Schizophrenia Flashcards
(43 cards)
Classification
the act of distributing things into classes or categories of the same type
Diagnosis
identification of disease by its signs and symptoms
Diagnosis of mental illnesses can be problematic
• Diagnosis may be subjective, low inter-rater reliability between doctors
• If a doctor sees them for an hour, it’s only a snapshot of their life, illnesses fluctuate, doctor may see them on a good day and give them too milder treatment
• Patient may exaggerate symptoms to make trip worthwhile
• Mental illnesses have overlapping symptoms – may be a side effect/major part of illness
• If behaviour is ambiguous, diagnosing behaviour can make them worse
o However, can be given reassurance
Advantages of a diagnostic system
- Justified explanation for making a diagnosis
* Gives an objective basis for proceeding on to treatment
Classification systems
• ICD (International Classification of diseases) is a classification system devised by the WHO (World Health Organisation, 1CD-10 distinguishes between 7 subtypes
• DSM produced by the American Psychiatric Association, dominant in the US
o Primary use by mental-health professionals is making diagnoses and conducting research
o Relationship between DSM and state of scientific knowledge on mental illness, DSM should lag just behind
o Argued that DSM pathologises human behaviour i.e. identifying more human behaviour as ‘disorders’, making psychiatrists money
o DSM-IV distinguished between 5 subtypes
o DSM continuously revised for to increase in knowledge of mental disorders/recognition of disorders that already existed/ become clearer of symptoms/renaming mental disorder/drug treatment may be more refined
• Scheider’s first rank criteria (same as first two symptoms of DSM-5)
• Crow made the distinction between two types of Sz
o Type 1: positive symptoms, symptoms taken away from the sufferer’s personality
o Type 2: negative symptoms, symptoms taken away from the sufferer’s personality
Symptoms; Diagnostic criteria from DSM-5 (2013) INTRO
- DSM-5 main goals: better recognition of disorders, provision of treatments, help doctors provide better care and increase quality of life
- Dropped the sub-types as trials have shown there is a lack of reliability in diagnosis of the sub-types
- 2 or more for a significant portion of time during a 1- month period
- At least one from 1-3.
- ‘Continuous signs of the disturbance’ for at least 6 months
- Level of functioning in one major areas, e.g., work, relationships, must have diminished
DSM-5 5 symptoms
- Delusions
• Fixed false beliefs resistant to change despite contrary evidence.
• Persecutory: belief that one will be harmed by someone
• Referential: belief that certain gestures/comments are directed at oneself
• Grandiose: belief that one has exceptional abilities/wealth/fame
• thought withdrawal: belief that one’s thoughts have been removed be some outside force
• thought insertion: belief that alien thoughts have been put into one’s mind
• delusions of control: belief that one’s body or actions are being acted on or manipulated by outside forces - Hallucinations
• Perception- like experiences without an external stimulus, not under voluntary control
• commonly auditory (voices), but in other sense modalities, e.g. visual/olfactory (smell)
• must occur in context of a clear sensorium – those that occur when falling asleep/waking up are considered part of normal experience
• They need to be distinguished from normal religious experience as can be seen a normal part of religious experience in certain cultural contexts - Disorganized thinking (speech)
• Disorganised thought inferred from speech.
• Involves (switching of topics), irrelevance and incoherence – due to severely disorganised speech / ‘word salad’.
• As disorganised speech is common, symptom must be severe enough to impair effective communication - Grossly disorganized or catatonic behaviour
• Disorganised behaviour includes unpredictable agitation or ‘silliness’.
• Catatonic behaviour is a marked decrease in reactivity to the environment, including rigid posture, lack of verbal or motor responses. - Negative symptoms
• Diminished emotional expression, reduction in eye contact, facial expressions, hand movements
• Avolition: decrease in motivated self- initiated purposeful activities
Issues in reliability of classification
• Reliability = consistency
• Range of classification systems
• Differences between DSM and ICD
o ICD-10 – distinguishes between 7 subtypes
o DSM-IV – distinguished between 5 subtypes, now DSM-5 has dropped the sub types and ICD-11 will drop them because trials have shown that there is a lack of reliability on diagnosis of the sub-types
• Inconsistent classification → inconsistent diagnosis and invalid classification
Issues in reliability of diagnosis
• Inter-rater reliability = consistency of diagnosis by different doctors
o Fairly easy to test but less commonly tested
• Kleitman’s 3 problems:
o Differences in procedures e.g. use of classification systems
• Different classification systems, likely to make different diagnoses
• DSM used in US, mixture used worldwide
• American and British psychologists shown the same video taped clinical interviews and asked to make a diagnosis
• Psychiatrists from New York diagnosed Sz twice as often
• Psychiatrists from London diagnosed mania and depression twice as often (Cooper 1972)
o Differences between clinicians, subjectivity
• Even if the same classification systems are being used, clinicians may interpret them differently
• Phrases in manuals are open to interpretation
• E.g. in DSM-5, delusions are defined as bizarre ‘if they are clearly implausible and not understandable to same-culture peers and do not derive from ordinary life experiences.’
