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Nerve Repair
Manual:
A Practical Approach to Injury
and Repair in the Brachial Plexus
and Upper Extremity
Scott
H.
Kozin,
MD
Brian O’Doherty, photographer
checkpointsurgical.com
The Checkpoint® Nerve Stimulator Locator is a single-use, sterile
device intended to provide electrical stimulation of exposed motor
nerves or muscle tissue to locate and identify nerves and to test
nerve and muscle excitability.
Do not use the Checkpoint Nerve Stimulator when paralyzing
anesthetic agents are in effect, as an absence of inconsistent
response to stimulation may result in inaccurate assessment of
nerve and muscle function.
For a complete list of warnings and precautions regarding the use of
the Stimulator, please see www.checkpointsurgical.com
This manual is designed to guide the diagnosis and treatment of
nerve injuries. The manual is not intended to replace sound clinical
judgment or meticulous surgical technique.
To access the videos throughout this manual please
download a QR reader App.
© Copyright 2016 Checkpoint Surgical Inc. All rights reserved.
Preface
Why make a manual solely devoted to nerve repair in the brachial plexus
and upper extremity? This answer is simple; find a perplexing problem and
simplify it. The diagnosis of nerve injury produces confusion, myth, and
misperception. The field of nerve injury crosses many specialties including
neurology, neurosurgery, plastic surgery, physiatry, orthopedic surgery, and
therapy. These areas of medicine publish in different arenas and present in
dissimilar venues. These specialties infrequently interact and therefore critical
information that may enhance the diagnosis and treatment of nerve injuries
is not shared. In addition, the quagmire of misinformation and the magnitude
of unsubstantiated treatment modalities are overwhelming for clinicians and
patients. The unvetted material on the internet has potentiated the problem
of “publishing” unreliable information. Hence, unproven and unsupported
treatment regimens are propagated and applied to treat patients with nerve
injuries. These modalities often delay treatment and miss a window of
opportunity to intervene and truly improve outcome.
The goal of this manual is to simplify and demystify nerve injuries based
upon our current understanding of anatomy, injury, treatment, and
outcome. This knowledge is derived from the credible peer reviewed
literature and twenty years of experience examining, treating, and
operating on patients with nerve injuries. These patients have been
informative and vital to enlighten my understanding of nerve injuries
from diagnosis thru treatment. Their participation in the “practice of
medicine” has been invaluable and instrumental in my learning during
my career as a nerve surgeon. Their contributions must be recognized
and appreciated as their willingness to discuss, interpret, and express
their thoughts has been priceless.
The goal of this project is to produce a readable and dependable multidisciplinary manual base upon what we “know now” (circa 2016). As
the knowledge based expands and innovation progresses forward, the
information and recommendations will change over time. As Socrates
said “the only true wisdom is knowing that you know nothing” and
I expect this manual to evolve over time as our knowledge of nerve
injury and pathophysiology is supplanted by ongoing research and
new discoveries. The ultimate goal is to eventually provide discrete
guidelines and apply innovative techniques to improve the lives of
patients with nerve injuries.
Scott H. Kozin, MD
Introduction
Nerve injuries are devastating to the patient and challenging to the
clinician. The anatomy can be perplexing as the nerves course
from the spinal cord to supply their respective muscles. The nerves
also provide critical sensation to the limb that differs from their
muscle innervation. The physical examination of specific nerves
requires diligence and a keen understanding of sensory and muscle
innervation. Following nerve injury, the pathoanatomy contains
puzzling terminology such as neurapraxia, axonotmesis, and
neurotmesis. The treatment following nerve injury is confounded
by numerous factors that lead the clinician astray and obscure
the time to intervene. Ancillary studies such as electrodiagnostic
testing, magnetic resonance, or ultrasound may provide valuable
information or produce indeterminate information that add further
confusion and further delays intervention. Nerve surgery can be
complicated with the variety of available options including neurolysis,
direct repair, conduit interposition, grafting (allograft or autograft) and
nerve transfer. This manual will demystify nerve injuries and provide
a practical approach to anatomy, injury, examination, and treatment
that will give the clinician the knowledge and confidence necessary
to diagnose and manage nerve injuries.
Anatomy
Central Nervous System
The central and peripheral nervous system is an array of neural
connections that allow transmission of a purposeful thought into
an immediate action. The central nervous system transmits efferent
signals from the brain (somatosensory motor cortex) to the spinal
column. These signals leave the brain and travel to the anterior horn
cells within the spinal column (motor cell bodies) and exit via the
brachial plexus to control all movement in the shoulder girdle and
the entire upper extremity. Similarly, afferent sensory signals travel
back from the limb into the spinal cord via the dorsal root ganglion
(sensory cell body) that resides in the intervertebral foramina. The
signal continues into the spinal cord and up to the brain to perceive
pain, temperature, pressure, proprioception, and touch.
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Brachial Plexus
The brachial plexus is a vexing complex of nerves that can be
simplified into basic anatomical elements. There are certainly
variations in brachial plexus anatomy; however, this description
applies to the vast majority of persons and this simplified explanation
can be relayed to patients and their families when describing the
anatomy and injury (Figure 1). The brachial plexus is structurally
similar to tree roots that provide the foothold for the tree that
Figure 1: Simplified diagram of the brachial plexus with relevant anatomy that is explainable to
patients and families. (Courtesy of Dan A. Zlotolow, MD)
subsequently outlet into branches. There are five roots (four cervical,
one thoracic) labeled C5, C6, C7, C8, and T1: the acronym C
refers to cervical or neck and T for thoracic or chest. The T1 nerve
root, however, originates from the spinal cord and travels above
the clavicle. Hence, all five nerve roots are in the neck. From these
five nerve roots, three trunks (upper, middle and lower) are formed.
The upper trunk is the combining of the C5 and C6 nerve roots.
The lower trunk is the conjoining of the C8 and T1 nerve roots. The
middle trunk is continuation of the C7 nerve root. The trunks pass
beneath the clavicle and travel into the arm sending nerve branches
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along the way to innervate the muscles within the shoulder girdle.
Ultimately, the trunks terminate into major peripheral nerves that
supply fundamental movement and sensation to the arm, forearm,
and hand. Each root is analogous to an internet cable with insulation
on the outside (myelin sheath) and fiber optic cables (axons) on the
inside. Each root contains approximately 20,000 axons (fiber optic
cables) for a total of 100,000 axons (five roots x 20,000 axons/root).
The diagram of the brachial plexus may be necessary to pass a
medical school test, but does not depict the anatomic innervation
related to the crisscrossing of nerve fibers. A simplified and practical
approach is the best method to understand the contributions of the
upper, middle, and lower trunks with respect to limb movement.
The upper trunk (C5, C6) controls shoulder (glenohumeral joint)
movement, primarily rotator cuff and deltoid muscles, that govern
shoulder abduction, external rotation, and internal rotation. The
upper trunk also controls elbow flexion, forearm supination, and
contributes to wrist extension. The middle trunk (C7) primarily
manages elbow extension, forearm pronation, wrist extension, finger
extension, and thumb extension. The lower trunk (C8, T1) is critical
for hand function and governs grasp and all fine motor tasks, such
as crossing one’s fingers and touching the tip of the thumb to the tip
of the small finger (opposition).
This basic understanding of “trunk” function can be expanded into
more detail. The upper trunk provides primarily nerve and muscle
input into the axillary nerve (deltoid and teres minor muscles),
suprascapular nerve (supraspinatous and infraspinatous muscles),
and musculocutaneous nerve (biceps and brachialis muscles).
The upper trunk also contributes to the radial nerve to innervate
the brachioradialis, supinator, and extensor carpi radialis longus
muscles. The middle trunk provides the primarily nerve and muscle
input into the radial nerve (triceps, extensor carpi radialis brevis,
extensor digitorum communis, extensor indicis propious, extensor
digiti minimi, and extensor carpi ulnaris). The middle trunk also
contributes to the median nerve to innervate the pronator teres and
flexor carpi radialis muscles. The lower trunk, provides the primary
nerve and muscle input into ulnar nerve (flexor digitorum profundus,
flexor carpi ulnaris, interossei, hypothenars, and adductor pollicis).
The lower trunk also contributes to the median nerve via the anterior
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interosseous nerve (pronator quadratus, flexor pollicis longus, and
flexor digitorum profundus to the index finger) and the recurrent
motor nerve (thenar muscles).
There are a few muscles that have segmental innervation from
numerous nerve roots. The pectoralis major receives innervation
from C5 thru T1 moving from top (clavicle origin) to bottom (ribs).
The subscapularis muscle receives innervation from upper and
lower subscapular nerves (C5 thru C7) moving from upper to lower.
The latissimus dorsi receives innervation from C6 thru C8 with C7
inputting the strongest contribution. The serratus anterior muscle
receives segmental innervation from C5 thru C7 from upper to
lower. The sensory examination is distinctly different than the motor
examination. The upper trunk provides sensation to the radial
sensory (first web space and radial dorsum of hand) and median
nerves (palmar aspect of thumb and index fingers). The middle trunk
inputs sensation into the median nerve that supplies the long finger
(palmar aspect of long finger). The lower trunk provides sensation
into the ulnar nerve (ulnar dorsum of hand and palmar aspect of ring
and small fingers).
