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.

Friday, May 22, 2020

Assessment and Modulation of Neural Plasticity in Rehabilitation With Transcranial Magnetic Stimulation

Assessments with NO REHAB PROTOCOL ARE COMPLETELY FUCKING USELESS. Until we get survivors in charge this crapola will not change.  We don't need potential mechanisms of recovery, we need actual EXACT mechanisms of recovery. Talk to some survivors sometime and ask if they are OK with only a potential recovery.

Assessment and Modulation of Neural Plasticity in Rehabilitation With Transcranial Magnetic Stimulation

Shahid Bashir1, Ilan Mizrahi1, Kayleen Weaver2, Felipe Fregni2,3, and Alvaro PascualLeone1,4 1Berenson-Allen Center for Noninvasive Brain Stimulation, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 2Laboratory of Neuromodulation, Spaulding Rehabilitation Hospital, Harvard Medical School, Boston, MA 3Núcleo de Neurociências e Comportamento, University of Sao Paulo, Brazil 4Institut Guttmann, Universitat Autonoma Barcelona, Spain
© 2013 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved. Corresponding author’s address: Alvaro Pascual-Leone, MD, PhD, Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess, Medical Center, 330 Brookline Ave, Boston, MA 02215, U.S.A., T: (617) 667-0203; Fax: (617) 975-5322. apleone@bidmc.harvard.edu & Felipe Fregni, MD, PhD, Laboratory of Neuromodulation, Spaulding Rehabilitation Hospital, 125 Nashua Street, Boston MA 02114, USA. T: 617 573-2326, Fregni.felipe@mgh.harvard.edu. NIH Public Access Author Manuscript PM R. Author manuscript; available in PMC 2014 March 13. Published in final edited form as: PM R. 2010 December ; 2(12 0 2): S253–S268. doi:10.1016/j.pmrj.2010.10.015.

Abstract 

Despite intensive efforts towards the improvement of outcomes after acquired brain injury functional recovery is often limited. One reasons is the challenge in assessing and guiding plasticity after brain injury. In this context, Transcranial Magnetic Stimulation (TMS) - a noninvasive tool of brain stimulation - could play a major role. TMS has shown to be a reliable tool to measure plastic changes in the motor cortex associated with interventions in the motor system; such as motor training and motor cortex stimulation. In addition, as illustrated by the experience in promoting recovery from stroke, TMS a promising therapeutic tool to minimize motor, speech, cognitive, and mood deficits. In this review, we will focus on stroke to discuss how TMS can provide insights into the mechanisms of neurological recovery, and can be used for measurement and modulation of plasticity after an acquired brain insult.
1. Introduction The impact of acquired brain injuries, for example stroke, upon individuals, families, and society continues to increase due to both the aging of the general population and the increasing length of post-insult survival (1). Unfortunately, functional outcomes remain often limited. Consider stroke: within the past decade, a significant amount of research has delineated the clinical course of post-stroke recovery and has begun to elucidate potential mechanisms of injury and recovery. Yet the mechanisms underlying stroke recovery remain fairly misunderstood and effective neurorehabilitation interventions remain insufficiently proven or widespread.


There are distinct phases in neurological recovery. For example, one can conceptualize an acute and a chronic phase. In the acute phase there is usually a rapid natural recovery, while in the chronic phase natural recovery is unlikely and secondary worsening of function is possible. In the acute phase, neurological deficits observed are partly due to the death of neuronal tissue in the affected region. Restoration of viable blood supply to this region, and resolution of perilesional edema and inflammation are factors possibly contributing to rapid recovery of function following stroke in the acute phase (2). Another important consideration is the disruption of neuronal networks in undamaged brain regions that are remote from the original injury yet functionally connected, such as subcortical regions or the contralesional motor cortex. In part this concept matches the notions of “diaschisis”, advanced by von Monakow as a principle contributing to explain the functional impact and eventual recovery from brain lesions, and more recently confirmed with modern neuroimaging techniques (3). In the chronic phase, natural recovery is less likely and in fact a decrease in functioning can be observed. In this phase, cortical reorganization plays a major role in determining neurological deficits. Plasticity in chronic stroke may not be beneficial and can lead to further worsening of function, including increased transcallosal inhibition from the unaffected to the affected motor cortex (4). Therefore, greater understanding of the pathophysiology of functional deficits at various times (phases) after a brain insult is critical to optimize interventions. For example, understanding the extent and purpose of cortical reorganization might guide treatments aiming to improve motor function. In addition, it might be possible to minimize damage or enhance recovery by modulating cortical excitability or modifying processes of diaschisis.
Transcranial Magnetic Stimulation (TMS) is a valuable non-invasive neurophysiologic tool to characterize the pathophysiologic processes involved in functional consequences after a brain insult and in harnessing such insights to maximize functional outcomes. In this review we shall focus on stroke and (1) Describe the neurophysiologic changes that occur after stroke; (2) Describe current rehabilitation techniques affecting brain activity and plasticity in order to compare them with TMS; and (3) Discuss the role of TMS in measuring cortical reorganization following stroke as well as the role of rTMS as an intervention in chronic stroke to enhance plasticity when used alone or in combination with other interventions to augment current pharmacotherapy and rehabilitation therapies for stroke rehabilitation

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