American Society for Peripheral Nerve

Spring 2015   •   Volume 5, Issue 1

The Newsletters is a publication of the American Society for Peripheral Nerve. Views expressed by various authors are not necessarily those of the ASPN.

Jonathan Isaacs, MD
Associate Editors:
Brent M. Egeland, MD
Jonathan M. Winograd, MD
Thomas Tung, MD, ASPN President
Message From The President

Dear Colleagues and Friends,

It is my honor to serve as President of the ASPN this year, following in the footsteps of great surgeons and scientists who have made significant contributions to nerve surgery. The annual meeting in the Bahamas was a huge success with unprecedented attendance and an amazing venue for both the scientific program and our families. Drs. Nash Naam and Greg Borschel put together a great program addressing the most pressing and controversial issues in our field and I am confident that everyone learned something to take away and apply at home in their practices.

This year is an exciting year for the ASPN as we move forward and continue to grow both in number and as a society representing an increasingly broad range of medical professionals of different training and backgrounds with a common interest in restoring function and sensation after surgery or trauma. To reflect the scope of our expanding membership, important proposals are under consideration to change the name and logo of our society. While many feel that it is time for change, it is important to listen to the conservative voices as well so that we remain true to the original identity and goals of our founding members. Therefore I urge all of you to respond to upcoming correspondences addressing these issues. We want everyone’s input! We hope this will encourage a productive exchange of ideas leading to positive discussion at next year’s annual meeting as these proposals come to a vote.

I would also like to recognize and thank PRRI, our new management company, for a smooth transition last year and facilitating additional changes to accommodate the society’s growth. We are confident that our society is in good hands to help us reach our goals. Next year’s annual meeting will be held at the Westin Kierland in Scottsdale, Arizona. It will be another great venue for the scientific program while family members can enjoy the amazing spa and the great outdoors. My program chair Ida Fox will be putting together an exciting program and the location will be easily accessible to everyone. I look forward to seeing everyone there!

Thomas H. Tung, MD
Associate Professor
Director of Microsurgical Reconstruction
Co-Director, Center for Nerve Injury and Paralysis
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
St. Louis, MO

Executive Council Members
Thomas H. H. Tung, MD
Saint Louis, MO

Martijn Malessy, MD, PhD
Leiden, Netherlands

Tessa Gordon, PhD
Toronto, ON, Canada

David L Brown, MD, FACS
Ann Arbor, MI

Gregory H. Borschel, MD
Toronto, ON, Canada

Christine Novak, PT, PhD
Toronto, ON, Canada

Allan J. Belzberg, MD
Baltimore, MD

Nash H. Naam, MD
Effingham, IL

Jonathan M. Winograd, MD
Boston, MA

Ida K. Fox, MD
St. Louis, MO

Michael W. Neumeister, MD
Springfield, IL

Industry Corner

Myoelectric Orthosis restores function to chronic brachial plexus injuries

In 2004, researchers at MIT sought to determine whether myoelectric control technology used in upper extremity prosthetics could be applied to orthotics as a means of supporting and restoring function to a paretic limb. Starting with Spinal Cord Injuries and progressing through chronic stroke, traumatic brain injury, Multiple Sclerosis and ALS, the technology has undergone several generations of improvement that have been commercialized by a spin out company, Myomo Inc. and a custom fabricated myoelectric orthosis, the MyoPro. Leading institutions such as the Mayo Clinic are increasingly using myoelectric orthotics as an assistive device for Brachial Plexus Injuries.

The MyoPro brace is a lightweight elbow orthosis consisting of a motor, myoelectric sensors, a wrist/hand orthosis appropriate for the users’ individual abilities, and a rechargeable battery. Patented EMG (electromyography) control software continuously monitors and senses, but does not stimulate, the affected muscles. The user self initiates and achieves natural movement patterns by their own muscular signals that indicate intention to move. The system senses even a very weak EMG muscle signal and then processes data to a motor on the device that enables desired motion. Based on the individual’s abilities, system parameters such as response time, sensitivity, and level of assistance are tuned and updated over time. The power assist applies an amount of force proportional to what users exert naturally and can lift upwards of 5 – 7 pounds (about the weight of a small bowling ball). The brace moves when and only to the extent that effort is exerted and has a battery life of several hours. Like myoelectric prosthetics, a myoelectric orthosis is a FDA Class I device. The MyoPro is registered with the FDA as a Limb orthosis (890.3475).

