topic 12: schizophrenia Flashcards
what is schizophrenia
a severe mental illness where contact with reality and insight are impaired, it is an example of psychosis
around 1% of people are diagnosed with it in their life
with who is schizophrenia more common and when
men > women
cities > countryside
working class > middle class
onset:
men - early to mid 20s
women - late 20s
but can develop at any stage in life
how is schizophrenia classified and what is classification
classification: the process of organising/grouping medical conditions into categories based on which symptoms cluster together in sufferers
schizophrenia has no 1 characteristic, it has a cluster of symptoms
2 major classification systems;
ICD-10 (WHO international classification of disease) - need 2 or more negative symptoms
DSM-5 (APA diagnostic and statistical manual) - need at lest 1 positive symptom
give examples of positive schizophrenic symptoms
positive symptoms: things that people wouldn’t usually experience
- hallucinations (all senses)
- delusions: thought based, believing things that aren’t true (delusions of grandeur, paranoia and persecution, think they’re being controlled)
- word salad
what are some negative schizophrenic symptoms
negative symptoms: when people are no longer displaying behaviours that should be there
- apathy
- speech poverty
- avolition: poor hygiene + lack of motivation + lack of energy
evaluate reliability and validity in the classification or diagnosis of Sz
– not reliable because of inconsistency
5 DSM editions and 10 ICD editions; criteria has changed numerous times making it unreliable eg. there are no longer subtypes in DSM, these changes are impactful because more can be diagnosed as there aren’t specific boxes.( can be good bc 10% of SZ that get help commit suicidal so the rate must be higher if not.
– low validity; validity is how accurately something Is measured and the DSM and ICD have different classification systems
DSM: 1 positive symptom
ICD: 2 negative symptoms, these are often found in depression –> more diagnoses of Sz
over diagnosis means ppl can be given meds they don’t need and have to suffer side effects, even be institutionalised
– co-morbidity
could be suggested that when there’s so much overlap, they aren’t even different conditions, this would lower validity because we weren’t measuring what we thought we measured
BUT, the treatment looks at the root symptom and so would be effective regardless, so it might not be that important
– cultural bias
+ gender bias evidence: 59 vs 20
women are more often undiagnosed
evaluate co-morbidity and symptom overlap in the diagnosis and classification of schizophrenia
– co-morbidity rates of conditions with Sz
depression 50%, substance abuse 47%
could be suggested that when there’s so much overlap, they aren’t even different conditions
if they were just one big conditions, validity would be much lower because we weren’t measuring what we thought we measured
BUT, the treatment looks at the root symptom and so would be effective regardless, so it might not be that important
evaluate gender and cultural bias in the diagnosis and classification of schizophrenia
– women can get undiagnosed, stopping them from receiving needed treatment
50 years ago Loring and Powell asked 290 psychiatrists to diagnose the same 2 pts with identical symptoms
male pt 50% - Sz
female pt- 20% Sz
links to validity how???
