Download Volume 11 Issue R7 Hand:Peripheral Nerves and Upper Extremity

Volume 11 • Issue R7
HAND: PERIPHERAL NERVES
AND UPPER EXTREMITY
FUNCTIONAL RECONSTRUCTION
Justin S. Chatterjee
Reconstructive
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Grafts and Flaps
Wound Healing, Scars, and Burns
Skin Tumors: Basal Cell Carcinoma, Squamous Cell
Carcinoma, and Melanoma
Implantation and Local Anesthetics
Head and Neck Tumors and Reconstruction
Microsurgery and Lower Extremity Reconstruction
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Lip, Cheek, and Scalp Reconstruction
Ear Reconstruction and Otoplasty
Facial Fractures
Blepharoplasty and Brow Lift
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Injectables
Lasers
Facial Nerve Disorders
Cleft Lip and Palate and Velopharyngeal Insufficiency
Craniofacial I: Cephalometrics and Orthognathic Surgery
Craniofacial II: Syndromes and Surgery
Vascular Anomalies
Breast Augmentation
Breast Reduction and Mastopexy
Breast Reconstruction
Body Contouring and Liposuction
Trunk Reconstruction
Hand: Soft Tissues
Hand: Peripheral Nerves
Hand: Flexor Tendons
Hand: Extensor Tendons
Hand: Fractures and Dislocations, the Wrist, and
Congenital Anomalies
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SRPS • Volume 11 • Issue R7 • 2015
HAND: PERIPHERAL NERVES
AND UPPER EXTREMITY
FUNCTIONAL RECONSTRUCTION
Justin S. Chatterjee, MBChB, MSc, EBOPRAS, FRCSGlasg(Plast),
FRCSEd(Plast), EurDiplHandSurg(FESSH), DipHandSurg(BSSH),
Birmingham Hand Centre, Birmingham, United Kingdom
PERIPHERAL NERVES
Anatomy
A nerve cell is called a neuron. A neuron consists
of a plasma membrane surrounding a cell body
with characteristic cytoplasmic extensions, the axon
(surrounded by a Schwann sheath), and the dendrite. The
axon of one neuron communicates with the dendrite or
cell body of another neuron through synapses. The axons
of peripheral nerves are surrounded by endoneurium and
are arranged in groups called fascicles or funiculi, each of
which is surrounded by a distinct perineurium (Fig. 1).1
Endoneurium
The perineurium is surrounded by a loose areolar
intraneural epineurium containing multiple vascular
channels. Bundles of fascicles surrounded by intraneural
epineurium are enclosed by an outer circumferential
epineurium encircling the entire peripheral nerve with its
fascicles (Fig. 2).1,2
Circumferential
epineurium
Perineurium
Fascicle
Intraneural
epineurium
A
Perineurium
around one
fascicle
Fascicular
bundle
Perineurium
Intraneural
epineurium
Circumferential
epineurium
Axon
B
Figure 1. Nerve fascicle surrounded by perineurium.
(Modified from Gutowski.1)
Figure 2. Human peripheral nerve. A, cross-section; B,
alternate view shows fascicular bundle. (Modified from
Gutowski.1)
1
SRPS • Volume 11 • Issue R7 • 2015
The neuroanatomy pertinent to surgical repair
includes the following:
•• Outer epineurium sutured in
epineurial repair
•• Inner epineurium sutured in fascicular
bundle and perineurial repair
•• Perineurium sutured in fascicular repair
The vascular supply of peripheral nerves is via
arteriae nervorum entering the nerve segmentally and
dividing into longitudinal superficial and interfascicular
arterioles. The arterioles communicate with each other
in a vascular plexus. Extrinsic vessels supply intrinsic
longitudinal vessels found in all layers of the epineurium,
and the intrinsic longitudinal vessels in turn communicate
with extensive capillary plexuses and deep epineurial
vessels (Fig. 3).1,3
The longitudinal capillary plexus pattern is
duplicated within each nerve fascicle, creating a
longitudinal epineurial and a separate longitudinal
perineurial vascular system, each with its respective
capillary network. Because of the duplication of
longitudinal vascular systems at the epineurial and
perineurial levels, intraneural dissection for fascicular
repair need not devascularize the perineurial longitudinal
blood supply.
Perineurial
plexus
Epineurial
vessels
Although connections do exist, they are not
numerous enough to preclude intraneural neurolysis,
fascicular repair, or interfascicular grafting. Williams and
Jabaley6 emphasized the importance of the internal neural
anatomy regarding nerve repair in the hand.
Capillary
within fascicle
Deep
epineurial
plexus
Figure 3. Microvasculature of peripheral nerve. (Modified
from Gutowski.1)
2
Peripheral nerves exhibit branching and fascicular
plexus formation. In the musculocutaneous nerve of the
arm, Sunderland,4 in 1945, identified fascicular branching
every few millimeters (Fig. 4, left).1 Many surgeons
assumed that pattern occurred at all levels in the forearm
and were consequently pessimistic about the chances of
successful intraneural dissection and nerve grafting in the
upper extremity. In 1980, however, Jabaley et al.5 dissected
the median, ulnar, and radial nerves in the forearm and
found discrete branches and bundles within the main
nerve trunk that could be traced for considerable distances
without disturbing adjacent fibers (Fig. 4, right).1
Figure 4. Peripheral nerve fascicular branching pattern
according to Sunderland4 (left) and according to Jabaley et
al.5 (right). (Modified from Gutowski.1)
SRPS • Volume 11 • Issue R7 • 2015
Physiology
Signals in peripheral nerves are conducted either by
localized potentials or action potentials. Localized
potentials occur over short distances, decrease over
distance, and are most important in intercellular junctions
or sensory nerve endings. Action potentials are conducted
impulses that do not decrease over distance. A compound
action potential is the net algebraic sum of individual fiber
action potentials in a multifiber nerve trunk.
Action potentials in unmyelinated fibers
progressively excite adjacent inactive areas, and the
rate of conduction is directly proportional to the crosssectional area of the axon. In contrast, current flow along
myelinated fibers is limited to sites where the myelin
sheath is interrupted (i.e., the nodes of Ranvier) (Fig. 5).1
The rapid conduction speeds in myelinated nerves are the
result of impulses jumping from one node of Ranvier to
the next, a process known as saltatory conduction.
Schwann cells exist in two separate groups, one
primarily involved with degeneration of myelinated fibers
after nerve transection and one responsible for protection
and remyelination of regenerating neurites. Schwann cells
within the endoneurial space produce new endoneurial
tubules or basement membranes,7 whereas those
proliferating in the distal stump most likely produce an
unidentified trophic substance to the regenerating axonal
buds.8 The speed of conduction of an impulse through a
nerve depends on the diameter of the nerve fiber and its
membrane properties (Table 1).9
The clinical interpretation of electrophysiological
recordings requires an understanding of the evoked
response, if any; the conduction velocity of the nerve
impulse; and the amplitude and shape of the wave
form, which can be altered experimentally.9 Terzis and
Publicover10 and Van Beek et al.11 reviewed techniques of
nerve stimulation and recording in the clinical setting.
Wilbourn12 provided a clinical review of electrodiagnostic
examination of peripheral nerve injuries, which should be
reviewed by surgeons for further information.
thoracic outlet known as the brachial plexus (Fig. 6).13 The
brachial plexus consists of spinal nerve roots (C5-T1),
trunks, divisions, cords, and terminal branches. Several
branches are given off at various points in the plexus,
and knowledge of their anatomic location is essential
in clinical assessment of a patient with brachial plexus
abnormality. The terminal branches include the ulnar,
musculocutaneous, median, radial, and axillary nerves.
The median nerve arises from the lateral and medial cords
(C5-T1). In the arm, the median nerve remains in the
anterior compartment and passes from lateral to medial
over the brachial artery. The ulnar nerve arises from the
medial cord (C8-T1). The ulnar nerve commences in
the anterior compartment of the arm and passes to the
posterior compartment through the medial intermuscular
septum. The radial nerve arises from the posterior cord
(C5-T1). The radial nerve commences in the posterior
compartment of the arm and passes to the anterior
compartment through the lateral intermuscular septum.
Matloub and Yousif14 reviewed the innervation patterns in
the forearm and hand.
Unmyelinated
axons
Myelin
Axon
neurofibrils
Schwann
cells
Node
of Ranvier
Unmyelinated
fiber
Myelinated
fiber
Nerves of the Upper Limb Brachial Plexus Forearm
and Hand
The spinal nerves of the upper limb undergo series of
unions and divisions between the spinal column and the
Figure 5. Unmyelinated nerve fiber compared with
myelinated nerve fiber. (Modified from Gutowski.1)
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SRPS • Volume 11 • Issue R7 • 2015
Table 1
Types of Nerve Fibers9
Fiber Type
A
Fiber Diameter (mm)
Conduction Velocity (m/s)
a
Proprioception, somatic motor sense
12−20
70−120
b
Touch, pressure
5−12
30−70
g
Motor to muscle spindles
3−6
15−30
d
Pain, temperature, touch
2−5
12−30
<
3−15
B
C
Function
Preganglionic sympathetics
dr*
Pain, reflex responses
0.4−1.2
0.5−2
S*
Postganglionic sympathetics
0.3−1.3
0.7−2.3
*dr, dorsal root; S, sympathetic.
Median Nerve
In the forearm, the superficial trunk of the median nerve
innervates the pronator teres (PT), flexor carpi radialis
(FCR), palmaris longus (PL), and flexor digitorum
superficialis (FDS) of the index finger. The deep trunk
innervates the flexor digitorum profundus (FDP) to the
index and middle fingers, flexor pollicis longus (FPL),
and pronator quadratus and provides sensation to the
radiocarpal joint through the anterior interosseous nerve.
The palmar cutaneous branch innervates the skin of the
palm and volar wrist. Hobbs et al.15 detailed the origin,
course, and distribution of the palmar cutaneous nerve
and related the nerve anatomy to the planning of incisions
around the palmar aspect of the wrist and palm.
The carpal tunnel is a gauntlet of inelastic
connective tissue through which pass the median nerve
and nine tendons, including the FPL, FDS, and FDP
on their way to the distal palm and digits.16 The median
nerve travels with the flexor tendons underneath the
transverse carpal ligament. At the distal edge of the flexor
retinaculum, the median nerve normally divides into six
branches: the recurrent motor branch, three proper digital
nerves, and two common digital nerves. Steinberg and
4
Szabo16 reported that the motor branch passed through
a separate fascial tunnel immediately before entering the
thenar muscles in 56% of the specimens studied. The
other branches of the radial trunk and the ulnar trunk
send common digital nerves to the radial side of the
thumb and the first, second, and third web spaces.
Sunderland17 reported that in 50% of cases, the
median nerve innervated the FDP of the index and
middle fingers whereas the ulnar nerve innervated those
of the ring and little fingers. In the other 50%, nerve
fibers overlapped so much that the median nerve often
encroached upon the territory of the ulnar nerve. In the
hand, the reverse is true, and the ulnar nerve tends to
extend radially into the median nerve territory. The most
variable muscles regarding innervation are the thenar
muscles, first dorsal interosseous, and third and fourth
lumbricals.
Martin-Gruber anastomoses are motor connections
between the median nerve and the ulnar nerve in the
proximal forearm or, more distally, between the anterior
interosseous nerve and the ulnar nerve (Fig. 7).14 The
connections can be of four types.14,18 Based on a review
of the literature, Leibovic and Hastings19 determined the
SRPS • Volume 11 • Issue R7 • 2015
frequency of each type of connection and cited a 17%
overall incidence of Martin-Gruber anastomoses.
Riche-Cannieu anastomoses are motor connections
between the median and ulnar nerves in the palm that are
present in as many as 70% of people (Fig. 8).14 Three types
of connections have been reported.
Motor anastomoses are noteworthy in that they
can mask the site of injury.20 For example, if both MartinGruber and Riche-Cannieu connections are present, a
complete low ulnar nerve lesion might be accompanied
by a normal appearing hand because the intrinsic muscles
of the hand are innervated by the anterior interosseous
branch of the median nerve (Fig. 9).20,21 Likewise, injury to
the median nerve at the elbow might result in the loss of
all intrinsic muscle functions of the hand, even if the ulnar
nerve remains intact.
Budak and Gönenç22 used electrophysiological
studies to determine the frequency of innervation
anomalies in the hand. Martin-Gruber anastomoses were
found in 18% of cases, and the finding was bilateral
in 73%. Martin-Gruber anastomoses most frequently
innervated both the first dorsal interossei muscle and
adductor digiti minimi muscle, with the next most
frequent being innervation of only the first dorsal
interossei muscle, and the third most frequent being
innervation of only the adductor digiti minimi muscle.
Dorsal scapular n.
Lateral pectoral n.
Lateral cord
Subclavian n.
Superscapular n.
Posterior cord
C4
C5
Medial cord
C6
Axillary n.
C7
T1
Radial n.
Long thoracic n.
Median n.
Upper
Trunks Middle
Lower
Ulnar n.
Lower
subscapular n.
Thoracodorsal n.
Medial brachial cutaneous n.
Upper
subscapular n.
Medial antebrachial cutaneous n.
Figure 6. Brachial plexus. n., nerve. (Modified from McCarthy et al.13)
5
SRPS • Volume 11 • Issue R7 • 2015
Riche-Cannieu anastomoses were found in 73% of cases,
suggesting that this communication should be accepted as
a normal anatomic variation rather than an abnormality.
Incidences of neural communication between the median
and ulnar nerves of 21% and 14% were observed for the
first dorsal interosseous and adductor digiti
minimi, respectively.
In addition to aberrant motor innervation patterns,
Stančić et al.23 described the Berrettini branch, or
superficial palmar communication between the median
and ulnar nerves. The Berrettini branch frequently
is found at the level of the transverse carpal ligament
or distally. Injury to this branch, particularly during
endoscopic carpal tunnel release (ECTR), can result in
altered sensation of the middle and ring fingers.
1
Median
nerve
2
3
4
5
6
Ulnar
nerve
Flexor
digitorum
profundus
7
Figure 7. Median to ulnar (Martin-Gruber) and ulnar to
median nerve anastomoses in the forearm. (Modified from
Matloub and Yousif.13)
6
Figure 8. Ulnar to median (Riche-Cannieu) nerve
anastomoses in the hand. 1, median nerve; 2, ulnar nerve; 3,
recurrent motor branch; 4, opponens pollicis; 5, superficial
head; 6, deep head. (Modified from Matloub and Yousif.13)
Figure 9. Complete low ulnar nerve lesion can present with
normal appearing hand when both ulnar to median nerve
and Riche-Cannieu connections are present. (Modified from
Mackinnon and Dellon.20)
SRPS • Volume 11 • Issue R7 • 2015
Ulnar Nerve
Classification
In the forearm, the ulnar nerve gives off branches to the
muscle bellies of the flexor carpi ulnaris (FCU) and the
FDP of the ring and little fingers. It also innervates the
ulnar artery by way of the nerve of Henle, which provides
sensory branches to the distal forearm and proximal
hypothenar eminence. The nerve of Henle was absent in
43% of dissections performed by McCabe and Kleinert.24
Sunderland17 and Seddon26 grouped nerve injuries into
five grades according to the disrupted internal structures.
Mackinnon and Dellon21 added a sixth degree of injury,
which is a mixed injury and likely more applicable in
most clinical settings (Table 2). The severity of the injury
progresses from minimal derangement of the axon in
neurapraxia (first degree) to complete disruption of all
neural structures in neurotmesis (fifth degree).
In the hand, the ulnar nerve divides at the level
of Guyon canal. The deep (motor) branch supplies the
hypothenar eminence and midpalm—all the interossei, the
two ulnar lumbricals, adductor pollicis, and deep head of
the flexor pollicis brevis (FPB). The superficial (sensory)
branch of the ulnar nerve supplies the radiocarpal joint
and ulnar aspect of the hand, the mid-longitudinal axis
of the ring finger, and the entire little finger. The dorsal
sensory branch of the ulnar nerve innervates the dorsum
of the hand in approximately the same distribution. The
palmar cutaneous branch of the ulnar nerve is absent when
the nerve of Henle is present.24
Radial Nerve
In the arm, the radial nerve gives off the posterior
antebrachial cutaneous nerve, which descends along the
lateral arm to supply the skin of the dorsal and lateral
forearm to the wrist. The radial nerve then divides at the
level of the elbow into a superficial (sensory) branch and
a deep (motor) branch. The deep branch is known as the
posterior interosseous nerve. This nerve gives off branches
to the supinator muscle in the forearm and innervates
the dorsal wrist capsule. Distal branches innervate all
the muscles of finger and thumb extension and provide
sensation to the radiocarpal and carpometacarpal joints.
The superficial branch of the radial nerve divides into a
lateral branch to the radial dorsal aspect of the thumb and
a medial branch, which in turn divides into four dorsal
digital nerves that supply the thumb, index finger, middle
finger, and radial side of the ring finger.
Nerve Injuries
Peripheral nerve injuries result in loss of sensory, motor,
and autonomic functions supplied by the involved nerve.25
McCabe and Kleinert24 indicated that neural
injuries can be classified according to their chronicity.
Acute injuries are caused by direct trauma, and the onset
of symptoms is immediate. Chronic lesions (also known
as entrapment neuropathies) are caused by repetitive
microtrauma or longstanding compression. With chronic
lesions, the onset of symptoms is gradual. The majority of
substantial peripheral nerve injuries are chronic.
Degree 1 and 2 injuries recover spontaneously
with function that is far better than that achieved with
surgical reconstruction. Degree 3 injuries also recover
spontaneously to a more variable degree, although
generally without the need for surgery. Degree 4 and 5
injuries will not recover without repair. Degree 6 injuries
recover to variable degrees, depending on the relative
degrees of injury involved.27
Ultrastructural Changes
In 1850, Waller28 presented his classic experiments on the
degeneration of peripheral nerves after transection. Ever
since, posttraumatic distal changes in a nerve have been
known as wallerian degeneration whereas changes in the
proximal portion of a nerve are called axonal degeneration.
Conventional wisdom holds that physical
disintegration of the axon and myelin sheath extends
only a few millimeters proximal to the point of injury.
Distally, the axon of the transected nerve undergoes
wallerian degeneration, while the sheath of Schwann,
endoneurium, and blood vessels remain intact. Schwann
cells in the distal stump proliferate into bands of Bungner
and form a conduit that helps guide regenerating axons.29
Simultaneously, the proximal nerve cell body enlarges
and its metabolism speeds up for 10 to 20 days. Axonal
budding begins during that time.17 Peripheral nerve injury
also results in substantial neuronal cell death proximally,
7
SRPS • Volume 11 • Issue R7 • 2015
Table 2
Classification of Nerve Injuries21
Histopathological Changes
Degree of Injury
Myelin
Axon
Endoneurium
Perineurium
I Neurapraxia
±
II Axonotmesis
+
+
III
+
+
+
IV
+
+
+
+
V Neurotmesis
+
+
+
+
VI
Epineurium
+
Various fibers and fascicles show various pathological changes
in the sensory neurons at the dorsal root ganglion and in
the motor neurons in the spinal cord.29 Sensory neuronal
death is more marked in distal injuries, and motor
neuronal death occurs in association with proximal
nerve injuries.30
Diagnosis
A complete history of the injury and a precise record of
all sensory and motor deficits must be obtained. Terzis31
offered a comprehensive approach to the preoperative
evaluation of peripheral nerve lesions. The requirement
for careful repeated clinical examination cannot be
understated in diagnosing a peripheral nerve lesion and
monitoring functional recovery. Investigations should be
considered an adjunct.
Muscle testing32 and electrophysiological studies33,34
help define the level of injury. Omer32 reviewed testing
and grading techniques for patients with peripheral
nerve injuries. He reported that the primary indication
for electrodiagnostic studies is inability to arrive at a
diagnosis. For unexplored closed injuries with suspected
nerve involvement, a waiting period of 6 weeks or longer
is appropriate before ordering electromyography (EMG)
and nerve conduction velocity (NCV) studies. If clinical
8
Tinel Sign
Present
Progresses Distally
−
−
+
+
+
+
+
−
+
−
+
±
evidence of muscle return is detected in the interim,
electrical studies are unnecessary.
The EMG and NCV findings in various types of
nerve lesions are listed in Table 3.35 Progress is monitored
by repeat testing, presupposing a nerve regeneration rate
of 1 mm per day (1 in/mo). Sable36 described the use of
electrodiagnostic studies in evaluating the median and
ulnar nerves at the level of the hand and wrist.
Compartment Syndrome
The differential diagnosis of peripheral nerve lesions in
open wounds of the hand must include compartment
syndrome. Clinical distinction between pain and
paresthesia from direct nerve trauma or secondary
to increased compartment pressure can be difficult.
Compartment syndrome develops when tissue pressure
progressively builds within a limiting fascial envelope,
squeezing the contained neuromuscular structures. As the
edema increases, the circulation is compromised37 and
the conscious patient experiences agonizing pain. If the
pressure is not released surgically, first muscle and then
nerve necrosis occurs as tissue pressures reach 30 mmHg.
The ischemic changes become irreversible after 6 hours in
muscle and after 8 to 10 hours in nerves.21,38 Treatment
SRPS • Volume 11 • Issue R7 • 2015
Table 3
Results of Electrical Studies According to Nerve Status35
Electromyogram
Fibrillations and
Positive Sharp Waves
Nerve Conduction Study
Voluntary Motor
Unit Potentials
Sensory and
Motor Latency
Amplitude
Normal
Absent
Present
Normal
Normal
Complete lesion
Present
Absent
Absent
Absent
Incomplete
lesion
Present
Decrease in numbers
Normal or slightly prolonged Reduced
Absent
Absent across block,
normal above
and below block
Neurapraxia
Absent
consists of urgent fasciotomies to relieve pressure in the
tissues (Fig. 10).39 Untreated compartment syndrome
can result in severe morbidity. Although the diagnosis
is essentially clinical, continuous compartment pressure
monitoring has been used as an adjunct by some authors.40
Continuous compartment pressure monitoring in the
lower extremity has a sensitivity of 94% and specificity of
98% for diagnosis of acute compartment syndrome.41
Factors Affecting Nerve Surgery
Both mechanical and biological factors affect nerve
regeneration. Neurotropic guidance of axonal regeneration
influences the extrinsic environment of the axon. In
contrast, neurotrophic enhancement implies an intrinsic
change in neuronal metabolism.42
At the nerve trunk level, axonal regeneration
is specific and presumably guided by tropic factors.43
Neuronal survival and regeneration might require a
continuous supply of neurotropic factors from their target
cells.44,45 Nevertheless, as Lundborg et al.46 discovered,
a well-organized nerve trunk can regenerate through
a preformed mesothelial chamber without preexisting
structural guidance as long as the gap is <15 mm. The
authors noted strong neurotrophic activity in fluid
collected from silicone chambers encasing the stumps of
Normal above
severed nerves.47,48 In cases in which axonal regeneration
of the severed trunk is unlikely,42 ganglioside preparations
have been used to stimulate collateral sprout formation
from intact nerve terminals.