Practical Anatomy for Brachial Plexus Injury Pattern
Trunk (Roots)
Muscles
Sensation
Upper Trunk
(C5 & C6)
Shoulder
(rotator cuff and deltoid)
Forearm supination
(biceps & supinator)
Elbow flexion
(biceps, brachialis,
brachioradialis)
Wrist extension (extensor
carpi radialis longus)
Median nerve
sensibility
thumb & index
finger
Middle Trunk
(C7)
Elbow extension (triceps)
Latissimus dorsi
Forearm pronation
(pronator teres)
Wrist extension (extensor
carpi radialis longus) Digital
extension (MCP joints)
Wrist flexion
(flexor carpi radialis)
Median nerve
sensibility long
finger
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Trunk (Roots)
Lower Trunk
(C8 & T1)
Muscles
Forearm pronation
(pronator quadratus)
Extrinsic finger and thumb
flexors (flexor digitorum
profundus and flexor pollicis
longus)
Wrist flexion
(flexor carpi ulnaris)
Digital extension (IP joints)
Intrinsic muscles
(interossei, thenars, hypo
thenars, adductor pollicis
Sensation
Ulnar nerve
sensibility
(ring and
small fingers)
Evaluation
Understanding the brachial plexus and peripheral anatomy
facilitates and simplifies the physical examination. The nervemotor evaluation should be concise, focused, and relatively brief
in the majority of cases. This succinctness is especially important
when examining children who have a short attention span and
are easily distracted. In acute isolated nerve injuries, passive
and active movements are performed and documented. Passive
movement should be full and painless. The lack of painless full
passive movement is a harbinger of another underlying problem,
such as fracture or dislocation. Over time, passive movement can
decrease and a joint contracture can develop without therapeutic
interventions, such as stretching and splinting. Cardinal active
movements are performed to illustrate and document specific
motions that demonstrate a functional or nonfunctional nerve.
The table below lists those active movements elicited and their
respective peripheral nerve and primary nerve root basis.
Table: Cardinal Movements and Nerve Innervation
Movement
Nerve
Root(s)
Axillary nerve- deltoid
Suprascapular nervesupraspinatous
C5, C6
C5, C6
Shoulder external
rotation
Suprascapular nerveinfraspinatous
Axillary nerve- teres minor
C5, C6
Shoulder internal
rotation
Subscapular nervessubscapularis
C5, C6,
C7
Shoulder abduction
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Peripheral
Nerve- Muscle(s)
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C5, C6
Musculocutaneous nervebiceps, brachialis
Radial nerve- brachioradialis
C6
Radial Nerve- triceps
C7
Forearm supination
Musculocutaneous nervebiceps
Radial nerve- supinator
C6
C6
Forearm pronation
Median nervepronator teres
Median nerve (AIN)pronator quadratus
Elbow flexion
Elbow extension
C6
C7
C8,T1
Wrist extension
Radial nerve- extensor
carpi radialis longus
Radial nerve- extensor
carpi radialis brevis
C6
C7
Wrist flexion
Median nerve- flexor
carpi radialis
Ulnar nerve- flexor carpi
ulnaris
C7
C8
Long finger flexion
Median and ulnar- flexor
digitorum profundus
C8, T1
Long finger and
thumb flexion
Median- flexor pollicis longus
C8, T1
Finger MCP joint
extension
Radial nerve- extensor
digitorum communis
C7
Finger IP joint
extension
Ulnar nerve- dorsal and
palmar interossei
C8,T1
Finger abduction and Ulnar nerve- dorsal and paladduction
mar interossei, respectively
Thumb abduction
and adduction
Median- abductor pollicis
Ulnar- adductor pollicis
C8,T1
C8,T1
C8,T1
AIN= anterior interosseous nerve
Certain cardinal movements require additional clarification to
fully understand nerve injury. The movements about shoulder,
elbow, forearm, and wrist are more easily understood. The hand
movements require further enlightenment. Digital (thumb and finger)
opening requires metacarpophalangeal and interphalangeal joint
extension. The primary metacarpophalangeal joint extensor muscles
originate in the forearm (extrinsic muscles) and are the extensor
digitorum communis, extensor indicis proprious, and extensor digiti
minimi muscles innervated by the radial nerve (C7). The primary
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interphalangeal joint extensor muscles originate in the hand (intrinsic
muscles) and are the interossei innervated by the ulnar nerve (C8,
T1). Digital (thumb and finger) closing or grasping requires both
metacarpophalangeal and interphalangeal joint flexion. The primary
interphalangeal joint flexor muscles originate in the forearm (extrinsic
muscles) and are the flexor digitorum profundus,
flexor digitorum superficialis, and flexor pollicis longus
muscles innervated by the median (C8, T1) and ulnar
nerves (C8, T1). The primary metacarpophalangeal
joint flexor muscles originate in the hand (intrinsic
Video 1: Intrinsic
muscles) and are the interossei and adductor pollicis versus Extrinsic
innervated by the ulnar nerve (C8, T1). Hence, full
digit extension and flexion of the digits requires a coordinated
effort between the extrinsic and intrinsic muscles innervated by
different nerves. This synchronized task is disrupted by injury to
the radial (C7) or ulnar (C8, T1)
nerve or nerve roots (Video 1).
This harmonized motion is also
necessary for crossing fingers,
as this seemingly simple task
is anything but simple. Full
metacarpophalangeal and
interphalangeal joint extension
coupled with interossei adduction
Figure 2A: Inability to cross fingers. 17 year-old
and abduction is necessary to
who sustained a right ulnar nerve laceration
complete this complicated task. above the elbow.
Special Tests
There are a variety of tests that are valuable in discerning nerve injury
patterns. As discussed, crossing one’s fingers is a synchronized
task that requires full metacarpophalangeal and interphalangeal
joint extension coupled with interossei adduction and abduction.
This infers functioning radial (C7) and ulnar (C8, T1) nerves or
nerve roots (C7,C8,T1) (Figure 2A). The Froment’s sign tests for
adductor pollicis muscle function and distal ulnar nerve (C8, T1)
function. In other words, the adductor pollicis is essential for lateral
pinch and functions similar to a palmar interossei. The adductor
pollicis adducts the thumb, flexes the metacarpophalangeal joint
and extends the interphalangeal joint. This combined movement
produces lateral pinch. The Froment’s sign is assessed by asking
the patient to forcefully perform lateral pinch to a piece of paper
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using both hands (Figure 2B). An
absent or weak adductor pollicis is
unable to generate enough force
for lateral pinch and the paper can
be easily pulled from the affected
side. In addition, the flexor pollicis
longus is recruited during lateral
pinch, which results in unopposed
interphalangeal joint flexion and
feeble pinch (Froment’s sign).
Figure 2B: Positive Froment’s sign.
Another maneuver to assess lower
trunk function is asking the patient
to form a “table top” with their fingers (Finger 2C). Specifically, full
metacarpophalangeal flexion and interphalangeal joint extension
indicates intact ulnar nerve or nerve roots (C8, T1).
There are also a variety of simple valid tasks that assess specific
peripheral nerves. Asking the patient to make an OK sign requires
flexion of the thumb and index interphalangeal joints (Figure 3). This
indicates intact anterior interosseous nerve function, which receives
its input from the median nerve
and C8 and T1 nerve roots.
Patients often enjoy extending
the index and small fingers while
grasping the second and third
fingers with the thumb (Figure
4). This maneuver demonstrates
functioning extensor indicis
propious and extensor digiti
Figure 2C: Unable to perform a table top with
fingers, specifically, full metacarpophalangeal
minimi muscles innervated by the their
flexion and interphalangeal joint extension at the
same time.
posterior interosseous branch of
the radial nerve (C7).
Sensory Examination
There are numerous methods to assess the status of sensation
or sensibility. Options include two-point discrimination, vibratory
testing, Semmes Weinstein monofilament testing, ten test, and
sharp/dull perception. I never perform sharp/dull perception as
you will quickly lose rapport with the patient, especially children.
Two-point is my preferred method of assessment in the office
setting as it is quick and efficient. A caliper or paper clip can be
used as the discriminator. The finger is touched with enough
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Figure 3: OK sign requires
flexion of the thumb and
index interphalangeal joints
and indicates intact anterior
interosseous nerve function
(median nerve and C8 and T1
nerve roots).
Figure 4: Asking the patients to extend
their index and small fingers while
grasping the second and third fingers
demonstrates functioning extensor
indicis propious and extensor digiti
minimi muscles (posterior interosseous
branch of the radial nerve (C7)).
pressure to blanch the skin. The patient always starts with their
eyes open and their non-injured limb to ensure understanding of the
test. Subsequently, their eyes are closed and the test completed
on the non-injured and injured limb. The test is performed on the
tip of the thumb (median and C6), long finger (median and C7),
and small finger (ulnar and C8). Two-point discrimination greater
than 15 millimeters after sharp injury infers nerve laceration. The
ten test (TT) is simple, reliable, and requires no test equipment. The
subject reports his/her light touch perception of the skin during
simultaneous stroking of the normal contralateral part and the area
under examination. The patient rates their sensation between 0/10
and 10/10 with 0 being no sensation and 10 perfect sensation. The
TT requires patient cooperation and comprehension, which may be
challenging for some patients.
