What should your doctor be doing the first week you are in the hospital?

What is your doctor's plan? The only plan is for 100% recovery, don't let your doctor talk of anything less.     SPECIFICALLY!  If your doctor hems and haws and uses the craptastic saying: 'All strokes are different, all stroke recoveries are different'. It means your doctor knows ABSOLUTELY NOTHING ON HOW TO GET YOU RECOVERED! But since  I'm not medically trained  you can't listen to anything I say. 

My doctor wrote 3 prescriptions for E.T.(Evaluate and Treat) to PT, ST, OT, and did nothing the first week allowing 5.4 billion neurons to die.   Meaning he knew ABSOLUTELY NOTHING ABOUT STROKE RECOVERY.

 

Your doctor should have very specific treatment plans for every one of these problems.  If your doctor doesn't know of all these and have treatment plans then you don't have a useful doctor, trade for something better.

 Your doctors and hospital  have known for decades that stroke recovery doesn't work.  Only 10% of patients get to full recovery.

Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

 Every single one of the following sections needs a SPECIFIC PROTOCOL FROM YOUR DOCTOR if they are competent at all.

First, create an objective diagnosis of exactly what area of the brain is dead or dying and map that to the deficits presented.

Start all the protocols necessary to stop the 5 causes of the neuronal cascade of death in the first days. I lost 5.4 billion neurons because my doctor did nothing that first week.  If I had only lost 177 million neurons in the 90 minutes it took me to get tPA I would have easily recovered by now.

 tPA only fully works to reverse the stroke 12% of the time. Known since 1996. What is your doctor doing to ensure that you still get to full recovery if tPA doesn't fully work?  Your doctor has had 26 years to work out a solution.  WHERE IS IT?

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30% of survivors having sleep problems.

What is your doctor's sleep protocol? Do sleeping pills even create good sleep?

 

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Stop brain atrophy due to lack of sleep and all other causes.  What is your doctor's brain atrophy prevention protocol?

Lack of sleep may shrink your brain September, 2014:

• brain atrophy (11 posts to July 2015)

• cerebral atrophy (2 posts to April 2016)

• Cortical atrophy (1 post to February 2019)
  

• Frontal Cortical Atrophy (1 post to June 2016)

• hippocampal atrophy (1 post to October 2019)

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You do have a 23% chance of stroke survivors getting PTSD.

What is your doctor's protocol to prevent that? And if not prevented what is the protocol to treat it?

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Only 10% of patients get to full recovery. How is your doctor ensuring you are one of them?

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Your risks of dementia, has your doctor told you of this?

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

Where are the  protocols to prevent your dementia?

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 How is your stroke doctor preventing your 39% chance of post stroke delirium?

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The researchers found that 21% of patients had developed cachexia one year later.

Weakness and wasting of the body due to severe chronic illness.

What is your doctors prevention protocol on this? 

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Post stroke anxiety(20% chance).  

What are your doctor's protocols to prevent that?

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Post stroke depression(33% chance).

What are your doctor's protocols to prevent that? The correct solution is to have EXACT STROKE PROTOCOLS LEADING TO 100% RECOVERY. Your survivor will be too busy counting reps and looking forward to recovery to get depressed. Treatment after already depressed is totally the wrong solution. PREVENT IT FROM OCCURRING!

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We've known for years that seizures can occur post stroke. What is your doctor doing to prevent them?

• 5% epiletic seizures after stroke (1 post to April 2021)

• 10% seizures post stroke (15 posts to April 2017)

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 What is your doctor doing to ensure you aren't having 69% sedentary time while in the hospital?  If you aren't doing direct therapy with therapists you should have thousands of hours of action observation videos.

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The occurrence of shoulder pain after stroke is quite common in hemiplegia with an estimated incidence between 16% and 84%. 

What is your doctors EXACT PROTOCOL to prevent such shoulder pain. PREVENT, not treat after the fact. 

