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:

Sunday, November 30, 2014

Harvard Unveils MRI Study Proving Meditation Literally Rebuilds The Brain’s Gray Matter In 8 Weeks

I bet your doctor won't create a stroke protocol based on this for at least 30 years. Don't do this on your own, you know how dangerous meditation is.
Test subjects taking part in an 8-week program of mindfulness meditation showed results that astonished even the most experienced neuroscientists at Harvard University.  The study was led by a Harvard-affiliated team of researchers based at Massachusetts General Hospital, and the team’s MRI scans documented for the very first time in medical history how meditation produced massive changes inside the brain’s gray matter.  “Although the practice of meditation is associated with a sense of peacefulness and physical relaxation, practitioners have long claimed that meditation also provides cognitive and psychological benefits that persist throughout the day,” says study senior author Sara Lazar of the MGH Psychiatric Neuroimaging Research Program and a Harvard Medical School instructor in psychology. “This study demonstrates that changes in brain structure may underlie some of these reported improvements and that people are not just feeling better because they are spending time relaxing.”
Sue McGreevey of MGH writes: “Previous studies from Lazar’s group and others found structural differences between the brains of experienced meditation practitioners and individuals with no history of meditation, observing thickening of the cerebral cortex in areas associated with attention and emotional integration. But those investigations could not document that those differences were actually produced by meditation.”  Until now, that is.  The participants spent an average of 27 minutes per day practicing mindfulness exercises, and this is all it took to stimulate a major increase in gray matter density in the hippocampus, the part of the brain associated with self-awareness, compassion, and introspection.  McGreevey adds: “Participant-reported reductions in stress also were correlated with decreased gray-matter density in the amygdala, which is known to play an important role in anxiety and stress. None of these changes were seen in the control group, indicating that they had not resulted merely from the passage of time.”
“It is fascinating to see the brain’s plasticity and that, by practicing meditation, we can play an active role in changing the brain and can increase our well-being and quality of life,” says Britta Hölzel, first author of the paper and a research fellow at MGH and Giessen University in Germany. You can read more about the remarkable study by visiting

Warfarin Pretreatment Reduces Cell Death and MMP-9 Activity in Experimental Intracerebral Hemorrhage

There is a slight problem here in that you would need to know you're going to have a hemorrhage so you can pretreat yourself. Or maybe you'd rather go to high altitudes for Training the Brain to Survive Stroke.

$39.95 / €34.95 / £29.95 *
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Little is known about the pathophysiology of oral anticoagulation-associated intracerebral hemorrhage (OAC-ICH). We compared hematoma volume, number of terminal deoxynucleotidyl dUTP nick-end labeling (TUNEL)-positive cells (indicating cell death), MMP-9 levels, and perilesional edema formation between warfarin-treated mice and controls. Intracerebral hemorrhage was induced by an injection of collagenase into the right striatum. Twenty-four hours later, hematoma volume was measured using a photometric hemoglobin assay. Cell death was quantified using TUNEL staining. MMP-9 levels were determined by zymography, and edema formation was assessed via the wet–dry method. Warfarin increased hematoma volume by 2.6-fold. The absolute number of TUNEL-positive cells in the perihematomal zone was lower in warfarin-treated animals (300.5 ± 39.8 cells/mm2) than in controls (430.5 ± 38.9 cells/mm2; p = 0.034), despite the larger bleeding volume. MMP-9 levels were reduced in anticoagulated mice as compared to controls (p  = 0.018). Perilesional edema formation was absent in warfarin mice and modestly present in controls. Our results suggest differences in the pathophysiology of OAC-ICH compared to intracerebral hemorrhage occurring under normal coagulation. A likely explanation is that thrombin, a strong inductor of apoptotic cell death and blood–brain barrier disruption, is produced to a lesser extent in OAC-ICH. In humans, however, we assume that the detrimental effects of a larger hematoma volume in OAC-ICH by far outweigh potential protective effects of thrombin deficiency.

Saturday, November 29, 2014

How Augmented Reflection Technology (ART) Can Assist Stroke Rehabilitation

You will need your doctor and therapists read this and see if anything here can be used right now to help you.
Augmented Reality (AR)
 Real-world view augmented by 3D virtual information,
which is computer-generated in real-time.
 The goal is to create the impression that the virtual objects
are part of the real environment.

Eating Junk Food Causes Irreversible Memory Loss

Be careful out there when feeding your mice, don't snack too much on their junk food.
Make sure your hospital diet is not causing your memory problems rather than your stroke.
Scientists in Australia are saying eating junk food for even a short amount of time can cause irreversible memory loss. The conclusions from tests with mice who ate a diet full of sugar and fat show the mice were unable to recognize places as well as mice who had had a healthier diet. Patrick Jones (@Patrick_E_Jones) has the rest.


An anonymous reply to one of my acupuncture  posts  pointed out the WHO paper suggesting that if WHO approves acupuncture it must work.
Here is the actual WHO paper. 87 pages in all,d.cWc
This line seems to indicate the only reason for the report is that it is widely used. Being widely used is no claim of efficacy.
In recognition of the increasing worldwide interest in the subject, the World Health Organization (WHO) conducted a symposium on acupuncture in June 1979 in Beijing, China. Physicians practising acupuncture in different countries were invited to identify the conditions that might benefit from this therapy. The participants drew up a list of 43 suitable diseases. However, this list of indications was not based on formal clinical trials conducted in a rigorous scientific manner, and its credibility has been questioned.
Page 29 has this
1. Diseases, symptoms or conditions for which acupuncture has been proved—through controlled trials—to be an effective treatment:
But they don't list the clinical trials that prove it works, thus with no proof there is no reason to believe it works. Appeal to WHO authority does not cut it for me.
Nowhere in here does it explain how acupuncture is supposed to work except as a placebo.

My reasons for not believing acupuncture does anything are here;

Neuro-Acupuncture and Stroke

and this:

Acupuncture is a theatrical placebo: the end of a myth - DC's Improbable Science

 It's up to you and your doctor how you want to handle this.

