New brain imaging technique offers hope for better stroke rehabilitation

 Which means the followup research needs to be how to get dendritic branching and axon pathfinding going to reconnect the areas of the brain. WHOM IS GOING TO DO THAT?

axon pathfinding (42 posts to March 2012)

dendritic branching (42 posts to February 2012)

Doesn't anyone in stroke have two functioning neurons to see the path forward to survivor recovery except for me?

The latest here:

New brain imaging technique offers hope for better stroke rehabilitation

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Georgetown University Medical CenterMar 3 2025

A new Georgetown University Medical Center study in collaboration with MedStar Health and the National Institutes of Health exploring a new brain imaging technique is bringing stroke experts a step closer to better tailoring rehabilitation.

Neurologists often use MRI images of the brain's white matter to glean information about a person's ability to recover, but a new imaging technique added to MRI allows clinicians to better see the condition of white matter tracts leading to the limbs, an observation usually only seen after death during an autopsy.

A white matter tract called the corticospinal tract provides the main wiring that goes from your brain down to your spinal cord to help power your arms and legs. If those cables are severed or atrophied, the person is not going to be able to regain meaningful use of their arms and legs – they wouldn't have much motor strength."

Matthew A. Edwardson, MD, study leader, associate professor of neurology at Georgetown University School of Medicine and vascular neurologist and a member of the stroke team atMedStar Georgetown University Hospital

The imaging technique used by Edwardson and his colleagues is called diffusion tensor-based morphometry (DTBM). It combines directional information about the structures in the brain with the shape and size of the structures being imaged. Previously it was difficult to separate the white matter cables from the gray matter using morphometry approaches because they did not include the directional information. This two-part technique allows researchers to map and quantify changes over time in the white matter tracts.

"To our knowledge, this is the first study to allow us to measure atrophy of these tracts in stroke survivors," says Edwardson, a member of the Center for Brain Plasticity and Recovery, a joint collaboration between Georgetown University and MedStar National Rehabilitation Network.

He and colleagues from the National Institutes of Health (NIH) describe their findings in March 3, 2025 in the journal Neurology ("Association between changes in white matter volume detected with diffusion tensor-based morphometry and motor recovery after stroke").

"Now, we can see if the cables have shrunk in size which would indicate that a stroke has caused enough damage to the brain to lead to the wiring becoming atrophied," says Edwardson. "That observation is strongly correlated with how well somebody will recover. If there's a lot of atrophy in the brain in those cables, they're not going to have much ability to recover their arm function after a stroke."

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Edwardson says further studies would be needed before the observations could be used to tailor stroke rehabilitation.

"It would be helpful for the therapist to know at the time of admission to inpatient rehabilitation whether there's some likelihood of their patient regaining function," he says. "If it is determined that the patient isn't likely to recover meaningful motor use, then the therapist could change their strategy to perhaps focus on the unimpaired side with strategies to compensate for the disability."

Along with Edwardson co-authors of the publication are Amritha Nayak, ME, M. Okan Irfanoglu, PhD; and Carlo Pierpaoli, MD, PhD; of NIH's National Institute of Biomedical Imaging and Bioengineering; and . Marie Luby, PhD; and Lawrence L. Latour, PhD; of NIH's National Institute of Neurological Disorders and Stroke.

The authors report having no personal financial interests related to the study.

Funding was received from the National Center for Advancing Translational Sciences (UL1TR000101), and Georgetown's Clinical and Translational Science Award.

Source:

Georgetown University Medical Center

Journal reference:

Edwardson, M. A., et al. (2025) Association Between Changes in White Matter Volume Detected With Diffusion Tensor–Based Morphometry and Motor Recovery After Stroke. Neurology. doi.org/10.1212/WNL.0000000000213408.

Insights into the dependence of post-stroke motor recovery on the initial corticospinal tract connectivity from a computational model

 Precisely how is this going to get survivors recovered? Useless research without that!

