Plastic Surgery Volume 6: Hand and Upper Extremity (4th Edition) – Peter C. Neligan

712
SECTION IV
CHAPTER 31 • Vascular anomalies of the upper extremity
experience is lacking in this entity mainly because it was not
recognized until recently.
Basic science/disease process
Most FAVA cases involve the leg. In the upper extremity, the
forearm is most commonly involved. Small lesions involve
portions of muscle whereas larger ones can involve an entire
muscle or muscle group. The hallmark clinical finding in this
lesion is pain that is worsened with activity. Contractures are
common in larger lesions as more muscle is involved.
Diagnosis/patient presentation
Lesions appear similar to venous malformations on MRI but
have larger fat and soft-tissue components. These lesions
replace normal muscle fibers with fibrofatty overgrowth and
phlebectasia (dilation of veins). Similar findings are noted on
gross specimens. On histology, lesions show dense fibrous
tissue, fat, and lymphoplasmacytic aggregates within atro­
phied skeletal muscle. There can be large, irregular, and
sometimes excessively muscularized venous channels and
smaller, clustered channels.
Diagnosis/patient presentation
Diagnosis is based on clinical findings and starts with physical
examination. Imaging can be tailored to specific areas as
involvement with multiple different kinds of vascular anoma­
lies is not uncommon. Differential diagnosis includes multiple
overgrowth syndromes but differentiation based on clinical
findings is usually possible. Guidelines for genetic PIK3CA
testing have been recently proposed.11
Treatment/surgical technique
Resection of the lipomatous component, staged debulking
and appropriate epiphysiodesis of the forearm and hand are
predictable and useful for the individual patient. Skeletal
angulation and rotation at all levels are corrected with
osteotomies. For massively overgrown digits that are non-
functional, the surgeon should consider amputation to allow
better function for the rest of the hand.
Fibro-adipose vascular anomaly (FAVA)
FAVA is a recently described vascular malformation that
appears in skeletal muscle in the extremities.24 Long-term
Fig. 31.24  Fibro-adipose vascular anomaly (FAVA) of forearm. (A) A 12-year-old
female with a large painful lesion of the entire volar forearm and progressive flexion
contractures of the wrist, thumb, and digits. (B) MRI post-contrast images show
extensive involvement of the flexor-pronator mass. (C) Intraoperative view after
excision of the lesion. The median nerve is involved. The mass was hard and densely
infiltrated with fibro-adipose tissue and clusters of phlebectasia. (D) Reconstruction
was performed with tendon transfers and free functional gracilis muscle transfer.
(E) Postoperative view.
A
B
C
D
E

713
Future directions
1. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations
in infants and children: a classification based on endothelial
characteristics. Plast Reconstr Surg. 1982;69:412–422. This classic
article helped clarify the delineation between hemangiomas and vascular
malformations. The classification is based on histologic differences in the
tissue; these endothelial characteristics are correlated with the natural
history of hemangiomas vs. vascular malformations.
2. Upton J, Taghinia A. Special considerations in vascular anomalies:
operative management of upper extremity lesions. Clin Plast Surg.
2011;38:143–151.
12. Kurek KC, Luks VL, Ayturk UM, et al. Somatic mosaic activating
mutations in PIK3CA cause CLOVES syndrome. Am J Hum Genet.
2012;90:1108–1115.
15. Upton J, Coombs CJ, Mulliken JB, et al. Vascular malformations of
the upper limb: a review of 270 patients. J Hand Surg. 1999;24:1019–
1035. This is a large series of patients with vascular malformations of the
upper limb. The diagnosis and treatment of various types is reviewed in
retrospective fashion.
24. Alomari AI, Spencer SA, Arnold RW, et al. Fibro-adipose vascular
anomaly: clinical–radiologic–pathologic features of a newly
delineated disorder of the extremity. J Pediatr Orthop. 2014;34:109–
117. Delineates a new anomaly termed fibro-adipose vascular anomaly,
FAVA.
25. Sapp JC, Turner JT, van de Kamp JM, et al. Newly delineated
syndrome of congenital lipomatous overgrowth, vascular
malformations, and epidermal nevi (CLOVE syndrome) in seven
patients. Am J Med Genet A. 2007;143A:2944–2958. This is a
presentation of the recently described CLOVES syndrome.
30. Tan W-H, Baris HN, Burrows PE, et al. The spectrum of vascular
anomalies in patients with PTEN mutations: implications for
diagnosis and management. J Med Genet. 2007;44:594–602.
32. Parkes Weber F. Right-sided hemihypertrophy resulting from
right-sided congenital spastic hemiplegia with a morbid condition
of the left side of the brain revealed by radiogram. J Neurol
Neurosurg Psych. 1922;37:301–311.
35. Upton J, Mulliken JB, Murray JE. Classification and rationale for
management of vascular anomalies in the upper extremity. J Hand
Surg. 1985;10:970–975.
51. Van der Horst CM, Koster PH, de Borgie CA, et al. Effect of the
timing of treatment of port-wine stains with the flash-lamp pumped
pulsed-dye laser. N Engl J Med. 1998;338:1028–1033. Treatment of flat
capillary vascular malformations is optimally treated with the flash-lamp
pumped pulsed-dye laser. This is because the wavelength of hemoglobin is
targeted. This article discusses optimal dosing and timing of treatment.
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Fig. 31.5 (C) CM plus overgrowth of thumb, long and ring digits in a child with
CLOVES. (D) Extensive CM plus lipomatous overgrowth, syndactyly, and no
skeletal overgrowth. (E) Limb of child with CM–AVM. (F) CM in an older man.
Fig. 31.9 (B) Lymphatic microcysts and small venous thromboses are studded
within dysplastic adipose tissue. (C) The neurovascular bundle has been
dissected with preservation vincular branches at the joint levels.
Fig. 31.11 Sclerotherapy. Radiographic studies of the vulnerable proximal third
of the forearm show a venous malformation (VM), which is ideal for
sclerotherapy.
Fig. 31.12 Venous malformation (VM) distal forearm.
Fig. 31.18 Parkes Weber syndrome: a 6-year-old child with a capillary
malformations of the wrist and hand, and a pulsatile mass of her distal forearm.
Fig. 31.20 Arteriovenous malformation with arteriovenous fistuli of thumb.
Fig. 31.21 Parkes Weber syndrome: teenager with type C arteriovenous
malformation, and his parents wanted to save the hand.
Fig. 31.22 High-flow PTEN lesion of the forearm.
Fig. 31.23 Right and left hands in a patient with CLOVES syndrome. These
pictures and radiographs demonstrate the prototypical CLOVES hands.
Table 31.2 Diagnostic work-up of vascular anomalies.
Table 31.7 Variations of venous malformations.
Table 31.8 Combined and fast-flow malformations.
Treatment/surgical technique
Sclerotherapy, cryotherapy, and steroid injections have not
been effective in treating this lesion. Pain may be relieved
temporarily, but usually recurs. Surgical therapy is the only
measure that provides long-lasting pain relief and improve­
ment of contractures. Unfortunately, it usually involves resec­
tion of the involved muscle tissue – which can cause loss of
function. In smaller lesions, functional compromise is less
likely. In larger lesions of the forearm (e.g., those that involve
most of the flexor/pronator mass) we have relied on local
tendon and free muscle (gracilis) transfers to replace diseased
muscle. The excision procedure is done in one procedure and
the free tissue transfer several days later (Fig. 31.24).
Future directions
Since the last publication of this chapter, several exciting
breakthroughs have been made in the molecular and clinical
understanding of these lesions. These have been referenced
liberally throughout the chapter and include discovery of
somatic mutation in PIK3CA12 and the mTOR11,39 pathway as
responsible for several overgrowth disorders, delineation of
the fibro-adipose vascular anomaly that mainly affects the
extremity (FAVA),24 and further understanding in the molecu­
lar basis of other vascular anomalies.81 There has been increas­
ing use of mTOR inhibitors (rapamycin) to treat difficult, large
malformations and early results have been promising with a
tolerable adverse-effect profile. Nevertheless, there has been
variability in response, and additional work is needed to
better understand these lesions and reasons why some
respond better than others. More basic science breakthroughs
are inevitable and they promise better understanding and
improved patient outcomes.

713.e1
References
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malformations. The classification is based on histologic differences in the
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2. Upton J, Taghinia A. Special considerations in vascular anomalies:
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SECTION V • Paralytic Disorders
32 
Peripheral nerve injuries of the
upper extremity
Simon Farnebo, Johan Thorfinn, and Lars B. Dahlin
SYNOPSIS
■ Nerve regeneration after injury is orchestrated by delicate processes in
neurons, non-neural cells, and other cells at various levels from the
periphery to the central nervous system.
■ The clinical effects of a nerve injury include not only impaired sensory
and motor function, but also symptoms such as impaired dexterity,
sensitivity to cold, and pain. Therefore, they have a severe impact on
activities of daily living.
■ Correct diagnosis and classification of the injury are crucial for
appropriate treatment.
■ The surgical approach and technique, as well as timing of surgery, are
factors of importance for outcome.
■ The type of injury, condition of the wound, and the vascularity of the
wound bed are key factors influencing surgical decision-making.
■ Various techniques for nerve repair are described, including epineurial,
fascicular, and end-to-side repair, and techniques for nerve
reconstruction.
■ Factors of importance for outcome, such as age, delay before repair,
and level of injury are discussed, as are means of evaluation after
surgery.
Introduction
A nerve injury may have a profound impact on the patient’s
activities of daily living, with subsequent effects on profes­
sional life and leisure time.1 Patients may have to change
profession, or be left with a permanently impaired ability to
work. Nerve injuries may, therefore, generate not only costs
for society within the healthcare system for treatment and
rehabilitation, but also outside the healthcare system resulting
from lost production.2 Nerve injuries most commonly affect
the upper extremity. The incidence of injuries to the hand has
been calculated as 7–37/1000 inhabitants/year in Europe.3
Similar data are available for children (incidence 2.7/1000
children/year). Most hand injuries are minor, but injuries to
the nerves (accounting for about 3% of hand injuries) usually
impair hand function.3,4 Few reports exist about the specific
incidence of nerve injuries, but the incidence has been reported
to be 13.9/100 000 person/year.5 Most of the injuries to the
hand (10%) and the wrist (63%) required less than a week in
hospital. However, few inpatient and outpatient data have
been reported. The incidence of a digital nerve injury is esti­
mated to 6.2/100 000 inhabitants/year. The general pattern of
distribution of both hand and nerve injuries between the sexes
is that it is usually young (median age 29 years) men (up to
75%) who are injured. The incidence of a radial nerve injury
associated with a fracture of the shaft of the humerus is
around 0.12/10 000 inhabitants and year.6 Based on these
reports one may estimate that 70 000 and 29 000 patients in the
European Community and in the US, respectively, injure a
nerve trunk annually.
The costs of treatment and rehabilitation, including those
for loss of production, after a nerve injury, may be substantial.
The costs for injuries to a median and an ulnar nerve are
roughly 70 000 USD and 45 000 USD, respectively 2; 87% of
these costs are the result of lost production. Costs are higher
for patients with coexisting tendon injuries (≥ 4 tendons). In
addition, costs within the healthcare sector are higher for
patients who had to change jobs after the injury and in patients
in whom both the median and the ulnar nerves were injured.
Up to 69% of patients with an ulnar or median nerve injury
are back in full-time work by 1 year after the nerve injury.2,7,8
Age is one important factor for outcome after nerve repair,2,9
which is probably based on better cerebral adaptation to the
injury, particularly in young children. The clinical effects of a
nerve injury include not only subjective impaired sensory and
motor functions, but also subjective complaints, such as
impaired dexterity, cold sensitivity, and pain10; thus, it can
have a severe impact on activities of daily living. Altogether,
nerve injuries can cause considerable problems for individual
patients and costs for society. In the present chapter, the
principles for repair and reconstruction of nerve injuries are
outlined, with emphasis on the fact that such injuries should
be treated promptly.
  Access video content for this chapter online at expertconsult.com