Friday, November 28, 2014

Stroke damage mechanism identified

This is rather appalling that they have only identified one out of five causes of the neuronal cascade of death. Don't they read stroke research at all? Do they really know which one it is? Don't we at least have common naming standards for stroke problems?
1.  glutamate poisoning
2.  excitotoxicity
3.  Capillaries that don't open due to pericytes
4.  Inflammatory action leaking through the blood brain barrier.
5. Lysosomal Membrane Permeabilization as a Key Player in Brain Ischemic Cell Death:
Researchers have discovered a mechanism linked to the brain damage often suffered by stroke victims—and are now searching for drugs to block it.
Strokes happen when the blood supply to part of the brain is cut off but much of the harm to survivors’ memory and other cognitive function is often actually caused by “oxidative stress” in the hours and days after the blood supply resumes.
A team from the University of Leeds and Zhejiang University in China studied this second phase of damage in laboratory mice and found a mechanism in neurons that, if removed, reduced the damage to brain function.
Co-author Dr Lin-Hua Jiang, of the University of Leeds’ School of Biomedical Sciences, said: “Until now, much of the drug research has been focussing on the direct damage caused by the loss of blood flow, but this phase can be hard to target. The patient may not even be in the ambulance when it is happening. We have found a mechanism that is linked to the next phase of damage that will often be underway after patients have been admitted to hospital.”
The study, published in the journal Cell Death and Disease and supported by a strategic partnership between the University of Leeds and Zhejiang University, looked at the damage caused by the excessive production of chemicals called “reactive oxygen species” in brain tissues immediately after blood supply is re-established. In a healthy brain, there are very low levels of reactive oxygen species, but the quantity dramatically increases after a stroke to levels that are harmful to neurons.
Dr Jiang said: “We identified an ‘ion channel’ in the membranes of neurons, called TRPM2, which is switched on in the presence of the reactive oxygen species. Basically, an ion channel is a door in the membrane of a cell that allows it to communicate with the outside world— TRPM2 opens when the harmful levels of reactive oxygen species are present and we found that removing it significantly reduced neuronal cell damage.”
The researchers compared the effects of strokes on mice with TRPM2 with a transgenic strain without it.
“In the mice in which the TRPM2 channel does not function, the reactive oxygen species are still produced but the neurons are very much protected. The neuronal death is significantly reduced. More importantly, we observed a significant difference in brain function, with the protected mice demonstrating significantly superior memory in lab tests,” Dr Jiang said.
“This study has pinpointed a very promising drug target. We are now screening a large chemical library to find ways of effectively inhibiting this channel. Our ongoing research using animal models is testing whether blockage of this channel can offer protection again brain damage and cognitive dysfunction in stroke patients,” Dr Jiang said.

Rehabilitation exercise assessment using inertial sensors: a cross-sectional analytical study

This makes so much sense that it won't occur unless you demand it. If you don't have an accurate objective description of your muscular problems there is absolutely no way your therapist can ever create a protocol and thus have something repeatable for future survivors. It's up to you. Do you want to pay it forward? Or just let your medical staff keep doing the useless crap they are doing now? And look at that, emails for your doctor to use.
Oonagh M Giggins1*
* Corresponding author
Kevin T Sweeney1,2
Brian Caulfield1,2
1 School of Public Health, Physiotherapy and Population Science, University
College Dublin, Dublin, Ireland
2 INSIGHT, University College Dublin, Dublin, Ireland
Accurate assessments of adherence and exercise performance are required in order to ensure
that patients adhere to and perform their rehabilitation exercises correctly within the home
Inertial sensors have previously been advocated as a means of achieving these
requirements, by using them as an input to an exercise biofeedback system. This research
sought to investigate whether inertial sensors, and in particular a single sensor, can accurately
classify exercise performance in patients performing lower limb exercises for rehabilitation
Fifty-eight participants (19 male, 39 female, age: 53.9 ± 8.5 years, height: 1.69 ± 0.08 m,
weight: 74.3 ± 13.0 kg) performed ten repetitions of seven lower limb exercises (hip
abduction, hip flexion, hip extension, knee extension, heel slide, straight leg raise, and inner
range quadriceps). Three inertial sensor units, secured to the thigh, shin and foot of the leg
being exercised, were used to acquire data during each exercise. Machine learning
classification methods were applied to quantify the acquired data.
The classification methods achieved relatively high accuracy at distinguishing between
correct and incorrect performance of an exercise using three, two, or one sensor
moderate efficacy scores were also achieved by the classifier when attempting to classify the
particular error in exercise performance. Results also illustrated that a reduction in the
number of inertial sensor units employed has little effect on the overall efficacy results.

Lab Technique May Lead to Better Understanding of the Fatigued Brain

Send your doctor after this researcher to see if this may explain the blasted fatigue most survivors deal with. See page 6.
Senior Author: Mary Harrington, PhD
Smith College
Northampton, Mass.
(413) 585-3925
Lab Technique May Lead to Better Understanding of the Fatigued Brain
Animal study shows fatigue from brain inflammation found to worsen with age
A procedure that induces fatigue in mice by activating the immune system has produced new insights into the underlying neural mechanisms that trigger fatigue, a common and often disabling symptom, according to research presented today at Neuroscience 2014, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
“It’s important to have a method to induce fatigue in mice so that we can develop better clinical treatments,” said senior author Mary Harrington, PhD, of Smith College in Northampton, Mass. “With this new procedure, we can now identify the brain cells that generate fatigue in mice and are beginning to map the brain pathways by which inflammation in the brain leads to that fatigue.”
It’s estimated that more than one-third of the workforce in the United States has experienced fatigue lasting longer than two weeks, costing employers more than $100 billion every year. Chronic fatigue is also common in people with neurological disorders. Up to 40 percent of people with Parkinson’s disease and multiple sclerosis, for example, cite fatigue as being the most disabling symptom of their disease.
The procedure developed by Harrington and her colleagues uses the cytokine IL-1 to initiate fatigue in mice without other symptoms, thus allowing researchers to explore the brain pathways related specifically to fatigue. With the procedure, Harrington and her team have recently discovered that the fatigue associated with inflammation within the mouse brain gets worse with age and that it does not require, as was previously suspected, a reduction in the activity of orexin neurons, which play a big role in keeping the brain alert and awake.
Research was supported with funds from the National Institute of Nursing Research.
Scientific Presentation: Tuesday, Nov. 18, 11 a.m.–noon, Room 147B

Just 1 Gram of This Spice Boosts Memory in Six Hours - tumeric

Puffery much? Notice the untreated pre-diabetes mention, nothing on regular people. Ask your doctor first, no self prescribing.
Article here:
Just 1 Gram of This Spice Boosts Memory in Six Hours

Research it is based upon here:
Turmeric Improves Post-Prandial Working Memory in Pre-Diabetes Independent of Insulin
Hope you can read Chinese.
Background and Objectives: Cognitive impairment develops with pre-diabetes and dementia is a complication of diabetes. Natural products like turmeric and cinnamon may ameliorate the underlying pathogenesis. Methods: People≥60 years (n = 48) with newly-recognised untreated pre-diabetes were randomised to a double-blind metabolic study of placebo, turmeric (1g), cinnamon (2g) or both (1g & 2g respectively), ingested at a white bread (119g) breakfast. Observations were made over 6 hours for pre- and post-working memory (WM), glycaemic and insulin responses and biomarkers of Alzheimer's disease (AD)(0,2,4 and 6 hours): amyloid precursor protein (APP), γ-secretase subunits presenilin-1 (PS1), presenilin-2 (PS2), and glycogen synthase kinase (GSK-3β). Differences between natural product users and non-users were determined by Students t and chi square tests; and between pre-test and post-test WM by Wilcoxon signed rank tests. Interaction between turmeric and cinnamon was tested by 2-way ANOVA. Multivariable linear regression (MLR) took account of BMI, glycaemia, insulin and AD biomarkers in...

