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.

Showing posts with label contralesional. Show all posts
Showing posts with label contralesional. Show all posts

Monday, January 5, 2026

Contralesional Motor Cortex: Key to Stroke Recovery?

 

But nothing here helps survivors get recovered. Describing something does no good, we need EXACT PROTOCOLS THAT DELIVER RECOVERY.

Contralesional Motor Cortex: Key to Stroke Recovery?

The human brain, with its intricate neural networks, continues to fascinate and baffle researchers, particularly in the realm of recovery following adverse events such as strokes. A recent scoping review highlighted in BMC Neuroscience delves into the role of the contralesional primary motor cortex in aiding upper limb recovery after a stroke. This development is particularly pivotal, given that strokes significantly impair motor functions, leading to long-term disability in numerous individuals. Studying the contralesional primary motor cortex offers a new lens through which we can understand post-stroke rehabilitation.

Strokes occur when the blood supply to part of the brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients. The consequences can be devastating, often resulting in the loss of motor functions, particularly in the limbs. Upper limb recovery becomes a critical goal in rehabilitation, as it heavily influences a person’s ability to carry out daily activities and ultimately impacts their quality of life. The contralesional primary motor cortex—the part of the brain that processes motor functions for the limbs opposite the side of body affected—holds promise in facilitating recovery from such debilitating conditions.

Researchers Hernan Fregni, Pattharawadee Suputtitada, and Victor Costa conducted this comprehensive review as part of their efforts to elucidate how the contralesional primary motor cortex contributes to functional recovery. Through the meticulous application of PRISMA-ScR guidelines—an established framework ensuring transparency and reproducibility in scoping reviews—they meticulously sifted through varied studies to extract pertinent findings. The synthesis of these studies offers critical insights into how contralesional regions can be harnessed to enhance rehabilitation strategies.

One of the most striking findings from this review is how the brain exhibits remarkable plasticity. Even after significant injury, the brain can adapt and reorganize itself to compensate for lost functions. This plasticity is particularly pronounced in the contralesional hemisphere, which, following the injury of the ipsilesional hemisphere—typically where the stroke occurs—can take over some motor tasks. This neural adaptation widens the horizon for therapeutic interventions, suggesting that targeted stimulation of the contralesional motor cortex could engender recovery pathways that were previously thought unattainable.

Moreover, the review meticulously highlights various therapeutic strategies aiming to exploit this contralesional connectivity. Rehabilitation techniques including transcranial magnetic stimulation (TMS) have emerged as frontrunners in modulating activity within the contralesional primary motor cortex. By using non-invasive brain stimulation techniques, therapists can enhance excitability in this area, thereby improving motor function. Such efficient stimulation protocols could provide a similar stimulus to the impaired areas of the brain, catalyzing the recovery process.

Additionally, the involvement of augmented feedback mechanisms in upper limb rehabilitation is worth noting. Studies included in the review reflect how feedback mechanisms, whether intrinsic or extrinsic, can significantly influence motor relearning and recovery. The contralesional primary motor cortex, capable of modifying its functional representation based on feedback from the environment, indicates that we might not only be able to recover lost motor functions but also optimize existing ones. Harnessing this feedback in therapeutic practices could lead to profound improvements in recovery trajectories.

Interestingly, the review also emphasizes the role of engaging patients in active rehabilitation practices. Motor imagery and mental practice, where patients visualize themselves performing movements, have been shown to engage the contralesional motor cortex, further underscoring the power of mental processes in recovery. These findings support a broader paradigm shift where cognitive engagement becomes a central tenet in rehabilitation, integrating both mental and physical stages in recovery protocols.

The clinical implications of this research are profound. With a clearer understanding of how the contralesional primary motor cortex facilitates recovery, therapists can tailor individualized rehabilitation protocols. These tailored approaches pivot from traditional methods, incorporating new dimensions such as virtual reality or gamified platforms that directly stimulate contralesional pathways, which can engage patients more effectively and promote better recovery outcomes.

A dynamic interplay between clinical techniques and neuroscience is evident, where researchers and practicing clinicians must collaborate closely. This scoping review nostalgically harkens to previous studies that highlighted the potential of the contralesional cortex, yet it provides a panoptic view of contemporary knowledge and outlines future directions for research. It poses essential questions regarding optimal stimulation parameters and the timing of interventions that are ripe for exploration.

