Israeli team uses silicon chip to deliver Alzheimer’s-busting protein to brain

Is your hospital competent enough to know about this and create a protocol? 

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

Nothing done?

Laziness? Incompetence? Or just don't care? No leadership? No strategy? Not my job?

Israeli team uses silicon chip to deliver Alzheimer’s-busting protein to brain

In Technion, Bar-Ilan trials, nanochip ferries ‘neural growth factor’ — which combats neurodegenerative diseases — and releases it where needed, overcoming blood-brain barrier

By Shoshanna Solomon 26 November 2019, 12:50 pm 2  

An illustrative image of neurons, or brain cells (whitehoune; iStock by Getty Images)

Researchers at the Technion–Israel Institute of Technology and Bar-Ilan University have developed technology they hope will help inhibit the progression of Alzheimer’s disease.
The study was published recently as a cover story in the journal Small. It was led by Prof. Ester Segal and PhD student Michal Rosenberg from the Technion Faculty of Biotechnology and Food Engineering with their partners, Prof. Orit Shefi and PhD student Neta Zilony-Hanin from the Bar-Ilan University Faculty of Engineering.

Alzheimer’s, the most common form of dementia, is a neurodegenerative disease whose symptoms include memory loss, speech impairment, orientation problems, and significant impairment of motor functions.

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It primarily strikes the elderly, and among those age 85 and up it reaches a prevalence of some 30%. Due to the increase in life expectancy, the overall incidence of the disease has grown and it is today referred to as the epidemic of the 21st century.

Prof. Ester Segal, of the Technion Faculty of Biotechnology and Food Engineering (Courtesy)

The major cause of the disease is the accumulation of a protein called amyloid beta (Aβ) in brain tissues. The protein blocks and kills nerve cells, also called neurons, in different regions of the brain. This leads, in part, to damage of the “cholinergic mechanisms,” the neurons in charge of brain function.
Research has previously shown that administering a specific protein, called “neural growth factor,” inhibits damage to the cholinergic mechanisms and slows the disease’s progression, said the Technion’s Prof. Segal in a phone interview.
“In people with neurodegenerative diseases, the expression of the neural growth factor protein is reduced,” she said.
The protein is known to have restorative qualities, but the problem is how to get it to the brain, she said.
Delivering the protein to the target area is not a simple task because the brain is shielded by the blood-brain barrier from infiltration by bacteria and harmful substances in the blood.

This protective barrier, however, also restricts the passage of drugs from the bloodstream to the brain, making it difficult for brain-curing medications to get through.

Thus, the neural growth factor proteins, if given in drug form, do not pass through the barrier, and even if they could, they would not live long enough to make the long journey to the brain, Segal said.

Some clinical trials have already started injecting these neural growth factor proteins directly into the brain via a catheter, but the procedure is complicated, invasive and very risky, Segal said.

Now, the Technion and Bar-Ilan University researchers say they have created nanoscale silicon chips that could meet this challenge.

The chips allow the insertion of the curative protein directly into the brain and its release at the targeted tissue.

These chips, developed in Segal’s lab, have a nanoscale porous structure that allows them to be loaded with large amounts of the protein. Through precise control of various features, including the dimension of the chips’ pores and the chemical properties of their surface, the researchers were able to create a silicone structure that retains the protein in its active form and then releases it gradually, over a period of about a month, to the target area in the brain. After releasing the drug, the chips safely degrade in the brain and dissolve, the Technion said in a statement.

With the use of the chips as a vehicle, the protein no longer needs to cross the blood-brain barrier, since the chip is inserted directly into the brain. This is done in one of two possible ways, explained Segal.

The first is by implanting the chip into the brain. Segal admits that this procedure is also invasive, as the skull needs to be drilled into. But, she said, it is less invasive than inserting a catheter, since the chip is not inserted into the brain itself but rather is placed on the outer layer of the brain — the dura mater, a dense connective tissue that surrounds the brain and spinal cord. The researchers aim to eventually be able to load the chip with medication that releases even more gradually, over the period of a year, to prolong the drug’s effect. Currently, in trials with mice, the chip releases the proteins over a period of a month.

The second way to get the proteins to the brain is by using a “gene gun” — a device that has been developed to inject DNA into plant cells in order to transform their genetic structure.

As part of the study, Prof. Shefi of Bar-Ilan reworked the gun, transforming it into “something like a nose spray” that injects the silicon chip with the protein particles into the brain via the nose, bypassing the blood-brain barrier.

The nose has direct pathways to the brain, explained Segal “Not for nothing drug addicts sniff cocaine via their noses,” she said.

This is the first time researchers have successfully used a gene gun to directly deliver particles into a live animal brain, she said.

In a series of experiments, the researchers showed that the two ways of delivering the platform into mice brains “led to the desired result,” said Technion doctoral student Michal Rosenberg. The technology has also been tested on a cellular model of Alzheimer’s disease, where the protein release led to the rescue of the nerve cells, she said.

