Schizophrenia (Sz) Flashcards

1
Q

Schizophrenia

A

A mental illness that usually occurs in late adolescence or early adulthood, but it can occur at any time in life. It is classified as a psychosis, as the sufferer has no concept of reality. Essentially the illness is due to a breakdown of the patient’s personality

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2
Q

Psychosis

A

A term used to describe a severe mental health problem where the individual loses contact with reality (unlike neurosis where the individual is aware that they have problems)

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3
Q

Symptoms of Schizophrenia

A
  • Multiple personalities
  • Lack of facial expression
  • Repetitive behaviours
  • Sudden weight loss
  • Loss of interest
  • Bizarre postures
  • Muddling of words
  • Neglect of hygiene
  • Hallucinations
  • Delusions of grandeur
  • Thought insertion
  • Compulsions
  • Avolition
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4
Q

Hallucinations

A
  • Involve disturbances in perception (rather than disturbances in thought) They are false perceptions that have no basis in reality
  • The most common hallucinations are auditory ones (hearing voices) but can include smell, touch and sight
  • Visual hallucinations
  • Seeing distorted facial expressions
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5
Q

Delusions

A

False beliefs that are firmly held despite being completely illogical, or for which there is no evidence

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6
Q

Delusions of persecution

A

The belief that others want to harm, threaten or manipulate you. Schizophrenics may believe that they are being spied on, that nasty rumours are being spread about them or that people are plotting to kill them

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7
Q

Delusions of grandeur

A

This is the idea that you are an important individual, even god-like and have extraordinary powers. One of the most frequent of this type of delusion is the belief that they are Jesus Christ

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8
Q

Delusions of control

A

Individuals may believe that they are under control of an alien force that has invaded their mind and/or body. This may be interpreted, for example as the presence of spirits or implanted radio transmitters

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9
Q

Negative symptoms

A

Cause a decline in functioning. They appear to reflect a loss of normal function.

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10
Q

Speech poverty

A

The inability to speak properly, characterised by a lack of ability to produce fluent words; this is thought to reflect slowing or blocked thoughts. It can manifest itself as short and empty replies to questions.

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11
Q

Avolition

A

The reduction, difficulty or inability to start and continue with goal-directed behaviour. It is often mistaken for apparent disinterest. E.g. no longer being interested in going out and meeting with friends. Sometimes called apathy

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12
Q

Compulsions

A

Behaviours that have to be done. These may be instructions from somebody else.

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13
Q

Mood disturbances

A

Affective flattening - lack of emotion in responses
Inappropriate affect - the wrong emotion for the topic/situation e.g. laughing at a funeral

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14
Q

Positive (adding) symptoms of Schizophrenia

A
  • Hallucinations
  • Delusions
  • Thought disorders
  • Disorganised speech
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15
Q

Negative (taking away) symptoms of Schizophrenia

A
  • Reduction in range and intensity of emotional expression
  • Avolition
  • Asocial behaviour
  • Speech poverty
  • Neglect of hygiene
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16
Q

Positive symptoms

A

Symptoms that are not usually present in a normal person. They reflect an excess or distortion of normal functioning.

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17
Q

DSM

A
  • Diagnostic and Statistical Manual of Mental Disorders (DSM)
  • Used in America
  • Used to recognise the subtypes but the most recent version (DSM-5) have dropped these
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18
Q

Clinical characteristics of Schizophrenia from DSM

A

Criterion A - Two or more of the following symptoms
- Delusions
- Hallucinations
- Disorganised speech
- Grossly disorganised or catatonic behaviour
- Negative symptoms
- Only one of these symptoms is needed if delusions are bizarre and hallucinations include a voice that constantly commentates

Criterion B - Social/occupational dysfunction

Criterion C - Duration
- Continuous signs of the disturbance persist for at least 6 months

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19
Q

ICD

A
  • International Statistical Classification of Diseases and Related Health Problems (ICD)
  • World Health Organisation
  • UK
  • ICD-10 featured subtypes but the current version (ICD-11) does not contain the subtypes
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20
Q

ICD-10 - Five main subtypes of Sz

A
  • Disorganised
  • Catatonic
  • Paranoid
  • Undifferentiated
  • Residual
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21
Q

Disorganised Schizophrenia

A
  • Generally disorganised behaviour
  • Thought disturbances
  • Absence of expressed emotion, incoherent speech, mood swings, loss of interest
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22
Q