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YOUR DOCTOR'S RESPONSIBILITY IS TO GET EXACT DIET PROTOCOLS CREATED. No protocols s/he needs to be fired. I take no prisoners in trying to get stroke solved by those who are responsible for solving it. In fact I would have the board of directors fired for incompetency also.

 

Diet: Your doctor is responsible for having the dietician create diets for ALL THESE:

For stroke prevention; for stroke recovery; for dementia prevention; for cognitive improvement; for cholesterol reduction; for plaque removal; for Parkinsons prevention; for inflammation reduction; for blood pressure reduction; for dementia prevention; for Alzheimer's prevention.

In case your doctor does nothing you can start guessing by reading all these:

• diet (433)

• diet diversity (1)

• diet drinks (8)

• diet protocols (3)

• diet soda (2)

• diet supplements (7)

• dietary cholesterol (2)

• dietary fats (2)

• dietary guidelines (11)

• dietary inflammatory index (2)

• dietary inflammatory potential (1)

• DASH diet (9)

• Atkins diet (1)

• protein diet (1)

• Portfolio diet (1)

• Plant-Based Diet (1)
  

• paleo diet (2)

• Nordic diet (2)

• MIND Diet (17)

• Mediterranean diet (67)

• low-salt diet (1)

• Low-carb diet (1)

• Ketogenic diet (18)
  

• high-sucrose diet (1)

• High-fructose diet (2)

• high-glycemic diet/ (1)

• high-fat diet (2)

• EVOO-enriched diet (1)

• Vegetarian Diet (4)

The role of diet in secondary stroke prevention

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20-25% apathy post stroke

 This is a secondary problem which is solved by having

EXACT STROKE PROTOCOLS LEADING TO 100% RECOVERY. Your survivor will be too busy counting reps and looking forward to recovery to be apathetic.

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The incidence of constipation for stroke was 48%.

What is your doctor's solution? You can't do marijuana until your doctor prescribes it.

Marijuana use linked with decreased constipation

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The results of the tests revealed that over 50% of the stroke patients had attention disorders that had not been diagnosed.  

Has your doctor diagnosed this and created a treatment plan for it?

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 These are your likely cognitive problems. Your doctor has a lot of work to do to prevent them.

5 lost years of brain cognition due to your stroke?

post-stroke cognitive impairment (PCI), the prevalence of which is high (from 24 to 70%)

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Fatigue is estimated all over the place. Fatigue and spasticity were my two worst problems to overcome. I bulled my way thru fatigue with tons of coffee. Spasticity hasn't lessened one bit in the past 15 years.  

At least half of all stroke survivors experience fatigue 

Or is it 70%?

Or is it 40%?

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Spasticity; the main reason I haven't recovered. No one in the world seems to know one damn specific thing about curing it, all we get are useless management strategies like botox or muscle relaxants..

Definition here: Spasticity is a condition in which there is an abnormal increase in muscle tone or stiffness of muscle, which might  interfere with movement, speech, or be associated with discomfort or pain. 

You might hear it called tone, which sounds so benign,it's not. 

Since 30% of survivors have spasticity you would think your doctor would have created a solution or at least initiated research into a solution. But I bet your doctor has done nothing in all the years of practice and survivors not getting cured of spasticity. Ask them what they are doing to CURE spasticity.

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And why doesn't your doctor have something like this for every stroke patient? Maybe call it a stroke protocol?

My doctor did absolutely nothing that first week letting 5.4 billion neurons die.

Of course your doctor will not listen to anything I have to say. Ask why the research I point to is invalid.

 

High-intensity, quicker rehab boosts stroke recovery, analysis shows

And I bet survivors would boost recovery even more by saving billions of neurons in the first week. Ask your doctor why the fuck they did nothing to save those neurons.

You're allowing billions of neurons to die in the first week because absolutely nothing has been done to solve the 5 causes of the neuronal cascade of death in the first week.

High-intensity, quicker rehab boosts stroke recovery, analysis shows

Stroke patients who take part in a high-intensity, early-start rehabilitation program show greater recovery than those receiving low-intensity rehab, according to an analysis by researchers in London and Barcelona. Their results suggest that the standard of care for stroke patients offered by many healthcare systems should be reevaluated. 

