schizophrenia Flashcards
(114 cards)
1
Q
schizophrenia definition
A
a severe mental disorder involving impaired insight and loss of contact with reality
2
Q
two main manuals used for classification of mental disorders
A
DSM- diagnostic and statistical manual of psychiatric disorders- mostly used in US
ICD- international classification of diseases- used in europe
3
Q
posotive symptoms of schizophrenia
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hallucinations
delusions
4
Q
hallucinations
A
bizzare unreal perceptions of the environment that are usually auditory but could be visual olfactory or tactile
5
Q
delusions
A
bizzare beliefs that seem real to the person with schizophrenia but arent real
these can be paranoid
6
Q
negative symptoms of schizophrenia
A
speech poverty
avolition
7
Q
speech poverty
A
lessening of speech fluency and productivity
thought to reflect slowing or blocked thoughts
8
Q
avolition
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reduction of interests and desires as well as an inability to initiate and persist in goal directed behaviour
9
Q
what are the differences in the DSM and ICD
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DSM one posotive symptom must be presented for diagnosis
ICD needs two or more negative symptoms for a diagnosis
10
Q
reliability in the role of classification and diagnosis of schizophrenia
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every clinician must be confident a classification system is consistent- two different clinicians should be able to reach the same conclusion about one patient (inter rater reliability)
or the same clinician must reach the same conclusion at two different times with the same patient (test retest reliability)
11
Q
how is validity an issue in diagnosis and classification of schizophrenia
A
validity- refers to the extent that a test/tool is measuring what it is intended to measure (as distinct from other disorders)
reliability and validity are interlinked because a test or measure of a behaviour or disorder cant be reliable if its not valid
12
Q
use of criterion validity in psychiatric diagnosis
A
limitation of the diagnosis of schizophrenia is its validity- use criterion validity in psychiatric diagnosis
schizophrenia is either over or under diagnosed= low criterion validity
study- 100 clients- found 68 diagnosed with schizophrenia under ICD and 39 under DSM
13
Q
co morbidity
A
if conditions occur together a lot of the time then this questions the validity of their diagnosis and classification as they may be a single condition
schizophrenia is commonly diagnosed with other conditions- half siagnosed with schizophrenia also had a diagnosis for depression or substance abuse
isse for classification of schizophrenia because it may not exist as a distinct condition q
14
Q
gender bias in diagnosis
A
since 1980s men are more commonly diagnosed than women- 1:4 ratio
women may be less vulnerable than men due to genetic factors
more likely that women are under diagnosed because they have closer relationships and hence get support so women with schizophrenia function better than men
under diagnosis is a gender bias and means women may not therefore be recieving treatment services that may benefit from
15
Q
culture bias in diagnosis of schizoprenia
A
limitation of schizophrenia is culture bias
symptoms especially hearing voices have different meanings in different cultures
afro carribean societies- hearing voices may be attributed to communication from ancestors
16
Q
symptom overlap
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limitation of sz diagnosis is symptom overlap with other conditions
both sz and biploar disorder involve posotive symptoms- delusions and negative symptoms- avolition
in terms of classification this suggests sz and bipolar disorders may be variatons of a single disorder
17
Q
key points of sz
A
experienced by 1% of the population
more commonly diagnosed in men than women
more diagnosis in cities and working class people
cluster condition
syndrome- lots of symptoms adding together
18
Q
biological explanations for sz
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genetic basis of sz
neural correlated of sz
19
Q
genetic basis of sz
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family studies
cadnidtae genes
the role of mutation
20
Q
family studies
A
confirmed that risk of sz increases in line with genetic similarity to a relative condition
21
Q
what did Gottesman find
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large scale study in 1991 and fiund if you have an auntie with sz you have a 2% chance of developing the disorder
if you have a sibling this increases to 9%
identical twin- 48%
strong support to genetic explanation of sz- importanbt to remember families share many aspects of environment
22
Q
candidate genes
A
no single responsible genetic variation
number of responsible genes- sz is polygenic
most likely genes appear to be those that code for the neurotransmitter dopamine
different studies have identified different candidate genes so sz is considered to be aetiologically heterogenous- means different combinations of factors including genetic variation can lead to the disorder
23
Q
what did Ripke find
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compared the genetic make up of 37,000 people with sz diagnosis to the genetic makeup of 113,000 controls
found 108 separate genetic variations associated with increased risk of disorder
24
Q
the role of mutation
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sz can develop in individuals with no family history of the disorder
