Schizophrenia Flashcards

1
Q

Mr Quemby’s friend

A

Was pregnant and didn’t quit smoking - have to slowly wean off drugs, can’t go cold turkey if heavily addicted

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2
Q

schizophrenia

def

A

A severe mental illness where contact with reality and insight are impaired – an example of psychosis

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3
Q

schizophrenia misconsepti0on

A

Schizophrenia is not, as many people think, a split
personality

The term comes from two Greek words: ‘schizo’, meaning
‘split’, and ‘phrena’ meaning ‘mind’

The ‘split’ in schizophrenia occurs between a person’s
thought processes and reality.

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4
Q

Who does it affect?

A
  • It affects 1% of the population

Men are more likely to be diagnosed than women

The onset is typically in late adolescence and early
adulthood

Commonly diagnosed in cities and the working class

The disorder severely affects daily life, which can
lead to homelessness and hospitalisation

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5
Q

Classification of a mental disorder

A

the process of organising symptoms into
categories based on which symptoms cluster together in sufferers

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6
Q

Classification of
schizophrenia

A

Schizophrenia doesn’t have a single defining
characteristic – it is a cluster of symptoms that seem to
be unrelated

We group them as positive symptoms and negative
symptoms

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7
Q

two main systems used to classify mental
disorders:

A

International Classification of Disease edition 10 – (ICD-10)

Diagnostic and Statistical Manual edition 5 – (DSM-5)

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8
Q

classification systems

Differences in classification

A
  • E.g. the DSM-5 system says that at least one ‘positive’ symptom must be present for diagnosis
  • Whereas the ICD-10 says that two or more ‘negative’ symptoms are sufficient for a diagnosis

The ICD-10 used to recognise subtypes of schizophrenia
- E.g. Paranoid schizophrenia (more positive symptoms)
- Old versions of the DSM recognised subtypes but these were dropped in DSM-5 due to inconsistent symptoms

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9
Q

postive syptoms

A

Atypical symptoms experienced in addition to normal experiences

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10
Q

Postive symptom 1

A

Hallucinations – sensory experiences of stimuli that either have no basis in reality or are distorted perceptions of things that are there

E.g. hearing voices, seeing animals/people that aren’t there

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11
Q

Postive sysmptom 2

A

Delusions – involve beliefs that have no basis in reality
Also known as paranoia or irrational beliefs
- Can involve conspiracy (government, politics, religion)
- Can involve being an important political or religious figure
- Can involve the body – beliefs of being controlled externally

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12
Q

Negative sysmpoms

A

Atypical experiences that represent the loss of a usual experience and
abilities

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13
Q

Negative symptom example 1

A

Avolition – involves the loss of motivation to carry out tasks and results in lowered activity levels

Sometimes called apathy, sufferers have difficulty starting or keeping at a goal-orientated task

Andreason (1982) identified 3 signs of avolition – poor
hygiene and grooming, lack of persistence at work/school,
lack of energy

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14
Q

Negative symptoms example 2

A

Speech poverty – involves reduced frequency and quality of speech – often accompanied with delay in responding to conversation

Speech disorganisation (more of a focus these days) is classified differently (as a positive symptom)

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15
Q

Reliability of classification and diagnosis

A

Diagnosis of schizophrenia for an individual needs to be consistent among clinicians (inter-rater reliability) and consistent over time (test-retest reliability)

Before the DSM-5, diagnosis had low reliability

Osório et al. (2019) found that when diagnosing a group of 180 individuals, inter-rater reliability was +.97 and test-retest reliability was +.92 between two clinicians

This shows that there is now high reliability in diagnosis

  • schitzophenic symptoms might be interpreted differently based on cultural norms leading to variability in diagnoses across different populations
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16
Q

cognitive explanation def

A

Explanations that focus on mental processes (thinking, language, attention)
to explain behaviour

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17
Q

cognitive explanation

dysfunctional thought processing

A

Information processing that doesn’t accurately represent reality and produces undesirable consequences

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18
Q

cognitive explanation

impared cognition

A

Impaired cognition can explain symptoms of schizophrenia

E.g. reduced thought processing in the ventral striatum is associated with negative symptoms. Reduced processing in the temporal gyri (crease that separates the temporal lobe) is
associated with positive symptoms.

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19
Q

cognitive explanations

There are two main types of dysfunctional thought processing

A

Metarepresentation dysfunction

Central control dysfunction

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20
Q

Metarepresentation dysfunction

A

Metarepresentation is one’s cognitive ability to reflect on thoughts and behaviours allowing us to :
have insight on our personal goals and intentions
interpret other people’s actions

Schizophrenic patients are likely to have dysfunctional meta representation which disrupts their ability to recognise that their thoughts and actions are their own rather than someone else’s.

— This is used to explain delusions and hearing voices as schizophrenic patients fail to recognise that these processes are projected in their mind by themselves and NOT by someone else.

