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FIGURE 8.1 Nerve anatomy. The normal peripheral nerve consists of myelinated and
unmyelinated axons organized into bundles of fascicles. Peripheral neural tissue is supported
by three major connective tissue sheaths: the endoneurium, perineurium, and epineurium.
BIOLOGY OF NERVE INJURY
Loss of axonal integrity (axonotmesis and neurotmesis) leads to Wallerian degeneration, which is then
followed by axonal regeneration.2 When axons are disrupted, they lose contact to their cell body
resulting in deprivation of signaling after 24 to 48 hours. This lack of input is followed by fragmentation,
disintegration, and phagocytosis of axons and myelin by Schwann cells (SCs) and macrophages.
Subsequently, SCs dedifferentiate, proliferate, and elongate along the now empty endoneurial tubes and
release growth factors to guide axons to the denervated end organ.3 Clinically, axonal growth occurs at
a rate of 1 to 3 mm/d and can be monitored by evaluation of a progressive Tinel sign along the nerve
path.
4,5
However, even if axonal transection is followed by surgical repair, motor and sensory recovery may be
limited. Axons oftentimes do not find their original endoneurial tube, which results in reinnervation of
muscles that were originally not innervated by the same axons.6 In addition, gene expression after injury
is transient and therefore axonal regeneration declines prior to reaching the end target in time to recover
function.7 Consequently, proximal injuries with a longer distance between the area of injury and the end
target have a lower chance of full recovery.
Furthermore, if the endoneurial tube is disrupted or the nerve is transected and not repaired, axons
sprout in an attempt to regenerate but do not find an end target resulting in formation of an end-stump
neuroma or neuroma in continuity.8 On histopathology, neuromas resemble tangled axons with
proliferation of the endo-, peri-, and epineurium and increased presence of myofibroblasts as compared
with control nerves.9 Symptomatic neuromas have been found to cause chronic neuropathic pain, as
well as phantom sensations. Any partial or complete nerve transection can result in formation of
neuroma, but not every neuroma will cause neuropathic pain. There is evidence that certain nerves
develop painful neuromas more commonly than others, but the pathobiology of painful neuroma remains
unclear.
10
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DIAGNOSTIC WORKUP FOR NERVE INJURY, NERVE COMPRESSION, AND
NEUROMA
Any patient presenting with suspected nerve injury, nerve compression, or neuroma should undergo a
thorough history and physical examination. It is pertinent to determine the mechanism of injury, the
onset and duration of symptoms, type of motor and sensory deficit, as well as pain/phantom pain
frequency, intensity, and quality. On examination, information regarding the nerve(s) affected, as well as
the degree and the level of nerve injury, can be determined. History and examination findings should be
further confirmed with additional diagnostic tools.
High-Frequency Ultrasound Imaging and Magnetic Resonance
Neurography
Technological advances in ultrasound (US) imaging and magnetic resonance imaging (MRI) and
magnetic resonance neurography (MRN) have provided the ability for identification of nerve injury,
compression, and neuroma, as well as precise anatomic localization in the acute phase of injury and/or
early phase of nerve compression when electrodiagnostic studies may not yield reliable results.
11
Strengths of high-resolution US imaging include high spatial resolution for superficial nerves, which
permits evaluation of nerve continuity, as well as stretch injury and early nerve compression.12 In
addition, techniques such as “sonopalpation” to induce a Tinel sign through pressure of the sonographic
probe can permit more accurate localization of injuries. Based on these advantages, some authors have
advocated for US to become the primary imaging modality for nerve injury of superficial nerves. One
study showed that, in patients with suspected brachial plexopathy or mononeuropathies, excluding
carpal/cubital tunnel syndromes, US imaging was more sensitive than MRI in detection of pathology
(93% vs 67%) with equivalent specificity (86%).13 The limitations of US imaging include the significant
experience required to identify nerve pathology, operator dependency, and limited visibility of deep
nerves.