As we look to the future, this research serves as an impetus for further studies aimed at unlocking the full potential of the contralesional primary motor cortex. Larger randomized controlled trials will likely refine the role of various rehabilitation strategies in exploiting this brain area effectively. The collective goal remains to enhance the quality of recovery for stroke patients, ultimately helping them regain independence and improve their quality of life.

In conclusion, the exploration of the contralesional primary motor cortex in relation to recovery from stroke represents an exciting frontier in neuroscience. The implications not only provide hope for individuals affected by strokes but also highlight a crucial intersection of clinical application and theory. Such advancements reinforce the necessity for continuous research and innovation, ensuring that recovery techniques remain ahead of the curve, aligning with our growing understanding of neuroplasticity and motor learning processes.

Subject of Research: The role of the contralesional primary motor cortex in upper limb recovery after stroke.

Article Title: The role of the contralesional primary motor cortex in upper limb recovery after stroke: a scoping review following PRISMA-ScR guidelines.

Article References:
Suputtitada, P., Costa, V. & Fregni, F. The role of the contralesional primary motor cortex in upper limb recovery after stroke: a scoping review following PRISMA-ScR guidelines.
BMC Neurosci 26, 31 (2025). https://doi.org/10.1186/s12868-025-00950-y

Image Credits: AI Generated

DOI: https://doi.org/10.1186/s12868-025-00950-y

Keywords: Stroke recovery, contralesional primary motor cortex, motor cortex plasticity, rehabilitation techniques, transcranial magnetic stimulation, motor imagery, neuroplasticity.

Tags: BMC Neuroscience scoping reviewbrain plasticity in stroke recoverycontralesional primary motor cortexenhancing quality of life post-strokeimpact of stroke on daily activitiesmotor function impairment due to strokeneural networks in stroke recoverypost-stroke rehabilitation strategiesrole of motor cortex in recoverystroke recovery mechanismsstroke-related long-term disabilitiesupper limb rehabilitation after stroke

Tuesday, June 14, 2022

Longitudinal Brain Changes After Stroke and the Association With Cognitive Decline

So you described something, but nothing here is going to get survivors better recovery. Useless.

 ipsilesional (not comparable) (pathology, medicine) On the same side as a lesion.

contralesional (not comparable) (medicine) Describing the half of a patient's brain or body away from the site of a lesion.

Longitudinal Brain Changes After Stroke and the Association With Cognitive Decline

  • 1Institute of Clinical Medicine, University of Oslo, Oslo, Norway
  • 2Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway
  • 3Regional Centre for Child and Youth Mental Health and Child Welfare, Department of Mental Health, NTNU – Norwegian University of Science and Technology, Trondheim, Norway
  • 4Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway
  • 5Department of Neuromedicine and Movement Science, Faculty of Medicine and Health Science, NTNU – Norwegian University of Science and Technology, Trondheim, Norway
  • 6Department of Geriatrics, Clinic of Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  • 7Department of Radiology and Nuclear Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway

Background: Cognitive impairment is common after stroke. So is cortical- and subcortical atrophy, with studies reporting more atrophy in the ipsilesional hemisphere than the contralesional hemisphere. The current study aimed to investigate the longitudinal associations between (I) lateralization of brain atrophy and stroke hemisphere, and (II) cognitive impairment and brain atrophy after stroke. We expected to find that (I) cortical thickness and hippocampal-, thalamic-, and caudate nucleus volumes declined more in the ipsilesional than the contralesional hemisphere up to 36 months after stroke. Furthermore, we predicted that (II) cognitive decline was associated with greater stroke volumes, and with greater cortical thickness and subcortical structural volume atrophy across the 36 months.

Methods: Stroke survivors from five Norwegian hospitals were included from the multisite-prospective “Norwegian Cognitive Impairment After Stroke” (Nor-COAST) study. Analyses were run with clinical, neuropsychological and structural magnetic resonance imaging (MRI) data from baseline, 18- and 36 months. Cortical thicknesses and subcortical volumes were obtained via FreeSurfer segmentations and stroke lesion volumes were semi-automatically derived using ITK-SNAP. Cognition was measured using MoCA.

Results: Findings from 244 stroke survivors [age = 72.2 (11.3) years, women = 55.7%, stroke severity NIHSS = 4.9 (5.0)] were included at baseline. Of these, 145 (59.4%) had an MRI scan at 18 months and 72 (49.7% of 18 months) at 36 months. Most cortices and subcortices showed a higher ipsi- compared to contralesional atrophy rate, with the effect being more prominent in the right hemisphere. Next, greater degrees of atrophy particularly in the medial temporal lobe after left-sided strokes and larger stroke lesion volumes after right-sided strokes were associated with cognitive decline over time.

