American Society for Peripheral Nerve

Fall 2014   •   Volume 4, Issue 2
Message From The President

It has been a great honor and a privilege to serve as President of the American Society for Peripheral Nerve this year. It has been a wonderful experience to contribute to this vibrant organization and watch it grow and get stronger. Our society is now the premiere society dedicated to education and research in the field of peripheral nerve in the world. Our challenge is to remain vibrant and relevant to our members and to our patients as well.

Many changes have taken place this year starting with changing our management service to PRRI, which has provided administrative stability to our society. We also placed the financial investments of our organization in the hands of professional financial advisors headed by Mr. Jeffery Palmer who also advises our sister organization, AAHS. Our membership drive has been successful with more than 25 new members in the pipeline this year. So, it is reassuring to know that our society is growing and its financial status is healthy.

We are very grateful to our partners; the American Society of Plastic Surgeons (ASPS) and the Plastic Surgery Foundation (PSF) for increasing the number of research grants to our society members to two each year. Each grant would provide up to $10,000 for research. This will enable ASPN to enhance its ability to pursue its research and educational mission.

As we come closer to our annual meeting in January at the Atlantis in the Bahamas, preparations for a stimulating and thought-provoking program are full steam ahead under the leadership of Greg Borschel, MD. You can review the program online. All the abstracts and posters will be posted online in the coming week. The Friday program will feature, for the first time, our ASPN/AAHS Joint Invited Guest Speaker, our Past President Susan Mackinnon, MD. She will speak on “Path to Innovation in Academic Surgery: The Good, The Bad and The Ugly.” The combined Saturday morning program with AAHS and ASRM will feature a timely panel discussion on “The Affordable Care Act and its Impact on the Surgeon.” Our Joint Presidential Keynote Speaker will be Ramez Naam who happens to be my son but I did not have anything to do with inviting him. The AAHS and ASRM presidents invited him to be our keynote speaker. He will lecture on the “Piercing the Veil: The Frontiers of Neuroscience.”

One of the most important features of our organization, being a relatively small one, is the intimate relationship between its members. So prepare yourself for a wonderfully stimulating program in the midst of one of the most beautiful places on earth. While the Northeast and Midwest deal with snowstorms and icy roads in January, we will be sipping our Margaritas on the beautiful sandy beaches of Nassau. So, get yourself ready to join all your friends and colleagues to have a great time filled with camaraderie, friendship, fun, sun and science.

I am looking forward to welcoming each and every one of you to the beautiful Bahamas. See you there.

Nash Naam

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


Jonathan Isaacs, MD

Associate Editors:
Jonathan M. Winograd, MD
Brent M. Egeland, MD

Staff Editor:
Sarah Boardman

American Society
for Peripheral Nerve

500 Cummings Center
Ste 4400
Beverly, MA 01915

Future ASPN Meetings
2015 Annual Meeting
January 23-25, 2015
Paradise Island, Bahamas

2016 Annual Meeting
January 15-17, 2016
Westin Keirland Hotel
Scottsdale, Arizona

2017 Annual Meeting
January 13-15, 2017
Hilton Waikoloa Village
Waikoloa, Big Island, Hawaii
Editor’s Notes

In an effort to keep the ASPN newsletter fresh and educational, I’ve started a repeating segment I’m calling “Industry Corner.” I will give different nerve related industries (Integra, Axogen, Checkpoint, etc.) an opportunity to teach us about some of their products. My goal is not to have “unpaid” advertising put to offer a venue in which you can learn about various products out there that may help your practice. Len Cosentino (President and CEO of Checkpoint) submitted the following piece on their intra-operative nerve-stimulating device. I asked him to make it as educational as possible and to try to avoid the “infomercial” undertones. Read the Industry Corner on the next page of the Newsletter.

