Schizophrenia Flashcards
1
Q
What are the two main classification systems for sz?
A
DSM (diagnostic and statistical manual) mostly used in the US
ICD (international classification of disease) mostly used in Europe
(Both have been extensively revised over the years to reflect social changes and developments in psychology)
2
Q
How has the DSM changed over the years?
A
1900 included 12 mental illnesses
Today 347 listed
(produced by American Psychiactric association)
Current edition DSM 5
3
Q
Who is the ICD produced by?
A
WHO (world health organization)
10th edition
4
Q
What are the diagnosis criteria for sz by the DSM 5?
A
For a diagnosis symptoms must have:
been present for at least 6 months
include at least one month of active symptoms
ruled out mood disorders (e.g. depression), drug abuse or brain tumours
Two of the required symptoms must be present
5
Q
What is sz characterised by in the DSM?
A
Delusions, hallucinations, disorganised and behaviour and other symptoms that cause social and occupational dysfunction
6
Q
What are the positive symptoms of sz?
A
Delusions, Hallucinations, Disorganised, Disorganised or catatonic (zoned out) behaviour
7
Q
What are delusions?
A
Bizarre or grandiose beliefs that can seem real to the person with sz
Can be paranoid e.g. believing there’s a plot to kill them
8
Q
What are hallucinations?
A
Distorted sensory experiences (not real)
Can come from any of the 5 senses
Often consist of voices commenting on their behaviour or telling them to things
9
Q
What is disorganised speech?
A
Incoherent or loosely connected speech indicates disorganised thinking
10
Q
What are the negative symptoms of sz?
A
Speech poverty, avolition, affective flattening
11
Q
What is speech poverty?
A
Producing fewer words ad using a less coplex syntax
Delay in responses
Reduction in speech fluency and productivity reflects slowing or blocked thoughts
12
Q
What is avolition?
A
Apathy: not able to initiate or persist in goal directed behaviour (e.g. sitting in the house for hours every day doing nothing)
Loss of motivation
Signs: poor hygiene, lack of energy/persistence
13
Q
What is affective flattening?
A
a reduction in the range and intensity of emotional expression
14
Q
What are positive symptoms?
A
Excess or distortion of normal functioning
15
Q
What are negative symptoms?
A
Loss or a severe reduction of normal functioning
16
Q
Why do we use classification systems?
A
classifications make it easier to identify, treat and break down the disorders
Should increase the reliability of diagnosis (Doctors are more likely to arrive at the same diagnosis using the same classification system)
17
Q
What is reliability?
A
For a diagnosis to be reliable it must be repeatable
18
Q
How is reliability tested?
A
Test-retest reliability: practitioner makes a consistent diagnosis on separate occasions from the same info
Inter-rater reliability: several practitioners make identical, independent diagnoses of the same patient
This level of agreement on diagnosis should be see over time and cross culturally
19
Q
What did Keefe et al find?
A
Assesed sz cognition rating scale (SCoRS) applied to 79 patients with sz assessed at 3 academic research centres in the US
Demonstrated excellent test-retest reliability of about 0.90 (90% reliable) in various circumstances
20
Q
What did Whaley find?
A
poor inter-rater reliability of classification systems: as low as 0.11 (11%)
21
Q
What did Cheniaux find in relation to inter-rater reliability of classification systems?
A
Had 2 psychiatrists independently diagnose 100 patients using both the DSM and ICD criteria
Both diagnosed 2x as many with sz using ICD compared to DSM
One diagnosed twice as many with sz than the other
22
Q
What are 3 possible reasons for the poor inter-rater reliability of sz diagnosis using classification systems?
A
-Clinical characteristics are open to interpretation e.g. as to the point when eccentricity becomes delusion
-The two system differ subtly:
DSM V requires 2 symptoms present for a month, ICD10 requires only one if its delusion
So symptom threshold is higher for DSM
-Cultural differences
23
Q
What did Keith et al find (cultural differences in sz)?
A
2.1% African-Americans diagnosed with sz compared to 1.4% white Americans.
But African-Americans also more likely to suffer poverty or marital separation
24
Q
What did Escobar suggest (racism in sz diagnosis)?
A
White psychiatrists may tend to over-interpret symptoms and distrust honesty of black people during diagnosis
25
What does the ethnic culture hypothesis suggest in terms of prognosis?
Predicts ethnic minorities experience less distress when diagnosed + living with a mental disorder because they live in more supportive social structures that don't abandon them
26
What did Brekke and Barrio find?
support for ethnic culture hypothesis in their study of 184 individuals diagnosed with sz. Found white-Americans had more symptoms than ethnic minority groups
27
What is validity in terms of sz?