The team is already conducting pre-clinical studies on animals, at Bar-Ilan , Segal explained, and hopes to expand them to clinical trials if all goes as hoped.
The research was conducted with the support of the Russel Berrie Nanotechnology Institute at the Technion.

Singing Showtunes Proven To Help Fight Off Dementia, Alzheimer’s Disease

Did your doctor setup singing  for stroke recovery? Why would you expect anything different from this research?  You need dementia prevention for these reasons:

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

5. Parkinson’s Disease May Have Link to Stroke March 2017

singing (7 posts to July 2013)

Singing Showtunes Proven To Help Fight Off Dementia, Alzheimer’s Disease

A new study finds that singing songs from classic musicals can boost the brain function of people with dementia and Alzheimer’s disease, the Guardian reports.
Researchers working with elderly residents at a U.S. care facility found that those who sang their favorite showtunes showed a marked improvement in mental performance compared to other residents who merely listened.

Over the course of a four-month study, the assisted living patients were led through familiar songs from musicals such as Oklahoma, The Wizard of Oz, and Pinocchio during 50-minute sessions, but only half of the participants sung along.
While listening sparked activity in the temporal lobe on the right side of the brain, singing led to more activity in the left side.

The Sound of Music/20th Century Fox

Patients who had sung the showtunes scored higher on cognitive and drawing tests after the study, as well as on a satisfaction-with-life questionnaire. The most improvement was seen among sufferers of moderate to severe dementia.
“A lot of people have grown up singing songs and for a long time the memories are still there,” explains neuroscientist Jane Flinn. “When they start singing it can revive those memories.”
“Even when people are in the fairly advanced stages of dementia, when it is so advanced they are in a secure ward, singing sessions were still helpful,” Flinn continues. “The message is: Don’t give up on these people. You need to be doing things that engage them, and singing is cheap, easy, and engaging.”
“Somewhere Over the Rainbow,” “The Sound of Music,” and “When You Wish Upon a Star” were among the showtunes sung during the study.

Gait rehabilitation machines based on programmable footplates

My conclusion is that NOTHING SPECIFIC is known about getting you walking properly again.  You will have to figure this out yourself. Why the hell are you paying your doctors and therapists? 

Gait rehabilitation machines based on programmable footplates

 HenningSchmidt*
1,2
, CordulaWerner
2
, RolfBernhardt
1
, StefanHesse
2
 and JörgKrüger
1
 Address:
1
Department of Automation and Robotics, Fraunhofer IPK, Pascalstrasse 8-9, 10587 Berlin, Germany and
2
Department of Neurological Rehabilitation, Charité University Hospital, Kladower Damm 223, 14089 Berlin, Germany Email: HenningSchmidt*-henning.schmidt@ieee.org; CordulaWerner-cowerner@zedat.fu-berlin.de; RolfBernhardt-rolf.bernhardt@ipk.fraunhofer.de ; StefanHesse-bhesse@zedat.fu-berlin.de; JörgKrüger-joerg.krueger@ipk.fraunhofer.de* Corresponding author

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 has to 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-mobilized patients 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 multi-centre 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

Wrong,  wrong,  wrong. Survivors need rehab protocols that deliver 100% recovery. This secondary problem wouldn't exist except for the complete failure of your stroke hospital in getting survivors recovered. Address the correct problem.  

Case study: ‘Survivors need more support after leaving hospital‘

Retired engineer Martin Hally has spoken of the intense struggle faced by many stroke survivors who are denied the chance to rebuild their lives because of a lack of support and therapy.
Mr Hally (74), from Dalkey, in Dublin, suffered a stroke while he was a patient in St Vincent‘s Hospital.
“I had enjoyed great health but one morning my wife noticed I was holding a spoon awkwardly and I felt drowsy.
“I was taken by ambulance to hospital and they found I had a transient ischaemic attack (TIA), or mini stroke.
“I was just about to be discharged from hospital when I suffered a full-blown stroke.”
The stroke affected his left side and he had to learn to walk again, helped by the physiotherapy and occupational therapy he received after being discharged to the Royal Hospital in Donnybrook for a few weeks.
“I left and was walking successfully with a stick.”
However, he believes that stroke survivors are denied the chance to reach their full potential in recovery because of a lack of rehab services in hospital and the community.
:
“It is something voiced by many survivors who attend the Irish Heart Foundation (IHF) support group in Dún Laoghaire, which provides us with a great chance to meet and share our experience.”

The IHF has pointed out that a stroke patient‘s life may be saved but they typically start to regress through poor access to basic therapies in hospital.
#bb-iawr-inarticle- { clear: both; margin: 0 0 15px; }
In therapy terms, patients “effectively walk off a cliff after they pass through the hospital gates – virtually no vital physical, communication or psychological services are available unless they can afford to pay themselves”.
Mr Hally echoed the warning, saying: “I don‘t regard myself as sick. But I have found it very difficult to get physiotherapists who specialise in stroke.
“The services are very thin on the ground.”
He has suffered cellulitis, a form of infection in his foot, and also from muscle tightening on his left side.
“When you are dependent on others your life collapses. We need more help to get us more mobile. I can walk about 50 metres with great difficulty.
“But once stroke survivors leave hospital they seem to be largely forgotten about. It makes good economic sense to provide these supports in order to prevent people unnecessarily becoming a burden on society.”