- JI

ASPN 2014-2015 Executive Council Members
Nash H. Naam, MD
Effingham, IL

Thomas H. H. Tung, MD
Saint Louis, MO

Martijn Malessy, MD, PhD
Leiden, Netherlands

David L. Brown, MD
Ann Arbor, MI

Gregory H. Borschel, MD
Toronto, ON, Canada

Gedge D. Rosson, MD
Baltimore, MD
Allan J. Belzberg, MD
Baltimore, MD

Robert Spinner, MD
Rochester, MN

Jonathan M. Winograd, MD
Boston, MA

Ida K. Fox, MD
St. Louis, MO

Lynda Yang, MD
Ann Arbor, MI
Industry Corner

Handheld Nerve Monitoring with the CHECKPOINT® Stimulator/Locator

Before the birth of Checkpoint Surgical in late 2009, our team began working with a small group of surgeons who had identified a need for a better way to locate and protect nerves intraoperatively in a significant set of nerve exploration/repair and complex reconstructive surgeries. These surgeons believed that too often in these procedures, nerves in the surgical field are at undue risk of intraoperative injury due to the prevalence of scar tissue or otherwise altered anatomy. These surgeons also had experience using available nerve stimulation and nerve monitoring technologies but found them inadequate and/or impractical. What they wanted was a “surgeon controlled” device that would be safe and effective, while also easy to use with a low technical burden.

Our team had substantial expertise in the development of neurostimulation technology, primarily in the arena of implantable devices. The challenge in developing ffthe desired device was to convert sophisticated implantable neurostimulation technology into a low cost, handheld device that would still be safe, reliable and accurate, while meeting the specific functional needs identified by the surgeons.

Out of this collaboration was born the CHECKPOINT® Stimulator/Locator, cleared by the FDA in late 2009 and introduced to market in 2010. The Checkpoint quickly proved an effective tool for locating and mapping nerves in the surgical field and verifying nerve integrity. Checkpoint also proved to be a helpful decision-making tool, aiding the surgeon in the assessment of neuromuscular function and determining the most appropriate course of intervention. The Checkpoint is now being used in a variety of surgical specialties in hundreds of hospitals across the United States and in four foreign countries.

The CHECKPOINT® offers the surgeon total independence from outside technical support in a simple to use, yet versatile tool for a variety of surgical procedures The Checkpoint circuitry is located on a single circuit board assembly with 77 components and proprietary embedded software. This micro-controller based circuit constantly monitors the internal circuitry of the Checkpoint with integrated self-testing operations to ensure the Checkpoint consistently produces safe, precise and reliable stimulus. The Checkpoint has three amplitude setting options (.5mA, 2mA and 20mA) and an adjustable pulse width control with a range of zero to 200 microseconds. The widely variable and reproducible stimulus intensity of the Checkpoint is useful whenever problems are encountered identifying and protecting the critical neurovascular structures in the surgical field. This may be as a result of altered anatomy due to previous surgery, trauma, or other conditions such as tumors or infection. The stimulator can be used to identify a suspect area that may contain a critical motor nerve and can then be used to identify precisely the nerve at risk and to confirm its identity by stimulating it and observing the distal motor response.

The Checkpoint circuitry is designed to be resistant to electrical impedance, which helps to avoid a false negative response. This component of the system generates a constant nerve-depolarizing field regardless of the type of impedance that is presented within the surgical environment. Therefore, the spatial field of excitation does not vary with the impedance of the tissue directly under the probe tip nor does it vary with the area of the probe tip in contact with tissue. This can be of significant value when working on nerves through surrounding tissue and at varying depths following trauma or previous surgery.

Checkpoint employs a biphasic waveform, which allows for repeated and continuous stimulation to an area of interest or directly on a nerve, without concern for diminished response or damage to the tissue area. The microcontroller-based circuit generates a controlled current, biphasic, capacitively coupled waveform. This precisely controlled biphasic stimulus, in combination with the stimulus frequency employed in the Checkpoint, elicits a tetanic muscle contraction that provides the surgeon unambiguous data. Other disposable stimulators employ direct current stimulation that elicits only a single muscle twitch and limits nerve contact to no longer than one second without risk of nerve injury. Furthermore, locating or activating nerves through surrounding tissue with these other stimulators is impractical.

The Checkpoint also may be used to evaluate the functional condition of the nerve using its variable pulse width setting. After the nerve is identified and initial dissection is performed, individual fascicle identification can also be done to further identify specific area of injury or for performing nerve transfers. Once the area of concern is identified, the nerve may be stimulated and the threshold parameter, which is the lowest stimulus intensity at which a muscle response, is noted. Without this variable pulse width control, establishing the threshold of nerve activation is challenging. Following a neurolysis, the nerve can be rechecked to see if the threshold stimulus intensity has dropped to the normal level confirming that nerve function has improved and eliminating the need to perform a graft which would require much longer recovery time. This type of use also may be helpful in a neuroma case to determine whether or not there is any functional axonal continuity or the neuroma must be resected and grafted or a nerve transfer procedure performed. Some response should be seen in the 2 mA range. Even a weak distal response indicates at least some functioning nerve fascicles and the capacity for further recovery, indicating that resection of the neuroma-in-continuity and grafting may not be necessary.

