Motor Cortex Activation During Treatment May Predict Therapeutic Gains in Paretic Hand Function After Stroke

 WHAT EXACT PROTOCOL WILL GUANANTEE THESE THERAPEUTIC GAINS?  If you can't provide that your research is mostly useless! The whole fucking point of stroke research is to get survivors recovered. This DOESN'T DO THAT! Look at all these supposedly smart Ph.D's that don't understand that.

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? What is your reason for doing stroke research? Getting published is not the correct answer.

Motor Cortex Activation During Treatment May Predict Therapeutic Gains in Paretic Hand Function After Stroke

Yun Dong, MD, PhD; Bruce H. Dobkin, MD; Steven Y. Cen, PhD; Allan D. Wu, MD; Carolee J. Winstein, PhD 

Background and Purpose—

Functional brain imaging after stroke offers insight into motor network adaptations. This exploratory study examined whether motor cortical activation captured during arm-focused therapy can predict paretic hand functional gains. 

Methods—

Eight hemiparetic patients had serial functional MRI (fMRI) while performing a pinch task before, midway, and after 2 weeks of constraint-induced therapy. The Wolf Motor Function Test (WMFT) was performed before and after intervention. 

Results—

There was a linear reduction in ipsilateral (contralesional) primary motor (M1) activation (voxel counts) across time. The midpoint M1 Laterality Index anticipated post-therapeutic change in time to perform the WMFT. The change in ipsilateral M1 voxel count (pre- to mid-) correlated with the change in mean WMFT time (pre- to post-). 

Conclusions—

The relationship between brain activation during treatment and functional gains suggests a use for serial fMRI in predicting the success and optimal duration for a focused therapeutic intervention. (Stroke. 2006;37:1552- 1555.) Key Words: magnetic resonance imaging  rehabilitation Functional MRI (fMRI) has revealed reorganization in the primary and secondary motor cortices during poststroke recovery and after therapeutic interventions. 

1 Few studies have explored the evolution of brain activation in relation to behavioral gains in a “one-to-one” correspondence during a specific rehabilitation intervention. 2 This exploratory study examined whether the brain activation midway through a 2-week arm-focused intervention might capture adaptations induced by the initial week of training and, in turn, could be used to anticipate post-therapeutic behavioral changes in paretic hand function. If so, this brain– behavior correspondence may offer guidance to determine an optimal duration for task-specific therapy. 2 Subjects and Methods Eight patients with hemiparetic stroke (Fugl-Meyer [FM] motor score 33 to 62) participated. Inclusion criteria were 3 months after stroke, ability to perform the fMRI task, and a minimum of 10° of voluntary wrist and finger extension.(Well, that excludes a huge portion of survivors that have spasticity, so massive cherry picking) Lesions varied in location, but all spared the hand motor representation (M1). No alternative therapy group was studied. Seven healthy volunteers were scanned twice to test the reproducibility of fMRI activation. Physical Therapy and Functional Measure All patients received constraint-induced therapy for 2 weeks as defined for the EXCITE trial. 3 The Wolf Motor Function Test (WMFT) 4 was performed before and after intervention. The behavioral outcome measure consisted of 6 dexterity items from the full 15-item WMFT (Lift Can; Lift Pencil; Lift Paper Clip; Stack Checkers; Flip Cards; Turn Key in Lock) that most directly captured fine motor control(If you can do most of these, you're a high-functioning survivor, thus more cherry picking). The change in mean WMFT (mWMFT) time for the 6-item subset was correlated with that for the 15-item test (r=0.98), indicating reliability and validity for the subset. The pre-mWFT–post-mWFMT (absolute time) difference was used as a proxy for functional change in motor skill. fMRI Acquisition fMRI acquisition parameters were described previously. 5 fMRI sessions were performed before intervention, midintervention, and after intervention, each with 4 30-s bouts of repetitive pinch alternating with 5 30-s rest periods. The pinch apparatus included a vertical plastic tube connected to a pressure transducer. The task required tube compression with the index and middle fingers against the thumb, creating enough pressure to match 50% of maximum, viewed through goggles as a target line, and paced by auditory cues at 75% maximum rate. These parameters were maintained constant across the 3 sessions. Practice before each fMRI session minimized unwanted movements and deviations from consistent task performance. Data Analysis fMRI data were analyzed as described previously. 5,6 Volumes related to head motion (2 mm), and associated movements (visually identified from videotape) were excluded. Z statistic images were thresholded at Z3.1, and significant clusters were defined at P0.01 (corrected for multiple comparisons). Regions of interest (ROIs) were set in bilateral M1 and dorsal premotor (PMd) areas. Percentage signal change (% SC) and voxel counts (VCs) within each ROI were measured and a Laterality Index [LI=(contra- lateral-ipsilateral)/(contralateral+ipsilateral)] (contralateral and ip- silateral activation to the hand movement. LI ranges from -1 [all ipsilateral activation] to 1 [all contralateral activation]) was calculated using VC for each ROI. Linear Mixed Model was used for intersession comparisons of fMRI variables (% SC, VC), pinch pressure, and rate, separately. Individual linear regression analyses were performed between LI, VC (M1 and PMd; independent variable) pre-, mid-, and post- and the post-pre–mWMFT time difference (dependent variable). Pearson correlation coefficient anal- ysis was used to assess the relationship between changes in fMRI measures and changes in mWMFT time. Preintervention fMRI from patients 5 and 6 was technically unusable. Results Prefunctional to postfunctional gains (mWMFT) varied across patients, but the group 6-item time decreased for the paretic hand after therapy (P=0.03; Table). No differences were detected in pinch pressure or rate across sessions (P0.1). Intersession comparisons of M1 activation in healthy volunteers showed no differences (Table). Group analysis for the paretic hand showed a continuous reduction of VC in ipsilateral M1 (P=0.02; P=0.006 linear trend) across time (Table). No differences in M1 activation across time were found for the less-affected hand (P0.1; data not shown). We observed 4 patterns of LI evolution for M1, including a progressive increase (patients 3, 4, and 7; Figure 1A), a midpoint-only increase (patient 8), a midpoint decrease (patient 1; Figure 1B), and nearly no change (patient 2). Among the 3 showing “progressive increase,” patients 3 and 4 (FM score 53 and 54, respectively) had either an increase in contralateral or a decease in ipsilateral M1 activation across time, whereas patient 7 (FM score 45) demonstrated a continuous reduction in bilateral M1 activation but more so ipsilaterally. The “midpoint decrease” in patient 1 (FM score 62), who was well recovered and showed the least functional improvement, was attributed to a pre- to mid- reduction in contralateral M1 activation. The “midpoint-only increase” in patient 8 (FM score 34), who showed the most functional improvement, resulted from a pre- to mid- decrease in ipsilateral M1 activation. There was no correlation between post-pre change in mWMFT time and change in activation (VC or % SC) in M1 or PMd (ipsilateral or contralateral), except for that between post-pre change in mWMFT time and pre- to- mid- change in ipsilateral M1 activation (VC; r=0.82; P=0.05). The mid-point and postintervention LI for M1 and midpoint ipsilateral M1 VC, but not that for PMd, did predict the post-pre mWMFT time change (6-item; Figure 2).

