Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Thursday, November 21, 2019

Oklahoma rehabilitation hospital introduces new therapy treatment for stroke patients

Failure, failure, failure. Notice they say 'better chance' and 'improve' NOT that you will get these results.  That is a complete failure to have EXACT STROKE PROTOCOLS producing recovery results.

Oklahoma rehabilitation hospital introduces new therapy treatment for stroke patients

OKLAHOMA CITY (KFOR) – Stroke survivors across the metro will now have a better chance at recovery thanks to a new therapy treatment program.
On Wednesday, Mercy Rehabilitation Hospital unveiled a new therapy treatment program for those who have suffered a neurological injury. Officials say neurological injuries are common after a stroke, which affects about 800,000 Americans each year.
In fact, the National Institute on Aging says that strokes are the number one cause of serious adult disability in the United States.
According to the Oklahoma State Department of Health, stroke was the fifth leading cause of death in Oklahoma in 2014.
After a stroke, patients will often undergo physical therapy to relearn simple motor activities like walking, sitting, standing, and lying down.
Now, a new therapy treatment hopes to improve the effects of physical therapy on Oklahoma stroke patients.Data pix.
The AI-powered InMotion Arm robotic therapy system from BIONIK helps stroke survivors record between 600 and 1,000 movements per session, which is a dramatic increase from traditional physical therapy.
"For the most part, this helps us get a lot of return with those patients. Our normal therapists can do about 40 to 60 reps of motion per session. This allows us to do about 600 reps per session with this bionic arm," said David Miller, director of therapy at Mercy Rehabilitation Hospital.
InMotion systems help patients throughout the United States and in more than 15 countries.

Stroke survivior earns a courage award

Recovery should not require courage. Your doctor and stroke hospital should have all the skills and stroke protocols that get you 100% recovered. Starting with stoppingthe 5 causes of the neuronal cascade of death in the first week.

Not getting you 100% recovered is failure on your doctor and stroke hospitals part.

 

Stroke survivior earns a courage award

LINCOLN, Neb. (KOLN) - Madonna Rehabilitation Hospital awarded stroke survivor Dave Melvin a courage award after volunteering his time to help other survivors.
Melvin had a stroke in 2016 and began rehab at Madonna. After his rehab, he wanted to help other people recover from their strokes.
"I was just very surprised," Melvin said. "I was told I was going to talk to another stroke survivor that was having a hard time. So I was looking forward to see if I couldn't help them."
According to the hospital, Melvin has put in more than 1,000 hours of volunteer work.
His wife, Terri, said she's always been proud of her husband for doing volunteer work.
"He's worked so very hard over the last three years. He never thought he was going to be a social butterfly, but he has truly been so good with patients," Terri said.
Melvin was nominated for the award by another stroke survivor - the first person to receive the award.

Robot-Assisted Stair Climbing Training on Postural Control and Sensory Integration Processes in Chronic Post-stroke Patients: A Randomized Controlled Clinical Trial

Maybe, just maybe your doctor can get this into your rehab since there already is a protocol for this. All she has to do is contact the researchers.  It will never occur.

Robot-Assisted Stair Climbing Training on Postural Control and Sensory Integration Processes in Chronic Post-stroke Patients: A Randomized Controlled Clinical Trial

Marialuisa Gandolfi1,2*, Nicola Valè1,2, Eleonora Dimitrova1,2, Maria Elisabetta Zanolin3, Nicola Mattiuz1,2, Elisa Battistuzzi1,2, Marcello Beccari1,2, Christian Geroin1, Alessandro Picelli1,2, Andreas Waldner4 and Nicola Smania1,2
  • 1Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy
  • 2UOC Neurorehabilitation, AOUI Verona, Verona, Italy
  • 3Unit of Epidemiology and Medical Statistics, University of Verona, Verona, Italy
  • 4Department of Neurological Rehabilitation, Private Hospital Villa Melitta, Bolzano, Italy
Background: Postural control disturbances are one of the important causes of disability in stroke patients affecting balance and mobility. The impairment of sensory input integration from visual, somatosensory and vestibular systems contributes to postural control disorders in post-stroke patients. Robot-assisted gait training may be considered a valuable tool in improving gait and postural control abnormalities.
Objective: The primary aim of the study was to compare the effects of robot-assisted stair climbing training against sensory integration balance training on static and dynamic balance in chronic stroke patients. The secondary aims were to compare the training effects on sensory integration processes and mobility.
Methods: This single-blind, randomized, controlled trial involved 32 chronic stroke outpatients with postural instability. The experimental group (EG, n = 16) received robot-assisted stair climbing training. The control group (n = 16) received sensory integration balance training. Training protocols lasted for 5 weeks (50 min/session, two sessions/week). Before, after, and at 1-month follow-up, a blinded rater evaluated patients using a comprehensive test battery. Primary outcome: Berg Balance Scale (BBS). Secondary outcomes:10-meter walking test, 6-min walking test, Dynamic gait index (DGI), stair climbing test (SCT) up and down, the Time Up and Go, and length of sway and sway area of the Center of Pressure (CoP) assessed using the stabilometric assessment.
Results: There was a non-significant main effect of group on primary and secondary outcomes. A significant Time × Group interaction was measured on 6-min walking test (p = 0.013) and on posturographic outcomes (p = 0.005). Post hoc within-group analysis showed only in the EG a significant reduction of sway area and the CoP length on compliant surface in the eyes-closed and dome conditions.
Conclusion: Postural control disorders in patients with chronic stroke may be ameliorated by robot-assisted stair climbing training and sensory integration balance training. The robot-assisted stair climbing training contributed to improving sensorimotor integration processes on compliant surfaces. Clinical trial registration (NCT03566901).

