Edexcel, A2 Psychology, Schizophrenia

Ella Middlemiss
Mind Map by Ella Middlemiss, updated more than 1 year ago
Ella Middlemiss
Created by Ella Middlemiss over 3 years ago
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Includes: symptoms, dopamine hypothesis, dopamine pathways explanation, genetic explanation, glutamate hypothesis, social adversity explanation, antipsychotics and assertive community treatment, Carlsson et al

Resource summary

Edexcel, A2 Psychology, Schizophrenia
1 What is it?
1.1 Overview
1.1.1 History
1.1.1.1 First began to be noticed in 1890's - was thought to be a type of mental deterioration that started in adolescence
1.1.1.2 Called schizophrenia in 1908, when it was found it didn't necessarily have to start in adolescence and it wasn't necessarily the start of mental deterioration
1.1.2 In men it often begins in their mid-20's; In women it often begins in their early 30's
1.1.3 Some schizophrenics can recover completely, but will always have to take drugs to keep symptoms under control and to allow them to live independently
1.1.3.1 15% will need help and support for the rest of their lives
1.1.3.2 15% will not respond to treatment
1.1.4 Affects about 1% of the population
1.1.4.1 Equally common between men and women
1.2 Symptoms
1.2.1 Psychotic disorders are characterised by major disturbances in thought, emotion and behaviour
1.2.1.1 For a diagnosis of schizophrenia to be given by a clinician, the patient must have described 2 or more of the key symptoms and for them to have been present for a high proportion of the last month
1.2.2 Positive Symptoms
1.2.2.1 Hallucinations
1.2.2.1.1 patient hears/sees things that don't exist
1.2.2.1.2 In the cases of hearing voices, most are harsh and critical
1.2.2.1.2.1 Critical voices provide a running commentary on what the person is doing
1.2.2.1.2.2 Controlling voices tell the person what to do
1.2.2.1.2.3 Sometimes the voices talk to one another
1.2.2.2 Characteristics that are added to the individual's behaviour
1.2.2.3 Delusions
1.2.2.3.1 Patient thinks their actions are being controlled by outside forces
1.2.2.3.2 A common delusion is the paranoid delusion where the person believes that someone is trying to mislead, manipulate or kill them
1.2.2.3.3 Delusions of grandeur is when the patient believes they are in a position of power
1.2.2.3.4 Delusions can lead to strange behaviour e.g. covering windows in foil to keep aliens out
1.2.2.3.4.1 Thought insertion (patient thinks thoughts are put in their head by someone else)
1.2.2.3.4.2 Thought withdrawal (belief that outside forces are taking thoughts from the mind)
1.2.2.3.4.3 Thought broadcasting (belief that thoughts are being broadcast to others
1.2.2.4 Disordered Thinking
1.2.2.4.1 When someone finds it hard to put their thoughts into logical sense
1.2.2.4.1.1 A patient's speech may be very muddled or stop mid-sentence (believe the thought has been taken out of their head)
1.2.2.4.1.1.1 Patients may also make up words that have no meaning
1.2.3 Negative Symptoms
1.2.3.1 Poverty of speech
1.2.3.1.1 patient uses as few words as possible
1.2.3.2 Social withdrawal
1.2.3.2.1 patient no longer interacts with friends or family
1.2.3.3 Flattening effect
1.2.3.3.1 lack of expression in their voice, does not show facial emotions
1.2.3.4 Characteristics that are missing in the individual's behaviour
2 Explanations
2.1 Biological
2.1.1 Dopamine Hypothesis
2.1.1.1 Excess levels of neurotransmitter, dopamine, may result in S/Z
2.1.1.2 In a normal brain: equal numbers of receptor sites and re-uptake channels
2.1.1.2.1 Schizophrenic brain: too many receptors on the post-synaptic membrane resulting in an over-receptivity to dopamine
2.1.1.2.1.1 Evaluation
2.1.1.2.1.1.1 Weaknesses
2.1.1.2.1.1.1.1 Social and environmental factors can be involved. Stressful life events can trigger the production of excess dopamine
2.1.1.2.1.1.1.1.1 Doesn't explain whether it's nurture or nature
2.1.1.2.1.1.1.2 Glutamate is also thought to cause psychotic symptoms if its production is blocked