When the user’s arm needs support for function, the rigid brace’s frame provides medial/lateral support, anterior/posterior support, rotational stability, and hyperextension prevention. Examples of how it is used include:

  • Support the weight of a laundry basket. The MyoPro also restricts the motion, in the elbow, to protect the arm and hold the basket. By supporting the arm at the desired angle, the brace then restricts downward motion (and thereby loss of control over the basket).
  • Assist in sit-to-stand for a patient’s arm that would otherwise buckle or hyperextend. In this case, the MyoPro restricts the motion of hyperextension, and also provides medial-lateral support.
  • Support a weak arm to hold a cooking pot in the kitchen. Without this support, the weak arm would not be able to support the pot at the required angle to avoid spilling. Many tasks require different angles when support to a weak arm is needed. In this case, the patient uses the motor to flex to the required angle, then stops. Next, during the carrying task, the brace restricts motion/collapsing of the weakened arm.
  • Carry a grocery bag. Simultaneous use of both arms is needed by many patients, especially if they are dependent on a walking aid for balance. Patients with arm weakness often are not able to carry objects because of the medial-lateral forces or hyperextension pressure. The rigid support from the MyoPro will protect the arm from these forces. If the patient lacks movement, the motor will provide assistance.

The concept of myoelectric orthotics & prosthetics is simple. The electrical activity naturally generated by contracting muscle in a paretic or residual limb is amplified, processed, and used to control the flow of electricity from a battery to a motor, which operates a myoelectric orthosis or prosthesis . Myoelectric control was first implemented by Reinhold Reiter in 1945 at Munich University . O&P practitioners have provisioned myoelectric orthotics on a limited basis for decades with the first publication dating back to 1967. Published research conducted since the late 1960s demonstrates myoelectric orthotics restore function to users with a variety of diagnosis and return of a wide range of ADL/IADLs ranging from feeding and grooming to occupational activitiesiii,iv,v,vi. What the MyoPro lends to this body of evidence is a streamlined, lightweight device that can be fabricated and tuned to individual needs.

The MyoPro is ordered by physicians and furnished by certified Orthotics & Prosthetics professionals. During the evaluation consultation, the Orthotist or Prosthetist will provide education regarding aspects of use, ensure the patient is a medically appropriate candidate, discuss insurance benefits, coverage and potential cost.

Each MyoPro brace is custom fitted to the patient using a plaster mold for optimum performance and comfort. Fabrication typically takes 2-4 weeks, the patient will then return for a fitting. During this fitting, the device will be calibrated to the user's individual muscle signal profile and minor adjustments to the brace can be made to optimize comfort. The user will be provided with initial training and a set of take home tasks to practice with the brace donned. Research studies have shown that orthotic and prosthetic users do better when they receive additional training on how to best use their accommodation device. Follow up training may take place at a MyoPro certified therapy or rehabilitation center or at the O&P practice.

Appropriate Candidates include:

  • Long term arm weakness or paralysis
  • Full Passive Range of Motion, Some Active Range of Motion
  • May have mild to moderate flexor tone
  • May have some shoulder subluxation
Disqualifying conditions include:
  • Elbow contracture or acute injury in the arm
  • Shoulder dislocation or subluxation of 3 fingers
  • Severe pain in shoulder or arm
  • Unable to cognitively participate in therapy activity
  • Flexor tone greater than a 3 on the Modified Ashworth Scale

Most commercial payers, Worker’s Comp, and the VA are reimbursing for myoelectric orthotics based on medical necessity. There is specific detail required in physician notes addressing patient goals, past interventions including passive orthotics, physical evaluation specific to an orthotic intervention, and justification for it as the least costly and most functional intervention.

For more information:,, 617.996.9058

  1. Springer (2004) Powered Upper Limb Prosthetics
  2. Pudulski (1969) The Boston Arm. Forum IEEE Spectrum 6
  3. Waring W Antonelli D (1967) Myoelectric Control for a Quadriplegic. Orthopedic and Prosthetic Appliance Journal, vol 21, no 4, pp 255-258
  4. Prentke E (1969) A Surface Electrode Design for Myoelectric Control. Orthopedic and Prosthetic Appliance Journal, vol 23, no 2, pp 63-67
  5. Sauter,WF, Bush G (1989) Myoelectrically controlled exoskeletal mobilizer for amytrophic lateral sclerosis (ALS) patients. Prosthetics and Orthotics International, 13:145-148
  6. Slack M, Berbrayer D. (1992) A myoelectrically controlled Wrist-Hand orthosis for Brachial Plexus Injury. Journal of Prosthetics and Orthotics, vol 4, no 3, pp 171-175
Expert Opinion

A virtual interview with Dr. Tessa Gordon, PhD, University of Toronto on stimulation axons

Editor: Dr. Gordon, despite decades of bench research, there has been no significant change in clinical outcomes for major peripheral nerve repairs. Some of the things you’ve been working on seem to hold promise for breaking this stalemate…. Would you agree and which of the concepts that you are currently working on do you think have the most potential for translation to the clinical arena?

