Schizophrenia

Question 1

Classification

Answer 1

the act of distributing things into classes or categories of the same type

Question 2

Diagnosis

Answer 2

identification of disease by its signs and symptoms

Question 3

Diagnosis of mental illnesses can be problematic

Answer 3

• 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

Question 4

Advantages of a diagnostic system

Answer 4

• Justified explanation for making a diagnosis

* Gives an objective basis for proceeding on to treatment

Question 5

Classification systems

Answer 5

• 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

Question 6

Symptoms; Diagnostic criteria from DSM-5 (2013) INTRO

Answer 6

• 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

Question 7

DSM-5 5 symptoms

Answer 7

1. 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
2. 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
3. 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
4. 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.
5. Negative symptoms
   • Diminished emotional expression, reduction in eye contact, facial expressions, hand movements
   • Avolition: decrease in motivated self- initiated purposeful activities

Question 8

Issues in reliability of classification

Answer 8

• 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

Question 9

Issues in reliability of diagnosis

Answer 9

• 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

Question 10

Issues in validity of diagnosis

Answer 10

• 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

Question 11

Issues in validity of classification

Answer 11

• 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

Question 12

Consequences of lack of validity

Answer 12

• 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.

Question 13

Biological explanations - genes

Answer 13

• 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

Question 14

AO2 biological, twin studies

Answer 14

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

Question 15

AO2 biological, adoption studies

Answer 15

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

Question 16

AO2 biological, separated twin studies

Answer 16

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

Question 17

AO2 biological, molecular genetics

Answer 17

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

Question 18

Dopamine hypothesis

Answer 18

• 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)

Question 19

AO2 dopamine hypothesis

Answer 19

• - 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)

Question 20

The dopamine hypothesis 111: the final common pathway model of dopamine (Howes & Kapur) INTRO

Answer 20

• 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

Question 21

the final common pathway model of dopamine AO1 and AO2

Answer 21

1. 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
2. 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.
3. 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
4. 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.

Question 22

the final common pathway model of dopamine AO2 only

Answer 22

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

Question 23

Psychological explanations

Background and history

Answer 23

• 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

Question 24

Stressful life events

Answer 24

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.

Question 25

stressful life events AO2

Answer 25

Norman & Malla
• found that the severity of symptoms over time was correlated with life events, suggesting that such events act as stressors for those who are already predisposed to schizophrenia
• It is notable that there is no evidence that those at risk have a higher number of stressful events than non- clinical populations
Horan et al
• found that patient samples have lower levels of such events than the general population
• suggested that it is not the number of events that matters but the ability of the patient to cope with such events
Day et al
• The main finding has been replicated in a cross- national study, which found higher rates of stressful events in the 2-3 weeks preceding the onset of schizophrenia.

• + consistent findings, from reviews of Western and cross- cultural studies, suggests that we can be confident that there is a genuine relationship between stressful life and events and schizophrenia
• + findings generally all in the right direction, triangualted evidence
• + prospective research by Ventura et al and Horan et al both suggest that the stressful events precede the onset of symptoms, as recorded at the time rather than retrospectively. These studies were both rather small, but they do address the causality issue reasonably well.
• + plausable mechanism - cortisol
• - isssue of causality
o it could be that patients retrospectively report more stressful events in the weeks preceding the onset of full symptoms
o Perhaps they are already experiencing a build- up of symptoms before full onset and this alters their recall of the events.
• - systematic problem with retrospective studes
• - mayve events proceed the onest of Sz
• - small size studies in prospective, with problems of attrition

Question 26

retrospective studies

Answer 26

asks participants to recall details from the past

Question 27

prospective studies

Answer 27

study follows particapants in the present

Question 28

Expressed Emotion (EE)

Answer 28

= a qualitative measure of the ‘amount’ of emotion displayed, typically in the family setting, usually by a family or caregivers. It is thought that a high level of EE in the home can worsen the prognosis or act as a potential risk factor for the development of schizophrenia.
• It appeared that some patients did better than others and that this was related to how their family treated them
• Relapse rates seemed to be higher in certain types of families

Brown: 3 elements of EE:
• Hostility: a negative attitude directed at the patient because the family feels that the disorder is controllable and that the patient is choosing not to get better.
• Critical comments may come about because the relative feels that the patient is wholly or at least partly responsible for their disorder.
• Emotional over-involvement is when a family member blames him or herself for the disorder, shows a lot of concern for the patient, the pity from the relative causes too much stress and the patient relapses to cope with the pity.
• EE can be seen as stressor in a diathesis- stress model, i.e. those at (genetic) risk will be affected by EE (other’s won’t)
• EE can be seen as one (among many) possible contributors to dopamine dysfunction within the ‘final common pathway’ model of the DH
• 3 factors lead to relapse being more likely due to a feeling of stress