ApoA-I Mimetic Peptide Reduces Vascular and White Matter Damage After Stroke in Type-2 Diabetic Mice

WHOM will your doctor contact to get this tested for stroke in humans?  No contact then you need to have that doctor fired for incompetency and dereliction of duty. We need to start clearing out a lot of dead wood in stroke, probably starting with your stroke hospital board of directors. And it is for hyperacute with a delayed time frame, so every survivor could get it.

 

ApoA-I Mimetic Peptide Reduces Vascular and White Matter Damage After Stroke in Type-2 Diabetic Mice

Xiaohui Wang1†, Rongwen Li1, Alex Zacharek1, Julie Landschoot-Ward1, Michael Chopp1,2, Jieli Chen1* and Xu Cui1*
  • 1Department of Neurology, Henry Ford Hospital, Detroit, MI, United States
  • 2Department of Physics, Oakland University, Rochester, MI, United States
Diabetes leads to an elevated risk of stroke and worse functional outcome compared to the general population. We investigate whether L-4F, an economical ApoA-I mimetic peptide, reduces neurovascular and white-matter damage in db/db type-2 diabetic (T2DM) stroke mice. L-4F (16 mg/kg, subcutaneously administered initially 2 h after stroke and subsequently daily for 4 days) reduced hemorrhagic transformation, decreased infarct-volume and mortality, and treated mice exhibited increased cerebral arteriole diameter and smooth muscle cell number, decreased blood-brain barrier leakage and white-matter damage in the ischemic brain as well as improved neurological functional outcome after stroke compared with vehicle-control T2DM mice (p < 0.05, n = 11/group). Moreover, administration of L-4F mitigated macrophage infiltration, and reduced the level of proinflammatory mediators tumor necrosis factor alpha (TNFα), high-mobility group box-1 (HMGB-1)/advanced glycation end-product receptor (RAGE) and plasminogen activator inhibitor-1 (PAI-1) in the ischemic brain in T2DM mice (p < 0.05, n = 6/group). In vitro, L-4F treatment did not increase capillary-like tube formation in mouse-brain endothelial cells, but increased primary artery explant cell migration derived from C57BL/6-aorta 1 day after middle cerebral artery occlusion (MCAo), and enhanced neurite-outgrowth after 2 h of oxygen-glucose deprivation and axonal-outgrowth in primary cortical neurons derived from the C57BL/6-embryos subjected to high-glucose condition. This study suggests that early treatment with L-4F provides a potential strategy to reduce neuroinflammation and vascular and white-matter damage in the T2DM stroke population.

Treadmill walking with partial body weight support versus floor walking in hemiparetic subjects

It seems there was no objective analysis of the walking disability. If so, nothing here is repeatable.  I found these body weight supported systems useless, my spasticity in my legs required my full body weight to counteract that.  But my therapists strapped me in these regardless. It is the one size fits all approach.

Treadmill walking with partial body weight support versus floor walking in hemiparetic subjects

Stefan Hesse, MD, Matthias Konrad, MD, Dietmar Uhlenbrock, MPhil

ABSTRACT.

Treadmill walking with partial body weight support versus floor walking in hemiparetic subjects. Arch Phys Med Rehabil 1999;80: 421-7. 
Objective: 
To compare the gait of hemiparetic subjects walking on a treadmill with various body weight supports and walking on the floor. 
Design: 
Hemiparetic subjects walked on a treadmill, secured in a harness, with no body weight support and with 15% and 30% body weight relief, and walked on a floor. Setting: Kinematic laboratory of a department of rehabilitation. 
Subjects: 
Eighteen hemiparetic stroke patients. 
Main Outcome Measures: 
Gait cycle parameters and kinesiologic electromyogram of six muscles of the affected side and of two muscles of the nonaffected side. 
Results: 
On the treadmill, patients walked more slowly because of a reduced cadence, with a longer single stance period of the paretic limb, more symmetrically, and with a larger hip extension (multivariate profile analysis, p < .05). The mean functional activities of the gastrocnemius muscle and of the first crest of the erector spinae of the paretic side were smaller on the treadmill (univariate test, p < .05). Further, the premature activity of the gastrocnemius muscle, indicating spasticity, was less on the treadmill (univariate test, p < .05); correspondingly the qualitative muscle pattern analysis re- vealed less co-contraction between the gastrocnemius and tibialis anterior muscles in 11 of the 18 subjects. 
Conclusions: 
Treadmill training with partial body weight support in hemiparetic subjects allows them to practice a favorable gait characterized by a greater stimulus for balance training because of the prolonged single stance period of the affected limb, a higher symmetry, less plantar flexor spasticity, and a more regular activation pattern of the shank muscles as compared with floor walking. 0 1999 by the American Congress of Rehabilitation Medi- cine and the American Academy of Physical Medicine and Rehabilitation 

Utility of Ability for Basic Movement Scale (ABMSII) in predicting ambulation during rehabilitation in post-stroke patients

Damn it all, there is not a survivor in the world that cares about predictions. They want to know the results of following EXACT STROKE PROTOCOLS.  When the hell will you get there? After hell freezes over?  Maybe when YOU become the 1 in 4 per WHO that has a stroke?