Thursday, November 27, 2014

New test to measure HDL cholesterol can predict cardiovascular risk

Do you want to know the risk and will your doctor offer the test?
A current study by the MedUni Vienna has shown that changes to the "good cholesterol" HDL (High-Density Lipoprotein) can be associated with cardiovascular diseases: by developing a new laboratory test, scientists at the Institute of Medical Genetics and the Department of Nephrology & Dialysis (University Department of Internal Medicine III) at the MedUni Vienna have demonstrated for the first time that the presence of certain proteins in the HDL can lead to an increased risk of cardiovascular disease and mortality.
HDL (High-Density Lipoprotein) is a class of proteins that plays a key role in the body's metabolism of cholesterol. HDL causes the cholesterol to be transported to the liver, where it is broken down. This gives rise to the popular name for HDL of "good cholesterol". A team led by Thomas Weichhart (Institute of Medical Genetics), Marcus Säemann and Chantal Kopecky (both from the Department of Nephrology & Dialysis at the University Department of Internal Medicine III) have demonstrated in a study involving over 1,200 patients that the presence of two specific proteins in the good HDL can be associated with a poorer prognosis in diabetic patients who require dialysis. The study has just been published in the Clinical Journal of the American Society of Nephrology.
High HDL levels are generally regarded as the best type to have and are believed to protect against cardiovascular diseases such as heart attacks and strokes. Clinical practice currently only measures the amount of cholesterol in the HDL (known as the HDL-C) and the protective effect against future cardiovascular disease is derived from this. This relationship may hold true for the healthy population. More recent research has shown, however, that in many chronic diseases such as coronary heart disease, diabetes mellitus or in patients receiving dialysis, the quantity of HDL-C in the blood cannot be used as a prognostic marker. As a result, new methods are needed in order to better estimate the risk of cardiovascular disease.
HDL is made up of only around 20 per cent cholesterol; over 50 per cent of HDL is made up of different proteins. And it is precisely this protein composition that changes in the presence of a number of different diseases. The researchers from Vienna have already demonstrated in an earlier study that two proteins in particular, namely Serum Amyloid A (SAA) and Surfactant Protein B (SP-B), are significantly raised in the HDL of dialysis patients, and these also contribute towards HDL losing its protective effect.
Test measures "dangerous" proteins
The scientists have now developed an innovative test that can quickly and directly measure the SAA and SP-B in the HDL. The HDL protein composition in over 1,200 patients requiring dialysis was analysed using this test. The results were clear. High levels of SAA in the HDL were associated with an increased occurrence of heart attacks, while high levels of SP-B in the HDL acted as a marker for a generally increased risk of mortality. This discovery could change the evaluation of HDL. "The HDL-C value continues to remain important, however the new test will also in future allow a much more precise risk prediction for cardiovascular diseases," explain the study authors, "allowing therapy to be commenced much earlier, for example through a modified lifestyle, in order to decisively improve the overall prognosis."
The laboratory test is currently being evaluated in other patient collectives in order to confirm the results in relation to other diseases such as coronary heart disease, in which the SAA and SP-B are also raised. The laboratory test is not yet being carried out routinely; an Austrian company is however currently working on its market launch.

The Application of Cycling and Cycling Combined with Feedback in the Rehabilitation of Stroke Patients: A Review

Have your doctor compare the effectiveness of recovery using cycling vs. ellipticals vs. treadmills.  You do expect your doctor to know this simple  recovery modality? Don't you? Oh my God, they mentioned test protocols.
, ,
Department of Industrial Electronics, University of Minho, Azurém, Guimarães, Portugal
Publication stage: In Press Corrected Proof
Stroke is a leading cause of long-term disabilities, such as hemiparesis, inability to walk without assistance, and dependence of others in the activities of daily living. Motor function rehabilitation after stroke demands for methods oriented to the recovery of the walking capacity. Because of the similarities with walking, cycling leg exercise may present a solution to this problem. The aim of this article is to review the state of the art applications of cycling leg exercise as a (1) motor function rehabilitation method and an (2) aerobic training method for stroke patients as well as the commonly used (3) assessment tools. The cycling characteristics and applications, the applied test protocols as well as the tools used to assess the state and the recovery of patients and types of cycling devices are presented. In addition, the potential benefits of the use of other therapies, like feedback, together with cycling are explored. The application of cycling leg exercise alone and combined with feedback in stroke rehabilitation approaches has shown promising results. Positive effects on motor abilities were found in subacute and chronic patients. However, larger and normalized studies and assessments are needed because there is a high heterogeneity in the patients' characteristics, protocols and metrics. This wil allow the comparison between different studies related with cycling.

Where are you sleeping tonight?

Last night as I walked around the neighborhood to get in my 10,000 steps for the day. This interesting sight was seen next to the curb. An army style cot with some charcoal and lighter fluid next to it. It got down to low 20's last night

I walked by again today and it is still there with the charcoal bag the same size. My speculation was  someone getting kicked out of the house or a place for a not welcomed Thanksgiving guest.

Gene that reduces risk of stroke discovered

I tore one of my carotid arteries, so I wonder if I don't have this gene or I was so violent that it overcame any protective effect this had.
There is also this blood clotting gene you may want to know about.

New stroke gene discovery could lead to tailored treatments

And this one;  alteration in a gene called HDAC9 which affects a person's risk of large artery ischemic stroke. 

Genetic variant increases risk of common type stroke

The newest article here;
Now new research by a team made up of Royal Holloway researchers together with colleagues drawn from the US and Europe offers some hope of reducing these appalling statistics.
Two pairs of major arteries in the neck, the carotid and the vertebral arteries, together called the cervical arteries, carry blood to the brain. The researchers found that people possessed of a specific variant of a gene, called Phosphatase and Actin Regulator 1 or PHACTR1 for short, are less likely to suffer a cervical artery dissection, a tear in the lining of one of these arteries. Such a tear can lead to compression of adjacent nerves and make a sufferer more likely to develop blood clots that can cause blockage of blood vessels thus restricting blood supply to the brain, so leading to a stroke.
The discovery of these beneficial properties of PHACTR1 could prompt the development of new treatments and prevention strategies for the disease, which is a major cause of stroke in young adults. The PHACTR1 gene variant has also been identified as one that protects against migraines and affects the risk of heart attack.