Measurement
• EE can be measured by interview or observation of family interactions in the home
• The Camberwell Family Interview is the main measurement tool used to assess EE
o Conducted with the carers of the patient
o Interviewer tries to create a picture of how things have been in the household in the months leading up to the onset of Sz
o Interview is taped and transcript is rated
o Obtain objective information about events and circumstances in the home in the months before onset
o Obtain subjective information about the relative’s feelings and attitude towards the patients when talking about the disorder
o Answers to questions and non-verbal cues are used to determine if someone has high EE
• Difficulties:
o Fluctuations in behaviour
o Interview is open to interpretation
o People lie
o Social desirability effects

Question 29

EE AO2

Answer 29

Brown
• initial identification of high levels of EE in homes where relapse was higher

Vaughn and Leff
• found relapse rates of 51% in high EE homes and 13% in low EE homes
• amount of face- to- face time spent with relatives also correlated with risk of relapse.

Butzlaff et al
• The conclusions of these initial studies have been conclusively replicated in many studies and collected in meta- analyses
• 27 studies, Butzlaff et al found relapse rates of 65% (high EE) and 35% (low EE) and a moderate effect size (0.3).
• findings highlight the importance of EE in the understanding and prevention of relapse in a broad range of psychopathological conditions

King et al
• Retrospective study tracked levels of EE and symptoms over time to see which occurs first, between symptom severity in Sz young adults and the EE of their mothers
• 28 patients and their mothers were interviewed 3 times, at 9 month intervals
• the more severe the hostile-uncooperative symptoms in the patient, the more critical the mothers became over time
• however, the greater the mother’s EOI (emotional over-involvement) at time 1, the less severe the patient’s hostile-uncooperative symptoms at time 3 – high EE causes symptom exacerbation
• found that some elements of EE are a response to, rather than a cause of, worsening symptoms – EE is a consequence of Sz in patients

• Survey studies of the EE-relapse relationship
o Two meta-analyses have found a close relationship between levels of EE and relapse rates in those returned to the family home
o Relapse rate are approximately twice as high in homes where EE is high than where it is low
o Issue of causality
• Treatment studies
o Meta-analysis of treatment studies using ‘family intervention’ show lower relapse rates, reduced hospital admissions and increased compliance with medication
o However it is a form if experiment, can not increase levels of EE, unethical, so must reduce them
• Prospective studies of the possible causal relationship between EE and relapse
o One study conducted that levels of some aspects of EE ‘appear to be more effect than cause’
o If accepted, this would be crucial evidence against claim that EE causes relapse
• - correlational research: it could be that EE is a response to symptom severity rather than a cause of relapse, weakening support for the theory.
• Intervention studies: levels of EE are manipulated by giving one set of families a therapy designed to reduce EE, and testing if this leads to a decrease in symptoms and relapse rates, have been successful in both reducing EE and relapse rates, but there are doubts about the use of random allocation in these studies.
• evidence overall is mixed. It seems likely that causality goes in both directions, i.e. from EE to relapse and from symptom severity to high EE.
• more, better quality, prospective and intervention studies are needed.

It doesn’t matter that high levels of EE are not specific to families of people with Sz as guilt can be a likely factor in relapse of a range of disorders.

Reasonable conclusion: EE can cause relapse of Sz where Sz initially cause EE as it originally developed.

Question 30

biological therapies

Methodology

Answer 30

• quality of data: studying the effectiveness of treatments in clinical trials aka RCTs, are field experiments, involving:
o random allocation
o blind procedures
o placebo or other control conditions
• quantity of data: treatments for Sz have been extensively researched, so there are many meta-analyses
• Cochrane reviews are an independent medical organisation who conduct reviews and meta-analyses of medical treatments, including for psychological illnesses, generally accepted as less likely to be biased than individual researchers
• File drawer problem
o Studies are often not published, especially those funded by drug companies
o There is no compulsion to publish trials, so much data goes unpublished

Question 31

biological therapies

history

Answer 31

• Until the middle of the 20th century, nothing worked, treatments for Sz were largely attempts to control and pacify patients
• In the middle of the 20th century, ECT had limited success
• ECT survives as treatment for catatonic and suicidal patients with Sz

Question 32

biological therapies

current practice

Answer 32

• The National Institute for Clinical Excellence (NICE) provide guidelines for clinical practice in the UK
• They currently state that patients should be offered drug treatment, CBT and where appropriate, family intervention
• ECT should only be sued for catatonic and suicidal patients
• No other treatments are currently recommended
• Drug treatments
o Patients tend to be switched between different drug treatments depending on their reaction to the treatment i.e. their symptoms and side effects
• ECT
o Rarely used now for Sz, more commonly used for major depression
o Tends to be used for those who have been sectioned i.e. hospitalised without their consent due to being a danger to themselves or others

Question 33

Effectiveness

Answer 33

Does the therapy work?