More at link with figures.

Motor Cortex Activation During Treatment May Predict Therapeutic Gains in Paretic Hand Function After Stroke

 It is vastly more important to DELIVER HAND FUNCTION than predict it! When the hell will stroke leadership get a strategy going to DELIVER 100% RECOVERY? I'm guessing never since survivors are not in charge.

Yeah, Bruce Dobkin is a superstar stroke researcher but I think even he is not actually solving stroke to get survivors recovered.  Hope he has 100% stroke recovery solved before he becomes the 1 in 4 per WHO that has a stroke!

Dr. Bruce H. Dobkin (15 posts to December 2011)

Motor Cortex Activation During Treatment May Predict Therapeutic Gains in Paretic Hand Function After Stroke

Yun Dong, MD, PhD, Bruce H. Dobkin, MD, Steven Y. Cen, PhD, Allan D. Wu, MD, and Carolee J. Winstein, PhDAuthor Info & Affiliations

Stroke

Volume 37, Number 6

https://doi.org/10.1161/01.STR.0000221281.69373.4e

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Abstract

Background and Purpose— Functional brain imaging after stroke offers insight into motor network adaptations. This exploratory study examined whether motor cortical activation captured during arm-focused therapy can predict paretic hand functional gains.

Methods— Eight hemiparetic patients had serial functional MRI (fMRI) while performing a pinch task before, midway, and after 2 weeks of constraint-induced therapy. The Wolf Motor Function Test (WMFT) was performed before and after intervention.

Results— There was a linear reduction in ipsilateral (contralesional) primary motor (M1) activation (voxel counts) across time. The midpoint M1 Laterality Index anticipated post-therapeutic change in time to perform the WMFT. The change in ipsilateral M1 voxel count (pre- to mid-) correlated with the change in mean WMFT time (pre- to post-).

Conclusions— The relationship between brain activation during treatment and functional gains suggests a use for serial fMRI in predicting the success and optimal duration for a focused therapeutic intervention.