715
Basic science and natural history
together with the medial cutaneous nerves to the arm (bra­
chial) and forearm (antebrachial). The radial and axillary
nerves originate from the posterior cord. There is a segmental
pattern of sensory and motor innervation (Fig. 32.2).
The anatomy of the plexus and the nerve trunks may vary
considerably from person to person. Variations are seen in the
forearm, where a “Martin Gruber” anastomosis may be found
in as many as 15%, particularly between the anterior interos­
seous nerve and the ulnar nerve. A similar anastomosis may
also be present more distally – Riche–Cannieu (branch
between the motor branch of the ulnar nerve and the thenar
branch of the median nerve in the thenar region in the hand:
Fig. 32.3).
The neuron and supporting cells
The cell bodies of the motor and sensory neurons are located
in the spinal cord and in the dorsal root ganglia, respectively,
with their axons extending out to their respective targets in
the periphery. The sensory neuron is pseudo-unipolar, with
one branch of the axon extending into the posterior part of
the spinal cord. The transition from the central to the periph­
eral nervous system takes place in the rootlets (or less often,
in roots of the nerves) of the transitional zone, which are
almost cone-shaped.11 In the central part, the neurons are
surrounded by oligodendrocytes and astrocyte processes,
whereas in the peripheral nervous system axons are closely
associated with Schwann cells. In myelinated nerve fibers,
each axon is embraced by a series of continuous Schwann cells
that create the myelin sheath. The border between individual
and enwrapping Schwann cells is called the node of Ranvier
(Fig. 32.4). Each nerve fiber is enclosed in a basal lamina (or
basement membrane). In contrast, several thinner axons run
in troughs in one Schwann cell – non-myelinated nerve fibers.
Each Schwann cell therefore embraces several axons. The
diameter of nerve fibers varies, and extends from 0.4 to
1.25 µm (non-myelinated) and from 2 to 22 µm (myelinated).12
The number of nerve fibers also varies with nerve trunks. In
addition, the number of nerve fibers decreases with age: as
many as 26% of the nerve fibers may disappear between the
second and eighth decades.
The nerve trunk
A number of nerve fibers are enclosed in bundles around
which there are flattened supporting cells and layers of col­
lagen that form the perineurium. These bundles of fibers
surrounded by the perineurium are called fascicles, which are
embedded in loose connective tissue (called epineurium); this
is composed of collagen fibers and fibroblasts (Figs. 32.4 &
32.5). The space inside the fascicles is called the endoneurial
space, in which the pressure is slightly positive (endoneurial
fluid pressure); it consists of collagen fibrils, and cells such as
fibroblasts and occasional macrophages and mast cells. Lym­
phocytes (CD4+ and CD8+) and macrophages are not gener­
ally found in the endoneurium (except after injury), but may
be present in the epineurium. The amount of connective tissue
varies among nerve trunks, and also within the same nerve
trunk. More abundant connective tissue is therefore located
in the nerve trunk at sites where extra protection is needed
(such as joints and superficial nerve trunks). The term “meso­
neurium” refers to the additional loose areolar tissue that is
Basic science and natural history
Anatomy
Gross anatomy: the upper extremity
The brain and the spinal cord (central nervous system) are
connected to targets by the peripheral nervous system, which
consists of cranial nerves, spinal nerves with roots and rami,
and peripheral nerve trunks with the peripheral components
of the autonomic nervous system. The anterior and posterior
nerve roots (that emerge from rootlets attached to the spinal
cord) merge into the spinal nerve, where the anterior primary
rami form the brachial plexus in the upper extremity (Fig.
32.1). The posterior primary ramus runs posteriorly, and sup­
plies the muscle and skin of the posterior part of the neck and
trunk; it does not enter the extremity. The anterior primary
rami of the cervical nerve roots C5–8 and the ramus of T1 form
the brachial plexus, from which the upper extremity receives
its innervation through various branches.
C5–6 roots form the upper trunk of the brachial plexus, C7
forms the middle trunk, and C8–T1 form the inferior trunks.
These trunks divide into anterior and posterior divisions in
which the lateral and medial cords are formed from the
anterior division, while the posterior divisions form the pos­
terior cord, which mainly innervates the extensor muscles in
the upper extremity. In contrast, the lateral and medial cords
innervate the flexor muscles in the extremity. The musculocu­
taneous nerve originates from the lateral cord. The median
nerve is formed by the joining of the lateral and medial cords,
whereas the ulnar nerve branches from the medial cord
Fig. 32.1  The anterior and posterior nerve roots, which emerge from rootlets
attached to the spinal cord.
Spinal cord
Dorsal root ganglion
Posterior primary
ramus
Anterior primary
ramus
Pia mater
Dura
Dura mater
Arachnoid
Spinal
nerve
Dorsal root
ganglion

716
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
intraneural blood supply, it is possible to mobilize a nerve
over an extended length without disturbing the blood supply.
In addition, the blood vessels adjacent to the nerve trunks
have a coiled appearance that allows excursion of the nerve
trunk. In addition to the vasa nervorum, there are also nervi
nervorum, such as free nerve endings in the epineurium,
perineurium, and endoneurium.
Physiology
To allow for propagation of the action potential, ions are
exchanged between the axon and the extracellular space at the
nodes of Ranvier (see Fig. 32.4). As this exchange occurs only
at the nodes of Ranvier in myelinated nerve fibers, the con­
duction velocity jumps from node to node. In myelinated
nerve fibers this saltatory conduction induces high conduc­
tion velocity. In contrast, the propagation of impulses is more
continuous in non-myelinated nerve fibers. After a nerve
has been injured, the process of Wallerian degeneration (see
located superficially to the epineurium. This tissue allows for
the gliding of the nerve trunk (excursion) during movements
of the extremity.
There is topographical segregation of fascicles and nerve
fibers in the nerve trunks, particularly in their peripheral
parts.13,14 The latter anatomical feature permits dissection of a
bundle of fascicles that can be used in nerve transfers.
Blood supply
Nerve trunks receive their blood supply from segmental
blood vessels (Fig. 32.6), which branch into plexuses in the
epineurium, perineurium, and in the endoneurial space. The
blood vessels inside the fascicles consist mainly of capillaries,
which are provided by circulation through blood vessels that
pierce the perineurium obliquely. The epineurial blood vessels
are more susceptible to trauma than the endoneurial vessels
and so epineurial edema develops more easily than endoneu­
rial edema. Because of the extensive reserve capacity of the
Fig. 32.2  The origin of the nerves of the brachial plexus (C5–Th1, top), and their target muscles.
Serratus anterior
Pronator
teres
Biceps
and
brachialis
Deltoid
Shoulder
rotators
Brachio-
radialis
Supinator
Palmaris longus
Flexor carpi radialis
Extensor
carpi
radialis
longus
Triceps
Abductor pollicis longus
Extensor pollicis brevis
Extensor pollicis longus
Extensor digitorum
Extensor carpi ulnaris
Flexor carpi ulnaris
Latissimus dorsi
Pectoralis major
Extensor
carpi
radialis
brevis
Extensor
indicis,
Extensor
digiti minimi
Flexor digitorum superficialis
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
Adductor pollicis
Flexor pollicis longus
Flexor digitorum profundus
(index and long finger)
Flexor digitorum profundus
(ring and little finger)
Hypothenar
Interosseus
C6
C5
C7
TH1
C8
N. ulnaris
N. medianus
N. radialis
N. thoracicus longus
N. thoracodorsalis
Nn pectoralis med and lat
N. suprascapularis
N. musculocutaneous
N. axillaris

717
Basic science and natural history
below) takes some time in humans, which explains why it is
possible to record propagation of an impulse in an injured
nerve by electrical stimulation at neurography for many days
after the injury. It is generally agreed, therefore, that neurog­
raphy should be done no earlier than 3–4 weeks after the
injury if signs of degeneration are to be found.
The cytoskeleton of the axon contains neurofilaments and
centrally located microtubules. Essential molecules are trans­
ported along the microtubules both from the cell body down
to the periphery (anterograde) and from the periphery up to
the cell body (retrograde) with energy-dependent axonal
transport. This transport has several functions, such as recy­
cling of materials that are not used in the periphery, provision
of membrane constituents, neurotransmitters, and necessary
cytoskeletal components to the axon. Transfer of important
molecules is essential for survival and signaling, both in the
normal state and after nerve injury. After cellular injury, these
signals are rapidly initiated from the environment by transla­
tion into intracellular messengers or commenced in the axon
at the site of injury. These changes involve profound altera­
tions in transcription, translation, and post-translational pro­
cesses in the cells after the injury.
Degeneration and regeneration
After a nerve injury, deep and intense processes are initiated
in the injured neurons and their axons and in the non-neuronal
cells, particularly the Schwann cells. In the cells a number of
temporary and spatially orchestrated mechanisms guide
survival and regeneration. In addition, there are mechanisms
that lead to apoptosis of the cells. The signal transduction
processes are not clarified, and this is a target of intense
research. After the peripheral nerve trunk has been injured by
transection or avulsion, the proximal part of the axon is
resealed to form a new surface on the tip of the axon – a
process that is influenced by the presence of calcium. There is
usually a slight retraction of the proximal axon, which is
related to the number of injured Schwann cells. At the tip of
the axon, signals are formed in the signal transduction pro­
cesses and transferred to the nucleus of the neuron where the
functions are changed from maintenance to survival and
growth.
The distal nerve segment
Schwann cells are extremely important for the function of the
peripheral nerve, both in the normal state and after injury.
After injury, there is disintegration of the axons and the myelin
sheath in the distal nerve segment, the latter released by
Schwann cells. It is important to remove myelin and
Fig. 32.3  An anatomical preparation of the Riche–Cannieu anastomosis in the
palm. This highly variable, although common, anastomosis between the median
nerve motor branch and the deep ulnar nerve provides a potential pathway for
enormous variation in intrinsic muscle innervation.
Fig. 32.4  Close-up of myelinated axon and the node of Ranvier.
Endoneurium
Basal lamina
Node of Ranvier
Axon
Schwann cell nuclei
Myelin sheath
Fig. 32.5  Schematic presentation of a peripheral nerve. Colors for identical
structures are the same as in Fig. 32.4.
Epineurium
Fascicle group
Perineurium
Endoneurium
Basal lamina
Fascicle
Myelin sheath
Schwann cell
Axon
Fig. 32.6  Principal blood supply of nerve segment, highlighted in red.

718
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
three groups of increasing severity (neuropraxia, axonotmesis,
and neurotmesis). This classification was modified by Sunder­
land21 and by Mackinnon22 to include six degrees of injury. In
Table 32.1 we summarize the differences between the three
classifications, and the specific neural changes are illustrated
in Fig. 32.9.
Neuropraxia
First-degree injury
In neuropraxia there is a physiological block of conduction,
but no disruption of the neural architecture at the site of
injury, and there are no degenerative changes within the
nerve. The pathogenesis is most often external compression,
surgical traction, or local ischemia. Complete recovery is the
general rule, and the healing time can vary from a few days
to 3–4 months. Tinel’s sign is not present over the site of injury.
Axonotmesis
Second-degree injury
In second-degree injuries, true degeneration of axons is initi­
ated. Axonal damage leads to distal (Wallerian) degeneration,
although the basal lamina of the Schwann cells remains intact.
The axons regenerate through their own endoneurial tubes
by axonal contact and guidance of the regenerating growth
cones at a rate of 1–3 mm/day. No topographical mismatch
will occur, and the integrity of sensory and motor nerve fibers
remains intact. Tinel’s sign is present, and the progress of
recovery can by followed by the gradual recovery of motor
the disintegrated axon to allow and prepare a conducive
environment for the regenerating axons. Both macrophages
and Schwann cells can therefore contribute to the cleaning up
mechanisms, where their relevance varies over time.
The timing of nerve repair is of crucial importance for a
successful outgrowth of axons after injury,15,16 which can be
related to a large number of factors that are up- and down­
regulated by Schwann cells after nerve injury. After the
Schwann cells have been activated, they proliferate along the
inside of their basal lamina, and form the bands of Büngner.
Neurotrophic factors and their receptors are upregulated
in Schwann cells after injury, and these may include neuro­
trophins (such as nerve growth factor and brain-derived
neurotrophic factor), fibroblast growth factors (such as
β-fibroblast growth factor), neuropoietic cytokines (such as
ciliary neurotrophic factor and leukemia-inhibitory factor),
and other groups of factors, such as insulin-like growth factor,
transforming growth factor, and interleukins.
Apoptosis (programmed death) of various cells, such as
macrophages and Schwann cells, an event that is initiated by
release of pro-apoptotic molecules from the mitochondria
(intrinsic pathway), can be activated through the death cell
surface receptors (extrinsic pathway; like Fas and tumor
necrosis factor receptor 1). The number of apoptotic Schwann
cells in the distal nerve segment is increased if the transected
nerve is repaired after a delay.17
All these changes in the injured neuron and its axon and
in the Schwann cells have the common goal of regrowth of
the axons into the distal nerve segments down to their targets.
Regrowth is a delicate process in which numerous sprouts
emerge from the distal part of each axon. On the tip of each
sprout there is a growth cone, which is formed as a small hand
on which the “finger-like” filopodia palpate the environment
with the purpose of finding guidance structures (Fig. 32.7).
Intricate mechanisms direct rate and direction of extension of
the growth cones, where actin filaments are polymerized and
organized.18,19 Microtubules are polymerized in the growth
cones. The growth is a dynamic process, where the filopodia/
growth cone is repulsed or attracted depending on the local
mechanisms and the structure of the environment.
The extracellular matrix is extremely important for the
outgrowth and advancement of the growth cone. Proteins,
such as laminin, fibronectin, galactins, tenascin, and collagens,
stimulate outgrowth. Laminin exerts its stimulatory effect
through cell surface glycoproteins called integrins, which
interact with the intracellular actin in the growth cone and in
the filopodia, thus navigating outgrowth of the axon. Precise
knowledge about how axons grow and how growth is directed
is still limited.
Diagnosis and presentation
Formal classification of injury
Nerve injuries can be divided into two main groups: those
that will temporarily block nerve conduction without loss of
axonal architecture, and those with severe damage that will
result in axonal degeneration distal to the injury (Fig. 32.8).
This may be one useful clinical way of approaching nerve
injuries, but more formal classifications have been presented
to describe the complexity of the lesions further, in particular
the Seddon classification,20 in which injuries were divided into
Fig. 32.7  As the nerve is severed (A), activated macrophages and Schwann cells
will immediately start the removal of myelin and remnants of the disintegrated axon,
to allow for a conducive environment for the regenerating axons (B). Within just a
few hours numerous sprouts emerge from the distal part of each axon and form the
sprout growth cone that will guide the regeneration process distally (C), until nerve
regeneration is complete (D).
Sprouts with growth cones
Transection
Macrophages
activated
A
B
C
D

719
Diagnosis and presentation
Table 32.1  Comparison between the Seddon, Sunderland, and MacKinnon classifications of nerve injury
Seddon
Sunderland
MacKinnon
Description
Neuropraxia
1
Local physiologic block with paralysis but no anatomic disturbance of the nerve. Full
recovery is expected
Axonotmesis
2
Nerve injury with degeneration of the distal segment. Intact endoneurium and perineurium.
Full recovery occurs at rate of 1.5 mm/day
3
Endoneurial damage with subsequent scarring and incomplete regeneration. Variable
recovery
Neurotmesis
4
Nerve damaged with complete internal structural disorganization. Nerve trunk remains
intact. No functional recovery unless operative intervention
5
Nerve trunk cut completely. Early operative intervention necessary for restoration of some
function
6
Mixed nerve injury
Fig. 32.9  Schematic of damaged structures within an axon
according to the classification of Sunderland grades 1–5.
Change in color (red) and pattern indicates damage to
each structure. Yellow represents an axon and its neuron.
Normal
Myelin sheath
Endoneurium
Perineurium
Epineurium
1
2
3
4
5
Fig. 32.8  Schematic flowchart of neuronal response to nerve compression and interruption of axonal continuity.
Inhibition of
axonal transport
Retrograde Anterograde
Metabolic
Signal block
Structural
Myelin damage
Compression
Incomplete
Complete
Neurapraxia
Sunderland I
Axonotmesis
Sunderland II-III
Neurotmesis
Sunderland IV-V
Decreased intraneural
microcirculation
Compartment
syndrome
Increased
intraneural
pressure
Ischemia
Surgery
Conservative treatment
Interruption of axonal continuity
or sensory function distal to the injury. Full recovery is
expected.
Third-degree injury
In a third-degree injury, the architecture within the perineu­
rium is disrupted together with axonal damage. The fascicles
remain intact, although progression of axonal regrowth will
be with less precision as the axonal guidance is impaired and
mismatch of fibers will occur. Axonal mismatch follows to a
larger extent in proximally based injuries as the fascicular
organization is usually of mixed motor and sensory patterns.
The clinical outcome is hard to predict, mainly because of
subsequent intrafascicular scarring and the failure of some