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21
Q

cognitive explanation

centeral control dysfunction

A
  • The ability to suppress automatic responses whilst doing a deliberate task.
  • Schizophrenics have trouble with dysfunctional central control which can explain speech poverty and disorganised thoughts.
  • Eg: delay in speech may be caused by interfering thoughts and automatic thoughts which are triggered by other parts of the conversation.
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22
Q

def

CBT

A

A method for treating mental disorders based on both cognitive and
behavioural techniques

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23
Q

CBT

A
  • Aims to identify and correct irrational and maladaptive thoughts (e.g. delusions are due to faulty interpretations)
  • Patients can be seen alone or in groups – and between 5-20 sessions – NICE recommend at least 16

-CBT helps patients make links between their thoughts, feelings, behaviours and symptoms

  • Enables alternative thought processing, distress reduction
    and improved functioning
  • It does not necessary reduce symptoms, it reduces distress if
    patients understand them better (normalisation)
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24
Q

Evaluation – research support CBT

CBT

A

Jauhar et al. (2014) did a review of 34 studies that used CBT to
treat schizophrenic patients – they concluded that CBT has
significant effects on both positive and negative symptoms

Furthermore, Pontillo et al. (2016) found CBT to reduce both
frequency and severity of symptoms in patients

This validates the effectiveness of CBT

It is also recommended by NICE – – all patients with schizophrenia
should be offered CBT

However, the research has been criticised as many patients
treated with CBT are usually treated with antipsychotics at the
same time - which one is actually helping