Compared with traditional MRI, MRN relies on high-resolution thin sections as well as suppression of
other surrounding structures such as fat and blood vessels to visualize the nerve independent from
other surrounding structures including hardware.14 This allows nerve imaging in difficult anatomic
locations and exact localization of nerve compression or nerve injury. Another advantage of MRN
includes early detection of muscle denervation as early as 4 days post injury, as compared with
electrodiagnostic studies that may take 2 to 3 weeks to detect muscle signal alterations.
15
Disadvantages of MRN include that it may not be available to all patients and studies are time
consuming as well as costly.
Electrodiagnostic Studies
Electromyography (EMG) and nerve conduction studies (NCSs) are typically performed together to
diagnose nerve injuries and nerve compression, to determine the severity of injury and to follow
improvement over time. NCSs are administered with cutaneous electrodes that measure conduction
velocities of signals traveling along sensory and motor nerves. For motor nerves, a stimulus is applied
proximally and the compound muscle action potential (CMAP) is measured at the distal muscle. For
sensory nerves, the compound sensory nerve action potentials (SNAPs) are measured in the distal
distribution of the sensory nerve. Small or absent CMAP/SNAP amplitudes indicate loss of
motor/sensory axons. In addition, a suspected conduction block (loss of myelin) is indicated by slower
than normal conduction velocities or increased latencies. During EMG studies, a needle is inserted into
the muscle(s) affected by nerve injury and muscle activity is measured. Approximately 2 weeks after
acute axonal injury, abnormal spontaneous muscle activity including fibrillations and positive sharp
waves can be detected, indicating axonal loss. In addition, motor unit potentials (MUPs) are a helpful
tool to monitor reinnervation over time. MUPs are generated by a single motor nerve and its associated
muscle fibers. MUPs are reduced immediately after injury but will reappear when the muscle fibers are
reinnervated prior to clinically visible spontaneous muscle activity. See Table 8.2 for a summary of
EMG/NCS results in Sunderland grade 1 to 6 nerve injuries.
TABLE 8.2. ELECTRODIAGNOSTIC FINDINGS BY DEGREE OF PERIPHERAL NERVE INJURY
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Sunderland
Classification of
Nerve Injury
Acute Nerve Injury Chronic Nerve Injury
Fibrillations/PSWs MUPs Fibrillations/PSWs MUPs
First degree No Normal No
a
Normal
Second degree Yes
b
Present:
secondary to
collateral
sprouting
No
a
Present:
secondary
to axonal
regeneration
Third degree Yes
b
Present:
secondary to
collateral
sprouting
No
a
Present:
secondary
to axonal
regeneration
Fourth degree Yes
b
No No
a
No
Fifth degree Yes
b
No No
a
No
Sixth degree
c
Yes
b
Variable No
a
Variable
a
Fibrillations and PSWs disappear after a period of chronic denervation.
b
Fibrillations and PSWs are not identifiable until 3 to 6 weeks after nerve injury.
c
Electrodiagnostic findings vary depending on the mixed severity and location of damage in sixth-degree nerve injuries.
MUPs, motor unit potentials; PSWs, positive sharp waves.
Diagnostic Nerve Blocks
Diagnostic local anesthetic blocks are a valuable tool in the diagnosis of neuropathic pain and neuroma.
The affected nerve is anesthetized proximal to the maximum point of pain to determine the level of
nerve injury/neuroma and plan the site of surgical management if indicated. Nerve blocks can be
performed using anatomic landmarks, as well as US and fluoroscopic guidance. The authors’ preference
is to use 1 to 3 mL of 1% lidocaine (1:100,000 epinephrine) and 1.5 mL of 0.5% bupivacaine (without
epinephrine). The amount of local anesthetic used should be the smallest amount required to
anesthetize the affected nerve. After the diagnostic portion of the nerve block examination is complete,
additional anesthetic can be injected to improve the therapeutic effect. However, injection of large
amounts of anesthetic will cloud the ability to identify specific pain points.