Sensory examination in children is more difficult. Two-point
discrimination is unreliable until about six to eight years of age.
There are other signs of absent sensibility in children. One clinical
clue is that children will bypass or ignore digits without sensation.
Another sign is dryness of the finger as nerve supply is necessary for
moisture. Lastly, water immersion will not produce wrinkling of the
fingers (“pruney fingers”) without an intact nerve supply.
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Ancillary Testing
Ancillary testing that may be helpful include imaging modalities
and electrodiagnostic testing. Imaging studies include ultrasound,
magnetic resonance imaging (MRI), and computerized tomography
(CT) myelography. Ultrasound and MRI can visualize peripheral
nerve continuity versus frank discontinuity. However, neither
imaging modality can discriminate between a neuroma-in-continuity
that will recover versus a neuroma in-discontinuity that will not
recover. Imaging studies may be useful in brachial plexus injuries,
especially adult injuries for assessment of potential nerve root
avulsion. Following nerve root avulsions, a meningeal pouch filled
with cerebrospinal fluid (pseudomeningocele) forms outside the
intervertebral foramen. CT myelography and MRI can visualize
these pseudomeningoceles (Figure 5). However, there are falsepositive and false-negative results with both imaging modalities.
More advanced techniques are under development to improve the
diagnostic accuracy but their validity remains to be established.
Magnetic resonance imaging currently offers the best evaluation of
the brachial plexus trunks and cords with potential identification of
a neuroma. Unfortunately, the MRI is unable to assess whether the
neuroma has axons in-continuity (axonotmesis) or there is complete
discontinuity (neurotmesis).
Electrodiagnostic testing
consists of two distinct
assessments: nerve conduction
and electromyography (direct
testing of muscle integrity). Nerve
conduction studies across an
injured nerve segment will be
abnormal immediately after
injury. However, the conduction
loss can be from a neurapraxia,
axonotmesis, or neurotmesis. A
neurapraxia type injury does not Figure 5: Coronal MRI reveals right sided
pseudomeningoceles that have formed outside
compromise the axons and the
the intervertebral foramen indicative of nerve
avulsion injury.
electromyography assessment
will always be normal. Following
more severe axonotmesis or neurotmesis injuries, an immediate
assessment with electromyography will also be normal. However,
as Wallerian degeneration ensues, the presence of denervation
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potentials (fibrillation potentials and positive sharp waves) within
the affected muscles will become evident with electromyography.
The presence or absence of muscle denervation cannot be
determined until Wallerian degeneration is complete, which
occurs one to four weeks following injury. The standard algorithm
for assessment with electromyography is to wait until at least
three weeks after injury. Denervation potentials, however, do not
discriminate between an axonotmesis versus neurotmesis. Hence,
early electrodiagnostic testing can never truly discriminate between
an axonotmesis that has the potential for spontaneous recovery
versus a nerve transection or neurotmesis that has no chance of
spontaneous recovery.
Nerve conduction studies can be helpful in determining nerve root
avulsions. The dorsal root ganglion (sensory cell body) remains
attached to the spinal nerve while the motor cell body is separated
from the distal downstream axons. The sensory loop is still able to
conduct neuron signals. The sensory nerve conduction is preserved
and normal in the absence of clinical sensation. This finding is
pathognomonic of nerve root avulsion.
Intraoperative Assessment
Nerve identification and intraoperative assessment are paramount
factors to optimize surgical outcome. Proper nerve identification can
be confirmed by nerve stimulation, especially during nerve transfer
surgery. In addition, confirming preoperative physical examination
and findings from electrodiagnostic testing can be enhanced with
intraoperative stimulation. The Checkpoint Nerve Stimulator provides
a valuable tool with its stimulation specifications, variable parameters,
and reliability, to enhance intraoperative decision-making. The device
can safely stimulate either continuously or repeatedly without fear
of diminished nerve or muscle response. The ability to control pulse
duration at each amplitude assures stimulation delivery through
varying tissues that surround the nerve and assists in preventing
“false negative” assessment of nerve integrity.
Injury
There are numerous mechanisms that can result in nerve injury. The
most common etiologies are laceration, traction, and compression.
Less common causes include infection (e.g., leprosy), idiopathic
(Parsonage Turner syndrome or Neuralgic amyotrophy), radiation,
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electric shock, and tumor (e.g., schwannomas or neurofibromas).
This manual will focus on nerve injuries related to open or closed
traumatic injuries, specifically laceration and traction. Laceration can
be caused by penetrating trauma (e.g., knife or gunshot wound),
fracture, and iatrogenic mechanisms. Traction injuries can result
from a myriad of events such as athletic endeavors, motorcycle
accidents, and during delivery of a baby (brachial plexus birth palsy).
Nerve laceration can be complete or partial involving only a
segment of the nerve. Complete transection injuries are relatively
straightforward to diagnose. There is complete loss of movement in
those muscles innervated by the nerve and there is absent sensation
in the skin innervated by the lacerated nerve. Timely surgery is
required and the repair techniques will be discussed under the
section entitled Nerve Surgery. Partial lacerations are much more
difficult to diagnose and treat. There is incomplete loss of movement
and/or sensation. A comprehensive physical examination, clinical
suspicion, and electrodiagnostic testing are necessary to confirm
the diagnosis. A useful sign to detect injured axons is the acute
TineI’s sign. Gentle tapping over the cut nerve will elicit an electrified
response from the exposed axons and sends the sensation of
tingling or pins and needles into the sensory distribution of the
injured nerve. This sign is decisive in the evaluation of a child with
a potential nerve injury. The child will describe electric shocks and
their heightened response when the cut nerve is tapped is often
dramatic. Treatment requires exploration and a split nerve repair
technique that is discussed under Nerve Surgery.
Closed traction injuries are more of a dilemma to diagnose and
treat. The traction induces strain (change in length) that injures the
nerve. The amount of ultimate strain has numerous components
that affect the extent of nerve damage including the magnitude of
the force and the vector along the nerve. The injury represents a
continuum with progressive injury to the nerve. Mild stretch disrupts
the myelin sheath and interrupts nerve conduction without loss
of continuity of the axon (neurapraxia). Recovery takes place via
remyelination without Wallerian degeneration. Ongoing stretch
exceeds the elastic limit of the nerve and damages the myelin
sheath and the underlying axons with loss of axon continuity
(axonotmesis). The connective tissue of the nerve is preserved
(epineurium, perineurium, and endoneurium). The entire nerve distal
to the injury undergoes Wallerian degeneration that usually begins
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within 24–36 hours after injury and is complete one to four weeks
later. The axonal degeneration is followed by degradation of the
myelin sheath and infiltration by macrophages. The debris within
the distal stump is removed to allow for regeneration. The motor
and sensory cell bodies transition from their normal role as signaling
centers to nerve cell growth promoting centers with upregulation
and an increase in cellular activity. The cell body actively increases
its synthesis of structural proteins necessary for axonal repair and
regeneration. Axonal sprouts emerge just proximal to the injury (first
node of Ranvier) and venture into the distal nerve stump. Many axon
collateral sprouts (5-20) enter the stump and those collateral sprouts
that make incorrect target contact are pruned. Ultimately, accurate
motor neurons project their axons into muscle and accurate sensory
neurons reach their sensory receptors. Axonal regeneration occurs
at a rate of one to three millimeters per day. This axonal regeneration
is a staggered response toward the motor and sensory cell targets.
There will be an advancing Tinel’s sign as the nerve regenerates in
a distal direction. In other words, tapping over leading edge of the
regenerating nerve will elicit tingling or pins and needles into the
sensory distribution of the injured nerve (Video 2). This advancing
Tinel’s sign is a barometer for the location of distal regeneration and
will advance as the nerve regenerates toward its
motor end plates and sensory receptors. The extent
of recovery is related to the robust response of the
axonal sprouting and the distance to the motor
end plate. Longer distances prognosticate lesser
recovery as the motor end plates within the muscle Video 2: Advancing
Tinel’s sign after
undergo irreversible end plate demise between
axonotmesis injury
18 and 24 months. Subsequent to this demise,
to the median nerve.
additional nerve regeneration will be ineffective in
reinnervating the muscle.
Continual stretch leads to complete disruption of the nerve
including the sheath, axon, and encapsulating connective tissue
(epineurium, perineurium, and endoneurium). This injury is
referred to as a neurotmesis and results in irreversible intraneural
scarring. The prognosis for recovery is bleak without surgical
reconstruction. The intervening scar must be resected and nerve
reconstruction performed to allow for nerve regeneration. Another
surgical option is nerve transfers distal to the injury that bypass
the neurotmesis altogether. These transfers are discussed under
the Nerve Surgery section.
