7 psychosis Flashcards
What is the general conceptualisation of psychotic disorders?
most severe form of mental health disturbance
debiliating symptoms - staying in touch with reality…
- inability to handly normal life activities
hearing voices
schizophrenia - most common
What are the different psychotic disorders the DSM-5 classifies?
SCHIZOPHRENIA
A. 2+ for more than 1 month
- delusions
- hallucinations
- disorganised speech
- disorganised behaviour
- negative symptoms
B. decrease in functioning
C. disturbance for 6+months
if less than a month
brief psychotic disorder
if less than 6 months
schizophreniform disorder
if psychotic symptoms already present + depressice or manic episode
schizoaffective disorder
only delusions
delusional disorder
only in context of depressive or manic episode
MDD or bipolar with psychotic or catatonic features
What are negative symptoms?
emotional expression
avolition
alogia
anhedonia
asociality
What are positive symptoms?
Delusions
fixed beliefs that are not amenable to change in light of conflicting evidence
Thought withdrawal or insertion
grandiose
persecutory
erotomanic
jealous
somatic
nihilistic
referential
+ with bizarre content
Hallucinations
perception-like experiences that occur without an external stimulus
positive vs. negative
auditory
visual
tactile
somatic
olfactory
gustatory
What is the difference between delusions and hallucinations?
hallucinations = negative automatic thoughts, intrusive thoughts BUT experienced as loud, external, real, true
delusions = beliefs or inferences about events or experiences, which affect mood and behaviour
What are clinical features of schizophrenia?
- breakdown in perceptual selectivity
- hallucinations
- delusions
- confused sense of self
- lack of insight
- formal thought disorder
- cognitive impairment
- prodromal anxiety or depression
- inappropriate, flattened or blunted affect
- post-psychotic depression
- prodromal excitation
- impaired goal-directed behaviour
- excited or catatonic behaviour
- poor self care
- poor work performance
- withdrawal from peer relationships
- comorbid disorders
- unhealthy lifestyle
How does assessment for psychotic disorders go?
- risk assessment and management
assess risk of self-harm or harm to others
prodromal impulsivity - dangerous behaviour
triggers, non-adherence to medication
always multimodal approach - diagnostic assessment
clarify symptomatology
standardised rating scales
multidisciplinary involvement - differential diagnosis
symptom prevalence
symptom severity
single symptom diagnosis?
affective symptoms
onset - insidious, if affective, more acute
How does formulation for psychotic disorders go?
interviewing
cope with trauma, stress, anomalous experiences
Low adherence to pharmacological and psychological treatment regimes, a poor alliance with service providers, lack of coordination among multidisciplinary or multi-agency service providers can maintain psychotic symptoms.
protective factors - good premorbid functioning, acute onset, clear awareness or insight into prodromal symptoms, low stress, social support, females rather than males have better outcome
formulation
general syndromal formulation
then other more specific ones on how they occurred and are currently maintained
How would treatment for psychotic disorders be conceptualised?
based on it being a recurrent episodic condition
only partially understood
no cure
Recovery-oriented case management to coordinate treatment and promote a return to as normal a life as possible.
Pharmacological therapy to control positive symptoms including delusions and hallucinations.
Individual or group-based cognitive-behavioural therapy focused on helping the service-user understand the disorder, cope with its symptoms and control environmental stress levels.
Preliminary cognitive remediation and social skill training may be offered for cases where significant cognitive or social skills deficits are present, and make it difficult for service-users to engage with CBT.
Family intervention to help family members understand the concept of psychosis and interact with the service-user in a way that is maximally supportive and minimally stressful. This may include group-work for parents, siblings or partners to provide them with education and support, and training in using contingency management to help service-users overcome negative symptoms.
Service-users may also be invited to join self-help or peer support groups to facilitate their recovery.
What are risk factors for schizophrenia?
positive family history of psychosis
schizotypy
maternal flu infection or malnutrition in 1st or 2nd trimester
father over 35years
obstetric complications
birth in late winter or early spring
male
unmarried
urban dwelling
migrant
low SES
trauma history
cannabis use
What are risk factors for specifically poor outcome schizophrenia?
family history of schizophrenia
male
obstretic complications
early age of onset
insidious onset
poor premorbid adjustment
longer duration of untreated psychosis
lack of an identifiable precipiating stressor
trait anxiety
external locus of control
severe negative symptoms and cognitive impairment
lack of depressive symptoms
poor treatment adherence
substance use
single
few friends
stressful life events
excessive family members
developing country
What is the difference between a diagnosis and a formulation?
what they have
how they got it
definition of symptoms
origin of symptoms
How can predisposing, precipitating, maintaining/perpetuating and protective factors be conceptualised?
predisposing = what is their “set up”? what are they working with initially?
precipitating = what acute event happened and how did it affect them?
maintaining/perpetuating = what chronic things are going on?
protective = what is protecting them? what is keeping them well?
