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.

Wednesday, July 13, 2016

Motor Recovery After Subcortical Stroke Depends on Modulation of Extant Motor Networks

Lots of big words meaning absolutely nothing to me. I got zilch out of this.
http://journal.frontiersin.org/article/10.3389/fneur.2015.00230/full?
  • 1Stroke Research Group, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK
  • 2MRC Unit for Lifelong Health and Ageing, University College London, London, UK
  • 3The National Hospital for Neurology and Neurosurgery, London, UK
  • 4INSERM U894, Centre Hospitalier Sainte-Anne, Sorbonne Paris Cite, Paris, France
Introduction: Stroke is the leading cause of long-term disability. Functional imaging studies report widespread changes in movement-related cortical networks after stroke. Whether these are a result of stroke-specific cognitive processes or reflect modulation of existing movement-related networks is unknown. Understanding this distinction is critical in establishing more effective restorative therapies after stroke. Using multivariate analysis (tensor-independent component analysis – TICA), we map the neural networks involved during motor imagery (MI) and executed movement (EM) in subcortical stroke patients and age-matched controls.
Methods: Twenty subcortical stroke patients and 17 age-matched controls were recruited. They were screened for their ability to carry out MI (Chaotic MI Assessment). The fMRI task was a right-hand finger-thumb opposition sequence (auditory-paced 1 Hz; 2, 3, 4, 5, 2…). Two separate runs were acquired (MI and rest and EM and rest; block design). There was no distinction between groups or tasks until the last stage of analysis, which allowed TICA to identify independent components (ICs) that were common or distinct to each group or task with no prior assumptions.
Results: TICA defined 28 ICs. ICs representing artifacts were excluded. ICs were only included if the subject scores were significant (for either EM or MI). Seven ICs remained that involved the primary and secondary motor networks. All ICs were shared between the stroke and age-matched controls. Five ICs were common to both tasks and three were exclusive to EM. Two ICs were related to motor recovery and one with time since stroke onset, but all were shared with age-matched controls. No IC was exclusive to stroke patients.
Conclusion: We report that the cortical networks in stroke patients that relate to recovery of motor function represent modulation of existing cortical networks present in age-matched controls. The absence of cortical networks specific to stroke patients suggests that motor adaptation and other potential confounders (e.g., effort and additional muscle use) are not responsible for the changes in the cortical networks reported after stroke. This highlights that recovery of motor function after subcortical stroke involves preexisting cortical networks that could help identify more effective restorative therapies.

Introduction

Stroke remains a leading cause of long-term disability and carries a significant social and economic cost (1, 2). After stroke, functional imaging studies of movement report widespread changes in activation of the cortical networks (38). The precise cognitive processes that determine these changes remain unclear. In this study, we used a data-led method to explore if the changes in movement-related networks are a result of processes specific to stroke patients (i.e., use of additional muscles) or whether they represent modulation of extent movement-related networks. Understanding this distinction in neuroplasticity is likely to help establish the driver of fMRI changes reported after stroke and help establish the most effective restorative therapies for patients (911).
Using a variety of tasks, numerous groups have reported changes in movement-related networks – importantly these remote changes relate to the recovery of motor performance. Movement-related fMRI activation in the ipsilesional primary motor cortex is associated with better recovery (4, 7, 8, 12, 13). Indeed it is on this model that many restorative intervention studies are based (14) changes in movement-related networks are being used to predict response to therapies (15). Yet it is possible that the changes in movement-related networks may represent an epiphenomenon of the increased difficulty involved in carrying out the task after a stroke (6).
There are several caveats when considering comparisons of patients with healthy volunteers (6). For instance, the kinematics of movements, EMG patterns, motor strategies (adaptation versus relearning), and whether movement involved different body parts in different subjects have not been monitored consistently in the MRI. In other words, it is possible that the differences reported represent a composite of cognitive processes specific to stroke patients that may not be directly related to the recovery process as such.
Understanding whether there are networks specific to stroke patients will greatly aid the understanding of the recovery process after stroke. It may allow a more targeted approach to rehabilitation as it could identify the most appropriate training programs. We explored the extent to which the widely described changes in motor networks after stroke are a result of specific processes (i.e., motor adaptation or use of different muscle) or whether they represent modulation of extant motor performance. There are two key aspects to our study.
First, to remove any biases produced by subtle differences in motor performance, we studied both motor imagery (MI) and executed movement (EM). MI is intrinsically linked to the motor system and can be used to study the motor system without actual movement (1619). In stroke patients with normal activations during EM, we have reported abnormal hemispheric lateralization during MI that related to recovery of motor function. In other words, by studying MI as well as EM, we are able to identify aspects of task-dependent activation that relate to motor execution and those more “upstream” (20).
Second, we use a data-led approach using tensor-independent component analysis (TICA) (21). Using TICA, we examine the cortical networks that are common to stroke patients and aged-matched controls or exclusive to either. Unlike the conventional mass univariate approach, TICA is a powerful data-led approach that explores similarities as well as differences in cortical networks. Importantly, both tasks (MI and EM) from both groups (stroke and aged-matched controls) are considered the same. We are able to use a “blinded task” during the production of the independent components (ICs) as they have the same temporal profile. In other words, we make no prior assumptions as to the extent of overlap, if any, between the task-related networks in stroke patients and controls or between the MI and EM. If the widely reported changes in movement-dependent networks are related to a stroke-specific cognitive process, then this analytic approach will likely produce separate components.
We hypothesize that in recovered subcortical stroke patients, the task-related motor networks identified for both EM and MI are shared with the age-matched controls. In keeping with our reports from healthy volunteers, we expect to find networks related exclusively to EM and others that are shared with MI. Finally, we expect that in stroke patients, the task-related networks would correlate with measures of motor recovery.

More at link.

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