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whats NICE
The National Institute of Health and Care Excellence
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# cognitive treatment Effectiveness is stage dependent
Research has shown that CBT is only effective when made available at certain stages of the treatment Addington and Addington (2005) – claim that self-reflection isn’t appropriate during the initial phase of schizophrenia - after theyv'e been stabalised Only once symptoms are stabilized with antipsychotic medication can patients benefit from normalising their experience with CBT Furthermore, research has consistently shown that CBT is more effective on patients that have had longer experience with their symptoms weakess?
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# cognotive treatment Lack of avalibility
Despite being recommended by NICE, only around 1 in 10 patients in the UK get access to CBT for schizophrenia – the average is found to be even lower in some parts of the country Haddock et al. (2013) found that out of 187 randomly selected patients form North West England, only 6.9% had been offered CBT for schizophrenia Colling et al. (2017) found that 34.6% of patients received at least one session and 26.4% at least two sessions of CBT Issue? However, Freeman et al. (2013) found that from those who are offered CBT, a significant number refuse or fail to turn up
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# def Family therapy
psychological therapy carried out on some/all family members to improve communication and reduce stress in the family environment
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Family therapy
Prioritised when there are persistent symptoms or a high risk of relapse Offered for between 3-12 months with at least 10 sessions Sessions aim to reduce EE, educate family members about schizophrenia and provide ways to support the patient Family members are to listen to one another and discuss solutions together Burbach’s model of practice: Phase 1: sharing info, 2: identifying resources, 3: create a safe space for expression, 4: identify unhealthy communication, 5: stress management skills, 6: relapse prevention planning, 7: future maintenance
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# family therapy research support
McFarlane (2016) carried out a review on family therapy and concluded that it is one of the most consistent treatments for schizophrenia For example, relapse rates typically reduce by 50-60% He also concluded that family therapy is highly effective when mental health is initially declining (early stages) Furthermore, NICE also recommends family therapy – they advise that all patients should be offered it once diagnosed with schizophrenia
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# family therapy Economic benefits
The NICE review of family therapy studies found that there is significant reduction in costs for standard care of patients This is because of lower relapse rates 🡪 less hospitalisation The cost of taking additional care of relapsed patients is much more expensive than family therapy Additionally, family therapy reduces relapse rates even after the intervention is completed – meaning even more money is being saved
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# family therapies Positive impact on family members
Family therapy is seen to have a positive impact on family members, as well as the patients themselves It can reduce negative impact schizophrenia has on family members and strengthens ability to support the patient Lobban et al. (2013) meta analysis on 50 family therapy studies that included intervention to support relatives 60% of studies reported a significant positive impact on relatives for at least one outcome category (problem-solving skills, relationship quality) Long term, keep using the resourses and not relasping However, methodological quality of those studies was generally poor, making it difficult to distinguish between effective/ineffective interventions
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Token economies def
A form of behaviour modification where desirable behaviours are encouraged via reinforcement
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token economy
A management technique based on operant conditioning Patients are given tokens whenever they engage in a target behaviour 🡪 tokens exchanged 🡪 rewards and privileges Ayllon and Azrin (1968) – female hospitalised patients 1. Neutral tokens given after functional tasks are completed (making bed, finishing meals) 2. tokens are then exchanged for a variety of rewards (e.g. TV, visits from family, etc.) 3. frequent exchange = frequent desirable behaviours No longer used as ‘treatment’ for ethical reasons
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Rationale
To correct bad habits developed due to prolonged hospitalisation Helps modify personal care (hygiene), condition-related behaviours (e.g. avolition) and social behaviour (interaction) Such modifications: Improve quality of life in hospital settings Normalise behaviours that will help patients adapt to demands in the outside world
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How and why does token ecoony work
- Based on operant conditioning – tokens are secondary reinforcers that allow for access to primary reinforcers (TV, snacks, visits, etc.) - Tokens that can be exchanged for a range of rewards are also known as generalised reinforcers (like money) - Tokens are awarded for target behaviours decided on a case by case basis - They work best when the reward is given directly after the token is received – immediate reward is more effective than delayed reward
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# rresearch support Token economy
- Glowacki et al. (2016) identified and reviewed 7 high quality studies published between 1999 and 2013 that tested the effectiveness of token economies on patients hospitalised with chronic mental disorders - All studies showed a reduction in negative symptoms and a reduction in unwanted behaviours - Counter - is this research as strong as it looks? - Reviews containing fairly small numbers of studies indicate that there is a file drawer problem This means that studies that show insignificant or mixed (unreliable) results are ‘filed away’ This reduces the number of studies available for review, leaving a bias selection of ‘high quality’ studies to draw conclusions from Although there is research that demonstrates the effectiveness of token economies, it may not be as credible as it seems
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# token economy Ethical issues
- Despite token economies no longer being in use as a ‘treatment’ for schizophrenia, ‘behaviour management’ in this way still raises ethical concerns (ristricts individual free will, failire to protect psychological harm) Token economies give the professionals with authority the power to control their patients’ behaviour This can become problematic when target behaviours are not decided sensibly – e.g. staff can modify behaviours to fit their norms instead of their patients’ norms Problem? It can become easy to restrict patients of their rights to choose their norms and behaviours, as well as restricting pleasure altogether E.g. a patient may enjoy to appear scruffy or sleep in late but staff can ‘modify’ those behaviours with reward Patients may lose out on basic pleasures like watching tv or speaking to family if they do not comply to the chosen system The benefits of token economies may be outweighed by the ethical concerns