• Mojtabi and Nicholson found weaker inter-rater reliability (0.4) between clinicians in judgements of whether hallucinations were ‘bizarre’ or not
o Differences between patients, presentation
• Patients may present themselves differently on different days depending on their mood and the variability of symptoms
• Patients may also react different depending on the doctor
• Improvements in reliability over time
o DSM 2 diagnostics had low reliability – Beck got two psychiatrists to diagnose 154 patients and only had inter-rater reliability for 54%
o DSM 3 showed an increase in reliability after removal of vague descriptions, clarifying how many symptoms and of which types were needed – American Psychiatric Association showed this e.g. diagnoses were consistent in 81% in a sample
• Unreliable diagnoses → invalid diagnoses
Reliability is necessary but not sufficient for validity of diagnosis as diagnoses may be the consistently wrong
Issues in validity of diagnosis
• A valid diagnosis is one that is correct
• If reliability of diagnosis is poor then so too is the validity
• If there is inconsistency in diagnosing Sz across two or more clinicians then at least one must be an incorrect (invalid) diagnosis
• The main problem with diagnosis is that what can be observed is an indirect sign of the illness
o In Sz there is no indicator that is accepted as showing the presence of the illness
o There is no laboratory test that objectively settles whether someone has Sz – all psychiatrists can do is observe behaviour and talk to patients, making genuine verification of the validity of a diagnosis very difficult
• Invalid diagnoses
o Type 1/false positive – inappropriate treatment however may reduce symptoms for something else, side effects, labelling can make it worse
o Type 2/false negative – no treatment when it’s needed
Issues in validity of classification
• Is Sz a genuine distinct illness?
• In the absence of a definitive physiological maker for the illness, we need to be confident that Sz has been classified in a valid way
• 3 criteria:
o descriptive validity – are the symptoms right?
• The diversity of symptoms makes it difficult to define precisely
• Bentall sees the term ‘schizophrenia’ as unhelpful as it masks large differences between patients
o Aetiological validity – can we identify causes and mechanisms?
• Disagreement on its causes and mechanisms involved
• Howes and Kapur argue that pre-synaptic dysregulation of dopamine is involved in all cases of Sz that involve psychotic symptoms i.e. hallucinations and delusions
• This suggests that if we restrict the term Sz to those with psychotic symptoms, and that such symptoms are caused by dopamine dysregulation, that the disorder can be defined in a clearer way i.e. such that there is a mechanism that is the same in all cases
o Predictive validity – what is the prognosis/reaction to treatment?
• In a well defined illness we should be able to describe how the illness progresses over time and predict how they will react to treatments
• In Sz there is great variability in prognosis - about 1/3 of patients remain chronically ill, about 1/3 recover from initial bouts of illness, about 1/3 have periods of illness and periods of being relatively ill
• Reaction to treatments for Sz, especially drug treatments, is mixed - all drugs that have any effectiveness are those that target dopamine receptors, but some are effective for some patients but not others, and prognosis is unpredictable
Consequences of lack of validity
• If psychiatrists are to treat schizophrenia properly they must be diagnosing it properly.
• If diagnoses are invalid two errors can occur:
o False positives
• if a patient is diagnosed with an illness that they do not have then they may receive treatment with powerful anti- psychotic drugs
• This may lead to the side effects of anti- psychotics, such as weight gain, sexual dysfunction and tardive dyskinesia
• Some argue that treating people with anti- psychotics when they don’t have Sz can sensitise dopamine receptors and induce the symptoms of Sz
• Perlman (2000) reported on patients (who it turned out had Asperger’s syndrome) diagnosed with undifferentiated schizophrenia, but did not fit the criteria properly: they had negative symptoms only. These patients were given unnecessary antipsychotics despite a lack of positive symptoms.
o False negatives
• If a patient is not diagnosed with an illness that they do have, then they will not receive treatment for an illness that they do have
• This leaves patients vulnerable and suffering unnecessarily
• Research
o If psychologists are to explain schizophrenia doctors to be diagnosing it properly, i.e., in a valid way
o If diagnoses are inconsistent or based on an invalid definition, explanations cannot be properly tested.
