Schizophrenia Flashcards
(287 cards)
1
Q
What is a delusion?
A
An unshakeable belief in something that is very unlikely, bizarre or obviously untrue.
2
Q
What is an hallucination?
A
Hearing or seeing things which are not there.
3
Q
What is avolition?
A
The reduction of, or the inability, to initiate and persist in goal related behaviour
4
Q
What is Alogia?
A
Lessening of speech fluency and productivity
5
Q
What is reliability?
A
Consistency of the measuring instrument such as a questionnaire
6
Q
What is validity?
A
Whether a measuring tool measures what it sets out to measure
7
Q
What is comorbdity?
A
Refers to the extent that two (or more) conditions co-occur.
8
Q
How can reliability be tested?
A
Reliability of such questionnaires or scales can be measured in terms of whether 2 independent assessors give similar diagnosis (inter-rater reliability) or whether tests used to deliver these diagnoses are consistent over time (test-retest reliability)
9
Q
What is inter-rater reliability?
A
Whether 2 independent assessors give similar diagnosis
10
Q
What is rest-retest reliability?
A
Whether tests used to deliver these diagnoses are consistent over time.
11
Q
What are the two most widely used classification systems for diagnosis of schizophrenia?
A
DSM-IV and ICD-10
12
Q
What are the differences between DSM-IV and ICD-10?
A
- Different time requirments
- Different factors considered
- Different subtypes
13
Q
How are DSM-IV and ICD-10 differ in terms of time requirments?
A
DSM-IV require people to have one or more of the clinical characteristics for at least 6 months, whilst ICD-10 requires it to be apparent for 1 month.
14
Q
What is the advantage of the ICD-10 over DSM-IV in terms of time requirements?
A
Sufferers do not have so much time in which they may me at risk to themselves and others. They also only have to live without help for one month before receiving diagnosis and appropriate treatment.
15
Q
How does DSM-IV and ICD-10 differ in terms of the factors they consider?
A
DSM is multi-axial; various factors (bio, psychological, social) considered. It takes account the individual and the situation rather than merely the symptoms as it assess the suffer’s social functioning, such as poverty and physiological state of health. ICD-10 place the emphasis on first rank symptoms, and ignores the social functioning/context of the individual.
16
Q
How does ICD-10 and DSM-IV differ in terms of subtypes?
A
ICD and DSM do not entirely agree on the number of subtypes of schizophrenia with the ICD suggest seven different subtypes and the DSM five.
17
Q
What is the problem with ICD-10 and DSM-IV differing in terms of subtypes?
A
The reliability here is questioned as a sufferer could be diagnoses as one type of schizophrenic according to the DSM and a different type according to the ICD which could result in incorrect treatment.
18
Q
Why could ICD-10 be considered more universal?
A
It can be applied to more diverse cultures at the World Health Organisation (creators of the ICD) are made up of representatives from 193 countries and therefore various cultures are represented.
19
Q
What did Copeland (1971) find about cultural differences in early classification system?
A
Gave 124 US and 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed schizophrenia. Only 2% of British psychiatrists diagnosed schizophrenia.
20
Q
What was done to try and solve the cultural differences in early classification systems?
A
Prior to 1970’s there was a significant difference in prevalence rates of SZ in different countries. To eliminate diagnostic differences attempts were made to bring the two systems (ICD-10 and DSM-TR-IV) into line with one another. Became similar, not identical
21
Q
What is the problem with the DSM system in terms of reliability?
A
Despite claims for increased reliability in DSM-III and later versions, 30 years later there is still little evidence that DSM is routinely used with high reliability by mental health clinicians.
22
Q
What are some other diagnostic tools to help diagnose schizophrenia?
A
St Louis Criteria, Schneider criteria Research Diagnostic Criteria etc.
23
Q
What is the difficulty with having multiple diagnostic tools?
A
It makes research comparisons difficult. Makes difficulty to describe what exactly is meant by SZ. If the catergories are poorly defined and arbitrary, consistent (reliable) diagnosis is likely to be low.
24
Q
What study did Prescott (1986) do on the use of diagnostic tools?
A
Used various measures to assess attention and information processing in 14 chronic schizophrenics. Performance on these measures (using test-retest reliability) was stable over a 6 month period.
25
Why could the DSM-IV be considered culturally biased?
It was created by Americans for Americans. Behaviour in one culture may not be regarded as a symptom of SZ but according to DSM it is. Thus could lead to incorrect diagnosis and treatment.
26
Why did Crow (1985_ believe that SZ is too broad a term?
Because at least two very different conditions exist:
Type 1 syndrome: Acute disorder characterised by positive symptoms
Type 2 syndrome: chronic disorder, negative symptoms.
27
What is the problem witht he use of Sub-types
Type 1 and Type 2 SZ respond very differently to psychological and biological treatment. Problem with division- people do not fit neatly into one category; blurred distinction between subtypes, soime people diagnosed in one category later develop symptoms from another, SZ has many different categories and symptoms
28
What is type 1 syndrome?
Acute disorder characterised by positive symptoms
29
What is type 2 syndrome?
Chronic disorder characterised by negative symptoms
30
How do treatments differ in success between type 1 and type 2 SZ?
Typical and Atypical phenothiazines have more success with relieving positive symptoms as does CBT.
31
Why might there be difficulties with reliability in diagnoses?
1. The same patient may give different information to different doctors
32
What is the Inter-rater reliability of diagnosis like?
Exceptionally low, less than 50%. Thus people who are incorrectly diagnosed may be included in research which may result in invalid conclusions about the cause of the 'illness' and/or treatment.
33
What did Beck et al (1961) find?
Found that agreement on diagnosis for 153 patients (where each was assessed by two psychiatrists from a group of four) was only 54%. This was often due to vague criteria for diagnosis and inconsistencies in techniques to gather data. –
34
What did Whaley (2001) find?
found inter-rater reliability correlations in the diagnosis of schizophrenia as low as 0.11
35
What is the problem with the characteristic 'delusions are bizarre'?
What seems bizarre to one psychiatrist might not seem bizarre to another. When 50 psychiatrists in the US were asked to differentiate between bizarre and non-bizarre delusions they produced inter-reliability correlations of only around +0.40
36
What did Cheniaux (2009) do?
investigated the inter-rater reliability of the diagnosis of schizophrenia according the DSM-IV and ICD-10. Although the inter-rater reliability was above +0.5 for both classification systems schizophrenia was more often diagnosed according to ICD-10 than DSM-IV criteria.
37
What are the aim of Rosenhan's study?
To test the hypothesis that psychiatrists cannot reliably tell the difference between people who are sane and those who are insane.
38
What was the method of Rosenhan's (1973) study?
8 people went to a psychiatric hospital and reported only 1 symptom- that a voice said only single words, like 'thud', 'empty' or 'hollow'. When admitted they began to act 'normally'.
39
What were the results of Rosenhan's (1973) study?
All were diagnosed with suffering from SZ (apart from 1). The individuals stayed in the institutions for between 7 to 52 days.
40
What were the conclusion of Rosenhan's (1973) study?
The reliability of the ability to detect the sane from the insane was proved to be inconsistent.
41
What is the problem with Rosenhan's study?
It was conducted over 30 years ago. Since then manuals have been improved and diagnostic practice is very different. Also the ICD and DSM have been brought in line with one another and so are now similar.
42
What does Validity refer to in regards to diagnosis?
Refers to the extent that a diagnosis represents something that is real and distinct from other disorders and the extent that a classification system measures what it claims to measure.