Functional MRI (fMRI) has revealed reorganization in the primary and secondary motor cortices during poststroke recovery and after therapeutic interventions.¹ Few studies have explored the evolution of brain activation in relation to behavioral gains in a “one-to-one” correspondence during a specific rehabilitation intervention.² This exploratory study examined whether the brain activation midway through a 2-week arm-focused intervention might capture adaptations induced by the initial week of training and, in turn, could be used to anticipate post-therapeutic behavioral changes in paretic hand function. If so, this brain–behavior correspondence may offer guidance to determine an optimal duration for task-specific therapy.²

Subjects and Methods

Eight patients with hemiparetic stroke (Fugl-Meyer [FM] motor score 33 to 62) participated. Inclusion criteria were >3 months after stroke, ability to perform the fMRI task, and a minimum of 10° of voluntary wrist and finger extension. Lesions varied in location, but all spared the hand motor representation (M1). No alternative therapy group was studied. Seven healthy volunteers were scanned twice to test the reproducibility of fMRI activation.

Physical Therapy and Functional Measure

All patients received constraint-induced therapy for 2 weeks as defined for the EXCITE trial.³ The Wolf Motor Function Test (WMFT)⁴ was performed before and after intervention. The behavioral outcome measure consisted of 6 dexterity items from the full 15-item WMFT (Lift Can; Lift Pencil; Lift Paper Clip; Stack Checkers; Flip Cards; Turn Key in Lock) that most directly captured fine motor control. The change in mean WMFT (mWMFT) time for the 6-item subset was correlated with that for the 15-item test (r=0.98), indicating reliability and validity for the subset. The pre-mWFT–post-mWFMT (absolute time) difference was used as a proxy for functional change in motor skill.

fMRI Acquisition

fMRI acquisition parameters were described previously.⁵ fMRI sessions were performed before intervention, midintervention, and after intervention, each with 4 30-s bouts of repetitive pinch alternating with 5 30-s rest periods. The pinch apparatus included a vertical plastic tube connected to a pressure transducer. The task required tube compression with the index and middle fingers against the thumb, creating enough pressure to match 50% of maximum, viewed through goggles as a target line, and paced by auditory cues at 75% maximum rate. These parameters were maintained constant across the 3 sessions. Practice before each fMRI session minimized unwanted movements and deviations from consistent task performance.

Data Analysis

fMRI data were analyzed as described previously.^5,6 Volumes related to head motion (>2 mm), and associated movements (visually identified from videotape) were excluded. Z statistic images were thresholded at Z>3.1, and significant clusters were defined atP<0.01 (corrected for multiple comparisons). Regions of interest (ROIs) were set in bilateral M1 and dorsal premotor (PMd) areas. Percentage signal change (% SC) and voxel counts (VCs) within each ROI were measured and a Laterality Index [LI=(contralateral−ipsilateral)/(contralateral+ipsilateral)] (contralateral and ipsilateral activation to the hand movement. LI ranges from −1 [all ipsilateral activation] to 1 [all contralateral activation]) was calculated using VC for each ROI. Linear Mixed Model was used for intersession comparisons of fMRI variables (% SC, VC), pinch pressure, and rate, separately. Individual linear regression analyses were performed between LI, VC (M1 and PMd; independent variable) pre-, mid-, and post- and the post-pre–mWMFT time difference (dependent variable). Pearson correlation coefficient analysis was used to assess the relationship between changes in fMRI measures and changes in mWMFT time. Preintervention fMRI from patients 5 and 6 was technically unusable.

More at link.

Does Spasticity Itself Raise the Cost of Stroke Care 4-Fold?

Well shit, spasticity does not need to be solved per the infuriating opinion of Dr. William M. Landau!

Spasticity After Stroke: Why Bother? Aug. 2004)

Yeah, Bruce Dobkin is a superstar stroke researcher but I think this letter is nit-picking.

Dr. Bruce H. Dobkin (15 posts to December 2011)

Quit discussing spasticity AND JUST FUCKING CURE IT!

Does Spasticity Itself Raise the Cost of Stroke Care 4-Fold?

Bruce H. Dobkin, MDAuthor Info & Affiliations

Stroke

Volume 41, Number 7

https://doi.org/10.1161/STROKEAHA.110.581561

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To the Editor:

The report from Lundstrom et al¹ headlines a relationship between spasticity and higher direct costs of stroke care over the first year after onset. The authors seem to be putting the cart’s contents, 1 of which is spasticity, before the horse of sensorimotor impairment. The authors used a modified Ashworth Score of ≥1 in any 1 of 7 arm and leg joints as the measure of spasticity. The modified Ashworth Score is a 6-point ordinal scale of resistance to passive movement across a joint, which can arise from reflexive clasp-knife resistance and from changes in connective tissues of the joint associated with severity of paresis, nonuse, and contracture. It is often used in studies, but its validity and reliability may be less than necessary to reflect a physiologically meaningful measure.² Clinicians involved in the care of patients with chronic stroke would not consider a modified Ashworth Score in any 1 joint of <3 to suggest a clinically important problem. No evidence exists that the modified Ashworth Score cutoff used for this study’s retrospective, database-driven findings could be detrimental after stroke. So what underlies the relationship described?