It is important to carefully monitor the patient’s response to nerve block. One simple tool to record
pain prior to and after the block is the visual analog scale that records pain on a scale of 0 to 10. Given
that patients who have had pain for a long time can have a delayed nerve block response, we
recommend recording pain 15 to 30 minutes after injection and contact with the patient ~24 hours later
to determine the transient benefit of the block. Although the literature is limited, a positive response to
nerve block has been shown to be a predictor for good outcomes after certain types of nerve
decompression surgery, such as headache surgery.
16,17
TIMING OF NERVE RECONSTRUCTION FOR FUNCTIONAL DEFICITS AND
NEUROPATHIC PAIN
The timing of nerve repair is critically important to achieve optimal outcome. If there is clear evidence of
either iatrogenic or traumatic nerve transection on imaging and/or electrodiagnostic studies, early
intervention is warranted within the first 24 to 72 hours to achieve the best functional results. However,
for patients who experience stretch injuries or blunt trauma that do not result in nerve transection or
avulsion, the optimal timing of surgical intervention remains a topic of debate. It is the authors’ practice,
in general, to investigate nerve injuries earlier rather than later and to perform early reconstruction if
possible.
Most authors agree that serial physical examinations, MRN, and electrodiagnostic studies can aid in
decision making for cases with an unclear degree of nerve injury and therefore uncertain potential for
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regeneration. If there is no return of nerve function on examination or imaging between 3 and 6 months
after injury, surgery is indicated depending on the level of injury and nerve(s) affected.
18
Timing of surgery for neuropathic pain and phantom sensation is less studied and less well
characterized. However, there is evidence to suggest that continuous acute neuropathic pain can lead to
central sensitization resulting in more complex pain that is difficult to treat.
19,20
Therefore, early
intervention for acute neuropathic pain is warranted if there is clear evidence of nerve pathology such as
compression or neuroma.
In addition, it is important to recognize the value of prophylactic interventions to avoid functional
deficits, neuropathic pain, and phantom sensations. For example, when nerve resection is not
preventable during extirpation of a tumor, nerve reconstruction and nerve transfers can prevent
permanent loss of function.21 Furthermore, following operations with expected nerve transection such as
amputations and breast cancer/transgender mastectomy, nerve reconstruction and/or reinnervation can
prevent numbness, neuropathic pain, and phantom sensation.22-24 Lastly, sensory neurotization should
be considered in free tissue transfer operations to further improve functional outcomes for patients.
NERVE RECONSTRUCTION
Primary Nerve Repair
Primary nerve repair is feasible in short segment injuries that permit coaptation of the severed nerve
ends under no tension. When nerves are placed under stretch, signs of tissue injury are apparent and
blood flow is reduced by 50% (5%-10% elongation), or no blood flow is present (>11% elongation). It is
important to debride the nerve ends sharply to an area of viable tissue prior to repair (visible fascicles,
bleeding vasa nervorum). Mobilization of the nerve through neurolysis and/or nerve transposition can be
helpful to gain additional length if needed. In addition, ensure that the area in which the nerve repair is
performed is in a neutral position and the repair is not under excessive tension when the joint is moved.
Although many different techniques for primary nerve coaptation have been described, epineural suture
repair remains the standard. The author’s preference is to perform a microsurgical coaptation with two
9.0 Nylon single interrupted sutures at 0° and 180°. The fascicles should be well aligned according to
their native topography as depicted in Figure 8.2. If nerve repair is performed in the first 72 hours, a
nerve stimulator can aid in identification of the topography of motor axons. Furthermore, the epineurial
vascular pattern can guide the correct alignment of fascicles.
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FIGURE 8.2 Direct nerve coaptation. A. In an epineural repair, the fascicles must be
appropriately trimmed so that they do not buckle, which will result in misdirection of the
regenerating fibers. B. Well-performed nerve repairs will result in good alignment of fascicles
without the need for fascicular sutures.
