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Behavioural Disorders
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31/08/2021 PBL 01: Dichotomy or continuum- Exam same format as with Brain Damage.
- Lectures some prerecorded and some online.
- He follows what we have discussed and takes into account the exam.
Notes on the problem:
- Some people have the benign symptoms of psychotic behaviour and it is of question
why in some people this expresses it as full-blown psychosis and why in other people
not.
- Coffee (more than 5 cups) may tip over people into showing psychotic symptoms.
- Auditory/visual hallucinations distinctly clinical from non-clinical and this depends on
age of onset/emotional valence of the voice etc.
Discussion:
- Age of onset and the more judgement there was more chance of developing a
psychosis
- More occuring is primary psychosis and less relevant is secondary psychosis.
- Prevalence is higher in urban areas and prevalence
- Excess in dopamine release > different dopamine pathways and some are
depleted/or some excess of dopamine, so drug-induced psychotic symptoms
- Highly inheritable and can skip generations and occurs together with schizophrenia.
- Genetic + environmental factors (attachment of parent and child)
- Caffeine as a trigger factor in people who are vulnerable
- Psychosis is more a symptom instead of disease on its own, since it is also a
symptom in schizophrenia for example. However, every healthy person can get
psychosis, but not everyone becomes schizophrenic and hallucinations are quite
common.
- Sex differences and response to drugs
- The more persisted, the more chance that you can develop such a disease (a drug
also can be).
- Maybe some of these religious visions may be related to seeing or hearing people >
combination of delusion and mindset or some bipolar disorder. Psychosis is more a
disorder, I would not consider it as a disorder.
a. One event is that called psychotic/life-changing would you call that as a
psychosis as a disease?
b. Occurs more often > brief psychotic disorder and could be 1 day/1 month
according to DSM > some distinction in time same for schizophrenia for
example
c. Only hallucinations without delusions etc. is that still psychosis
- DSM hallucinations and delusions to consider it as a psychosis and disrupts normal
life.
- More of a symptom because it is related to multiple disorders (depression) > brain
disease leading towards psychotic symptoms.
- It depends on the degree of impairment, you cannot compare psychosis in relation to
depression or psychosis on it’s own
- Drugs/stress/trauma/grief are environmental factors that could be of influence to get
full-blown psychosis
, - Hallucinations are part of psychosis.
- Biopsychosocial look to combine
- Coffee:
a. Environmental and genetic predisposition plays a role
b. Psychotic symptoms is different from diagnosis psychosis
c. Sleep deprivation lead to coffee and also lead to psychotic like experiences
- Arch of the bow in the disease model:
a. Psychosis comes in peaks
b. Psychotic limitations > cognitive aspects of psychosis
Keywords tutor:
- Age-related changes
- Model
- What leads to expression of disease from symptoms to disease
- Non-medical/medical
- Environment + genetic risk factors
- Continuum spectrum
- Sex differences
- Degree of severity
- Schizophrenia
- Dopamine
- Drugs/drug-induced
- Hallucination vs psychosis
- Visions/religious vs disorder
- How to diagnose psychosis
Questions:
1. What is psychosis? What is the difference with other
disorders/hallucinations/delusions and how is it described in DSM-5?
2. Different disorders/diseases where it plays a role in?
3. What does this model entail and what does it say about psychosis and the
development of it?
4. Environmental factors that lead to developing psychosis?
5. Biological explanation of psychosis with the two dopamine tracks?
6. How comes heredity into play in psychosis?
7. Main differences between primary and secondary psychosis?
8. Treatment of diagnosis?
9. What characteristics divide clinical from non-clinical patients?
10. What is the advantage of more diagnosing on a continuum spectrum instead of
dichotomy?
Learning goals:
1. What is psychosis and what is not psychosis?
a. Which biological and environmental factors play a role?
2. How can psychosis best be diagnosed?
a. In which pathologies play a role?
b. Is the spectrum dichotomous or continuous?
c. Differences between clinical and non-clinical cases of psychoses?
, d. Possible intervention?