Researchers compared the results of two independent rehabilitation studies involving a total of 455 stroke patients who had lost some motor function in their arms. In the first study, UCL’s Queen Square Upper Limb Neurorehabilitation program offered patients three weeks of six-hour-a-day therapy — approximately 90 hours in total. In the second study, the Institute for Bioengineering of Catalonia’s Rehabilitation Gaming System offered patients 20 to 30 minutes a day of therapy for between three and 12 weeks, or 7.5 hours to 30 hours in total.

After measuring each patient’s improvement rate per week relative to their respective recovery potential, results showed that the recovery of those who received six hours of therapy per day was significantly greater than those who received just 20 to 30 minutes. These findings also backed up previous studies showing that the advantages of rehabilitation decrease the later that therapy starts following a stroke. Despite this, researchers observed that the benefits of receiving high-intensity therapy were enough to overcome the detrimental effects of starting late.

Current healthcare guidelines in many parts of the world still dictate that rehabilitation should not begin too early after a stroke, that the duration of each individual session should be short, and that patients should be discharged early, the study authors noted. They also predicted that patients who received high-intensity therapy would have shown even greater improvements if the duration of their program had gone longer than their weeks. 

“Many protocols follow a three-to-six-month window of recovery, but we believe that it could actually be much longer than that — perhaps even years,” concluded study author Belén Rubio Ballester with IBEC.

Full findings are published in the Journal of Neurology, Neurosurgery & Psychiatry.

 

 

Death After Reperfusion Therapy for LVO Stroke: When and Why?

So over half(31% +23%) died during the first week. The neuronal cascade of death

 occurs during the first week. If the stroke medical world would solve the

5 causes of the neuronal cascade of death in the first week you could probably save a lot of those people. But that will require destroying the existing fucking failures of stroke associations  and have them run by survivors.  

The latest here:

 Death After Reperfusion Therapy for LVO Stroke: When and Why?

Christine Judge

Over half of stroke-related deaths following treatment for large-vessel occlusion (LVO) stroke occurred within the first 7 days, and underlying causes of death changed over time, according to data from a comprehensive stroke center.

In a retrospective analysis, among 3520 patients receiving intravenous tissue plasminogen activator (IV-tPA) and/or endovascular thrombectomy after LVO stroke, 218 died within 90 days (91% from stroke-related illness). Nearly one third of deaths occurred during days 3 to 7 after presentation, and another 23% within days 0 to 2.

Underlying cause of death within the first 7 days was nonhemorrhagic/noninfectious sequelae of stroke in 58% and symptomatic intracerebral hemorrhage in 25%. Throughout the 90-day follow-up, infection became a more common underlying cause of death. Read more about the study.

 

A First Step Toward the Operationalization of the Learned Non-Use Phenomenon: A Delphi Study

 In my opinion your ideas on learned non-use are completely wrong. It is much more likely that you are slowly losing functionality because your doctor DID NOTHING  to stop the neuronal cascade of death in the first week.

  You are losing billions of neurons,  miles of myelinated fibers, and tons of dead synapses that first week. I'd suggest charging your stroke hospital $1,000 a dead neuron, that might finally get your stroke hospital to solve stroke. 

I only lost 5.4 billion neurons that first week. If I had only lost 177 million neurons, the 90 minutes it took to deliver tPA, then I would be completely recovered by now.

A First Step Toward the Operationalization of the Learned Non-Use Phenomenon: A Delphi Study

Show all authors

Theresa Hirsch, MSc*, Maria Barthel, MSc*, Pauline Aarts, PhD, ...

First Published March 11, 2021 Research Article 

https://doi.org/10.1177/1545968321999064

Article information

 

Abstract

Background

The negative discrepancy between residual functional capacity and reduced use of the contralesional hand, frequently observed after a brain lesion, has been termed Learned Non-Use (LNU) and is thought to depend on the interaction of neuronal mechanisms during recovery and learning-dependent mechanisms.