720
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
dysfunctional nerve and a wound overlying the course of a
nerve is regarded as having a transected nerve until proved
otherwise (Fig. 32.10).
Functional evaluation
Motor and sensory function should be carefully examined
and documented in all patients with injured extremities.
Motor evaluation should include pinch and grip strength, and
assessment of weakness and atrophy of individual muscles.
Sensory function should be evaluated with the patient unable
to see what the examiner is doing. Acutely, it may be easy to
assess the patient’s ability to feel pain, such as that applied by
forceps, in the innervation area of an individual nerve such
as a digital nerve. Assessment of two-point discrimination
and the patient’s ability to separate sharp and blunt objects
for testing of protective sensation can also be used. Loss of
sympathetic function, with vasomotor and sudomotor paraly­
sis, gives the loss of ability to produce sweat in the innervated
segment of skin, which will look red, dry, and “polished.”
Tinel’s sign is present, and continuous severe pain over the
region of injury usually indicates a more severe injury.
Electromyography/neurography
In case of confusing diagnostic signs, electrophysiological
studies can help to establish the diagnosis and to identify
injured nerve branches, although the results must be inter­
preted with caution during the first 3–4 weeks. It may take up
to 4 or even 6 weeks after the injury before signs of nerve
degeneration and muscular denervation can be detected.23 It
is stressed that waiting for an electrophysiological examina­
tion should not delay exploration of an injured nerve if indica­
tion for surgery is strong.
Intraoperative conduction studies can be of help, particu­
larly in the case of a previously closed injury that has failed
to show satisfactory recovery at follow-up. Intraoperative
examination enables a higher grade of specificity as the
observed nerve or even individual nerve fascicles can be
anatomically isolated, and action potentials across the scarred
area can be evaluated.24 If electrical recovery is recorded over
the area of interest, the patient can be classified as Sunderland
grade II or III, in which case spontaneous full recovery is
expected. If no electrical recovery can be seen, the patient
should be graded Sunderland grade IV or V and will most
likely benefit from nerve resection and grafting. However, in
the case of a neuroma in continuity (sixth-degree injury), the
picture is more complex. Some fascicles will need resection
and grafting, whereas others are actually grade II–III and will
recover spontaneously. In these cases, postoperative outcome
may be uncertain and the decision to operate is hard as inter­
vention may result in a tedious and potentially damaging
dissection with internal and external neurolysis and resection
of damaged sections. However, it may sometimes be possible
to distinguish injured fascicles that require nerve grafting
from intact healthy fascicles intraoperatively. Intraoperative
electrophysiology is therefore warranted and extremely
helpful in decision-making during the procedure.
Wound inspection
Peripheral nerve transections rarely occur in isolation.
Depending on the extent of the injury, surrounding structures
axons to regenerate. Tinel’s sign is present and progresses
distally with recovery. Microsurgical resection and grafting
may not be beneficial in these cases.
Neurotmesis
Fourth-degree injury
In a fourth-degree lesion, the epineurium is intact, but all
other parts of the nerve are damaged. The formation of an
intraneural scar impairs both axonal regeneration and rein­
nervation, and typically forms a neuroma at the site of injury.
A more profound retrograde neuronal effect than in a third-
degree injury is expected, and this causes a higher incidence
of neuronal death. Tinel’s sign is usually present over the site
of the injury, but there are no signs of recovery, or proximal-
to-distal progression of regeneration. The injury requires
complete excision of the neuroma and microsurgical nerve
repair, usually with nerve grafting.
Fifth-degree injury
In a fifth-degree injury, the nerve is completely transected.
Recovery of function is dependent on surgical repair, with or
without nerve grafting. These injuries are most commonly
associated with injuries that include the surrounding struc­
tures, such as tendons, muscles, bones, or blood vessels.
Sixth-degree injury
The sixth-degree injury was added by Mackinnon to take
account of mixed injuries,22 for example those that occur after
closed traction damage to a nerve, or gunshot or stab wounds
that cause partial injuries to a nerve. This type of injury is
often referred to as a neuroma in continuity, in which all
degrees of nerve injury, from normal to neurotmesis, may
coexist within the scarred nerve. A neuroma in continuity
typically results from failure of the regenerating nerve growth
cone to proceed beyond the injury to reach its peripheral
targets. It occurs within an intact nerve with continuity in
response to internally damaged axons and fascicles, resulting
in a distal portion of the nerve that no longer, more or less,
functions properly. Surgical exposure is often necessary and
intraoperative electrodiagnostic studies can help to distin­
guish fascicles with signs of recovery from those without
(grades IV and V).
Clinical examination
A correct diagnosis is crucial. Confirmation of a nerve injury
is usually not hard, even though every nerve injury is unique
in its character and highly variable in its symptoms. Lack
of active movement, such as against resistance, because of
paralysis of the muscles supplied by the nerve, can be seen
immediately after the injury if the nerve is completely tran­
sected. However, when motor defects are minor or overshad­
owed by more striking sensory deficits, the diagnosis can
sometimes be overseen, particularly in an incoherent patient.
The patient’s history and understanding of the mechanism
of the injury are therefore important for the evaluation of
the injury and identification of those that will be improved
by operation. It is important that every patient with a

721
Clinical examination
Sharply transected nerves are easier to manage than
crushed or avulsed ones. In a sharp transection, the zone of
injury is limited, and the nerve can usually be prepared and
repaired at the primary operation. If, however, the nerve is
seriously crushed or longitudinally avulsed, the zone of injury
is harder to establish and delayed excision of the damaged
nerve followed by repair may improve outcome.
may be crushed, lacerated, avulsed, or otherwise damaged.
Extensive tissue damage and an unclear zone of injury
together with a contaminated wound are factors that influ­
ence management and may result in delayed neural repair.
Extensive debridement and cleaning of the wound are essen­
tial for a satisfactory final outcome, and to decrease the risk
of a complicating infection and subsequent scarring.
Fig. 32.10  Algorithm for open and closed nerve injuries. Flowchart showing timing of surgical exposure and nerve repair.
>3cm
<3cm
Tidy wound
Nerve in continuity
End-to-end coaptation
Nerve graft
Tubular graft or nerve graft
Open injury
Closed injury
Sunderland class I
Recovery
Recovery
Partial recovery
No recovery
No recovery
No recovery
No recovery
Clinical examination
Neurological examination
Neurological examination
Neurological examination
Irreversible denervation of target organs
Sunderland class I or II
Continued observation
Repeated neurophysiology
can be considered
Surgical exploration
Surgical exploration
Clinically unacceptable outcome
Sunderland class I or II
Secondary repair
Secondary repair
Surgical exploration
End-to-end coaptation
Nerve graft
Nerve defect
Sunderland class V
Clear cut
Sunderland class V
Untidy wound
-unclear zone of injury
-wound contamination
>1 week
4-6 weeks
3 months
4 months
12 months

722
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
call for careful debridement before any nerve repair is tried.
In addition, when the patient presents with signs of an incom­
plete injury for which there is a chance that spontaneous
recovery can yield a better outcome than immediate repair,
reconstruction is preferred at a later stage only if the clinical
results of conservative treatment are not satisfactory. There­
fore, one of the most challenging aspects of a nerve injury will
be the decision-making regarding timing of nerve exploration
and reconstruction in complex cases such as open crush
injuries or gunshot wounds. In these cases, the primary goal
should always be to go for careful debridement and viable
tissue coverage. Nerve reconstruction can thus only be con­
sidered when the surrounding tissue provides a viable envi­
ronment for the nerve (see condition of the wound, below).
In case of an open injury, where the patient presents with a
sensory and/or motor function deficit, but with a macroscopi­
cally intact nerve upon surgical exposure, a close follow-up is
essential for assessment of the nerve function. Such cases,
which include open wound crush injuries and gunshot
wounds, should, as the surrounding tissue envelope has
healed, be treated the same way as closed traction injuries
(Table 32.2). Neurological examination is performed regularly,
sometimes together with recurrently performed neurophysi­
ological testing, and surgery is usually performed if no signs
of regeneration or reinnervation occur (e.g., for some injuries,
exploration after 3 or 4 months). It is, however, important to
stress that all open wounds, where the patient presents with
a sensory or motor loss, should be explored in the acute
setting, in order to obtain the best outcome.
Condition of the wound
The state of the wound is important. A clean wound calls for
an early repair, whereas an untidy wound needs careful
debridement to remove non-viable tissue before any nerve
reconstruction is undertaken. In severe cases, there may be a
need for multiple debridements. In these cases, the nerve
repair is better planned as a secondary reconstruction that can
be done when other structures have healed with better chances
of satisfactory soft-tissue coverage of the reconstructed nerve.
Such a reconstruction is preferable within 3 weeks. At the time
of re-exploration, the zone of injury is likely to be better
defined, and scar tissue can more easily be extracted.
Ideally the repaired nerve should be surrounded by a well-
nourished soft-tissue bed, muscle, or fat. In severe cases, this
implies that the damaged soft tissues surrounding the injured
nerve need to be replaced by a soft-tissue transfer to reconsti­
tute a gliding surface either before secondary reconstruction
or in connection with the primary reconstruction.
Patient selection
All patients with a suspected nerve injury should be judged
individually as a number of factors must be considered before
the decision to explore is made (see Fig. 32.10). When one is
considering sharp lacerations, traction injuries, blast injuries,
or a combination, some key factors must be considered that
will be of decisive importance in the timing of operation and
the approach, including the type of injury and condition of
the wound, and the vascularity of the wound bed.25,26
Type of nerve injury
In cases where there are clinical signs of nerve injury, but there
is no wound, the treatment should be conservative for the first
4–6 weeks, when clinical signs of recovery of function can be
investigated. If at this point there has still not been a complete
spontaneous recovery, electrophysiological examination can
be done. This may be repeated if there is only partial, but
insufficient, recovery before any operation is considered. In
case of a closed injury where no recovery has been seen at all
after 3 months, clinical and electrophysiological examination
should be considered.27 If there are no signs of spontaneous
recovery during this period, exploration of the injured nerve
is indicated. However, if there is partial recovery during the
first 3 months, regular re-evaluation may be indicated for up
to another 3 months.28 The important point is to see if any
recovery at all is present.
Nerve injuries with open wounds should always be
explored. If the nerve is in continuity, it should be treated as
a closed injury, and the clinical and electrophysiological func­
tion should be evaluated for up to 3 months. In contrast, a
clear-cut injury with the nerve ends closely approximated is
suitable for immediate repair, whereas a crush injury usually
is not. In the latter case, there might be difficulties in distin­
guishing between viable and non-viable tissue, which would
Table 32.2  Differing treatments for different types of nerve injury
Type of nerve injury
Neurography/EMG
Exploration
Revision
Repair or reconstruction
Sharp transection
–
Immediate
Immediate
Immediate
Open wound – nerve crush injury
4–6 weeks§
Immediate
Immediate
Immediate*
Delayed†
Closed traction injury
4–6 weeks
Delayed
–
3–4 months‡
Open wound – gunshot wound
4–6 weeks§
Immediate
Immediate
Immediate*
Delayed†
*If there is macroscopic nerve discontinuity on exploration, repair or reconstruction should be performed after repeated revision to ensure that the wound is tidy.
†If there is nerve continuity on exploration, the nerve injury should be treated as a closed injury so that repair or reconstruction is performed only when there is no sign of
nerve regeneration (Tinel’s sign), e.g., for some injuries, exploration after 3–4 months.
‡Repair or reconstruction is performed after 3–4 months if there are no clinical signs of nerve regeneration or reinnervation.
§If the nerve is in continuity on exploration, neurography/EMG can be performed in the same manner as for closed injuries.
EMG, electromyogram.

