SCHIZOPHRENIA Flashcards
(103 cards)
1
Q
form of psychosis
A
severe mental disorder where thoughts and emotions are significantly impaired and there is loss of touch with reality
2
Q
culturally universal
A
1% of world population
seen in all cultures - not due to culture
more commonly diagnosed in urban than rural areas
* Slightly more commonly diagnosed in men than in women.
Onset for men tends to be between 15-24 years.
Onset for women is more prevalent between 25-34 years.
3
Q
positive symptoms
A
- Behaviours not generally seen in ‘normal’ people.
Something extra
A behaviour or reaction that you didn’t have before.
hallucinations
delusions
4
Q
hallucinations
A
- Bizarre, unreal perceptions of the environment that other people don’t experience.
- Usually auditory (hearing voices), but can be visual (seeing things), olfactory (smelling things) or tactile (e.g. feeling bugs crawling).
- Many report hearing a voice or several voices telling them to do something or commenting on their behaviour.
5
Q
delusions
A
- Bizarre beliefs that seem real but aren’t.
- Can be paranoid in nature.
- Often involves a belief that the person is being followed or spied upon by someone.
- May also involve inflated beliefs about the person’s power and importance (delusions of grandeur) e.g. may believe they are famous or have special powers.
- May also experience delusions of references, where events in the environment appear directly related to them.
6
Q
negative symptoms
A
- Associated with disrupted to normal emotions and behaviour.
Reflect a reduction or loss of normal function.
avolition
speech poverty (alogia)
disorganised speech
flattened/blunted affect
anhedonia
7
Q
avolition
A
- Reduction in interests and desires and inability to initiate and persist in goal-oriented behaviour.
- Distinct from poor social function or disinterest.
- Reduction in self-initiated involvement in activities available to the patient.
8
Q
speech poverty (alogia)
A
- Lessening of speech fluency and productivity, thought to reflect slowing or blocked thoughts.
- Fewer words in a given time on a verbal fluency task – difficulty of spontaneously producing them.
- Reflected in less complex syntax e.g. fewer clauses, shorter utterances.
- Associated with long illness and earlier onset of the illness.
9
Q
disorganised speech
A
- Result of abnormal thought processes, where the individual has problems organising thoughts.
- May slip from one topic to another (derailment) even midsentence.
- Speech may be incoherent and sound like gibberish.
10
Q
flattened / blunted affect
A
- Reduction in range and intensity of emotional expression, including facial expression, voice tone, eye contact and body language.
- Individuals show fewer body and facial movements and less co-verbal behaviour.
- Deficit in prosody (paralinguistic features) that provide extra information not explicitly contained in a sentence and gives cues to the listener as to emotional or attitudinal content and turn-taking.
11
Q
anhedonia
A
- Loss of interest and pleasure in all or almost all activities, or a lack of reactivity to normally pleasurable stimuli. May be pervasive or confined to certain aspect of experience.
- Physical anhedonia is inability to experience physical pleasures e.g. food, bodily contact.
- Social anhedonia is inability to experience pleasure from interpersonal; situations such as interacting with other people.
12
Q
comorbidity
A
Simultaneous presence of two or more diseases or medical conditions.
May cause misdiagnoses.
13
Q
symptom overlap
A
People diagnosed with one mental disorder simultaneously show symptoms of another psychological disorder.
May cause misdiagnoses.
14
Q
diagnostic criteria
A
- To diagnose psychological disorders, qualified practitioners will consult classification systems / diagnostic criteria that outline symptoms required to be evidenced by patient.
- DSM-5 (Diagnostic and Statistical Manual of Psychiatric Disorders) created by American Psychiatric Association.
- ICD-11 (International Classification of Diseases) developed by World Health Organisation and is commonly used in Europe and in the rest of the world.
Suggest similar persistent symptoms
Differences in criteria – symptoms for 1 or 6 months.
Criteria lacks consistency, reducing reliability and validity of diagnoses.
15
Q
reliability of diagnoses
A
- Reliability refers to consistency and how consistently the same diagnosis is made.
- Test-retest reliability – diagnose somebody, then repeat and compare results to check consistency.
- Inter-rater reliability – make diagnosis and ask somebody else to see if they would make same diagnosis.
Measured statistically using a Kappa score (coefficient used for qualitative analysis.
Score of 0.7 is generally deemed acceptable. - Read found that diagnosis of schizophrenia only had a 37% concordance rate when diagnoses were made on two separate occasions.
194 British and 134 US psychiatrists gave diagnoses based on a case description. 69% of US psychiatrists diagnosed schizophrenia compared to 2% of British psychiatrists.
Used test re-test. Low reliability due to 0.37 concordance rate (0.7 acceptable).
Poor inter-rater reliability – differs across countries.
16
Q
validity of diagnoses
A
- Validity refers to accuracy.
- Correctly diagnosing schizophrenia as a distinct disorder and not misdiagnosing a different disorder.
- Descriptive validity – diagnosis is valid if symptoms differ significantly from those of other diagnosable conditions. Can therefore be considered a distinct disorder.