What biological theories of schizophrenia exist?
genetic hypothesis
neurodevelopmental hypothesis
neutrotransmitter dysregulation hypotheses
two syndrome hypotheses
What does the genetic hypothesis of schizophrenia posit?
A genetic predisposition renders some young people vulnerable to schizophrenia
-> psychoeducation and medication
What information supports the genetic hypothesis of schizophrenia?
inherited vulnerability
80% heritable
MZ - risk 48%
DZ - 17%
children of affected parent - 13%
grandchildren - 5%
general population - 1%
polygenetically transmitted
candidate genes have been identified
neuregulin 1 (NRG1) - synapse formation and synaptic signalling
disrupted-in-schizophrenia (DISC1)
catechol-O-methyltransferase
(COMT) - regulates dopamine in frontal cortex
D-amoni acid oxidase activator (DAOA) - glutamate signalling
dysbindin (DTNBP1)
regulator of G-protein signalling 4 (RGS4)
calcineurin (PP3CC) - dopamine and glutamate neurotransmission
What does the neurodevelopmental hypothesis of schizophrenia posit?
prenatal and perinatal adversities which cause neuroanatomical abnormalities lead to schizophrenia in genetically vulnerable populations
-> multimodal interventions
What information supports the neurodevelopmental hypothesis of schizophrenia?
obstetric complications - maternal infection with influenza or rubella, malnutrition diabetes mellitus, smoking, bleeding during pregnancy, problematic labour or delivery, anoxia of asphysxia
20-30% have history of OC
5-10% of unaffected population
foetal hypoxia
How does synaptic prunning interact with the neurodevelopmental hypothesis of schizophrenia?
synaptic connection within the brain increase up to 2 years and decline gradually before puberty and decrease markedly in adolescence
synaptic pruning
emergence of sophisticated cognitive skills
synaptic prunning is excessive → fragmented brain and consequent psychotic symptoms
What are five neuroanatomical abnormalities found in schizohprenia?
reduced overall brain volume and enlargement of cerebral ventricles associated with brain atrophy
reduced size and activation within frontal lobes
dorsolateral prefrontal cortex particularly affected - neuronal packing density
reduced temporal lobe volume inducing reduction in size of amygdala, hippocampus → emotional processing and memory
decreased thalamic volume and disorganisation of thalamocortical pathways → attention
disorganisation of white matter tracts and reduced connectivity between many areas of the brain
psychophysiology - sleep architecture, REM latency reduced, evoked potentials are abnormal, eye movements are abnormal, highly heritable!
What does the neurotransmitter dysregulation hypothesis posit?
Dysregulation of the dopaminergic and glutamatergic neurotransmittion system causes symptoms of schizophrenia
-> antipsychotic medication
What information supports the neurotransmitter dysregulation hypothesis?
DOPAMINE
medication that blocks dopamine receptors alleviate symptoms
overactivity of mesolimbic dopamine pathway - positive symptoms
underactivity of the mesocortical dopamine pathway - negative symptoms
Downar and Kapur (2008) - dopamine gives neural networks associated with thoughts or perceptions salience
overactivity of mesolimbic dopamine pathway probably results in many thoughts and perception being misinterpreted as highly salient or important
GLUTAMATE
underactivity of NMDA receptors underpins cognitive impairments and delusions
drugs that reduce efficiency of NMDA induces psychotic symptoms
major excitatory neutrotransmitter in central nervous system
attention, perception, cognition
development of nervous system → synaptic pruning
other neurotransmitters need to be included in research for more sophisticated theories
What does the two syndrome hypothesis of schizophrenia posit?
Type 1 - genetically determined and leads to positive symptoms associated with dysregulation of dopamine system
Type 2 - due to prenatal or perinatal brain damage and leads to negative symptoms
-> antipsychotic for +
-> rehabilitative intervention for -
What information supports the two syndrome hypothesis of schizophrenia?
