Schizophrenia 3 Flashcards
Diagnosis and classification A01
*more common in men, city dwellers and lower socio-economic groups
*medical approach for classification- identity symptoms that go together= disorder. Diagnosis- identify symptoms and use classification system to identify disorder
*ICD-10 (two negative ) and DSM-5 (one positive, USA) major system for classification
Positive and negative symptoms
*positive: additional symptoms beyond normal experience including hallucinations (unusual sensory experiences, distortion of reality) and delusions (beliefs not based on reality, bizarre behaviour)
*negative: loss of usual abilities including speech poverty (reduced amount and poor quality speech, disorganised) and avolition (loss of motivation, low activity)
Issues in classification and diagnosis A03
*good reliability, DSM-5 reliability has improved- Osorio inter rated reliability=+.97, test retest reliability +.92
*low validity: Cheniaux had 2 psychiatrists independently assess100 clients ,68 diagnosed with SZ using ICD-10 and 39 with DSM-5, low criterion validity either over or under diagnosed
*co-morbidity, Buckley: around half of clients have another diagnosis eg depression or substance abuse
*gender bias, 1980s more men diagnosed than women so there is a bias with women under diagnosis due to support for, closer relationships and better functioning
*culture bias, African Caribbean 9x more likely to be diagnosed than white British as misinterpreted by white clinicians eg hearing voice in hatit is communication with ancestors, discrimination by culturally bias systems
*symptom overlap, both bipolar and SZ include delusions and avolition so may be variation of single condition hard to distinguish from bipolar, may not be distinct condition & hard to diagnosis
Genetic basis of schizophrenia
*Gottesman found in large scale family study that a relative with SZ increases chances eg aunt =2%, 9%= sibling and 48% if identical twin, share environment so correlation represents both but good genetic basis
*candidate gene: SZ is polygenic mostly likely for genes coding neurotransmitters eg dopamine, Ripke combined data from genome-wide studies of 37,000 with diagnosis compared to control found 108 separate variations that increase risk, also aetiologically heterogeneous (different combinations of factors)
*mutation: parental gene can be mutated by radiation, poison or viral infection, evidence from positive correlation between paternal age and risk of SZ increasing around 0,7% under 25 fathers and 2% in over 50
Genetic basis A03
*research support, strong evidence base Gottesman-increase risk with genetic similarity, Tienari-biological parents with SZ increase risk even in different environments, Hilker-concordance rate for 33% for MZ and 7% for DZ, ppl more vulnerable to SZ because of genetic make up
*environmental factors also increase risk, biological = brith complications and smoking THC rich cannabis in teens, psychological= childhood trauma, Morkved: 67% of SZ ppl and psychotic disorder have at least one childhood trauma compared to 38%, partial explanation
*generic counselling can advise parents of genetic risk but risk estimate is average figure and environmental risk unknown
Neural correlates A01
original dopamine:drugs to treat SZ caused symptoms like Parkinson disease (low DA levels) so SZ is result of high DA in subcortical areas eg excess of DA receptors in subcortex to Broca’s area explains speech poverty
Updated: Davis said high DA in subcortex and low DA in cortex explains negative symptoms, cortical hypoDA lead to subcortical hyperDA, DA levels affected by both genetic vulnerability, childhood and adolescence stress
Neural correlates A03
*Evidence that DA is involved in SZ, 1. amphetamines increases DA and worsens symptoms can induce symptoms in people (Curran), 2. antipsychotic drugs reduce DA activity and reduce intensity of symptoms, 3. candidate genes acts on production of DA and DA receptors, DA is involved
*evidence for central role of glutamate, post-mortem and live scanning found raised levels of glutamate in regions of brain in SZ people, candidate genes involved in glutamate production/processing, strong case
*Tenn induced SZ like symptoms in rats using amphetamine and relived using drugs that reduce DA however other drugs that decrease DA did not cause SZ, amphetamine psychosis closely mimics SZ
Psychological explanations: Family dysfunction
*Fromm-Reichmann said psychodynamic explanation where patients had cold, rejecting and controlling SZ mother (causing SZ) creating a tension and secretive family climate that leads to paranoid delusions and SZ
*double-bind:Bateson empathised role of communication where child fears doing wrong but receives mixed msgs & unable to comment on fairness/ clarification, punished for wrong by less love so understands world as confusing+dangerous = disorganised thinking and paranoid delusions, risk factor not only cause