- Criterion validity – the extent to which using different classification symptoms produces the same diagnosis in the same patient.
- Cheniaux asked 2 psychiatrists to diagnose a hundred patients using the ICD and DSM.
One diagnosed 26/100 patients with schizophrenia using the DSM and 44/100 using the ICD. The other diagnosed 13 with the DSM and 24 using the ICD.
Suggests criteria is not valid – less diagnoses with DSM than ICD.
Challenges criterion validity as both produce different diagnoses. Cannot accurately diagnose, do not know that schizophrenia is distinct from other disorders. Lacks descriptive validity.
17
Q
Rosenhan aims
A
- To test the hypothesis that psychiatrists cannot reliably tell the difference between people who are sane and those who are insane.
18
Q
Rosenhan procedure
A
- Field experiment, participant observation.
- Participants were hospital staff in 12 hospitals.
- 8 sane people tried to gain admission to hospitals. Complained that they had been hearing voices, which was of the same sex as themselves, unfamiliar and unclear. Gave false name and job but other details were true.
- After admission, stopped simulating abnormality, took part in activities and conversations as they would ordinarily. They said they felt fine and no longer had symptoms. Told they could leave by convincing staff they were sane.
- None were detected and all but one were admitted with a diagnosis of schizophrenia and were eventually discharged with ‘schizophrenia with remission’. Normal behaviours were seen as aspects of supposed illness.
- In second study, staff were told that a pseudo-patient would be admitted and asked psychiatrists to rate every new patient on a 10-point scale for the likelihood of them being a pseudo-patient.
19
Q
Rosenhan results
A
- Psychiatrists cannot reliably tell the difference between people who are sane and those who are insane.
- Main experiment illustrated a failure to detect sanity and secondary study demonstrated a failure to detect insanity.
- Suggests that psychiatric labels stick and everything a patient does is interpreted in accordance with the diagnostic label once it has been applied.
- Suggests that diagnoses may lack reliability and that misdiagnoses are common.
- Psychiatrists were not making accurate diagnoses – even though only had one symptom, they were diagnosed with schizophrenia. Should not be enough to make any diagnosis.
- Diagnoses were consistent – all pseudo-patients who complained of symptoms were misdiagnosed – suggests reliability but not valid.
20
Q
comorbidity
A
- Presence of multiple disorders existing at the same time.
- Schizophrenia is commonly comorbid with depression, PTSD, OCD, and substance abuse.
- Buckley reported that an estimated 50% of schizophrenia patients had co-morbid depression, 29% had PTSD and 23% OCD. 47% had co-morbid substance abuse.
- Reduces descriptive validity – do not know whether we are actually looking at schizophrenia and a comorbid disorder, rather than a completely separate disorder that encompasses symptoms from both diagnosable disorders.
- Reduces reliability (test-retest / inter-observer) – if a person exhibits two different disorders at the same time, this could impact diagnoses at different points or between psychiatrists depending on which symptoms of which disorder are more prevalent at each point of diagnosis.
- Implications (affecting treatment and prognosis) – practitioners cannot know which treatment is best if diagnosis is complicated by the presence of multiple disorders.
More likely to be adverse health outcomes, as one may go untreated in favour of the other being treated, possibly due to the avoidance of interactions between differing treatments.
21
Q
symptom overlap
A
- Where symptoms used in the diagnosis of one disorder are also present as part of the diagnostic criteria for a different disorder.
- Schizophrenia overlaps with bipolar – both share positive symptoms like delusions and negative symptoms like avolition.
- Ophoff assessed genetic material from 50,000 participants to find that of 7 gene locations on the genome associated with schizophrenia, 3 were also associated with bipolar disorder, suggesting a genetic overlap.
- Also overlaps with cocaine intoxication and dissociative identity disorder (DID).
- Reduces descriptive validity – hard to discern which of the possible disorders is more accurate if showing symptoms of more than one disorder.
- Reduces inter-rater reliability – different psychiatrists may diagnose different disorders if symptoms can be attributed to more than one disorder.
- Ketter suggested that misdiagnosis due to symptom overlap can lead to years of delay in appropriate treatment.
- However, Serper found that despite there being considerable symptom overlap in patients with schizophrenia and cocaine abuse, it was possible to make accurate diagnoses.
22
Q
gender bias
A
- Longenecker found that men have been diagnosed with schizophrenia more often than women.
Psychiatrists have historically been more male than female.
Diagnoses may be predominantly from a male perspective of what constitutes ‘abnormal’ behaviour (androcentrism).
Females tend to have a higher level of functioning than males which could mask symptoms and lead to underdiagnosis. E.g. males tend to experience more negative symptoms than females, leading to greater impairment of functioning. - Loring and Powell randomly selected 290 male and female psychiatrists to read two case articles of patients’ behaviour.
When participants were described as male or there was no information about their gender, 56% were diagnosed with schizophrenia.
When they were female, only 20% were diagnosed.
The gender bias did not appear to be evident amongst the female psychiatrists.
