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Peripheral Nerve Repair and Reconstruction

Article  in  The Journal of Bone and Joint Surgery · December 2013

DOI: 10.2106/JBJS.L.00704 · Source: PubMed

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C OPYRIGHT Ó 2013 BY T HE J OURNAL OF B ONE AND J OINT S URGERY, I NCORPORATED

Current Concepts Review

Peripheral Nerve Repair and Reconstruction
Justin W. Griffin, MD, MaCalus V. Hogan, MD, A. Bobby Chhabra, MD, and D. Nicole Deal, MD

Investigation performed at the Department of Orthopaedic Surgery, University of Virginia Health System, Charlottesville, Virginia

ä When possible, direct repair remains the current standard of care for the repair of peripheral nerve lacerations.

ä In large nerve gaps, in which direct repair is not possible, grafting remains the most viable option.

ä Nerve scaffolds include autologous conduits, artificial nonbioabsorbable conduits, and bioabsorbable conduits
and are options for repair of digital nerve gaps that are <3 cm in length.

ä Experimental studies suggest that the use of allografts may be an option for repairing larger sensory nerve gaps
without associated donor-site morbidity.

Nerve injuries result in approximately $150 billion spent in
annual health-care dollars in the United States1. Most patients
are young males, with the radial nerve in the upper extremity
and the peroneal nerve in the lower extremity most commonly
injured2. Selecting the proper treatment continues to pose a
challenging problem with a wide variability in approach and
outcome. Direct tensionless end-to-end repair, when possible,
achieves the most predictable outcomes. In nerve injuries when
the nerve ends cannot be approximated without tension, nerve
grafts represent the most commonly used method of recon-
struction. The development of nerve conduits to enhance nerve
repair remains an important research area and future clinical
developments in the area of nerve regeneration and repair
potentially could improve patient outcomes.
Anatomy
Nerves are surrounded by the epineurium, perineurium, and
endoneurium, each with a vital function. The epineurium serves
to wrap the nerve in a supportive barrier against outside stresses.
The perineurium lies beneath the epineurium as a thin sheet of
flat cells with tight junctions to regulate diffusion surrounding
individual fascicles and has a high tensile strength. The endo-
neurium has a loose collagenous matrix surrounding individ-
ual nerve fibers3 (Fig. 1).
One important clinical aspect of nerve anatomy is that
individual fasciculi do not run in a straight line, but instead
form plexuses along a nerve fiber. An increased number of
fascicles increases the strength of the nerve and concomitantly
increases the complexity of repair as the fascicle location varies
over short distances. It has been suggested that matching these
fascicles could improve outcomes. Kato et al. noted excellent
results with fascicular orientation using electrical stimulation
to help ensure sensory and motor fascicular alignment4. Al-
though time-consuming, matching recently cut nerve endings
in terms of motor and sensory function has been described5.
Despite these efforts, certain nerves possess greater variability
in cross-sectional arrangement along their length3,6,7.
Classification
Nerve injuries are described with use of the Seddon classifi-
cation terms8. Three degrees of injury were initially described.
Neurapraxia is often the result of a compressive or crush injury
to the nerve where conduction is blocked due to myelin damage,
resulting in a focal conduction block without Wallerian de-
generation as the axon itself remains intact with recovery generally
evident in three to six weeks when myelin continuity is restored.
The complete interruption of axons is termed axonotmesis.
Neurotmesis is the complete physiologic transection of axons

Disclosure: One or more of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in
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prior to submission of this work, with an entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written
in this work. No author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to
influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the
online version of the article.