Insights into the dependence of post-stroke motor recovery on the initial  from a computational model

• Dongwon Kim,
• Leah M. O’Shea &
• Naveed R. Aghamohammadi 

Journal of NeuroEngineering and Rehabilitation volume 22, Article number: 8 (2025) Cite this article

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Abstract

There is a consensus that motor recovery post-stroke primarily depends on the degree of the initial connectivity of the ipsilesional corticospinal tract (CST). Indeed, if the residual CST connectivity is sufficient to convey motor commands, the neuromotor system continues to use the CST predominantly, and motor function recovers up to 80%. In contrast, if the residual CST connectivity is insufficient, hand/arm dexterity barely recovers, even as the phases of stroke progress. Instead, the functional upregulation of the reticulospinal tract (RST) often occurs. In this study, we construct a computational model that reproduces the dependence of post-stroke motor recovery on the initial CST connectivity. The model emulates biologically plausible evolutions of primary motor descending tracts, based on activity-dependent or use-dependent plasticity and the preferential use of more strongly connected neural circuits. The model replicates several elements of the empirical evidence presented by the Fugl-Meyer Assessment (FMA) subscores, which evaluate the capabilities for out-of-synergy and in-synergy movements. These capabilities presumably change differently depending on the degree of the initial CST connectivity post-stroke, providing insights into the interactive dynamics of the primary descending motor tracts. We discuss findings derived from the proposed model in relation to the well-known proportional recovery rule. This modeling study aims to present a way to differentiate individuals who can achieve 70 to 80% recovery in the chronic phase from those who cannot by examining the interactive evolution of out-of-synergy and in-synergy movement capabilities during the subacute phase, as assessed by the FMA.

Introduction

Clinical observations suggest that the extent of potential motor recovery following stroke primarily depends on the residual connectivity of the ipsilesional corticospinal tract (CST) observed within the first few weeks [5, 66, 67]. The ipsilesional CST is the primary motor descending pathway that conveys motor commands to motoneurons [49]. Stroke survivors generally fall into two groups: one group significantly recovers to the level of mild impairment with substantial hand/arm dexterity, and the other group remains at the level of severe-to-moderate impairment, limiting the restoration of hand/arm dexterity [11]. The success or failure to retrieve hand/arm dexterity may depend on whether CST connectivity is resilient during the subacute phase where spontaneous motor recovery occurs [62]. If CST connectivity is not resilient, alternative pathways, including the contralesional reticulospinal tract (RST), may be employed, leading to improvements in gross motor function [10, 15, 62].

The proportional recovery (PR) rule was not originally devised to account for the initial CST connectivity in motor recovery post-stroke [68]. However, this rule is known to broadly differentiate individuals with stroke into two groups: one group with sufficient initial CST connectivity (fitters) and one group with insufficient or no initial CST connectivity (non-fitters) [5]. The PR rule describes that individuals spontaneously recover an average of 70–80% from the first week of stroke to the follow-up (typically 3 or 6 months) in terms of the Fugl-Meyer assessment (FMA) total score, regardless of sex, age and race [46, 72, 74]. Though there are questions about the PR rule due to issues such as mathematical coupling [28], this rule emphasizes the influence of the initial connectivity of the CST, distinguishing ‘fitters’ from ‘non-fitters’. Fitters achieve 70 to 80% recovery, typically surpassing the threshold of the FMA total score of 40 ~ 42 [33, 64], achieving substantial spontaneous recovery of hand/arm dexterity upon entering the chronic phase. The CST is assumed to be the dominant motor descending pathway in fitters. Meanwhile, non-fitters fail to achieve 70 to 80% recovery. The main reason may be that out-of-synergy test items that require the sufficient functional capability of the CST are difficult for non-fitters to score well on (i.e. Score “2” for each test item) [18, 39, 64]. The CST in this group barely achieves a functional capability level that allows for restoring of hand/arm dexterity.

