A level - Schizophrenia - Mindmap in A Level and IB Psychology

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Created on: 06-02-18 18:21

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Schizophrenia
- Diagnosis and classification of Schicophrenia
  - Symptoms
    - Positive
      - Experienced in addition to normal experience
      - Delusions
        Bizarre beliefs the person believe are real
      - Hallucinations
        False perceptions that affect the different senses
        Visual, Auditory, Tactile, Olfactory
    - Negative
      - Represent the loss of a usual experience
      - Alogia
        Losing ability to speak fluently
      - Avolition
        Reduction in engadgmet of good behaviour
  - Following the DSM-V (2013) Diagnosis of schizophrenia
    - Criterion A) Display 2 or more symptoms
      - Criterion B) Social/ occupational dysfunction, affecting areas of functioning (work, relationships)
        Criterion C) Duration, disturbance persist for at least 6 months, including 1 month of symptoms from criterion A
  - Reliability and Validity of diagnosis and classification
    - Validity issues
      - Symptom overlap
        Many of the symptoms are found in other disorders (depression and bipolar)
        
        Ellason and Ross (1995) found that people with dissociative identity disorder (DID) have more schiz. symptoms than people diagnosed with schiz., meaning they could receive at least one other diagnosis (Read, 2004)
        
        After treatment, not everyone has same outcome, 20% go back to how they were before treatment, 30% have relapse, only 10% have lasting improvements
      - Gender bias
        When accuracy of diagnosis is dependent on gender of individual
        Gender biased diagnostic criteria or clinicians basing their judgement on stereotypical beliefs held about gender
        DSM diagnostic criteria argue some diagnostic categories are biased toward pathologising one gender rather than the other
        
        Broverman (1970) found that US clinicians equated mentally healthy 'adult' behaviour with mentally healthy 'male' behaviour, resulting in a tendency for women to be perceived as less mentally healthy
        
        Longenecker (2010) reviewed studies, found that since the 1980s, men have been diagnosed with schiz. more often than women, may be that men are more genetically vulnerable, and that females typically function better (more likely to work, have good family relationships)
        Cotton (2009) this high functioning may explain why women are less likely to be diagnosed, where men with similar symptoms have been
        
        Loring and Powell (1988) had 290 male and female psychiatrists, read case studies of patients behaviour, make judgement using standardised diagnostic criteria (DSM), when described as 'male' or no gender info given, 56% of psychiatrists gave schiz. diagnosis, if 'female' only 20% gave diagnosis, gender bias no evident is female psychiatrists, suggesting gender bias affected by gender of patient and clinician
      - Co-morbidity
        Refers to the extent that 2 or more conditions can occur at the same time
        Common among schiz. patients, substance abuse, anxiety, depression
        Buckley (2009) estimated that co-morbid depression occurs in 50% of patients, 47% have lifetime diagnosis of co-morbid substance abuse
        
        If conditions occur together, it may be that the individual has actually one condition, weakness of diagnosis classification
        Weber (2009) Viewed nearly 6 million hospital discharge records to calculate co-morbid rates, found co-morbid psychiatric disorders with schiz. 45%, and non-psychiatric disorders (asthma, hypertension, type 2 diabetes)
        Concluded those with psychiatric disorders, tend to receive a lower standard of medical care, affects prognosis of patient
      - Measuring what your supposed to, is diagnosis an accurate reflection of the disorder, diagnosis distinct from other disorders
    - Reliability issues
      - Cultural differences in diagnosis
        Research suggests variation between countries when diagnosing sch.
        
        Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient, 69% US diagnosed schiz. 2% British gave same diagnosis, found one of the main characteristics of schiz. was 'hearing voices', also appears to be influenced by cultural environment
        
        Luhrmam (2015) interviewed 60 adults diagnosed with schiz. 20 each in Ghana, India and US, each asked about voices they heard, African and Indian reported as positive experience (playful or offering advice), American (violent or hateful), suggests schiz. has a lack of consistent characteristics
      - Inter-rater reliability
        2 different clinicians must reach the same conclusion, measured using a kappa score (1 perfect, 0 indicates zero agreement) 0.7 or above considered good
        Originally though DSM and ICD could be used as a standardised method of recognising mental disorders, however behaviour of individual is up for interpretation
        DSM-V diagnosis of schiz. has a kappa score of 0.46
        
        Whaley (2001) found inter-rater reliability for diagnosing schiz. as low as 0.11
        
        For diagnosis, only one symptom required 'if delusions are bizarre'
        50 US senior psychiatrists asked to differentiate 'bizarre' from 'non-bizarre' delusions, produced correlation of around 0.4
        
        Test-retest reliability
        The same clinician must reach the same conclusion at 2 different points in time
      - Meaning diagnosis of schiz. must be repeatable
  - Affects 1% of population, 4 in 1000 people, diagnosed between ages of 15 - 35, men women affected equally
- Mental disorder (type of psychosis) characterized by disruption of cognition and emotion
  - Affecting language, thought, perception, emotion and sense of self
- Biological Explanation
  - Doesn't deny importance of psychological factors, accepting the 'diathesis-stress' model
  - Genetics
    - Family studies
      - Gottesman (1991) Found children with **** parents 46%, one parent with schiz. 13%, siblings with schiz. 9%
    - Twin studies
      - Joseph (2004) calculated pooled data for all schiz. twin studies (prior 2001) found MZ 40.4%, DZ 7.4%
    - Adoption studies
      - Tienari (2000) Study in Finland of 164 adoptees, whose biological parents had been diagnosed with schiz.
        11 (6.7%) diagnosed compared to non-schizo. mothers adoptees (control) 4 (2%) of 197
    - Tends to run in families, (not one gene) combination of genes makes individual more susceptible to schiz.
      - Look at the extent to which the disorder is inherited
    - Evaluation
      - Common rearing patterns may explain family similarities, rather than genetics
        Research shows schiz. tends to run in families, however researchers now admit that this may be due to common rearing patterns (or other factors) rather than heredity
        Research on Expressed Emotion, shows that negative emotional climate is families may lead to stress beyond an individual coping mechanisms, thus triggering a schiz. episode
      - MZ twins encounter more similar environments
        Joseph (2004) identified that MZ twins are treated more similarly than DZ twins (more likely to do things together), and experience more 'identity confusion' (treated as twins rather than separate identities)
        Therefore it may be argued that the differences in concordance rates between MZ and DZ twins, may reflect the environmental differences
  - Dopamine Hypothesis
    - Excess of the neurotransmitter Dopamine in certain regions of the brain (associated with positive symptoms)
      - Message from neurons that transmit dopamine fire too easily / too often, leading to positive symptoms
        Thought that schiz. patients have abnormally high number of D2 receptors on receiving neurons, resulting in more dopamine binding, therefore more neurons firing
        Evidence
        Drugs that increase dopaminergic activity
        Amphetamine (dopamine agonist) stimulating release of extra dopamine, causing synapse to be flooded with dopamine
        "Normal' individuals who use dopamine-releasing drugs, can develop the characteristic hallucinations and delusions of a schiz. episode (usually disappears with the abstinence of the drug)
        Grilly (2002) found that patients with Parkinson's disease, a neurodegenerative disease characterised by low levels of dopamine, who take L-Dopa increase their dopamine levels, and found to develop schiz. type symptoms
        