Nerve Repair With Conduits
Nerve conduits are synthetic tubes to guide nerves across short segmental nerve gaps when primary
repair cannot be accomplished in a tension-free manner. These constructs have been shown to support
successful nerve regeneration across short sensory nerve gaps and work best for small gaps. Benefits
of conduits include that the regenerating axons are not required to cross two suture lines and no donor
tissue is required. Disadvantages are complications specific to the conduit (such as extrusion and
possible foreign body reactions) as well as limited understanding of the maximum nerve gap length that
will provide good or excellent outcomes. Several studies have analyzed conduit repair for segmental
nerve defects of varying lengths. Clinical outcomes for short gap repairs with conduits (<6 mm) have
been shown to be equivalent to primary nerve repair.25 Above 6 mm, results vary between studies with
failure rates between 40% and 100%.
26,27
In addition, a recent review article found that conduits led to
significantly lower rates (62.2%) of meaningful recovery (MR) defined as ≥S3 and ≥M3 based on MRCC
scales as compared to autograft (81.6%) and allograft (87.1%).28 Therefore, the use of currently
commercially available conduits should be critically evaluated on a case-by-case basis and approached
with caution. A significant amount of research has gone into creation of neural conduits with
neurotrophic factors that may improve functional outcomes.
Nerve Repair With Autograft and Allograft
Long segmental nerve gaps require autograft or allograft interposition. Similar to primary repair, tensionfree coaptation is important and should be taken into consideration when harvesting a nerve graft or
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choosing an allograft. In addition, nerve donor to recipient diameter should be approximated as closely
as possible. The same suture techniques as for primary repair can be used. Common autograft donor
nerves include the sural nerve, medial and lateral antebrachial cutaneous nerves, posterior interosseous
nerve, cutaneous branches of intercostal nerves, and the posterior and lateral cutaneous nerves of the
thigh.29 Nerve autografts are immunogenically inert scaffolds with neurotrophic factors and SCs. No
clear benefit has been shown in the use of vascularized versus nonvascularized nerve autografts. After
harvest, the autograft should be placed in reversed orientation at the repair site to prevent loss of
regenerating axons along branches. Large-diameter nerves may require multiple autograft cable grafts
to provide optimal nerve regeneration. The grafts should be made 10% to 20% longer than the nerve
gap to avoid undue tension. Advantages of nerve autograft include the availibility of growth factors and
SCs that provide growth guidance cues. In addition, no foreign material is introduced and the financial
cost is limited. The disadvantages include donor site morbidity including scar, numbness, and potential
for neuroma formation, as well as a limited supply of donor nerves.
Acellular nerve allograft is an alternative to autograft use. Nerve grafts are harvested from deceased
donors and decellularized to avoid an immune response. Advantages of nerve allograft include no donor
site morbidity, reduced surgical time, and unlimited supply. Disadvantages include the financial cost.
Autograft repair remains the standard for nerve reconstruction for long segmental nerve gaps.
Experiments in rodents have shown that axon regeneration across nerve defects is accelerated with
autografts versus currently available clinical alternatives.
30,31
However, clinical trials in humans have
shown that allograft repairs have similar clinical outcomes. One large prospective multicenter study (385
subjects and 624 nerve repairs) found that 82% MR was achieved across sensory, mixed, and motor
nerve repairs with segmental gaps of up to 70 mm with nerve allograft repairs.32 Another systematic
review article found that functional outcomes for MR for both sensory and motor function were not
significantly different between autograft (n = 670) and allograft (n = 711) (sensory 71.8% vs 81.9%
P = .186; motor 56.0% vs 58.3% P = .500).28 However, further prospective head-to-head comparison
studies are required to determine the outcomes for autograft versus allograft in specific nerve locations.
