Schizophrenia

Schizophrenia

Treatments
1. Psychological
  1. Cognitive Behavioural Therapy (CBT)
    1. Based on cognitive explanation of schizophrenia
    2. Focus is to identify and eventually correct impaired thought processes
      1. To do this they're encouraged to 'reality-test' their hallucinations and delusions
        Think of in A Beautiful Mind where he says the girl can't be real because she hasn't aged
    3. Also use role-pay to test 'faculty thinking' and let them see the consequences of thinking differently
      1. Patients will often be given 'homework' to help them apply this in everyday life and develop good thought processes and habits
    4. Sensky (2000( found it to be particularly effective for people who did not respond to drug treatments
      1. This is particularly important as it improved both positive and negative symptoms for over 9 months
        One of the only treatments shown to be effective in improving symptoms for long term
    5. Only treats the symptoms and not the cause
    6. Patient can become dependent on therapist
  2. Psychoanalysis
    1. The aim is to bring unconscious conflicts to the conscious mind where they can be dealt with
    2. First stage is to create an alliance with the patient by helping them with what they think is the issue, then moving onto the task of uncovering the real unconscious issue
      1. Freud himself said that this was near impossible with most schizophrenic patients as they could not form a 'transference' with the therapist
    3. Very few psychiatrists specialise in this
  3. Token economy
    1. Based no operant conditioning
    2. Encourages people in psychiatric institutions to improve socially acceptable behaviour
      1. Lacks ecological validity as cannot work outside of institutions
      2. Improves self care and desirable behaviour like getting dressed
        Even in chronic institutionalised schizophrenics
    3. Effectiveness shown by Ayllon & Azrin (1968)
      1. Patients in psychiatric institution improved from 5 chores a day to 40 (average)
    4. Superficial
      1. Only treats symptoms and ignores the cause of schizophrenia
      2. Doesn't necessarily help patient psychologically but rather makes them easier to handle for staff
2. Biological
  1. Drugs
    1. Conventional
      1. Chlorpromazine
      2. Agonists (inhibit the dopamine system)
      3. Dopamine agonists bind to (but don't stimulate) D2 receptors, displacing the dopamine in the synaptic gap
        Based on dopamine hypothesis
        By reducing stimulation, positive symptoms are reduced or eliminated
      4. Has a lot of side effects
      5. Hill et al
        Studies side effects and found that 30% of patients had developed tardive dyskinesia and that 75% of these cases were irreversible
        HUGE ethical issues
        Hill analysed the cost to benefit and found negative results showing it's not worth the side effects
        There was even a case of US where someone got sued for inhumane treatment for the side effects of the tardive dyskinesia
    2. Atypical
      1. Chlozapine
      2. Based on dopamine system
      3. Are thought to block serotonin AND dopamine receptors although Kapur & Remington (2001) disagrees with this
      4. Only temporarily block the receptors then allowing normal dopamine transmission.
        This reduces side effects
        tardive dyskinea - involuntary movements of the mouth and tongue
    3. Effective at reducing POSITIVE SYMPTOMS
      1. Not effective at reducing negative symptoms
    4. Most effective and widely used treatment for scizophrenia
  2. ECT
    1. First they are injected with a short acting chemical so that they are unconscious before the shock is administered
      1. Then given a nerve blocking agent to paralyse them (to prevent injury to patient and staff)
        A small electric current is passed between two scalp electrodes to induce a seizure.
        Around 0.6 amp
    2. Patients require 3-15 treatments
    3. There are significant risks associated with ECT
      1. Maybe even death
      2. Brain damage
      3. Memory dysfunction
      4. Because of this, the use of ECT as a treatment for schizophrenia has declined in UK
      5. Should only be used as a last resort for the most severe cases
Explanations
1. Psychological
  1. Psychodynamic (Freud 1924)
    1. Result of past experience - harsh upbringing/parents
      1. Person regresses (defence mechanism) to a pre-ego state
    2. Symptoms either due to
      1. Lack of ego control
        Delusions of grandeur
      2. Attempts to regain ego control
        Hallucinations and delusions
    3. Unfalsifiable! Roles of ego, superego and id cannot be isolated or measured
    4. Some studies support idea of schizophrenia stemming from childhood
      1. Fromm-Reichmann (1948) found 'schizophrenogenic mothers' contribute to their child developing schizoophrenia
        Correlational (no cause and effect)
        Parents could be displaying particular behaviour due to the child being schizophrenic
  2. Socio-cultural
    1. Family relationships
      1. Double-bind
