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, September 23, 2023

Motor and Premotor Cortices in Subcortical Stroke: Proton Magnetic Resonance Spectroscopy Measures and Arm Motor Impairment

What a waste, measuring impairment,  NOT CREATING RECOVERY!

Motor and Premotor Cortices in Subcortical Stroke: Proton Magnetic Resonance Spectroscopy Measures and Arm Motor Impairment

Abstract

Background
 
Although functional imaging and neurophysiological approaches reveal alterations in motor and premotor areas after stroke, insights into neurobiological events underlying these alterations are limited in human studies. 
 
Objective
 
We tested whether cerebral metabolites related to neuronal and glial compartments are altered in the hand representation in bilateral motor and premotor areas and correlated with distal and proximal arm motor impairment in hemiparetic persons.  
 
Methods
 
In 20 participants at >6 months postonset of a subcortical ischemic stroke and 16 age- and sex-matched healthy controls, the concentrations of N-acetylaspartate and myo-inositol were quantified by proton magnetic resonance spectroscopy. Regions of interest identified by functional magnetic resonance imaging included primary (M1), dorsal premotor (PMd), and supplementary (SMA) motor areas. Relationships between metabolite concentrations and distal (hand) and proximal (shoulder/elbow) motor impairment using Fugl-Meyer Upper Extremity (FMUE) subscores were explored.  
 
Results
 
N-Acetylaspartate was lower in M1 (P = .04) and SMA (P = .004) and myo-inositol was higher in M1 (P = .003) and PMd (P = .03) in the injured (ipsilesional) hemisphere after stroke compared with the left hemisphere in controls. N-Acetylaspartate in ipsilesional M1 was positively correlated with hand FMUE subscores (P = .04). Significant positive correlations were also found between N-acetylaspartate in ipsilesional M1, PMd, and SMA and in contralesional M1 and shoulder/elbow FMUE subscores (P = .02, .01, .02, and .02, respectively). 
 
Conclusions
 
 Our preliminary results demonstrated that proton magnetic resonance spectroscopy is a sensitive method to quantify relevant neuronal changes in spared motor cortex after stroke and consequently increase our knowledge of the factors leading from these changes to arm motor impairment.(You do know you  want to know what the factors are leading to arm recovery? Or are you that blitheringly stupid?)

Introduction

Human imaging studies have revealed that early after subcortical stroke, restoration of paretic arm function is associated with a greater involvement of radiologically normal-appearing (or spared) motor (primary motor cortex or M1) and premotor (dorsal premotor cortex or PMd, supplementary motor area or SMA) areas in both injured (ipsilesional) and uninjured (contralesional) hemispheres.1-3 Later, successful recovery occurs in stroke survivors who exhibit relatively normal patterns of ipsilesional activation and less contralesional motor activation, whereas patients, who often show bilateral cortical activation, typically have less complete recovery.4-6 These results should be viewed in the context of the anatomic structures and pathways of these areas. Although M1 motor pathways are critical, the premotor areas also contribute to motor control and might be recruited during motor recovery after stroke. The parallel nature of the direct (corticospinal) pathways from premotor areas and M1 emphasizes that PMd and SMA are, in some respects, at a similar level of hierarchical organization as M1,7 although these projections to spinal cord motor neurons are less numerous and less efficient than those from M1.8-10 Another possibility is the indirect (corticoreticulospinal) projections to cervical propriospinal premotoneurons, which have divergent projections to muscle groups operating at multiple joints.11,12 Finally, corticocortical connections between these areas might also play an important role in poststroke recovery.7,13-15 Thus, understanding the neural events associated with the functional changes in these areas could provide critical insight into successful treatments of patient’s impairment.
Proton magnetic resonance spectroscopy (1H-MRS) provides a noninvasive means to measure concentrations of certain metabolites associated with a specific cell type16 after stroke.17 Most clinical stroke studies report lower levels of N-acetylaspartate (NAA, putative marker of neuronal integrity) in spared ipsilesional M1 and PMd.18-21 In some instances, the NAA levels were related to clinical severity. In a series of studies of stroke survivors, we also found higher myo-inositol (mI, putative marker of glial cells) in ipsilesional and contralesional M1.21 However, none of these studies addressed the changes in key metabolites related to neuronal and glial compartments, that is, NAA and mI, in motor and premotor areas in stroke.
The first aim of the current study was to quantify NAA and mI concentrations in ipsilesional and contralesional motor and premotor areas in chronic subcortical stroke. Since neuronal integrity might be compromised in these remote areas,21,22 we expected NAA to be lower, especially in the ipsilesional areas. Given the role of glia in plastic brain changes,23-25 we also expected mI to be higher. The second aim was to explore correlations between metabolite concentrations and arm motor impairment. Since the premotor projections are significantly stronger on the proximal muscles than distal muscles compared with M18,9, we predicted that metabolite measures in ipsilesional PMd and SMA would be correlated with proximal (shoulder/elbow) motor impairment whereas those in M1 would be correlated with both proximal and distal (hand) impairments. Since both direct and indirect pathways from the contralesional M1 project to axial and proximal muscles rather than hand muscles,26,27 relationships between contralesional M1 metabolites and proximal impairment were also expected.
 
More at link.


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