Suggests that women are better at diagnosing without bias.
Gender bias affects who is diagnosed. - Women are more likely to go underdiagnosed, and therefore face delay in treatment, which can lead to the disorder becoming more progressed.
23
Q
culture bias
A
- Tendency to over-diagnose schizophrenia in ethnic minority cultures.
- Cochrane reported incidence of schizophrenia in the West Indies and Britain to be similar (~1%), but people of Afro-Caribbean descent were seven times more likely to be diagnosed when living in Britain.
Imposed etic - British standardised culture and social norms are used as a reference for diagnosis.
Suggests that diagnoses are not accurate or valid across cultures.
Low inter-rater reliability – psychiatrists in different cultures would not make the same diagnoses. - Rack suggested that in many cultures it is normal to see and hear recently deceased loved ones (often part of the grieving process).
Glossolalia (speaking in tongues) is a common religious practice among Pentecostal Christians, a branch common amongst ethnic minorities, including Afro-Caribbean.
Such practices are unfamiliar in Western culture and so can lead to incorrect interpretation of behaviour as being symptoms of schizophrenia when they are normal practices. - Escobar pointed out that white psychiatrists may tend to over-interpret the symptoms of black people during diagnosis.
Increased risk of over-diagnosing people from a particular culture.
Could then result in unnecessary or inappropriate treatments that can sometimes have serious negative effects.
Could be prejudice and discrimination against particular ethnicities due to a lack of understanding of cultural practices.
Risk pathologising behaviour because it is different to our own culture. - Research into schizophrenia should take a culturally relativist approach.
People should be diagnosed by psychiatrists from their own cultures so they understand the complexities of their culture.
Would lead to greater accuracy.
24
Q
biological explanations
A
genetic explanations
neural correlates
dopamine hypothesis
drug treatments
25
genetic explantions
* Schizophrenia is hereditary – the trait is transmitted from parents to offspring.
* Based on concordance rates of schizophrenia between family members.
Measure of similarity between family members.
If one family member has schizophrenia, the percentage likelihood that other family members will have it too.
* Twin studies and comparing concordance rates between monozygotic and dizygotic twins can be used to study genetics as a potential cause.
Monozygotic twins share 100% of DNA
Dizygotic twins share 50% of DNA – share as much DNA as regular siblings.
Adoption studies can help determine whether due to nature or nurture by twins having different shared environments.
26
Gottesman
* Studied 57 pairs of twins.
Concordance rate for MZ twins was 42%.
Concordance rate for DZ twins was 9%.
* Carried out family studies, where concordance rates are assessed between relations of different degrees.
Suggests that schizophrenia has some genetic components.
Higher occurrence of schizophrenia when higher degrees of relatedness.
However, cannot be only factor as not 100% or 50% concordance rates.
27
polygenetic
* Caused by many different genes, and not one single schizophrenia-causing gene, or genes may provide a genetic vulnerability.
* Ripke found that 108 separate genetic combinations were associated with increased risk of schizophrenia.
* Accepted that schizophrenia is aetiologically heterogeneous – number of different combinations of genes can lead to it.
* E.g. COMT gene
28
genetic explanations strengths
practical applications
Being able to identify candidate genes that may be involved in the onset of schizophrenia could lead to clear applications.
Gene mapping – process of establishing the locations of genes on chromosomes. By following inheritance patterns, the relative positions of genes can be determined.
Can lead to benefits like monitoring and recognising symptoms earlier and having earlier diagnosis due to figuring out who has a genetic vulnerability for schizophrenia. Can receive treatment and can slow or reduce severity of symptoms. Disorder is more manageable, help improve quality of life.
Therefore the genetic explanation is useful.
However, this could be socially sensitive (research leading to prejudice, discrimination, or cause offence) as it can place responsibility and blame on the parents if their child has schizophrenia as they have given them the gene.
29
genetic explanations weaknesses
shared environments
Issue of shared environments could cast doubt on the role of genetics, particularly in twin studies.
Gottesman found a higher concordance rate for schizophrenia in MZ (42%) than in DZ twins (9%).
Could be due to shared environment as MZ twins are identical, so are more likely to treated the same, due to others’ perception of them being similar.
Higher degrees of relatedness, more of a shared environment (confounding variable).
Questions validity of concluding that higher concordance rates for schizophrenia are due to degree of genetic relatedness as other environmental factors could influence this.
Can’t always separate nature and nurture.
* However, there is evidence from adoption studies to support the role of genetics in schizophrenia.
Tienari found that adopted children of biological mothers with schizophrenia were more likely to develop the disorder themselves than adopted children of mothers without schizophrenia.
Reinforces the idea of inherited genetics having a larger influence on schizophrenia than environmental influences, therefore the theory is valid and credible.
30
genetic explanations weaknesses
concordance rates
If schizophrenia has an entirely genetic basis, we expect concordance rates to be 100% for monozygotic twins and 50% for dizygotic twins.
Should be in line with degrees of genetic relatedness if purely genetic e.g. first line family members with 50% shared genetics should have 50% concordance rates (6-17%).