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Neurapraxia is an entity separate and distinct from the more severe
injuries of axonotmesis and neurotmesis. Traction axonotmesis and
neurotmesis lesions, however, are a continuum with an overlap
similar to a Venn diagram. Complex nerve injuries, such as brachial
plexus injuries often have elements of each type of injury that
may be intertwined. In reality, a trunk may have axonotmesis and
neurotmesis within the zone of injury, complicating terminology
and decision-making to determine which nerve will spontaneously
recover and which will not recover. The clinician may interpret these
injuries as “partial ruptures” or “ incomplete neurotmesis,” terms that
add ambiguity into the delineation of the exact injury pattern.
Another confounding factor in brachial plexus injuries is the
location of injury. The vast majority of brachial plexus injuries are
supraclavicular (above the clavicle). Axonotmesis typically occur at
the level of the trunk within the neck. Neurotmesis injury can occur
at the level of the trunk and is called a rupture. This injury separates
the motor and sensory cell bodies from their distal downstream
connections. Neurotmesis can also occur when the spinal nerve
is pulled from the spinal cord and is called an avulsion; similar to
pulling a plug from the wall and disconnecting the wire (spinal nerve)
from the plug (spinal cord). This injury separates the motor cell body
from the distal downstream axons. In contrast, this injury is proximal
to the dorsal root ganglion (preganglionic) and the sensory distal
downstream axons are not separated from their cell body (located in
the dorsal root ganglion) and downstream axons. The sensory loop
is disrupted from the spinal cord, but preserved in its connection
to the periphery. The sensory loop is unaware of its disconnection,
which preserves its ability to conduct neuron signals back and forth.
As discussed previously, an electrodiagnostic study of sensory
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conduction will demonstrate preservation of signal conduction in
the absence of clinical sensation. The physical finding of absent
sensation combined with the electrodiagnostic findings of normal
sensory conduction is pathognomonic of root avulsion. As of
2016, there is no reliable technique to restore continuity between
an avulsed nerve root and the spinal cord. The injury is similar to
a spinal cord injury with limited ability to recover notwithstanding
surgical alternatives. Surgery can bypass the injury discussed
under nerve repair techniques, but no direct repair to the spinal
cord is possible.
Treatment Principles
Timing
The timing of intervention is based upon fundamental principles of
nerve regeneration and muscle viability. Nerve regeneration is slow
with a rate between one to three millimeters per day. In addition,
muscles do poorly without nerve input. Visual examination can
assist in determining viable muscle. A healthy muscle with an intact
nerve supply has a bright red color. When a muscle loses its nerve
supply, the color degrades to pale and a chronically denervated
muscle has even poorer color and lacks contractibility. This lack of
contractibility can be confirmed during surgery, using the Checkpoint
Nerve Stimulator at the 20mA muscle testing setting. If the muscle
innervation is intact, the stimulator can be placed directly on muscle
tissue at the 20mA setting and increasing the pulse width slider
switch should demonstrate a proportional increase in muscle
contraction. A chronically denervated muscle will have minimal to no
contractibility at the 20mA muscle testing setting.
The reconstructive goal is to avoid the pale non-contractile muscle
that occurs following prolonged denervation and irreversible
endplate demise 18 to 24 months after injury. Chronically denervated
muscle eventually becomes fibrotic and electrically inactive. In
contrast, the encapsulated sensory receptors retain their capacity
for reinnervation for many years. When making a decision regarding
surgical intervention, application of these essential principles guides
treatment. The objective is to intervene as soon as possible in
neurotmesis to allow ample time for nerve regeneration and muscle
reinnervation. The obstacle is deciphering an axonotmesis with
ample spontaneous recovery from a neurotmesis that necessities
surgical intervention.
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Potential ancillary testing to enhance accurate diagnosis was
discussed previously. The underlying problem is that no test
is 100% accurate in distinguishing an axonotmesis from a
neurotmesis without obvious discontinuity on an imaging study.
Clinical signs that infer an axonotmesis are an advancing Tinel’s
sign and recovery of the most proximal muscle that is distal to
the nerve injury. As the nerve regenerates via axonal sprouting,
this muscle would be reinnervated first. A useful ancillary test
that can detect early signs of recovery following axonotmesis is
electromyography. Axonal regeneration leads to the formation
of nascent potentials that are low in amplitude, polyphasic in
configuration, and variable in duration. These initial immature
nascent potentials may precede clinical recovery as they are
incapable of generating a detectable contraction or force. This
finding may obviate the need for surgical intervention as they
prognosticate additional functional recovery over time.
Nerve Surgery
There are a variety of nerve surgeries depending upon the injury
pattern, time from injury, extent of injury, and available surgical
options. The surgical team needs to be prepared with ample
equipment including magnification (loupes and/or microscope),
nerve stimulator, micro suture and/or fibrin glue. This section will
discuss the various possibilities from simple to complex.
Nerve Repair
The most straightforward surgical option is direct repair following
a sharp laceration, such as a knife. The surgical approach always
begins outside the zone of injury to identify uninjured nerve based
upon the normal anatomy. The uninjured nerve is traced toward
the injury from both a proximal and distal direction. The sharply
transected nerve is identified and mobilized to allow a tension
free repair or coaptation. The orientation of the nerve is essential
to approximate sensory to sensory and motor to motor proximal
and distal fascicles. The vaso nervorum (vessels located on the
epineurium) can guide the surgeon to correctly orient the nerve and
the size of the group fascicles. In acute injuries, the Checkpoint
Nerve Stimulator can identify motor fascicles on the distal transected
nerve and facilitate orientation. The epineurium should be gently
approximated to coapt the cut nerve ends ensuring that the nerve
ends are not too tight (strangulated) or too loose (Figure 6 A&B).
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We equate nerve repair to
kissing your mother versus
kissing your girlfriend. A gentle
kiss on the cheek will afford
the best possible condition
for nerve regeneration. Tightly
squeezing the nerve ends
will “bunch” the axons and
impede nerve regeneration.
The coaptation can be secured
with a few microsutures and/
or fibrin glue dependent upon
the surgeon preference; the
results following sutures and
glue are similar. There have
been numerous attempts
to perform individual group
fascicle repair to directly
coapt the motor to motor and
sensory to sensory fascicles.
However, these techniques
have not been shown to be
superior to epineurial repair
and lead to increased scarring
within the repair.
Figure 6A: 6 year-old who lacerated left median
nerve and palmar cutaneous branch (Courtesy of
Allan Peljovich, MD).
Figure 6B: Primary nerve repair with gentle
coaptation of the cut nerve ends.
Neurolysis
The role of neurolysis following nerve injury is debatable. A
recovering nerve should be left alone as neurolysis may cause
additional scarring, disrupt circulation, and diminish functional
recovery. The primary role of neurolysis is outside of the nerve itself
and is to remove extrinsic compression such as encasing bone or
enveloping cicatrix. Other indications are crush injuries or Volkmann’s
ischemic contracture whereby subsequent fibrosis may squeeze
the nerve thus compounding the initial injury. In these cases, the
Checkpoint Nerve Stimulator can assist in locating the nerve within
the scar and to evaluate nerve function. The Checkpoint Nerve
Stimulator probe can be placed directly on the scarred area at 0.5
mA and the pulse width slowly increased with ongoing assessment
of any motor response. If no motor response is appreciated after
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reaching the maximum 200 microseconds, the process can be
repeated at the 2.0 mA amplitude. Once identified, the nerve
location and its course can be mapped by sweeping the probe
across the tissue observing the motor response.
Intraoperative Nerve Assessment
The concept of intraoperative nerve assessment via nerve action
potential across the neuroma is controversial regarding the ability
to predict a neuroma in-continuity that will recovery (axonotmesis)
versus a neuroma in-discontinuity (neurotmesis). Authorities debate
as to whether a less than 50% conduction across a neuroma-incontinuity should be treated with neuroma resection and grafting,
versus a less severe nerve injury with greater than 50% conduction
across the neuroma could be treated with neurolysis alone.
Currently, the answer is unknown and we rely on our preoperative
examination and assessment of functional recovery.
The Checkpoint biphasic stimulation has variable stimulation
parameters that may add additional information during the decision
making process. In addition, the Checkpoint Nerve Stimulator is
invaluable during nerve surgery such as nerve transfer procedures.
The device has three amplitude settings, 0.5, 2.0 and 20 mA.
The stimulator also has a variable pulse duration slider switch that
adjusts from 0 to 200 microseconds, allowing variable output at
each amplitude, much like a dimmer switch controlling the output
from a wall switch. The device employs a fixed frequency of 16 Hz
enabling the device to produce a tetanic contraction of muscle.
