Schizophrenia Flashcards
1
Q
What is schizophrenia?
A
A severe mental disorder where contact with reality and insight are impaired - causing profound disruption of cognition and emotion.
2
Q
What is meant by classification of mental disorder?
A
The process of organizing symptoms into categories based on which symptoms frequently cluster together.
3
Q
What is the process of diagnosing a disorder?
A
- We need to distinguish one disorder from the next.
- We identify clusters of symptoms that occur together - which can then be classified as one disorder.
- Diagnosis can then occur, identifying symptoms and deciding what disorder the person has.
4
Q
What are the two current classification of mental disorder systems?
A
- The international classification of disease (ICD-10)
- Diagnostic and statistical manual edition 5 (DSM-5)
5
Q
How does the ICD-11 and DSM-5 differ in classification of schizophrenia?
A
- In the DSM-5 one or more POSITIVE symptoms are required for diagnosis whereas in the ICD-11, two or more NEGATIVE symptoms are sufficient for diagnosis.
- The DSM-5 requires delusion, hallucination or disorganised speech to be present for diagnosis.
- The DSM-5 requires symptoms to persist over 6 months, whereas the ICD-11 requires symptoms present most of the time for psychotic episodes lasting at least 1 month.
6
Q
What % of the worlds population have schizophrenia?
A
1%
7
Q
Define positive symptoms of schizophrenia
A
Atypical symptoms experienced IN ADDITION to normal experiences
8
Q
Define negative symptoms of schizophrenia.
A
Atypical experiences that involve the loss of usual experiences and abilities.
9
Q
What are the two positive symptoms of schizophrenia?
A
- Hallucinations
- Delusions (paranoia)
10
Q
What are hallucinations (a positive symptom of schizophrenia)
A
- Unusual sensory experiences that can either have no relation to reality or may be distorted perceptions of things that are there.
Hallucinations can be experienced with any sense, for example: hearing commentary voices that can also converse. In addition, they may see distorted facial expressions or people/animals that are not there.
11
Q
What are delusions (a positive symptom of schizophrenia)
A
- Beliefs that have no basis in reality and are irrational - these make sense to the individual but seem bizarre to others.
12
Q
What are common delusions in schizophrenia?
A
- Being an important historical, political or religious figure such as Napoleon or Jesus.
- Belief that they are being persecuted by the government or aliens and belief they have superpowers.
- Belief that they are under external control.
13
Q
What are the two negative symptoms of schizophrenia?
A
- Avolition
- Speech poverty (alogia)
14
Q
What is avolition? (a negative symptom of schizophrenia)
A
- Loss of motivation and lowering of activity.
- They have sharply reduced motivation for goal-directed activity (actions performed to produce a consequence)
15
Q
What 3 signs of avolition did Andreasen outline?
A
- Poor hygiene and grooming
- Lack of persistence in work or education
- Lack of energy
16
Q
What is speech poverty/alogia? (a negative symptom of schizophrenia)
A
- Change in patterns of speech, being a reduction quality and amount of speech.
- This is accompanied by a delay in verbal responses during conversation
17
Q
List the ‘issues in diagnosis and classification’ for schizophrenia
A
- Good reliability
- Low validity
- Co-morbidity
- Gender bias
- Culture bias
- Symptom overlap
18
Q
Evaluate validity and reliability in diagnosis and classification of schizophrenia
A
- Good reliability.
One strength of diagnosing schizophrenia is reliability, or consistency. For a psychiatric diagnosis to be deemed reliable, different diagnosing clinicians need to reach the same diagnosis for the same individual (inter-rater reliability). In addition, test-retest reliability also determines diagnostic reliability where the same clinician reaches the same diagnosis for the same individual on two occasions. Prior to the DSM-5, reliability in diagnosing schizophrenia was low but has since improved.
A study reported excellent reliability for the diagnosis of schizophrenia in 180 individuals using the DSM-5. Pairs of interviewers achieved inter-rater reliability of +.97 and test-retest reliability of +.92. This means we can be reasonably sure that diagnosis is consistently applied. - Low validity.
A limitation into the diagnosis and classification of schizophrenia is validity. In general, validity refers to whether we are assessing what we are intending to assess. For diagnosis, criterion validity is used to assess the validity of diagnosis. A study had two psychiatrists independently assess the same 100 clients with one using the DSM-IV and the other using the ICD-10. For the ICD-10, 68/100 were diagnosed with schizophrenia compared with only 39/100 being diagnosed under the DSM-5 criteria. This suggests schizophrenia is either over or under diagnosed according to the diagnostic system - suggesting low criterion validity. - COUNTERPOINT TO VALIDITY.
Despite a disconcordance in diagnosis between two classification systems, it was reported that there was excellent agreement between clinicians when they used measures to diagnose schizophrenia from the DSM-5. This means that criterion validity for diagnosing schizophrenia is actually good provided it takes place under a singular diagnostic system.
19
Q
Evaluate co-morbidity and symptom overlap in issues with the diagnosis and classification of schizophrenia
A
- Co-morbidity
Another limitation of schizophrenia diagnosis is co-morbidity with other conditions. Co-morbidity, as a definition is where conditions can occur together. If conditions occur together frequently, it questions the validity of diagnosis and classification due to giving the impression that it could be a single condition as opposed to two. Schizophrenia, for example, is commonly diagnosed alongside other conditions. For example, 1/2 of those with schizophrenia are diagnosed with depression or substance abuse. This poses a problem for classification as it means schizophrenia may not exist as a distinct condition. As a result, diagnosis is a problem as some diagnosed with schizophrenia may display unusual cases of conditions such as depression. - Symptom overlap.