Conclusion: Atrophy in the ipsilesional hemisphere was greater than in the contralesional hemisphere over time. This effect was found to be more prominent in the right hemisphere, pointing to a possible higher resilience to stroke of the left hemisphere. Lastly, greater atrophy of the cortex and subcortex, as well as larger stroke volume, were associated with worse cognition over time and should be included in risk assessments of cognitive decline after stroke.

Introduction

Although the chances of surviving a stroke have become high, its aftermath often involves the development of cognitive problems (1). About 30% of stroke survivors develop cognitive impairments after a first-ever stroke, with the incidence of dementia within the first year after a major stroke being almost 50 times higher than in the general population, and nearly 6 times higher after a minor one (1). Stroke and dementia both pose risks for each other and share many of the same neurodegenerative and cerebrovascular risk factors (2), with pre-existing structural brain pathology being a frequent finding in stroke patients (3). Early onset (<3 months) of post-stroke dementia (PSD) has been found to be primarily associated with stroke lesion volume and white matter hyperintensity (WMH) load (47). The likelihood of developing cognitive impairment after a stroke does however remain elevated for many years after the incident (8), with late onset (>6 months) being mainly associated with the presence of lacunes and a history of ischemic heart disease and stroke (9). Moreover, early deficits in cognition after a stroke does not necessarily mean long-term problems and some studies report that about ¼ of patients with cognitive impairment at time of discharge show improvement already within the first year after a stroke event (10). Discovering reliable methods of identifying stroke patients at risk of dementia vs. only transitory cognitive impairment therefore has major implications in the development of tailorized follow-up strategies for patients, thereby decreasing both the personal and the societal disease burden of PSD.

Accelerated post-stroke cortical and subcortical atrophy is common, but the pattern it occurs in remains somewhat unclear. Stroke has been found to be associated with an overall accelerated atrophy rate for at least 3–12 months after a stroke incident, with the atrophy taking place irrespective of stroke lesion location (11). This could either be explained by distant neurophysiological changes, also called diachisis (12) or by secondary atrophy, also called Wallerian degeneration, affecting descending fiber tracts from the locus of the stroke, leading to structural changes also in areas distal to the stroke (13). In stroke there may also be a greater atrophy rate in the ipsi- (same side as the stroke) than the contralesional (opposite side of the stroke) hemisphere. Ipsilesional cortices and subcortical structures have been found to decrease more than its contralesional counterparts (11, 14), although some structures, such as the hippocampus, have also been reported to shrink equally in both hemispheres (15). Additionally, some studies report that the ipsilesional hemisphere atrophies more than the contralesional hemisphere only if the stroke was located to the middle cerebral artery territory (16). These somewhat diverging findings call for further clarification.

Although the exact spatial pattern of atrophy remains unclear, the effects of a stroke has been shown to last for years, with findings showing persistent greater brain atrophy up to 6 years after a stroke insult (17). Moreover, ipsilesional cortical and subcortical atrophy as opposed to contralesional atrophy rates have been found to be 2–4 times greater at 1 year compared to at 3 months after a stroke (11). These findings suggest that a stroke leads to protracted atrophy in the ipsilesional cortex more so than in other parts of the brain. Still, the temporal profile of the atrophy is yet to be fully understood. Longitudinal designs are therefore required to map out a potential difference in atrophy pattern trajectories between anatomical regions following a stroke.

Both cortical and subcortical atrophy have been shown to be associated with cognitive decline (14, 18). The brain changes reported as providing the greatest risk of cognitive decline in cross-sectional and longitudinal studies lasting up to 3–12 months are global brain atrophy, medial temporal lobe (including hippocampal) atrophy, and WMH load (4, 1922). Since accelerated brain atrophy is demonstrated for a longer time period, potentially important changes in brain structure-function relationship over time may be overlooked due to relatively short follow-up times in previous studies. The current study therefore aimed to use a longitudinal follow-up design including both cognition and structural brain imaging assessed three times across 36 months in contrast to the typical 3–12 months follow-up.