the bias is thought to be linked to women having better interpersonal skills, such as working and maintaining a good family relationship
– in 1971, Copeland gave a pt description to 134 American and 194 British psychiatrists
US - 69% Sz
UK - 2% Sz
shows cultural influence in inter-rater reliability of Sz, a reason for the difference was not found but it suggests that one of the countries has psychiatrists misinterpreting symptoms of ethnic minorities
But, diagnostic criteria has improved a lot over the last 50 years
outline the genetic explanation of schizophrenia
candidate genes: genes that may be implicated in obtaining a disorder
combined all previous genome-wide Sz study data, comparing 37,000 Sz ppl to 113,000 controls
found 108 seperate genetic variations linked to an increase Sz risk
also gave evidence for Sz being etiologically heterogenous bc diff studies found diff combos it’s also obv polygenic
family studies have also suggested a link between Sz and genes
Gottesman large scale family study found:
p vs sibling - 9%
p vs fraternal twin - 17%
p vs identical twin - 48%
vs 1% with general population
outline the neural explanation of schizophrenia
neural correlates - measurements of brain structure in correlation with an experience eg. hallucinations
ventral striatum - part of the brain thought to be involved in reward anticipation
Sz pts found to have lower ventral striatum activity levels compared to controls and the lower the activity the worse the severity of negative symptoms seems to be; avolition
auditory hallucinations
Allen scanned brains and compared to control of pts with auditory hallucinations while asking them to identify pre-recorded speech as theirs or others
found lower primary auditory cortex and pre-frontal lobe activity levels in hallucination group, who also made more errors
evaluate the genetic explanation of Sz
+ evidence from adoption studies
Tienari compared 144 Sz offspring and 178 nonSz offspring; both adopted by others
found 10% Sz family kids to develop Sz
found 1% nonSz family kids to develop Sz
– env. factors increase Sz risk
eg. birth complications (biological), smoking THC rich cannabis as teen
childhood trauma (psychological) - study showed approx 65% of ppl with Sz reported min. 1 childhood trauma vs 40% in matched group w/ non-psychotic mental health issues
+ reliable and valid
clinical and objective methods used, not affected by bias like individual differences
– genetic factors alone can’t provide a complete explanation for Sz
if no other influencing factors; identical twins would be 100% concordant
evaluate the neural explanation of Sz
– data is all correlational, just bc auditory hallucinations occur in people with reduced activity in their prefrontal and auditory cortices doesn’t mean it’s causation
both could be caused by a 3rd, unidentified variable
– over simplistic and reductionist
looks at brain activity and size but for such a complex disorder other aspects eg. neurotransmitters eg dopamine and life stressors could be involved
diathesis stress model is better
+ neural correlate data has high reliability
carried out n highly controlled env. with high specialist equipment eg. MRI’s and PET scans so accurate reading can be taken, suggests that if research was retested, the results would be the same
what is the dopamine hypothesis (DH)
dopamine (DA) is the best known neural correlates for Sz, DA is a neurotransmitter associated with reward
the original DH: hyperdopaminergia causes Sz with too much DA in subcortical brain regions e.g. excess dopamine receptors in Broca’s area has been linked with speech poverty and auditory hallucinations
because the biological treatment was antipsychotics, which reduce DA
more recent DH: hypodopaminergia can also explain Sz symptoms, Rakic found low levels of dopamine in the prefrontal cortex to correlate with negative symptoms eg. avolition has been linked to low dopamine uptake in cortical regions
evaluate the dopamine hypothesis
+ evidence support
DA agonists (eg amphetamines) increase DA levels, worsening Sz and producing Sz symptoms in non-sufferers
antipsychotic drugs work by reducing DA activity, so we can see the correlation between DA and schizophrenia symptoms
– inconsistent results
apo-morphine increase DA levels but doesn’t cause Sz like symptoms, so other factors must be involved in the correlation between DA and Sz symptoms
– post mortems and brain scan studies consistently found that Sz pts had raised levels of neurotransmitter glutamate in several brain regions, giving evidence that other neurotransmitters could be involved
agonist vs antagonist
agonist binds to a receptor to activate it
antagonist binds to prevent the agonist from binding
evaluate the different ways of taking medication
tablets
+ convenient, at home
+ pre-measured dose
– avolition, could forget to take
syrup
+ easy to consume
+ absorbed by body quickly, works faster
+ convenient, at home
injections
+ directly to bloodstream, works fastest
+ lasts 2-4 wks, no remembering daily
– professional has to administer
outline typical antipsychotics