In this study, we construct a computational model to explain the differential motor recovery of non-fitters versus fitters. This model evaluates how the degree of the initial CST connectivity impacts motor recovery after stroke. We reproduce several key features of subscore distributions of the FMA for the upper extremity in fitters and non-fitters. This allows us to gain insight into the interactive evolutions of motor tract (i.e. CST and RST) dynamics depending on the degree of the initial CST connectivity post-stroke. The subscores of the FMA, derived from 27 subtests for in-synergy and out-of-synergy movements, reveal clues about the functioning neural substrates, potentially distinguishing uses of the CST and RST. We apply a strict assumption that while the type of in-synergy movements (tested using the flexion synergy and extension synergy test items) is mediated primarily by either the CST or RST, the type of out-of-synergy movements (tested using the synergy-mixing and out-of-synergy test items) is mediated predominantly by the CST. Individuals with no neurological deficit can conduct elbow flexion while performing shoulder abduction (which is considered as an abnormal synergistic movement following a stroke) by exciting the biceps and abductors individually (via the CST); they do not use involuntary coactivation to perform the movement. We incorporate a stochastic gradient descent algorithm into the Hebbian theory to reflect activity- or use-dependent plasticity [19]. This algorithm successfully replicated the evolution of the torque generation of the elbow joint during flexion, indicating upper- extremity functional activity following stroke. It also revealed that more strongly connected motoneurons are optimized with priority (Reinkensmeyer, Guigon, and Maier [56]). We aim to present a way to differentiate individuals who can achieve 70 to 80% recovery in the chronic phase from those who cannot, by examining the interactive evolution of out-of-synergy and in-synergy movement capabilities during the subacute phase, as assessed by the FMA. Our efforts in this study will provide insights into clinically observed motor improvement during the subacute phase and therapy design.

Modulation of the Association Between Corticospinal Tract Damage and Outcome After Stroke by White Matter Hyperintensities

 I could see ABSOLUTELY NOTHING in here that will help survivors recover! Useless.

Modulation of the Association Between Corticospinal Tract Damage and Outcome After Stroke by White Matter Hyperintensities

Jennifer K. Ferris, MSc, PhD https://orcid.org/0000-0003-3624-6996, Bethany P. Lo, BSc, Giuseppe Barisano, MD, PhD https://orcid.org/0000-0001-5598-1369, Amy Brodtmann, MBBS, PhD, FRACP https://orcid.org/0000-0001-9466-2862, Cathrin M. Buetefisch, MD, PhD, Adriana B. Conforto, Miranda R. Donnelly, MS https://orcid.org/0000-0002-1983-3008, … Show All … , and Sook-Lei Liew, PhD, OTR/L, FAOTA https://orcid.org/0000-0001-5935-4215Authors Info & Affiliations

May 28, 2024 issue

102 (10)

https://doi.org/10.1212/WNL.0000000000209387

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Abstract

Background and Objectives

Motor outcomes after stroke relate to corticospinal tract (CST) damage. The brain leverages surviving neural pathways to compensate for CST damage and mediate motor recovery. Thus, concurrent age-related damage from white matter hyperintensities (WMHs) might affect neurologic capacity for recovery after CST injury. The role of WMHs in post-stroke motor outcomes is unclear. In this study, we evaluated whether WMHs modulate the relationship between CST damage and post-stroke motor outcomes.

Methods

We used data from the multisite ENIGMA Stroke Recovery Working Group with T1 and T2/fluid-attenuated inversion recovery imaging. CST damage was indexed with weighted CST lesion load (CST-LL). WMH volumes were extracted with Freesurfer's SAMSEG. Mixed-effects beta-regression models were fit to test the impact of CST-LL, WMH volume, and their interaction on motor impairment, controlling for age, days after stroke, and stroke volume.

Results

A total of 223 individuals were included. WMH volume related to motor impairment above and beyond CST-LL (β = 0.178, 95% CI 0.025–0.331, p = 0.022). Relationships varied by WMH severity (mild vs moderate-severe). In individuals with mild WMHs, motor impairment related to CST-LL (β = 0.888, 95% CI 0.604–1.172, p < 0.001) with a CST-LL × WMH interaction (β = −0.211, 95% CI −0.340 to −0.026, p = 0.026). In individuals with moderate-severe WMHs, motor impairment related to WMH volume (β = 0.299, 95% CI 0.008–0.590, p = 0.044), but did not significantly relate to CST-LL or a CST-LL × WMH interaction.

Discussion

WMHs relate to motor outcomes after stroke and modify relationships between motor impairment and CST damage. WMH-related damage may be under-recognized in stroke research as a factor contributing to variability in motor outcomes. Our findings emphasize the importance of brain structural reserve in motor outcomes after brain injury.