Objective

Albeit the LNU phenomenon is generally accepted to exist, currently, no transdisciplinary definition exists. Furthermore, although therapeutic approaches are implemented in clinical practice targeting LNU, no standardized diagnostic routine is described in the available literature. Our objective was to reach consensus regarding a definition as well as synthesize knowledge about the current diagnostic procedures.

Methods

We used a structured group communication following the Delphi method among clinical and scientific experts in the field, knowledge from both, the work with patient populations and with animal models.

Results

Consensus was reached regarding a transdisciplinary definition of the LNU phenomenon(Where the fuck is that definition then? Not publicly available, then it doesn't exist. Useless.). Furthermore, the mode and strategy of the diagnostic process, as well as the sources of information and outcome parameters relevant for the clinical decision making, were described with a wide range showing the current lack of a consistent universal diagnostic approach.

Conclusions

The need for the development of a structured diagnostic procedure and its implementation into clinical practice is emphasized. Moreover, it exists a striking gap between the prevailing hypotheses regarding the mechanisms underlying the LNU phenomenon and the actual evidence. Therefore, basic research is needed to bridge between bedside and bench and eventually improve clinical decision making and further development of interventional strategies beyond the field of stroke rehabilitation.

Keywords experience-dependent non-use, sensorimotor learning, rehabilitation, perceptual disorders, diagnosis

Access Options

 

Addressing inactivity after stroke: The Collaborative Rehabilitation in Acute Stroke (CREATE) study

If you want to increase activity post stroke there are two possibilities I see:

1. Have your doctor stop the 5 causes of the neuronal cascade of death in the first week. That would save billions of neurons. I only lost 5.4 billion neurons that first week because my doctor did nothing that first week. At $1000 a neuron that should have cost the hospital 5.4 trillion dollars. That would concentrate the hospital leadership.

2. Have EXACT STROKE PROTOCOLS WITH EXACT REPETITIONS THAT DELIVERS 100% RECOVERY. With that motivation to exercise would not be a problem. Survivors would be too busy counting and exercising to sit on their butts.

Your solution is incorrect because it is just a guideline NOT a protocol. So NO DEFINED OUTCOME.

Addressing inactivity after stroke: The Collaborative Rehabilitation in Acute Stroke (CREATE) studyj

Show all authors

Fiona Jones, Karolina Gombert-, Stephanie Honey, ...

First Published November 2, 2020 Research Article 

https://doi.org/10.1177/1747493020969367

Article information

   

Abstract

Background

Stroke patients are often inactive outside of structured therapy sessions – an enduring international challenge despite large scale organizational changes, national guidelines and performance targets. We examined whether experienced-based co-design (EBCD) – an improvement methodology – could address inactivity in stroke units.

Aims

To evaluate the feasibility and impact of patients, carers, and staff co-designing and implementing improvements to increase supervised and independent therapeutic patient activity in stroke units and to compare use of full and accelerated EBCD cycles.

Methods

Mixed-methods case comparison in four stroke units in England.

Results

Interviews were held with 156 patients, staff, and carers in total; ethnographic observations for 364 hours, behavioral mapping of 68 patients, and self-report surveys from 179 patients, pre- and post-implementation of EBCD improvement cycles.

Three priority areas emerged: (1) ‘Space’ (environment); (2) ‘Activity opportunities’ and (3) ‘Communication’. More than 40 improvements were co-designed and implemented to address these priorities across participating units. Post-implementation interview and ethnographic observational data confirmed use of new social spaces and increased activity opportunities. However, staff interactions remained largely task-driven with limited focus on enabling patient activity. Behavioral mapping indicated some increases in social, cognitive, and physical activity post-implementation, but was variable across sites. Survey responses rates were low at 12–38% and inconclusive.

Conclusion

It was feasible to implement EBCD in stroke units. This resulted in multiple improvements in stroke unit environments and increased activity opportunities but minimal change in recorded activity levels. There was no discernible difference in experience or outcome between full and accelerated EBCD; this methodology could be used across hospital stroke units to assist staff and other stakeholders to co-design and implement improvement plans.