Dr. Gordon: I do agree. Together with Ming Chan, we recently wrote a review in which we considered several agents that have potential to promote nerve regeneration. These include FK506 that has positive effects on nerve regeneration but studies remain to be carried out to provide good evidence of effect. Studies in Susan Mackinnon’s laboratory have shown positive effects when the agent is administered prior to the injury but of course, the question is whether FK506 can promote nerve regeneration when applied after surgical repair of an injured nerve. Studies that I carried out with Dr. Wale Sulaiman some time ago demonstrated the efficacy of systemic FK506 in promoting the regeneration after delayed nerve repair but currently in our laboratory in Toronto more localized administration of FK506 is having a dramatic effect of regeneration after immediate nerve repair.

In our review, we also considered our findings with my PhD graduate student at the time Abdul Al-Majed, and with Tom Brushart that brief low frequency electrical stimulation of a transected nerve proximal to the site of immediate coaptation, has a dramatic accelerating effect on nerve regeneration. We published these findings in 2000 and 2002 in Journal of Neuroscience. What was very revealing to us in the study published in 2000 was that axon regeneration across the suture site is much slower than previously thought. The latent period of a few days actually pans out to be much longer with axons growing in a haphazard fashion across the suture site through disorganized extracellular matrix and Schwann cells that migrate into the site rather slowly.

Editor: Can you briefly review the theory behind the neurostimulatory effects of electrical stimulation?

Dr. Gordon: Our original rationale for determining the effect of brief electrical stimulation on nerve regeneration was based on findings of Nix and Hoft (1983) and Pockett and Gavin (1985). These authors published short papers that demonstrated that the electrical stimulation accelerated the recovery of muscle contractile force reflex and the return of a withdrawal, respectively. Whilst these studies were enticing and informing, the latter study indicating that electrical stimulation was most effective when administered within a half-hour of the injury and the former that a continuous low frequency stimulation regime was effective, neither study elucidated whether the stimulation affected nerve regeneration itself as opposed to the process of target reinnervation. It was for these reasons that we began our valued collaboration with Tom Brushart whose expertise in backlabeling of regenerated axons allowed the quantative assessment of the numbers of neurons that regenerated their axons to the point of application of the fluorescent dye. This expertise allowed us to count the numbers of motor and sensory neurons that regenerated their axons across the suture site as well as some distance into the distal nerve stump. Further collaboration with Melitta Schachner’s group demonstrated the accelerated recovery of function after electrical stimulation of the injured and repair nerve proximal to the site of the nerve repair (Eberhardt et al., 2006).

I must add that the rationale for the continuous 20Hz electrical stimulation for a 2 week period that we adopted was in light of the timing of preferential nerve regeneration that Tom Brushart had described for regeneration of femoral axons down the motor and sensory branches of the nerve. Brushart (1993) had demonstrated that the regenerating motor nerves that grow a distance of 25 mm into the quadriceps and the saphenous nerves within the first two weeks do so in a random fashion with equal numbers of motoneurons sending their axons into both branches. He reported that by 8 weeks, there was preferential motor nerve regeneration into the quadriceps branch to the denervated quadriceps muscle. We therefore began our studies with a continuous two week 20Hz stimulation paradigm. This paradigm being effective, we progressively reduced the period of stimulation with a 1 hour period being equally effective (Al-Majed et al, 2000). The 1 hour paradigm has been adopted in many studies that followed with the efficacy of the electrical stimulation being confirmed in several nerves. Kathryn Jones in her several papers on the efficacy of electrical stimulation accelerating regeneration and reinnervation of facial muscles has adopted a daily stimulation period of 20Hz electrical stimulation for a period of 30 minutes each daily after a crush injury to the facial nerve (Sharma et al, 2010; Hetzler et al, 2008).

When you ask about ‘the theory behind the neurostimulatory effects of electrical stimulation’ I understand your question to include the basis for the neurostimulatory effects of electrical stimulation. As a continuation of Dr. Al-Majed’s PhD thesis, he demonstrated the accelerated expression of brain derived neurotrophic factor and its receptor followed by accelerated expression of the regeneration associated genes of tubulin and actin that are cytoskeletal proteins essential for the elongation of the growing axons (Al-Majed et al, 2000b; 2004). In continuing studies we demonstrated a central role of cAMP and now, Drs Jones (Foecking et al, 2012; Sharma et al, 2008) and Art English (Liu et al, 2014; Thompson et al, 2014) are also demonstrating a role of androgens in the cascade to accelerated expression of regeneration associated genes and, in turn, accelerated axon outgrowth.