Most importantly, the Checkpoint’s biphasic waveform, unlike other
stimulators, employs waveform that has no direct current. The
stimulator excites the nerve while maintaining recruiting efficiency via a
large fast pulse (cathode phase or “stimulating phase”) that stimulates
the nerve and follows that stimulation by a smaller amplitude anode
phase or “recovery phase” that lasts longer and recovers all the
charge introduced by the larger fast pulse. In essence, the biphasic
waveform removes the same amount of energy that it’s introducing,
thus delivering a net zero charge to the tissue. The Checkpoint Nerve
Stimulator has a design that is inherently safe and cannot deliver any
net direct current to the patient and most importantly, the Checkpoint
can be used to deliver stimulus current to nerve tissue indefinitely
without risk of tissue damage.
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Nerve Graft
A delay in surgical intervention following a sharp laceration results
in additional obstacles for successful repair. A complete laceration
results in nerve retraction and subsequent neuroma formation as the
nerve attempts to regenerate. Surgical exploration reveals retraction
coupled with proximal and distal neuromas. Resection of the hard
“woody” neuromas is necessary to expose unscarred viable axons
that can regenerate. This resection increases the intervening gap.
Primary repair is no longer possible as the nerve ends cannot be
approximated with a tension free repair. The intervening gap must
be bridged by a scaffold to allow nerve regeneration across the
defect. There are a variety of options to bridge the gap including
autograft, allograft, and synthetic conduits. The gold standard is
autograft, although the use of conduits and allografts are viable
options. Conduits are best for short gaps as the regenerating nerve
can navigate across the defect. Larger defects, especially major
peripheral nerves, require better guidance. I prefer sural nerve
allograft in the vast majority of
cases and reserve conduits and
allografts for deficits that cannot
be bridged by available autograft.
However, I do recognize that
ongoing research into the perfect
conduit or allograft may one day
supersede the use of autograft
especially as nerve growth factors
that promote nerve regeneration
Figure 7A&B: 9 year-old fell off slide six
are identified and incorporated into months ago sustaining a left both bone
forearm fracture. Treated with hematoma
the product. A conduit or allograft block and closed reduction. Subsequently
laced with these nerve factors may developed absent median motor and
sensation in hand. Nerve conduction studies
ultimately be superior to nerve
revealed median absent sensory and motor
autograft, avoid the potential donor conduction.
morbidity, and save operating
room time.
The technique of nerve grafting across the brachial plexus or a
peripheral nerve requires meticulous technique to maximize outcome
(Figure 7A&B). The neuroma is resected and the proximal and distal
segments are sharply cut until viable nerve ends are visible (Figure
7C-H). The extremity or neck is positioned to maximize the gap
between the proximal and distal nerve ends. This positioning avoids
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Figure 7C: Nerve exploration revealing
nerve entering and exiting fracture site.
Checkpoint Nerve Stimulator showed
no distal response.
Figure 7D: Nerve cut proximal with
nerve cutting device.
Figure 7E: Nerve cut distal with nerve
cutting device.
Figure 7F: Intervening neuroma
removed.
Figure 7G: Good proximal axons.
Figure 7H: Good distal axons.
any tension along the grafts once the extremity or neck is repositioned
following the reconstruction. For autograft, the primary donor is the
sural nerve for large gaps. However, depending upon the injury and
need for graft material, other alternatives may be available such as the
medial antebrachial cutaneous and radial sensory nerves. The defect
between the proximal and distal nerve ends is measured. The grafts
are cut to size and positioned across the defect to obtain a similar
graft diameter as the cut nerve ends (Figure 7I). The grafts are carefully
secured with microsutures and/or glue (Figure 7J). Conduits or nerve
connectors can be used to facilitate nerve alignment at the proximal
and distal coaptation sites. Conduits or nerve connectors should not
cover the entire cable graft as imbibition (absorption of nutrients) and
inosculation (vessel ingrowth) occur from the recipient bed.
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Partial Nerve Injuries
Partial nerve injuries are difficult to
diagnose and challenging to treat. Within
the injury, there are intact and disrupted
fascicles. Acute partial nerve laceration is
managed by repair of the cut portion while
protecting the undamaged segment.
The unharmed segment prevents nerve
retraction, which facilitates a tension free
repair (Figure 8).
Figure 7I: 3 cm defect bridged
with sural nerve cable grafts
augmented by nerve connectors
to facilitate alignment.
Delayed partial nerve injuries, especially
the combination of axonotmesis
and neurotmesis within the zone of
injury, are puzzling to diagnose. Careful
deliberation coupled with a thorough
comprehensive examination is necessary
to make an accurate diagnosis. The
Figure 7J: Fibrin glue applied to
secure coaptation sites.
axonotmesis section will recover at
a rate of one to three millimeters per
day and will produce an advancing Tinel’s sign. The neurotmesis
portion will form a neuroma and will not regenerate. Hence, an odd
recovery pattern will develop over time with reinnervation of only
those muscles innervated by
the regenerating axons. A key
clinical sign is a non-anatomical
or unexplainable recovery as the
nerve regenerates. For example,
an axonotmesis injury to the
radial nerve above the elbow
Figure 8: Acute partial nerve laceration treated should result in reinnervation
by repair of the cut portion while protecting
of the brachioradialis (elbow
the undamaged segment (Courtesy of Dan A.
Zlotolow, MD).
flexor) followed by the wrist
extensor muscles (extensor carpi
radialis and extensor carpi brevis) followed by the finger extensors
(extensor digitorum communis). Recovery of finger extensor
before wrist extensor infers a partial nerve injury with axonotmesis
and neurotmesis subdivisions. Delayed partial nerve lacerations
are treated with preservation of the intact nerve and resection
of the damaged segment (Video 3). A biphasic nerve stimulator
(Checkpoint Nerve Stimulator) is crucial during dissection of the
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partially cut nerve to discriminate intact functional
axons from lacerated non-functional scar that
requires resection. A biphasic waveform allows for
repeated stimulation and contact with the nerve
without the concern of nerve injury or fatigue. The
visual motor response can be continually monitored. Video 3: Split nerve
grafting
The defect across the lacerated non-functioning
nerve is bridged via nerve grafting techniques discussed previously.
Delayed partial nerve lacerations can also be treated with nerve
transfers that completely bypass the injured segment.
Nerve Transfers
The concept, indications, and techniques of nerve transfers have
expanded greatly over the last decade. The concept of nerve
transfer involves taking a non-critical normal donor nerve (part or
whole) and transferring this donor nerve into a non-functioning
recipient nerve to provide motor and/or sensory innervation. The
general principles for the selection of donor nerves are similar to
tendon transfers. The donor nerve must be normal, expendable,
and preferably synergistic. Normal implies uninjured and not a
reinnervated nerve. Expendable means the patient can function
without the donor nerve. Synergistic infers the donor nerve fires in
phase with the recipient nerve/muscle. In addition to these motor
nerve transfers, sensory nerve transfers are also available and follow
similar principles of normal and expendable. Any loss of sensation
from the donor sensory nerve must be acceptable to the patient.
From a surgical perspective, the donor and recipient nerves should
be in close proximity to avoid any intervening graft and to allow a
tension free coaptation.
There are distinct advantages of nerve transfers compared to nerve
grafting. Nerve transfer involves motor to motor and sensory to
sensory coaptation avoiding potential misdirected fibers. Because
nerve transfers are typically performed distal to the site of injury,
the motor nerve transfer is closer to the muscle end plate and
reinnervation is quicker. However, the regeneration rate is still one to
three millimeters per day and and motor end plate viability degrades
at 18 to 24 months. Nerve transfers are particularly applicable to
proximal injuries, such as brachial plexus injuries or major peripheral
nerves above the elbow, as the slow rate of nerve regeneration
often precludes muscle recovery before irreversible motor end plate
demise. Nerve transfers are also invaluable in late presenting nerve
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injuries that have missed the window of opportunity for repair or
reconstruction but still have adequate time for regeneration via nerve
transfer that is closer to the motor endplates.
The donor options for motor nerve transfers have expanded over
the last decade with research and investigation into possible
donors. The donor list is likely to grow and increase the available
options. The nerve transfer can be end-to-end or end-to-side into
the recipient nerve. In most circumstances, end-to-end repair is
preferred as the results are superior. In my practice, end-to-side
transfers are reserved for dire straits where there are no other
options. There are two distinct types and techniques of nerve
transfer. In the more straightforward procedure, an expendable
donor nerve is cut as distal as possible (donor distal) and the
recipient is cut as proximal as possible (recipient proximal) to
provide adequate length of nerve for the transfer and coaptation.
Subsequently, the cut nerve ends are repaired end-to-end without
tension (e.g., spinal accessory to suprascapular nerve transfer).
Available Donor Motor Nerves via Distal Dissection
Nerve
Spinal accessory
nerve
Descriptor
Distal to upper
trapezius muscle
function.
