REVA
Inhoud
REVA....................................................................................................................... 1
🔹 Appendix 1 – Overzicht van leerstrategieën uit het raamwerk (vertaald) ....30
1. Foutloos leren (Errorless Learning – EL)...................................................30
2. Analogie leren (Analogy Learning – AL)....................................................31
3. Observerend leren (Observational Learning)...........................................32
4. Motorische mentale oefening (Mental Practice – MP)...............................32
5. Proefondervindelijk leren (Trial-and-Error Learning).................................33
6. Instructiegestuurd leren (Instructed Learning).........................................33
7. Dubbele taak leren (Dual-Task Learning).................................................34
🧠 Samenvatting van het Artikel: Revisiting the Symptoms and Signs of
Cerebellar Syndrome......................................................................................... 56
American Association of College of Nursing:................................................89
Week 1 Kennisclip MS
Doelstellingen:
- De medische symptomatologie bij MS verklaren.
- De incidentie en prevalentie cijfers reproduceren.
- De verschillende vormen van MS onderscheiden.
MS: oorzaak, symptomen en medische behandeling.
,MS is een Demyelinating disease of the central neurosystem. This includes the
brain and the spinal cord. Myelin is the protective sheets thatsurrounds the axon
of neurons. Allowing them to quickly sends electrical impulses. This myolin is
produced by Oligodendrocyte, which are a group of cells that supports neurons.
In multiple sclerosis de-myelations happens when the immune system
innapropriatly attacs the myelin, which makes communications between neurons
break down, ultimately leading to all sorts of sensory, motor and cognitive
problems.
The brain and the neurons in the brain is protected from things in the blood by
the blood brain barriere. Which only lets certain molecules and cells thru from the
blood. For immune cells like T- and B-cells that means they have to have the right
lygin or service molecule to get trhu the blood brain barriere. This is kind of like
having a VIP pass to get into a exclusive club. Once a T-cell can make its way in it
can get activeded by something it encounters. In the case of MS it can get
activated by myelin.
Once the T-cell gets activated it changes the
blood brain barriere cels to get more
receptors and this allowes immune cells to more easily bind and get in. its kind of
like bribing the bouncer to let in a lot of people.
MS is a Type 4 hypersensitivity reaction. Cell – mediated hypersensitivity.
This means those myolen specific T-cells release cytokines, which dyolate the
blood vessels, which allowes more immune cells to get in. as it directly causes
damage to the elecrodendocytes.
,these cytokines also attracted B-cells and macrophages as part of the
inflammatory reaction.
Those B-cells start to make anti-bodys that mark the myoline sheet proteins. And
then the macrophages use the anti-body markers to engulf and destroy
oligodendrocytes, without oligodendrocytes there is no myolin to cover the
neurons and this leaves behind areas of scar tissue, also called plaques or sclera.
In MS these attacs typaccly happen in bouts. In other words an autoimmune attac
on the oligodendrocytes might happen and regulatory T-cells come in to inhabet
or calm down the othes immune cells leading to a reduction in the inflammation.
Early on in MS the oligodendrocytes will heal and extend out new myolins to
cover the neurons, which is a process calles remyelination. Unfortinatly tho as
time goes by the oligodendrocytes die off, the remyelation stops and the damage
becomes irreversible with the loss of axons. Just like other autoimmune diseases,
the exact cause of multiple scleroses is unknown, but its linked to both genetic
and enviromental factors.
- Genetic risk factor include being female and having genes that encode a
specific type of immune molecule called hla-dr2, which is used to identify
and bind foreign molecules
- Enronmental factors; are caused by infections of vitimine – D deficiency,
which is an interesting one because it might help explain why the rates of
MS are highe at the northern and southern poles, compared to the equator
where there is a lot more sunlight. Together these genetic and
environmental influences might lead too the body not killing off immune
cells that target myolin.
It turns out that there are 4 main types of MS, based on the pattern of symptoms
over time.
1. Relapsing – remitting (RRMS)
Attacs happen months or even years apart and causing an increase in the
level of dysability. For example a peron might lose some vision, but it
might be followed by improvement if there is remyolation. Unfortunately
more oftan than not the remyolation prosess is not completed, so there is
often some residual disability that remains. That means that with eacht
attac the central nervous system gets irriversibally damaged. In this type
there is typically no increase in disability between bouts, the line stays flat
during that time.
2. Secundairy progressive MS (SPMS)
, This one is pretty similar to the relapsing – remitting type, but over time
the immune attack becomes constant, which causes a steady progression
in dysability..
3. Primary progressive MS (PPMS)
Basically one constant attack on myolin, which causes a steady
progression on dysability over a perons lifetime.
4. Progressing – relapsing MS (prms)
Which is also one constant attack but this time its super imposed, which
means the disability happens even faster.
Specific symptoms very a lot from person to person, and lagerly depends on the
location of the plaques
* MS typaccly effects between age 20-40 yrs old
* Worsen over weeks and linger for months without treatment
Charcots neurologic traid
This includes dysartria (difficulty speaking) due to plaques in the brainstem
that effacts neurofibers that control muscles of the mouth and throat this can
innerfere with conscious movement like eating and talking and could lead to
things like stutter.