The authors found a significantly higher National Institutes of Health Stroke Scale score in the group considered to have any degree of spasticity. It would seem, then, that they would want to examine for a correlation between cost of care and level of impairment based on the National Institutes of Health Stroke Scale. They did show that poorer modified Rankin Scale scores (which intermix aspects of impairment and disability) were significantly related to higher costs. If indeed, greater resistance to passive movement across a singe joint has a relationship to cost, the primary relationship is probably to the degree of sensorimotor impairment that induces greater disability and, in turn, higher in-hospital costs from complications of greater impairment such as immobility.

The discussion from the authors seems to repudiate the primacy of their correlation. If “our study does not provide evidence that spasticity as such is responsible for the (4-fold) increase of costs” and “spasticity reflects a more severe motor disorder,” how can the authors suggest that their data offer, at best, a baseline for “the cost-effectiveness of interventions, including botulinum toxin” … ? This particular intervention is likely to drive up costs if injected into patients with a modified Ashworth Score <3 but will not alter sensorimotor impairments. From a healthcare priority point of view, their findings suggest the need for more outpatient physiotherapy, which was provided to only 4% of their subjects. A rehabilitation intervention to maintain range of motion, prevent painful contractures and dystonic postures, and to improve motor control and skills might reduce disability, costs, and burden of care for those who are most impaired by paresis.

References

1.

Lundstrom E, Smits A, Borg J, Terent A. Four-fold increase in direct costs of stroke survivors with spasticity compared with stroke survivors without spasticity: the first year after the event. Stroke. 2010; 41: 319–324.

Neurobiology of Rehabilitation - BRUCE H. DOBKIN, MD

While an excellent writeup on stroke. NOTHING WILL COME OF IT, we have NO stroke leadership and NO stroke strategy.

Neurobiology of Rehabilitation - BRUCE H. DOBKIN, MD

Department of Neurology, Director, Neurologic Rehabilitation and Research Program, Geffen School of Medicine, University of California Los Angeles,  Reed Neurologic Research Center, Los Angeles, California 90095-1769, USA

ABSTRACT

:Rehabilitation aims to lessen the physical and cognitive impairments and disabilities of patients with stroke, multiple sclerosis, spinal cord or brain injury, and other neurologic diseases. Conventional approaches beyond compensatory adjustments to disability may be augmented by applying some of the myriad experimental results about mechanisms of intrinsic biological changes after injury and the effects of extrinsic manipulations on spared neuronal assemblies. The organization and inherent adaptability of the anatomical nodes within distributed pathways of the central nervous system offer a flexible substrate for treatment strategies that drive activity-dependent plasticity. Opportunities for a new generation of approaches are manifested by rodent and non-human primate studies that reveal morphologic and physiologic adaptations induced by injury,by learning-associated practice, by the effects of pharmacologic neuromodulators, by the behavioral and molecular bases for enhancing activity-dependent synaptic plasticity, and by cell replacement, gene therapy, and regenerative biologic strategies. Techniques such as functional magnetic resonance imaging and transcranial magnetic stimulation will help deter-mine the most optimal physiologic effects of interventions in patients as the cortical representations for skilled movements and cognitive processes are modified by the combination of conventional and biologic therapies. As clinicians digest the finer details of the neurobiology of rehabilitation, they will translate laboratory data into controlled clinical trials. By determining how much they can influence neural reorganization, clinicians will ex-tend the opportunities for neurorestoration.

15 more pages at link.

Evolution of FMRI activation in the perilesional primary motor cortex and cerebellum with rehabilitation training-related motor gains after stroke: a pilot study

 But with no specific protocols listed and no objective damage starting point this is still almost completely useless

Evolution of FMRI activation in the perilesional primary motor cortex and cerebellum with rehabilitation training-related motor gains after stroke: a pilot study

 Yun Dong,MD,PhD,Carolee J.Winstein,PhD,Richard Albistegui-DuBois,PhD,and Bruce H.Dobkin,MD
Background
Previous studies report that motor recovery after partial destruction of the primary motor cortex (M1) may be(weasel words are useless to survivors.) associated with adaptive functional reorganization within spared M1.
Objective
To test feasible methodologies for evaluating relationships between behavioral gains facilitated by rehabilitative training and functional adaptations in perilesional M1 and the cerebellum.
Methods
Four patients with hemiparesis for more than 3 months after a cortical lesion partially within M1 and 12 healthy volunteers participated.Functional magnetic resonance imaging (fMRI) using a finger-tapping task and concurrent behavioral assessments, including the Fugl-Meyer Motor Assessment of the upper extremity and the Wolf Motor Function Test,were conducted before and after 2 weeks of arm focused training;2 patients were further examined 6 and 12 months later to evaluate long-term persistence of brain behavior adaptations.
Results
All patients showed higher activation magnitude in perilesional M1 than healthy controls before and after therapy.Further long-term functional gains paralleled the decrease of activation magnitude in perilesional M1 in the 2 more impaired cases.
Conclusion  

The evolution of suggestive correlations between serial scans of fMRI adaptive activity within the primary motor cortex and the cerebellum in relation to relevant behavioral changes over the course of 2 weeks of task specific therapy and then no formal therapy suggests that repeated assessments may be best for monitoring therapy induced neuroplasticity.This approach may help develop optimal rehabilitation strategies to maximize post stroke motor recovery as well as improve the search for brain behavior correlations in functional neuroimaging research.