Does it reduce symptoms/prevent relapse/how long do effects last?

Question 34

Appropriateness

Answer 34

Is it right to give this therapy?

Side effects/ethical issues/do patients want treatment/what is the cost?

Question 35

Drug treatments biological therapies

Answer 35

Conventional/typical antipsychotics e.g. Chlorpromazine
• 1950s developed
• Use: reduces the positive symptoms of Sz
• Rationale: Sz results from an excess of dopamine activity at synaptic sites
• Aim: to reduce dopamine activity at receptor sites
• Process (mode of action): typical anti- psychotics are dopamine antagonists, which means that they bind to dopamine receptors and block rather than stimulate their action, reducing the release of dopamine and therefore the hallucinations and delusions experienced by schizophrenic patients.

Clozapine /atypical antipsychotics e.g Clozapine
• Later, developed
• Newer antipsychotics have been introduced over the past 15 years, and shown to be as effective as chlorpromazine but with fewer side effects.
• Clozapine appears effective in controlling positive symptoms in those resistant to other neuroleptics.
• It also has the advantage of reducing negative symptoms
• Use: to treat positive and negative symptoms with fewer side effects
• Rationale: Sz results from an excess of dopamine activity at certain synaptic sites and that an imbalance in neurotransmitters, e.g., serotonin, are linked to Sz
• Aim: to target serotonin and dopamine receptors in the brain.
• Process: atypical anti- psychotics combine the blocking of dopamine receptors achieved by typical anti- psychotics with a similar blocking of serotonin receptors

Question 36

Evaluation of drug treatments

Answer 36

Effectiveness
• Typical anti- psychotics are effective for about 60% of patients
• Adams et al
o review of 50 high quality RCTs found chlorpromazine to be more effective than placebo across symptoms
o fewer people allocated to chlorpromazine left trials early compared with placebo
o reduction in relapse rates in short/medium term heterogeneous (varied)
o reduction in relapse rates in longer term favouring chlorpromazine homogeneous (similar)
o Out of the 349 trials considered, 299 were excluded because of flaws in the research methods or the reporting of data
• Atypical anti- psychotics are marginally better than typicals as they are effective in slightly more patients, including many resistant to typicals
• Essali et al
o review of RCTs found fewer relapses, more improvement in functioning and negative symptoms with clozapine than typicals from BPRS scores
o Improvements in those who did not improve on typical antipsychotics – 34% of treatment-resistant participants had a clinical improvement with clozapine treatment
• These were both Cochrane reviews, so the data should be of high quality
• However, there are major issues of publication bias due to drug companies burying unfavourable data, results may exaggerate benefits.
• Typical: in trials comparing Chlorpromazine to placebo, it has been found to: reduce relapse rates, improve functioning – findings confirmed by meta-analyses
• Atypical: in trials and meta-analyses comparing clozapine to typical anti-psychotics, it has been found to lead to: reduction of positive and negative symptoms, fewer relapses
Appropriateness
• Typical:
o Major side effects include extrapyramidal side effects (EPS) – movement and coordination disorders:
• tardive dyskinesia – involuntary movements of the tongue and jaw (20%), parkinsonianism e.g. stiffness
o also weight gain and sexual dysfunction (both 50%), with higher rates for typicals, patients may not take the drugs
• Atypical:
o A small % of those who take clozapine have reduced white cell count, but this is easily monitored.
o Fewer side effects than typical anti-psychotics, although more: drowsiness, hyper-salivation, temperature increase

Conclusion:
• Clozapine may be more effective in reducing symptoms of Sz than typical but data is weak and prone to bias (better conduct and reporting of trials could have increased confidence in results)
• Short-term benefits of clozapine have to weighed against the risk of adverse effects

