1
Q
Diagnosis and classification
A
- In order to classify mental disorders you need to be able to differentiate between them, this is done by organising symptoms which often occur/cluster together and classifying this as one disorder
- The two major systems for classifying disorders is DSM-5 and ICD-10
- ## These differ in their classification of schizophrenia, for example in DSM 5 one of the postive symptoms must be present for a diagnosis, whereas ICD doesnt have this criteria
2
Q
positive symptoms
A
Symptoms experienced in addition to normal experience
3
Q
negative symptoms
A
symptoms that represent a loss of a normal experience
4
Q
Hallucinations
A
- positive symptom
- Unusual sensory experiences
- most often auditory or visual but can involve all senses
- Sometimes can be in relation to external stimuli, therefore representing a distorted view of reality, or can have no reference at all
- The voices are often critical
5
Q
delusions
A
- positive symptom
- irrational beliefs
- grandeur delusions, famous historical, political or religious control delusions, they may believe they are under external control
6
Q
Speech poverty
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- negative symptom
- lack of verbal abilities, delayed speech
7
Q
avolition
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- negative symptom
- Loss of motivation to complete any task goal related, eg Nancy Anderson identified, lack of personal hygeine, no perseverance in work or education and lack of energy
8
Q
Catatonic behaviour
A
- hyper kinetic - constantly moving
- hypo kinetc - not moving in reaction external stimulus
9
Q
disorganised speech
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- incoherent speech
10
Q
reliability of diagnosis
A
- improved since DSM-5 and ICD 10
- Osorio et al. reported high inter rater reliability between psychiatrists diagnoses of shizophrenic patients using DSM 5
11
Q
validity of schizophrenia diagnosis study
A
- Chieneaux et al. found 2 psychiatrists to diagnose 100 patients, one using DSM 4 and the other ICD 10
- 68 were diagnosed using ICD and 39 using DSM
- This demonstrates how the diagnostic systems of ICD and DSM may not be valid in testing for schizophrenia
12
Q
co-morbidity
A
- Often schizophrenia occurs with another condition
- Bucky et al. found 50% diagnosed with schizophrenia also had depression, 47% had a history with substance abuse and OCD 23%
- this calls into question the validity of a schizophrenia diagnosis
13
Q
Culture bias in schizophrenia diagnosis in Britain
A
- In britain african-carribean people are 9 times more likely to be diagnosed with schizophrenia
- but in the carribean they are not diagnosed as much so its not a genetic vulnerability
- this could be because they often beleive in hearing voices from their ancestors
14
Q
gender bias
A
- men are more likely to be diagnosed with schizophrenia
- could be because of genetics
- Cotton et al. suggests more likely that women receive more support
15
Q
symptom overlap
A
make diagnosis less valid, as sysmptoms may be a reuslt of a different disorder
16
Q
polygenic
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phenotype (schizophrenia) influenced by more then one gene (DISC1 or neurogulin etc.) these genes are called candidate genes
17
Q
twin studies by Gottesman and Sheilds
A
- 42% of monzygotic twins and 9% of dizygotic twins shared schizophrenia, they followed the twins for up to 13 years to see if they would develop schizophrenia in later life
- Joseph 2004 metanalysis similar results
- genes do not play a defining role in the development of schizophrenia
18
Q
Gottesman family studies
A
- the closer related the higher chance of developing schizophrenia
- however first cousins and general population have a very similar chance and are both very low
- genes play a small role in the development of schizophrnia
19
Q
tienari et al. adoption studies
A
- 303 adoptees
- some high risk (mother with schizophrenia)
- some low risk (control group)
- both adoptive families tested for healthy households via OPAS ratings, low ratings=healthy household
- findings: only 14 developed schizophrenia 11 from high risk and 3 from low risk
- found that healthy households had a protective effect on high risk adoptees
20
Q
how many people diagnosed with schizophrenia have no known relative with schizophrenia
A
80%
21
Q
hyderdopaminergia
A
high levels of dopamine
22
Q
hypodopaminergia
A
low levels of dopamine
23
Q
neural correlate
A
patterns of brain activity or structure that is associated with symptoms or experiences of a specific mental disorder
24
Q
original and updated dopamine model
A
original:
- caused by hyperdopaminergia in the subcortical areas, specifically between the subcortex and Broca’s area, this explains the hallucinations and dillusions as symptoms of schizophrenia
Updated
- caused by both hyper and hypodopaminergia, high levels in the subcortical areas but also low levels in the prefrontal cortex. This explains speech poverty and avolition
25
genetic counselling as a strength for the biological explanation of schizophrenia
- identify high risk patients and provide them with treatment early on
- just a probability
26
support for the dopamine model
- amphetamines increase dopamine, worsen symptoms in patients with schizophrenia, but induce symptoms in patients without
- some candidate genes act on dopamine receptors and production of dopamine
- antipsychotic drugs induce dopamine and reduce intensity of symptoms
- Tenne et al. induced schizophrenia like symptoms in rats using amphetamines, then treated the symptoms using drugs that reduced dopamine activity
- however studies have shown that other drugs that increase dopamine dont cause schizophrenia-like symptoms
27
limitation of dopamine hypothesis
- ignores role of neurotransmitter glutamate
- post mortem and living scans of patients with schizophrenia have consistently showed increase activity of glutamate in areas of the brain
28
the schizophrogenic mother
- psychodynamic approach to the causation of schizophrenia proposed by Frieda Fromm-Reichmann
