schizophrenia Flashcards
what is schizophrenia
neurodevelopmental disorder of thought characterised by positive and negative symptoms
Marked by extreme heterogeneity in psychopathology, treatment response and outcome both within and between people.
Treatment resistance is common
what is the diagnostic critieria for schziophreni
2+ symptoms in the last month, with at least one of these positive
positive symptoms: delusions, hallucinatins, disorder of speech, catatonic movement
negative symptoms: alogia, avolition, flat affect
what are the stages of development of schizophrenia
premorbid: abnormal brain development between birth and puberty
prodomal: early symptoms and signs concentration and memory problems, unusual behaviour and ideas, withdrawl
onset/deterioration: acute episode of hallucinations and delusions causing agitation and distress
residual: attenuation of positive symptoms with persistent negative symptoms
due to neurochemical dysregulation such that there is sensitisation by dopamine and excitatory neurotoxicity of glutamate
potentially neurdegenerative
what are the issues with the definition of schizophrenia
there is extreme heterogeneity within and between people in psychopathology, treatment response and outcome
better conceptualised as part of the same spectrum syndrome
distinct genetic brain disease which is not seen in other psychosis disorders so it is seen as somewhat separate
what is the content of hallucinations
hearing voices, lights changing, feeling spiders etc
auditory, visual, touch
what is the nature of delusions
thoughts are broadcasted internally
there is a withdrawal from thought
feeling of external tampering with thought,
delusions of control (an external force moved me etc)
delusions of persecution (something being after you)
delusions of gradneur
delusions of reference (e.g facebook status contains a secret message for me to decipher)
what is the epidemiology of schizophrenia
associated with substantial morbidity and with personal and societal costs
the typical age of onset is in adolescene and early adulthood but can be later
more common in ubran, socially disadvataged and BAME groups
more common in winter and early spring (leading to the idea of flu during pregnancy as a contributing factor)
equally common in men and women
what are the outcomes for schizophrenia patients
sustained recovery occurs in less than 14% within the first 5 years following a psychotic episode (Robinson et al., 2004)
an additional 16% show late-phase recovery (Harrison et al., 2001)
less than 20% in Europe with schizophrenia are employed
20% are homeless within a year
3x more likely to end up in criminal justice system than hospital in USA
more likely to be victims of violent attacks than purportrators
what are the levels of explanation for schizophrenia
behaviour: signs and symptoms
cognition: endophenotypes
biological: brain structure and dynamics - neurotransmitter function, blood flow, metabolism
genes x environment interaction
what are the genetic explanations for schizophrenia
the average risk of schizophrenia increases with increasing closeness to a biological relative with schizophrenia proband
MZ twins: 48%
offspring of two parents: 46%
still not entirely genetic
non-shared environmental factors
being raised by parents with schizophrenia will introduce key environmental influences
why is schizophrenia described as polygenic
studies have found small effects for 150 common variants
however only a small proportion of these have obvious functional effects
DRD2 encodes the D2 subtype of DA receptor
also genes involved in glutamatergic neurotransmission
what is the social defeat hypothesis of schizophrenia (Selten et al., 2005)
common denominator of four key environmental influences
urban upbringing
migration - higher risk for 2nd gen migrants, not about ethnicity
low IQ
drug use
common and long-term experience of social defeat may lead to long-term neurophysiological changes
sensitisation of mesolimbic dopamine system
how do most risk factors for schizophrenia show similar associations with psychotic experiences
parental: genes, pregnancy and birth complications e.g early birth, low weight, illness, trauma
childhood: social cognition, neurodevelopment
adolescence: trauma and victimisation, social environment, cannabis use
impact on adulthood
developmental view - timing of when things are occurrig
are there early cognitive deficits associated with schizophrenia
children show no obvious impairment
late onset measn we should of this as a neurodevelopmental condition
what is the relationship between the environment and schizophrenia
individuals with genetic vulnerabilities may be more sensitive to particular environments
a disorder of adaptation to social context
degrees of relatedness
what evidence is there for vulnerable subgroups and gene-environment interactions using proxy measures of genetic risk
with low genetic risk you do not see the same elevated risk due to environmental factors
consistent with cognitive fitness
what is the dopamine hypothesis
schizophrenia arises as a consequence of hyperactivity of the dopamine system - this explains the positive symptoms through a mechanism of aberrant salience
antipsychotic drugs have a common mechanism on DA release targeting D2 receptors
drugs that limit DA result in psychosis like experiences e.g amphetamine and cocaine
Griffith et al., (1972): experienced amphetamine users received 10mg d-amphetamine every hour for five days. All 7 volunteers became psychotic within 2-5 days.