Catatonic Schizophrenia

A
  • Severe motor abnormalities
  • Unusual gestures or use of body language
  • Repetitive movements
  • Total immobility for hours at a time, with the patient simply staring blankly
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23
Q

Paranoid Schizophrenia

A
  • Delusions (persecution or grandeur)
  • Patient remains emotionally responsive and are more alert
  • Argumentative
  • Least serious but most well known
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24
Q

Undifferentiated Schizophrenia

A

Includes patients who do not clearly belong in any other category

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25
Q

Residual Schizophrenia

A

Describes people who, although they have had an episode of Schizophrenia during the past 6 months and still exhibit some symptoms but these are not strong enough to put the patient in another category. Symptoms are mild.

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26
Q

Rosenhan (1973) Aim

A

To investigate how situational factors affect a diagnosis of schizophrenia. Sane confederates went into psychiatric hospitals and told medical health professionals they had a hallucination, and observed whether staff would realise that they were sane. If staff did not detect their sanity, it would have implications for methods of diagnosing mental illness and show that situational factors affect diagnosis.

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27
Q

Rosenhan (1973) Method

A
  • 8 confederates acted as pseudo patients, going to 12 different hospitals. The real participants were the hospital staff who did not know about the experiment.
  • The pseudo patient called the hospital for an appointment.
    -When they arrived they complained of hearing voices saying “empty”, “hollow” and “thud”. They said that the voices were unclear, unfamiliar and of the same sex as the pseudo patient. Pseudo patients gave false names, occupations and symptoms, but gave real life histories.
    -Once on the ward, the pseudo patients stopped pretending symptoms, behaved normally and wrote observations. Pseudo patients were discharged only when they convinced staff that they were sane.
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28
Q

Rosenhan (1973) Results

A

On admission, staff diagnosed 11 pseudo patients with schizophrenia, and one with manic-depression. Staff never detected their sanity. Nurses reported their behaviour as showing “no abnormal indications”, but did interpret their behaviour in the context of their diagnosis. The average hospital stay was 19 days. All pseudo patients were discharged with diagnosis of schizophrenia ‘inremission’. 35 real patients detected sanity (e.g., saying “You’re not crazy”).

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29
Q

Rosenhan (1973) Conclusion

A

Rosenhan’s research showed that psychiatrists cannot reliably tell the difference between an insane and sane person, calling into question the reliability of a schizophrenia diagnosis. ‘Normal’ behaviour was misinterpreted as ‘abnormal’ to support their idea that the pseudo patients had a mental illness. This suggests the validity of psychiatric diagnoses was low and the DSM was flawed.

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30
Q

Follow up study - Rosenhan

A
  • Staff in on hospital were asked to rate patients, seeking admission on a 10 point scale from ‘highly likely to be a pseudo patient’ (1 or 2) to ‘least likely to be a pseudo patient’
  • At this point, they were aware of the previous study and were told that one or more pseudo patients would be sent their way unannounced
  • 41 out of 193 patients received a 1 or 2 score
  • No pseudo patients were actually sent
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31
Q

Is Rosenhan’s study reliable?

A

Yes, as all the psychiatrists agreed that the pseudo patients had Schizophrenia

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32
Q

Is Rosenhan’s study valid?

A

No, as the pseudo patients were not actually ill.

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33
Q

Loring and Powell (Gender bias in the diagnosis of SZ)

A

Loring and Powell (1988) randomly selected 290 male and female psychiatrists to read two case articles of patients’ behaviour and then asked them to offer their judgment on these individuals using standard diagnostic criteria. When the patients were described as ‘male’ or no information was given about their gender, 56% were given a diagnosis of schizophrenia. However, when the patients were described as ‘female’, only 20% were given a diagnosis of schizophrenia. This gender bias did not appear to be evident amongst the female psychiatrists. This suggests that diagnosis is influenced not only by the gender of the patient but also the gender of the clinician.

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34
Q

Criterion validity

A

Do different assessment systems arrive at the same diagnosis for the same patient?

