Week 11 - Schizophrenia and Psychotic Disorders Flashcards
(22 cards)
Overall introduction
Lifetime prevalence - 26.6 per 100 000
Onset - early adulthood
Psychotic disorders very impairing (14 years lower life expectancy, worse cog function, social function, job function, QOL)
Large variation in prognosis, course, treatment response
80-90% preceded by clinical high-risk phase (mild symptoms, functional decline)
Approx. 20% transition to psychosis if untreated (prediction here uncertain)
Positive symptoms
Excesses and distortions (only in acute phase)
Hallucinations - sensory experience without stimulation
- auditory more common than visual (arguing, voicing commenting on behaviour)
Delusions - persistent beliefs contrary to reality
- can be bizarre or non-bizarre
- types - grandiose, ideas of reference, thought insertion/ withdrawal/broadcasting, persecution, erotomatic, jealous, somatic, nihilistic, control
Negative symptoms
Deficits in motivation, pleasure, social closeness, emotional expression
Persistent (not just acute phase)
Affects QOL more than positive sxs
Types - blunted affect, avolition, anhedonia, asociality, alogia (speech)
Disorganised symptoms
Disruptions in behaviour
Disorganised thinking (speech) - erratic speech and emotions that can’t be understood
- loose association or derailment
Disorganised motor behaviour - odd behaviour, difficulty organising tasks
- catatonia (decrease in reactivity) - instruction resistant, catalepsy, waxy flexibility, excitement, mutism, stupor
Cognitive symptoms
Separate from positive and negative, but linked to disorganised
Begins prior to schizophrenia onset, stabilises after onset, worsens after 65
Neurocognition - attention, concentration, memory, PS, EF
Social cognition - emotion recognition, ToM
Self-reports don’t match test results - those with schizophrenia feel less impaired than high-risk individuals (disorganised sxs, self-certainty)
Often not part of formal assessment/care
Cog. impairments correlate with functioning
Schizophrenia phases
Prodromal - early stage, often unrecognised until later
Active/acute - visible phase w/positive symptoms
Residual - fewer obvious symptoms
Schizophrenia DSM
A. 2+ present for significant time over 1-month period (at least one of 1, 2 or 3)
- 1. Delusions, 2. Hallucinations, 3. Disorganised speech, 4. Grossly disorganised/catatonic behaviour, 5. Negative symptoms
B. Reduction in work, social or self-care function
C. At least 6+ months, including 1 month of criterion A and may include prodromal or residual periods (only 1 neg. symptom or attenuated A)
D. Not schizoaffective, depressive or bipolar disorder
E. Not attributable to something else
F. If history of ASD or communication disorder, diagnosis only possible if hallucinations and delusions, plus other symptoms more than 1 month
Schizophreniform disorder
Only lasts between 1 and 6 months
Relatively good function, most patients resume normal life
Brief psychotic disorder
Positive sxs and/or disorganised symptoms
>1 day but <1 month
Shortest duration, often preceded by trauma or stress
Schizoaffective disorder
Schizophrenia + major mood episode (manic/depressive)
Psychotic sxs must occur outside mood disturbance for at least 2 weeks
Mood disorder present for majority of active/residual phases
Similar prognosis to schizophrenia (don’t improve on their own)
Delusional disorder
Key feature is delusions, no other positive or negative or disorganised sxs
Functioning generally not impaired, better prognosis
Differential diagnosis
Psychotic symptoms can be due to many things (other disorders, substances, medication)
Can’t only observe symptoms but must observe everything else going on
What it’s like stories
Concentration and social problems prior to onset
Onset in early adulthood
Depersonalisation (common in schizophrenia)
Schizophrenia prevalence, conceptualisation and morbidity
Prevalence - 1% of population (equal in M and F), can emerge at any time (early adulthood typical)
Conceptualisation - past (neurodegenerative - dementia praecox), current (neurodevelopmental)
Morbidity
- chronic course, most have moderate/severe impairment (21.5% employed, 85% need government assistance)
- life expectancy less than average (double mortality rate, 42-63% abuse substances, 5% die by suicide)
- often co-occurring conditions - heart disease, COPD, obesity, diabetes
Genetic risk
Main driver - 60-80% from twin studies (risk increases with genetic relatedness)
Negative symptoms stronger genetic component than positive
Healthy environment is protective however
Common variants - SNPs (342 linked to schizophrenia, increase risk by 1.06x)
Rare variants - CNVs and SNVs (approx. 12, increase risk by 2-80x)
Dopamine hypothesis
Schizophrenia due to overactive DA
- Drugs increasing DA cause symptoms and vice versa
- Studies show DA drives positive and disorganised sxs
Theory too simplistic however - other NTs involved (underactive glutamate, NMDA, GABA)
Other biological influences
Enlarged ventricles common (brain cell loss) - not specific to schizophrenia or unanimous however
Reduced grey matter and PFC volume (less activation > greater neg. severity)
Impairments in (de)activation of brain networks
Increased pro-inflammatory cytokines and oxidative stress markers
Environmental influences
Stress - pregnancy/delivery complications, abnormal foetal growth, maternal respiratory issues, maternal nutritional deficiencies, older fathers, abuse, weed
Gene-environment interaction
Abnormally low glutamate and GABA in schizophrenia postmortems (gene activity changes)
Life experiences can reduce these (which may confer risk)
Recovery
Varies from full recovery to debilitating impairment (impacted by comorbidities, long periods of untreated psychosis, social factors)
Prevention
Identify at-risk children, foster stable environments
Offer treatment at prodromal stages (including social skills training)
Treatment
Short-term hospital stays, medication, psychosocial treatment
Antipsychotics (neuroleptics)
- First generation - DA D2 antagonists (chlorpromazine/haloperidol, gave extrapyramidal side effects, tardive dyskinesia (permanent sucking motions))
- Second generation - DA D2 partial agonists, atypical antipsychotics (clozapine, leads to weight gain/sedation)
Medication compliance problematic - side effects, financial, low doctor trust
CBT - manage early relapse signs, reduce stress, reduce positive sxs preoccupation, social skills
Family therapy - reduces relapse, psychoeducation, blame avoidance reduction, communication, social network expansion
Token economies (inpatients)
Case management - connect people to services
Vocational rehab - get people working
Psychoeducation + social skills training + cognitive remediation improve functioning