- based on stories from her patients childhood, she identified a type of mother which led to the development of schizophrenia - cold, rejecting and controlling
- leads to distrust which develops into paranoid delusions and eventually schizophrenia
29
double bind theory
- Bateson emphasises that communication within the the family is also a factor, even if not the main
- When a child grows up in a home where he is punished(specifically with withdrawal of love), but also unclear on exactly what was wrong but is scared to ask, this leads to the perception that the world is dangerous and confusing, leading to paranoid delusions and eventually schizophrenia
- he emphasises that this only a risk factor
30
expressed emotion
- particular negative emotions expressed to patients with schizophrenia or a genetic risk, by their caregiver can cause a relapse or the onset of schizophrenia:
- emotional overinvolvement, including needless self sacrifice
- verbal or physical abuse or criticism
- hostility, including anger or rejection
31
dysfunctional thinking
- reduced thought processing in the ventral striatum is associated with negative symptoms
- reduced information processing in the temporal and cingulate gyri is associated with hallucinations
32
meta-representation dysfunction
- Firth et al. identified this as a dysfunctional cognitive process linked to schizophrenia
- metarepresentation allows us insight into our intentions and goals
- this would explain hallucinations specifically of voices and insertion delusions (that someone else is forcing thoughts into your mind), as a schizophrenic patient is unable to recognise their actions as their own
33
Central control dysfunction
- firth et al also identified another dysfunctional cognitive process
- Central control dysfunction is responsible for suppressing automatic responses whilst performing deliberate actions
- this would would explain speech and though derailment
34
typical antipsychotics
- dopamine antagonists - reduce DA activity, eg chlorpromazine, links to dopamine hypothesis model
- mild side effects, weight gain, itchy skin, nausea, dizziness
- extreme side effects; TD(50% of patients), involuntary muscle spasms specifically of the mouth, NMS, blocks dopamine action in the hypothalamus, inability to regulate body temperature
35
A-typical antipsychotics
- Clozapine and Risperidone
- acts on serotonin receptors as well as dopamine, clozapine also acts on glutamate receptors
- mild side effects; weight gain, itchy skin, nausea, dizziness
- Serious side effects, clozapine can cause agranulocytosis, lowered white blood cell count, reduced immunity
36
appropriateness of drug therapy to treat schizophrenia
- side effects, both have mild, typical has TD and NMS, clozapine has agranulocytosis
- chemical cosh argument, subduing a disruptive patient, but helps with treatment as more willing to engage with CBTp
37
effectiveness of drug therapy as a treatment for schizophrenia
- Thornley et al. on typical antipsychotics, 13 trials with 1121 patients found that chlopromazine were affective in reducing symptoms and better functioning compared with a placebo group
- Meltzer found that a-typical antipsychotics are more effective than typical
- However Healey suggests flaws with the evidence such as only investigating short-term effects and not considering that antipsychotics have a calming affect which confound the results
38
Why does high levels of EE lead to relapse in schizophrenia
- causes high amounts of stress
- revert back to the symptoms as defence mechanisms
39
phases of CBTp
- Initial assessment - patient expresses his or her thoughts, and realistic goals are discussed
- Engagement - the therapist empathises with the patients feelings and perspectives and stresses that explanations for their distress together
- the ABC model - consider activating effects that appear to cause their emotions and behavioural consequences
- Normalisation - information that other individuals also experience hallucinations under different circumstances
- Critical collaborative analysis - logically questioning the reality of the delusions
- Developing alternate explanations
40
Aims of family therapy
- improve quality of communication
- Making family life less stressful
- reduce relapse and rehospitalisation
- support for carers
41
Strategies in family therapy
Pharoah et al.
- reduce levels of EE to reduce stress and therefore relapse
Form a therapeutic alliance - agree on aims
- Improve beliefs about and behaviour towards the patient
- Achieve a balance between caring for the patients and maintaining their own lives
42
token economies as a way of managing schizophrenia
- increases socially desirable behaviours
- tokens (secondary reinforcers) can redeem tangible rewards (primary reinforcers
- combats institutionalised behaviour
- positive reinforcement
43
evaluation of token economies as a way of managing schizophrenia
- ethical issues, restricting availability of rewards, social workers have considerable power, imposing norms
- evidence for effectiveness - Glowacki et al. metanalysis of 7 studies finding decrease in negative symptoms and in unwanted behaviours
- other ethical options - art therapy identified by Chiang to be effective - NICE recommends
- limited effectiveness, not transferrable to life after hospitalisation
44
diathesis stress model as an explanation for schizophrenia
- gene causes a vulnerability, traumatic experience causes onset
- diathesis - many genes interact to cause schizophrenia, Read et al. suggests that trauma can act as the diathesis, severe enough trauma can cause an overactive hypothalamic-pituitary-adrenal system
- the stress doesn't only have to be psychological, for example cannabis use increase the risk of developing schizophrenia
45
Meehl's model as an explanation for schizophrenia
- if one does not have the gene no amount of stress can cause schizophrenia
46
evaluation of interactionist approach as an explanation for schizophrenia
support:
- Tienarri et al. adoption studies
- Tarrier et al. combining psychological and biological treatments more effective than just biological treatments however treatment causation fallacy
limitation:
- oversimplistic, so many different factors interact together