Keywords Stroke, inactivity, co-design

Introduction

Evidence that increasing the frequency and intensity of stroke rehabilitation can improve outcomes has driven numerous international guidelines and other major developments in hospital-based stroke care to achieve larger doses of therapy provided over seven days.^1,2 However, outside of the scheduled therapy, inactivity is common and observational studies show stroke patients can be inactive and alone for more than 60% of waking hours, an issue largely unchanged for decades.^3,4

There is now more understanding that rehabilitation intensity and outcomes cannot be improved by national targets alone – the stroke unit environment and how time is spent outside of scheduled face-to-face therapy are of critical consideration. Attempts to address inactivity have had mixed results. Dose-driven interventions including circuit class therapy and seven-day therapy have increased therapy provision but not patient activity outside of sessions.⁵ Some progress has been made by applying environmental enrichment evidence from animal models.⁶ Studies conducted in Australia have utilized controlled pre- and post-designs and evaluated the impact of more stimulating environments on inpatient activity.^3,7 Behavior mapping showed an increase in activity levels across all domains and some changes were sustained at six months post intervention. However, the environmental enrichment was driven by the perspectives of researchers and professionals without patient and carer involvement and no specific quality improvement (QI) methodology. Improvement research is now recognized to be critical to ‘cumulate, synthesize and scale learning’ to expedite the translation of evidence into practice.⁸ We believed that a robust QI methodology could address the intractable issue of patient inactivity.

Across healthcare internationally, there is increasing evidence of improvement methodologies which involve patients and staff working collaboratively to help co-design solutions and deliver healthcare services.⁹ Experience-based co-design (EBCD) is an approach which enables staff and patients to co-design services in partnership. Experiences are gathered from patients and staff through in-depth interviewing, observations and group discussions, to identify key ‘touch points’ or emotionally positive or negative issues. An edited ‘trigger’ film is created from patient interviews to convey experiences of the service. Staff and patients are then brought together to explore the findings and to work in small groups to identify, co-design and implement activities that will improve the service or the care pathway.^10,11 EBCD now has widespread use and led to improvements across multiple healthcare settings, including acute hospitals – but can lack detailed evaluation of feasibility and impact.¹² To date EBCD has not been used as an improvement method in stroke units to address inactivity.

Aims

The Collaborative Rehabilitation in Acute Stroke study (CREATE) aimed to (1) evaluate the feasibility of patients, carers and staff collaborating to develop and implement changes to increase supervised and independent therapeutic patient activity in acute stroke units; and (2) understand if improvements developed by two initial stroke units could be transferred to two further units and implemented within a shortened time frame using an accelerated form of EBCD (AEBCD).

Figure 1 provides an overview of the stages of EBCD and AEBCD, data collected, and cohorts included pre- and post-implementation of improvements. Full EBCD and AEBCD took nine and six months to complete, respectively.

Figure 1. Showing accelerated and full experienced-based co-design with pre- and post-implementation data collection.

 

Characterizing upper extremity motor behavior in the first week after stroke

Useless, describes something but offers NO SOLUTION. 

good side therapy (6)

 

 

 Characterizing upper extremity motor behavior in the first week after stroke

PLoS ONE , Volume 15(8) , Pgs. e0221668.

