CLINICAL

Cards (47)

  • Dopamine hypothesis

    Research has developed into 3 parts:
  • Too high levels of dopamine

    • Makes someone more likely to have poor impulse control and be impulsive
    • Linked with hallucinations (explains positive symptoms, not negative)
  • Too many dopamine receptors
    • Excess number of receptors at synapses in the brain leads to schizophrenia development
  • Varying amounts of dopamine in different brain areas
    • Overactivity in the mesolimbic pathway contributes to positive symptoms, dysfunction in mesocortical pathway contributes to negative symptoms
  • Lindstroem et al (1999)
    • Radioactively labelled L-DOPA and administered it to 10 schizophrenia patients and 10 controls, schizophrenia patients took it up quicker, suggesting they produce more dopamine
  • Biological research is always in the form of correlational observation, cannot establish cause and effect
  • Serotonin is another neurotransmitter thought to affect schizophrenia
    Clozapine, one of the most effective treatments for schizophrenia patients, affects serotonin
  • Genetic explanation
    Explains why some people may develop schizophrenia, dopamine hypothesis explains how symptoms may occur
  • Antipsychotic drugs developed from biological explanations have nasty side effects (weight gain, sexual problems, risk of diabetes)
  • Critics reject drugs and state that schizophrenia patients should not think of themselves as 'sick' and instead brace symptoms and learn to live with them
  • Genetic explanation
    Explains why some people may develop schizophrenia
  • Gottsman and Shields (1996)

    • Found higher concordance rate in development of schizophrenia amongst monozygotic twins (75%) compared to dizygotic twins (24%)
  • Kety et al (1998)
    • Found 13% concordance rate for biological relatives, and 2% for adoptive relatives of schizophrenia patients
  • Sekar et al (2016)
    • Identified component 4 (C4), a gene which is part of the immune system, as being associated with increased likelihood of developing schizophrenia
  • C4 gene
    • May cause overexcessive pruning of synapses during adolescence, which could explain why symptoms show after adolescence and why schizophrenia patients' brains appear to 'shrink'
  • Concordance rates are not 100% for monozygotic twins

    Suggests there are other factors besides genetics
  • Genetic factors

    Predispose someone to having schizophrenia but a trigger is needed e.g. environment
  • Individuals related to schizophrenia patients and those with the particular form of the C4 gene are aware of their high risk and can avoid possible triggers
  • If high-risk individuals are aware, they can consult professional help at early stages (before a psychotic episode) which would make treatment more effective
  • Cognitive explanation - Attention Deficit Theory
    Preconscious thought contains a lot of information from our senses which is usually filtered, but if it is not filtered, it causes sensory overload. Thoughts which would usually be filtered out are noticed and treated as more significant by schizophrenia patients, accounting for positive symptoms
  • Frith's Theory of Mind
    • Metarepresentation (a disorder of understanding others and the self)
    • Central control (a disorder of controlling actions)
  • Hemsley's theory

    Schizophrenia patients' schemas do not activate during situations and are disconnected from what they see/hear, therefore they do not know what to filter out
  • McGuigan (1966)
    • Found that schizophrenia patients' vocal cords were tense during auditory hallucinations, suggesting they mistook their inner voice as an external source
  • Not clear whether cognitive dysfunction causes schizophrenia or schizophrenia causes cognitive dysfunction
  • Many brain-damaged patients have cognitive deficits
    Yet do not show symptoms of schizophrenia, suggesting other factors play a role
  • Frith (1992) using PET scans

    Observed decreased blood flow in the frontal cortex of schizophrenia patients, associated with negative symptoms
  • Genetic explanation
    Credible as it is supported by research showing a genetic component, could be paired with cognitive explanation
  • Cognitive Behavioural Therapy (CBT)

    Patient and therapist work closely together to figure out triggers and existing coping strategies, and improve them. Patients are given 'homework' to put them into use. Reality testing is also used where patients demonstrate their delusions
  • Tarrier et al (1998)

    • Investigated 87 schizophrenia patients, some receiving normal treatment and some receiving CBT. 3 months after, those who received CBT had fewer symptoms and spent less time in hospital
  • CBT is designed to treat positive symptoms instead of negative
  • Benefits of CBT
    May occur from the close relationship developed with the therapist, rather than just the 'homework'
  • Participants continue to improve after CBT sessions, e.g. Bradshaw's 1998 study of Carol
  • CBT may be more difficult for patients than drugs

    As it requires patients to think and communicate clearly, which schizophrenia interferes with
  • However, CBT may be seen as more beneficial in the long-term, as patients continue to benefit after treatment
  • National Institute for Clinical Excellence (NICE) 2004 stated that CBT shows improvement in both negative and positive symptoms, and suggested the NHS includes this as part of their integrated treatment
  • Rosenhan (1973) study

    Aimed to test the reliability of mental health diagnosis and see if medical professionals could tell the sane from the insane in a clinical setting, and to investigate the effects of labelling on medical diagnosis
  • Rosenhan's procedure
    8 pseudopatients rang different psychiatric hospitals for urgent appointments and described the same symptoms, 7 were admitted for schizophrenia, 1 for manic depression with psychosis. During their stay, they wrote notes about observations
  • Type 1 error

    False positive
  • Type 2 error

    False negative
  • A follow up study was conducted, where a hospital was informed 1 or more pseudopatients would be admitted over the next 3 months (none were), 19 actual patients were rated as pseudopatients by both staff and psychiatrists