Key Words:
Stroke rehabilitation—fMRI—Wol fMotor Function Test—Primary motor cortex—Constraint-induced movement therapy—Adaptive reorganization.
Post stroke recovery of motor function with and without specific rehabilitation training has been attributed in part to adaptive functional reorganization within the central nervous system.^1,2The under-lying neurophysiological mechanisms may include changes in neuronal membrane excitability,synaptic strengthening, synaptogenesis, dendritic arborization,fiber sprouting from surviving neurons,and recruitment of nearby and remote neuronal ensembles after focal brain injury.^3,4Functional reorganization within the intact area surrounding an infarct restricted to the primary motor cortex (M1) was observed over the temporal course of recovery from stroke using functional magnetic resonance imaging (fMRI). The studies supported the notion that human M1 is capable of functional adaptation comparable to that seen in primate experiments.^5,6Growing evidence from both animal and human studies suggests the importance of perilesional adaptive reorganization and the potential modulative effects of focused,intensive rehabilitative training in facilitating this use-dependent reorganization.^7,8With the use of advanced neuroimaging technologies,rehabilitation therapy-induced adaptive reorganization within putative motor networks has been investigated in chronic stroke patients who received constraint induced movement therapy (CIMT).^9-12The correlates between motor functional gains and changes in physiological signals have differed across studies,however.To best elucidate the mechanisms mediating cerebral adaptations after stroke,studies must account for inter subject variability in initial impairment level(Yeah, like an objective damage diagnosis?),lesion location and size,trajectory of behavioral gains associated with time and motor learning experience,and dose of rehabilitation therapy.¹³ between intensive training-related motor functional improvement and adaptive reorganization in perilesionalM1 in patients with partial M1 damage.We performed consecutive fMRI scans with concurrent behavioral assessments in 4 patients who had a single stroke involving a portion ofM1 before,immediately after 2 weeks of CIMT,and,in 2 willing subjects,6 and 12 months later.The aims of the study were 2-fold:1) to test the hypothesis that rehabilitative training-related behavioral gains are associated with specific functional adaptations within the intact perilesional M1 and the remotely connected cerebellum and 2) to test methods for evaluating direct brain-behavior correlates and generate preliminary data for larger scale studies.

The Clinical Science of Neurologic Rehabilitation

You can read the 500+ pages yourself, I'm certainly not going to, it would be a waste of time, NO PROTOCOLS will be discussed.  

And Dr. Dobkin is relatively famous in stroke circles.

• Dr. Bruce H. Dobkin (12)

The Clinical Science of Neurologic Rehabilitation

June 1989 Focused Stroke Rehabilitation Programs Do Not Improve Outcome

When this first came out in 1989 did your hospital do ANYTHING AT ALL  to address the problem? Or is your hospital relying on spontaneous recovery, pointing to those gains and attributing them to their rehab programs?

Focused Stroke Rehabilitation Programs Do Not Improve Outcome

A Rehabilitation-Internet-of-Things in the Home to Augment Motor Skills and Exercise Training

Even Dr. Dobkin doesn't point to any protocols for stroke rehab.
http://journals.sagepub.com/doi/abs/10.1177/1545968316680490

Bruce H. Dobkin, MD

First Published March 1, 2017 research-article

Abstract

Although motor learning theory has led to evidence-based practices, few trials have revealed the superiority of one theory-based therapy over another after stroke. Nor have improvements in skills been as clinically robust as one might hope. We review some possible explanations, then potential technology-enabled solutions. Over the Internet, the type, quantity, and quality of practice and exercise in the home and community can be monitored remotely and feedback provided to optimize training frequency, intensity, and progression at home. A theory-driven foundation of synergistic interventions for walking, reaching and grasping, strengthening, and fitness could be provided by a bundle of home-based Rehabilitation Internet-of-Things (RIoT) devices. A RIoT might include wearable, activity-recognition sensors and instrumented rehabilitation devices with radio transmission to a smartphone or tablet to continuously measure repetitions, speed, accuracy, forces, and temporal spatial features of movement. Using telerehabilitation resources, a therapist would interpret the data and provide behavioral training for self-management via goal setting and instruction to increase compliance and long-term carryover. On top of this user-friendly, safe, and conceptually sound foundation to support more opportunity for practice, experimental interventions could be tested or additions and replacements made, perhaps drawing from virtual reality and gaming programs or robots. RIoT devices continuously measure the actual amount of quality practice; improvements and plateaus over time in strength, fitness, and skills; and activity and participation in home and community settings. Investigators may gain more control over some of the confounders of their trials and patients will have access to inexpensive therapies.

