Biological explanations for schizophrenia

• Biological explanations for schizophrenia

  Genetic causes

  Brain areas

  Neural correlates (neurotransmitters)
• Family studies (genetic basis)

  Gottesman


  Schizophrenia is more common when a biological relative also has schizophrenia.

  
  

  Closer the genetic relatedness the higher the likeliness.

  
  

  Gottesmans study- children with two schizophrenic parents had a concordance rate of 46%

  
  

  Children with one schizophrenic had a rate of 13%

  
  

  With a brother or sister = 9%
• Twin studies and schizophrenia

  Gottesman


  Monozygotic and dizygotic twins (100% and 50% of genes)

  
  

  40 twin studies

  
  

  Identical twins (monozygotic) = 48% concordance rate

  
  

  Non identical (dizygotic) = 17%
• Adoption studies and schizophrenia

  Tienari

  Observe the effects of genes with a different environment

  
  

  Tienari study in Finland- 164 adoptees

  
  

  Mothers with schizo =6.7% had schizo

  
  

  Compared to the control group

  
  

  In which 2% had shizo
• Evaluation of genetics

  Joseph

  Gottesman and Shields


  Never a 100% concordance rate so there must be other factors at play

  
  

  Joseph- those monozygotic twins are more likely to be treated similarly, do things together and be confused as each the other twin, so it is more an affect of environmental factors.

  
  

  Gottesman and Shields- both genes and environment are important in development of schizo
• Biological approach


  Brain Areas
• Brain areas


  Ventricular enlargement

  Damage to dorsolateral prefrontal cortex

  Occipital lobe

  "Where" system in Wernickes area
• dorsolateral prefrontal cortex

  Gur et al

  Ito et al


  Damage to this area reduces the ability to solve problems and organise thoughts

  
  

  Also be involved in the perception of lies and deception (Ito)
• Occipital lobe

  Jibiki et al


  Visual info messed up

  
  

  Leads to misreading of facial expressions and emotions which could further lead to deluded thinking
• Wernickes area

  Plaze et al

  The where system allows us to differentiate between internal and external voices, this is one of the key aspects of auditory hallucinations

  
  

  ( why are the audio hallucinations bad)

  Combine it with the previous point about the deluded thinking.
• Neurotransmitters

  Dopamine hypothesis

  Started with amphetamines and cocaine which affect the dopamine release

  
  

  Also schizophrenics had high numbers of D2 receptors

  
  

  These are called dopamine agonists as they release excess dopamine and this also leads to schizo type symptoms

  
  

  Also L-dopa raises dopamine (its given to people with Parkinson's) this also lead to schizo type symptoms (Grilly)

  
  

  Also drugs that decrease dopamine transmission lead to a reduction in symptoms

  (Dopamine antagonists)
• Revised dopamine hypothesis

  Davis and Kahn

  (Patel support)

  Positive symptoms are due to an excess in the mesolyombic pathway

  
  

  Negative symptoms are due to a lack of dopamine in mesocortical pathways

  
  

  Patel used pet scans to assess levels of dopamine in the dorsolateral prefrontal cortex ( schizophrenic people had lower levels)
• Evaluation of the dopamine hypothesis

  Leucht et al


  Leucht meta analysed 212 studies that analyses the effectiveness of antipsychotics and placebos.

  
  

  All the drugs had a higher effectiveness than placebo (treated the positive and negative symptoms)
• Evaluation of dopamine hypothesis

  Moncrieff (negative)


  Cocaine and amphetamines affect dopamines as well as many other neurotransmitters.

  
  

  Dopamine levels in post mortem studies have been negative ( goes against the hypothesis)
• Evaluation of dopamine hypothesis

  Noll

  In 1/3 of cases the antipsychotic drugs do not reduce the symptoms.

  
  

  Regardless of the levels of dopamine the symptoms were present.
• Schizophrenia runs in families

  There is a strong relationship between genetic similarity of family members and likelihood of both developing schizophrenia.
• Gottesman's (1991) family study 


  Found MZ twins have a 48% shared risk of schizophrenia, DZ twins have a 17% shared risk and sibilings (about 50% of genes shared) have a 9% shared risk. All of these are higher than the shared risk of the general population which is about 1%
• Genetic explanation for schizophrenia

  • Strong evidence base
• Family studies


  • Gottesman study showing risk increases with genetic similarity to a family member with schizophrenia
• Adoption studies


  • Tienari et al 2004 study showing biological children of parents with schizophrenia are at heightened risk even if they grow up in an adoptive family
• Twin studies


  • Hickler et al 2018 study showing 33% concordance rate for identical twins and 7% for non-identical twins
• Some people are more vulnerable to schizophrenia as a result of their genetic make up
• Genetic counselling


  Application of understanding the role of genes in schizophrenia
• If one or more potential parents have a relative with schizophrenia, they risk having a child who would go on to develop the condition
• The risk estimate provided by genetic counselling is just an average figure and will not really reflect the probability of a particular child going on to develop schizophrenia because they will experience a particular environment which also has risk factors
• Genetic explanation for schizophrenia


  • Has limitations
  • Environmental factors also increase risk of developing schizophrenia
• Environmental factors that increase risk of schizophrenia


  • Biological risk factors
  • Psychological risk factors
• Biological risk factors


  • Birth complications (Morgan et al 2017)
  • Smoking THC-rich cannabis in teenage years (Di Forti et al 2015)
• Psychological risk factors


  • Childhood trauma which leaves people more vulnerable to adult mental health problems in general
• There is now evidence for a particular link between childhood trauma and schizophrenia
• In one study by Morkved et al 2017, 67% of people with schizophrenia and related psychotic disorders reported at least one childhood trauma as opposed to 38% of a matched group with non-psychotic mental health issues
• Genetic factors alone cannot provide a complete explanation for schizophrenia
• One strength = strong evidence

  • Gottesman 1991 - clearly shows genetic similarity + shared risk of SZ are closely related
  • Adoption studies (Tienari et al 2004) - people with SZ are still at a heightened risk of developing SZ even if adopted into families without history of SZ
  • So SZ may not be entirely genetic but there is overwhelming evidence that genetic factors make some people more vulnerable
• The original hypothesis was based on the discovery that drugs used to treat schizophrenia (ANTIPSYCHOTICS, which reduce DA) caused symptoms similar to those in people with Parkinson's diseases, a condition associated with low DA levels  (Seeman 1987). Therefore schizophrenia might be the result of high levels of DA (hyperdopaminergia) in subcortical areas of the brain. For example, an excess of DA receptors in pathways from the subcortex to Brocas area (responsible for speech production) may explain specific symptoms of schizophrenia such as poverty of speech and/or auditory hallucinations.
• Cortical hypodopaminergia


  Abnormally low dopamine in the brain's cortex
• Cortical hypodopaminergia


  Can explain symptoms of schizophrenia
• Low dopamine in the prefrontal cortex


  Responsible for thinking, could explain cognitive problems (negative symptoms of schizophrenia)
• Cortical hypodopaminergia


  Leads to subcortical hyperdopaminergia
• Both high and low levels of dopamine in different regions of the brain are part of the updated version of the dopamine hypothesis
• The dopamine hypothesis tries to explain the origins of abnormal dopamine function