Question 37

Electro- convulsive therapy

Answer 37

• Use: originally developed to treat Sz, now more for depression, often for those with catatonic schizophrenia or if the patient is suicidal or pregnant
• Rationale: there is abnormal activity of neurotransmitters and / or hormones
• Aim: the shock disrupts/corrects this abnormal neurotransmitter activity
• Procedure:
o small electric current (70-130 mv) for 0.5 to 5 seconds induces mini- seizure by producing electrical convulsions in brain
o Several sessions over a number of weeks
o Anaesthetic and muscle relaxants are administered before the shock
o Electrical current is applied via electrodes positioned on the head
o Current is given either bilaterally (one electrode on each side or more usually unilaterally (on the same side)
o When given unilaterally it is usually to the non-dominant cerebral hemisphere
• It is possible to give ECT without the patient’s consent when they are:
o Suicidal
o Convinced they are too wicked to be treated
o Eating or drinking too little to stay alive for much longer

Question 38

ECT AO2

Answer 38

Effectiveness
• ECT was initially believed to be very effective in Sz, but was soon replaced by drug treatments for most patients
• Good evidence that ECT is most effective for those who are suicidal
• Best with those who are catatonic/have a catatonia
• Effectiveness is unclear when there is a combination with drug treatment
• Ineffective in treating the negative symptoms of depression, and less effective in the long-run than in the short-run
• - Mechanism is unclear
• - reporting of research is unclear, as well as there being big gaps in the research
• Tharyan & Adams
o review of 26 RCTS found that ECT led to fewer relapses (than sham ECT) in the short term, but not evidence that this is maintained in the medium/longer term
• Sham – no actual electric shocks given, to do with participant reactivity, however a problem is that there are no side effects
o This might prevent suicide in severe patients and give time for drug or psychological treatments to work.
o When ECT was compared with antipsychotic drug treatment, results favoured drug treatment
o Limited evidence that ECT and drug treatment resulted in greater improvement than antipsychotic drugs alone – however the combination could be considered an option for people with Sz, especially where rapid global improvement and reduction of symptoms is required
o Cochrane review – non profit-organisation, unlikely to be bias
• Greenhalgh et al
o found no decent evidence for its effectiveness in catatonic schizophrenia, older people, children and adolescents, despite NICE recommending it for such patients
o there is a need for further high-quality RCTs of the use of ECT in specific subgroups
o little good quality of quantitative evidence of the short and longer term cognitive side effects
o cognitive functioning should be measured using well validated instruments
o quality of reporting of trials in this area would be vastly improved by strict adherence to the Consolidated Standards of Reporting Trials (CONSORT) recommendations
• Both reviews report that much of the evidence is poor, making definitive conclusions difficult.
• Wykes et al
o Found an effect size of 0.4 (moderate-weak) for CBT compared to no treatment
o However, studies with lack of blinding had higher effect sizes i.e. person doing assessment knew whether they had CBT or not
o In ‘good’ studies i.e. those with blinding, the effect size was reduced to 0.22 (weak)
Appropriateness
• major short- term side effect of ECT is memory loss, though it is unclear, because of lack of research, whether this continues over the longer term.
o Arguably justifiable if patients know about possible side effects, understand that the long term is unknown, more justifiable for those who are suicidal
• Improvements in procedure have eliminated the fractures caused by earlier treatments
• The main remaining issue is that of consent: patients given ECT are often serious cases who are treated without their consent.

Have a point of view in answer:
• i.e. side effects not as bad as being suicidal
• two doctors, social worker, independent psychiatrist must agree that the treatment is necessary
Future:
• need more studies on the subgroups particularly catatonic/suicidal patients
• are there good measures of suicidal intent?

Question 39

Psychological therapies

Answer 39

• The enthusiasm for drug treatments meant that for many years psychological treatments were not seen as appropriate for Sz.
• Some of the trials conducted have used a repeated measures design i.e. compared pre- and post-treatment measures, less useful than trials with independent groups design i.e. comparing CBT with a control group or comparison treatment
• Effect size = a statistic developed to bring together results from different studies that have used different measurement scales
o Cohen: 0.2 is a small effect, 0.5 is a medium effect, 0.8+ is a large effect

Question 40

Cognitive- behavioural therapy

Answer 40

• Use: to treat most patients with Sz
o NICE recommend that it is offered to all patients.
o It may be that patients will also require drug treatment, especially if their symptoms are particularly severe.
o As the treatment was developed for use with patients with depression it is easily applied to negative symptoms (which often resemble symptoms of depression), but it is routinely used for those with positive (psychotic) symptoms.
• Rationale: Sz is caused, or at least maintained, by the beliefs that patients have about their experiences. They can be helped to deal with their symptoms by changing their beliefs, thus leading to less catastrophic symptoms.
• Aim: to identify and change patients beliefs which contribute to their symptoms.
• Process: the agendas set are generally more flexible than traditional CBT, the patient generally has between 12 and 20 sessions.
o Make patient aware of the role of cognitions (e.g., beliefs about their experiences) and how they impact on their functioning.
o Question, challenge and try to change patient’s beliefs.
o Test patient’s beliefs against reality.
o Achieved through experimentation, role- play and ‘homework’.
o Allow patient to become aware of irrationality of beliefs.

