schizophrenia

• APAs diagnostic and statistical manual of mental disorders

  • DSM only needs one positive symptom
  • subtypes removed
• WHOs International Classification of Diseases

  • needs two or more negative symptoms
  • 5 subtypes recognised e.g paranoid and catatonic
• positive symptoms of schizophrenia

  • hallucinations
  • delusions
  • disordered thinking
• hallucinations


  sensory experiences that have no basis in reality or are distortions of stimuli that are genuinely there. These can be experienced in relation to any sense
• types of hallucinations


  • auditory
  • visual
  • olfactory
  • tactile
• delusions


  irrational beliefs involving a misinterpretation of perceptions or life experiences
• types of delusions

  • paranoia
  • control
  • grandeur
• disordered thinking


  concentration problems mean sufferers struggle to maintain their train of thought

  e.g tangential speech, incoherent speech, switching topics and racing thoughts
• negative symptoms of schizophenia


  • avolition
  • speech poverty
  • attentive flattening
• avolition


  lack of purposeful behaviour. sufferers have reduced motivation to carry out activities shown by a lack of self-care, motivation and energy
• speech poverty 


  characterised by changes in patterns of speech - usually a reduction in both the amount and quality of speech. alogia is where speech is blocked, echolalia, neologisms and word salads are all classic characteristics of speech poverty
• attentive flattening 


  reduction of a person's range of emotions lacking non-verbal cues and eye contact
• what are the issues with classification and diagnosis of sz

  • reliability
  • validity
  • co-morbidity
  • symptom overlap
  • cultural bias
  • gender bias
• reliability as an issue of classification and diagnosis of sz

  • there are issues with inter-rater reliability when it comes to the diagnosis of sz
  • Cheniaux et al (2009) has 2 psychiatrists independently diagnose 100 patients using both psychiatric manuals. she found one psychiatrist diagnosed 26 (DSM) and 44 (ICD) the other diagnosed 13 (DSM) and 24 (ICD)
  • therefore, diagnosis will vary depending on who is making the assessment and fundamental lack of agreement with healthcare providers
• validity as an issue of classification and diagnosis of sz

  • there are issues with validity when it comes to the diagnosis of sz
  • in the Cheniaux study, it is clear there are issues with criterion validity. Both psychiatrists reached a diagnosis of sz more frequently when using ICD compared to DSM. This means that at least one of the manuals is incorrect. Either ICD is overdiagnosing or DSM is underdiagnosing.
  • there is an incorrect assesment not measuring sz accurately as different manuals are used in different countries the hen a large number of patients will be negatively impacted by this
• co-morbidity as an issue of classification and diagnosis of sz

  • high co-morbidity rates in sz suggest a lack of understanding about the illness
  • Buckley et al (2009) reviewed diagnoses of sz and found 50% of sz patients were diagnosed with depression, 47% with substance abuse, 29% PTSD and 23% OCD
  • this would suggest there may be an issue where psychiatrists are unable to tell the difference between 2 disorders or 2 disorders appear in tandem where is may be a singular disorder
  • regardless, we still do not fully understand issues and symptoms
• symptom overlap as an issue of classification and diagnosis of sz

  • another issue with diagnosing sz is the degree of similarity between this and other disorders
  • the symptoms of sz overlap with many disorders, for exmaple bipolar involves positive symptoms such aas delusionary thinking and negative symptoms like avolition
  • this not only makes it difficult to distinguish between 2 disorders but also questions whether these 2 similar disorders are the same
• cultural bias as an issue of classification and diagnosis of sz

  • diagnosing sz is weakend by high cultural bias evident by the highest rates of diagnosis of African-Caribbean or American people
  • Pinto and Jones (2008) found that British people of Afro-Caribbean orgin are 9 times more likely to be diagnosed sz than white British people, yet this is not true is Afro-Carribbean countries
  • this suggests its unlikely to be a genetic vulnerability and is in fact due to cultural bias where psychiatrists are misinterpreting culturally specific behaviour as sz symptoms
• gender bias as an issue of classification and diagnosis of sz

  • another weakness of diagnosing sz is much of the reseach is based on gender sterotypes as women are viewed as having better interpersonal functioning
  • men are more likely to be diagnosed with sz compared to women with a ratio 1:4:1. Cotton et al (2009) suggests this is bevause women have closer relationships and greater support
  • this strong interpersonal functioning could mask sz severity questioning validity
• biological explanations for sz

