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.

Sunday, October 2, 2016

Same Intervention–Different Reorganization The Impact of Lesion Location on Training-Facilitated Somatosensory Recovery After Stroke

Fucking useless research without a stroke protocol writeup for survivors. This simple task is what our fucking failures of stroke associations is unable to do because it is too much like work. And survivors will continually get screwed until that changes.
http://nnr.sagepub.com/content/30/10/988?etoc
  1. Leeanne M. Carey, PhD1,2
  2. David F. Abbott, PhD2
  3. Gemma Lamp1,2
  4. Aina Puce, PhD2,3
  5. Rüdiger J. Seitz, MD2,4,5
  6. Geoffrey A. Donnan, MD2
  1. 1La Trobe University, Bundoora, Victoria, Australia
  2. 2The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia
  3. 3Indiana University, Bloomington, IN, USA
  4. 4LVR-Klinikum Düsseldorf, Düsseldorf, Germany
  5. 5University Hospital Düsseldorf, Heinrich Heine University, Düsseldorf, Germany
  1. Leeanne M. Carey, PhD, Occupational Therapy, School of Allied Health, College of Science, Health and Engineering, La Trobe University, Bundoora, Victoria, 3086, Australia. Email: l.carey@latrobe.edu.au

Abstract

Background. The brain may reorganize to optimize stroke recovery. Yet relatively little is known about neural correlates of training-facilitated recovery, particularly after loss of body sensations. Objective. Our aim was to characterize changes in brain activation following clinically effective touch discrimination training in stroke patients with somatosensory loss after lesions of primary/secondary somatosensory cortices or thalamic/capsular somatosensory regions using functional magnetic resonance imaging (fMRI).  
Methods. Eleven stroke patients with somatosensory loss, 7 with lesions involving primary (S1) and/or secondary (S2) somatosensory cortex (4 male, 58.7 ± 13.3 years) and 4 with lesions primarily involving somatosensory thalamus and/or capsular/white matter regions (2 male, 58 ± 8.6 years) were studied. Clinical and MRI testing occurred at 6 months poststroke (preintervention), and following 15 sessions of clinically effective touch discrimination training (postintervention).  
Results. Improved touch discrimination of a magnitude similar to previous clinical studies and approaching normal range was found. Patients with thalamic/capsular somatosensory lesions activated preintervention in left ipsilesional supramarginal gyrus, and postintervention in ipsilesional insula and supramarginal gyrus. In contrast, those with S1/S2 lesions did not show common activation preintervention, only deactivation in contralesional superior parietal lobe, including S1, and cingulate cortex postintervention. The S1/S2 group did, however, show significant change over time involving ipsilesional precuneus. This change was greater than for the thalamic/capsular group (P = .012; d = −2.43; CI = −0.67 to −3.76). 
Conclusion. Different patterns of change in activation are evident following touch discrimination training with thalamic/capsular lesions compared with S1/S2 cortical somatosensory lesions, despite common training and similar improvement.

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