Lecture 12 - Psychosis Flashcards
What are the main points this lecture looks at
*What are psychosis and
schizophrenia?
*Risk and causal factors
*Treatment, course, and
outcomes
What are the different themes that come into this topic?
Themes:
1. Nature vs Nurture
2. Socio-cultural Context
3. Individual differences
4. Bi-directional effects
What are some diagnoses points for Schizophrenia?
Involves a cluster of ‘positive symptoms’ (delusions, hallucinations, disorganised speech) and ‘negative symptoms’ (flattened speech, reduced affect, lack of initiative)
Commonly conceptualised as an illness (either you have it or you do not)
What are some diagnoses points for psychosis?
Can be used to describe a collection of ‘symptoms’
Describes a loss of contact with reality (not just hearing voices, but having a belief about where these voices are from)
Can be conceptualised as an experience that is on a continuum
What are the three A B C criteria that need to be met for a Schizophrenia diagnoses?
Criterion A: Characteristic symptoms: Two or more of the following, each
present for a significant portion of time during a one-month period. At least
one of these should include 1-3.
1. Delusions
2. Hallucinations
3. Disorganized speech
4. Grossly disorganized or catatonic behaviour
5. Negative symptoms, i.e., diminished emotional expression or avolition
Criterion B: Social/occupational dysfunction: One or more major areas of
functioning such as work, interpersonal relations, or self-care, are markedly
below the level achieved prior to the onset
Criterion C: Duration: Disturbance persist for at least six months
Exclusions: Mood disorders, substances, developmental delay or autism
What are some criticisms around the diagnosis approach
What is an environmental risk factor for developing schizophrenia?
Cannabis linked to schizophrenia (Arsenault et al., 2002: 2004) –
Dunedin Cohort
*Prospective longitudinal study in New Zealand
*Early use by 15 led to greatest risk increase. 10.3% of <15 at onset of
cannabis had psychosis/schizophrenia.
*Heavy use by age 18 associated with risk increase 6xs
*Issues of causality:- those at risk of schizophrenia ↑ likely to use cannabis?
*THC versus CBD?
*Meta-analysis of 8167 people with schizophrenia - those who used cannabis
in adolescence but not alcohol had earlier onset symptoms (Large et al.,
2011)
*Genetic susceptibility
What are some other risk factors for developing schizophrenia?
Other risk factors
*Gender: more common in males (ratio 4:1)
*Social class (?): Highest rates in lowest socioeconomic class, and
found in inner city areas
*Urbanisation (?): Prevalence of schizophrenia in Chicago. Rates
increase as get closer to city centre (Faris & Dunham, 1939).
*Immigrant groups (?): Unusually high rates of schizophrenia found for
variety of immigrant groups. In UK 2-18xs increased levels (Not
reflected by home country rates) (This is very high – more than cannabis rate??)
What do these findings reflect? Trauma? Social Inequalities? Gene x
Environment interaction?
How does epigenetics give us insight into nature-nurture interaction and schizophrenia?
Epigenetics
MZ twins who are discordant for a diagnosis of schizophrenia show differences in
gene expression (Petronis et al., 2003).
Could environmental stress or events (e.g. oxygen deprivation at birth) turn on
genes for certain traits in one twin and not the other? Or could the effects on the
brain push the affected twin over the threshold (cumulative adversity?)
Does genetic susceptibility predispose people to experience more adverse effects
from environmental stress? E.g. cannabis
Fetal oxygen deprivation is associated with brain abnormalities in later life, but the
effects might depend on genetic predisposition (Cannon et al., 2002 review of
prospective studies)
People whose mothers had been exposed to the flu in the second trimester were significantly more likely to develop schizophrenia.
Biology: genetics and schizophrenia
- ‘Schizophrenia’ is heterogeneous – what phenotype are we looking for? Need
research directed toward symptom clusters? - Twin studies – could the MZ rates be over-estimated because identical twins
share the same prenatal environment? Concordance rates for MZ twins who
share a placenta are 60% vs. 11% for MZ twins with separate placenta
Neurochemistry - Time lag in actions of drugs: Blockage of the dopamine system from medication
occurs in hours, any benefit takes weeks, why? (see Bentall, 2004) - About 1/3 patients don’t respond to treatment – why?
- Pharmacology more effective for positive than negative symptoms
- Not all studies find differences in DA receptors and/or alternations in brain
functioning (Buchsbaum et al., 1992; Heinrichs, 2001) – related to environmental
differences, e.g. trauma?
Neurochemistry: the dopamine hypothesis and schizopphenia
- Pharmacology: Drugs that block dopamine receptors (e.g. Chlorpromazine) helpful for Schizophrenia
- Amphetamines: Linked to excess dopamine. Amphetamine abuse can lead to a psychosis including paranoia and auditory hallucinations (Kalant, 1966)
- Parkinson’s Disease: Drug L-Dopa used to increase dopamine -> side effect can be
psychosis. Dates back to 1960’s – link to positive symptoms
What are some critiques of the biological approaches (genetics and neurochemistry)?
Genetics
1. ‘Schizophrenia’ is heterogeneous – what phenotype are we looking for? Need
research directed toward symptom clusters?
2. Twin studies – could the MZ rates be over-estimated because identical twins
share the same prenatal environment? Concordance rates for MZ twins who
share a placenta are 60% vs. 11% for MZ twins with separate placenta
Neurochemistry
3. Time lag in actions of drugs: Blockage of the dopamine system from medication
occurs in hours, any benefit takes weeks, why? (see Bentall, 2004)
4. About 1/3 patients don’t respond to treatment – why?
5. Pharmacology more effective for positive than negative symptoms
6. Not all studies find differences in DA receptors and/or alternations in brain
functioning (Buchsbaum et al., 1992; Heinrichs, 2001) – related to environmental
differences, e.g. trauma?
What about cognitive factors and schizophrenia?
Lincoln et al. (2011): negative symptoms of schizophrenia associated
with lower self-esteem and negative self-concept about interpersonal
abilities
Kesting and Lincoln (2013): psychotic disorders appear to reflect low
self-esteem and that this might make people feel they ‘deserve’ to be
persecuted
Cognitive process
Moritz and Woodward (2006): study showing people with diagnosis of
schizophrenia appear to have a bias against disconfirmatory evidence
Dudley et al. (2016): meta-analysis showing people with psychosis
require less information to make decisions (‘jumping to conclusions bias’) [this last part – jar of green and yellow marbles. Ask them if there is more green or yellow marbles in the jar. They take 2 out. They go well there are more yellow marbles cos you took 2 out but many would say I need to see more marbles]
From the cognitive perspective - how can you help as a therapist?
Cognitive models of psychotic experiences [How do you help as a therapist?]
A variety of models exist that explain psychosis and associated
experiences from a cognitive perspective, explaining how
biological and environmental factors lead to cognitive features in
the first place, and the role of stress as a trigger for developing
psychosis in this context (i.e., a diathesis-stress model)
o Garety: a model explaining the development and maintenance of
positive symptoms
o Morrison: a model explaining how people interpret anomalous
experiences and how this ultimately maintains these experiences
o Freeman: a model explaining persecutory delusions
You don’t say you don’t have a chip in your brain, you go via socratic questioning. Patients may leave therapy still thinking chip there but doing less harm than thought. How does it work if a voice is not negatively interpreted? Just positive ones maybe? In that case can therapy help???? Maybe not.
CBT for psychosis is not about getting rid of the psychosis but more about challenging the worst aspects they have.