  • genetics
  • dopamine hypothesis
  • neural correlates
• genetics 


  there is clear evidence that sz runs in families as there are cases where more than one family member suffers from the illness. Gottesman conducted a large-scale family study which looked at genetic similarity and the likelihood of developing sz
• what are the statistics of developing sz for each genetic relative

  general population 1%

  cousins 2%

  uncles/aunts 2%

  nephews/nieces 4%

  grandchild 5%

  half siblings 6%

  parents 6%

  siblings 9%

  children 13%

  fraternal twins 17%

  identical twins 48%
• candidate genes 


  • there are specific genes which may be asociated with the risk of inheritence. There have been a number identified, which each confer a small increased risk of sz but as there is no single gene, this suggests sz is polygenic which means it requires a number of factors to work in combination
  • because a several studies have identified different genes, this also suggests sz is aetiologically heterogeneous, which means different combination of factors can lead to the condition
• research support for candidate genes

  • ripke (2014) carried out a large-scale study combining data from genome-wide studies which are looking at the whole human genome as pposed to particular genes
  • they found 108 genetic variations in the sz sample of 37000 compared with 113000
• what are the 2 dopamine hypothesises

  • hyperdopaminergia
  • hypodopaminergia
• hyperdopaminergia


  • high levels of dopamine in the brain's subcortex
  • an excess of dopamine receptors in Broca's Area (speech production) may be associated with positive symptoms of sz such as auditory hallucinations
• hypodopaminergia

  • more recent versions of the dopamine hypothesis have focused on abnormal levels (low) dopamine in the prefrontal cortex
  • prefrontal cortex is responsible for thinking and decision-making (negative symptoms) like speech poverty, avolition and affective flattening
• neural correlates of positive symptoms

  Allen et al (2007) compared sz sufferers who were experiencing auditory hallucinations with a control group. they gave pps the task of identifying whether pre-recording speech was that of their own or others. They simultaneously scanned pps brains. The experiemental group showed lower activation in the superior temporal gyrus and anteriror cingulate gyrus
• superior temporal gyrus 


  sound processing
• cingulate gyrus 


  inability to recongise own voice and thoughts
• neural correlates of negative symptoms

  avolition is the loss of motivation. motivation involves anticipation of reward. Juckel et al (2006) measured activity levels in the ventral striatum (an area of the brain involved in reward anticipation) and found lower activity in sz sufferers than in controls. there was negative correlations show between activity in the ventral striatum and severity of negative symptoms
• ventral striatum 


  an area of the brain involved in reward anticipation
• biological explanations A03 genes (fraternal vs identical twins)

  • although Gottesman's study provides support for heredity in the risk of developing sz some of the findings actually detract from the role of genes
  • it states that an identical twin has a 48% risk of developing sz and half sibilings + parents share 1/2 of genes but have the same risk %
  • this is a problem as identical twins share 100% of genes but there's only 48% risk
  • therefore indicates although there is a clear genetic pattern sz cannot solely be dependent on genetics so there must be environmental factors affecting development
• biological explanations A03 genes (adoption)

  • Tienari's research supports the genetic explanation
  • she found that 155 adopted children born to sz mothers had a concordance of 10% compared to 1% in adopted childrern without sz mothers
  • this shows that despite being removed from a schizophrenogenic household the risk was greater for those who were born to sz mothers
  • study shows adoption is not an extraneous variable as adopted children have 1% chance
  • adds support for genetic vulnerability giving suggestions on how to reduce the risk of those who are vulnerable by placing them in homes with no sz
• amphetamines effect on dopamine

  stimulants wich act as dopamine agonists - increase dopamine levels
• side effect of amphetamines

  experience positive symptoms of sz such as delusions and hallucinations
• L-Dopa effect on dopamine

  Levodopa is a drug which increases dopamine levels of Parkinson's suffers who experience tremors due to low dopamine
• L-Dopa side effects


  users who don't get the balance right may end up with too much dopamine production and therefore experience positive symptoms
• antipsychotic effect on dopamine

  they inhibit dopaminergic neurotransmission blocking 72% of D2 dopamine receptors in the brain
• antipsychotic side effects

  Tardive Dyskinesia - sudden, jerky or slow twisting movements in your face or body