Nerve growth factor (NGF) is a protein that
supports cell survival and elicits neuritic outgrowth.44-51
NGF has been isolated from some sympathetic or
adrenergic nerves and axons originating from sensory
ganglion cells but not from somatic efferent or
parasympathetic fibers.
Neuronal changes occur after axonal injury, and
they switch the neurons from a state of transmission to a
growth state, resulting in upregulation of genes involved
in cell survival and neurite outgrowth.25 Retrograde
transport is also disrupted and provides negative signals to
inform the cell body of the disconnection. NGF transport
therefore decreases and provides an important negative
feedback to the cell body. Artificial application of NGF to
axotomized sensory neurons can delay axonal regrowth.
Interested readers are directed to an in-depth publication
illustrating current concepts in neurobiology of peripheral
nerve regeneration.25 Other neurotrophic factors involved
in promotion of cell survival include brain-derived
neurotrophic factor, neurotrophin 4/5, glial derived
neurotrophic factor, ciliary neurotrophic factor, leukemia
inhibitor factor, and glial growth factor.29
9
SRPS • Volume 11 • Issue R7 • 2015
Figure 10. Preferred fasciotomy incisions for compartment
decompression in upper extremity. (Modified from
Rowland.36)
Time of Repair
The functional results of primary and early secondary
nerve repair are equal when conditions are optimal and
similar skills apply.52 Primary repair is probably best under
the following circumstances:
•• For proximal injuries
•• In which the distal nerve ends can
be pinpointed
•• That are minimally contaminated
•• Without associated injuries precluding
skeletal stabilization or compromising tissue
viability or skin coverage
•• In an otherwise healthy patient
•• When performed by a well-trained,
well-rested operative team working with
appropriate facilities53
If these conditions are met within 7 days, delayed
primary repair seems reasonable; if not, secondary repair
is indicated. Nerve stumps are approximated during the
initial débridement procedure, and a specific date is set
for reexploration and definitive repair. This approach
ensures patient compliance and avoids further delay in
case minimal return should tempt one to prolong the
observation period. Delayed repairs within 6 months of
injury yield better functional return than those performed
after 6 months.54
10
The zone of injury for a nerve depends on the
mechanism of injury: sharp, crush, saw, or avulsion.
Avulsion is by far the worst mechanism, as discussed by
Zachary et al.55 In their study, the histological injury in
nerve avulsions continues to progress along the nerve up
to 21 days after injury and requires aggressive resection
if immediate reconstruction is performed. The zone of
injury can extend up to 2 cm proximally and distally
beyond the transection site. Therefore, primary repair is
not recommended for injuries with any notable blunt
or avulsive component. Waiting for 3 weeks allows the
surgeon to define the damaged area of nerve and to
resect judiciously based on gross appearance at the time
of reconstruction. Resection of injured nerve ends at the
time of definitive reconstruction must remove all damaged
tissue to ensure regeneration can occur without injured or
scarred tissue impeding growth. A conduit or nerve graft
might be required to avoid inappropriate tension across
the repair, as repair site tension induces additional scarring
and decreased nerve regeneration. In other words, use of
nerve conduit or graft for a tensionless repair is superior to
primary nerve suture under excessive tension.56
The experimental data regarding the best time
for suture of sharply lacerated peripheral nerves are
contradictory. Cabaud et al.57 recommended repair as early
as possible to take advantage of early axonal sprouting
and to minimize scarring in the distal endoneurial space.
Similarly, Ducker et al.58 and Sunderland17 supported
primary or delayed primary repair within the first 10 days.
Grabb59 and Kline and Hackett60 reported improved motor
reinnervation after primary nerve repair in primates, and
Van Beek et al.61 and Hatano62 reported greater end-organ
recovery (muscle strength and reinnervated muscle weight)
with primary sciatic nerve repair in the rat.
Seddon,26 on the other hand, noted that fibrosis
at 3 weeks offered mechanical advantages for optimal
nerve suturing. Kleinert and Griffin63 recommended
nerve repair at 7 to 18 days to coincide with maximal
axoplasmic synthesis and to facilitate axonal sprouting
across the gap. Citing the same reasons, Holmes and
Young64 recommended nerve repair at 2 to 3 weeks after
injury. As indicated by Zachary et al.,55 it is preferable to
wait 3 weeks if the presence of an avulsive (versus sharp)
mechanism of nerve injury is suspected.
SRPS • Volume 11 • Issue R7 • 2015
Patient Age
Tension of Repair
When other variables are the same, functional results of
peripheral nerve repair are better in direct correlation
with younger patient age. Onne52 noted that for median
and ulnar nerve repairs, regained 2-point discrimination
(TPD) value in millimeters was approximately the same
as the age of the patient, up to 20 years. Between ages 20
and 31 years, recovery was variable but generally poor,
and after age 31 years, all sutured nerves showed poor
functional recovery, with TPD >30 mm. In contrast,
digital nerve repairs in that series showed good results up
to age 50 years.
Elasticity of neural tissues can be used to advantage to
bridge the space between the stumps when a nerve is
sutured primarily. Millesi54 stated that human nerve tissue
tolerates elongation of 20%, at which point it reaches its
elastic limit, beyond which nerve conductivity diminishes.
Young et al.65 found useful TPD in 80% of patients
younger than 20 years who underwent digital nerve
repairs; protective sensation, but no TPD, was achieved by
patients older than 40 years. Sunderland,17 on the other
hand, noted good functional results in older patients and
denied any correlation between patient age and outcome.
The excellent function observed in children after nerve
repair is ascribed to easier reeducation of central, cortical,
sensory, and motor pathways and to a stronger tropic
influence of one cell on another.
Condition of Wound
The degree of intraneural damage (contusion, hematoma,
devitalized tissue, infection, scarring) is a factor of the
traumatic agent. Severe intraneural damage is reflected
at the neuron cell body level, where increased proximal
degeneration is present and the regeneration potential
is consequently reduced. Traction injuries, high-velocity
missile wounds, shotgun wounds, and other types of severe
trauma adversely affect the outcome of nerve repair.
Level of Injury
The more proximal the injury, the worse the prognosis for
sensory and motor functional return.17,66 In proximally
innervated muscles, recovery is faster and more complete
when the nerve fibers are large and localized to the nerve
trunk. Crossover during nerve regeneration might not
adversely affect function if it occurs between synergistic
muscle groups but can play havoc with muscles responsible
for precise independent movements, such as the intrinsics.
The experimental data are contradictory. Highet
and Sanders67 studied the effects of stretching on canine
popliteal nerves and noted no permanent elongation but
rather long-term damage from continual stresses on the
nerves. Likewise, Miyamoto et al.68 showed that tension of
50 g (or stretch >2 cm) impaired transverse anastomoses
and later intraneural vascularization of fibular nerves in
dogs. In contrast, Rydevik et al.69 working with rabbit
tibial nerves, noted that endoneurial capillaries remained
well perfused some days after neurolysis despite laceration
of regional vessels and mobilization of fascicles for at least
2 cm. Those findings supported the contention held by
Smith70 that nerves can probably be mobilized up to 6 to
8 cm and stand as empirical evidence for the existence of
a duplicate longitudinal vascular supply at the fascicular
level. Vasconez et al.71 noted functional recovery in rhesus
monkeys that had 5 to 15 mm of median or ulnar nerve
removed. Working with rats, Terzis et al.72 concluded that
whereas severe tension predictably diminished functional
recovery, mild stretching produced results similar to
properly fitted nerve grafts.
Gap Size
Several authors59,70 have remarked on the worsening results
of neurorrhaphy when the gap between the proximal
and distal ends of the nerve exceeds 2.5 cm. The major
reason for a nerve gap is elastic retraction on both sides
of the injury. In the absence of primary repair,73 a fibrotic
reaction takes place around the interfascicular epineurium
that effectively anchors the nerve ends in a
retracted position.
The maximum gap that can be tolerated depends
on the normal excursion for that nerve. For example,
McLellan and Swash74 established that the greatest
excursion for the median nerve is 3.5 cm, produced by
extension of the wrist and fingers and flexion of the elbow.
If the gap after resection of the injured portion is 2 cm, the
nerve lacks 1.5 cm to accommodate full excursion and the
gap should be bridged.
11
SRPS • Volume 11 • Issue R7 • 2015
Techniques for bridging a nerve gap include direct
repair, grafting, nerve transfer(transfer of a redundant
nerve or fascicle to reinnervate a critical sensory or motor
territory), various tubes and conduits,75 nerve allografts,
and tissue expansion.75 The ideal nerve conduit should
be readily available, biodegradable, nonantigenic, easily
vascularized, and porous enough to facilitate oxygen
transport.75 Mackinnon75 reviewed experimental and
clinical experience with polyglycolic acid (PGA) (Dexon;
Covidien, Mansfield, MA) and Vicryl (Ethicon, Inc., West
Somerville, NJ) tubes, autogenous veins, and degenerated
muscle grafts in bridging nerve gaps. The authors reported
that the best sensory results are obtained with muscle
grafts in an acute setting and with PGA tubes if the nerve
reconstruction is delayed.
The first randomized, prospective, multicenter
evaluation of a bioabsorbable conduit for nerve repair
was presented by Weber et al.77 In that study, 136 nerve
transections were randomized into either a standard repair
(end-to-end or nerve graft) or repair using a PGA conduit.
At 12 months of follow-up, no significant differences
were observed between the two groups. Excellent or good
results were obtained in 86% and 74% of the control and
PGA conduit groups, respectively. Results were stratified
retrospectively to groups with nerve gaps of <4 mm, 5 to 7
mm, and >8 mm, but differences among group sizes made
it difficult to draw definitive conclusions. Conduits were
superior to “standard” repair in the <4 mm and >8 mm
groups but equivalent in the 5 to 7 mm group.
The RANGER multicenter study evaluated digital
nerve gaps of 5 to 15 mm that were reconstructed with
nerve allograft. Ninety-two percent were found to achieve
meaningful sensory recovery (grades S3-S4) and were
reported to be as good as historical autograft controls.
However, statistical significance was not reported.78
Mechanism of Injury
Taha and Taha79 evaluated functional outcome and return
to work after suture of radial, median, and ulnar nerves
injured by low-velocity missiles. The authors found that
nerve suture repair of injuries between the wrist and
axilla often required supplemental techniques, such as
permanent splints, tendon or muscle transfers, or fusions,
to achieve good results and expectations for return to
12
work, with the exception of combined median and ulnar
nerve injuries. Specifically, supplemental techniques
were required after suture repair in 11% of radial, 45%
of median, 72% of ulnar, and 100% of combined
median and ulnar nerve injuries. After suture repair and
supplemental techniques, if needed, patients returned to
work in 100% of radial, 55% of median, 57% of ulnar,
and 0% of combined median and ulnar nerve injury cases.
Surgical Management
Frykman et al.35 offered an algorithm for managing
peripheral nerve injuries that is predicated on the results
of clinical examination and electrodiagnostic
studies (Fig. 11).
Nerve Repair
The goals of nerve repair are to align the severed nerve
ends as accurately as possible with the fewest possible
number of sutures and to dissect nerve ends only to the
extent necessary to achieve proper alignment with minimal
tension. Optimal function is possible only if the motor
and sensory fascicles of a nerve are precisely and correctly
matched. Anatomic, electrophysiological, histochemical,
and immunohistochemical methods are now available for
fascicular motor sensory differentiation intraoperatively
and contribute to good surgical results of primary repair
after nerve injuries.80
Nerve repairs are of three general types. To date,
comparative analyses have not proved any one type to
be superior to the others. The following descriptions are
largely excerpted from the review presented by Daniel and
Terzis.81
Epineurial Repair—Epineurial repair is the conventional
technique for suturing divided peripheral nerves. It is used
primarily for small digital nerves that can be aligned with
two or three 9-0 or 10-0 nylon sutures. The advantages
and disadvantages of epineurial repair are presented in
Table 4.81
Perineurial (Fascicular or Funicular) Repair—
Fascicular repair was described in 1917 by Langley and
SRPS • Volume 11 • Issue R7 • 2015
Nerve is injured
Nature of nerve
lesion is known
Yes
Nerve is in
continuity
No
No
Repair as soon
as appropriate
Yes
Yes
Wait to allow
2.5 cm/month for
re-innervation
Wait 3 weeks
or more
Examine for return
of muscle activity
Yes
Re-examine every
1–3 months
Progressive return
of muscle activity
Yes
Congratulations
No
No
Electrical Studies Results:
EMG
[
NCV
[
FIBS, PSW
NO VMP
NO MOTOR
NO SENSORY
Explore surgically
and repair
EMG
[
FIBS, PSW
↓NO VMP
NCV
[
AMPLITUDES ↓
SENSORY AND
MOTOR LATENCIES
NORMAL OR
SLIGHTLY ↑
Expect further return
EMG
[
NCV
[
NO FIBS OR PSW
VMP ABSENT
MOTOR AND
SENSORY
NORMAL ABOVE
AND BELOW
BLOCK
Expect full return
EMG
[
NO FIBS OR PSW
NO VMP UNLESS
PATIENT IS TRICKED
NCV
[
NORMAL
Normal nerve
No injury
Figure 11. Algorithm for management of peripheral nerve injuries. EMG, electromyogram; FIBS, fibrillation potentials; PSW,
positive sharp waves; VMP, voluntary motor potentials; NCV, nerve conduction velocity. (Modified from Frykman et al.32)
13
SRPS • Volume 11 • Issue R7 • 2015
Table 4
Advantages and Disadvantages of Epineurial Repair74
Advantages
Disadvantages
Short execution time
Compromise of precise fascicular alignment
Technical ease
Sutured epineurium lying in same vertical plane as cut axonal interphases
Minimal magnification
Tension from normal retraction of cut nerve ends even if no nerve tissue is lost
Intraneural contents not invaded
Many sutures required to achieve structural integrity of repair
Sutures placed only in
outer investing sheath
Controversial outcome
Applicable to both primary and
secondary repairs
Likelihood of performance by improperly trained personnel
Hashimoto.82 The superiority of fascicular over epineurial
repair is still in question. Some investigators find no
difference between the techniques,65,83-85 whereas others
tend to favor perineurial repair over the funicular
suture.86-91 Orgel85 stated that suture of the outer
epineurium is the technique of choice for most acute nerve
lacerations. The author found it to be easier, to be faster,
and to require less manipulation of the delicate internal
neural structure. Fascicular repair, on the other hand, is
more likely to restore usable pathways when branched
fiber systems are well localized at the nerve ends. It yields
superior results, as judged by morphological and
neurophysiological parameters.92
Jabaley93 defined the respective indications for
epineurial and perineurial repair. Funicular repair is the
technique of choice in nerve grafting and is applicable to
nerves with fewer than five fascicles but is contraindicated
for multi-fascicled nerves. Theoretical advantages are
considerably more myelination of the stumps, better
fascicular alignment by coaptation of perineurial tubes,
more regenerating axons entering endoneurial tubes
of the distal nerve, and greater functional recovery of
motor and sensory end organs.82 Disadvantages include
longer operative times, increased fibrosis at the suture
site, possible vascular compromise of isolated fasciculi,
inability to restore funicular continuity on a one-to-one
14
basis, crowding of the suture line with suture material,
greater trauma to nutrient vessels at the nerve ends, and
inability to approximate very small funiculi.83 In addition,
identifying motor and sensory fascicles in the proximal
and distal stumps to accurately match the transected ends
might not be possible.53
Group Fascicular Repair—Group fascicular repair is
possible when a nerve is transected at a level where the
branches responsible for different functions are well
formed and readily identified within the main trunk.
Considering these conditions, motor and sensory
components can be accurately coapted to avoid motor
sensory cross-innervation. Although histochemical staining
can distinguish between motor and sensory axons94-96
to aid in matching the appropriate fascicles, the lengthy
process is not clinically practical at this time.
Jabaley93 presented a list of specific indications
for group fascicular suture at various levels in the upper
extremity. Regarding the median nerve, the suitable
length of nerve trunk for group fascicular repair extends
from approximately 5 cm above the wrist crease to its
termination in the palm and for several centimeters below
the elbow. In the ulnar nerve, a likely area extends 7 to 8
cm proximal to the wrist crease.
SRPS • Volume 11 • Issue R7 • 2015
Repair of Upper Extremity Peripheral Nerve Defects
Trumble and McCallister97 described four techniques for
achieving direct coaptation of nerve ends when repairing
defects in peripheral nerves: nerve stump mobilization,
nerve rerouting and transposition, joint positioning, and
bone shortening. The authors provided a decision pathway
for using these methods of reconstructing peripheral nerve
injuries (Fig. 12).
In addition to the four methods, the authors
described neurotization, which involves embedding the
distal end of a nerve directly into the recipient muscle and
the use of autologous nerve grafts from adjacent nerves
that have been irreparably damaged.
Nerve mobilization can reduce tension at the repair
site and requires release of constricting fascia, division of
mesoneurial attachment, division or dissection of tethering
nerve branches, and sometimes epineurolysis. Trumble and
McCallister97 reviewed the literature regarding decrease in
nerve blood flow as a result of stretching the nerve itself.
The authors found a range of 4% to 25% nerve elongation
through direct stretching to be safe, based on clinical and
experimental studies.
Mobilization as described above must be performed
judiciously because nerve mobilization, even without
stretching the nerve, can decrease nerve vascularity. Maki
et al.98 found, in a rabbit sciatic nerve model, that a nerve
can be maintained on its proximal intrinsic blood supply
after transection and circumferential dissection along a
length equal to 63 times its diameter. The nerve could also
be supported on a single extrinsic blood vessel with nerve
transection both proximally and distally (eliminating the
intrinsic blood supply) for a length equal to 45 times its
diameter. The results support the clinical use of extensive
nerve mobilization to gain additional length for nerve
repair in a tensionless fashion.
Peripheral nerves can also be rerouted and
transposed to decrease tension at the repair site. Anatomic
locations in the upper extremity best suited to nerve
transposition include the following:97
1.Ulnar nerve at the elbow
2.Recurrent motor branch of the ulnar nerve
at the wrist as it enters the carpal tunnel
3.Median nerve at the elbow with release of
the lacertus fibrosus, PT muscle, and
FDS muscle
Positioning of the joints nearest the site of injury
results in the greatest reduction of tension across the repair
site. As described, correcting joint position postoperatively
starts no earlier than 2 to 3 weeks after repair and increases
joint motion by 10% each week.97 However, concern
exists regarding scarring as a result of tension at the nerve
repair site. Nerve grafts or conduits can be used in an
acute or chronic setting to avoid tension of nerve repairs
in all extremes of joint position at the time of repair.56,99
However the number of axons within the regenerating
front that succeed in crossing a neurorrhaphy site reduces
with each additional suture line. Therefore, a degree of
joint positioning might result in a higher number of axons
reaching their target end organ if it allows a direct end-toend nerve repair.
Bone shortening in the upper extremity is another
technique of bridging nerve gaps.97 Humeral shortening,
commonly indicated when multiple nerves have been
injured in the setting of a comminuted fracture, facilitates
end-to-end repair of both the median and ulnar nerves.
Additional indications for humeral shortening include
segmental defects of the ulnar nerve in children and
adolescents and cases in which concomitant repair of
the median and radial nerves is possible. By using these
four techniques (nerve mobilization, rerouting and
transposition, joint positioning, and bone shortening),
Trumble and McCallister97 provided maximum lengths
attainable for median, ulnar, and radial nerve repairs. The
authors provided a detailed description of the anatomic
specifics of the maneuvers.
Functional Recovery
Nerve Regeneration and the Reinnervation Process
When the ends of a severed nerve are approximated,
Schwann cell processes projecting from the distal nerve
segment accept the progressing axonal buds and serve as
conduits to bridge the gap. The regenerating axons are
said to grow at a rate of approximately 1 to 3 mm per
day through the old endoneurial conduits in the distal
segment.17,53,100 According to Huber,101 regeneration of the
peripheral end of a severed nerve depends on the outcome
of the struggle between the down-growing axis cylinders
15
SRPS • Volume 11 • Issue R7 • 2015
Can the injury be repaired primarily
without having to overcome a
segmental defect in the nerve?
Yes
No
Proceed with primary repair.
Are the end organs (skin, muscle)
supplied by the nerve
irreparably damaged?
Yes
No
Is the proximal portion of the
nerve available for repair?
Proceed with neurovascular
island flaps or tendon transfers.
No
Yes
Consider nerve transfer
(e.g., intercostal nerve transfer
to the musculocutaneous nerve).
No
Is the distal end of the
nerve available for repair?
Yes
Consider neurotization.
Can the nerve ends be
approximated with mobilization,
transposition, bone shortening,
or joint positioning?
No
Bridge nerve defect
with intercalary graft.
Yes
Repair end to end.
Figure 12. Algorithm for management of peripheral nerve injuries. (Modified from Trumble and McCallister.93)
16
SRPS • Volume 11 • Issue R7 • 2015
and the developing connective tissue between the
severed ends.
Experimental studies revealed accelerated
axonal regeneration of 4 to 5 mm per day in animal
models.57,102-104 Cabaud et al.,57 working with rhesus
monkeys, documented remyelination beginning at 1 to
2 weeks; by 3 weeks, it was far distal to the site of injury.
Moreover, most new fibers passed down new endoneurial
tubules, rarely using old conduits. Wallerian degeneration
continued for 6 weeks.
The rate and quality of the recovery depend on
appropriate reinnervation of the muscles. Progress of the
regenerating nerves is measured by Tinel sign, repeated
sensory and motor testing, and electrodiagnostic studies.
Clinically successful reinnervation depends to a large
extent on the proximity of the lesion from its end organ
and the denervation interval.31,105,106
Gutmann and Young106 studied the process of
muscular reinnervation in the rabbit after variable
periods of denervation. The proportion of end plates
successfully reinnervated was inversely related to the
length of denervation; even so, the authors found intact
motor end plates 1 year and more after denervation. The
number of end plates returning to function was thought to
correspond with the proximity of the nerve injury to
the muscle.
Brushart and colleagues,91,107 working with rat sciatic
nerves, documented reinnervation of peroneal muscles
by appropriate motor neurons and by motor neurons
that previously served their antagonists. Disappointing
functional results, therefore, are not only caused by
sensory-motor crossover but also by inappropriate motor
reinnervation.
Sunderland,17,105 citing cases in which excellent
recovery was achieved 12 months or longer after injury,
concluded the following:
•• Restoration of muscle function requires
more than reestablishment of axonal
continuity with the terminal endings in
the muscle.