The current prospective 36-months follow-up study of stroke patients aimed to investigate the longitudinal associations between (I) brain structure atrophy and stroke hemisphere, and (II) cognitive impairment and brain structure atrophy after stroke. We expected to find that (I) cortical thickness and hippocampal-, thalamic-, and caudate nucleus volumes declined more in the ipsilesional than the contralesional hemisphere at both 18- and 36 months after stroke. We also expected that (II) cognitive decline was associated with a larger stroke volume, and with greater cortical thickness and hippocampal-, thalamic-, and caudate nucleus volume atrophy at each timepoint.

More at link.

 

Sunday, July 25, 2021

The role of multiple contralesional motor areas for complex hand movements after internal capsular lesion

So ask your doctor to decipher this into EXACT INSTRUCTIONS FOR RECOVERY. And your doctor hasn't managed to accomplish this in 15 years? Sounds like you need to call the president and ask when competence will exist in their hospital.

The role of multiple contralesional motor areas for complex hand movements after internal capsular lesion

6096 The Journal of Neuroscience, May 31, 2006
 •
 26(22):6096–6102
 
MartinLotze,1,2
JochenMarkert,1
PaulSauseng,3
JuliaHoppe,1,4
ChristianPlewnia,5
andChristianGerloff 1,4
1 Department of General Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, D-72076 Tuebingen, Germany,
 2 Institute of Medical Psychology and Behavioral Neurobiology, University of Tuebingen, D-72074 Tuebingen, Germany,
 3 Department of Psychology, University of Salzburg, A-5020 Salzburg, Austria,
 4 Department of Neurology, University Medical Center Hamburg–Eppendorf, D-20246 Hamburg, Ge Germany, and
5 Department of Psychiatry and Psychotherapy, University of Tuebingen, D-72072 Tuebingen, Germany
Imaging techniques document enhanced activity in multiple motor areas of the damaged and contralesional (intact) hemisphere(CON-H) after stroke. In the subacute stage, increased activity within motor areas in the CON-H during simple movements of the affected hand has been shown to correlate with poorer motor outcome. For those patients in the chronic stage who recovered well, the functional relevance of an increased activation within the CON-H is unclear. Using trains of repetitive transcranial magnetic stimulation TMS) during performance of complex finger movements, we tested the behavioral relevance of regional functional magnetic resonance imaging(fMRI) activation within the CON-H for sequential finger movement performance of the recovered hand in seven patients who had experienced a subcortical stroke. TMS was navigated over fMRI activation maxima within anatomically preselected regions of the CON-H, and effects were compared with those of healthy controls.  Stimulation over the dorsal premotor cortex(dPMC), the primary motor cortex(M1),and the superior parietal lobe(SPL) resulted in significant interference with recovered performance in patients. Interference with the dPMC and M1 induced timing errors only, SPL stimulation caused both timing and accuracy deficits. The present results argue for a persistent beneficial role of the dPMC, M1, and SPL of the CON-H on some aspects of effectively recovered complex motor behavior after subcortical stroke.

Sunday, July 11, 2021

Enhanced Cortical Activation in the Contralesional Hemisphere of Chronic Stroke Patients in Response to Motor Skill Challenge

 WHOM is going to do the needed followup  to create protocols for that that deliver recovery? Not just this intermediate step of Enhanced Cortical Activation. This just describes what occurred for those lucky enough to recover, NOT HOW TO RECOVER.

As adjectives the difference between ipsilesional and contralesional

is that ipsilesional is on the same side as a lesion while contralesional is (medicine) describing the half of a patient's brain or body away from the site of a lesion.

Enhanced Cortical Activation in the Contralesional Hemisphere of Chronic Stroke Patients in Response to Motor Skill Challenge

Cerebral Cortex, Volume 18, Issue 3, March 2008, Pages 638–647, https://doi.org/10.1093/cercor/bhm096
Published:
29 June 2007

Abstract

The brain processes involved in the restoration of motor skill after hemiparetic stroke are not fully understood. The current study compared cortical activity in chronic stroke patients who successfully recovered hand motor skill and normal control subjects during performance of kinematically matched unskilled and skilled hand movements using functional magnetic resonance imaging. We found that cortical activation during performance of the unskilled movement was increased in the patients relative to controls in the contralesional primary sensorimotor cortex. Performance of the skilled movement elicited increased activation in the patients relative to controls in the contralesional primary sensorimotor cortex, ventral premotor cortex, supplementary motor area/cingulate, and occipitoparietal cortex. Further, the activation change in the contralesional occipitoparietal cortex was greater in the patients relative to controls with the increase in motor skill challenge. Kinematic differences, mirror movements, and residual motor deficits did not account for the enhanced activation in the contralesional cortices in the patients. These results suggest that activation in the contralesional cortical network was enhanced as a function of motor skill challenge in stroke patients with good motor recovery. The findings of the current study suggest that successful recovery of motor skill after hemiparetic stroke involves participation of the contralesional cortical network.