The extent to which sz is a unique syndrome with a shared set of characteristics distinct from other disorders.
The extent that a classification system such as ICD or DSM measures what it claims to measure
(diagnosis also can't be valid if its not reliable)
28
What are the issues of validity of classification and diagnosis in sz?
Low reliability undermines validity
Symptoms, development of sz, repsonse to treatment all vary enormously
often difficult to define boundaries between sz and other disorders
29
What is gender bias?
The extent to which a diagnosis is dependent on the gender of the person
30
What did longnecker et al find?
reviewed studies of prevalence of sz- concluded that since the 1980s men have been diagnosed with sz more often than women...so:
Men may be more genetically vulnerable to sz?
Gender bias in diagnosis of sz?
31
What did Loring and Powell find in relation to gender bias of sz?
Randomly selected 290 male + female psychiatrists
Two case studies of patient's behaviour:
56% diagnosed sz when patients described as 'male' (or no gender)
20% diagnosed sz when 'female'
Gender bias less evident in female psychiatrists suggesting gender bias is also dependent on gender of the psychiatrist
32
What did Cotton et al suggest as a reason for gender bias?
Female patients typically function better than men-
more likely to work + have good family relationships
Could explain women's lower diagnosis rate compared to men with similar symptoms
Better functioning may bias clinicians to under-diagnose due to:
Symptoms masked by higher functioning
Higher functioning makes case seem too mild for diagnosis
33
What s symptom overlap?
Where many symptoms of a disorder are also found within another disorder e.g. sz, bipolar and depression all overlap
most people with sz also have enough symptoms to receive another diagnosis
34
What is co-morbidity?
extent that two or more conditions occur together
if conditions occur together a lot of the time it calls into question their validity as separate disorders
sz commonly diagnosed with other conditions
35
What are the co-morbidity rates for sz? (Buckley et al)
50% also have diagnosis of depression
47% also have diagnosis of substance abuse
29% also have PTSD
24% also have OCD
(not a coincidence that 1% of pop. have sz and 2-3% pop. OCD but that they often occur together)
36
What is the problem with co-morbidity in sz?
Such high levels of co-morbidity pose a challenge to classification and diagnosis of sz:
if 1/2 sz also diagnosed with depression maybe we are bad at differentiating them
maybe in classification severe depression looks a lot like sz so are they on a continuum? are they one condition?
37
What are the differences in prognosis for those diagnosed with sz?
20% recover their previous level of functioning
10% achieve significant and lasting improvement
30% show some improvement with intermittent relapse
Diagnosis therefore has little predictive validity
38
What are the ethical issues of sz diagnosis?
Labelling: label of sz is permanent on medical records- not seen as curable, Scheff highlighted possibility of self fulfilling prophecy 'living the label'
other people are also often suspicious of such labels
39
What biological factors may affect sz?
genetic pre-disposition, neural correlates, early life factors e.g. pregnancy complications as well as environmental stressors such as drug use
40
What are the methods for studying genetic the factors of sz?
Family studies, twin studies, adoption studies
41
What are neural correlates?
The connection between brain structure/ function and symptoms of sz)
42
What have family studies shown about sz as a genetic disorder? (genetic factors of sz)
Family studies have established that sz is more common in those with genetic relatives who have sz (closer relation= more likelihood of sz)
43
What did Gottesman's study into family genetic component of sz find? (genetic factors of sz)
Children with 2 sz parents- concordance rate of 46%
Children with 1 sz parent- 13%
Children with sz sibling- 9%
44
What did Gottesman's twin study meta-analysis find? (genetic factors of sz)
Summarised 40 twin studies and found that if 1 twin had sz concordance rate was:
48% MZ twins
17% DZ twins
Suggests likelihood of sz has a large genetic component
45
Why are adoption studies used in psychology? (genetic factors of sz)
In order to separate genetic and environmental influences for those that share genes
46
What did Tienari's study find? (1991 study) (genetic factors of sz)
Studied 155 adopted children with sz biological mothers compared to 155 adopted children with non-sz biological mothers
10% children with sz biological mothers developed sz
1% children with non-sz biological mothers developed sz
47
What do the results of Tienari's stud suggest? (genetic factors of sz)
Supports the suggestion that the likelihood of development of sz has a genetic basis
(Although clearly does not predict that a child will certainly have sz- just increases likelihood)
48
What are the overall evaluation points (strengths) for the role of genetic factors in sz?