Gottesman found that concordance rates for monozygotic and dizygotic twins are 48% and 17% respectively.
Suggests that genetics cannot provide a complete explanation but there must be other factors influencing the occurrence of schizophrenia.
Therefore the genetic explanation is reductionist.
May provide a genetic vulnerability to schizophrenia, but other factors may influence whether it actually occurs.
31
genetic explanations weaknesses
family history
Schizophrenia can occur in the absence of any family history.
Brown found a positive correlation between paternal age and risk of schizophrenia. The risk increased for 0.7% in fathers under 25 to 2% in fathers aged over 50.
A potential explanation is a mutation in parental DNA e.g. mutations are more likely with age in paternal sperm cells.
Age of parents and mutations determines presence of candidate gene.
Contradicts the suggestion of schizophrenia being hereditary but is caused by a mutation due to genes.
Limits validity of genetic explanations.
However, Brown’s research is correlational.
Cannot establish cause and effect.
32
neural correlates
* When structures or neurochemical processes in the brain can be associated with a particular disorder, function or characteristic.
* Assumption is that they may be implicated in originating the experience.
* Thought that specific structures and neurochemical imbalances in the brain are linked to different positive and negative symptoms.
33
superior temporal gyrus
* Linked with auditory hallucinations (positive)
* Allen carried out brain scans of schizophrenics and a control group while they were tasked with identifying speech as either their own or someone else’s.
Found lower activity in the part of the brain.
More mistakes were made by schizophrenics.
34
ventral striatum
* Linked with avolition – loss of motivation (negative)
* Juckel found lower levels of activity in this part of the brain (involved in reward anticipation) in schizophrenics compared to a control group.
Observed a negative correlation with functioning in this part of the brain and severity of symptoms.
35
dopamine hypothesis
hyperdopaminergia in subcortex
* High levels of dopamine activity in the central areas of the brain, notably the subcortical and limbic brain regions.
Mesolimbic pathway
* Thought to be due to hyperactivity of dopamine D2 receptors in these regions.
* More associated with positive symptoms e.g. hallucinations, delusions.
* Dopamine is excitatory – increased volume, more activation and impulses sent through the brain results in higher level of activity.
* Version 1 of the theory – proposed in the 1970s after success of antipsychotic drugs treating psychosis. Carlson identified that these drugs worked via dopamine receptors.
36
dopamine hypothesis
hypodopaminergia in cortex
* Goldman found low levels of dopamine in the prefrontal cortex (thinking and decision making) and linked this to negative symptoms.
Mesocortical pathway
* Believed to be hypofunctionality (reduced function) of dopamine D1 receptor neurotransmission in the prefrontal cortex.
* Linked to avolition – less activation results in lower level of functioning, low motivation and lack of speech production.
* Version 2 of the theory – added in 1991 by Davis who proposed regional specificity in addition to the original version.
37
dopamine hypothesis strengths
drug evidence
* Evidence from effects of different drugs to support the role of dopamine in psychotic symptoms associated with schizophrenia.
Curran found that dopamine agonists (drugs which increase activity) such as amphetamines produce schizophrenia-type symptoms in patients.
Supports idea of neural correlates and hyperdopaminergia as increased dopamine leads to schizophrenia symptoms.
Suggests the theory has validity.
Leads to better evidence of cause and effect – manipulating levels through drugs and observing symptoms.
However, this contradicts the idea of hypodopaminergia – suggests may depend on which dopaminergic pathway in the brain is affected.
38
dopamine hypothesis weaknesses
correlation
Neural correlates only show an association between areas of the brain and symptoms of schizophrenia.
Superior temporal gyrus associated with auditory hallucinations.
Cause and effect cannot be established.
Bidirectional – schizophrenia may cause changed function or neurotransmitter activity, or this may cause schizophrenia.
Therefore validity is limited.
39
dopamine hypothesis weaknesses
other neurotransmitters
May be other neurotransmitters involved in the onset of schizophrenia.
Glutamate alternatively linked to schizophrenia.
Acts as a brake or accelerator of dopamine so may be levels of glutamate that lead to either hyper- or hypodominergia in different brain regions.
Suggests that the dopamine hypothesis is too simplistic and we need to look at the interaction of other neurotransmitters.
Therefore our understanding of schizophrenia is still developing and is more complex than we originally thought.
40
dopamine hypothesis weaknesses
physiologically reductionist
Biological explanations such as neural correlates can be seen as physiologically reductionist.
Doesn’t consider cultural, societal, cognitive or behavioural influences on schizophrenia symptoms. Narrows it down to the role of neurotransmitters, structures within the brain and dopamine levels.
Focusing on biological structures and processes and neglects to consider the influence of other factors such as psychological or societal factors.
Such explanations could be oversimplifying schizophrenia by only considering its cause to be at its lowest level (neuroanatomical) and not considering how multiple factors interconnect to provide a more complex account of the disorder.
41
drug treatments
* Antipsychotic drugs (neuroleptics) are the most common treatment of schizophrenia.