Editor: What do you see as the major obstacles to moving your electrical stimulation work from the lab to clinical settings? It seems to me that for any idea like this to achieve widespread adoption, a company needs to make a packaged “kit” or device…. Many surgeons just want a tool

Dr. Gordon: In answer to your question, I would say that I am very hopeful that electrical stimulation of repaired peripheral nerves will move to clinical setting. Our work with Ming Chan on the electrical stimulation of median nerve after carpal tunnel release surgery required simply that one of the two stainless steel wires that were bared of their insulation at the end, were inserted close to the nerve proximal to the site of release. These wires were simply pulled out after the 1 hour 20Hz electrical stimulation was carried out within 15 minutes of the release surgery. These proof of principle studies provided amazing acceleration of reinnervation of the musculature of the median eminence with all the median nerves reinnervating the muscle within 6-8 months in contrast to no significant increase in the numbers of motor nerves innervating the muscle even after 12 months. The major outcome of the release surgery of relief of pain and the movement of the hand muscles being adequately compensated by the unaffected muscles in the lower arm apparently did not impress all surgeons. A paper in Annals of Neurology by Wong et al (2015) is currently in press that reports accelerated recovery of sensation after surgical repair of transected and surgically repaired digital nerves. Such recovery is more obvious but it is clear that the efficacy of the electrical stimulation in human nerve repair is certain and we are definitely ready for more widespread adoption. As you suggest, a packaged kit or device is the way to go and we are certainly going that way.

Editor: Are there settings where electrical stimulation of repaired nerves might not be appropriate?

Dr. Gordon: Electrical stimulation of repaired nerves, being feasible, can be applied within the operating room. We had in our experimental series in rats, demonstrated that it is essential for action potentials to be conducted toward the neuronal cell bodies, the effect of the electrical stimulation being eliminated when action potential conduction was prevented by application of a sodium channel blocker, tetrodotoxin (Al-Majed et al, 2000). We had used suprathreshold stimulation to stimulate the injured rat nerves but the electrical stimulation was adjusted for comfort of the awake patient in the study in which we performed the electrical stimulation after carpal tunnel release. Whilst it remains to be determined whether all the nerves need to be activated for effect, in surgery, the electrical stimulus should be of minimum duration (~100µs) and, under conditions where a branch of the nerve is intact the stimulus current can be adjusted to evoke muscle contractions. Because it is the electrical stimulation must be given to the nerve proximal to the injury, it is feasible to electrically stimulate the nerve some distance from the site of nerve repair. The questions of secondary incision sites come up and of course all conditions of safety are paramount. We are currently evaluating these issues.

Editor: The other area that you have been working on lately that is very exciting is supercharging or side-to-side grafting (or I call it reverse end-to-side nerve transfer). Can you briefly describe the theory behind why you think this will help improve nerve regeneration?

Dr. Gordon: The technique that you refer to as reverse end-to-side nerve transfer is exciting, especially because I believe that it can readily be translated to the clinical arena. I frequently give the intact ulnar and injured median nerves as examples of possible translation because, especially for brachial nerve injuries the period of time for regenerating nerves to ‘reach’ the lower arm are extremely long and certainly well beyond the short window of time when the regenerative power of the injured neuron and the regenerative support of the denervated Schwann cells are prime. The expression of growth associated genes in the neurons and the Schwann cells is short lived with the highest expression declining within 3 months, many declining in even shorter periods of time. The basis for examining whether donor nerves that regenerate into a nerve stump can sustain a growth permissive state for longer periods of time was based on the release of many mitogens (agents that promote cell division) that promote cell division of Schwann cells. These mitogens are normally released from the growing nerve and promote a second phase of Schwann cell division when they encounter the cells in the distal nerve stump. This was an early finding of Pellegrino and Spencer, 1985).

We first examined the efficacy of the end-to-side nerve transfer in Edmonton where Dr. Ladak, an MSc student at the time compared the effect of one and three cross-bridges as we called them. Essentially, we used common peroneal autografts to insert 6 mm cross-bridges between the intact donor tibial nerve and the recipient denervated common peroneal nerve stump at right angles to the nerves. Small perineurial windows were opened to insert these cross-bridges. We found that 3 bridges were better than a single bridge and that common peroneal nerve regeneration through the 4 month chronically denervated common peroneal nerve stump was better when the bridges were inserted as compared to when they were not (Ladak et al, 2011). Further experimentation in Toronto explored the question of the whether or not a perineurial window was necessary and how many cross-bridges are optimal. We are just submitting the revised manuscript (Gordon et al, 2015). We are finding that, indeed a perineurial window is necessary with the number of tibial axons regenerating through the bridges increasing as a function of the diameter of the perineurial window. The issue is that an optimum number of axons is required. Because the capacity of nerves to sprout and reinnervate muscle is considerable with 20% of remaining nerves in partially denervated muscles being able to sprout and reinnervate denervated muscle fibers, many donor axons can enter into the recipient denervated nerve stump.

Editor: How close are we to clinical trials of some of these concepts?

Dr. Gordon: I believe that the first sentences in answer to your previous question, answer the currant question.

Editor: One last question… which area of the complex regeneration process do you think the next major breakthrough in nerve surgery will be and why?