Introduction

Stroke often causes hemiparesis due to direct damage and/or secondary functional disruption of brain areas controlling movement. Recovery of motor function, when it occurs, typically starts with regaining limb synergies characterized by gross, undifferentiated movements of the stroke-affected limb (Twitchell 1951; Brunnstrom 1966). Recovery may proceed by regaining the ability to perform skilful, nonsynergistic limb movements in which intralimb joints can be controlled independently. Recovery of hand motor function also follows this trajectory, with early restoration of synergistic movements in which the digits can grasp and release in unison and later restoration of dexterous, nonsynergistic movements in which the digits can be moved independent of one another. Recovery of nonsynergistic hand movements is critical to functional use of the hand in daily activities, such as tool usage and object manipulation.

The changes in brain activity mediating recovery of motor function after stroke are beginning to be unraveled. Early after hemiparetic stroke in patients, performance of a gripping task (i.e., a synergistic movement) by the affected hand has been shown to increase activity in several cortices within the ipsilesional and contralesional hemispheres to a greater degree than in normal control subjects (Ward et al. 2003a). Progressive normalization of cortical activity elicited by hand gripping appears to occur during the recovery process in stroke patients (Ward et al. 2003a). Further, cortical activity associated with hand gripping in chronic stroke patients with good motor recovery has been shown to be indistinguishable from that in normal controls (Ward et al. 2003b). In contrast, during index finger or sequential finger tapping (i.e., nonsynergistic movements), cortical activity in chronic stroke patients with good motor recovery has been observed to be enhanced relative to that in normal controls, most commonly in the primary motor cortex, premotor cortex, and parietal cortex of the contralesional hemisphere (Chollet et al. 1991; Weiller et al. 1993; Cramer et al. 1997; Cao et al. 1998; Foltys et al. 2003; Gerloff et al. 2006; Lotze et al. 2006). These observations suggest that differences in motor task–related cortical activity between well-recovered stroke patients and normal controls are more pronounced as the skill demanded by the motor task is increased. However, the relationship between cortical activity and motor skill challenge in stroke patients has not been tested directly. This is partly due to previous studies, with the exception of a few, having stroke patients perform only a single motor task, either synergistic or nonsynergistic. In the few studies in which more than one motor task was performed (Cramer et al. 2001; Foltys et al. 2003; Nair et al. 2007), comparison between resultant activation patterns was confounded by the tasks not being matched for kinematic parameters of performance (e.g., force, amplitude, frequency, range of motion, number of body segments moved, and which body segments moved).

The purpose of the current study was to gain insight into the cortical processes involved in the restoration of motor skill after stroke. To meet this goal, cortical activity in chronic stroke patients who successfully recovered motor skill was compared with that in normal control subjects using functional magnetic resonance imaging (fMRI). The fMRI was conducted while the subjects performed a pair of kinematically matched hand motor tasks that were developed by Ehrsson et al. (2002) to examine differences in the neural control of synergistic versus nonsynergistic movements in normal healthy subjects. The synergistic task involved movement of all 5 digits in unison, whereas the nonsynergistic task involved independent movement of the thumb relative to the unified movement of the other 4 digits. As the nonsynergistic task involved independent digit movement, this task required more skill than the synergistic task. Understanding the effect of motor skill challenge on cortical activation in stroke patients could ultimately lead to the development of interventions aimed at maximizing motor recovery after hemiparetic stroke.


 
 

Wednesday, May 19, 2021

Contralesional motor deficits after unilateral stroke reflect hemisphere specific control mechanisms

 But nothing here helps survivors get recovered. Talking does no good, we need EXACT PROTOCOLS THAT DELIVER RECOVERY.