        Drugs that decrease dopaminergic activity
        Antipsychotic drugs (dopamine antagonists) block dopamine activity, be deceasing activity in dopamine neural pathways, decreasing positive symptoms
    - The revised dopamine hypothesis
      - Davis and Kahn (1991) proposed positive symptoms caused by increased dopamine in subcortical areas of the brain, in the 'mesolimbic pathway'. Negative symptoms caused by decreased of dopamine in areas of the PFC, in the 'mesocortical pathway'
    - Evaluation
      - Supporting evidence by drugs that change levels of dopamine activity in the brain
        Leucht (2013) carried out meta-analysis of 212 studies, that compared effectiveness of antipsychotic drugs with a placebo, found drugs more effective
        Shows dopamine directly involved in schiz,, However atypical drugs bind to serotonin receptors, meaning they may have an effect as well
      - Drugs dont work for everyone
        Noll (2009) found antipsychotic drugs dont work for everyone, and 1/3 experience positive symptoms despite taking drugs
        This lead to further research, meaning other drugs and CBTp can be developed
        Dopamine may not be the only reasonable cause of schiz.
  - Neural Correlates
    - Looks at areas of the brain that are influential in the onset development of schiz.
    - PFC
      - Area involved in executive control (planning, reasoning, judgment) research shows this area is impaired in schiz. patients
        Weinberger and Gallhofer (1997) hypothesised cognitive symptoms in schiz, are the result of deficits within PFC, and its connections with other areas of the brain, 'hippocampus'
    - Hippocampus
      - Found in temporal lobe, Conrad (1991) found deficits in the nerve connections between the PFC and hippocamus, correlate with the degree of working memory impairment (central cognitive impairment)
        Suggesting that hipppocampal dysfunction might influence level of dopamine release in basal ganglia indirectly, affecting the processing of information within PFC
    - Research about brain matter in relation to schiz.
      - Grey matter (mostly cell bodies and unmyelinated axons)
        Reduced grey matter in the brain, mainly temporal and frontal lobes
        Cannon (2014) found schiz. patients showed increased loss of grey matter and greater expansion of vesicles
      - White matter (found in brain and spinal-cord, made up of nerve fibers myelinated, increasing the efficiency of conducting information across the CNS
        Du (2013) found decreased myelination in white matter pathways between PFC and hippocampus
      - Ventricle (brain cavities filled with cerebrospinal fluid)
        Enlarged ventricles linked with negative symptoms
        Hartberg (2011) concluded it was due to nearby parts of the brain, not developing properly or being damaged
- Psychological explanations
  - Family dysfunction
    - Double bind
      - Gregory Bateson (1956) suggest children who frequently receive contradictory messages, more likely to develop schiz. (on a verbal and non-verbal level)
        The child finds themselves in situations, where they fear doing the wrong thing, but receive mixed messages on what that is, they also feel unable to comment on the unfairness of the situation or seek clarification
        When they 'get it wrong' (which is often) they are punished by a withdrawal of love
        Leaves them with an understanding of the world as dangerous and confusing, this is reflected in their symptoms like disorganised thinking and paranoid delusions
      - Not main factor, just risk factor to developing schiz.
    - Expressed emotion
      - Explanation for relapse, although it may be stress that can trigger the onset of schiz. who is already vulnerable
        The family factor associated with schiz. is a negative emotional climate (high degree of EE)
        EE refers to family communication style, in which the family members of a psychiatric patient talk about the patient in a critical or hostile way, that indicates emotional over-involvement or over-concern with the patient or their behaviour
        Kuipers (1983) found that high EE relatives talk more and listen less, high EE more likely to cause relapse. Linszen (1997) A patient returning to a family with high EE is 4x more likely to relapse that low EE family
        
