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.

Saturday, April 17, 2021

Multimodal imaging of brain reorganization in motor areas of the contralesional hemisphere of well recovered patients after capsular stroke

 In 15 years has ANYTHING AT ALL been done with this to create recovery protocols?  Or is your doctor using the fucking statement; 'All strokes are different, all stroke recoveries are different' to justify inaction?

Multimodal imaging of brain reorganization in motor areas of the contralesional hemisphere of well recovered patients after capsular stroke

  Christian Gerloff, 1,2
Khalaf Bushara, 2
Alexandra Sailer, 1
Eric M. Wassermann, 4
Robert Chen, 2
Takahiro Matsuoka, 2
Daniel Waldvogel, 2
George F. Wittenberg, 3
Kenji Ishii, 2
Leonardo G. Cohen 3
and Mark Hallett 2
1 Cortical Physiology Research Group, Department of Neurology, Eberhard–Karls University Medical School, Tuebingen,Germany; Sections of
 2 Human Motor Control and 3 Human Cortical Physiology, Medical Neurology Branch and
 4 BrainStimulation Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
Correspondence to: Christian Gerloff, MD, Department of General Neurology, Hertie Institute for Clinical Brain Research,University of Tuebingen, Hoppe-Seyler Street 3, 72076 Tuebingen, Germany E-mail: christian.gerloff@uni-tuebingen.de orMark Hallett, MD, NINDS, National Institutes of Health, 10 Center Drive, MSC-1428, Bethesda, Maryland 20892, USA,E-mail: hallettm@ninds.nih.gov
 
 
Clinical recovery after stroke can be significant and has been attributed to plastic reorganization and recruitment of novel areas previously not engaged in a given task. As equivocal results have been reported in studies using single imaging or electrophysiological methods, here we applied an integrative multimodal approach to a group of well-recovered chronic stroke patients (n=11; aged 50–81 years) with left capsular lesions. Focal activation during recovered hand movements was assessed with EEG spectral analysis and H215O-PET withEMG monitoring, cortico–cortical connectivity with EEG coherence analysis (cortico–cortical coherence) and corticospinal connectivity with transcranial magnetic stimulation (TMS). As seen from comparisons with age-matched controls, our patients showed enhanced recruitment of the lateral premotor cortex of the lesioned hemisphere [Brodmann area (BA) 6], lateral premotor and to a lesser extent primary sensorimotor andparietal cortex of the contralesional hemisphere (CON-H; BA 4 and superior parietal lobule) and left cerebellum (patients versus controls, Z  > 3.09). EEG coherence analysis showed that after stroke cortico–cortical connections were reduced in the stroke hemisphere but relatively increased in the CON-H (ANOVA, contrast analysis, P <0.05), suggesting a shift of functional connectivity towards the CON-H. Nevertheless, fast con-ducting corticospinal transmission originated exclusively from the lesioned hemisphere. No direct ipsilateral motor evoked potentials (MEPs) could be elicited with TMS over the contralesional primary motor cortex(iM1)in stroke patients. We conclude that (i) effective recovery is based on enhanced utilization of ipsi- and contralesional resources, (ii) basic corticospinal commands arise from the lesioned hemisphere without recruitment of (‘latent’) uncrossed corticospinal tract fibres and (iii) increased contralesional activity probably facilitates control of recovered motor function by operating at a higher-order processing level, similar to but not identical with the extended network concerned with complex movements in healthy subjects.Keywords
: Plasticity; stroke; recovery; motor control; motor cortex
 

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