 Contralesional motor deficits after unilateral stroke reflect hemisphere specific control mechanisms

 

Brain, Volume 136, Issue 4, April 2013, Pages 1288–1303, https://doi.org/10.1093/brain/aws283
Published:
28 January 2013
Article history

Abstract

We have proposed a model of motor lateralization, in which the left and right hemispheres are specialized for different aspects of motor control: the left hemisphere for predicting and accounting for limb dynamics and the right hemisphere for stabilizing limb position through impedance control mechanisms. Our previous studies, demonstrating different motor deficits in the ipsilesional arm of stroke patients with left or right hemisphere damage, provided a critical test of our model. However, motor deficits after stroke are most prominent on the contralesional side. Post-stroke rehabilitation has also, naturally, focused on improving contralesional arm impairment and function. Understanding whether contralesional motor deficits differ depending on the hemisphere of damage is, therefore, of vital importance for assessing the impact of brain damage on function and also for designing rehabilitation interventions specific to laterality of damage. We, therefore, asked whether motor deficits in the contralesional arm of unilateral stroke patients reflect hemisphere-dependent control mechanisms. Because our model of lateralization predicts that contralesional deficits will differ depending on the hemisphere of damage, this study also served as an essential assessment of our model. Stroke patients with mild to moderate hemiparesis in either the left or right arm because of contralateral stroke and healthy control subjects performed targeted multi-joint reaching movements in different directions. As predicted, our results indicated a double dissociation; although left hemisphere damage was associated with greater errors in trajectory curvature and movement direction, errors in movement extent were greatest after right hemisphere damage. Thus, our results provide the first demonstration of hemisphere specific motor control deficits in the contralesional arm of stroke patients. Our results also suggest that it is critical to consider the differential deficits induced by right or left hemisphere lesions to enhance post-stroke rehabilitation interventions.

Introduction

A large body of research has now established that the two cerebral hemispheres show a considerable degree of lateralization or a specialization for controlling different aspects of behaviour. Although such neural lateralization has been characterized primarily through studies of perceptual and cognitive processes, behavioural and neuroimaging studies have raised the possibility that the right and left hemispheres play different roles in the motor control of either arm. Based on our work in young healthy individuals, we have proposed a model of motor lateralization, in which each hemisphere has become specialized for different aspects of motor control, such that the ‘dominant/left’ hemisphere is critical for predicting limb and task dynamics, and the opposite, ‘non-dominant/right’ hemisphere is critical for specifying steady-state limb positions through impedance control mechanisms (see Sainburg, 2010 for a review). Our recent work in patients with unilateral brain damage (Schaefer et al., 2007, 2009a, b; Mutha et al., 2010, 2011a, b; Schaefer et al., 2012) and findings from other previous studies (Haaland and Harrington, 1989; Harrington and Haaland, 1991; Bernspang and Fisher, 1995; Winstein and Pohl, 1995; Haaland et al., 2004) have provided a confirmation for hemispheric specialization for movement control. For example, our study examining movement coordination in right-handed stroke patients (Schaefer et al., 2009b) showed a clear double dissociation between hemisphere status (healthy/hemisphere damage) and arm (right/left) for different features of movement. Patients with left hemisphere damage, but not right hemisphere damage, showed errors in direction and linearity of reaching movements that were associated with poor coordination of intersegmental dynamics. In contrast, patients with right hemisphere damage made well-coordinated and fairly straight movements, but they showed large and highly variable final position errors. In more recent studies, we have significantly expanded on these initial results by demonstrating differential deficits in motor adaptation and error correction mechanisms in left and right hemisphere damage stroke patients (Schaefer et al., 2009a; Mutha et al., 2011b; Schaefer et al., 2012). These studies have consistently revealed a deficit in predictive control after left hemisphere damage and final position control after right hemisphere damage, in line with the predictions of our model.