one explanation can be gene mutation in the DNA of a parent which can be caused by mutation or viral infection
posotive correlations found between paternal age (increased risk of sperm mutation) and sz where the risk has been found to increase from 0.7% with a father under 25 to 2% in fathers over 50
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neural correlates of sz
the original dopamine hypothesis
the revised dopmaine hypothesisn
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the dopamine hypothesis
theory developed when it was found that antipsychotics used to treat sz (that reduced da) caused symptoms similar to those of parkinsons disease- associated with low da
parkinsons sufferers given L-dopa to increase da levels developed sz symptoms
considered that sz may be the result of high da levels (hyperdopaminergia)
eg excessive D2 receptors in pathway from subcortex to Brocas area (responsible for speech) could explain symptoms of speech poverty and auditory hallucinations
high number of D2 receptors on recieving neurons results in more neurons firing and more frequently leading to hallucinations and delusions that are charachteristics of sz
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the revised dopamine hypothesis
hypothesis updated in 1991 to include cortical hypodopaminergia (low DA in the brains cortex) eg low DA in the prefrontal cortex- responsible for thinking could explain the negative symptom of cognitive problems
suggested cortical hypodopaminergia leads o subcortical hyperdopaminergia so both high and low da in different regions of the brain lead to sz
version also includes psychological origins of the disorder in terms of individuals experience of stress and how this can make some people more vulnerable to cortical hypodompainergia and hence subcortical hyperdopaminergia
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neural correlated of negative symptoms
avolition- involves loss of motivation/anticipation of reward which is associated with the ventral striatum area of the brain
abnormality here may be involved in development of avolition
research found lower levels of activity in ventral striatum of sz sufferers than in controls
a negative correlation therefore between activity levels in the vs and severity of symptoms
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neural correlates of posotive symptoms
hallucinattions
lower activation levls in the superior temporal gyrus has been found in sz patients who had auditory hallucinations when they were given task of identifying speech as their own or that of others compared to activity levels of conrtols doing same task
therefore reduced activity in the superior temporal gyrus is a neural correlate of auditory hallucinations
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what is a limitation of the dopamine hypothesis
evidence for central role of glutamate
post mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with sz
means an equally strong case can be made for the role of other neurotransmitters
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psychological explanations for sz
family dysfunction
cognitive explanations
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family dysfunction
double bind theory
expressed emotion
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cognitive explanations
metarepresentation dysfunction
central control dysfunction
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double bind theory
bateson 1950s
children who constantly recieve contradictory messages from their parents are more likely to develop sz
interactions prevent development of an internally coherent construction of reality in long term can create sz symptoms- flattened affect and withdrawal- avoloyion-negative
- dont know which to respond to
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expressed emotion
negative emotional climate or a high degree of expressed emotions
a family communication style
family members talk about the psyciatric patient in a critical or hostile manner
in a way indicating emotional over investment/ over concern with the patient and their behaviour
a patient returning to a family with high EE is over 4 times more likely to relapse
family members talked more and listened less
causes stress beyond (already impaired) coping ability, caused by the negative emotional environment
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the schizophrenogenic mother
Frieda Fromm Reichman
patients noted particular charachteristics of their mothers- cold rejecting controlling
creates family environments of secrecy and tension
later leads to distrust and paranoia later developing into delusions (persecution complex) and ultimately sz
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dysfunctional thinking
focus on role of mental processes such as reduced thought processing in ventral striatum associated with negative symptoms and reduced processing of information in temporal and cingulate gyri associated with hallucinations
low level of info processing suggests impaired cognition
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metarepresentation dysfunction
Frith identified two types of dysfunctional thought processes:
metarepresenttation is the cognitive ability to reflect on thoughts and behaviour allowing self insight to goals and intentions also to interpret behaviour of others
dysfunction of this would impair the ability to recognise our own actions and thoughts as belonging to ourselves
this explains hallucinations and delusions as being like thought insertion- having thoughts projected into the mind by others
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central control dysfunction