Nerve Transfers and Functional Muscle Transfers
Also see Chapters 81-83, 41: Principles and Applications of Nerve Transfers, Management of Brachial
Plexus injuries, Tetraplegia, Facial Paralysis.
Prolonged denervation in proximal nerve injuries results in muscle atrophy, fibrosis, and loss of motor
end plates as regenerating axons cannot reach their end target in time. If nerve injury occurs very
proximal and/or there is no evidence of improvement of nerve function on examination and/or EMG after
a 3-month period, distal nerve transfers are an option to keep the muscle viable while axons travel the
long distance to the muscle target. There are several commonly performed nerve transfers for a variety
of conditions from head to toe. In the face, the masseteric nerve branch of the mandibular nerve is
frequently coapted to the buccal branch of the facial nerve for smile restoration. Regularly performed
transfers in the upper extremity include the double fascicular transfer of the median fascicle to biceps
branch and ulnar fascicle to brachialis branch, as well as the long head of triceps to the anterior axillary
nerve branch and the anterior interosseous nerve to the ulnar nerve. Lower extremity nerve transfers
are less frequent but include the obturator to femoral nerve transfer as well as the tibial nerve branch to
tibialis anterior transfer.
When patients present in a delayed fashion after nerve injury and irreversible muscle atrophy has
already occurred, nerve transfers are no longer a treatment option, as the muscle will not regenerate. In
these cases, functional muscle transfer should be considered. The gracilis flap is the most common free
functional muscle flap used to reconstruct upper and lower extremity dysfunction, as well as facial palsy.
However, other functional muscle transfers such as the latissimus dorsal flap and rectus abdominis flap
have been described.
TREATMENT OF NEUROPATHIC PAIN
Also see Chapters 9, 82, 45: Management of Neuroma Pain, Management of Compression
Neuropathies of the Upper Extremity, Migraine Management and Surgery.
Patients suffering from neuropathic pain require a multidisciplinary team to manage different aspects
of care including pharmacological treatment (pain medicine, neurology), injections (pain medicine,
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neurology), neurostimulation (pain medicine), psychological care, as well as musculoskeletal and nerve
therapies (surgery, rehabilitation medicine, physical and occupational therapy). As part of the pain team,
surgeons are tasked to identify and treat the three main sources of neuropathic pain: nerve
compression, nerve injury (neuroma), and musculoskeletal injury/inflammation.33 All three conditions can
occur from head to toe and cause severe pain and disability. Physical examination, high-frequency US
imaging, MRI/MRN, and electrodiagnostic studies, as well as local anesthetic blocks, can be helpful in
confirming the diagnosis.
Common nerve compression syndromes that can cause severe neuropathic pain include occipital
neuralgia, supraorbital/supratrochlear neuralgia, carpal tunnel syndrome (median nerve compression),
cubital tunnel syndrome (ulnar nerve compression), and pudendal and tibial nerve compression (tarsal
tunnel syndrome). Once identified, patients should undergo early workup and intervention to prevent
long-term weakness, numbness, and centralization of pain. Surgical principles of nerve decompression
include identification of all nerve compression points, complete nerve release from surrounding
structures, and prevention of recurrence with techniques that vary depending on the surgical site.
Neuroma formation occurs after nerve injury and can affect any partially or fully transected nerve.
There is evidence to suggest that certain nerves such as the radial sensory nerve, the digital nerves of
the upper and lower extremity, as well as the sural nerve have a high propensity to develop painful
neuromas.10 Symptomatic neuromas cause severe pain in the distribution of the affected nerve, and
early treatment is warranted to avoid long-term morbidity. The diagnosis of symptomatic neuroma
includes presence of all the following symptoms: (1) pain with at least three of these characteristics:
burning, sharp, shooting, electric, paresthesias, numbness, and cold intolerance; (2) symptoms in a
defined neural anatomical distribution; (3) history of nerve injury or suspected nerve injury. In addition,
one of the following must be present: (1) positive Tinel sign (for a cutaneous nerve); positive response to
local anesthetic injection; (2) US or MRI confirmation of neuroma.
