Biological explanations of sz

• Explanation 1: Genetics

  Twin studies (eg. Gottesman, 1991) have identified strong concordance rates:

  MZ = 0.48 (48% risk)

  DZ = 0.17 (17% risk)

  General Population = 0.01 (1% risk)

  Point of interest: If your partner has schizophrenia your risk is twice that of the general population
• Explanation 2: Dopamine hypothesis

  Dopamine is a chemical substance 

  (neurotransmitter) manufactured in the 

  brain that transmits messages between 

  neurons (brain cells).

  Dopamine appears to work differently in 

  patients with schizophrenia. 

  Dopamine is particularly important in the functioning of several brain systems that may cause symptoms of schizophrenia – in particular the cortex and subcortex.
• Explanation 2: Dopamine hypothesis

  Hyperdopaminergia in the 

  Subcortex

  The original version of the hypothesis

  focused on abnormal dopamine

  activity in the subcortex. 

  An excess of dopamine receptors in 

  Broca’s area (responsible for speech 

  production) may be associated with poverty of speech and/or auditory hallucinations
• Explanation 2: Dopamine hypothesis

  Hypodopaminergia in the cortex

  More recent versions of the theory

  focus on abnormal systems in the

  cortex 

  Low levels of dopamine in the

  Prefrontal cortex (responsible for

  thinking and decision-making) may play a role in the negative symptoms of schizophrenia (Goldman-Rabic et al., 2004)
• Explanation 2: Dopamine hypothesis

  It may be the case that both hyper and hypo dopaminergia are correct 

  Hyperdopaminergia = Excessive levels of dopamine in the Subcortex & Broca’s Area 

  Hypodopaminergia = Low levels of dopamine in the prefrontal cortex.
• Explanation 3: Neural correlates

  Neural correlations = patterns of structure or activity in the brain that occur with a schizophrenic experience. As they occur simultaneously this could lead us to believe that the patterns observed are implicated in causing schizophrenia. 

  Avolition which involves motivation, has been associated with one of the main reward centres in the brain. The Ventral Striatum is crucial in the anticipation of reward. Juckel et al (2006) measured activity levels here and found lower levels of activity in schizophrenics compared to controls.
• Explanation 3: Neural correlates

  Negative correlation between 

  activity levels and severity of 

  avolition. As activity levels 

  increase, avolition decreases. 

  As activity decreases, avolition 

  increases. 

  Ventral striatum is a neural 

  correlate of negative symptoms.
• Explanation 3: Neural correlates

  Positive symptoms also have neural correlates. Allen et al (2007) scanned patients with auditory hallucinations, compared to a control. Lower activation levels were found in superior temporal gyrus and anterior cingulate gyrus of hallucination group. 

  Reduced activity in these parts of the brain is a neural correlate for auditory hallucinations.