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35
Q

Research evidence for criterion validity as an issue surrounding the diagnosis and classification of schizophrenia

A
  • There is a debate as to what causes sz. Research evidence suggests that sz may be the result of a range of differing factors.
  • Sz seems to develop differently in different patients. Some don’t recover whereas some respond well to treatment
  • Evidence indicates that 10% of patients with sz make a significant recovery and have lasting improvement, 20% recover to previous levels and 30% have some improvement but with relapses
  • Ellison and Ross (1995) found that patients with Dissociative Identity Disorder had more symptoms of sz than people diagnosed with sz. Symptom overlap.
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36
Q

Morbidity

A

How common an illness is

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37
Q

Co-morbidity

A

If conditions occur together a lot of the time, then this calls into question the validity of their diagnosis and classification because they might actually be one a single (combined) condition

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38
Q

Research evidence for co-morbidity as an issue surrounding the diagnosis and classification of schizophrenia

A
  • People with sz often disorders as well as sz. This creates difficulty in making a valid diagnosis and in making decisions about treatment.
  • Buckley (2009) found that 50% of people with sz also have depression. 47% of people with sz also have substance abuse
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39
Q

Harrison (1997) Culture bias in the diagnosis of sz

A

Found that the incidence rate of sz in African-Caribbean groups in the UK and USA is up to eight times higher than white groups. This may be down to more stressors and worse social conditions, but might be a result of cultural misunderstanding and misdiagnosis by clinicians. For example, some Caribbean cultures believe people should talk to dead friends and relatives; a clinician from another culture may misinterpret this as a symptom of sz

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40
Q

Gottesman (1991)

A

Found that genetic similarity and shared risk of schizophrenia are closely related.
Concordance rates

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41
Q

What are the concordance rates found in Gottesman’s study

A

General population -1%
MZ twins - 48%
Parents - 6%
Siblings - 9%
DZ twins - 17%

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42
Q

Evaluation of twin studies (genetic explanations of twin studies)

A
  • 48% concordance rate is not 100% - must be other factors involved
  • Twins are very rare in the general population and so is schizophrenia. Therefore it is unusual to find twins with schizophrenia. Small samples limit the findings
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43
Q

Tienari (2004) adoption study - Finland

A
  • 19,000 Finnish children whose biological mothers had been diagnosed with Schizophrenia
  • Compared to a control group adoptees without a family history of Schizophrenia (low genetic risk)
    Adoptive parents had been assessed for child-rearing were strongly associated with the development of schizophrenia but only in the high genetic risk group
  • Highlights a combination of genetic vulnerability and family stress in the risk factors for schizophrenia
  • This study is only partial evidence because Sz tended to only develop amongst adopted children who were experiencing a particular parenting style
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44
Q

Ripke et al (2014)

A
  • The biological location of a specific gene for the cause of schizophrenia has not yet been identified, although several have been implicated in the development of the disorder
  • 37,00 patients vs 113,000 controls
  • 108 separate genetic variations were associated with increased risk of schizophrenia
  • Genes associated with increased risk for sz include those genes which are responsible for coding the functioning of a number of neurotransmitters including dopamine.
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45
Q

Evaluation of candidate genes

A

Strength: This is strong evidence for genetic factors being involved in the cause of Sz. The idea that genetic
factors increasing vulnerability for Sz “has overwhelming evidence”.

Limitations: However – as ever, it’s not completely clear
cut. Different studies have identified different genes that are responsible. Aetilology means “cause”.
It seems that Sz is “aetiologically heterogeneous”, ie:

The idea that Sz is aetiologically heterogenous
is supported by the findings of 108 different
combinations of genes being found in those 37,000 cases

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46
Q

Genetic causes of schizophrenia without history of the disorder in the family

A

Schizophrenia can also have a genetic origin in the absence of a family history of the disorder. One explanation for this is mutation in parental DNA can be caused by radiation, poison or viral infection

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47
Q

Environmental causes against genetic explanations

A

Birth complications
Smoking THC-rich cannabis as a teenager
Childhood trauma

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48
Q

Dopamine (DA) Hypothesis

A

The brain’s chemical messengers appear to work differently in the brain of a patient with Sz. In particular, dopamine is widely believed to be involved.

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49
Q

Hyperdopaminergia

A
  • Excess of dopamine
  • In the subcortex (central areas of the brain)
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50
Q

Excess of dopamine in Broca’s area

A

May be associated with poverty of speech and/or the experience of auditory hallucinations

51
Q

Hypodopaminergia

A
  • Lack of dopamine
  • In the cortex/prefrontal cortex
  • These areas are responsible for thinking and decision making
52
Q

Strengths of the dopamine hypothesis (Hyperdopaminergia)

A

Post-mortems:

Amphetamines (enhance the actions of
dopamine) – these support the idea of DA being
involved in Sz
If a healthy individual takes lots of these drugs:
Larger does of these drugs can induce positive symptoms very similar to sz in healthy individuals

This supports the idea that high dopamine levels lead to hallucinations.