Introduction

Upper extremity motor impairment is one of the most common consequences of stroke¹ and typically results in long-term disability.² The degree of damage to the corticospinal tract (CST) relates strongly to motor impairment after stroke,^3,4 indicating a primary insult to the motor system. However, motor recovery after stroke is variable even after accounting for CST damage.⁵ Recovery after stroke is likely mediated by compensation of surviving neural substrate.⁶ This suggests that the integrity of structures beyond the CST might be prognostic of motor recovery^7,8 because overall brain health may be important in explaining why 2 individuals with similar stroke lesions can experience very different trajectories of recovery.⁹

White matter hyperintensities (WMHs) of presumed vascular origin are the most common form of age-related cerebrovascular damage.¹⁰ They are present in more than half of people older than 60 years.¹¹ Individuals with WMHs are more likely to experience a stroke¹² in part because of common cardiometabolic risk factors between WMHs and stroke.¹³ There is growing evidence that WMHs can also affect functional outcomes after stroke.¹⁴ The relationship between WMHs and post-stroke cognitive impairment has been well established¹⁴; however, there have been few investigations of the specific impact of WMHs on motor outcomes after stroke. WMHs modulate relationships between stroke lesion volume and overall functional outcome.^15,16 Motor outcomes after stroke may similarly be modulated by concurrent WMHs because of the widespread impacts of WMHs on cerebral networks,^17,18 which may create preexisting damage in compensatory pathways and, therefore, decrease the brain's capacity for motor recovery.

We tested whether the relationship between post-stroke motor impairment and CST damage is affected by concurrent WMH damage, controlling for age, time after stroke, and stroke lesion volume. We hypothesized that the relationship between motor impairment and CST damage would be attenuated in individuals with higher WMH volumes, indicating a greater influence of concurrent WMHs on motor outcomes after stroke.

 

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Exploring the Structural Plasticity Mechanism of Corticospinal Tract during Stroke Rehabilitation Based Automated Fiber Quantification Tractography

 No clue! Absolutely useless for survivors to bring to their medical staff for recovery. But great word salad though!

Exploring the Structural Plasticity Mechanism of Corticospinal Tract during Stroke Rehabilitation Based Automated Fiber Quantification Tractography

Haojie Zhang, MD https://orcid.org/0000-0001-6889-0853, Jun Zhao, MD, […], and Tong Zhang, MD tommzhang@163.com+7View all authors and affiliations

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https://doi.org/10.1177/15459683241249115

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Abstract

Background

Corticospinal tract (CST) is the principal motor pathway; we aim to explore the structural plasticity mechanism in CST during stroke rehabilitation.

Methods

A total of 25 patients underwent diffusion tensor imaging before rehabilitation (T1), 1-month post-rehabilitation (T2), 2 months post-rehabilitation (T3), and 1-year post-discharge (T4). The CST was segmented, and fractional anisotropy (FA), axial diffusion (AD), mean diffusivity (MD), and radial diffusivity (RD) were determined using automated fiber quantification tractography. Baseline level of laterality index (LI) and motor function for correlation analysis.

Results

The FA values of all segments in the ipsilesional CST (IL_-CST) were lower compared with normal CST. Repeated measures analysis of variance showed time-related effects on FA, AD, and MD of the IL_-CST, and there were similar dynamic trends in these 3 parameters. At T1, FA, AD, and MD values of the mid-upper segments of IL_-CST (around the core lesions) were the lowest; at T2 and T3, values for the mid-lower segments were lower than those at T1, while the values for the mid-upper segments gradually increased; at T4, the values for almost entire IL_-CST were higher than before. The highest LI was observed at T2, with a predominance in contralesional CST. The LIs for the FA and AD at T1 were positively correlated with the change rate of motor function.

Conclusions

IL_-CST showed aggravation followed by improvement from around the lesion to the distal end. Balance of interhemispheric CST may be closely related to motor function, and LIs for FA and AD may have predictive value for mild-to-moderate stroke rehabilitation. Clinical Trial Registration. URL: http://www.chictr.org.cn; Unique Identifier: ChiCTR1800019474.

