Lecture 20: schizophrenia Flashcards
Define delusions? What are the 4 types in schizophrenia?
delusions: false beliefs
- persecutions
- reference
- influence
- grandeur
Persecution delusion description?
False conviction that others are conspiring against you
Reference delusion description?
False belief that everything occurring around them is related to and about them
- People are writing about them, laughing about them
Influence delusion description?
other people or external agents are exerting powers over themselves covertly
Grandeur delusion description?
false attribution to the self of great ability, knowledge, importance, or worth
What are the 6 hypotheses of schizophrenia?
- Genetics
- Brain anatomy changes
- Dopamine hypothesis
- Glutamate hypothesis
- Serotonin hypothesis
- Inflammatory hypothesis
Genetics hypothesis?
- genetics plays an important role, but isn’t the ultimate determiner
- much more likely to get schizophrenia if close members of your family have had it though
- important gene = COMT
DA hypothesis?
- originally thought it was overactive DA system
- amphetamines caused high DA –> made people psychotic
- drugs that decrease DA decrease symptoms
- drugs that block access to D2 receptors reduce “positive” symptoms
What are the problems with the DA hypothesis of schizophrenia?
- elevated DA levels can only explain why they experience positive symptoms, not negative symptoms
- not all schizophrenics have high levels of DA
- drugs don’t work for negative and cognitive symptoms
instead… - DA dysregulation model –> hyper activity in some areas and hypo activity in others
Why is it important that the gene encoding COMT might be dysregulated in schizophrenia? (think of the role of this gene in dopamine and the dopamine hypothesis)
- COMT is involved in dopamine breakdown
- if there is dysregulation in COMT in people with schizophrenia, it supports that they have excess dopamine (because it is not being properly broken down)
Glutamate hypothesis?
- hypofunction of glutamate (NMDA) receptors
- PCP (NMDA antagonist) induces effects, works on pos. and neg. symptoms
- effective in animal studies
- treatment has not shown conclusive results
How does the understanding of the mechanism of PCP help in the understanding of the biological basis of schizophrenia
- increase glutamate and dopamine release in the prefrontal cortex
- there is NMDA hypoactivity in the prefrontal cortex
- improve negative symptoms by increasing the DA and glutamate in the prefrontal cortex
Serotonin hypothesis?
- hyperactivity of 5HT2A receptors in glutamate neurons in the cortex
- serotonin antagonists to block the receptors treats psychosis in parkinson’s patients, seems like it would work for schizophrenia
- relevant for hallucinations
Inflammatory hypothesis?
- schizophrenics have higher rates of autoimmune diseases
- higher levels of cytokines
What anatomical changes can be observed in the ventricles, limbic system and thalamus? What is the significance of those changes in the success of the treatments?
- enlarged ventricles
- loss of brain tissue
- larger ventricles = less effective treatment
- limbic system
–> smaller hippocampus & amygdala - smaller thalamus
- reduced blood flow
- hypofrontality