Our stroke studies were initiated as a critical test of this framework of hemispheric specialization for movement. We reasoned that if a hemisphere contributes its specialization to the movements of both arms, then motor deficits after damage to that hemisphere should be evident even if the ipsilesional arm in stroke patients is used to perform the task. Our studies, therefore, almost always required subjects to use their ipsilesional arm. However, given the crossed organization of the motor system, motor deficits after stroke are most prominent on the contralesional side. Therefore, most studies in stroke patients have, unsurprisingly, been dedicated to understanding the nature of these contralesional motor deficits. These studies have shown that although weakness and spasticity are common with contralesional hemiparesis (Bobath, 1990), discoordination is also a major problem, particularly during point-to-point reaching tasks. For example, Beer et al. (2000, 2004) demonstrated systematic direction errors and poor interjoint coordination with the contralesional arm in a 16-direction centre-out reaching task. In this task, all four directions comprised a quadrant in task space, and deficits were largest in the two quadrants where intersegmental coordination requirements were greatest. Similarly, Levin (1996) and Cirstea and Levin (2000) showed that when stroke patients made horizontal plane reaching movements with the paretic arm, their movements were characterized by high variability and poor synchrony between elbow and shoulder joint motions. In light of these significant contralesional deficits, motor rehabilitation after stroke has also focused on improving the functioning of the contralesional arm. In fact, newer therapeutic approaches, such as constraint-induced movement therapy (Taub et al., 1993; Mark and Taub, 2004), emphasize forced and repetitive use of the contralesional arm while also preventing use of the ipsilesional arm as a means to improve contralesional arm performance.

Despite such strong emphasis on understanding contralesional deficits and improving contralesional arm function, previous studies have not been coupled with the growing body of work that addresses hemispheric specificity for movement control mechanisms. One potential reason for this could be the concern that spasticity, weakness and variability in degree of impairment in the contralesional limb could mask any performance asymmetries. Nevertheless, understanding whether neural lateralization results in contralesional deficits that differ depending on the hemisphere of damage is of critical importance for assessing the impact of brain damage on function and also for designing rehabilitation protocols specific to the impaired limb. In this study, we ask whether the motor deficits in the contralesional arm of unilateral stroke patients reflect hemisphere-specific control mechanisms. Our model of lateralized control predicts clear differences in contralesional motor deficits depending on the laterality of stroke; therefore, this study also serves as a critical test of our model. We overcome the potential limitation of contralesional spasticity and reduced motor abilities by examining patients with only mild to moderate hemiparesis, defined by a score >45 (of a maximum possible 66) on the Fugl-Meyer Assessment of Upper Extremity Function.


Sunday, November 15, 2020

Contralesional Motor Cortex Activation Depends on Ipsilesional Corticospinal Tract Integrity in Well-Recovered Subcortical Stroke Patients

 The takeaway from this is that YOU need to have the correct stroke and resulting integrity. The stroke medical world seems to be ignoring the real world of stroke. Good luck planning your stroke to fit the research and interventions that exist currently. YOUR RESPONSIBILITY! This makes it much easier for your doctor to blame you for not recovering, rather than looking at what they should be doing to get you 100% recovered.

Contralesional Motor Cortex Activation Depends on Ipsilesional Corticospinal Tract Integrity in Well-Recovered Subcortical Stroke Patients

2012, Neurorehabilitation and Neural Repair
 Martin Lotze, MD 1, 
Willy Beutling 1, 
Moritz Loibl 1, 
Martin Domin 1, 
Thomas Platz, MD 2, 
Ulf Schminke, MD 1, 
and Winston D. Byblow, PhD 3

Abstract

Background.
 The relationship between structural and functional integrity of descending motor pathways can predict the potential for motor recovery after stroke. The authors examine the relationship between brain imaging biomarkers within contralesional and ipsilesional hemispheres and hand function in well-recovered patients after subcortical stroke at the level of the internal capsule.
Objective.
 Measures of functional activation and integrity of the ipsilesional corticospinal tract might predict paretic hand function.
 Methods.
 A total of 14 patients in the chronic stable phase of motor recovery after subcortical stroke and 24 healthy age-matched individuals participated in the study. Functional MRI was used to examine BOLD contrast during passive wrist flexion–extension and paced or maximum-velocity active fist clenching. Functional integrity of the corticospinal pathway was assessed by transcranial magnetic stimulation to obtain motor-evoked potentials (MEPs) in the first dorsal interosseus muscle of the paretic and nonparetic hands. Fractional anisotropy and the proportion of traces between hemispheres in the posterior limb of both internal capsules were quantified using diffusion-weighted MRI.
Results.
 Patients with smaller MEPs had a weaker paretic hand and more primary motor cortex activation in their affected hemisphere.  Asymmetry between white matter tracts of either hemisphere was associated with reduced precision grip strength and increased BOLD activation within the contralesional dorsal premotor cortex for demanding hand tasks.
Conclusion.
 There may be beneficial reorganization in contralesional secondary motor areas with increasing damage to the corticospinal tract after subcortical stroke. Associations between clinical, functional, and structural integrity measures in chronic stroke may lead to a better understanding of motor recovery processes.
 