The 20 mA setting, in addition to regional stimulation for nerve location, can be used to stimulate entire muscles and thus evaluate their viability or to test them during muscle and tendon transfer procedures allowing precise evaluation of both tendon excursion and setting the tension in tendon transfers. At 20 mA, there is significant stimulus spill into adjacent tissues. 20 mA is not used to directly stimulate nerves, although it may be used to stimulate a region of tissue surrounding a nerve to try to determine if a nerve is present within the tissue mass.

Checkpoint Surgical is headquartered in Cleveland, Ohio, a leading center for neurodevice research and development. The CHECKPOINT® Stimulator/Locator is the flagship product of Checkpoint Surgical, an emerging leader in the intraoperative nerve protection and repair market.

To learn more about Checkpoint visit

Expert Opinion

An Interview with Dr. Dellon on Diabetic Neuropathy

Editor: Dr. Dellon, I have been doing the lower extremity nerve releases you described in the early 1990’s and been impressed by at least the subjective improvement my patients have almost universally reported. Are you still doing this procedure and how has you attitude toward the procedure changed since you first described it?

Dr. Dellon: Yes I still do this procedure. Since I first proposed the theory in 1988 that there was optimism for patients with diabetic neuropathy who also had nerve compressions in the lower extremity, my confidence in this theory has increased. The original basic science research done in rats in our lab has been confirmed in Maria Siemionow’s lab at the Cleveland Clinic and in labs in Turkey and Romania. After many individual retrospective case series reports, there has been a 38 center prospective multicenter study including 800 diabetics that showed a significant decrease in prevention of ulcers, amputations, and hospital admissions for foot infections, and a significant decease in pain, with the observational period being 3 years. The positive predictive value of the positive Tinel sign has been confirmed at 80%. The prevalence of diabetics with a positive Tinel sign and neuropathy has been observed to be 50 to 60% in the upper and lower extremity in a community based endocrinology practice. The first Level I study has demonstrated a significant decrease in pain. An economic cost benefit analysis using a decision-tree experimental design has been published demonstrating a significant savings if this “Dellon Approach” were implemented. Finally, I am proud to say that this surgery is being done in 21 countries outside the U.S.A.

Editor: Can you describe briefly for the readers the theory behind the surgical procedure?

Dr. Dellon: Part of the metabolic disease of diabetes is increased production of sorbitol from the excess serum glucose, by the enzyme aldose reductase. The increased sorbitol in the axoplasm causes water to be pulled into the nerve, causing increased nerve volume. If the peripheral nerve becomes swollen in an anatomic narrow space, like the carpal tunnel, fibular tunnel or tarsal tunnels, then there is relative ischemia, productive of paresthesias and, in time, chronic nerve compression. This is well accepted. It is the basis of the double crush hypothesis in diabetes, and the reason that diabetics with neuropathy have a high prevalence of nerve compressions. If we as surgeons can relieve carpal tunnel symptoms in the diabetic patient with neuropathy in the upper extremity, then, my hypothesis was, that we should be able to do this by decompressing anatomic sites of narrowing in the lower extremity. For those interested, I can supply the references for these studies; email me at

Editor: Can you offer some thoughts on patient selection?

Dr. Dellon: Patient selection for nerve decompression in a person with diabetes and numbness, tingling, (with or without pain) for more than 6 months in the lower extremities;

  1. Patient must approach good sugar control, with HbA1c < 6.5 if possible
  2. Patient must have tried neuropathic pain medication and still have symptoms or be intolerant of the drugs
  3. Patient should weight under 300# or must reduce weight prior to surgery (preferable by diet or water walking, swimming)
  4. Patient must have no pedal edema
  5. Patient must have sufficient circulation in the feet for healing (palpable pulse, or Doppler measured ankle/brachial index > .7, or percutaneous PO2 > 40.
  6. Patient must meet normal criteria for elective surgery (cardiac and renal function)
  7. Patient must have a positive Tinel sign over the tibial nerve in the tarsal tunnel (positive predictive value of 80% for successful surgery)

Editor: Can you describe in general terms the actual surgery?