Crow (1985) -
type 1 type 2 distinction → genetic marker
1: acute onset, clear precipitants, predominantly positive symptoms, good response to antipsychotic medication and good inter-episode judgment
2: poor premorbid functioning, insidious onxet, chronic course, neuropsychological deficits, predominantly negative symptoms, poor response to medication
→ fits good proportion of available data but probably oversimplification
What psychological theories of schizophrenia exist?
neurotoxicity hypothesis
diathesis-stress model
family theory and therapy
cognitive theory and CBT
cognitive deficit theory and cognitive remediation
social skill and social cognition theory
prodromal hypothesis
recovery model
What does the neurotoxicity hypothesis of schizophrenia posit?
extended period of untreated psychosis causes neurobiological pathology
-> early intervention
(better outcomes in cases with short duration of psychosis
minimum duration threshold that must be reached to have a neurotoxic effect)
What does the diathesis-stress model of schizophrenia posit?
psychosis occurs when neurobiologically vulnerable individual are exposed to psychosocial stress
-> multimodal interventions
What information supports the diathesis-stress model of schizophrenia?
onset, course, severity is related to stress and trauma
Physical and sexual child abuse, neglect, family violence and serious injury
renders people vulnerable to the development of psychosis, and there is a dose-response relationship with greater levels of trauma being predictive of more severe symptoms.
Low socio-economic status, migration to a new country and living in an urban rather than a rural setting all confer risk for the development of schizophrenia, and all entail increased stressful demands on coping resources.
The onset of schizophrenia is typically triggered by a build-up of stressful life events (illness, injury, bullying, life-transitions, loss, etc.).
continuous stress after onset may compromise recovery
symptoms are intrinsically stressful
HPA axis overactivity - cortisol levels
Raised cortisol levels indicative of HPA axis hyperactivity are more common in first-episode psychosis.
Heightened physiological arousal associated with HPA overactivity probably exacerbates psychotic symptoms, particularly positive symptoms such as hallucinations, delusions and thought disorder.
Elevated cortisol levels arising from HPA axis overactivity compromise the efficiency of the immune system and increase vulnerability to cardiovascular and metabolic disease, common in schizophrenia.
ppl with schizophrenia tend to not use adaptive strategis for emotion management or cognitive appraisal
What does the family theory and therapy of schizophrenia posit?
expressed emotion (criticism and overinvolvement) affect the course of psychosis, particularly the timing and rate of relapse
-> psychoeducational family therapy
(half of medicated clients relapse
relapse rates are higher with unsupportive environment: high levels of expressed emotion, criticism, hostility, emotional overinvolvement)
What does the cognitive theory and CBT of schizophrenia posit?
When neurobiologically vulnerable individuals are exposed to stress
-> physiological arousal
-> reduction of cognitive resources
-> increase in delusions and hallucinations
CBT to challenge dysfunctional thinking and promote adaptive coping strategies
What does the cognitive deficit theory and cognitive remediation of schizophrenia posit?
Functional impairment in psychosis is due to cognitive deficits affecting attention, memory, processing speed, cognitive flexibility, social cognition and executive functioning
-> cognitive remediation to ameliorate cognitive deficits and improve functional impairment
What information supports the cognitive deficit theory and cognitive remediation of schizophrenia?
three-quarters show significant cognitive deficits
average IQ is one SD down the normal IQ of an average population
but considerable heterogeneity
mild premorbid cognitive deficits, followed by a steep decline in cognitive functioning during psychotic episodes, with some amelioration of cognitive deficits during remission and relative stability over the long term
rehabilitation theory - set of cognitive drills to enhance attention, memory and executive functions
What does the social skill and social cognition theory of schizophrenia posit?
impairment mainly due to social cognition deficits
-> social skills and social cognition training
What information supports the social skill and social cognition theory of schizophrenia?
limitations in those areas account for much of functional impairment seen in psychosis
accurately perceiving social situations, understanding and planning what to do in them, maintaining social appropriateness
failure to learn social skills during normal course of development due to deficits in social cognition, emotion perception, social perception, attributional style, theory of mind
social skill theory - ppl with psychosis may fail to use social skills that have been acquired because psychotic symptoms interfere with their use
development of communication, conversation, assertiveness, medication management and social problem-solving skills. Modelling, rehearsal, shaping and reinforcement are used during the training process.
The main emphasis in on practising skills rather than talking about them
What does the prodromal hypothesis of schizophrenia posit?
the onset of of a psychotic episode is heralded by a clearly identifiable prodromal dysphoric syndrome
-> early intervention and plans to manage symptoms
What information supports the prodromal hypothesis of schizophrenia?
high risk - prodromal set of symptoms, largely perceptual hypersensitivity, cognitive information processing deficits
exacerbated by inferences, attributions made about controllability and origins of unusual
four stages of psychosis - Birchwood, 1996
1 - feeling of loss of control over cognitive and perceptual processes
sense of anxiety
2 - depression characterised by low mood, self-esteem, social withdrawal, poor vocational performance and vegetative features (sleep disruption)
3 - disinhibition, impulsive behaviour, agression, self-destruction, sexual urges, wishes to travel, …
4 - pre-psychotic thinking, perceptual misinterpretations, delusional explanations, paranoid ideation, ideas of reference
What is the recovery model of schizophrenia?