723
Treatment and surgical techniques
can be done several months later, but the regenerative response
of neurons and particularly of Schwann cells decreases over
time (see sections on physiology, above, and autografts,
below).38
Treatment and surgical techniques
Immediate compared with delayed
nerve repair
General principles
Any nerve injury may be repaired immediately, or after a
certain delay. If the conditions are favorable, immediate
primary suture is the method of choice, resulting in the most
favorable outcome,29 as based on the neurobiological tempo­
rally diverse events outlined above. One of the most important
prerequisites for primary repair is that it must be completed
with little or no tension,30–32 otherwise a nerve graft should be
considered.33 Several authors have argued that more than 80%
of all nerve lesions can be sutured immediately with a primary
end-to-end coaptation.34,35 In these studies, it had to be pos­
sible to coapt the nerve endings with a single 9-0 nylon suture,
without either separating the endings from each other or
tearing the epineurium, to qualify for a primary end-to-end
suture.
Primary immediate repair is technically easier than delayed
repair, as approximation by rotation of the distal and proximal
ends is more obvious when the epineurial vessels are present
and clearly visible.36 The elastic recoil of nerve endings that
inevitably occurs as the nerve is injured is also easier to
overcome in the acute phase. As time passes, the nerve endings
will become embedded in fibrous scar tissue and end-to-end
coaptation will be more difficult without tension or more
extensive mobilization.
Clinical tips
• Ensure optimal condition of the wound bed.
• Careful debridement of injured and lacerated tissue is
imperative.
• If the zone of injury of the nerve is unclear, go for
secondary nerve reconstruction.
Clinical tips
• Open wounds should always be explored as soon as
possible if a nerve injury is suspected.
• Delay in nerve repair or reconstruction causes impaired
functional outcome.
• If the nerve is in continuity, it should be treated as a closed
injury.
Timing
Immediate repair is preferable within the first 48 h, but some
authors have suggested that it may also be done successfully
during the first 1–3 weeks 37; however, recent experimental
neurobiological data have clearly pointed out the advantage
of early nerve repair. This implies that patients who present
with uncomplicated open nerve injuries that happened more
than 48 h previously benefit from nerve repair that is delayed
in the sense that it is done after the wound has healed com­
pletely. Practically, the implication is that the nerve should be
repaired as soon as possible, preferably within 2–3 weeks of
the injury. The rationale for this approach is to reduce the risk
of iatrogenic infection secondary to operation on a contami­
nated wound. A longer delay will also cause difficulties in
doing primary repair due to scar formation and retraction of
nerve endings, but most importantly, injured parts of the
nerve ends should be resected to obtain viable nerve ends for
optimal coaptation.
A delayed nerve repair, i.e., more than 3 weeks after the
injury, usually requires a nerve graft. Nerve graft procedures
Surgical approach
The incisions follow the general principles of plastic surgery
in that the main objective is to prevent contractures and scars
in areas of maximum sensory perception (Fig. 32.11). Wide
exposure is often recommended to obtain a detailed anatomi­
cal overview, and it offers a safer dissection as the area of
injury can be approached from healthy tissue outside the zone
of injury. This often means that the traumatic wound needs to
be extending proximally and distally, which is particularly
important in secondary reconstructions.
Clinical tips
• Wide exposure and careful dissection to obtain well-
vascularized tissue flap are vital for nerve coverage.
• Approach the nerve injury from viable tissue – thus, “from
the known to the unknown.”
• Use of a tourniquet is always advised.
Fig. 32.11  Small stab wound on the radial side of the index finger. Loss of
sensation distal to the wound calls for exploration. A modified Bruner incision is
used.
Principles of nerve repair
General principles
Proper and thorough microsurgical technical skills are crucial
in nerve repair. An atraumatic approach with minimal tissue
damage, using microsurgical instruments under either loupe
magnification or a microscope, is essential (Video 32.1
).

724
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
retained and the nerve can therefore be approximated with
minimal tension.
Second, the ultimate aim is a tension-free repair to enable
the nerve to heal in optimal conditions. Usually, some dissec­
tion of the nerve trunk is necessary to achieve this. Even a
small elongation through longitudinal traction will have a
potentially devastating effect on the vascular supply to the
nerve endings, with subsequent effects on the viability of the
Schwann cells,29 as stretching of a nerve trunk has been shown
to impair intraneural microcirculation.41 Nerve blood flow
decreases approximately 50%, with substantial recovery in
30 min after 8% elongation, whereas 15% elongation produces
approximately an 80% reduction in blood flow with minimal
recovery.30 Some dissection of the nerve trunks proximal and
distal to the injury is therefore often needed to alleviate
tension, and this can be done without interfering with the
segmentally approaching blood vessels. Other means of alle­
viating tension, such as transposing the ulnar nerve anteriorly
First, the injured nerve ends must be identified. Non-viable
tissue must be resected, preferably with a surgical blade or
using microsurgical scissors, to allow visualization of healthy
fascicles that help the adaptation in primary nerve repair
(Figs. 32.12–32.14 and Video 32.2
). When repairing a nerve
it is preferable to align the nerve according to its fascicular
pattern, which may help topographical arrangement and
improve outcome. If later reconstruction is planned (second­
ary reconstruction), the nerve ends may be tagged with a
non-resorbable suture, and sutured to other structures in the
wound. This is primarily to prevent the retraction of the nerve
that inevitably happens after transection, but also to facilitate
identification at a secondary procedure. If the nerve is allowed
to retract, it will become tethered in fibrous scar tissue and lose
its elasticity and normal excursion. The normal longitudinal
excursion of the nerve needs to be taken into consideration,
as the immediate demand for suitable length will depend
on it. The normal excursion of the median and ulnar nerves
is thought to be around 1.5 cm at the wrist when taking the
wrist from full extension to full flexion.39,40 This length should
preferably be added to the nerve deficit when estimating the
total defect and assessing whether a nerve graft is needed
or not. In a primary repair, the longitudinal extension is
Fig. 32.12  A lacerated nerve and the cut-off line for debridement. The dashed line
illustrates suggested resection line to reach healthy nerve tissue.
Fig. 32.13  Standard epineurial repair with nylon sutures. To get proper fascicular
alignment, nerve endings are aligned based on the pattern of the blood vessels
within the epineurium.
Fig. 32.14  Peripheral nerve repair of a digital nerve using standard epineurial
end-to-end coaptation. (A) Nerve injury with minimal gap. (B) Epineurial suture.
(C) Complete coaptation with minimal tension.
A
B
C

725
Treatment and surgical techniques
nerve endings generally need trimming, which means that
some nerve tissue has to be resected to reach viable parts.
Under the microscope this is seen as “mushrooming” of the
fascicles together with slight retraction of the epineurium
from the neural stumps (Fig. 32.15B). It is hard to give a
general rule for how much tension is acceptable in each
individual case, but if flexion of a joint is necessary to shorten
the distance between the nerve ends, the resulting tension will
usually be too great, and further dissection or nerve grafting
should be considered (Figs. 32.16A & 32.17A).
Third, the nerve endings should be rotated to their correct
positions by matching fascicles, branches, or the longitudinal
and therefore increasing excursion over the elbow, can be
considered to enable a tension-free direct suture. It is, however,
important to bear in mind that mobilization by dissection can
theoretically impair the blood supply to the nerve endings.
This issue has been an issue of debate,42–44 although clinical
experience from ulnar nerve transposition points to the fact
that intraneural microcirculation can resist considerable
mobilization, and that gentle handling of the nerve can be
acceptable.43,44
As complete lesions almost always result in some retraction
of the nerve endings, there is in most instances a gap between
the ends that makes a completely tension-free suture rare. The
Fig. 32.15  Patient with a median nerve injury that is repaired with standard
epineurial end-to-end coaptation at minimal tension. (A) Nerve injury with minimal
gap. (B) Mushrooming seen when healthy nerve tissue is reached after resection.
(C) Complete coaptation with minimal tension.
A
B
C
Fig. 32.16  Patient with a lacerated median nerve that, after resection of the
destroyed part, remains with a nerve deficit (A) that is bridged with multiple cables
of sural nerve grafts (B,C). Note that the individual cables are about 15% longer than
the gap.
A
B
C

726
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
Epineurial compared with fascicular repair
The nerve trunks may be adapted either at the level of the
epineurium (see Fig. 32.12) or the fascicles (Fig. 32.19). Which
method is preferable has been a matter of debate, probably
because the scientific evidence is not entirely clear as the data
are based on experimental studies in rats and primates with
their inherent methodological problems.48,49
The theoretical advantage of the fascicular repair over the
epineurial repair is that it facilitates regeneration with a better
chance of keeping the axonal specificity to sensor or motor
end organs. However, fascicular repair requires a more pro­
found dissection to identify the individual fascicles at the two
ends, which in turn may increase the risk of compromising
the vascular supply. An epineurial repair with careful rotation
of the nerve trunks is therefore thought to be as effective,
particularly more distally. The dissection is technically more
difficult as the individual fascicles are hard to identify clearly
distally. A group fascicular adaptation is preferable, for
example with lesions of the ulnar nerve at the wrist. Great
care should be taken to make sure that sensory and motor
fascicles are located both proximally and distally through
dissection, and coapted separately (Fig. 32.20).
epineurial vessels of the two nerve endings, which decreases
the risk of mismatch between bundles of axons (Figs. 32.15A
& 32.18). Correct coaptation facilitates a good postoperative
outcome.
Nerve endings are commonly coapted with interrupted 9-0
or 10-0 nylon sutures. It is generally thought that a minimal
amount of suture material is preferable, and the number of
sutures should be no greater than the minimum number
required to ensure coaptation of the nerve stumps. It is impor­
tant that the nerve ends are not closed too tightly so that the
fascicles become malaligned and crumple in the process.45
Outward-pointing fascicles are sometimes found, and should
be cut with microscissors. They are then able to retract to
within the coaptation and will subsequently probably be able
to regenerate sufficiently.
Other means, apart from nylon sutures, of maintaining the
primary repair can be considered, particularly if the repair is
to be made by a relatively inexperienced surgeon. The use of
fibrin glue as an alternative, or as an adjunct, to epineurial
sutures has been evaluated in rats after transection of the
sciatic nerve.46,47 The results showed that fibrin glue is as good
as suturing in experienced hands, and superior to sutures
when the surgeon is inexperienced.43,46
Fig. 32.17  (A) Digital nerve laceration. (B) The nerve gap was bridged with a
single autograft from the lateral cutaneous antebrachial nerve.
A
B
Fig. 32.18  End-to-end coaptation. Note that the epineurial vessels match.
Clinical tips
• Proper magnification, appropriate equipment, and
microsurgical skills are crucial.
• Resect non-viable tissue carefully, possibly stepwise, to
visualize healthy nerve endings – look for mushrooming.
• Important for tension-free coaptation – if flexion of joints is
needed, consider nerve reconstruction.
• Aim at fascicular match – look for intraneural vessels to
help with alignment in repair and reconstruction.
Fig. 32.19  Group fascicular repair with nylon sutures. Corresponding groups of
fascicles are sutured through the interfascicular epineurium.
Clinical tips
• Epineurial repair is preferable as long as it is technically
possible.
• Apply a limited number of sutures, maybe with fibrin glue
as an adjunct to sutures.
• Group fascicular repair is a good option when sensory and
motor fascicles are distinct, such as with the ulnar nerve at
the wrist level.

727
Treatment and surgical techniques
Nerve reconstruction
Fig. 32.20  Ulnar nerve injury at the wrist level. Note how the motor and sensory
fascicles are anatomically separated. A group fascicular coaptation is performed.
End-to-side nerve repair
When conventional surgical methods are unavailable, particu­
larly if the proximal stump is absent, or after injuries to nerve
proximally in the extremity (such as in high ulnar nerve
injuries), the distal end of an injured nerve can be attached to
an “uninjured” donor nerve.50,51 Collateral or terminal sprout­
ing of donor nerve axons occurs, and donor site morbidity
associated with the harvest of a nerve graft is avoided. In
addition, the distance traveled by regenerating axons to reach
their targets is shortened. Theoretically this implies that a
single neuron possesses the ability to innervate two targets,
but one of the branches is probably pruned away.51 Several
studies have indicated that the outgrowth of axons from the
donor nerve requires an axonal injury to induce sprouting.52
At present, experimental and clinical experience with end-to-
side coaptation has, at best, achieved mixed results, depend­
ing on the type of reinnervated nerve and donor nerve.53 More
extensive clinical and laboratory experiments are presently
produced, which is required before end-to-side suturing
generally can be included with the more established tech­
niques of nerve repair.54,55 However, for reinnervation of
muscles from motor donor nerves, the end-to-side techniques
have been reported to be useful.56
Wound closure and immobilization
The wound should be closed with interrupted sutures and a
local anesthetic may be given before dressing. It is preferably
given through a blunt cannula inserted between the stitches.
Sharp needles should be avoided to reduce the risk of neuro­
vascular damage proximal to the injury if the site of repair/
reconstruction is located superficially.
A plaster should be applied, primarily to restrict excessive
movement, avoiding tension in the repair, and still allow
some range of movement for controlled early mobilization.
The plaster should position the extremity in such a way that
it both releases tension and prevents excessive movement. For
digital nerve injuries, the wrist is immobilized at 30° of flexion
and the metacarpophalangeal joints at 70°. The splint is
usually extended just past the proximal interphalangeal joints
to prevent hyperextension. Immobilization with plaster of
Paris, with controlled restricted range of movement, is usually
maintained for 3 weeks before full range of movement is
allowed in digital nerve repairs. In repairs of larger nerve
trunks a prolonged protection of the suture line may be rec­
ommended up to 6 weeks postoperatively, to avoid extensive
extension of the wrist or elbow.
Clinical tips
• Always consider a nerve reconstruction to alleviate tension
at the coaptation site when trauma or debridement has left
a nerve deficit or when joint movements are expected.
• Autologous nerve grafts are still considered the gold
standard compared to artificial conduits.
Autografts
Nerve reconstruction involves the use of a nerve graft to
overcome a lack of continuity after an injury (see Figs. 32.16
& 32.17). The use of autologous grafts is still the method of
choice despite the fact that other strategies, such as nerve and
muscle allografts or synthetic materials, have been proposed,
but they demand a more complex approach than a primary
nerve repair to be successful.
The rationale for using a nerve autograft in reconstruction
is to alleviate all tension at the site of suture. If tension is
completely avoided, axonal sprouting to cross the two sites of
repair will be easier than over a primary repair site under
unfavorable conditions.57 The axonal outgrowth through the
nerve graft depends on the diameter of the graft and the
vascularity of the tissue bed. The selection of donor nerve will
therefore be much influenced by size, as survival is dependent
on diffusion from the surrounding tissues. Neovasculariza­
tion will occur through capillary ingrowth from the periphery
and nerve ends.57,58 Smaller nerves (for example, the sural, and
the medial and lateral antebrachial cutaneous nerves) will
therefore revascularize easily, and thicker nerves will carry
the risk of central necrosis and scarring as a result of poor
diffusion. Only one cable is needed when smaller nerves, such
as digital nerves, are bridged (see Fig. 32.17), whereas multiple
cables may be needed to bridge the gap in larger damaged
nerve trunks (see Figs. 32.16 & 32.21).
Approach and preparation
The initial steps in preparing the nerve tissue are no different
from those for primary nerve repair. However, when the ends
are being resected to create a clean-cut surface, it is important
to expose the nerve carefully, including the whole zone of
injury. This enables proper evaluation of the viability and
vascularization of the nerve and surrounding tissues. In crush
or high-velocity injuries, this principle is central. As with all
tissue injuries in which the zone of injury is not clear, late
effects on viability call for second looks and re-evaluations.
When the nerve is explored after the surrounding tissue has
healed, it is important to remove any scar tissue carefully, or
preferably to approach the nerve lesion through a separate
incision. This includes raising a flap that at closure of the
wound will enable good tissue coverage.
Nerve ends
A good way to find out whether the nerve endings are viable
is to look for “mushrooming” (see Fig. 32.15B), which is a sign
of transected viable axons that will be able to sprout after