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Corticospinal tract: a new hope for the treatment of post-stroke spasticity

We don't need 'hope'. Survivors want recovery and results! WHOM is going to do the followup research to find concrete answers?  With NO leadership and NO strategy in stroke; NOTHING WILL BE DONE.

Corticospinal tract: a new hope for the treatment of post-stroke spasticity

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Corticospinal tract: a new hope for the treatment of post-stroke spasticity

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• Linxing Huang,
• Lizhen Yi,
• Huiyuan Huang,
• Sheng Zhan,
• Ruixue Chen &
• Zenghui Yue 

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Abstract

Stroke is the third leading cause of death and disability worldwide. Post-stroke spasticity (PSS) is the most common complication of stroke but represents only one of the many manifestations of upper motor neuron syndrome. As an upper motor neuron, the corticospinal tract (CST) is the only direct descending motor pathway that innervates the spinal motor neurons and is closely related to the recovery of limb function in patients with PSS. Therefore, promoting axonal remodeling in the CST may help identify new therapeutic strategies for PSS. In this review, we outline the pathological mechanisms of PSS, specifically their relationship with CST, and therapeutic strategies for axonal regeneration of the CST after stroke. We found it to be closely associated with astroglial scarring produced by astrocyte activation and its secretion of neurotrophic factors, mainly after the onset of cerebral ischemia. We hope that this review offers insight into the relationship between CST and PSS and provides a basis for further studies.

Introduction

Stroke is the third leading cause of death and disability worldwide [1]. Post-stroke spasticity (PSS) is the most common complication of stroke but is only one of the many manifestations of upper motor neuron syndrome. Over time, PSS continues to develop without effective interventions, and the disease worsens [2]. Twelve months after stroke, 43.2% of survivors develop spasticity [3]. Spasticity is as high as 97% among survivors of chronic stroke with moderate-to-severe dyskinesia [4]; this places a heavy economic burden on patients’ families and wider society. Therefore, more effective therapies are required to promote recovery from PSS.

Treatment of PSS has largely focused on reducing the area of cerebral ischemia and rescuing neurons from damaged areas of the brain; however, the effects of putative neuroprotectants are less pronounced in clinical trials [5]. Several recent clinical studies report that the degree of corticospinal tract (CST) damage correlates with the severity of spasticity in patients with chronic stroke [6,7,8] and that there is a significant correlation between motor function improvement and CST remodeling in patients with PSS [9]. A few experimental studies have also observed that by destroying the corresponding CST, the upper motor neurons lose control of the spinal cord, causing spasticity of the contralateral limb [10]. While the pathogenesis of PSS is more complex, the more established mechanism is that PSS is a maladaptive manifestation of the loss of supraspinal inhibitory modulation of spinal reflex pathways, which occurs through a functional reorganization at different levels, involving a physiological mechanism of mutual inactivation of motor centers and excitation of peripheral spinal cord segmental neurons; it is one of the syndromes of upper motor neurons [2, 11]. The CST, as an upper motor neuron [12], is the only direct descending motor pathway and is the main pathway innervating spinal motor neurons closely related to the recovery of limb function after stroke [13]. This suggests that CST is closely related to the pathological mechanisms of PSS. Many studies have demonstrated that motor recovery after stroke depends mainly on the plasticity of the damaged lateral primary motor area, evident through stroke patients and experimental animal studies [14,15,16], or on the homologous CST axon integrity [17,18,19,20]. Spasticity is a common disorder that coexists with dyskinesia after stroke [21,22,23,24], and it does interfere with motor recovery after stroke as PSS and other dyskinesias are essentially clinical manifestations of abnormal neuroplasticity and manifestations of common processes [25]. Therefore, promoting axonal regeneration of the damaged side of the CST may be a novel avenue for the treatment of post-stroke spasticity; however, only a few studies exist on the specific link between the CST and PSS, the remodeling of CST after stroke, and the recovery promotion of PSS.

This review aimed to provide an overview of the pathophysiological mechanisms of PSS, including the types of spastic hemiparesis, the close correlation between CST and PSS, and the relationship between PSS and motor recovery. We further reviewed the therapeutic strategies to promote axonal regeneration of the CST after stroke. We found that the astroglial scar and its secreted neurotrophic factors, mainly associated with the activation of astrocytes after the onset of cerebral ischemia, are important for remodeling the CST after stroke. This provides potential novel avenues for the treatment of PSS. Finally, we briefly describe the clinical treatment of PSS in cases where the cerebral cortex is severely damaged, and the cortical inputs are not re-established.