53
Q

Strengths of the dopamine hypothesis (Hypodopaminergia)

A

Phenothiazines – these are drugs to treat Sz which come under the category of antipsychotic drugs.
Phenothiazines are DA antagonists, so they reduce the action of dopamine and can reduce the symptoms of Sz
They are effective in alleviating many of the symptoms of Sz.

Lindstroem’s Radioactive labelling study
found chemicals needed to produce dopamine
are taken up faster in the brains of Sz sufferers
than controls, suggesting they produce more

54
Q

Weaknesses of the dopamine hypothesis

A

Cause and effect issue with post-mortems:
The theory is that dopamine levels cause Sz but we do not know this for sure as it could be the other way round

Moghaddam & Javitt 2012 – It ain’t just
DA!!
Suggested dopamine does not provide a complete explanation for Sz. Some of the genes identified as linked to Sz also link to other neurotransmitters.
Suggest other neurotransmitters could also involved.
Moghaddam and Javitt suggested the neurotransmitter glutamate is linked.
Shows research is overall mixed.

55
Q

Neural correlates

A

Structures or activity in the brain that occurs with Sz symptoms. Because they occur simultaneously they could be implicated in causing Sz

56
Q

Neural correlates for negative symptoms

A

Motivation involves the anticipation of reward.
The ventral striatum is involved with anticipation.
Negative correlation: The lower the brain activity in the ventral
striatum, the higher the amount of negative symptoms the Sz

57
Q

Neural correlates for positive symptoms

A

Positive symptoms such as auditory hallucinations:
Allen (2007) – brain scans of SZ patients with auditory
hallucinations
Asked them if pre-recorded speech was their own, or someone
else’s.
The Sz patients made more errors than the control group.
The Sz patients had lower levels in their superior temporal gyrus
and their anterior cingulate gyrus.
So there’s a correlation here between a lack of brain activity in
these areas and occurrence of positive symptoms.

58
Q

Typical antipsychotics - Chlorpromazine

A
  • Tablets, syrup or injection
  • Max dose 1,000mg, typically 800mg
  • Usage declined in last 50 yrs
  • Chlorpromazine is a dopamine antagonist
  • Blocks dopamine receptors in synapses
  • Production of dopamine is therefore reduced, as are symptoms such as hallucinations
  • Effective sedative – calms patients, so good for when first admitted to psychiatric hospital
59
Q

Strengths of Chlorpromazine

A
  • Thornley et al (2003) reviewed studies where the experience of
    over 1,100 patients was identical apart from a placebo
  • Chlorpromazine associated with better overall functioning and reduced symptoms
  • Data from 3 trials with 512 patients showed a lower relapse rate when Chlorpromazine was taken.
60
Q

Weaknesses of Chlorprozamine

A
  • Antipsychotic drugs have side-effects from mild to serious (and fatal).
  • Dizziness, agitation, weight gain, itchy skin and tardive dyskinesia (caused by dopamine supersensitivity and
    manifests as grimaces, blinking & lip-
    smacking (ie involuntary facial
    movements).
  • Most serious is NMS – neuroleptic malignant syndrome. Caused by the drug blocking dopamine in areas of the brain that regulate bodily systems.
  • NMS = high temperature, delirium, coma, death. Fortunately rare: 0.1 to 2% of cases
61
Q

Atypical antipsychotics - Clozapine

A
  • Was initially withdrawn after launch following the deaths of some patients – blood condition (could not fight infection).
  • Re-marketed in the 1980s when found to be more effective than
    Chlorpromazine. People have regular blood tests to make sure
    they are OK.
  • Not available as an injection due to potentially fatal side effects.
    Lower dosage than above: 300-450mg a day.
  • Works by binding to dopamine receptors but acts on serotonin
    and glutamate receptors too.
62
Q

Strengths of clozapine

A
  • Clozapine much less risky than typical antipsychotics.
  • The mood-enhancing effects are good additional feature to the symptom reduction.
  • 2012 – a review found Clozapine is more effective than other drugs and is effective in 30-50% of cases where other drugs have failed
  • Improves anxiety mood as well as symptoms – good for those at risk of suicide. NB: this is important when 30-50% of people with Sz attempt suicide.
63
Q

