Biological explanations of Schizophrenia

Genetic factors: Twin studies
1. A01
  1. Concordance rates suggest there is a genetic influence to Sz as MZ twins share 100% genes while DZ twins share 50%
    1. CR appears higher for MZ twins
  2. Joseph
    1. Pooled data from no of studies + found CR of 40.4% for MZ twins + 7.4% for DZ twins
      1. Suggests while you may expect CR to be 100% if Sz was 100% bio there is evidence of genetic influence
2. A02
  1. Environmental differences rather than bio ones
    1. MZ twins are treated more similarily
      1. Leading to experience of more 'identity confusion', as they are commonly viewed as 'the twins' rather than 2 separate people
        With this in mind, Joseph argued higher CR may simply be distinguishing environmental differences of 2 types of twins
  2. Studies focusing on other genetic relatives show greater genetic relatedness = greater risk for person to develop disorder if relative has it
    1. Gottesman
      1. One researcher who wanted to determine whether bio relatives are similarly affected more often than non-bio relatives when there is diagnosed Sz in fam
    2. Research has shown children w/ 2 Sz parents have CR of 46%, children w/ 1 Sz parent 13% + siblings 9%
Genetic factors: Adoption studies
1. A01
  1. Further develop theory of Sz having genetic basis as they separate biological + environmental influences
    1. Allows researchers to differentiate between influence of indivi. genes + environment they were raised in - away from Sz family member
  2. Can be used to defend findings of twin + fam studies because they remove environmental influences
    1. Means if results are similar it further supports all other results
2. A02
  1. Research support
    1. Tienari et al
      1. Conducted study looking at differences between adopted children w/ bio mothers who had Sz compared to those who didn't
        Found out of 164 adoptees whose bio mothers had been diagnosed w/ Sz 11 were also diagnosed with disorder
        These findings were compared to control group of 197 adoptees born to non-Sz mothers were only 4 received diagnosis of Sz
  2. Knowledge of adoptive parents is questionable
    1. Would have likely been informed about child's genetic predisposition + may have treated them differently due to this
      1. May have meant adoptive environment either helped or hindered them as adoptive parents may have been apprehensive about predisposition
    2. Kringlen
      1. Pointed out that 'one might wonder who would adopt such a child'
        Suggesting they may have had high levels of expressed emotion due from adoptive parents or double-bind due to parents knowlesge
        Diathesis stress model
Dopamine hypothesis
1. A01
  1. DH claims Sz have chemical imbalance caused by messages from neurons that transit dopamine being fired too easily or too often
    1. High levels of D associated w/ characteristic symptoms of disorder
      1. Suggests by controlling levels of D in brain one might be able to lessen symptoms of Sz
2. A02
  1. Research support
    1. Amphetamines
      1. Are a D agonist which stimulates nerve cells containing D causing synapse to be flooded
        Large doses of these cause characteristic hallucinations + delusions of a Sz episode
    2. Antipsychotics
      1. Block activity of D in brain
        By reducing stimulation of D system these drugs eliminate symptoms such as hallucinations + delusions
    3. Effects of these drugs demonstrate role D plays in Sz episode + also demonstrate how effects can be counteracted
  2. Post-mortem studies
    1. Shown antipsychotics may actually have opposite effect than that desired + may actually cause D levels to rise further
      1. Haracz
        Found these anomalies in post-mortems of those Sz who had received antipsychotic drugs shortly before death showed elevated levels of D
        Those who hadn't received medication had normal levels of D
      2. Suggests D's role in symptoms of Sz could be over exaggerated + potentially misleading
Brain structure: ventricles
1. A01
  1. Ventricles in Sz have been found to be bigger while other areas are smaller (frontal + temporal lobes) than that of a normal indivi.
    1. Torrey
      1. Found ventricles were 15% larger in sufferers of Sz
        However, suggested ventricles were not cause of Sz but that decreased brain tissue due to size of ventricles was cause
  2. Suggests certain brain structures may cause onset of Sz
2. A02
  1. Ho et al
    1. Conducted research which supports theory as they found that Sz had larger ventricles + their brains made more cerebrospinal fluid compared to a control group
    2. Due to longitudinal nature of study they found that larger ventricles became less easy it was for patients to cope w/ their symptoms
      1. Suggests symptoms experiences by Sz could get worse as they grow older as ventricles generally become larger in males + older people
  2. Cause and effect?
    1. Idea is inconclusive as psychologists can't state whether enlarged ventricles are cause or consequence of Sz
      1. Due to fact that you can't operationalise ventricle size from 1 person to next as we all develop differently
      2. 'Enlargement' itself is questionable as ventricles naturally get bigger in everyone
        So what counts are Sz-causing enlargement and what doesn't?
        Suggests some bio explanations are inconclusive

Próximo

Biological explanations of Schizophrenia

Descrição

Resumo de Recurso

Semelhante

	Criado por bebe97 mais de 9 anos atrás