        Children receive contradictory messages from parents
        E.g, "I love you" while turning away in disgust
        Prevents coherent construction of reality, resulting in symptoms of schizophrenia
        Evidence
        SUPPORTS - Berger (1965)
        Found that schizophrenics recalled more double-bind statements from their mothers than non-schizophrenics
        DISPROVES - Hall & Levin (1980)
        Meta-analysis found no difference in degree which verbal and non-verbal communication were in agreement
    2. Labelling theory
      1. Social groups construct rules (norms) for members to follow
      2. The symptoms of schizophrenia deviate from these norms and so the person is labelled 'schizophrenic'
        Label the becomes a self-fulfilling prophecy that promotes more symptoms to develop
        Rosenhan (1973)
        Once the label had been applied, the diagnosis influenced behaviour of staff towards the patient even when this was not necessary
  3. Cognitive
    1. Hemley (1993)
      1. Arises from a disconnection between stored memory and sensory input
        Those with schizophrenia therefore cannot differentiate schemas and so do not know where to allocate their focus
        This leads to becoming overwhelmed with information.
        This even extends to internal sensory input as tactile and auditory hallucinations are said to be internal events which are misinterpreted as sensation
    2. Schizophrenia caused by impaired thought processes. They cannot filter their attention selectively and so are overwhelmed with information, making it difficult to process for meaning
      1. Like trying to understand this mindmap by looking at it as a whole rather than individual elements!
      2. When turning to others to validate their experience, others fail to confirm what the person is experiencing which leads to delusions as they believe others must be hiding the truth
    3. Lindenberg (2002) found link between excess dopamine in prefrontal cortex and working memory which would cause cognitive defecits
2. Biological
  1. Neuroanatomy
    1. Enlarged ventricles (Particularly left hemisphere)
      1. Andreason et al (1990) found significant enlargement of ventricles in schizophrenic patients
        Very well controlled study which used modern technology (CAT scans)
        HOWEVER the study was unrepresentative and only found this correlation in men
        Results cannot be generalised as it is not applicable to women
      2. Research is all correlational; we cannot identify cause and effect
        Enlarged ventricles causing schizophrenia or Schizophrenia causing enlarged ventricles?
    2. Disturbances to the limbic system cause agitation seen in schizophrenics
  2. Dopamine Hypothesis
    1. Dopamine is a neurotransmitter responsible for levels of attention and perception (Comer 2003)
    2. Excess dopamine in the synaptic gap may be cause of the symptoms of schizophrenia
      1. This can happen three ways
        Oversensitive receptors
        Excess D2 receptors
        When dopamine is released from the vesicles, not all receptors receive dopamine
        Brain is signalled to make more, resulting in excess dopamine
        Excess dopamine in synaptic gap
    3. Evidence for effect of too much AND too little dopamine
      1. Parkinson's disease drugs (Grilly 2002)
        A degenerative disease
        Those with Parkinson's tend to have low levels of dopamine
        Take L-dopa to increase dopamine levels
        Develop schizophrenic-type symptoms
      2. Antipsychotic drugs
        They all block the activity of dopamine in the brain (dopamine agonists)
        Reducing stimulation of dopamine system eliminates positive symptoms
    4. Neuroimaging hasn't found convincing evidence of altered dopamine activity in the brains of those with schizophrenia (Copolov & Crook 2000)
  3. Genes
    1. You can only get AO1 for genes!
    2. May be due to a genetic factor
    3. Cannot be sole cause of schizophrenia as no 100% concordance rates found
      1. Gottesman & Shields (1966)
        Monozygotic twins = 48%
        Dizygotic twins = 17%
Clinical characteristics
1. Symptoms
  1. Positive
    1. Traits that those with Sz have and normal people don't
      1. Hallucinations
      2. Delusions
  2. Negative
    1. Traits that those with Sz don't have but normal people do
      1. Catatonic behaviour
      2. Lack of motivation
2. Classified
  1. ICD
    1. British
    2. 1 month
  2. DSM
    1. American
    2. 6 months
3. Issues
  1. Cultural differences in diagnosis
    1. ICD & DSM are different, resulting in unreliable daignosis
    2. Copeland (1971)
      1. Gave patient description to US&UK psychiatrists - 69% US diagnosed schizophrenia but only 2% UK
  2. Validity
    1. Symptoms can be found in other disorders
      1. Ellason & Ross (1995) point out that people with DID may have more of these symptoms than a schizophrenic
    2. The extent that diagnosis represents something that is real and distinct from other disorders

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	Created by Emmy Taylor about 9 years ago