Weaknesses of clozapine

A
  • A side effect is agranulocytosis where white blood cells are affected, meaning they cannot fight infection. Regular blood tests are important
  • Myocarditis (inflammation of the heart muscle) can be fatal
64
Q

Atypical antipsychotics - Risperidone

A
  • The most recent type of drug. Been around since the 1990s.
  • An attempt to produce an effective drug without the potential for the dangerous blood condition associated with Clozapine
  • Tablets, syrup or injection – lasts for 2 weeks
  • Small dose – builds up to 12mg
  • Only a small dose is needed since it binds more strongly to the dopamine receptors than other drugs. Some evidence that this leads to fewer side effects.
65
Q

Strengths of Risperidone

A
  • Main strengths are the smaller dose and fewer side effects.
  • The fact it is available as injection suggests that it is relatively safer than Clozapine.
66
Q

Weaknesses of Risperidone

A
  • Most common side effects include feeling sleepy, having headaches or experiencing problems with movement. However these symptoms are very rare and vary depending on who is taking them
  • Extreme risks include cardiovascular disease but this is very rare
67
Q

General evaluation for drug treatments of schizophrenia

A
  • The problem with all of these drugs is that they all work by reducing dopamine activity. Remember then that they are only addressing the original dopamine hypothesis. Know the more recent theory that Sz may be caused by dopamine levels being too low rather than too high. On that basis, it is not always clear how or why antipsychotics work. Indeed, in theory, sometimes they should not work.
  • The calming effects of antipsychotics has been mistaken for a reduction in the severity of psychosis.
  • Studies do not always study benefits in the long-term. Some positive studies have been published several times, skewing the data.
  • Critics say they are to make the lives of staff easier, rather than to help the patients. As such, opinion varies from recommended practice to human rights abuse (a ‘chemical straitjacket’)
68
Q

Schizophrenogenic mother (family dysfunction)

A
  • Cold, dominant, created conflict, caused schizophrenia to emerge in the child (1948)
  • Early theorists were influenced by Freudian ideas
  • These mothers were said to be rejecting, overprotective, self-sacrificing , moralistic about sex and fearful of intimacy
  • Tension and secrecy in the household
  • The distrust, resentfulness and instability caused by such a parent was thought to induce a schizophrenic reaction (paranoid delusion)
69
Q

Evaluation of the schizophrenogenic mother explanation

A
  • By the 1980s research concluded that there was no such criticisms
  • It had become apparent that only a small percentage of women who might arguably fit the criteria of a schizophrenogenic mother had actually produced schizophrenic children
  • Many schizophrenics were found to have mothers who did not fit the criteria
  • The theory has been criticised for hindering progress in psychiatry
70
Q

Double bind theory

A
  • Bateson 1950s
  • A communication style
  • Children are being ‘punished’ for what was asked (giving a hug then being pushed away) and then being punished again when the parent gives no reason for pushing them away
  • Mixed messages (e.g. that joke was quite funny.. for you)
  • Can’t seek clarification
  • Punished when they get it wrong
  • This theory suggests that children will become confused and lose their grip on reality
  • Negative symptoms of social withdrawal and flat affect may be an appropriate and logical response to double bind situations
71
Q

Evaluation of double bind theory

A
  • Berger (1965) found that schizophrenics reported a higher recall of double bind statements by their mothers than non sz
  • This evidence may not be reliable as patients’ recall may be affected by their sz
  • Other studies find little support: Liem (1994) and Hall and Levin (1980) found no difference in the patterns of parental communication in families with a sz child in comparison to normal families
72
Q

Expressed emotion

A
  • High expressed emotion is a family communication style
  • It involves critical comments through both tone and content, occasionally accompanied by violence, hostility towards the patient (including anger and rejection), and emotional over-involvement in the life of the patient , including needless self-sacrifice
  • If these factors are high, there is a high risk of relapse
73
Q

Brown (1966) Supporting evidence for expressed emotion

A
  • Families where communications are commonly to do with criticism, hostility and disapproval are said to have high EE
  • People recovering from Sz and discharged from hospital were followed up over a 9-month period
  • Interviews with family members were conducted to determine the level of expressed emotion
  • 58% of relapse in EE families compared to only 10% of those from low expressed emotion families
74
Q

Support for family dysfunction as a risk factor

A
  • Read (2005) reviewed 46 studies of child abuse and sz in adulthood. Found that 69% of adult in-patients with a diagnosis for schizophrenia had a history of child abuse - the figure for men was 59%
  • Adults with insecure attachments to their primary caregiver are also more likely to develop sz
75
Q