Irish Independent

Implications of the AHA/ASA Updated Definition of Stroke for the 21st Century

Absolutely nothing here will help survivors recover. So useless and a waste of time.

Implications of the AHA/ASA Updated Definition of Stroke for the 21st Century

Abridged from original article by Scott E. Kasner, MD,  and Ralph L. Sacco, MD published 13 July 2018 in World Neurology Vol 28 No. 4

Note: The views expressed by the authors are their own and do not represent an official statement by the American Heart Association/American Stroke Association.

---

Stroke was defined by the World Health Organization (WHO) more than 40 years ago as “rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin.”¹ This was a working definition created for a study assessing the prevalence and natural history of stroke, and it served its purpose at the time.
The ensuing decades have witnessed major advances in basic science, pathophysiology and neuroimaging that have dramatically improved our understanding of ischemia, infarction and haemorrhage in the central nervous system (CNS). There is little doubt that permanent injury occurs well before the 24-hour threshold, and therefore purely time-based definitions are inaccurate and obsolete. Further, neuroimaging has demonstrated that clinically transient symptoms are often associated with evidence of acute cerebral infarction and that infarction may occur without overt symptoms.
In 2009, the American Heart Association/American Stroke Association (AHA/ASA) published a scientific statement redefining transient ischemic attack (TIA) as, “a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia without acute infarction.”² This statement formally addressed only one side of the proverbial coin, but clearly implied that objective evidence of infarction should be considered as a defining feature of stroke.

The new definition harmonizes with our understanding of the pathophysiology of infarction and with the recent redefinition of TIA, but also necessitates the inclusion of silent infarction and silent hemorrhage within the broad definition of stroke.

In the spring of 2013, the AHA/ASA published an expert consensus document with a new definition of stroke to reflect these advances.³ Authors with expertise in the fields of neurology, neurosurgery, neuroradiology, neuropathology, clinical research methods, epidemiology, biomarkers, policy and global public health were invited from within the AHA/ASA, as well as the American Academy of Neurology, the American Association of Neurological Surgeons and Congress of Neurological Surgeons, U.S. Centers for Disease Control and Prevention, the National Institute of Neurological Disorders and Stroke, the European Stroke Organization (ESO), the World Stroke Organization (WSO) and others to establish a universal definition of stroke.
The major fundamental change compared with older definitions is that the new broader definition of stroke includes any objective evidence of permanent brain, spinal cord or retinal cell death due to a vascular cause based upon pathological or imaging evidence with or without the presence of clinical symptoms.  Ultimately, the leaders of the ESO and WSO withdrew from participation and declined to endorse the statement because they disagreed about the inclusion of silent cerebral infarction and silent cerebral haemorrhage within the lexicon of stroke. (See “Stroke Definition in the ICD-11 at the WHO.“)
The AHA/ASA defined CNS infarction based on pathological, imaging or other objective evidence of infarction. In the absence of this evidence, the persistence of symptoms of at least 24 hours or until death remained a method to define stroke. At present, imaging is not always available and also is not perfect. In much of the developing world and in rural parts of more developed regions, neither [CT or MRI] may be available in the acute setting, if at all, which limits the global applicability of an imaging-based definition of stroke.
Silent lesions have been recognized pathologically as infarctions and haemorrhages since the 1960s but were deemed of uncertain importance. However, they may not be entirely asymptomatic, as patients may have subtle cognitive, gait or other functional impairments in the absence of a typical acute presentation. To some extent, the “silence” of an infarction or haemorrhage depends on the eye of the beholder. Patients may not be aware of their symptoms due to neglect, denial or simply may attribute them to another cause and not seek a medical opinion. Physicians and other health care providers may vary in their ability to detect mild neurologic abnormalities, or they, too, may ascribe them to an alternative cause.
The AHA/ASA included silent CNS infarctions and haemorrhages within the broadest definition of stroke for multiple reasons.