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The interactionist approach def
A way of explaining behaviour using a range of factors, such as biological and psychological factors
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interactionalist approach
Most importantly, an interactionist approach focuses on how different factors combine to explain behaviour, rather than simply adding/including various factors together (the ways in which factors combine cannot be predicted by each factor separately) The interactionist approach to explaining schizophrenia acknowledges the role of biological, psychological and social factors to explain its development (e.g. genetic vulnerability, stress and poor familial communication respectively)
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The diathesis-stress model def
An interactionist approach to explain behaviour that suggests that a vulnerability and a stress-trigger are needed to develop a condition
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The diathesis-stress model
For schizophrenia, diathesis can include one or more factors that make someone vulnerable to developing it (historically this just included genetics, but now we understand trauma to be a diathesis) But the onset of symptoms of schizophrenia is triggered by stress The diathesis-stress model explanation can be split into two – the original model (Meehl’s model) and the modern model
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Meehl’s model (original) 1962
The original diathesis-stress model suggested that the diathesis for schizophrenia is purely genetic (schizogene) This led to the development of a biologically based ‘schizotypic’ personality – characterised by sensitivity to stress Furthermore, an individual without the schizogene would never develop schizophrenia, regardless of any stressful events But an individual that possesses the schizogene could develop schizophrenia if they experience chronic stress during childhood – in particular, if they have a schizophrenogenic mother
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Modern understanding of the diathesis-stress model
Diathesis – we now know there is no one ‘schizogene’ Different variations of candidate genes only increase vulnerability to schizophrenia by a fraction Early psychological trauma is also considered a diathesis now (rather than an environmental stressor) Read et al.’s neurodevelopmental model (2001) suggests that severe early trauma (e.g. child abuse) can alter many aspects of brain development For example, it can cause overactivity in the hypothalamic-pituitary-adrenal (HPA) (too much adrenaline) system, making the individual more vulnerable to later stress
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Modern understanding of stress
In Meehl’s original model, stress was mainly psychological and related to parenting Although still important, ‘stress’ in this model is now considered to include anything that risks triggering schizophrenia Example: Cannabis Cannabis has been found to increase risk of developing schizophrenia by up to 7 times (particularly THC-rich doses) Research indicates that cannabis interferes with the dopamine system Many people that smoke cannabis do not develop schizophrenia, suggesting that most do not have the vulnerability for triggering it in the first place
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# interactionalist Research support - Tienari
Hospital records were reviewed from 19,000 Finnish adoptees with biological mothers that had a diagnosis of schizophrenia (high genetic risk) They were compared with a control group of adoptees with no family history of schizophrenia (low genetic risk) They also assessed the parenting style of the adoptive parents They found that a parenting style involving high levels of criticism and hostility and low levels of empathy were strongly associated with the development of schizophrenia in the children But this relationship was only found to be the case for children in the high genetic risk group – so? This suggests that a combination of genetic vulnerability and family stress may cause schizophrenia – validating the interactionist approach
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# iteractionalist simplistic models
The original model has been criticised for being too simplistic – there is no one schizogene or stressor that causes schizophrenia There are multiple genes found to increase vulnerability to schizophrenia (they have very little effect on their own) Stress can also come in many forms – stress can be biological as well as psychological Houston et al. (2008) – found that childhood sexual trauma was a major vulnerability factor, whereas cannabis use was a major trigger for developing schizophrenia Shows that diathesis is not strictly biological and stressors are not strictly psychological Problem? This invalidates the original model and supports newer versions But still suggests more research and understanding is needed to effectively apply the diathesis-stress model to schizophrenia
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# interactionalist approach effective treatment
There has been support for the effectiveness of combined treatment Biological and psychological treatments combined are more effective than biological treatment alone Tarrier et al. (2004) – randomly allocated 315 patients to either medication+CBT, medication+counselling or medication only (control) They found that both combined groups showed lower symptom levels than the control group Strength? However, they found no differences in hospital readmissions
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# interactionalist however... treatment -causation fallacy
Researchers have critiqued the popular assumption that ‘effective treatment = valid explanation’ This is known as the ‘treatment-causation fallacy’ Successful treatment does not justify it’s matching explanation E.g. drinking alcohol reduces shyness – does this make lack of alcohol the cause of shyness? No. But the same logic is applied explanations and treatments for disorders like schizophrenia Just because combined treatment is the most effective doesn’t necessarily mean combined (interactionist) explanation is the most valid
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# of classification Validity
Just because clinicians are consistent in diagnosis (while using the same system) doesn’t mean they are accurately diagnosing schizophrenia As the ICD-10 and DSM-5 use different criteria to diagnose, the same patient may not get a consistent diagnosis across clinicians Cheniaux et al. (2009) had two psychiatrists diagnose 100 patients independently using DSM-5 and ICD-10 criteria They found that one psychiatrist diagnosed 70/100 patients (26 using DSM and 44 using ICD) and the other diagnosed only 37/100 patients (13 using DSM and 24 using ICD) This also means 68 were diagnosed using the ICD and only 39 were diagnosed using the DSM in total There is low criterion validity – at least one of the systems is wrong when diagnosing schizophrenia – this means patients may be misdiagnosed depending on the system their clinician uses.