728
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
length and a few millimeters of extra epineurium is removed
from the ends of the graft.
Coaptation and maintenance
The nerve graft is preferably reversed at the time of placement
to decrease the risk of diversion of regenerating axons through
these cut-off branches. Depending on the size of the nerve
trunk, the whole nerve or individual fascicles can be sutured
using 9-0 or 10-0 nylon, if possible with fibrin glue as an
adjunct. A sufficient number of fascicles are used to bridge the
defect, preferably with one cable for each severed group of
fascicles (see Figs. 32.16C & 32.21). The coaptation should not
be too tight, as this can easily lead to crumpled nerve endings.
Fibrin glue may be interposed to reinforce and lessen the risk
of separation between the graft and nerve endings. Fibrin glue
may also give an instant better match between the graft and
the nerve end. The number of sutures should be kept to one
or two. If multiple cables are used, the individual grafts are
positioned so that they do not adhere too closely to each other.
This is to allow diffusion of oxygen and other nutrients, and
allow for rapid revascularization from the recipient bed. It
must be stressed therefore that the viability of the tissue bed
is of crucial importance for optimal survival of Schwann cells
and successful axonal regeneration.
Donor nerves
Sural nerve
The sural nerve is often thought to be the main donor nerve
for free grafting, because it can easily be harvested in lengths
between 30 and 40 cm61; it originates from the tibial nerve
dorsal to the knee joint (Fig. 32.22), and it has communicating
branches from the peroneal nerve at levels distal to this. These
communicating branches need to be identified and transected
before the nerve is pulled out.
The sural nerve is identified through a short longitudinal
incision halfway between the lateral malleolus and the Achil­
les tendon. If the nerve is gently pulled distally, the proximal
course of the nerve can be palpated and extracted through 3–5
small transverse incisions that usually pose a minor aesthetic
problem for the patient (Fig. 32.23). Alternatively a long dorsal
incision can be used, which enables an easier dissection of the
nerve and its small branches. It is preferable to cut the nerve
beneath the fascia to reduce the risk of a troublesome neuroma.
Nerve strippers can be used and endoscopic harvest has been
suggested to reduce aesthetic morbidity at the donor site.62
The area of diminished or absent sensation after the graft has
been harvested is shown in Fig. 32.24, but is usually consid­
ered to be of minor importance to the patient.60
Medial and lateral antebrachial cutaneous nerves
The medial cutaneous nerve can be harvested from the distal
border of the axillary groove to below the elbow (10–12 cm).
In the forearm it is located medially (8–10 cm), close to the
brachial vein, where it divides into three branches (Fig. 32.25).
These branches correspond well in size to digital nerves. The
consequences are usually of minor importance to the patient
(Fig. 32.26).
The lateral cutaneous nerve (10–12 cm) is the terminal
branch of the musculocutaneous nerve. It is identified at the
reconstruction from the resection site, indicating that the
nerve is a suitable recipient for a nerve graft.
The gap
To harvest a proper graft it is essential to calculate the
maximum gap that is going to be bridged, and this has to be
done in relation to any movement of a joint that might occur
later on.
Length of graft
Because the graft may shrink slightly, it should be about 15%
longer than the maximum gap.59 Nerve excursion must be
considered, and length is best assessed with all adjacent joints
fully extended (or in certain cases, such as radial nerve injury
at upper arm, in a flexed position).
Harvest of the graft
The size of the nerve trunk to be bridged is the main factor to
be considered when deciding which donor nerve will be most
suitable to use as a graft. Donor site morbidity and functional
deficit also have to be considered when choosing the proper
donor nerve (Table 32.3).60 Patients should be well informed
about these aspects before the harvest. The most common
grafts are the sural nerve, the medial antebrachial cutaneous
nerve, the lateral antebrachial cutaneous nerve, or the terminal
branch of the posterior interosseous nerve.
Gentle handling is of great importance and must follow the
same principles as handling of all nerves. As the graft is
harvested, great care must be taken that it is kept moist in a
gauze soaked in saline. The grafts are sharply cut to proper
Fig. 32.21  Schematic presentation of autograft repair. Each segment is coapted to
the corresponding group of fascicles of the nerve endings. Note how the individual
grafts are applied quite loosely.
Table 32.3  Common nerves used as autografts
Donor nerve
Length (cm)
Sensory defect
Sural nerve
30–40 cm
Dorsal aspect of lower
leg and lateral foot
Medial antebrachial
cutaneous nerve
10–12 cm*
8–10 cm†
Medial forearm
Lateral antebrachial
cutaneous nerve
10–12 cm
Lateral forearm
Superficial sensory
branch of the
radial nerve
25 cm
Radial dorsal hand
*Above elbow.
†Below elbow.

Fig. 32.23  Incisions to enable harvest of the sural nerve, shown by dotted lines.
Fig. 32.24  Area of diminished or absent sensation after harvest of the sural nerve.
Fig. 32.25  Medial antebrachial cutaneous nerve shown in orange, and basilic vein.
Basilic vein
Medial antebrachial
cutaneous nerve
Fig. 32.22  Course of the sural nerve in the lower leg, shown in orange.
Sural nerve
Small saphenous vein
Lateral malleolus
Sural branch of
the peroneal nerve

730
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
Superficial sensory branch of the radial nerve
The superficial sensory branch is formed as the radial nerve
is divided into a deep (the posterior interosseous nerve) and
a superficial branch at the elbow level. The superficial branch
runs beneath the brachioradialis muscle to surface distally
about 8 cm from the tip of the radial styloid between the
tendon of brachioradialis and the tendon of extensor carpi
radialis (Fig. 32.30). It provides a 25 cm-long nerve graft, but
is rarely used because it tends to cause painful neuromas. It
is primarily used when large quantities of nerve grafts are
needed in brachial plexus injuries. In the presence of a median
or ulnar nerve injury, it is considered a relative contraindica­
tion to use it as a donor for nerve grafts (Fig. 32.31).
Other
The saphenous nerve (40 cm) has been used primarily in
plexus injuries and as a vascularized nerve graft. The lateral
femoral cutaneous nerve (20 cm) can be used as a last choice,
but has the disadvantages of comparatively large sensory loss,
and painful neuromas.
lateral border of the biceps tendon where it parallels the
cephalic vein (Fig. 32.27).
A few short incisions are generally sufficient to harvest
these nerves adequately. The consequences are usually
regarded as more troublesome for the patient after lateral
antebrachial cutaneous nerve harvest than after harvest of the
medial antebrachial cutaneous nerve (Figs. 32.28 & 32.29).
The terminal branch of the posterior
interosseous nerve
The terminal branch of the posterior interosseous nerve is
simple to harvest dorsally just proximal to the wrist, lying
on the interosseous membrane.63 Generally, one can harvest
a 4–5-cm long segment (1–3 fascicles), which may fit into
a small digital nerve defect. Harvest causes no complica­
tions or loss of function, which is beneficial, especially in
reconstructions of digital nerve defects. This was recently
exemplified in a retrospective study, where posterior interos­
seous nerve grafts were shown superior to the medial cutane­
ous nerve of the forearm, especially in terms of donor site
morbidity.64
Fig. 32.26  Area of diminished or absent sensation after harvest of the medial
antebrachial cutaneous nerve.
Fig. 32.27  Lateral antebrachial cutaneous nerve shown in orange and cephalic
vein.
Lateral antebrachial
cutaneous nerve
Cephalic vein

731
Treatment and surgical techniques
Fig. 32.28  Area of diminished or absent sensation after harvest of the dorsal
aspect of the lateral antebrachial cutaneous nerve.
Fig. 32.29  Areas of diminished or absent sensation after harvest of volar aspect of
the lateral antebrachial cutaneous nerve.
Tubular repair and artificial conduits
Autologous nerve grafts are still considered to be the gold
standard for bridging defects in nerves. The superiority in
outcome is thought to be mainly the result of their ability to
provide a biocompatible scaffold that contains both Schwann
cells and their basal lamina. These factors promote regenera­
tion through natural production of growth factors and adhe­
sion molecules, which will help stimulate neurite elongation
and direction on site.65 However, there are disadvantages with
autografts, some of which have been mentioned above. Har­
vesting requires an extra surgical incision to obtain an other­
wise healthy sensory nerve. There are limited sources of graft
material, and the injured nerve and donor nerve may be
mismatched at grafting.66
Our present inability to gain full functional recovery with
autografts has been the main driving force behind the devel­
opment of alternative means to bridge nerve defects. Tissue
engineering has in recent years offered the opportunity to
develop biodegradable guiding materials with tailored prop­
erties that imitate normal biological features. Structural stabil­
ity is enabled, and both growth factors and supportive cells,
such as Schwann cells or stem cells, can be added to give
physical guidance to the regenerating axons. However, the
latter procedure is far from clinical practice, but may be a
possibility in the future. Formation of a longitudinally ori­
ented fibrin matrix and accumulation of various tropic and
trophic factors will ensue within the conduit, and this will
further improve the physical conditions for nerve regenera­
tion. Obviously, donor morbidity after graft harvest will be
eliminated.
Biological conduits
The first attempt to bridge a nerve defect with a tube was
published by Glück, who used a piece of decalcified bone to
bridge a nerve gap.67 Since then, several biological scaffolds
have been used, including veins,68,69 arteries,70 muscles,70
tendons,71 and combinations such as vein–muscle grafts,72,73
and acellular nerve allografts,74–76 with variable outcomes. The
main theoretical advantage of using biological constructs with
a core matrix is the availability of a longitudinally oriented
basal lamina and extracellular matrix components that direct
and improve the regeneration of axons. In contrast, bridging
methods using only tubular material, such as vein grafts
or non-degradable or degradable nerve conduits (several
are commercially available) lack this function and may be
less attractive, at least theoretically. The use of composite

732
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
have been proven to be safe and effective in sensory nerves
up to 30 mm; however, the maximal length of the nerve defect
is not yet established.78–81
The three-dimensional structure of these acellular scaffolds
contains many of the beneficial characteristics of nerve auto­
grafts. This includes not only the physical structure of the
epineurium, and fascicles with endoneurial tubes, but also
protein structures and guidance molecules specific for nerve
tissue. It is hypothesized that the grafts thereby function as a
guide for tissue regeneration, by stimulating a rapid revascu­
larization and repopulation with host Schwann cells.
Today, commercially available processed nerve allografts
are all manufactured from donated human peripheral nerve
tissue. A detergent protocol is used to remove all cells and
cause a pre-Wallerian degeneration of the nerve tissue in
order to cleave growth inhibitors. The tissue is then sterilized
prior to use as an off-the-shelf product.
In a large multicenter observational study, the RANGER
Study registry, 71 nerve gaps in sensory, mixed, and motor
nerves were reconstructed in 56 subjects. Overall, a meaning­
ful level of recovery, defined as motor nerve function of M3
to M5 and sensory function of S3 to S4, was achieved in 86%
of the patients with repairs with graft lengths up to 50 mm.
Meaningful levels of recovery were also found in 89% of
biological conduits, such as combinations of veins and
muscles, has therefore been explored. The main rationale for
using this combination, apart from it being of autologous
origin, has been that a collapse of the vein is prevented by
filling the lumen, and that the vessel wall prevents the risk of
axons sprouting outside the muscle. Nerve regeneration is
propagated along the longitudinally oriented muscle fibers
and no foreign material is used in the bridging process. In
a recent retrospective study of nerve reconstructions of
up to 6 cm-long digital nerve defects, comparing autografts,
muscle-in-vein grafts, and direct nerve repair,77 it was found
that muscle-in-vein grafts yielded similar outcome as the
nerve autografts, which have been slightly, but not signifi­
cantly, worse than the ones after direct nerve suture. One
advantage of muscle-in-vein grafts is the lack of donor site
sensory morbidity.
Processed nerve allografts
Processed nerve allografts provide decellularized and
predegenerated human nerve tissue as an alternative to
conventional nerve autografts or tube conduits for nerve
reconstruction. These grafts have shown promising results
both in animal studies and early clinical studies, where they
Fig. 32.30  Superficial sensory branch of the radial nerve.
Superficial sensory branch
of the radial nerve
Fig. 32.31  Area of diminished or absent sensation after harvest of the superficial
sensory branch of the radial nerve.