34
The treatment algorithm for symptomatic neuromas has changed over the past years with a paradigm
shift toward more advanced nerve reconstruction techniques.35 For decades, the standard for treatment
and prevention of neuroma was excision and implantation of the nerve end in muscle and traction
neurectomy. This technique yielded good to excellent outcomes in 82% of patients, but results were not
consistent across studies.36 New research insights that expanded our understanding of peripheral nerve
regeneration led to the implementation of alternative techniques that have been shown to be highly
effective in the treatment and prevention of neuroma pain.
In general, contemporary surgical techniques vary based on whether the patient has a neuroma in
continuity (distal nerve end available) or an end stump neuroma (distal end not available).
35
For neuromas in continuity, the function of the affected nerve and the expected deficit after partial or
complete excision must be considered and weighed on a case-by-case basis. In patients with mild pain
who have a high likelihood of significant motor and sensory deficits after neuroma excision, an
intervention may not be justified. However, in cases of incapacitating pain, neuroma excision and
reconstruction may be acceptable. After excision of a neuroma in continuity, the nerve gap can be
reconstructed with a conduit, autograft, or allograft depending on the defect size.
Treatment of end stump neuromas typically involves excision and reconstruction of the nerve end to
prevent recurrence.35 The principles of neuroma excision include transection of the nerve proximal to the
area of pain, debridement of the neuroma to normal and healthy appearing nerve tissue, and sharp
transection of the nerve end.
Various techniques for reconstruction have been described. Regenerative peripheral nerve interface
(RPNI) and targeted muscle reinnervation (TMR) are novel surgical techniques that have become
increasingly popular for the treatment and prevention of neuroma pain. Both techniques rely on the
principle that the regenerating nerve will grow into a denervated segment of muscle. Thereby, the nerve
endings have “somewhere to go and something to do” instead of forming a neuroma and this improves
the risk of developing neuropathic pain. RPNI is a technique in which a denervated segment of muscle
is wrapped around the transected nerve end.37 When performing TMR, a small motor branch is found in
a muscle adjacent to the transected nerve and the affected nerve is coapted to the small motor
branch.
38
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Another common technique is relocation nerve grafting.35 An autograft or allograft is coapted to the
transected nerve end, and the distal end of the graft is placed in an area remote from the original pain
and buried in muscle. Given that only a limited number of axons will reach the end target that is buried
deep in muscle, this is intended to limit development of neuropathic pain. Capping of nerve ends has
further been investigated with different materials and shown to be effective in prevention of neuroma
formation.39This technique assumes that the nerve end will grow to the end of the cap but will not form a
neuroma given the limited space present within the cap.
Currently, there are no direct comparison studies of techniques employed for the reconstruction of end
stump neuromas. However, a recent meta-analysis that included 54 studies found that surgical
management of symptomatic neuromas resulted in clinically meaningful pain reduction in 77% of cases.
In patients with symptom duration <23 months, the type of surgical technique used to address the
neuroma did not lead to significantly different outcomes. In patients with symptom duration over
24 months, excision and transposition into muscle, bone, or vein (74% patients improved [95%
confidence interval (CI): 0.65-0.83]), as well as neurolysis and coverage with vascularized tissue (91%
patients improved [95% CI: 0.80-1.00]), led to significantly improved outcomes as compared with
excision only and excision and repair (20% patients improved [95% CI: 0.05-0.34], P < .05).
40
PERIOPERATIVE CARE
The perioperative care of patients with nerve injuries is multidisciplinary and includes pain management,
psychiatry, physical therapy, and occupational therapy. Patients should be optimized prior to surgery to
avoid adverse outcomes.
Immediately preoperatively, it is important to mark the exact area of suspected nerve injury and if
applicable the area of maximum pain/pain distribution. Given that certain nerves have a high degree of
anatomic variability, these markings are invaluable to identify the correct nerve intraoperatively. During
nerve procedures in general, optimal pain control with nerve blocks and local anesthetic injections is
critical to improve the postoperative patient experience.