Utility of Ability for Basic Movement Scale (ABMSII) in predicting ambulation during rehabilitation in post-stroke patients

Shoji Kinoshita, MD1, 2; Masahiro Abo, MD, PhD2; Takatsugu Okamoto, MD, PhD1, 2; Naojiro Tanaka, RPT1 5

  1Department of Rehabilitation Medicine, Nishi-Hiroshima Rehabilitation Hospital,
6-265, Miyake, Saeki-ku, Hiroshima, Hiroshima 731-5143, Japan 2Department of Rehabilitation Medicine, The Jikei University School of Medicine,
3-25-8, Nishi-Shimbashi, Minato-Ku, Tokyo 105-8461, Japan 10


Running title: ABMSII and ambulation in post-stroke patients
Word count: main text excluding references: 2,439, abstract: 213 

Corresponding author: Prof. Masahiro Abo, MD, PhD, Department of 15

Rehabilitation Medicine, The Jikei University School of Medicine, 3-25-8,
Nishi-Shimbashi, Minato-Ku, Tokyo 105-8461, Japan. Phone: +81-3-3433-1111. Fax:
+81-3-3431-1206, Email address: abo@jikei.ac.jp 

ACKNOWLEDGMENTS: We express our deepest gratitude to the staff of 20

Nishi-Hiroshima Rehabilitation Hospital.

Disclosure: The authors declare no conflict of interest.
ABMSII and ambulation in post-stroke patients. Page 2

ABSTRACT

Objective:
To test the hypothesis that the revised version of Ability for Basic 25

Movement Scale (ABMSII) can predict ambulation during rehabilitation in
post-stroke patients.
Subjects and Methods: 
The study included first-ever stroke patients who were
admitted to the rehabilitation ward and were dependent in walking. ABMSII were
assessed by physical therapists on admission to the hospital. Functional ambulation 30

category (FAC) was assessed every two weeks during hospitalization. The primary
outcome was independent ambulation, defined as ≥4 points of FAC. 
Results: After setting the inclusion criteria, data of 374 stroke patients (mean age:
70.0 years, 153 women) were eligible for the analysis. Of these, 193 patients achieved
independent ambulation during hospitalization. The ABMSII score was significantly 35

higher in the patients who regained independent walking than those who required
assistance in walking. Based on receiver-operating characteristics curve analysis,
ABMSII score of ≥16 points had a sensitivity of 93% and specificity of 71%.
Kaplan-Meier curve analysis after log-rank test demonstrated significantly higher
event rate in patients with ABMSII score ≥16 compared to those with ABMSII score 40

<16. Univariate and multivariate Cox regression analyses identified ABMSII score as
a significant and independent predictor of ambulation during rehabilitation.
Conclusions:
Our results suggest that ABMSII score is a potentially useful test to
predict ambulation during rehabilitation in post-stroke patients.

A tactile sensing approach in stroke rehabilitation

You'll have to ask your doctor how this is going to get you recovered and how you will do enough repetitions in the therapy sessions to actually recover. 

A tactile sensing approach in stroke rehabilitation

Mikov, Nikolay; Mohagheghia, Amir; Kilbride, Cherry; Du, Xinli
Date: 2019

Abstract:

The paper describes an experimental, mechanically simple, tactile sensing solution in the form of a sensing chair for discriminating human motion in a reaching task. This cost-efficient technical approach was employed for the assessment of selective arm movements in stroke survivors. The sensing system classifies trunk motion in a seated stroke survivor during a goal-directed task where there is direct correlation with the level of severity of arm movement. The system interprets motion mechanically from coupled sensory data transients using artificial neural networks and shows tolerance to patients’ sitting posture and performance variability. The accuracy of classification was typically greater than 94% across three categories when applied to a group of stroke survivors of wide-ranging motor abilities. The mechanical simplicity, versatility of approach for use in other classes of movement, and potential low cost of manufacturing provides opportunity to employ the system at clinics and homes for assessment and training.

Light-Emitting Diode Photobiomodulation After Cerebral Ischemia.

Well fuck, we really need someone to write and distribute a protocol on this. All this previous research; OR ARE WE WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM?     

