Recovery of post stroke proximal arm function, driven by complex neuroplastic bilateral brain activation patterns and predicted by baseline motor dysfunction severity

Once again, no clue. The researchers don't even know what they are measuring. We have no definition of what chronic means.
http://journal.frontiersin.org/article/10.3389/fnhum.2015.00394/abstract
Svetlana Pundik^{1, 2*}, Jessica McCabe⁴, Ken Hrovat⁴, Alice E. Fredrickson¹, Curtis Tatsuoka², I Jung Feng³ and Janis J. Daly^{5, 6}

• ¹Neurology, Cleveland Department of Veterans Affairs Medical Center, USA
• ²Neurology, Case Western Reserve University School of Medicine, USA
• ³Biostatistics, Case Western Reserve Univeristy, USA
• ⁴Research, Cleveland Department of Veterans Affairs Medical Center, USA
• ⁵Brain Rehabilitation Research Center of Excellence, MR Gainesville Department of Veterans Affairs Medical Center, USA
• ⁶Neurology, University of Florida, College of Medicine, USA

Objectives: Neuroplastic changes that drive recovery of shoulder/elbow function after stoke have been poorly understood.(This may not be neuroplasticity, this could still be spontaneous recovery, depending on the time since the stroke) The purpose of this study was to determine the relationship between neuroplastic brain changes related to shoulder/elbow movement control in response to treatment and recovery of arm motor function in chronic stroke survivors.
Methods: Twenty-three chronic stroke survivors were treated with 12 weeks of arm rehabilitation. Outcome measures included functional Magnetic Resonance Imaging (fMRI) for the shoulder/elbow components of reach and a skilled motor function test (Arm Motor Abilities Test (AMAT)), collected before and after treatment.
Results: We observed two patterns of neuroplastic changes that were associated with gains in motor function: decreased or increased task-related brain activation. Those with significantly better motor function at baseline exhibited a decrease in brain activation in response to treatment, evident in the ipsilesional primary motor and contralesional supplementary motor regions; in contrast, those with greater baseline motor impairment, exhibited increased brain activation in response to treatment. There was an linear relationship between greater functional gain (AMAT) and increased activation in bilateral primary motor, contralesional primary and secondary sensory regions, and contralesional lateral premotor area, after adjusting for baseline AMAT, age, and time since stroke.
Conclusions: Recovery of functional reach involves recruitment of several contralesional and bilateral primary motor regions. In response to intensive therapy, the direction of functional brain change (i.e. increase or decrease in task-related brain recruitment) for shoulder/elbow reach components depends on baseline level of motor function and may represent either different phases or different strategies of neuroplasticity that drive functional recovery.