Dr. Dellon: The actual surgery is a neurolysis of the common peroneal nerve at the knee, the release of the four medial ankle tunnels, and the neurolysis of the deep peroneal nerve over the dorsum of the foot. In about 25% of the patients, there is also compression of the superficial peroneal nerve in the leg. In about 20% there is also compression of the tibial nerve at the soleal sling. Photos of these procedures are available at, in my book PAIN SOLUTIONS, written for patients, by clicking on the book cover, and then downloading chapter 2 for free. Also at, at the top of the page is Free Booklets. There you can download free the booklets on Foot Drop, on Tarsal Tunnels Syndrome, on Neuropathy, page 7 of each 8 page brochure has the published evidence base for the surgery. The surgery is done as an outpatient, and usually takes less than 2 hours of general anesthesia. The patient walks immediately after the surgery using a walker. Further surgical details are available in a review (Dellon, AL, The Dellon Approach to Neurolysis in the Neuropathy Patient with Chronic Nerve Compression, Handchir Mikrochir, Plast Chir, 40:1-10, 2008.) and will be present in a Supplement on “Pain” in Plastic and Reconstructive Surgery in the October 2014 issue.

Editor: Any special surgical tips?

Dr. Dellon: For the common peroneal nerve at the knee, there is a fibrous band almost always present beneath the peroneus muscles that must be released (Dellon AL, Ebmer J, Swier P: Anatomic variations related to decompression of the common peroneal nerve at the fibular head. Ann Plast Surg, 48: 30-34, 2002.). For the four medial ankle tunnels, it is critical to release the medial and lateral plantar tunnels into the bottom of the foot and to remove the septum between the tunnels in order to reduce the pressure upon the nerves (Barker, A.R., Rosson, G.D., Dellon, A.L., Pressure Changes in the Medial and Lateral Plantar, and Tarsal Tunnels Related to Ankle Position: A Cadaver Study, Foot & Ankle Internat., 28:250-254, 2007). For the superficial peroneal nerve, remember that one in four patients can have a high division of the nerve with a branch in the anterior compartment so both the lateral and anterior compartments must be released (Barrett SL, Dellon, AL, Rosson GD, Walters, L.: Superficial Peroneal Nerve: Clinical Implications of its Anatomic Variability, J Foot & Ankle Surgery, 45:174-176, 2006.).

Editor: I have had a couple of patients experience persistent wound drainage and healing problems especially with the posterior medial ankle incision. Any tips on how to avoid these pitfalls? By the way, both patients I’m thinking of asked me to do their contralateral limb once the wounds healed!

Dr. Dellon: When I teach the surgery for release of the four medial ankle tunnels, I demonstrate special attention to wound closure. Remember that walking immediately post-op with a walker is critical for nerve gliding and a good result. Wound healing starts with not cauterizing the skin edges. The bipolar coagulator is set on a low number, usually about 12. The skin edge is everted and the dermal bleeders are not cauterized in the dermis, but as they enter the dermis. Often poor healing is due to injury to the skin during this phase of hemostasis. Of course there must be excellent hemostasis. For wound closure, I use a row of interrupted intradermal 4-0 monocryl sutures first, and then both interrupted and continuous 5-0 nylon sutures are placed. Then I personally show the patient and accompanying person that they must “march” when using the walker, wearing the large, bulky, supportive dressing, a Robert Jones type of dressing with cotton. No black boots which inhibit ankle movement. When they walk, the must lift from the knee so reduce ankle motion to less than about 15 degrees of movement.

Editor: I get asked a lot about non-diabetic neuropathy…. What indications other than diabetic neuropathy are you offering the surgery? Chemotherapy induced neuropathy?

Dr. Dellon: The published results show the same success for idiopathic neuropathy as for diabetic neuropathy (Valdivia Valdivia, JM, Weinand, M, Maloney, CTJr, Blount, A, Dellon, AL, Surgical treatment of superimposed, lower extremity, peripheral nerve entrapment in patients with diabetic and idiopathic neuropathy, Ann Plastic Surg, 70:675-679, 2013.). We have reported similar results with neuropathy induced by the “platins” and “taxols” (Dellon AL, Swier P, Maloney CT, Levingood M, Werter, S., Chemotherapy-induced neuropathy: Treatment by decompression of peripheral nerve. Plast Reconstr Surg, 114:478-483, 2004.)

Editor: I think an important question is how does this surgical release affect the natural history of diabetic neuropathy? Do you have any thoughts on this?

