schizophrenia

• schizophrenia

  a psychotic disorder in which patients often lose contact with reality and insight
• classification - ICD 10


  Europe - at least two negative symptoms
• classification - DSM V

  America - must have at least one positive symptom
• positive symptoms


  behaviour is added to the normal range of bvrs showing loss of touch with reality, often includes hallucinations and delusions - delusions can be paranoial or grandiose - positive sumptoms usually occur in short episodes
• negative symptoms


  behaviour removed from the normal range of behaviours e.g avolition (loss of motivation) and speech poverty - these often have longer lasting episodes and are more resistant to medication having a negative effect on the quality of life
• diagnoses and classification AO3

  • high inter-rater reliability - within classification system, Osorio et al - 180 individuals DSM-V pairs of interviewers IRR 0.97 and test-retest 0.92 - diagnoses accurate and consistent
  • low criterion validity - cheniaux et al two psychiatrists, 100 clients 68 diagnosed ICD 10 39 with DSM-V - shows uncertainty of diagnoses may be over/under diagnosed
  • comorbidity and symptom overlap - diagnosed commonly alongside depression, substance abuse - problem for classification as not distinct, symptom overlap w/ bipolar - false diagnoses - reduces validity
• biological explanation - genetic basis AO1

  family studies - confirmed risk of Sz in line with genetics - Gottesman 1991 - Mz 48%, sibling 9%, aunt 2% - not fully genetic as not 100% for MZ

  candidate genes - polygenic, Ripke found 108 different genes associated with the risk of Sz

  absence of family history - the role of mutations of parental DNA - epigenetics
• biological explanations - neural correlates AO1

  original dopamine hypothesis - link with high levels of DA in subcortical areas of the brain, excess DA receptors in Broca's areas explain auditory hallucinations

  • updated version - overactive mesolimbic pathways due to increased DA - positive symptoms and decreased DA in mesocortical - negative symptoms
  • both low and high levels of DA in different regions contribute
• biological explanations AO3

  • strong evidence base for genetic - family studies e.g Gottesman shows high risk with genetic similarities, adoption studies - Tienari bio parents with Sz 4x greater risk in adopted children
  • h/ environmental factors evidence - diathesis-stress
  • evidence for dopamine - amphetamines increase dopamine and worsen SZ symptoms and induce in those without, antipsychotics lower DA and reduce symptoms
  • h/ evidence for a central role of glutamate, post mortem and live scanning - high levels glutamate in brains of Sz and several candidate genes involve glutamate production
• psychological explanations - family dysfunction AO1

  • schiziophrenogenic mother - cold, maladaptive relationship, rejecting, controlling, family environment governed by tension and secrecy - leads to distrust and paranoial delusions
  • expressed emotion - high levels of negative emotion towards Sz, hostility, verbal criticisms/ overinvolvement - cause of stress
  • double bind theory - contradictory info from parents on right and wrong, fear of doing what is wrong but cannot clarify leads to confused understanding of world as dangerous and disorganised thinking
• cognitive explanations for Sz AO1

  • dysfunctional thinking - disruption to normal thought and processing, cognition impaired and lack of ability to suppress thought Frith et al proposed two ways:
  • metarepresentation dysfunction - disrupts the ability to recognise own actions as carried out by ourselves rather than someone else - explains hallucinations and thought insertions
  • central control dysfunction - issues with the cognitive ability to suppress automatic thoughts and responses - speech poverty
• family dysfunction AO3


  • research support - Read et al - adults w/ Sz disproportionally likely to have insecure att, 69% of women and 59% men with Sz have a history of abuse suggests family dysfunction - h/ correlational
  • evidence lacks support - theory of schizophrenogenic mother and double bind based on clinical obs, informal assessments cannot account for link in explanation
• cognitive explanations AO3