733
Treatment and surgical techniques
increasing numbers of studies have reported promising
results regarding recovery of both sensory93–95 and motor
function.96,97
In a level II study, Boeckstyns et al. randomized ulnar or
median nerve injuries to repair with a collagen nerve conduit
or with conventional microsurgical techniques. The use of
collagen conduits was found to have a recovery of sensory
and motor functions that were equivalent to that after direct
suture when the nerve gap was 6 mm or less, as evaluated at
24 months after repair. At 12 months, however, there was a
significantly better motor recovery in the direct suture group.
Also, ulnar nerve lacerations were found to have a poorer
prognosis compared to median nerve lacerations.98
Another recent prospective long-term follow-up on digital
nerve reconstructions with collagen nerve conduits found that
sensibility continued to improve in most cases after 12 months.
Also, it was shown that the improvement of sensibility was
associated with a significantly shorter nerve gap length with
significantly better results if the gap length was < 10 mm.99
Fillers
The main purpose of inserting filler structures in the conduits,
whether in the form of guidance channels, hydrogels, or
others, is to apply hapotactic cues (contact-mediated) to
support axonal regeneration or chemotactic cues (diffusible)
to guide the regenerating axons.100 The most commonly used
haptotactic cues are extracellular matrix proteins such as col­
lagen, laminin, and fibronectin. Neurotrophic factors, such as
nerve growth factor, glial-derived neurotrophic factor, and
neurotrophin NT-3, are additives that act as chemotactic cues
that will promote neuronal regrowth and sprouting.65 Addi­
tion of cellular components, such as Schwann cells101 and stem
cells,102 can further be used to improve the regeneration by
creating a more optimal microenvironment. In the future, it is
possible that “off-the-shelf” conduits may be filled with
autologous supporting cells that are harvested and immedi­
ately prepared from the patient’s injured nerve segments.103
Other techniques
Preclinical studies have indicated that shorter digital nerve
defects can be bridged by applying longitudinal resorbable
sutures that will act as a guide for the fibrin matrix that is
formed to fill the defect. Schwann cells and axons will follow
this matrix and thereby overcome the defect. The newly
formed nerve trunk, which can be made in a branched pattern,
is subsequently surrounded by a new perineurium-like struc­
ture and provides functional recovery.104
Nerve transfers
In recent years there has been an increasing interest in the use
of nerve transfers in nerve reconstruction.105 This technique
has primarily been used in brachial plexus injuries, and is
based on the assumption that less important nerves can be
sacrificed, transected, and rerouted to be attached to a func­
tionally more important nerve segment.106,107 It can also be
used after other proximal nerve injuries, and the procedure
transfers a proximal nerve injury to a distal one. This is a
tempting and valuable method that can be used when patients
present late with nerve injuries, even in young patients.108 The
topic is further discussed in Chapter 33.
digital nerve repairs, 75% of median nerve repairs, and 67%
of ulnar nerve repairs.79,82 In a follow-up study of short-gap
(i.e., 5–15 mm) sensory recovery, using the same material, it
was shown that the outcome for nerve allografts were equiva­
lent to previous data on autograft and exceeded those of
conduits.83
Non-degradable conduits
The first artificial conduits used in preclinical and human
trials were composed of non-resorbable polymers based on
silicone and polytetrafluoroethylene84,85 (Fig. 32.32). Silicone
was chosen because of its inert material properties and
because it is tolerated well by the recipient.86 It has been used
successfully in hand surgery for arthroplasty and two-stage
tendon-grafting procedures for the last two decades. As sili­
cone tubes are non-degradable and impermeable to large
molecules, they also provide the necessary biological isolation
from scar-forming elements of the wound and allow for
accumulation of growth factors. A longitudinally oriented
fibrin matrix containing macrophages is formed and there is
migration of Schwann cells, ingrowth of axons, and neovas­
cularization of the newly formed nerve trunk. Silicone tubes
were used in a clinical prospective randomized study that
compared tube repair and microsurgical nerve repair in
median and ulnar nerve injuries.87 Results showed no signifi­
cant differences in outcome between the two methods, except
for a decrease in cold intolerance in the conduit group at the
5-year follow-up.88 The authors concluded that tubular repair
may be preferable in the future when appropriate bioresorb­
able materials are available. However, utilization of a silicone
tube is not an alternative when there is a nerve defect.
Biodegradable conduits
Increasing interest has turned towards the use of biodegrad­
able materials as conduits. Ideally, the material from which
the tube is made should be highly biocompatible and allow
degradation to non-toxic end products. They should be
mechanically stable, yet still flexible and porous to ensure
supply of nutrients and provide a microenvironment that
allows for the production of functional tissue.65,89–91
Polymer-based materials, such as collagen, polyglycolic
acid polymer, and polylactide-caprolactone polymer, and
other available materials such as chitosan conduits,91 offer a
high degree of flexibility in chemical and physical properties
and are available commercially. Future inclusion of fillers,
such as Schwann cells, or incorporation of biologically active
substances in the polymers that are released as the tube is
degraded are areas of massive research. Yet, at present, clinical
experience in terms of randomized trials is lacking,92 although
Fig. 32.32  A nerve defect bridged by a nerve conduit.

734
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
Sensory re-education
Cortical reorganization
After an acute nerve transection, the brain must compensate
for the loss of sensory input.113 First, a gross decrease in the
number of fibers is seen, as well as a topographical mismatch.
A “silent area” is created in the nerve’s representational area
in the brain. However, adjacent cortical areas expand instantly
and occupy this former nerve territory.114–117 These changes
are mediated by the unmasking of normally inhibited syn­
aptic connections in the vicinity of this “silent area”, and a
reorganization of the somatosensory cortex occurs through
processes of brain plasticity. This period is referred to as
phase 1 during rehabilitation – before any reinnervation has
occurred in the hand. During this phase some training may
be initiated.
Because of the mismatch and misdirection of the regenerat­
ing axons that happens at the repair site, areas of skin in the
hand and muscles will not be reinnervated by their original
axons to a large extent.118 The original well-organized hand
representation in the sensory and motor cortex alters into a
distorted and mosaic-like pattern with disappearance of, and
overlapping of, fingers.114 As a result of misdirection and
remapping of the representation of the cortical hand, “the
hand speaks a new language to the brain” (phase 2 during
rehabilitation). A sensory relearning program that helps the
brain to decipher the signals may assist it in interpreting the
new language, which works well and improves outcome.119
Recent data have indicated that it is beneficial for this process
to begin when the reorganization in the sensory cortex has
already started (phase 1)116 and that this should not be post­
poned until touch can be perceived in the hand, as was earlier
believed. Effectiveness in the relearning process is probably
greatly influenced by the individual motivation of each
patient. Coping strategies that are individualized for each
patient should be considered, as adaptation to the condition
is an evolving process by which the patient’s own resources
can be used to overcome problems in daily activities.
Sensory re-education in phase 1
During the early postoperative period (phase 1), various
“babysitting” methods can be used until the hand becomes
reinnervated by the outgrowing axons. Functional similarities
exist between perception and imagery (the premotor cortex
can be activated by just imagining a movement – so-called
“motor imagery”). The corresponding phenomenon for
sensory function is “sensor imagery”. Imagining the hand
being touched activates the same cortical areas as if the hand
is really being touched.
Activation of “mirror motor neurons” in the premotor
cortex by mere observation of hand motor actions by others
plays a fundamental part in action, imitation, and action
understanding.120 Reading or listening to action words related
to hand movements activates hand representational areas
in the motor cortex and observation of touching a hand acti­
vates the corresponding representational areas in the sensory
cortex. The patient’s observation of the denervated hand
being touched is already initiated during the first days post­
operatively, which may activate the cortical hand area as a
result of visuotactile interaction.121
Postoperative care
General aspects
The role of early active mobilization after microsurgical nerve
repair has been debated. It has been hypothesized that it may
cause a change in tension at the site of nerve repair, which in
turn will result in impaired functional outcome.109,110 Experi­
mental studies have indicated that intraneural scarring at the
repair site can impede revascularization and reduce axonal
regeneration across the suture line as a result of tension.32,111
However, immobilization may result in an increase in scar
tissue that surrounds the reconstructed nerve. Tethering of the
nerve by scar tissue may lead to additional pain on move­
ment.112 Maintenance of full range of movement of the neuro­
muscular unit and preservation of movement of small joints
are of importance in the postoperative phase. Intermittent,
controlled mobilization in a protected splint is therefore
thought to be beneficial for the patient. Most importantly, the
nerve grafts should be applied at minimal tension with joints
in an extended position and in a manner that allows subse­
quent full range of motion without causing tension over the
repair sites. Surgeons should supervise physiotherapy and
occupational therapy, check advancement of Tinel’s sign
and return of muscle function, which is recovered during
rehabilitation.
Postoperative movement training
Dorsal splinting may be maintained for 3 weeks in a manner
that allows intermittent early gentle mobilization within a
protected range without putting the microsurgical repair at
risk or tension. Although some authors have advocated that
the nerve should be allowed to rest for 8 days before active
and passive mobilization,33 an earlier start to training may be
appropriate within the limits of bandages and restrictive
splinting. It is thought that early active movements may
reduce the risk of the nerve being tethered in scar tissue,59,112
which is a possible effect if rigid immobilization is adopted.
Elevation of the hand is recommended for the first week
postoperatively. Sutures and plaster are usually removed at 3
weeks and active exercises of the fingers can then be initiated.
Prolonged protection of the suture line may be recommended
up to 6 weeks postoperatively, to avoid extensive extension in
the wrist. These general principles apply for digital nerves as
well as major nerve trunks and nerve grafts.
Clinical tips
• Current literature supports the use of conduits or acellular
nerve allografts for reconstructions of nerve defects when
the defects are limited, for example in digital nerves and
larger nerves (median and ulnar nerves). In larger defects,
conduits and allografts should be used with caution, and
until proven effective for longer distances, we suggest
nerve grafting for long defects.
• For sensory digital nerve defects, especially if the proximal
stump is absent, cross-over end-to-side neurorrhaphy is a
reconstructive option.

735
Outcome
In early sensory training, the multimodality of the brain
is activated; the cortical audiotactile interaction is used to
activate cortical sensory areas by listening to the sound of
touch. A sensor glove, provided with minimicrophones at its
fingertips, can be applied to the denervated hand.122 Active
touch of items is associated with a specific “friction sound”,
depending on the texture touched, which is transmitted to
earphones. The patient can “listen to what the hand feels.”
If the sensor glove is used in the early phase after nerve
repair, tactile discrimination may be improved considerably.
To conclude, early re-learning, i.e., starting within the first
week after a median or an ulnar nerve injury and conven­
tional nerve repair, by using this described guided plasticity
seems to have a potential to improve outcome during the first
6 months.121
Improving effects of sensory re-education –
phase 2
A relearning process is required to adapt to the new and
distorted afferent sensory input caused by axonal misdirec­
tion when familiar objects are touched. For this purpose,
sensory re-education is routinely used in phase 2, when the
hand has started to reinnervate, to regain tactile gnosis. Ways
of touching, and the capacity to localize touch, are trained,
followed by touching and exploration of items, presenting
shape and textures of varying and increasing difficulty with
eyes open and closed. Vision assists training and improves the
deficient sense.
Repeated sessions of cutaneous anesthesia of the forearm
increase the effects of sensory re-education and result in
expansion of representation of the cortical hand122 (Fig. 32.33).
The hand is given more “brain space”, which enables the
improved processing of sensory impulses. Repeated applica­
tion of a cutaneous anesthetic cream (lidocaine/prilocaine:
EMLA), combined with intensive sensory re-education,
increases the effects of sensory re-education with a
considerable improvement in tactile gnosis (functional sensi­
bility) in patients with repaired median nerves.123,124
Outcome
Assessment of outcome
Final evaluation of sensory and motor function should not be
made until after rehabilitation has finished. Depending on the
type of injury, the rehabilitation period may last for 12–24
months postoperatively to allow for reinnervation and sensory
re-education,125 although some authors claim that a follow-up
time of at least 3 years is necessary to evaluate the final
outcome.126
General aspects
Even though extensive amounts of data have been published
on the results of nerve repair, there is no consensus on how
to evaluate the outcome in a standardized manner. Different
protocols for assessing the outcome have been proposed,125,127–129
but none has been adapted uniformly. The evaluation instru­
ment most widely accepted is the Highet Scale from 1954,
adopted by the British Medical Research Council (MRC)
(Table 32.4).
The outcome after nerve repair depends on to what extent
the regeneration of the axons is successful, and how many
of the axons reach their end target. Several factors that influ­
ence the results after nerve repair have been documented.
MRC scale
Several modifications of the British Medical Research Coun­
cil’s scale for nerve recovery have been described,130 and the
modification by Dellon et al. is probably the most used.131 The
sensory function is evaluated according to how the patient
describes levels of recovery (see Table 32.1). Critics claim that
Table 32.4  The Highet Scale from 1954, adopted by the British Medical Research Council
Motor grade
Level of recovery
M0
No recovery
M1
Perceptible contraction in proximal muscles
M2
Perceptible contraction in proximal and distal muscles
M3
Contraction possible against gravity
M4
Contraction possible against resistance
M5
Full recovery in all muscles
Sensory grade
Level of recovery
S0
No recovery
S1
Recovery of deep cutaneous sensibility
S1+
Recovery of superficial pain and sensibility
S2
Recovery of superficial pain and some touch
S2+
S2 recovery with hypersensitivity
S3
Recovery of pain and touch without hypersensitivity
S3+
S3 recovery with localization and some two-point discrimination
S4
Complete recovery with normal two-point discrimination

736
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
Rosen and Lundborg presented a protocol that illustrated
patients’ functional limitation in activities of daily living.128
This protocol is based on previous studies that investigated
what methods are most effectively used to study the temporal
aspects of the outcome after nerve repair.125 Three domains
of function were described: (1) sensory; (2) motor function;
and (3) pain and discomfort. A total score is calculated
that correlates significantly with the MRC scale, which was
shown in a study of 70 patients who had been treated for
the MRC scale is based on subjective findings without any
attempt to standardize defined methods of evaluation, which
complicates our ability to compare different sets of patients as
well as results from different observers.
The Rosen score
To enable improved interpretation of patients’ functional
outcome after nerve repair (median and ulnar nerves),
Fig. 32.33  Brain plasticity. Repeated sessions of cutaneous anesthesia of the forearm increase the effects of sensory re-education and result in expansion of representation
of the cortical hand. The hand is given more “brain space”, which enables the improved processing of sensory impulses.