Dr. Dellon: In the early basic science on rats made diabetic, even with blood sugars of 400 for one year (half of their lab lifetime), they walked like normal rats IF they had their tarsal tunnels released before they were made diabetic (Dellon ES, Dellon AL, Seiler WA IV: The effect of tarsal tunnel decompression in the streptozotocin-induced diabetic rat. Microsurg 15:265-268, 1994.). This study clearly shows a change in the natural history of diabetic neuropathy in a rat model. In a clinical retrospective review of 50 patients followed for a mean of 4.5 years (range 2 to 7 years), each patient had one leg that had a “Dellon Triple” procedure (neurolysis of three areas as described above). The other leg was observed for its natural history… obviously the blood sugar was the same in each leg! No ulcers or amputations occurred in the index limb of these patients. In contrast, there were 12 ulcers and 3 amputations in 15 different patients in contralateral limbs. This difference was significant at P < 0.001. It is concluded that decompression of lower extremity nerves in diabetic neuropathy changes the natural history of this disease, representing a paradigm shift in health care costs. (Aszmann OC, Tassler PL, Dellon AL: Changing the natural history of diabetic neuropathy: Incidence of ulcer/amputation in the contralateral limb of patients with a unilateral nerve decompression procedure, accepted Ann Plast Surg, 53:517-522, 2004. ).

Editor: One last question… many people have reported success with this procedure yet it does not seem as widely accepted as you would expect for a treatment that seems to so dramatically help patients that are really suffering. In fact, most of my referrals are still word of mouth… a satisfied patient refers their friends so to speak. How do you explain this reluctance to embrace this procedure and how do you think we “break through” to the “nonbelievers”?

Dr. Dellon: You are correct in your observations. Education about peripheral nerve problems and their surgical approach is poorly taught. We must begin to educate young doctors, even at the medical school level where they are still NOT taught about the presence of nerve compression in patients in general, except carpal tunnel syndrome, and certainly not about the prevalence of these in people with diabetes. My work has been published entirely in surgical journals. We must seek professionally to make internal medicine doctors, diabetologists, and endocrinologists aware of the evidence now available. Neurologist are a big part of the problem with patients NOT being referred, as they believe no one should have a nerve decompression unless there is a confirming electrodiagnostic study documenting nerve compression. However, they fail to admit in public that it is very difficult in a non-neuropathy patient to document the presence of tarsal tunnel syndrome, and it is extremely difficult, due to the already impaired nerve function, to demonstrate a tibial nerve compression in the presence of an axonal neuropathy. I often suggest to young surgeons that they speak to their nearest vascular surgeon, who sees a steady stream of patients with painful neuropathy who have normal vascular studies; these patients likely have a nerve compression and he can refer them to the peripheral nerve surgeon. Finally, whenever the patients come back to me with relief after surgery, I ask them to please let their family practice know and their diabetologists know that they are better.

Clinical Experience In Nerve Repair

Acellular Nerve Allografts: An Evolution in My Clinical Practice
Bauback Safa, MD, MBA
The Buncke Clinic
San Francisco, CA

The last few years have seen a gradual, yet dramatic, shift in my peripheral nerve practice. As a surgeon at the Buncke Clinic, one of the most common procedures I perform is the repair of transected nerves resulting from various mechanisms, including lacerations, avulsions, crush or blast injuries, and often with the presence of a significant gap. A great majority of these nerve injuries occur in the setting of complex emergent hand trauma with concomitant injuries to additional structures, and often in the setting of devascularization.

The nerve gap has long presented a challenge to peripheral nerve surgeons. We have all been taught that primary nerve coaptation is preferred to nerve repair with modalities such as hollow tube conduits or nerve grafts, assuming there is negligible tension at the repair site. In an effort to achieve primary coaptation, however, many surgeons attempt radical mobilization of the nerve, perhaps even achieving repair with joints in flexion. While there may be minimal tension at the repair site with the joints flexed, post-operative motion likely places excessive tension at the repair site during the healing phase, thereby resulting in suboptimal nerve regeneration. It is my belief that the desire to achieve primary coaptation at “time zero” in a complex trauma creates a potential subconscious incentive for surgeons to perhaps repair nerves primarily in a less-than-ideal fashion.