  • r. support - Stirling et al - 30 Sz and 30 control group stroop test, Sz twice as long due to cognitive processing impaired and lack of central control so unable to suppress colours
  • proximal explanation - only explains what is happening now not the origins and initial cause - partial explanation
• drug therapy AO1


  typical antipsychotics - 1950s e.g chlorpromazine, dopamine antagonists, reduce dopamine activity by clocking DA receptors, reduce symptoms such as hallucinations in the mesolimbic pathway, H/ mesocortical pathways increased negative symptoms - sedative effect due to effect on histamine receptors

  atypical - 1970s, e.gt clozapine - maintains effects and reduces negative side effects - main side effect agranulocytosis blood disorder h/ regular blood tests to ensure doesnt develop, atypicals bind to DA and serotonin receptors and glutamate to increase mood and reduce depression
• drug therapy AO3


  • evidence for effectiveness - both typical and atypical, Ben Thornly et al - studies of chlorpromazine across 13 trials overall increased function and reduced symptoms
  • serious side effects - tardive dyskinesia, long term irreversible dopamine sensitivity, neuroleptic malignant syndrome can be fatal
  • chemical cosh - sedative effect, chemical straight jacket to restrain institutionalised patients - ethics, h/ can make them engage better in therapy
• psychological therapy AO1


  • CBT - targets dysfunctional thinking, 5-20 sessions, identifies irrational thoughts and makes sense of them - explains auditory hallucinations as malfunctioning speech centre to reduce anxiety and normalised bvr as an extension of norm e.g hearing voices as extension of thinking in head
  • family therapy - aims to improve communication in the family to reduce levels of expressed emotion and stress, focuses on relapse prevention by finding what the family can do to help and how to cope with stress and create a safe space in order to maintain good health
• CBT AO3


  • evidence for effectivness - Jauhar et al - 24 studies using CBT with Sz, clear evidence on effects for both positive and negative symptoms, clinical advice by NICE
  • quality of evidence - CBT techniques and Sz symptoms vary from case to case therefore different studies in the role of different CBT techniques, means hard to say how effective
  • does CBT cure - improves the quality of life but is not a 'cure'
• family therapy AO3

  • evidence for effectiveness - McFarlane, most consistently effective in particular for relapse prevention which was reduced 50-60%, likely to benefit at both early and late stages but when initial decline most effective
  • benefits to the whole family - Lobban 2016 effects important as the family provides the bulk of care, increases functions of whole family, strengthens supports and reduces stress
  • economic benefits if the family can provide care
• token economies AO1


  rewards system to manage and modify bvr of patients in institutions

  • Ayllon and Azrin - trial in wards of Sz women, every time carried out desired bvr e.g shower, given a token to be swapped for rewards e.g film
  • improves quality of life, normalises bvr and is easier to adapt back after institutionalisation
  • operant conditioning, token given immediately to associate w/ task, tokens secondary reinforcers swapped for more meaningful rewards primary reinforcers
• token economies AO3


  • evidence for effectiveness - Glowaki et al - 7 studies from 1999-2013, found effectiveness in all studies for reducing negative symptoms h/ only 7 over 14 years - file drawer problem, bias towards positive published findings
  • ethical issues - professionals control over bvr, if targets bvrs not identified sensitively can abuse power, furthermore restricting pleasures has negative effects on those already vulnerable - has led to legal action by families of Sz patient
  • alternate approaches perhaps more suitable - art therapy, low risk high gain
• interactionist approach to Sz - AO1

  meehls original diathesis-stress model - diathesis single schizogene, entirely genetic, stress dysfunctional parenting from childhood

  • modern understanding - diathesis is polygenic - ripke 108 genes, range of factors beyond genetics also effect such as psychological trauma can be a diathesis as can alter brain development - read et al, stress can be anything triggering in envt, link to cannabis use and increased risk
  • treatment acknowledges both in combination
• interactionist approach to Sz - AO3

  • real world application - combined treatment most effective, Tarrier 2004, combined CBT and drug therapy reduced symptoms most
  • support for vulnerability and triggers - Tienari 2004 - 24000 Finnish women with Sz, 145 children adopted away, found high genetic risk in healthy family but Sz not developed h/ in maladaptive parents risk of Sz greater - supports a combination of diathesis and stress increases Sz risk
  • diathesis stress complex - meehls original model too simplistic now known range of factors influence - supports modern understanding