2.1.1.2.1.1.1.3 PET scans show that blocking dopamine receptors doesn't always remove symptoms
2.1.1.2.1.1.2 Strengths
2.1.1.2.1.1.2.1 Neuroleptic drugs that block dopamine seem to reduce the symptoms of S/Z. E.g. phenothiazine blocks dopamine at the synapse, & typically reduces many symptoms - however does have more effect on positive than negative symptoms
2.1.1.2.1.1.2.2 Randup & Mankvad (1966) raised dopamine levels of rats by injecting them with amphetamine. The rats showed positive symptoms of psychosis
2.1.1.2.1.1.2.2.1 Rats= can't generalise to humans
2.1.1.2.1.1.2.2.2 Outdated
2.1.1.2.1.1.2.2.3 Limited/weak research
2.1.1.2.1.1.2.2.3.1 Lowers validity
2.1.1.2.1.1.2.3 The drug L-dopa increases dopamine levels, and can produce many symptoms of S/Z
2.1.2 D2 Pathways
2.1.2.1 overactivity of the mesolimbic pathway= positive symptoms
2.1.2.1.1 mesocortical pathway dysfunction (extending from hypothalamus to frontal lobe) = negative symptoms
2.1.3 Glutamate Hypothesis
2.1.4 Genetic
2.1.4.1 Family, twin & adoption studies support the role of genetic influences in S/Z
2.1.4.1.1 Immediate biological relatives of people with S/Z have about 10 times greater risk than that of the general population
2.1.4.1.1.1 Evaluation
2.1.4.1.1.1.1 Strengths
2.1.4.1.1.1.1.1 Gottesman & Shields (1966) used a sample of 61 patients. They found on average for MZ twins, concordance rate was 42%. In DZ the average was 17%. In severe cases the average for MZ twins rose to between 75-91%
2.1.4.1.1.1.1.1.1 42% is still low
2.1.4.1.1.1.1.1.1.1 weak research
2.1.4.1.1.1.1.2 Tienari et al (2000) found that almost 7% of adoptees with S/Z had a biological mother with the same disorder compared to only 2% of schizophrenic children born to mothers without S/Z
2.1.4.1.1.1.1.2.1 still low number
2.1.4.1.1.1.1.3 Sullivan et al (2003) conducted a meta-analysis of twin studies and found a figure of 81% heritability
2.1.4.1.1.1.1.3.1 high figure
2.1.4.1.1.1.1.3.1.1 high reliability/validity
2.1.4.1.1.1.1.3.2 meta-analysis increases validity and eliminates research problems
2.1.4.1.1.1.2 Weaknesses
2.1.4.1.1.1.2.1 Tiwari et al (2010) points out that fewer than 1/3 of people with S/Z have a family history of the disorder
2.1.4.1.1.1.2.1.1 suggests an environmental basis
2.1.4.1.1.1.2.2 Twin and family studies fail to control for environmental influences
2.1.4.1.1.1.2.2.1 Generally have low validity/reliability as there's little control - subjective
2.1.4.2 Twin studies involve comparing MZ (share 100% of genes) and DZ (share 50% of genes) twins to see what differences there are in the incidence of a certain characteristic
2.1.4.2.1 If S/Z is genetic then we would expect MZ to have a higher concordance rate than DZ
2.2 Social
2.2.1 Environmental/Social Breeder Hypothesis
2.2.1.1 A link between low socio-economic status and s/z
2.2.1.1.1 Statistics show that the majority of schizophrenics in the UK come from lower classes, or from groups such as immigrants.
2.2.1.1.1.1 Research suggests that social class is a cause or involved in the development of s/z
2.2.1.1.1.1.1 Social drift = S/Z makes you lower class. Social breeder = lower class increases risk of S/Z
2.2.1.1.1.1.1.1 Eaton et al. (1988) conducted a meta-analysis of 17 studies showing there are more lower class people with s/z and that the disorder is more common in the lower class.
2.2.1.1.1.1.1.1.1 Sufferers of a lower class experience the illness and treatment differently
2.2.1.1.1.1.1.1.1.1 They are more likely to be taken by the police or social services for treatment than those of upper classes
2.2.1.1.1.1.1.1.1.1.1 Also more likely to become mandatorily committed or become long-term sufferers.
2.2.1.1.1.1.1.1.1.1.1.1 It's hard to separate those factors which might be causing s/z with those that are being caused by s/z, it may be that lower social class, economic status and the lack of a job are all consequences of the disorder, not the other way around.
2.2.1.1.1.1.1.1.1.1.1.2 Cooper (2005) found that the tendency for s/z came from what happens in early childhood rather than developing because of lower socioeconomic status.