* They work by regulating the action of the neurotransmitter dopamine in areas of the brain associated with schizophrenia.
* They reduce symptoms to allow for some degree of functioning to become possible, but they do not offer a cure.
42
typical antipsychotics
* Referred to as ‘first generation’ as they were the first to be used in the 1950s.
* Reduce dopamine activity by blocking dopamine receptors at synapse. Lower levels can excite the neurone.
* Calms dopamine system in brain, reducing positive symptoms e.g. hallucinations and delusions and have a general sedative effect.
* Antagonists – bind to but do not stimulate dopamine receptors.
Particularly D2 receptors in mesolimbic dopamine pathway.
Limits the effect of dopamine on the post synaptic neurone.
* E.g. chlorpromazine
43
atypical antipsychotics
* Used from 1970s.
* Block dopamine receptors and act on other neurotransmitters e.g. glutamate and serotonin (dual-action).
* Mainly positive symptoms but also target negative symptoms such as flattened affect and anhedonia.
* Agonistic
* Activate dopamine neurones in mesocortical pathway, leading to more dopamine release in the prefrontal cortex.
* E.g. clozapine has partial agonistic action at dopamine D2 receptors, stimulating neurones, leading to an increase of dopamine.
44
drug treatments strengths
research evidence
* There is research evidence to support that drug therapies are effective.
Leuch et al carried out a meta-analysis who had been stabilised on antipsychotics. Some were taken off the drugs and given a placebo instead.
Within 12 months, 64% of the patients given the placebo had relapsed, compared with 27% who had stayed on the drug.
This is a strength as it demonstrates effectiveness.
Meta-analysis demonstrates high consistency and reliability. Results can be compared against placebo to establish cause and effect.
Therefore this suggests that drug therapies are valid and have practical applications.
45
drug treatments weaknesses
negative outcomes
There are potential negative outcomes/consequences of the treatment.
Typical antipsychotics can also lead to Tardive Dyskenesia which is an involuntary neurological disorder causing involuntary movements e.g. facial tics and grimaces.
Impacts adherence to taking meds (potential revolving door effect) and drugs create undesirable side effects which makes it unlikely for people to continue to take the drugs.
Therefore, this suggests that psychological therapies may be better due to no side effects and more likely to finish course than drug therapies.
46
drug treatments weaknesses
evidence to refute
There is evidence to question the effectiveness of the treatment.
Ross and Read suggest that drugs reduce the effects but not the cause, and therefore they decrease the motivation of the patient to find their cause of schizophrenia, leading to motivational deficits.
Schizophrenia may be affected by environmental factors, such as family environment, and drugs reduce symptoms but do not address the issue.
Limits effectiveness and practical applications.
47
drug treatments weaknesses
alternative treatments
There are alternative treatments that highlight issues with drug treatment.
Xiong randomly allocated schizophrenics into standard drug care or drug care with family therapy. After 1 year, 61% of standard drug care relapsed, compared to 33% of standard care with family therapy patients.
Suggests that drugs are not effective in addressing the issue as cannot treat cognitive and environmental influences which play a role.
This suggests that the theory is reductionist and we should consider an interactionist approach.
48
drug treatments weaknesses
practical implications
There are practical implications of time/cost/inconvenience relating to drug treatment.
CAMH highlighted that it can take up to 4-6 weeks for antipsychotics to take full effect.
Patients may lack motivation towards to taking drugs if not experiencing improvements and suffering side effects. Not taking the drugs mean the patient does not improve.
This suggests that drug therapy can be ineffective and impractical.
49
drug treatments weaknesses
moral implications
There are potential moral implications that could be raised by this treatment.
In 2011, 3 million Americans were prescribed antipsychotics, generating $18 billion in profits. Prescriptions for atypical antipsychotics increased by 93% between 2001 and 2011, though the incidence rate for schizophrenia remained the same.
Pushing use of drug therapies more than is required. Focus is on the profit of large pharmaceutical companies over the benefit of the individual.
Drug therapies may be overprescribed without the individual in mind – may not be most effective treatment.
50
psychological explanations
family dysfunction
51
family dysfunction
* Family dysfunction theory links schizophrenia to experiences of living within a dysfunctional family.
Poor communication
Cold parenting
High levels of expressed emotion (negatively directed at individuals)
52
double bind theory
* When communication produces a mixed message.
E.g. if a mother tells her son that she loves him, yet at the same time turns her head away in disgust, the child receives conflicting messages about their relationship on different communication levels.
Affection on the verbal level
Animosity on the non-verbal level
* Child’s ability to respond to the parent is incapacitated by such contradictions because one message invalidates the other.
* Prolonged exposure prevents development of an internally coherent construction of reality. In the long run, this manifests itself as typically schizophrenic symptoms such as flattened affect, delusions and hallucinations, incoherent thinking and disorganised speech and paranoia.
53
double bind theory strengths
evidence to support
There is evidence to support double bind theory.
Berger found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics.
Higher recall indicates prolonger exposure and higher occurrence of double bind statements. Suggests they are linked with schizophrenia.