A further limitation in diagnosing schizophrenia is symptom overlap. In schizophrenia’s case, symptom overlap is where there is considerable overlap between symptoms of schizophrenia and symptoms seen in other conditions. Using an example, both schizophrenia and bipolar disorder involve similar symptoms such as delusions and avolition - also having similar characteristics like having cyclic patterns of symptoms. In terms of classification, this suggests schizophrenia and bipolar disorder may not be two different conditions but variations of a single condition. For diagnosis, it means schizophrenia is hard to distinguish from bipolar disorder resulting in a false diagnosis. As with co-morbidity, symptom overlap means that schizophrenia may not exist as a single condition and even if it is, it is harder to diagnose as classification and diagnosis are flawed.
20
Q
Evaluate gender bias and culture bias in issues with the diagnosis and classification of schizophrenia
A
- Gender bias
A limitation of diagnosing and classifying schizophrenia is the existence of gender bias. Since the 1980s, men are more commonly diagnosed with schizophrenia, at a figure of 1.4:1 ratio compared to women. This can be explained by the fact women are less vulnerable than men, potentially due to genetic factors. Despite this, it is more likely that women are under diagnosed due to having closer relationships and therefore, more support. This means that women with schizophrenia may be better functioning than men. This under diagnosis is a gender bias and means women may not therefore be receiving treatment and services that benefit them. - Culture bias
Another limitation of schizophrenia diagnosis is culture bias. Some symptoms of schizophrenia, such as hearing voices, have different meanings in different cultures. For example - in Haiti, hearing voices is believed to be communication from ancestors. In the UK, British people of Afro-Carribean origin are 9x more likely to be diagnosed with schizophrenia compared to white British people. This does not correlate with the fact that people living in African or Carribean countries are not, ruling out genetic vulnerability. To explain this, it is likely that culture bias occurs in diagnosis of clients. Psychiatrists of different cultural backgrounds could over interpret symptoms in Black British people due to ethnocentrism. In summary, due to culture bias, British African-Carribean people may receive discrimination due to a culturally-biased diagnosis system.
21
Q
Define classification
A
The process of organizing symptoms into categories based on which symptoms frequently cluster together
22
Q
What is the difference between co-morbidity and symptom overlap?
A
- Co-morbidity is the occurrence of two or more disorders together.
- Symptom overlap is where two or more conditions share symptoms (bipolar and schizophrenia example)
23
Q
What are the two biological explanations of schizophrenia?
A
- Genetics
- Neural correlates
24
Q
What are the 3 genetic explanations for schizophrenia?
A
- Family studies
- Candidate genes
- Role of mutation
25
What psychologist carried out family studies into schizophrenia?
Gottesman
26
For different family members diagnosed with schizophrenia, what is an individuals chances of developing it? (GOTTESMAN FAMILY STUDY)
- Aunt: 2% chance
- Sibling: 7%
- Identical twin: 48%
27
What is the role of mutation in schizophrenia (biological explanation)
- Mutation in DNA is believed to be a factor in developing schizophrenia, regardless of family history.
- A study found positive correlations between paternal age (associated with risk of sperm mutation) and risk of schizophrenia.
0.7 risk in fathers under 25, 2% in fathers over 50.
28
What are candidate genes in schizophrenia?
Candidate genes are genes that create vulnerability for developing schizophrenia.
29
Who studied candidate genes as a genetic explanation for schizophrenia (biological explanations for schizophrenia)
Ripke et al.
30
Is schizophrenia polygenic?
- It appears so.
Modern research supports that multiple genes are involved in the development of schizophrenia.
These genes are most likely involved in coding for neurotransmitters.
31
What did Ripke do and find in his genome-wide study on candidate genes?
- Ripke combined data on the genetic makeup of 37000 people diagnosed with schizophrenia and compared these to a control of 113000 people.
- Ripke found 108 separate genetic variations were associated with an increased risk of schizophrenia.
32
Why is schizophrenia aetiologically heterogenous?
Different studies identified different candidate genes.
It is aetiologically heterogenous as different combination of factors, including genetic variation can lead to the condition.
33
What is meant by neural correlates? (a biological explanation for schizophrenia)
- Patterns of structure or activity in the brain that occur simultaneously with an experience, and can be implicated in the origin of this.
34
What is the best-known neural correlate of schizophrenia?
- Dopamine (DA)
35
What are explanations under neural correlates?
- The original dopamine hypothesis
- The updated versions of the dopamine hypothesis
36
Outline the original dopamine hypothesis (biological explanations)
- The original dopamine hypothesis was founded on the discovery that anti-psychotic drugs used to treat schizophrenia caused symptoms similar to Parkinson's disease, a condition characterized by low DA levels).
- Therefore, the original dopamine hypothesis concluded that schizophrenia may be associated with high levels of dopamine in subcortical levels of the brain.
37
In short, what is the main claim of the original dopamine hypothesis?
- Schizophrenia may be the result of **hyperdopaminergia** in **subcortical** areas of the brain.
38
How does the original dopamine hypothesis explain symptoms such as speech poverty and auditory hallucinations? (biological explanations for schizophrenia)
- An excess of DA receptors in pathways from the **subcortical areas** to the **Brocas area** (responsible for speech production) explain these symptoms.