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Co-morbidity
‘morbidity’ refers to how common a medical condition is Co-morbidity refers to the idea that two or more conditions occur together - Schizophrenia is often diagnosed with other conditions A review by Buckley et al. (2009) found that half of patients diagnosed with schizophrenia are also diagnosed with depression (50%) or substance abuse (47%) PTSD also occurred in 29% and OCD in 23% - Validity issues with diagnosis – there may be issues telling the difference between different conditions – misdiagnosis Validity issues with classification – if the symptoms overlap with other conditions, schizophrenia may not be a distinct condition People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
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Similarly, symptom overlap
Even if an individual does not have two conditions (co-morbidity), the symptoms of schizophrenia still overlap with symptoms of other disorders For example, symptoms of bipolar disorder also include delusions (a positive symptom) and avolition (a negative symptom) This again means we may be classifying and diagnosing schizophrenia incorrectly for patients – validity issue Not only may we misdiagnose patients, it also implies that schizophrenia may not be a distinct disorder e.g. an individual may just have a rare variation of bipolar disorder People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
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# Symptom overlap (extra/alternative research) Ellason and Ross (1995)
found that people with dissociative identity disorder (DID) have more symptoms of schizophrenia that people diagnosed with schizophrenia
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# Symptom overlap (extra/alternative research) Read (2004)
most people diagnosed with schizophrenia have enough sufficient symptoms to be diagnosed with at least one other disorder
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Gender bias in diagnosis
Men are diagnosed with schizophrenia more often than women This could be due to genetic factors, but it is more likely due to social factors Women are more likely to have close relationships and social support – leading to better functioning in society Cotton et al. (2009) – women generally function better and at a higher level than men (better interpersonal skills, etc.) Higher functioning may be why women’s symptoms are easily overlooked, leading to under-diagnosis Schizophrenia is not properly understood in women – samples are more likely to be men – treatments will therefore be tailored for men – leading to more bias in the medical field
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Biological explanations
Genetics Neural correlates
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Genetics
genes consisting of DNA that contain instructions for physical features of an organism, which can also influence psychological features (e.g. disorders)
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# the genetic basis Family studies – Gottesman (1991)
- He found that someone with an aunt with schizophrenia had a 2% chance of developing it - A 9% chance if their sibling had it - And a 48% chance if they had a MZ twin that had it - This clearly shows a relationship between genes and schizophrenia
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Candidate genes
- Schizophrenia is suggested to be polygenic – no one specific gene has been found to explain schizophrenia - The genes involved are most likely to be related to dopamine - Ripke et al. (2014) did a review of genome-wide studies on schizophrenia (studies that look at one’s full genetic makeup) - After comparing 37,000 people with schizophrenia to 113,000 controls, he found 108 different genetic variations that are associated with increased risk of schizophrenia - This suggests that schizophrenia is aetiologically heterogeneous – Different combinations of genes (and other factors) can lead to schizophrenia
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# genetic explanation Research support
Twin studies – Hilker et al. (2018) found a concordance rate of 33% for MZ twins that shared schizophrenia compared to 7% of DZ twins that shared it The difference is best explained by the amount of genes shared (100% vs 50%) Adoption studies – Tienari et al. (2004) studied adopted children from Finland and found that of those that had schizophrenia, many of them had a biological mother that also had schizophrenia This shows that even without being raised by a schizophrenic parent, you can still develop the disorder (best explained by genes)
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# Genetic explanation Environmental factors
- Although research shows that genetics have a role in the development of schizophrenia, there is also a lot of evidence for environmental factors being involved - Examples include birth complications, childhood trauma and smoking cannabis during adolescence - Morkved et al. (2017) found that 67% of people with schizophrenia and other related psychotic disorders reported at least one experience of childhood trauma compared to 38% of a control group with non-psychotic disorders - incomplete explanation, as ignores enviromental factors,
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Neural correlates def
Patterns of structure or activity in the brain that occurs in conjunction with (correlates with) an experience
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# neural correlates Dopamine
a neurotransmitter found to be important in several brain systems related to schizophrenia It is excitatory and linked to pleasure Very low levels are associated with Parkinson’s disease Because there is no hard evidence to pinpoint exactly what the role of dopamine is in the development of the disorder, hypotheses have been generated to explain the link
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The dopamine hypothesis (the original)
Research showed that drugs used to treat schizophrenia (antipsychotics which reduce dopamine levels) also cause symptoms similar to those that people with Parkinson’s disease experience – PD is also associated with low dopamine levels… Therefore, from this it was hypothesised that schizophrenia may be caused by high levels of dopamine in subcortical areas of the brain (hyperdopaminergia – hyper=high) For example, speech poverty and auditory hallucinations may be caused by an excess of dopamine receptors between the subcortex and Broca’s area
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The updated dopamine hypothesis
Davis et al. (1991) hypothesised that low levels of dopamine in the cortex may cause schizophrenia (cortical hypodopaminergia – hypo=low) Low levels of dopamine in the pre-frontal cortex can explain negative symptoms associated with cognitive functioning (However, this does not oppose the original hypothesis) It is suggested the low levels of dopamine in the cortex may cause high levels in the subcortex Howes et al. (2017) suggests that this caused by genetic variations and early experiences of stress These factors may make people more sensitive to cortical hypodopaminergia and eventually 🡪 subcortical hyperdopaminergia
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# biological explanation research support