Suggests theory has validity.
However, memory is not always reliable or accurate, especially schizophrenics who have a distorted perception of reality, and so their recall might not be accurate to reality e.g. recall in persecutory or paranoid way.
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double bind theory weaknesses
evidence to contradict
There is evidence to contradict double bind theory.
Hall and Levin analysed data from previous studies and found no difference in the extent to which there was discrepancy between verbal and non-verbal communication between families with a schizophrenic and those without.
No greater prevalence of double bind in families with schizophrenics than without.
Questions validity of theory.
55
expressed emotion
* When negative emotions dominate communication patterns within the family and therefore affect how they act.
Verbal criticism
Hostility towards the patient including anger or aggression
Emotional over-involvement
Overly moralistic, secret alliances encouraging paranoid symptoms such as delusions of persecution.
* Is primarily an explanation for relapse but has also been suggested as a source of stress that could trigger the onset of schizophrenia in someone who is genetically vulnerable (diathesis-stress).
Influence relapse rates of recovering schizophrenics who return to their families after treatment.
High stress levels this creates triggers a schizophrenic episode.
56
expressed emotion strengths
evidence to link to relapse
Evidence to link expressed emotion to relapse rates.
Kavanagh reviewed 26 studies and found that mean relapse rate for schizophrenia when returning to high expressed emotion families was 48%, compared to 21% in low expressed emotion.
Supports role of expressed emotion in creating relapse, adds validity.
However, only explains relapse rates and not the cause of schizophrenia.
Usefulness of theory limited, does not offer causal explanation.
57
expressed emotion strengths
treatments
Understanding role of expressed emotion in schizophrenia has lead to effective treatments.
Family therapy focuses on improving communication and reducing hostility and has proven successful in reducing relapse.
Treatment is effective, so theory has validity.
Theory is useful and has lead to significant benefits improving lives.
58
expressed emotion weaknesses
individual differences
Role of individual differences affecting vulnerability to expressed emotion.
Altorfer found that ¼ of patients show no physiological responses to stressful comments from relatives.
Different people may have different reactivity and response levels to stressful environments.
Cannot say it is true of all individuals, nomothetic – assuming have same effect on everybody.
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family dysfunction weaknesses
contradicting evidence
Contradicting evidence
Liem and Hall found that there was no difference in patterns of parental communication in families with a schizophrenic child compared to normal families.
Contradicts the role of negative communication in schizophrenia.
Decreases validity of theory.
60
family dysfunction weaknesses
no cause and effect
Do not know whether family dysfunction is the cause or effect of having a family member with schizophrenia.
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schizophrenogenic mother
* Based on ideas from accounts about childhood from schizophrenic patients.
* Characteristics include: overprotective, cold, rejecting, controlling, environment of tension and secrecy
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schizophrenogenic mother strengths
research evidence
Mednick studied 207 children at high risk to developing schizophrenia due to being raised in dysfunctional families, specifically with mothers who were cold, temperamental, rejecting and emotionally controlling. After 10 years, 17 developed schizophrenia compared to only 1 in the control group.
Suggests theat characteristics of the mother influences the likelihood of developing schizophrenia, validating the concept.
63
schizophrenogenic mother weaknesses
lacks temporal validity
Lacks temporal validity
Family structures do not always have a traditional mother as a primary caregiver.
May not account for all families, who do not place as much emphasis on the mother.
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schizophrenogenic mother weaknesses
recalled accounts
Theory based on recalled accounts from schizophrenic patients about their experiences in childhood.
May have inaccurate or delusional perception of reality, memory likely to be inaccurate.
Theory not based on reliable evidence.
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schizophrenogenic mother weaknesses
socially sensitive
Socially sensitive
Places blame upon mother.
Gynocentric, alpha bias (exaggerating differences between males and females).
Psychic determination - childhood experiences shape later behaviour.
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schizophrenogenic mother weaknesses
unfalsifiable
Unfalsifiable – cannot prove it wrong so is unscientific.
67
cognitive explanations
Frith
schizophrenics have dysfunctional thought processing
68
metarepresentation
* Cognitive deficit – schizophrenics have difficulty processing information.
* Refers to ability to reflect on own thoughts and behaviour.
Allows us to understand intention and motivation of our actions and others’.
* Faulty in schizophrenics who struggle to recognise actions and thoughts as their own and so attribute them to ‘someone else’.
* Linked to auditory hallucinations and delusions of persecution.
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central control
* Cognitive bias – schizophrenics have issues with selective attention.
* Refers to ability to suppress and not immediately act upon impulses whilst consciously trying to focus on someone else.
* Automatic thoughts can become intrusive and distract from efforts to consciously control over thoughts and behaviour.
* Linked to thought derailment and disorganised speech.
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stroop test
* Schizophrenics tend to perform poorly as cannot focus on one task.
* Henick and Salo suggested that schizophrenics exhibit increased interference, consistent with the distractibility they exhibit in everyday life.
Shows a cognitive deficit in ability to remain focused on one task and not to be distracted by the other.