Dr. Gordon: This is an interesting and important question. Dr. Susan Mackinnon frequently talks of major steps (-novel leaps forward but I can’t quite remember her terminology), in which she includes nerve transfers. At this point I would like to comment that surgeons repeatedly refer to the irreversible replacement of chronically denervated muscles by fat. I have personally fought this idea for some time. My reason for doubting the conclusion of the irreversible fate of the denervated muscles comes from the studies of my graduate students Drs. Susan Fu and Mukaila Raji in 1995 and 2010 (Fu and Gordon, 1995a,b; Gordon et al, 2011). Their studies demonstrated that the short duration of the regenerative capacity of injured neurons and of the regenerative support of chronically denervated Schwann cells can together fully account for the poor nerve regeneration and/or the failure of functional recovery after delayed nerve repair and/or after repair requiring very long period for nerves to regenerate to reach denervated targets. Clearly denervated muscles atrophy but I always remember a wonderful chapter on muscle denervation by Sunderland in his 1978 book. He considered the ischemia in denervated limbs after nerve injury as an important and neglected issue when considering the atrophy of denervated muscles. This is a key question concerning the fate of denervated muscles and must be addressed. Recently Dr. Michael Willand has electrically stimulated muscles to find that the daily stimulation accelerates nerve regeneration (Willand et al, 2014). I personally was amazed by this finding. I know from the work of Kerns and others that electrical stimulation of denervated muscle can sustain the muscle fibers and the question I would address at this point in time is the consequence of the electrical stimulation in sustaining the blood flow to the denervated muscles in addition to the direct effect in sustaining the dimensions of the muscle fibers.

With respect to the direct question of nerve surgery, I anticipate that the work on delivery of agents to the nerves via microspheres is an interesting and important current endeavor. Whilst I am in favor of such approaches, my bent is always to ‘use’ the biology of the system in order to attempt to replicate the optimal conditions that the body so often presents. My respect for the biology of living things is boundless.

Case Discussion - Difficult Nerve Injury

Difficult Nerve Injury Case presentation to ASPN Experts:
Jonathan Isaacs, MD
Director, Upper Extremity and Peripheral Nerve Center
Professor and Chief, Division of Hand Surgery
Department of Orthopaedic Surgery
Virginia Commonwealth University
Richmond, Virginia

Commentary by:
Zhongyu John Li, MD, PhD
Associate Professor
Department of Orthopaedic Surgery
Wake Forest Baptist Medical Center
Winston-Salem, North Carolina

Greg Borschel, MD
Associate Professor
University of Toronto Dept of Surgery
and the Hospital for Sick Children Division of Plastic and Reconstructive Surgery

Thomas H. Tung, MD
Associate Professor
Director of Microsurgical Reconstruction
Co-Director, Center for Nerve Injury and Paralysis
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
St. Louis, MO

Seventy one year old male presented to our trauma center after an accidental self inflicted shot gun injury to his nondominant left brachium while intoxicated. Other than alcoholism which evidently is cured after this incident (he reports that he no longer consumes alcohol), he is otherwise healthy. He undergoes emergent brachial artery reconstruction by our trauma and vascular teams. The median nerve is reported to be intact but contused and the ulnar nerve is not inspected. Both are clinically out post operatively though radial nerve appears to be functioning. The soft tissue envelope is stable despite the high-energy insult. Patient presents to the Peripheral Nerve Clinic three months post injury. Hand is viable but stiff. He is insensate in the median and ulnar nerve distributions and has no active wrist or finger flexion, pronation, or intrinsic function.

What would you do next? Further imaging, testing, therapy, surgery?

Li: We would start therapy emphasizing passive stretching and active ROM, pain control and neuromuscular electrical stimulation therapy. We would also obtain a baseline EMG/NCV and nerve ultrasound. Neurologists would routinely perform nerve ultrasound with EMG/NCV in our institution. Ultrasound would be very help in determining nerve continuity and neuroma formation in this case.

Borschel: He needs aggressive hand therapy to improve his PROM. I would plan on EMG/NCS in about 1 month before considering surgery, for at least 4 months of observation since many GSWs will have some spontaneous recovery but may take just a little longer. I do not believe that any imaging studies would be informative at this time as the median nerve was already observed to be intact, it wouldn’t change management at this time, and surgery appears to be likely.

Tung: In the setting of ballistic trauma it is suspicious that the radial nerve is functioning but the adjacent median and ulnar nerves are not, even though they lie in close proximity in this anatomic location. This finding suggests that the ulnar nerve may be disrupted. If high resolution ultrasound is available it may help confirm that suspicion. The main diagnostic tool is the history and physical examination, which indicates no clinical return of function of median and ulnar nerves at three months post injury. Is there a Tinel sign anywhere along the course of the median or ulnar nerves? MRI may also be useful in helping make that determination, and EMG/NCS is warranted to check for motor unit action potentials. At a minimum I would consider a release the anatomic compression points, including the cubital tunnel, arcade of Struthers, the carpal tunnel and Guyon’s canal. I would also want to explore the ulnar nerve and the median nerves at the level of the injury itself to see whether they are in fact intact.

