So WHOM is doing the followup research that will determine the EXACT interventions that drive arm recovery? This is just the first step. Leaders would create the followup research; IF WE HAD ANY!
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.
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.
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