Creates difficulty processing visual and auditory information.
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cognitive explanations strengths
evidence to support
Stirling compared 30 schizophrenics to 18 controls on Stroop test. Schizophrenics took twice as long to name ink colours.
Supports Frith’s idea of dysfunction with central control as were unable to supress automatic impulses.
Provides validity to link between cognitive impairment and schizophrenia.
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cognitive explanations strengths
practical applications
CBT found to have a significant effect in reducing both positive and negative symptoms.
Significant positive impact and useful in improving schizophrenia.
Cognitive theories have predictive validity as treatments based on cognitive assumptions are effective in improving symptoms.
Theory suggesting that faulty cognitions must have accuracy.
73
cognitive explanations strengths
better considered complementary
Cognitive explanations may be better considered not as an alternative to biological explanations but instead as complementary.
Frith found that cognitive deficits are linked to abnormalities in areas of the brain that use dopamine, especially the prefrontal cortex. He showed that schizophrenics have reduced blood flow to these areas (indicating reduced brain activity) during certain cognitive tasks.
Since the PFC handles attention and self-monitoring, supports the link between biological and cognitive explanations.
Use objective, reliable and empirical methods e.g. brain scans to scientifically evidence faulty cognition.
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cognitive explanations weaknesses
causality
Assumes cognitive dysfunction causes schizophrenia but could be the other way around.
Only able to establish a link and cannot state which has causation.
Explanation more descriptive than explanatory.
Describes faulty mental processes but fails to fully explain where faults originate from.
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CBTp
* Helps patient identify and correct faulty interpretations/beliefs, such as believing that their behaviour is being controlled by someone or something else.
* Helps establish links between thoughts, feelings or actions and their symptoms and general level of functioning.
Better able to consider alternative ways of explaining why they feel and behave in the way that they do.
Reduces distress and so improves functioning.
* Encouraged to trace back origins of delusions and hallucinations and to consider how they can test the validity of their faulty beliefs.
* Can be in groups but usually on a one-to-one basis.
* Recommend 16 sessions for schizophrenia.
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CBTp behaviour assignments
Help improve general level of functioning.
Learning of maladaptive responses is result of distorted thinking and mistakes in assessing cause and effect e.g. assuming something terrible happened because they wished it.
Patient develops own alternatives to previous maladaptive beliefs by looking at alternative explanations and coping strategies already present.
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CBTp strengths
research evidence
Research evidence to support effectiveness of CBTp over antipsychotic medications.
NICE review found reduction in hospitalisation 18 months following end of treatment compared to antipsychotic. Also reduces symptom severity and improvements in social functioning.
Suggests effectiveness in reducing relapse and severity. Aids patients and helps live better life.
However, most studies into CBTp have been conducted at the same time as antipsychotic medication.
Difficult to assess the effectiveness independently.
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CBTp strengths
can adjust
Effective can vary depending on stage of disorder, but treatment can be adjusted.
Addington claims that in the initial acute phase, self-reflection is not appropriate. After stabilisation of symptoms, with antipsychotics, individuals can benefit from group CBTp.
Can help normalise experience by meeting with others with similar issues.
Research shows that individuals with more experienced schizophrenia and greater realisation of problems benefit more from individual CBTp.
Suggests stage and individual differences can affect effectiveness.
Not always effective for all or for all stages, limiting effectiveness.
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CBTp weaknesses
lack of availability
Lack of availability.
Only 1 in 10 who could benefit get access to CBTp.
Haddock found that only 13/187 schizophrenics had been offered it. A significant number either refused or failed to attend sessions.
Not widely or easily accessible, lacks equality. Leads to some going untreated.
Limits effectiveness.
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CBTp weaknesses
study quality
Meta-analyses provide unreliable conclusions about effectiveness as fail to account for study quality.
Some fail to randomly allocate to CBTp or control. Some affected by bias and demand characteristics as interviewers assessing symptoms know which condition. All studies are grouped together.
Cannot trust effectiveness and validity due to methodological issues.
Perhaps not as effective as we thought.
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CBTp weaknesses
research as sole treatment
Research into effectiveness as sole treatment is low.
Jauhar revealed only a small therapeutic effect on hallucinations and delusions. Even these effects disappeared when symptoms assessed blind.
Does not provide a big enough difference in symptoms to be effective.
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token economy
* Based on principles of behaviourism – operant conditioning and positive reinforcement (reward behaviour to encourage repetition).
* Mainly used with long-term hospitalised patients with schizophrenia, aiming to improve overall level of functioning to allow them to live more independently.
* Targets negative symptoms e.g. avolition (low levels of functioning).
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token economy process
Identify target behaviours e.g. personal hygiene: showering, brushing teeth.
A token given each time target behaviour demonstrated.
Once a certain number of tokens acquired, can be exchanged for a desirable reward e.g. sweets, magazines, access to activities like watching a film or taking a walk outside.
Through repetition, the tokens become associated with the actual reward and become reinforced.
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token economy secondary reinforcers
* Tokens are secondary reinforcers as are symbolic of the actual reward of the primary reinforcer.
