Schizophrenia

• Schizophrenia: classification

  • ICD-10 & DSM 5 (organised categories to diagnose, looks at pos/neg symptoms)
  • ICD-10 subtypes: PARANOID- powerful hallucinations & delusions ; HEBEPHRENIC- primarily negative symptoms ; CATATONIC- disturbed movement (immobile or overactive)
• positive symptoms of schizophrenia

  • addition to normal experiences
  • hallucinations: unusual sensory experiences, can relate to any sense, can be related to environment (e.g hearing voices or seeing distorted faces)
  • delusions: paranoia, irrational beliefs, common ones involve historical, political or religious figure (e.g jesus), some are believed to be harassing or persecuting, others believe in an external control or their delusion is part of them, can lead to aggression (aliens, government controlling them)
• negative symptoms of schizophrenia

  • takes away from normal experiences
  • avolition: difficult to keep up with goal-directed activities, ANDREASON identified 3 signs - poor hygiene & grooming, lack of persistence in work or education, lack of energy
  • Speech poverty: reduced quality and amount of speech production (slurring), delayed responses, unclear speech, changes topic mid-sentence
• evaluation of classification in schizophrenia

  (-) co-morbidity: 2+ conditions occur together, common- invalid (could be one condition), BUCKLEY ET AL found 50% depression, 23% OCD, 29% PTSD, challenges classification (one condition) & diagnosis (poor judgement in differences)

  (-) system overlap: same symptoms as bipolar (delusions, avolition), diagnosis differs (ICD & DSM classification)

  (-) gender bias: since 1980s men more diagnosed, could be due to higher genetic vulnerability, women’s higher functioning in relationships & work (COTTON ET AL), under-diagnosis (mask or underestimates)
• Biological explanations for schizophrenia

  • runs in families, argued that shared experiences could be mistaken for full genetic links
  • GOTTESMAN: found 48% risk for MZ twin, 13% for children, 9% for sibling
  • candidate genes: polygenic condition (combination), aetiologically heterogenous (different combinations)
  • RIPKE ET AL: compared genome-wide studies data (whole human genome not specifics), 37,000 diagnosed to 113,000 controls, found 108 variations associated with increased risk (including dopamine- abnormal levels)
• biological explanations for schizophrenia continued

  • dopamine hypothesis: HYPERDOPAMINERGIA in subcortex (excess dopamine receptors in Broca’s area, linked to speech avolition & auditory hallucinations) ; HYPODOPAMINERGIA in cortex (low levels in prefrontal cortex, thinking & decision making, linked to negative symptoms)
  • Neural correlates: measurements of structure or function of brain that correlates with experience (schizophrenia)
• biological explanations for schizophrenia: neural correlations research

  • NEGATIVE SYMPTOM CORRELATIONS: avolition (involves loss of motivation), requires anticipating rewards (linked to ventral striatum), JUCKEL ET AL found lowers levels of activity - reduced levels in ventral striatum is neural correlate of avolition
  • POSITIVE SYMPTOM CORRELATIONS: ALLEN scanned auditory hallucinators’ brains whilst identifying pre-recorded speech as theirs/others, lower activity levels in superior temporal gyrus & anterior cingulate gyrus (made more errors) - reduced activity is neural correlate of A.Hs
• biological explanations for schizophrenia A03

  (-) correlation-causation issue: cant determine whether factors are cause or result of schizophrenia, research isn’t applicable in this sense

  (-) doesn’t consider psychological environment (functioning family)

  (-) mixed evidence on dopamine hypothesis: some antipsychotic drugs show reduction in symptoms in cases, others show worsened effects or bring on schizophrenia symptoms for those undiagnosed, mixed evidence means isn’t reliable as is a different situation for different individuals (not specified how or why, can’t tackle it)
• Psychological explanations for schizophrenia

  • family dysfunction: links to childhood & adult experiences
  • schizophrenogenic mother: FROMM-REICHMANN studied clients about particular parent (means schizophrenia-causing), cold, rejecting, controlling, secrecy & tense family climate, schizophrenic develops paranoia from this distrust (develops into delusions like persecution - schizophrenia)
• psychological explanations for schizophrenia continued

  • double bind theory: BATESON emphasised communication role (fears doing something wrong but doesn’t know what, mixed signals of what’s right, feels like cant confront unfairness of situation, cant seek clarification) ’gets it wrong’ often - punished (withdrawal of love), sees world as jealous & confusing (shows in paranoid delusions)
  • expressed emotions: carer towards schizophrenic, verbal & violent criticism( can be violent), hostility (anger & rejection), emotional over-involvement (needless sacrifice)
• cognitive explanations for schizophrenia