Ellis’ REBT involves use of the ABC model and important processes such as normalisation and decatastrophisation.

Question 41

CBT AO2

Answer 41

Effectiveness
• Rector & Beck and Gould et al found that CBT reduces positive symptoms, but the effects are smaller in proper RCTs rather than pre/post treatment studies.
• Wykes et al:
o found an effect size of 0.4 between CBT and no treatment
o but only an effect size of 0.22 in good quality trials
• Jones et al:
o review of RCTs found that CBT was no more effective than other psychological treatments on any criteria (functioning, relapse, hospitalisation), despite NICE recommending it as the front- line psychological treatment for Sz.
o However suggested that there might be some longer term advantage in CBT for dealing with emotions and distressing feelings
o Also number of people leaving the study lower in those participating in CBT
o The original enthusiasm for CBT may have been based on inadequate trials, including some with weak blinding, and (in the case of NICE) the relative cost of CBT compared to other psychological treatments.
o Trials often small and of limited quality
o However, studies reliably selected, assessed for methodological quality, had to review authors, who worked independently extracting data
• Argued that CBT could be used on its own with patients who are drug resistant, especially if they are experiencing some side effects of medication
Appropriateness
• low cost and relative speed of CBT make it appropriate for the NHS, where cost to the tax- payer is a consideration
• The absence of side- effects compared to drug treatments is a major advantage
• probably has fewer issues of dependence on the therapist compared to other therapies, in which the relationship between patient and therapist is important.
• Ethically CBT is more collaborative than other talking therapies: therapist and patient work together to bring about improvement, encouraging independence in the patient, advantage over other talking therapies e.g. psychoanalysis as it is less likely to lead to dependence on the therapist
• Patients seem to like CBT
o Trials of CBT tend to have lower attrition rates than drug trials/other talking therapies
o Advantage because even if it is no more effective in those than other therapies, it is better that patients stay in therapy and get these benefits

Question 42

Family interventions

Answer 42

• Use: with family members of (i.e. those who live with) people with Sz as well as the patient
• Rationale: Sz is maintained, i.e. relapse is made more likely, by communication and emotional problems, particularly high levels of EE, within the family of people with schizophrenia and that EE problems are not seen as the sole cause of Sz but as a factor affecting the course of the illness
• Aim: provide the family with practical coping skills that enable them to manage difficulties, reduce levels of EE within families, reduce the risk of relapse
• Process: educate the family about Sz, e.g. its causes, course and symptoms, improve communication within families, develop cooperative and trusting relationship within the family, adjust expectations of family members to avoid imposing guilt etc on the patient, recognise early signs of relapse, expand social networks of family to allow communication with other parents of people with schizophrenia

Question 43

family interventions AO2

Answer 43

Effectiveness
• Leff et al
o first showed, in a RCT, that training families to reduce levels of EE reduced relapse rates from 78 to 14%.
o Programme involved: education sessions dealing with the nature of Sz and its symptoms, group meetings which took place with families who coped well with their Sz family member, family sessions where social workers and other professionals met the whole family at home to discuss the family’s particular concerns
o Effects evaluated during the following 2 years
o Patients in both groups taking antipsychotic medication throughout
• A NICE review (2009) found average relapse rates of 26% in the treatment condition and 50% in control groups
• Pharaoh et al
o reviewed 53 randomised studies, with positive results in relation to relapse, hospital admission and compliance with medication.
o Improves general social impairment and levels of expressed emotion within the family
o However, there are major issues about bias due to the lack of random allocation and blind assessments in many of the studies that were conducted in China, likely to exaggerate the effectiveness
• - researcher bias, putting those who are more likely to respond positively to therapy in one condition to fit hypothesis
Appropriateness
• probably best used as a complement to drug treatments (as occurs in trials).
• A problem is that family members may not want or be able to take part, due to guilt or lack of time respectively
o McCreadie who found that only half of relatives of Sz volunteered to take part in FI and only half of them actually turned up
o May think the patient needs to change and not them
o Feel that they have been blamed for it
o Too overwhelmed
• Not applicable for those living alone/with friends/without a family/aren’t exposed to a family

With any therapy, there is a generalised placebo effect – just through participating in any treatment can improve a patient’s conditions.

In Cochrane reviews, less bias because it is an independent organisation unlike those who have a professional reputation to worry about.