 

A new treatment protocol using photobiomodulation and muscle/bone/joint recovery techniques having a dramatic effect on a stroke patient's recovery: a new weapon for clinicians Sept. 2012      

 

Interplay between up-regulation of cytochrome-c-oxidase and hemoglobin oxygenation induced by near-infrared laser June 2017      

 

Photobiomodulation therapy promotes neurogenesis by improving post-stroke local microenvironment and stimulating neuroprogenitor cells Oct. 2017    

The latest here which of course NOTHING will happen with, no followup will occur.  Your stroke hospital is completely fucking incompetent.

 

Light-Emitting Diode Photobiomodulation After Cerebral Ischemia

Author information

1
Clinical Neurosciences Research Laboratory, Health Research Institute of Santiago de Compostela (IDIS), Clinical University Hospital, Universidade de Santiago de Compostela, Santiago de Compostela, Spain.
2
Optics Area, Department of Applied Physics, Faculty of Physics, Universitdade de Santiago de Compostela, Santiago de Compostela, Spain.
3
Faculty of Optics and Optometry, Universitdade de Santiago de Compostela, Santiago de Compostela, Spain.

Abstract

Photobiomodulation (PBM) therapy is a promising therapeutic approach for several pathologies, including stroke. The biological effects of PBM for the treatment of cerebral ischemia have previously been explored as a neuroprotective strategy using different light sources, wavelengths, and incident light powers. However, the capability of PBM as a novel alternative therapy to stimulate the recovery of the injured neuronal tissue after ischemic stroke has been poorly explored. The aim of this study was to investigate the low-level light irradiation therapy by using Light Emitting Diodes (LEDs) as potential therapeutic strategy for stroke. The LED photobiomodulation (continuous wave, 830 nm, 0.2-0.6 J/cm2) was firstly evaluated at different energy densities in C17.2 immortalized mouse neural progenitor cell lines, in order to observe if this treatment had any effect on cells, in terms of proliferation and viability. Then, the PBM-LED effect (continuous wave, 830 nm, 0.28 J/cm2 at brain cortex) on long-term recovery (12 weeks) was analyzed in ischemic animal model by means lesion reduction, behavioral deficits, and functional magnetic resonance imaging (fMRI). Analysis of cellular proliferation after PBM was significantly increased (1 mW) in all different exposure times used; however, this effect could not be replicated in vivo experimental conditions, as PBM did not show an infarct reduction or functional recovery. Despite the promising therapeutic effect described for PBM, further preclinical studies are necessary to optimize the therapeutic window of this novel therapy, in terms of the mechanism associated to neurorecovery and to reduce the risk of failure in future clinical trials.

Want to Live Longer? Get Some Friends

So your doctor needs to get you 100% recovered immediately before you lose the first two groups of friends that Aristotle describes.  DEMAND results or your doctor will use the craptastic saying; 'All strokes are different, all stroke recoveries are different'. You can't allow your doctor to hide and cower behind that useless saying.

Aristotle believes that there are three different kinds of friendship; that of utility, friendship of pleasure, and virtuous friendship. 

and that you will likely lose all of the first two post stroke?

 

Want to Live Longer? Get Some Friends



Americans Lose Touch, Report Fewer Close Frien
Exercise and quitting smoking are thought to be important steps for a long, healthy life, but a new study suggests another potential tip for extending lifespan: make some friends.
The results show people with strong social relationships increased their odds of survival over a certain time period by 50 percent, the researchers say. That's on par with ceasing smoking, and nearly twice as beneficial as physical activity in terms of decreasing your odds of dying early.

The findings underscore just how important friendships are to our health, the researchers say.
"I think we make a compelling case that social relationships should also be taken quite seriously in terms of reducing risk of mortality," said study researcher Julianne Holt-Lunstad, a psychologist at Brigham Young University in Utah.
Assessing social networks
The researchers reviewed 148 studies that examined the link between social relationships and mortality. The studies involved more than 308,000 participants in total, and subjects were followed for an average of 7.5 years.
The studies measured social relationships in a number of ways. Some simply looked at the size of a person's social network or whether or not they were married or lived alone. Others assessed peoples' perceptions about their relationships, such as whether or not they felt others were there for them. And still others looked at how integrated people were in their social networks or communities.
Overall, high scores on measures indicative of strong social relationships were associated with increased odds of survival. The results held regardless of the person's age, gender, health status and cause of death.
In general, studies that took into account more than one aspect of a person's relationship (for instance, social network size and how integrated a person is with that network) were better predictors of mortality than those that only assessed one measure (such as whether someone lives alone).
Why are friends beneficial?
Our relationships can influence our health in a variety of ways, Holt-Lunstad said. For instance, they can help us deal with stress – a deadly pastime.
"As we encounter potentially stressful events in our lives, if we know that we've got people we can count on or that we can turn to, we may be less likely to even perceive it as stressful, because we know we can handle it," Holt-Lunstad said. "But also, let's say we're already in the throes of some kind of stressful event, our relationships can also help us cope with it and buffer that reaction to the stress."
Our friendships can also encourage healthy behaviors (and unhealthy ones) that have a direct impact on well-being. For example, our friends might encourage us to eat better, exercise, get more sleep or visit the doctor, Holt-Lunstad said.
Social relationships also provide meaning to our lives and might influence us to take better care of ourselves or take fewer risks, she said.
The work suggests such relationships are important from a public health perspective, and medical care professionals might consider recommending or promoting better social connections, the researchers say. Hospital and clinic staff might also try to involve their patients in social support networks during recovery, they say.
The results are published this week in the journal PLoS Medicine.