The Specific Requirements of Neural Repair Trials for Stroke

The relatively famous Dr. Bruce Dobkin and Dr. Carmichael entering into the need for better stroke interventions. Now if we had a stroke leader that would put this all together into a strategy. But this will again fall through the cracks and nothing will get done. You are once again fucking screwed.
9 posts on Dobkin. 5 posts on Carmichael.

http://nnr.sagepub.com/content/30/5/470?etoc

1. Bruce H. Dobkin, MD1
2. S. Thomas Carmichael, MD, PhD1⇑

1. ¹David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

1. S. Thomas Carmichael, MD, PhD, Department of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA 90095-1769, USA. Email: scarmichael@mednet.ucla.edu

Abstract

Novel molecular, cellular, and pharmacological therapies to stimulate repair of sensorimotor circuits after stroke are entering clinical trials. Compared with acute neuroprotection and thrombolysis studies, clinical trials for repair in subacute and chronic hemiplegic participants have a different time course for delivery of an intervention, different mechanisms of action within the milieu of the injury, distinct relationships to the amount of physical activity and skills practice of participants, and need to include more refined outcome measures. This review examines the biological interaction of targeted rehabilitation with neural repair strategies to optimize outcomes. We suggest practical guidelines for the incorporation of inexpensive skills training and exercise at home. In addition, we describe some novel outcome measurement tools, including wearable sensors, to obtain the more detailed outcomes that may identify at least some minimal level of success from cellular and regeneration interventions. Thus, proceeding in the shadow of acute stroke trial designs may unnecessarily limit the mechanisms of action of new repair strategies, reduce their impact on participants, and risk missing important behavioral outcomes.

Cancer Research UK invests £15 million to unite finest minds across UK to develop better treatments

The key point here is uniting the finest minds. In stroke nobody seems to want to attempt that. The WSO had their World Stroke Organization Synergium in 2010 and you can see why in my opinion it is totally worthless. You as a stroke survivor are totally screwed until the complete stroke leadership is deposed and removed from any part of this.
My list of finest minds:
Dr. Steven Wolf;
Peter Levine; 
Dr. S. Thomas Carmichael;
Dr. Bruce H. Dobkin;
Dr. Dale Corbett;
Dr. Michael Tymianski, of the Toronto Western Hospital Research Institute in Canada;
Dr. Michael A. Moskowitz ;
Dr. Watson, IBM computer;
Dr. Google;
myself;
Dr. Amy Shissler;
Barb Polan;
Jo Murphy;  
Rebecca Dutton; 
My list of those that should NOT be invited:
Dr. William M. Landau - his ideas on spasticity are appalling;
Matt Lopez, president of the NSA;
Dr. Mariel Jessup, president of the ASA;
WSO President - Steve Davis (Australia); 
Immediate Past-president WSO - Bo Norrving (Sweden)

http://www.alphagalileo.org/ViewItem.aspx?ItemId=157007&CultureCode=en

Feedback about walking activity does not increase walking activity levels during inpatient rehabilitation after stroke

I know Dobkin is famous in stroke circles but I don't see how this conclusion could come about.
This one makes it sound like feedback works:

Effects of a novel walking training program with postural correction and visual feedback on walking function in patients with post-stroke hemiparesis 

As compared to this latest one. Ask your doctor which way s/he swings.

Feedback about walking activity does not increase walking activity levels during inpatient rehabilitation after stroke 

• Abstract
• Full Text

Summary of: Dorsch AK, Thomas S, Xu X, Kaiser W, Dobkin BH, on behalf of the SIRRACT investigators. SIRRACT: An international randomized clinical trial of activity feedback during inpatient stroke rehabilitation enabled by wireless sensing. Neurorehabil Neur Rep. 2015;29:407-415.

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The Specific Requirements of Neural Repair Trials for Stroke

I hope they finally get to objective measurements.
http://nnr.sagepub.com/content/early/2015/09/08/1545968315604400.abstract?