Limitations of family dysfunction as an explanation for schizophrenia

A
  • Parent blaming - Parents who have already suffered at seeing their child’s descent into sz underwent further trauma by receiving blame for the condition
  • Cause and effect - it could be the other way round as sz in the family could cause this these communication styles and a high stress environment. Also, it is difficult to pinpoint an exact cause due to there being many contributing factors.
76
Q

Evaluation of expressed emotion

A
  • High EE communication patterns are not specific to sz (depressive illness, eating disorders)
  • More evident in Western families
  • There is a problem with how EE is measured which is usually via one interview. This is too short of an assessment.
77
Q

How is schizophrenia linked to the cognitive approach

A

The idea of abnormal information processing

78
Q

Ventral striatum

A
  • Lack of activity in ventral-striatum - negative symptoms (avolition due to lack of anticipation of reward)
  • If you don’t expect a reward when you would normally get one then that is abnormal processing
79
Q

Cingulate gyrus

A
  • Reduced level of information processing in the cingulate gyrus is associated with hallucinations
  • Linked to many factors such as maternal bonding, regulation of aggressive behaviour and decision making
80
Q

Central control

A
  • The cognitive ability to suppress (put a lid on) automatic responses while we perform deliberate actions instead
  • For example, not being able to suppress word associations and automatic thoughts
  • Sz sufferers suffer derailment of their speech and thinking
81
Q

Diathesis stress model

A
  • It might not be that faulty mental processing is the direct cause of sz
  • It could be that certain people are more vulnerable to sz than others
  • Their sz may be triggered by factors such as their biology or environment - and this in turn affects their thinking
82
Q

Metarepresentation

A
  • The cognitive ability to reflect on thoughts and behaviour
  • Gives insight into our intentions/goals
  • If misrepresentation goes wrong, we may come to believe that our actions and thoughts are carried out by someone else rather than ourselves
  • Explains thought insertion and auditory hallucinations
83
Q

Stirling - stroop test - supporting evidence for sz

A
  • Stroop test - having to say the font colour not the word
  • Sz patients vs control group
  • Sz patients took twice as long - struggled to suppress saying the word rather than the colour
  • However it tells us nothing about the origins of sz. The cognitive explanation can explain symptoms but the true cause may lie elsewhere
84
Q

Limitation of cognitive explanations of sz

A
  • Cognitive explanations are proximal (an explanation of what is happening now)
  • The symptoms are happening now so they are explained. This is different to explaining what actually causes the condition that causes the symptoms
85
Q

Family therapy

A
  • Takes place with families as well as the identified patient (a term used in family therapy which describes one member of a dysfunctional family who expresses the family’s conflict)
  • Aims to improve the quality of communication and interaction between family members
  • Many people with sz are cared for at home and that can place a strain on the family
  • Involves a series of informal meetings that take place over 6 months
  • Tries to understand alliances within the family
86
Q

How family therapy helps

A
  • Pharoah et al (2010) identified a range of strategies that family therapists use to try to improve the functioning of a family that has a member with schizophrenia
  • Reduces negative emotion - Family therapy aims to reduce levels of expressed emotion. Reducing stress is important to reduce the likelihood of relapse.
  • Improves the family’s ability to help - The therapist encourages family members to form a therapeutic alliance whereby they all agree on the aims of therapy. A further aim is to ensure that family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives.
87
Q

Who proposed a model for working with families dealing with schizophrenia?

A

Burbach (2018)

88
Q

Phase 1 (Burbach’s model for family therapy)

A

Sharing basic information and providing emotional and practical support

89
Q

Phase 2 (Burbach’s model for family therapy)

A

Involves identifying resources including what family members can (and cannot) offer

90
Q

Phase 3 (Burbach’s model for family therapy)

A

Aims to encourage mutual understanding, creating a safe space for all family members to express their feelings

91
Q

Phase 4 (Burbach’s model for family therapy)

A

Involves identifying unhelpful patterns of interaction

92
Q

Phase 5 (Burbach’s model for family therapy)

A

About skills training such as learning stress management techniques

93
Q

Phase 6 (Burbach’s model for family therapy)

A

Looks at relapse prevention planning

94
Q

Phase 7 (Burbach’s model for family therapy)

A

Maintenance for the future

95
Q

Evaluation of family therapy (evidence of effectiveness)