43
How are reliability and validity linked?
Reliability and Validity are linked because if scientists cannot agree who has SZ (low reliability) then questions of what it actually is (i.e. validity) become essentially meaningless.
44
What is meant by comorbidity?
Comorbidity refers to the extent that two or more conditions co-occur. Psychiatric co-morbidities are common among patients with schizophrenia. These include substance abuse, anxiety and symptoms of depression.
45
What did Buckley et al (2009) estimate?
Estimates that comorbid depression occurs in 50% of patients and 47% of patients also have a lifetime diagnosis of comorbid substance abuse.
46
Why does comorbidity make things more difficult?
It makes diagnosis difficult and also treatment difficult to advise. Also, as a consequence of being diagnosed with SZ they receive a low standard of care which affects their prognosis.
47
What might poor levels of functioning in many SZ be a result of?
Could be less the result of their psychiatric disorder and more to do with their untreated comorbid physical disorder.
48
What did Weber et al (2009) find?
Examined nearly 6 million hospital discharge records to calculate comorbidity rates. Found psychiatric and behaviour related diagnosis accounted for 45% of comorbidity. Many patients diagnosed with SZ also had non-psychiatric problems, such as hypothyroidism, asthma, hypertension and diabetes. Concluded that being diagnosed with a psychiatric disorder meant patient receive a lower standard of medical care, which adversely affects their prognosis.
49
What is meant by schizophrenia like disorder?
ICD/DSM include schizophreniform psychosis, schizoaffective disorder, schizotypal disorder, schizoid personality disorder- many variations-, where individuals diagnosed present SZ type symptoms but do not meet criteria.
50
What is the problem with Shizophrenia-like disorders?
Doubt about the validity of some of these classifications, as the boundary between them is blurred.
51
What did Ellason and Ross argue?
They point out that many people with dissociative identity disorder have more SZ symptoms than people diagnosed as being schizophrenia.
52
What did Klosterkotter et al (1994) find?
Assessed 489 admissions to a psychiatric unit in Germany to determine whether positive or negative symptoms were more valid for a diagnosis. They found positive symptoms were more useful than negative.
53
What is the problem with Prognosis for SZ?
People with SZ rarely share the same symptoms or the same outcomes. A diagnosis of SZ therefore has little predictive validity.
54
What are some of the prognosis percentages for SZ?
20% full recovery
10% significant improvement
30% some improvement with lapses
55
What is the problem with the social stigma that surrounds SZ?
A system for diagnosing schizophrenia cannot be considered accurate if many cases go undiagnosed- due to certain social stigmas and repercussions attached to diagnosing someone with schizophrenia.
56
Where is SZ more likely to be undiagnosed due to social stigma?
Japan where SZ literally translates to "disease of the disorganised mind"
57
What did Kim and Berrios (2001) find?
They found that in Japan the idea of a "disorganised mind" is so stigmatised that psychiatrists are reluctant to tell patients of their condition. As a result only 20% are aware of it, and the rest are left undiagnosed.
58
What is the problem with labelling someone with a mental illness?
They have to disclose that information in certain situations such as job interviews, and they risk carrying the stigma of their condition for the rest of their lives.
59
What are the cultural variations in SZ?
It occurs across culturals, but in USA/UK it is more frequent among African American and African-Carribean populations.
60
Why could there be cultural variations in the diagnoses of SZ?
Could reflect greater genetic vulnerability, psychosocial factors, minority groupings or misdiagnosis. Clinicals could misinterpret cultural differences in behaviour and expression as symptoms. Doctors don't understand black culture and misdiagnose SZ.
61
How do Psychiatrists in Pakistan, China and India differ from the West?
They think that the West place too much emphasis on separation of mind and body.
62
What is schizophrenia?
It is characterised by a profound disruption of cognition and emotion, which affects language, thought, perception and sense of self.
63
What are the prevalence rates of schizophrenia?
The lifetime prevalence of SZ is 1%. Men are more likely to suffer. The onset is typically in late adolescence and early adulthood.
64
What are positive symptoms?
Those that appear to reflect an excess or distortion of normal functions
65
What are negative symptoms?
Those that appear to reflect a diminution or loss of normal functions.
66
What are the positive symptoms of SZ?
1. Delusions (paranoia, grandiosity)
2. Experiences of control- thoughts and actions are believed to be under external control
3. Auditory hallucinations- bizarre, unreal perceptions, usually auditiory
4. Thought disturbance and disordered thinking 0thoughts have been inserted or withdrawn from the mind
5. Language impairments
6. Disorganised behaviour
67
What are the positive symptoms of SZ?
1. Reduction in range and intensity of emotion expression, including facial expression, tone of voice etc.
2. Avolition- reduction or inability to take part in goal directed behaviour
3. reactivity is not expected
4. Thought blocking
5. Asocial behaviour
6. Emotional blunting
7. Alogia- poverty of speech, lessening of speech fluency and productivity.
68
What is paranoid type?
(35-40%-less severe) Preoccupation with one or more delusions or frequent auditory hallucinations. No disorganised speech, disorganised or cataonic behaviour, or flat or inappropriate affect.
69
What is catatonic type?
(10%) Immobility or stpor excessive motor activity that is apparently purposeless, extreme negativism, strange voluntary movement as evidenced by posturing, stereotyped movements, prominent mannerisms, or prominent grimacing.
70
What is undifferentiated type?
(20%) Variation between symptoms, not fitting into a particular type.
71
What is residual type?
(20%) Absence of prominent delusions, hallucinations, disorganised speech and grossly disorganised or catatonic behaviour. Plus presence of negative symptoms or two or more symptoms listed in criterion A for SZ.
72
What is disorganised type?
(10%) Must have all; disorganised speech, disorganised behaviour, flat or inappropriate affect and not meet the criteria for catatonic type.
73
What is the DSM?
Diagnostic and statistical Manual of Mental Disorders) is produced by the American Psychiatric association. It contains a list of symptoms for each disorder and guidelines for clinicians who make diagnosis.
74
What is the ICD?
International Classification of Diseases) is produced by the World Health Organisation for both physical and mental illnesses. Its aim is to follow the epidemiology of diseases worldwide.
75
What is Schizophrenia?
It is characterised by a profound disruption of cognition and emotion, which affects language, thought, perception and sense of self.
76
What is the prevalence of SZ?
The lifetime prevalence is 1%. Men are more likely to suffer than women. The onset is typically in late adolescence and early adulthood.
77
How does the prevalence of SZ support a biological view?
Prevalence of schizophrenia is the same all over the world (about 1%). Risk rises with degree of genetic relatedness. This supports a biological view as prevalence does not vary with environment.
78
What did Kendler et al find about biological explanations for schizophrenia?
Found that 1st degree relatives of those with schizophrenia are 18 times more at risk than the general population.
79
What study did Kety et al do on biological explanations for schizophrenia?
Identified 207 offspring of mothers diagnosed with schizophrenia, along with a matched control of 104 children, matched on age, gender, parental socio-economic status, and urban/rural residence. Children aged 10-18 at start of study. SZ diagnosed in 16.2% of high risk group compared to 1.9% in control group.
80
How can twin studies help to demonstrate the impact of genetics on Schizophrenia?
Both identical (MZ) and fraternal (DZ) twins share the same environment, but only MZ twins have identical genetics- if schizophrenia is genetically related, the concordance rate of SZ should be much higher in MZ twins.
81
What did Gottessman and Shields find about biological explanations for SZ?