Implications for World Neurology

The new tissue-based definition of CNS infarction depends on either early objective (currently neuroimaging) evidence of infarction or persistence of symptoms for at least 24 hours. If early imaging is not available, then clinicians are left with a diagnostic dilemma in those first 24 hours since the event cannot be clearly classified as stroke.
Ultimately, diagnostic techniques and/or time will help define infarct or haemorrhage based on objective imaging, or TIA in the absence of positive imaging and resolution of symptoms within 24 hours from onset. A major challenge for the future will be the achievement of access to diagnostic and treatment tools in the developing world, where a substantial portion of the global burden of stroke occurs.
The inclusion of silent infarcts and microhemorrhages within the AHA/ASA definition of stroke opens many questions for clinicians. In regions with little or no access to neuroimaging, this change in definition may prove irrelevant for many years to come. However, for those with such access, silent lesions are likely to be detected as a result of the widespread use of MRI for non-cerebrovascular symptoms such as headache or dizziness.
Updating the definition of the disease can have prominent effects on disease surveillance and assessments of public health.  In the case of adding a large number of silent infarction cases to the existing number of stroke cases, this will increase the total number of stroke cases while likely decreasing the mortality rate due to the addition of a number of minor/silent cases.⁴ Updating the definition of stroke could result in reclassification of stroke cases for incidence, prevalence, and mortality in national and international statistics, disease classification coding systems and existing health surveys. This is particularly problematic if definitions are applied differently in each region of the globe, and this is a major concern of all stroke organizations. Therefore, the AHA/ASA recommended that symptomatic and silent infarctions and haemorrhages should be counted separately to allow for valid analyses of temporal and geographic trends in stroke. Although the WSO, ESO and WHO will not include the silent lesions within the definition of stroke, they recognize their importance and are going to start counting them within the scope of cerebrovascular disorders in the ICD-11.

Read the full article 

---

At the time of print, Kasner is with the University of Pennsylvania and Sacco is with the University of Miami.
References

1. Aho K, Harmsen P, Hatano S, Marquardsen J, Smirnov VE, Strasser T. Cerebrovascular disease in the community: results of a WHO collaborative study. Bull World Health Organ. 1980;58:113-130.
2. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, Higashida RT, Johnston SC, Kidwell CS, Lutsep HL, Miller E, Sacco RL. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40:2276-2293.
3. Sacco RL, Kasner SE, Broderick JP, Caplan LR, Connors JJ, Culebras A, Elkind MS, George MG, Hamdan AD, Higashida RT, Hoh BL, Janis LS, Kase CS, Kleindorfer DO, Lee JM, Moseley ME, Peterson ED, Turan TN, Valderrama AL, Vinters HV. An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;44:2064-2089.
4. Pia Sormani M. The Will Rogers phenomenon: the effect of different diagnostic criteria. J Neurol Sci. 2009;287 Suppl 1:S46-49.

Understanding gait control in post-stroke: Implications for management

Survivors don't give a shit about 'management'. They want EXACT STROKE PROTOCOLS that deliver 100% recovery. WHEN THE HELL will you get there? Useless generalities. 

Understanding gait control in post-stroke: Implications for management

 Rajesh  Verma, DM (Neurology), DNB (Neurology), Professor, Kamal Narayan Arya, MOT, PhD (Scholar), Sr. Occupational Therapist*,Pawan Sharma, MD (Medicine), Sr. Resident, DM (Neurology)-III,R.K. Garg, DM (Neurology), Professor & HOD
Department of Neurology, CSM Medical University (KGMU), Lucknow 226003, UP, India
Received 7 September 2010; received in revised form 2 December 2010; accepted 3 December 2010
KEYWORDS
Gait; Locomotion; Stroke; Hemiparesis; Rehabilitation
Summary
 The role of the brain in post-stroke gait is not understood properly, although the ability to walk becomes impaired in more than 80% of post-stroke patients. Most, however, re-gain some ability to walk with either limited mobility or inefficient, asymmetrical or unsafe gait. Conventional intervention focuses on support of weak muscles or body part by use of foot orthosis and walking aids. This review provides an overview of available evidence of neuro-kinesiology & neurophysiology of normal and post-stroke gait. The role of the spinal cord has been explored, more in animals than humans. Mammalian locomotion is based on a rhythmic, “
 pacemaker
” activity of the spinal stepping generators. Bipedal human locomotion is different from quadripedal animal locomotion. However, knowledge derived from the spinal cord investigation of animals, is being applied for management of human gait dysfunction. The potential role of the brain is now recognized in the independent activation of muscles during walking. The brain modifies the gait pattern during the complex demands of daily activities. Though the exact role of the motor cortex in control of gait is unclear, available evidence may be applied to gait rehabilitation of post-stroke patients.
ª
 2010 Elsevier Ltd. All rights reserved.
Introduction
Stroke is the second leading cause of death and one of theleading causes of adult disability in the world today(Gresham et al., 1997). Ability to walk gets impaired inmore than 80% of post-stroke patients (Duncan et al., 2005;
* Corresponding author. Pt. Deendayal Upadhyaya Institute for the Physically Handicapped, University of Delhi, Ministry of SocialJustice & Empowerment, Govt. of India, New Delhi 110002, India.
E-mail address:
 kamalnarya@yahoo.com (K.N. Arya).
available at www.sciencedirect.comjournal homepage: www.elsevier.com/jbmt
Journal of Bodywork & Movement Therapies (2012)
 16
, 14
e
211360-8592/$ - see front matter
 ª
 2010 Elsevier Ltd. All rights reserved.doi:10.1016/j.jbmt.2010.12.005

Benefits of stem cell heart therapy may have nothing to do with stem cells, a study on mice suggests

Will this change the moon shot of stem cells for stroke?  WHOM in control in stroke will evaluate this to see where stem cell research should go? WITH NO STROKE LEADERSHIP nothing will occur. 