39
What psychologist contributed to the UPDATED dopamine hypothesis?
Davis et al.
40
What does the updated dopamine hypothesis claim?
- The updated dopamine hypothesis claims that HYPOdopaminergia can also be implicated in schizophrenia. - so low DA in the prefrontal cortex (responsible for thought) could be an explanation, in addition to the original dopamine hypothesis claim that it is explicitly due to HYPERdopaminergia in subcortical areas of the brain
- In addition, it sees that cortical hypodopaminergia can lead to hyperdopaminergia - so both high and low dopamine levels in different sections of the brain causes symptoms.
- Lastly, in addition to explaining links with abnormally low DA levels - the updated hypothesis attempts to explain the origin of this.
For example, it is accepted that genetic variations and early experiences of stress increase sensitivity to *cortical hypodopaminergia* and, subsequently hyperdopaminergia.
41
What did Davis et al propose as part of the updated dopamine hypothesis?
- Cortical **hypodopaminergia** can be implicated in the symptoms of schizophrenia (abnormally low levels of DA in the cortex)
42
How does **hypodopaminergia** as part of the updated dopamine hypothesis explain symptoms of schizophrenia?
Low DA in the prefrontal cortex (responsible for thought) can explain cognitive problems in schizophrenia such as avolition.
43
In short, what is the main claim of the UPDATED dopamine hypothesis?
- Both Cortical **hyperdopaminergia** and **hypodopaminergia** can cause schizophrenic symptoms.
It is about the disparity of dopamine in different sections of the brain (high DA in subcortical, low DA in prefrontal cortex)
44
Hypodopaminergia can lead to hyperdopaminergia, true or false?
True
45
Evaluate the genetic basis as a biological explanation for schizophrenia
- Research support
One strength of the genetic explanation as a biological explanation for schizophrenia is the strong evidence base.
Gottesman's, alongside other family studies demonstrate that risk increases with genetic similarity to a family member with schizophrenia.
Adoption studies are utilised as research support, showing how biological children of parents with schizophrenia are at heightened risk regardless of the environment they were adopted into. A recent twin study showed that there was a concordance rate of 33% for monozygotic twins and 7% for dizygotic twins.
This supports the notion that some people are more vulnerable to schizophrenia as a result of genetic makeup.
- Environmental factors.
A limitation for the genetic explanation of schizophrenia is that there is distinct evidence to show environmental factors increase the risk of schizophrenia. Environmental factors consider both biological and psychological influences. Biological risk factors include birth complications and the intake of THC-rich cannabis in teenage years. Psychological risk factors include childhood trauma, leaving people more vulnerable to adult mental health problems - having links to schizophrenia. In one study 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched control group.
This evidence suggests that genetic factors alone cannot provide a complete explanation for schizophrenia.
46
Evaluate neural correlates as a biological explanation for schizophrenia
- Evidence for the role of dopamine
A strength of using neural correlates to explain schizophrenia is evidence to support the dopamine hypothesis - that DA is involved with the disorder. It has been found amphetamines increase DA and worsen symptoms experienced by people with schizophrenia - also inducing symptoms in people without the disorder. Oppositely, anti-psychotic drugs that reduce DA activity have been found to reduce intensity of symptoms. This strongly suggests that dopamine is involved in the symptoms of schizophrenia.
- Glutamate ignored.
One limitation of the dopamine hypothesis is that it disregards the role of glutamate, even with evidence for it having a central role.
Both post-mortem and live scanning studies have found consistency in raised levels of glutamate (another neurotransmitter) in several brain regions of people with schizophrenia. In addition, several candidate genes are believed to be involved in glutamate production and processing. This means that an equally strong case can be made for the role of glutamate, not just primarily dopamine.
47
What is the main biological therapy for schizophrenia?
Drug therapy - anti-psychotics.
48
What are anti-psychotics?
Drugs to reduce the intensity of symptoms, in particular the **positive** symptoms of schizophrenia and other psychotic disorders.
49
What are the two types of anti-psychotics?
- Typical anti-psychotics
- Atypical anti-psychotics
50
What are **typical** anti-psychotics?
- The first generation of drugs for schizophrenia, acting as dopamine-antagonists
51
What is another word for typical anti-psychotics?
- Dopamine-antagonists
52
Name one typical anti-psychotic
Chlorpromazine
53
How does chlorpromazine work?
- It acts as an antagonist in the dopamine system
It reduces the action of dopamine, working by blocking dopamine receptors in the synapses of the brain - reducing the action of dopamine.
54
What are dopamine antagonists?
Chemicals that reduce the action of the neurotransmitter dopamine.
55
What happens when an individual starts to take chlorpromazine and why?
- Initially, dopamine levels build up, then production levels reduce in response
- This is because chlorpromazine, a dopamine antagonist, has an effect of normalising neurotransmission of effected areas of the brain - reducing symptoms such as hallucinations
56
Chlorpromazine, a typical anti-psychotic, works as a sedative - true or false?
True.
57
Why is chlorpromazine used as a sedative?
It has an effect on histamine receptors - calming individuals.
58
What are atypical anti-psychotics?
Drugs for schizophrenia developed after typical anti-psychotics - targeting a range of neurotransmitters such as dopamine and serotonin
59
What is the difference between atypical anti-psychotics and typical anti-psychotics
- Typical anti-psychotics target dopamine receptors
- Atypical anti-psychotics target both dopamine and other neurotransmitters such as serotonin.