A
  • A strength is that there is evidence for the effectiveness of family therapy
  • A review of studies by William McFarlane (2016) concluded that family therapy was one of the most consistently effective treatments for sz
  • Relapse rates were found to be reduced, typically by 50-60%
  • He also concluded that using family therapy as mental health initially starts to decline is particularly promising
  • NICE recommends family therapy for everyone with an sz diagnosis
  • This means that family therapy is likely to be of benefit to people with both early and ‘full-blown’ sz
96
Q

Evaluation of family therapy (benefits the whole family)

A
  • Family therapy for sz benefits all family members
  • A review of evidence by Fiona Lobban and Christine Barrowclough (2016) concluded that these effects are important because families provide the bulk of care for people with sz
  • By strengthening the functioning of a whole family, family yhterapy lessens the negative impact of sz on other family members and strengthens the ability of the family to support the person with sz
  • This means that family therapy has wider benefits beyond the obvious positive impact on the identified patient
97
Q

Evaluation of family therapy (economy)

A
  • As family therapy reduces relapse rates and makes families better able to provide the bulk of care, it has huge economic benefits
  • The state does not need to pay so much
98
Q

Cognitive behavioural therapy (CBT) for schizophrenia

A
  • Usually takes place over 5-20 sessions (this is longer than for other conditions)
  • Aims to deal with both thoughts and behaviour
  • CBT can help a client make sense of how their irrational cognitions (e.g. delusions and hallucinations) impact on their feelings and behaviour
  • Just understanding where symptoms come from can be hugely helpful for those with symptoms like auditory hallucinations. e.g. if a client hears voices and believes the voices represent demonic forces, they will naturally be very afraid. If a therapist can convince them that the voice actually comes from the malfunctioning speech centre in their own brain and that it cannot hurt them, this is much less frightening
  • Provides coping mechanisms by asking for evidence to challenge their beliefs and searching for alternatives
99
Q

Evaluation of CBT for schizophrenia (effectiveness)

A
  • There is evidence for the effectiveness of CBT
  • Jauhar (2014) reviewed 34 studies of using CBT with sz, concluding that there is clear evidence for small but significant effects on both positive and negative symptoms
  • Pontillo (2016) found reductions in frequency and severity of auditory hallucinations
  • NICE recommends CBT for schizophrenia
  • This means that both research and clinical experience support the benefits of CBT for schizophrenia
100
Q

Evaluation of CBT for schizophrenia (quality of evidence)

A
  • One limitation of CBT for schizophrenia is the wide range of techniques and symptoms included in studies
  • CBT techniques and sz symptoms vary widely from one case to another
  • Neil Thomas (2015) points out that different studies have involved the use of different CBT techniques and people with different combinations of positive and negative symptoms
  • The overall modest benefits of CBT for schizophrenia probably conceal a wide variety of effects of different CBT techniques on different symptoms
  • This makes it hard to say how effective CBT will be for a particular person with schizophrenia
101
Q

Chadwick - effectiveness of coping strategy enhancement (CSE)

A
  • Support for effectiveness of CSE comes from Chadwick (1992) who worked with a schizophrenic who had a delusion that his thinking could influence the future.
  • However, he failed to predict what would happen in 50 video clips highlighting how he didn’t know what was going to happen in the future
102
Q

Evaluation of CBT for schizophrenia (cure)

A
  • CBT may improve the quality of life for people with schizophrenia but not actually ‘cure’ them
  • As schizophrenia appears to be largely a biological condition, we would expect that a psychological therapy like CBT just benefits people by improving their ability to live with schizophrenia
  • On the other hand, studies report significant reductions in the severity of both positive and negative symptoms.
  • This suggests that CBT does more than enhance coping
103
Q

Coping strategy enhancement (CSE)

A

Building on schizophrenics’ existing coping strategies

104
Q

An example of a cognitive coping strategy

A

Distraction

105
Q

An example of a behavioural coping strategy

A

Breathing techniques

107
Q

Token economies

A
  • A method of helping institutionalised patients to manage/control their impulses and behaviour
  • Coloured counters = privileges
  • A behavioural treatment based on operant conditioning
108
Q

Examples of how tokens are earned

A
  • Making bed
  • Good hygiene
  • Speaking coherently
  • Keeping room and belongings tidy
  • Doing chores
  • Participating in hospital activities
109
Q

Examples of what tokens can be ‘cashed in’ for

A
  • Food
  • More family visits
  • Arts and crafts
  • Films
110
Q

What could the reinforcement schedule be in a token economy?