737
Outcome
Digital nerves
In several studies of primary repair of the digital nerves, the
results of immediate repair of digital nerves were “normal”,
“excellent”, or “good” in 37–68% of the nerves repaired after
a follow-up of 8–32 months.132–134,145,146 In terms of static two-
point discrimination (S2PD), “normal” sensory function has
been defined in these studies as the equivalent to the unin­
jured digit or S2PD of 5 mm or less, whereas “excellent”
function has been defined as a S2PD of 7–10 mm. To sum­
marize, after microsurgical repair of a digital nerve injury,
about half improve to have normal or fair sensation.
Nerve trunks
The motor outcome of lesions to the larger nerve trunks seems
to be dependent on their target organ. This is indicated by the
results in a series of 1837 nerve lesions that outcome after
repair (primary suture, secondary suture, or graft repair) of
the median nerve was superior to the outcome of repair of
lesions to the radial nerve, which in turn was better than that
after ulnar nerve repair.147 The better outcome of motor func­
tion in median nerves than in ulnar nerves is also supported
by others.126,148,149 Recovery of sensation, on the other hand,
has not been shown to differ between the median and ulnar
nerves,126 and combined median and ulnar nerve inju­
ries.126,150,151 The theoretical explanation may be that the ulnar
nerve innervates the delicate intrinsic muscles of the hand,
and the demand of an accurate innervation is theoretically
greater than that of the median or radial nerves that innervate
muscles that do not undertake delicate movements to the
same extent. However, it is difficult to compare the outcome
after injury to various nerve trunks due to their individual
characteristics.
Level of injury
Lesions that are more proximal have a worse outcome than
more distal lesions.138 This may be explained by the fact that
a proximal injury induces a more severe impact on the indi­
vidual neuron, with higher risk of neuronal cell death, and
that the axons have to regenerate over a large distance to reach
the targets.152,153
Type of repair
In a study of 654 lesions of the ulnar nerve, the functional
outcome (grade 3 or better) after suture repair (72%) was
superior to that after graft repair (67%).147,154 In the same series,
neurolysis was done for patients with ulnar entrapment, and
in comparison these patients achieved a functional outcome
of grade 3 or better in 92% of the repairs, indicating the
importance of preserving the continuity of nerve trunks if
possible. A nerve repair therefore achieves better results than
a nerve graft.155
Type of injury
Injuries with the nerve in continuity have a good prognosis,
and so a nerve crush leads to better functional recovery than
a transected nerve trunk. However, a transection injury can
often be treated by a primary repair, whereas a crush injury,
if it does not recover spontaneously, may require a nerve graft,
which will lead to an impaired outcome.
nerve transection at the wrist or distal forearm level. The
total score also correlated strongly with the patients’ overall
estimation of the impact of the injury on activities of daily
living.128
Factors that affect outcome
General aspects
Ruijs et al. presented an excellent meta-analysis of 23 papers
based on data from individual patients about motor and
sensory recovery after microsurgical repair of the median
and ulnar nerves.125 Prognostic factors that have an impact
on outcome varied for motor and sensory recovery. For
motor recovery, age, delay before repair, level of injury,
and type of injured nerve were important, and for sensory
recovery, age and delay before repair were the most
important.
Age
In several studies of digital nerve repairs, there was a close
positive correlation between the younger age of the patient
and the recovery of sensation.132–134 For more proximal injuries
of the median, ulnar, or radial nerves in the forearm, age also
seems to be the factor that played the most important part in
the outcome. Children (mean age 6 years) that were evaluated
a minimum of 1 year after primary repair of injury to the
median nerve were all considered to have regained normal
function.135 In comparison, 95 patients (age 15–55 years) with
primary or secondary repair, or grafting, of injuries of the
median and ulnar nerves30 showed that only the younger
patients who had primary distal repair had excellent results,
with normal sensitivity and motor function. These findings
are supported by other authors in similar case series.127,136–138
Patients under 16 years are four times more likely to have
satisfactory outcome in motor recovery, and also a signifi­
cantly increased chance of satisfactory sensory recovery, with
lower age.126
The superior results in children may, to some extent,
be explained by better peripheral nerve regeneration and
shorter regeneration distances. However, it is likely that
a greater adaptability of the brain is of predominant
importance for the functional outcome in children.139,140 This
hypothesis is confirmed by recent data that showed that early
sensory re-education programs improve functional outcome
in adults because of improvements in training-induced
plasticity.141
More importantly, in a recent long-term follow-up, the age
factor was extensively investigated indicating that children
with injured median and ulnar nerves during childhood
recovered significantly better than those injured during ado­
lescence.142 However, in spite of excellent clinical recovery
among the children injured during childhood, the electroneu­
rography response was poor,143 indicating that a better cerebral
plasticity is the crucial factor for outcome. Recently, a func­
tional magnetic resonance imaging (fMRI) study showed that
the children that had their median nerve injured at the age of
1–13 years had an activation pattern in the brain similar to
healthy subjects and that changes in both cerebral hemispheres
may explain differences in clinical outcome between children
injured during childhood and adolescence.144

738
SECTION V
CHAPTER 32 • Peripheral nerve injuries of the upper extremity
reported as the most frequent symptom (80%). Other symp­
toms were stiffness (77%), weakness (72%), pain (63%), change
in skin color (50%), and swelling (33%). Most of the patients
(59%) were considered to have abnormal cold intolerance. In
this group, a larger proportion (70%) had combined ulnar and
median nerve injuries, whereas isolated nerve injuries were
less common (median nerve 57% and ulnar nerve 56%). Even
though there was no difference in sensory recovery between
women and men, cold intolerance was more common in
women than in men. Importantly, time since injury did not
correlate with the presence of cold intolerance (follow-up time
2–10 years).168 This is also supported by other investigators,165
indicating that cold intolerance is a stationary condition when
the maximum sensory recovery has been achieved.
There is currently no treatment available that is specifically
directed against cold intolerance, although possible effects of
treatment by Pavlovian conditioning, a behavioral treatment
for digital cold sensitivity where whole-body cold exposure
becomes associated with warm hands, has been reported
recently in patients with hand injuries.173 In addition, CRPS
may be a severely disabling condition that may be treated
with substances like gabapentin and pregabalin174 and other
strategies.175 This poses a pedagogic challenge to the treating
physician when addressing the patient’s expectations of the
final outcome after nerve repair.
Future directions
Nerve injuries, extending from minor digital nerve injuries up
to severe injuries to the brachial plexus in the upper extremity
as well as less common injuries in the lower extremity, repre­
sent one of the most challenging clinical problems for the
treating surgeons and physicians. A variety of factors influence
outcome and each individual nerve injury is unique in its
entity; thus each case also requires consideration of factors
such as motivation for rehabilitation and coping strategies of
the patient. Efforts to improve diagnostic tools and treatment
strategies have to be directed towards all components. In the
future, improved imaging techniques, like three-dimensional
high-resolution magnetic resonance imaging with diffusion
tensor imaging and tractography and pre- and intraoperative
high-resolution sonography, may improve the diagnostic
accuracy; however, an initial and appropriate basic clinical
examination is still the key for early treatment. Proper evalua­
tion systems are needed to examine fully new surgical and
rehabilitation techniques, such as the nerve transfers, end-to-
side repair and the EMLA concept (see above), respectively. In
addition, a continuous search for the secrets of intracellular
signaling in neurons, Schwann cells, and other cells may
provide the knowledge needed for the introduction of pharma­
cological treatment, not only of any neuropathic pain, but also
to improve regeneration as an adjunct to surgical repair and
reconstruction. Hopefully genomic and proteomic develop­
ment may lead to improved repair and reconstruction strate­
gies, with or without utilization of stem cells in the future.176
Acknowledgments
Financial support for this work was received from the Swedish Research
Council (MEDICINE). We appreciate all the help from Professor Jørgen
Tranum Jensen and his colleagues at the Panum Institute, University of
Medicine and Dentistry, Copenhagen, Denmark.
Postoperative dysfunction
General aspects
Peripheral nerve injuries often have a dramatic impact on a
person’s capacity to function adequately, as the functional
outcome often fails to reach the level of motor or sensory
function present before the injury, at least in adults.138,156 As
most nerve injuries in the upper extremity are seen in young
men,34,157 there is a high probability of disability and subse­
quent social consequences.8 The accompanying amount of
post-traumatic stress after hand and forearm injuries has been
evaluated and shown to be comparable with the psychologi­
cal distress found among survivors of big disasters.158 Other
symptoms, such as pain, dysesthesia, and cold intolerance,10
may also affect the outcome, and cause lifelong impairment
of hand function. However, patients may have different
strategies to cope with their injuries, whether it is a nerve
injury or another serious hand injury.159
Complex regional pain syndrome
Complex regional pain syndrome (CRPS) is a clinical diagnosis
that involves regional pain together with autonomic dysfunc­
tion, functional impairment, and atrophy. According to the
classification, CRPS type 1 occurs with no evidence of periph­
eral nerve injury, whereas CRPS type 2 requires known damage
to nerve structures. CRPS can be a disabling condition in many
cases, and about half of patients with untreated symptoms for
more than a year will have extensive residual dysfunction.
Cigarette smokers and women are at increased risk of CRPS,
and even though it may occur at any age, most patients are
around 45 years. During operation, common sites of injury to
peripheral nerves that may elicit CRPS are damage to the
dorsal branch of the ulnar nerve, the palmar cutaneous branch
of the median nerve, and the superficial branch of the radial
nerve. However, CRPS may be initiated after any type of nerve
injury. The symptoms are pain that is often described as burning
or aching, and it is usually induced by a small stimulus that in
the normal patient would not result in such a response to pain.
It may affect the tissues surrounding the area of injury, or the
whole extremity. In addition, there may be some kind of trophic
changes, such as edema and stiffness, together with changes of
the skin, nails, and hair. The limb may be perceived as different
in temperature from the opposite side.
Other
Numbness, weakness, and abnormal pain with or without
discoloration after exposure to mild to severe pain can be
problematic after peripheral nerve injury.160–162 In fact, cold
intolerance is regarded by many authors as the most disabling
symptom after nerve repair or other trauma to the upper
extremity.10,163–165 The mechanism behind hypersensitivity to
cold is not known, but its presence has been inversely corre­
lated to sensory recovery.166–168 In addition, predictors associ­
ated with cold intolerance are coexisting injury to major
vessels,167,169,170 crush injury,170,171 early postoperative pain,162,172
and the level of the nerve injury.164
In a study by Ruijs et al. on 107 patients with median or
ulnar nerve injury, or a combination of the two, numbness was

739
Future directions
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138. Bolitho DG, Boustred M, Hudson DA, et al. Primary epineural
repair of the ulnar nerve in children. J Hand Surg Am.
1999;24:16–20.
139. Lundborg G, Rosen B. Sensory relearning after nerve repair.
Lancet. 2001;358:809–810.
140. Fornander L, Nyman T, Hansson T, et al. Age- and time-dependent
effects on functional outcome and cortical activation pattern in
patients with median nerve injury: a functional magnetic
resonance imaging study. J Neurosurg. 2010;113:122–128.
141. Lundborg G, Rosen B. Hand function after nerve repair. Acta
Physiol (Oxf). 2007;189:207–217.
142. Chemnitz A, Björkman A, Dahlin LB, et al. Functional outcome
thirty years after median and ulnar nerve repair in childhood and
adolescence. J Bone Joint Surg Am. 2013;95:329–337.
143. Chemnitz A, Andersson G, Rosén B, et al. Poor electroneurography
but excellent hand function 31 years after nerve repair in
childhood. Neuroreport. 2013;24:6–9.
144. Chemnitz A, Weibull A, Rosén B, et al. Normalized activation in
the somatosensory cortex 30 years following nerve repair in
children: an fMRI study. Eur J Neurosci. 2015;42:2022–2027.
145. Sullivan DJ. Results of digital neurorrhaphy in adults. J Hand Surg
[Br]. 1985;10:41–44.
146. Wang WZ, Crain GM, Baylis W, et al. Outcome of digital nerve
injuries in adults. J Hand Surg Am. 1996;21:138–143.
147. Murovic JA. Upper-extremity peripheral nerve injuries: a
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review with comparison of the operative outcomes of 1837
Louisiana State University Health Sciences Center median, radial,
and ulnar nerve lesions. Neurosurgery. 2009;65(suppl):11–17.
148. Deutinger M, Girsch W, Burggasser G, et al. Peripheral nerve
repair in the hand with and without motor sensory differentiation.
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149. Rosen B, Lundborg G. The long term recovery curve in adults
after median or ulnar nerve repair: a reference interval. J Hand
Surg [Br]. 2001;26:196–200.
150. Kabak S, Halici M, Baktir A, et al. Results of treatment of the
extensive volar wrist lacerations: “the spaghetti wrist”. Eur J Emerg
Med. 2002;9:71–76.
151. Noaman HH. Management and functional outcomes of combined
injuries of flexor tendons, nerves, and vessels at the wrist.
Microsurgery. 2007;27:536–543.
152. Hart AM, Terenghi G, Wiberg M. Neuronal death after peripheral
nerve injury and experimental strategies for neuroprotection.
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153. Ygge J. Neuronal loss in lumbar dorsal root ganglia after proximal
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154. Kim DH, Han K, Tiel RL, et al. Surgical outcomes of 654 ulnar
nerve lesions. J Neurosurg. 2003;98:993–1004.
155. Bontioti EN, Kanje M, Dahlin LB. Regeneration and functional
recovery in the upper extremity of rats after various types of nerve
injuries. J Peripher Nerv Syst. 2003;8:159–168.
156. Allan CH. Functional results of primary nerve repair. Hand Clin.
2000;16:67–72.
157. Noble J, Munro CA, Prasad VS, et al. Analysis of upper and lower
extremity peripheral nerve injuries in a population of patients
with multiple injuries. J Trauma. 1998;45:116–122.
158. Jaquet JB, Kalmijn S, Kuypers PD, et al. Early psychological stress
after forearm nerve injuries: a predictor for long-term functional
outcome and return to productivity. Ann Plast Surg. 2002;49:82–90.
159. Cederlund RI, Ramel E, Rosberg HE, et al. Outcome and clinical
changes in patients 3, 6, 12 months after a severe or major hand
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161. Engkvist O, Wahren LK, Wallin G, et al. Effects of regional
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163. Backman C, Nystrom A, Bjerle P. Arterial spasticity and cold
intolerance in relation to time after digital replantation. J Hand
Surg [Br]. 1993;18:551–555.
164. Nancarrow JD, Rai SA, Sterne GD, et al. The natural history of
cold intolerance of the hand. Injury. 1996;27:607–611.
165. Povlsen B, Nylander G, Nylander E. Cold-induced vasospasm
after digital replantation does not improve with time. A 12-year
prospective study. J Hand Surg [Br]. 1995;20:237–239.
166. Kay S. Venous occlusion plethysmography in patients with cold
related symptoms after digital salvage procedures. J Hand Surg
[Br]. 1985;10:151–154.
167. Koman LA, Nunley JA. Thermoregulatory control after upper
extremity replantation. J Hand Surg Am. 1986;11:548–552.
168. Ruijs AC, Jaquet JB, van Riel WG, et al. Cold intolerance following
median and ulnar nerve injuries: prognosis and predictors. J Hand
Surg Eur Vol. 2007;32:434–439.
169. Craigen M, Kleinert JM, Crain GM, et al. Patient and injury
characteristics in the development of cold sensitivity of the hand: a
prospective cohort study. J Hand Surg Am. 1999;24:8–15.
170. Irwin MS, Gilbert SE, Terenghi G, et al. Cold intolerance following
peripheral nerve injury. Natural history and factors predicting
severity of symptoms. J Hand Surg [Br]. 1997;22:308–316.
171. Isogai N, Fukunishi K, Kamiishi H. Patterns of thermoregulation
associated with cold intolerance after digital replantation.
Microsurgery. 1995;16:556–565.
172. de Medinaceli L, Hurpeau J, Merle M, et al. Cold and post-
traumatic pain: modeling of the peripheral nerve message.
Biosystems. 1997;43:145–167.
173. Carlsson I, Cederlund R, Holmberg J, et al. Behavioural treatment
of post-traumatic and vibration-induced digital cold sensitivity.
Scand J Plast Reconstr Surg Hand Surg. 2003;3:371–378.
174. Gordh TE, Stubhaug A, Jensen TS, et al. Gabapentin in traumatic
nerve injury pain: a randomized, double-blind, placebo-controlled,
cross-over, multi-center study. Pain. 2008;138:255–266.
175. Vranken JH. Mechanisms and treatment of neuropathic pain. Cent
Nerv Syst Agents Med Chem. 2009;9:71–78.
176. Dahlin L, Johansson F, Lindwall C, et al. Chapter 28: Future
perspective in peripheral nerve reconstruction. Int Rev Neurobiol.
2009;87:507–530.