More at link.

New research supporting stroke rehabilitation

Ask your doctor to create a stroke protocol based on this. You do expect your hospital to have thousands of videos to watch for every possible muscle movement? Don't you?
Using world-leading research methods, the team of Dr David Wright and Prof Paul Holmes, working with Dr Jacqueline Williams from the Victoria University in Melbourne, studied activity in an area of the brain responsible for controlling movements when healthy participants observed a video showing simple hand movements and simultaneously imagined that they were performing the observed movement.
Using - a technique where a coil placed over the scalp delivers a stimulation to the , activates neurons in the underlying area, and causes a muscular contraction in the participant's hand - the researchers found that combining (imagining the feelings associated with performing the movement) with observation (watching the movement) created the strongest activity in the brain.
Using electrodes on the participant's hand, the researchers found that muscle contractions in response to the cortical stimulation were larger when participants were concurrently imagining themselves moving their muscle whilst watching a video of a hand moving on screen, compared to when they used the imagery or observation techniques alone. or engaged in various control conditions.
This research, which is published in the open-access journal Frontiers in Human Neuroscience, may provide useful applications for the care of stroke patients who have restricted use of their upper limbs. If stroke patients practice the recommended techniques, it could potentially help maintain activity in movement-related brain areas, especially when used alongside more traditional physiotherapy techniques where the same movements are also practiced physically.
Dr Wright said: "The idea is that because imagery and observation techniques share some characteristics with physical movement in terms of activating similar areas of the brain, if someone can't perform the movements themselves physically, it might be possible to keep those areas of the brain active through imagery and observation techniques. This might help contribute to the recovery of motor function."
Currently, imagery and, less frequently, observation are used separately alongside physical therapy during the rehabilitation of , but Prof Holmes suggested that combining the two techniques may support re-learning of movement patterns for some patients.
He said: "After a stroke, parts of the brain die and will not recover. To compensate, other parts of brain can alter their function to take control of the lost behaviour - a form of brain plasticity. We think that combining imagery and observation, in addition to physical therapy, may allow the brain to speed up this plastic change as well as benefitting more psychological aspects of recovery such as movement confidence". He continued, "the research team's work in this area has the potential to make a real impact on the way physiotherapists, occupational therapists and nurses work with the stroke community"
"These changes may happen without the intervention - it is certainly not a miracle cure - but the combined imagery and action observation approach should speed up the process of relearning movements that have been lost."
The research was funded by Manchester Metropolitan University's Knowledge Exchange Innovation Fund and a Research Accelerator Grant awarded to Dr Wright (an early career researcher in the Motor Cognition Research section of the Centre of Health, Exercise and Active Living).
Future research by the Group will seek to establish optimal methods for delivering these psychological interventions for stroke rehabilitation by investigating the effects of different types of instruction given to participants and different video presentation methods on activity in the brain during combined imagery and observation. The team also expect to release a stroke rehabilitation App in early 2015.
More information: Combined action observation and imagery facilitates corticospinal excitability , Frontiers in Human Neuroscience , DOI: 10.3389/fnhum.2014.00951

Cholesterol-lowering supplements: What works?

Good luck asking your doctor about these rather than statins. But it is from the Mayo Clinic.
Here are some supplements that you might hear about for high cholesterol, and what's known about them.



Fish oil


Garlic extract

  • Green tea extract


Black psyllium

Red yeast

Sitostanol and beta-sitosterol

 Details at link. Don't do this without your doctors ok.

Wednesday, November 26, 2014

Could motor unit control strategies be partially preserved after stroke?

I hate these papers that ask questions but never provide answers or stroke protocols to address the problems described.
S. Jayne Garland1*, Courtney L. Pollock2 and Tanya D. Ivanova1
  • 1Department of Physical Therapy, University of British Columbia, Vancouver, BC, Canada
  • 2Graduate Program in Rehabilitation Sciences, Department of Physical Therapy, University of British Columbia, Vancouver, BC, Canada


There is considerable evidence on the impairments that a cerebral stroke will have down-stream of the stroke, i.e., in the spinal motoneuron and the muscle. Motor impairment following stroke has been documented as force production that is slow, weak, and lacking in precision (Garland et al., 2009) and is associated with difficulty in fully activating the muscle (Klein et al., 2013). Furthermore, in functional tasks such as standing balance and gait, there is evidence of deficits in intra-limb coordination of muscles even on the non-paretic side (Marigold and Eng, 2006; Raja et al., 2012). In this opinion paper, we will first briefly review the changes observed at the level of the motor unit (MU) after stroke and second reflect upon whether some changes in the intrinsic properties of motoneurons, typically considered to be maladaptive, might also reflect a positive adaptation that could assist in force production. Lastly, this paper will explore the control of MUs between limbs during standing balance and suggest that, while some impairment may exist, there remains the possibility of a preservation of fundamental motor control strategies after stroke that might be a target for rehabilitation.

Motor Unit/Muscle Characteristics

At the level of the MU, studies have demonstrated a loss of spinal motoneurons following stroke (McComas et al., 1973; Hara et al., 2004; Lukacs, 2005; Li et al., 2011), particularly those that innervate type II MUs (Lukacs et al., 2008). It has been suggested that chronically paretic muscle is made up of fewer, but larger, MUs due to collateral sprouting of the remaining motoneurons to innervate a greater number of muscle fibers (Lukacs, 2005; Kallenberg and Hermens, 2011; Li et al., 2011) and this process could result in a mismatch of muscle fiber type and motoneuron characteristics (Young and Mayer, 1982; Dattola et al., 1993). Ultimately both of these changes may result in muscle contractions with slower rates of force development and decreased levels of force production (Garland et al., 2009).

Several pages between here at the link.

Concluding Remarks

There is no doubt that there are changes in the MU discharge characteristics after stroke. But the AHP and common drive data suggest that residual motor control strategies may remain after stroke, albeit diminished, and may reveal a need to consider functional task-dependency in future research to explore MU impairment and adaptation post-stroke. It remains to be seen whether treatments that challenge the neuromuscular system could prevent the muscle remodeling and any compensatory MU control adaptations.

