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.

Showing posts with label It's too hard. Show all posts
Showing posts with label It's too hard. Show all posts

Saturday, May 11, 2019

Sleep as a model to understand neuroplasticity and recovery after stroke: Observational, perturbational and interventional approaches

Useless piece of crap. Nothing here will help survivors recover. You should all be fired. 

Sleep as a model to understand neuroplasticity and recovery after stroke: Observational, perturbational and interventional approaches

Abstract

Our own experiences with disturbances to sleep demonstrate its crucial role in the recovery of cognitive functions. This importance is likely enhanced in the recovery from stroke; both in terms of its physiology and cognitive abilities. Decades of experimental research have highlighted which aspects and mechanisms of sleep are likely to underlie these forms of recovery. Conversely, damage to certain areas of the brain, as well as the indirect effects of stroke, may disrupt sleep. However, only limited research has been conducted which seeks to directly explore this bidirectional link between both the macro and micro-architecture of sleep and stroke. Here we describe a series of semi-independent approaches that aim to establish this link through observational, perturbational, and interventional experiments. Our primary aim is to describe the methodology for future clinical and translational research needed(So you want someone else to do the actual hard work of solving this? Too hard for you? Not your job?) to delineate competing accounts of the current data. At the observational level we suggest the use of high-density EEG recording, combined analysis of macro and micro-architecture of sleep, detailed analysis of the stroke lesion, and sensitive measures of functional recovery. The perturbational approach attempts to find the causal links between sleep and stroke. We promote the use of transcranial magnetic stimulation combined with EEG to examine the cortical dynamics of the peri-infarct stroke area. Translational research should take this a step further using optogenetic techniques targeting more specific cell populations. The interventional approach focuses on how the same clinical and translational perturbational techniques can be adapted to influence long-term recovery of function.

KEYWORDS:

Brain damage; EEG; Functional recovery; Sleep; Slow waves; Stroke; Translational
PMID:
30571989
DOI:
10.1016/j.jneumeth.2018.12.011
Free full text

Wednesday, February 21, 2018

Pre-therapy neural state of bilateral motor and premotor cortices predicts therapy gain after subcortical stroke: A pilot study

You fucking bastards are once again wasting time and money on predictions rather than solving all the problems in stroke. Your mentors and senior researchers need to be keel-hauled. If solving stroke is too hard for you take up macrame and let better people into the field. 
https://search.naric.com/research/rehab/redesign_record.cfm?search=2&type=all&criteria=J77787&phrase=no&rec=135758&article_source=Rehab&international=0&international_language=&international_location=
American Journal of Physical Medicine and Rehabilitation , Volume 97(1) , Pgs. 23-33.

NARIC Accession Number: J77787.  What's this?
ISSN: 0894-9115.
Author(s): Cirstea, Carmen M.; Lee, Phil; Craciunas, Sorin C.; Choi, In-Young; Burris, Joseph E.; Nudo, Randolph J..
Publication Year: 2018.
Number of Pages: 12.
Abstract: Study investigated whether neural state of spared motor and premotor cortices captured before therapy predicts therapy-related motor gains in chronic subcortical stroke. Ten stroke survivors with chronic, moderate upper-limb impairment underwent proton magnetic resonance spectroscopy, magnetic resonance imaging, clinical, and kinematics assessments before a 4-week impairment-oriented training. Clinical/kinematics assessments were repeated after therapy, and motor gain was defined as positive values of clinical upper-limb/elbow motion changes and negative values of trunk motion changes. Candidate predictors were N-acetylaspartate-neuronal marker, glutamate-glutamine-indicator of glutamatergic neurotransmission, and myo-inositol-glial marker, measured bilaterally within the upper limb territory in motor and premotor (premotor cortex, supplementary motor area) cortices. Traditional predictors (age, stroke length, pre-therapy upper-limb clinical impairment, infarct volume) were also investigated. Results indicated poor motor gain was associated with lower glutamate-glutamine levels in ipsilesional primary motor cortex and premotor cortex, lower N-acetylaspartate in ipsilesional premotor cortex, higher glutamate-glutamine in contralesional primary motor cortex, and lower glutamate-glutamine in contralesional supplementary motor area. These predictors outperformed myo-inositol metrics and traditional predictors. The findings suggest that glutamatergic state of bilateral motor and premotor cortices and neuronal state of ipsilesional premotor cortex may be important for predicting motor outcome in the context of a restorative therapy.
Descriptor Terms: BIOCHEMISTRY, BIOENGINEERING, BODY MOVEMENT, BRAIN, IMAGING, LIMBS, MOTOR SKILLS, OUTCOMES, STROKE, THERAPEUTIC TRAINING.


Can this document be ordered through NARIC's document delivery service*?: Y.

Citation: Cirstea, Carmen M., Lee, Phil, Craciunas, Sorin C., Choi, In-Young, Burris, Joseph E., Nudo, Randolph J.. (2018). Pre-therapy neural state of bilateral motor and premotor cortices predicts therapy gain after subcortical stroke: A pilot study.  American Journal of Physical Medicine and Rehabilitation , 97(1), Pgs. 23-33. Retrieved 2/21/2018, from REHABDATA database.

Wednesday, July 27, 2016

One researcher’s journey to understand the molecular basis of aging, using blood

Not that I'm suggesting you do this but the first order of business is to ask your doctor what the corresponding age of humans is to the young mice used in these experiments. You have to know how young your grandchildren have to be. Then, since 16 is the age to legally donate blood via the Red Cross you probably have to find a black market phlebotomist. Don't do this, it is not proven yet.  Or you can wait decades until the TGF-β1 molecule is tested and fabricated. Or maybe if you have a cool $100 million to spend you can hire your own researchers to solve this. Our fucking failures of stroke associations will do nothing about this. 'It's too hard.'
http://scopeblog.stanford.edu/2016/07/27/one-researchers-journey-to-understand-the-molecular-basis-of-aging-using-blood/