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Two diagnostic materials used for schizophrenia
DSM
ICD-10
Positive symptoms of schizophrenia
Excess of normal functions → pathological excess or distortion = add to person’s personality
Delusions
Hallucinations
Positive symptoms of schizophrenia: delusions
Irrational false beliefs
Remain unchanged even when individual is presented with conflicting evidence
Completely disconnected from reality → often appears bizarre to others
Positive symptoms of schizophrenia: hallucinations
Sensory perceptions → occur in absence of external stimulus
Vivid + involuntary + perceived as being located in external space (rather than in individual’s imagination)
Can happen in any of the senses = any modality
Negative symptoms of schizophrenia
Loss of normal functions → often persist more + more resistant to traditional antipsychotic treatments
Avolition
Speech poverty
Negative symptoms of schizophrenia: avolition
Total lack of motivation to initiate + persist in self-directed + purposeful activities = apathy
Signs of avolition = Andreasen identified clear indicators ~ failure to maintain personal hygiene, lack of persistence in work or school
Negative symptoms of schizophrenia: speech poverty
Alogia
Significant reduction in amount or fluency of speech
Reflects disruption in thought process rather than physical inability to speak
Comorbidity
Occurrence of two or more distinct clinical conditions in single patient
Schizophrenia rarely exists in isolation = complicates “descriptive validity” of disorder
Schizophrenia comorbidity: Buckley et al
A → quantify prevalence of comorbid psychiatric conditions in schizophrenic patients
P → review clinical data from patients diagnosed with schizophrenia
F → 50% = comorbid depression, 47% = substance abuse, 29% = PTSD, 23% = OCD
C → high comorbidity = suggests scz may not be distinct category → may lead to inconsistent diagnosis + inefficient treatment
Schizophrenia comorbidity: AO3
Reduces validity in diagnosing + treating schizophrenia → due to overlapping symptoms
Bias in scz diagnosis: gender bias
Men : women scz diagnosis = 4:1
Diagnostic criteria = applied inconsistently between men vs women → often leads to under-diagnosis in females
Suggests validity of diagnosis of scz = poor
Gender bias in diagnosis: Loring and Powell
A → test if patient’s gender influences psychiatrist’s diagnosis
P → 290 psychiatrists evaluated identical case studies → only gender was changed
F → patient labelled male = 56% diagnosed scz vs patient labelled female = 20% diagnosed scz
C → women = under-diagnosed → often maintain higher interpersonal functioning = masks severity of symptoms to clinicians
Bias in scz diagnosis: culture bias
Misinterpretation of cultural norms as scz symptoms
Assuming British cultural standards are ‘correct’
Afro-Caribbean descent = 7 times more likely to be diagnosed vs white citizens ~ Cochrane (in Britain)
Western clinicians → label “hearing voices” = hallucination
Spiritual norm in some African cultures
Leads to unfair institutionalisation of minority groups
Symptom overlap
Different disorders share identical clinical features.
Patients could be diagnosed with multiple conditions simultaneously → depends on which symptoms clinician prioritises
Ambiguity = results in misdiagnosis + delays in appropriate pharmacological intervention
Symptom overlap: Cheniaux et al
A → investigate reliability + validity of scz diagnosis
P → two psychiatrists independently assessed 100 patients → using DSM + ICD-10
F → diagnosed 26 with scz using DSM + 44 using ICD vs diagnosed 13 with DSM + 24 with ICD
C → lower inter-rater reliability is low
Biological approach to schizophrenia
Asserts scz = physical illness
Focuses on:
Genes
Dopamine
Brain structure
Biological approach to schizophrenia: genetic correlates
Polygenic = many genes contribute → no single gene responsible
Large number of genes = ones that affect dopamine neurotransmitter production
Aetiologically heterogeneous = different genetic combinations can produce same symptoms
Ripke → found 108 separate genetic variations associated with scz
Biological approach to schizophrenia: genetic explanations → twin studies
Gottesman → mz twins = 48% concordance rate vs dz twins = 17% concordance rate
Indicates genetic factor involved → not purely biological
MZ twins = 100% same genetic data + similar environment
DZ twins = ~50% same genetic data + similar environment
Difference between concordance rate should be entirely due to genetic factors → not demonstrated in this study
Biological approach to schizophrenia: genetic explanations → adoption study
Tienari → Finnish adoption study = longitudinal study with 19000 ppts