60
Name two atypical anti-psychotics
- Clozapine
- Risperidone
61
Why were atypical anti-psychotics developed?
To improve the suppression of symptom whilst minimising the side-effects.
62
How does clozapine work?
- Clozapine binds to dopamine receptors, and IN ADDITION, it works on serotonin and glutamate receptors.
This improves mood by reducing depression and anxiety in patients and improves their ability of cognitive functioning.
63
Why was risperidone produced?
The first atypical anti-psychotic, clozapine, had side effects such as agranulocytosis - risperidone was developed to be as effective as clozapine but without serious side effect.
64
How does risperidone work?
Similar to clozapine, it binds to dopamine receptors and serotonin receptors.
A difference is that it binds more strongly to dopamine receptors compared to clozapine so is therefore more effective in smaller doses.
65
Evaluate biological therapy for schizophrenia
- Evidence for effectiveness
One strength of using anti-psychotics is evidence to support effectiveness.
There is a sufficient body of evidence to support that both typical AND atypical anti-psychotics are at least moderately effective in tackling symptoms of schizophrenia. A review studied comparisons between chlorpromazine effects to control conditions. Data from 13 trials with over 1000 participants displayed that chlorpromazine (a typical anti-psychotic) was associated with overall better functioning and reduced symptom severity compared to a placebo.
There is further evidence for effectiveness of atypical antipsychotics where it was concluded clozapine is more effective than typical anti-psychotics and other atypical ones.
Clozapine is effective in 30-50% of cases where typical anti-psychotics fail.
This implies, as far as we can tell, anti-psychotics work on schizophrenia.
- Flaws in evidence base
A limitation in claiming evidence for effectiveness is that it is seriously flawed.
Most studies into the effectiveness of anti-psychotics are only conducted on short-term effects and successful trials may have had data published multiple times which exaggerates the evidence for positive effects. Also, due to the antipsychotic property of having powerful calming effects, it is easy to claim they have a positive effect on those experiencing symptoms. This however, is not the same as claiming a reduction in the severity of psychosis. This means that evidence for anti-psychotic effectiveness is less sufficient than it initially appears
- Serious side effects
A limitation of the use of anti-psychotic drugs as a biological therapy is the likelihood of side effects. Typical anti-psychotics are associated with various side effects such as dizziness, agitation, weight gain and itchy skin. Long term usage creates more advanced medical issues such as TARDIVE DYSKINESIA, caused by dopamine super sensitivity, characterised by involuntary facial movements such as grimacing and blinking. The most fatal side effect is NEUROLEPTIC MALIGNANT SYNDROME where the anti-psychotic blocks dopamine reception in the hypothalamus. The hypothalamus is associated with various body system regulations which, if subject to NMS causes fever, delirium, coma and death. This suggests anti-psychotics may be harmful in addition to their positive effects, making individuals avoid them and therefore, treatment may be ineffective.
- Unclear mechanism
A further limitation of anti-psychotics is that we do not have a complete picture of their function. Understanding of the mechanism closely corresponds with the original dopamine hypothesis which states high DA in the subcortex causes schizophrenia symptoms. However, since the dopamine hypothesis has been updated it is accepted that the original was simplified. Now, the hypothesis sees that unequal dopamine levels in the brain are associated with schizophrenia. If using the updated dopamine hypothesis as a theory, most anti-psychotics should therefore not work. Given the questioning of anti-psychotic effectiveness anyway, this adds to the argument of their ineffectiveness. This means at least some of the anti-psychotics may not be the best treatment as another factor may be involved in their apparent success.
66
What are the two psychological explanations for schizophrenia?
- Cognitive explanations
- Family dysfunction
67
What is included in the family dysfunction explanation of schizophrenia? (psychological explanations)
- The schizophrenogenic mother
- Double bond theory
- Expressed emotion
68
Define family dysfunction
Processes within a family such as poor communication, cold parenting and high levels of expressed emotion that are risk factors for the development and maintenance of schizophrenia
69
What psychologist proposed the “schizophrenogenic mother”
Fromm-Reichmann
70
How did Fromm-Reichmann identify the ‘schizophrenogenic mother’ as a psychological explanation for schizophrenia
- Fromm-Reichmann found many patients described a particular type of parent when recounting their childhood.
71
What approach / explanation is the schizophrenogenic mother?
- Psychodynamic explanation (family dysfunction)
72
What did Fromm-Reichmann describe the schizophrenogenic mother as and how does this explain schizophrenia?
- Cold
- Rejecting
- Controlling
- Creates a family environment of tension and secrecy
- This leads to distrust that later develops into paranoid delusions and ultimately schizophrenia.
73
Who proposed double bind theory? (family dysfunction psychological explanation)
Bateson
74
What is double-bind theory?
The idea that family communication style is important in the development of schizophrenia.
75
What occurs under double bind theory to cause risk of development of schizophrenia?
- A dysfunctional communication style is present within the family
- A developing child finds themselves trapped in situations where they fear that they’re doing the wrong thing, yet receive mixed messages about what this is.
- The child feels unable to comment on any unfairness or seek clarification.
- When the child “gets it wrong” they’re punished with withdrawal of love
- As a consequence, they develop a picture that the world is confusing and dangerous which is reflected in symptoms of **disorganised thinking** and **paranoid delusions**
76
Is double bind theory a risk factor or a primary cause of schizophrenia?
- A RISK FACTOR, not a primary cause !!
77
What is meant by expressed emotion?