•• Reinnervated human muscles are capable
of regaining almost complete function
even after a year of denervation, provided a
sufficient number of axons can be directed
to their original or functionally similar end
organs and the muscle has been maintained
in good condition with therapy.
•• Any functional deficit remaining after
muscle reinnervation is often the result
of an insufficient number of reinnervated
muscle fibers, fiber mixing at the site of
nerve repair, or persisting retrograde and
transsynaptic central neuronal changes
impairing activity patterns.
Lundborg and Rosén108 assessed 54 patients after
repair of transected median or ulnar nerves at the wrist
level. The best results for recovery of hand sensibility were
achieved in patients younger than 10 years. A rapid decline
then occurred until age 18 years, at which time a plateau
was reached. The authors concluded that the critical age
period for regaining functional sensibility after nerve repair
ends in the late teenage years.
A growing body of evidence supports the role of
an intact distal target in promoting nerve regeneration.
This is relevant in nerve graft reconstruction, with which
a proximal nerve end or donor nerve can be coapted to
a nerve graft without a distal recipient neuromuscular
unit being present. Such a scenario commonly occurs in
cases of cross-facial nerve grafting, nerve pedicle transfer,
and contralateral C7 transfer using pedicled vascularized
ulnar nerve grafts. Goheen-Robillard et al.109 reported a
significant increase in regenerating axons when a nerve
graft is coapted to its distal nerve and/or muscle target
at the time of proximal graft coaptation. The number
of fibers crossing the neurorrhaphy site was double with
coaptation to a distal target. The finding was also suggested
by Hadlock et al.110 in a facial nerve injury model and by
Rab et al.111 in an extremity model.
Postoperative Rehabilitation
Most authors agree that sensory and motor recovery
after peripheral nerve injury, especially recovery to useful
function, continues to improve for more than 2 years
postoperatively. Immediately after surgery, immobilization
for 7 to 10 days is sufficient in most cases.31 Wilgis112
suggested a slightly longer period of immobilization and
charted his protocol for rehabilitation of nerve injuries
(Fig. 13).
17
SRPS • Volume 11 • Issue R7 • 2015
Rapidly accumulating evidence indicates that a
prolonged period of immobilization is not mandatory
after digital nerve repair in the setting of an associated
flexor tendon repair.113,114 In a cadaver model, the Duran
protocol was performed without disruption of nerve
coaptations when the nerve gap was 5 mm or less (Figs.
14 and 15).115,116 This is in direct contradiction to the
conventional wisdom that dictates 3 to 4 weeks of casting
after digital nerve repair.117 Once passive motion of the
extremity begins, physiotherapy, direct muscle stimulation,
and sensory reeducation are essential for optimal return
of function.
s
ye
a
r
on
th
1
m
6
on
th
m
3
ks
w
ee
6
3
0
w
ee
ks
s
The use of early tactile stimulation after digital nerve
repair has been reported by Cheng and colleagues118,119 to
provide better sensibility compared with no early tactile
stimulation. Tactile stimulation was started 3 weeks after
nerve repair using a rotating tactile stimulator disc in
addition to standard rehabilitation techniques.
Additional innovations for rehabilitation after
sensory nerve repair in the hand come from the research
conducted by Rosén and colleagues120,121 in Sweden.
During the early phase of sensory recovery, as sensation
returns to the digits, repeated sessions of forearm
anesthesia by topical application of EMLA cream
(AstraZeneca, London, United Kingdom) might augment
sensation for up to 4 to 6 weeks through rapid cortical
reorganization. The durability of this early difference is
not certain based on current evidence, considering that
four treatments over a 2-week period did not have lasting
effects after 8 to 11 months.122 It was recently reported
that extension of the cutaneous anesthesia protocol along
with sensory rehabilitation over the course of a year
allowed reversal of “alexia” for Braille in a blind patient.123
Temporary cutaneous anesthesia of neighboring sensory
territories remains a promising modality to augment
sensory recovery after nerve repair, although a predictable
and tested protocol has yet to be determined.
Protection of repair
Prevention of secondary deformity
Splintage
Increased range of motion
Increased strength
Sensory reeducation:
Start when 256 cycles per second recovery and
Tinel advancement to end plate
Figure 13. Course of rehabilitation after peripheral nerve repair. (Modified from Wilgis.108)
18
SRPS • Volume 11 • Issue R7 • 2015
Figure 14. Mean gap at which disruption occurred for each digital nerve. No statistically significant difference was shown
between mean disruption gaps for each of 10 digital nerves. For each nerve, n = 10. R, radial digital nerve; U, ulnar digital
nerve within each digit; crosshatched bars, splinted; white bars, unsplinted. (Reprinted with permission from Chao et al.112)
Figure 15. Effect of mobilization on nerve repairs and grafts. Percentage of nerves that remained intact for certain gaps
after modified Duran and unsplinted protocols decreased with increasing gap. Increased rupture rates for unsplinted nerves
at 5- and 7.5-mm gaps were shown to be statistically significant. n = 100 for each bar except as indicated for three bars.
Crosshatched bars, splinted; white bars, unsplinted. (Reprinted with permission from Chao et al.112)
19
SRPS • Volume 11 • Issue R7 • 2015
Evaluating the Results
by touch.
Grading Systems
Jerosch-Herold133 argued that to accurately assess the
functional outcome of peripheral nerve suture in the hand,
the evaluation must “include an additional measure of
performance on daily living tasks.” The author’s conclusion
was based on a study of the relevance of sensory tests to
everyday functional activities. Analysis of the data revealed
that the tests of sensibility do not predict patients’ ability
to use their hands in everyday activities because patients
are able to compensate for sensory deficit through the use
of vision and bilateral use of the hands.
To compare the published clinical results of peripheral
nerve repair, one must rely on standardized, universally
recognized, objective criteria. In 1946, Zachary and
Holmes124 proposed a system that was based on a scheme
presented by Highet and Sanders.67 The scheme was later
modified by the Nerve Committee of the British Medical
Research Council (Tables 5 and 6).21 The grading scale,
although useful, does not fully reflect hand function. For
example, an M3 level might be sufficient for effective
motor function in some muscle groups but not in others,
and the sensory criteria do not include meaningful
sensation such as object recognition. Furthermore,
MacAvoy and Green125 reported marked limitations in
the ability of the Medical Research Council system to
discern motor activity in the functional range (Grades
3−5), considering Grade 4 encompasses 96% of potential
elbow flexion strength. The other 4% of detectable elbow
strength must therefore be distributed among Grades 2,
3, and 5. Although Grade 2 (contraction with gravity
removed) generally is not functional in daily use, the level
of movement is clinically detectable.
Non-obstetric Brachial Plexus Injury
Brachial plexus injuries are most common in young men.
The majority of injuries are sustained in motor vehicle
accidents (traction or crush); less frequently, they occur as
sequelae of penetrating wounds, tumors, obstetric trauma,
or radiation.134,135 Brachial plexus injuries can occur at
several levels134-136 and usually involve multiple structures
of the thorax and upper extremity.137
Static TPD tests, such as described by Onne52 in
1962, are best at predicting hand activities that depend
on the sensation of something being held between the
fingers and correctly assessing the pinch strength needed
to maintain grasp. This is a test of innervation density in
slowly adapting fibers. In 1978, Dellon and colleague126,127
suggested a moving TPD test and correlated test results
with object recognition or tactile gnosis. This is a test of
innervation density in rapidly adapting fibers.
Evaluation of a patient suspected of having brachial
plexopathy must include a detailed medical history,
clinical assessment of motor and sensory function in the
upper extremity, and determination of the status of the
diaphragm, pectoralis, serratus, latissimus, trapezius, and
paraspinous muscles.138 To determine suitability of the
intercostal nerves for transfer, any history of rib fractures
is also elicited. Concomitant injuries to the spine, clavicle,
ribs, shoulder girdle, and upper limb are important clues
to the energy transfer involved and the likely grade
and level.
In routine use, the “ten test” described by Strauch
and colleagues128,129 is a simple, practical, trackable,
reliable, and repeatable examination with which the
patient develops a ratio between light moving touch and
diminished moving touch on a scale of 1 to 10. It is most
likely a test of pressure threshold in rapidly adapting
fibers. A more common assessment of pressure threshold
in slowly adapting fibers is the use of Semmes-Weinstein
monofilaments, which come as a calibrated set of at least
five and as many as 20 filaments.130 Moberg131,132 proposed
a “pick-up” test that has patients picking up objects from
a table and placing them in a small box. The patient is
subsequently blindfolded and asked to identify the objects
The literature regarding brachial plexus injury
is extensive, and a substantial proportion is historical.
Contemporary management is determined by several
factors, including the level of injury, grade of injury,
timing of injury, evidence of neuronal regeneration, and
intra- and extraplexal donor nerves available. Regarding
level of injury, it is critical to determine whether the injury
is pre- or post-ganglionic.139 An avulsion indicates that
the spinal nerve has been avulsed from the spinal cord,
with no connection between the central and peripheral
nervous system, and is termed preganglionic. A rupture
describes division of the peripheral nerve, usually caused
by tractional force, which can occur at any level of the
20
SRPS • Volume 11 • Issue R7 • 2015
Table 5
Classification of Sensory Recovery21
Grade
Recovery of Sensibility
S0
No recovery of sensibility in the autonomous zone of the nerve
S1
Recovery of deep cutaneous pain sensibility with the autonomous zone of the nerve
S1+
Recovery of superficial pain sensibility
S2
Recovery of superficial pain and some touch sensibility
S2+
As in S2 but with overresponse
S3
Recovery of pain and touch sensibility with disappearance of overresponse*
S3+
As in S3 but localization of stimulus is good and recovery of 2-point discrimination is imperfect†
S4
Complete recovery‡
*Classification modified to include classic 2-point discrimination range: S3 has 2-point discrimination >15 mm.
†Classification modified to include classic 2-point discrimination range: S3+ includes 7- to 15-mm range.
‡Classification modified to include classic 2-point discrimination range: S4 includes 2- to 6-mm range.
Table 6
Classification of Motor Recovery21
Grade
Motor Recovery
M0
No contraction
M1
Return of perceptible contraction in proximal muscles
M2
Return of perceptible contraction in both proximal and distal muscles
M3
Return of function in both proximal and distal muscles to such a degree that all
important muscles are sufficiently powerful to act against gravity
M4
All muscles act against strong resistance, some independent movements are possible
M5
Full recovery in all muscles
21
SRPS • Volume 11 • Issue R7 • 2015
brachial plexus and indicates disruption distal to the dorsal
root ganglion (DRC) with an intact connection between
the central and peripheral nervous system and is therefore
postganglionic (Fig. 16).139 Preganglionic lesions have
no proximal source of axons for nerve regeneration and
therefore preclude repair or interpositional nerve grafting.
Postganglionic lesions have a proximal source of axons
for nerve regeneration and therefore interpositional nerve
grafting can be considered.
Level of injury is also anatomically classified as
supraclavicular (75%) or infraclavicular (25%), with
supraclavicular injuries involving the roots and trunks and
infraclavicular injuries involving the divisions, cords, and
terminal branches.140 Several other classifications have been
published, including that presented by Terzis et al.141 who
classified injury levels into supraclavicular preganglionic,
supraclavicular postganglionic, and infraclavicular. In
2010, Chuang142 published a further classification of level
of injury based on a review of 819 adult brachial plexus
injuries operated on by a single surgeon. It should be
noted that injury might involve more than one level.
Clinical examination can indicate the level of
injury based on dermatomal and myotomal neurological
findings. Signs of Horner syndrome indicate sympathetic
chain disruption and likely avulsion of the lower roots
(C8−T1). Computed tomographic (CT) myelography
can define pseudomeningocele from a dural tear; however,
it is not pathognomonic for root avulsion and not used
universally.143 Magnetic resonance imaging (MRI) can
be useful when considering root avulsion. It offers the
advantages of visualization of the whole brachial plexus
and no radiation exposure. However, CT myelography
remains the gold standard imaging for assessing root
avulsion and is most accurate 3 to 4 weeks after injury.140
EMG and nerve conduction studies are routinely
performed.144 They aid in diagnosing, localizing, and
defining the extent of axonal loss, but they should be
delayed for 3 to 4 weeks because Wallerian degeneration
is responsible for the emergence of spontaneous electrical
discharge.139,143 Sensory nerve action potentials require
continuity between the axon and cell body, which is
located in the dorsal root ganglion. Therefore, action
Avulsion
B
Dorsal
root
ganglion
C
Stretch
A
D
Rupture
Figure 16. A, Transverse section through the cervical spine shows the dorsal root ganglion, dorsal and ventral rootlets,
spinal cord, and osseous anatomy. B, With avulsion injuries, the rootlets are torn from the spinal cord. They are preganglionic
injuries, as the injury occurs proximal to the dorsal root ganglion. C, If the injury occurs distal to the ganglion, it is
postganglionic. Such injuries include stretch injuries (shown in panel C) and ruptures of the nerve (shown in panel D).
(Modified from Giuffre et al.135)
22
SRPS • Volume 11 • Issue R7 • 2015
potentials are preserved in preganglionic lesions but
not postganglionic lesions or combined pre- and
postganglionic lesions. Somatosensory evoked potentials
can also help to distinguish between preganglionic and
postganglionic lesions.145
Grade of nerve injury has been classified by
Sunderland146 and described earlier. From a clinical
perspective, it is important to determine whether the
injury is a conduction block (neurapraxia) or axonal injury.
A conduction block requires no surgical intervention,
and full recovery can be expected. Axonal injury results in
Wallerian degeneration and prolonged recovery, the extent
of which is determined by the distance from injury to
end organ and the extent of connective tissue disruption.
Three clinical findings can help to determine whether
the patient has conduction block or axonal injury: Tinel
sign, sweating, and neuropathic pain. Conduction block
typically presents with absent Tinel sign, intact sweating
(sympathetic supply), and no neuropathic pain. These
injuries are common in cases of low-energy trauma.
Axonal injury typically presents with Tinel sign, intact
sweating, and neuropathic pain. Complete nerve division
(rupture) presents with Tinel sign, absent sweating, and
neuropathic pain (Table 7). Of note, severe neuropathic
shooting pain into an anaesthetic territory is suggestive of
a preganglionic injury.
Timing of operative intervention is controversial,
with a shift to a more proactive approach with earlier
intervention.147,148 Timing of nerve injury has substantial
impact on management and outcome. Patients often
are referred to the Brachial Plexus Unit several weeks
after initial injury, at which point suboptimal conditions
exist for exploration, resulting in delayed surgical
intervention. A recent publication reported that 25% of
delayed explorations occurred in patients with injuries
that would have been suitable to explore within the first
2 weeks.147 Earlier intervention is currently advocated
on the basis of biological, technical, and pain-related
factors.148 Birch148 argued that because neurons rely on
neurotrophic factors to survive after axonotomy and
proximal nerve injuries result in cell death in both the
ventral horn and the dorsal root ganglion, reestablishing
the nerve cells with neurotrophic factors in the peripheral
nerve by early intervention should improve outcome.
Some units have designed a protocol system for timing
of exploration for brachial plexus injuries (Fig. 17). It is
generally accepted that open injuries, vascular injuries,
and iatropathic injuries dictate immediate exploration.
Patients with adverse features, such as Tinel sign,
autonomic dysfunction, and neuropathic pain, might
benefit from early surgical exploration (<12 weeks). This
strategy allows diagnosis, decompression, and neurolysis
and, where indicated, nerve grafting or nerve transfer.
Even where an incontinuity lesion exists, decompression
optimizes the conditions for axonal regeneration and
can greatly improve neuropathic pain. Patients without
indication for immediate exploration should be regularly
assessed by a peripheral nerve injury service to establish
the pattern, grade, and extent of injury, which nerves have
potential for spontaneous recovery, and what potential
donor nerves are available for transfer. Once a diagnosis
of rupture or avulsion is established, early exploration can
be performed to confirm the diagnosis and reconstruction
can then be accomplished with nerve grafting or transfer.
Late intervention (>3 months) is indicated for those cases
in which the expected progress has not been achieved,
in cases that are not fit for earlier intervention, and in
cases that were referred late. Conservative treatment for
3 months is recommended for patients with upper type
injuries who have no clinical evidence of
preganglionic lesions.
Reinnervation of muscle is generally considered
necessary by 12 months before irreversible motor end
plate degeneration takes place. The timing of intervention
depends on the type of procedure and the distance from
the injury to end organ. Nerve transfer can convert a
high-level injury to a low-level injury such that it can be
considered at 10 months.149 However, proximal injuries
treated with nerve grafting require intervention at an
earlier time point to allow for the longer distance for
axonal regeneration to the end organ. In a large series of
patients with complete traumatic brachial plexus injuries,
Bentolila et al.150 found that operative delay of less than
6 months from time of injury was a significant factor
regarding recovery of the function of the biceps (P =
0.003).
Ferenz151,152 reviewed the literature of brachial
plexus injuries and discussed the current management
trends for both acute and chronic injuries of the brachial
plexus. Because up to 60% of brachial plexus injuries
below the clavicle resolve gradually without medical
intervention,153 surgery is postponed 2 to 5 months to
23
SRPS • Volume 11 • Issue R7 • 2015
Table 7
Clinical Signs of Injury Type
Injury Type
Tinel Sign
Sweating
Neuropathic Pain
Conduction block
−
+
−
Axonal injury
+
+
+
Rupture
+
−
+
−, absent; +, present.
await the spontaneous return of nerve function.136,144 The
later the operative repair is performed, however, the more
difficult the procedure is and the worse the results are.135
Patients should be examined for the availability of
both intraplexal and extraplexal donors for reconstruction
via nerve transfer and for donor nerve site for nerve
grafting. Direct coaptation for the brachial plexus is
limited to open sharp injuries. High energies involved in
closed traction-type stretch or rupture injuries produces a
zone of injury that precludes direct repair. This results in
a requirement for functional reconstruction with a focus
on reconstruction of key components of upper extremity
function by nerve grafting, nerve transfer, tendon transfer,
and free functioning muscle transfer. These techniques are
discussed in detail later in the monograph.
Terzis and Papakonstantinou154 drew on many
years of experience with brachial plexus injuries in adults
when they suggested the following aims of reconstructive
procedures:
1.Stability of the shoulder with focus on
return of function in the supraspinatus
and deltoid muscles: Shoulder fusion is
not advocated.
2.Restoration of biceps function: A hand that
has been spared from injury will be useless
unless elbow flexion is restored.
3.Reinnervation of the triceps to provide
elbow joint stability: Not all authors
attempt to regain triceps function, and,
24
in some cases, the triceps muscle can be
transferred to provide elbow flexion.
4.Restoration of median nerve function to
allow both sensory protection and finger
flexion: Sensory protection can be achieved
by neurotization of the median nerve
from sensory intercostal nerves or from
supraclavicular sensory nerves.
5.Lower root involvement: In cases of lower
root involvement, it might be prudent
to leave banked nerves at the elbow level
for future free muscle transplantation for
hand reanimation.
Terzis et al.141 reported outcomes of brachial plexus
reconstruction in 204 patients with adequate follow-up
during an 18-year period. Most patients were young
(mean patient age, 26 years), and 55% of injuries were
caused by high-velocity motor vehicle accidents involving
nerve avulsions. Nerve reconstruction included 577
nerve repairs (140 direct neurotizations and 437 nerve
grafts). Microneurolysis was performed in 89 cases, and
vascularized free nerve grafts were used in 120 repairs.
Muscle transfers (29 pedicled and 78 free) were performed
to enhance hand function. The results were good or
excellent in 75% of suprascapular nerve reconstruction,
40% of deltoid reconstruction, 48% of biceps
reconstruction, 30% of triceps reconstructions, 35% of
finger flexion reconstructions, and 15% of finger extension
reconstructions. The majority of patients experienced
protective sensation and pain relief postoperatively.
SRPS • Volume 11 • Issue R7 • 2015
Immediate
• Open injuries
• Vascular injuries
• Latropathic injuries
Early (<12 weeks)
• Closed injuries with adverse features
• Associated injury needing intervention
• Evidence of avulsion and/or rupture clinically
Late (>12 weeks)
• Not fit initially
• Failure to make expected progress
• Late referral
Figure 17. Birmingham peripheral nerve injury service
protocol. Early is defined as within 12 weeks of injury. Late
is defined as more than 12 weeks after injury.
Complications of Nerve Injury
Neuromas
occurs at the site of the nerve injury or if partial injury
exists, painful sequelae can develop because a portion of
the nerve is transmitting relatively normal impulses and
the remainder of the nerve is transmitting
abnormal impulses.
A pragmatic approach to neuroma prevention in
patients with irreparable nerve division is simple resection
to allow the cut ends to retract proximally into healthy soft
tissue.155 If the soft-tissue bed is not adequate, the nerve is
transected proximally where local trauma can
be minimized.
Neuromas can occur after injury or surgical repair.
They can be classified according to their site: lateral,
incontinuity, end, or amputation stump neuromas.
Conventionally, neuromas are divided into those that
occur after complete transection and those that occur after
partial transection.
Complete Transection
The management of painful neuromas is controversial. In
the event of an established, painful neuroma that cannot
be repaired primarily, en bloc relocation to an unscarred,
protected site is preferred.156,157 Alternatives are crushing,158
epineurial closure and ligation,159 transposition (either
in-continuity or after resection),112 relocation of the
intact neuroma,157 and resection and proximal nerve end
implantation into muscle or bone.160
Neuromas behave unpredictably, particularly those
forming in proximal peripheral nerves. Patients’ activities
of daily living and work can be restricted because of the
severity of the symptoms. Neuromas are also difficult
to diagnose because of the fascicular arrangement of
proximal nerves. Mackinnon and Dellon21 stated that
when a peripheral nerve is divided, nerve fibers in the
proximal nerve stump form regenerating units that
contain numerous axon sprouts. If the sprouting fibers
make appropriate sensory or motor distal connections,
functional recovery occurs. If they do not make
appropriate distal connections, loss of function occurs.
Pain can develop at the level of the thwarted regeneration.
Physical and chemical measures, such as freezing,
cauterization, electrocauterization of the nerve stump,
silicone-rubber capping, and corticosteroid injection,
have been tried with variable success.161-163 Martini and
Fromm164 described managing 68 painful neuromas by
shortening the fascicles and sealing the epineurial cuff with
Histoacryl topical skin adhesive (B. Braun Medical, Inc.,
Bethlehem, PA) to plug the nerve ends and prevent escape
of regenerating axons. All except three of 36 patients were
cured or improved.