+ Strong research evidence
+Genetic science appears close to identifying genes involved in sz (same genes as involved in bipolar disorder- could explain difficulty in diagnosis of both)
The genes most clearly implicated code for proteins that may impact glutamate receptor function (which also affects dopamine receptors)
49
What are the overall evaluation points (weaknesses) for the role of genetic factors in sz?
- not 100% concordance & 2/3 szs have no sz relatives (other factors must be involved)
- methodological weaknesses: sample size often small & studies often retrospective
50
If genetic factors play a role in sz what could this imply? (neural correlates)
```
The genes may influence the 'hardware' of the brain:
biochemical abnormalities (dopamine hypothesis)
Problems in brain structure (enlarged ventricles)
```
51
What does the original dopamine hypothesis suggest?
Excess of dopamine causes hallucinations + delusions (positive symptoms)
Szs thought to have to have abnormally high numbers of D2 receptors on receiving neurons--> more dopamine binding --> more neurons firing
52
What support is there for the original dopamine hypothesis?
Drugs that increase dopaminergic activity
| Drugs that decrease dopaminergic activity
53
How do drugs that increase dopaminergic activity support the original dopamine hypothesis?
Amphetamines: a dopamine agonist- increases dopamine levels causing hallucinations + delusions. Which generally disappear with absence from drug
L-Dopa: given to Parkinson's patients (who have low dopamine levels) raises dopamine levels. Can cause sz type symptoms
54
How do drugs that decrease dopaminergic activity support the original dopamine hypothesis?
Antipsychotic drugs- work by blocking dopamine receptor sites + reduce many of the positive symptoms
55
What does the revised dopamine hypothesis suggest causes positive symptoms?
Dopamine excess in sub-cortical areas- particularly mesolimbic pathway (also called 'reward pathway') (as in original version)
56
What does the revised dopamine hypothesis suggest causes negative symptoms?
Defecit of dopamine in areas of the Prefrontal cortex (the mesocortical pathway)
57
Who suggested the revised dopamine hypothesis?
Davis and Kahn
58
What support is there for the revised dopamine hypothesis?
Patel- neural imaging study
| Wang & Deutch- rat study
59
What was Patel's neural imaging study? (AO3 revised dopamine hypothesis)
PET scans. Lower levels of dopamine found in dorsolateral prefrontal cortex of sz patients compared to normal controls
60
What was Wang & Deutch's rat study? (AO3 revised dopamine hypothesis)
Created dopamine depletion in prefrontal cortex of rats
Caused cognitive impairment in rats e.g. poor memory
Reversed this effect using atypical anti-psychotic drug thought to work on negative symptoms in humans
61
What are the issues with the revised dopamine hypothesis?
Evidence to suggest that dopamine does not offer a complete explanation of sz:
Some genes identified in genome-wide studies code for production of other neurotransmitters suggesting they also impact sz
Newer antipsychotic drugs
Much current research shifting to glutamate influence
62
How are newer antipsychotic drugs an issue for the revised dopamine hypothesis? (AO3)
Newer anti-psychotic drugs e.g. Clozapine block dopamine less yet work better, possibly because they also affect serotonin
63
What is the focus for the glutamate theory?
Focuses on under-activity of glutamate receptors (ivolved in positive symptoms) and it affects other neural circuits (involved in negative symptoms)
64
What is the evidence supporting the glutamate theory?
newer anti-psychotics e.g. Clozapine work on dopamine + glutamate receptors & have shown to have some effect on negative symptoms
65
What are the positives of new drugs being developed based on the glutamate theory?
Target glutamate receptors: fewer side effects, as effective on positive symptoms and some effect on negative symptoms
66
What is the enlarged ventricles explanation for sz?
Enlarged ventricles (liquid filled cavities in the brain)
Torrey: On average 15% bigger than normal in szs & brains also lighter than normal
Enlarged ventricles associated with negative symptoms- linked with cognitive disturbances & poor responsiveness to drug therapy.
67
What further support is there for the enlarged ventricles hypothesis?
Andraesen: well-controlled CAT scan study. Found significant enlargement of ventricles in szs compared to controls
68
What are the issues with the enlarged ventricles explanation for sz?
Have been found in ppl without sz. MRI scans mainly done on those already diagnosed. Does sz (& medication given) cause these abnormalities?
Lyon: found as medication increased brain tissue density decreased leading to enlarged ventricles
69
What is the issue with assuming sz is a completely biological disorder?
Exact genes/mechanisms not identified. MZ concordance not 100%. 2/3 sz patients have no family history of sz.
Diathesis stress: biological vulnerability only develops if environmental stressors present
70
What are the historic treatments of sz?
