Stroke subtype and motor impairment influence contralesional excitability
Gary W Thickbroom1, Mar Cortes1, Avrielle Rykman1
1From the Laboratory for Non-Invasive Brain Stimulation and Human Motor Control (G.W.T., M.C., A.R., D.J.E.), Burke Medical Research Institute, White Plains; Department of Neurology (M.C., D.J.E.), Weill Cornell Medical College, New York; Feinstein Institute for Medical Research (B.T.V.), Manhasset, NY; Laboratory of Neuromodulation (F.F.), Spaulding Rehabilitation Hospital, Harvard Medical School, Boston; Mechanical Engineering Department (H.I.K.), Massachusetts Institute of Technology, Cambridge; Department of Neurology and Division of Rehabilitation (H.I.K.), School of Medicine, University of Maryland, Baltimore; Department of Physical Medicine and Rehabilitation (H.I.K.), Fujita Health University, Nagoya, Japan; Institute of Neuroscience (H.I.K.), University of Newcastle, Newcastle upon Tyne, UK; and Berenson-Allen Center for Non-Invasive Brain Stimulation (A.P.-L., D.J.E.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
Objective:
The nonlesioned motor cortex (M1NL) is thought to be hyperexcitable in patients with subacute or chronic stroke and offers a promising therapeutic target. However, whether M1NL excitability behaves the same for subcortical and cortical strokes is unknown. The aim of the present study was to determine whether cortical, or purely subcortical, strokes have a different effect on M1NL excitability.
Methods:
We looked for correlations between the Fugl-Meyer (FM) score and M1NL resting motor threshold (RMTNL) in 34 stroke survivors classified according to lesion location (cortico-subcortical or purely subcortical). In addition to the FM, the Wolf Motor Score and motor power were measured.
Results:
FM correlated with RMTNL for subcortical (r = 0.82; p = 0.001) but not for cortical strokes (r = 0.11; p = 0.62). Likewise, Wolf Motor Score (r = -0.62; p = 0.03) and motor power (r = 0.64; p = 0.023) were correlated with RMTNL for the subcortical group, but not for the cortical group.
Conclusion:
We show that the impact on M1NL depends on lesion location and conclude that protocols aimed at reducing M1NL cortical excitability may be worth exploring for subcortical but not for cortical stroke.