Per Mackinnon and Dellon,21 the inevitable
consequence of complete division of a peripheral nerve is
formation of a neuroma at the proximal site of the nerve
division if the neuron’s attempt to regenerate distally
is thwarted. Not all of these neuromas are painful. No
consensus exists regarding why one neuroma is clinically
symptomatic and another is not. If partial regeneration
Novak et al.165 surveyed 70 patients to evaluate the
long-term subjective outcome of surgical treatment of
upper extremity neuroma. In all cases, the neuromas (n =
112) were resected and the involved nerve was transposed
into proximal muscle away from overlying scar and
denervated skin. Forty-five patients (64%) reported good
pain relief and were able to return to work after surgery.
25
SRPS • Volume 11 • Issue R7 • 2015
No significant difference was observed in functional
outcome that could be related to patient sex, postinjury
time, follow-up time, number of previous operations,
or site of nerve injury. Mackinnon and Dellon166 offered
an algorithm for the surgical management of painful
neuromas (Fig. 18).
Partial Transection
When no definite evidence of nerve severance is present,
a 1-month waiting period for evidence of spontaneous
recovery is reasonable. Serial examinations of the injured
extremity to include Tinel test and electrodiagnostic
studies (nerve conduction velocity and evoked response)
should be correlated with the clinical picture to determine
whether and at what point exploration is necessary. The
findings at exploration will determine the course of action,
as follows:81
•• In the event of residual sensory and motor
function and a lateral neuroma, care
should be taken not to convert a partial
lesion into a complete one. Management
is by appropriate resection and repair of
the disrupted perineurium of the involved
fascicles only. The resulting gap determines
whether nerve graft is indicated.
•• Where exploration reveals a spindleshaped neuroma and fascicular continuity,
intraneural neurolysis (not resection and
repair) should be performed regardless of
the functional loss.
•• Spindle-shaped neuromas associated with
complete transection and no sensory or
motor return should undergo subsequent
resection and coaptation at the site
of injury.
Woodhall et al.167 noted significant functional
recovery in 75% of patients with nerve injuries who had
initial paralysis but no overt nerve severance. Evidence
of regeneration was delayed beyond the expected time
in half the patients, and those cases were subsequently
explored. In that group, nerve regeneration and eventual
recovery was better when the neuroma was not excised
and the nerve not sutured. Because motor end plates tend
to disintegrate after denervation and to lose most of their
26
reinnervation potential with time, 12 months should be
considered the outer time limit for surgical intervention in
suspected neuromas of the motor system.
Certain anatomic sites are common for neuroma
formation, including superficial radial nerve or branches,
Palmar cutaneous branch of the median nerve, and
digital nerves after amputation. Nonsurgical management
should be considered in the initial treatment of neuromas
and includes physical therapy, desensitization, and
pharmacological treatment (gabapentin or pregabalin).168
A recent review advocated dividing surgical management
into three categories:168
1.If appropriate distal nerve and sensory
receptors are available, nerve grafting
can direct regenerating nerve fibers from
proximal to distal segment.
2.If a distal nerve is not available but
critical function is required distally, free
functioning neurocutaneous flap can be
used to accept regenerating sensory nerve
fibers in the proximal segment.
3.If the local environment is not suitable
for nerve grafting or if multiple previous
operations have been performed, resection
of the neuroma and transposition of the
proximal stump into muscle, vein, or bone
is advised. Centro-centralization technique
involves suturing two nerve fascicles in the
proximal segment to each other and has
shown clinical success.
Autologous tissue wrapped around the nerve has also been
used to help provide a well-vascularized tissue with the
aim of producing a gliding surface and preventing fibrosis,
adherence, and irritation to the peripheral nerve.
Elliot169 reported complete resolution of all
modalities of pain in eight of 14 patients undergoing
teno-neurolysis and fascial nerve wrap. The author
recommended the use of local flaps, including the Becker
fasciocutaneous flap and the anterior forearm fascial flap.
This usually is reserved for large forearm nerves (median or
ulnar) in continuity to treat pain rather than
distal sensation.169
SRPS • Volume 11 • Issue R7 • 2015
Arm
Wrist
Forearm
Neuroma resection
Bone
Critical sensation
Nerve graft
Noncritical
Brachioradialis
muscle
Distal nerve stump
available
Nerve graft
No distal nerve
Provide innervated
free tissue
Distal nerve
available
Nerve graft
No distal nerve
Bone
Critical sensation
Hand
Noncritical
Lower
extremity
Critical sensation
Nerve graft
Bone
Noncritical
Soleus muscle
Figure 18. Surgical algorithm for management of painful neuroma. (Modified from Mackinnon and Dellon.161)
Complex Regional Pain Syndrome
Complex regional pain syndrome (CRPS) is a contemporary
term to replace numerous historical terms including
algodystrophy, algoneurodystrophy, Sudeck atrophy, reflex
neurovascular dystrophy, causalgia, reflex sympathetic
dystrophy, shoulder-hand syndrome, and fracture disease.
For the sake of clarity, the term CRPS is used to replace
previous terminology in much of the following section.
Here is a history of CRPS based on reviews
presented by Schutzer and Gossling,170 Wilder et al.,171 and
Inhofe and Garcia-Moral.172 The history of CRPS began in
1864, when Mitchell and colleagues reported the sequelae
of nerve injuries in victims of the Civil War and called the
disorder causalgia. Sudeck, in 1900, described refractory
pain, swelling, stiffness, vasomotor instability, trophic
skin changes, and osteoporosis of the affected extremity.
Hence Sudeck atrophy is the term used to describe
demineralization of the bone. Lankford and Thompson
categorized CRPS as either minor causalgia, which involves
sensory nerve injury alone, and major causalgia, which
involves mixed nerve injury. This somewhat confusing
classification is not currently advocated.170-172
In 1991, the American Association for Hand
Surgery appointed an ad hoc committee to define the
disorder known as reflex sympathetic dystrophy (RSD) and
to make recommendations regarding its diagnosis and
management. Much of this summary of RSD is taken
largely from that committee’s report173 and from reviews
conducted by Schutzer and Gossling,170 Wilder et al.,171
and Inhofe and Garcia-Moral.172
According to the ad hoc committee of the American
Association for Hand Surgery,173 reflex sympathetic
dystrophy was the term given to a complex syndrome of
posttraumatic pain. The pain typically is accompanied
by loss of function, and evidence exists of “autonomic
dysfunction” in the affected limbs. Based on the evidence,
committee members thought that a more appropriate
name for RSD would be sympathetic maintained
pain syndrome.
Traditionally, three diagnostic criteria were
required for the diagnosis of RSD of the hand: 1) diffuse,
intense, or unduly prolonged pain; 2) delayed functional
recovery with some degree of loss of hand mobility; and
3) sympathetic dysfunction manifested by vasomotor
27
SRPS • Volume 11 • Issue R7 • 2015
disturbances and various associated trophic changes.170,173
Both over-diagnosis and under-diagnosis
commonly occurred.
The cause of CRPS is unknown. Most researchers
think that chronic irritation of the peripheral sensory
nerve(s) causes afferent input, resulting in continuous
stimulation of sympathetic and motor efferent fibers. The
altered sympathetic activity produces subsequent motor
tone changes that culminate in CRPS. Some authors think
that patients who are emotionally labile and have a low
pain threshold are predisposed to CRPS, which, in those
persons, might have a psychogenic origin.
Other investigators think an excessive inflammatory
response is behind the development of CRPS.174 To test
that hypothesis, Oyen et al.174 obtained scintigrams by
using indium-111-labeled immunoglobulin G in 23
patients with a diagnosis of CRPS of the hand. The
results suggested that a flow-independent inflammatory
component characterized by increased vascular
permeability for macromolecules plays a role in the
development of CRPS.
Veldman et al.175 surveyed the signs and symptoms
of CRPS in 829 patients. In its clinical presentation,
CRPS exhibits three phases: 1) an initial warm phase for
the first 2 to 3 months, 2) a phase of vasomotor instability
that can last for several months, and 3) a terminal cold
end phase.176 During its early phase, CRPS is characterized
by pain and regional inflammation that is exacerbated by
exercise. Both hypo- and hyperesthesia are present in up
to 75% of patients. During the second and third phases,
tissue atrophy, involuntary movements, muscle spasms,
and pseudoparalysis can occur. Tremors and muscular
incoordination are noted in approximately half the patient
population. Sympathetic signs are infrequent and have
no diagnostic value. The authors noted that the early
symptoms of CRPS are those of an exaggerated regional
inflammatory reaction and not those of a disturbance of
the autonomic nervous system. A three-phase radionuclide
bone scan is highly sensitive and specific in the diagnosis
of CRPS.21
Heerschap et al.176 conducted a nuclear MRI study
of the skeletal muscles of the leg in 11 patients with
CRPS. The authors reported that the average tissue pH
of the muscles of affected legs was significantly increased
over that of control legs, as was the average inorganic
28
phosphate:phosphocreatine ratio of the muscles. The
findings were in agreement with those of previous studies
documenting reduced oxygen extraction and impairment
of high-energy phosphate metabolism in cases of CRPS.
Because the pathogenesis of CRPS is unclear,
treatment is perforce empiric. Nonoperative measures
include elevation of the extremity, physical therapy,
transcutaneous electrical nerve stimulation, steroids, local
and regional anesthetic blocks, and administration of a
variety of drugs such as antidepressants, anticonvulsants,
nonsteroidal antiinflammatory agents, vasodilators,
calcitonin, and beta-adrenergic antagonists. Surgical
management consists primarily of
cervical sympathectomy.170
Watson and Carlson177 developed a program
of progressive “stress loading” for treatment of CRPS
in the hand, consisting of two simple activities called
scrub and carry. The authors avoided the use of all other
modalities, including immobilization and aggressive joint
mobilization, until the pain began to subside. The patients
exhibited improvement in pain, vasomotor activity,
edema, motion, and strength, with 95% returning to
normal activities and 84% returning to their pre-CRPS
occupations.
Although conservative treatment is said to be
successful in approximately half of all cases of CRPS, a
survey by Inhofe and Garcia-Moral172 showed that the
long-term results are not so encouraging. Five years or
more after diagnosis, a significant number of patients
reported worsening of symptoms (56%), a negative impact
on their daily lives (78%), and either a downgrading of
their jobs or unemployment as a direct result of
their condition.
Wilder et al.171 presented an excellent review
of CRPS in children, which has become increasingly
common and is thought to be precipitated by the stress
of sports activities. Appropriate treatment requires a
multidisciplinary approach and consists primarily of
noninvasive regimens, such as active physical therapy,
transcutaneous electrical nerve stimulation, and
biobehavioral intervention. Adjunctive sympathetic
blocks are highly successful in relieving symptoms and
accelerating the rate of mobilization.
CRPS has become the preferred descriptor for
SRPS • Volume 11 • Issue R7 • 2015
pain syndromes.178 The name was developed at the 1993
consensus workshop of the International Association
for the Study of Pain. The new terminology emphasizes
the current understanding that sympathetic dysfunction
might not be present in every case of chronic pain. Two
subgroups are defined, with Type I developing after minor
or orthopaedic trauma without any detectable nerve
injury and Type II occurring after a recognizable nerve
injury. Type I corresponds to RSD, whereas Type II was
traditionally called causalgia.
In 2011, The Royal College of Physicians published
guidelines for the diagnosis, referral and management of
CRPS.179,180 CRPS is defined as “a debilitating condition,
characterised by pain in a limb, in association with sensory,
vasomotor, sudomotor, motor and dystrophic changes.”
Diagnosis is undertaken using the Budapest criteria, and
readers are directed to this guideline for a comprehensive
contemporary approach to treatment, which is based on
“four pillars” using an interdisciplinary approach:
1.Patient information and education
2.Pain relief (medication and procedures)
3.Physical and vocational rehabilitation
4.Psychological intervention
Functional Reconstruction of the Upper Extremity
Reconstruction of function in the upper limb after
peripheral nerve injury should be undertaken using
a systematic approach in a manner similar to the
reconstructive ladder for soft-tissue reconstruction. A
number of procedures are available depending on the
timing of the injury, nerve recovery, and expendable donor
muscle-tendon units, nerve fascicles, or muscles available.
This armamentarium can be considered a functional
reconstructive ladder (Table 8, Fig. 19). Ascension of the
ladder involves interventions of greater complexity.
Nerve Grafting
Mackinnon and Dellon reviewed the history of nerve
grafting, which they traced to Philipeaux and Vulpian
in 1817. The modern era of nerve grafting dates to
experiments conducted by Millesi and colleagues181-185
during the early 1970s. The authors recommended nerve
21
autografts for any gap >2 cm and, despite adverse surgical
conditions, obtained excellent functional results in lesions
of the radial, median, and ulnar nerves. Since those reports
were published, nerve grafting has become accepted as
a clinically feasible alternative to primary repair. Nerve
grafting can be considered only when a proximal source of
axons is available and a distal organ with the potential for
full functional recovery is present.
The following are highlights of the technique
presented by Millesi185 for interfascicular nerve grafting:
•• The fascicles are dissected both proximal
and distal to the lesion in normal
unscarred tissue.
•• Not every single fascicle is dissected; rather,
the dissection involves the connective tissue
between groups of fascicles.
•• When in doubt, resect; only healthy looking
tissue should be preserved.
•• Nerve junctures should be placed at
different levels along the fascicular groups.
•• A drawing of the cut surfaces helps in
matching the stumps.
•• Autografts are harvested as single strands
and joined to fascicular groups of
corresponding diameter.
•• The grafts are cut slightly longer than the
defect to be bridged.
•• Only one or two 10-0 nylon stitches are
needed to secure each fascicle or
fascicular group.
•• Each suture incorporates the perineurium of
the fascicle of the proximal and distal stump
and the epineurium of a single nerve graft.
•• Four or five autografts are necessary for the
ulnar and radial nerves and five or six for
the median nerve.
Recovery was more complete when the nerve grafts
were performed between 6 and 12 months after injury,
but the relationship between graft length and function was
less clear. The sural nerve was the most common source
of autograft, and the medial antebrachial cutaneous nerve
was the next most common.
29
SRPS • Volume 11 • Issue R7 • 2015
Table 8
Upper Extremity Functional Reconstructive Ladder
Complexity
Procedure
4
Free functioning muscle transfer
3
Tendon transfer
2
Nerve transfer
1
Nerve grafting
Figure 19. Upper extremity functional reconstructive ladder. FFMT, free function muscle transfer.
Nunley et al.186 reported grafting the anterior
branch of the medial antebrachial cutaneous nerve for the
repair of defects of the digital nerve in 21 cases, including
all fingers and thumb. Indications for nerve grafting
were a gap in the digital nerve of >1 cm or excessive
tension needed to oppose the severed nerve ends. At an
average follow-up of 57 months, all except one finger had
recovered the ability to distinguish between sharp and dull
stimuli and all except three had TPD values between 5 and
15 mm. No painful neuromas were evident at the
donor site.
30
Although grafts from sensory nerve donors have
been the norm, a growing body of experimental evidence
supports the use of nerve grafts from motor nerve donors
for reconstruction of motor and mixed motor and sensory
nerves.187 This concept has been termed preferential motor
reinnervation.188 The difference seems to be a combination
of neurotrophic,188 cellular,189 and physical190 factors that
facilitate axonal regeneration across motor nerve grafts
when compared with sensory nerve grafts. Although
motor nerve grafts have traditionally been considered
nonexpendable, the common use of muscle flaps in
microsurgery indicates that some muscles, and thus
SRPS • Volume 11 • Issue R7 • 2015
some motor nerves, are expendable when viewed from a
different paradigm. Examples include the motor branch of
the obturator nerve to the gracilis and the descending or
transverse branch of the thoracodorsal nerve.
In 1976, Taylor and Ham191 transferred a free
vascularized nerve graft of the radial nerve to bridge a
defect of the median nerve. Eight years later, Bonney et
al.192 presented a report of 30 patients with brachial plexus
injuries treated by vascularized ulnar nerve grafts. Koshima
and Harii193,194 experimentally showed a significantly
greater number of large-caliber, myelinated axons and
earlier regeneration (4 versus 8 weeks) of vascularized
nerve grafts compared with standard nerve grafts (P <
0.05). Breidenbach and Terzis195 noted that vascularized
nerve grafts might be of benefit in scarred recipient beds,
in proximal nerve lesions, in large nerve gaps, or as carriers
for nonvascularized nerve grafts.
Rose and Kowalski100 described features of the deep
peroneal nerve-dorsalis pedis artery complex that make
it ideal as a donor of segmental vascularized nerve grafts
for digital sensory nerve reconstruction. Townsend and
Taylor196 presented a discussion of the use of composite
arterialized neurovenous systems in selected clinical cases.
In 1982, Chiu et al.197 presented experimental
evidence of nerve regeneration through a segment of
autogenous interpositional vein graft. Eight years later,
Chiu and Strauch198 evaluated their clinical results
achieved with the technique in the repair of 15 palmar
digital nerve gaps. Although all patients reported
symptomatic relief and satisfactory sensory return,
TPD values indicated superiority of direct repair and
conventional nerve grafts over the vein graft technique.
Nevertheless, the authors reported that autogenous vein
grafts as nerve conduits are effective when selectively
applied to bridge small (<3 cm) gaps in nonessential
peripheral sensory nerves.
Bain199 reported the use of peripheral nerve
allotransplantation in seven patients. Six achieved good
sensory recovery, three experienced motor recovery, and
one had no recovery because of rejection. All patients
required immunosuppression with combinations of
cyclosporin A, azathioprine, prednisone, and FK506.
Immunosuppression was withdrawn after Tinel sign
progressed into the distal segment of the reconstructed
nerve. No clinically significant complications of systemic
immunosuppression were reported; however, the allograft
was rejected in one patient. No patient experienced
deterioration of nerve function after withdrawal of
immunosuppression, and no evidence of chronic rejection
was observed.
Wyrick and Stern200 reviewed secondary nerve
reconstruction and discussed alternatives to nerve grafting,
such as tubulization (insertion of conduits for the passage
of axons), elongation with tissue expanders, and direct
muscular neurotization.
Most brachial plexus injuries were previously
managed primarily by nerve grafting.134-136 Millesi136
reported 64.5% “useful recovery” in complete lesions
and 82.4% in incomplete lesions. Narakas134,135 noted
61% fair results achieved in cases of supraclavicular
lesions. Chuang et al.201 presented a report of 15 patients
with total root avulsion of the brachial plexus who were
treated with cross-chest C7 nerve graft and then free
muscle transplantation at a later stage in eight patients.
After a long period of rehabilitation, useful function
of the reconstructed limb was achieved, although no
independent movement of the transferred muscles could
be documented.
Nagano202 recommended that nerve grafting should
be performed if a ruptured root shows positive evoked
spinal cord potentials or somatosensory evoked potentials
in the trunk or in the cord. Exploration of the brachial
plexus should be extended distally as far as possible
to achieve good results after nerve grafting. When the
exploration is thus extended, more than M3 power of the
infraspinatus, deltoid, and biceps can be achieved in more
than 70% of patients.
Nerve Transfers
Mackinnon and Colbert27 provided a contemporary
update of indications and techniques in the rapidly
expanding application of nerve transfers. The theoretical
basis for nerve transfers is similar to that for tendon
transfers: trivial or redundant motor units are surgically
redistributed to reconstruct a critical missing function.
Nerve transfers, however, have the capacity for
reconstruction of sensation. Common clinical situations
include high injuries to the radial, ulnar, and median
nerves and to the brachial plexus. The technique of
31
SRPS • Volume 11 • Issue R7 • 2015
reconstruction using a distal motor nerve transfer is
now considered superior to the use of long nerve grafts
to the brachial plexus for brachial plexus and high-level
nerve injuries.203 The management philosophy regarding
nerve transfers is that of converting high-nerve injury
to low-nerve injury. Nerve transfer also requires a distal
organ with potential for functional recovery. Choosing
nerve transfer for motor reconstruction is therefore time
sensitive. Principles include the following:
1.Maintain anatomic and physiological
integrity of musculotendinous units.
2.Minimize regeneration distance and time.
3.Target function of the transferred nerves.
4.Dissect in an unscarred field.203,204
Although nerve transfers have been described for proximal
injuries, their successful use distal to the elbow opens
a new spectrum of options for reconstruction. Table 9
provides a comprehensive list of commonly used
nerve transfers.27
Proximal nerve transfers have involved donor nerves
such as the thoracodorsal,205 medial pectoral,206 spinal
accessory,207,208 phrenic,209,210 and intercostal nerves.211
The donor nerves can be divided into intraplexal (based
on brachial plexus branches) or extraplexal (based on
nerves outside the brachial plexus), with only the latter
being available after total brachial plexus avulsion injuries.
All these donor nerves must be noted as terminal nerve
trunks, which are essentially sacrificed at the time of
transfer with total loss of muscle function in their native
territory. A paradigm shift occurred when Oberlin et al.212
began to use a single proximal fascicle of the intact ulnar
nerve for reinnervation of the biceps. Doing so allowed the
sacrifice of a highly selected fascicle of the ulnar nerve as
a donor for transfer, with minimal to undetectable loss of
function in the remaining ulnar nerve distribution because
of highly redundant function among proximal fascicles.
Similar strategies have since been used, with good success
for distal transfers using an expendable fascicle from the
median nerve as a donor for elbow flexion213 or radial
nerve palsy (Fig. 20).214,215 The double fascicular transfer
was described in 2005 as means of innervating both biceps
and brachialis muscles to improve outcome in elbow
flexion reconstruction.216
The contralateral C7 nerve root has been used
32
as a donor for multiple-root avulsion injuries of the
brachial plexus. First described by Gu et al.217 in 1992,
the contralateral C7 nerve root has been identified
as expendable in the setting of a normal uninjured
contralateral brachial plexus because of redundancy in
function among the adjacent C6 and C8 nerve roots.218
Reports have indicated that the predominant morbidity
after transfer is a transient sensory disturbance in the
thumb, index, or long fingers, generally lasting 3 to 6
months.219 Either the entire C7 nerve root or a hemi-C7
donor can be selected, based on the needs at the recipient
nerve. When selecting which portion of the C7 root to
use in a hemi-C7 transfer, the anterior division generally
is used for flexor functions and the posterior division for
extensor functions. The posterior division of C7 contains
a greater number of motor axons compared with the
anterior division.201,220,221 A nerve graft usually is required
because of the long distance between the donor and
recipient nerves; pedicled or free vascularized ulnar nerve
grafts are preferred, but sural or saphenous nerve grafts
can also be used (Figs. 21-23).222 The contralateral C7
transfer has also been applied in children.223 Concerns
remain regarding synkinesis of the contralateral donor
arm to activate motion of the reconstructed recipient arm
in a majority of patients, and attempts at elucidating the
relevant neurophysiological adaptations are ongoing.224
Nagano202 recommended intercostal nerve transfers
to restore elbow flexion in root avulsion type injury, and
M3 or greater strength can be achieved in 70% of patients.