used to combat positive symptoms, work as antagonists by blocking and therefore reducing the amount of dopamine in the DA pathways and receptors, eventually reducing dopamine production
1st generation drugs containing only dopamine
- chlorpromazine, from 1950s
side effects: tremors+muscle rigidity+unstablegout ( Parkinson’s like symptoms), weight gain, sedation, low bp
outline atypical antipsychotics
treat positive and negative symptoms by being dopamine antagonists and serotonin agonists
clozapine
binds to dopamine receptors + works on serotonin and glutamate receptors
working on serotonin increases mood, lowering chances of developing depression and anxiety and may improve cognitive functioning, so clozapine is often prescribed to pts w/ suicide risk
side effects: can cause agranulocytosis, (attack white blood cells), blood tests are used to confirm it isn’t developing
risperidone
it binds v strongly to dopamine receptors so doses can be small and some evidence suggests this reduces side effects
evaluate drug therapy as treatment for schizophrenia
— serious side effects
eg. dizzy, agitated, weight gain, itchy skin
clozapine also needs regular blood tests to identify agranulocytosis asap
side effects can be worse than symptoms so ppl don’t take the drug —> part of the 10% of Szs that commit suicide
+ it has been effective
chlorpromazine vs placebo trials: 13 trials data, chlorpromazine found to give better overall functioning, reduced symptom severity and lower relapse rate
clozapine is up to 50% more effective at treating treatment-resistant cases
+ drugs is less work for the pt
pts with avolition etc. struggle with CBT and family therapy
atypical antipsychotics (clozapine) bind to dopamine+serotonin receptors
improve mood, reduce depression+anxiety, may improve cognitive function
pts can then access the other treatment and be treated holstically
— chemical cost argument; ethical concerns w/ sedatives eg. chlorpromazine
sedative calm Sz pts and makes conditions easier for ppl around them (staff/friends/family)
pt is spaced out and may have lower quality of life, but paranoid Sz are prevented from harming themselves and others
outline a family dysfunction explanation of Sz relating to the mother
family dysfunction
Fromm-Reichman coined the term ‘schizophrenogenic mother’ - the mother cold and controlling because of maternal overprotection and rejection; this can cause a climate of tension and secrecy which causes the patient to become distrusting (leads to paranoid delusions) and resentful of others
outline a family dysfunction explanation of Sz relating to mixed signals
family dysfunction
double bind communication - a pair of messages being mutually contradictory; suggested by Batesman
eg. mother tells child they aren’t affectionate but when child shows affectionate they’re pushed away and shamed for babyness; child cannot win (can be especially hard for small children)
this ongoing confusion can cause internal conflict, and prolonged exposure could harm the child’s chance at developing any coherent construction of reality ; by the time the child is old enough to become aware of the situation, it has already been internalised and can’t be confronted
the only solution - escape from the conflicting logical demands into a world of delusions
outline a family dysfunction explanation of Sz relating to emotions
Brown et al. Expressed Emotion (EE) Sz theory, a qualitative measure of how much emotion is displayed in a family setting
suggested to be more imp in Sz maintenance that cause
high EE: worsens Sz pt prognosis, increases chance of relapse and readmission, it involves:
- hostility to pt because family feels disorder is controllable and pt isn’t trying to get better
- emotional over-involvement; family blames themselves and makes pt feel guilty and cause stress leading to relapse
outline a cognitive explanation of Sz
based around abnormal info processing
Frith put forward two ideas
-
meta-representation dysfunction - inability to recognise your actions and thoughts as your own and then reflect on them
hallucinations of voices and thought insertion delusions -
lack of central control - lack of the cognitive ability to suppress automatic responses whilst we instead perform deliberate actions
derailment of thoughts and sentences as associations are triggered by each word and the automatic responses to these can’t be supressed by the pt
evaluate family dysfunction explanations of Sz
– unethical to blame parents/loved ones
blaming family can cause parents to feel guilty leading to stress and anxiety
this is considered outdated/unfair by most psychologists and psychiatrists
Schizophrenogenic mum, EE+double bind only have weak, correlational evidence
+ evidence support
65% Sz had at least one childhood trauma vs 40% of non-psychotics
– retrospective information
there could be bias; one of Sz’s symptoms is impacting the pt’s grip w/ reality, so relying on their memory might not be the most secure method as there is no way of verifying if their memories are accurate
– nature causes
evidence suggests that there are also biological causes, so although family-dysfunction might trigger Sz, it might not be the root cause
MZ 48% DZ 17%, so not just nature bc MZ>DZ