Before the introduction of commercially available acellular nerve allografts, the options available for bridging a nerve gap included hollow-tube conduits, vein grafts, and autologous nerve grafts. Most surgeons, however, are reluctant to use nerve autografts emergently in the setting of an acute trauma. And since vein grafts, despite good clinical results (Chiu DT et al. Plast Reconstr Surg. 1990 Nov; 86(5):928-34), had not gained much popularity, nerve conduits were the only readily available alternative for bridging nerve gaps acutely.

The use of conduits was ushered in by early clinical studies that showed success in short gaps (Weber et al. Plast Reconstr Surg. 2000 Oct;106(5):1036-45). Indeed, hollow tube conduits were used very commonly in our hand trauma practice prior to 2008, primarily for common and proper digital nerves. However, our results in defects exceeding 10mm were, in general, suboptimal with this modality. Upon closer examination, the average nerve gap in these early studies was less than 10mm and in retrospect, this would explain our less-than-ideal clinical results for longer gaps. Indeed, pre-clinical studies using conduits for long gaps have shown that the lack of microtubular structure results in a thin, hourglass-shaped regenerate within the nerve conduit (Lundborg et al. Exp Neurol. 1982;76:361–75). Studies have also shown axon density to be significantly lower in conduit groups compared to nerve allograft and autograft (Whitlock et al. Muscle and Nerve, 2008).

For the above reasons, I had a low threshold for using an acellular nerve allograft in acute traumas when I was first presented with the opportunity. Early clinical data had shown excellent recovery in digital nerves (Karabekmez, F., Duyman, A., Moran, S. HAND 2009 Sep;4(3):245-9) and there were no good alternatives to be used in an acute setting. With the volume of hand trauma at the Buncke Clinic, our center eventually became the lead site for the RANGER study, a retrospective registry study evaluating outcomes data in patients from, at this time, 18 centers around the country. The RANGER study has resulted in numerous publications and nerve allografts have been shown to achieve meaningful recovery in over 80% of patients across all gap and nerve function cohorts (Cho et al. J Hand Surg Am. 2012 Nov;37(11):2340-9). The RANGER study is not without its weaknesses however. It is purely a retrospective registry study with no control arm, and comparisons can only be made to data from existing historical controls from other studies using nerve conduits and autograft.

Despite our excellent early clinical results with the acellular nerve allograft, many questions remain. While regeneration in mixed and motor nerves have demonstrated equivalent outcomes to those of historical autograft controls, these cases represent smaller cohorts compared to that of sensory nerves. Furthermore, pre-clinical studies have demonstrated the importance of cellular elements in motor nerve regeneration. The fact that allografts have been cleared of all cellular elements in the decellularization process represents a potential disadvantage. And while animal studies have shown that native Schwann cell migration into an allograft occurs rapidly across a critical gap, there is no data for the length at which Schwann cell migration begins to taper off in humans.

However, while cellular elements have been cleared out from acellular nerve allografts, so have inhibitors of nerve regeneration, such as chondroitin sulfate proteoglycans (CSPGs). The absence of this inhibitor could potentially provide a counterweight to the theoretical disadvantage of absent cellular elements. Also, cable grafting a large mixed nerve (current modality with autografts) introduces copious amounts of collagen and connective tissue into the coaptation site. This could theoretically fail to provide an equivalent number of microtubules when compared to the native nerve (e.g. isograft). Since allografts are available in as large as 5mm in diameter, there is also a potential advantage in using one large similarly-sized graft as opposed to multiple cables, thereby maximizing the number of microtubules available for regeneration.

The RANGER study is the largest database of peripheral nerve repair to date, with nearly 400 patients currently enrolled. Due to the limitations of the study, however, further work is needed to better delineate the role of processed nerve allografts in peripheral nerve repair. Better animal models are needed in order to test longer human allografts to auto/isografts. Indeed, early primate studies comparing 70mm human allograft compared to isograft in a mixed nerve have shown promising results. Also, additional clinical studies are needed, ideally in a prospective fashion, in order to compare acellular nerve allografts to both nerve conduits as well as autografts.

Nerve autografts continue to play a prominent role in our hand practice, especially in nerve gaps exceeding 7cm in length. In recent years, however, acellular nerve allografts have replaced a bulk of our nerve reconstructions in sensory, mixed, and motor nerves less than 7cm in length.

Figures: Ulnar nerve repair using allograft. Note excellent return of intrinsic function.