2.2.2 Social Adversity
2.2.2.1 S/z is more common in urban communities rather than rural areas
2.2.2.1.1 Features in environment:
2.2.2.1.1.1 adversity in adult life
2.2.2.1.1.2 unemployment and poverty
2.2.2.1.1.3 social isolation
2.2.2.1.1.4 poor housing
2.2.2.1.1.5 Overcrowding
2.2.2.1.1.6 high levels of crime and drug-use
2.2.2.1.1.7 separation from parents as a child
2.2.2.1.2 Harrison (2001) suggests being brought up in declining inner-city areas could lead to s/z, as this is where the bulk of sufferers lie
2.2.2.1.2.1 Hjem et al. (2004) National cohort study in Sweden, census data from 1970 to 1990. Childhood socioeconomic indicators: rented apartments, low socioeconomic status, single-parent households, unemployment and households receiving welfare benefits.
2.2.2.1.2.1.1 Those with 4 measures of adversity had a 2.7 fold higher risk of s/z than those with none.
2.2.2.1.2.1.1.1 Social adversity leads to the development of s/z later in life
2.2.3 Immigrant Populations
2.2.3.1 UK census data shows higher incidence of s/z in the Afro-Caribbean and black immigrant population (1991 & 2001).
2.2.3.1.1 Estimate of 4X as many incidences in these populations as in the white indigenous population
2.2.3.1.1.1 Genetic reason for this: the risk for s/z is greater not only for Afro-Caribbean immigrants but also for African-born black immigrants and to an extent Asian immigrants.
2.2.3.1.1.1.1 In Caribbean countries, the incidence of s/z is similar to that for the indigenous UK population - lower than for immigrants in the UK
2.2.3.1.1.1.1.1 The rate for 2nd generation Afro-Caribbean immigrants is higher than for 1st generation immigrants
2.2.3.1.1.1.1.1.1 It is not thought that those who came into the UK as immigrants in the 1950's and 60's had weaker mental health; it is thought that immigrants would have been upwardly striving individuals
2.2.3.1.1.1.1.1.1.1 Afro-Caribbean people with s/z are likely to be unemployed, living in poor inner-city areas and in a worse situation than other Afro-Caribbean people. They're likely to be living alone and to have been separated from their parents when younger
3 Treatments
3.1 Social
3.1.1 In 1963, the government ordered many patients to be released and treated in their communities
3.1.1.1 Outpatient therapy in the community
3.1.1.2 Preventative care: manage their symptoms through therapy and medication
3.1.1.3 Aftercare: meet other people suffering the same disorder
3.1.1.4 Emergency care: number they can phone
3.1.2 Assertive Community Treatment (ACT)
3.1.2.1 Weaknesses of ACT
3.1.2.1.1 Gomory (2001) pointed out that the client is offered little choice and surrenders all responsibility for making decisions and taking care of themselves
3.1.2.1.1.1 Lack of right to withdraw
3.1.2.1.1.2 It's suggested about 11% of clients feel forced into the treatment
3.1.2.1.2 Harvey et al (2012) raised questions about the difficulties for staff of running the programme, which should be considered when looking at effectivness
3.1.2.1.2.1 Adequate staffing is needed to undertake this hands-on therapy (urban areas)
3.1.2.1.2.1.1 may not be provided in rural areas where there aren't many cases of S/Z due to cost implications
3.1.2.1.2.1.2 Inadequate treatment can be dangerous if the patient is having suicidal thoughts
3.1.2.1.3 Doesn't address biological causes, often combined with chemotherapy
3.1.2.1.3.1 Does not seem to have an actual effect on functioning and reducing positive and negative symptoms
3.1.2.2 Strengths of ACT
3.1.2.2.1 Nishio et al. (2012) in Japan, found some measures of success in their study and concluded that ACT could be successful, although their study focused on serious mental illness, not just S/Z
3.1.2.2.2 Van Vugt et al (2011) found, in the Netherlands, that, provided the model was adhered to, ACT could be effective,and that it was the team structure that was important
3.1.2.2.3 Bond et al. (2001) summarised 25 controlled studies that looked at the effectiveness of ACT. Concluded that it was highly effective as it engaged clients, prevented re-hospitilisations, increased housing stability and quality of life
3.1.2.2.4 Addresses social causes
3.1.2.2.5 ACT is used in severe mental health cases, not only S/Z
3.1.2.2.6 Bond (2002) points out that by preventing hospitalisation the treatment increases a client's choice, and by helping them to live in the community, the treatment increases their freedom.