- The level of emotion, particularly negative emotion, expressed TOWARDS a person with schizophrenia by caters or family members.
78
What are the three components of expressed emotion? (family dysfunction)
- Hostility
- Criticism
- Emotional over involvement
79
How do high levels of expressed emotion cause schizophrenia?
- High levels of expressed emotion directed at an individual is a serious source of stress
- It is the primary explanation for the relapse of schizophrenia
- High levels of expressed emotion have been suggested to trigger the onset of schizophrenia to someone already vulnerable.
80
Evaluate family dysfunction as an explanation for schizophrenia
- Research support
One strength of family dysfunction as a psychological explanation is evidence linking this to schizophrenia.
Indications of family dysfunction include insecure attachment and exposure to childhood trauma, in particular, abuse.
A review found that adults with schizophrenia are *disproportionately* likely to have insecure attachment styles, specifically type C or D. Furthermore, it was reported 69% of women and 59% of men with schizophrenia had a history of physical and/or sexual abuse. Concluding the review, most people with schizophrenia in a study reported at least one trauma in childhood, concerning abuse.
This strongly implies family dysfunction has a role in creating vulnerability to schizophrenia.
- Flawed evidence for family dysfunction.
One limitation of the family dysfunction explanation is the poor evidence base. There is a presence of an excess evidence base to outline an association between childhood family-induced stress and schizophrenia development in adulthood - however, there is lack of evidence to support the traditional family explanation theories such as the *schizophrenogenic mother* and *double-bind*.
Both theories are based on clinical observations of people with schizophrenia, having an informal assessment of their mothers personalities, but NO SYSTEMATIC EVIDENCE. This means that the full extent of family explanations have not been able to properly account for the link between schizophrenia and childhood trauma.
81
What are the cognitive explanations for schizophrenia (psychological explanations)
- Dysfunctional thinking (including…)
- Metarepresentation dysfunction
- Central control dysfunction
82
What are cognitive explanations?
Explanations that focus on mental processes such as thinking, language and attention
83
What is meant by dysfunctional thinking in schizophrenia?
- A cognitive explanation that focuses on information processing that does not represent reality accurately, producing undesirable consequences.
84
What does schizophrenia have to do with dysfunctional thinking in the brain?
- Schizophrenia is characterised by disruption to normal thought processing
85
Which parts of the brain are associated with positive symptoms, and which parts are associated with negative symptoms?
- Negative symptoms:
Reduced thought processing in the **VENTRAL STRIATUM**
- Positive symptoms:
Reduced processing of informations in the **TEMPORAL** and *CINGULATE GYRI** - creates hallucinations.
(overall, lower than average levels of information processing suggests cognitive impairment)
86
Who identified the two dysfunctional thought processes of metarepresentation dysfunction and central control dysfunction?
Frith et al.
87
What are the two dysfunctional thought processes, proposed by Frith?
(cognitive explanations as part of psychological explanations for schizophrenia)
- Metarepresentation dysfunction
- Central control dysfunction.
88
What is meant by metarepresentation dysfunction?
- Metarepresentation is our cognitive ability to reflect on thoughts and behaviour, allowing insight into our intentions and goals, as well as interpreting others.
- Metarepresentation dysfunction is where there is a disruption in our ability to recognise our own thoughts and actions as being our own, rather than others.
This explains auditory hallucinations and thought insertion.
89
What is meant by central control dysfunction?
- Central control, in general, is the ability to suppress automatic responses while we perform deliberate actions
- Central control dysfunction is where a person with schizophrenia has the inability to suppress automatic thoughts and speech triggered by other thoughts. This leads to speech poverty and thought disorder, as well as derailment as each word triggers association and the individual cannot control automatic responses
90
Evaluate cognitive explanations as part of psychological explanations for schizophrenia
- Research support
One strength of cognitive explanations for schizophrenia is evidence for dysfunctional thought processing, specifically central control dysfunction. A study compared performance on a range of cognitive tasks in 30 people with schizophrenia compared to a control. Tasks included the Stroop task in which participants had to name the font colours of colour-words, meaning they have to suppress the tendency to read the words aloud. As predicted by Frith's central control theory, people with schizophrenia took longer - more than 2x the time for the control group to name the font colours. This means that the cognitive processes of people with schizophrenia are impaired.
- Proximal explanation
A limitation of cognitive explanations for schizophrenia is that they only explain the proximal origin of symptoms. Cognitive explanations for schizophrenia are deemed as proximal explanations due to explaining what is happening CURRENTLY to produce symptoms. This is distinct from distal explanations that explain what initially caused the condition. Possible distal explanations are genetic and family dysfunction. What currently remains unclear, and is not well addressed, is how genetic variation or childhood trauma may lead to problems with metarepresentation and central control. This means cognitive theories explaining schizophrenia, on their own, only provide a partial explanation.
91
What are the the 2 psychological treatments / therapy for schizophrenia?
- Family therapy
- Cognitive behavioral therapy (CBT)
92
What is cognitive behavioral therapy?
A method of treating mental disorders using both cognitive and behavioral techniques.
Cognitive techniques include challenging negative thoughts
93
In what ways can CBT help schizophrenia?
- CBT, overall, helps a client make sense of how their irrational cognitions (hallucinations and delusions) impact their feelings and behavior.
- Understanding the origin:
Simply understanding where symptoms come from such as auditory hallucinations can be helpful. A therapist can convince a client that a 'demonic voice' cannot harm them, and it is the result of a malfunctioning speech center in the brain - making symptoms less frightening and debilitating.
