Functional MRI and ApoE4 genotype for predicting cognitive decline in amyloid-positive individuals

 What are the next steps to prevent this cognitive decline? No next steps, I'd fire all of you. Useless.

Functional MRI and ApoE4 genotype for predicting cognitive decline in amyloid-positive individuals

Jun-Ding Zhu https://orcid.org/0000-0003-0718-4087, Chi-Wei Huang, […], Hsin-I Chang, Shih-Jen Tsai, Shu-Hua Huang, Shih-Wei Hsu, Chen-Chang Lee, Hong-Jie Chen, Chiung-Chih Chang, and Albert C. Yang accyang@nycu.edu.tw, +7 -7View all authors and affiliations

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https://doi.org/10.1177/17562864221138154

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Abstract

Background:

In light of advancements in machine learning techniques, many studies have implemented machine learning approaches combined with data measures to predict and classify Alzheimer’s disease. Studies that predicted cognitive status with longitudinal follow-up of amyloid-positive individuals remain scarce, however.

Objective:

We developed models based on voxel-wise functional connectivity (FC) density mapping and the presence of the ApoE4 genotype to predict whether amyloid-positive individuals would experience cognitive decline after 1 year.

Methods:

We divided 122 participants into cognitive decline and stable cognition groups based on the participants’ change rates in Mini-Mental State Examination scores. In addition, we included 68 participants from Alzheimer’s Disease Neuroimaging Initiative (ADNI) database as an external validation data set. Subsequently, we developed two classification models: the first model included 99 voxels, and the second model included 99 voxels and the ApoE4 genotype as features to train the models by Wide Neural Network algorithm with fivefold cross-validation and to predict the classes in the hold-out test and ADNI data sets.

Results:

The results revealed that both models demonstrated high accuracy in classifying the two groups in the hold-out test data set. The model for FC demonstrated good performance, with a mean F₁-score of 0.86. The model for FC combined with the ApoE4 genotype achieved superior performance, with a mean F₁-score of 0.90. In the ADNI data set, the two models demonstrated stable performances, with mean F₁-scores of 0.77 in the first and second models.

Conclusion:

Our findings suggest that the proposed models exhibited promising accuracy for predicting cognitive status after 1 year in amyloid-positive individuals. Notably, the combination of FC and the ApoE4 genotype increased prediction accuracy. These findings can assist clinicians in predicting changes in cognitive status in individuals with a high risk of Alzheimer’s disease and can assist future studies in developing precise treatment and prevention strategies.

Gait in Cerebral Small Vessel Disease, Pre-Dementia and Dementia: A Systematic Review

With no next steps on what EXACTLY THE FOLLOWUP RESEARCH should be. Useless.  Whenever I came upon a problem in programming, if I didn't have an exact plan to fix it I would have been fired immediately. The same should apply here.

Gait in Cerebral Small Vessel Disease, Pre-Dementia and Dementia: A Systematic Review

Helena M Blumen, Oshadi Jayakody, Joe Verghese

First Published July 7, 2022 Research Article 

https://doi.org/10.1177/17474930221114562

Article information

Abstract

Background: 

The interrelationships between gait, cerebral small vessel disease (CSVD), and cognitive impairments in aging are not well-understood – despite their common co-occurrence.

Objective: 

To systematically review studies of gait impairment in CSVD, pre-dementia, and dementia and to identify key gaps for future research and novel pathways toward intervention.

Methods:  

A PRISMA-guided search strategy was implemented in PubMed to identify relevant studies. Potential articles (n=263) published prior to December 1st, 2021 were screened by two reviewers. Studies with sample sizes >20 and including some adult over >65 years (n=202) were included.

Results: 

The key findings were that 1) adverse gait and cognitive outcomes were associated with several (rather than select) CSVD pathologies distributed across the brain, and 2) poor gait and CSVD pathologies were more strongly associated with dementia with a vascular, rather than an Alzheimer’s disease-related, cause.