*expressed emotions: negative emotions to SZ persons including verbal criticism (violence too), hostility (anger and rejection) and emotional involvement in life (needless self sacrifice), sources of stress explains relapses but stress may also trigger SZ in vulnerable person (genetic make up)
Family dysfunction A03
*research support, Read said SZ adults are disproportionately likely to have insecure attachment, 69% of women and 59% of SZ men have history of sexual/ physical abuse, Morkved adults reported 1 childhood trauma
*explanations lack support, evidence for association of childhood family stress and SZ but none to support importance of SZ mother and double bind, based on clinical observations of SZ people and informal assessments of personality not systematic, can’t account for link of trauma and SZ
*Parent blaming, socially sensitive especially for mothers, has to watch symptoms and be blamed
Cognitive explanations A01
*dysfunctional thinking: reduced thought processing in ventral striatum=negative, reduced thought in temporal and cingulate gyri= hallucinations
Frith: 2 kinds of dysfunctional thoughts
1. Metarepresentation- ability to reflect own thoughts, cannot recognise own thoughts, explains hallucination of hearing voices and delusions like thought insertion
2. Central control dysfunction- cognitive ability to suppress automatic responses while performing deliberate actions triggers other thoughts and leads to speech poverty and derailment of thought
Cognitive explanations A03
*research support, Stirling 30 SZ ppts took twice as long on stroop test than 30 control as cannot suppress tendency to read worlds aloud, evidence for dysfunctional thought processing, impaired
*proximal explanation, explains what is happening now to produce symptoms not what caused condition (distal explanation, may be genetic), partial explanations
*psychological or biological
Biological therapy for Schizophrenia A01
*typical antipsychotics: chlorpromazine, orally=1000mg daily, dosages usually smaller up to 400-800mg max
Dopamine antagonists: block dopamine receptors to reduce symptoms
Sedation effect: affects histamine receptors, not fully understood, calming effect, syrup
*atypical: 1970’s, improve effectiveness in suppressing symptoms and minimise side effects
Clozapine:risk of fatal agranulocytosis, more effective than typical so used when other treatments fails w/ regular blood tests, fatal side effects so 300-450mg/day, binds to dopamine receptors but also acts on serotonin+glutamate, improves mood+cognitive, reduce depression, avoids suicides (30-50% of SZ attempt)
Risperidone: recent, effective with less side effects, 4-8mg daily max12mg, same function as clozapine but stronger so effective in smaller dosages, some evidence for less side effects
Biological therapy for Schizophrenia A03
*effectiveness, Thornley found chlorpromazine had better functioning, less symptoms compared to control of data from 13 trials, Meltzer found clozapine is 30-50% more effective than typical failure cases, works
Counter: Healy, flawed evidence, short term effects, calming effects easy to show positive effects, severity?
*Side effects, dizziness&weight, LT=tardive dyskinesia, neuroleptic malignant syndrome(0.1-2%) less DA in hypothalamus(regulation of body systems) causes coma, can do harm and good
*mechanism unclear, tied w/ dopamine hypothesis but this is not full explanation for SZ, some parts too low so drugs shouldn’t work, question on effectiveness adds to them being ineffective, other factors in success
Psychological therapy for schizophrenia: Cognitive behaviour therapy A01
*therapist helps client make sense of how irrational cognitions (symptoms) impact behaviour and feelings eg understand origin of voices is not demonic but a malfunctioning speech centre in brain
*doesn’t eliminate symptoms but help cope reducing distress and improve ability to function adequately
*normalisation reduces anxiety, voice hearing is extension of ordinary experience of thinking in words
*reality testing to challenge delusion, likelihood of beliefs being true
*Turkington: Mafia example
Psychological therapy for schizophrenia: Cognitive behaviour therapy A03
*effectiveness, Jahuhar found from 34 studies of CBT treatment that there is clear evidence for small but significant effects of positive and negative symptoms, Pontillo=less frequent auditory hallucinations, NICE
*quality of evidence, Thomas: studies involved different CBT techniques, people with negative & positive symptoms, benefits conceal wide variety of different techniques and symptoms, hard to say it’s effective
*it doesn’t cure them, improve quality but is a biological condition