Stem cell-based treatments against stroke: observations from human proof-of-concept studies and considerations regarding clinical applicability

Ask you doctor to analyze this and dertermine when stem cells might become useful for you.
Thorsten R. Doeppner* and Dirk M. Hermann
  • Department of Neurology, University of Duisburg-Essen Medical School, Essen, Germany
Ischemic stroke remains a heavy burden for industrialized countries. The only causal therapy is the recanalization of occluded vessels via thrombolysis, which due to a narrow time window still can be offered only to a minority of patients. Since the majority of patients continues to exhibit neurological deficits even following successful thrombolysis, restorative therapies are urgently needed that promote brain remodeling and repair once stroke injury has occurred. Due to their unique properties of action, stem cell-based strategies gained increasing interest during recent years. Using various stroke models in both rodents and primates, the transplantation of stem cells, namely of bone marrow derived mesenchymal stem cells (MSCs) or neural progenitor cells (NPCs), has been shown to promote neurological recovery most likely via indirect bystander actions. In view of promising observations, clinical proof-of-concept studies are currently under way, in which effects of stem and precursor cells are evaluated in human stroke patients. In this review we summarize already published studies, which due to the broad experience in other medical contexts mostly employed bone marrow-derived MSCs by means of intravenous transplantation. With the overall number of clinical trials limited in number, only a fraction of these studies used non-treated control groups, and only single studies were adequately blinded. Despite these limitations, first promising results justify the need for more elaborate clinical trials in order to make stem cell transplantation a success for stroke treatment in the future.

Resting-state functional connectivity in anterior cingulate cortex in normal aging

Ask your doctor to compare your brain connectivity post-stroke to what is normal at your age and if any deficits are found propose a stroke protocol to correct them.  Your doctor has no stroke protocols and has no idea what this means? Why the hell are you seeing such as worthless doctor?
But don't listen to me, as a non-medical stroke-addled person I can have no coherent thoughts on what the fucking hell is wrong  with stroke rehabilitation.  Does your doctor have a single coherent thought on stroke rehab? I dare you to challenge your doctor to explain exactly how you are going to 100% recover. No excuses from your doctor.

Weifang Cao1, Cheng Luo1*, Bin Zhu1, Dan Zhang1, Li Dong1, Jinnan Gong1, Diankun Gong1, Hui He1, Shipeng Tu1, Wenjie Yin2, Jianfu Li1, Huafu Chen1 and Dezhong Yao1*
  • 1The Key Laboratory for NeuroInformation of Ministry of Education, University of Electronic Science and Technology of China, Chengdu, China
  • 2Radiology Department, Chengdu First People's Hospital, Chengdu, China
Growing evidence suggests that normal aging is associated with cognitive decline and well-maintained emotional well-being. The anterior cingulate cortex (ACC) is an important brain region involved in emotional and cognitive processing. We investigated resting-state functional connectivity (FC) of two ACC subregions in 30 healthy older adults vs. 33 healthy younger adults, by parcellating into rostral (rACC) and dorsal (dACC) ACC based on clustering of FC profiles. Compared with younger adults, older adults demonstrated greater connection between rACC and anterior insula, suggesting that older adults recruit more proximal dACC brain regions connected with insula to maintain a salient response. Older adults also demonstrated increased FC between rACC and superior temporal gyrus and inferior frontal gyrus, decreased integration between rACC and default mode, and decreased dACC-hippocampal and dACC-thalamic connectivity. These altered FCs reflected rACC and dACC reorganization, and might be related to well emotion regulation and cognitive decline in older adults. Our findings provide further insight into potential functional substrates of emotional and cognitive alterations in the aging brain.

Examining the potential of creating new synapses in old or damaged brains

Only a 12 minute video by Stanford neurobiologist Carla Shatz, PhD.  What is your doctor going to takeaway from this to update your 100% recovery protocol?
Synapses are the structures in the brain where neurons connect and communicate with each other. Between early childhood and the beginning of puberty, many of these connections are eliminated through a process called “synaptic pruning.” Stroke, Alzheimer’s disease, and traumatic brain injury can also cause the loss of synapses. But what if new synapses could be created to repair aging or damaged brains?

Stanford neurobiologist Carla Shatz, PhD, addresses this question in the above Seattle+Connect video. In the lecture, she discusses the possibility of engaging the molecular and cellular mechanisms that regular critical developmental periods to regrow synapses in old brains. Watch the video to learn how advances at the neural level around a novel receptor, called PirB, have implications for improving brain plasticity, learning, memory and neurological disorders.

Previously: Drug helps old brains learn new tricks, and heal, Cellular padding could help stem cells repair injuries and Science is like an ongoing mystery novel, says Stanford neurobiologist Carla Shatz and “Pruning synapses” and other strides in Alzheimer’s research

Effect of “Deqi” during the Study of Needling “Wang’s Jiaji” Acupoints Treating Spasticity after Stroke

This does make the assumption that acupuncture actually does something. Trial was not double-blind.
I however, don't believe  because of this;

Neuro-Acupuncture and Stroke

and this:

Acupuncture is a theatrical placebo: the end of a myth - DC's Improbable Science


It's up to you and your doctor how you want to handle this.

Effect of “Deqi” during the Study of Needling “Wang’s Jiaji” Acupoints Treating Spasticity after Stroke

Huanqin Li,1 Huilin Liu,1 Cunzhi Liu,1 Guangxia Shi,1 Wei Zhou,2 Chengmei Zhao,3 Tao Zhang,1 Xuefei Wang,1 Guiling Wang,1 Yin Zhao,1 Jingqing Sun,1 Jing Wang,1 and Linpeng Wang1

1Acupuncture and Moxibustion Department, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, 23 Meishuguanhou Street, Dongcheng District, Beijing 100010, China
2Acupuncture and Moxibustion Department, Huguosi Hospital of Traditional Chinese Medicine Affiliated to Beijing University of Chinese Medicine, 83 Mianhua Alleyway, Huguosi Street, Xicheng District, Beijing 100035, China
3Traditional Chinese Medicine Department, Fangshan Hospital of Traditional Chinese Medicine, 151 Chengguan South Street, Fangshan District, Beijing 102400, China

Received 10 April 2014; Revised 1 September 2014; Accepted 6 September 2014; Published 12 November 2014

Academic Editor: David Mischoulon

Copyright © 2014 Huanqin Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Background. Acupuncture has been shown to reduce spasticity and prevent the onset of spasticity after stroke. The purpose of this study is to assess the effect of “Deqi” during needling “Wang’s Jiaji” acupoints treating spasticity in the early stage of stroke. Methods. This study is a multicenter, prospective, randomized, controlled trial. 238 patients with stroke (<21 days) participated and were randomly allocated to the verum-acupuncture () group or sham-acupuncture group (). The verum-acupuncture group received verum acupuncture required to produce the sense of “Deqi” while the sham-acupuncture group received sham acupuncture without “Deqi.” Patients in both groups followed the same 30 min acupuncture regimen 5 times per week for a period of 4 weeks. Scales of MAS, FMA, ADL, MBI, NIHSS, SS-QOL, and MRS were measured at baseline and at 2, 4, and 12 weeks after intervention. Results. Significant differences were observed between two groups. The MRS rating composition has the statistical difference after 4 weeks (). The score of MAS, FMA, Barthel, and SSQOL in verum-acupuncture group has increased significantly compared with the sham-acupuncture group after 12 weeks. There was 14% reduction of higher muscle tension in the verum-acupuncture group. Conclusion. Acupuncture “Wang’s Jiaji” points with sensation of “Deqi” in the early stage may reduce the occurrence and decrease the severity of spasticity after stroke.