We initiated therapy to loosen up fingers and obtained a base line EMG/NCS which showed no conduction in motor or sensory components of ulna and median nerves. Selected muscles (PT, FPL, 1st Dorsal interosseus) showed increased insertional activity, +4 fibs, and no recruitment on EMG.

He’s now about 4 months out…What now? More studies? Time? Surgery?

Li: This is obviously a challenging situation. We might continue therapy and follow signs of recovery as the median nerve was reported in continuity. We would consider exploration if there is no signs of recovery in 6 months.

Borschel: I would proceed with surgery at this point to explore the nerves, and plan potential nerve graft reconstruction for sensation and distal nerve transfers for motor reconstruction.

Tung: Plan for surgery as outlined above.

We took him to the OR with plans to explore and do intraoperative studies.

Both nerves (ulnar and median) intact (no images) but feel “firm” in several places.

Now what?

Li We would release all fibrous tissue that was compressing the nerves, neurolysis including removal of the thickened epineurium. We would hope for some recovery as both nerves were in continuity. We are not sure if large gap nerve graft would provide any better chance of functional recovery than neurolysis alone in a 71 years old with high median and ulnar nerve injuries.

Borschel: If neuroma in continuity is found, I would resect the neuroma and plan reconstruction.

If no neuroma is found, but the nerves demonstrate ‘firm’ scarring, intra-operative nerve studies would verify if there is any regeneration through the lesions.

We did intra-operative nerve studies which showed no conduced action potentials across either nerve.   Do you use these studies? Why or why not?

Li: We use intra-operative nerve stimulations and conduction studies. We have no experience in nerve active potential (NAP) evaluation.

Tung: I have not used these studies , and it may be premature to expect conduction across the entirety of the nerve. If there is a lot of blast injury then the growth cones may not have extended very far. It may be worth looking very proximally and checking for conduction.

Based on the studies we resected back to normal nerve:

Case Presentation Image 1
Click to view larger image

Median nerve defect right around 7cm and ulnar nerve defect around 5cm. How would you fix these? Or would you do something else?

Li: We most likely would stop after neurolysis as we are not sure the results of nerve graft would be any better than neurolysis. Sometimes we see surprising recoveries in patients who we thought having no chance to recover based on the intraoperative findings. It is not unusual to see partial recoveries in motor and sensory function after neurolysis in patients with enlarged, firm nerves that were not responsive to the intraoperative electrical stimulation.

If nerve repair is indicated as in this case, we would cable graft both the nerves and transfer a supinator branch of radial nerve to the AIN. We would have more tendon transfer options if the transfer works and the graft fails.

Borschel: I would reconstruct the median nerve with cabled sural nerve grafts and wait to see if he reinnervates his proximal forearm flexors, pronator. If not, then I would consider radial to median (ECRB to pronator teres, supinator to AIN) nerve transfers, and perform EIP opponensplasty in 1-1.5 years. I would harvest ipsilateral MABC to obtain at least 2 cables from proximal and distal to the injury level, and reconstruct the ulnar nerve. If not enough is obtainable, I would harvest the ipsilateral LABC distal to the brachialis branch of the MCN for at least one cable. Reconstruction of the ulnar nerve would be for sensation and to prevent pain and neuroma formation.  He will need an anti-claw procedure and possible thumb adductorplasty since there is no chance of intrinsic recovery. He is also likely to need in the future a side-to-side flexor tenodensis for ring and small finger flexion if this is not recovered by the cabled autograft reconstruction of the ulnar nerve.

Tung: I would graft both with sural nerve, and also release all downstream compression points including the cubital tunnel, Guyon’s canal and the carpal tunnel.

We fixed the median with sural nerve cable graft and the ulnar with 5mm diameter by 5cm long acellular nerve allograft:

Case Presentation Image 2
Click to view larger image

Editor discussion:
The median nerve needed autograft based on length of defect but also (at this level) greater importance (more proximal muscles to benefit from reinnervation and more important sensory distribution). Unlikely that hand intrinsics will be reinnervated by either nerve regardless or grafting technique so ulnar nerve was relatively less important. We had already harvested sural from one leg and decided not to give him a third surgical site on his contralateral leg. Local nerve graft options such as medial anterbrachial and medial brachial were damaged from the trauma but even if they were not, I prefer not to take more sensation from a compromised limb. Therefore, we decided to use allograft. Of course, when you use the argument I’m going to try acellular allograft because I don’t think even an autograft will work… then you are setting yourself up for failure and must be careful not to blame the tool!