Used the Maudsley twin register and found 58% (7/12 MZ twins raised apart) were concordant for SZ.
82
What is the issue with genetics as an explanation for SZ?
1. No twin study has yet shown 100% concordance in MZ twins.
2. Studies conducted so far don't tell us which genes might be important for the transmission of SZ.
83
Who developed the dopamine hypothesis?
Comer
84
What is the dopamine hypothesis?
Dopamine neurons play a key role in guiding attention, so it is thought that disturbances in this process may lead to the problems of attention and thought found in people with schizophrenia.
85
How do Dopamine substitutes support the Biochemical explanation?
Dopamine substitutes such as L-Dopa increase the positive symptoms of SZ. L-Dopa is used to treat Parkinson's disease which is characterised by a lack of dopamine. Too much L-Dope produces psychotic symptoms in Parkinson's patients.
86
What are dopamine agonists?
Drugs such a L-Dope, cocaine, amphetamine and methylphenidate act as 'dopamine agonists'- mimicking the effects of dopamine because of their similar molecular shapes.
87
What evidence did Davis find for the biochemical explanation?
Injected schizophrenics with methylphenidate (which increases dopamine) and found a marked increase in symptoms.
88
What is the issue with the biochemical approach?
- Ethical issues
- Increases in dopamine leads to increases in positive symptoms, but not negative symptoms. Negative symptoms are better explained by structural brain abnormalities.
89
How else could dopamine contribute to SZ?
It might not just be about having too much dopamine. Schizophrenics are thought to have an abnormally high number of D2 receptors on their receiving neurons, resulting in more dopamine binding and therefore more neurons firing.
90
What did Torrey find about brain structure and SZ?
Using PET, MRI and Cat scans researchers have discovered that many schizophrenics have enlarged ventricles, cavities in the brain that supply nutrients and remove waste. The ventricles of a person with schizophrenia are on average about 15% bigger than normal
91
What did Brown et al find about brain structure and SZ?
found decreased brain weight and enlarged ventricles, which are the cavities in the brain that hold cerebrospinal fluid
92
What did Flaum et al find about brain structure and SZ?
also found enlarged ventricles, along with smaller thalamic hippocampal and superior temporal volumes.
93
WHat did Buchsbaum find about brain structure and SZ?
found abnormalities in the frontal and pre-frontal cortex, the basil ganglia, the hippocampus and the amygdale.
94
How does research on brain structure support the belief that there are two types of SZ?
Structural abnormalities have been found more often in those with negative/chronic symptoms, rather than positive/acute symptoms, lending support to the belief that there are two types of schizophrenia: Type 1 (acute) and Type 2 (chronic).
95
What did Suddath et al find about brain structure and SZ?
1990)used MRI to obtain pictures of the brain structure of MZ twins in which one twin was schizophrenic. The schizophrenic twin generally had more enlarged ventricles and a reduced anterior hypothalamus. The differences were so large the schizophrenic twins could be easily identified from the brain images in 12 out of 15 pairs.
96
What is the strengths of biological brain structure explanation for SZ?
1. High reliability; tested and retested, in highly controlled environments
2. Wider academic credibility
97
What are the limitations of biological brain structure explanations for SZ?
- Enlarged ventricles could be the effect rather than the cause
- if the reduction in brain volume is the cause of the schizophrenic symptoms then it cannot explain why after 30 years of the initial onset, 35% of the schizophrenics are classified as "much improved".
98
What are the strengths of the biological approach?
- HUmane, poses no blame on the individual or their family
- tends to provoke little fear or stigma
- effective treatments
- well established scientific treatments
99
What are the limitations of the biological approach?
- Reductionist
- Animal Studies
- Relies on self report
- Treats symptoms, not causes
100
What did Beng-Choon Ho find about brain structure and SZ?
in a longitudinal correlational study of 211 schizophrenics found that antipsychotic drugs have measurable influence on brain tissue loss over time.
101
What did Lewis find about brain structure and SZ?
administered antipsychotic drugs to primates and found a brain volume loss of 10% . However this was a correlational study so it does not show cause and effect and this study was carried out on animals so we cannot extrapolate to humans without caution.
102
How do phenthiazines aid in the treatment of SZ?
They bind with the D2 receptors on the neurons and therefore prevent the excess dopamine binding and causing SZ symptoms.
103
How may the psychodynamic approach use childhood events to explain SZ?
If you have a cold and uncaring environment than the child may focus on themselves resulting in a weakened ego so they lose touch with reality and the selfish ID is left in charge of the personality.
104
How may the psychodynamic approach use the idea of regression and a poorly developed ego to explain SZ?
the ego may be overwhelmed by the demands from the Id or by feelings of guilt from the super ego & so the individual regresses to the safety and security of the oral stage. In the 1st stage the ego has not yet properly developed & the child can’t distinguish between itself & its fantasies & the external world.
105
How may the psychodynamic approach explain paranoia?
Paranoia may be a consequence of projection – If you have aggressive feelings you may not want to admit you’re like this so it gets pushed onto other people. So you’re worried that other people want to harm you rather than you yourself harming someone. Hence paranoia.
106
What did Fromm-Reichmann say about the psychodynamic approach and SZ?
Schizophrenogenic mothers are likely to develop SZ in a child. Interviewed patients with SZ about their childhoods. Many patients had mothers that were cold, manipulative, domineering and unable to show affection (the child is still expected to be emotional/affectionate). The families tend to have high levels of conflict between them/high levels of emotional tension and poor methods of conflict resolution.
107
What did Brown et al find about the psychodynamic approach and SZ?
found that SZ’s who return to families with high levels of expressed emotion are almost 6 times as likely to suffer a relapse as those who return to families with low levels of expressed emotion. This offers support for the idea of a Schizophrenogenic family.
108
What is the issue with the idea of a schizophrenogenic family?
- Data is retrospective
- Research suggests that most people with SZ don't come from this type of family
- Some people with SZ will suffer a relapse even if they've been moved from their families
- Blames parents for their children's problems.
109
How does the cognitive explanation view SZ?
Distorted thought processes may be a cause of SZ. Cognitive explanations focus on the conscious thought processes rather than the unconscious. SZ is seen as a consequence of poor information processing e.g. A faulty attentional system.
110
How does Hemsley use the cognitive approach to explain SZ?
1. Failure to activate schemas
2. The relationship between stored schemas and incoming information breaks down- an individual can't make sense of context, don't know what to expect.
3. Inability to attend selectively results in sensory overload- All information is seen as equally important so now there's too much to cope with
4. Superficial information appears relevant- this could cause delusions of reference, paranoia etc.
5. Internally generated thoughts are attributed to external forces- can't distinguish between stored schemas and external reality. Hence hallucinations.
111
How does Frith use the cognitive explanation to explain SZ?
1. A breakdown in ‘meta-representational ability’ – our ability to become aware of our own goals & intentions & the ability to understand the beliefs and intentions of others.
2. This can lead to delusions of control – SZ’s may not realise that their own actions are a result of their own intentions. This gives rise to the belief that they are under alien control and their thoughts are being implanted in their heads.
3. It can cause delusions of reference – SZ’s can’t interpret other peoples social signals or understand their intentions. They can’t tell if someone is talking to them or not.
4. It can cause hallucinations & paranoia – they can’t tell whether a sound that they hear is an attempt of communication or not. So non speech sounds may be communicated as an attempt of communication so you hear voices. When others say they can’t hear what you hear they believe it’s a lie and manipulation (hence paranoia).
112
What are the strengths of cognitive explanations?