second type of thought disorder identified by Frith is problems with ability to suppress automatic responses when carrying out deliberate actions resulting in speech poverty and thought eg sufferers experience thought derailment because every word triggers an association and an automatic response to that which cant be suppressed
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evidence that supports the view of family dysfunction as an explanation for the development of sz
adoption study by Tienari 1994
adopted children with schizophrenic biological parents were more likely to become ill than children with non sz parents
suggests illness develops under appropriate environment conditions so genetic vulnerability isnt sufficient
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limitation of family dysfunction as an explanation for sz
explanations lack support for the link between childhood trauma and sz
Liem 1974
measured patterns of parental communication in families with a sz child and found no difference compared to normal families
inconsistencies in research
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effectivness of CBT as support for congitive explanations
symptoms of sz have origin in faulty cognition is reinfforced by the success of cognitive based therapies
effectiveness of CBT shown in national institute for health and care excellence review of treatment for sz
found evidence that when compared with antipsychotic medication cbt was more effective in reducing symptom severity and improving levels of social functioning
supports view that faulty cognitions have an important influence in development of sz
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support for Friths central control theory
evidence from experiments using stroop test support friths central control theory
stroop test- ps have to name the font colours of colour words so have to supress the tendancy to read words aloud
compared 30 people with sz to 30 controls
as predicted by friths central control theory people with sz took over twice as long on average to name font colours- suggests the congitive processes of people with sz are impaired
takes a lot of cognitive processing
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vbiological treatments for sz
typical antipsychotics
atypical antipsychotics
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antipshycotic drugs
drugs used to treat symptoms of psychotic illness
they work by reducing dopamine activity in the brain
given tablet/syrup or may be an injection
not necessarily given all life or straight away
things may settle down and be weened off
some take all life time
nasty side affects
have such wide ranging side effects- people stop taking them-symptoms come back
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typical antipsychotics
1950s
eg chlorpromazine
first generation
none help negative symptoms
designed for hallucinations
maximum dose of 1,000mg
work on dopamine hypothesis
work as dopamine antagonists
reduce amount of dopamine in the brain
binds to receptor site on poststynaptic neuron so dopamine cant bind to it- dopamine levels increased at first
reduce hallucinations
have a sedative effect
sleepy, low in energy
related to effect on histomine receptors
unethical- reason- trying to manage their behaviour
tardine dyskonesia symptoms- tics
hypersensitivity to dopamine
47
atypical antipsychotics
1970s+
dont have tardine dyskonesia effect
can kill you
minimise lots of side affects
eg clozapine
agranulocytosis- deadly blood disease- can kill you- people get regular blood tests
brought back in 1980s
much lower dosage 300-400
cant take as injection
binds to dopamine receptors, acts as glutamate and seretonin receptors
30-50% of people with sz attempt suicide
seretonin and glutomate attempt to lift mood of symptoms associated wiyj co morbid depression
dont bind as strongly to dompaine receptors
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second generation atypical antipsychotics- eg risperidone
wont kill you
no life threatening side affects
tablets/syrup injection
typical dose 4-8mg max 12mg
better for body small doses
similar to clozapine
stronger in way it binds to dm receptors
more effective
less side effects
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evidence for the effectiveness of antipsychotics
moderaely effective
compared against placebo
chlorpromazine
wide evidence to suggest they are effective
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serious side affects of antipsychotics
dizziness agitation sleepiuness weight gain itchy skin stiff jaw
tardine dyskonesia
ethical issue
condition may be better than side effects
agranulocytosis- life threatening
question ethics of taking these- tadine dyskonesia sufferer awarded settlement under health and human rights act saying no one should suffer degrading human treatment
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support for drug therapy
support for the effectiveness of antipsychotics from studies comparing relapse rates for antipsychotics and placebos
some patients taken off antipsychoticss and given placebos instead
after 12 months 64% given placebos had relapsed compared to 27% on antipsychotics
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psychological treatments for sz
CBT
family therapy
token economies
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main assumption of CBT
assumes schizophrenia results from dysfunctional thought processes
role is to challenge irrational beliefs- logically disputing the reality of delusions and helping to develop alternatives
55
role of ABC model by ellis in CBT