A

A fixed ratio - consistently doing a behaviour (5 times) gets rewarded with a token

111
Q

What type of reinforcers are tokens?

A

Secondary reinforcers as they don’t have value on their own

112
Q

Strengths of token economies (Sz)

A
  • It has been proven effective in reducing psychotic behaviours
  • Glowacki (2016) - 7 studies - effective for chronic mental health issues in care a hospital setting
113
Q

Paul and Lentz (1977)

A
  • Ran a token economy in a mental hospital for schizophrenia
  • After 4 1/2 years 98% of patients improved and could leave the hospital
  • This figure is compared to 45% with patients who had basic hospital
  • Concurrently the drug does of these patients were reduced
114
Q

Limitations of token economies

A
  • The file drawer problem
  • Good behaviour quickly ceases when the rewards go away which makes this therapy hard to transpose into the outside world
  • Hallucinations, disorganised speech and delusions have not been shown to improve from this therapy
  • It has been argued that patients in token economies merely mimic ‘normal’ behaviour and do not actually believe it
  • It is hard to quantitatively measure improvements in an ecological validity fashion
  • ‘Desired’ behaviours are decided in most cases by the hospital or institution - ethical issues
  • In reality, not many patients with Sz actually live in institutions anymore. It is hard to create token economies in the real world
115
Q

Diathesis

A

Means vulnerability
A predisposition to develop a medical conditions

116
Q

Stress (diathesis-stress model)

A

Any environmental factor that could trigger the disorder

117
Q

Meehl’s model (1962)

A
  • Diathesis was entirely genetic, the result of a single ‘schizogene’
  • This led to the idea of a biologically based schizotypic personality
  • According to Paul Meehl, if a person does not have the schizogene then no amount of stress would lead to schizophrenia
118
Q

Modern understanding of diathesis

A
  • It is now clear that many genes appear to increase genetic vulnerability only slightly, there is no single ‘schizogene’ (Ripke 2014)
  • Modern views of diathesis also include a range of factors beyond the genetic, including psychological trauma (Ingram and Luxton 2005) - trauma becomes the diathesis rather than the stressor
119
Q

Modern understanding of stress

A
  • Although psychological stress, including that resulting from parenting may still be important, a modern definition of stress includes anything that risks triggering schizophrenia
  • E.g. In terms of the diathesis-stress model cannabis is a stressor because it increases the risk of schizophrenia by up to 7 times according to dose
  • Most people do not develop schizophrenia after smoking cannabis presumably because they lack the requisite vulnerability factors
120
Q

An example of an interactionist treatment

121
Q

Evaluation of the diathesis-stress model of schizophrenia (Tienari)

A
  • Tienari (2004) adoption study
  • Investigated the impact of both genetic vulnerability and a psychological trigger (dysfunctional parenting)
  • The study followed 19,000 Finnish children whose biological mothers had been diagnosed with schizophrenia and a control group
  • Assessed family functioning in the adoptive families using the Oulu Family Rating Scale (OPAS Scale)
  • The scale measures parent-offspring conflict and lack of empathy
  • The interviewing psychiatrists were kept blind as to whether the biological mothers had was schizophrenic or not
  • A stressful family environment was only strongly associated with Sz in the high genetic risk group
  • Combination of stress and genetic vulnerability
122
Q

Evaluation of the diathesis- stress model of schizophrenia (Real-world application)

A
  • The interactionist approach has a strength in the combination of biological and psychological treatments
  • A practical application of acknowledging biological and psychological factors in schizophrenia has been the combination of drug treatment and psychological therapies
  • Studies show that combining treatments enhances their effectiveness e.g. Nicholas Tarrier (2004) randomly allocated 315 participants to (1) medication + CBT, (2) medication + counselling, or (3) control group (medication only)
  • Combination groups showed lower symptoms than control groups
123
Q

Evaluation of the diathesis model of schizophrenia (oversimplified)

A
  • The original diathesis-stress model is oversimplified
  • However modern understanding other diathesis-stress demonstrate its complexity
124
Q

Enlarged ventricles

A
  • Ventricles provide a protective cushioning effect for the brain
  • Enlarged ventricles are associated with people with schizophrenia
  • Johnstone (1976) found from CT scans that people with schizophrenia had larger than average ventricles
  • However, this research is correlational