Best results were obtained in patients younger than 30
years and in those who have been treated surgically within
6 months of injury. However, using the intercostal nerve
as a donor dictates a longer regeneration distance to biceps
in comparison with intraplexal distal donor nerves, which
might explain poorer results after 6 months.
Tendon Transfers
The surgical practice of tendon transposition is based
on the concept that the power of a functioning muscle
can be used to activate a nonfunctioning nerve-muscletendon unit. Tendon transfers are justified for restoration
of functional motion of the hand, not just motion.
The surgical alternatives to tendon transfer include
neurorrhaphy, tenorrhaphy, tenodesis, tendon graft,
arthrodesis, and amputation.
SRPS • Volume 11 • Issue R7 • 2015
Table 9
Common Nerve Transfers of the Upper Extremity27
Injured Nerve
Missing Function
Donor Nerve
Recipient Nerve
Motor
Suprascapular
Shoulder abduction,
stabilization, external rotation
Distal spinal accessory
Suprascapular
Axillary
Shoulder abduction
Triceps branch of radial nerve
Axillary
Musculocutaneous
Elbow flexion
Ulnar nerve fascicle to FCU, median nerve
fascicle to FCR
Brachialis branch, biceps branch
Spinal accessory
Shoulder elevation, abduction
Medial pectoral
Spinal accessory
Spinal accessory
Shoulder elevation, abduction
C7 redundant fascicle
Spinal accessory
Ulnar
Intrinsic hand
Terminal AIN (branch to
pronator quadratus)
Ulnar nerve fascicles to deep
motor branch
Median and ulnar
Intrinsic hand
Radial nerve branches to ECU, EDQ
Ulnar nerve deep
motor branch
Median
Thumb opposition
Terminal AIN (branch to
pronator quadratus)
Median (recurrent) motor
Median
Finger flexion
Ulnar nerve fascicle to FCU
AIN
Median
Pronation
Ulnar nerve fascicle to FCU, intact
branches to PL or FCR, radial nerve branch
to ECRB
Median nerve branch to pronator teres
Radial
Wrist extension,
finger extension
Median nerve branches to FCR, FDS, PL
Radial nerve branch to ECRB, PIN
Median sensory
Thumb-index finger key pinch
area sensation
Median common sensory branch to third
web space in upper trunk (C5, C6) injury
Median common sensory branch to
first web space
Median sensory
Thumb-index finger key pinch
area sensation
Ulnar common sensory branch to fourth
web space
Median common sensory branch to
first web space
Median sensory
Thumb-index finger key pinch
area sensation
Dorsal sensory branch of ulnar nerve
Median common sensory branch to
first web space
Median sensory
Thumb-index finger key pinch
area sensation
Sensory branch of radial nerve
Median common sensory branch to
first web space
Median sensory
Noncritical median
distribution sensation
Ulnar common sensory branch to fourth
web space (side to end)
Median common sensory branch to
second and/or third web space
Ulnar sensory
Ring and small finger sensation
Median common sensory branch to third
web space
Ulnar common sensory branch to
fourth web space, ulnar digital nerve
to small finger
Ulnar sensory
Ulnar border of hand sensation
Median sensory at distal forearm
(side to end)
Ulnar sensory nerve at distal forearm
Ulnar sensory
Ulnar border of hand sensation
Lateral antebrachial cutaneous
Dorsal sensory branch of ulnar nerve
Median sensory at distal forearm
(side to end)
Dorsal sensory branch of ulnar nerve
Sensory
Ulnar sensory
FCU, flexor carpi ulnaris; FCR, flexor carpi radialis; AIN, anterior interosseous nerve; ECU, extensor carpi ulnaris; EDQ, extensor digitorum
quinti; PL, palmaris longus; ECRB, extensor carpi radialis brevis; FDS, flexor digitorum superficialis; PIN, posterior interosseous nerve.
33
SRPS • Volume 11 • Issue R7 • 2015
Injury
Open
Surgical Reconstruction
Explore
No Improvement/Nerve Conduction Studies
No Injury
Observe
(3 months)
Improvement
Done
No Improvement/Nerve Conduction Studies
Closed
Surgical Reconstruction
Observe
(3 months)
Improvement
Done
Figure 20. Radial nerve palsy algorithm. (Reprinted with permission from Lowe et al.209)
When injury to a nerve renders a muscle-tendon
unit useless, nerve repair often is indicated. The prognosis
for function depends on the type of injury, time since
injury, distance from lesion to muscle, patient age, type of
nerve, etc. (see above). de Medinaceli et al.225 reviewed the
results of primary nerve repair in 2181 fresh nerve injuries
of the upper extremity at a reconstructive surgery center
in France. Digital injuries accounted for 68% of all cases.
Forty-one percent of patients had injury of only one nerve,
whereas the other 59% had injury of two or more nerves.
In 18% of cases, the injured limb was lost or beyond
repair. Of the remaining 1800 or so injuries, end-to-end
suture was successful 87% of the time and not possible
in 11%, even with nerve graft. The authors concluded
that primary neurorrhaphy was possible in a very large
majority of peripheral nerve injuries of the upper limb and
consequently that true loss of substance was rare in
civilian practice.
Direct suture of an injured tendon is not applicable
in every case but should not be ignored in the decision.
When the prognosis for function after tendon transfer
is poor, tenodesis is a definite consideration. The mere
provision of a fixed point of origin for a tendon will
34
sometimes position a joint so that it moves acceptably.
The best approach to an irreparable tendon injury
often lies between a tendon graft and a tendon transfer.
Tendon grafts use muscles that already have the correct
power, amplitude, and direction, require no relearning of
task, and involve no loss of other function. On the minus
side, tendon grafts require two junctures rather than one,
have no blood supply, and are more prone to adhesions.
Fusing a joint occasionally provides sufficient
stabilization to simulate the desired muscle action (e.g.,
the interphalangeal [IP] joint of the thumb after loss of the
FPL). Amputation of a ray or digit might be indicated in
extreme cases to shorten the rehabilitation time and restore
useful function.
Tendon transfer might be indicated for
functional reconstruction:
•• After nerve injury
•• After loss of muscle-tendon unit (acute
or chronic)
•• As a rebalancing procedure
SRPS • Volume 11 • Issue R7 • 2015
Procedure Selection—Several factors need to be assessed
when considering undertaking tendon transfers:
1.General factors
2.Patient factors
3.Recipient factors
4.Donor factors
Figure 21. Custom-made metal passers for cross-chest
tunneling of nerve grafts. Upper, passer for ulnar nerve;
lower, passer for saphenous nerve. (Reprinted with
permission from Terzis and Kokkalis.217)
5.Surgical factors and technique
General Factors
Task Analysis
The patient’s need or desire to perform a certain task is of
paramount importance in planning a transfer procedure.
To accomplish that task (e.g., open a door), the fingers
must be positioned in the proper way to engage the
doorknob and must have the power to grasp and twist it. A
transfer designed to restore intrinsic function to the fingers
for grasp is of little use unless it also carries enough power
for closing around the knob and turning it. Transfers,
therefore, should be designed to accomplish tasks rather
than motions.
Figure 22. Selected bundles of anterior and posterior
divisions of C7 have been neurectomized and coapted
in end-to-end manner to two cross-chest saphenous
nerve grafts. (Reprinted with permission from Terzis and
Kokkalis.217)
Nature of the Disease
If the functional loss is caused by systemic or local disease,
it should be controlled before restoration is attempted. If
the disability is secondary to trauma, tendon transfer after
neurorrhaphy can maintain muscle function until nerve
recovery is complete.
Patient Factors
Motivation
Figure 23. “Banked” cross-chest saphenous nerve
grafts are depicted. Orange, upper graft connected to
selected bundles of posterior division will be used for
neurotization of free-muscle graft for finger extension
restoration; green, lower graft is connected to selected
bundles of anterior division and is destined for
neurotization of free muscle for finger flexion. (Reprinted
with permission from Terzis and Kokkalis.217)
For any method of functional restoration to succeed, the
patient must first be aware of the loss and be willing to do
something about it. Patients who are unconcerned about
the disability are unlikely to retrain the muscle that is
newly empowered by a transferred tendon.
Age
Tendon transfers are relatively contraindicated in the
elderly because joint stiffness during splinting increases
with age. The process of relearning or teaching a muscle
35
SRPS • Volume 11 • Issue R7 • 2015
to perform a new task is not only lengthier but also more
difficult at an advanced age, and the corresponding need
for power movements also decreases.
Cognition
The patient must be capable of understanding both the
nature of the surgery and its limitations. Additionally he
or she must understand the motor reeducation program
necessary for movement of the recipient tendon by
activation of the transferred tendon.
by approximately one motor grade when the muscle is
detached from its normal insertion and is placed opposite
a new antagonist. Reinnervated muscles are not ideal and
should have a Medical Research Council grade of 4 or
greater and be used only in exceptional circumstances. In
general, muscle power corresponds to muscle cross-section,
but by placing the tendon insertion farther from the joint
axis and as close to 90 degrees as possible, the effective
power of the muscle can be increased during transfer.
Excursion
Compliance
The patient’s adherence to the required immobilization
and activity limitation during the period of healing and
to the therapy regimen necessary for retraining of the
transferred tendon and mobilization of stiffened joints
must be reasonably certain. Assessing patient compliance
to preoperative physiotherapy can provide a useful
predictor of compliance postoperatively.
Recipient Site Factors
•• Soft tissue: The soft tissue should be pliable
and free from scar tissue and overlying
skin graft.
•• Skeletal Stability: Joints should be stabile to
maximize the efficiency of the transfer.
•• Sensation: Normal neurovascular status is
required to provide useful function.
•• Supple joints: Joints should be supple with a
full range of motion. A tendon transfer will
not rehabilitate a stiff joint.
Ideally, the donor muscle should have the same amplitude
or excursion as the muscle it replaces. Stretching the
donor tendon over a number of joints improves total
excursion. Wrist flexors and extensors have excursions of
approximately 3 cm, finger extensors 5 cm, and finger
flexors 7 cm. Effective amplitude can be increased by the
effect of tenodesis or by freeing of fascial attachments to
the muscle-tendon unit. A muscle of too much power and
too little excursion can be inserted closer to the joint axis
to minimize the distance it must contract to produce the
desired motion.
One Tendon, One Function
Ideally, each tendon transfer should be designed to
perform a single action. Effectiveness of a tendon transfer
is reduced when designed to produce two different
functions. Additionally, the donor muscle should be
independently innervated (e.g., the sublimis) and not act
in concert with other motors (e.g., the lumbrical).
Performance
Donor Muscle Factors
A useful mnemonic with which to remember the donor
muscle factors is PEOPLES: Power and control; Excursion;
One tendon, one function; Performance; Line of pull;
Expendability; Synergism.
Power and Control
The donor muscle power should be similar to that which
it replaces and must be adequate for the function it will
assume after transfer, remembering that it will diminish
36
A donor muscle must be able to perform under voluntary
control. Muscles prone to spasticity or involuntary
contraction will function poorly.
Line of Pull
Tendon transfers work more efficiently when traveling in a
direct line of pull from its origin to new insertion. Where
this is not possible, the tendon should pass through no
more than one Pulley and the design should avoid
acute angulation.
SRPS • Volume 11 • Issue R7 • 2015
Expendability
The replacement tendon must be carefully selected to
avoid substantial functional deficit as a consequence of
transfer.226-239 One must be confident that transfer will
not result in loss of a critical hand movement from lack of
the donor function. For example, in cases of radial nerve
palsy, transfers for wrist and finger flexion should ensure
that at least one functioning wrist flexor remains intact.
Smith and Hastings239 offered an algorithm for selecting
appropriate donor muscles to restore function in the hand.
Synergism
Muscles transferred within synergistic groups that
produce composite movement are generally easier to
retrain. Synergistic muscles include the fist group (wrist
extensors, finger flexors, digital adductors, thumb flexors,
and forearm pronators) and the open hand group (wrist
flexors, finger extensors, digital abductors, and forearm
supinators). The operative plan must also be designed to
avoid hand imbalance at any of the affected joints.
A tendon transfer can benefit a patient who has
lost a certain movement. The substitute tendon is chosen,
aligned, and inserted according to the patient’s need for a
specific motion rather than based on a standard prescribed
formula. For complex functional problems or multistage
reconstructions, the surgeon should list the potential
donor muscles for each desired function to maximize the
benefit of the available donors and prevent using a muscle
to power one action only to find out later that it could
have been better used in another capacity. Consideration
must be given to the balance of the transfer. An overly
powerful muscle will overcompensate and, in time, deform
the joint.
Timing of tendon transfers depends on the
cause and prognosis of the motor imbalance, the
neurophysiological problems for the patient, and the
condition of the involved extremity.240 In cases in which
stiffness and deformity can be expected to increase with
time, however, the transfer should be performed early,
such as after median nerve injury with a poor chance of
recovery, in which case a tendon transfer to secure thumb
opposition will prevent the supination and/or adduction
deformity that is likely to develop as the patient substitutes
new motions in an attempt to preserve function.
Surgical Factors and Techniques
•• Incisions: When creating incisions,
avoid crossing the path of the transferred
tendon. The tendon should course through
subcutaneous tissue free of scar to avoid
adhesions that might tether it and limit
its function.
•• Operate in reverse order: Have the
recipient site and tunnel ready before raising
the muscle.
•• Avoid interference with critical structures:
Ensure that the transferred tendon does not
compress nerves.
•• Apply correct tension: The tension at
the insertion should be set to produce
the necessary movement of the joint
with maximal muscle contraction.
Because it tends to “stretch” slightly,
some initial overcorrection is indicated
by many surgeons for certain transfers
(extensor indicus-extensor pollicis longus
[EPL]). However, it has been shown that
overstretching the muscle into the passive
tension portion of the Blix curve decreases
the potential contractile force to 28% of its
maximum force.241 Therefore, setting the
donor muscle near its normal length might
be optimal for force generation.241
•• Tendon insertion: Tendon insertion should
be at an angle of 90 degrees to the joint of
motion to maximize power and excursion.
The insertion can be moved away from the
axis of the joint to improve power but at
the cost of diminished excursion. A single
insertion is best; when dual insertions are
contemplated, motion will be effected at
the tighter one (can occasionally be used
to advantage in complex movements, with
which one insertion is tighter during one
phase of motion and the other takes over
during another phase).
•• Tendon coaptation: Methods include
Pulvertaft weave, side-to-side, and bone
fixation. Whichever method is used, it
37
SRPS • Volume 11 • Issue R7 • 2015
should be robust enough to allow early
active mobilization and to minimize
adhesions. A recent in vitro study using
human cadaver tendons comparing the
Pulvertaft weave and side-to-side methods
showed average detected failure loads of 182
N and 96 N, respectively.242
•• Joint immobilization: The affected joint
should be immobilized for an appropriate
length of time in a position that relieves
tension at the insertion.
Specific Deficits
Low Median Nerve Palsy
Palsy of the median nerve of the hand often occurs after
a forearm injury that typically includes disruption of the
tendons, blood vessels, and ulnar nerve. When isolated,
the median nerve injury produces sensory loss in the palm,
sensory loss in the radial side of the hand and fingers,
and loss of motor innervation to much of the thenar
musculature.
Loss of sensation to the pulp of the thumb, index
finger, or long finger severely inhibits pulp-to-pulp pinch,
a delicate motion which, unlike gross pinch, requires
constant receptor input. Under optimal conditions,
only 25% to 30% of patients achieve satisfactory thumb
position (M3) and TPD of <15 mm (S3) with direct nerve
repair,243 dictating the need for tendon transfer to improve
hand function. Sensory restoration to the contact surfaces
of the digits using neurovascular island flaps244 or digital
nerve transfers245 might be necessary to complete the
feedback loop for successful control of pinch.
The principal motor deficit associated with a low
median nerve injury is loss of thumb opposition. Thumb
opposition is a composite of two movements: one rotates
the pulp of the thumb to face the pulp of the index ray,
and the other abducts the thumb metacarpal ray from the
palmar plane.246 The combined action normally is brought
about by the opponens pollicis (rotation and/or pronation
of the thumb ray) and the abductor pollicis brevis, assisted
by the superficial head of the FPB (some pronation,
palmar abduction, and metacarpophalangeal [MP]
flexion).247 Although placing the thumb in opposition
38
prepares the thumb for pinch, pinch is not a power move
that requires a large and powerful muscle. Synergistic
muscles include the finger flexors, wrist extensors, PL, and
hypothenar muscles.
The standard transfer places the FDS of the
ring finger248 through a pulley249 in the region of the
pisiform246 to its insertion. Other possible transfers for
thumb opposition in cases of low median nerve palsy were
summarized by Smith and Hastings (Table 10).239
Bunnell246 suggested pulling the thumb metacarpal
toward the carpal pisiform by a tendon coming from that
direction to create the proper vector of motion. Littler250
reported preference for a pull in the direction of the
adductor pollicis brevis (APB), and Thompson249 chose a
more transverse route across the palm.
The transferred tendon must insert on the radial
side, either at the APB250 or halfway into the APB and
halfway into the EPL, in a dual insertion,251 to increase the
extension of the IP joint and help balance the flexor force
of an intact FPL at that joint. The dual insertion transfers
some of the force of the FPL to the more proximal joints
and helps stabilize the MP joint. A modification splits
the insertion between the EPL and the adductor pollicis
longus (APL) to try to neutralize the adductor and/or
supinator forces.252 Tension at the insertion is adjusted
to move the thumb into full opposition with the wrist in
neutral. With the wrist in neutral position, a minimum of
25 to 30 mm of tendon excursion is needed for adequate
thumb ray function, even more if the transfer is to
function in all wrist positions.
In 1929, Camitz253 described the PL abductorplasty
for severe thenar atrophy secondary to carpal tunnel
syndrome (CTS). The concept was later revisited by Littler
and Li254 and by Braun.255 More recently, Terrono et al.256
reviewed the outcomes of the PL transfer described by
Camitz in 33 hands (29 patients). Surgery was secondary
in three patients and primary (at the time of initial release
of the carpal tunnel) in 26. At a mean follow-up duration
of 17 months, 94% of the patients were satisfied with the
results of surgery because their thumb function
had improved. SRPS • Volume 11 • Issue R7 • 2015
Table 10
Low Median Nerve Palsy: Transfers for Opposition239
Donor
Pulley
Graft
Insertion on Thumb
FDS (ring)
Distal FCU
None
Dorsal-ulnar base PP
FDS (ring)
FCU
None
APB
FDS (ring)
FCU
None
APB and EPL at PP
FDS (ring)
Guyon canal
None
APB and EPL
EIP
Ulnar side of wrist
None
PP
ADQ
None
None
APB
PL
Carpal tunnel
Rerouted EPB
EPB
PL
None
Palmar fascia
Radial side MP joint
Half FPL
Around radial side of thumb
None
Dorsal PP
FPL
Translocated dorsally
None
PP
FPL
Transverse carpal ligament
None
PP and FDP
APL
PL
None
Base metacarpal
ECU
Ulnar side of wrist
Rerouted EPB
EPB
ECRL or ECRB
Ulnar side of wrist
Free graft
EPL
FDS, flexor digitorum superficialis; FCU, flexor carpi ulnaris; PP, pronator profundus; APB, adductor pollicis brevis; EPL, extensor
pollicis longus; EIP, extensor indicis proprius; ADQ, abductor digiti quinti; PL, palmaris longus; EPB, extensor pollicis brevis;
MP, metacarpophalangeal; FPL, flexor pollicis longus; FDP, flexor digitorum profundus; APL, adductor pollicis longus; ECU,
extensor carpi ulnaris; ECRL, extensor carpi radialis longus; ECRB, extensor carpi radialis brevis.
A tendon transfer designed to restore thumb ray
opposition must include release of any long-standing
adduction contracture and lengthening of the web fascia.
The EPL and APL act to supinate the thumb in an
adducted position, so much so that a substitute for pinch
in the absence of median nerve abduction involves rotating
of the thumb into this position, which is relatively stable,
and bringing the index pulp to meet it.
Effective powerful pinch requires a stable MP joint
to avoid collapse, which in turn demands careful balance
of extensor and flexor forces. The FPB prevents extension
of the joint as the thumb pulp contacts the index pulp.
In isolated low median nerve injuries, the tendon retains
marked ulnar innervation in approximately half the
cases257 so that MP joint stabilization is not needed; when
complicated by low ulnar palsy, however, any effective
transfer for power pinch must include MP flexion and/or
stabilization.258,259
An alternative method for restoring opposition
after median nerve injury was suggested by Ustün et al.260
Based on a cadaver study, the authors recommended
transfer of the motor branch to the pronator quadratus
muscle from the anterior interosseous nerve to the thenar
motor branch. They noted that this would allow for
reestablishment of some motor function with a minor loss
of function after denervation of the pronator quadratus
muscle. This technique has been brought to clinical
fruition by Vernadakis et al.261 who used a nerve graft from
the distal anterior interosseous nerve (pronator quadratus
branches) to the thenar motor branch.
39
SRPS • Volume 11 • Issue R7 • 2015
High Median Nerve Palsy
Injuries to the median nerve above the level of the forearm
increase the likelihood of ulnar nerve damage, limiting
the transfer alternatives to radially innervated muscles. In
addition to severe motor and sensory deficit of the index
finger and thumb, loss of forearm pronation and loss of
flexion of the index and long fingers and the FPL of the
thumb occur. The goal for the reconstruction is gross key
pinch rather than fine discriminatory tasks.
Loss of forearm pronation creates a marked
disability. A hand that is allowed to supinate for a long
time after nerve injury will develop a contracture that is
difficult to reverse. It is therefore important to maintain
range of motion of the forearm. If reinnervation of the
pronators is unlikely or delayed, one should consider
rerouting the biceps.
Smith and Hastings239 listed various options for
tendon transfer in high median nerve palsy.255,262-268
Because the powerful finger flexors that contribute to wrist
flexion have been lost, two wrist flexors can be transferred
to the digits without compromising wrist balance. When
the two deep flexors on the ulnar side of the hand still have
power, all the profundus tendons can be sutured together
to achieve mass finger flexion.
If strong radial hand motion is required, the
extensor carpi radialis longus (ECRL) can be transferred
to the profundi of the index and long fingers. Disparate
excursions of the ECRL and profundus tendons demand
fine adjustment of tension at the insertion to enable finger
flexion without contracture from this dynamic tenodesis.
The brachioradialis can be used to duplicate the action of
the FPL. Once again, the tension of the transferred tendon
can be set loose enough to prevent flexion contracture
while the wrist tenodesis serves to flex the thumb.