J Bone Joint Surg Am. 2013;95:2144-51 d http://dx.doi.org/10.2106/JBJS.L.00704

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Fig. 1
Illustration of a cross-sectional anatomy of the peripheral nerve. (Reprinted from Lundborg G. Nerve Injury and Repair. New York: Churchill Livingstone;
1988, p 33, with permission from Elsevier.)
as well as all supporting tissue. Neurotmesis results in changes
within the nerve cell body and degeneration with a variable re-
covery course.
The Sunderland classification describes five degrees of in-
jury based on histology, and allows a better prediction of outcomes
following injury6. First-degree injury is equivalent to neurapraxia
with no loss in axon integrity. Second-degree injury describes
axonal injury within an intact endoneurial tube allowing re-
growth within the endoneurial tube. In third-degree injury the
endoneurial tube is damaged and the resultant reinnervation is
not identical to the original and may result in intrafascicular
fibrotic block, growth of axons into unfamiliar endoneurial tubes,
and swelling. In fourth-degree injury, only the epineurium remains
intact and fascicular damage occurs in addition to endoneurial
damage. Interfascicular regrowth, disorganization, and fibrous block
occur that often necessitate surgical excision and reconstruction.
Fifth-degree injury damages the nerve trunk and is equivalent to
neurotmesis by the Seddon classification.
Pathophysiology of Nerve Degeneration and
Regeneration
Nerve Degeneration
Axonal degeneration follows a sequence of events with the zone
of injury extending both proximally and distally. Proximal to
the site of injury, traumatic degeneration occurs, traveling to
the level of the intact node of Ranvier, or, in some cases, further
proximal. The swollen cell body begins production of elements
essential to axonal repair and growth9.
Distal to the site of injury, Wallerian, or secondary, de-
generation occurs within twenty-four to forty-eight hours
P E R I P H E R A L N E R V E R E PA I R AND RECONSTRUCTION
following injury and begins with axonal breakdown. Wallerian
degeneration is antegrade degeneration in which the part of the
axon separated from the neuron’s cell body degenerates distal
to the injury10. Affected Schwann cells throughout the distal
segment begin to catabolize the myelin. This distal degenera-
tion, combined with macrophages recruited to the area, leads
to phagocytosis of axonal and myelin debris. These events ul-
timately result in myelin tube collapse9.
Nerve Regeneration
From the proximal stump, axonal sprouting begins within
twenty-four hours after injury. The growth cone protrudes
from the axonal sprout elongating down the path of the intact
basal lamina and within the regenerative promoting environ-
ment. With an intact endoneurial tube, such as in axonotmesis,
the regenerating sprouting axon has a direct path to the end
organ. This is a slow migration process occurring at approxi-
mately 1 mm per day11.
The growth cone is under the influence of neurotrophic
and neurite-promoting factors, also referred to as neuro-
trophins12. Nerve growth factor is an essential neurotrophic
factor and one of great interest in nerve injury and the devel-
opment of future options for peripheral nerve repair13-15. Nerve
growth factor plays an important role in the growth, mainte-
nance, and survival of target neurons and supports peripheral
nerve regeneration in a rat model. Glial nerve growth factor,
ciliary neurotrophic factor, and a number of other growth
factors play a critical role in the nerve regeneration process13.
Also aiding in the axonal elongation and growth process are
a number of neurite-promoting factors and matrix-specific
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substances, which serve as building blocks for nerve develop-
ment10. A complete understanding of neurotrophins is beyond
the scope of this review, but it is clear that these factors play
a crucial role in neuron cell survival, neurite outgrowth, cell
differentiation, and cell migration, and promote controlled
neurogenesis.
Reinnervation
After nerve injury, muscle atrophy occurs at the motor end
plate, followed by fibrosis. If reinnervation does occur, both old
and new motor end plates will be activated. Although the muscle
is atrophied and fibrotic, it can remain viable for up to eighteen
months16; however, if reinnervation does not occur within one
year, the chance of functional recovery diminishes17. Patient age
is the most important factor to consider in evaluating the success
of nerve recovery following repair18 while the level of injury also