-May help understand the origins of particular symptoms
113
What are the limitations of the Cognitive explanations?
- Don't explain why the symptoms are there in the first place
- Different SZ have different parts of the brain suggested and show different symtpoms
- Ignores environmental factors.
114
What is the argument against the limitation that cognitive explanations don't explain why the symptoms are there in the first place?
Hemsley suggested that the hippocampus may be at fault. Frith proposed a disconnection between the frontal and posterior areas of the brain. Thus, brain mechanisms have been suggested.
115
Who suggested the Double-Bind theory?
Bateson et al.
116
What does the Double-Bind theory suggest?
that children who frequently receive contradictory messages from their parents are more likely to develop schizophrenia.
117
What did Bateson et al argue about the Double-Bind Theory?
argued that the child’s ability to respond to the mother is incapacitated by such contradictions because one message effectively invalidates the other.
Prolonged exposure to such interactions prevents the development of an internally coherent construction of reality; in the long run, this manifests itself as typically schizophrenic symptoms such as flattening affect, delusions and hallucinations, incoherent thinking and speaking, and in some cases paranoia.
118
What is expressed emotion?
A family communication style that involves criticism, hostility and emotional over-involvement.
119
What did Linszen et al find about expressed emotion?
A patient returning to a family with high EE is about 4 times more likely to relapse than a patient whose family is low in EE.
120
What did Torabi et al find out about expressed emotion?
Studied the relapse rate in Iran. found that the high prevalence of EE in Iranian culture (overprotective mothers and rejecting fathers) was one of the main causes of relapse. The negative emotional climate in these families seems to arouse the patient and lead to stress beyond his or her already impaired coping mechanisms
121
What did Berger find about double-bind theory?
They found that schizophrenics reported a higher recall of double bind statements by their mothers than non-schizophrenics. However, evidence may not be reliable as patient’s recall may be affected by their schizophrenia.
122
What therapy did Hogarty develop in response to research into expressed emotion?
produced a type of therapy session, which reduced social conflicts between parents and their children which reduced EE and thus relapse rates. This suggests that gaining an insight into family relationships allows psychiatric professionals to help improve the quality of patient’s lives.
123
What did Mischler and Waxler find about SZ and family relationships?
found significant differences in the way mothers spoke to their schizophrenic daughters compared to their normal daughters, which suggests that dysfunctional communication may be a result of living with the schizophrenic rather than the cause of the disorder.
124
What did Liem find about SZ and family relationships?
They measured patterns of parental communication in families with schizophrenic child and found no difference compared with normal families.
125
What did Hall find about SZ and family relationships?
analysed data from previous studies and found no difference between families and without a schizophrenic member in the degree to which verbal and non-verbal communication were in agreement. This suggest that there is refuting evidence for the double bind theory causing schizophrenia
126
What did Brown and Birley find about SZ and sociocultural factors?
found that prior to a schizophrenic episode, patients who had previously experienced schizophrenia reported twice as many stressful life events compared to a healthy control group.
127
How could stress factors trigger SZ?
The mechanisms through which stress factors trigger SZ are not known but high levels of physiological arousal associated with neurotransmitter changes are thought to be involved.
128
What did Scheff say about SZ and labelling?
Schizophrenic symptoms are seen as deviant from the rules of ‘normal behaviour’. If a person displays these behaviours they may be labelled schizophrenic leading to them displaying more of the symptoms.
129
What did Comer say about SZ and labelling?
suggest that labelling causes a self-fulfilling prophecy, which promotes the development of other symptoms.
130
What did Rosenhan find about SZ and labelling?
found that once a label of schizophrenia had been applied it influenced that way the staff behaved towards the patient.
131
How does learning theory attempt to explain SZ?
1. A consequence of direct reinforcement or observational learning. Abnormal behaviour is shown by direct reinforcement or is imitated by others.
2. Abnormal behaviour is learnt in the same way as normal behaviour; if you get attention for behaving in bizarre ways or others get attention for behaving in bizarre ways.
132
What are the issues with learning theory?
1. Behaviours can't explain the cognitive aspects of SZ.
2. It is not clear how symptoms are acquired if not observed in others
3. Mechanistic/deterministic; if it is a learned behaviour then it should be possible to unlrean it.
133
What are the two biological therapies?
1. Antipsychotic drugs
| 2. Electroconvulsive therapy (ECT)
134
What are the two psychological therapies?
1. Cognitive Behavioural therapy (CBT)
| 2. Family intervention.
135
What are the two main types of antipsychotics?
1. Typical antipsychotics; the first generation of antipsychotics (developed during the 50's)
2. Atypical antipsychotics: a newer generation of antipsychotics (developed during the 1990's)
136
How is dopamine thought to be linked with SZ?
Dopamine is involved with perception. If a person has too much dopamine activity in one part of the brain, this will produce too much 'perception', seeing and hearing things not there.
137
How do typical antipsychotics work?
1. Block dopamine receptors by fitting into the receptor space usually reserved for dopamine.
138
What are the issues with antipsychotics?
1. If a drug blocks all dopamine receptors it can upset muscle control (Parkinson's type symptoms).
1. If you block acetylcholine receptors, it reduces your learning, produces mild sedation and confusion etc.
3. If you block noradrenalin it sometimes upsets your blood pressure e.g. you feel dizzy when you stand up etc.
4. If you block some serotonin receptors, it may have an effect on your appetite and hence weight gain can occur.
139
How do atypical antipsychotics work?
. Atypicals such as Clozapine work differently from typicals in that they only attach to the specific D2 dopamine receptors (with a transient blocking action on excessive perceptionisation).
140
What is tardive dyskinesia?
*Involuntary movement of lips & tongue; incidence as side affect of conventional antipsychotics is 30% and irreversible in 75% of these cases (Hill, 1986)
141
Why are atypical antipsychotics preferred?
Atypicals are preferred to conventional antipsychotics because they produce less side affects (eg. tardive diskinesia*)
142
What did Leucht et al find about atypical antipsychotic?
Good for ‘positive’ symptoms, however comparative affects on ‘negative’ schizophrenia are marginal
143
When is ECT used?
ECT is not considered a first line treatment but may be prescribed in cases where other treatments have failed. It is only measurably effective where symptoms of catatonia are present and in terms of treatment for drug-resistant catatonic schizophrenia, NICE* recommends its use in the UK.
144
How do they think ECT work?
ECT works by using an electrical shock to cause a seizure (a short period of irregular brain activity). This seizure releases a ‘rush’ of chemical neurotransmitters and temporarily alters function (eg. perception/memory etc)
145
How often is ECT treatment usually given?
ECT is given up to 3 or 4 times a week and usually for a maximum of 12 treatments.
146
How are ECT treatments given?
Before each treatment, an intravenous line is attached and through it the patient will be given an anesthetic (to induce sleep) and a muscle relaxant. Then an electrical shock is applied to the patient’s head (via electrodes). The shock will last only 1 or 2 seconds (high voltage / low amperage) and will make the brain have a seizure. This seizure is controlled by the medicines to stop/reduce the body having a grand muscular spasm.
147
What are the side effects of ECT?
-Common side effects include temporary short-term memory loss, confusion, paranoia, nausea, muscle aches and headache.
Some people may have longer-lasting/permanent problems with memory/paranoia.
Nowadays, rare cases result in death.
148
How can psychological treatments help people with SZ?
Help people with SZ to cope better with the symptoms of hallucinations or delusions. Can also help to treat some of the negative symptoms of schizophrenia, such as apathy or a lack of volition/hedonism.