        Verbal criticism (accompanied by violence), Hostility (including anger and rejection), Emotional over-involvement in the patients life
      - Suggests schiz. have lower tolerance to environmental stimuli (emotional comments and interactions with family) The negative climate arouses the patient, and leads to stress beyond their impaired coping mechanisms, thus triggering an episode
        Noll (2009) Whilst a supportive and emotionally undemanding family, may help reduce dependence of drug and reduce relapse
    - Caused by abnormal patterns of communication within family
    - Evaluation
      - Patients may be more genetically vulnerable who have biological mother with schiz.
        Family may be a stressor, triggering symptoms
      - Schiz patients, had higher recall of double bind experience as a kid
        Recall may not be accurate, as thoughts may be affected by schiz.
        Study found no difference in communication whether the family had a schiz. patient or not
      - Individual difference with coping with EE, 1/4 do not respond negatively to stressful environments, so people who deal well with emotion do better in recovery
  - Cognitive
    - Abnormalities in cognitive functions, can bias an individual toward developing cognitive schemas that see the world in a more threatening way
    - Research found evidence of dysfunctional though processing in schiz. patients, particularly in patients displaying positive symptoms
    - Christopher Frith (1992) identified 2 kinds of dysfunctional thought processing
      - Meta-representatio
        Cognitive ability to reflect on own thoughts and behaviour, this gives us insight into our own intentions and goals, as well as interpret others actions
        Dysfunction in the Meta-representation, would disrupt our ability to recognise our own thoughts and behaviour as being carried out by ourselves rather than someone else
        This explains auditory hallucinations and delusions like though insertion (experience of having thoughts projected into the mind by others)
      - Central control
        Cognitive ability to suppress automatic responses while we perform deliberate actions instead
        Disorganised speech and thought disorder could result from the inability to suppress automatic thoughts and speech triggered by other thoughts
        Schiz. tend to experience derailment of thought and spoken sentences, because each word triggers associations and the patient cannot suppress automatic responses to these
    - Evaluation
      - Supporting evidence for the cognitive model of schiz.
        Sarin and Wallin (2014) reviewed research relating to the cognitive model of schizophrenia, they found evidence for positive symptoms having their origins in faulty cognition
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- Biological therapies
  - Drug therapies
    - Antipsychotics
      - Typical (chlorpromazine) Combat positive symptoms
      - Atypical (clozapine) combat positive symptoms and negative symptoms
    - Dopamine discovered in 1952, drugs discovered which decreased dopamine levels, which help functions and increase feelings of well-being
      - Combined with therapy
    - Reduce dopaminergic transmission, reducing action of dopamine in areas of the brain associated with schiz.
    - Evaluation
      - Antipsychotics vs placebo
        Leucht (2012) meta-analysis of 65 studies (published between 1959 and 2011) involving 6000 patients, using either typical, atypical or placebo
        Within 12 months, 64% of those given a placebo had relapsed, compared to 27% of who stayed on drug
      - Side effects
        Drugs cause movement problems, known as 'extra-pyramidal' effects, as the drugs affect the 'extra-pyramidal' area of the brain, which control motor activity
        When using drugs for long period, they may cause 'tardive dyskinesia', involuntary movements of the tongue, face and jaw
        May need to be given other drugs to calm them down, or they may stop using antipsychotics
      - Atypical drugs better
        Crossley (2010) meta-analysis of 15 studies, to test the efficacy and side effects of typical and atypical drugs in early treatment of schiz.
        Found no difference in terms of their effect on symptoms, but noticed different side effects, patients on atypical gained more weight, whilst those on typical experienced more extra-pyramidal side effects
      - Ethical problems
        Critics argue that if side effect, deaths and psycho-social consequences were taken into account, a cost-benefit analysis of its advantages would most probably be negative
      - Advantages of atypical over typical
        Fewer side effects, olanzapine and quetiapine are less likely to produce extra-pyramidal effects, meaning patients more likely to continue with treatment
    - Kapur (200) suggested drugs need to bind to at least 60-75% of D2 receptors in the mesolimbic pathways and the same amount in the brain, which is dangerous
- Psychological therapies
  - CBTp
    - Assumes people have distorted beliefs, which influence their feelings and behaviours, believe their behaviour is controlled by someone or something else. Delusions are thought to result from faulty interpretations of events. CBTp used to help patients identify and correct these faulty interpretations
      - Help people establish link between their thoughts, feelings or actions and their symptoms and general level of functioning. By monitoring their thoughts, feelings or behaviour with respect to their symptoms, patients are better able to consider alternative views of explaining why they feel and behave the way they do. This reduces distress, improving functioning
        Encouraged to trace back to the origins of their symptoms, to find out how they may have developed. Also encouraged to evaluate the content of their delusions or voices, and consider ways that may test the validity of their faulty beliefs. Replacing thoughts with more helpful and rational ones
    - Groups, usually 1-1, recommended 16 sessions
  - Family therapies
    - Family intervention
      - Research consistently showed family environment may play a role in development of schiz. (relationship between patient and those who care for them)
    - Family therapy
      - 3-12 months (usually 10 sessions), Family-based interventions aimed at reducing the level of EE within the family
        Garety (2008) estimated relapse rate for individuals who received family therapy as 25%, compared to 50% who received standard care alone
    - Psycho-education, form alliance with relatives who care for patient, reduce emotional climate within family, enhance relatives abilities to anticipate and solve problems, reduce expression of anger and guilt by family members for patient performance, encourage relatives to set appropriate limits whilst maintaining some degree of separation when needed
  - Token economy
    - Suffer negative symptoms, apathy and social withdrawal, leading to reduced interest in aspects of normal healthy life, washing, eating and maintaining their physical appearance
      - Research look at decreasing negative symptoms, and increasing patients engagement in positive behaviour, with the use of token economy
        Primary reinforcers - something that gives pleasure (reward)
        