Low Ulnar Nerve Palsy
In the absence of normal ulnar innervation, hand function
is severely limited. Most fine hand movements depend on
muscles innervated by the ulnar nerve. Sensory loss along
the ulnar border of the hand constitutes a substantial
disability, even though it is less of a problem than the
40
motor deficit. The affected muscles are the four dorsal and
three volar interossei, the ring and small finger lumbricales,
the APL and deep head of the FPB, and the hypothenar
mass. In cases of low ulnar nerve palsy, the deficit in the
moment potential of MP joint flexion decreases by varying
amounts, depending on the digit.269 The middle, ring,
and small fingers lose moment potential by 7%, 13%,
and 28%, respectively. Each muscle should be specifically
tested before embarking on surgical reconstruction,
however, because of frequent anomalous communications
between the median and ulnar nerves. These crossconnections might alter the severity of the deficit and
negate the standard patterns of ulnar = ring and small
fingers and median = index and long fingers. Functionally,
the deficit manifests as follows:
•• Coordinated finger flexion and IP joint
extension are lacking because of loss of
the lumbricals and interossei, causing the
fingers to roll into the palm in an ineffective
grasp rather than encircle an object. The loss
of active digital abduction and/or adduction
produces the typical “claw” deformity as
the extrinsics hyperextend the MP joints
while trying to extend the IP joints. This
is sometimes accompanied by an abducted
little finger (Wartenberg sign) resulting
from unopposed abduction by the extensor
digiti minimi.270
•• Thumb-index finger pinch of all kinds
are diminished from the combined loss of
effective support to the thumb MP joint
and adductor pollicis and loss of the first
dorsal interosseous, which severely limits
abduction strength in the index finger. Sideto-side movement of the fingers, necessary
for fine manipulation of objects within the
hand, is prevented by loss of the interossei.
•• Power grip is absent because of loss of the
intrinsics for grasping and the hypothenar
mass for cupping an object.
•• Sensation in the palm along the ulnar
border is lost, and the loss might extend
to the dorsal surface in cases of lesions
proximal to the origin of the dorsal sensory
SRPS • Volume 11 • Issue R7 • 2015
branch of the nerve (approximately 6–8 cm
above the wrist).
Clawhand is an indication for intrinsic muscle
transfer in all four fingers. Various tendon transfers, with
and without tendon grafts, have been suggested for the
correction of clawhand.239 Common sites of insertion are
the lateral bands, proximal phalanx, and A2 pulley.
Hastings and Davidson270 analyzed the results
achieved in 34 patients with ulnar nerve palsy and clawing
who underwent reconstruction by various techniques of
tendon transfer. Of the 14 digits treated for low ulnar
deficit, correction of clawing was achieved in all instances
with Brand and Riordan transfers and in two-thirds to
three-fourths of those treated by Stiles-Bunnell transfer
and Zancolli lasso transfer. Grasp strength was not
substantially improved by any of the procedures, however,
leading the authors to conclude that only the addition of a
tendon motor from the wrist will add power.
Limiting full finger extension at the MP joint
theoretically allows the extrinsic extensors to exert force
for active IP extension and prevents recurrence of clawing.
In a strong hand, the extensor muscles tend to stretch
with time and eventually become ineffective. Mikhail271
suggested placing a bone slab on the dorsal side of the
MP joint to limit extension. Bunnell272 reported that
MP arthrodesis achieves a similar effect, with obvious
restriction of full finger flexion into the palm. These
techniques achieve neither coordinated finger flexion
to grasp a large object nor improved grip strength and
should be strictly reserved for patients with limited motor
resources from multiple paralyses.
Zancolli273 originally advanced the volar plate of
the MP joint proximally while excising volar palmar skin
to passively restrain the MP joint. Modifications of the
Zancolli procedure have since been described.274,275
Bunnell276 incised the A1 and part of the A2 pulleys
on their volar aspect to bowstring the flexor tendons and
increase their power at the MP joint. The basic technique
of tenodesis routes a tendon (ECRL or extensor carpi
ulnaris) attached to the proximal phalanx or dorsal hood
through the intermetacarpal spaces to end beneath the
deep transverse metacarpal ligament.251,277-280 Wrist flexion
is made possible by attaching the proximal juncture to the
wrist dorsum.280
An unstable thumb MP joint, loss of thumb
adduction, and insufficient index finger abduction all
contribute to inadequate pinch in ulnar palsy. Tendon
transfers succeed in increasing available power to only
30% to 50% of normal strength.281 Some of the more
common transfers designed to improve pinch include the
tendon loop presented by Bunnell276 (extensor digitorum
communis [EDC] to index finger with a tendon graft
around the ulnar border of the hand to the adductor
tubercle of the thumb), the extensor indicis proprius
(EIP) transfer presented by Brown281 (passed between the
metacarpals to insert on the adductor tubercle), and the
brachioradialis or ECRL presented by Boyes282 (to insert
on the adductor pollicis).
Another pinch-improving strategy aims at increasing
the abduction power of the index for use against the
thumb. Brand283 reminded us that most people can
support a key-pinch simply by flexing all the adducted
fingers together, so that the thumb presses against a fistful
of fingers.
High Ulnar Nerve Palsy
Injuries to the ulnar nerve above the elbow affect the
ring and small finger FDP and the FCU in addition to
producing the disabilities described under low ulnar nerve
palsies. The major functional problem resulting from the
injuries is further weakening of power grip.
Despite high ulnar injury, finger flexion on the ulnar
side might still be possible because of variable innervation
of the FDP and intramuscular fascial connections. Patients
with high ulnar injury can be treated with suturing of the
FDP of all fingers in the forearm to distribute the available
power more evenly across the full width of the hand.
FCU loss can be similarly ignored in most cases, although
the tendon plays an important role in certain motions
involving wrist flexion and ulnar deviation (e.g., swinging
a hammer).283
A forearm muscle being used to motor the proximal
phalanx must cross the wrist, affecting it in some way. In
cases of high ulnar palsy, the wrist is already overpowered
on the radius/extensor side; it therefore makes sense to use
a radial wrist extensor as the donor tendon to counteract
that force. When the transfer approaches the insertion
from the volar wrist, the moment arm is increased by
41
SRPS • Volume 11 • Issue R7 • 2015
flexion, raising the power of the motion correspondingly.
Various authors250,274-285 have suggested transferring
the ECRL through the interosseous membrane across the
volar aspect of the wrist to insert proximally. Alternatively,
the extensor carpi radialis brevis (ECRB) elongated by a
graft can be passed across the dorsal wrist and through
the intermetacarpal spaces.286 Fowler280 and Riordan278
reported a preference for the EIP, and Fritschi287
recommended the PL. Brand283 advocated transferring the
brachioradialis or FCR tendon to supplement the function
of the FCU in selected cases.
Combined Median and Ulnar Nerve Palsy
Tendon transfers in cases of combined nerve palsies are
more complicated than those in cases of isolated nerve
injuries because of the usually complex upper extremity
trauma, poor proprioception, weakness of muscles
available for transfer, and need for multistage procedures.
finger extension is best motored by the synergistic FCR;
the EPL remains motored by the PL. Green294 presented
details and illustrations of the various transfer techniques
that can be used in radial nerve palsy, and Smith and
Hastings239 listed the options.
Beasley295 reported a preference to adjust the
tension in the fingers and thumb first. With the wrist in
full extension, the fingertips should reach the palm on
passive flexion; with the wrist in full flexion, complete MP
extension should be possible. The tension on the wrist
extension transfer is set last and should be as tight
as possible.
Lowe et al.296 described the use of nerve transfers
to the radial nerve as an alternative to tendon transfers in
radial nerve injuries. The authors presented the cases of
two patients who underwent transfers of motor branches
to the PL and FDS off the median nerve to branches of
the posterior interosseous nerve and motor branch to the
ECRB muscle. At 13 to 14 months postoperatively, both
patients had a motor strength score of 4 of 5 at the wrist
and fingers.
Radial Nerve Palsy
Injuries to the radial nerve impair the hand tremendously
by voiding extension power to the wrist, fingers, and
thumb and preventing radial abduction of the thumb.
Wrist extension is critical for stability, which in turn is
essential for grip and for function of the many tendons
passing over it to mobilize distant joints.
Tendon transfers for radial nerve palsy are well
defined and highly effective. The “standard” transfers
include PT to ECRB for wrist dorsiflexion;288 FCU to
EDC to fingers II through V; and PL to EPL for thumb
extension.289,290 Boyes and colleagues291,292 suggested an
alternative superficialis transfer (PT to ECRB and ECRL
for wrist extension, long finger FDS to EDC for finger
extension, ring finger FDS to EIP and EPL for thumb and
index extension, and FCR to APL and extensor pollicis
brevis for thumb radial abduction). The author reasoned
that the FCU should be preserved because the normal
direction of wrist flexion is from dorsoradial to volar ulnar,
a motion to which the FCU substantially contributes.
The transfer preferred by Brand293 for cases of radial
nerve palsy consists of PT to ECRB for wrist extension,
FCR to EDC for finger extension, and PL to EPL for
thumb extension. The logic behind this protocol is that
42
Other Transfers
Peripheral nerve injuries in the upper extremity are the
primary reason why tendon transfers are undertaken.
In addition, loss of muscle power in the hand occurs
from many other causes, and restoration of some degree
of function can be attempted by performing transfers.
Omer240 noted that in poliomyelitis, 50% of the residual
strength of a muscle is recovered within 3 months of
onset and 75% within 6 months. If voluntary muscle test
at 3 months shows only a trace of activity in a pertinent
muscle-tendon unit, tendon transfer is indicated.
High Cervical Quadriplegia and/or Tetraplegia
Freehafer297,298 described his experience with tendon
transfers in tetraplegic patients. During a 30-year period,
272 of 285 patients experienced improvement in upper
extremity function after tendon transfers after high-level
spinal cord injuries. Recommended transfers to achieve
independence in those patients included wrist extension
procedures, posterior deltoid transfers, opponens transfers,
and transfers for finger flexion. The author reported that
patients with C6, C7, and C8 complete neurological
SRPS • Volume 11 • Issue R7 • 2015
injuries were almost as independent after the tendon
transfers as paraplegics. They could transfer from a chair,
insert a catheter, write, type, hold a book, take care of their
toilet needs, bathe themselves, eat, drink, dress themselves,
and perform other activities of daily living. A few patients
with C5 neurological level required automatic grasp
or used a wrist-driven splint. After the procedures, the
patients achieved active wrist extension, elbow extension,
thumb pinch, and finger grasp.
A key concept in hand reconstruction for tetraplegia
is the use and surgical augmentation of tenodesis
motion, whereby active extension and passive flexion
with gravity at the wrist are parlayed into digital motion
by rebalancing the digital flexor and extensor tendons
through shortening and/or bone attachment. This is the
principle behind the Moberg key pinch and House series
grasp reconstructions.299 Other authors have reported their
experiences and made recommendations for patients with
spinal cord injury.300-312
Rehabilitation
Physical therapy is essential to regain joint mobility lost
during splinting and to train the tendon to glide in its
new course. Even more important is teaching patients to
activate the replacement muscle when they want a certain
response, a process that must be repeated many times
to establish the new neural pathways before it becomes
automatic. The more the patient feels the disability, the
greater the motivation and the easier the retraining.
Despite a long history of tendon transfer surgery
and the multiple surgical procedures described, there is a
paucity of literature regarding management of the hand
after tendon transfer. Toth313 outlined the basic principles
of rehabilitation as follows:
Preoperatively, it is imperative to obtain maximum
passive range of motion, quality of soft tissues, and
strength of donor muscles. Postoperative care is
administered in four stages:
1.The protective phase begins at surgery
and lasts 3 to 5 weeks. During that time,
therapeutic objectives are to protect the
transfer by immobilization (protective
splinting), control edema, and mobilize the
uninvolved joints.
2.During the mobilization phase, which
begins when tendon healing is adequate to
begin activation of the transfer (usually 3 to
5 weeks postoperatively), one should strive
to mobilize the tendon transfer, immobilize
the soft tissue, continue mobilization of
uninvolved joints to prevent joint stiffness
from disuse, reinforce preoperative teaching
and patient education, continue edema
control, continue protective splinting, and
begin a home hand rehabilitation program.
3.The intermediate phase begins 5 to 8 weeks
after transfer. At that time, the patient
gradually increases hand activity (active
and passive range-of-motion exercises),
and limited functional movements
are permitted.
4.During the final resistive phase, beginning
at 8 to 12 weeks when tendon junctions
are strong enough to withstand increasing
resistance, the therapeutic objective is
to increase endurance and strength of
transferred muscles. Work-related simulated
tasks are begun to patient tolerance.
Toth313 further delineated the management of
specific tendon transfers in his excellent article, which
is highly recommended to all hand surgeons. Surgical
execution is only part of the key to the success of a tendon
transfer; postoperative rehabilitation is in large measure
responsible for the eventual functional outcome.
The volume of evidence for rehabilitation after
tendon transfer compared with tendon repairs is relatively
small. A recent systematic review of rehabilitation
regimens administered after tendon transfers found
that although early mobilization offers some short-term
benefits (superior range of motion, grip strength, pinch
strength, and tendon transfer integration), the benefit for
long-term outcome is not conclusive.314
Free Functioning Muscle Transfer
Local muscle transfers used for functional reconstruction
in the upper extremity include a Steindler flexorplasty,
a pectoralis major transfer, a latissimus dorsi transfer,
and a triceps transfer. However, a muscle loses a grade of
43
SRPS • Volume 11 • Issue R7 • 2015
power on transfer and a lack of choice of donor muscle
often occurs because of neurological injury concomitant
to the brachial plexus injury. Free functioning muscle
transfer (FFMT) is becoming increasingly popular in
upper extremity reconstruction, and results from these
procedures are superior to those achieved with local muscle
transfers. FFMT are particularly useful in cases of global
plexopathy.315,316 Indications for FFMT include acute or
chronic root avulsion, rupture with failed nerve transfer,
muscle loss caused by trauma, electrical burns, and tumor
resection. If time from nerve injury to intervention is
approaching a year, FFMT should be considered.139 Elbow
flexion is a critical function in the upper limb and the
most common indication for FFMT. Other key functions
that should be considered include shoulder abduction,
elbow extension, and finger flexion and extension. Donor
muscles include gracilis, latissimus dorsi, and rectus
abdominis muscles. Chuang316 undertook 647 FFMT
between 1987 and 2003 and provided insight into the use
of FFTM in brachial plexus avulsion injuries.
Doi et al.258 from Japan presented the results of
reinnervated free muscle transplantation in 24 patients
with brachial plexus injuries. Time from injury was longer
than 1 year in 21 patients. After conventional diagnostic
maneuvers, including physical examination, myelography,
and electromyography, all patients underwent surgical
exploration of the brachial plexus and intraoperative
electrodiagnosis. Twenty-one of 23 traumatic injuries
showed complete avulsion of the C5 to T1 nerve roots,
two had avulsion of the C5 to C7 nerve roots, and one
had avulsion of the C5 and C6 nerve roots. The donor
muscles (gracilis, latissimus dorsi, and rectus femoris
muscles) were selected according to their length (i.e., the
transplanted muscle had to reach from clavicle to forearm).
Both the accessory nerve and the intercostal nerve were
used to motor the transplanted muscles. Restoration of
functions, such as elbow and finger flexion, required up
to 20 muscle transplants in combination with multiple
nerve transfers. Venous thrombosis with subsequent partial
or total muscle loss developed in four cases and delayed
reinnervation considerably. Analysis of results showed no
significant difference in time to reinnervation among the
three donor muscles (P > 0.002), but muscles reinnervated
by the intercostal nerves took approximately 2 months
longer to show EMG signs of reinnervation (average, 5.25
months) than those reinnervated by the spinal accessory
44
nerve (average, 3.3 months). The authors reported that the
combination of the latissimus dorsi muscle reinnervated
by the spinal accessory nerve led to the most powerful
contraction and greatest range of joint motion.
Another report by Doi et al.317 described the use
of double free muscle transfer in a large series of patients
with complete avulsion of the brachial plexus. Twenty-six
of 32 patients were followed for at least 24 months after
the second free muscle transfer. In most cases, the gracilis
muscles were used for both the first and second muscle
transfer; however, in some cases, latissimus dorsi or rectus
femoris muscle was used. After initial exploration of the
brachial plexus, the first free muscle transfer was used
to restore elbow flexion and finger extension and was
reinnervated by the spinal accessory nerve. The second
muscle transfer, to restore finger flexion, was reinnervated
by the 5th and 6th intercostal nerves. The motor branch
to the triceps brachii was reinnervated by the 3rd and 4th
intercostal nerves to restore elbow flexion. Hand sensibility
was restored by suturing the sensory rami of the intercostal
nerves to the median nerve or the ulnar nerve component
of the medial cord. Secondary reconstructive procedures,
such as arthrodesis, were also used.317
In the series presented by Doi et al.,317 96% of
patients had satisfactory elbow flexion and 65% had
satisfactory prehension (more than 30 degrees of total
active motion of the digit). In addition, 54% of patients
could position the hand in space, negating simultaneous
flexion of the elbow, while moving fingers at least 30
degrees. They could also use the reconstructed hand for
activities requiring the use of two hands, such as holding
a bottle while opening the cap and lifting a heavy object.
The authors concluded that the double free muscle
procedure can provide reliable and useful prehensile
function for patients with complete avulsion of the
brachial plexus.
In an earlier study, Doi et al.318 used a free gracilis
muscle transfer to restore hand function after injuries to
the lower brachial plexus. The authors presented the results
achieved in three patients who had good outcomes after
intercostal nerve transfers to the transferred gracilis muscle
at long-term follow-up.
SRPS • Volume 11 • Issue R7 • 2015
•• When the history and physical examination
suggest that more than one nerve might
be compressed in a single extremity and
no history of trauma is reported, a more
proximal source of compression should
be considered.
Compression Neuropathies
Diagnosis
Nerve compression is a common cause of peripheral
neuropathy in the upper extremity. In a comprehensive,
thoughtful treatise, Dellon319 discussed patient
evaluation and treatment considerations for patients with
compression neuropathies. Among the highlights of his
review are the following points:
•• When obtaining the history of the problem,
begin with questions related to which areas
are numb, tingling, or a source of pain,
because they might relate to the innervation
pattern of a specific peripheral nerve. In
particular, ask questions regarding the small
finger, because it is the only digit without
any median nerve innervation.
•• The most common misconception is to
assume that “weakness” or “dropping
things” is causally related to CTS.
Symptoms related to weakness or loss
of coordination are causally related to
ulnar nerve dysfunction, most often to
entrapment of the ulnar nerve at the elbow.
•• Nocturnal disturbance is a hallmark of
CTS. Neck pain should not be present.
•• Neck pain deserves extensive evaluation,
especially when concomitant with bilateral
upper extremity symptoms.
•• Chronic compression of a peripheral nerve
results in a predictable sequence of events.
The key to understanding the physical
examination and to successfully diagnosing
and managing the problem is to translate
the physiological events into
clinical manifestations.
•• Testing with the tuning fork is the simplest
and most efficient screening test for the
hand surgeon to use in the office.
•• Physical examination of a patient who
has isolated peripheral nerve compression
should reveal localized signs of entrapment
of that nerve at the known area of anatomic
narrowing (e.g., Phalen sign, Tinel sign).
•• The diagnosis of chronic peripheral nerve
compression in a single extremity should
not represent a challenge in most cases.
Bianchi et al.320 described the use of a highfrequency ultrasonographic examination of the hand
and wrist and suggested that the modality could be used
to depict the median nerve at the wrist level. Anatomic
variants such as accessory branches, proximal bifurcations,
and the presence of a persistent median artery can be
identified, which is important before endoscopic release
to avoid injury to the aberrant structures. Flattening or
deformity of the nerve within the carpal tunnel, bulbous
swelling of the nerve proximal to the tunnel, and palmar
bowing of the flexor retinaculum might also suggest
median nerve compression. Ultrasound can also be used
to identify space-occupying lesions, which could be
contributing to nerve compressions at the wrist. Color
Doppler sonography can identify reactive hyperemia
resulting from severe compression.321 The cross-sectional
area of the median nerve shown by ultrasonographic
examination has been positively correlated with
electrophysiological derangements routinely associated
with CTS.322,323 Although ultrasonography is still
considered to be far from a standard diagnostic modality,
a growing body of evidence suggests ultrasonography as an
adjunct for diagnosis of CTS.324-326
Yassi327 reviewed the field of repetitive strain injuries
and categorized the disorders according to affected part
(tendon, muscle, joint, peripheral nerve, or
blood vessel):
Tendon-related disorders
Tendonitis
Tenosynovitis
Stenosing tenosynovitis
Periodontitis
Ganglion cyst
Epicondylitis (lateral or medial)
45
SRPS • Volume 11 • Issue R7 • 2015
Muscular disorders
Focal dystonia
Fibromyositis
Tension-neck syndrome
Myositis
Myalgia
Peripheral nerve entrapment
Carpal tunnel syndrome
Guyon tunnel syndrome
Radial tunnel syndrome
Pronator teres syndrome
Cubital tunnel syndrome
Joint and joint capsule disorders
Osteoarthritis
Bursitis
Synovitis
Adhesive capsulitis
Neurovascular and vascular disorders
Hand-arm vibration syndrome
(Raynaud syndrome)
Ulnar artery thrombosis
The review article provides a comprehensive overview
of the spectrum of repetitive strain injuries, their costs
to society, and the role of the physician in preventing,
recognizing, and managing these problems.
It is important to differentiate nerve compression
syndromes from other disorders that present with similar
sensory disturbances. Careful attention should be given
to patients who have experienced hand-arm vibration
exposure, usually in work-related settings. Such patients
are likely to complain of cold intolerance and difficulty
with handwriting, picking up small objects, opening
46
lids, lifting, and carrying. Hand-arm vibration syndrome
is a chronic condition that might not reverse when
vibration exposure stops. Because it cannot be treated
pharmacologically or surgically, prevention is the
best approach.328-330
Pathophysiology
The sequence of events that follows chronic compression
of a peripheral nerve is clinically observed in the sensory
system first as numbness or tingling, which can be
measured by noting alterations in the cutaneous pressure
threshold or cutaneous vibratory threshold.331 In the motor
system, the first change noted by the patient is weakness of
pinch and grip.331 Muscle atrophy occurs with progression
of the compression.
Rydevik et al.69 studied the effects of gradual
compression on intraneural blood flow. At pressures
of 20 to 30 mmHg, interference with venular flow
occurred; at 40 to 50 mmHg, impairment of arteriolar
and interfascicular capillary flow occurred; and at 60 to 80
mmHg, complete blockage of nerve perfusion occurred.
The authors surmised that acute compression of a nerve
can cause mechanical injury to the intraneural vessels and
result in long-term impairment of circulation to
that nerve.