3. What does the model actually state/explain the figure > psychosis-proneness-persistence-
impairment’ model?
a. Is it a realistic model or outdated?
b. Is it used in the clinic or in research?
01/09/2021 HC 01: Intro into Brain Imaging
Overview of field and course
Recent developments have developed, so a lot of knowledge that we had, was obtained via
studying post-mortem brains > of course very delayed > only can we see what happened
after a person died. We know a lot about single neurons, but this is all based on animal
studies, but we want to study this in humans.
Last decades > major shift with new techniques (neuroimaging) and allow to study the brain
non-invasively in alive human subjects while they perform tasks > major change in the field.
fMRI was developed in the 80's and 90’s and is the most important technique used. Also a
major shift by studying how different regions interact and took off in the last 10 years. Major
shifts in how we study the brain and impacts our knowledge and how we assess brain
disorders.
1. Field started off with physics and basic research on neuroimaging technique > what
kind of analysis where you can show brain connectivity/how it exactly works etc.
2. Cognitive neuroscience > primarily focuses on different general cognitive functions
(emotions, fear) which brain mechanisms are involved > within subject design (1
person does tasks A and B and looks at the contrast and identifies which brain
regions are involved) > how particular functions are represented in the brain.
3. Clinical neuroscience > shift in focus and are interested in people deviating from the
norm, we want to not look at the population in general, but how these people differ. Is
based on basic research of the steps above.
To really understand clinical neuroscience, you need the basics above.
Clinical neuroimaging:
- Many studies linking brain and behaviour did not replicate
- But now we have much larger datasets that become available (Human Brain Initiative
+ large cohort studies)
- One of the things shown > looking at brain-behaviour relations we need those large
sample sets and is the same with those genetic studies. We found genetic markers >
a lot of these do not replicate > brain-wide genetic studies (looking at all genes)
shows that this is only possible with big datasets > if you want brain-behavioural
phenotype across the brain, you really need large datasets.
These datasets are now becoming available. Depending on where you place the electrode
with deep brain stimulation, the participant will respond with it’s own network and depends
on location of electrode.
The way we studied the brain previously does not give you a really good insight in how the
brain works > another example that the field is really changing. If you look at a particular
brain area it is involved in almost all mental functions. Disorders are heterogeneous and see
a wide variety of symptoms in patients and are labeled under the same label > but how in
, the brain, the heterogeneously is a disadvantage and currently we give a treatment only
good for a subset of patient, so the question is, is it the right way to group those patients
under one label?
Intro into neuroimaging
Main technique is MRI and involves a big magnet and a participant lies with its head in the
coil and there are different sequences where you can study different ways the brain
(structure/function (depends on what the person is doing).
A wide field of research techniques and most dominant way to relate brain processes to
behavioural traits:
- Performance on cognitive tasks > focus on the task in general and the brain regions
involved (cognitive neuroscience).
- Inter-individual differences > a lot of differences in healthy people, quite a distribution
across properties across healthy people.
- Disease conditions > difference in brain activity deviates from the distribution in
healthy participants.
A lot is possible and definitely has its advantages, but there are pitfalls/limitations and makes
you a critical user.
Techniques:
- MEG & EEG
- Radioactive ligand imaging (SPECT, PET)
- Near-infrared spectroscopy
- Optical imaging
- fMRI
- Structural MRI
- Diffusion weighted MRI > another form of structural and study the pathways in the
brain
- MR spectroscopy
Structural imaging:
- Magnetic resonance based
a. Structural MRI, diffusion MRI, MR spectroscopy
b. X-rays
c. Ultrasound echography
d. Metabolic (PET/SPECT)
Functional imaging:
a. Electrophysiology based > EEG and MEG (local field potentials)
b. Measuring blood oxygen level dependent (fMRI)
c. Metabolic > radioactive metabolic compounds
When looking at those techniques, we can pair them based on spatial and temporal
resolution (time and spatial skill allow us to study brain functioning).
- EEG and MEG have low spatial resolution and only study for the whole brain or
different brain regions (maps), but it has high temporal resolution and can study
processes that happen really fast.
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