Intercostal nerves
Radial nerve
branch to triceps
Nerve can be
harvested via anterior
or posterior approach
Phrenic nerve must be
working
Medial, lateral, or
long head branch
Brachialis motor
nerve
Biceps must be
functioning
Medial pectoral
nerve
Dissect from medi- Upper and/or lower
al cord
pectoral nerves must
be working
Thoracodorsal
nerve
Distal branch
Flexor digitorum
superficialis motor
nerve
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Caveats
Flexor digitorum
profundus must be
working
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Extensor carpi
radialis brevis
motor nerve
Extensor carpi radialis longus must be
working
Anterior
Distal at level
interosseous nerve of pronator
quadratus
Pronator teres should
be working
Flexor carpi ulnaris
motor nerve
Flexor carpi radialis
should be working
Flexor carpi radialis
motor nerve
Flexor carpi ulnaris
should be working
In the more complex nerve transfer, a proximal nerve with redundant
motor fibers is carefully separated into group fascicles via intrafascicular dissection (Figure 9). The Checkpoint biphasic wave
form nerve stimulator on low amplitude (0.5 milliamps) and low
pulse duration selectively stimulates each group fascicle and the
motor response noted. A redundant group fascicle, preferably with
synergistic movement, is selected and cut distal (donor distal) to the
recipient nerve. The recipient motor
nerve is cut as proximal as possible
(recipient proximal) and the nerve
ends are repaired end-to-end
without tension. The differences
between these techniques are
illustrated in the videos.
Figure 9: The ulnar nerve is carefully
separated into group fascicles via intrafascicular dissection to identify appropriate
donor group fascicle.
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Available Donor Motor Nerves
via Intra-fascicular Dissection
Nerve
Descriptor
Caveats
Ulnar motor
fascicle
Lower trunk must
be working
For elbow flexion,
select a fascicle that
innervates the flexor
carpi ulnaris for synergistic movement
Median motor
fascicle
Lower trunk must be
working
Avoid anterior interosseous nerve harvest
Medial pectoral
nerve
Can dissect
directly from
middle trunk
Upper and/or lower
pectoral nerves must
be working
The numerous nerve transfer options prevent an all-encompassing
description of every technique and the surgeon should fully
understand the technique prior to performing the procedure. The
nerve transfer options can be divided according to the function to
be restored.
Nerve Transfer Options for Particular
Motor Function
Function
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Nerve transfer options
Shoulder
Spinal accessory to
suprascapular nerve
Triceps branch to
axillary nerve
Pectoral fascicle to long
thoracic nerve
Thoracodorsal to long
thoracic nerve
Pectoral fascicle to spinal
accessory nerve
Elbow flexion
Median/ulnar fascicles to
biceps/brachialis motor nerves
Elbow extension
Ulnar fascicle to triceps motor nerve
Axillary branch (posterior division) to
triceps motor nerve
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Forearm pronation
Flexor digitorum superficialis
to pronator teres nerve
Extensor carpi radialis brevis
to pronator teres nerve
Wrist extension
Median (flexor carpi radialis and flexor
digitorum superficialis) to radial
(posterior interosseous nerve and
extensor carpi radialis brevis) nerve
Fingers and thumb
flexion (Median nerve)
Flexor digitorum superficialis to anterior
interosseous nerve
Brachialis to anterior interosseous
nerve
Extensor carpi radialis brevis to anterior
interosseous nerve
Extensor carpi radialis brevis to
pronator teres and supinator to anterior
interosseous nerve
Fingers and thumb
extension (Posterior
interosseous nerve)
Median (flexor carpi radialis/ flexor
digitorum superficialis) to radial
(posterior interosseous/ extensor
carpi radialis brevis) nerve
Supinator nerve to posterior
interosseous nerve
Hand intrinsic function
(Ulnar nerve)
Anterior interosseous to ulnar
motor nerve
Nerve Transfer Options For Hand Sensation
Nerve transfers to restore
hand sensation utilize noncritical sensory territories to
reinnervated critical sensory
regions. These critical areas
include the thumb-index finger
for object manipulation and the
Figure 10: Sensory nerve transfer in a median
ulnar border of the hand for
nerve injury that sacrifices the ulnar nerve
protection. The donor nerve
sensation to the ring-small interspace to
regain sensation to the ulnar side of the thumb depends upon availability. In a
and the radial side of the index sensory nerves
(Courtesy of Dan A. Zlotolow, MD).
median nerve injury, the most
common transfer sacrifices the
ulnar nerve sensation to the ring-small interspace by transferring
these sensory nerves to the ulnar side of the thumb and the radial
side of the index sensory nerves (Figure 10). In an ulnar nerve injury,
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the sensory nerve to the long-ring interspace third web space is
transferred to the ulnar digit nerve of the small finger. Other transfers
have been described using the superficial radial nerve, lateral
antebrachial cutaneous nerve, and dorsal cutaneous branch of the
ulnar nerve as donor nerves. Different from motor nerve transfers,
sensory nerve transfers are not time sensitive and sensation may be
restored many years after injury as sensory receptors remain viable.
Selected Techniques of Nerve Transfer
This section will highlight currently common motor nerve transfer
procedures. Nerve transfers to restore shoulder and elbow function
are frequently performed. Nerve transfer to restore intrinsic muscle
function after proximal ulnar nerve injury is also gaining popularity.
Therefore, these techniques will be described in this inaugural manual.
Nerve Transfers to Restore Shoulder Function
Nerve transfers to restore shoulder function should address the
deficits in both rotator cuff function (suprascapular nerve) and
deltoid function (axillary nerve). Therefore, two donor nerves are
necessary. The spinal accessory nerve is the preferred donor for the
suprascapular nerve and a branch of the radial nerve to the triceps
the preferred donor for axillary nerve. The spinal accessory nerve
can be harvested via an anterior supraclavicular approach or a
posterior approach along the scapular spine. The anterior approach
is preferred during brachial plexus exploration as
the incision and locale is the same (Video 4). The
posterior approach is preferred during isolated nerve
transfer surgery as the donor is more distal and the
recipient nerve closer to the muscle end plate. In
addition, the superior transverse scapular ligament
Video 4: Anterior
approach for
can be divided to decompress the suprascapular
spinal accessory
notch and eliminate any potential site of compression
to suprascapular
nerve transfer.
on the regenerating nerve.
The posterior approach is performed with the
patient in the lateral decubitus or prone position
(Figure 11A)(Video 5). Lateral decubitus is preferred
as concomitant nerve transfers for elbow flexion
can be performed without repositioning the patient.
The affected hemithorax and arm are prepped
and draped. An incision is performed just above
the scapula spine that extends from medial to the
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Video 5: Spinal
Accessory to
suprascapular
nerve transfer
Figure 11A: Incision drawn for posterior
approach for spinal accessory to
suprascapular nerve transfer.
scapula to the acromion. The
underlying trapezius muscle is
elevated from the spine of the
scapula with electrocautery.
The underlying supraspinatous
muscle is identified. A rake
retractor is placed into the
supraspinatous muscle and
pulled in an inferior direction
while the trapezius muscle is
elevated in a superior direction.
This combination of retraction opens up
the space above the scapula. The superior
border of the scapula is palpated and the
superior transverse scapular ligament and
suprascapular notch identified just lateral
to the omohyoid muscle’s insertion into
the scapula. The ligament is incised while
protecting the underlying suprascapular
nerve (Figure 11B &C). The nerve is then
traced in a proximal direction and ultimately
cut (recipient proximal).
Attention is then directed to identifying
the spinal accessory nerve (Figure 11D).
The undersurface of the trapezius muscle
is explored just medial to the scapular
border. The nerve resides between the
midline (spine) and the border of the
scapula. The nerve is verified using the
Checkpoint Nerve Stimulator and traced
in a distal direction to gain length. The
nerve is transected as distal
as possible (donor distal).
The spinal accessory and
suprascapular nerves are
brought in proximity along the
superior border of the scapula.
Tension free coaptation is
Figure 11 B&C. B: Trapezius muscle
elevated from scapular spine and
suprascapular nerve identified
entering scapular notch. C: Close
up of suprascapular nerve.
Figure 11D: Spinal accessory nerve isolated deep
to trapezius muscle and traced in a distal direction.
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performed with microsutures and/
or fibrin glue. (Figure 11E & F)
Figure 11E&F. E: Nerve transfer spinal
accessory to suprascapular secured with
suture and fibrin glue. F: Close-up of nerve
coaptation.
Figure 12A&B. A: Axillary incision drawn
for radial to axillary nerve transfer for
elbow flexion. B: Axillary incision and
deep dissection to identify radial and
axillary nerve.
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The radial to axillary nerve transfer
has two possible approaches:
posterior or axillary. Both approaches
accomplish the transfer and the
choice is based upon concomitant
procedures and surgeon preference.
An axillary incision with medial
extension down the arm is currently
preferred (Figure 12A & B). This
approach allows for a radial to axillary
nerve transfer along with a single or
double fascicular transfer for elbow
flexion. The patient is placed in the
lateral decubitus and the affected
hemithorax including the arm is
prepped and draped. The axillary
incision is designed within a skin
fold from the posterior acromion to
the mid-axilla. The incision is then
extended down the medial aspect
of the arm over the intermuscular
septum. Dissection is performed
through the fat and fascia to identify
the following muscles from anterior
to posterior: latissimus dorsi, teres
major, long head of the triceps, and
deltoid. The axillary nerve resides
deep to the latissimus dorsi and teres
major muscles and is isolated anterior
(emanating from the posterior cord)
and posterior (toward the deltoid)
to these muscles (Figure 12C). The
motor and sensory parts of the
axillary nerve must be separated.
