Family Intervention Studies:

A

Problem with randomisation: All 53 studies claimed to use random allocation, it emerged than in China it actaully wasn’t. (Wu 2006)
Lack of blinding: Researchers were not blind to conditions meaning researcher bias could have occurred.

102
Q

Evaluating appropriateness of family intervention

A

McCreadie et al:
Findings:
-63 relative of 52 schizophrenics offered family intervention in an NHS setting.
-32 relative refused.
-14/31 other relatives turned up after agreeing to participate.
Conclusions:
-FI lacks appropriateness as this study demonstrates it is hard for everyone to commit, many also do not wish to participate.
-It may make relative feel responsible for the schizophrenia.

103
Q

economic benefits of FI

A

Expensive therapists, however relapse rate is lowered = lowered costs, also reducing wasted medication

104
Q

How many symptoms must you have and for how long to be diagnosed with schizophrenia according to the DSM 5

A

2 symptoms

at least 1 from hallucinations, delusions, disorganised thoughts (speech)