P3: Schizophrenia Flashcards
Describe the diagnosis and classification of schizophrenia
Schizophrenia: Contact with reality/insights are impaired.(No single defining trait) -For diagnosis:
DSM-5:1 positive symptom must be present
ICD-10: 2 or more negative symptoms must be present
SYMPTONS:
-Positive: Additional experiences beyond ordinary life
1) Hallucinations: Unusual sensory experiences=No basis in reality/distorted perception of things.
2) Delusions: Irrational beliefs=No basis in reality ∴bizarre behaviour but rational to them.
-Negative: Loss of usual abilities/experiences
1) Avolition: Loss of motivation=everyday tasks ∴lowered activity Lvl/unwillingness to do goal-related behaviours
2) Speech Poverty: Reduced frequency/quality of speech. Delays in verbal responses.
DSM=disorganised/incoherence
ISSUES IN DIAGNOSIS
-Reliability: Extent of which diagnosis of schizo=constant
-Validity: Do diagnosis techniques measure schizo
-Co-morbidity: 2 illnesses=confused diagnosis/treatment
-Symptom overlap: 2 or more conditions sharing symptoms ∴ validity of classification questioned
Evaluate diagnosis and classification of schizophrenia
- Diagnosis reliability: Low-inter-rater reliability using different professionals=bias/inconsistency between classifications=over/under diagnosis(bad validity)
(Criterion Validity=Different assessment arrive at same diagnosis) - Gender bias: More men diagnosed VS women ∵genes?Females escape diagnosis ∵better interpersonal functioning ∴bias under-diagnosis=bad ∵same symptoms(both sex)=different diagnosis
- Co-morbidity: 50% of schzio have depression/47% substance abuse. Look similar, maybe=1 condition ∴creating confusing pic=limitation
Describe and Explain The Biological Explanations for Schizophrenia
GENETIC BASIS Schizo runs in family ∵gene similarity -MZ twins= 48% Shared risk, -DZ twins=17%, -Siblings=9% -Polygenetic/Aetidogically heterogeneous (each gene=small risk increasedDifferent combos=schzio). Of 37,000ppl=108 variations associated with risk. Link to dopamine transmitter DOPAMINE HYPOTHESIS (Linked to schizo symptoms) -Hyperdopaminergia(in sub cortex): High DA activity linked to hallucinations/poverty of speech.(Excess DA receptors in Broca's area) -Hyperdopaminergia(in prefrontal cortex):(NEW) Lvls of DA in prefrontal linked to decision making/thinking NEURAL CORRELATES -Measurements of structure/function of brain=correlated to pos/neg symptoms. -Avolition: Low Lvl activity=loss anticipation of reward in Ventral Striatum(Negative correlation) -Hallucinations: Brain scans show. Auditory hallucinations=lower activation Lvl in superior temporal gyrus
Evaluate the Biological Explanations for Schizophrenia
+ Research Evidence(Genetic basis): ppl with schzio history=risk if adopted into families without history of schzio. Not entirely genetic but lots of evidence=gene=vulnerable
- Mixed Evidence(Dopamine Hyp): DA Agonists that increase DA=induce schzio like symptoms in regular ppl. Antipsychotic drugs(lower DA)=reduce symptoms. Other candidate genes found =glutamate (Neurotransmitter) ∴DA hyp= partial explanation
+ Mutation: Schzio occur in absence of family history= Parental age=higher risk.0.7%=under 25. 2%=over 50. ∴genes play big factor
- Interactionist approach: Even identical twin= less than 50% chance of developing ∴environmental factors play a role(childhood) ∴Schizo= combo of bio/psych
Describe the psychological explanations for schizophrenia
FAMILY DYSFUNCTION
-Schizophrenogenic mother: cold/rejecting=family tension= distrust.paranoid delusion/schzio
-Double-Bind Theory: Conflicting family communication (Right/wrong)=unable to express feelings of unfairness of situation ∴ world=confusing/dangerous =disorganised thinking/delusions
-Expressed Emotions(EE): Negative emotions expressed towards schizo.e.g.hostility, verbal criticism
Primary reason for relapse in patients
COGNITIVE EXPLANATION
-Dysfunctional thought process: Lower Lvls of processing in areas of brain.e.g.Ventral Striatum
-Metarepresentation:(Ability to reflect on thoughts /behaviour) ∴unable to recognise own thoughts= Hallucination/delusions
-Dysfunction of central control: Ability to suppress automatic responses while preforming deliberate actions ∴ get derailment(speech poverty) Each word triggers new association which cannot be suppressed
Evaluate the Psychological Explanations for Schizophrenia
- Research Evidence(Family Dysfunction): Little evidence to support. Based on observation ∴Bias. Insult to injury(blaming suffering parents) ∴lack of creditability
- Methodology(Family dysfunction): All retrospective. 69%females/59%males(with Schizo)=history of physical /sexual abuse in childhood. Maybe distorted/memory decay(gather after diagnosis) ∴ issue with validity
- Causation Direction: e.g. does dysfunctional metarepresentation reduce DA Lvls in superior temporal gyrus or direction reversed ∴ Validity Questioned
+ Research support: Schizo mind=functions differently. Stroop Test(e.g.White)=schizo took 2x long to name colour ink. Unsure if its cause/symptom of schizo
Describe the Biological Therapies for Schizophrenia: Drug Therapy
Antipsychotics: Reduce intensity of symptoms(mainly. pos)
TYPICAL ANTIPSYCHOTICS
-Dopamine Antagonists:(Chlorpromazine) Reduce DA by blocking receptors in synapses ∴normalises neurotransmission in key areas of brain ∴ reduces hallucinations. Also has a sedation effect on histamine receptors∴used for anxious patients too
ATYPICAL ANTIPSYCHOTICS (2nd gen)(Clozapine)
-Target DA/serotonin, binds to DA receptors/acts on serotonin/glutamine receptors ∴ reduces depression/anxiety n improves cognition/mood.