Rempel et al.332 reviewed the pathophysiology of
nerve compression syndromes and provided the following
conclusions from the literature regarding the role of tissue
loads in the pathogenesis of peripheral nerve entrapment:
•• Elevated extraneural pressures can, within
minutes or hours, inhibit intraneural
microvascular blood flow, axonal
transport, and nerve function. This results
in endoneurial edema with increased
intrafascicular pressure and displacement
of myelin.
•• On the basis of animal models, lowmagnitude, short-duration extraneural
pressure can initiate a process of nerve
injury and repair and can cause structural
tissue changes that persist for at least 1
month. The cascade of biological response
to compression includes endoneurial edema,
demyelination, inflammation, distal axonal
SRPS • Volume 11 • Issue R7 • 2015
degeneration, fibrosis, growth of new
Median Nerve
axons, remyelination, and thickening of the
CTS
perineurium and endothelium.
•• In healthy people, non-neutral positions of
the fingers, wrist, and forearm and loading
of the fingertips can elevate extraneural
pressure in the carpal tunnel in a doseresponse manner.
•• In a rat model, exposure of the hind limb
to vibration causes intraneural edema,
structural changes in myelinated and
unmyelinated fibers of the sciatic nerve, and
functional changes both in nerve fibers and
non-neuronal cells.
•• Exposure of vibrating hand tools at work
can lead to permanent nerve injury with
structural neuronal changes in the finger
nerves and in the nerve trunks just proximal
to the wrist.
Mackinnon and Dellon21 and other authors319,333-335
reviewed current concepts of the pathophysiology of nerve
compression and discussed the presenting symptoms,
appropriate diagnosis, and management of entrapment
neuropathies (Table 11).
Mackinnon and Novak336 commented on the
pathogenesis and treatment of cumulative trauma
disorders, which, in their view, are complex disorders
with multiple components. The authors hypothesized
a multifactorial origin for cumulative trauma disorders,
including organic causes such as neuropathic compression,
myofascial pain, and muscle imbalance. These are overlaid
by psychological and sociopolitical considerations having
to do with repetitive tasks, low-prestige occupations, and
insurance reimbursement patterns. Mackinnon and Novak
recommended a correspondingly broad treatment plan
that takes into account all areas of possible dysfunction
and deals with them accordingly.
Much has been written about CTS, which is now the most
common entrapment disorder affecting peripheral nerves.
Between 1% and 10% of the United States population
will exhibit symptoms of carpal tunnel compression at
some time. CTS results from repetitive prolonged wrist
extension causing mechanical irritation, synovitis, and
eventually compressive neuropathy of the median nerve.
Certain occupations such as cashier, checker, butcher,
and baker are associated with increased frequency of
CTS symptoms (23% of grocery store workers).337 The
condition also frequently occurs in rowers and bicyclists.338
The normal anatomy of the nerves and tendons
at the level of the carpal tunnel was illustrated by
Eversmann.339 As described, the carpal tunnel is bordered
by the transverse carpal ligament volarly and by the
bones of the wrist dorsally. The median nerve shares this
space with nine flexor tendons. At the level of the carpal
tunnel, the median nerve gives off a motor branch to the
thenar eminence muscles, a branch to the first and second
lumbricals, and sensory branches to the radial three and a
half digits.16,340
Olave et al.341 performed a biometric study of the
superficial palmar arch and of the communicating branch
between the ulnar and median nerves as related to the
flexor retinaculum. The authors found that in men, the
distance between the distal wrist crease and the site at
which the communicating branch originates from the
ulnar component had an average of 34 ± 6 mm on the
right side and 30 ± 8 mm on the left. The difference
between the distal wrist crease and the junction of the
communicating branch with the common palmar digital
nerve of the third interosseous space was 44 ± 7 mm on
the right and 40 ± 6 mm on the left. Conversely, in 15%
of cases, the communicating branch was observed to
emerge from the common palmar digital nerve of the third
interosseous space. The distance between the retinaculum
and the superficial palmar arch in the axial line of the
fourth metacarpal bone was on average 7 ± 4 mm on the
right and 8 ± 4 mm on the left. At the same level, the
distance between the retinaculum and the communicating
branch was 6 ± 4 mm on the right and 5 ± 3 mm on
the left. The measurements in women were consistently
smaller throughout (Tables 12 and 13).341 These
47
SRPS • Volume 11 • Issue R7 • 2015
Syndrome
Median nerve
Carpal tunnel syndrome
Pronator syndrome
Anterior interosseous
nerve syndrome
Table 11
Nerve Compression Syndromes
Site of Compression
Carpal tunnel
Numbness radial three and a half
digits, thenar atrophy, positive Tinel
sign at wrist, positive Phalen sign,
increased symptoms with tourniquet,
decreased NCV
Where median nerve passes deep to both Reproduction of proximal forearm pain
heads of pronator teres, at thickening of
on resistance to forearm pronation and
lacertus fibrosus or flexor superficialis arch wrist flexion, possible median numbness,
Tinel sign, EMG changes
Where nerve crosses tendinous
origin of deep head of pronator teres
Supracondyloid process syndrome Bony spur 3 to 5 cm above medial
epicondyle, ligament of Struthers
between spur and condyle (1%), fascial
band from biceps to volar forearm fascia
Radial nerve
Radial tunnel syndrome
Signs and Symptoms
Proximal to radial tunnel by fibrous
bands, at takeoff of radial recurrent artery
(vascular leash of Henry), at tendinous
origin of ECRB, or at arcade of Frohse
“Pinch attitude” of hand caused by
paralysis of FPL and FDP to index and
long fingers, no sensory component,
varies if Martin-Gruber anastomosis
is present
Possible median nerve symptoms
after trauma
EDC to finger(s) paralyzed
Posterior interosseous
nerve syndrome
Localized to the arcade of Frohse were the All EDC and FCU paralyzed, loss of MP
posterior interosseous nerve pierces the
extension, wrist in dorsoradial extension,
two heads of the supinator
no sensory component
Superficial radial nerve syndrome
Variable
Pain in proximal forearm, hypesthesia of
dorsal thumb
At first rib or costoclavicular area
Pain with neck rotation, variable sensory
and/or motor symptoms
Arcade of Struthers syndrome
Where the ulnar nerve passes into the
posterior compartment of the distal arm
Variable sensory and/or
motor symptoms
Cubital tunnel syndrome
Distal to medial epicondyle where nerve
passes through tow heads of flexor carpi
ulnaris, at common origin of FCU, FDP,
and FDS
Pure motor or sensory loss of ulnar one
and a half fingers or combination sensory
and motor impairment, possible
slowed NCV
Guyon canal syndrome
In Guyon canal at pisiform or hook
of hamate
Loss of intrinsic muscle function to small
and ring fingers with or without
sensory loss
Ulnar nerve
Cervical syndromes
NCV, nerve conduction velocity; EMG, electromyogram; FPL, flexor pollicis longus; FDP, flexor digitorum profundus; ECRB,
extensor carpi radialis brevis; EDC, extensor digitorum communis; FCU, flexor carpi ulnaris; MP, metacarpophalangeal; FDS,
flexor digitorum superficialis.
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SRPS • Volume 11 • Issue R7 • 2015
Table 12
Distance from Distal Wrist Crease to Exit Level and to Junction Level of Communicating Branch341
Sex
Junction Level
(mean ± SD in mm)
Exit Level
(mean ± SD in mm)
Right
Left
Right
Left
Male
33.9 ± 5.5
30.2 ± 8.2
43.6 ± 6.9
40.2 ± 6.2
Female
28.5 ± 6.2
27.1 ± 3.3
40.7 ± 7.8
34.4 ± 1.6
Table 13
Distance from Distal Margin of Flexor Retinaculum to Communicating Branch341
Communicating Branch Level
(mean ± SD in mm)
Sex
Right
Left
Male
6.2 ± 3.7
5.1 ± 2.8
Female
5.3 ± 3.7
4.0 ± 1.9
measurements can be used as a reference during surgical
procedures in the palmar tunnel, particularly ECTR.
Lanz342 studied the anatomy of the median
nerve at the carpal tunnel and identified three major
patterns of branching of the recurrent motor branch:
extraligamentous (46%–90%), subligamentous (31%),
and transligamentous (23%).
Amadio343 confirmed the anatomic work presented
by Lanz342 in his own series of 275 carpal tunnel releases
and noted that anomalies within the carpal tunnel are
common. More recently, Szabo and Pettey344 reported
a bilateral group III variation in which the radial-most
branch of each median nerve occupied an accessory
ligamentous compartment beneath its transverse
carpal ligament.
Green and Morgan345 further emphasized the
anatomic variability of and potential for iatrogenic injury
to the thenar motor branch. In their series of 1400
consecutive patients who underwent open carpal tunnel
release (OCTR) through a thenar crease incision, 25.5% of
patients displayed an extraligamentous or transligamentous
course, which rendered the thenar motor branch more
vulnerable to injury. The authors recommended caution
when thenar muscle fibers are located superficial to or
within the transverse carpal ligament, considering the
incidence of anomalous motor branch was 93% in those
cases. They reported numerous representative cases in
which motor branch nerve fibers were clearly located
within the standard field for OCTR and were vulnerable
to inadvertent injury. Based on the findings presented by
Green and Morgan, the precise location of the incision
is extremely important in avoiding the vulnerable thenar
49
SRPS • Volume 11 • Issue R7 • 2015
motor branch nerve fibers.
Kaplan346 presented a classic description of the
thenar motor branch as lying at the intersection of axes
defined by the radial border of the long finger and the
“cardinal line,” which extends from the apex of the first
web space parallel to the middle palmar crease. The
location was recently clarified by Eskandari et al.347 in
patients undergoing OCTR. Based on the radiographic
measurements presented by Eskandari et al., the thenar
motor branch is 12.6 mm ulnar and 4.4 mm proximal to
the location described by Kaplan. Therefore, the motor
branch is more in line with the mid-axis of the long finger
than with its radial border, which is a cause for caution
when using the traditional landmarks for OCTR. Finally,
the anatomic definition of the cardinal line presented by
Kaplan was reinvestigated by Vella et al.,348 indicating that
it is best drawn from the apex of the first web space to the
hook of the hamate. The authors confirmed the finding
reported by Eskandari et al. that the cardinal line described
by Kaplan is not a reliable landmark for localizing the
thenar motor branch, but they indicated that the cardinal
line is consistently 18 mm proximal to the superficial
palmar arch. Whereas this topography is important for
the safety of open releases, knowledge of the limitation
of these landmarks is crucial in limited-incision and
endoscopic techniques.
Sugimoto et al.349 evaluated the blood supply to the
median nerve using dynamic, contrast-enhanced MRI.
The authors found significant circulatory disturbances
in the median nerve of patients with CTS, suggesting
that chronic hypoxia in the nerve rather than nerve
compression alone produces the symptoms of CTS.
The role of the lumbrical muscles in the cause of
carpal tunnel disorder has been sporadically investigated
for many years. In the 1970s, Eriksen350 and Jabaley351
reported symptoms of CTS associated with hypertrophy
of a lumbrical muscle the origin of which was high enough
to crowd the carpal tunnel during active finger flexion.
Desjacques et al.352 noted that in nearly all cases of CTS
that showed complete denervation of the thenar muscles,
the first and second lumbricals maintained part of their
innervation. Cobb et al.353 from the Mayo Clinic evaluated
the significance of lumbrical muscle incursion within
the carpal tunnel. The authors documented a progressive
increase in carpal tunnel pressure for each degree of finger
50
flexion in cadaveric hands with intact lumbricals. This
stood “in sharp contrast to a relatively stable carpal tunnel
pressure during finger flexion for the group without
lumbrical muscles.” The authors concluded that lumbrical
muscle incursion into the carpal tunnel can result in
elevation of carpal tunnel pressure and could be a cause of
work-related CTS.
Braun et al.354 described provocative stress testing
for patients suspected of having CTS. Of 40 patients who
were evaluated, 34 had increased hand volume but only 17
had impaired sensibility associated with the swelling, and
those 17 were considered to have dynamic CTS
requiring surgery.
Osamura et al.355 began to elucidate the role of
alterations in material properties of the carpal tunnel
subsynovial connective tissue (SSCT) in patients with
idiopathic CTS. They reported a mean shear modulus of
22.8 kPa in patients with CTS versus 2.7 kPa in normal
control patients and mean maximum shear strength of
54.6 kPa in the CTS group versus 23.3 kPa in the
control group.
A more recent study using human cadaveric wrist
models investigated the effect of high- (60 mm/s) and
low- (2 mm/s) velocity tendon excursion of the SSCT.
The results showed that increasing velocity lowers the
threshold for SSCT damage with resistance energy greater
at all excursions (P < 0.031).356 The authors suggested that
this finding might be important in understanding SSCT
and occupational links with CTS. Associated evidence
suggests that digital motion at extremes of wrist flexion
and extension might lead to shear injury to the SSCT and
volume changes within the carpal tunnel.357
Much controversy exists regarding the most
appropriate surgical technique for decompression of the
carpal tunnel. A number of operative procedures have
been recommended, from simple operative release of the
flexor retinaculum at the wrist, to release and exploration
of either the motor branch to the thenar muscles or
the palmar cutaneous branch of the median nerve, to
release and neurolysis of the median nerve. The various
approaches are passionately defended by
their practitioners.
Open Carpal Tunnel Release—Steinberg and Szabo16
SRPS • Volume 11 • Issue R7 • 2015
argued for the traditional approach of open surgical
decompression of the median nerve with full visualization
of the transverse carpal ligament because of the potential
for anomalous branching patterns of the nerve. Details of
the “classic” technique they prefer are presented in their
article. Ariyan and Watson358 reviewed their extensive
experience with CTS and described their operative
technique. Heckler and Jabaley359 emphasized that the
treatment of CTS is nerve dissection and decompression
rather than transverse carpal ligament release. Jakab
et al.360 described a technique of transverse carpal
ligament reconstruction in surgery for CTS that resulted
in complete resolution of symptoms in 93% of 104
hands. The authors described the operation as requiring
substantially more dissection, with release of Guyon canal
and mobilization of the ulnar nerve and artery.
Serra et al.361 described the site of a short incision
through which it is possible to completely section the
carpal ligament without damaging the carpal contents.
The technique involves a specially designed, blunt-tipped,
rigid cannula and three Senn-Miller retractors to guide the
scalpel and avoid injury to the median nerve. The resulting
incision is 1.5 to 2 cm long. The authors note that their
approach combines the advantages of the endoscopic
technique—minimal scar, no tenderness, early recovery—
with those of the classic open technique—exploration of
the carpal contents.
First reported by Lee and Strickland362 in 1998,
the Indiana Tome (Biomet Orthopaedics, Inc., Warsaw,
IN) is an instrument that allows sectioning of the
transverse carpal ligament through a limited palmar
incision. The approach used is extrabursal (outside the
synovial confluence of flexor tendons and median nerve),
proceeding from distal to proximal over a protective
guide. The technique was designed as a hybrid technique
that offers the advantages of both open and endoscopic
techniques by allowing direct visualization of the carpal
tunnel contents and a limited incision. The results
achieved with this technique were comparable to those
achieved with other techniques, with 72.6% of patients
experiencing complete relief and 19.6% experiencing
near-complete relief. In the initial report of 694 hands,
one partial and one complete median nerve transection
occurred (0.29%) because of a second pass of the tome
after difficulty with the initial pass. After that move was
eliminated, no other transections occurred.
Lee et al.363 reported 13-year outcomes for 1332
patients who had undergone carpal tunnel release with the
Indiana Tome. The complication rate was 0.83%. Third
common digital neurapraxia occurred most commonly.
One can assume higher grade injury to the third common
digital nerve in four patients (0.30%). Two of those cases
were confirmed by surgical exploration, and two were
unexplored but displayed persistent increase in TPD. The
authors unequivocally stated the following:
“The key to reducing complication in any
minimally invasive technique, including the
Indiana Tome, is to have a low threshold
of converting to a standard open approach
whenever the anatomy appears unclear or
the technique does not proceed easily. It is
the responsibility of all surgeons, whatever
their degree of experience, to recognize this
potential for complications and to do what
is necessary to ensure patient safety.”
Lowry and Follender364 evaluated the benefits of
adjunctive interfascicular neurolysis in the treatment of
severe CTS and found no significant difference between
the study group (n = 25) and the control group (n =
25) who underwent standard ligament release alone.
The authors concluded that no benefit is derived from
adjunctive interfascicular neurolysis in carpal tunnel
surgery. In the absence of substantial adhesions to the
nerve, Seiler et al.365 also noted no improvement in nerve
blood flow after epineurotomy.
Mackinnon et al.366 agreed with that opinion on
the basis of a prospective, randomized study comparing
carpal tunnel release with and without internal neurolysis.
The authors stated that the addition of internal neurolysis
to division of the transverse carpal ligament does not add
notable improvement in the sensory or motor outcomes
for patients with primary CTS. A similar prospective
comparative study by Blair et al.367 found no difference
between the epineurotomy and non-epineurotomy
groups in terms of TPD, physical and neurophysiological
findings, and patient perception of outcome. These studies
do not support the use of routine epineurotomy as an
adjunctive procedure during carpal tunnel decompression.
Similarly, it has been reported that simultaneous
release of Guyon canal is no longer recommended for
patients with carpal tunnel and paresthesias in the little
51
SRPS • Volume 11 • Issue R7 • 2015
finger. MRI findings showed that the dimensions of
Guyon canal enlarge with carpal tunnel release alone.368
This finding has been clinically substantiated.16,369
Singh et al.370 surveyed the results of surgical
decompression of the carpal tunnel in 265 patients (303
hands) who were diagnosed as having CTS. The femaleto-male ratio was 6:1, and 40 patients had bilateral
involvement. Only 39% of hands showed numbness
and paresthesias along the distribution of the median
nerve. Tinel sign was positive in 63% of hands, and
Phalen maneuver was positive in 67%. EMG studies were
universally positive for carpal tunnel compression but
were not conducted in every case (i.e., some patients were
operated on solely on the basis of the clinical findings).
A variety of operative procedures were performed, and all
patients reported improvement in symptoms regardless of
the type of surgery. The most common complication was a
sensitive palmar scar, which bothered 62% of patients for
up to 5 months postoperatively. Follow-up duration was 4
to 32 months (mean, 22 months).
Lindau and Karlsson371 presented a 6-year followup of 91 patients undergoing OCTR. The results are
presented in Table 14.
Other complications of carpal tunnel release include
infection, transection of the motor branch of the median
nerve, injury to the palmar cutaneous branch of the
median nerve, partial severance of the carpal ligament,
pisotriquetral pain syndrome, RSD, interpillar pain,
and transection of digital sensory nerves. The diagnosis
and management of these and other complications were
reviewed by Kuschner et al.372
Shurr et al.373 reported improvement in all clinical
and electrodiagnostic studies after carpal tunnel release:
motor and conduction velocities and TPD studies were
significantly improved as early as 2 weeks postoperatively;
sensory and motor latencies improved by 3 and 6 months;
and pinch and grip strengths improved by 6 and 9 months
(P < 0.05).374,375 In addition, ulnar nerve symptoms,
present in 33% of patients with CTS, improved with
carpal tunnel release alone.369
Wintman et al.376 correlated the severity of
preoperative symptoms of CTS with surgical outcomes
in 54 hands. The authors measured hand, wrist, and
forearm pain, night pain and paresthesias, intermittent
52
paresthesias, hand clumsiness, hand weakness, constant
numbness, and difficulty with work-related tasks
before and after carpal tunnel release. Although all
symptoms showed considerable improvement 3 months
postoperatively, patients whose hand weakness, pain,
numbness, and clumsiness were rated more severe showed
less improvement of function and less satisfaction with
overall symptom relief. Patients with preoperative night
symptoms and intermittent paresthesias tended to be more
satisfied with the results of surgery.
Cartotto et al.377 reported two unusual but
extremely serious complications of carpal tunnel release.
One patient had massive necrosis of the palm, which
required free flap coverage, and another had complete
severance of the median nerve for which direct repair
failed, necessitating grafting.
Endoscopic Carpal Tunnel Release—Okutsu et al.378 and
Chow379 first introduced ECTR in 1987 and 1989. Initial
reception of the endoscopic approach was colored by
clinical series performed with the original Agee device and
using the transbursal technique, which were associated
with complication rates four times higher than those
associated with the current extrabursal technique.380 Since
that time, a single-portal operation with the retooled Agee
device381 and a dual-portal technique presented by Chow379
have been used extensively in the United States for carpal
tunnel decompression.
Nagle382 reviewed the literature of ECTR and
compared its surgical outcomes with those of OCTR.
Overall, the author found no difference between the two
approaches in terms of tendon, artery, or nerve lacerations,
hematomas, incomplete releases, or time to resolution of
paresthesias or pain. In general, ECTR is more commonly
associated with neurapraxia and stitch infection than is
OCTR, but ECTR also leads to more rapid recovery of
pinch and grip strength and wrist range of motion and less
midpalm tenderness than does OCTR. In a presentation
at the annual meeting of the American Society for Surgery
of the Hand in 1995, Palmer and Toivonen383 reported
the results of a survey of the membership regarding
complications of ECTR and OCTR (Table 15).
Brown et al.384 analyzed the results of carpal tunnel
release through the open and endoscopic methods in
SRPS • Volume 11 • Issue R7 • 2015
Table 14
Open Carpal Tunnel Release: Preoperative and 6-Year Postoperative Findings371
Preoperative
(n = 85)
6 Years
Postoperative
(n = 91)
Relative Risk
(95% confidence interval)
Numbness at night
78
29
0.35 (0.14−0.85)
Numbness during day
63
29
0.43 (0.22−0.83)
Weakness of grip
17
39
2.14 (1.09−4.21)
Occasional pain at rest
24
19
0.74 (0.37−1.48)
Decreased sensibility
15
11
0.68 (0.30−1.59)
Decreased wrist motion
0
28
Sensitivity to cold
0
33
Pain with loading
0
35
Positive Phalen sign
61
9
0.14 (0.06−0.32)
Positive Tinel sign
55
7
0.12 (0.05−0.29)
Thenar atrophy
5
10
1.87 (0.61−5.71)
Dysesthesia in scar
0
8
Pain in scar
0
1
Subjective symptoms
Objective findings
Table 15
Nerve Laceration Complications Associated with
Endoscopic Carpal Tunnel Release and Open Carpal Tunnel Release383
Endoscopic
(708 surgeons)
Open
(616 surgeons)
100
147
Ulnar nerve
88
29
Digital nerve
77
54
Tendon
69
19
Superficial arch
86
21
Ulnar artery
34
11
Laceration
Median nerve
53
SRPS • Volume 11 • Issue R7 • 2015
169 hands and found no significant differences between
the two groups regarding sensation, motor strength, or
subjective relief of symptoms. The open technique was
associated with more tenderness of the scar than was the
endoscopic method. The open approach also resulted
in longer time to return to work (median, 28 days)
than did the endoscopic technique (median, 14 days).