ABC model by ellis- provide a process to cognitively restructive irrational beliefs (delusions)
A- activating event
B- beliefs
C- consequences
D- disputing irrational beliefs (logical)
E- restructured belief (effect)
reality testing- demonstrate irrational thoughts
based on the idea sz is a cognitive issue
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key points of CBT
CBT often used in conjunction with drug treatment
long length of treatment
difficult process
requires engagement
negative symptoms= unwillingness to take part
posotive symptoms= distrust of process
ending treatment early is common
antipsychotic medication + CBT- reduces initial symptoms severity so CBT can be completed
cost of CBT-expensive- cost of keeping people in hospitals is also high- has to be cost effective- quality of therapist makes a difference
doesnt produce nasty symptoms/side effects
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what does NICE recomend
everyone with a sz diagnosis should be offered CBT- alongside drug treatment- as the drug treatment often still leaves patient with persistent posotive and negative symptoms
CBT aims to help with cognition (thoughts) and behaviour
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aim of CBT
to help people cope with their symptoms eg convincing them their voices dont come from demons but from a malfunctioning speech centre in their brain
this helps them feel less frightened and more able to cope on a daily basis
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how is 'reality testing' used in CBT
individual encouraged to examine the likelehood of the beliefs being true- this is not always effectuve but can still be used to help the anxiety and depression that comes with sz
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what phases does CBT proceed through
assessment
engagement
ABC model
normalisation
critical collaborative analysis
development of alternative explanations
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assessment
expression of yhoughts and realistic goals are set
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engagement
therapist empathy important and reassurance of explanations
makes them feel non judged and valued
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normalisation
reassurance that it happens to many in different circumstances- this relieves stress
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critical collaborative analysis
Q&A to help patients see irrationalities eg why can no one else hear voices
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development of alternative explanations
patient encouraged to consider healthier explanations
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does CBT provide a cure
treatments improve quality of life but dont cure- aims to make sz more managable and improve the patients quality of life
help patients make sense of and challenges symptoms
dont fully cure symptoms- neither do biological treatments- only reduces severity of symptoms
has an underlying biological cause- hard to suggest a psychological therapy would provide a cure- does reduce symptoms
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evidence that CBT is effective
Juaher concluded from 34 studies of CBT and SZ that CBT has a significant but small effect on posotive and negative symptoms
some studies focusing on symptoms found reductions in the frequency and severity of auditory hallucinations
NICE reccomends CBT ofr sz
evidence to show CBT reduces relapse rates compared to standrard treatment- antipsychotics
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quality of evidence used for if CBT is effective
wide range of techniques and symptoms included in studies- different studies involve different CBT techniques- people with different combinations of posotive and negative symptoms- only look at overall effects whereas different CBT techniques may have different effects on different symptoms- makes it hard to identify how effective CBT will be for a particular person with sz
patients usually recieving CBT and drug therapy- hard to establish cause and effect- which is actually reducing the severity of the symptoms
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methodoligcal issues with evidence for the effectiveness of CBT
meta analysis- lots of differernt researchers- cant identify quality of individual researchers- some didnt even have random allocation to conditions or carried out subsequent assessments on participants
found more rigororus studies, weaker effect of CBT- rigorous in their methodologies- however they still have a small effect
70
family therapy
evidence shown the long term outcomes for those with sz are better (less chance of relapse) if they are in a supportive family environment
research shown more frequent relapse rate for individuals in a family of high expressed emotion and criticism and over involvement than for those who live in families of less expressed emotion
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when do NICE recommend family therapy
that this intervention is given a priority where theres a high risk of relapse
reccomended it is given as priority where theres a high risk of relapse
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what is the aim of family therapy
reduced expressed emotion among famiy members and hence reduce relapse rates for the individual
aim to reduce negative emotions by reducing high expressed emotions such as anger and guilt
aim to improve families ability to help by encouraging members to agree on aims of therapy and the beliefs about behaviour towards sz also encouraged to achieve a balance between caring for the diagnosed individual whilst maintaining their own lives
