schizophrenia Flashcards

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1
Q

what are positives symptoms

A

hallucinations
delusions

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2
Q

what are negative symptoms

A

avolition
speech poverty

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3
Q

what is avolition

A

lose of ability to perform basic actions

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4
Q

definition of reliability in term of diagnosis

A

If diagnosis is reliable then a diagnosis is consistent over time and by different psychiatrists. When two independent psychiatrists agree on a diagnosis of schizophrenia this is referred to as high inter-rater reliability. If a diagnostic system is to be valid, it must also have high reliability. Clearly if a disorder cannot be agreed upon (so low reliability) then all of the different views cannot be correct (so low validity).

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5
Q

definition of validity in term of diagnosis

A

One way to assess the validity of a diagnosis of schizophrenia is criterion validity. This refers to using two different measures which diagnose schizophrenia and seeing if they arrive at the same diagnosis.
in the UK the two diagnostic systems are ICD (International Classification of Diseases and Related Health Problems) and DSM (Diagnostic and Statistical Manual of Mental Disorders). Their criteria have some differences.

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6
Q

criterea for DSM-5 for schizophrenai

A

Two or more of the following for at least a one-month (or longer) period of time
* Delusions
* Hallucinations
* Disorganized speech
* Grossly disorganized or catatonic behaviour
* Negative symptoms, such as diminished emotional expression
* One of the positive symptoms – hallucinations, delusions or speech disorganisation must be present for a diagnosis
No subtypes in DSM 5 – although did exist in previous versions

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7
Q

criterea for ICD-10 for schizophrenai

A

Minimum of one very clear symptom (and usually two or more if less clear-cut)

Therefore, a key difference with the DSM and the ICD is that two negative symptoms are sufficient under ICD.

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8
Q

opposing evidence for validity/reliability

rosenhan

A

Pseudopatients presented to 12 different psychiatric institutions with single symptom of hearing a voice saying ‘hollow, empty, thud’. Once admitted they behaved normally. All but one of the patients were given the label of paranoid schizophrenia with the other patient being labelled as bipolar.
Rosenhan did a follow up study where he told the psychiatric institutions that he would send them more pseudopatients. **After three months they were confident that about a third of the new patients they were sent were pseudopatients, however none had been sent.
**

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9
Q

opposing evidence for validity/reliability

Cheniaux et al

A

Two psychiatrists independently diagnosed 100 patients using DSM and ICD. One psychiatrist diagnosed 26 with Schizophrenia according to DSM and 44 according to ICD.

The other diagnosed 13 using DSM and 24 according to ICD. Not only do the two diagnostic systems not agree but different psychiatrists interpret the criteria differently.

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10
Q

4 factors affecting reliability and validity

A
  1. comorbidity
  2. gender bias
  3. symptom overlap
  4. cultural bias
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11
Q

comorbidity

factors affecting reliability and validity

A

Schizophrenia is commonly diagnosed alongside other conditions. 50% of schizophrenic patients also have depression, 47% also have substance abuse, 29% have PTSD, 23% have OCD

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12
Q

symptom overlap

factors affecting reliability and validity

A

There is considerable overlap between symptoms of schizophrenia and other conditions.
For example, both SZ and bipolar disorder have symptoms of delusions and avolition.
Using the ICD a patient is more likely to be diagnosed with schizophrenia, but the same patient may be seen as bipolar using the DSM.

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13
Q

gender bias

factors affecting reliability and validity

A

Men are more likely to receive a diagnosis of SZ than women. This may simply be because men are more genetically vulnerable than women.
However,* before 1980 there was no gender difference* in rates of schizophrenia which suggests there could be gender bias in how schizophrenia is now diagnosed.
Women with schizophrenia tend to function better, more likely to work and maintain good family relations. This could lead to women being underdiagnosed.

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14
Q

cultural bias

factors affecting reliability and validity

A

People of Afro-Caribbean origin are significantly more likely to be diagnosed with schizophrenia.
However, rates of schizophrenia in Africa and the Caribbean are not any higher than in Europe, suggesting that this is not due to an increased genetic vulnerability.
There must be cultural bias in how schizophrenia is diagnosed.
Hearing voices is acceptable in African cultures because of cultural beliefs about communication with ancestors.