Two groups of adopted children → schizophrenic bio mother vs non scz bio mother
Studied whether genetics or environment influence scz
Scz bio mother = 7% developed scz
Non scz bio mother = 1.5% developed scz
Supports genetic influence → but evident other factors are involved
Supports stress-diathesis model
Biological approach to schizophrenia: dopamine hypothesis
Imbalance of neurotransmitter of dopamine → drives symptoms of scz
Hyperdopaminergia (excess) → especially in subcortex + Broca’s area
Linked to positive symptoms ~ auditory hallucinations → over-active neurons
Hypodopaminergia (deficit) → especially in prefrontal cortex
Linked to negative symptoms ~ avolition
Biological approach to schizophrenia: dopamine hypothesis → empirical validation
Curran et al
A → observe effects of dopamine agonists on scz symptoms
P → amphetamines (inc dopamine levels) administered to scz + control group
F → induced psychotic symptoms in healthy controls + significantly increased existing symptoms in scz patients
C → indicate elevated dopamine levels = physiological trigger for scz
Biological approach to schizophrenia: neural correlates
Patterns of structures + activity in brain associated with scz experience
Ventricle enlargement
Ventricles = fluid-filled cavities in brain
Research has consistently shown → scz patients often have significantly larger ventricles vs healthy controls
Suggests that the surrounding brain tissue has shrunk or failed to develop, particularly in the pre-frontal cortex.
Regional activation + symptoms
Ventral striatum = one of main reward centres → anticipation of reward
Juckel measured activity levels here → lower levels of activity in scz
Avolition
Auditory hallucinations → Allen et al found lower activation levels in superior temporal gyrus during hallucinatory episodes.
Speech poverty → reduced activity in Wernicke’s area (speech comprehension) is negatively correlated with the severity of thought disorders
Biological approach to schizophrenia: AO3
+ Scientific credibility → empirical + reliable + replicable methods
- Issue of causation ~ brain scans show enlarged ventricles → causing scz or caused by scz?
- Environmental influence → mz twins only have a 48% concordance rate = scz is not solely biological ~ environmental factors interact + trigger the vulnerability to scz
- Reductionist → ignores cognitive factors in the explanation of scz
Biological treatments: drug therapy
Antipsychotics = drugs that reduce psychotic symptoms ~ hallucinations
Biological treatments: drug therapy → typical psychotics
Primary treatment for scz → introduced 1950s
Chlorpromazine
Dopamine antagonists → block dopamine receptors in brain
Targets D2 receptors in mesolimbic pathway (reward + sensory)
Drastically reduces psychotic symptoms ~ hallucinations
Influence histamine receptors → secondary interaction = used to calm highly anxious + aggressive patients
Side effects:
Increased heart rate
Tardive dyskinesia = involuntary facial movements
Biological treatments: drug therapy → atypical psychotics
Secondary/modern → introduced 70s then 90s
Clozapine + risperidone
Clozapine = comorbid depression → reduces suicidal tendencies up to 80% (30-50% scz attempt suicide)
Risperidone = higher affinity → as useful in lower doses
Bind to dopamine receptors + modulate serotonin
Block dopamine + increase serotonin
Clozapine = glutamate agonist → increases
Glutamate = brain’s primary excitatory neurotransmitter → responsible for 90%+ of excitatory signalling + essential for learning + memory + normal neural communication
Side effects
Weight gain
Clozapine → agranulocytosis = autoimmune condition affecting WBC → fatal seizure risk
Biological treatments: drug therapy → Bagnall study
A → compare efficiency + tolerability of atypical vs typical antipsychotics
P → systematic review of 232 studies involving various drug trials
F → atypical = more effective overall + lower patient attrition rates
C → atypical = more sustainable + effective treatment path
Psychological explanations to schizophrenia: cognitive explanations
Focuses on role of IMP
Dysfunctional thought processing:
Metarepresentation
Central control
Psychological explanations to schizophrenia: cognitive explanations → metarepresentation
Cognitive ability to reflect on thoughts + behaviours + identify them as internal
Dysfunction:
Disrupt ability to recognise own thoughts + actions
Thought insertion = belief thoughts are being projected into the mind by others
Psychological explanations to schizophrenia: cognitive explanations → central control
Ability to suppress automatic responses while performing deliberate actions instead
Dysfunction:
Cannot stop tangential thoughts from intruding into speech = word salad or derailment
Disorganised speech + thought disorder = inability to suppress automatic thoughts
Psychological explanations to schizophrenia: cognitive explanations → Stirling study
Stirling et al
A → investigate central control in scz ppts
P → 30 scz ppts vs 18 non-scz ppts did range of cognitive tasks ~ stroop test
F → scz ppts took 2x to name ink colour + supress impulse of reading words
C → supports central control as proximate correlation in scz
C → does not provide evidence central control is cause
Psychological explanations to schizophrenia: cognitive explanations →
Psychological explanations to schizophrenia: family dysfunction
Social stressor
Maladaptive patterns of communication
High levels of interpersonal conflict within home
Primary environmental triggers → in combination with underlying genetic vulnerability
Psychological explanations to schizophrenia: family dysfunction → schizophrenogenic mother
Fromm-Reichmann
Schizophrenogenic mother → primary cause of paranoid delusions
Schizophrenogenic mother = simultaneously cold + rejecting + overly controlling
Creates climate of secrecy + tension → leads to profound distrust in developing child
Child eventually breaks from reality → develops into paranoid delusion + schizophrenia
Marital schism = psychological disturbance due to marital problems
Psychological explanations to schizophrenia: family dysfunction → double bind theory
Bateson
Explain disorganised thinking
Social withdrawal
Double bind = communication paradox → person receives two or more conflicting messages
Verbally convey one message + non-verbally conveys opposite message
Child cannot solve contradiction + fear punishment either way = become confused + lose grip on reality
Psychological explanations to schizophrenia: family dysfunction → expressed emotion (EE)
Psychological explanations to schizophrenia: family dysfunction → expressed emotion (EE) study
Vaughn and Leff
Expressed emotion = measure of level of negative emotion directed toward patient by caregivers
Three main elements → verbal criticism + hostility & rejection + emotional over-involvement
Psychological explanations to schizophrenia: family dysfunction → Read et al
Read et al
Reviewed 46 studies of child abuse + scz
69% of in-patients diagnosed with scz → had a history of abuse
Psychological explanations to schizophrenia: family dysfunction → Tienari
Psychological
Interactionist approach to schizophrenia
Combines biological + psychological + environmental factors → explain + treat schizophrenia
Holistic
Interactionist approach to schizophrenia: limitations of single explanations
Biological → ~ half of MZ twins = discordant
Share genes yet not both have schizophrenia
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Interactionist approach to schizophrenia: diathesis-stress model
Inherit a vulnerability to scz ~ genetic risk, biological predisposition = diathesis
Combined with environmental stressors = develop disorder → pushes person past the threshold
Environmental stressor ~ drug use + family conflict + traumatic life event
Explains why MZ do not have a 100% concordance rate
Interactionist approach to schizophrenia: diathesis-stress model → Meehl
Meehl’s model → original diathesis-stress model
Diathesis = entirely genetic → result of single ‘schizogene’
Meehl suggested no schizogene = no scz → even despite chronic stress
Have schizogene + chronic stress in childhood ~ schizophrenogenic mother = develop scz
Interactionist approach to schizophrenia: diathesis-stress model → modern understanding
No single ‘schizogene’ → range of biological factors + genetic predispositions
Modern view of diathesis → also includes factors beyond genetic ~ psychological trauma
Read → proposed neurodevelopmental model
Early trauma alters developing brain
Early + severe trauma ~ child abuse = seriously affect many aspects of brain development
Hypothalamic-pituitary-adrenal (HPA) → become over active = increases vulnerability to stress
Interactionist approach to schizophrenia: diathesis-stress model → Tienari
Interactionist approach to schizophrenia: modern understanding of stress
Original diathesis-stress model → stress = psychological in nature ~ stress resulting from parenting
Modern definition of stress = anything that risks triggering schizophrenia → Houston
Cannabis as a stressor → increases risk of scz up to x7
Interferes with dopamine system
Interactionist approach to schizophrenia: treating scz
Combining antipsychotic medication + psychological therapies → CBT
Turkington → points out belief in biological causes of scz can co-exist with use of CBT to relieve psychological symptoms