There are typically three group
fascicles within the axillary nerve. The
most superior group fascicle follows
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Figure 12C: Axillary nerve
divided into group fascicles
and traced in a proximal
direction.
Figure 12D: Radial nerve
traced in a distal direction.
the posterior humeral circumflex vessel and
innervates the anterior and middle deltoid.
This group fascicle is the recipient nerve. The
middle group fascicle branch innervates the
posterior deltoid. The inferior group fascicle
branch innervates the teres minor. Vessels
loops are placed proximal and distal to the
intended area of microdissection. Elevation of
the vessels loops places tension across the
nerve and eases dissection. The epineurium
is gently opened by spreading with micro
forceps and the underlying group fascicles are
exposed. The Checkpoint Nerve Stimulator
set at two milliamps may facilitate identification
by stimulating any remaining muscle fibers
visualized as slight twitching of the deltoid.
Lack of stimulation requires distal dissection
to directly identify fascicles entering the deltoid
muscle (motor) versus entering the skin
(sensory).
Attention is next directed at identifying the radial nerve just anterior
to the latissimus dorsi and teres major tendons (Figure 12D). The
radial nerve and the branches to the triceps muscle are isolated.
The Checkpoint Nerve Stimulator on low amplitude (0.5 milliamps)
is used to stimulate the individual triceps branches. Occasionally,
a common trunk from the radial nerve divides into three individual
branches (long head, lateral head, and medial head). This anatomic
variation requires intrafascicular dissection to ensure preservation of
elbow extension after nerve transfer.
The branch to the long, lateral, or medial head can be selected
as the donor depending upon nerve caliber, location, and ease of
dissection. The medial head branch provides more distal length
(donor distal); however, the long or lateral are suitable options. Once
an appropriate sized radial nerve branch to the triceps is identified,
the branch is dissected in a distal direction to gain donor nerve
length. The adjacent group fascicle of the axillary nerve (usually
the group fascicle to the anterior deltoid) is dissected in a proximal
direction (recipient proximal). After adequate proximal recipient and
distal donor dissection have been achieved, the group fascicles are
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cut. The recipient axillary nerve branch to the
deltoid and donor radial group fascicle nerve,
are then brought in proximity and a tension
free coaptation performed with microsutures
and/or fibrin glue (Figure 12E).
Nerve Transfers to Restore
Elbow Flexion
Nerve transfers to restore elbow flexion can
address the deficit in brachialis and/or biceps
muscle function. The standard donor for the
biceps motor nerve is a group fascicle from
the ulnar nerve (Video 6). The standard donor
for the brachialis is a group fascicle from the
median nerve (Video 7). A single or double
fascicular transfer can be performed.
Surgery is performed with the patient supine
and the arm extended. A medial arm incision
is performed along the intermuscular septum
(Figure 13A). The basilic vein and medial
antebrachial cutaneous nerve are isolated and
protected. The musculocutaneous nerve is
identified deep to the biceps muscle (Figure
13B). The biceps motor nerve is proximal to
the brachialis motor nerve. The location of the
biceps motor nerve is heralded by a vascular
leash. The motor nerve is identified and traced
in a proximal direction using intra-fascicular
dissection to gain length. If a double fascicular
transfer is planned, the musculocutaneous
nerve is traced in a distal direction to identify
the brachialis motor nerve that is dissected in
Figure 13B: Motor branch from
musculocutaneous nerve to biceps muscle.
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Figure 12E: Radial to
axillary nerve transfer.
Video 6: Ulnar to
musculo-cutaneous
nerve transfer
Video 7: Median to
musculo-cutaneous
nerve transfer.
Figure 13A: Right arm
with medial incision. Red
vessel loop is around
biceps motor branch from
musculocutaneous nerve,
yellow vessel loop is around
ulnar nerve.
a similar fashion. After both recipients
are identified, attention is directed
toward the donor nerves.
The ulnar nerve adjacent to the biceps
motor nerve and the median nerve
opposite the brachialis motor nerve
Figure 13C: A longitudinal
are isolated. Vessel loops are placed
epineurotomy along the ulnar nerve to
identify the individual group fascicles
proximal and distal to the intended
and to isolate an expendable motor
area of microdissection to simplify the component. Adjacent parallel nerve is
medial antebrachial cutaneous.
dissection. Elevation of the vessels
loops places tension across the nerve
and eases dissection. The epineurium
is gently opened by spreading with
micro forceps and the underlying
group fascicles are exposed (Figure
13C). Using the Checkpoint Nerve
Stimulator on low amplitude (0.5
Figure 13D: Group fascicle of ulnar
milliamp), the group fascicles are
nerve to extrinsic muscles is divided
individually stimulated. For the ulnar
and transferred toward the biceps
motor branch.
nerve, the group fascicle that yields
primarily extrinsic function and preferably wrist flexion (flexor carpi
ulnaris) is chosen. For the median nerve, the group fascicle that
yields primarily extrinsic function (flexor carpi radialis, flexor digitorum
superficialis, or palmaris longus) is selected and care is taken to
preserve anterior interosseous nerve. The donor group fascicle is
dissected in a distal direction (donor distal) to gain nerve donor
length. Once adequate proximal recipient and distal donor dissection
has been achieved, the group fascicles are cut (Figure 13D). The
recipient and donor nerves are brought in proximity and a tension
free coaptation performed with microsutures and/or fibrin glue.
Nerve Transfers to Restore Elbow Extension
This nerve transfer is similar in dissection to the transfer for elbow
flexion. The difference is in the selection of the recipient nerve being
a radial nerve branch to the triceps. The ulnar
nerve is typically used as the donor nerve
(Video 8). Another option is using the posterior
branch of the axillary nerve as the donor nerve.
This transfer is gaining popularity in persons
with spinal cord injury. There are typically three
8: Ulnar motor
group fascicles within the axillary nerve. The most Video
to triceps motor nerve
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transfer.
33
superior group fascicle follows the posterior humeral circumflex
vessel and innervates the anterior and middle deltoid. This group
fascicles should be preserved. The middle group fascicle branch
innervates the posterior deltoid and is the donor nerve. The inferior
group fascicle branch innervates the teres minor.
Using the ulnar nerve as the donor nerve, the Checkpoint Nerve
Stimulator on low amplitude (0.5 milliamp) verifies the group fascicle
that yields primarily extrinsic function. Subsequently, an appropriate
sized radial nerve branch to the triceps is identified and dissected
in a proximal direction to gain length. The adjacent group fascicle of
the ulnar nerve is dissected in a distal direction (donor distal). After
adequate proximal recipient and distal donor dissection has been
achieved, the group fascicles are cut. The recipient radial nerve
branch to the triceps and donor ulnar group fascicle nerves are then
brought in proximity and a tension free coaptation performed with
microsutures and/or fibrin glue.
Nerve Transfer to Restore Intrinsic Function
Surgery is performed with the patient supine and
the arm extended (Video 9). Under tourniquet
control, an incision is performed from the distal
ulnar forearm into the palm across Guyon’s canal.
Skin flaps are raised and the ulnar neurovascular
structures isolated deep to the flexor carpi ulnaris.
Video 9: Anterior
The ulnar neurovascular structures are traced in a
interosseous nerve
distal direction. The volar carpal ligament is divided to ulnar motor nerve
transfer.
to open Guyon’s canal. The deep motor branch
of the ulnar nerve is identified and dissected in a
proximal direction separating the motor nerve from the sensory
branches. The dissection proceeds into the forearm. The anterior
interosseous nerve is isolated proximal to the pronator quadratus
and traced into the muscle to gain length. Since the pronator
quadratus will be denervated following the transfer, the muscle is
simple divided by bipolar electrocautery. The anterior interosseous
nerve is traced as distal as possible (donor distal). After adequate
proximal recipient and distal donor dissection has been achieved,
the group fascicles are cut. The recipient deep motor branch of
the ulnar nerve and the anterior interosseous nerve are brought in
proximity and a tension free coaptation performed with microsutures
and/or fibrin glue.
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Nerve Reconstruction versus Nerve Transfer
versus Tendon Transfer
A discussion regarding the choice between nerve reconstruction
(repair or graft), nerve transfer, and tendon transfer is necessary.
The chosen procedure depends on the clinical scenario with
consideration of numerous patient and injury factors including
patient age, time from injury, extent of injury, available donors, and
surgeon preference. These procedures are not mutually exclusive
and can be used in combination. For example, an ulnar nerve
laceration proximal to the elbow may be treated with nerve grafting
for sensation and extrinsic muscle recovery (flexor carpi ulnaris and
flexor digitorum profundus) and nerve transfer for intrinsic muscle
recovery. Another example would be a radial nerve laceration
proximal to the elbow treated with tendon transfer for wrist extension
and nerve transfer to the posterior interosseous nerve for distal
recovery (thumb and finger extension). There are often multitudes of
plausible surgical options; however, all must abide to the principles
previously detailed. Tendon transfer remains the gold standard
for chronic nerve lacerations that have passed the window of
opportunity for nerve reconstruction.