plays a role, with distal injuries having better recovery results
than proximal injuries19,20.
Clinical Evaluation
Evaluation of the patient with peripheral nerve injury begins
with determination of the mechanism of injury. Crush injuries
can produce a variety of nerve injuries but often lead to
neurapraxia. Penetrating injuries can lead to partial or full
nerve transection, gunshot-related nerve deficits tend to be due
to neurotmesis and the degree of injury depends on the velocity
of the weapon involved, and fracture-related injuries must be
correlated with their mechanism. High-energy blunt trauma
can lead to a variety of injury patterns requiring further ex-
amination to determine regeneration potential. Twisting, trac-
tion, and crush-type injuries can result in nerve entrapments
and tension-type stress on the nerve, leading to neurotmesis
and axonotmesis20,21.
Neurophysiologic Studies
When considering the need for surgical intervention, closed
fractures with nerve injury often result in nerve recovery in
a greater majority of patients without operative intervention
and should be followed expectantly22. The standard of care in
decision-making in peripheral nerve surgery has been the use
of serial neurophysiologic studies over months combined with
serial physical examinations. The degree of muscle degenera-
tion that occurs after nerve injury cannot be determined until
Wallerian degeneration is complete. This process may take up
to four weeks. Although early studies can help to localize in-
juries, the typical waiting period to allow a baseline to be ob-
tained is approximately six weeks. Electrodiagnostic studies
may differentiate acute injury from chronic injury. They may
also assist in determining the type of nerve fiber affected. When
obtained serially over time, they may map nerve recovery23.
Nerve conduction studies are generally used initially as a
screening test and the addition of electromyography (EMG)
provides valuable information in the form of reduced action
potentials23. Clinical or electrodiagnostic evidence of pro-
gressive recovery of sensorimotor function indicates an injury
with a neurapraxic or axonotmetic component, which warrants
P E R I P H E R A L N E R V E R E PA I R AND RECONSTRUCTION
further observation because spontaneous recovery normally
occurs within the first few months11.
Imaging
Ultrasound and magnetic resonance imaging (MRI) remain the
most used imaging studies for peripheral nerve injury. Ultrasound
is inexpensive and safe and has recently become more commonly
utilized in the diagnosis of nerve injury. One prospective study24
utilized high-resolution ultrasound to evaluate twenty-six patients
with documented motor or sensory peripheral nerve deficits that
were due to either trauma or entrapment. Of those twenty-six
patients, nineteen underwent operative exploration and ultra-
sound diagnoses were then correlated with neurological exami-
nation and intraoperative findings. Ultrasound provided reliable
visualization of nerve injury in all patients and findings such as
axonal swelling, neuroma formation, and partial laceration had
high correlation with intraoperative findings24. However, ultra-
sound use in the setting of extensive edema and/or obesity can be
challenging and can limit diagnostic accuracy.
MRI can provide useful information for diagnosis and
surgical planning. Grant et al.25 showed that MRI can provide
resolution of fascicular patterns and can demonstrate nerve
edema. In addition, their study of sciatic nerve injury in a rat
model showed that high-resolution MRI can differentiate
neurotmesis from high-grade axonotmesis. However, a clinical
study evaluated short T1 inversion recovery (STIR) MRI
compared with EMG and found that MRI was less sensitive
than EMG, with 11% of cases of nerve injury not recognized on
MRI being confirmed on EMG26.
Timing of Repair
Operative exploration should occur in a timely fashion in open
injuries. A transected nerve should be repaired within two to
three days postinjury to decrease fibrosis, to minimize tension
due to retraction, and to maximize biologic regrowth19,27. The
surgeon must consider reduction attempts when nerve palsy is
accompanied by a fracture. However, peripheral nerve injury
by examination is not considered a reason for exploration
immediately without other indication11.
Much of the research on the timing of exploration has
focused on one of the most common peripheral injuries, the
radial nerve in humeral shaft fractures. Böstman et al.28 retro-
spectively examined seventy-five patients with radial nerve