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15
Q

supporting evidence for schizophrenia being polygenic

A

Ripke et al (2014) carried out a meta-analysis of genome-wide studies (studies looking at the whole human genome and not focusing on particular genes) of schizophrenia. **The genetic makeup of 37,000 patients with schizophrenia was compared to that of 113,000 controls. **
They found that there were 108 separate genetic variations linked with increased risk of schizophrenia. These candidate genes associated with increased risk included those coding for the functioning of a number of neurotransmitters including dopamine.

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16
Q

evidence to support the gentic explanation

meta-analysis

A

**Gottesman **(1991) carried out a very large –scale family study. He pooled the data from 40 European studies published between 1920 and 1987. He conducted a meta-analysis of the genetic influences on schizophrenia. he recorded relationship to person with SZ and risk of developing SZ
1. identical twins - 48%
2. fraternal twins - 17%
3. children - 13%

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17
Q

evidence to support the gentic explanation

adoption

A

Tienari et al (2004) found that children of schizophrenia sufferers are still at a heightened risk of developing the disorder even if adopted into families with no history of schizophrenia.

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18
Q

However, schizophrenia can occur in people without a family history of the disorder +supporting evidence

opposing to genetic explanation

A

One explanation for this is mutation in their parent’s DNA, e.g. in the father’s sperm cells. This could be caused by radiation, poison or viral infection. This mutated DNA is then passed on to the child, leading them to develop schizophrenia later on.
This is supported by Brown et al (2002) who found a positive correlation between paternal age (associated with an increased risk of sperm mutation) and risk of schizophrenia, increasing from around **0.7% with fathers under 25 to over 2% in fathers over 50. **

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19
Q

what is dopamine

A

Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centres. It is excitatory in that it increases brain activity. Stimulant drugs such as caffeine, cocaine and amphetamines increase dopamine activity in the brain, increasing feelings of alertness.
Dopamine also helps regulate movement and emotional responses. It enables us not only to see rewards, but to take action to move toward them (motivation)

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20
Q

original dopamine hypothesis

A

was based on the discovery that** anti-psychotic drugs that were used to treat schizophrenia (by decreasing dopamine levels) **helped to reduce symptoms e.g., hallucinations and delusions. They also led to symptoms similar to Parkinson’s disease (associated with low levels of dopamine)
Evidence for this also comes from that fact that amphetamines increase the amounts of dopamine. Large doses of amphetamine given to people with no history of psychological disorders produce behaviour which is very similar to paranoid schizophrenia. Small doses given to those with Schizophrenia can worsen symptoms.
This led to a belief that Schizophrenia is related to high levels of dopamine (Hyperdopamingergia).

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21
Q

what is high levels of dopamine callled

A

Hyperdopamingergia

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22
Q

what is low levels of dopamine callled

A

hypodopaminergia

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23
Q

updated version of the dopamine hypothesis

A
  • Abnormally high levels of dopamine (hyperdopaminergia) in the subcortex. Symptoms of speech poverty and auditory hallucinations can be explained by an excess of dopamine receptors in Broca’s area (responsible for speech)
  • Abnormally low levels of dopamine (hypodopaminergia) in the prefrontal cortex. This is the area responsible for thinking and decision making). This is ***associated with avolition and lack of motivation.
    *
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24
Q

supporting evidence for hyperdopamingeria

A

Wise & Stein (1973) carried out **post mortems of schizophrenia patients and found abnormally low levels of Dopamine Beta Hydroxylase (DBH)** in the brain fluid. DBH is an enzyme whose function is to break down the neurotransmitter dopamine after release.

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25
Q

supporting evidence for hypodopamingeria

A

Meador-Woodruff et al (1997) carried out post-mortem investigation of 16 patients who had suffered from schizophrenia and compared them to 9 controls. They found **dramatic decreases in dopamine receptors in the prefrontal cortex. **

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26
Q

However, there is evidence to suggest that dopamine does not provide a complete explanation for schizophrenia.

genetic

A

Some of the genes identified in Ripke’s genome study code for the production of other neurotransmitters, so** although dopamine plays an important role so do other neurotransmitters**. Current research is focused in investigating the role of a neurotransmitter called glutamate.

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27
Q

cause and effect is not clear

genetic SZ

A

We can’t assume that imbalances in dopamine in the brains of people with schizophrenia are causing the disorder. It could be that the abnormal thinking caused by the disorder affect the biochemistry of the brain.

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28
Q

neural correlates

A

patterns of structure or activity in the brain that occur alongside an experience (in this case symptoms of schizophrenia). Negative and positive symptoms have different neural correlates.

