clinical revision Flashcards
what are the. 4Ds
deviance
dysfunction
danger
distress
explain deviance
deviant behaviours are those that are unusual , undesirable or bizarre.
An understanding of statistical and social norms is necessary to determine unusual behaviours and desirability within a social/ cultural group
explain dysfunction
symptoms which distract, confuse or interfere with a persons ability to carry out their usual roles and responsibilities may be seen as dysfunctional
explain danger
hostile or hazardous behaviour which jeopardises the safety of the individual and/or others may be considered grounds for diagnosis
explain distress
when symptoms cause emotional pain or anxiety- this is a sign that a diagnosis may be beneficial
sometimes psychological distress may be manifested as physical symptoms
strength of the 4Ds
✅using ALL 4 might help to avoid errors in diagnosis
E.G. if deviance from statistical or social norms were the only consideration when making a diagnosis - those eccentric but harmless may be seen as abnormal
BUT those with common but debilitating symptoms of depression may be missed
A valid system should be neither over or under inclusive
2 weaknesses of the 4Ds
❌lack of objectivity
ratings are made from feelings so objectivity is unlikely
also affects reliability
4Ds involve making comparisons to a reference between the individual and others in society
decisions would be better if they were made in comparison to a reference group rather than the subjective view of the clinician
this shows that if the 4Ds are applied meaningfully, clinicians require detailed information not only on the person but also their community
❌we end up with labels for ppl with mental health issues
using ‘danger’ as a criteria leads ppl to equate mental illness with being dangerous .
this becomes distorted in the media
most ppl with sz are not actually more dangerous than ppl without (FAZEL ET AL)
such attitudes may become ‘self fulfilling prophecy’ - stereotypes that lead ppl to act in the way predicted by the stereotype
what is the DSM
the DSM describes symptoms, features and associated risk factors of over 300 mental and behavioural disorders arranged into 22 categories
what is the DSM based on
a classification system that was used to identify disorders experienced by world war 2 soldiers
when was the DSM first published
1952
what does erroneous diagnosis lead to
labelling, stigmatisation, ineffective treatment
when was the DSM-5 published
2013
what sections are the manual divided into ?
• 1 : guidance for using the new system
• 2: details the disorder and is categorised according to current understanding of underlying causes and similarities between symptoms
• 3: suggestions for new disorders which currently require further investigation
ALSO info on the impact of culture on the presentation of symptoms and the way they are communicated, especially when the clinician is from a different cultural background
how do clinicians gather info about a patient
observations
unstructured interviews
Describe the diagnostic process
this involves ruling out disorders which do not match the patients symptoms sufficiently
before deciding which disorder offers the ‘best fit’
how is reliablity of the DSM assessed
- SPITZER introduced the use of cohens Kappa to improve reliability of the DSM-III
what does the cohens kappa refer to
the proportion of ppl who receive same diagnosis when assessed then re assessed
what cohens kappa value indicates good agreement
0.7
what type of validity refers to when 2 ppl with the same diagnosis exhibit similar symptoms
descriptive validity
what type of validity refers to when 2 ppl share similar causal factors
aetiological validity
what type of validity refers to when a clinician uses more than 1 method to reach diagnosis and both lead to the same diagnosis
concurrent validity
what type of validity refers to the ability to accurately predict outcomes for an individual from diagnosis
predictive validity
Strength of the DSM in terms of reliability
✅ field trials demonstrated impressive levels of agreement between clinicians for a variety of disorders
REIGER (2013) reported that 3 disorders, including PTSD had kappa values ranging from 0.60-0.79 ( very good)
while 7 more diagnoses (including SZ) had kappa values of 0.40-0.59 (good)
important bcs the criteria for PTSD has changed in terms of symptoms required to make a diagnosis, it is clear clinicians have adapted well to these changes
weakness of the DSM in terms of reliability
❌what counts as an acceptable level of agreement has plummeted over the last 35 yrs
COOPER explains that the DSM 5 task force classified levels as low as 0.2-0.4 as ‘acceptable’
one of the least reliable diagnosis (0.28) was for major depressive disorder
suggests that the DSM may be less reliable than previous versions and that diagnoses of MDD for example may have been made in error
while other cases may have been missed all together
strength of the DSM in terms of validity
✅ evidence supports the validity of certain disorders
KIM COHEN ET AL demonstrated the concurrent validity of conduct disorder through :
- interviewing children and their mothers
- observing the childs anti social behaviour
- using questionnaires completed by the child’s teacher
specific risk factors were common (low income, male, parental disorders) suggesting sound aetiological validity
predictive validity also demonstrated- 5 yrs old children with CD were more likely to display behavioural and educational difficulties aged 7
important bcs accurate diagnosis could reduce adult mental health problems which are frequently preceded by the symptoms of CD
weakness of the DSM in terms
of validity
❌ naming or classifying a disorder does not actually tell us anything about the causes
arguments are circular
results of diagnosis is a label that tells us nothing useful
what does the ICD include
both mental and physical disorders
when was the ICD 10 published
1992
how are mental disorders coded in the ICD
- each disorder has a code, starting with F
- disorders are listed consecutively and there are 11 sections
- each section has a few ‘leftover codes’ allowing new disorders to be added without having to recode other disorders
- codes are used for indexing medical records making it easy when conducting research to find examples of ppl with specific conditions
- the system attempts to be be comprehensive enough to include all known conditions but also to avoid repetition or overlap
how would a clinician make a diagnosis using ICD 10
- ICD contains both physical + psychological disorders and both are coded in the same way
- the clinician selects key words from an interview with a client that relate to their symptoms (hallucinations, delusions, incoherent speech, lack of emotion)
- the clinician can look up these symptoms in an alphabetical index or may go straight to an obvious section such as schizophrenia
- the clinician then uses symptoms to locate a subcategory
strength of the ICD in terms of reliability
✅improvements in reliability
PONIZOVSKY ET AL compared reliability of the ICD 9 and 10
about 3000 patients were assessed at each time point (1996,1989,2003)
stability (reliability) of diagnosis was measured using positive predictive value (PPV)
This is the proportion of ppl who get the same diagnosis when they’re re-assessed.