Motor learning during poststroke gait rehabilitation: a case study

No protocol but more paretic propulsion stuff. It must be important. What the fuck protocol does your doctor have you doing to improve your paretic propulsion? NONE I BET. 

Motor learning during poststroke gait rehabilitation: a case study

Trisha M. Kesar, PT, PhD, Michelle J. Sauer, BE, Stuart A. Binder-Macleod, PT, PhD, and Darcy S. Reisman, PT, PhD
 

Introduction: 
To develop more effective gait rehabilitation strategies, it is important to understand the time course of motor learning that underlies improvements achieved with gait training. The purpose of this case study was to evaluate motor learning through the measurement of within-session and across-session changes in gait biomechanics during the first and sixth weeks of a 6-week clinical gait training program. 
Case Description: 
A47-year-old man with post stroke left hemiparesis participated in the study(15.5 months post stroke, lower extremity Fugl-Meyer score of 12). 
Intervention:  
The subject participated in 6 weeks of training with 3 sessions per week, comprising fast treadmill walking and functional electrical stimulation to plantar and dorsiflexors. In one training session during the first and sixth weeks, paretic propulsion and swing phase knee flexion were measured during a pretest (before the training session), post test (after the training session), and retention test (48 hours after training). 
Outcomes: 
After 6 week of training, the subject’s gait speed increased from 0.38 to 0.57 m/s; there was a 55.4% improvement in paretic propulsion and 25% increase in swing phase knee flexion. Examination of change scores revealed greater within session gains and greater retention during the first versus sixth weeks of gait training for both paretic propulsion and knee flexion. 
Discussion: 
We demonstrate the feasibility and advantage of using within and across session changes for evaluating motor learning during clinical gait rehabilitation. An understanding of the time course of motor learning that underlies gait training can guide the development

Wednesday, November 20, 2019

Gait rehabilitation machines based on programmable footplates

WHOM is going to write a protocol for gait training based on the thousands of research articles on gait? Or do you prefer your therapist shooting in the dark about your chances of getting 100% recovered? Guidelines do not count, I consider them worthless. 

This is but a fraction of gait research; your doctor should have an index of all gait research and access so you can read them.

Gait rehabilitation machines based on programmable footplates

Abstract

Background:
Gait restoration is an integral part of rehabilitation of brain lesioned patients.Modern concepts favour a task-specific repetitive approach, i.e. who wants to regain walking hasto walk, while tone-inhibiting and gait preparatory manoeuvres had dominated therapy before.Following the first mobilization out of the bed, the wheelchair-bound patient should have the possibility to practise complex gait cycles as soon as possible. Steps in this direction were treadmill training with partial body weight support and most recently gait machines enabling the repetitive training of even surface gait and even of stair climbing.
Results:
With treadmill training harness-secured and partially relieved wheelchair-mobilisedpatients could practise up to 1000 steps per session for the first time. Controlled trials in stroke and SCI patients, however, failed to show a superior result when compared to walking exercise on the floor. Most likely explanation was the effort for the therapists, e.g. manually setting the paretic limbs during the swing phase resulting in a too little gait intensity. The next steps were gait machines, either consisting of a powered exoskeleton and a treadmill (Lokomat, AutoAmbulator)or an electromechanical solution with the harness secured patient placed on movable foot plates(Gait Trainer GT I). For the latter, a large multicentre trial with 155 non-ambulatory stroke patients (DEGAS) revealed a superior gait ability and competence in basic activities of living in the experimental group. The Haptic Walker continued the end effector concept of movable foot plates,now fully programmable and equipped with 6 DOF force sensors. This device for the first time enables training of arbitrary walking situations, hence not only the simulation of floor walking but also for example of stair climbing and perturbations.
Conclusion:
Locomotor therapy is a fascinating new tool in rehabilitation, which is in line with modern principles of motor relearning promoting a task-specific repetitive approach. Sophisticated technical developments and positive randomized controlled trials form the basis of a growing acceptance worldwide to the benefits or our patients.

Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia

Well shit, enriched environment has been out there since 2011. Is your stroke hosital using this intervention? Or is incompetence reigning supreme?

Hasn't it been proven enough by this enriched environment talked about by Dr. Dale Corbett in 2011?