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what did Garety find about family therapy
relapse rates in families where this intervention had taken place was 25% compared to 50% in families where there had been no intervention
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what does family therapy involve
involves the diagnosed individual because a charachteristic of psychosis is suspicion so by involving them suspicion is reduced
family members encouraged to learn about sz to listen to each other and discuss issues together
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main strategies in family therapy for sz
psychoeducation
forming an alliance with the person caring for them- between family members
reducing emotional climate within the family and burden of care for family members- reduces paranoia and builds environment of trust
improving families ability to anticipate and solve problems
reducing anger and guilt expressed by family members
maintaining reasonable expectations among family members for patient performance
individual with sz is encouraged to talk to their family and explain what help they find the most helpful and what things make it worse for them
maintenance for future- identify potential problems and help to resolve them
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what is psychoeducation
helping the person and their carer to understand and be better able to deal with their illness- stress management techniques- carers
form a less EE family, understand illness- reduce hostility anger negative environment
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comparison of the strategies in family therapy to burbachs model
phase 1- psychoeducation and phase 2
phase 3- i,proving families ability to anticipate and solve problems
phase 4- identify unhelpful patterns of interaction- reducing anger and guilt expressed by family members
phase 1 phase 2 and 3- individual with sz encouraged to talk to their family and explain what support is most helpful and what might make it worse
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how many phases are in Burbachs model for family therapy
7 phases
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phase 1 of burbachs model
sharing basic information and providing practical and emotional support
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phase 2 of burbachs model
identifying resources that members can and cant offer
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phase 3 of burbachs model
encourage mutual understanding by identifying the safe space for members to express feelings
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phase 4 of burbachs model
identify unhelpful patterns of interaction
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phase 5 of burbachs model
skills training eg stress management techniques
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phase 6 of burbachs model
relapse prevention planning
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phase 7 of burbachs model
maintenance for the future
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who did a key study for family therapy
Pharoah et al 2010
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what was the procedure of Pharoahs study
reviewed 53 studies from europe, asia and north america that compared outcomes for family therapy v standard care
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findings of pharoahs study
mental state of patients was mixed findings- some found imrpoved outcomes, others didnt
compliance with medcation was increased by family therapy
social functioning showed some improvement on general functioning but no difference in more concrete outcomes such as living independently
relapse was reduced in therapy families and also a reduction in hospital admission
89
criticisms of Pharoahs study
cause and effect- could the improvements simply be the fact that family therapy increased medicinal compliance- so the drugs are working- hard to differentiate
in 10 of the 53 studies in Pharoahs meta analysis the raters werent blinded so they knew which type of treatment participants had recieved- risk rater bias- shouldve been a blinded study
90
how are only certain people suitable for family therapy
have to be careful with sample
50% relapsed in 9 months compared to 8% who recieved family therapy- risen to 50% with family therapy and 75% with standrad patient care
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limitation of family therapy
may not be able to maintain this- maintain patterns of behaviour in the long term
length of treatment- can take up to a year- patients can drop out- family situation can change
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token economies
desirable behaviours are selectively reinforced to encourage them- tokens given in response to socially desirable behaviour
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target behaviours
tokens given in response to socially acceptable behaviours to encourage these behaviours
eg getting dressed/making beds/cleaning
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key points of token economies
not about reducing symptoms- about encouraging more socially acceptable behaviour- negative symptoms- avolition
based on operant conditioning- behavioural approach
target desirable behaviours in individuals
reward has to be given quickly after token- for association to be made
tokens=secondary reinforcer
reward=primary reinforcer