Benefits of stem cell heart therapy may have nothing to do with stem cells, a study on mice suggests

“Paradigm-shifting” study shows stem cells don’t even have to be alive to heal the heart.

In this microscope image, immune cells (shown in red and green) flock to the injured region of a damaged mouse heart three days after researchers injected adult heart stem cells within the yellow dotted area. Researchers found that injecting living or dead stem cells triggers a healing immune response. (Cincinnati Children's)

By Carolyn Y. Johnson 

November 27, 2019 at 1:00 PM EST

For 15 years, scientists have put various stem cells into seriously ill patients’ hearts in hopes of regenerating injured muscle and boosting heart function. A new mouse study may finally debunk the idea behind the controversial procedure, showing the beneficial effects of two types of cell therapy are caused not by the rejuvenating properties of stem cells, but by the body’s wound-healing response — which can also be triggered by injecting dead cells or a chemical into the heart.

The discovery will have to be repeated and investigated in human tissue, but the emergence of a likely explanation for how heart cell therapy can have modest benefits comes after years of hype, hope and disagreement about stem cells’ potential to heal broken hearts. Experimental therapies have been tested in hundreds of patients with heart disease, even as doubts have grown about the underlying scientific rationale. The idea that the cells could regenerate the heart was intuitively attractive and captured a field searching for therapies to offer desperate patients, and many scientists started companies to try to commercialize different cell types. The new work provides a long-awaited explanation — one that some outside scientists argued does not support more trials with the cells.

“It’s sort of an ‘Aha!’ feeling,” said Christine Mummery, a developmental biologist at the Netherlands’ Leiden University Medical Center not involved in the study. “My personal view is that we’ve done so many of these studies, particularly for the heart, I think it would be a waste of time starting up any new ones. Whether or not the old ones should be continued — I call it expensive homeopathy."

Stroke Care 2 Stroke rehabilitation

I have seen nothing that supports that multidisciplinary units are doing anything other than taking credit for spontaneous recovery and

the Hawthorne effect.

Other than that this is all generalities, so useless. 

Stroke Care 2 Stroke rehabilitation

Series
www.thelancet.com

Vol 377 May 14, 2011
1693
Lancet
 2011; 377: 1693–702
See
Editorial
page 1625See
World Report
 page 1639This is the second in a
Series
 of two papers about stroke care
Academic Section of Geriatric Medicine, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Royal Infirmary, Glasgow, UK
 (Prof P Langhorne PhD)
; Stroke Division, Florey Neuroscience Institutes, Melbourne, VIC, Australia
(Prof J Bernhardt PhD)
; La Trobe University, Bundoora, VIC, Australia
 (J Bernhardt)
; Department of Rehabilitation Medicine, Research Institute MOVE, VU University Medical Centre, Amsterdam, Netherlands
(G Kwakkel PhD)
; and Rudolf Magnus Institute, University Medical Centre Utrecht, Utrecht, Netherlands
(G Kwakkel)Correspondence to:Prof Peter Langhorne, Academic Section of Geriatric Medicine, Institute of Cardiovascular and Medical Sciences, Level 4, Walton Building, Royal Infirmary, Glasgow G4 0SF, UK
peter.langhorne@glasgow.ac.uk
Stroke Care 2Stroke rehabilitation
Peter Langhorne, Julie Bernhardt, Gert Kwakkel
Stroke is a common, serious, and disabling global health-care problem, and rehabilitation is a major part of patient care. There is evidence to support rehabilitation in well coordinated multidisciplinary stroke units or through provision of early supported provision of discharge teams. Potentially beneficial treatment options for motor recovery of the arm include constraint-induced movement therapy and robotics. Promising interventions that could be beneficial to improve aspects of gait include fitness training, high-intensity therapy, and repetitive-task training. Repetitive-task training might also improve transfer functions. Occupational therapy can improve activities of daily living; however, information about the clinical effect of various strategies of cognitive rehabilitation and strategies for aphasia and dysarthria is scarce. Several large trials of rehabilitation practice and of novel therapies (eg, stem-cell therapy, repetitive transcranial magnetic stimulation, virtual reality, robotic therapies, and drug augmentation) are underway to inform future practice.

Alternative Motor Task-Based Pattern Training With a Digital Mirror Therapy System Enhances Sensorimotor Signal Rhythms Post-stroke

Survivors don't care about cortical activation, they want to know about protocols that deliver recovery results.  This peripheral research shit needs to stop. If we had a stroke strategy and were following it, this waste of time wouldn't occur. 