overarching framework for mental health services internationally
Kraepelins (1899) - neurobiological disorder with chronic declining course
→ institutional care and reliance on medication
→ reduced emphasis on trauma
→ stigmatisation and marginalisation in society
→ reduced value of psychosocial interventions
⇒ recovery movement arose from service-user
personal journey from psychosis to mental health
priviledges the concepts of optimism, wellbeing, personal strengths, supportive relationships, collaboration, personal choice, adaptive coping, developing a meaningful life, civil rights, empowerment and inclusion
chronic decline in schizophrenia is not inevitable
trauma and stress play important role in aetiology
psychosocial interventions facilitate recovery
→ inclusive place in society, innovative community-based approaches
What are some cognitive strategies to manage psychotic symptoms?
+ distraction or attention switching
+ focusing or attention narrowing
+ self-instruction to act in a particular way
+ self-instruction to re-attribute the cause of a particular event
What are some behavioural strategies to manage psychotic symptoms?
+ increase physical activity
+ increase social activity
+ modulating social activity (breaks!!)
+ testing out beliefs by checking if the facts fit with beliefs about causes or interpretations of events
+ relaxation techniques
What is the main aim of CBT for schizophrenia?
aims to help service-users manage stressful situations that might exacerbate psychotic symptoms;
minimize distress associated with hallucinations and other psychotic experiences;
reduce the negative impact of delusional beliefs;
manage negative symptoms;
and prevent relapse
What does CBT for psychosis start with?
CBT for psychosis begins with a thorough fine-grained ABC contextual assessment of each specific symptom, taking account of
antecedent activating events (As);
beliefs and associated cognitive distortions and misattributions (Bs);
and resultant distressing emotional responses or maladaptive behavioural consequences (Cs).
During this fine-grained cognitive-behavioural analysis, 10-point visual analogue scales are a particularly useful way to assess the magnitudes of beliefs (Bs) and consequences (Cs) arising from these beliefs.
What is stimulus control in CBT for schizophrenia?
identifying specific situations which precipitate distressing hallucinations
systematic problem-solving approach: identify pros and cons of each of these; select the most promising; try this; evaluate outcome and modify to improve its effectiveness if necessary
What specific techniques are used in CBT for schizophrenia?
cognitive interventions
weaken conviction of maladaptive beliefs being the reality
self-efficacy
internal locus of control
eliciting these beliefs and creating a processing hierarchy
coping-skills training
list of distressing and frequently occuring symptoms
→ one at a time is selected for focus training
cognitive remediation
tasks are assigned to improve specifically targeted cognitive deficits
social skills training
group therapy context
modelling, rehearsal, shaping, reinforcement
How is relapse prevention done in CBT?
relapse drills to manage potential relapse situations
To deal with relapses, service-users may be invited to write down
their relapse drill which includes (1) a detailed description of the cognitive, emotional and behavioural elements of their personal relapse signature; (2) the specific strategies that they will use to cope with prodromal symptoms; and (3) phone numbers of key workers they can call to help them implement their strategy.
Lack of insight, lack of syndrome stability and a ‘sealing over’ recovery style may preventservice-users from learning and using their relapse signatures to implement relapse drills to prevent relapses or minimize their impact
How can delusions be managed?
- addressing distress associated with delusions through empathetic exploration
- Sometimes a lack of real-world information can contribute to the development of delusions, and an intervention to explain how things work in the real world can sow a patient’s doubt of the delusion or change how a patient responds to a delusional belief.
- A third area in which one can intervene is by narrowing the sphere of delusional thinking with specific questions.
- A fourth area is to evaluate the evidence for and against a particular delusion by asking the patient to think of himself as a prosecutor and present evidence for the delusion
- A fifth area of intervention is to ascertain the origin of the delusion
- A sixth intervention is to address the utility of the delusion for the individual
- A seventh area of intervention is judicious self-disclosure
- The final intervention is to address the theme underlying the delusional belief
How can hallucinations be managed?
coping skills to deal with negative emotions
deal with stress
search for evidence of actual existence
set up predictor experiments
evaluate pros and cons of behaviour
providing normalising rationale for voices
What are some principles contributing to positive treatment outcomes?
connect -> enhances engagment
understand -> clarficiation, reduction of barriers
teach -> practical skills
practice -> generalised and easier application
ask -> collaboration, active role of patient
review -> reinforcement of learnings