1. Bruce H. Dobkin, MD1
2. S. Thomas Carmichael, MD, PhD1

1. ¹David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

1. S. Thomas Carmichael, Department of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA 90095-1769, USA. Email: scarmichael@mednet.ucla.edu

Abstract

Novel molecular, cellular, and pharmacological therapies to stimulate repair of sensorimotor circuits after stroke are entering clinical trials. Compared with acute neuroprotection and thrombolysis studies, clinical trials for repair in subacute and chronic hemiplegic participants have a different time course for delivery of an intervention, different mechanisms of action within the milieu of the injury, distinct relationships to the amount of physical activity and skills practice of participants, and need to include more refined outcome measures. This review examines the biological interaction of targeted rehabilitation with neural repair strategies to optimize outcomes. We suggest practical guidelines for the incorporation of inexpensive skills training and exercise at home. In addition, we describe some novel outcome measurement tools, including wearable sensors, to obtain the more detailed outcomes that may identify at least some minimal level of success from cellular and regeneration interventions. Thus, proceeding in the shadow of acute stroke trial designs may unnecessarily limit the mechanisms of action of new repair strategies, reduce their impact on participants, and risk missing important behavioral outcomes.

Walking Quality During Inpatient Stroke Rehabilitation Assessed by Wireless Sensing

With this your PT could objectively determine your specific walking problems and use specific muscle stroke protocols to correct those problems. Instead of the crappy 'Walk this way' demonstration that I got. That was totally useless. And it has the fairly famous Bruce Dobkin.
http://www.neurology.org/content/84/14_Supplement/P5.176.short

1. Andrew Dorsch₂,
2. Seth Thomas₁ and
3. Bruce Dobkin₃

+Show Affiliations

1. Neurology April 6, 2015 vol. 84 no. 14 Supplement P5.176

• Abstract

Abstract

OBJECTIVE: Demonstrate that the quality of gait, in addition to walking speed and distance, can be derived from inertial sensors worn at both ankles.  (better yet would be at the knees, toes and hips)

BACKGROUND: The international Stroke Inpatient Rehabilitation Reinforcement of ACTivity (SIRRACT) trial deployed wireless sensors and activity-recognition algorithms to monitor and provide feedback about the quantity of stroke patients’ daily walking activity (epub, Neurorehabil Neural Repair, 2014). This follow-up study aimed to characterize the quality of walking by calculating spatiotemporal gait metrics. 

DESIGN/METHODS: In SIRRACT, 135 trial participants wore sensors throughout the average 3-week inpatient rehabilitation admission. Stopwatch-timed 10-meter walks (performed weekly for system calibration) were selected for the current analysis. Individual steps were delimited by identifying heel strike and toe-off times. Metrics including gait cycle duration, symmetry of stance and swing times, and double-limb support time were calculated for both the paretic and non-paretic limbs. The magnitude of peak lower leg acceleration during the swing phase of gait was also calculated. 

RESULTS: Data from five trial participants are presented as exemplars. Walking speeds averaged 0.24 ± 0.14m/s on study entry and 0.81 ± 0.35m/s at the time of discharge. Gait cycle duration decreased during rehabilitation (median:334ms [211,853]), as did double-limb support time (median:188ms [72,681]). Stance and swing time asymmetries were present throughout rehabilitation. Peak swing-time acceleration of the paretic leg was greater at discharge (median:0.20g-units [0.15,0.31]). 

CONCLUSIONS: The laboratory-quality gait metrics calculated by our wireless sensor system were sensitive to functional improvements during a period of known clinical recovery. Commercial sensor systems, for which steps counts are inaccurate at the slow speeds typical of hemi-paretic walking, have difficulty producing outcomes related to motor control in persons disabled by neurologic disease. Measurement of the quantity and quality of movements performed during daily activities enables clinicians and researchers to supervise gait training and skills practice during rehabilitation.

Improving Stroke Rehab, One Monitored Step at a Time

Some cool stuff from Bruce Dobkin, wrote The Clinical Science of Neurologic Rehabilitation.

Improving Stroke Rehab, One Monitored Step at a Time

An International Randomized Clinical Trial of Activity Feedback During Inpatient Stroke Rehabilitation Enabled by Wireless Sensing

What a novel idea. Objective measurements of muscle activity. What took so fucking long to think of this?
Would this
3-D Body Suit Put to Use in Healthcare Research
have been even better?
Or this?
Rapid Rehab Smart Insole Will Train Athletes and Assist Rehab Patients
And Bruce Dobkin is known for this book:
'The Clinical Science of Neurologic Rehabilitation'.
 From this lack of using the most up-to-date technology for research our stroke researchers are failing us.

An International Randomized Clinical Trial of Activity Feedback During Inpatient Stroke Rehabilitation Enabled by Wireless Sensing

1. Andrew K. Dorsch, MD1
2. Seth Thomas1
3. Xiaoyu Xu, PhD1
4. William Kaiser, PhD1
5. Bruce H. Dobkin, MD1
6. on behalf of the SIRRACT investigators

1. ¹University of California, Los Angeles, CA, USA

1. Bruce H. Dobkin, Department of Neurology, Geffen School of Medicine, University of California Los Angeles, RNRC, Room 1-129, 710 Westwood Plaza, Los Angeles, CA 90095, USA. Email: bdobkin@mednet.ucla.edu

Abstract

Background. Walking-related disability is the most frequent reason for inpatient stroke rehabilitation. Task-related practice is a critical component for improving patient outcomes.  