Biological explanations - genes
- We inherit 50% of our genes from each parent
- Genes contain our DNA which codes the proteins to build bodies including, crucially, the brain structure
- The brain is the source of all mental states
- Schizophrenia is a disorder of mental states
- Schizophrenia may be heritable, i.e., have a genetic basis
- Genes for Sz may influence dopamine production
Liability threshold model
• Most geneticists believe that there are a number of genes that each have a small effect, though some have more of an effect than others, more genes – more risk, some riskier than others
Diathesis- stress model
• The genes are the diathesis, as they put someone at risk; stressors are the environmental factors
that determine who develops the disorder and when
Combining the models
• Those with a higher liability threshold will be more at risk and it may take relatively minor environmental effects to trigger the illness
AO2 biological, twin studies
Gottesman review: Concordance rates;
MZs ≈ 40 %, DZs ≈ 15% across a range of reviews
Large difference between figures for the two types of twins, but MZs nowhere near 100% Consistent evidence from a series of reviews of twins studies for a strong genetic effect
As genes clearly not the only factor, provides room for environmental effects, possibly in a diathesis- stress model
AO2 biological, adoption studies
Tienari: Concordance rate between mothers with Sz and adopted- away offspring = 7 – 10 %, but 0 - 1.5 % when biological mother does not have Sz
Wahlberg: re-examined data from Tienari and found a strong effect of environmental factors where those at risk of developing Sz were adopted into families with poor communication – diathesis-stress model
Schizophrenia more likely in households with dysfunctional communication
Consistent evidence, from a series of studies, for a moderately strong genetic effect, but not so many studies
Influence of dysfunctional households provides more direct support for diathesis- stress model
AO2 biological, separated twin studies
Gottesman: In the only study of 14 pairs of separated MZ twins the concordance rate was 58% Evidence for a strong effect, but a very small study
AO2 biological, molecular genetics
Many studies have found links to a large variety of genes all of which have small effects, many related to dopamine production
Glatt et al: meta-analysis identifies an association between the dopamine D2 receptor gene and Sz, the risk of developing Sz was shown to increase by 30% in relation to a defect in the gene coding for the D2 receptor Provides support for the liability threshold model, as not just one gene involved and increases in risk are small
Dopamine hypothesis
• Different versions claim Sz is due to: excess of dopamine, excess of dopamine receptors or super- sensitivity of dopamine receptors
• However, the evidence is correlational, so a causal claim cannot be made
• dopamine dysfunction causes Sz, or Sz causes dopamine dysfunction.
• Even if dopamine dysfunction does precede and cause Sz, what causes the dopamine dysfunction in the first place?
• suggested causes for dopamine in Sz:
o L- dopa, which increases dopamine levels, leads to Sz- like symptoms in previously unaffected (Parkin’s) disease
o recreational use of amphetamines, which also increase dopamine activity, also induce Sz- like symptoms (and worsen symptoms in those with Sz)
AO2 dopamine hypothesis
• - does not seem to apply to all Szs
o drug treatments do not help all patients, tend to help around 60%
o not all users of amphetamines or L- dopa develop Sz- like symptoms
o dopamine does not seem to be involved in Type 2/ negative symptoms of Sz
• + explains why drugs are effective, but not for all patients
• + solves the problem of initial causes of dopamine dysfunction: due to a variety of factors
• + explains why negative symptoms are unrelated to dopamine dysfunction and only leads to psychosis (hallucinations and delusions)
The dopamine hypothesis 111: the final common pathway model of dopamine (Howes & Kapur) INTRO
• Dopamine is the ‘common (biological) pathway’ through which psychosis develops i.e. positive or type 1 symptoms, whether through genetic or environmental causes i.e. nature-nurture including EE and stressful life events
o Different to diathesis-stress model which suggests that all cases of Sz have some genetic basis
o Nature-nurture suggests that Sz could develop without any genetic influence, as long as the ‘hits’ on dopamine functioning were powerful enough
• All those with Sz who have psychotic symptoms (and those with a different disorder who have such symptoms) have pre-synaptic dopamine dysfunction
the final common pathway model of dopamine AO1 and AO2
- Initial causes:
Multiple factors, both genetic and environmental, interact, resulting in dopamine dysregulation
• The genes that most raise the risk of developing Sz are those associated with dopaminergic pathways
• Environmental factors associated with increased risk of Sz: unemployment, lack of close friends and childhood abuse, are linked to social isolation and subordination
• In animal studies, these factors lead to dopamine dysfunction.
