Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Monday, September 5, 2016

Correlates of Post-Stroke Brain Plasticity, Relationship to Pathophysiological Settings and Implications for Human Proof-of-Concept Studies

Yes, yes, we know neuroplasticity exists and can help us recover so why don't you figure out exactly how to make it repeatable so we can recover. Instead you write with big words telling us nothing. But we get useless crap instead.
http://journal.frontiersin.org/article/10.3389/fncel.2016.00196/full?
  • Department of Neurology, University Hospital Essen, Essen, Germany
The promotion of neurological recovery by enhancing neuroplasticity has recently obtained strong attention in the stroke field. Experimental studies support the hypothesis that stroke recovery can be improved by therapeutic interventions that augment neuronal sprouting. However plasticity responses of neurons are highly complex, involving the growth and differentiation of axons, dendrites, dendritic spines and synapses, which depend on the pathophysiological setting and are tightly controlled by extracellular and intracellular signals. Thorough mechanistic insights are needed into how neuronal plasticity is influenced by plasticity-promoting therapies in order not to risk the success of future clinical proof-of-concept studies.

Introduction

Following ischemic stroke, neuronal networks in the vicinity and at distance to the stroke are reorganized. Axons and axon collaterals are enabled to sprout (Reitmeir et al., 2011, 2012) and dendritic and synaptic processes are reshaped (Li et al., 2010; Overman et al., 2012) leading to an overall reorganization of the representational map that mediates the recovery of motor functions in a large number of settings ranging from rodents to primates and humans (Nudo and Milliken, 1996; Nudo et al., 1996; Wang et al., 2010; Overman et al., 2012). These reorganization processes enroll regions of the contralateral hemisphere (Mohajerani et al., 2011; Reitmeir et al., 2011) and have been shown to persist at least for several months post-stroke (Rossini et al., 2003; Sawaki et al., 2014). A wide variety of molecules are involved in these plasticity processes, including cell adhesion and guidance molecules, growth inhibitors, neurotransmitters and transport proteins (Bacigaluppi et al., 2009; Li et al., 2010; Sánchez-Mendoza et al., 2010; Reitmeir et al., 2011) that may activate or inactivate highly complex molecular pathways that enhance or inhibit neuronal sprouting and therefore local and remote connections (Li et al., 2010; Hermann and Chopp, 2012). Unfortunately, the natural capacity of the brain to rewire is insufficient. Though a degree of spontaneous sprouting exists (Li et al., 2010; Reitmeir et al., 2011, 2012) and some spontaneous recovery has been reported in humans (Duncan et al., 2000), neurological deficits persist in the large majority of stroke events even following localized or mild ischemic injuries (Hummel et al., 2005).
The intrinsic capacity of brain repair can be efficiently stimulated by exogenous therapeutic interventions, e.g., by physical exercise, delivery of growth factors, cell-based biologicals or pharmacological compounds, which in rodent and primate models of stroke were shown to enhance neurological recovery (Bacigaluppi et al., 2009; Reitmeir et al., 2011, 2012; Jaeger et al., 2015; Wang et al., 2016). Neurological recovery in the experimental setting can be defined as regain of lost function of the paretic limb as compared to a baseline defined previous to the stroke, which should not be confused with neurological compensation (Murphy and Corbett, 2009), in which other parts of the limbs (e.g., shoulder or the non-paretic limb) are recruited to complete a task. Neurological recovery and compensation can be discriminated by specific tests that allow the study of the paretic limb in isolation, e.g., pellet withdrawal in rodents or digit testing in primates that measure fine motor skills (Nudo and Milliken, 1996; Biernaskie et al., 2004), and tests measuring overall motor function, such as the rotarod, tight rope or hand grip tests (Doeppner et al., 2014a). There seems to be a critical time window after stroke in which various interventions, such as voluntary motor stimulation, pharmacological treatment or transcranial brain stimulation, can improve neurological recovery (Nudo et al., 1996; Biernaskie et al., 2004; Hummel et al., 2005; Sawaki et al., 2014; Wahl et al., 2014). In contrast to acute neuroprotective therapies, plasticity-promoting therapies have proven efficacy over weeks or even months post-stroke in animal and human studies.
Within this perspective article, we would like to briefly integrate some findings regarding brain remodeling and plasticity after stroke, elucidating: (a) structural surrogates of successful neurological recovery depending on the localization of ischemic lesions; (b) reorganization and plasticity processes of the cellular, subcellular and network level; (c) critical time windows for various therapeutic interventions; and (d) modes for the delivery of biologicals or drugs. We will shortly present (e) selected molecular signals that are likely mediators of plasticity processes, since we believe that understanding these signals is a major hallmark to prevent the failure of treatments in future clinical studies.

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