''generalised reinforcers''- able to choose- exchanged for a variety of rewards- much preferred by patients- behaviour modification
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token values
tokens are exchanged for rewards (primary reinforcers)
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behaviour modification
encourages desirable behaviour- should reduce maladaptive behaviour
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what three key areas are adressed by a token economy
personal care
condition-related behaviour
social behaviour
98
what two key benefits does modifying behaviour by token economies have
improving quality of life- reintroducing personal care
helps patients integrate back into society-especially after hospital/institution care
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aim of a token economy
to improve patients quality of life and assist their transition back into society by reducing maladaptive behaviour and encouraging desirable behaviour
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benefits for patients of token economies
target behaviours should improve daily quality of life
patients get rewards eg outdoor walk
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how do token economies work
tokens act as secondary reinforcers- given after desirable behaviour and are then given a reward (primary reinforcers)- operant conditioning the rewards increase the occurence of the behaviour
102
evidence for the effectiveness of token economies
strong evidence for their effectiveness
Larista Glawacki- looked at 7 studies- 1999-2013
all studies showed a reduction in negative symptoms and a decline in the frequency of the unwanted behaviour
however 7 studies (high quality) is a small evidence base- file drawer problem- bias towards posotive published findings and undesirable results being filed away- look for effectiveness with therapies
103
ethical issues of token economies
ethical issues raised gives proffesionals considerable power to control the behaviour of patients- imposing personal values
involves imposing a persons/instiutions norms on others which can be problematic if target behaviours arent identified sensitively- behaviour modification
restricting availability ofpleasures/rewards may increase distress in patients who are already facing extreme distrress- stress is a trigger for sz episodes
human rights issue- food is a reinforcer when it is a basic human right
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the interactionist approach to sz
acknowledges there are biological, psychological and environmental factors that affect the development of sz
105
diathesis stress model
a genetic vulnerability and a stress trigger are necessary to develop the condition
106
what did Meehl propose in the original diathesis stress model in 1962
thought there was a single schizogene- that made people vulnerable to the disorder and exposure to chronis stress through childhood and adolescence especially with a schizophrenogenic mother makes the individual most vulnerable to sz
107
modern view of the diathesis stress model
now understood there are many genes which can increase genetic vulnerability
also thought that psychological trauma can be the diathesis rather than the stressor- proposed by Read- where they describe a neurodevelopmental model where severe trauma can affect brain development eg the hypothalamtic-pituitary-adrenal system can become overactive which makes individual very vulnerable to stress
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what is additivity
diathesis and stress add together to produce sz
they can add in different ways
low vulnerability + major stress= sz
high vulnerability+ low stress= sz
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what was the aim of Tienaris study
tested if genetic factors make you more susceptible to environmental risks associated with adoptive family functioning
110
procedure of Tienaris study
145 adoptees from mums with sz/psychosis compared to 158 adoptees without risk
assessed after 12 years, follow up after 21
used OPAS scale to measure family functioning- to see of stressful families were more likely to trigger the biological vulnerability
111
findings of tienari
303 adoptees- 14 developed sz- 11 from high risk group
those raised in healthy adoptive family had a protective effect even for those at a high genetic risk of sz- high genetic risk but low opas rating were less likely to develop sz
high genetic risk adoptees with high OPAS ratings were more likely to develop sz
in adopties with high genetic risk of sz but not those with low genetic risk adoptive family stress was a significant predictor of development of sz
high stress= predictor if highly vulnerable- not a prediction if less vulnerable
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limitations of the Tienari study
assessment of adoptive family functioning by psychiatrists was only given at one point in time- fails to see any developmental changes that may happen over time in family functioning
difficult to assess the source pf stress when observing family intercations- coming from adoptees or from the adoptive family?
113
evaluation of the interactionist approach- treatment causation fallacy
treatment causation fallacy
implications for treatment- combine antipsychotics and CBT however argued this is the treatment causation fallacy
treatment causation fallacy- cant automatically assume the success of combined therapues means interactionist explanations are correct
just because a treaztment succesfully treats something doesnt mean its caused by a lack of that thing
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