Borschel: There is no evidence that acellular allografts beyond 2-3 mm diameter size and 3 cm length work. In fact, I would be concerned about neuroma formation and pain which we have seen with ‘over-extended’ allograft reconstruction, potentially requiring resection and proximal transposition in the future. I have no concerns about taking MABC or LABC from this limb since he already has a compromised limb both in terms of function and sensation, and losing some forearm sensation is of little consequence to hand or overall extremity function.

If you believe autograft reconstruction of the median nerve has a good chance of recovering proximal forearm flexors/pronator, then the same should apply to the ulnar nerve for recovery of ring/small finger FDP and FCU, and autograft reconstruction should be considered, even though the primary reason is for sensation and the prevention of neuroma formation and pain. As stated above, recovery of hand intrinsics is of course not expected and is managed by distal tendon transfer.

We also wrapped our repairs with collagen matrix (porcine intestinal submucosa):

Case Presentation Image 3
Click to view larger image

Do you believe that this has any benefit?

Li: Cost is obviously a concern. Although it appears to be a common practice nowdays, but we do need more scientific studies to prove the benefit of using collagen matrix wraps at the nerve repair sites.

Borschel: No. I do not believe there is any convincing supportive data.

Tung: I am not sure if there is data to suggest its use in this clinical situation.

Any other comments?

Tung: It may be worth considering radial to median nerve transfers to try to obtain some flexion in the digits and wrist. It may also be worth considering tendon transfers now, given the age of the patient. For example, using some of his expendable wrist and digital extensors to power digital flexors.

The use of a Best Practice Alert in the electronic health record following peripheral nerve repair.
Loree K. Kalliainen, MD, MA, FACS
Department of Plastic and Hand Surgery
Regions Hospital
St. Paul, MN
Zeke McKinney, MD
Department of Occupational Medicine
Regions Hospital
St. Paul, MN

A review of our group’s use of collagen nerve conduits was published in 2011 in Hand. Several findings were concerning to me: the loss of 33% (32 of 96 patients) of our patients to long-term followup (>30 days), and a relatively poor degree of postoperative improvement (43% of 96 patients). With respect to follow-up, nerve growth is likely just starting to advance by the end of the first postoperative month. Longer follow-up is important to determine efficacy of surgery and to optimize therapeutic interventions such as cortical remodeling, desensitization, nerve glide exercises, and, scar management. Inadequate follow-up could have contributed to our relatively low rate of subjective or objective improvement. To address this issue, I worked with our Epic (electronic health record) specialist to create a Best Practice Alert (BPA) that would fire when a nerve injury code (955.x) was entered into the patient’s electronic medical record. The goal of the BPA was to remind physicians to refer the patient to hand therapy. The BPAs started on 2/1/11 and data was gathered on patients from that time until 7/21/13.

The charts of 120 nerve-injured patients were reviewed for firing of the BPA, duration of follow-up by a surgeon, hand therapy visits, the use of the hand therapy nerve recovery protocol, and notation of recovery of nerve function.

The BPA only fired for 32/120 patients. Our Epic specialist is looking into this, but it could be due to a member of the care team not entering an appropriate diagnostic ICD-9 code in Epic. Our surgeons are not asked to enter operative codes into Epic at the time of surgery; this is done by the billing and coding department. In postoperative clinic visits, though, a diagnosis code must be entered by the surgeon or mid-level practitioner to close the chart. Entering a nerve injury code could be avoided if a postoperative event code (V67.00 or Z09) were entered or if a different injury diagnosis code (eg, open wound, tendon injury, fracture). In these situations, the reminder to refer to hand therapy would not appear.

Despite the poor rate of BPA firing, loss of patients to long-term followup (>30 days) was slightly improved: 89 patients (74%) had follow-up greater than 30 days with short-term follow-up only in 31 patients (26%). The average followup with the surgeon was 122 days (range, 0-991) and with the hand therapists was 86 days (range, 0-352). 92% of all patients (109/120) were seen by hand therapy postoperatively, and in 63% (76/120), the cortical remodeling protocol was used. The nerve recovery protocol has been used for the past five years by our hand therapists and incorporates early sensory and auditory stimulation along with mirror therapy as has been discussed by Lundborg and Rosen. Nerve recovery was noted in 83% of our patients treated with the nerve recovery protocol and only in 54% of patients in whom the nerve recovery protocol was not used. As opposed to our earlier study of collagen conduits, there was evidence of nerve recovery in 74% of our patient with collagen conduits, similar to 78% of patients in patients who had primary repair.

One of the concerns raised about alerts in the EHR is “alert fatigue”, so it is reasonable to ask whether the BPA was effective or useful. The 7% improvement in long-term followup may be partially due to the BPA, and occasionally seeing the BPA may have served as a reminder to our practitioners to order hand therapy for all patients with nerve injuries. In addition to the BPA, awareness has increased in general in our department about postoperative options for nerve-injured patients. We have had internal presentations about the cortical remodeling protocol, one of our hand therapists presented our data at last year’s AAHS meeting, and an article has been submitted for publication to the Journal of Hand Therapy. There have been no voiced departmental complaints about seeing the BPA, and so keeping it is unlikely to be unpopular. It may serve to remind rotating trainees to refer patients to hand therapy. We are pleased, though, that the use of the cortical remodeling protocol may have improved nerve repair outcomes. We will be looking into this in more depth.  