Enriched Environment Promoted Cognitive Function via Bilateral Synaptic Remodeling After Cerebral Ischemia

Chuanjie Wang1,2, Qun Zhang3, Kewei Yu3, Xueyan Shen3, Yi Wu3* and Junfa Wu3*
  • 1Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai, China
  • 2Department of Rehabilitation Medicine, Jinshan Hospital, Fudan University, Shanghai, China
  • 3Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai, China
Ischemic stroke is the second leading cause of death worldwide. Ischemia-induced cognitive dysfunction may result in a poor quality of life. Synaptic plasticity plays a key role in cognition promotion. An enriched environment (EE), which can attenuate cognitive deficits in chronic cerebral hypoperfusion, has been shown to facilitate synaptic plasticity. However, the effect of EE on synaptic plasticity in bilateral cerebral hemispheres in stroke remains unclear. This study used a permanent middle cerebral artery occlusion mouse model, which was divided into standard housing and EE groups. The Morris water maze test was performed to detect the cognitive function. Electron microscopy was used to determine the synapse numbers. The expression of SYN and GAP-43 was then quantified by immunofluorescence staining and Western blot analysis. Compared with the standard housing, EE promoted the cognitive function recovery in the mice with stroke. Moreover, EE increased the synapse numbers and the expression of SYN and GAP-43 in both the ipsilateral and contralateral hemispheres (P < 0.05). A further correlation analysis revealed a positive correlation between the cognitive function outcomes and the relative expression of GAP-43 and SYN. Furthermore, the correlation of the expression of GAP-43 and SYN with cognitive function was higher in the contralateral brain than in the ipsilateral brain. In conclusion, an EE may promote cognitive function via bilateral synaptic remodeling after cerebral ischemia. Also, the contralateral brain may play an important role in the recovery of cognitive function

Aerobic Training and Mobilization Early Post-stroke: Cautions and Considerations

TLDR. This is for your doctor to read and understand. I bet there is almost zero chance that your doctor has read ANY of the 282 supporting references. 

Aerobic Training and Mobilization Early Post-stroke: Cautions and Considerations

  • 1KITE, Toronto Rehab-University Health Network, Toronto, ON, Canada
  • 2Department of Exercise Sciences, Faculty of Kinesiology and Physical Education, University of Toronto, Toronto, ON, Canada
  • 3Canadian Partnership for Stroke Recovery, Toronto, ON, Canada
  • 4Schlegel-University of Waterloo Research Institute for Aging, University of Waterloo, Waterloo, ON, Canada
  • 5Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada
  • 6Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada
  • 7School of Kinesiology and Health Studies, Queen's University, Kingston, ON, Canada
  • 8Sunnybrook Health Sciences Center, Toronto, ON, Canada
Knowledge gaps exist in how we implement aerobic exercise programs during the early phases post-stroke. Therefore, the objective of this review was to provide evidence-based guidelines for pre-participation screening, mobilization, and aerobic exercise training in the hyper-acute and acute phases post-stroke. In reviewing the literature to determine safe timelines of when to initiate exercise and mobilization we considered the following factors: arterial blood pressure dysregulation, cardiac complications, blood-brain barrier disruption, hemorrhagic stroke transformation, and ischemic penumbra viability. These stroke-related impairments could intensify with inappropriate mobilization/aerobic exercise, hence we deemed the integrity of cerebral autoregulation to be an essential physiological consideration to protect the brain when progressing exercise intensity. Pre-participation screening criteria are proposed and countermeasures to protect the brain from potentially adverse circulatory effects before, during, and following mobilization/exercise sessions are introduced. For example, prolonged periods of standing and static postures before and after mobilization/aerobic exercise may elicit blood pooling and/or trigger coagulation cascades and/or cerebral hypoperfusion. Countermeasures such as avoiding prolonged standing or incorporating periodic lower limb movement to activate the venous muscle pump could counteract blood pooling after an exercise session, minimize activation of the coagulation cascade, and mitigate potential cerebral hypoperfusion. We discuss patient safety in light of the complex nature of stroke presentations (i.e., type, severity, and etiology), medical history, comorbidities such as diabetes, cardiac manifestations, medications, and complications such as anemia and dehydration. The guidelines are easily incorporated into the care model, are low-risk, and use minimal resources. These and other strategies represent opportunities for improving the safety of the activity regimen offered to those in the early phases post-stroke. The timeline for initiating and progressing exercise/mobilization parameters are contingent on recovery stages both from neurobiological and cardiovascular perspectives, which to this point have not been specifically considered in practice. This review includes tailored exercise and mobilization prescription strategies and precautions that are not resource intensive and prioritize safety in stroke recovery.

Neuroprotective Effects of Serpina3k in Traumatic Brain Injury

WHOM will your doctor contact to get this tested for stroke in humans?  No contact then you need to have that doctor fired for incompetency and dereliction of duty. We need to start clearing out a lot of dead wood in stroke, probably starting with your stroke hospital board of directors.