        Secondary reinforcers - initially have no value to individual but acquire reinforcing properties (token)
- Interactionist approach
  - Schiz. result of genetics interacting with the environment
    - Genetically vulnerable, requires environmental stressor to trigger schiz. symptoms
      - Family studies suggest people have varying levels of inherited genetic vulnerability to schiz. however whether they develop schiz. is dependent on the level of stress experienced over their lifetime
      - Stress - childhood trauma, or the stresses of living in a highly unbiased environment
        Varese (2012) found children who experienced severe trauma before age of 16, were 3x more likely to develop schiz. compared to general population
        
        Higher level of urbanisation associated with increased risk of developing schiz. Vassos (2012) risk of schiz. in most urban environments was 2.37x than in most rural environments, however only small minority will develop schiz.
Evaluation
- Research support for the influence of grey-matter deficits in schiz.
  - Vita (2012) meta-analysis, analysed results of 19 studies, 813 schiz., 718 controls
    - Schiz. patients showed increased reduction in cortical grey matter over time, affecting frontal, temporal and parietal lobes
      - Also found, the process was most active during first stages of disease
- Implications for treatment
  - Early detection and intervention may prevent development of later stages of the disorder
    - Addington (2015) used number of different assessments (neuroimaging) to predict who will convert to schizophrenia
      - Suggests, with better understanding of how schiz. develops, researchers can detect loss of brain tissue early, and treat patients at risk, before psychosis develops
Evaluation
- Token economy
  - Ayllon and Azrin (1968) used token economy in female ward with schiz., giving them a token for good behaviours (making their bed, domestic chores), which could be exchanged for privileges (watch a movie), they found token economy increased the number of desirable behaviours performed by the patient each day
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Additivity - minor stressor, high vulnerability or major stressor, low vulnerability
Key study, Tienari (2004)
- Reviewed records of 20,000 women, who finished psychiatric hospitals between 1960-1979, identifying those who where diagnosed at least once with schiz.
  - List was checked to identify mothers who had one or more of their children adopted away
    - 145 adopted away (high-risk group), matched with 158 adoptees, without genetic risk (low risk group)
      - Both groups assessed at 12, then followed up at 21, psychologists also assessed family functioning (OPAS scale)
        14 out of total 303 developed schiz, 11 from high-risk, 3 from low-risk
        However being reared in a 'healthy' adoptive family appeared to have a protective effect even for those who had a high genetic risk

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A level - Schizophrenia

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