149
What idea is CBT based on?
based on the idea that most unwanted thinking patterns, and emotional and behavioural reactions are learnt over a long period of time.
150
What is the aim of CBT?
to identify the thinking patterns that are causing you to have unwanted feelings and behaviour, and to learn to replace this thinking with more realistic and useful thoughts.
151
How is CBT usually used?
Most people will require between eight to 20 sessions of CBT over the space of six to 12 months. CBT sessions usually last for about an hour.
152
Who developed psychoanalysis?
Psychoanalysis was first developed by Freud (1880’s) and further developed by the Neo-Freudians.
153
What does psychoanalysis refers to?
refers to treatment including: free association, TAT tests, hypnotic regression and dream analysis. From these the analyst uncovers the unconscious conflicts causing the patient's symptoms and interprets them for the patient to create a subjective resolution of the problem (much as with CBT).
154
What does the cognitive explanation see as the cause of SZ?
The focus is on the faulty and maladjusted thinking that occurs with the positive symptoms of disturbed language, attention thought and perception; faulty information processing is therefore seen as the cause of the disturbances which are characteristic of the condition.
155
What is the aim of cognitive therapy?
to help the sufferer to identify and correct the faulty and maladjusted thinking and to identify the thinking patterns that are causing the unwanted feelings and behaviour, and to learn to replace this thinking with more realistic and useful thoughts.
156
What idea is cognitive behavioural therapy based on?
on the idea that most unwanted thinking patterns, and emotional and behavioural reactions are learnt over a long period of time.
157
What is meant to happen in cognitive therapy?
, disordered and delusional thinking can be replaced with thought processes that are more constructive and more in line with reality
158
How does CBT work?
1. Patients are asked to trace back the origins of their symptoms and understand how they started
2. The sufferer is taught to recognise their own examples of delusional thinking.
3. CBT challenges the patient’s interpretation of events, and helps them to change their habit of thinking about things in a pathological way.
4. The therapist encourages patient to come up with their own coping strategies for when they experience any symptoms
5. They may then receive help and advice about how they can avoid acting on these thoughts.
159
How long does CBT last?
Most people will require between eight to 20 sessions of CBT over the space of six to 12 months. CBT sessions usually last for about an hour.
160
What are outcome studies?
These measure how well a patient does after a particular treatment, compared with the accepted form of treatment for that condition.
161
What do outcome studies suggest about CBT?
Patients who receive cognitive therapy experience fewer hallucinations and delusions and recover their functioning to a greater extent than those who receive anti-psychotic medication alone.
162
What did Drury et al find about CBT?
found benefits in terms of a reduction of positive symptoms and a 25-50% reduction in recovery time for patients given a combination of antipsychotic medication and CBT
163
What did Kuipers et al find about CBT?
confirms that this sort of therapy is effective in reducing some of the delusional symptoms of schizophrenia.
164
What did Gould et al find about CBT?
found that all seven studies in their meta-analysis reported a statistically significant decrease in the positive symptoms of SZ treatment.
165
Why can it be difficult to assess the effectiveness of CBT?
most CBT runs alongside antipsychotic medication, it is therefore difficult to assess the effectiveness of CBT independent of antipsychotic medication.
166
How does CBT work?
CBT works by trying to generate less distressing explanations for psychotic experiences, rather than eliminating them completely.
167
What did Kingdon and Kirschen find about CBT?
In a study of 142 SZ’s in Hampshire, they found that many patients were not deemed suitable because they felt that they would not engage with the therapy. Older patients were deemed less suitable than younger patients.
168
What is the aim of family intervention?
To make the family environment less stressful and reduce hospitalisation and relapse, by reducing levels of expressed emotion and stress, and by increasing the capacity of relatives to solve related problems.
169
What are common family intervention strategies?
1. Form alliances with relatives who care for the person with SZ
2. Reduce the emotional climate within the family and the burden of care for family members
3. Enhancing relatives' ability to anticipate and solve problems.
4. Reducing expressions of anger and guilt by family members
5. Maintaining reasonable expectations among family members for patient behaviour
6. Encouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed.
170
What did NICE find about family intervention?
meta-analysis involving 32 studies and nearly 2500 participants found significant evidence for the effectiveness of family intervention. Compared with patients who received standard care alone there was a reduction in hospital admissions and severity of symptoms during and up to 24 months following intervention. Relapse was 26% with intervention compared to 50% control.
171
What is a significant benefit of family intervention?
Cost of family intervention offsets the cost of hospitalisation due to lower relapse rates. Meaning cost savings.
172
What is a significant limitation of family intervention?
– Lots of research comes from outside the UK for example China. The NICE study expressed the view that hospitalisation levels may differ across countries depending upon the clinical practice in those countries. Therefore this data may not be applicable to the UK.
173
What is schizophrenia?
A severe mental disorder characterised by a profound disruption of cognition and emotion. This affects a person's language, thought, perception, affect and even their sense of self.
174
What is inter-rater reliability?
Whether two independent assessors give similar diagnoses.
175
What is test-retest reliability?
Whether tests used to deliver these diagnoses are consistent over time.
176
What did Carson claim about the DSM-III?
Claimed that it had fixed the problem of inter-rater reliability once and for all.
177
What did Wilks et al find about the reliability of cognitive screening tests for schizophrenia?
Administered two alternate forms of the test to schizophrenic patients over intervals varying from 1-134 days. The rest-retest reliability (correlation of scores across the two test periods) was high at .84.
178
What is validity?
Refers to the extent that a diagnosis represents something that is real and distinct from other disorders and the extent that a classification system such as ICD or DSM measures what it claims to measures.
179
WHat did Buckley et al find about schizophrenia?
Estimate that comorbid depression occurs in 50% of patients, and 47% of patients also have a lifetime diagnosis of comorbid substance abuse.
180
What issue does comorbidity create for the validity of diagnosis of mental illness?
Creates difficulties in the diagnosis of a disorder and also in deciding what treatment to advice.
181
What did Klosterkotter et al find about the diagnosis of schizophrenia?
Assessed 489 admissions to a psychiatric unit in Germany to determine whether positive or negative symptoms were more valid for a diagnosis of SZ. They found that positive symptoms were more useful for diagnosis than were negative symptoms
182
What did Bentall et al find about the prognosis of SZ?
THe prognosis for patients varies with about 20% recovering their previous level of functioning, 10% achieving significant and lasting improvement, and about 30% showing some improvement with intermittent relapses.
183
Why does SZ have little predictive validity?
People diagnosed as SZ rarely share the same symptoms, nor is there evidence that they share the same outcomes, thus the prognosis varies.
184
What are hallucinations?
Bizarre, unreal perceptions of the environment that are usually auditory, but may also be visual, olfactory, or tactile.
185
What is affective flattening?
A reduction in the range and intensity of emotional expression, including facial expression, voice tone, eye contact and body language.
186
What are the clinical positive symptoms characteristics of SZ?
1. Delusions
2. Experiences of control
3. Hallucinations
4. Disordered thinking
187
What are the clinical negative symptoms of SZ?
1. Affective flattening
2. Alogia
3. Avolition
188
What did Whaley find about the reliability of SZ diagnosis?
Found that inter-rater reliability correlations in the diagnosis of SZ as low as +0.11
189
What study did Rosenhan do on diagnosis of SZ?
Neurotypical people prsented themselves to psychiatric hospitals in the US claiming they heard an unfamiliar voice in their head saying 'empty', 'hollow' and 'thud'. They were all diagnosed as having SZ and admitted. Throughout their stay, none of the staff recognised that they were actually neurotypical
190
What study did COpeland do on diagnosis of SZ?