 

Neuroprotective Effects of Serpina3k in Traumatic Brain Injury

Yao Jing1, Dianxu Yang1, Yimu Fu2, Wei Wang1, Guoyuan Yang3, Fang Yuan1, Hao Chen1, Jun Ding1*, Shiwen Chen1* and Hengli Tian1*
  • 1Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
  • 2Department of Emergency, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
  • 3School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China
Traumatic brain injury (TBI) is a major cause of disability and mortality worldwide, in part resulting from secondary apoptosis of neurons in peri-contusion areas. Serpina3k, a serine protease inhibitor, has been shown to inhibit apoptosis in injury models. In this study, we investigated the anti-apoptotic function of serpina3k in vivo using a mouse model of TBI, as well as the underlying neuroprotective mechanism in vitro using the SH-SY5Y human neuroblastoma cell line. TBI was induced in adult male C57BL/6 mice using controlled cortical impact. Serpina3k protein was intravenously administered at a concentration of 0.5 mg/kg twice daily for up to 14 days. SH-SY5Y cells were subjected to biaxial stretch injury and then treated with different concentrations of serpina3k. We found that endogenous serpina3k protein levels were elevated in peri-contusion areas of the mouse brain following TBI. Serpina3k-treated mice had fewer apoptotic neurons, lower levels of oxidative stress, and showed greater recovery of neurological deficits relative to vehicle-treated mice. Meanwhile, in the SH-SY5Y cell injury model, serpina3k at an optimal concentration (150 nM) inhibited the generation of intracellular reactive oxygen species, abrogated changes of the mitochondrial membrane potential, and reduced the phospho-extracellular regulated protein kinases (p-ERK)/ERK, phospho-P38 (p-P38)/P38, B cell lymphoma (Bcl)-2-associated X protein/Bcl-2, and cleaved caspase-3/caspase-3 ratios, thereby reducing the apoptosis rate. These results demonstrate that serpina3k exerts a neuroprotective function following TBI and thus has therapeutic potential.

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

WHOM will your doctor contact to get this tested for stroke in humans?  No contact then you need to have that doctor fired for incompetency and dereliction of duty. We need to start clearing out a lot of dead wood in stroke, probably starting with your stroke hospital board of directors.

Methylene Blue Reduces Neuronal Apoptosis and Improves Blood-Brain Barrier Integrity After Traumatic Brain Injury

Jun Shen1,2,3,4, Wenqiang Xin2,3,4, Qifeng Li2,3,4, Yalong Gao2,3,4, Lili Yuan5* and Jianning Zhang2,3,4*
  • 1Department of Neurosurgery, Yijishan Hospital of Wannan Medical College, Wuhu, China
  • 2Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China
  • 3Tianjin Neurological Institute, Tianjin, China
  • 4Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, China
  • 5Department of Neurology, Yijishan Hospital of Wannan Medical College, Wuhu, China
Objective: To investigate whether methylene blue (MB) treatment can reverse neuronal mitochondrial dysfunction caused by oxygen glucose deprivation/reoxygenation (OGD) injury and then investigate whether MB treatment can reduce neuronal apoptosis and improve blood-brain barrier (BBB) integrity in traumatic brain injury (TBI) animals.
Methods: Reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) were used to evaluate mitochondrial function. The terminal deoxynucleotidyl transferase-dUTP nick end labeling (TUNEL) assay was used to assess neuronal apoptosis in vitro. TUNEL and immunofluorescence staining for neuronal nuclei (NeuN) were combined to assess neuronal apoptosis in vivo. An Evans blue (EB) permeability assay and brain water content (BWC) were used to measure BBB permeability in vivo. The Morris water maze (MWM), rotarod test, and modified Neurological Severity Score (mNSS) test were employed to assess the prognosis of TBI mice.
Results: MB treatment significantly reversed neuronal mitochondrial dysfunction caused by OGD injury. Both in vitro and in vivo, MB treatment reduced neuronal apoptosis and improved BBB integrity. In TBI animals, treatment with MB not only improved cognitive and motor function caused by TBI but also significantly improved overall neurological function.
Conclusions: Our findings suggest that MB is a potential candidate for the treatment of TBI. Future research should focus on other therapeutic effects and mechanisms of MB in secondary brain injury.

Introduction

Traumatic brain injury (TBI) is the most common cause of mortality and disability among working-age adults and young individuals worldwide (1). In the United States, ~2 million people suffer a TBI each year, and TBI accounts for nearly one-third of all trauma-related mortality (1, 2). TBI damages brain tissue through two pathological processes, primary and secondary injury. Primary injury is characterized by immediate bleeding and loss of brain tissue when a blunt or sharp object impacts the head. Secondary injury involves complicated cellular and biochemical cascade reactions, including oxidative stress, excitotoxicity, neuroinflammation, free radical-induced injury, and calcium-mediated damage, which lead to blood-brain barrier (BBB) damage, elevated intracranial pressure, cerebral hypoxia, brain edema, and neuronal apoptosis (38). Mitochondrial dysfunction has been demonstrated to be a key participant in the pathological processes of secondary brain injury (9, 10).
Methylene blue (MB) is an FDA-approved drug used to treat cyanide poisoning, carbon monoxide poisoning, and methemoglobinemia (11). Previous studies have demonstrated that MB can improve mitochondrial function (12). Under pathological conditions, MB acts as an alternative electron carrier that bypasses complex I/III blockage and efficiently transfers electrons from NADH to cytochrome c (cyt c). This process reduces electron leakage, enhances adenosine triphosphate (ATP) production, and decreases the overproduction of reactive oxygen species (ROS) (13). In recent years, MB has been shown to attenuate pathological and neurobehavioral impairments in animal models of Alzheimer's disease (AD) (14, 15), Parkinson's disease (PD) (16), ischemic stroke (17, 18), and TBI (1921). After TBI, MB treatment can attenuate neuroinflammation, reduce lesion volume, and improve neurological damage (1921).
Since MB treatment can reduce the release of ROS and increase the production of ATP, it may have the potential to reduce neuronal apoptosis and improve BBB integrity. However, these effects of MB on TBI have not been investigated. In the present study, we first investigated whether MB treatment can reverse neuronal mitochondrial dysfunction and then investigated whether MB treatment can reduce neuronal apoptosis and improve BBB integrity after TBI.