Discussion:  

A better understanding of the interrelationships between gait performance in CSVD, pre-dementia and dementia requires studies examining a) comprehensive patterns in the clinical manifestations of CSVD, b) racially/ethnically diverse samples, c) samples followed for extended periods of time or across the adult lifespan, d) non-traditional CSVD neuroimaging markers (e.g., resting-state fMRI), and e) continuous (e.g., wearable sensors) and complex (e.g., dual-task) walking performance.

Keywords

Cerebral Small Vessel Disease, Gait, Cognition, Aging, Cognitive Impairment, Dementia, Gait Abnormalities

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Reclassification and risk stratification of embolic stroke of undetermined source by ASCOD phenotyping

 EXACTLY how is this going to get survivors 100% recovered? After this research what are the next steps to 100% recovery? Don't know or don't have that, then this was fucking useless research. Please explain how your mentors and senior researchers are so clueless about the only goal in stroke; 100% recovery.

Reclassification and risk stratification of embolic stroke of undetermined source by ASCOD phenotyping

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Takao Hoshino, Takafumi Mizuno, Ayako Nishimura, ...

First Published April 14, 2022 Research Article 

https://doi.org/10.1177/17474930221096953

Article information

Abstract

Background:

Vascular diseases underlying stroke, including atherosclerosis, small-vessel disease (SVD), and cardioembolic pathology, can be present in patients with embolic stroke of undetermined source (ESUS), although these are not direct causes of stroke.

Aims:

To describe the frequency and degree of the 3 major diseases using ASCOD phenotyping and to assess their prognostic implications in ESUS.

Methods:

In this prospective observational study, 221 patients with ESUS within 1 week of onset were consecutively enrolled and followed up for 1 year. Vascular diseases associated with stroke were assessed using the ASCOD classification. The primary outcome was a composite of major adverse cardiovascular events (MACEs).

Results:

Among 221 patients, 135 (61.1%), 102 (46.2%), and 107 (48.4%) had any grade of atherosclerosis (A2 or A3), SVD (S3), and cardiac pathology (C2 or C3), respectively. ESUS patients graded as A2 or A3 (i.e., ipsilateral atherosclerotic plaque, contralateral ≥50% stenosis, or aortic arch plaque) were at a significantly higher risk of MACE than those graded as A0 (i.e., no atherosclerotic disease) (adjusted hazard ratio [95% confidence interval], 2.40 [1.01–5.72]). No differences were observed in the event risk between patients with S3 (i.e., magnetic resonance imaging evidence of SVD) and S0 (i.e., no SVD) and between those with C2 or C3 (i.e., presence of any cardiac pathology) and C0 (i.e., no cardiac abnormalities).

Conclusions:

ASCOD grade A2 or A3 was predictive of MACE in ESUS patients. Reclassification of ESUS using ASCOD phenotyping provides important clues for risk prediction and may guide optimal management strategies.

Keywords

ASCOD, Atherosclerosis, Cardioembolism, Embolic stroke of undetermined source, Etiology, Small vessel disease

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Health-Related Quality of Life Among Patients With Acute Ischemic Stroke and Large Vessel Occlusion in the ESCAPE Trial

YOU have a hell of a lot to solve to get these patients 100% recovered. HOW ARE YOU GOING TO DO THAT? Writing this paper is just the beginning.  WHAT THE FUCK ARE YOUR NEXT STEPS?  And the answer is NOT; Let the survivors figure it out. 

Health-Related Quality of Life Among Patients With Acute Ischemic Stroke and Large Vessel Occlusion in the ESCAPE Trial

Raed A. Joundi

,

Alexander D. Rebchuk

,

Thalia S. Field

,

Eric E. Smith

,

Mayank Goyal

,

Andrew M. Demchuk

,

Dar Dowlatshahi

,

Alexandre Y. Poppe

,

David J. Williams

,

Jennifer L. Mandzia

, … See all authors

Originally published11 Mar 2021https://doi.org/10.1161/STROKEAHA.120.033872Stroke. ;0:STROKEAHA.120.033872

Abstract

Background and Purpose:

Endovascular thrombectomy (EVT) reduces(NOT GOOD ENOUGH!) 90-day disability in patients following acute ischemic stroke due to large vessel occlusion. Patient-reported outcome measures after EVT, such as health-related quality of life and specific functional domains, are less well described.

