schizophrenia Flashcards
features
1 in 100 affected onset 15-25 years old unlikely to occur in childhood more prevalent in men 1 in 4 attempts suicide with 10% dying
difference between positive symptoms and negative symptoms
positive symptoms add to the experience and negative symptoms take away from normal behaviour
positive symptoms (4)
Hallucinations = perceptual disturbances, seeing or hearing things that aren’t there (auditory)
Delusions = disturbances of thought including false beliefs
Thought or language disorder = speech difficult to follow, thought insertion, disorganised and incomprehensible speech
abnormal motor behaviours = disorganised behaviour that can affect daily life
- catatonia = fall in responsiveness to environment
- echopraxia = involuntary echoing of an observed persons movements of speech
types of delusions
paranoid delusions
- belief you are being persecuted or conspired against
delusions of grandeur
- believe you are famous or very important
referential delusions
- belief that language or behaviour of others is directed at them
negative symptoms
- lack of energy and apathy
- social withdrawal
- lack of emotion
- avolition
- not looking after self
evaluate negative symptoms
many people show evidence of negative symptoms without positive does not mean they are schizophrenic
why are negative symptoms different to positive
negative are tougher to treat and often start before positive symptoms (predromal period)
types of schizophrenia
- paranoid: delusions and hallucinations
- disorganised: disorganised speech and moods
- catatonic: withdrawn, isolated, little physical movement
- residual: few positive and some psychotic symptoms
- undifferentiated: person doesn’t fit any other types
schizoaffective disorder: not schizo but schizo mood and symptoms
neurotransmitter theory explanation
- D2 receptors are responsible for how we react to dopamine
- schizophrenics overreact as they tend to have hypersensitive dopamine receptors
- D2 receptors have greater affinity to dopamine meaning they are more likely to bind to neurotransmitters when present in the synapse
neurotransmitter theory supporting evidence
randrup and munkvad 1966 - injected rats with amphetamines which increases dopamine in brain and rats were more aggressive and isolated
lieberman et al 1975 - 75% of schizophrenics showed increased or new symptoms when using amphetamines or methylphenidate
brown and birley 1968 - 50% of patients reported a major life event 3 weeks prior to relapse (social factors)
owen et al 1978 - post mortum studies found overwhelming increase in density levels of dopamine receptors in cerebral cortex. This demonstrates that they may be hypersensitive to dopamine levels
amphetamines
groups of drugs that increase activity of certain chemicals in the brain
evaluation for neurotransmitter theory
SE- drugs phenothiazine blocks dopamine receptors and alleviates schizo symptoms as less dopamine is taking up
EV - drugs block dopamine receptors almost immediately but any calming effect is not seen until several days after. Suggests that other causes and hypothesis is highly reductionistic
SE - amphetamines can cause excess dopamine resulting in symptoms of psychosis (similar to + symptoms) suggests that dopamine is linked to schizophrenia
EV - amphetamines only produce positive and fails to take into account negative so dopamine hypothesis is not a sufficient explanation
SE - scanning shows when those with schizophrenia are given amphetamines there is a greater release of dopamine than non schizo. Suggests that those with schizo are more sensitive to dopamine and tend to overreact
CE - social and environmental factors also involved. Stressful event can cause excess dopamine and trigger schizoz Brown and Birley 1968. There is a link between social class and schizophrenia but correlation does not equal causation
conclusion for neurotransmitter theory
these factors suggest the holistic explanation for schizophrenia may be far more complex and multi-faceted than suggesting it is only down to neurotransmitter functioning and sensitivity
genetic explanation for schizophrenia
heritability factors are significant in development of schizophrenia. Those with family members who have schizophrenia may have a stronger predisposition to also developing it
Gottesman and shields 1966 - twin studies to determine concordance rates, population has less than 1% likelihood
MZ = 48%
1st degree relative = 6-17%
2nd degree relative - 2-6%
diathesis stress model
- genetic factors mean someone may have a high vulnerability but environmental trigger is required to activate it
Tienari et al 2002 - 7% adoptees who had biological mother with schizophrenia also developed the disorder. 2% of adoptees with schizophrenia whose mother not diagnosed
genetic explanation evaluation
SE - Gottesman and Shield 1966
EV - MZ twins have 100% DNA so should have 100% concordance rate so other factors must (reductionistic)
CE - diathesis stress model (Brown and Birley 1968)
EV - difficult to separate out influence of nature vs. nurture
social causation hypothesis
= higher rate of schizophrenia in lower classes
1% rate of schizophrenia in general population
4% concordance rate = white low social class and immigrant groups
(unemployed and living in deprived areas more at risk and tend to have different course and different treatment)
60s SCH suggested social class was the cause now other factors such as stress are included
Hjem et al 2004 - social adversity in childhood linked with developing schizophrenia later in life
Cooper 2005 - social class 5, unskilled labourer = 4.1x likely social class 1, higher managerial = less likely afro caribbean and black immigrants 4x likely as they are disadvantaged in education, housing, social class and discrimination
Veiling et al 2008 - immigrants in areas where there own ethnicity did not dominate = higher incidence of psychotic disorder
social causation hypothesis evaluation
strengths
- diathesis stress model - good face validity for SCH
- SE from studies
weakness
- social drift hypothesis = schizophrenia causes people to drift down social classes
- too many factors to isolate
family therapy A01 and A03
A01
aims to provide SUPPORT NETWORK for patient and help develop a COLLABORATIVE RELATIONSHIP. enables patient to OPENLY TALK about symptoms and patient becomes EXPERT ON SCHIZOPHRENIA. e.g. explain how it feels to experience hallucinations so family can be supportive
Goldstein and miklowitz 1995 - family intervention effective when takes place alongside drug therapy. reduction in relapse rates
A03
- not a treatment and will not cure the disorder, just to help families cope and create manageable environment
- research shows FT reduces relapse rate when used alongside medication
- relies on whole family to be mentally/ cognitively involved
drug therapy
typical - old 1950s
- first antipsychotics developed
- fluphenazine
- unpleasant side effect; muscle spasms and tremors tardive dyskenesia
atypical - new 1990s
- second generation antipsychotics developed
- olanzapine
- improve - symptoms and cognitive functioning
Bar et al 1997 - clozapine most effective/ popular as it addresses positive and some negative
how do antipsychotics work?
- reduce dopamine levels in brain by blocking D2 dopamine receptors which prevents dopamine binding to receptors in synapse and evens dopamine
- newer antipsychotics bind less tightly to receptors and block 5HT2A (serotonin) receptors which is what scientist think supports reduction in unpleasant side effects from earlier
evaluation for drug therapy
Pros
- earlier treatments were sterilisation or shock therapy so more humane and positive
- drug therapy medicalises schizos behaviour and takes away faults of behaviour
- strong biological evidence, dopamine hypothesis explains why drugs should work when blocking D2 receptors. Strong face validity
Cons
- bad side effects for typical antipsychotics so patients stop taking meds (tardive dyskenesia)
- atypical clozapine increases risk of developing agranulocytosis (increased risk of infections by decreasing WBC count)
