SZ exam summary

• AO1- Diagnosis and classification:

  • Positive symptoms- additional experiences beyond those of ordinary experiences, e.g. hallucinations and delusions
  • Negative symptoms- loss of usual abilities and experience, e.g. avolition and speech poverty
  • Issues in diagnosis, reliability (extent to which diagnosis of sz is consistent), validity (extent to which diagnosis techniques measure what they are designed to), co-morbidity (occurrence of 2 illnesses together, confuses diagnosis and treatment), and symptom overlap (two or more conditions share symptoms, questioning validity of the classification)
• AO3- Diagnosis and classification:

  • Limitation- Cheniaux et al. had psychiatrists diagnose patients using DSM and ICD criteria, inter-rater reliability poor, one diagnosed 26 using DSM and 44 using ICD and other 13 with DSM and 24 with ICD
  • Limitation- poor criterion validity, do different assessment systems arrive at same diagnosis. Cheniaux et al- sz more likely to be diagnosed using ICD than DSM
  • Limitation- co-morbidity, Buckley et al., 50% with sz have depression and 47% with sz experience substance abuse
  • Limitation- culturally relative, African-Americans and English of African origin more likely to be diagnosed with sz, positive symptoms normal in African cultures, e.g. hearing voices in ancestor communication, some from cultural backgrounds more likely to be diagnosed than others
• AO1- Biological explanations (genetic basis and dopamine hypothesis):

  • Polygenic and aetiologically heterogenous
  • Runs in families (genetic)- Grottesman's family study, MZ 48% shared risk, DZ 17% and siblings 9%. Ripke et al. found 108 separate genetic variations associated with increased risk
  • High dopamine activity in subcortex associated with hallucinations and poverty of speech, e.g. excess of dopamine receptors in Broca's area
  • Low level of dopamine in prefrontal cortex (thinking and decision-making)
• AO1- Biological explanations (neural correlates):

  • Neural correlates= measures of structure or function of brain that correlate with positive or negative symptoms of sz
  • Ventral striatum involved in anticipation of reward (linked to motivation), so loss of motivation (avolition) in sz may be explained by low activity levels in ventral striatum
  • Supported by Juckel et al.- found a negative correlation between ventral striatum activity and overall negative symptoms
  • Allen et al.- found patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus
• AO3- Biological explanations:

  • Strength- Grottesman study demonstrates genetic similarity, and adoption studies (Tienari et al.) show children of people with sz still at hightened risk if adopted into family without history of sz
  • Limitation correlation-causation problem, negative correlation may suggest low activity in ventral striatum causes avoliton, but avolition could cause this low activity
  • Strength- mutation support, sz can take place in absence of family history (e.g. mutation of paternal DNA through radiation). Brown et al. found link between paternal age and risk of sz: 0.7% in under 25, 2% in fathers over 50
  • Limitation- possibility of developing even if twin has it is 50%, so environment must play role (e.g. family functioning in childhood), may be combination of biological and psychological approaches (as suggested by interactionist approach)
• AO1- Psychological explanations:

  • Family dysfunction- Fromm-Reichmann's schizophrenogenic mothers (cold, rejecting and controlliing, create a climate of tension and secrecy leading to distrust and paranoid delusions, and then sz),