• factors interact, e.g. early experiences that affect dopamine regulation ‘prime’ the brain for more extreme reactions to later experiences.
• The ‘hits’ from these factors will be of different strengths and combine in diverse ways
• Unique symptoms will result from unique pathwyas from the initial cause to the presynaptic dopamine dysfunction - Locus of dysfunction:
The locus of the dopamine dysregulation is presynaptic, involving increased synthesis and tendency to release the transmitter • So excess dopamine is produced and released but the dysfunction is presynaptic rather than at the dopamine receptor
• This means that current drugs are acting ‘downstream’ rather than ‘upstream’, they are not treating the primary location, so partially successful for some people but can make things worse for others
• In a meta- analysis of brain scanning studies H&K (2012) found very high rates of presynaptic dopaminergic function in Sz while other dopamine dysfunction (i.e. at synapses) seems to be less pronounced. - Effect on psychotic symptoms: Dopamine dysregulation is linked specifically to the dimension of positive, psychotic symptoms and ‘psychosis proneness’, regardless of diagnosis • Sz patients with psychotic symptoms display dopamine dysfunction, while those without do not.
• Non- schizophrenics who experience psychotic symptoms also have dopamine dysfunction.
• Drugs that reduce positive symptoms all work on the dopamine system.
• So the theory is really an explanation of psychosis rather than Sz - Psychological effects: Dopamine dysregulation alters the appraisal of stimuli through the process of aberrant salience • People with Sz have difficulties telling the difference between relevant and irrelevant information
• Try to make sense of experiences in the usual way, but because they do not filter out irrelevant information, thoughts become confused
• The difference between people without Sz is that delusions incorporate experiences that are not actually relevant (salient)
• Some studies have linked dopamine systems to motivational salience.
the final common pathway model of dopamine AO2 only
Testing this version of the DH?
• Trials of drugs that work pre-synaptically and see if they are more effective than those that work on the receptors
• Genes linked to Sz likely to be those related to the dopamine system
• Environmental factors linked to Sz would be expected to lead dopamine dysfunction
o Brain scans to identify precise location of dysfunction: compare Szs with non-Szs, expect to find biggest differences pre-synaptically
Howes at al
• Investigated the nature of the dopaminergic dysfunction in Sz using meta-analysis of in vivo studies (living patients)
• 44 studies identified comparing 618 patients with Sz with 606 controls, using positron emission tomography to measure in vivo striatal dopaminergic function
• studies grouped into those of presynaptic function, dopamine transporter and receptor availability
• Results:
o a highly significant elevation of p
Psychological explanations
Background and history
• Until the 1960s, the main theories of Sz were psychological/environmental
• However theories were rejected due to: growing evidence for the biological basis for Sz and the limitations for the environmental theories
o E.g. critics argued that at best, the evidence showed a correlation between family factors and Sz
o Problems within families were a result of the difficulties of dealing with someone with Sz, rather than the actual cause of Sz
• By the 1970s, it became clear that Sz could not be explained entirely in biological terms
• The challenge is to provide convincing evidence that the environmental factors play a genuine causal role in Sz/how biological and environmental explanations can combine
Stressful life events
Models of stressful life events
• Holmes & Rahe’s Social Readjustment Rating Scale (SRRS)
o Stressors include: bereavement, losing your job or home, a divorce or the end of a relationship, or physical, sexual, emotional or racial abuse
o LCU – life change units
o For younger people, key stressors include exams, starting or ending relationships and first jobs.
o May interpret positive events as negative e.g. marriage
• diathesis- stress model
o genes are the diathesis making people vulnerable to Sz
o some genes have more penetrance than others, giving a higher risk
o Stressful life events can be seen as stressor i.e., those at (genetic) risk will be affected by stressful life events (others won’t).
o This may work via the HPA (hypothalamic- pituitary- adrenal) axis (what we called the pituitary adrenal system in the AS)
o dysregulation in the stress hormone cortisol has been associated with psychosis and higher levels of cortisol predicts severity of symptoms.
o Howes and Kapur: a range of interacting biological and environmental factors can cause Sz, all of which affect the pre-synaptic functioning of the dopamine system
• dopamine hypothesis – final common pathway
o stressful events, among many other possible contributers are one of the factors that lead to dopamine dysregulation, which then leads to psychosis.