Lecture 2 - Psychosis & Schizophrenia Spectrum Disorders Flashcards
1
Q
psychosis
A
- characterised by delusions, hallucinations, disorganised thinking/speech, disorganised behaviour, social/emotional flatness
- out of character for how one usually behaviours
- loss of contact with reality
2
Q
positive symptoms
A
- e.g. delusions & hallucinations.
- add something to how behaviour usually is
3
Q
disorganisation
A
- e.g. disordered thinking/speech & behaviour
- disruption of what normally happens
4
Q
negative symptoms
A
- e.g. social/emotional flatness
- take away from how individual usually behaves
- occur longer in the course than pos or disorganised symptoms do.
5
Q
delusions
A
- false beliefs over time and remain fixed despite evidence. can be bizarre or non-bizarre.
- persecutory, grandiose, nihilistic, erotomanic, somatic, referential
- can also be thought broadcasting (people sharing their thoughts) thought insertion (thoughts are being inserted) and thought withdrawal (thoughts being taken away)
- typically late adolescence and especially in men
- often reflect socio-political themes of an era and religion
6
Q
Hallucinations
A
- vivid, clear sensory perceptions experienced in the absence of external stimulation
- can be auditory (most common), visual, tactile, somatic, gustatory, olfactor
- voices may be known and often have relevance at affective or behavioural level
- Allen et al. (2008) - patients with speech hallucinations have reduction in brain GM in L hem auditory and speech perception areas. inc activity in brocas.
7
Q
Luhrmann et al. (2015)
A
- asked about hallucination content in different settings
- USA: voices intrusive, unreal thoughts
- South India: voices provided guidance
- West Africa: voices morally good and causally powerful.
- varying experiences can mean varying distress.
8
Q
motor symptoms
A
- catatonic behaviour: dec in reactivity to the environ.
- resisting instructions & requests (negativism)
- holding rigid bizarre posture
- absence of verbal or motor response
- purposeless or excessive motor activity
- stereotyped movements e.g. staring, grimacing
- involuntary movements.
9
Q
disorganised thinking/speech
A
- aka thought disorder
- sounds communicative but gives little understanding and may use new words (Neologisms)
- includes: poverty of speech (slow/vague), derailment (switching topics), tangentiality (unrelated) perseveration (repetition of words), clanging (stringing together rhyming words) flight of ideas (leaping from ideas)
10
Q
Other cognitive symptoms
A
- impairments in EF, focussing/attention, WM, verbal learning & memory
11
Q
using language and cognitive skills to detect schizophrenia early
A
- initial difficulties with language and cognition may be early warnings for onset of Sz spectrum disorder.
- in high risk adolescents deficits in verbal reasoning/learning, wm, attention and processing speed predicted sz. some evidence of abrupt decline in months preceding.
12
Q
negative symptoms
A
- symptoms that flatten or remove usual responses. can reduce expressive behaviour or experience of pleasure.
- include: diminished emotional expression, avolition (dec in motivated self directed goals), anhedonia (inability to experience pleasure of things that usually are), asociality (lack of interest in social situations), alogia (dec speech)
- persists beyond episodes
13
Q
schizophrenia spectrum and psychotic disorders
A
- delusional disorder - hold delusions but behaviour does not show disorganisation and performance deficiencies of Sz. may include erotomania
- brief psychotic disorder - sudden onset of psychotic symptoms or disorganisation but not recurrent episodes.
- schizophreniform disorder - schizophrenia-like psychoses that last 1-6m
- schizophrenia
- schizoaffective disorder - not only features of sz but also mood disorder.
14
Q
schizophrenia DSM criteria
A
- 2 or more of following, at least one MUST BE 1, 2 or 3.
1. delusions
2. hallucinations
3. thought disorder
4. abnormal motor behaviour
5. negative symptoms - impaired function for proportion of time
- symptoms at least 6m
- ruled out schizoaffective & bipolar
- not explained by substance use
- if ONLY ONE of 1-3 present need to also be motor abnormalities or negative symptoms.
15
Q
prevalence of schizophrenia
A
- lifetime prevalence is 0.48 per 100. approx 0.7% according to Saha et al. 2005?
- every 7m 4f
- inc risk of dying
- earlier diagnosis for men than women.
- peak onset 18-30, in men peak 20-24 same for women but women have second peak age 40-60.
- tend to be more severe in men (Leung & Chue 2000). sex hormones play protective role in women? oestigen low = worse symptoms.
16
Q
The course of schizophrenia
A
- first episode is followed by many episode and preceded by prodrome.
- if intervention happens after first episode can see remission (critical period) or see partial response/no response to treatment & relapse.
17
Q
prodromal phase of schizophrenia
A
- gradual emergence of psychotic symptoms (sudden onset is rare) which gradually becomes more obvious
- subtle changes e.g. unusual thoughts, abnormal perceptions, lack of interest in usual activities. early sign = lack of attention to personal care. behaviours inc speech affected, often seen as a ‘phase’
- a key stage to try an intervene but often not picked up due to people isolating themselves
18
Q
neurodevelopmental condition
A
- differences in cognition, communication, behaviours & motor skills from abnormal brain development
- people with Sz show dif in brain structure/function but is not purely caused by these differences - life exposures can shape the brain & behaviour
- genes can also be turned on/off by environment
19
Q
diathesis stress model
A
- diathesis is a pre existing risk/disorder
- neurological vulnerability may be dopamine involvement in sz
- favourable environments may reduce chance a genetic predisposition results in sz.