- Normalization
People with auditory hallucinations can be taught that hearing voices is an extension of the ordinary experience of thinking in words - called normalization.
- Reality testing
Delusions can be challenged by a process called reality testing. The therapist and client jointly examine the likelihood that beliefs are true. Even if delusions are resistant to reality testing, CBT still tackles the anxiety and depression people with schizophrenia face.
94
What are the 3 ways / techniques used for schizophrenia in CBT?
- Understanding what causes symptoms
- Normalization
- Reality testing
95
Evaluate cognitive behavioral therapy as a psychological treatment for schizophrenia.
- Evidence for effectiveness of CBT
One strength of CBT for schizophrenia is evidence for it's effectiveness. A review was taken on 34 studies using CBT as therapy for schizophrenia - it was concluded that there were small but significant effects on both positive AND negative symptoms. Other studies focusing on symptoms outlined reduction in frequency and severity of auditory hallucinations. Clinical advice from NICE (National Institute for health and Care Excellence) recommends CBT as a treatment for schizophrenia. This demonstrates both research and clinical experience support the benefits of CBT for schizophrenia.
- Lack of standardization across studies.
A limitation of CBT for schizophrenia is that studies include a wide range of techniques for different symptoms. This is a limitation as CBT techniques and schizophrenic symptoms vary widely from one case to another. It has been pointed out that different studies involve the use of different CBT techniques, and those who receive differing techniques may present with different combinations of positive and negative symptoms. The overall modest benefit of CBT for schizophrenia may conceal a wide variety of effects that depend on CBT technique and symptom presentation. This makes it hard to conclude how effective CBT will be in the case of a single particular person.
96
What is family therapy?
A psychological therapy for schizophrenia carried out with all or some family members - it has the aim of improving communication and reducing the stress of living as a family.
97
Who does family therapy always include?
The *identified patient* - this is a term that describes the member of the family who expresses the family's conflict.
98
In what 2 ways does family therapy help schizophrenia, according to Pharoah?
- Reduces negative emotions
Family therapy aims to reduce levels of expressed emotion (EE)
This reduces the level of emotion generally, especially negative emotions such as anger and guilt.
Reducing family stress caused is important to reduce risk of relapse.
- Improves the family ability to help
The therapist can encourage family members to form a therapeutic alliance whereby they all agree with the aims of therapy. From this, the therapist will attempt to improve the family's beliefs and behavior towards schizophrenia.
It also ensures, for the family members, balance is achieved between caring for the individual with schizophrenia and maintaining their own lives.
99
Who created the 'model of practice' in family therapy for treating schizophrenia?
Burbach.
100
List the 7 stages of Burbach's 'model of practice' in family therapy as a psychological therapy for schizophrenia.
- Phase 1:
Share basic information, providing emotional and practical support.
- Phase 2:
Identify resources, including what different family members can and CANNOT offer.
- Phase 3:
Encourage mutual understanding to create a safe space to express feelings
- Phase 4:
Identify unhelpful patterns of interaction
- Phase 5
Skills training ----> learn stress management techniques
- Phase 6:
Relapse prevention planning
- Phase 7:
Maintenance for the future
101
Evaluate family therapy as a psychological therapy for schizophrenia
- Evidence for effectiveness
One strength of family therapy for schizophrenia is evidence for it's effectiveness.
A review of studies concluded that family therapy was one of the most consistently effective treatments available for schizophrenia. Studies particularly looked at relapse rates, and these were found to be reduced typically by 50-60%. It was further concluded that using family therapy as mental health initially starts to decline is particularly promising in preventing relapse. Clinical advice from NICE recommends family therapy for everyone with schizophrenia.
This means family therapy is likely to be of benefit to people with early and 'full-blown' schizophrenia.
- Benefits to whole family
A further strength of family therapy for schizophrenia is that it's benefits extend to the family. Therapy provided by family therapy is not just for the benefit of the identified patient, but also for the family providing the care. A review of evidence found that these effects are important as family tends to provide the bulk of care for individuals with schizophrenia. By strengthening the functioning of the family, family therapy lessens the negative impact of schizophrenia on other family members and strengthens the ability to support their effected family member. This means that family therapy has wider benefits beyond the obvious positive impact on the identified patient.
102
What is used in the MANAGEMENT of schizophrenia?
Token economies
103
What are token economies?
A form of behavioral modification where desirable behaviors are encouraged via selective reinforcement
104
How were token economies first developed?
- Token economies were initially trialed in a ward of women diagnosed with schizophrenia.
- Every time the participants carried out a task such as making their bed or cleaning they were given a token that could be exchanged for ward privileges - for example: more time outside or being allowed to watch a movie.
- It was found that the number of tasks carried out increased **significantly**
105
What are the reasons for using a token economy in the management of schizophrenia?
- To tackle institutionalization
Token economies tackle institutionalization (due to prolonged hospitalization faced).
Due to institutionalization, people develop habits of neglect - ceasing to maintain hygiene or socialize with others in response to living without ordinary routine.
106
Who identified 3 categories of institutional behavior that is tackled by token economies?
Matson
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What are the 3 institutional behaviors tackled with token economies?
- Personal care
- Condition related behavior (e.g: apathy)
- Social behavior
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What are the 2 benefits of modifying schizophrenic behaviors with a token economy?