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29
Q

examples of neural correlates of SZ

A
  1. an excess of dopamine recpetors in brocas may be responsible for speech disruption and auditory hallucinations
  2. low levels of dopamine in the frontal cortex [responsible for thinking/decision making] may be responsible for the negative symptoms of sz
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30
Q

research evidence to support the neural correlates of schizophrenia

x2

A
  1. **Juckel et al **(2006) measured activity levels in the **ventral striatum **in schizophrenic patients and found lower levels of activity in this area compared to a control group. They also observed a negative correlation between activity levels in the ventral striatum and the severity of overall negative symptoms. They concluded that activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia.
  2. Allen et al (2007) scanned the brains of patients experiencing auditory hallucinations and compared them to a control group. The scans were conducted whilst the subjects identified pre-recorded speech of theirs or others. Results showed that lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group. They concluded that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.
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31
Q

correlation-causation problem

neural explantions of SZ

A

**Does the abnormal activity in a region of the brain CAUSE the symptom? Or do symptoms of SZ change the functioning of the brain? **For example there is a correlation between activity in the ventral striatum and negative symptoms. It could be that something wrong with the ventral striatum causes the symptoms. Or it could be that the *negative symptoms means that less information is processed by the ventral striatum, resulting in reduced activity. * Or there could be a third factor which influences both the ventral striatum and the negative symptoms.

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32
Q

psychological explantions - family dysfunction

briefly explained

A

Some psychologists have linked schizophrenia to family dysfunction. This means abnormal processes within a family such as poor family communication, cold parenting and high levels of negative emotion.

33
Q

Schizophrenogenic mother

psychological explantions of SZ

A

Fromm-Reichmann (1948) noted that many of her patients spoke of having a **particular type of mother. A schizophrenogenic (schizophrenia causing) mother is cold, rejecting and controlling, and creates a family climate characterised by tension and secrecy**. This leads to distrust that later develops into paranoid delusions (the belief that someone/something is out to get you) and eventually schizophrenia.

34
Q

double bind

psychological explantions of SZ

A

This theory emphasises the role of communication style within a family. The child regularly finds themselves in a situation where they fear doing the wrong thing, but receive mixed messages about what this is, and feel unable to ask for clarification. When they* ‘get it wrong’ (which is often) they are punished by the withdrawal of love. This leaves them feeling that the **world is confusing and dangerous, leading to symptoms of disorganised thinking and paranoid delusions. ***

35
Q

expressed emotion

psychological explantions of SZ

A

This is the level of emotion, particularly negative emotion, expressed towards an individual. This includes verbal criticism and sometimes violence, hostility, anger and rejection, emotional over involvement and needless self-sacrifice. These expressed emotions are very stressful and may **lead to relapse or indeed trigger schizophrenia in high risk individuals. **

36
Q

supporting evidence for family dysfunction

x2

A
  1. **Read et al **found that 69% of females and 59% of males with SZ had experinced SA, physical abuse or both during childhood [HOWEVER DOESN’T EXPLAIN WHY ONSET IS 18-22]
  2. Linzen et al found that a patient who returned to a family high in hostility, criticism and emotional over-involvement are 4x more likely to relapse
37
Q

opposing evidence for family dysfunction

x2

A

1.** Mischler and Waxler** found significant difference in the way mothers spoke to their SZ daughters compared to their healthy daughters. this suggests dsyfunctional communication may be the result of living with a person with SZ
2. reseach into family dsyfunction tends to be carried out after development of symptoms. the experince of having SZ [so can sudder from delusions] could distort recall of childhood experinces

38
Q

what are the two cognitive explanations for SZ

A
  1. Problems with Metarepresentation
    2.Problems with Central control
39
Q

Problems with Central control

cognitive explanations for SZ

A

Central control is the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Automatic thoughts pop into our heads all the time but we are able to choose not to express them and can dismiss them. This ability seems to be malfunctioning in the brains of individuals with schizophrenia.
They have disorganised speech because they can no longer suppress every little thought. Each word can trigger new associations and ideas and therefore they experience derailment of thoughts and speech.