IMPORTANT∵ up to 50% of schizo commit suicide.
-Linked to blood condition (Agranulocytosis)=death
SO Risperidone Developed. Binds more strongly/ weaker side effects ∴ smaller dosage needed=better
Evaluate Biological Therapies for Schizophrenia: Drug Therapy
+ Research Evidence: Better than placebos. Chlorpormazine=better functioning/reduced symptoms. Clozapine 30-50% more effective in treatment resistant case ∴ Antipsychotics work decent
- Side effects: Typical= dizziness /agitation /sleepiness /weight gain. Most serious=Neuroleptic malignant syndrome(NMS) ∵ blocking DA in hypothalamus(fatal)
- Reliance on DA hypothesis: Evidence that some ares = too low(prefrontal cortex) ∴DA shouldn’t work ∴ undermined faith= positive effects due to antipsychotics
- Ethics: Chlorpormazine=Sedative ∴used in hospital= easier to work with patients VS benefiting the patients ∴can be seen as abuse of human rights
Describe the 3 Psychological Therapies for Schizophrenia
COGNITIVE BEHAVIOUR THERAPY(CBT)
AIM: Identify/challenge irrational thoughts=help patients understand symptoms ∴realising beliefs aren’t based in reality
FAMILY THERAPY
AIM: Reduce EE in family ∴improving communication /interactions. Via strategies .e.g.
- Reduce stress of caring for relative with schizo
- Improve families ability to anticipate/solve problems
- Reduce guilt/anger in family members
- Improve beliefs/behaviour towards schizo
TOKEN ECONOMIES
AIM: reinforce desirable behaviours(secondary reinforcers)
No value outside of psychiatric ward but can be swapped later for a tangible reward
Evaluate Psychological Therapies for Schizophrenia
- Research Evidence: CBT=significant but small effect. Tokens=1/3 that used random allocation=improvement.
Family therapy= moderated reduction of readmission. Overall inconsistent ∴only modest evidence - Help but not cure: CBT=help make sense. Family therapy= reduced stress of living together. Token=socially acceptable behaviour. BIO therapies=no cure but reduce symptoms ∴more desirable
- Ethics: Tokens= severely ill patients=less privileges ∴discriminated. CBT challenges belief. Might interfere with freedom of thought(modify politics) ∴controversial
- Under-researched: NICE recommend Art therapy if there is an expert available. But not sure how effective this is ∴should under-researched therapies be provided to patients
Describe the Interactionist Approach to schizophrenia
Diathesis-stress model(Vulnerability+stress=schizo)
MEEHL’S MODEL (OG DIATHESIS-STRESS MODEL)
Schizo Gene+stress=schizo ∴ no gene=cannot get schizo /Just gene+no stress=no schizo
MODERN UNDERSTANDING OF DIATHESIS
Polygenetic/aetiologically hetrogeneous
Doesn’t have to be genetic. Can be early childhood trauma affecting brain development.e.g.Child abuse affects hypothalamic-pituitary-adrenal(HPA) system ∴more vulnerable to stress
MODERN UNDERSTANDING OF STRESS
Anything that risks triggering Schizophrenia.e.g. Weed=7x increased risk(depending on dosage) ∵interfere with DA system
TREATMENT ACCORDING TO INTERACTIONIST
Antipsychotics Medication + CBT
UK more interactionist VS US ∴standard in UK for interactionist VS US= conflict between models ∴slower adoption of interactionist approach
Evaluate the Interactionist Approach to Schizophrenia
+ Research Evidence: Studied parenting styles of kids adopted away from schizo mums=hight conflict/
criticism/low empathy= schizo for high risk kids ∴supports Diathesis-stress model
- Simplistic: OLD=multiple genes=bigger risk, stress= many forms.e.g.dysfunctional parenting.NEW=Stress can include Bio factors.e.g.childhood trauma=diathesis, cannabis= trigger ∴OLD=Bio=vulnerability/Psych=trigger is too simplistic
+ IRL application: Random allocated groups.1)Medication+CBT,2)Medication+Counselling group,3)Control(Medication). 1/2=lower symptoms VS control but no difference in hospital readmissions ∴Practical advantage to Interactionist approach