To avoid postoperative tension on the nerve repair site, movement should be restricted in the first
week after surgery. Patients may require braces and other assist devices to bridge the time to functional
recovery. In addition, patients with pain should not wean off medications independently but continue
their work with psychiatry and pain management to discontinue medications responsibly.
QUESTIONS
1. Which of the following states of nerve injury will lead to no spontaneous recovery of motor or
sensory function?
a. Wallerian degeneration
b. Neurotmesis
c. Neuropraxia
d. Axonotmesis
2. A 23-year-old otherwise healthy patient with no prior surgeries sustains a nerve injury to the
femoral nerve resulting in a 8-cm nerve gap. What is the best option for nerve repair?
a. Direct repair
b. Nerve reconstruction with nerve conduit
c. Nerve reconstruction with nerve allograft
d. Nerve reconstruction with nerve autograft
3. A 50-year-old patient presents with burning, electric pain, and numbness, as well as cold
intolerance of the thigh, following below-the-knee amputation 1 year ago. What diagnostic workup
is indicated to establish a diagnosis for suspected symptomatic neuroma?
a. Electromyography and nerve conduction studies
b. Ultrasound and/or MRI and diagnostic local anesthetic injection
c. Psychiatric evaluation
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d. Nerve biopsy
ANSWERS AND EXPLANATIONS
1. Answer: b. Neurotmesis means that there will be no spontaneous recovery of nerve function in
the absence of nerve repair or reconstruction. Wallerian degeneration describes a process that
occurs with both axonotmesis and neurotmesis. When axons are disrupted, they lose contact with
their cell body resulting in deprivation from signaling after 24 to 48 hours. This lack of input is
followed by fragmentation, disintegration, and phagocytosis of axons and myelin by Schwann cells
(SCs) and macrophages. Subsequently, SCs dedifferentiate, proliferate, and elongate along the
now empty endoneurial tubes and release growth factors to guide axons to the denervated end
organ. Neurotmesis means that there will be no spontaneous recovery of nerve function.
Neuropraxia leads to full spontaneous recovery. Axonotmesis results in variable recovery.
2. Answer: d. The current standard technique for long gap nerve repairs is nerve autograft. Other
principles of nerve repair include that the nerve tissue should be trimmed back to healthy tissue
(good vascular supply, visible fascicles) prior to tension-free repair. In an epineurial repair, the
axons should be well aligned. If the axons buckle and come out of the repair site, they should be
trimmed to avoid axonal escape. If tension-free primary repair is not possible, conduits, autografts,
and allografts can be used to bridge the nerve gap. Conduits are best suited for short gap repairs.
However, conduits should not be used in long nerve gaps, as autografts and allografts have been
shown to have better outcomes. The current standard technique for long gap nerve repairs is nerve
autograft.
3. Answer: b. Diagnostic criteria for neuroma include all the following: (1) pain with at least three
of these characteristics: burning, sharp, shooting, electric, paresthesias, numbness, and cold
intolerance; (2) symptoms in a defined neural anatomical distribution; (3) history of nerve injury or
suspected nerve injury. In addition, one of the following must be present: (1) positive Tinel sign (for
a cutaneous nerve); (2) positive response to local anesthetic injection; (3) US or MRI confirmation
of neuroma.
34
ACKNOWLEDGMENTS
Kyle Eberlin, MD, is a consultant for Axogen, Integra, Checkpoint, and Tissium. Lisa Gfrerer, MD, PhD,
is a consultant for Sientra and Cytrellis. This work was supported by the American Association of Plastic
Surgeons Academic Scholar Program to Lisa Gfrerer, MD, PhD. The content is solely the responsibility
of the authors and does not necessarily represent the official views of the American Association of
Plastic Surgeons.
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