Statins and delirium: Is there a role?

If we are going to use statins immediately post-stroke because of this then your doctor needs to know the downside.
Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons

The downside?
 Statins and delirium: Is there a role?
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Delirium is a serious but potentially avoidable complication in critically ill patients. Various pathophysiological processes have been associated with delirium development; however, neuroinflammation hypothesis and pleiotropic effects are the reasons why HMG-CoA reductase inhibitors have been evaluated for delirium prevention. Statin therapy is associated with favorable outcomes in critically ill patients, but significant variability of results exists in patients who received these agents postoperatively. Study design methodological weaknesses, inconsistent delirium assessment, and lack of information on sedation regimens may have confounded these outcomes. Furthermore, no evidence exists on the type of statin, lipophilic or non-lipophilic, that is associated with the most benefit or when therapy with a statin should be initiated. Thus, the efficacy of HMGM-CoA reductase inhibitors on delirium prevention has not been fully established and non-pharmacological methods should remain mainstay of therapy.

How To Use Music To Boost Athletic Performance

Whom is going to study exactly which music benefits stroke recovery? We need a specific music stroke protocol that has proven results. Otherwise we are in dangerous territory because survivors will choose their own music not knowing how dangerous that can be.
Don't do this on your own. Danger, danger Will Robinson.
And jazz is not the only music that’s been linked to athletic performance, as one of the study’s authors Dr. Ali Boolani explains:
“Other research has shown that country music improves batting, rap music improves jump shots and running is improved by any up-tempo music.
But the benefit of music in fine motor control situations was relatively unknown.
Hopefully, this is the first step in answering this question.”
You can train your doctor in music therapy with these 3 posts on music therapy.
Or these 53 posts on music.

More at link.

Relation between abnormal synergy and gait in patients after stroke

Yes, yes, we know synergy exists after stroke and is a problem. What do you suggest we do about this f*cking problem? Solutions anyone?
Kaoru Sakuma12*, Koji Ohata1, Keisuke Izumi3, Yu Shiotsuka4, Tadashi Yasui5, Satoko Ibuki1 and Noriaki Ichihashi1
1 Department of Physical Therapy, Human Health Sciences, Graduate School of Medicine, Kyoto University, 53, Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan
2 Japan Society for the Promotion of Science, 5-3-1 Kojimachi, Chiyoda-ku, Tokyo 102-0083, Japan
3 Department of Rehabilitation, Biwako Gakuen Medical and Welfare Center, Kusatsu, 8-3-113 Kasayama, Kusatsu-shi, Shiga 525-0072, Japan
4 Department of Rehabilitation, Hakuhoukai Tagawashinsei Hospital, 3638 Ooazanatsuyoshi, Tagawa-shi, Fukuoka 825-0004, Japan
5 Manufacturing Technology Section, Kawamura Gishi Co., Ltd, 1-12-1 Goryo, Daito-shi, Osaka 574-0064, Japan
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Journal of NeuroEngineering and Rehabilitation 2014, 11:141  doi:10.1186/1743-0003-11-141
The electronic version of this article is the complete one and can be found online at:

Received:11 June 2014
Accepted:18 September 2014
Published:25 September 2014
© 2014 Sakuma et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.



The abnormal synergy seen in patients after stroke is considered to limit the ability of these patients. However, in the lower extremity, antigravity torque generation rather than precise movement is needed for functions such as sit-to-stand movement and gait. Therefore, the ability to generate torque may be important either as a primary movement or as an abnormal synergy. We attempted to quantify the torque generation in the lower limb, selectively and as an abnormal synergy, and its relation with gait.


Selectively generated plantar flexion torque in the ankle and plantar flexion torque secondarily generated accompanying maximal hip extension (i.e., torque generated with abnormal synergy) were measured in subjects after stroke and control subjects. In subjects after stroke, secondary torque generation while controlling hip extension torque as 25%, 50%, and 75% of the maximal hip extension was also measured. The relation of torque generation with the gait speed and timed-up-and go test (TUG) was also analyzed.


In subjects after stroke, there was no difference between the amount of plantar flexion torque generated secondarily and the selectively generated torque, whereas the selective torque was significantly greater in control subjects. Pearson product–moment correlation coefficient analysis revealed that TUG speed is related to secondarily generated torque accompanying maximal hip extension but not with selectively generated torque.


Secondarily generated torque was found to be a factor that affects TUG speed, and the ability to generate torque even through abnormal synergy may help for gait ability in subjects after stroke. 


The results of this study revealed that in subjects after stroke, the increase in the percentage of maximum hip extension torque generated by the subjects increased the%STo. The subjects after stroke exhibited lower torque than the control group in the PTo but not in the STo. The PTo was significantly higher than the STo in the control group but not in the subjects after stroke. Our hypothesis was supported by the observation that there is a correlation between TUG and the STo in the subjects after stroke, and the principal finding of this study is that the STo was the determinant of TUG, as revealed by stepwise analysis. This is the first study that quantitatively demonstrated the inability to selectively generate voluntary torque in the lower limb, and showed that STo affects TUG in patients after stroke.

Relation between secondary torque generation and percent hip extension torque in the subjects after stroke

Controlling agonist activity is a fundamental function required in activities of daily living. Therefore, in this study, we chose a task that requires generating a certain percentage of maximum voluntary torque. The subjects after stroke showed explicit increase in the %STo as the percentage of required hip extension increased, which is consistent with the characteristics of abnormal synergy described in previous studies [8,9]. Therefore, the STo measured in this study is considered to reflect the feature of abnormal synergy.