Alternative Motor Task-Based Pattern Training With a Digital Mirror Therapy System Enhances Sensorimotor Signal Rhythms Post-stroke

Chao-Sheng Chang^1,2, Ying-Ying Lo¹, Chien-Liang Chen³, Hsin-Min Lee³, Wei-Chi Chiang⁴ and Ping-Chia Li^4*

• ¹Department of Healthcare Administration, I-Shou University, Kaohsiung, Taiwan
• ²Department of Emergency Medicine, E-Da Hospital, Kaohsiung, Taiwan
• ³Department of Physical Therapy, I-Shou University, Kaohsiung, Taiwan
• ⁴Department of Occupational Therapy, I-Shou University, Kaohsiung, Taiwan

Mirror therapy (MT) facilitates motor learning and induces cortical reorganization and motor recovery from stroke. We applied the new digital mirror therapy (DMT) system to compare the cortical activation under the three visual feedback conditions: (1) no mirror visual feedback (NoMVF), (2) bilateral synchronized task-based mirror visual feedback training (BMVF), and (3) reciprocal task-based mirror visual feedback training (RMVF). During DMT, EEG recordings, including time-dependent event-related desynchronization (ERD) signal amplitude in both mu and beta bands, were obtained from the standard C3 (ispilesional hemisphere, IH), C4 (contralesional hemisphere, CH), and Cz scalp sites (supplementary motor area, SMA). The entire ERD curve was separated into three time-phases: P0 (−2 to 0 s), P1 (0 to 2 s), and P2 (2 to 4 s). Four-way and subsequent repeated-measures analyses of variance were used to examine the effects of group (stroke vs. control group), test condition (NoMVF, BMVF, and RMVF), time-phase (P0, P1, and P2), and brain area (IH, CH, SMA) on the ERD areas (%) in mu and beta bands. For the mu band, generally, ERD areas (%) were larger in the control than in the stroke group. The ERD areas (%) were largest under the RMVF condition, followed by BMVF and NoMVF conditions. Similar results were found in the beta bands. The main effects of group, time-phase, and test condition on the ERD areas (%) were significant for the three brain areas, except the main effect of group in the SMA (Cz) and CH (C4) brain area. The ERD areas (%) were larger in the control than in the stroke group. The ERD area (%) was significantly larger during P1 than during P0 and P2 (ps < 0.02), and during P2 than during P0 (ps < 0.01). The ERD area (%) under the RMVF condition was significantly larger than that under the BMVF condition and NoMVF condition (ps < 0.05). The present study suggests that cortical activation particularly in the SMA (Cz) of the brain increases in the RMVF condition in both healthy subjects and stroke patients. This result supports the hypothesis that stroke patients may benefit from RMVF training.

Gait Training Induced Change in Corticomotor Excitability in Patients With Chronic Stroke

I got nothing out of this. NO PROTOCOL,  nothing distributed worldwide. No definition of what type of treadmill; rotating, split-belt, type of BWSTT. 'May' is not good enough, we need specifics. 

Gait Training Induced Change in Corticomotor Excitability in Patients With Chronic Stroke

Chu-Ling Yen, MS, PT, Ray-Yau Wang, PhD, PT, Kwong-Kum Liao, MD, Chia-Chi Huang, MS, PT, and Yea-Ru Yang, PhD, PT

Background. 

Numerous studies have reported the effects of gait training on motor performance after stroke. However, there is limited information on treatment-induced changes in corticomotor excitability. Objectives.

The purpose of the study was to investigate the effects of additional gait training on motor performance and corticomotor excitability and to demonstrate the relationship between motor improvement and corticomotor excitability change in patients with chronic stroke. 

Methods. 

Fourteen patients were randomly assigned to the experimental or control group. Participants in both groups participated in general physical therapy. Those in the experimental group received additional body weight− supported treadmill training for 4 weeks. All participants received baseline and posttreatment assessments. The outcome measures included assessment of the Berg Balance Scale (BBS) and gait parameters. Focal transcranial magnetic stimulation was used to measure the motor threshold, map size, and location of the amplitude-weighted center of gravity of the motor map for the tibialis anterior (TA) and abductor hallucis (AH) muscles. 

Results.

After general physical therapy, we noted that the patients showed an improvement only in walking speed and cadence, and there were no significant changes in corticomotor excitability. After additional gait training, participants improved significantly on BBS score, walking speed, and step length. Moreover, the motor threshold for TA decreased significantly in the unaffected hemisphere.The map size for TA was increased in both hemispheres, whereas that for AH was increased only in the affected hemisphere. There were significant differences between the change scores of the

groups in terms of walking speed, step length, and motor threshold for TA in the unaffected hemisphere and map size for AH in the affected hemisphere. Additionally, the changes in corticomotor excitability correlated with functional improvement. 

Conclusions. 

Additional gait training may improve balance and gait performance and may (NOT good enough)induce changes in corticomotor excitability.