Thursday, September 24, 2020

Low-Frequency Repetitive Transcranial Magnetic Stimulation Over Contralesional Motor Cortex for Motor Recovery in Subacute Ischemic Stroke: A Randomized Sham-Controlled Trial

So nothing useful found but more research requested. You'll have to ask what the definition of subacute is?

Low-Frequency Repetitive Transcranial Magnetic Stimulation Over Contralesional Motor Cortex for Motor Recovery in Subacute Ischemic Stroke: A Randomized Sham-Controlled Trial

First Published August 18, 2020 Research Article 

Low-frequency repetitive transcranial magnetic stimulation (rTMS) over the contralesional motor cortex (M1) has demonstrated beneficial effects on motor recovery, but evidence among patients with subacute stroke is lacking. We aimed to investigate whether 1-Hz rTMS over the contralesional M1 versus sham rTMS could improve arm function in patients with subacute ischemic stroke when combined with rehabilitative motor training.

In total, 77 patients who were within 90 days after their first-ever ischemic stroke were enrolled and randomly allocated to either real (n = 40) or sham rTMS (n = 37). We delivered 1-Hz 30-minute active or sham rTMS before each daily 30-minute occupational therapy sessions over a 2-week period. The primary endpoint was changes in the Box and Block Test (BBT) score immediately after the end of treatment (EOT). Secondary analyses assessed changes in Fugl-Meyer assessment, Finger Tapping Test (FTT), Brunnstrom stage, and grip strength.

ClinialTrials.gov (NCT02082015).

Changes in BBT immediately after the end of treatment did not differ significantly between the 2 groups (P = .267). Subgroup analysis according to cortical involvement revealed that real rTMS resulted in improvements in BBT at 1 month after EOT (17.4 ± 9.8 real vs 10.9 ± 10.3 sham; P = .023) and Brunnstrom stage of the hand immediately after EOT (0.6 ± 0.5 real vs 0.2 ± 0.5 sham; P = .023), only in the group without cortical involvement.

The effects of real and sham rTMS did not differ significantly among patients within 3 months poststroke. The location of stroke lesions should be considered for future clinical trials.

 

Saturday, September 19, 2020

Low-Frequency Repetitive Transcranial Magnetic Stimulation Over Contralesional Motor Cortex for Motor Recovery in Subacute Ischemic Stroke: A Randomized Sham-Controlled Trial

 Contralesional:Adjective. (not comparable) (medicine) Describing the half of a patient's brain or body away from the site of a lesion.

Or is c-tDCS (2 posts) better for contralesional stimulation?

Low-Frequency Repetitive Transcranial Magnetic Stimulation Over Contralesional Motor Cortex for Motor Recovery in Subacute Ischemic Stroke: A Randomized Sham-Controlled Trial

First Published August 18, 2020 Research Article Find in PubMed 

Low-frequency repetitive transcranial magnetic stimulation (rTMS) over the contralesional motor cortex (M1) has demonstrated beneficial effects on motor recovery, but evidence among patients with subacute stroke is lacking. We aimed to investigate whether 1-Hz rTMS over the contralesional M1 versus sham rTMS could improve arm function in patients with subacute ischemic stroke when combined with rehabilitative motor training.

In total, 77 patients who were within 90 days after their first-ever ischemic stroke were enrolled and randomly allocated to either real (n = 40) or sham rTMS (n = 37). We delivered 1-Hz 30-minute active or sham rTMS before each daily 30-minute occupational therapy sessions over a 2-week period. The primary endpoint was changes in the Box and Block Test (BBT) score immediately after the end of treatment (EOT). Secondary analyses assessed changes in Fugl-Meyer assessment, Finger Tapping Test (FTT), Brunnstrom stage, and grip strength.

ClinialTrials.gov (NCT02082015).

Changes in BBT immediately after the end of treatment did not differ significantly between the 2 groups (P = .267). Subgroup analysis according to cortical involvement revealed that real rTMS resulted in improvements in BBT at 1 month after EOT (17.4 ± 9.8 real vs 10.9 ± 10.3 sham; P = .023) and Brunnstrom stage of the hand immediately after EOT (0.6 ± 0.5 real vs 0.2 ± 0.5 sham; P = .023), only in the group without cortical involvement.

The effects of real and sham rTMS did not differ significantly among patients within 3 months poststroke. The location of stroke lesions should be considered for future clinical trials.

Access Options