On the other hand, endoscopic release was associated
with more frequent complications, such as partial nerve
transections, contusions, and wound hematomas. The
authors concluded that although function is restored
faster when the endoscopic method is used, the higher
rate of complications is a sign that intraoperative safety
needs to be improved before ECTR can be performed on
a widespread basis. Murphy et al.385 also reported a case of
transection of the median nerve and pseudoaneurysm of
the superficial palmar arch after ECTR.
A review of the literature disclosed marked
differences in return-to-work times of patients after
carpal tunnel release by either the endoscopic or the open
approach.380,381,386-389 Jimenez et al.389 provided an extensive
review of published articles on ECTR and OCTR. The
authors concluded that the reported success, complication,
and failure rates of ECTR are acceptable and comparable
to those of OCTR in adequately selected patients.
Furthermore, many patients who underwent ECTR
returned to work and activities of daily living sooner than
did the patients who underwent OCTR.389 In addition,
the patients who underwent ECTR reported less pain and
tenderness during the postoperative period. The authors
were unable to recommend one procedure over the other
but preferred subligamentous or extrabursal techniques to
transverse methods. Ultimately, surgeons should perform
the procedure with which they are most comfortable.
Thoma et al. compared cost and effectiveness of
ECTR and OCTR using a decision analysis economic
model. Based on medical costs from a Canadian
university hospital, the calculation strongly favors OCTR
performed in a day surgery unit when compared with
ECTR performed in the main operating room. When
both OCTR and ECTR are performed in the day surgery
unit, the findings are equivocal depending on the variable
occurrence of increased scar sensitivity (OCTR) or
increased RSD (ECTR). Although the results were based
on a cost structure and operating room setup that were
390
54
unique to a specific institution, the study indicated the
important factors of surgery resource utilization, operating
room equipment availability, and logistics when weighing
the two procedures in the setting of limited
health resources.
A meta-analysis of randomized controlled trials
conducted by Thoma et al.391 compared ECTR and
OCTR (Fig. 24). Based on the 13 available Level I trials in
the world literature, including five non-English language
publications, the authors found support to favor ECTR
in reduction of scar tenderness and increase in grip and
pinch strength at 12-week follow-up examinations. Data
were inconclusive for symptom relief and return to work.
Reversible nerve damage was three times more likely to
occur in ECTR cases, but irreversible nerve damage was
rare with either technique (Fig. 24).391 The authors called
for a multicenter randomized controlled trial to obtain a
definitive comparison between the techniques.
More recently, Atroshi et al.392 conducted a
randomized trial comparing outcomes of OCTR and
ECTR performed in 63 patients each with 5-year followup. No difference in outcomes was shown by the validated
Carpal Tunnel Questionnaire (CTQ). Of note, persistent
palm and scar tenderness were equal in both groups.
A number of validated outcome assessment
questionnaires have been used to compare outcomes in
cases of CTS. Hand-specific outcome instruments include
the CTQ, Michigan Hand Outcomes Questionnaire, and
Disability of Arm, Shoulder and Hand Questionnaire
(DASH). These have all been compared and shown to be
responsive to change after carpal tunnel release.393-395
CTS in Children—Lamberti and Light396 reviewed the
literature and described 64 cases of pediatric CTS. The
most frequent age of diagnosis and treatment was between
6 and 8 years; however, some patients were as young
as 2 years. Fifty percent of the cases were secondary to
lysosomal storage disease, whereas 25% were considered
idiopathic. Most children presented with modest
complaints and were often described as being clumsy with
their hands. Other complaints included wrist and hand
pain, and older children often complained of paresthesias
and nocturnal symptoms similar to those of adults with
CTS. More than half the patients had evidence of thenar
SRPS • Volume 11 • Issue R7 • 2015
Figure 24. Graphs show effect size and odds ratio for outcomes. OCTR, open carpal tunnel release. ECTR, Endoscopic carpal
tunnel release. (Reprinted with permission from Thoma et al.384)
55
SRPS • Volume 11 • Issue R7 • 2015
atrophy, and, in some cases, it was severe enough to
suggest the possibility of congenital absence or hypoplasia
of the thenar muscles.
Findings of provocative tests, such as Tinel and
Phelan tests, often are normal for children with longstanding nerve compression, and electrodiagnostic studies
are essential to establish the diagnosis. Pediatric cases tend
to include bilateral electrophysiological abnormalities
even if only one hand is clinically involved. Therefore, it is
recommended that electrodiagnostic studies be performed
bilaterally in all suspected pediatric cases.
Causes of CTS in the review presented by
Lamberti and Light396 include genetic abnormalities such
as lysosomal storage disease, mucopolysaccharidosis,
mucolipidosis, primary familial CTS, Schwartz-Jampel
disorder, and hemophilia. Nongenetic causes include
massive hemangiomatosis, macrodactyly, melorheostosis,
sports-related activities, and aberrant anatomy.
Sixty of the 64 cases underwent carpal tunnel
release, and the vast majority of patients experienced either
partial or complete recovery of sensation and strength. The
authors implied that operative release is the only treatment
documented to be effective in cases of pediatric CTS.
Choudry et al.397 summarized a series of 32 children
(age 16 years or younger) with CTS at the Mayo Clinic
between 1974 and 2005. Overuse syndrome was the most
frequent (44%) cause of CTS in that series, with less
frequent causes being genetic conditions (25%), familial
CTS (16%), trauma (13%), and ganglion cyst (3%). The
mean patient age was 14 years, with a range of 5 to 16
years. The experience mirrors the findings presented by
Lamberti and Light396 regarding surgery as the preferred
treatment for CTS secondary to genetic disorders and
trauma. However, Choudry et al. found conservative
therapy to be effective in 79% of cases related to overuse
syndrome, with only 14% of those cases requiring surgery.
Recurrent CTS—Although the vast majority of patients
are relieved of their symptoms after carpal tunnel
decompression, Hunter398 noted an increasing number of
patients (approximately 20% of those undergoing carpal
tunnel surgery) who failed to return to the work force
postoperatively because of recurrent CTS. Approximately
50% of those patients had histories of previous injury to
the wrist, and Hunter speculated that something other
56
than simple compression neuropathy of the median nerve
was at work. The median nerve might have been fixed in
adhesions, either from the trauma or the failed surgery,
and rapid-pace recovery programs might have aggravated
the problem by forcing the hand into pronation and
causing radial neuropathy. Such a complex of events could
even lead to brachial plexus traction disorders. Hunter
stated that the best approach to recurrent CTS is complete
mobilization of the median nerve through the hand
and wrist.
O’Malley et al.399 recommended reexploration
for patients with unrelieved carpal tunnel symptoms
after release if they have positive Phalen test findings,
nocturnal symptoms, symptoms exacerbated by activities,
or a short or transverse initial incision. In the absence of
these criteria, reexploration will not result in a satisfactory
outcome. Rose et al.400 added a palmaris brevis turnover
flap to internal neurolysis of the chronically scarred
median nerve in cases of recurrent CTS. With that
protocol, they documented improvement in strength,
bulk, and sensibility in all hands in their study.
Botte et al.401 identified the common causes of
recurrent CTS and prescribed treatment as follows:
•• For incomplete release of a transverse carpal
ligament, conduct reexploration and repeat
release of the transverse carpal ligament or
perform incision or excision of the reformed
transverse carpal ligament.
•• For fibrous proliferation or scarring within
the carpal tunnel, perform epineurolysis
or use local muscle flaps or local or remote
free fat grafts with or without internal
neurolysis, perform excision or Z-plasty of
painful scar, or insert a nerve barrier (e.g.,
silicone sheet, vein wrapping).
•• For recurrent or exuberant flexor
tenosynovitis, repeat tenosynovectomy or
appropriate chemotherapy.
Anterior Interosseous Syndrome
Eversmann333 and Howard402 reviewed the anatomy,
diagnosis, and treatment of the anterior
interosseous syndrome.
SRPS • Volume 11 • Issue R7 • 2015
Pronator Syndrome
Olehnik et al.403 presented their experience with median
nerve compression in the proximal forearm. The nerve
might be impinged upon by the lacertus fibrosus, by
vascular leashes across the nerve canal, or by abnormalities
of the PT muscle or the FDS muscle. Less commonly, the
median nerve is pinched beneath the ligament of Struthers
from a supracondylar process on the distal humerus. Nerve
conduction testing is ineffective for confirming clinical
impression of proximal median nerve entrapment. The
treatment of choice for this disorder is surgical release of
the median nerve in the proximal forearm.
Radial Nerve
At the level of the elbow, the radial nerve can be
compromised at four different sites along its submuscular
course by the following: 1) fibrous bands proximal to
the radial tunnel; 2) the vascular leash of Henry (radial
recurrent artery); 3) the tendinous margin of the ECRB;
or 4) the arcade of Frohse (the proximal edge of the
superficial supinator), where the posterior interosseous
nerve travels between the superficial and deep heads of
the supinator.333,404
Radial Tunnel Syndrome
Compression of the radial nerve at the level of the elbow
manifests clinically as radial tunnel syndrome.333,402 This
condition is distinct from lateral epicondylitis, or “tennis
elbow,” which also exhibits pain in the region of the
mobile wad and common extensor origin.405 Anatomically,
the radial tunnel contents include both the superficial
radial nerve (the primary sensory branch) and the motor
component of the radial nerve (nerves to brachioradialis,
ECRL, ECRB, supinator, and posterior interosseous
nerve). Symptoms are exertional pain in the extensorsupinator muscle mass in the proximal forearm that
can radiate distally, with paresthesia in the dorsal radial
aspect of the hand; patients also frequently complain of
a weak grip.332,402 EMG studies are not diagnostic unless
marked denervation is present,333 but radial nerve block
is prognostically helpful: Ritts et al.404 noted excellent
surgical results in patients who experienced relief of pain
when their radial nerve was anesthetized.
In a recent study of the long-term results of surgical
decompression of the radial tunnel by a brachioradialis
muscle-splitting approach, Jebson and Engber406 noted
that complete pain relief and return to activities after
radial tunnel surgery is not as predictable as previous
studies indicated. The authors tracked the functional
results of surgical release in 24 extremities for an average
of 8 years after surgery. The criteria outlined by Roles and
Maudsley407 and Ritts et al.404 were used to determine
outcomes. Based on the method presented by Roles and
Maudsley, eight extremities (33%) were judged to be
fair or poor. Based on the method presented by Ritts et
al., seven extremities (29%) were judged to be fair or
poor. Five patients changed their occupations because of
continued discomfort. These findings are in line with the
30% fair or poor results reported by Lawrence et al.408 in
a retrospective review of 30 decompressions of the
radial nerve.
Posterior Interosseous Nerve Syndrome
Compression of the posterior interosseous nerve at
the fibrous arcade of Frohse gives rise to the posterior
interosseous nerve syndrome. The nerve supplies branches
to the extensor digitorum, extensor digiti minimi, extensor
carpi ulnaris, abductor pollicis longus, EPL, extensor
pollicis brevis, and EIP muscles.402 Symptoms are paresis
of the hand with loss of finger extension, loss of thumb
abduction, and radial deviation of the hand during wrist
extension.
The radial tunnel and arcade of Frohse can
be approached anteriorly or posteriorly. When the
compression neuropathy can be localized to the arcade of
Frohse, Mackinnon and Dellon21 prefer a lazy-S musclesplitting incision extending posteriorly between the
brachioradialis muscle and the ECRL (Fig. 25).404 Patients
with radial nerve entrapment syndrome that cannot be
localized to the arcade of Frohse are best served by a
zigzag anterolateral incision to expose the radial tunnel for
exploration.333
Kotani et al.409 reported four cases of posterior
interosseous nerve paralysis with multiple constrictions.
At the time of surgery, the constrictions were found
between the arcade of Frohse and a point of bifurcation
of the supinator motor branch. External neurolysis with
epineurotomy under the microscope was performed in all
cases, and full recovery was obtained.
57
SRPS • Volume 11 • Issue R7 • 2015
7
1
2
3
8
9
4
10
5
6
Figure 25. Sites of compression of the posterior
interosseous nerve in association with radial tunnel
syndrome. 1, radial nerve; 2, brachialis; 3, brachioradialis;
4, arcade of Frohse; 5, extensor carpi radialis brevis; 6,
superficial radial nerve; 7, bicep; 8, median nerve; 9, radial
recurrent artery; 10, fibrous bands. (Modified from Ritts
et al.397)
Ulnar Nerve
Mackinnon and Dellon,21 Eversmann,333 and Leffert410
reviewed the anatomy, diagnosis, and treatment of
ulnar neuropathies.
Cubital Tunnel Syndrome
The ulnar nerve lies on the medial head of the triceps
muscle, enters the cubital tunnel behind the medial
epicondyle, and continues distally beneath the arcade
of fascia joining the heads of the FCU (Fig. 26).338,411
The nerve might be constricted in its course through
the cubital tunnel at the level of the elbow. Ulnar nerve
constriction manifests as pain on the medial side of
the proximal forearm and paresthesias, dysesthesias, or
anesthesia in the little and ring fingers.412 Clinical signs
and a positive percussion test over the ulnar nerve are
diagnostic of entrapment; nerve conduction velocity
studies are inconclusive.333
When the ulnar nerve is squeezed by the
aponeurosis of the FCU, surgical decompression
58
Figure 26. Zigzag incision for anterolateral approach to
radial tunnel when compression cannot be localized to
arcade of Frohse. (Modified from Eversmann.327)
alone is sufficient for treatment.333-413 Patients for whom
decompression has failed or whose ulnar neuropathy
is the result of trauma, cyst, or congenital anomaly are
candidates for anterior transposition of the ulnar nerve.
Learmonth414 described the submuscular technique
of anterior transposition, and Leffert410 recounted his
experience with anterior submuscular transposition of
the ulnar nerve in 38 patients. Ulnar nerve mobilization
necessitates decompression of the cubital tunnel,
fasciotomy of the FCU, and dissection along the
ulnar nerve for at least 8 cm proximal to the medial
epicondyle.413 Controversy surrounds the selection of
an appropriate technique for ulnar nerve decompression
in each individual patient.415 Numerous prospective
randomized controlled trials have shown comparable
results between simple decompression and either
SRPS • Volume 11 • Issue R7 • 2015
submuscular or subcutaneous transposition.416-419 Bartels
et al.416 found that simple decompression has a lower
complication rate when compared with subcutaneous
transposition (9.6% versus 31.1%), with sensibility
loss around the scar and superficial infection occurring
most commonly. In a companion study, the same group
showed that total costs were substantially lower for
simple decompression (1124 Euros versus 2730 Euros).420
Limitations of those studies were failure to include
all treatment modalities and inadequate distribution
of patients with mild, moderate, and severe symptom
staging. A meta-analysis was conducted by Mowlavi et
al.421 Based on an evaluation of 30 studies, the authors
determined that patients with mild stage cubital tunnel
syndrome benefit equally from nonoperative and all
surgical treatments, those with moderate stage respond
best to submuscular transposition, and those with severe
stage show inconsistent efficacy for all available modalities,
with medial epicondylectomy displaying the poorest result.
Lowe and Mackinnon422 emphasized that all procedures
have pitfalls that can lead to an overall recurrence or
failure rate of 25% after surgery. The authors inferred the
importance of expert technique and awareness of potential
problems in performing the surgical modality of choice.
Race and Saldana423 described the anatomic course
of the medial cutaneous nerves of the arm, the fibers of
which overlie the medial epicondyle and supply the skin
over the olecranon. Because the standard incision used
for ulnar nerve transposition severs the terminal branches
of these cutaneous nerves, the authors recommended a
posterior approach for transposition of the ulnar nerve.
Lowe et al.424 further characterized these branches in
clinical practice by using a standard approach posterior to
the medial humeral epicondyle. In those cases, a branch
of the medial antebrachial cutaneous nerve crossed the
incision line 1.8 cm proximal to the epicondyle 61% of
the time and 3.1 cm distal to the epicondyle 100% of the
time (Fig. 27). Meticulous dissection is required at the
time of surgery to preserve these branches despite use of a
posterior approach.
Ulnar Tunnel Syndrome
In its passage from forearm to hand, the ulnar
neurovascular bundle crosses the wrist by way of Guyon
canal. The roof of the space is the volar carpal ligament,
which begins at the pisiform and extends radially to the
hook of the hamate and attaches to the transverse carpal
ligament. The floor of Guyon canal consists of the muscles
of the hypothenar eminence, their fibers of origin, and
the flexor retinaculum. Fatty tissue separates the proximal
and distal segments of the roof of the canal.1376,333,334
Compression of the ulnar nerve in Guyon canal at the
wrist is known as ulnar tunnel syndrome. Clinical signs are
varied, and the site of the lesion determines whether both
motor and sensory abnormalities exist or whether only
motor or sensory paralysis is present.425 The latter is rare.425
The most common cause of Guyon canal
entrapment is a carpal ganglion, and the second most
common cause is repeated trauma to the hypothenar area,
usually related to occupation.425 Treatment is by surgical
exploration of Guyon canal, decompression, and resection
of any obstructing mass (e.g., a ganglion).425
König et al.426 studied the hypothenar region in 23
cadaveric hands and noted that the contents of Guyon
canal exit through two distinct areas termed the deep distal
hiatus and the superficial distal hiatus. The deep motor
branch of the ulnar nerve, with its deep branch of the
ulnar artery and venae comitantes, which anastomose with
the deep palmar vascular arch, runs beneath the opponens
digiti minimi and flexor digiti minimi through the deep
distal hiatus. This deep ulnar neurovascular bundle exits
deep toward the midpalmar space, where the finger flexors
lie and, in 61% of specimens, is bound by a potentially
compressive fibrous arcade. The clinical implication of
this finding is that when a release of the ulnar nerve is
indicated, surgery should not only open the roof of Guyon
space to release the superficial sensory branch to the ring
and small fingers but also the fibrous arcade of the deep
distal hiatus to release the deep motor branch to the
intrinsic muscles. Otherwise, intrinsic weakness is very
likely to be incompletely treated.
Traction Neuritis
Occasionally, patients develop persistent pain after
OCTR or transposition of the ulnar nerve at the elbow.
The pain might be the result of a neuroma of one of
the subcutaneous nerves in the area, incomplete release
of the anatomic structure causing compression of the
nerve, scarring of the nerve to adjacent structures, or
59
SRPS • Volume 11 • Issue R7 • 2015
Figure 27. Standard 8-cm surgical incision for primary cubital tunnel surgery. a, average distance of proximal crossing branch
from medial epicondyle is 1.8 cm; b, average distance of distal branch from medial epicondyle. (Reprinted with permission from
Lowe et al.417)
devascularization of the nerve. Conventional treatment
involves initial reexploration of the nerve and external
neurolysis and then epineurotomy, epineurectomy, or
internal neurolysis. Most patients improve after surgery,
but a small group of patients are virtually crippled by
debilitating pain. The pain usually is exacerbated by direct
pressure over the incision or by flexion and extension
of the adjacent joints. The patients who experience this
pain have developed traction neuritis because of adhesive
scarring of the nerve, either to the overlying skin or to the
underlying tendons, which can progress to interfascicular
scarring and segmental devascularization of the nerve.
Typical examples include the following: 1) traction
60
neuritis of the median nerve after OCTR, sometimes
referred to as adhesive median neuritis427 or epineural fibrous
fixation,398 which is treated by secondary reexploration
and neurolysis; and 2) traction neuritis of the ulnar nerve
after unsuccessful cubital tunnel decompression, treated
by either medial epicondylectomy, subcutaneous, or
submuscular transposition.428
The concept of circumferential wrapping of a
peripheral nerve involved in end stage traction neuritis
with highly vascularized free flaps or pedicled flaps
evolved out of frustration with the failure of conventional
treatment and the successful precedent of relieving the
SRPS • Volume 11 • Issue R7 • 2015
pain of brachial plexus neuritis by coverage with greater
omentum. Circumferential wrapping might cushion the
nerve from external pressure on the overlying skin, might
isolate the nerve from the traction forces of adjacent
moving tendons to allow improved gliding of the nerve,
and might promote revascularization of a scarred nerve.
In a report by Jones et al.428 nine patients with chronic
severe pain caused by end stage traction neuritis of an
intact peripheral nerve underwent external neurolysis and
epineurectomy or epineurectomy and internal neurolysis
and then circumferential wrapping of the devascularized
segment of nerve. The flap was transferred on a pedicle
or by microvascular anastomosis and consisted of
subcutaneous adipose tissue, fascia, or muscle. During
a follow-up period ranging from 1 to 5 years, seven
patients experienced substantial relief of pain whereas
two patients had no decrease in pain. The two patients
without improvement had pure-fascia radial forearm
fascial flaps without any overlying skin. Jones et al.428
expressed reservations regarding the effectiveness of such
a flap compared with subcutaneous fatty tissue or muscle
and discussed the pros and cons of various flap tissues
and territories for circumferential nerve wrapping in the
treatment of traction neuritis.
Recent enthusiasm for using collagen-based
nonvascularized materials for wrapping nerves affected
by traction neuritis remains relatively unsubstantiated
in clinical or scientific practice.429 Experimental
studies conducted by Magill et al.430 using a rat model
indicated that Seprafilm (Genzyme Corporation,
Cambridge, MA), an antiadhesive hyaluronic acid and
carboxymethylcellulose membrane sheet, is safe for use
in nerve wrapping and might have benefits for decreasing
perineurial scar bands.
Multiple Nerves
The term double crush syndrome is used to characterize
the case of a single nerve compressed at two separate
levels.431,432 According to a definition presented
by Mackinnon,433 multiple crush syndrome implies
compression of a single nerve at multiple sites or multiple
structures compressing a nerve within a single anatomic
area. The three major nerves of the upper extremity can be
subject to multiple compressions as they pass through the
structures of the forearm into the wrist and hand.431
Mackinnon433 reported that the histological
changes in chronic nerve compression are slow but
progressive. According to Mackinnon, once the changes
are established, unless the cause is a systemic one that can
be alleviated, the process will progress. Ideally, patients
with multiple entrapment neuropathy or multiple
crush syndrome are treated with job modification and
education to avoid positions that exacerbate pressure on
the entrapment sites. Should the modifications fail to
eliminate the complaints, more distal surgical procedures
are recommended and frequently obviate the more
complex thoracic outlet decompression.433
Multiple compressions along a nerve have a
cumulative effect on conduction, both antegrade and
retrograde. The proximal source of compression can be
subclinical yet partially responsible for the compression
symptoms of more distal parts. Strict attention to the
patient’s history and physical findings permits separation
of the multiple points of compression and facilitates the
choice of a site for surgical decompression.431
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