1) Improves quality of life within a hospital setting
2) 'Normalizes behavior' - making adaptation back to normal life easier for those who spend prolonged times in hospital.
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How is the token economy system used (basic)
- Desirable behaviors are decided for the individual, tailored to them.
- Tokens are given **immediately** to individuals when they carry out a desirable behavior.
- Tokens are exchanged for tangible awards - these should be **immediate** as delayed rewards are less effective.
110
Explain the theoretical operation of token economies
- Tokens are **secondary reinforcers** - this is because they only have value AFTER the receiver has learned they can be used to obtain meaningful rewards. Therefore, rewards are **primary reinforcers**
- As tokens are exchanged for a range of different primary reinforcers (rewards) - they are particularly powerful **secondary reinforcers** - being called **generalised reinforcers**
- In order for tokens to become secondary reinforcers, they are paired with rewards (the primary reinforcers) and administered together.
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What is behavioral modification?
A behavioral therapy based on operant conditioning
112
What are token economies examples of?
Behavioral modification
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Evaluate token economies for the management of schizophrenia
- Evidence for effectiveness
One strength of token economies in management of schizophrenia is evidence for their effectiveness.
Seven high quality studies published between 1999-2013 were identified that examined the effectiveness of token economies for those with hospitalized with chronic mental health issues. All studies showed a reduction in negative symptoms (avolition and speech poverty) and a further decline in frequency of unwanted behaviors.
This supports the value of token economies.
- COUNTERPOINT: evidence base criticized.
A counterpoint of research evidence supporting token economies is that the evidence base may be considered insufficient. A common issue with small numbers of studies, in this case 7, is potential for the 'file-drawer problem' The 'file-drawer problem' creates the consequence of potential bias towards positive findings, whilst undesirable results are 'filed away'
This may be a problem particularly for reviews that include only a small evidence base of studies. This means that there is a serious debate over evidence for effectiveness of token economies.
- Ethical issues
A limitation of using token economies to manage schizophrenia is ethical issues raised. The use of token economies is ethically sensitive due to it giving professionals considerable power to control patients behavior. Token economies, inevitably, involve imposing the institutions norms on others - this is problematic when target behaviors are not identified in a sensitive manner. If someone prefers to get up late or remain in pajamas, they may have their personal freedoms curtailed. With more serious implications, restricting pleasures (rewards) to people who don't behave as desired means severely ill people who already have distressing symptoms are denied enjoyment. This proposes the argument that the token economy system favors those displaying mild symptoms.
This criticism of the token economy has led to decline of it's usage - therefore, token economies benefits are outweighed by their impact on personal freedom and potential reduction in quality of life in hospitals.
- Alternative approaches
A further limitation of token economies is the existence of more ethical alternatives. Although token economies can be helpful for managing schizophrenia there are other approaches with a comparable evidence base that do not raise the same ethical issues. A review concluded that art therapy may be a good alternative. The evidence base is regularly small, and has some methodological limitations, however it appears to show that art therapy is a high gain and low risk approach to managing schizophrenia. Even if art therapy benefits are modest, this is generally true for all approaches to treatment and management of schizophrenia, and unlike alternatives, art therapy is a pleasant experience without risk of side effects or ethical disputes.
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What comes under the diagnosis and classification topic of schizophrenia?
- Diagnosis and classification
- ICD-11 and DSM-5
- Positive symptoms (hallucinations and delusions)
- Negative symptoms (avolition and speech poverty)
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What comes under the *issues* in diagnosis and classification topic of schizophrenia?
- Good reliability
- Low validity
- Co-morbidity
- Culture bias in diagnosis
- Symptom overlap
- Gender bias in diagnosis
116
What comes under the biological explanations for schizophrenia?
- **Genetic basis** (includes...)
- Family studies
- Candidate genes
- Role of mutation
- **Neural correlates** (includes...)
- Original dopamine hypothesis
- Updated dopamine hypothesis
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What comes under psychological explanations for schizophrenia?
- **Family dysfunction** (includes..)
- Schizophrenogenic mother
- Double-bind theory
- Expressed emotion
- **Cognitive explanations** (includes...)
- Dysfunctional thinking -----> central control dysfunction and metarepresentation dysfunction.
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What comes under the biological therapy topic for schizophrenia?
- Typical anti-psychotics (sedation effect and dopamine antagonists)
- Atypical anti-psychotics
119
What comes under the psychological therapy for schizophrenia?
- **Cognitive behavioral therapy** (includes...)
- How CBT helps
- **Family therapy** (includes...)
- How family therapy helps
- Burbach's model of practice
120
What comes under the management of schizophrenia topic?
- How token economies were developed
- The reasons for using token economy
- What is involved in a token economy
- Theoretical understanding of TC: behavioral modification and reinforcers.
121
What comes under the interactionist approach topic?
- The interactionist approach definition
- Meehl's **diathesis stress model**.
- Modern understanding of diathesis
- Modern understanding of stress.
- Treatment according to the interactionist approach.
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Define "the interactionist approach"
A way of explaining the development of behaviour by combining a range of factors - including *biological* and *psychological*.
The most important part of this is that such factors don't simply add together, they combine in a way that cant be predicted by each one separately - they **interact**.
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What is the diathesis-stress model?
An interactionist approach to explaining behaviour.
In the diathesis-stress model, schizophrenia is explained as a result of both..
- Underlying vulnerability ---> *diathesis*
- A trigger ---> *stressor*
**Both of these are necessary for the onset of schizophrenia**
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Who created the original diathesis stress model?