Methods:

We report outcomes on the EuroQol-5D (EQ-5D) from the ESCAPE (Endovascular Treatment for Small Core and Anterior Circulation Proximal Occlusion With Emphasis on Minimizing CT to Recanalization Times) randomized controlled trial at 90 days after stroke. Death was assigned an index value of 0 for EQ-5D. We used quantile regression to evaluate the association between EVT and EQ-5D index scores and logistic regression for the association between EVT and symptom-free status among 90-day survivors for each EQ-5D dimension (self-care, usual activities, mobility, pain/discomfort, and anxiety/depression), assessing for modification by age or sex and adjusting for baseline factors including stroke severity, affected hemisphere, and receipt of alteplase. Lastly, the association between severe disability at 90 days and EQ-5D was evaluated with assessment for modification by EVT, age, and sex.

Results:

There were 165 patients randomized to EVT and 150 patients randomized to control. Median EQ-5D was significantly higher for those who received EVT compared with best medical management (0.80 versus 0.60; P<0.001). After accounting for the greater number of deaths in the elderly, there was evidence of modification of treatment effect by age, with older age associated with a larger effect size difference in EQ-5D with EVT. Those receiving EVT had higher odds of symptom-free status in self-care, usual activities, mobility for those aged 60 to 79 years, and pain/discomfort for women, but there was no association with anxiety/depression. Severe disability at 90 days was associated with lower EQ-5D in older compared with younger individuals, and the association was not modified by EVT.

Conclusions:

Patients treated with EVT report substantially improved(NOT GOOD ENOUGH!) health-related quality of life, with relatively greater impact in older individuals and observed benefit across multiple dimensions.

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Association of Matrix Metalloproteinase 9 and Cellular Fibronectin and Outcome in Acute Ischemic Stroke: A Systematic Review and Meta-Analysis

 With no proposed next steps on what to do with this information, this is completely and totally fucking useless.

Association of Matrix Metalloproteinase 9 and Cellular Fibronectin and Outcome in Acute Ischemic Stroke: A Systematic Review and Meta-Analysis

Lu Wang^1,2†, Linghui Deng^3†, Ruozhen Yuan¹, Junfeng Liu¹, Yuxiao Li¹ and Ming Liu^1*

• ¹Department of Neurology, West China Hospital, Sichuan University, Chengdu, China
• ²Center of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, China
• ³National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University, Chengdu, China

Introduction: The role of matrix metalloproteinase 9 (MMP-9) and cellular fibronectin (c-Fn) in acute ischemic stroke is controversial. We systematically reviewed the literature to investigate the association of circulating MMP-9 and c-Fn levels and MMP-9 rs3918242 polymorphism with the risk of three outcome measures after stroke.

Methods: We searched English and Chinese databases to identify eligible studies. Outcomes included severe brain edema, hemorrhagic transformation, and poor outcome (modified Rankin scale score ≥3). We estimated standardized mean differences (SMDs) and pooled odds ratios (ORs) with 95% confidence intervals (CIs).

Results: Totally, 28 studies involving 7,239 patients were included in the analysis of circulating MMP-9 and c-Fn levels. Meta-analysis indicated higher levels of MMP-9 in patients with severe brain edema (SMD, 0.76; 95% CI, 0.18–1.35; four studies, 419 patients) and hemorrhagic transformation (SMD, 1.00; 95% CI, 0.41–1.59; 11 studies, 1,709 patients) but not poor outcome (SMD, 0.30; 95% CI, −0.12 to 0.72; four studies, 759 patients). Circulating c-Fn levels were also significantly higher in patients with severe brain edema (SMD, 1.55; 95% CI, 1.18–1.93; four studies, 419 patients), hemorrhagic transformation (SMD, 1.75; 95% CI, 0.72–2.78; four studies, 458 patients), and poor outcome (SMD, 0.46; 95% CI, 0.16–0.76; two studies, 210 patients). Meta-analysis of three studies indicated that the MMP-9 rs3918242 polymorphism may be associated with hemorrhagic transformation susceptibility under the dominant model (TT + CT vs. CC: OR, 0.621; 95% CI, 0.424–0.908; P = 0.014). No studies reported the association between MMP-9 rs3918242 polymorphism and brain edema or functional outcome after acute stroke.