For sz PPV increased from 68% in 1989 to 94.2% in 2003
Higher values for 2003 show improved reliability and suggest that the increased number of disorders has not detracted from reliability of diagnosis
Reliability for ICD 10 competing argument
- high reliability is meaningless without validity
concepts of reliability and validity of psychiatric diagnosis are often conflated
a demonstration of high stability of diagnosis does not mean that the system is valid
reliability on its own tells us nothing about the true meaning of the diagnosis
strength of the ICD in terms of validity
✅MASON ET AL have shown that the diagnosis of schizophrenia using the ICD 10 has good predictive validity
The study compared different ways of making a diagnosis.
The ICD 9 and 10 were “reasonably good at predicting disability” in 99 people with schizophrenia 13 yrs later
shows the initial diagnosis was useful and meaningful in terms of its ability to accurately predict future outcomes
what are 4 key symptoms of schizophrenia
- thought insertion
- hallucinations
- delusions
- disorganised thinking
explain thought insertion
when a person believes their thoughts do not belong to them and have been implanted by an external source
they experience a “blurring” effect of the boundary between the self and others
explain hallucinations
involuntary, vivid and clear perceptual experiences that occur in the absence of any external stimuli
auditory hallucinations are most common
explain delusions
fixed beliefs that are not amendable to change up in the light of conflicting evidence
explain disorganised thinking
inferred from a persons speech which may be characterised by derailment
the person may switch from one topic to another and jumble seemingly unrelated ideas
explain a strength of diagnosis of schizophrenia
- can be made with a high degree of sonsistence and this is true of diagnosis made with both the DSM 5 and ICD 10
- field trials of the DSM 5 reported a kappa value of 0.46 which is interpreted as good
- SARTORIOUS ET AL quote a very high kappa value of 0.86
- only 3.8% of clinicians said they lacked confidence in their diagnosis of sz
explain a weakness of diagnosis of sz
- identifying disorders can be difficult if the client is from a different cultural background from the psychiatrist
- Rastafarians often use neologisms which are a play on English words such as ‘over stand’ for ‘understand’
a clinician who is unaware of this may see this as a sign of disorganised thinking when interviewing a person
this demonstrates an accurate diagnosis of sz requires an awareness and sensitivity to cultural and linguistic differences
explain hypodopaminergia in terms of the dopamine hypothesis
hypodopaminergia refers to there being a dopamine deficiency
DAVIS ET AL suggests that the positive symptoms of sz may result from excess of dopaminergic activity in the mesolimbic pathway
whereas negative symptoms may results in hypodopaminergia (lack of dopamine in mesocortical pathway)
explain hyperdopaminergia in terms of the dopamine hypothesis
hyperdopaminergia = excess dopamine
in the 1950’s 2 antipsychotic drugs called chlorpromazine and reserpine were found to be helpful in alleviating sz symptoms
both drugs induced tremors and muscle rigidity –> symptoms of Parkinson’s
- sz symptoma may be linked to high dopamine levels
explain serotonin and negative symptoms in terms of the dopamine hypothesis
2000’s research on role of neurotransmitters and GABA, glutamate and serotonin
attention turned to newer antipsychotic = clozapine which minds to D1 and D4 , also WEAKLY to D2
- clozapine also binds to serotonin receptors and reduces both pos and neg symptoms of sz
explain dopamine dysfunction in terms of the dopamine hypothesis
HOWES AND KAPUR =
describe dopamine dysregulation in the striatum as the common pathway to psychosis
also suggested that attention should be turned to high pre-synaptic dopamine levels as opposed to irregularities of D2 receptors
- they focus on interactions between genetic, environmental and social cultural factors
and believe that the dopamine hypothesis should be softened and viewed as an explanation of psychosis proneness, not sz.