palsy, sixteen with deficit after manipulation and fifty-nine
with initial palsy. Early exploration and internal fixation were
performed in thirty-seven patients. Thirty-eight patients were
watched expectantly. Of those thirty-eight patients observed,
twenty-six (68%) experienced spontaneous recovery and
twelve (32%) underwent delayed nerve exploration. Böstman
et al. concluded that early exploration was not advisable. Of
those patients who underwent initial exploration, twenty-seven
(73%) of thirty-seven had recovery of radial nerve function
compared with thirty-three (87%) of thirty-eight who were
managed nonoperatively. Ring et al.29 retrospectively reviewed
twenty-four patients with humeral shaft fractures. Eleven of the
twenty-four humeral shaft fractures were open. Fourteen of the
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twenty-four patients were explored at the time of presentation,
and three patients in this group had closed fractures. Ring et al.
found that all eight of the patients with intact explored nerves
and nine of the ten patients with unexplored nerves with an
initial deficit recovered fully within a six-month period. Five of
the six patients in the transection group underwent repair and
none showed functional recovery. Signs of nerve recovery did
not appear until approximately seven weeks.
Direct Nerve Repair
Direct nerve repair is indicated in cases of sharp nerve division
with minimal gap. The ideal setting for direct repair is an injury
zone with good blood supply and soft-tissue coverage. The
proper alignment of nerve ends is critical to optimize nerve
recovery, and gaps of >2.5 cm at the site of injury will com-
monly necessitate nerve grafting. Tension-free suture repair
remains the preferred treatment option for nerve injury. If this
is not possible because of either gap formation or poor quality
of tissue for repair, alternative methods should be utilized30.
Simple direct repair entails suturing the nerve together in
a tension-free fashion (Fig. 2). End-to-side repair may be
favorable when the proximal aspect of the injured nerve is
not salvageable. The distal portion of the injured nerve can
be sutured to an adjacent nerve with subsequent collateral
sprouting31. Yu et al. evaluated end-to-side neurorrhaphy in the
ulnar nerve as the donor and in the musculocutaneous nerve as
the recipient and noted collateral sprouting of intact axons of
the ulnar nerve with limited functional reinnervation32. The
development of novel microsurgical techniques and instru-
mentation led some to promote grouped fascicular repair.
Fig. 2
Photograph showing a median nerve laceration in forearm repaired by direct end-to-end repair.
P E R I P H E R A L N E R V E R E PA I R AND RECONSTRUCTION
This technique is similar to epineural repair, but in addition
the perineural sheaths of individual fascicles are repaired
under microscopic magnification. This approach attempts
more accurate approximation of regenerating axons but re-
quires more dissection and potential soft-tissue disruption. In
nerves with defined motor and sensory topography, such as
median or ulnar nerves in the forearm and the sciatic nerve in
the thigh, such repair is often used11. With both epineural and
fascicular repair, most surgeons advocate the use of 8-0 or 9-0
monofilament suture in adult patients. Direct muscular neu-
rotization involves placing the proximal nerve stump into the
muscle belly. This technique is not preferred as functional re-
covery is weakest with this treatment, but it remains an option
when direct repair and/or reconstruction are not possible27.
Fibrin glue can be considered as an adjunct or alternative to
epineurial repair and is viewed by many as quick and easy to
use33,34. Multiple studies have shown that fibrin glue is equiva-
lent to suture repair and may improve resistance to gapping34.
Use of Conduits
A tensionless repair has been cited as one major factor to the
successful recovery of sensorimotor function35. When tension-
less direct repair cannot be achieved, interposed autologous
nerve grafting is the gold standard for segmental defects27,36.
However, autologous grafting carries with it donor-site mor-
bidity, requirement for two anastomotic sites, increased oper-
ative time, and elevated costs, thereby justifying the ongoing
search for options37. Potential advantages of nerve conduits
include absorbability, lack of donor-site morbidity, and lack of
axonal escape.
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TABLE I Options for Bridging Nerve Gaps
Nerve
Autografts
Allografts