At the beginning, tokens may need to be given more frequently to train the patient to make the association between token, desirable behaviour and reward.
Issuing of tokens and exchange for rewards also needs to be done in a timely manner to make the association.
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token economy strengths
research evidence
Research evidence to support effectiveness.
Glowacki identified 7 studies that showed a reduction in negative symptoms of schizophrenia and a decline in unwanted behaviour due to use of token economies.
Suggests a consistency of findings, demonstrating reliability and effectiveness in dealing with negative symptoms and improving functioning.
However, only addresses negative symptoms such as avolition and does not aid with positive symptoms.
If patients are suffering from positive symptoms, it may make it hard to engage with the strategy and does not address the cause of schizophrenia.
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token economy weaknesses
doesn't deal with all symptoms
McGonagle found that token economy is particularly aimed at negative symptoms.
Only addresses negative symptoms such as avolition, and does not aid with positive symptoms, which may make it hard to engage with strategy.
Just manages some symptoms, does not actually treat schizophrenia.
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token economy weaknesses
unethical
Can be viewed as unethical.
Patients with severe symptoms may not be able to engage with it, as cannot perform desirable behaviours to get rewards.
Seen as discriminatory and idea of restricting rewards to people with mental disorders has been frowned upon and raises connotations of social control and the potential for causing distress and psychological harm.
Could be argued that benefits outweighed by potential negative impact.
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token economy weaknesses
short-lived
Improvement in functioning may only be short-lived.
Once token economy has ceased (usually upon release from hospitalisation), the effects can be diminished and functioning can decline again, leading to high re-admittance rates.
Without consistent reinforcement, the overall effectiveness is reduced.
Individual reliant upon external motivation for improvement as opposed to sustaining change in behaviour themselves.
Does not offer a long-term solution.
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token economy weaknesses
methodological issues
Methodological issues with research into token economy.
Comer suggests that studies tend to be uncontrolled. Implementation does not involve a control group for comparison, so judgement usually based on comparison with an individual’s past behaviour.
May be misleading, as other factors like increased staff attention could act as a confounding variable and be influencing improvement rather than token economy itself.
True effectiveness is hard to ascertain.
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family therapy
based on family dysfunction
aims to reduce stress to prevent relapse
increase positive communication and tolerance levels
decrease criticism, guilt and responsibility for illness
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family therapy process
therapist meets with patient and family, talk openly about symptoms and progress
support as caregivers, specific roles in rehab
emphasis on openness
3 months --> year, 10 sessions
aimed at reducing expressed emotion
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family therapy strengths
reduces relapse rates
Pharaoh found that family therapy reduces relapse rates and hospital readmissions compared to standard care and increased compliance to medication, lowered risk of relapse for 2 years
suggests effective with a long term effect
however, some argue that findings are less to do with improvements and more than increases medication compliance --> not due to family therapy
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family therapy strengths
useful for some
useful for patients who lack awareness into illness or cannot speak coherently as family members can assist by giving info
have insight in behaviour and moods
effective in increasing depth of info provided to therapist by another's perspective, aids treatment
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family therapy weaknesses
may cause problems
openness may cause family tensions, may not be honest or engage fully, does not tackle faulty communication
may not work for all, individual differences, limits usefulness
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family therapy weaknesses
based on nurture
can be caused by genes, drug therapy effective, not for all
reductionist --> only looks at environment
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interactionist approach
more holistic
considers role of biological, societal and psychological factors in schizophrenia development
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diathesis-stress model
Meehl
both vulnerability / predisposition and triggering environmental disorder needed to develop schizophrenia
proposed a schizogene --> single gene causing schizophrenia
diathesis
purely genetic - leading to biologically based schizotypic personality (sensitivity to stress)
stress includes chronic stress in childhood - family dysfunction
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revised diathesis stress model
many candidate genes creating vulnerability
psychological trauma as diathesis as early trauma alters developing brain e.g. hypothalamic-pituitary-adrenal system overactivity, more vulnerable to stress
stress not just psychological (parenting), now includes risks triggering Sz e.g. smoking cannabis, interferes with dopamine
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interactionist approach
treatment
antipsychotics and CBT used together --> drugs reduce symptoms, better engage in therapy
hallucinations, delusions
avolition, anhedonia using CBT
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interactionist approach strengths
practical applications
Tarrier found that drugs and CBT had lower symptoms than just drugs or control group
effectiveness - both helpful but more so together, role of both bio and psych influences
treatment-causation fallacy - just because treatment works, does not mean cause has been identified, just managing symptoms
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interactionist approach strengths
holistic view
both bio, psych, societal factors (urbanicity, cannabis use) using diathesis-stress
more comprehensive understanding, better treat
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interactionist approach strengths
supporting evidence
Gottesman studied 57 twins
mz = 42%, dz = 9%
shows role of genetics, and other factors
nature and nurture
valid
however, shared environment, confounding, cannot separate
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interactionist approach weaknesses
original too simplistic
single schizogene
polygenetic
reductionist