Pre-treatment- restraint during acute psychosis
Frontal lobotomies during 1930s-50s
Psychosurgery- abandoned in favor of drug therapy in 1950s.
ECT- electroconvulsive therapy: under general anaesthesia small electric currents passed through brain to trigger brief seizure- short lied results (also abandoned in 1950s)
71
What is anti-psychotic medication?
Reduce intensity of symptoms (particularly positive) They are dopamine antagonists (block dopamine action). Usually initial treatment for sz & later combined with psychological therapy to manage disorder
72
What are the two main types of anti-psychotics?
Typical (conventional) drugs e.g. Chloropromazine
| Atypical drugs e.g. Clozapine
73
What do 'typical' anti-psychotic drugs do?
Dopamine antagonists: bind to dopamine receptors on post synaptic neuron preventing puffs of dopamine sticking to receiving neuron. Resultingly receiving not stimulated & so reduces effect of dopamine. Particularly affect D2 receptors in subcortex but also must block others = side effects
74
What is the effectiveness of typical anti-psychotic drugs?
Reduce symptoms in approx 60% cases- allowing sz sufferers to return to community. Effect on negative symptoms i minimal. Relapse occurs if medication stopped so maintenance dose may be life long.
75
How was the effectiveness of typical anti-psychotic drugs tested through relapse rates?
Davis: meta-analysis 29 studies (3519 ppl) Found:
| 55% placebo group patients relapsed, 14% treatment group relapsed
76
What are the relapse rates shown by Vaughn + Leff (one group in Davis' meta analysis)?
If hostile home environment: 92% placebo patients relapsed & 53% treatment patients relapsed
If supportive home environment: 15% placebo patients relapsed & 12% treatment patients relapsed
(shows importance of environmental factors)
77
What are the side effects of anti-psychotic medication?
Stiffness of joints/movement, dry mouth, drowsiness, low blood pressure, constipation, extrapyramidal side effects
78
What are extrapyramidal side effects?
Motor control and coordination- side effects may include: Akathisia: restlessness, tapping fingers, rocking etc
Parkinsonism: same symptoms as Parkinson's - tremor, slow thought process, rigid muscles
Approx 25% cases: Tardive Dyskinesia
79
What is tardive dyskinesia?
Damage to brain tissue (caused by antipsychotic medication) can result in facial tics, inoluntary movement of tongue, lip smacking
80
What are some of the ethical concerns of the use of typical antipsychotics?
Are these drugs chemical straightjackets? de-humanising? Informed consent often an issue- side effects vary and in acute sz episode person may not understand
81
What are atypical (second generation) antipsychotics?
Also block D2 receptors, but only temporarily occupy receptors then rapidly disassociate from receptors allowing normal dopamine transmission. may explain why these have fewer side effects.
82
What is an example of an atypical antipsychotic and how does it work?
Clozapine: binds to dopamine receptors but also works on serotonin and glutamate. They not only reduce positive symptoms but effect negative symptoms and cognitive impairment
83
What is the effectiveness of atypical antipsychotics?
Marginally more effective than typical. Does reduce some negative symptoms. Meta analysis -Leucht: 2 studies found them slightly more effective + 2 studies found no more effective than typical.
NICE now recommends atypical over typical
84
What are the side effects of atypical anti-psychotics?
Far less risk of tardive dyskenesia (Jeste: found it in 30% on typical drugs but only 5% on atypical)
weight gain, damage to immune system, clozapine in particular can lower white blood cell count. (important to do regular blood checks)
85
What are the two key cognitive explanations for sz?
dysfunctional thought processing and family dysfunction
86
Why do we need psychological explanations when sz has so clearly a biological basis?
MZ studies don't show 100% concordance; supports environmental, psychological factors
Are useful in explaining how genetic vulnerability comes to be triggered, how sz comes to be maintained
87
What is the psychodynamic explanation of sz?
conflicts/traumas cause sz to regress to oral stage- pre-ego stage (e.g. parents harsh/uncaring)
Great self-interest/delusions of grandeur
ego not yet developed - no reality testing can occur
88
What are the two key theories of family dysfunction as a factor in sz?
Double-bind theory, expressed emotions
89
Why would family dysfunction affect sz?
Family can be seen as set of entities interacting with each other. Problematic behaviour may result from problems in wider family system.
90
What is the double bind theory?
Parents predispose children to sz through contradictory communications.
Such contradictions leave child with impression of world as confusing/dangerous reflected in symptoms such as disorganised thinking, paranoid delusions + withdrawal
91
What evidence is there to support double bind theory?