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Corticospinal Excitability Quantification During a Visually-Guided Precision Walking Task in Humans: Potential for Neurorehabilitation

 Useless for us, healthy participants were used. So nothing will ever occur to help stroke survivors.  WE HAVE NO STRATEGY AND NO LEADERSHIP IN TRYING TO SOLVE STROKE!

Corticospinal Excitability Quantification During a Visually-Guided Precision Walking Task in Humans: Potential for Neurorehabilitation

Charline Dambreville, PhD, Cécilia Neige, PhD, […], Catherine Mercier, PhD https://orcid.org/0000-0002-2037-6916, Andreanne K. Blanchette, and Laurent J. Bouyer, PhD https://orcid.org/0000-0003-2034-4516 laurent.bouyer@rea.ulaval.ca, +2 -2View all authors and affiliations

Volume 36, Issue 10-11

https://doi.org/10.1177/15459683221124909

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Abstract

The corticospinal tract has been shown to be involved in normal walking in humans. However, its contribution during more challenging locomotor tasks is still unclear. As the corticospinal tract can be a potential target to promote gait recovery after neurological injury, it is of primary importance to quantify its use during human walking. The aims of the current study were to: (1) quantify the effects of precision walking on corticospinal excitability as compared to normal walking; (2) assess if corticospinal modulation is related to task difficulty or participants’ performance. Sixteen healthy participants walked on a treadmill during 2 tasks: regular walking (simple task) and stepping onto virtual targets (precision task). Virtual targets appeared randomly at 3 different step lengths: preferred, and ±20%. To assess corticospinal excitability, 25 motor evoked potentials (MEPs) were recorded from the tibialis anterior muscle in each task during walking. Performance for each participant (global success score; % of target hit) and task difficulty related to step length adjustments (success score for each step length) were also calculated. MEP size was larger during the precision task in all participants (mean increase of 93% ± 72%; P < .05) compared to the simple task. There was a correlation between MEP facilitation and individual performance (r = −.64; P < .05), but no difference in MEP size associated with task difficulty (P > .05). In conclusion, corticospinal excitability exhibits a large increase during the precision task. This effect needs to be confirmed in neurological populations to potentially provide a simple and non-invasive approach to increase corticospinal drive during gait rehabilitation.

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

You tell us what helps recovery but give us NOTHING on how to achieve that. Useless.  Predicting failure to recover doesn't help survivors one bit.

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

  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.

 

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Corticospinal Tract Lesion Load Originating From Both Ventral Premotor and Primary Motor Cortices Are Associated With Post-stroke Motor Severity

So what? You described a problem, offered no solution. Useless.

Corticospinal Tract Lesion Load Originating From Both Ventral Premotor and Primary Motor Cortices Are Associated With Post-stroke Motor Severity

 

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Kaori L. Ito, PhD, OTR/L, Bokkyu Kim, PhD, PT, Jingchun Liu, MD, ...

First Published December 24, 2021 Research Article Find in PubMed 

https://doi.org/10.1177/15459683211068441

Article information

Abstract

Lesion load of the corticospinal tract (CST-LL), a measure of overlap between a stroke lesion and the CST, is one of the strongest predictors of motor outcomes following stroke. CST-LL is typically calculated by using a probabilistic map of the CST originating from the primary motor cortex (M1). However, higher order motor areas also have projections that contribute to the CST and motor control. In this retrospective study, we examined whether evaluating CST-LL from additional motor origins is more strongly associated with post-stroke motor severity than using CST-LL originating from M1 only. We found that lesion load to both the ventral premotor (PMv) cortex and M1 were more strongly related to stroke motor severity indexed by Fugl-Meyer Assessment cut-off scores than CST-LL of M1 alone, suggesting that higher order motor regions add clinical relevance to motor impairment.

Keywords

corticospinal tract, stroke, Fugl-Meyer, motor, ventral premotor cortex, M1

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