40
Q

Problems with Metarepresentation

cognitive explanations for SZ

A

Metarepresentation is our ability to reflect upon our own thoughts and behaviour. This allows us to understand why we say and do things and also helps us to make sense of the behaviour of others. If this processing system stops functioning we fail to recognise our thoughts and actions as being our own. We lose self-awareness.
Therefore, individuals may interpret a tune in their head as coming from an external source such as the radio or believe that a moment of self-doubt is a voice from outside. **They may believe that their own inner speech is being sent from outside themselves and is therefore experienced as a hallucination. **

41
Q

supporting evidence for dysfunctional information processing.

cog

A

**Stirling et al **(2006) compared 30 patients with schizophrenia with 18 people without schizophrenia on the Stroop test which involves naming incongruent ink colours of colour words by suppressing the impulse to read the words. The schizophrenic patients took more than twice as long to name the ink colours than the control group suggesting they had central control dysfunction.

42
Q

descriptive

cog explanation of SZ

A

While the links between faulty cognitions and symptoms of schizophrenia are clear, it only really describes what the cognitive processing of someone with schizophrenia is like. It doesn’t tell us anything about the cause of these dysfunctional cognitions. Genetic, neurochemical and neuroanatomical factors might better explain why some people have a tendency to think like this and others don’t.

43
Q

causality

cog explanation of SZ

A

These cognitive factors could be causing the symptoms of schizophrenia or the faulty thinking could be a symptom or effect of having the disorder.

44
Q

practical apllications in terms of a study

cog explanation of SZ

A

Yellowlees et al. (2002) developed a machine that produced virtual hallucinations, such as hearing the television telling you to kill yourself or one person’s face morphing into another’s. The intention is to show schizophrenics that their hallucinations are not real.
They found that 76% of users said that it improved their understanding of their auditory hallucinations and 69% thought it improved their understanding of visual hallucinations.
This suggests that understanding the effects of cognitive deficits allows psychologists to create new initiatives for schizophrenics and improve the quality of their lives.

45
Q

what are typical antipsychotics

biological therpay

A

These are older types of drugs, used since the 1950s. They work as dopamine antagonists (reduce dopamine activity) by blocking dopamine receptors in the synapses in the mesolimbic pathway, reducing positive symptoms such as auditory hallucinations. An example of a typical antipsychotic is Chlorpromazine which not only treats the symptoms of schizophrenia, it also acts as a sedative and was often used to keep patients calm.

46
Q

what are atypical antipsychotics

biological therapy

A

These have been used since the 1970s. They were developed in response to concerns about the serious side effects associated with the typical antipsychotics. There are several different atypical drugs which work in different ways. For example:
Clozapine binds to dopamine receptors in the same way typical antipsychotics do but also act on serotonin and glutamate receptors. This not only treats psychotic symptoms but also improves mood and reduces depression and anxiety in patients. This is often prescribed when a patient is considered at high risk of suicide.

47
Q

evidenc for effectiveness of typical antipsychotics

A

Thornley – placebo and Chlorpromazine, 1121 patients, 13 trials - Chlorpromazine associated with better overall functioninbbg and reduced symptom severity, in 312 patients relapse rate was lower

48
Q

side effects of Chlorpromazine

eval.

A
  1. can result in **tardive dysleinsia **which is caused by dopamine supersensitivity which is involuntary facial movements e.g blinking
  2. neuroleptic malignant syndrome - drug blocks dopamine in the hypothalamus which results in high temp, delirium and coma’s
49
Q

evidenc for effectiveness of atypical antipsychotics

A

meltzer conclude clozapine more effective than typical - effective in 30-50% of treatment resistant cases

50
Q

side effects of clozapine

eval.

A

led to agranulocytosis- low amount of white blood cells, WBC’s fight infections and disease

51
Q

Problems with the evidence for effectiveness of drug therapy

A
  1. some results are inconclusive bc some patients respond better to particular medication than others
  2. data published multiple times - bc makes the drug seems more effective than they are
  3. anti-psychotics have calming effects, so benefits may not be as good as we think – e,g may improve sleep not hallucinations
52
Q

the ‘chemical cosh’ arg

drug therpay

A
  • ‘chemical straightjackets’ - unethical, people who’ve been senctioned can be forced to take drugs – MAY BE USED AS A FORM OF SOCIAL CONTROL TO KEEP DIFFICULT PEOPLE PASSIVE; patient may not want it but be forced to take it
53
Q

CBT for SZ

specific form of cbt

A

Tarrier et al (1990) devised a specific form of CBT for schizophrenia known as Coping Strategy Enhancement (CSE) which focuses on building on schizophrenic patients’ existing coping strategies. Tarrier noted that even before therapy patients were able to identify triggers for schizophrenic episodes and had devised their own coping strategies. Examples of triggers would be things like certain people (e.g. a parent), being on their own, being put under stress. The aim of CSE is to develop and apply coping strategies for the psychotic symptoms and the accompanying stress they produce.