Characteristics of primary torque and secondary torque in the subjects after stroke and the control group

In a previous study that measured the secondary torque in the ankle joint during maximum voluntary hip extension in both controls and subjects after stroke, the secondary torque was seen in both groups and no differences were found in the rate of the secondary torque to maximum voluntary ankle plantar flexion torque between the groups [13]. Similarly in this study, there were concurrent ankle plantar flexion torques measured as the STo during the generation of the maximum voluntary hip extension torque in both the controls and the subjects after stroke, and there were no differences between the controls and subjects after stroke in the STo torque normalized to body weight. In the current study, the control group could generate considerably higher PTo than STo, whereas the subjects after stroke could only generate PTo torque equivalent to their STo torque. Moreover, the gastrocnemius and the soleus, which are the agonist muscles in ankle plantar flexion, were more activated during STo than during PTo in the subjects after stroke; the opposite was observed in the controls. This is probably due to the disorganization of motor unit recruitment, rate modulation patterns [31,32], antagonist muscle weakness [33], and the abnormal corticospinal responses [34-36] that might affect the contribution of agonist activity to the voluntary torque seen in the subjects after stroke. It should also be noted that the tibialis anterior muscle activity during STo was higher than that during PTo in the subjects after stroke. The co-activation of the antagonist muscle, i.e., the tibialis anterior muscle might have inhibited the generation of plantar flexion torque as STo. However, the gastrocnemius and soleus activities during STo were not higher than those during PTo. Therefore, we conclude that the tibialis anterior muscle activity did not affect the results of this study. In the subjects after stroke, because of the inability to selectively activate the agonist muscle, the STo becomes relatively higher than the PTo.

Correlation with gait ability

The stepwise analysis revealed that the STo, and not the PTo, was the determinant of TUG. Although there was no significant relation between the STo and gait speed, the correlation coefficient was high. Therefore, we consider that there might be a relation between the STo and gait ability. In previous studies, the relation between the Brunnstrom recovery stage [19] or the Fugl-Meyer assessment [23] and gait speed was reported. However, because these clinical assessments evaluated both recovery from abnormal synergy and improvement of voluntary movement, it was unclear whether abnormal synergy or voluntary movement was related to gait speed. In this study, by quantifying the abnormal synergy measuring the joint torque, the relation between abnormal synergy and gait was revealed for the first time, showing that STo was the determinant of TUG. On the other hand, a previous study showed that the paretic ankle plantar flexion torque was correlated with gait speed in the patients after stroke [27]. We consider that because TUG consists not only of gait but also of sit-to-stand movement, which requires a large torque [37,38], abnormal synergy might be a related factor. Our results suggest that in subjects after stroke, STo might be adopted to compensate for the inability to generate the voluntary torque during gait.


Three limitations of this study need to be mentioned. First, the PTo and STo measured in this study might be affected by other factors such as co-activation and spasticity. Nevertheless, we could at least assess one aspect of abnormal synergy quantitatively as the joint torque generated concurrently with the intended voluntary torque.
Second, the subjects after stroke recruited in our study were community-dwelling, able to walk. Therefore, our results may not be applicable to patients in a more severe condition after stroke who are unable to live in the community or have greater disability in gait.
Finally, this study did not evaluate abnormal synergy during gait, or the relation of abnormal synergy with each element in gait. Therefore, the influence of abnormal synergy on each factor in gait remains unknown.


We found that the amount of secondarily generated plantar flexion torque (STo) was as large as the selectively generated plantar flexion torque (PTo), and that the STo was negatively correlated to TUG speed. This suggests that torque generation as abnormal synergy may help for patients after stroke who cannot sufficiently generate selective torque.
More details at link since you will need to figure out how to solve this yourself.

Accelerometer measurement of upper extremity movement after stroke: a systematic review of clinical studies

A study of studies. Whoopee. Create a dammed protocol for using these accelerometers and them maybe we can discuss real results.
Marika Noorkõiv12*, Helen Rodgers1 and Christopher I Price1
1 Stroke Research Group, Institute of Ageing and Health, Newcastle University, Newcastle upon Tyne, UK
2 Adeli International Rehabilitation Centre, Valge 13, Tallinn 11415, Estonia
For all author emails, please log on.
Journal of NeuroEngineering and Rehabilitation 2014, 11:144  doi:10.1186/1743-0003-11-144
The electronic version of this article is the complete one and can be found online at:

Received:29 May 2014
Accepted:2 October 2014
Published:9 October 2014
© 2014 Noorkõiv et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.


The aim of this review was to identify and summarise publications, which have reported clinical applications of upper limb accelerometry for stroke within free-living environments and make recommendations for future studies. Data was searched from MEDLINE®, Scopus, IEEExplore and Compendex databases. The final search was 31st October 2013. Any study was included which reported clinical assessments in parallel with accelerometry in a free-living hospital or home setting. Study quality is reflected by participant numbers, methodological approach, technical details of the equipment used, blinding of clinical measures, whether safety and compliance data was collected. First author screened articles for inclusion and inclusion of full text articles and data extraction was confirmed by the third author. Out of 1375 initial abstracts, 8 articles were included. All participants were stroke patients. Accelerometers were worn for either 24 hours or 3 days. Data were collected as summed acceleration counts over a specified time or as the duration of active/inactive periods. Activity in both arms was reported by all studies and the ratio of impaired to unimpaired arm activity was calculated in six studies. The correlation between clinical assessments and accelerometry was tested in five studies and significant correlations were found. The efficacy of a rehabilitation intervention was assessed using accelerometry by three studies: in two studies both accelerometry and clinical test scores detected a post-treatment difference but in one study accelerometry data did not change despite clinical test scores showing motor and functional improvements. Further research is needed to understand the additional value of accelerometry as a measure of upper limb use and function in a clinical context. A simple and easily interpretable accelerometry approach is required. 


Real-world usage of the upper extremity during stroke rehabilitation is still not yet well described and we require better knowledge of how to interpret different variables of accelerometry against clinical measures which holds meaning for clinicians and patients. Recommendations from this review of recent studies are:
– Clinical measures are still required to provide context for interpretation in case the individual’s recovery is not reflected through real world accelerometer data e.g. due to learned non-use
– The ratio between impaired and unimpaired sides is the standard approach for upper limb accelerometry but hand dominance might require further consideration depending upon individually chosen rehabilitation goals
– Diaries should be used for at least a proportion of the monitoring period in order to relate individual accelerometer data to background levels of activity.
– Simple, user-friendly cost-effective and easily interpretable upper limb accelerometry methods are still required if this is to be a useful tool to monitor patients’ progress alongside clinical assessments of motor recovery.
More detail at link.