20
Q
dopamine hypothesis
A
- og theory excess dopamine due to a pathway being blocked? a functional dopamine excess.
- phenothiazines block dopamine receptors and reduce agitated symptoms. amphetamines inc dopamine receptors & sz symptoms.
- believed high levels of postsynaptic dopamine D2 receptor binding led to functional excess of dopamine but no evidence of higher levels of D2 receptors.
- new theory is inc dopamine synthesis
- mesolimbic system = overactive, positive symptoms
- mesocortical system = a dysfunction, negative symptoms
21
Q
questioning the dopamine hypothesis
A
- 1/3 don’t respond to dopamine focussed treatments. maybe some more factors. e.g. antipsychotics block dopamine but relief takes ages
- glutamate and serotonin important
- glutamate excitatory & PCP blocks receptors inducing Sz symptoms. lower glutamate levels in Sz.
- dopamine receptors inhibit release glutamate. overactive dopaminergic system could result in excessive suppression of glutamate leading to underactivity of nmda receptors
22
Q
structural differences in the brain
A
- enlarged ventricles (25%). often indicates reduction in brain tissue in area nearby.
- reduced brain volume (2%) and mostly in frontal lobe
- possibly related to problems in development
- also some WM loss & abnormal structuring - cor with cog impairments (Kubicki et al. 2007)
- but does not tell us what the brain does.
23
Q
- unusual activation of pfc sometimes over & under active. in early stages and at high risk. associated with planning, inhibition. hypothesised pfc fails to appropriately deactivate = difs in cognition?
- thought to account for some of the neg symptoms too
A
24
Q
genetic risk of schizophrenia
A
- MZ 48% DZ 17% & is polygenic
- adversity in family predicted problems in adopted children but only those who were raised in dysfunctional families AND had high genetic risk developed Sz related disorders. our genetic makeup may control how sensitive we are to environ.
- there are shared genetic risks for schizophrenic spectrum and bipolar disorders - overlap of disorders?
- ## the indiv genes in sz are linked to other neurodevelopmental disorders
25
Q
reciprocity between genes and environment
A
- we seen gene-environment interactions going both ways
- environ can activate pre existing genetic risk.
- genetic features can also determine how we shape and select our environment
- could have inherited predisposition but depending on environment not express as sz
26
Q
non-genetic factors
A
- higher risk of sz for:
> men
> urban environments
> migrated (2nd gen higher)
> social adversity in upbringing
> cannabis users (THC inc dopamine)
> head injury
> immune disorders - possible cumulative effects
27
Q
antenatal risk factors
A
risk factors include:
> pregnancy complications
> abnormal foetal growth
> delivery complications
- antenatal factors affecting risk also include
> maternal stress/bereavement
> maternal poor nutrition
> maternal viral exposure - N hemisphere more with Sz born between january and march (waddington et al. 1999)
- likely that metabolic, endocrine and oxygen related alternations to uterine affect foetal development.
28
Q
early life immune risk factors for schizophrenia
A
- Sz incidence may be higher for people born at certain times of year
> in N hem, highest rates for people born january-march (viral activity) - exposure to viruses in general affect levels of c-reactive protein(immune marker of infection) in amniotic fluid predict later Sz in offspring.
29
Q
Trauma
A
- trauma history common in people with psychotic symptoms
- e.g. abuse, violence, neglect, victimisation, often chronic
- victims dissociate from reality as a self protective mechanism but may predispose to other reality dissociated experiences such as hallucinations
- traumatic events can also trigger the onset of psychotic episodes
- trauma is also a risk factor for a range of other disorders
30
Q
cognitive differences in schizophrenia. reality monitoring impairments.
A
- may have impaired ability to distinguish internal/external events
- to do with reality mentoring of where sources come from. may explain why hallucinations feel external
- sz people poorer at judging original source of material to be external vs internal
- functionally linked to pfc
31
Q
endophenotypes in schizophrenia
A
- can have similar genetics but differences in how symptoms present. they are discrete stable and measurable traits that are thought to be under genetic control.
- e.g. Genain quadruplets had varied presentation and level of functioning
- given pre existing risk one determinent of outcome is family environment e.g. favourable treatment?
32
Q
1st generation antipsychotics
A
- e.g. phenothiazines. helpful with positive symptoms.
- block dopamine receptors to reduce obvious symptoms including hallucinations & delusions (dopamine antagonists)
- extra-pyramidial side effects (motor control problems) common but fade
- BUT tardive dyskinesia can result from LT use (involuntary chewing and eye movements, facial grimacing, involuntary movements)
- 30% don’t respond to them
33
Q
2nd generation antipsychotics
A
- atypical antispsychotics
- fewer extrapyramidal side effects
- e.g. clozapine, risperidone, olanzapine
- may require regular blood checks with clozapine
- side effects: weight gain, metabolic disorders linked to heart disease
- act on serotonin receptors too
- also used in bipolar disorder
- some effectiveness against negative symptoms and pos.
34
Q
relapse and maintenance
A
- antipsychotics help control not cure
- often supplemented with psychological treatment
- maintenance doses needed and relapse possible even when on antipsychotics
- about 20% lifetime remission after one episode of sz
- most experience further episodes. greatest risk of relapse for those who stop antipsychotics
- inc use of talking therapies to identify meaning in symptoms and spot triggers
35
Q
talking therapies
A
- aim to empower & de-stigmatise
- may take due to side effects of medication
- mixed evidence
- NICE recommended CBT but in reality medication often relied on in NHS
- may need more research on if talking therapies is the correct form of CBT
- new approach is avatar therapy