Conclusion: Our meta-analysis showed that higher MMP-9 levels were seen in stroke patients with severe brain edema and hemorrhagic transformation but not poor outcome. Circulating c-Fn levels appear to be associated with all three outcomes including severe brain edema, hemorrhagic transformation, and poor functional outcome. The C-to-T transition at the MMP-9 rs3918242 gene appears to reduce the risk of hemorrhagic transformation.

Introduction

Ischemic stroke is one of the most severe neurological disorders and one of the leading causes of disability worldwide (1, 2). The main reasons of deterioration were neurological complications including severe brain edema and hemorrhagic transformation, which may share the common pathophysiological mechanism of blood–brain barrier (BBB) breakdown (3). At present, neuroimaging tests are the main method for diagnosing severe brain edema and hemorrhagic transformation, but these tests are usually performed in the presence of signs of neurological worsening. The neuroimaging tests may delay the effective treatment. Given the limitations of current methods for early detection, new methods are needed to identify these two neurological complications in order to optimize timing of management administration (4).

A change of biomarker levels may precede the appearance of clinical deterioration. Clinical studies have identified that biomarkers of BBB breakdown, such as matrix metalloproteinase 9 (MMP-9) and S100-B, may be associated with clinical deterioration (5–8). Among these biomarkers, MMP-9 has sparked the most interest (9). MMP-9 belongs to a family of zinc-dependent proteolytic enzymes. In animal models, MMP-9 is upregulated in the cerebral ischemic area (10) and degrades the basal lamina around blood vessels in the brain including type IV collagen, fibronectins, and lamina (11–13). As the substrate of MMP-9, fibronectins are located between cell and cell or matrix and consist of cellular fibronectin (c-Fn) and plasma fibronectin (p-Fn). C-Fn is situated nearly exclusively in the endothelium and increases rapidly when vascular damage occurs (14, 15). After stroke onset, high levels of MMP-9 and c-Fn may represent severe damage of the neurovascular unit in injured brain tissue, and when reperfusion begins in the occluded vessels, the disruption of the extracellular matrix may further cause BBB leakage, brain edema, and even hemorrhagic complications in the infarction area (16).

No uniform conclusions have been drawn thus far about associations of circulating MMP-9 levels with the risk of severe brain edema, hemorrhagic transformation, and poor outcome after acute ischemic stroke. Previous systematic reviews suggested a correlation between MMP-9 levels and risk of hemorrhagic transformation (17, 18). While a recent study did not indicate that MMP-9 plasma concentrations were associated with any outcomes including symptomatic intracerebral hemorrhage (sICH), death, and functional outcome (19). Besides, studies focused on c-Fn are very limited, although one study suggested a device that quantified the c-Fn levels was able to stratify patients who developed hemorrhagic transformation (20). In addition, previous studies reported that MMP-9 gene polymorphism, especially the rs3918242 polymorphism (at−1562 locus C/T), regulates expression and thereby influences the levels of circulating MMP-9 (21). Stroke patients with the CT and TT genotypes had significantly higher MMP-9 levels than those with the CC genotypes at the rs3918242 polymorphism (22). MMP-9 rs3918242 polymorphism has already been associated with stroke susceptibility (23–25); however, it is unclear whether or not MMP-9 rs3918242 polymorphism is associated with stroke outcome. Considering these limitations, we aimed to systematically review all the relevant data to investigate (1) whether circulating MMP-9 levels and c-Fn levels might constitute markers of severe brain edema, hemorrhagic transformation, and poor outcome after ischemic stroke; (2) whether variations in the MMP-9 rs3918242 gene were associated with susceptibility to severe brain edema, hemorrhagic transformation, and poor outcome after ischemic stroke.