Rehabilitation
The initial post-operative protocol following nerve repair, grafting,
or transfer are similar. The coaptation site is allowed to heal
via immobilization without tension across the repair site. The
regimen may vary according to concomitant injuries, such as
tendon lacerations. In general, following nerve repair, transfer, or
reconstrution, the limb is immobilized for three weeks duration
followed by gradual mobilization. The initial goal of therapy is
to maintain supple joints and prevent contracture. The inherent
imbalance that occurs after motor nerve injury predisposes joints
to contracture. Passive range of motion and splinting are essential
modalities. In patients with loss of sensation, splint fabrication must
be meticulous to avert skin breakdown.
Patient education is an important part of the rehabilitation. Sensory
loss can lead to inadvertent injury. The patient needs to be extremely
careful with regards to hot and cold temperatures. The patient must
be educated about nerve injures and the slow regenerative process.
Unfortunately, neither the patient nor therapist can speed up the
process of watchful waiting at one to three millimeters per day.
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As the nerve regenerates to the motor end plates, the focus on
therapy changes to late phase rehabilitation and includes motor
and sensory re-education. The patient must reactivate or relearn
to move the muscle. Movement can be enhanced using auditory
or visual biofeedback. Relearning a direct nerve repair or grafting
is a straightforward process. Relearning a nerve transfer is more
challenging and the rehabilitative techniques are similar to tendon
transfer. An experienced therapist is invaluable as the learning
process can be frustrating and difficult. The exact process of
relearning after nerve injury/reconstruction is largely unknown, but
certainly involves brain plasticity and reorganization of the primary
somatosensory cortex to learn how to fire a muscle innervated by a
different motor nerve.
As the nerve regenerates to the sensory receptors,
the initial sensation may be uncomfortable
(e.g. tingly or itchy) and hypersensitive. Tactile
hyperesthesia refers to recovery that results in
an abnormal increase in sensitivity to touch. The
Video 10:
therapist uses sensory reeducation or retraining to
Desensitization for
improve both the patient’s cognitive and adaptive
hyperesthesia using
various textures.
response to stimulation of the affected skin region
(Video 10). The early phase of sensory retraining is
aimed at reeducating constant (localization) versus moving touch
perceptions. For regions with hyperesthesia, desensitization with
gentle stroking using various textures and stimulation of A-Beta
touch receptors is performed to lessen the response. In the later
phase of retraining, the focus shifts to reeducate the directionality
of movement (e.g. left to right or distal to proximal). Over time, the
program dampens the tactile hyperesthesia and improves object
identification and manipulation. Patients regain the ability to perform
various activities of daily living and
improve in their stereognosis (ability
to recognize an object in their hand
without any visual cues).
Tactile hyperesthesia in infants, such
as babies with brachial plexus palsies,
manifests as biting (Figure 14). The
biting can be severe and result in
infection and even nibbling away of the
affected fingertips. Regrettably, there
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Figure 14: Infant with brachial plexus
birth palsy biting right index finger.
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is no intellectual reasoning with infants and the parents feel horrible
about the biting. Numerous medical and home remedies have
been tried to no avail as the infants continue to gnaw at their digits.
Fortunately, as the sensory recovery progresses and the tactile
hyperesthesia lessens, the biting diminishes. The result is often
physical scarring to the child and emotional scarring to the parents.
Outcome
The outcome following nerve surgery has numerous confounding
factors. The results are difficult to decipher as published reports
conglomerate a mixed sample of injuries into a single paper. The
best results are in distal sharp lacerations in young persons that
are repaired with a tensionless technique. However, that may be
similar to searching for a herd of unicorns. In clinical practice, the
mechanism of injury is often a combination of sharp and blunt
trauma with or without an element of traction. In addition, there may
be associated injuries such as tendon laceration, artery transection,
or bony fracture. Hence, the number of isolated truly sharp
transections is relatively low.
There are certain variables that improve the
chances of success including young age (children),
distal injuries closer to the motor end plates,
timely repair or reconstruction, and meticulous
microsurgical technique using appropriate
equipment (magnification, micro forceps, and
microsutures) (Video 11). In contrast, poor
prognostic factors include older age, proximal
injuries far from the motor end plates, delayed
presentation, and suboptimal technique with
inadequate equipment.
Video 11: 5 year-old
s/p acute nerve
grafting of radial
and ulnar nerves
in the arm due to
segmental loss.
In general, timely nerve repair or reconstruction “works” about 85
to 90 percent of the time to reinnervate downstream muscle fibers
and/or sensory end organs. However, the patient may not achieve
full function and this expected outcome needs to be conveyed to
the patient and family prior to surgery. This discussion frequently
modifies their expectations. The concepts of slow regeneration and
motor end plate demise must be discussed honestly with the patient
and family. The discussion equates the nerve to an internet cable,
which imparts colloquial understanding into the complexities of
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Figure 15: 14 year-old male depicted in Figure 11 3 years s/p shoulder nerve transfers (spinal
accessory to suprascapular and radial to axillary) and elbow nerve transfers (median to
brachialis and ulnar to motor nerve transfers for elbow flexion and forearm supination.
Figure 15B: Good muscle bulk and
elbow flexion.
Figure 15A: Elbow
flexion.
Figure 15D: Overhead
motion.
Figure 15C: Shoulder external rotation.
nerve anatomy and nerve surgery. The lengthy time to recovery must
also be communicated prior to the surgical procedure along with the
possible complications.
The outcomes following nerve transfer surgery have similar
challenges but can overcome the factors related to proximity
to sensory receptors or motor end plates (Figure 15) . The
outcome, however, still relies upon age, timeliness, and meticulous
microsurgical technique. Nerve transfer surgery has other numerous
benefits including operating out of the zone of injury and preferential
direction of nerve fibers (motor fibers to motor fibers and sensory
fibers to sensory fibers). Nerve transfer surgery is becoming the
preferred technique in many situations especially proximal injuries,
such as upper trunk (C5, C6) brachial plexus lesions and proximal
peripheral nerve injuries. However, nerve transfer surgery is limited
by the number of available expendable donors that is narrowed in
patients that have sustained multiple nerve injuries.
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Future
The future is bright for advances in nerve surgery from diagnosis to
treatment and subsequent rehabilitation. The diagnostic advance
will be related to the immediate determination of the extent of the
nerve injury. Nerve imaging with or without an injectable substance
will discriminate whether the injury is a neurapraxia, axonotmesis,
or neurotmesis type injury. This diagnostic advance will obviate
the current practice of “watching and waiting ” that will become
obsolete. The physician will be able to ascertain the diagnosis and
recommend the appropriate management without wasting time.
The immediate or early diagnosis will allow prompt intervention
for neurotmesis avoiding the delay in surgical intervention that
jeopardizes motor end plate survival.
The surgical management of nerve injuries will be augmented as
the pharmacology of nerve regeneration is better elucidated. Nerve
repair or reconstruction will be enhanced by the addition of a local
or systemic pharmacologic treatment that will promote nerve
regeneration. In addition, a period of intraoperative nerve stimulation
following repair or reconstruction may ignite nerve regeneration.
These pharmacologic agents and intraoperative modalities will enrich
nerve regrowth via superior axonal sprouting to the denervated
starving motor end plates and sensory receptors. This augmented
regeneration may also stimulate motor to motor and sensory to
sensory directionality.
The other impactful scientific advance that will improve nerve
surgery and rehabilitation is further understanding the brain. Imaging
studies have revealed remarkable rapid changes after nerve injuries
or limb loss that can be reversed with nerve recovery or limb
replantation. Cortical plasticity and motor relearning play a pivotal
role during nerve recovery. Harnessing the plasticity of the brain will
directly affect rehabilitation after nerve injury. Techniques such as
transcranial magnetic stimulation (TMS), electroencephalography,
magnetoencephalography (MEG), functional MRI (fMRI), structural
MRI (sMRI), and positron emission tomography (PET) are unveiling
the mysteries of human cortical plasticity. Rehabilitation that
modulates the processes of pruning of ineffective connections and
sprouting of intact afferents from nearby cortical and/or subcortical
territories will improve nerve recovery. How soon will these advances
occur? Remember what Albert Einstein said, “I never think of the
future- it comes soon enough.”
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Scott Kozin, M.D.
Chief of Staff, Shriners Hospital for Children
Clinical Professor, Department of Orthopaedic
Surgery, Lewis Katz School of Medicine at
Temple University
Adjunct Clinical Professor in the Department of
Orthopaedic Surgery, Sidney Kimmel Medical
College at Thomas Jefferson University
Dr. Kozin has a financial interest and/or other relationship with
Checkpoint Surgical Inc. This manual was funded by Checkpoint
Surgical Inc. and is not peer reviewed.
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Checkpoint Surgical, Inc.
22901 Millcreek Blvd., Suite 110
Cleveland, Ohio 44122
Toll-free: 877.478.9106
Local: 216.378.9107
Fax: 216.378.9116
Email: [email protected]
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