VA, DoD update guideline for rehabilitation after stroke

Useless, guidelines NOT PROTOCOLS.  No talk of results from using these guidelines so useless.

VA, DoD update guideline for rehabilitation after stroke

(HealthDay)—In a systematic review and clinical practice guideline, published online Nov. 19 in Annals of Internal Medicine, recommendations from the U.S. Department of Veterans Affairs and the U.S. Department of Defense are presented for stroke rehabilitation and nonpharmacologic and pharmacologic treatments for motor deficits and mood disorders in adults who have had stroke.
James Sall, Ph.D., from the Department of Veterans Affairs in Los Angeles, and colleagues provide recommendations for rehabilitation care of patients after stroke. Recommendations were developed in six areas, including timing of rehabilitation treatment, motor therapy, dysphagia management, cognitive rehabilitation approaches, mental health treatment, and community reintegration such as returning to work and driving. Stroke rehabilitation requires an interdisciplinary, holistic approach to poststroke sequelae, according to the authors.
Kristen E. D'Anci, Ph.D., from the ECRI Institute in Plymouth Meeting, Pennsylvania, and colleagues summarized evidence on the benefits and harms of nonpharmacologic and pharmacologic treatments for motor deficits and mood disorders in adults who have had stroke. Data were included from 19 systematic reviews and 37 randomized controlled trials. The researchers found that most interventions did not improve motor function. Based on high-quality evidence, fluoxetine use was not supported for improving motor function. There was moderate-quality evidence for use of cardiorespiratory training for improving maximum walking speed and repetitive task training or for improving activities of daily living. Based on low-quality evidence, antidepressants may reduce depression, although the frequency and severity of related adverse events is unclear; cognitive behavioral therapy and exercise may reduce symptoms of anxiety and depression.
"We recommend using these guidelines as an adjunct to the American Heart Association/American Stroke Association for Adult Stroke Rehabilitation and Recovery," Sall and colleagues write.

Pathway-specific modulatory effects of neuromuscular electrical stimulation during pedaling in chronic stroke survivors

Since we don't know how NMES works we can't get a stroke protocol out of it. This is a prime candidate for further research which will never occur since we have NO STROKE LEADERSHIP AND NO STROKE STRATEGY.

Pathway-specific modulatory effects of neuromuscular electrical stimulation during pedaling in chronic stroke survivors


Abstract

Background

Neuromuscular electrical stimulation (NMES) is extensively used in stroke motor rehabilitation. How it promotes motor recovery remains only partially understood. NMES could change muscular properties, produce altered sensory inputs, and modulate fluctuations of cortical activities; but the potential contribution from cortico-muscular couplings during NMES synchronized with dynamic movement has rarely been discussed.

Method

We investigated cortico-muscular interactions during passive, active, and NMES rhythmic pedaling in healthy subjects and chronic stroke survivors. EEG (128 channels), EMG (4 unilateral lower limb muscles) and movement parameters were measured during 3 sessions of constant-speed pedaling. Sensory-level NMES (20 mA) was applied to the muscles, and cyclic stimulation patterns were synchronized with the EMG during pedaling cycles. Adaptive mixture independent component analysis was utilized to determine the movement-related electro-cortical sources and the source dipole clusters. A directed cortico-muscular coupling analysis was conducted between representative source clusters and the EMGs using generalized partial directed coherence (GPDC). The bidirectional GPDC was compared across muscles and pedaling sessions for post-stroke and healthy subjects.

Results

Directed cortico-muscular coupling of NMES cycling was more similar to that of active pedaling than to that of passive pedaling for the tested muscles. For healthy subjects, sensory-level NMES could modulate GPDC of both ascending and descending pathways. Whereas for stroke survivors, NMES could modulate GPDC of only the ascending pathways.

Conclusions

By clarifying how NMES influences neuromuscular control during pedaling in healthy and post-stroke subjects, our results indicate the potential limitation of sensory-level NMES in promoting sensorimotor recovery in chronic stroke survivors.

Foot slap

I have a pretty good case of this, pretty damn noisy walking in the tiled halls of airports. I should be able to go to any physical therapist in the world and be able to get EXACT STROKE PROTOCOLS to correct this problem. 

The standard explanation for this is lack of dorsiflexon. Not for me, I can dorsiflex just fine. According to my analysis it goes back to the fact I don't have a free swinging lower leg .  Initial, mid and terminal swing don't exist due to spasticity. I swing my leg like a log.  Fix my spasticity and I can recover normal walking easily. 

Understanding Phases of the Gait Cycle