Berger: found sz had higher recall of double-bind statements by mothers than non-sz
92
What are the issues of the double bind theory?
researcher bias: families studied after sz diagnosis
unhelpful/destructive to blame families
research post-1970s: Liem: found no evidence to support theory
93
What is expressed emotion?
communication style where families talk about patient in a critical or hostile manner or in a way that suggests emotional over-involvement or over-concern (high EE)
94
Why does high EE trigger relapse?
Arouses stress beyond patients coping ability which can trigger a sz episode
95
How is EE measured?
Counting number of: Critical comments made by relative, statements of dislike/resentment towards patient, comments suggesting emotional over-involvement/over-protectiveness of/to patient
96
What role does EE play in relapse? (study)
Vaughn & Leff: measured relapse rates pf sz 9 months after returning home from hospital (128 patients)
Families rated for EE
Low EE: 12% relapse on medication, 15% if not
High EE: 53% relapse on medication, 92% if not
97
Why is the cause and effect of EE an issue for the explanation? (AO3)
More support for this theory than double bind but...
Correlational evidence: which came first? EE or sz?
High EE less common in first sz episodes...
98
What support is there for the role of family environment in onset and maintenance of sz? (AO3)
Prospective studies shown high risk children who develop sz more likely to come from families with negative rships. Israeli 'high risk' study found no sz in high risk children who'd received 'good parenting' from an sz parent.
Suggests bad parenting may trigger underlying vulnerability to sz (not cause sz though)
99
How are individual EE vulnerability differences an issue for the EE explanation? (AO3)
Altofer et al: 1/4 patients studied showed no physiological response to stressful comments of relatives. Lebell: some patients don't perceive high EE behaviour as stressful- such ppl can do well regardless of living in high EE family
(suggests not all families will benefit from family therapy)
100
How has EE explanation led to effective form of therapy?(AO3)
High EE relatives shown how to reduce levels of EE through family therapy. Found to significantly reduce relapse rates. Endorsed by NICE. Suggests significant EE role in relapse.
101
What are the two key theories of the cognitive explanation?
Attention not functioning normally
| Dysfunctional meta representation or central control
102
What is the role of attention normally?
We're constantly bombarded with incoming stimuli
| We're able to filter and process this, interpret what it means and only attend to relevant things
103
How does attentional impairment affect those with sz?
Filtering/processing systems may be faulty in brains of sz. Become: overwhelmed with sensory input, let in too much irrelevant info and can't interpret it
104
What does this attentional impairment lead to?
Confusion: difficulty focusing on individual things at a time, turning insignificant stimuli into highly meaningful messages
105
What evidence supports attentional impairment theory?
Szs perform badly in lab experiments requiring attention on some stimuli and ignoring others (e.g. visual tracking task)
Ability to focus attention on selected things is impaired
106
What is meta-representation?
Allows us insight into our own intentions
| Allows us to interpret actions of others
107
How does dysfunction in meta-representation link to sz?
| Frith
Would cause inability to recognise actions as our own
Could explain hallucinations (own thoughts perceived as coming from outside) and delusions e.g. thought insertion (feeling that other ppl are putting thoughts in our mind)
108
What evidence is there to support the idea of dysfunction in meta-representation?
Szs perform badly on theory of mind tasks: can't understand that ppl have different point of view/separate mental state. Suggesting problems with meta-representation - can't monitor own or other's mental state (e.g. box of matches example)
109
What is central control dysfunction? (Frith)
Szs struggle to suppress automatic responses while performing deliberate actions: e.g. speech may become derailed by associations with different words that can't be suppressed --> disorganised speech
110
What support is there for the role of central control dysfunction?
Stroop test: Stirling: compared 30 sz with 18 controls
(pps have to read colour of the word and ignore word itself)
sz took 2x as long to perform the task supporting Frith's theory of central control dysfunction
111
What is an issue with the cognitive explanation? (AO3)
Doesn't explain basic cause of faulty processing - which almost certainly has biological basis. e.g. Why do sz have trouble filtering info?
May be better explained by salience theory
112
What is salience theory? (AO3 cognitive explanations)
Salience= importance we attach to stimuli
Dopamine= chemical that tells us something is salient
Excess of dopamine may lead to excess of salience making szs attach inappropriate importance to stimuli
113
How are cognitive explanations supported by the success of CBTp? (CBT for psychosis) (AO3)
NICE found CBTp more effective than anti-psychotics in reducing symptom severity and improving social functioning. In CBTp patients encouraged to evaluate content of delusions/hallucinations + consider how to test validity of these faulty beliefs.
Success of CBTp suggests faulty cognitions do play a clear role in sz