Objective. To test the feasibility of providing quantitative feedback about daily walking performance and motivating greater skills practice via remote sensing. 

Methods. In this phase III randomized, single blind clinical trial, patients participated in conventional therapies while wearing wireless sensors (triaxial accelerometers) at both ankles. Activity-recognition algorithms calculated the speed, distance, and duration of walking bouts. Three times a week, therapists provided either feedback about performance on a 10-meter walk (speed only) or walking speed feedback plus a review of walking activity recorded by the sensors (augmented). Primary outcomes at discharge included total daily walking time, derived from the sensors, and a timed 15-meter walk.  

Results. Sixteen rehabilitation centers in 11 countries enrolled 135 participants over 15 months. Sensors recorded more than 1800 days of therapy, 37 000 individual walking bouts, and 2.5 million steps. No significant differences were found between the 2 feedback groups in daily walking time (15.1 ± 13.1 vs 16.6 ± 14.3 minutes, P = .54) or 15-meter walking speed (0.93 ± 0.47 vs 0.91 ± 0.53 m/s, P = .96). Remarkably, 30% of participants decreased their total daily walking time over their rehabilitation stay.  

Conclusions. In this first trial of remote monitoring of inpatient stroke rehabilitation, augmented feedback beyond speed alone did not increase the time spent practicing or improve walking outcomes. Remarkably modest time was spent walking. Wireless sensing, however, allowed clinicians to audit skills practice and provided ground truth regarding changes in clinically important, mobility-related activities.

The Evolution of Neurorehabilitation and Neural Repair - Bruce H. Dobkin, MD

Dr. Dobkin I wish you would realize that  Neurorehabilitation and Neural Repair would be immensely easier after stroke if you stop the neuronal cascade of death. Don't you think about cause and effect at all?
http://nnr.sagepub.com/content/28/1/3.full?etoc

Over the past 8 years that I have served as the editor of Neurorehabilitation and Neural Repair, many well-designed, conceptually driven, randomized clinical trials have been published in this journal, as well as in others. This positive turn reveals a growing interest in the scientific bases of neurorehabilitation that was barely apparent as recently as 15 years ago.

Consider this. In 1999, Gert Kwakkel and colleagues published a randomized clinical trial in the New England Journal of Medicine, a journal not prone to publishing rehab studies at the time. They reported that therapy focused on the upper extremity improved dexterity but not walking and that therapy focused on the leg improved walking outcomes, but not arm functioning; both strategies were better than no therapy in patients who started treatment within 14 days of stroke. That focused, intensive enough therapy can improve outcomes at almost any time after stroke has been shown many times since then. Indeed, it is now unlikely that an experimental intervention would be tested against a control group that did not receive an equally intensive training paradigm.

Energy abounds around the world in neurologic rehabilitation, evidenced by a citation factor of 4.8 for Neuro-rehabilitation and Neural Repair over the past 5 years. What has changed since 1999?? It is the rising tide of scientific insights and promising strategies. Treatments being tested include action-observation and imagery, virtual reality applications, transcranial magnetic stimulation and direct current neurostimulation to modulate learning, electromechanical assists for arm and leg practice, brain-computer interfaces to control the environment, and exoskeletons to assist movement. Mobile health and tele-rehabilitation strategies to monitor practice, give feedback, and for more clinically meaningful outcome measurements may compliment these. A new era of pharmacologic interventions to enhance learning, neural repair by cellular and axon/dendrite growth promoters and neuromodulators, genetic insights, imbedded electrodes to activate brain or spinal networks, and adaptive robotic training are among those that will come into testing over the next 5 to 10 years.

It is my pleasure to congratulate Randolf Nudo, PhD, Professor of Molecular and Integrative Physiology at the University of Kansas, as the new editor of Neurorehabiliation and Neural Repair. He has been a major contributor to modeling physiologic and structural neural adaptations in relation to rehabilitation interventions. He and his editorial staff will have the opportunity to influence the clinical and basic science innovations, through their interaction with researchers, that will make the next 10 years exciting for clinicians and hopeful for our patients.

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Left to right: Gert Kwakkel, Tom Carmichael, Mickey Selzer (editor, 2000-2005), Bruce Dobkin (editor, 2006-13), Randy Nudo (incoming editor).

Thanks to Gert Kwakkel, my European managing editor, Tom Carmichael, my managing editor for the neurobiology of repair, the associate editors and editorial board, the indefatigable authors and peer reviewers, the American Society of NeuroRehabiliation, the World Federation of NeuroRehabilitation, and the staff at SAGE Publications for all their help. All of us will be there to help Randy Nudo nurture the journal into the future of neurologic rehabilitation.

Bruce H. Dobkin, MD
Outgoing Editor-in-Chief