 

Pathophysiology of Intracranial Aneurysms

With this knowledge, WHAT ARE THE NEXT STEPS TO PREVENT THESE ANEURYSMS FROM BURSTING? No next steps, useless research.

Pathophysiology of Intracranial Aneurysms

COX-2 Expression, Iron Deposition in Aneurysm Wall, and Correlation With Magnetic Resonance Imaging

Jan Rodemerk ,
Andreas Junker ,
Bixia Chen ,
Daniela Pierscianek ,
Philipp Dammann ,
Marvin Darkwah Oppong ,
Alexander Radbruch ,
Michael Forsting ,
Stefan Maderwald , … See all authors

Originally published10 Jul 2020https://doi.org/10.1161/STROKEAHA.120.030590Stroke. ;0

Abstract

Background and Purpose:

The pathophysiology of development, growth, and rupture of intracranial aneurysms (IAs) is only partly understood. Cyclooxygenase 2 (COX-2) converts arachidonic acid to prostaglandin H₂, which, in turn, is isomerized to prostaglandin E₂. In the human body, COX-2 plays an essential role in inflammatory pathways. This explorative study aimed to investigate COX-2 expression in the wall of IAs and its correlation to image features in clinical (1.0T, 1.5T, and 3.0T) magnetic resonance imaging (MRI) and ultra-high-field 7T MRI.

Methods:

The study group comprised 40 patients with partly thrombosed saccular IAs. The cohort included 17 ruptured- and 24 unruptured IAs, which had all been treated microsurgically. Formaldehyde-fixed paraffin-embedded samples were immunohistochemically stained with a monoclonal antibody against COX-2 (Dako, Santa Clara, CA; Clone: CX-294). We correlated Perls Prussian blue staining, MRI, and clinical data with immunohistochemistry, analyzed using the Trainable Weka Segmentation algorithm.

Results:

Aneurysm dome size ranged between 2 and 67 mm. The proportion of COX-2 positive cells ranged between 3.54% to 85.09%. An upregulated COX-2 expression correlated with increasing IA dome size (P=0.047). Furthermore, there was a tendency of higher COX-2 expression in most ruptured IAs (P=0.064). At all field strengths, MRI shows wall hypointensities due to iron deposition correlating with COX-2 expression (P=0.022).

Conclusions:

Iron deposition and COX-2 expression in IAs walls correlate with signal hypointensity in MRI, which might, therefore, serve as a biomarker for IA instability. Furthermore, as COX-2 was also expressed in small unruptured IAs, it could be a potential target for specific medical treatment.

Footnotes

For Sources of Funding and Disclosures, see page xxx.

Correspondence to: Jan Rodemerk, Department of Neurosurgery, University Hospital Essen, Hufelandstraße 55, 45122 Essen, Germany. Email jan.rodemerk@uk-essen.de

Effect of Additional Rehabilitation After Botulinum Toxin-A on Upper Limb Activity in Chronic Stroke

So now we need followup to find out EXACTLY what upper limb interventions are effective. This just launches us to next steps which stroke leadership should be doing.  BUT WE HAVE NO LEADERSHIP, so nothing will occur.

Effect of Additional Rehabilitation After Botulinum Toxin-A on Upper Limb Activity in Chronic Stroke

The InTENSE Trial

Natasha A. Lannin, PhD,^1,10 Louise Ada, PhD,³ Coralie English, PhD,⁵ Julie Ratcliffe, PhD,⁶ Steven G. Faux, MBBS,^8,9 Mithu Palit, MBBS,¹⁰ Senen Gonzalez, MBBS,¹¹ John Olver, MBBS,² Ian Cameron, PhD,⁴ and Maria Crotty, PhD⁷, on behalf of the InTENSE Trial Group^*

Author information Article notes Copyright and License information Disclaimer

This article has been corrected. See Stroke. 2020 February; 51(2): e45.

Go to:

Background and Purpose—

The aim of this trial was to determine the effect of additional upper limb rehabilitation following botulinum toxin-A for upper limb activity in chronic stroke.