Meehl
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What did Meehl's original diathesis-stress model say about schizophrenia?
- Diathesis (vulnerability) was entirely *genetic* - the result of a single **schizogene**, this led to the idea of a biologically based **schizotypic personality**, characterized by 'sensitivity to stress'.
- Meehl also stated, about diathesis that if one does not have the **singular schizogene**, NO amount of stress would lead to schizophrenia.
- For people with the gene, chronic stress through childhood and adolescence, in particular with the presence of a *schizophrenogenic mother* could result in the disorder developing.
126
What researchers contributed to the 'modern understanding of diathesis?*
- Ingram and Luxton (extending diathesis into psychological)
- Read (proposing how trauma alters the brain)
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How does the modern understanding of *diathesis* differ from Meehl's original diathesis stress model?
Modern understanding of diathesis sees that...
- Multiple genes appear to increase genetic vulnerability slightly.
- There is NO '*schizogene*'
- Diathesis now includes a range of factors beyond genetic, including psychological trauma - so trauma can be the **diathesis** rather than **stressor** (INGRAM AND LUXTON)
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What proposition supports Ingram and Luxton's idea that diathesis can be psychological?
- Read et al.
- Read et al. proposed a neurodevelopmental model to account for how early trauma can alter the developing brain.
- In this early, and severe enough, trauma - such as child abuse - severely impacts the brains development.
- A brain section affected is the **Hypothalamic-Pituitary-Adrenal System** (HPA) - it becomes overactive, making a person much more vulnerable to later stress.
129
How does the modern understanding of *stress* differ from Meehl's original diathesis stress model?
- Stress was originally seen as psychological in nature, in relation to parenting under Meehl's model.
- In current understanding of stress, this can still be important, however the modern definition of stress in the diathesis-stress model includes *anything* that risks triggering schizophrenia.
130
Against Meehl's idea that the schizogene was the only diathesis, what is an alternative diathesis (vulnerability) in our understanding modernly?
- Psychological trauma, such as child abuse - so trauma is the diathesis rather than stressor.
131
Against Meehl's idea that the psychological factor of parenting is a stressor, what is an alternative 'stressor' in our understanding modernly?
- Cannabis use
- HOWEVER, note that parenting can still be a stressor!
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Why can cannabis be deemed as a 'stressor' - including research.
- Research into factors 'triggering' schizophrenia concerns cannabis use - in the modern diathesis-stress model for schizophrenia, cannabis use is a **stressor** as it increases the risk of schizophrenia up to **7x more**.
- To explain this, this is because cannabis interferes with the dopamine system. However, most do not develop schizophrenia after cannabis use, presumably because they lack the required vulnerability factors needed to interact and cause it.
133
What treatment should be administered for schizophrenia, according to the interactionist approach.
- The interactionist model of schizophrenia acknowledges BOTH biological and psychological factors, so it is therefore compatible with **both biological and psychological treatments**
So the model accepts combining *anti-psychotic medication* (a biological treatment) with psychological therapies such as *CBT*
134
Who pointed out that it is possible to believe in biological causes of schizophrenia and still practice CBT to relieve psychological symptoms? and what is the issue with this?
Turkington.
- The issue with this is: this requires adopting the interactionist model, it is not possible to have a purely biological approach, and inform those diagnosed that there is a purely biological cause with no psychological significance, and then treat them with CBT.
135
What is the difference between Britain and America in how they utilize the interactionist approach to treat people with schizophrenia?
- **Britain**: In Britain, it is standard practice to treat people diagnosed with schizophrenia using a *combination* of anti-psychotics and CBT.
- **USA**: In the USA, there is a history of conflict with biological and psychological models of schizophrenia - hence, there is a slower adoption of the *interactionist approach*. So - medication without an accompanying psychological treatment, and vice-versa, is more common here.
136
Evaluate the interactionist approach to schizophrenia.
- Support for vulnerability and triggers (YAH FINLAND).
One strength of the interactionist approach to schizophrenia is evidence supporting the role of both vulnerability and triggers.
There was a *large scale* study investigating the impact of both genetic vulnerability and a psychological trigger (dysfunctional parenting). The study followed 19000 Finnish children whose biological mothers had received a schizophrenia diagnosis. In adulthood, the high genetic risk group were compared to a control group of adoptees without a family history of schizophrenia (low risk). Adoptive parents had been assessed for child rearing style and it was found that high levels of criticism and hostility, along with lack of empathy were STRONGLY associated with the onset of schizophrenia, *but only in the high genetic risk group*.
This shows that a combination of genetic vulnerability and family stress can lead to a greatly increased risk of onset, predicted by the interactionist model.
- Diathesis and stress are complex.
One limitation of the original diathesis-stress model (Meehl) is oversimplicity. In modern models, it is now clear that Meehl's portrayal diathesis as one single 'schizogene' and stress as schizophrenogenic parenting is hopelessly simplistic.
Multiple genes in multiple combinations influence diathesis, and stress also comes in many forms, including, *but not limited to* dysfunctional parenting. In fact, diathesis can also be influenced by psychological factors meanwhile stress can be both biological and psychological.
A study outlined this - supporting modern theories. The study saw childhood sexual abuse emerge as the major influence on underlying vulnerability, and cannabis was a major trigger. This means that there are multiple factors, both psychological and biological that work as diathesis and stress, supporting the modern understanding rather than the original diathesis-stress model.
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