Gave 134 US and 194 British psychiatrists a description of a patient. 69% of the US psychiatrists diagnosed SZ, but only 2% of the British psychiatrists gave the same diagnosis.
191
What study did Mojtabi and Nicholson do on diagnosis of SZ?
50 senior psychiatrists in the US were asked to differentiate between 'bizarre' and 'non-bizarre' delusions; they produced inter-reliability correlations of only around +0.40, forcing the researchers to conclude that even this central diagnostic requirement lacks sufficient reliability for it to be a reliable method of distinguishing between schizophrenic and non-schizophrenic patients.
192
What did Cheniaux et al find about diagnosis of SZ?
Investigated the inter-rater reliability of the diagnosis of SZ according to both DSM-IV and ICD-10. Although the inter-rater reliability was above +0.50 for both classificatory systems, SZ was more frequently diagnosed according to ICD-10 than DSM-IV criteria.
193
What did Kessler et al find about comorbidity?
Found the rate for attempted suicide rose from 1% for those with SZ alone to 40% for those with at least one lifetime comorbid mood disorder.
194
What did Harrison et al find about SZ?
Reported that the incidence rate for SZ was eight times higher for African-Caribbean groups than for white groups.
195
How could the higher rates of SZ among African-Carribbeans compared with white populations be explained?
As a result of poor housing, higher rates of unemployment and social isolation. However, possible that misdiagnosis may in part result from factors such as cultural differences in language and mannerisms and difficulties in relating between black patients and white clinicians.
196
What did Ellason and Ross point out about the diagnosis of SZ?
Point out that people with dissociative identity disorder (DID) actually have more SZ symptoms than people diagnosed as being SZ.
197
What study did Davis et al do on biological explanations for SZ?
Carried out a meta-analysis of 29 studies that analysed the effectiveness of antipsychotic treatment compared with a placebo. They found that at the end of the clinical trial, relapse occurred in 55% of the patients whose drugs were replaced by a placebo, but only 19% of those who remained on the drug.
198
What is the diathesis-stress relationship explanation for SZ?
A biological predisposition (the diathesis) for SZ only developing into the disroder if other significant psychological stressors are present in the person's life.
199
What have family studies found about concordance rates of SZ?
THey have established that SZ is more common among biological relatives of a person with SZ, and that the closer the degree of genetic relatedness the greater the risk. For example, children with two SZ parents have a concordance rate of 46%, children of one SZ parent 13%, and siblings 9%
200
Why are twin studies used to study SZ?
If monozygotic (identical) twins, who share 100% of their genes, are more concordant in terms of a trait like SZ than dizygotic (fraternal) twins this suggests that the greater similaritiy is due to genetic factors.
201
What did Joseph find about biological explanations of SZ?
Calculated that the pooled data for all SZ twin studies carried out prior to 2001 shows a concordance rate for monosygotic twins of 40.4% and for dizygotic twins of 7.4%.
202
What did Tienari et al find about biological explanations of SZ?
Of 164 adoptees whose biological mothers had been diagnosed with SZ, 11 (6.7%) also received a diagnosis of SZ compared to just 4 (2%) of the 197 control adoptees (born to non-sz mothers). The investigators concluded that these findings showed that the genetic liability to SZ had been 'decisively confirmed;"However, the difference only emerged in situations where the adopted family was rated as disturbed. Genetic vulnerability alone was not sufficient.
203
What does the dopamine hypothesis state?
That messages from neurons that transmit dopamine fire too easily or too often, leading to the characteristic symptoms of SZ. SZ are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more more neurons firing. Dopamine neurons play a key role in guiding attention, so disturbances in this process may well lead tot he problems relating to attention, perception and thought.
204
What do amphetamines do?
It is a dopamine agonist, stimulating nerve cells containing dopamine causing the synapse to be flooded with this neurotransmitter. Large doses of the drug can cause the characteristic hallucinations and delusions of a SZ episode.
205
How are antipsychotic drugs thought to work?
They are dopamine antagonists- theyblock the activity of dopamine in the brain. By reducing stimulation of the dopamine system these drugs eliminate symptoms, such as hallucinations and delusions.
206
What did Grilly find about biological explanations of SZ?
Low levels of dopamine activity are found in Parkison's disease. FOund that some people who were taking the L-dopa drug to raise their levels of dopamine were developing SZ-type symptoms.
207
What is a major methodological problems with heredity studies into SZ?
Most SZ adoption studies would not have found statistically significant differences between the adoptees born to SZ and non-SZ parents without broadening the definition of SZ to include non-psychotic 'schizophrenia spectrum disorders'
208
What did Kety et al find about biological explanations of SZ?
FOund that no cases of full SZ were found among the first-degree relatives of adopted children identified with a schizophrenia spectrum disorder
209
What evidence is there that SZ is a biological disorder that originated in distant ancestral humans?
Found even in the most remote racial enclaves. For example, AUstralian Aboriginies became isolated from the rest of humankind about 60,000 years ago, yet SZ has been observed in this racial group (Torrey)
210
What hypothesis have Stevens and PRice proposed for the persistence of SZ?
THey suggest that schizoid personalities have acted in the past to perform the valuable function of dividing trival communities when they become too large. As a group grows in size, there comes a point when the optimum group size is exceeded and splitting the group will increase the reproductive fitness of each individual.
211
Why do Stevens and Price argue that SZ is adaptive?
It would be an adaption whose function is to facilitate group splitting. This would be achieved through the influence of a charismatic leader, who, because of his psychotic thinking, can separate himself from the dogma fo the main group and create a new community with a new world view. Schizoid symptoms such as mood changes, bizarre belies, hallucinations and delusions of granduer would induce discontented group members to leave.
212
WHat is the problem with assuming that SZ runs in families?
It may have nothing to do with genetics and more to do with common rearing patterns or other factors that have nothing to do with heredity.
213
What did JOseph point out about the concordance rates between monozygotic and dizygotic twins?
Points out that it is widely accepted that MZ twins are treated more similarly, encounter more similiar environments and experience more 'identity confusion' than DZ twins. Thus, the differences in concordance rates could reflect nothing more than the environmental differences that distinguish the two types of twin.
214
Why did Joseph criticise adoption studies?
Claims that in countries like Denmark and the US, potential adoptive parents would have been informed of the genetic background of children prior to selection for adoption, thus there may be differences between adoptive parents who adopt children whose background is normal and others who don't.
215
What is a major problem with the dopamine hypothesis?
The drugs used to treat SZ by blocking dopamine activiity can actually increase it as neurons struggle to compensate for the sudden deficieny.
216
What did Haracz find about biological explanations for SZ?
In a review of post-mortem studies of SZ, found that most of those studied who showed elevated dopamine levels had received antipsychotic drugs shortly before death. Post-mortems of SZ who had not received medication, on the other hand, showed that these individuals had normal levels of dopamine.
217
What did COpolov and Crook find about biologically explanations for SZ?
Found that neuroimaging studies have, as yet, failed to provide convincing evidence of altered dopamine activity in the brains of individuals with SZ.
218
What did Brown and Birley find about psychological explanations for SZ?
Found that about 50% of people experience a stressful life event in the three weeks prior to a SZ episode, while only 12% reported one in the nine weeks prior to that. A control sample reported a low and unchanging level of stressful life events over the same period, suggesting that it was the life events that triggered the relapse.