3.1.2.2.6.1 A review of evidence, found that ACT was extremely effective in most mental health disorders, across gender, age and culture, and suggests it allows client choice
3.1.2.2.7 Social skills and family training can help someone to improve their interactions with others
3.1.2.3 How does it work?
3.1.2.3.1 real-life settings
3.1.2.3.2 visiting and helping them, rather than offering medication
3.1.2.3.3 Enough staff to offer this support
3.1.2.3.4 Help with independence, rehabilitation and recovery, and to avoid homelessness and re-hospitilisation
3.1.2.3.5 Work with other professionals such as psychiatrists, nurses, social workers and people with whom the treatment has worked
3.1.2.3.5.1 A commitment to spend as much time as necessary to support them. offering a holistic treatment
3.1.2.4 Psychological
3.2 Biological
3.2.1 Chemotherapy
3.2.1.1 Weaknesses of Chemotherapy
3.2.1.1.1 Drugs have been described as a chemical straight jacket and some people think that such control by society is unacceptable
3.2.1.1.2 Generally more effect on positive symptoms than negative ones because anti-psychotics block dopamine receptors
3.2.1.1.3 Side effects
3.2.1.1.4 Guo et al. (2011) found few differences when they compared 7 anti-psychotic drugs,in particular when they measured discontinuation over a year
3.2.1.1.5 Hartling et al (2012) looked at many studies and found that for core symptoms there were generally few differences
3.2.1.1.6 It doesn't address social causes such as social adversity etc.
3.2.1.1.6.1 Can result in revolving door syndrome in which the patient keeps getting readmitted into hospital
3.2.1.2 Strengths of Chemotherapy
3.2.1.2.1 Effective for treating Anorexia Nervosa aswell
3.2.1.2.2 Meltzer et al. (2004) found that haloperidol (anti-psychotic) gave significant improvements in all areas of functioning compared with a placebo, which is a starting point for saying that anti-psychotics work
3.2.1.2.3 For a disorder that has more biological causes, this biological treatment is likely to be more effective
3.2.1.3 Anti-psychotic Drugs
3.2.1.3.1 Works to affect levels of neurotransmitters
3.2.1.3.1.1 Phenothiazines
3.2.1.3.1.1.1 Decreases dopamine activity,
3.2.1.3.1.1.2 Reduces positive symptoms
3.2.1.3.1.1.3 No effect on negative symptoms
3.2.1.3.1.1.4 Side effects
3.2.1.3.1.1.4.1 dizziness
3.2.1.3.1.1.4.2 nausea
3.2.1.3.1.1.4.3 sexual impotence
3.2.1.3.1.1.4.4 tardive dyskinesia
3.2.1.3.1.1.4.4.1 involuntary facial movements
3.2.1.3.1.2 Clozapine
3.2.1.3.1.2.1 Blocks less dopamine activity and blocks more serotonin
3.2.1.3.1.2.2 Reduces both positive and negative symptoms
3.2.1.3.1.2.3 Can produce a potentially lethal blood disorder by lowering the white blood cell count
3.2.1.4 Physical therapy
3.2.1.4.1 May have placebo effect (psychological)
4 Carlsson et al. (1999/2000) Network interactions in schizophrenia - therapeutic implications (contemporary study)
4.1 A review
4.1.1 Research focuses on other studies and forms conclusions by looking at a broad set of results.
4.2 Background
4.2.1 Research has shown how there is a dopaminergic dysfunction in S/Z (the dopamine hypothesis). In PET scans, an increase in dopamine correlates with positive symptoms
4.2.1.1 More recently there is evidence to suggest that dopamine interacts with other neurotransmitters. Glutamate is one of these.
4.2.1.1.1 Glutamate: the most common neurotransmitter accounting for 90% of synaptic connections. It's involved in learning and memory. It regulates development and creation of nerve contacts. Glutamate bonds to NMDA receptors.
4.2.1.1.2 Dopamine: controls the brains reward and pleasure centres. It is responsible for feelings of pleasure, addiction, movement and motivation. People repeat behaviours that lead to dopamine production.
4.2.1.1.3 Serotonin and Glutamate are linked in perception and a lack of them can result in paranoia, insensibility, anxiety
4.3 The Glutamate Hypothesis
4.3.1 Glutamate deficiency/ defect could be linked to S/Z
4.3.2 When people take the drug PCP, it produces schizophrenic-like symptoms
4.3.2.1 PCP blocks glutamate receptors
4.3.2.1.1 People with S/Z must either have a defect in the receptor so it can't be properly stimulated by glutamate or they have a deficiency of glutamate.
