SCHIZOPHRENIA - Explanations for causes of schizophrenia
- Created by: EmilyEther
- Created on: 21-11-18 14:34
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- Explanations for causes of schizophrenia
- Biological
- Genetics
- def: transmission of abnormality by hereditary means
- sch is p***ed on genetically - hereditary condition
- gene mapping: study into genetic material among sufferers - recent knowledge about human genomes
- not completely understood
- certain genes / variations / mutations of genes which are involved with sch
- no one particular gene causes sch: combination of genes
- Types of studies
- Family studies
- look at young children/adults with sch - look at their parents or siblings (maybe grandparents) and see what level of sch they had
- concordance rates (matching rates) between person with sch and parents
- high concordance rate: more likely you have child with sch with parents who have sch. High con.rates in family members
- the more closely genetically related they are, the higher the concordance rate will be (parents over grandparents, for example)
- Gottesman (1991) - children with 2 sch parents had con.rate of 46%, children with 1 sch parents - con.rate of 13%, siblings (bro or sis) - 9%
- Evaluation of family studies
- family members have same environment - growing up with 2 sch parents will make you more sch (NATURE NOT NURTURE)
- Twin studies
- monozygotic (MZ) - identical and dyzigotic (DZ) - non-identical
- testing concordance rate between two pairs of twins. Should by 100%
- difference: MZ should be higher con.rate bc they are genetically identical
- Joseph (2004) - meta-analysis of sch twin studies after 2001: con.rate for MZ twins = 40.4% and 7.4% for DZ
- Evaluation
- very rare to have 100% con.rate for MZ twins (Joseph found 40.4%)
- some studies use blind diagnosis - researchers don't know if they are testing MZ or DZ twins - those studies have found lower con.rate
- MZ twins will be treated in the same way (environment) - higher con.rate bc of this, not bc of the genetic similarity
- Adoption studies
- use people who are genetically similar - bros and sis but have been raised separately - adopted by diff families
- sometimes they use twins - difficult to find
- if shows people raised differently but are genetically similar - shows that it is the genetics not the environment that caused sch
- adoption studies arguably better than twin and family studies
- Tienari (2000) - Finland, 164 adoptees whose biological mums had be diagnosed with sch, 11 (6.7%) had been diag with sch, compared to 4 (2%) of the 197 control adoptees (born to non-sch mums)
- Evaluation
- adopted children could be placed selectively - Denmark/US - parents are informed about the genetic background. If they know it - who would want to adopt them? They will then go into similar environments
- very small sample sizes - difficult to make generalisations and representativeness, some people may be distant relatives (half-siblings etc.)
- Gene-mapping
- DNA of 40,000 schs, and 113,000 non-schs. Identified 128 genetic variations and 108 locations on the human chromosomes the contribute mostly to developing sch
- difficult to criticise - scientific methods
- Gurling (2006) - gene mapping family study. Identified PCM1 gene which made people more vulnerable to sch
- Family studies
- Dopamine hypothesis
- def: the development of sch is related to abnormal levels of the hormone and neurotransmitter dopamine
- additional excess of the drug in the brain
- dopamine increases the rate of communication between neurotransmitters across the synaptic gap
- Snyder (1976) - most connected to the positive symps, eg hallucinations, delusions etc
- schs have more D2 receptors on receiving neurons
- more dopamine sticks to neurons - more neurons are fired and messages p***ed on
- too many messages and stimulus in the brain
- more dopamine sticks to neurons - more neurons are fired and messages p***ed on
- Evidence used to come up dopamine hypothesis
- Anti psychotic drugs
- reduce dopamine activity in the brain
- proven to be fairly effective
- Dopamine antagonist drugs
- Drug: L-Dopa
- used to treat Huntingtons disease
- dopamine agonist (increases impact of dopamine in brain - creates sch)
- schizophrenic side effects
- Amphetamines
- eg. speed (recreational drugs)
- dopamine agonist
- Davis (1991) - updated Snyder's theory - high levels of dopamine are not found in sch, and drug clozapine (dopamine-blocking drug) works well
- Davis suggested: high levels of dopamine in mesolimbic dopmine system (***. with positive symps)
- high levels in the mesocortical dopmaine system are ***. with negative symptoms
- neuortransmitter glutamate involved: reduced function of the NMDA glutamate receptor in sch. Dopamine receptors reduce release of gluatmate
- Anti psychotic drugs
- Patel (2010) - PET scans to ***ess dopamine levels in sch and normal individs. Lower levels of dopamine in dorsolateral prefrontal cortex of sch individs than normal controls
- Wang & Deutch (2008) - induced dopamine depletion in the prefrontal cortex in rats. Resulted in cognitive impairment (memory deficit) that researchers able to reverse using olanzapine (atypical antipsychotic drug - has beneficial effects of neg symps in people)
- Leucht (2013) - meta-analysis of 212 studies that analysed the effectiveness of diff anti psychotic drugs compared with placebo. All tested drugs were significantly more effective than placebo in treatment of pos and neg symps
- Moncrieff (2009) - evidence is not conclusive. Although some drugs have been shown to induce sch episodes. but are known to effect other neurotransmitters.