Methods—

We conducted a multicenter phase III randomized trial with concealed allocation, blinded measurement, and intention-to-treat analysis. One hundred forty stroke survivors who were scheduled to receive botulinum toxin-A in any muscle(s) that cross the wrist because of moderate to severe spasticity after a stroke >3 months ago, who had completed formal rehabilitation and had no significant cognitive impairment. Experimental group received botulinum toxin-A plus evidence-based movement training while the control group received botulinum toxin-A plus a handout of exercises. Primary outcomes were goal attainment (Goal Attainment Scaling) and upper limb activity (Box and Block Test) at 3 months (end of intervention). Secondary outcomes were spasticity, range of motion, strength, pain, burden of care, and health-related quality of life.

Results—

In terms of goal attainment, the experimental group scored the same (mean difference, 2 T-score [95% CI, −2 to 7]) as the control group on the Goal Attainment Scale. In terms of upper limb activity, by 3 months the experimental group moved blocks at the same speed (mean difference, 0.00 blocks/s [95% CI, −0.02 to 0.01]) as the control group on the Box and Block Test. There were no differences between groups on any secondary outcome except strength, in favor of the experimental group (mean difference, 1.4 kg [95% CI, 0.2–2.7]).

Conclusions—

Findings suggest that additional intensive upper limb rehabilitation following botulinum toxin-A in chronic stroke survivors with a disabled upper limb is not effective.

Registration—

URL: https://www.clinicaltrials.gov. Unique identifier: ACTRN12615000616572.

Early Reperfusion After Brain Ischemia Has Beneficial Effects Beyond Rescuing Neurons

What is the followup needing to be done to translate this to humans? Next steps?
http://stroke.ahajournals.org/content/48/8/2222?etoc=

Masaki Tachibana, Tetsuro Ago, Yoshinobu Wakisaka, Junya Kuroda, Masahiro Shijo, Yoji Yoshikawa, Motohiro Komori, Ataru Nishimura, Noriko Makihara, Kuniyuki Nakamura, Takanari Kitazono

https://doi.org/10.1161/STROKEAHA.117.016689

Stroke. 2017;48:2222-2230

Originally published June 16, 2017

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Abstract

Background and Purpose—Recent studies show that successful endovascular thrombectomy 6 to 12 hours after stroke onset enhances functional outcomes 3 months later. In this study, we investigated the effects of reperfusion after ischemia on repair processes in the ischemic areas, as well as on functional recovery, using mouse stroke models.

Methods—We examined time-dependent histological changes and functional recovery after transient middle cerebral artery occlusion of different durations, including permanent middle cerebral artery occlusion, using the CB-17 (CB-17/lcr-+/+Jcl) mouse strain, which has poor pial collateral blood flow.

Results—Large microtubule-associated protein 2-negative areas of neuronal death were produced in mice subjected to ≥60 minutes of ischemia followed by reperfusion on day 1, while restricted microtubule-associated protein 2-negative regions were observed in mice subjected to a 45-minute period of ischemia. A substantial reduction in microtubule-associated protein 2-negative areas was observed on day 7 in mice given early reperfusion and was associated with better functional recovery. Klüver–Barrera staining demonstrated that white matter injury on day 1 was significantly lesser in mice with reperfusion. Immunohistochemistry and electron microscopy revealed that a greater number of endothelial cells were present in the infarct areas in mice with earlier reperfusion and were associated with a more rapid recruitment of platelet-derived growth factor receptor β-positive pericytes and subsequent intrainfarct fibrosis. Early reperfusion also resulted in a greater accumulation of glial fibrillary acidic protein–positive astrocytes in peri-infarct areas. Peri-infarct astrogliosis was attenuated in platelet-derived growth factor receptor β heterozygous knockout mice.

Conclusions—Early reperfusion after ischemia enhances the survival of endothelial cells and pericytes within ischemic areas even after the infarct is established, resulting in efficient intrainfarct fibrosis and peri-infarct astrogliosis. These effects might be associated with efficient peri-infarct reorganization and functional recovery.