  1. Wangensteen KJ, Kalliainen LK. Collagen tube conduits in peripheral nerve repair: a retrospective analysis. Hand. 5(3):273,2010.
  2. Lundborg G, Rosen B, Lindberg S. Hearing as substitution for sensation: a new principle for artificial sensibility. J Hand Surg 1999;24A:219–224.
  3. Lundborg G. Brain plasticity and hand surgery: an overview. J Hand Surg (Br), 2000;25(3):242-252.
  4. Kesselheim AS, Cresswell K, Phansalkar S, Bates DW, Sheikh A. Clinical decision support systems could be modified to reduce ‘Alert Fatigue’ while still minimizing the risk of litigation. Health Affairs, 2011;30(12):2310-2317.
Assistant or Associate Professor: Neural Regeneration
VARITAS Logo Department of Otolaryngology
Harvard Medical School
Division of Facial Plastic and
Reconstructive Surgery
Massachusetts Eye and Ear
Mass Eye & Ear Logo
The Department of Otolaryngology at the Harvard Medical School and the Massachusetts Eye and Ear (MEE) seek applications from researchers interested in neural regeneration. The MEE provides an interdisciplinary and collaborative intellectual environment within an active clinical setting. The research base in our Department includes 30 NIH-funded investigators studying diverse aspects of hearing, balance, smell, facial movement, and their disorders. MEE researchers participate in a variety of teaching programs for graduate students, medical students and residents, at both Harvard and MIT.

Candidates should have an outstanding record of research accomplishment and a strong desire for research collaboration, especially in areas relevant to disorders of the facial nerve. Applications will be accepted until the position is filled, however initial evaluation will take place by June 1, 2015. Interested candidates should send a CV and Statement of Research Interests to:

Tessa Hadlock, M.D.
c/o Missy Allen
Division of Facial Plastic and Reconstructive Surgery
Massachusetts Eye and Ear
243 Charles St., Boston MA 02114
The Massachusetts Eye and Ear Infirmary and Harvard Medical School are Equal Opportunity/Affirmative Action Employers. Women and minorities are encouraged to apply.
Program Chair’s Report

Dear friends,

I am delighted to report that our recent meeting held in the Bahamas was exceptionally well attended, with a final registration of 234 people from 20 different countries – the highest ever for ASPN!

I would like to thank all those who made this meeting successful. I was humbled by the thoughtfulness, creativity, innovation and quality of our presenters. We enjoyed an exceptional set of instructional courses and invited speakers – thank you for freely sharing your approaches to problems in nerve injury and regeneration.

The meeting had eight scientific paper sessions with 59 podium presentations and a poster session that showcased 20 posters. For the first year we decided to include electronic posters as well. I would like to thank members of the Scientific Program Committee for the huge amount of time and effort they spent to review and grade the numerous abstract submissions and for judging the presentations during the meeting. Congratulations to Gwendolyn Hoben (Schwann Cell Senescence: A Key Role in Reducing Axon Regeneration) and Chelsea Snider (Transient Receptor Potential Vanilloid-1 Channel Blockade in the Peripheral Nerve Terminal by Resiniferatoxin for the Treatment of Chronic Pain) for the Best Research Presentations; and to Joseph Catapano for the Best Clinical Presentation, entitled “Corneal Reinnervation: a Minimally Invasive Approach.” Our poster award winner was Alison Snyder-Warwick for her work entitled “Morphologic Characterization and Lifespan of Terminal Schwann Cells.”

The AAHS/ASPN Joint Invited Speaker, Susan Mackinnon, spoke on “Pathway to Innovation in Academic Surgery: The Good, The Bad and The Ugly,” in which she recounted her personal journey of innovation and progress in nerve surgery and nerve injury research. International Guest Speaker, Fausto Viterbo, discussed the evolution of end to side nerve transfer, including its contemporary rediscovery and subsequent scientific investigations. President Nash Naam delivered a lecture on “The Magic Power of Touch.” I am personally indebted to Nash for his wisdom, leadership, and hands-on engagement during the shaping of this year’s program. Joint Presidential Keynote Lecturer Ramez Naam discussed “The Wired Brain: The Frontiers of Neural Prosthetics” from his unique perspective as a software engineer, author and futurist.

I am truly delighted to have served as your Program Chair of our 2015 meeting. Thank you again for making it such a success!

Gregory H. Borschel
2014-2015 ASPN Program Chair
Associate Professor
University of Toronto Dept of Surgery
and the Hospital for Sick Children Division of Plastic and Reconstructive Surgery

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