- points out that other sources of dopamine release have not been considered - stress / smoking etc. Suggests current evidence doesn't support dopamine hypothesis
- evidence in post-mortem brain tissue has either been negative or inconclusive
- Noll (2009) -
- NOT ON SYLLABUS - Neural correlates (neuro-anatomical)
- problems with the brain structure
- eg enlarged ventricles (gaps in the brain filled with fluid) - common among sch sufferers
- some schs have large ventricles, some don't - no consistent evidence
- problems with the brain structure
- Genetics
- Psychological
- Family dysfunction
- too much expressed emotion (EE)
- family communication style of expressing (hostile / critical) emotion to each other
- can help to cause initial sch
- once someone is sch, it can lead to higher relapse rates
- if someone in family is sch, they will treat you differently
- suggests people with sch have lower tolerance for intense environmental stimuli
- Kuipers (1983) - high EE relatives talk more and listen less
- double bind theory
- suggested by Bateson (1956)
- contradictory messages from parents
- affects child badly - confusing, don't know how to express and show emotions themselves
- develops into affective flattening and withdrawal
- R.D.Laing - sch is a reasonable response to an insane world
- case study of sch girl 'Jane' - when Laing first met her - emotionally flat and she had reoccurring fantasy - she saw herself as a tennis ball involved in a game of mixed doubles
- Laing discovered parents' relationship was awful but still living together. Dad's mother used to get involved. Mum's father used to get involved - mixed doubles
- Laing also found in past, Jane used to be a go-between (go tell your mum this etc.)
- too much expressed emotion (EE)
- Cognitive
- includes dysfunctional thought processing (part of general cognitive approach)
- maladaptive (irrational) thought processes cause sch
- faulty thought processing (wrongful interpretation)
- problems with meta-cognition
- def: when an individ is thinking about their thinking
- healthy person can think about how our thinking can affect out thinking and behavs
- sch people have problems with their met-cognition
- problems with our executive functioning
- healthy person = efficient ex.funct
- cognitive processes that control and manage other cognitive and behavioural processes
- cognitive explanations of delusions
- degree to which an individ perceives him or herself as the central component in events
- sch tendency to relate irrelevant events to themselves
- muffled voices criticise them, flashing light is from God
- degree to which an individ perceives him or herself as the central component in events
- cognitive explanations for hallucinations
- hallucinating individs focus excessive attention on auditory stimuli
- Aleman (2001) - hallucination-prone individs find distinguishing between imagery and sensory-based perception
- Baker and Morrison (1998) - hallucinating patients with sch are more likely to misattribute the source of self-generated auditory
- Research
- O'Carroll (2000) - 75% cognitive impairment of schs - particularly memory, attention, motor skills, executive function and intelligence.
- Elevag & Goldberg (2000) - sch is better characterised by cognitive deficits rather than symps. Memory and attention are the main cognitive deficits.
- Knoblich (2004) - schs are impaired in their ability to detect mismatch between self-generated movement and their consequences when drawing. Suggests cognitive inability to self-monitor
- Bowie & Harvey (2006) - cognitive impairments are core feature of sch: impact memory, attention, verbal learning and executive functions. Impairments pre-date disorder
- Takahashi (2013) - compared electrical brain activity of sch when exposed to auditory tones. Ability to detect changes in tone was limited.
- Evaluation (A03)
- Cognitive theories don't explain the cognitive impairments -> can't been seen as explaining causes for sch
- explanation can account for positive and negative symptoms
- theory can be combines with other theories (biological)
- Sarin & Wallin - found supporting evidence of claim that positive symptoms have origin of faulty cognition
- high success rate of cognitive based therapies (CBT)
- Howes & Murray - early vulnerability factors (genes etc.) combined with social stressors causes an increase in dopamine.
- Family dysfunction
- Interactionist (diathesis stress model)
- certain genes would make someone vulnerable to sch - but not necessarily develop it
- will develop sch with an environmental trigger (typically a stressor)
- certain genes would make someone vulnerable to sch - but not necessarily develop it
- Biological
- A01
- A03
- Evidence (studies)
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