Curran et al. (2004) found that when amphetamines are given to patients with schizophrenia, they increase dopamine levels and worsen symptoms of the disorder Amphetamines also induce similar symptoms in people without schizophrenia! Tauscher et al. (2014) also found that antipsychotics decrease dopamine levels and symptoms of schizophrenia Both studies suggest that dopamine levels (in particular high levels) are associated with schizophrenia Furthermore, some candidate genes identified also affect dopamine production and dopamine receptors Amphetamines are stimulant drugs. They make the messages between your brain and body move faster. As a result, you are more alert and physically active. Some people use amphetamines to help them stay awake on the job or to study for a test. Others use them to boost their performance in sports
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Role of other transmitters?
Research has also found glutamate (another excitatory neurotransmitter) to be associated with schizophrenia McCutcheon et al. (2020) found increased levels of glutamate in several brain regions of schizophrenic patients across brain-imaging and post-mortem studies Furthermore, some of the candidate genes identified affect the production of glutamate as well - neural explanation, brain activity can be investigated to find schitzophernia, practical value as can make it easier to diagnose
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Two psychological explanations
Family dysfunction Cognitive explanations
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Family dysfunction
Abnormal patterns of communication within the family, such as cold parenting, poor communication and high expressed emotion Such aspects of the family dynamic are suggested to be risk factors for both the development and maintenance of schizophrenia
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3 key factors to family dysfunction
- Schizophrenogenic mother (cold parenting) - Double-bind theory (poor communication) - Expressed emotion
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The schizophenogenic mother
Fromm-Reichmann (1948) Noted that many of her patients spoke about a particular type of parent – she named the ‘schizophenogenic’ mother This means ‘schizophrenia-causing’ This is a mother that is cold, rejecting and controlling She creates a family dynamic characterised by tension and secrecy This is suggested to cause distrust which later develops into paranoid delusions, and eventually, schizophrenia This is a psychodynamic explanation – how childhood experiences can affect you psychologically
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# family dysfunction Double-bind theory
Bateson et al. (1972) Children receive contradictory messages from parents E.g. verbal and non-verbal contrasts Children then fear doing the wrong thing, even when they don’t understand what the wrong thing is (due to mixed messages) They feel unable to protest about the unfairness of a situation, nor do they feel able to seek clarity on it They learn that doing the wrong thing leads to a withdrawal of love, causing them to understand the world to be confusing and dangerous Bateson argues that this is what leads to paranoid delusions and disorganised thinking patterns Bateson et al. clarified that this was not a generalisable sole cause for schizophrenia, just a risk factor EE includes elements of verbal criticism, sometimes accompanied by violence, hostility including anger and rejection and over-involvement
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Expressed emotion (EE)
EE refers to the level of emotion expressed towards the schizophrenic patient by family members/carers A high level of negative expressed emotion is suggested to be a significant source of stress and can trigger the onset of the disorder (in those already vulnerable), as well as relapse
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EE contains the following elements
- Verbal criticism and sometimes violence towards the patient - Hostility, anger and rejection - Emotional over-involvement in the patient’s life
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# family dysfunction Research support
There is a range of research to suggest that issues within the family dynamic play a role in schizophrenia Insecure attachment – Read et al. (2005) found that adults with schizophrenia are disproportionately likely to have had insecure resistant or disorganised attachment as a child Abuse – Read also found that 69% of women and 59% of men have a history of physical and/or sexual abuse Trauma – Morkved et al. (2017) found that 67% of patients with a psychotic disorder reported at least one childhood trauma All of the research suggests that family dysfunction can make you more vulnerable to developing schizophrenia
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# family dysfunction Weak explanations
Although research shows a link between childhood family-based stress and schizophrenia (generally) there is little evidence to support specific explanations such as schizophrenogenic mother and double-bind theory Research on these explanations come from clinical observation of individual patients and informal assessments of the mother’s personalities Furthermore, research that does exist contradicts the explanations Liem (1974) found no differences in parental communications between schizophrenic and non-schizophrenic patients Hall and Levin’s (1980) meta analysis found no differences in contradictory statements made in families with and without a schizophrenic patient Low explanatory power – FD may not be good enough to explain the link between childhood experiences and schizophrenia Low validity – contradictory suggests FD is an incorrect explanation
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Cognitive explanations def
Explanations that focus on mental processes (thinking, language, attention) to explain behaviour
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# Psychological explanation Research support | cognitive
Stirling et al. (2006) gave the stroop test to 30 schizophrenic patients and 30 controls (the task was to say the colour of the font of the word rather than reading the word) The schizophrenic patients took twice as long as the control group to complete the task correctly – so? This suggests that those with schizophrenia struggled to supress the tendency to read the words instead of the colours, showing dysfunctional central control This validates the role of central control dysfunction in schizophrenia
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# Psychological explanati0on Only a proximal explanation | cognitive
A proximal explanation only goes as far to explain present circumstances as opposed to explaining how the circumstances developed in the first place (distal explanations) Biological and family dysfunction explanations can explain how symptoms of schizophrenia develop initially But cognitive explanations offer no insight on how dysfunctional thought processing develop initially Furthermore, cognitive explanations are difficult to link with the others – genetic variations nor childhood trauma can explain how dysfunctional thought processing develops Low explanatory power- only a partial explanation
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drug treatments spec
Drug therapy – antipsychotics Typical antipsychotics Atypical antipsychotics