Biological conduits
Vein
Artery
Synthetic conduits
Collagen
Polyglycolic acid
Caprolactone
Nerve scaffolds include autologous grafts, artificial non-
bioabsorbable conduits, and bioabsorbable conduits (Table I).
Three main types of bioabsorbable conduits are currently ap-
proved by the U.S. Food and Drug Administration (FDA) for
use. With variations in tubes currently available, it is helpful to
review the evidence surrounding the selection of tubes. Most
regard the upper limit of nerve conduit length to be 3 cm38. In a
rabbit peroneal nerve study, Strauch et al. compared results of
using vein conduits from 1 to 6 cm with deteriorating results at
a length of >3 cm39.
Autogenous Conduits
Veins are the most common type of autogenous conduit used
for reconstruction of nerve defects, and are often referred to
as autogenous or autologous vein nerve conduits. Chiu and
Strauch conducted a prospective study of twenty-two patients
with defects of £3 cm, finding that autogenous vein nerve
conduits produced results as good as those of sural nerve digital
grafts40. Rinker and Liau41 in their recently published prospective
Fig. 3
Photograph showing a collagen conduit used to bridge traumatic nerve laceration.
P E R I P H E R A L N E R V E R E PA I R AND RECONSTRUCTION
randomized study compared autogenous vein nerve conduits
with synthetic polyglycolic acid conduits for digital nerve gaps
of 4 to 25 mm. Forty-two patients with seventy-six repairs were
enrolled in the study, with thirty-seven patients with sixty-eight
repairs undergoing repair with either polyglycolic acid conduits
or autogenous vein nerve conduits (thirty-six with synthetic
polyglycolic acid, and thirty-two with vein conduits). The au-
thors analyzed sensory recovery at six and twelve months after
repair, the time and cost of repair, and the complication profile
between the two treatment groups and found equivalent results
with similar cost profiles and sensory recovery outcomes41.
Collagen Conduits
Type-I collagen and Type-IV collagen remain the most com-
monly used nerve conduit design, with Type-I collagen being
most biocompatible42. Figure 3 demonstrates a commonly
available collagen conduit used to bridge a nerve laceration.
Animal studies with collagen conduits have demonstrated
equivalent efficacy when compared with autograft; however,
clinical studies are lacking43,44. To date, only case series have
been published with no documented Level-I studies available.
Bushnell et al.43 reported a Level-IV case series of twelve digital
nerve gaps from 10 to 12 mm over a two-year period. Out-
comes in this study were measured with use of American So-
ciety for Surgery of the Hand (ASSH) guidelines with static
2-point discrimination, Disabilities of the Arm, Shoulder and
Hand (DASH) scores, and Semmes-Weinstein testing. In their
study of twelve patients, three of whom were excluded, of the
remaining nine patients, four (44%) had excellent results, four
(44%) had good results, and one (11%) had fair results with an
average DASH score of 10 points. Five patients had full sensory
recovery, two patients had diminished sensory recovery, one
patient had diminished protective sensation, and one patient
had loss of sensation. Lohmeyer et al.45 performed a prospective
cohort study with collagen conduits to repair twelve digital
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nerves with an average 12.7-mm gap. At the one-year follow-
up, of the twelve patients, four (33%) had excellent sensory
recovery, five (42%) had good sensory recovery, one (8%)
exhibited poor sensory recovery, and two (17%) had no sen-
sory recovery. However, grading of outcomes using 2-point
discrimination remains nonstandardized and no studies have
examined motor recovery with collagen tubes42.
Polyglycolic Acid Conduits
The polyglycolic acid conduit is regarded as more flexible, and
the porous nature allows oxygen to diffuse in and aid in re-
generation with conduit resorption occurring in six months42.
In a prospective case series of fifteen patients undergoing sec-
ondary nerve reconstructions of digital nerve gaps measuring
approximately 17 mm with polyglycolic acid tubes, Mackinnon
and Dellon 46 found that five patients (33%) had excellent
sensory recovery, eight patients (53%) had good recovery, and
two patients (14%) had poor or no recovery. Sensory data were
gathered with use of the British Medical Research Council
sensory nerve grading scale with moving and static 2-point
discrimination. Although that study was an early Level-IV
study, Mackinnon and Dellon concluded that polyglycolic acid