4.3.2.1.2 NMDA receptor antagonists such as the drug PCP, block NMDA receptors.
4.3.2.1.2.1 This means glutamate can no longer bind to these receptors which means less or no electrical impulses can be initiated
4.3.3 Glutamate and GABA are long-distance neurotransmitters which act on the whole cortex and down into the spinal cord
4.3.4 The genes that relate to S/Z seem to impact on the function of glutamate/ cause glutamate dysfunction.
4.4 Aim: to better understand the relationship between neurotransmitter functioning and psychosis in S/Z and to produce drugs that are more effective.
4.5 Method: A review doesn't have a procedure or ppts as the data isn't gathered directly. The method is to review the methods and findings of other studies in this area. They then used this to build a body of knowledge about S/Z.
4.5.1 Findings:
4.5.1.1 PCP
4.5.1.1.1 Acts as an antagonist of a glutamate receptor
4.5.1.1.2 Glutamate deficiency more likely to be result in psychosis (Moghaddam & Adams 98) - shown in PET scans
4.5.1.2 Glutamate failure (PET)
4.5.1.2.1 in the cerebral cortex may lead to negative symptoms
4.5.1.2.2 in the basal ganglia may lead to positive symptoms
4.5.1.2.2.1 Weaknesses of PET scans
4.5.1.2.2.1.1 May be unreliable as areas of activity in the brain are often delocalised so can be difficult to pinpoint the activity
4.5.1.2.2.1.2 Small sample sizes as it's so expensive
4.5.1.2.2.1.3 Panicking in PET scanner may cause different brain activity results (stressful and anxiety-provoking)
4.5.1.2.2.1.3.1 Type I error
4.5.1.2.2.2 Strengths of PET scans
4.5.1.2.2.2.1 Scientific, objective evidence
4.5.1.2.2.2.1.1 High internal validity and reliability
4.5.1.2.2.2.2 Provides evidence for positive and negative symptoms
4.5.1.2.2.2.2.1 Less reductionist
4.5.1.3 Clozapine is a highly effective drug for S/Z
4.5.1.3.1 fewer reported side effects
4.5.1.3.2 reduces levels of dopamine and serotonin
4.5.1.3.2.1 serotonin is related to glutamate
4.5.1.3.2.2 Weaknesses of Secondary Data
4.5.1.3.2.2.1 Often meant for other purposes and hypotheses so not always suited to this explanation for S/Z
4.5.1.3.2.2.1.1 Low validity
4.5.1.3.2.2.1.1.1 Clozapine research - don't know how controlled the studies were etc.
4.5.1.3.2.2.2 Biased in which studies were included in the review (may have chosen studies that fit hypothesis
4.5.1.3.2.3 Strengths of Secondary data
4.5.1.3.2.3.1 Easier and quicker to collect
4.5.1.3.2.3.1.1 Gather lots of data efficiently
4.5.1.3.2.3.2 Assess reliability and validity across a whole number of studies and group them together
4.5.1.3.2.3.3 Large sample size
4.5.1.3.2.3.3.1 Increased population vailidity
4.5.1.3.3 more effective in patients who have not previously responded to treatment
4.5.1.4 Animal Studies
4.5.1.4.1 Research done on mice in early 2009 has shown that administering NMDA antagonists in late/post foetal stage increases neuronal death which is linked to adult S/Z like behaviour
4.5.1.4.1.1 This led to symptoms (such as disturbed social function, inability to adapt to predictable future stressors) that overlap with S/Z
4.5.1.4.1.1.1 Strengths of Animal Research
4.5.1.4.1.1.1.1 Able to do things that would be unethical to do with humans
4.5.1.4.1.1.1.1.1 Able to test where you otherwise wouldn't
4.5.1.4.1.1.1.1.1.1 Wider range of data available - can gather more data on effects of glutamate
4.5.1.4.1.1.2 Weaknesses of Animal Research
4.5.1.4.1.1.2.1 May be unable to generalise to humans
4.5.1.4.1.1.2.1.1 Rats symptoms of psychosis are different to humans
4.5.1.4.1.1.2.1.1.1 Lacks reliability
4.5.1.4.1.1.2.2 Often unethical
4.6 Conclusion
4.6.1 Further research is needed in developing drugs to treat S/Zto avoid negative side effects
4.6.2 Drug therapies need to consider the role of other neurotransmitters. Different types of S/Z could be due to abnormal levels of different neurotransmitters not just dopamine
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