NARIC Accession Number: J84365.  What's this?
ISSN: 1932-6203.
Author(s): Barth, Jessica ; Geed, Shashwati ; Mitchell, Abigail ; Lum, Peter S. ; Edwards, Dorothy F. ; Dromerick, Alexander W..
Project Number: 90REGE0004.
Publication Year: 2020.
Number of Pages: 14.
Abstract: Study characterized the motor behaviors of the less-affected upper extremity (UE) during the first week after stroke. Data were obtained from 25 patients at a mean of 4.5 days after stroke and 12 control subjects who were hospitalized for non-neurological conditions. Outcome measures were accelerometry, the Upper-Extremity Fugl-Meyer, Action Research Arm Test, Shoulder Abduction/ Finger Extension Test, and National Institutes of Health Stroke Scale. Accelerometry indicated total paretic UE movement was reduced compared to controls, primarily due to a 44-percent reduction of bilateral UE use. Unilateral paretic movement was unchanged. Thus, movement shifted early after stroke; bilateral use was reduced and unilateral use of the non-paretic UE was increased by 77 percent. Low correlations between movement time and motor performance prompted an exploratory factor analysis revealing a 2-component solution; motor performance tests load on one component (motor performance) whereas accelerometry-derived variables load on a second orthogonal component (quantity of movement). Findings suggest that early after stroke, spontaneous overall UE movement is reduced, and movement shifts to unilateral use of the non-paretic UE. Two mechanisms that could influence motor recovery may already be in place 4.5 days post stroke: (1) the overuse of the less affected UE, which could set the stage for learned non-use and (2) skill acquisition in the non-paretic limb that could impede recovery.(But what about the research suggesting use of the non-affected side promotes recovery of the affected side? You don't know about that?) Accurate UE motor assessment requires two independent constructs: motor performance and quantity of movement. These findings provide opportunities and measurement methods for studies to develop new behaviorally based stroke recovery treatments that begin early after onset.
Descriptor Terms: BIOENGINEERING, BODY MOVEMENT, HEMIPLEGIA, LIMBS, MOTOR SKILLS, STROKE.


Can this document be ordered through NARIC's document delivery service*?: Y.
Get this Document: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0221668.

Citation: Barth, Jessica , Geed, Shashwati , Mitchell, Abigail , Lum, Peter S. , Edwards, Dorothy F. , Dromerick, Alexander W.. (2020). Characterizing upper extremity motor behavior in the first week after stroke.  PLoS ONE , 15(8), Pgs. e0221668. Retrieved 9/19/2020, from REHABDATA database.

Enhancing Nervous System Recovery through Neurobiologics, Neural Interface Training, and Neurorehabilitation

Yet, you are totally missing the most important component of better stroke recovery. Maybe you might just want to prevent to death of billions of neurons in the first week. By stopping the 5 causes of the neuronal cascade of death in the first week. I lost 5.4 billion neurons in that first week that my doctor did absolutely nothing to try to prevent that. In my opinion that is complete incompetence. If I had only lost the 171 million neurons in the 90 minutes it took to get tPA I would have easily recovered by now. If you don't understand this concept and are working to solve it you don't belong in stroke.

 

Enhancing Nervous System Recovery through Neurobiologics, Neural Interface Training, and Neurorehabilitation

Max O. Krucoff^1*, Shervin Rahimpour¹, Marc W. Slutzky^2,3, V. Reggie Edgerton⁴ and Dennis A. Turner^1,5,6

• ¹Department of Neurosurgery, Duke University Medical Center, Durham, NC, USA
• ²Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
• ³Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
• ⁴Department of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA
• ⁵Department of Neurobiology, Duke University Medical Center, Durham, NC, USA
• ⁶Research and Surgery Services, Durham Veterans Affairs Medical Center, Durham, NC, USA

After an initial period of recovery, human neurological injury has long been thought to be static. In order to improve quality of life for those suffering from stroke, spinal cord injury, or traumatic brain injury, researchers have been working to restore the nervous system and reduce neurological deficits through a number of mechanisms. For example, neurobiologists have been identifying and manipulating components of the intra- and extracellular milieu to alter the regenerative potential of neurons, neuro-engineers have been producing brain-machine and neural interfaces that circumvent lesions to restore functionality, and neurorehabilitation experts have been developing new ways to revitalize the nervous system even in chronic disease. While each of these areas holds promise, their individual paths to clinical relevance remain difficult. Nonetheless, these methods are now able to synergistically enhance recovery of native motor function to levels which were previously believed to be impossible. Furthermore, such recovery can even persist after training, and for the first time there is evidence of functional axonal regrowth and rewiring in the central nervous system of animal models. To attain this type of regeneration, rehabilitation paradigms that pair cortically-based intent with activation of affected circuits and positive neurofeedback appear to be required—a phenomenon which raises new and far reaching questions about the underlying relationship between conscious action and neural repair. For this reason, we argue that multi-modal therapy will be necessary to facilitate a truly robust recovery, and that the success of investigational microscopic techniques may depend on their integration into macroscopic frameworks that include task-based neurorehabilitation. We further identify critical components of future neural repair strategies and explore the most updated knowledge, progress, and challenges in the fields of cellular neuronal repair, neural interfacing, and neurorehabilitation, all with the goal of better understanding neurological injury and how to improve recovery.