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Drug therapy - antipsychotics def
Drugs used to reduce the intensity of symptoms of a psychotic disorder (usually positive ones)
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when was drug therapy introduced
Introduced in the 1950s – no treatment before this
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antipsychotics use
- ecommended for initial treatment - then used in combination with psychological therapies later on -some use them in the short term without symptoms returning - but most need to take them for life
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Two types of antipsychotics:
typical antipsychotics aytpical antipsychotics
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typical antipsychotics
used primarily for positive symptoms
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Atypical antipsychotics
also combat positive symptoms, but has some beneficial effects on negative symptoms as well
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Typical antipsychotics history
The first generation of antipsychotic drugs, having been used since the 1950s. They work as dopamine antagonists. E.g. Chlorpromazine
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Typical atypsychotics
Antagonists are blockers – they block the activity of neurotransmitters Typical antipsychotics are dopamine antagonists which bind to D2 receptors on neurons, blocking their action (blocking transmission of dopamine) At first dopamine levels build up (because transmission is blocked) but over time, less and less dopamine is produced elimination of hallucinations and delusions happens after a few days Other positive symptoms may take longer (several weeks) The effectiveness eventually led to the original dopamine hypothesis Can be taken via tablet , syrup or injection – up to 1000mg a day (avg 400-800mg for most patients)
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# typical antipsycotics Sedation effects
Typical antipsychotics like chlorpromazine also work as a sedative (although not properly understood why) They can be given to patients with other conditions to calm them E.g. patients that are very anxious may be given them when they are first admitted to hospital They are most likely given as syrup for these purposes as they are absorbed faster than tablets Kapur et al. (2000) – estimated 60-75% of D2 receptors must be blocked in the mesolimbic pathway But this means D2 receptors in other areas are blocked too This can lead to undesirable/possibly harmful side effects
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harmful effects of typical antipsychotics
Kapur et al. (2000) – estimated 60-75% of D2 receptors must be blocked in the mesolimbic pathway But this means D2 receptors in other areas are blocked too This can lead to undesirable/possibly harmful side effects
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# drug therapy Clozapine | atypical
First trialled in the 1970s – despite some patients later dying from a blood condition after taking them (agranulocytosis), they were remarketed in the 80s as the treatment to use if other treatments failed – and were found to be more effective than typical antipsychotics (today regular blood tests are taken and dosages are kept low) - Clozapine binds to D2 receptors, as well as serotonin and glutamate receptors - This consequently improves mood and reduces anxiety and depression - As well as suicidal thoughts (which can occur in 30-50% of patients) No injections as side effects can be fatal
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Risperidone | atypical
Developed in the 90s – develop to reduce side effects that come with Clozapine It binds to more dopamine receptors than Clozapine so smaller doses are needed – and it can be taken in any form Some evidence suggests it has fewer side effects than the other antipsychotics
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difference between typical and atypical
typical proved effect on positive sysmptoms atypiclal claimed effect on cognitive imparmnet and negative symptoms
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Atypical antipsychotics context
Drugs that developed after typical antipsychotics (1970s). They typically target both dopamine and serotonin. E.g. Clozapine and Risperidone | AKA second-generation antipsychotics
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Three main differences between typical and atypical
atypical : less extrapyramidal side effects, more beneficial for negative symptoms, better for treatment-resistant patients
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atypical antipsycotics examples
Clozapine and Risperidone
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# drug therapy a03 Research support
Lots of research compares relapse rates for antipsychotics and placebos Leucht et al. (2012) did a meta-analysis of 65 studies from 1959-2011, involving ~6000 stabilised patients They were stabilised with either typical/atypical drugs Some were taken off their medication and given a placebo instead Within 12 months, 64% given the placebo relapsed, compared to 27% who stayed on the antipsychotic drug - suggests the drug is effective, high practical use
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# drug therapy AO3 Side effects
Typical antipsychotics are more likely to produce side effects than atypical ones - Including dizziness, sleeplessness, weight gain, stiff jaw and itchy skin More long-term effects include tardive dyskinesia which Involves involuntary facial movements (blinking, grimacing) This is caused by dopamine supersensitivity The most serious side effect is neuroleptic malignant syndrome (NMS) which causes delirium, coma and sometimes death (up to 2% risk), suggested to be caused by the blocking of dopamine to the hypothalamus - may not be worth the risk, Typical antipsychotics have been criticised for its overall cost-benefit analysis This is because the drugs have led to many harmful side-effects, deaths and psychosocial consequences E.g. Chari et al. 2002 – covered a large out-of-court settlement for a patient suffering from tardive dyskinesia in the US Based on the Human Rights Act 1988, the patient was compensated for the side effects experienced – as it states ‘no one shall be subjected to inhuman or degrading treatment or punishment’ Further suggesting that drug therapy may do more harm than good in real life (for patients, professionals and economy)
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# Drug therapy A03 Poor clarity
- It is not fully understood why antipsychotic drugs work to reduce symptoms - The use of drugs is heavily tied with the original dopamine hypothesis (that schizophrenia is caused by subcortical hyperdopamineria) but we now know that the original dopamine hypothesis is not the full explanation – the updated hypothesis suggests that low levels of dopamine in the cortex may also cause the condition - - Therefore, drugs that ultimately decrease dopamine levels overall should not work – so why do they? - low explanatroy power
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Token economy used to go together with the other therapies but due to much critique...
it is now considered a method of management as opposed to treatment