strength of the dopamine hypothesis
- research on rats treated with amphetamines
- TENN ET AL found that rats given 9 amphetamine injections over 3 weeks showed various sz like symptoms
- manifested as stereotypical movements and social withdrawal
- dopamine antagonists were successful in reversing effects
- suggests that increased dopamine may be a cause of sz in humans
competing argument of dopamine hypothesis
- DEPATIE AND LAL showed that apomorphine , a dopamine agonist, does not induce psychotic symptoms
- nor does it exacerbate already existing symptoms
- challenges the suggestion that hyperdopaminergia is responsible for pos symptoms
dopamine hypothesis weakness
- neurochemical explanations cannot explain WHY certain groups in society are more prone to sz diagnosis
- netherlands - VELING ET AL showed that Morrocan immigrants were more likely to be diagnosed with sz than turkish immigrants
- correlated with the amount of actual and percieved discrimination faced by each group
- suggests environmental factors such as social stress may interact with internal neurochemistry , making some ppl more prone to psychosis.
2nd strength of the dopamine hypothesis
- support for the role of D2 receptors
research from SNYDER - found that chlorpromazine acts as an antagonist at many dopamine receptors, especially D1 AND D2
- has an antipsychotic affect
HALOPERIDOL = dopamine antagonist with a narrower range of biochemical effects yet is more effective in reducing symptoms
suggests = excess activity on specific just not ALL receptors is implicated in the development of symptoms
explain genetics as an explanation of sz
- SZ is a heritable condition
- recent estimates for heritability = 79%
(HIKER ET AL) - this suggests a large role for genetic factors in determining the disorder
- WRIGHT (2014) has indicated as many as 700 genes have been linked to SZ and by now this figure is likely to be in the thousands
explain genetic mutations in regards of the genetic explanation of sz
- sz can appear in the absence of a family history of the disonder.
- The DNA code in 1 or more genes may spontaneously change (mutate).
- Thess Change may result from an environmental factor or error during cell division, such as deletion or duplication
- e.g DiGeorge syndrome caused by deletion of around 30-40 genes.
25% ppl with this condition later develop sz
name the 2 candidate genes
- COMT GENE
DISC 1 GENE
describe the COMT gene
link between sz + DiGeorge syndrome may be due to the deletion of the COMT Gene.
CoMT genes provides instructions for the creation of an enzyme which breaks down neurotransmitters such as dopamine
deletion would mean dopamine levels were poorly regulated
describe the DISC 1 Gene
ppl with abnormality to the DISC1 gene are 1.4x more likely to develop sz (KIM ET AL)
this gene codes for the creation of GABA
( a neurotransmitter which regulates other neurotransmitters)
explain the diathesis stress model
its most likely that genes create a vulnerability to sz rather than causing it
you may possess sz genes (diathesis) but the condition is only triggered by other biological or environmental effects —> genes are the required element
‘stress’ refers to anything that triggers Sz
strength of the genetic explanation of sz
✅research support
GOTTESMAN (1991)
analysed the concordance rate for ppl of different genetic similarity.
—> clear relationship between genetic similarity and an increase in 2 related ppl having sz
GOTTESMAN AND SHIELDS (1966) : identified a concordance rate of 42% MZ, 9% DZ
—> shows that while sz is not entirely a genetic disorder, the fact that concordance rate for MZ is higher shows that biology plays a significant role
weakness of genetic explanation of sz
Concordance rate is far from 100%, even for MZ twins.
Pederson + Mortensen (2006) research demonstrates that the longer a person has been exposed to city life + the denser the population →
the greater risk of SZ
Suggests that rural dwelling may help protect a person from developing a disorder to which they’re genetically
predisposed
2nd strength of the genetic explanation of sz
✅candidate genes as an explanation has a wealth of research evidence
- in a review of 14 studies , DAHOUN ET AL concluded that DISC1 is associated with presynaptic dopamine dysregulation
EGAN ET AL propose a link between decreased dopamine activity and one form of COMT gene - ‘val’ allele
—> they conclude inheriting 2 copies increase sz risk by 50%
what are the factors in the non bio explanation of sz
• Urbanicity
• social isolation
• immigration and minority status
• social adversity
explain social adversity in the social causation explanation
all humans have the same basic needs:
• physical: shelter, warmth
• emotional
• intellectual
• social
some children grow up in environments less favourable than others, making them vulnerable to mental health disorders .
ppl from lower socioeconomic groups may not be able to access treatment for sz, leaving them even more vulnerable and further exacerbating their problems
explain urbanicity in the social causation hypothesis for sz
EATON suggested that city life is more stressful than rural life + longterm exposure to such stress may trigger an episode of sz
many stressors link to city life - noise, light pollution, faster pace, criminality
collectively these factors make a person more vulnerable to sz
increased population density also makes life more competitive which arguably increases the experience of chronic social defeat
(a stressor which may elicit sz)
what were carlsson et als 8 steps
- the dopamine hypothesis revisited
- Beyond dopamine
- glutamatergic control of dopamine release
- glutamate - dopamine interactions
- the thalamic filter
- Comparing the two experimental schizophrenia models
- is the therapeutic potential of dopaminergic agents exhausted
- concluding remarks
what was carlssons aim
to review evidence for and against the dopamine hypothesis
