biological explanations and treatments

• a01 - genetic

  • gottesman - family studies show that risk of developing sz is greater for those closely related to the sz patient
  • MZ twinns have higher concordance rate of SZ

  twin studies

  • joseph - collected data from sz data

  concordance rates - MZ twins - 40.4% - DZ 7.4%

  • rosenthal - studies identical quadruplets who all developed sz

  however they all suffered from poor environment and home life

  
  

  candidate genes

  • sz is polygenic
  • ripke - looked at genetic makeup of 37k patients and compared to 113k controls found 108 separate genetic variation associated with higher risk of sz
• a01 - dopamine hypothesis

  • sz have higher levels of dopamine
  • hyperdopaminergia - in the subcortex where there is excess of dopamine receptors in broca area - explains speech poverty
  • hypodopaminergia - goldman-rakic - low levels of dopamine in the prefrontal cortex influence negative symptoms

  may be both hyper and hypodopaminergia are correct explanations - both high and low levels of dopamine in different brain regions are involved in sz
• neural correlates

  • measurements of the structure or function of the brain that correlates with an experience ie sz

  negative symptoms

  • motivation involves anticipation of rewards which is highlighted in the ventral striatum
  • Juckel et al - lower level in the ventral striatum in sz patients which is related to avolition
  • observed a negative correlation between activity levels in VS and the severity of overall negative symptom

  positive symptoms

  • allen et al - lower levels of superior temporal gyrus and anteriol cingulate gyrus activity for individuals with auditory hallucinations
• a03 - adoption studies

  • tienari et al - children of sz parents that have been adopted into a family with no history of sz are still at a higher risk of the onset of sz
  • alsi use ripke and gottesman - overwhelming evidence that genetic factors increase the vulnerability of sz and that although no entirely gentically based, genetic suspectibility is an important factors
• a03 - mixed evidence for dopamine hypotheis
• a03- correlation causation problem
• biological treatment a01

  typical antipsychotics

  • work on positive symptoms
  • work on dopamine
  • they occupy receptors but dont activate them (antagonists)
  • drugs bine to dopamine receptors and work by blocking them
  • reduced stimulation of dopamine positive symptoms are reduced
  • most common is chlorpromazine
• biological treatment ao1

  atypical antipsychotics

  • reduce effects of both dopamine and serotnin
  • blocks both dopamine and serotnin receptors
  • as they reduce the stimulation of dopamine and sertonin - hallucinations and low moods are reduced and eliminated
  • most common is clozapine
  • risperidone was produced later and combines to receptors more strongly therefore requiring smaller doses
• chlorpromazine

  • typical
  • positive symptoms
• clozapine

  • atypical
  • positive and negative symptoms - works on serotonin receptors to improve mood
• risperidone

  • atypical
  • positive and negative symptoms
  • binds more effectively to D2 receptors therefore lower dosage needed
• a03 - evidence for effectiveness

  • thornley et al - compared chlorpromazine to a placebo
  • chlorpromazine was associated with better ability to reduce symptoms severity and increase functioning
  • relapse rate was lower

  meltzer - clozapine is more effective than typical and any other atypical drugs.

  although many studies have tried to compared the atypical drugs the results have been inconlcsuive perhaps bc some people resond better to one drug than the other
• a03- side effects

  typical antipsychotics have been associated with tardive dyskinesia which is caused by dopamine supersensitivity.

  
  

  The most serious side effect is NMS which is caused bc the drug blocks dopamine action in the hypothalamus; an area which regulates a number of body systems.

  
  

  although they are effective (Meltzer) side effects are serious and ppl taking clozapine have to take regualr blood tests
• a03 - problem with evidence for effectiveness

  despite the mass of evidence for effectiveness Healy suggested that successful trials have had their data published more than once, exaggerating the evidence.

  also suggested that bc drugs have a calming effect it is easy to show the positive effect of them and it is not the same as saying that they reduce the severity of the psychosis. furthermore most studies assess the short term effect rather than the long term benefits