219
What did Hirsch et al find baout psychological explanations of SZ?
Followed 71 SZ patients over a 48-week period. It was clear that life events made a significant cumulative contribution in the 12 months preceding relapse rather than just having a more concentrated effect in the period just prior to the SZ episode (as suggested by the retrospective studies.)
220
How did Freud see SZ?
Saw it as an infantile state, with some symptoms (e.g. delusions of grandeur) reflecting this primitive condition, and other symptoms (e.g. auditory hallucinations) reflective the person's attempts to re-establish ego control.
221
What did Freud believe that SZ was a result of?
Two related processes, regression to a pre-ego stage and attempts to re-establish ego control. If the world of the SZ has been particularly harsh, they may regress to this early stage in their development before the ego was properly formed and before they had developed a realistic awareness of the external world.
222
What does the cognitive approach suggest about SZ?
It acknowledges the role of biological factors in causing the initial sensory experiences of SZ, but claims that further features of the disorder appear as individuals attempt to understand those experiences.
223
How does the cognitive approach say SZ develops?
When SZ first experience voices and other worrying sensory experiences, they turn to others to confirm the validity of what they are experiencing. Other people fail to confirm the reality of these experiences, so the SZ comes to believe that others must be hiding the truth. They begin to reject feedback from those around them and develop delusional beliefs that they are being manipulated and persecuted by others.
224
What are the psychological theories for SZ?
1. Psychodynamic
| 2. Cognitive
225
What are the socio-cultural factors of SZ?
1. Life events
2. Family relationships:
- Double-bind theory
- Expressed emotion
3. Labelling theory
226
What are the biological explanations of SZ?
1. Genetic factors
| 2. The dopamine hypothesis
227
What does Falloon et al suggest about stressful life events and SZ?
The mechanisms through which stress factors trigger SZ are not known, but they suggest high levels of physiological arousal associated with neurotransmitter changes are thought to be involved.
228
What does Bateson et al (double-bind theory) suggest about socio-cultural factors of SZ?
Suggest that children who frequently receive contradictory messages from their parents are more likely to develop SZ. The child's ability to respond to the parent is incapacitated by such contradictions. THese interactions prevent the development of an internally coherent construction of reality and in the long run, this manifests itself as SZ symptoms.
229
Who developed the double-bind theory?
Bateson et al.
230
What is expressed emotion?
A family communication style that involves criticism, hostility, and emotional over-involvement.
231
What did Linszen et al find about socio-cultural factors of SZ?
High levels of expressed emotions are most likely to influence relapse rates. A patient returning to a family wiht high EE is about four times more likely to relapse than a patient returning to a family with low EE.
232
What did Kalafi and Torabi find about socio-cultural factors of SZ?
Found that the high prevalence of expressed emotion in Iranian culture (overprotective mothers and rejective fathers) was one of the main causes of SZ relapses.
233
How is expressed emotion thought to be linked to SZ?
It appears that the negative emotional climate in these families arouses the patient and leads to stress beyond their already impaired coping mechanisms, thus triggering a SZ episode.
234
Who popularized the labelling theory of SZ?
Scheff
235
What does the labelling theory of SZ say?
The symptoms of SZ are seen as deviant from the rules we ascribe to 'normal' experiences. If a person displays these unusual forms of behaviour, they are considered deviant, and the label of schizophrenic may be applied. Once this diagnostic label is applied it becomes a self-fulfilling prophecy that promotes the development of other symptoms of SZ.
236
What did Jenkins and Karno find about expressed emotions?
Although findings on expressed emotion have been replicated cross-culturally, expressed emotion is much less common in families of people with SZ outside the West.
237
What possible explanation is there for the lower level of expressed emotion found outside the West?
Non-Western cultures are less individualist and less committed to concepts of personal responsibility than Western societies, such as the US and UK. Thus, the are less likely to blame someone with SZ for their actions.
238
What did Fromm-Reichman suggest are important contributory influences int he development of SZ?
Described 'schizophrenogenic mothers' or families who are rejecting, overprotective, dominant and moralistic, as important contributory influences
239
What is a major weakness of the psychodynamic explanation?
There is no research evidence to support Freud's specific ideas concerning SZ/
240
What did Oltmanns et al find about psychological theories of SZ?
Showed that parents of SZ patients do behave differently from parents of orhter kinds of patient, particularly in the presence of their disturbed offspring (like to be a consequence tho)
241
What treatment has Yellowlees et al proposed for SZ?
Developed a machine that produced virtual hallucinations, with the interntion to show SZ that their hallucinations are not real. Supports cognitive explanation, but there is no evidence yet that this will provide a successful treatment.
242
What did Van Os et al find about socio-cultural factors of SZ?
Reported no link between life events and the onset of SZ. Patients were not more likely to have had a major stressful life event in the three months preceding the onset of their illness. In a prospective part of the study, those patients who had experienced a major life event went on to have a lower liklihood of relapse.
243
What are the problems with linking life events and SZ?
Only correlational. Life events after the onset of the disorder may be a consequence rather than a cause. It could also be that the beginnings of the disorder, erratic behaviour etc., were the cause of the major life events.
244
What did Berger find about socio-cultural factors of SZ?
Found that SZ reported a higher recall of double-bind statements by their mothers than non-SZ.
245
What did Liem find about socio-cultural factors of SZ?
Measured pattersn of parental communication in families with a SZ child and found no difference when compared to normal families.
246
What did Hall and Levin find about socio-cultural factors of SZ?
Analysed data from various previous studies and found no difference between families with and without a SZ member in the degree to which verbal and non-verbal communication were in agreement.
247
What did Hogarty et al find about socio-cultural factors of SZ?
Found that therapy where high-EE relatives are showed how to reduce levels of expressed emotion can significantly reduce relapse rates.
248
What did Scheff find about socio-cultural factors of SZ?
Evaluated 18 studies explicitly related to labelling theory. He judged 13 to be consistent with the theory and 5 to be inconsistent, thus concluding that the theory was supported by the evidence.
249
What did Rosenhan find in support of labelling theory?
Found that once the 'label' of SZ had been applied, the 'diagnosis' continued to influence the behaviour of staff toward the patient, even when this was no longer warranted.
250
What are the biological therapies for SZ?
1. Antipsychotic medication
| 2. Electrovonvulsive therapy (ECT)
251
What are the psychological therapies for SZ?
1. Cognitive-behavioural therapy (CBT)
| 2. Family intervention
252
What are biological therapies?
Are any form of treatment focused on producing physical changes in the brain, and so decreasing the symptoms of SZ.
253
How do conventional antipsychotic drugs work?
They are dopamine antagonists, in that they bind to dopamine receptors (particularly the D2 receptors) but do not stimulate them, thus blocking their action. By reducing stimulation of the dopamine system in the brain, they can help eliminate the positive symptoms experienced by people with SZ.
254
How do atypical antipsychotic drugs work?
Also act on the dopamine system, but help by only temporarily occupying the D2 receptors and then rapidly dissociating to allow normal dopamine transmisison This is thought to be responsible for the lower levels of side effects compared to conventional antipsychotics. Also thought to block serotonin receptors in the brain too.
255
What do Kapur and Remington argue about atypical antipsychotic drugs?
Suggest that these drugs do not involve serotonin or other neurotransmitters, but only the dopamine symstems and the D2 receptors in particular.
256
How did ECT develop?
Followed reports that dementia praecox (an early name for what we now know as SZ) was rare in patients with severe epilepsy and that seizures in patients with dementia praecox somehow reduced the symptoms of the disorder.