Post-mortem studies show abnormalities in the metabolites of dopamine
what did Howes et al., 2007 find about dopamine in schizophrenic’s brains
radio labelled L-dopa
track DA release across synaptic cleft
scz patients have elevated presynaptic striatal DA synthesis capacity
suggests patients produce more DA than controls
elevated dopamine synthesis capacity is seen in the nigral origin of dopamine neurons as well as their striatal terminals in schizophrenia, and is linked to symptom severity in patients.
what is abnormal about presynaptic dopamine in patients with dementia
Review of 44 PET studies found the locus of the largest dopaminergic abnormality in scz is presynaptic
Affects DA synthesis capacity , baseline synaptic DA, DA release
No evidence of alterations in DA transporter availability
Small elevation in D2/3 receptor availability but not evidence in drug-naive patients
All current drug treatment act on receptors failing to target abnormalities
how do abnormalities of DA transmission cause schizophrenia symptoms
DA: incentive/motivational salience and reward prediction
DAergic abnormalities may lead to aberrant assignment of salience to external objects/internal representations
Hallucinations = abnormal salience attributed to internal representations
Delusions = cognitive explanation for these bizarre experiences
Filtered through patient’s existing cognitive and sociocultural schemas
Way they are rationalised will vary from patient to patient
what is the idea of dopamine as the final common pathway
multiple hits interact to result in striatal dopamine dysregulation to alter the appraisal of stimuli and resulting in psychosis
do patients with schizophrenia have cognitive impairments
1.5SD below normative sample
composite score of processing speed, attention, working memory, verbal learning, visual learning, reasoning and social cognition
however cannot reliably be used to diagnose schziohrenia
need to have a focus on individual change pre and post onset - it is less hlepful as a between group identifier
what is the course of cognitive impairments over time
Pre-morbid - small differences
Sudden decline before onset
Antipsychotics do not improve cognitive decline (argument that they may slow down this decline)
Argument that they may contribute - ‘dampening’ / slow down side effects
what information processing biases are seen in schizophrenia
interpretation and reasoning are impaired, and this extends to memory and attention
there is a tendency for the information processing system to consistently favour stimuli material of a particular type or content
interpretation biases could be external attributions
what is Morrison’s 1998 interpretation of triggers
in those most vulnerable, internal and external triggers such as stress, sleep deprivation and isolation can result in auditory hallucinations
these cause safety behaviours to prevent these things happening again however stress is not attributed as the cause
instead there is worry that there is a perceptual abnormality to blame which subsequently affects mood and physiology
this results in a cycle of worsening sleep and increasing stress
what is the bias of jumping to conclusions (Fine et al., 2007)
rather than just being a consequence of the symptoms of schizophrenia, the tendency to jump to a conclusion without full evidence may contribute to schizophrenia patients accepting hypotheses that other people reject as implausible
BUT
No evidence that scz patients have a bias against disconfirmatory evidence
Unsupported delusion maintenance
Limited number of typical scz delusions
Role of insight into experience and condition
how is schizophrenia treated
antipsychotics/ neuroleptics
these dampen down the system but have a limited impact on negative symptoms
appear better to doctors in terms of compliance
often see weight gain, eye twitch, strange movements, increased risk of cardiovascular problems
compliance in taking medication is poor, some people do not respond in the first place and some symptoms persevere
can also use family or cognitive therapy
how can CBT be used to treat psychosis
need to challenge the origins of delusions
highlight irrational and inconsistent features
offer alternative perspectives (such as making friends with the voice)
reduce feelings of persecution and paranoia
focus on personal impact
suggest behavioural tests
how effect is CBT for positive symptoms (Zimmermann et al., 2005)
effective with antipsychotics
most so for acute episodes over chronic conditions
summary
Neurodevelopmental syndrome over one psychotic illness
Can explain scz in terms of genetic risk factors in combination with environment
And dopamine striatal release
Neurocognitive and neuropathological conditions
Antipsychotics treat downstream effects
CBT may be important factor
