You will need to demand answers from your doctor how this is different from the current theories on how neuroplasticity works. Then get new stroke protocols. Be insistent, your doctor is supposed to help you recover, not just sit on the sideline. Your doctor needs to be able to predict how synapses form and what it will take to do that. God, this is so blasted simple, does your doctor have any brains at all?
http://www.alphagalileo.org/ViewItem.aspx?ItemId=135224&CultureCode=en
The human brain keeps changing throughout a person’s lifetime. New
connections are continually created while synapses that are no longer in
use degenerate. To date, little is known about the mechanisms behind
these processes. Jülich neuroinformatician Dr. Markus Butz has now been
able to ascribe the formation of new neural networks in the visual
cortex to a simple homeostatic rule that is also the basis of many other
self-regulating processes in nature. With this explanation, he and his
colleague Dr. Arjen van Ooyen from Amsterdam also provide a new theory
on the plasticity of the brain – and a novel approach to understanding
learning processes and treating brain injuries and diseases.
The brains of adult humans are by no means hard wired. Scientists
have repeatedly established this fact over the last few years using
different imaging techniques. This so-called neuroplasticity not only
plays a key role in learning processes, it also enables the brain to
recover from injuries and compensate for the loss of functions.
Researchers only recently found out that even in the adult brain, not
only do existing synapses adapt to new circumstances, but new
connections are constantly formed and reorganized. However, it was not
yet known how these natural rearrangement processes are controlled in
the brain. In the open-access journal PLOS Computational Biology, Butz
and van Ooyen now present a simple rule that explains how these new
networks of neurons are formed (DOI: 10.1371/journal.pcbi.1003259).
“It’s very likely that the structural plasticity of the brain is the
basis for long-term memory formation,” says Markus Butz, who has been
working at the recently established Simulation Laboratory Neuroscience
at the Jülich Supercomputing Centre for the past few months. “And it’s
not just about learning. Following the amputation of extremities, brain
injury, the onset of neurodegenerative diseases, and strokes, huge
numbers of new synapses are formed in order to adapt the brain to the
lasting changes in the patterns of incoming stimuli.”
Activity regulates synapse formation
These results show that the formation of new synapses is driven by
the tendency of neurons to maintain a ‘pre-set’ electrical activity
level. If the average electric activity falls below a certain threshold,
the neurons begin to actively build new contact points. These are the
basis for new synapses that deliver additional input – the neuron firing
rate increases. This also works the other way round: as soon as the
activity level exceeds an upper limit, the number of synaptic
connections is reduced to prevent any overexcitation – the neuron firing
rate falls. Similar forms of homeostasis frequently occur in nature,
for example in the regulation of body temperature and blood sugar
levels.
However, Markus Butz stresses that this does not work without a
certain minimal excitation of the neurons: “A neuron that no longer
receives any stimuli loses even more synapses and will die off after
some time. We must take this restriction into account if we want the
results of our simulations to agree with observations.” Using the visual
cortex as an example, the neuroscientists have studied the principles
according to which neurons form new connections and abandon existing
synapses. In this region of the brain, about 10 % of the synapses are
continuously regenerated. When the retina is damaged, this percentage
increases even further. Using computer simulations, the authors
succeeded in reconstructing the reorganization of the neurons in a way
that conforms to experimental results from the visual cortex of mice and
monkeys with damaged retinas.
The visual cortex is particularly suitable for demonstrating the new
growth rule, because it has a property referred to as retinotopy: This
means that points projected beside each other onto the retina are also
arranged beside each other when they are projected onto the visual
cortex, just like on a map. If areas of the retina are damaged, the
cells onto which the associated images are projected receive different
inputs. “In our simulations, you can see that areas which no longer
receive any input from the retina start to build crosslinks, which allow
them to receive more signals from their neighbouring cells,” says
Markus Butz. These crosslinks are formed slowly from the edge of the
damaged area towards the centre, in a process resembling the healing of a
wound, until the original activity level is more or less restored.
Synaptic and structural plasticity
“The new growth rule provides structural plasticity with a principle
that is almost as simple as that of synaptic plasticity,” says co-author
Arjen van Ooyen, who has been working on models for the development of
neural networks for decades. As early as 1949, psychology professor
Donald Olding Hebb discovered that connections between neurons that are
frequently activated will become stronger. Those that exchange little
information will become weaker. Today, many scientists believe that this
Hebbian principle plays a central role in learning and memory
processes. While synaptic plasticity in involved primarily in short-term
processes that take from a few milliseconds to several hours,
structural plasticity extends over longer time scales, from several days
to months.
Structural plasticity therefore plays a particularly important part
during the (early) rehabilitation phase of patients affected by
neurological diseases, which also lasts for weeks and months. The vision
driving the project is that valuable ideas for the treatment of stroke
patients could result from accurate predictions of synapse formation. If
doctors knew how the brain structure of a patient will change and
reorganize during treatment, they could determine the ideal times for
phases of stimulation and rest, thus improving treatment efficiency.
New approach for numerous applications
“It was previously assumed that structural plasticity also follows
the principle of Hebbian plasticity. The findings suggest that
structural plasticity is governed by the homeostatic principle instead,
which was not taken into consideration before,” says Prof. Abigail
Morrison, head of the Simulation Laboratory Neuroscience at Jülich. Her
team is already integrating the new rule into the freely accessible
simulation software NEST, which is used by numerous scientists
worldwide.
These findings are also of relevance for the Human Brain Project.
Neuroscientists, medical scientists, computer scientists, physicists,
and mathematicians in Europe are working hand in hand to simulate the
entire human brain on high-performance computers of the next generation
in order to better understand how it functions. “Due to the complex
synaptic circuitry in the human brain, it’s not plausible that its fault
tolerance and flexibility are achieved based on static connection
rules. Models are therefore required for a self-organization process,”
says Prof. Markus Diesmann from Jülich’s Institute of Neuroscience and
Medicine, who is involved in the project. He heads Computational and
Systems Neuroscience (INM-6), a subinstitute working at the interface
between neuroscientific research and simulation technology.
Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 29,112 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
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