Changes in activation timing of knee and ankle extensors during gait are related to changes in heteronymous spinal pathways after stroke

I'm sure there is something important in here that will help your walking, your therapist should be able to modify your stroke walking protocol to accommodate the newest information. I really hate these types of research, they describe a problem but give nothing on how to address it. We as survivors have to figure out all this crap ourselves.
Joseph-Omer Dyer12*, Eric Maupas3, Sibele de Andrade Melo12, Daniel Bourbonnais12, Sylvie Nadeau12 and Robert Forget12
1 Centre de recherche interdisciplinaire en réadaptation, Institut de réadaptation Gingras-Lindsay de Montréal, Montréal, Canada
2 School of Rehabilitation, Faculty of Medicine, Université de Montréal, P.O. Box 6128, Station Centre-Ville, Montréal, Quebec H3C 3 J7, Canada
3 UMT-Centre de Rééducation Fonctionnelle, Laboratoire de Physiologie de la Posture et du Mouvement PoM, Université Champollion, Albi - Université de, Toulouse, France
For all author emails, please log on.
Journal of NeuroEngineering and Rehabilitation 2014, 11:148  doi:10.1186/1743-0003-11-148
The electronic version of this article is the complete one and can be found online at:

Received:24 January 2014
Accepted:12 October 2014
Published:24 October 2014
© 2014 Dyer et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.



Extensor synergy is often observed in the paretic leg of stroke patients. Extensor synergy consists of an abnormal stereotyped co-activation of the leg extensors as patients attempt to move. As a component of this synergy, the simultaneous activation of knee and ankle extensors in the paretic leg during stance often affects gait pattern after stroke. The mechanisms involved in extensor synergy are still unclear. The first objective of this study is to compare the co-activation of knee and ankle extensors during the stance phase of gait between stroke and healthy individuals. The second objective is to explore whether this co-activation is related to changes in heteronymous spinal modulations between quadriceps and soleus muscles on the paretic side in post-stroke individuals.


Thirteen stroke patients and ten healthy individuals participated in gait and heteronymous spinal modulation evaluations. Co-activation was measured using peak EMG activation intervals (PAI) and co-activation amplitude indexes (CAI) between knee and ankle extensors during the stance phase of gait in both groups. The evaluation of heteronymous spinal modulations was performed on the paretic leg in stroke participants and on one leg in healthy participants. This evaluation involved assessing the early facilitation and later inhibition of soleus voluntary EMG induced by femoral nerve stimulation.


All PAI were lower and most CAI were higher on the paretic side of stroke participants compared with the co-activation indexes among control participants. CAI and PAI were moderately correlated with increased heteronymous facilitation of soleus on the paretic side in stroke individuals.


Increased co-activation of knee and ankle extensors during gait is related to changes in intersegmental facilitative pathways linking quadriceps to soleus on the paretic side in stroke individuals. Malfunction of intersegmental pathways could contribute to abnormal timing of leg extensors during the stance phase of gait in hemiparetic individuals. (WHAT!)
Hemiparesis; Gait; Sensory afferents; Leg extensors; Spinal pathways; Propriospinal


Following stroke, impaired coordination is frequently observed and manifests by the incapacity to activate muscles selectively [1]. This lack of voluntary control produces abnormal coupling of joint movements on the paretic side that can hamper motor task performance [1-3]. Altered motor coordination in the paretic leg among stroke patients is associated with functional deficits [4]. As a result of this lack of coordination, these patients often produce stereotypical co-activation of several muscles on the paretic side as they voluntarily attempt to move [1,5]. These co-activations, which are commonly referred to as abnormal synergies, are defined as the simultaneous recruitment of muscles at multiple joints resulting in a stereotypical pattern of movement [6]. In the paretic leg of stroke patients, prevalent extensor synergy consisting of the co-contraction (i.e., co-activation) of the majority of the leg extensor muscles is often present throughout most of the stance phase of gait [7,8]. This co-activation can be observed in EMG tracings showing the simultaneous activation of leg extensors during stance [6]. In the present study, the term “co-activation” will be used to describe the simultaneous EMG activity in knee and ankle extensor muscles [9]. This co-activation is a key component of extensor synergy [7] since it can produce abnormal coupling of knee and ankle extension, often resulting in an altered gait pattern after stroke [7,10].
Since knee and ankle extensors are both anti-gravity muscles with out-of-phase activation during healthy gait, their abnormal co-activation could contribute to hemiparetic gait disabilities. The quadriceps muscle normally reaches its peak activation during the early stance phase in order to support body weight [11]. In turn, calf muscles demonstrate maximal activity during the late stance phase in order to control ankle dorsiflexion and produce push off [12]. In hemiparetic gait, prolonged activation of the quadriceps at the end of the stance phase [8,13] may impede knee flexion in preparation for the swing phase. Premature activation of ankle extensors early in the stance phase [14,15] could hamper body weight support upon initial foot contact [7]. These changes are consistent with abnormal co-activation of leg extensors on the paretic side during the stance phase of gait [14,16].
Although the co-activation of leg extensors has been widely described in clinical literature, few studies have quantified its extent in the paretic leg during gait. The paucity of studies assessing muscular co-activation via EMG approaches may stem from limitations related to the normalization of EMG signals [17] and the determination of the timing of muscular activation [18], variables which allow inter-subject comparisons to be made. Analyses of EMG activity by factorization procedures have been used to objectively identify shared patterns of activation among different muscle groups in the paretic lower limb during gait [19,20]. Through the use of a factorization procedure, it has been shown that the number of EMG modules required to describe muscle activation patterns in the paretic leg correlates with walking performance measures in post-stroke individuals [19].
Furthermore, the underlying mechanisms of leg extensor co-activation after stroke are not fully understood. Supraspinal and spinal mechanisms may both contribute to motor deficits in the paretic leg [21-23]. Spinal interneuronal systems are basic sensorimotor mechanisms that can integrate influences from sensory and descending pathways to modulate the activity of motoneurones (MNs) [9,21]. Intersegmental or propriospinal pathways can regulate the activity of muscles acting at different joints [21,24]. In humans, these pathways are assessed with electrophysiological methods, whereby conditioning stimulation is used to modulate the activity of a heteronymous muscle [25-27]. For example, intersegmental excitatory and inhibitory pathways linking quadriceps (Quads) to soleus (Sol) can be assessed by measuring the effects of femoral nerve (FN) stimulation on Sol activity [9,21]. More precisely, FN stimulation induces early, short-term facilitation and later longer-lasting inhibition of both Sol H reflex and voluntary EMG, which have been attributed to projections from Quads to Sol group excitation and recurrent inhibition, respectively [28,29]. An increase in early heteronymous facilitation and a decrease in later inhibition of Sol activity after FN stimulation have been found in stroke subjects [21]. Moreover, based on the results of this study, increased facilitation was correlated with level of motor coordination of the paretic leg [21]. This raises the question of whether co-activation of knee and ankle extensors in the paretic leg during gait is related to transmission changes in intersegmental pathways linking Quads to Sol. This study aims to (1) compare co-activation of knee and ankle extensors during gait between stroke and healthy individuals, (2) assess whether this co-activation is related to clinical measures of motor deficits after stroke, and (3) determine whether it is related to changes in heteronymous modulations of Sol voluntary EMG after FN stimulation in the paretic leg. 

More at link.