Skilled Reach Performance Correlates With Corpus Callosum Structural Integrity in Individuals With Mild Motor Impairment After Stroke: A Preliminary Investigation

I bet my inability to do any kind of reaching is due to spasticity. This research was useless in helping survivors get better, more followup needed. Next steps is missing, how would you go about solving the problem you describe?
http://journals.sagepub.com/doi/abs/10.1177/1545968317712467

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Jill Campbell Stewart, PhD, Michael O’Donnell, BS, Kaci Handlery, DPT, ...

First Published June 6, 2017 Research Article

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Abstract

Background. Recovery of arm function after stroke is often incomplete. An improved understanding of brain structure–motor behavior relationships is needed for the development of novel and targeted rehabilitation interventions. Objective. To examine the relationship between skilled reach performance and the integrity of two putative white matter motor pathways, corticospinal tract and corpus callosum, after stroke. Methods. Eleven individuals with chronic stroke (poststroke duration, mean 62.5 ± 42.4 months) and mild motor impairment (upper extremity Fugl-Meyer score, mean 54.2 ± 7.6) reached to six targets presented at three distances and two directions. Fractional anisotropy (FA) obtained from diffusion tensor imaging was used to determine the structural integrity of the corticospinal tract and the corpus callosum. Results. Overall reach performance was decreased in the paretic arm compared with the nonparetic arm. While FA was decreased in the ipsilesional corticospinal tract, FA in the corticospinal tract did not correlate with variability in reach performance between individuals. Instead, FA in the premotor section of the corpus callosum correlated with reach performance; individuals with higher FA in premotor corpus callosum tended to reach faster with both the paretic and nonparetic arms. Conclusions. The structural connections between the two premotor and supplemental cortices that traverse the premotor corpus callosum may play an important role in supporting motor control and could become a target for interventions aimed at improved arm function in this population.

Abnormal EEG Responses to TMS During the Cortical Silent Period Are Associated With Hand Function in Chronic Stroke

There should always be a next steps section to propose what still needs to be done to make an intervention that actually gets survivors to 100% recovery. But since we have NO stroke leadership and NO stroke strategy this will never occur. Survivors will be screwed forever until we get that. 
http://journals.sagepub.com/doi/abs/10.1177/1545968317712470

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Whitney A. Gray, Jacqueline A. Palmer, PhD, Steven L. Wolf, PhD, ...

First Published June 12, 2017 Research Article

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Abstract

Background. Abnormal brain excitability influences recovery after stroke at which time a prolonged transcranial magnetic stimulation (TMS)–induced electromyographic silent period is thought to reflect abnormal inhibitory interneuron excitability. Cortical excitability can be probed directly during the silent period using concurrent electroencephalography (EEG) of TMS-evoked responses. Objective. The primary study objectives were to characterize TMS-evoked cortical potentials (TEPs) using EEG and to investigate associations with persistent hand and arm motor dysfunction in individuals with chronic stroke.  
Methods. Thirteen participants with chronic stroke-related mild-moderate arm motor impairment and 12 matched controls completed a single TMS-EEG cortical excitability assessment. TEPs recorded from the vertex during cortical silent period (CSP) assessment and while at rest were used to evaluate differences in cortical excitability between stroke and control participants. Associations between TEPs and CSP duration with measures of upper extremity motor behavior were investigated. Results. Significantly increased TEP component peak amplitudes and delayed latencies were observed for stroke participants compared with controls during CSP assessment and while at rest. Delayed early TEP component (P30) peak latencies during CSP assessment were associated with less manual dexterity. CSP duration was prolonged in stroke participants, and correlated with P30 peak latency and paretic arm dysfunction.  
Conclusions. Abnormal cortical excitability directly measured by early TMS-evoked EEG responses during CSP assessment suggests abnormal cortical inhibition is associated with hand dysfunction in chronic stroke. Further investigation of abnormal cortical inhibition in specific brain networks is necessary to characterize the salient neurophysiologic mechanisms contributing to persistent motor dysfunction after stroke.