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Discuss issues associated with the classification and / or diagnosis of schizophrenia. (16)
AO1 – identify the issues Introduce the classification systems (ICD-10 and DSM-5) Explain how diagnosis differs depending on the system used Start introducing the issues (it makes sense to start with reliability and validity issues if none are specifically named in the question) AO3 – discuss the issues (what implications do they have for patients, the economy and the medical field?) Discuss why having low reliability/validity is a problem when diagnosing/classifying schizophrenia Discuss the issues of co-morbidity, symptom overlap, gender bias and culture bias
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The issues with classification/ diagnosis
Reliability Validity Symptom overlap Co-morbidity Gender bias Culture bias
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# The reliability and validity of diagnosis and classification AO3 validity
Just because clinicians are consistent in diagnosis (while using the same system) doesn’t mean they are accurately diagnosing schizophrenia As the ICD-10 and DSM-5 use different criteria to diagnose, the same patient may not get a consistent diagnosis across clinicians Cheniaux et al. (2009) had two psychiatrists diagnose 100 patients independently using DSM-5 and ICD-10 criteria They found that one psychiatrist diagnosed 70/100 patients (26 using DSM and 44 using ICD) and the other diagnosed only 37/100 patients (13 using DSM and 24 using ICD) This also means 68 were diagnosed using the ICD and only 39 were diagnosed using the DSM in total There is low criterion validity – at least one of the systems is wrong when diagnosing schizophrenia – this means patients may be misdiagnosed depending on the system their clinician uses.
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# The reliability and validity of diagnosis and classification AO3 Co-morbidity
‘morbidity’ refers to how common a medical condition is Co-morbidity refers to the idea that two or more conditions occur together - Schizophrenia is often diagnosed with other conditions A review by Buckley et al. (2009) found that half of patients diagnosed with schizophrenia are also diagnosed with depression (50%) or substance abuse (47%) PTSD also occurred in 29% and OCD in 23% Why is this a problem? Validity issues with diagnosis – there may be issues telling the difference between different conditions – misdiagnosis Validity issues with classification – if the symptoms overlap with other conditions, schizophrenia may not be a distinct condition People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money
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# The reliability and validity of diagnosis and classification symptoms overlap
Even if an individual does not have two conditions (co-morbidity), the symptoms of schizophrenia still overlap with symptoms of other disorders For example, symptoms of bipolar disorder also include delusions (a positive symptom) and avolition (a negative symptom) This again means we may be classifying and diagnosing schizophrenia incorrectly for patients – validity issue Not only may we misdiagnose patients, it also implies that schizophrenia may not be a distinct disorder e.g. an individual may just have a rare variation of bipolar disorder People may receive treatment for the wrong thing, unnecessary labels, waste of research, waste of money Ellason and Ross (1995) found that people with dissociative identity disorder (DID) have more symptoms of schizophrenia that people diagnosed with schizophrenia Read (2004) – most people diagnosed with schizophrenia have enough sufficient symptoms to be diagnosed with at least one other disorder
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# The reliability and validity of diagnosis and classification Cultural bias in diagnosis
hearing voices is a symptom that may be interpreted differently in different countries Black British people are up to 10 times more likely to be diagnosed with Schizophrenia than white British people, even though rates of schizophrenia in African and Caribbean countries are not particularly high Escobar (2012) suggested that (overwhelmingly white) psychiatrists may tend to over-interpret symptoms and distrust the honesty of ethnic minorities during diagnosis Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient 69% of the US psychiatrists diagnosed the patient, but only 2% of the British ones did! This suggests that there are huge cultural differences in how doctors diagnose patients
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# The reliability and validity of diagnosis and classification AO3 Gender bias in diagnosis
Men are diagnosed with schizophrenia more often than women This could be due to genetic factors, but it is more likely due to social factors Women are more likely to have close relationships and social support – leading to better functioning in society Cotton et al. (2009) – women generally function better and at a higher level than men (better interpersonal skills, etc.) Higher functioning may be why women’s symptoms are easily overlooked, leading to under-diagnosis Schizophrenia is not properly understood in women – samples are more likely to be men – treatments will therefore be tailored for men – leading to more bias in the medical field
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aetiologically heterogeneous
Different combinations of genes (and other factors) can lead to schizophrenia
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token economies def
A form of behaviour modification where desirable behaviours are encouraged via reinforcement A management technique based on operant conditioning Patients are given tokens whenever they engage in a target behaviour 🡪 tokens exchanged 🡪 rewards and privileges
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# token economy Ayllon and Azrin (1968) – female hospitalised patients
1. Neutral tokens given after functional tasks are completed (making bed, finishing meals) 2. tokens are then exchanged for a variety of rewards (e.g. TV, visits from family, etc.) 3. frequent exchange = frequent desirable behaviours No longer used as ‘treatment’ for ethical reasons
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why do token economies exist
To correct bad habits developed due to prolonged hospitalisation Helps modify personal care (hygiene), condition-related behaviours (e.g. avolition) and social behaviour (interaction)
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# token economies examples of modicfation
- Improve quality of life in hospital settings -Normalise behaviours that will help patients adapt to demands in the outside world
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# token economies How and why does it work?
- Based on operant conditioning – tokens are secondary reinforcers that allow for access to primary reinforcers (TV, snacks, visits, etc.) - Tokens that can be exchanged for a range of rewards are also known as generalised reinforcers (like money) - Tokens are awarded for target behaviours decided on a case by case basis - They work best when the reward is given directly after the token is received – immediate reward is more effective than delayed reward
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# token economies research support