tubes could produce results equivalent to the classic nerve graft
without donor-site morbidity with gaps up to 3 cm.
In a cohort study, Battiston et al.47 examined the utility of
polyglycolic acid tubes compared with biologically constructed
muscle-vein conduits reporting equivalent results. Thirty pa-
tients were treated for digital nerve injuries. Of these patients,
muscle-vein combined conduits were used in thirteen patients
and polyglycolic acid conduits were used in seventeen patients.
The authors compared outcomes with use of the Mackinnon-
Dellon modification of the British Medical Research Council
scale. Results showed no notable differences between the two
groups with respect to evaluation testing used, although the
polyglycolic acid group achieved S4 sensation (excellent sensi-
bility) in 12% (two of seventeen) compared with 38% (five of
thirteen) of the vein conduit group. The evidence must be
weighed with the fact that certain patients underwent immediate
repair while others were delayed.
Weber et al.48 compared polyglycolic acid conduits with
primary repair or autograft for digital nerve injuries in a Level-
II study. Ninety-eight patients with 136 digital nerve repairs
were prospectively randomized to either a group undergoing
direct end-to-end repair or utilizing a nerve graft or a group
undergoing repair with a polyglycolic acid conduit. The au-
thors reported that conduits were superior in gaps of £4 mm or
>8 mm. That study provided evidence that polyglycolic acid
nerve conduits produce equivalent results to nerve repairs or
autologous grafts for short or moderate digital nerve gaps.
Caprolactone Conduits
Poly(DL-lactide-e-caprolactone) was first demonstrated in rat
models to bridge 10-mm sciatic nerve gaps; these guides were
reported to degrade completely in one year. Poly(DL-lactide-e-
caprolactone) is another bioabsorbable conduit that may be used
to bridge nerve gaps49. Bertleff et al.50 performed a multicenter,
P E R I P H E R A L N E R V E R E PA I R AND RECONSTRUCTION
blinded, randomized controlled trial of thirty patients with
thirty-four nerve injuries using caprolactone Neurolac nerve
tubes (Polyganics, Groningen, the Netherlands) compared with
primary repair for digital nerve lacerations in gaps of 6 to 8 mm.
Moving and static 2-point discrimination was 7 to 10 mm for
both the experimental and control groups38.
Relative indications for nerve tubes based on the above
studies include nerve gaps of <3 cm in length when tension
would result from primary repair coupled with patient or sur-
geon preference to avoid harvesting an autologous nerve graft.
Longer nerve gaps may lead to decreased sensory recovery48. In a
recent study, Shin et al.51 evaluated sciatic nerve motor recovery
in a rat model with a 10-mm defect using autograft, capro-
lactone, collagen, and polyglycolic acid conduits. They found
that caprolactone conduit and autograft repairs were equivalent
in motor function as measured by action potentials, muscle
weight, histomorphometry, and isometric force.
Grafting
For larger nerve gaps in which primary repair would cause ten-
sion, autografting remains the standard of care, especially for
the recovery of motor function. Recent advances in allografting
technique and biomaterials continue to produce interesting
prospects for the future of peripheral nerve repair.
Use of Autograft
In patients with larger nerve gaps, use of autograft remains the
most reliable repair technique. Sensory donor nerves are most
often used, with the sural nerve being the most commonly har-
vested. Autografting methods include single-stranded, cable,
and vascularized, and in all cases the graft is left 10% to 20%
longer than the gap for ensuring a tension-free repair. Although
no large clinical studies exist comparing these techniques, the
most commonly used is cable grafts with multiple small di-
ameter nerve grafts sewn between fascicles parallel to one an-
other to match the diameter of the severed nerve52.
Use of Allograft
Like autograft, nerve allograft provides a framework for nerve
regeneration but with the potential for shorter operative time,
abundant supply, and lack of donor site morbidity. A recent
multicenter retrospective study53 evaluated seventy-six nerve
repairs performed at various centers in a relatively heteroge-
neous group (forty-nine sensory, eighteen mixed, and nine
motor) using a processed human nerve allograft. Subgroup anal-
ysis was performed to determine the influence of nerve type,
gap length, patient age, time to repair, age of injury, and mech-