As well as uncounsious movement like swallowing
Inhoud
REVA....................................................................................................................... 1
🔹 Appendix 1 – Overzicht van leerstrategieën uit het raamwerk (vertaald) ....30
1. Foutloos leren (Errorless Learning – EL)...................................................30
2. Analogie leren (Analogy Learning – AL)....................................................31
3. Observerend leren (Observational Learning)...........................................32
4. Motorische mentale oefening (Mental Practice – MP)...............................32
5. Proefondervindelijk leren (Trial-and-Error Learning).................................33
6. Instructiegestuurd leren (Instructed Learning).........................................33
7. Dubbele taak leren (Dual-Task Learning).................................................34
🧠 Samenvatting van het Artikel: Revisiting the Symptoms and Signs of
Cerebellar Syndrome......................................................................................... 56
American Association of College of Nursing:................................................89
Week 1 Kennisclip MS
Doelstellingen:
- De medische symptomatologie bij MS verklaren.
- De incidentie en prevalentie cijfers reproduceren.
- De verschillende vormen van MS onderscheiden.
MS: oorzaak, symptomen en medische behandeling.
,MS is een Demyelinating disease of the central neurosystem. This includes the
brain and the spinal cord. Myelin is the protective sheets thatsurrounds the axon
of neurons. Allowing them to quickly sends electrical impulses. This myolin is
produced by Oligodendrocyte, which are a group of cells that supports neurons.
In multiple sclerosis de-myelations happens when the immune system
innapropriatly attacs the myelin, which makes communications between neurons
break down, ultimately leading to all sorts of sensory, motor and cognitive
problems.
The brain and the neurons in the brain is protected from things in the blood by
the blood brain barriere. Which only lets certain molecules and cells thru from the
blood. For immune cells like T- and B-cells that means they have to have the right
lygin or service molecule to get trhu the blood brain barriere. This is kind of like
having a VIP pass to get into a exclusive club. Once a T-cell can make its way in it
can get activeded by something it encounters. In the case of MS it can get
activated by myelin.
Once the T-cell gets activated it changes the
blood brain barriere cels to get more
receptors and this allowes immune cells to more easily bind and get in. its kind of
like bribing the bouncer to let in a lot of people.
MS is a Type 4 hypersensitivity reaction. Cell – mediated hypersensitivity.
This means those myolen specific T-cells release cytokines, which dyolate the
blood vessels, which allowes more immune cells to get in. as it directly causes
damage to the elecrodendocytes.
,these cytokines also attracted B-cells and macrophages as part of the
inflammatory reaction.
Those B-cells start to make anti-bodys that mark the myoline sheet proteins. And
then the macrophages use the anti-body markers to engulf and destroy
oligodendrocytes, without oligodendrocytes there is no myolin to cover the
neurons and this leaves behind areas of scar tissue, also called plaques or sclera.
In MS these attacs typaccly happen in bouts. In other words an autoimmune attac
on the oligodendrocytes might happen and regulatory T-cells come in to inhabet
or calm down the othes immune cells leading to a reduction in the inflammation.
Early on in MS the oligodendrocytes will heal and extend out new myolins to
cover the neurons, which is a process calles remyelination. Unfortinatly tho as
time goes by the oligodendrocytes die off, the remyelation stops and the damage
becomes irreversible with the loss of axons. Just like other autoimmune diseases,
the exact cause of multiple scleroses is unknown, but its linked to both genetic
and enviromental factors.
- Genetic risk factor include being female and having genes that encode a
specific type of immune molecule called hla-dr2, which is used to identify
and bind foreign molecules
- Enronmental factors; are caused by infections of vitimine – D deficiency,
which is an interesting one because it might help explain why the rates of
MS are highe at the northern and southern poles, compared to the equator
where there is a lot more sunlight. Together these genetic and
environmental influences might lead too the body not killing off immune
cells that target myolin.
It turns out that there are 4 main types of MS, based on the pattern of symptoms
over time.
1. Relapsing – remitting (RRMS)
Attacs happen months or even years apart and causing an increase in the
level of dysability. For example a peron might lose some vision, but it
might be followed by improvement if there is remyolation. Unfortunately
more oftan than not the remyolation prosess is not completed, so there is
often some residual disability that remains. That means that with eacht
attac the central nervous system gets irriversibally damaged. In this type
there is typically no increase in disability between bouts, the line stays flat
during that time.
2. Secundairy progressive MS (SPMS)
, This one is pretty similar to the relapsing – remitting type, but over time
the immune attack becomes constant, which causes a steady progression
in dysability..
3. Primary progressive MS (PPMS)
Basically one constant attack on myolin, which causes a steady
progression on dysability over a perons lifetime.
4. Progressing – relapsing MS (prms)
Which is also one constant attack but this time its super imposed, which
means the disability happens even faster.
Specific symptoms very a lot from person to person, and lagerly depends on the
location of the plaques
* MS typaccly effects between age 20-40 yrs old
* Worsen over weeks and linger for months without treatment
Charcots neurologic traid
This includes dysartria (difficulty speaking) due to plaques in the brainstem
that effacts neurofibers that control muscles of the mouth and throat this can
innerfere with conscious movement like eating and talking and could lead to
things like stutter.
As well as uncounsious movement like swallowing