257
What did Karagulla find about ECT?
THe first studies of the clinical use of this technique specifically for the treatment of SZ were disappointing, with lower rates of recovery for ECT patients compared to those who did not receive ECT.
258
What happens in ECT?
. AN electrode is placed above the temple of the non-dominant side of the brain, and a second in the middle of the forehead. The patient is first injected with a short-acting barbiturate, so they are unconscious before the electric shock is administered. They are then given a nerve-blocking agent, paralyzing the muscles to prevent them contracting during the treatment and causing fractures. A small amount of electric current (approx 0.6 amps), lasting about half a second, is passed through the brain. This produces a seizure lasting up to a minute, whih affects the entire brain. A patient usually requires 3-15 treatments.
259
What did Tharyan and Adams find about ECT?
Carried out a review of 26 studies. They found that when ECT was compared with placebo of stimulated ECT, more people improved in the real ECT condition. However, there was no indication that this advantage was maintained over the medium-or long-term. When ECT was compared with antipsychotic mediation treatments, results favoured the medication groups. THere was some limited evidence to suggest that when ECT was combined with antipsychotic medication, this resulted in a greater improvement in mental states.
260
What did Tharyan and Adams conclude about ECT?
Concluded that a combination of ECT and medication may be appropriate when rapid reduction of symptoms is required, or when patients show limited response to medication alone.
261
Why does Ross and Read criticise placebo studies into SZ treatment?
Argue that studies, like Davis et al, using placebo conditions are not a fair comparison of treatment vs. non-treatment, because in the placebo condition the patient is actually in a drug withdrawal state. Consequently, a proportion of the relapses in the placebo condition can be explained by the withdrawal effects of the drugs.
262
What study did Davis et al do on antipsychotics?
Analysed the results of 29 studies. They found that relapse occurred in 55% of the patients whose drugs were replaced by a placebo, and 19% of those wo remained on the drug.
263
Why do Ross and Read argue that Davis et al's study on antipsychotics is misleading?
As they also indicate that 45% of those on a placebo did benefit. Likewise, of the 81% who benefited drom the drug, the data suggests that a large proportion (i.e. 45%) would also have benefitted from a placebo.
264
What did Vaughn and Leff find about antipsychotics?
Found that antipsychotic medication did make a significant difference, but only for those living with hostility and criticism in their home environment. In such conditions, the relapse rate for those on medication was 53%, but for those in the placebo condition the relapse rate was 92%. FOr individuals living in more supportive home environments there was no significant difference between those on medication and those in a placebo condition.
265
What is tardive dyskinesia?
Uncontrollable movements of the lips, tongue, face, hands and feet.
266
What did Hill find about conventional antipsychotics?
About 30% of the people taking antipsychotic medication develop tardive dyskinesia, and it is irreversible in 75% of cases.
267
Why do Ross and Read argue about the use of antipsychotic medication?
Argue that being prescribed medication reinforces the view that there is 'something wrong with you'. This prevents the individual from thinking about possible stressors that might be a trigger for their condition. In turn this reduces their motivation to look for possible solutions that might alleviate these stressors and reduce their suffering.
268
What did Leucht et al find about antipsychotic medication?
A meta-analsyis of studies published in 1999 revealed that the superiority of atypical drugs compared to conventional antipsychotics was only moderate. This analsysis found that two of the new drugs tested were only 'slightly' more effective than conventional antipsychotics, while the other two were no more effective.
269
What are the ethical issues with antipsychotic medication?
Critics argue that if side effects deaths and psychosocial conditions were taken into account, a cost-benefit analysis of its advantages would most probably be a negative.
270
What did Jeste et al find about antipsychotic medication?
Found tardive dyskinesia rates in 30% of people after nine months of treatment with conventional antipsychotics, but just 5% for those treated with atypical antipsychotics.
271
What did Sarita et al find about ECT?
Found no difference in symptom reduction between 36 SZ patients given either ECT or simulated ECT.
272
What are the ethical issues with ECT?
There are significant risks associated with ECT, including memory dysfunction, brain damage and even death.
273
What is the basic assumption of CBT?
That people often have distorted beliefs which influence their behaviour in maladaptive ways. Delusions are thought to result from faulty interpretations of events, and cognitive therapy is used to help the patient to identify and correct these.
274
What happens in CBT?
Patients are encouraged to trace back the origins of their symptoms. Encouraged to evaluate the content of their delusions or of any internal voices they hear, and to consider ways in which they might test the validity of their faulty beliefs. The therapist lets the patient develop their own alternatives to these previous maladaptive beliefs, ideally by looking for alternative explanations and coping strategies that are already present in the patient's mind. May be set behavioural assignments with the aim of improving their general level of functioning.
275
What are outcome studies?
These measure how well a patient does after a particular treatment compared with the accepted form of treatment for that condition.
276
What did Drury et al find about CBT?
Found benefits in terms of a reduction of positive symptoms and a 25-50% reduction in recovery time for patients given a combination of antipsychotic medication and CBT.
277
What did Kuipers et al find about CBT?
Confirmed benefits in reduction of positive symptoms and recovery time, but also noted that there were lower patient drop-out rates and greater patient satisfaction when CBT was used in addition to antipsychotic medication.
278
What did Brown et al find about the effect of family environment on SZ?
SZ in families that expressed high levels of criticism, hostility, or over involvement had more frequent relapses than people with the same problems who lived in families that were less expressive in their emotions.
279
What is the main aim of family intervention?
TO make family life less stressful and so reduce re-hospitalisation.
280
What strategies may family intervention make use of?
1. FOrming an alliance with relatives who care for the SZ
2. Reducing the emotional climate within the family & burden of care for family members
3. Enhancing relatives' ability to anticipate and solve problems
4. Reducing expressions of anger and guilt by family members
5. Maintaining reasonable expectations among family members for patient behaviour
6. ENcouraging relatives to set appropriate limits whilst maintaining some degree of separation when needed.
281
What did Pharoah et al find about family intervention?
Reviewed 53 studies published between 2002-2010 conducted in Europe, Asia and North America. Compared outcomes from family intervention to 'standard' care along. Some studies reported an improvement in the overall mental state of patients compared to those receiving standard care, whereas others did not. The use of family intervention increased patients' compliance with medication. Family intervention did not appear to have much of an effect on more concrete outcomes such as living independelty or employment.
282
What were the methodological issues of Pharoah et al study on family intervention?
1. A large number of studies used were from the People's Republic of China. Evidence has emerged that in many Chinese studies, randomisation bad been stated as having been used, yet was not (Wu et al)
2. Lack of blinding- ten studies reported no form of blinding was used, a further 16 did not specify whether it had been used.
283
What are the ethical issues in SZ research?
Potential for harm associated with medication discontinuation, the use of placebo conditions and capacity for informed consent.
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What did Gould et al find about ECT?
Found that all seven studies in their meta-analysis reported a statistically significant decrease in the positive symptoms of SZ after CBT>
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Why is it difficult to assess the effectiveness of CBT?
Most studies of CBT have been conducted with patients treated at the same time with antipyschotic medication, so it is difficult to assess the effectiveness of CBT indepedent of medication.
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What did NICE found about family intervention?
A meta-analysis involving 32 studies and nearly 2500 participants found significant evidence for the effectiveness of family intervention in the treatment of SZ.
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What reason does Pharoah et al give for the effectiveness of CBT?
Suggest that the main reason for its effecitveness may have less to do with any improvements in these clinical marks annre more to do with the fact that it increases medication compliance.