anism of injury on outcomes. Brooks et al. reported meaningful
recovery in 87.3% of subjects across subgroups using both
qualitative and quantitative outcome measures with no response
to treatment in eight of the subjects. There were no graft-related
adverse effects. Additionally, they showed functional recovery
in nerve gaps up to 50 mm53.
Immunogenicity has historically been a concern with
allografts. Although graft Schwann cells display major histo-
compatibilty complexes that incite T-cell response, host Schwann
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cell proliferation and irradiation of the graft improve regen-
eration and histologic outcome in animal models54. Karabekmez
et al.55 retrospectively studied short-term sensory recovery after
decellularized cadaveric nerve transplantation in seven patients
with ten nerve gaps, eight digital and two ulnar sensory. They
examined 2-point discrimination and found that all patients
recovered 10 mm or better static 2-point discrimination with
five good results and five excellent results with no cases of
infection or rejection. Although larger randomized studies are
needed, for small gaps up to 3 cm, allograft outcomes may be
comparable with that of conduits in sensory outcome43,48. Ray
et al.56 reported success in a mouse model with cold preserva-
tion for four weeks to decrease immunogenicity. Whereas most
studies have focused on sensory recovery, a recent study design
compared motor recovery of autograft to allograft and collagen
conduit in rat sciatic nerve gap lesions and found autograft
superior to allograft at sixteen weeks postoperatively in terms
of isometric strength recovery57. Allograft and autograft
were superior (p < 0.05) to collagen conduit. Although head-
way has been made, more development is needed prior to
recommending allograft use over autograft for longer nerve
gaps.
Evaluating Recovery and Outcomes
Rehabilitation after nerve injury may include adjacent joint
motion and motor and sensory training including biofeed-
back or re-sensitization focusing on central nervous system
reeducation19. Most studies to date have graded the success of
nerve repair using the British Medical Research Council’s
system or its modified versions for the evaluation of motor
and sensory return. Physical examination allows grading of
sensory recovery from S0 to S5 and motor from M0 to M5.
Subjective patient-perceived outcome measures are also
helpful in terms of assessing perceived disability, pain, and
functional outcome58,59. One recent retrospective review sug-
gested that high DASH scores may be predictive of greater
long-term disability59. Injury severity, patient age, site of repair
relative to target muscle, and time of repair remain the best
predictors of outcome following nerve injury20,31. However, a
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P E R I P H E R A L N E R V E R E PA I R AND RECONSTRUCTION
standardized, validated method to assess neural recovery fol-
lowing repair has not been established. Most nerve injuries
result in some level of nerve deficit and the development of a
standardized evaluation tool is made more difficult by the va-
riety of factors known to play a role in the recovery process
including the level of injury, age of patient, comorbidities,
timing of repair, and type of nerve injured.
Summary
Peripheral nerve injury often results in substantial disability.
Patient factors including age, degree of injury, and type of
nerve involved often predict the outcome. Although tension-
free direct repair remains the standard of care in easily ap-
proximated nerve ends, the armamentarium of the peripheral
nerve surgeon has increased in the past decade. Conduits,
grafting, and biologic agents can improve recovery when pri-
mary repair is not possible. Nerve and tendon transfers pro-
vide additional means of dealing with peripheral nerve injuries
in the right situation. Future advances in bioengineering,
allografts, and operative technique will lead to improved
options. n
Justin W. Griffin, MD
A. Bobby Chhabra, MD
D. Nicole Deal, MD
Department of Orthopaedic Surgery,
University of Virginia Health System,
400 Ray C. Hunt Drive,
Suite 330, P.O. Box 800159,
Charlottesville, VA 22908-0159
MaCalus V. Hogan, MD
Division of Foot and Ankle Surgery,
Department of Orthopaedic Surgery,
Universiy of Pittsburgh School of Medicine,
UPMC Shadyside Hospital,
5200 Centre Avenue, Suite 415,
Pittsburgh, PA 15232
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V O L U M E 95-A N U M B E R 23 D E C E M B E R 4, 2 013
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