54
Q

examples of strategies in CBT for sz

A
  1. relaity testing and challengeing delusions - finding evidnece to dispute
  2. behaviour tasks eg distraction tasks – listening to music
  3. psychoeducation - help client understand their hallucinations are a resuklt of malfunctioning metacognition
55
Q

different aspects to CBT for SZ

+brief explanaitions

A
  1. Develop a rapport with the client. As paranoia is common with schizophrenia, it is essential that trust is established between client and therapist.
  2. Identify triggers of psychotic symptoms as well as reviewing existing coping strategies and developing new ones. Clients will have periods when their symptoms are chronic. The therapist and client will work together to establish patterns and triggers for these chronic episodes. Clients may keep a diary in between sessions to help them recognise what happens on a ‘good day’ or a ‘bad day’. E.g. social isolation might be associated with ‘bad days’ and could trigger a psychotic episode.
  3. Target specific symptoms and find strategies to deal with them. These might include distraction techniques such as listening to music to cope with the voices or doing an activity which is engaging.
    4.** Help the patient to identify irrational thoughts and reality test them by discussing how likely it is that the beliefs are true**. The therapist and client might also find alternative and less threatening possibilities.
56
Q

how does CBT help SZ

A

During CBT, patients can be helped to make sense of how their delusions and hallucinations impact on their behaviour and where these symptoms may come from i.e. their experiences, their triggers and their beliefs.
This greater understanding and explanations for their delusions and hallucinations can help to reduce fear and anxiety in the patient. The aim is not to eliminate symptoms but to help individuals cope with their experiences, reduce distress and improve their ability to function.

57
Q

evidence for effectiveness of CBT

A

Jauhar et al (2014) reviewed the results of 34 studies of CBT for schizophrenia. They concluded that CBT has a significant but fairly small effect on both positive and negative symptoms.

58
Q

CBT can be combined with drug therapy

eval of CBT

A

Tarrier et al (2004) compared 315 patients who were randomly allocated to different groups. A combination of** medication and CBT or medication and counselling or medication only**. Patients in the two combination groups showed fewer symptoms than the medication only group, supporting the usefulness of CBT in treating schizophrenia as part of a combined therapy.

59
Q

CBT doesnt cure SZ

eval of CBT for SZ

A

CBT aims to make schizophrenia more manageable and improve patients’ quality of life. CBT helps by allowing patients to make sense of and challenge some of their symptoms. However, none of these cure schizophrenia.

60
Q

reality testing may not work

eval of CBT for SZ

A

Delusions are a key characteristic of symptoms for many clients. Delusions, by nature, can be very resistant to logic. For example, if a client has paranoid delusions then challenging these delusions may make the client begin to mistrust the therapist too. They may believe the therapist is conspiring with the persecutors. This is a real risk and a therapist that challenges the delusions too vigorously may lose the trust and cooperation of the client. So, drug therapy might be more appropriate and effective in some cases.

61
Q

alternatiev psychological therapies

eval of CBT for SZ

A

There are other therapies available that can be helpful for some people with schizophrenia that are less likely to be available to patients. For example, the National Institute for Health and Clinical Excellence recommends art therapy. However, there are few qualified art therapists with experience of working with people with schizophrenic available.

62
Q

aim of family therapy

A

aims to improve quality of communication between family members and to reduce the family dysfunction which may be the root cause of schizophrenia. Family therapists are especially concerned with reducing stress within the family which could contribute to a patient’s risk of relapse, in particular levels of expressed emotion.

63
Q

range of strategies in family therapy

[dont need all, name 3]

A
  • Forming a therapeutic alliance with all family members
  • Reducing stress of caring for relative with schizophrenia
  • Improving ability of family to anticipate and solve problems
  • Reduction of anger and guilt in family members
  • Helping achieve a balance between caring for someone with schizophrenia and maintaining own lives.
  • Improving families’ beliefs and attitudes towards schizophrenia.
64
Q

supporting evidence for family therapy

+ added benefit

A

* Pharoah et al (2010) found that family therapy significantly reduces hospital readmission over the course of a year and improves quality of life for patients and their families.
* Anderson et al. (1991) found a* relapse rate* of almost 40% when patients had drugs only, compared to only 20 % when Family Therapy was used and the relapse rate was less than 5% when both were used together.

