Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Monday, September 5, 2016

Contralesional Cortical Structural Reorganization Contributes to Motor Recovery after Sub-Cortical Stroke: A Longitudinal Voxel-Based Morphometry Study

Who gives a shit about what might help us recover, we want to know what will help us recover. Damn it all solve the problem, don't just describe the problem.
Jianxin Cai1, Qiling Ji2, Ruiqiang Xin1, Dianping Zhang1, Xu Na1, Ruchen Peng1* and Kuncheng Li3*
  • 1Department of Radiology, Beijing Luhe Hospital, Capital Medical University, Beijing, China
  • 2Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing, China
  • 3Department of Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China
Although changes in brain gray matter after stroke have been identified in some neuroimaging studies, lesion heterogeneity and individual variability make the detection of potential neuronal reorganization difficult. This study attempted to investigate the potential structural cortical reorganization after sub-cortical stroke using a longitudinal voxel-based gray matter volume (GMV) analysis. Eleven right-handed patients with first-onset, subcortical, ischemic infarctions involving the basal ganglia regions underwent structural magnetic resonance imaging in addition to National Institutes of Health Stroke Scale (NIHSS) and Motricity Index (MI) assessments in the acute (<5 days) and chronic stages (1 year later). The GMVs were calculated and compared between the two stages using nonparametric permutation paired t-tests. Moreover, the Spearman correlations between the GMV changes and clinical recoveries were analyzed. Compared with the acute stage, significant decreases in GMV were observed in the ipsilesional (IL) precentral gyrus (PreCG), paracentral gyrus (ParaCG), and contralesional (CL) cerebellar lobule VII in the chronic stage. Additionally, significant increases in GMV were found in the CL orbitofrontal cortex (OFC) and middle (MFG) and inferior frontal gyri (IFG). Furthermore, severe GMV atrophy in the IL PreCG predicted poorer clinical recovery, and greater GMV increases in the CL OFG and MFG predicted better clinical recovery. Our findings suggest that structural reorganization of the CL “cognitive” cortices might contribute to motor recovery after sub-cortical stroke.


Brain damage after ischemic stroke can cause a greater variety of functional deficits. These deficits can be caused by direct damage to the cortices or fiber tracts, For example, injuries to the right inferior parietal lobe, superior temporal gyrus and inferior frontal gyrus (IFG) are frequently associated with neglect (Corbetta and Shulman, 2011), and lesions to the corticospinal tract (CST) can cause hemiplegia (Lo et al., 2010). In addition to the direct damage caused by lesions, indirect atrophy of lesion-related remote cortices has also been reported (Rowan et al., 2007; Gauthier et al., 2012; Fan et al., 2013; Zhang et al., 2014; Cheng et al., 2015). For example, a recent research has demonstrated that cortical atrophy in remote cortices is also correlated with the magnitude of residual motor deficits in chronic sub-cortical stroke patients (Gauthier et al., 2012). In addition to the evidence of secondary cortical atrophy, many early studies also reported secondary degeneration of remote white matter tracts after damage to the motor pathway due to sub-cortical stroke (Thomalla et al., 2004, 2005; Liang et al., 2008; Yu et al., 2009; Rüber et al., 2012), and the severity of the degeneration predicts poor motor recovery (Yu et al., 2009; Lindenberg et al., 2010). These findings indicate that the secondary neurodegeneration of the motor pathways might be responsible for the atrophy of remote cortical regions and might consequently influence motor performance.
Although secondary structural impairment of remote cortex has frequently been reported, the structural plasticity of the remaining cortex after stroke has yet to be fully clarified. In a review of previous neuroimaging literature that focused on the cortical changes after stroke, we found that the majority of studies adopted either a retrospective or cross-sectional design, and heterogeneities in lesion location and duration were frequently present (Schormann and Kraemer, 2003; Kraemer et al., 2004; Schaechter et al., 2006; Rowan et al., 2007; Stebbins et al., 2008; Gauthier et al., 2012). Individual variability in cross-sectional studies might mask subtle changes in the cortex or induce some false positive results, and lesion heterogeneity increases the complexity of interpreting the underlying neuronal mechanism. In a recent study of longitudinal changes in cortical thickness 3 months after sub-cortical stroke (Brodtmann et al., 2012), the authors found thickening of the contralesional (CL) cortices; however, these authors did not find any atrophy of the ipsilesional (IL) cortices. In another similar longitudinal study, Cheng et al. (2015) failed to identify any changes in cortical thickness in the CL lesion-connected or lesion-unconnected cortices, although they observed a strong decrease in the cortical thickness of the IL lesion-connected cortex. The discrepancy between the two studies may have been caused by the following factors: (1) the relative shorter follow-up duration (3 months after stroke); (2) the insensitivity of the region-of-interest (ROI) analysis method; and (3) the constraint of the cortical thickness in completely characterizing cortical atrophy and plasticity without accounting for changes in cortical surface area.
In this study, we recruited a subset of motor-deficit stroke patients with first onset, subcortical ischemic infractions that involved the basal ganglia regions. In contrast to early longitudinal studies (Brodtmann et al., 2012; Cheng et al., 2015), we used a whole-brain voxel-based morphometry (VBM) method to identify the potential changes in gray matter volume (GMV) after stroke. Moreover, the follow-up duration in the present study was extended to 1 year. Because the GMV contains information about both cortical thickness and cortical surface area, any changes in these two metrics can be reflected by the GMV. Based on the features of the VBM method and the longer follow-up duration, we hoped to identify both atrophy and augment in the GMV of the remote cortices after 1 years. Specifically, based on early studies that revealed secondary cortical atrophy of the IL cortices and its association with clinical performance, we hypothesized that the GMVs of the IL motor-related cortices would be decreased after 1 year, and the severity of the atrophy of these cortices would be associated with clinical recovery. Because early studies also demonstrated wide-spread of functional reorganization of multiple brain network (Wang et al., 2010, 2014; Rehme et al., 2012), we also hoped to observed increases in the GMVs of the remaining cortices and significant association between GMV increases and clinical recovery.

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