Ulnar nerve repair using allograft 1

Ulnar nerve repair using allograft 2

Ulnar nerve repair using allograft 3

Ulnar nerve repair using allograft 4

Ulnar nerve repair using allograft 5

Ulnar nerve repair using allograft 6

CASE PRESENTATION – Complex Nerve Trauma

Jonathan Winograd, M.D.
Assistant Professor Harvard Medical School

Mr. F is a 59 year old gentleman who was transferred from an outside hospital with a work related injury. While grasping a piece of wood on a conveyor belt, his arms became caught within the conveyor and he was trapped against the belt for several minutes. He sustained multiple deep burns to his bilateral upper extremities and chest, as well as left both bone open forearm fractures, an open humerus fracture with shoulder dislocation, left rib fractures, a left hemothorax, a left total brachial plexus palsy, and a right medial elbow burn directly over the cubital tunnel with exposure and severe contusion of the ulnar nerve. He was stabilized at the outside hospital, underwent washout and reduction of the humerus fracture and forearm fractures with external fixation, a chest tube placement, and subsequently was transferred to MGH.

His neurologic exam on arrival demonstrated a complete brachial plexus palsy with an insensate upper extremity on the left side as well as numbness in the ulnar nerve distribution on the right side with intrinsic muscle paralysis as well as flexor digitorum longus palsy of the small and ring fingers. His humerus fracture and his both bone forearm fractures underwent washout and ORIF by the orthopedic trauma service. His shoulder was not able to be stably reduced. He was then evaluated by the plastic surgery hand service. Treatment of his brachial plexus injury was deferred at that point given the severity of his shoulder injury, both bony and soft tissue and the need for nerve conduction studies and EMG evaluation. His burns were treated with excision and grafting except in the left arm, where there was medial exposure of his brachial artery and vein and brachial plexus, and his right elbow, where the ulnar nerve was exposed over a 5 cm span and appeared necrotic.

At that point, he was taken to the OR by the plastic surgery hand service for soft tissue reconstruction of his bilateral upper extremities and for ulnar nerve reconstruction at the right elbow. At that time, it was noted that his ulnar nerve, despite careful wound care, appeared frankly necrotic at the level of the cubital tunnel. His left musculocutaneous nerve was also noted at the time to be frayed at the mid biceps level.

Right elbow with exposed necrotic ulnar nerve and left arm with exposed brachial vessels and frayed musculocutaneous nerve.

Treatment Dilemma: treatment options for his brachial plexus injury of the left upper extremity and his ulnar nerve injury of the right elbow both for 1) soft tissue and 2) nerve injuries?

The brachial vessels and terminal branches of the brachial plexus were covered with a latissimus dorsi flap and split thickness skin grafting, with the idea of both covering the exposed vessels and nerves as well as allowing for future reconstruction if necessary. His right elbow wound was further debrided and the ulnar nerve, after excision of grossly necrotic nerve at the elbow, was left with a 7 cm gap at the cubital tunnel after the nerve ends proximally and distally were transposed out of the cubital tunnel. The nerve was grafted with five cables of sural nerve autograft. The large wound was covered with a pedicled radial artery forearm flap. The radial forearm was selected because of its low profile and excellent pliability for elbow motion restoration. Additionally, an end to end AIN to deep motor branch nerve transfer was performed and the donor site in the distal forearm was skin grafted. The patient subsequently healed all of the above wounds. He did require some additional grafting by the burn service for his wounds, which all healed uneventfully.

Clockwise from upper left. Left arm coverage with latissimus dorsi flap, with delayed skin grafting. Right ulnar nerve cable grafts x 5. AIN to deep motor branch transfer. Distal forearm neurolysis of deep motor branch from ulnar nerve in preparation for transfer.

Radial forearm flap elevated and transposed. Radial forearm flap in place with adjacent split thickness skin graft.

Diagnostic and Treatment Dilemma: What additional testing is needed at this point for the patient in regard to his brachial plexus injury and his reconstructed ulnar nerve? Is there a role for supercharged end-to-side transfer vs. end to end transfer? Outcome data to guide the clinician is lacking at this point.

In follow up, 2 months post injury, he began to recover left brachial plexus function, with diminished but present sensation to light touch present in the MABC, LABC, radial sensory nerve and axillary nerve distributions, as well as flexion and extension of his fingers. By six months, his brachial plexus injury has recovered significantly, with return of voluntary elbow, wrist, and hand movement, and diminished sensation to light touch in the palmar skin of the radial three digits with absent sensation in the ulnar digits. Of note, his nerve conduction studies and EMG were deferred originally because of concerns over his recent latissimus dorsi flap and skin grafts. By two months, he began to exhibit clinical recovery and his studies were deferred again. By six months, they did not appear to be necessary.