Key Words: Body weight–supported treadmill training—Balance and gait—Transcranial magnetic stimulation—Corticomotor excitability—Stroke.
From the Institute and Faculty of Physical Therapy, National YangMing University, Taipei, Taiwan (CLY, RYW, YRY); the Neurological Institute (KKL), and Physical Therapy, Department of Physical Medicine and Rehabilitation (CCH), Taipei Veterans General Hospital, Taipei, Taiwan; and the Department of Education and Research (RYW), and Section of Physical Therapy (YRY), Taipei City Hospital, Taipei, Taiwan.
Address correspondence to Yea-Ru Yang,PhD, Institute and Faculty of Physical Therapy, National Yang-Ming University, Taipei,Taiwan,155, Sec. 2, Li-Nong St, Beitou District, Taipei, 112, Taiwan. E-mail: yryang@ym.edu.tw.
Yen C-L, Wang R-Y, Liao K-K, Huang C-C, Yang Y-R. Gait training–induced change in corticomotor excitability in patients with chronic stroke. Neurorehabil Neural Repair 2008;22:22-30.

Toyota launches new version of walking rehabilitation robot

Do you really think your stroke hospital will purchase this? I see nothing here that suggests that stroke survivors can get walking 100% recovered using this while in the hospital. 

Your doctor should be comparing this to all these:
the Esko exoskeleton
the Walk Again Project
the HULC exoskeleton system ready for soldier tests
Is this better than Cyberdyne Hal from Japan?
Or maybe the Delta6 Accelerator from  G.I. Joe: The Rise of Cobra?

Toyota launches new version of walking rehabilitation robot

Toyota has launch the new version of its Welwalk WW-2000, a robot designed to provide rehabilitation support to individuals with lower limb paralysis as a result of stroke and other causes.
Orders for the new model commenced in November 2019 and planned to be delivered in February 2020.
The Welwalk WW-2000 upgrades the various features of the prior model (the Welwalk WW-1000), namely the rehabilitation support functions based on motor learning theory and the ease of use in clinical settings.
Specifically, it adds functions that display assistance settings in real time to improve abnormal gait as well as a game function that helps maintain motivation so patients continue their rehabilitation efforts.
The adoption of these new functions reduces burdens on therapists compared to the previous model while providing more efficient walking training to patients.

The prior model was provided on a rental basis to medical institution, but in light of requests from healthcare institutions and market assessments, the Welwalk WW-2000 will be made available for purchase with the aim of improving overall quality of service.
In addition, production will be implemented at the Motomachi Plant, with a sales target of 50 units sold to medical institutions annually.
In line with the vision of “freedom of mobility for all, and the joy of self-reliance”, Toyota has been developing rehabilitation assist robots in collaboration with Fujita Health University in Toyoake City, Aichi Prefecture since the end of 2007, with the robots used in pilot testing in healthcare settings and clinical research at medical institutions starting in 2011.
In 2017, rental of the Welwalk WW-1000, which was the first Toyota product to receive approval as a medical device, commenced.
The Welwalk WW-1000 received the 8th Robot Award in 2018, and to date, it has been used at approximately 80 medical institutions in Japan.
With the launch of the Welwalk WW-2000, Toyota hopes to bring the “joy of walking with one’s own feet” to even more patients while reducing burdens on therapists.
Prices being quoted by Toyota are $215,000 to purchase the hardware and then $450 a month in maintenance starting from the second year.

Kessler Foundation participates in new study to test innovative treatment for hand paralysis

What is your doctor doing CURRENTLY to get your hand back? Or will this maybe BE AVAILABLE for your children and grandchildren?  

Kessler Foundation participates in new study to test innovative treatment for hand paralysis

• Download PDF Copy

Reviewed by Kate Anderton, B.Sc. (Editor)Nov 26 2019

Kessler Foundation is participating in a phase II multi-site study of an innovative treatment to improve hand function in stroke survivors. Olga Boukrina, PhD, research scientist in the Center for Stroke Rehabilitation Research, is the site's principal investigator. The study is funded through a five-year $3.2 million grant from the National Institutes of Health awarded to the principal investigator, Jayme S. Knutson, PhD, director of Research and associate professor of Physical Medicine and Rehabilitation at the MetroHealth System and Case Western Reserve University.
This is the first multi-site clinical trial of contralaterally controlled functional electrical stimulation (CCFES), a new rehabilitation intervention for hand recovery following stroke developed by Knutson and colleagues. With CCFES, electrical stimulation is applied to the muscles of the weak hand through surface electrodes, causing the weak hand to open, a function that is often lost in stroke survivors. The patient controls the stimulation to their weak hand through a glove with sensors worn on their opposite, unaffected hand. Opening their unaffected hand delivers a proportional intensity of electrical stimulation that opens their weak hand, and enables them to practice using their hand in therapy. Researchers will enroll 129 patients who are 6 to 24 months post stroke who have upper extremity hemiparesis and limited hand movement.