  1. economic benefits as it reduces relapse rates, so patients are less likely to take up hospital beds and resources
65
Q

not a cure

family therapy

A

Family therapy helps by reducing the stress of living with schizophrenia for both the patients and their families. It doesn’t cure schizophrenia but may be effective in preventing relapse in patients who have also received another type of therapy such as antipsychotic drugs or CBT.

66
Q

increasing awareness

family therapy

A

This may result in other family members who develop schizophrenia getting help earlier, or it could prevent schizophrenia developing in other family members due to reduced expressed emotion and better communication within the family.

67
Q

what is token economy

A

Token economy is based upon the principles of operant conditioning and it involves the use of positive reinforcement for behaviours performed.

68
Q

token economy applied to SZ patients

A

used to manage the behaviour of patients with schizophrenia, in p**articular those who have developed maladaptive behaviour as a result of becoming institutionalised **due to spending a long time in a psychiatric institution. For example, they may have developed bad hygiene or stay in their pyjamas all day.
Token economy doesn’t aim to cure schizophrenia, but to improve the patients’ quality of life and help them to adapt to living outside a hospital setting.

69
Q

criticims of Studies looking at the effectiveness of token economies

A

McMonagle and Sultana (2009) found only 3 studies where patients had been randomly allocated to conditions and only one of these studies found an improvement in symptoms.

69
Q

evidence for effectiveness of token economy for SZ

A

Allyon and Azrin (1968) used a token economy system to alter the behaviours of patients with schizophrenia who had suffered with the condition for more than 15 years. Patients were rewarded for positive, prosocial behaviours like tidying the room, talking to other patients, being helpful to others and not being violent to staff or other patients.
The token economy system worked to improve a range of prosocial behaviours in chronic schizophrenics, but the system did not reduce the frequency or intensity of hallucinations or delusions. The researchers stated that the system worked successfully, as the goal of their study was to improve the daily behaviour within the hospital not cure the symptoms.

70
Q

unethical

eval of token economy

A
  • **Privileges become more available to patients with mild symptoms and less so for those with more serious symptoms which could be seen as discriminatory. **
  • Token economy is often brought in across a whole institution and all patients are expected to participate. This raises issues of consent to treatment.
  • Token economy helps by making patients’ behaviour more socially acceptable so they can reintegrate into society better but it doesn’t cure the SZ. When patients leave the institution their behaviour may regress due to lack of reinforcement.
71
Q

interactionist approach to SZ

A

states that schizophrenia is a **complex mix of biology **(genes, neurochemical messages, neurological abnormalities) psychology (thinking patterns, emotional components and resilience) and **societal factors like daily hassles and life changing events. **
This approach states that all of these factors interact together and the consequence of this complex mix is schizophrenia.

72
Q

the original diathesis stress model

A

By Meehl
* Diathesis (vulnerability) is entirely genetic (caused by a schizogene which leads to a schizotypic personality).
* In carriers of the schizogene, stress in childhood (e.g. caused by schizophrenogenic mother) could result in schizophrenia.
* This is now considered to be too simplistic

73
Q

modern diathesis stress model

A
  • Diathesis: No single schizogene. Many combinations of candidate genes increase genetic vulnerability. Early psychological trauma can affect brain development, making people more vulnerable to the effects of later stress.
  • Stress: Not just childhood stress. Modern research is focused on role of cannabis (increases risk of schizophrenia seven times). Cannabis interferes with the dopamine system.
74
Q

treatment for SZ according to the diathesis stress model

A

combination therapy — drugs AND CBT

75
Q

why is the original diathesis stress model oversimplified

A

Multiple genes + no single schizogene
Vulnerability and stress dont have one singu source
can be biological Stress > Houston et al
found childhood SA trauma was a vuinerability factor whilst cannabis use was
a trigger

76
Q

supporting evidence for combination therpay

diathesis-stress

A

**
Tarrier et al** › 315 patients were randomly allocated to a medication+ CBT group OR medication + Counseling OR control groups
* P’s in combo groups showed less symptom levels than those with medication only

77
Q

childrearing on SZ

diathesis stress model

A

Children adoptive from 19,000 finnish mothurs with schizophrenia were followed up
- adoptive parents were assessed for child rearing style and rates of SZ were compared to those in a control group as adoptees without any genetic risk of sz:
Child rearing that invoured high levels
Of crit+conflict, low levels of empathy were implicated in the development of SZ, but only in the group with genetic risk and not control