His right elbow wound healed well after the pedicled radial forearm flap. He can extend his elbow to -20º, with full flexion. His right hand and wrist has a full range of motion but he has no voluntary contraction of his FDP at this time. He has no clawing but does have guttering and first web space atrophy at 6 month follow up. He has grip strength with a Jamar dynamometer of 40 lbs., and tip, chuck and lateral pinch of 8, 9, and 9.5 lbs. respectively. He remains insensate in the ulnar nerve distribution of his right hand.

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ASPN/PSF Combined Pilot Research Grant Reminder

The Plastic Surgery Foundation (PSF) and the ASPN recognize the importance of promoting innovative research in peripheral nerve surgery. These organizations are dedicated to fostering the development of surgeon scientists and are committed to increasing the amount of research dollars, in order to fund pilot research studies that set the stage for investigators to apply to larger funding agencies. Apply by the December 1 deadline for consideration. Applicants must be an Active or Candidate member of ASPS or a member of ASPN. View grant guidelines and application.

Membership Recruitment

ASPN has seen a steady increase in membership numbers and continues its efforts to grow. Please encourage your colleagues to join ASPN, a diverse group of professionals ranging from neurosurgeons to plastic surgeons and physical therapists to general scientists. Applicants are accepted on a rolling basis. The next application deadline is November 21st. Learn more about ASPN Membership categories.

Membership benefits include access to research grant funding, significantly reduced registration rates for ASPN Annual Meetings which are held in warm, family-friendly locations each January, opportunities to hold office and serve on ASPN committees, complimentary access to the Plastic Surgery Education Network (PSEN), and access to the ASPN newsletter.

Program Chair’s Message

Dear Colleagues,

In honor of the 25th Anniversary of ASPN, we have planned a unique program for the 2015 ASPN Annual Meeting. We have fully integrated our educational, scientific and social activities with the AAHS and ASRM to create an outstanding program.

The 2015 ASPN program will begin Friday January 23, 2015 with combined ASPN/AAHS instructional courses, a clinical nerve scientific podium session and later in the morning an integrated panel on nerve transfers. We have also planned an ASPN scientific paper session, our Joint AAHS/ASPN Invited Speaker Susan Mackinnon (“The Path to Innovation in Academic Surgery: The Good, The Bad and The Ugly”) followed by an interactive poster session lunch.

On Saturday, we have combined the extraordinary strengths of the three societies with combined instructional courses, a combined panel on affordable health care, an outstanding paper session and our Joint Presidential Keynote Lecture by noted technology author, futurist, and inventor Ramez Naam. The AAHS/ASPN/ASRM Welcome Reception will be held that evening.

On Sunday, the ASPN program will begin with early morning instructional courses followed by a combined ASPN/ASRM panel on free muscle based reconstruction of brachial plexus injuries, followed by a combined ASPN/ASRM scientific paper session. The morning will continue with ASPN scientific paper sessions, International Guest Speaker Fausto Viterbo’s lecture on End-to-Side Nerve Repair, a special Founding Member and Past President Panel, a special International Invited Panel, and conclude with the ASPN business meeting.

The Atlantis Paradise Island is a fantastic venue in which to enjoy the Bahamas. We will have activities at the resort for you to enjoy with your family and friends. The 25th Anniversary program promises to be an exciting educational and fun learning experience. I invite you, your colleagues, and your families to join us in the Bahamas!

View Preliminary Program

With very best wishes,

Gregory H. Borschel, MD, FAAP, FACS
2015 ASPN Program Chair

Schedule At a Glance thumbnail
View Schedule At a Glance


Atlantis Resort Paradise Island
Make your reservation online or contact the hotel directly at 954-809-2100 and refer to group code: AAHS/ASPN/ASRM or, GQWDEU5. Rooms and rates are limited and will be confirmed on a space available basis until Friday, December 5, 2014 or until the block is full, whichever occurs first. We encourage you to make your reservation as soon as possible to ensure room rate and availability.

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If you plan on attending the American Society for Peripheral Nerve Meeting please use the buttons below to register. Please register on or before November 21, 2014 to receive the early bird registration rate.

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American Society for Peripheral Nerve
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