  • role of mental processes: abnormalities provide explanations, e.g reduced processing in ventral striatum - negative symptoms, reduced process of activity in cingulate & temporal gyri - hallucinations (impaired cognitions)
• cognitive explanations: FRITH ET AL’S types of dysfunctional processing

  • METAREPRESENTATION- cognitive ability to reflect thoughts & behaviour, insight owns intentions/goals, interpret actions of others, dysfunction- unable to recognise own actions & thoughts as own, explains hallucinations of voices & delusions (thought insertion- thoughts of others in own mind)
  • CENTRAL CONTROL- suppresses automatic responses while performing deliberate actions, dysfunction- disorganised speech, thought disorder, spontaneous speech when triggered by other thoughts (derailment), cant suppress
• Biological therapies to schizophrenia

  • ANTIPSYCHOTICS:
  • typical- chlorpromazine, smaller doses (average max 400-800mg), any form taken, acts as antagonist (reduces action of neurotransmitter, i.e dopamine), blocks dopamine receptors in synapse to reduce symptoms like hallucinations, also effective sedative
  • atypical: 300-450mg a day, improve effects & minimise side effects, clozapine, does same and also acts on serotonin & glutamate (reduce anxiety & depression, improve mood & cognitive functioning) risperidone (alternative, less Sid effects, binds serotonin & dopamine)
• Biological therapies to schizophrenia A03

  (+) THORNLEY found reduced symptom severity, better functioning & lower relapse rate

  (-) side effects: dizzy, agitation, drowsy, stiff jaw, weight gain, coma, fatal

  (-) atypical drug clozapine can cause a blood condition that results in deaths (agranulocytosis), so requires regular blood testing
• psychological therapies to schizophrenia

  • CBT: identify & challenge irrational thoughts (discuss likelihood), help cope with anxiety (answers & understanding of how hallucinations & delusions effect their behaviour- takes away power of things like voices causing fear)
  • FAMILY THERAPY: improve communication, considers schizophrenogenic mother & double bind, PHAROAH ET AL strategies - form a therapeutic alliance with family, reduce stress of care, improve ability of family to anticipate & solve problems (help), reduced expressed emotions, educate family
• psychological therapies continued

  • TOKEN ECONOMY: reward system, improve avolition traits, for a better life and try get out of institution, token as reinforcement (getting dressed etc.), rewards (operant conditioning & secondary reinforcer as value learned from earning tokens), materialistic or privlieges used as rewards
• psychological therapies to schizophrenia A03

  (-) JAUHAR found small effects in CBT

  (-) helps improve quality of life and make manageable but doesn’t cure (family therapy helps better coping together and CBT helps coping within self)

  (+) proving explanations in CBT can be beneficial for a schizophrenic to understand themselves better
• interactionist approach to schizophrenia

  • range of factors (biological & psychological)
  • factors: biological (genes, neurons), societal (poor interactions, life events, daily hassles)
  • DIATHESIS-STRESS MODEL: biological vulnerability + negative psychological experience (stress trigger) = condition
  • MEEHL: genetic vulnerability leads to schizotypic personality (no schizogene = no amount of Stress could lead to developing condition) but gene accompanied by chronic stress (schizophrenogenic mother) can result in condition
• interactionist approach to schizophrenia continued

  • modern understanding of diathesis: RIPKE- genes (not a singular schizogene) can increase risk slightly, psychological trauma becomes diathesis (predisposed) rather than stressor, READ- found early trauma alters brain development, HPA system overacts making vulnerable to later stress
  • modern understanding of stress: related to nature (particularly parenting), cannabis use x7 risk (interferes with dopamine system)
  • treatment: both- antipsychotics & CBT
• interactionist approach to schizophrenia A03


  (-) original diathesis-stress model over simplified: no ‘schizogene’, multiple stress forms so cant be identifiable to one gene/ no singular source

  (+) evidence supporting diathesis: TIERNARI studied adoptees of Finnish mothers, no genetic risks (control group) tested against those with a genetic risk, tested a specific child-rearing style (criticism severe, conflict, low empathy), genetic vulnerability found to have a higher rate of developing schizophrenia

  (+) considers multiple factors - holistic approach