Summary of the Parkinson's lesson given by prof Gilat of the neuroscientific aspects course. It is a summary of the powerpoint slides and additional items noted during the lesson. The slides were in English and my own notes are always in Dutch as much as possible. It is therefore a mix of the 2 lan...
Why do we need to know about neural correlates and brain mechanisms as neurotherapists?
- 1. Behaviour alone can mask recovery as patients put in effort – true neural (lack of) recovery hidden?
Als we kijken naar het gedrag van de P weten we niet wat er in de hersenen gebeurd
Gedrag kan ervoor zorgen dat ze zich beter voordoen dan dat ze eigenlijk zijn (hersenen)
- 2. Knowledge of neural mechanisms thinking more deeply about the goals of therapy
- 3. Provide inspiration for a different approach to therapy
But knowledge to date is very incomplete and comes from different sources!
Interpretation into one coherent picture is difficult.
- Really improved after practice, motor improvement -> yet, the connections in
the brain that are damaged are not altered
Behaviour can hide things!
Is it good to generate hyperactivity in the non-affected side of the stroke patient?
- It can be good but also bad… different patients with different patterns
- Reducing hyperactivity can be good in severely affected patients, bad in the early phase of recovery
- What is happening in the brain? Overstimulate unaffected side or opposite?
Difficult part: this or that? One clear picture on what’s happening in the brain not possible at this moment
- Different sources and methodologies to know more (zie eerdere lessen)
- Coherent picture now not possible, try to make it as coherent as possible
1. METHODS non-invasive
← indicates methods prone to network analyses (most likely for network)
The brain is an connection-organ network analyses are increasing and combined methods (multimodal)
- Connection-organ -> specific lesion can have an effect on another region
- Network analyses! And combining methods to get an overall view
Figuuur
- EEG= electrische activiteit
- MRI
Perfusie
Bold response= spatial spec
- White matter integrity
Axonen
- Grey matter thickness
Nuclei
- Functional near infrared spectroscopy
Perfusie op cortical niveau
1.1. DIRECT MEASURES OF BRAIN ACTIVITY
EEG
- High density cap (really covered with 128 electrodes) to pick up brain activity
- Now already able to use EEG (high density) during active tasks
More and more mobile method
Transcranial Magnetic Stimulation
- Directly measuring activity of neurons -> localized measure
- Transcranial: brain facilitated or inhibited
Nala Melis Pagina 1
, Neural networks: parkinson’s disease
1.2. INDIRECT MEASURES OF BRAIN ACTIVITY
Magnetic resonance imaging
- Functional
During a task -> task based functional imaging
- Resting state
Just look at how the brain is active in rest
Learn about tendency of the brain, connect certain areas and others not
Diffusion tensor and structural imaging
- Diffusion tensor: White matter integrity
- Structural imaging: Gray matter thickness
Functional Near-Infrared Spectroscopy (mobile)
- Looking at circulation of the brain during activity
- We do not need a scanner
P can be active during the measurement
For completion:
- Molecular imaging – indirect measures of brain activity PET using radio-tracers
Glucose metabolic tracers
- Measures of neurotransmitter metabolism PET imaging using radiotracers (PD!)
Dopamine transporters
2. Invasive methods
Molecular imaging – indirect measures of brain activity PET using radio-tracers
- Glucose metabolic tracers (usually 18F-FDG)
Gelijkaardig aan bold response
o Hoe actiever region, ↑ suiker, ↑activiteit PET
- PD= ↓ glucose metabolisme
Measures of neurotransmitter metabolism PET imaging using radio-tracers
- Dopamine transporters (DAT)
Regio’s dopamine vrijgeven zien
- Figuur
Healthy
o Cirkel= putamen
PD
o Frontale zijde licht op= post. Putamen 1st aangedaan
o L>R activiteit= unilateral onset PD
- Veel nigrastriataal dopamine geprojecteerd naar putamen
- Post. Putamen=auto bewegingen
- Ant. Putamen= goal directed bewegingen+ cognitie
Jin et al. 2023 PaRD
- Careful first evidence to suggest that regular physical activity can slow down this process. Needs
verification in larger study (SPARX3)
- Actievere groep behouden dopamine activiteit beter als minder/ niet actieve groep
Fysieke activiteit helpt afremmen progressie
INTERPRETATION OF NEURAL MARKERS OF COMPENSATION – RECOVERY
Neurogenesis
- only possible in hippocampus/striatum in humans, sometimes generated from
neural stem cells and mediated by brain-derived neurotrophic factor (BDNF)
- generatie nieuwe neuronen
- BDNF
Stim. Neuronale groei, olectric spine groei
Nala Melis Pagina 2
, Neural networks: parkinson’s disease
1. GREY MATTER
Change of cortical thickness or shape of subcortical nuclei
- Exact neuronal cellular processes that underlie these changes are
unknown. Exercise- induced cortical thickness appears to occur
rapidly in M1, through arborization of dendrites and dendritic spine
growth → synaptogenesis or metabolic changes?
- We denken geen neurogenesis in cortex
Wat is corticale dikte ↑ dan?
Hippocampus = KT-geheugen
Striatum= rol in motor learning
BDNF ≠ neuro imaging
- Van CSF/bloed
- Meer = ↑ learning & plasticiteit algemeen
- Depressie= dalen tot min. + flutueren
Grey matter can be visualized with MRI (M1 = grey matter and CSF) measure the cortical
thickness in the brain. Possibly a marker of recovery.
We can expect that after exercise there is in the connections of the neurons: dendritic spine
growth and become more prominent. Dendritic spine growth is possible but the exact
process is unknown
What are the neural markers that indicate recovery? Is neurogenesis a marker?
- It is possible in the hippocampus and also in the striatum = learning centers
- It is likely that there are new neurons generated in these regions
- BDNF = molecule helps generation of neurones
these levels in the blood can be seen as a marker of recovery
very careful with this interpretation! Depression: BDNF = low, it can also fluctuate
not really a reliable marke
2. WHITE MATTER
Axonen + myelinisatie axonen
Decreased WM integrity probably refers to poor neural efficiency but multimodal
studies are not providing consistent results
White matter fibre structure changes are difficult to measure
Increased WM integrity desirable outcome (usually slow) of rehabilitation. It can also
indicate adaptive or maybe maladaptive compensation. Therefore, comparison between
pathological groups and healthy controls is therefore very important!
- Second marker could be with matter changes, but if you combine studies (WM &
functional changes) -> lower activity
- Reversed story: after recovery/exercise we can see increase WM = slow process
- Difficulty of interpretation:
Sometimes increase WM can also be an adaptive change, other areas are used more
(compensation) -> more WM light up
Compensation can be a good thing but also maladaptive (overuse of unaffected side in stroke)
Therefore: comparison of groups -> control with healthy people
WMF changes = difficult to measure, not neatly going up or down, cross fibres.
↓WM in vb MS, mogelijks bij verouderen
- Of zegggen connecties verloren= minder WM integrity
Soms zien ↓ WM tracts & bij meten met fMRI niet perse ↓ BOLD-respons
- ↓tracts ≠ ↓activiteit perse
Efficiënter?
Steeds interpreteren met andere info vb gedrag / ziekte ernstigheid/…
- ↑ziekte + ↑sympt= slecht
- ↓WM+ ↑performance (gerelateerd aan spontane/ neuroplast) = beter = efficiënter
Echter WM / GM ∆ duren lang+ veel oefenen voor meetbare ∆
3. EXAMPLE OF BETWEEN GROUP WM CHANGES
Nala Melis Pagina 3
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