Introduction

Historically, for patients suffering from spinal cord injury (SCI), stroke, or traumatic brain injury (TBI), the prognosis for recovery has been poor, and patients with more complete and chronic injuries have shown the least potential for improvement (Jennett et al., 1976; Waters et al., 1992, 1996; Curt et al., 2008; Perel et al., 2008; Steyerberg et al., 2008; Lloyd-Jones et al., 2010). Researchers have been dedicated to improving the quality of life for these patients in several ways, e.g., (1) biological manipulation of the cellular milieu to encourage neuronal repair and regeneration (Magavi et al., 2000; Chen et al., 2002; Lee et al., 2004; Freund et al., 2006; Benowitz and Yin, 2007; Park et al., 2008; Maier et al., 2009; de Lima et al., 2012b; Dachir et al., 2014; Li et al., 2015; Omura et al., 2015), (2) creation of neural- or brain-machine interfaces designed to circumvent lesions and restore functionality (Wolpaw and McFarland, 1994; Kennedy and Bakay, 1998; Leuthardt et al., 2004; Monfils et al., 2004; Hochberg et al., 2006, 2012; Moritz et al., 2008; O'Doherty et al., 2009; Ethier et al., 2012; Collinger et al., 2013; Guggenmos et al., 2013; Ifft et al., 2013; Memberg et al., 2014; Zimmermann and Jackson, 2014; Grahn et al., 2015; Jarosiewicz et al., 2015; Soekadar et al., 2015; Bouton et al., 2016; Capogrosso et al., 2016; Donati et al., 2016; Hotson et al., 2016; Rajangam et al., 2016; Vansteensel et al., 2016), and (3) new rehabilitation techniques that include electrical stimulation and pharmacological enhancement of spinal circuitry to stimulate recovery (Carhart et al., 2004; Levy et al., 2008, 2016; Dy et al., 2010; Harkema et al., 2011, 2012; Dominici et al., 2012; van den Brand et al., 2012; Gad et al., 2013b, 2015; Angeli et al., 2014; Gharabaghi et al., 2014a,c; Wahl et al., 2014; Gerasimenko et al., 2015b). Unfortunately, the path to clinical relevance for these individual approaches remains long, and each field tends to operate largely in its own sphere of influence. Nonetheless, there is now emerging evidence that these methods may synergistically enhance recovery of native motor function that can persist even after the training period and is beyond what was previously thought possible (van den Brand et al., 2012; Guggenmos et al., 2013; Angeli et al., 2014; Wahl et al., 2014; Gad et al., 2015; García-Alías et al., 2015). Some animal models are even displaying functional axonal regrowth, sprouting, and rewiring never seen before in the central nervous system (CNS) of mammals (Bregman et al., 1995; Chen et al., 2002; Liebscher et al., 2005; Freund et al., 2006; Maier et al., 2009; van den Brand et al., 2012; Wahl et al., 2014; García-Alías et al., 2015). Throughout much of this work, evidence is emerging that combinatorial therapy across fields may actually be necessary to achieve significant and lasting neurological repair (Wahl et al., 2014; Gad et al., 2015). This paper explores the state of the art in each of these disciplines, identifies essential components of rehabilitation strategies, and argues why synthesizing approaches across specialties will be essential to realizing clinical applicability.

More at link.