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The effectiveness of CCFES will be compared with two other treatments -- cyclic neuromuscular electrical stimulation (CNMES), which has pre-set duration and intensity of stimulation and operates independent of patient control, and traditional task-based training without stimulation. Participants will be randomly assigned to one of the three treatment options for 12 weeks. The research teams will administer the treatments and conduct blinded outcome assessments. The durability of functional improvements will be evaluated at 6-month follow-up. Study sites include the MetroHealth System (Jayme Knutson, PhD), the Cleveland Clinic (Ela Plow, PT, PhD), Emory University (A.M. Barrett, MD), and Johns Hopkins University (Preeti Raghavan, MD).

Because hand function is integral to so many activities of daily living, advances that improve function can have significant effect on the lives of stroke survivors. This study will help determine the optimal method for restoring hand function. We anticipate that putting the patients in control of stimulating their weak hand with CCFES may activate neuroplastic changes that lead to greater and longer lasting functional gains."

Dr. Olga Boukrina, research scientist in the Center for Stroke Rehabilitation Research

Source:

Kessler Foundation

By age 85, half of you reading this article today will have developed Alzheimer’s disease, with or without a family history.

This is it, what is your doctor doing to prevent it? 

 I'm doing this.

Dementia prevention 19 ways

Don't follow me, I'm not medically trained.

A clue to a cure for Alzheimer’s disease

Posted November 27, 2019, 10:30 am

Andrew E. Budson, MD
Contributor

Are you worried about Alzheimer’s disease? Does one of your parents or siblings have the disease? If so, your risks are between two and four times that of the general public. What about people without a family history of the disease? Unfortunately, everyone is at risk for it. By age 85, half of you reading this article today will have developed Alzheimer’s disease, with or without a family history.

Sounds pretty scary, doesn’t it?

I’m writing today to give you some good news. A new study from the lab of Harvard researcher Yakeel Quiroz, PhD, has suggested a new target for drugs that might have the potential to slow down or even stop Alzheimer’s disease in its tracks.

A family with early-onset disease — and one exception

Dr. Quiroz, her longtime colleague Dr. Francisco Lopera, and first author Dr. Joseph Arboleda-Velasquez have been studying a large family in Colombia, South America, some of whom have a mutation in the presenilin 1 gene that causes early-onset Alzheimer’s disease. Over 1,000 people in this family are affected by the mutation. Among these family members, early symptoms of Alzheimer’s, such as memory loss and word-finding difficulties, almost always develop around age 44, and dementia follows at around age 49. Sometimes individuals may develop these symptoms or dementia one, two, or even three years later. But not 10 or 20 years later — and certainly not 30 years later. Yet one individual — a woman in her 70s with this genetic mutation — is only now starting to show symptoms.

The study, reported in the November 2019 issue of Nature Medicine, is a case report and extensive analysis of this one woman.

The APOE gene can modify your risk of Alzheimer’s

Many people have read or heard about variations in the APOE gene as a risk factor for Alzheimer’s. Interestingly, in their inquiry into why this woman with a mutation for early-onset Alzheimer’s had not yet developed dementia, the researchers found that she had an additional mutation in her APOE gene.

APOE has been linked to ordinary, late-onset Alzheimer’s disease and comes in three common forms. Most people, about 70% to 75%, have APOE3. About 15% to 20% of people have an APOE4 gene, and about 5% to 10% of people have an APOE2 gene.

• If you have one APOE4 gene, your risk of developing Alzheimer’s disease is three to four times more likely than if you only have APOE3 genes.
• If you have one APOE2 gene, your risk of developing Alzheimer’s disease is somewhat less than if you only have APOE3 genes.

This woman’s mutation of her APOE gene is an unusual variant called APOE3Christchurch (APOE3ch), named after the New Zealand city where it was first discovered. Even more unusual is the fact that she had two versions of this mutation, meaning that both her father and her mother gave it to her. The researchers wondered if this APOE3ch mutation could be the cause of her resistance to Alzheimer’s disease.

Resistance to tau

Another piece of the puzzle relates to an abnormal protein called tau. Tau is associated with the destruction of brain cells in Alzheimer’s disease. Tau is thought to accumulate in the brain after amyloid protein — the pathologic hallmark of Alzheimer’s disease — forms plaques. Although her brain was full of abnormal amyloid plaques — even more so than most people with full-blown Alzheimer’s dementia — she had relatively little tau.

Now the question was, could the APOE3ch mutation be related to the small amounts of tau protein? Although the answer is far from settled, the researchers did uncover some clues through laboratory experiments. Their findings suggest that the APOE3ch mutation may reduce the uptake of tau in brain cells. In addition, they were able to produce similar beneficial results using a special protein they created in the laboratory to try to mimic the effects of the APOE3ch mutation.

Where we are now

In brief, these Harvard researchers have a viable hypothesis to explain why this woman has been highly resistant to developing Alzheimer’s disease dementia. Moreover, their work suggests a possible path to a treatment that could be beneficial for all forms of Alzheimer’s disease.

We are still years away from a human treatment. The next step will be to try to treat laboratory models of Alzheimer’s disease in rodents, and then clinical trials in people with the disease after that. But in my view, this paper has provided the scientific community with a clue that may lead us to an eventual cure for Alzheimer’s disease.