SECTION V • Paralytic Disorders
33 
Nerve transfers
Kirsty Usher Boyd, Ida K. Fox, and Susan E. Mackinnon
SYNOPSIS
■ Nerve injuries are often devastating, with associated pain and impaired
function.
■ Motor nerve injuries must be managed expeditiously, because
regenerating axons must reach target muscle prior to degeneration and
fibrosis – “time is muscle”.
■ Nerve transfers offer an advantageous method of reconstruction by
delivering regenerating nerve fibers to the target end organ more
quickly, thus converting a proximal injury to a more distal injury.
■ Nerve transfers allow for dissection outside the original zone of injury,
providing a safer and more technically straightforward procedure.
■ Unlike tendon transfers, the muscle–tendon biomechanical structure is
preserved, thus excursion, origin, insertion, and length–tension
relationships are undisturbed.
■ Nerve transfers require time for the nerve to regenerate and extensive
physical therapy for retraining.
■ Intraneural dissection is technically demanding, and nerve transfers
require intimate knowledge of nerve topography.
Introduction
While peripheral nerve reconstruction is an evolving field,
nerve transfers have become a more broadly accepted recon­
structive option.1–3 As our understanding of internal nerve
topography improves, we are able to recognize redundant
or non-essential potential donor nerves and fascicles. Recent
contributions in basic science are broadening options for nerve
transfer with new and improved techniques. Clinical research
focusing on outcomes, applications to novel populations, and
areas of debate continue to advance the field. This chapter
will outline the history and principles of nerve transfers as
they pertain to upper extremity nerve reconstruction. The
recent literature as it relates to current techniques, debates,
and advances in nerve transfers will be reviewed. Current
commonly performed nerve transfers are detailed with focus
on both motor and sensory nerve transfers, their indica­
tions, rehabilitation and postoperative protocols, and a basic
overview of selected surgical techniques4 (see key points,
above).
Access the Historical perspective section online at

Table 33.1 appears online only.
Key points
• Nerve transfers are a relatively recent development in
peripheral nerve surgery.
• Nerve transfers can be performed to restore sensory or
motor deficits.
• Nerve transfers essentially convert a proximal injury to a
distal injury, providing a source of regenerating axons in
close proximity to the end target.
• Nerve transfers are associated with minimal to no
downgrade in donor function.
• Nerve transfers preserve the original biomechanical
muscle–tendon relationship.
• Nerve transfers may provide superior results to tendon
transfer, with the ability to restore individual and separate
muscle function.
• Nerve transfers are replacing other techniques as the gold
standard for brachial plexus and other peripheral nerve
injury in the authors’ practice.
• New applications of nerve transfers to pediatrics, lower
extremity injury, partial injury (through supercharging or
other end-to-side techniques), and central nervous system
disorders (spinal cord injury and transverse myelitis) are
exciting.
  Access video lecture content for this chapter online at expertconsult.com

740.e1
Historical perspective
Historical perspective
The classification of nerve injury is perhaps the single most
important factor when determining management (Table 33.1).
The six degrees of nerve injury have been well described.
First- and second-degree injuries recover spontaneously, as do
third-degree, albeit recovery is variable and less than normal,
depending on scar tissue. Fourth- and fifth-degree injuries are
significant and recovery is not expected. These injuries should
be managed with prompt surgical intervention to prevent
degeneration and fibrosis of the motor end plates. Sixth-
degree injuries encompass a variety of nerve injuries within
a single nerve, and the need to operate is determined on an
individual basis.
Table 33.1  Classification of nerve injury highlighting the six degrees of nerve injury and the anticipated rate and likelihood of recovery
Degree of injury
Tinel’s sign present
Recovery
Rate of recovery
Surgical procedure
I
Neurapraxia
No
Complete
Up to 12 weeks
None
II
Axonotmesis
Yes
Complete
1* per month
None
III
Yes
Varies*
1* per month
None or neurolysis
IV
Neuroma-in-continuity
Yes, but no advancement
None
None
Nerve repair, graft, or transfer
V
Neurotmesis
Yes, but no advancement
None
None
Nerve repair, graft, or transfer
VI
Mixed injury (I–V)
Some fascicles (II, III)
Some fascicles (II, III)
Depends on degree
of injury (I–V)
Neurolysis, nerve repair,
graft, or transfer
*Recovery can vary from excellent to poor depending on the amount of scarring and the sensory versus motor axon misdirection to target receptors.

741
Basic science
Once surgical intervention has been deemed necessary, there
are a number of surgical options. Traditionally nerve repair or
grafting was used with tendon transfers to augment poor
recovery or delayed presentation. The difficulty with proximal
nerve injuries is that the distance from the injury to the motor
end plate is significant, and recovery is prolonged. In addi­
tion, delayed intervention may result in denervation and
fibrosis prior to muscle reinnervation. Axonal regeneration
has been shown to occur at the rate of approximately 1 inch
(2.5 cm) per month and reinnervation of denervated muscle
is not possible after 12–18 months; therefore nerve transfers
offer a valuable means of providing regenerating axons in
closer proximity to the motor end plate. Essentially, a nerve
transfer converts a proximal nerve injury to a distal one,
enabling faster recovery and quicker return to function.
Function
Number of nerve fibers
Time of denervation
α
Nerve transfers were described very early; however they were
traditionally reserved for otherwise unsalvageable root avul­
sions and proximal pan-plexus injuries. Approximately 20
years ago, nerve transfers were revisited and applied to a
significantly broader patient population, with applications in
partial plexus injuries to recreate specific essential functions
in the upper extremity.5–7 As our understanding of internal
nerve topography has broadened, techniques and equipment
for performing microsurgery have improved, and our diag­
nostic ability for brachial plexus and peripheral nerve injury
has progressed, the field of nerve transfers has exploded.
Nerve transfers have become the standard of care for treat­
ment of peripheral nerve injuries in the authors’ practice, and
have largely replaced other modalities.
Basic science
There have been dramatic increases in our knowledge of
nerve injury, healing, and regeneration. The majority will be
touched on in Volume 1, Chapter 22, and Chapter 32 of this
volume. The most relevant recent basic science advances
pertaining to nerve transfers relate to end-to-side transfers
(Fig. 33.1). End-to-side neurorrhaphy involves the coaptation
of the distal end of an injured recipient nerve into the lateral
aspect of an intact nerve, which serves as a proximal source
of axons to regenerate into the injured nerve. Reports of end-
to-side transfers occurred as early as the late 1800s and then
made a resurgence in the 1990s. There has, however, been
controversy regarding the success of these transfers, and
sensory recovery has typically been more impressive than
motor recovery. The sprouting of axons in an end-to-side
coaptation, thus eliminating the need for a proximal nerve
stump, makes nerve transfers an option for proximal nerve
injuries and has been well demonstrated in the literature.8,9
While sensory nerves are able to sprout spontaneously (col­
lateral sprouting), donor nerve axonotmetic injury is required
for motor neuronal regeneration (regenerative sprouting)
across the end-to-side repair (Fig. 33.2).8 An epineurotomy in
the donor nerve is required, and partial axotomy will result
in more significant regenerative sprouting into the recipient
nerve, albeit at the potential expense of a measurable down­
grade in donor nerve function.
Fig. 33.1  The various options for coaptation in nerve transfer. (A) End-to-end
coaptation between the donor nerve (red) and the recipient nerve (blue).
(B) End-to-side coaptation, where the distal end of the divided recipient nerve
(blue) is transferred to the side of the intact donor nerve (red). In this transfer,
fascicles from the donor will “sprout” into the distal donor nerve. The recipient
nerve essentially “pulls” the donor fascicles into the distal nerve. (C) Reverse
end-to-side coaptation. In this transfer, the donor nerve (red) has been divided and
transferred to the side of the intact recipient nerve (blue). The donor essentially
“pushes” regenerating fascicles into the distal donor nerve. (© Washington
University in St. Louis.)
Donor
Recipient
Donor
Recipient
Donor
Recipient
A
B
C
Fig. 33.2  The difference between regenerative and collateral sprouting. Traumatic
regenerative sprouting occurs following injury to the proximal nerve. The damaged
axons degenerate and then regenerate at the rate of 1 mm/day into the distal
recipient nerve. Collateral sprouting occurs spontaneously, and does not require
proximal nerve injury. Axons from the donor nerve simply sprout into the distal end
of the recipient nerve. Only sensory nerves will undergo spontaneous collateral
sprouting. Motor nerves require an axonotmetic injury to facilitate regenerative
sprouting. (© Washington University in St. Louis.)
Recipient nerve
Donor nerve
Donor nerve
Target
Traumatic regenerative sprouting
Recipient nerve
Target
Spontaneous collateral sprouting
Reverse end-to-side nerve transfers involve the complete
transection of the donor nerve, which is then coapted into
the side of the intact recipient nerve. This maximizes the
potential number of available motor axons from the donor
nerve. This procedure does not interrupt any recovery in
the injured recipient nerve because the nerve remains in
continuity; however the additional axons recruited from the
donor nerve improve distal target reinnervation, a concept

742
SECTION V
CHAPTER 33 • Nerve transfers
Diagnosis and patient presentation
The value of a complete history and physical examination in
the patient with a potential brachial plexus or proximal nerve
injury of the upper extremity cannot be overstated. Patients
should be evaluated promptly after injury, both to provide a
baseline for future serial examinations and to facilitate timing
of surgical intervention where necessary.
Patient history
On history, details of the mechanism and timing of injury are
crucial. When seeing a patient in a delayed fashion, it is also
useful to ascertain any interval recovery of function. The
mechanism of injury will determine timing of intervention,
with prompt exploration of penetrating sharp trauma, and
more expectant management of closed injuries and gunshot
wounds. Specific patient symptoms such as loss of function,
both sensory and motor, and pain should be precisely elicited,
as this will help focus the subsequent physical examination.
The pain diagram and questionnaire are particularly useful
for eliciting this information (Fig. 33.4). Other factors, such as
patient age, handedness, occupation, and comorbidities, will
factor into management decisions. Attention to patient goals
and expectations allows for individually tailored and nuanced
approaches that may or may not involve nerve transfer
surgery techniques, which form “a part of the armamentar­
ium”12 when caring for patients with complex upper extremity
injury. Further information on steadily improving quality of
life and other gradual but continuing changes over time after
nerve transfer in brachial plexus injury patients may further
influence treatment choices and patient preference-specific
choices.13
Physical examination
A complete physical examination of the upper extremity
includes assessment of sensory and motor function, joint
suppleness, range of motion, and a functional assessment
with attention paid to adaptive strategies and use patterns.
Particularly in patients with late presentation, the presence of
fixed joint contractures may preclude functional recovery.
Perfusion, bony pathology, presence of edema, scar, previous
incisions, and other soft-tissue trauma are factors that influ­
ence treatment choices.
Function should be graded at each joint. Manual muscle
testing and examination by direct palpation is imperative for
assessing the presence of redundant function when checking
for expendable donor muscles. Shoulder function should be
assessed by examining deltoid, supraspinatus, infraspinatus,
trapezius, latissimus dorsi, serratus anterior, and pectoralis
major. The patient’s ability to abduct/adduct, flex/extend,
and internally/externally rotate must be assessed. The elbow
should also be assessed for flexion and extension. Here it is
important to differentiate between flexion secondary to biceps
brachii and brachialis (musculocutaneous nerve) and brachio­
radialis (radial nerve). The forearm and wrist should be
assessed for flexion/extension and pronation/supination.
Palpation of the individual tendons with wrist flexion is
essential to determine which nerves are involved, as well as
known as “supercharging”.10 In a proximal partial nerve
injury, with a long distance required for reinnervation,
this technique can protect target muscles from denervation
atrophy and fibrosis.9,10 Clinically, the most relevant place to
consider this strategy is for preservation of intrinsic hand
function in proximal severe ulnar neuropathy with use of the
end-to-side distal anterior interosseous (branch to pronator
quadratus) to deep motor branch of ulnar nerve end-to-side
coaptation.10
More recently, work on side-to-side, “cross-grafting” nerve
transfers in animal models has also been completed and
shows some role for preservation and protection of the dener­
vated end organ (Fig. 33.3).11 These strategies, however,
remain under debate and deserve continued laboratory study
and clinical evaluation.
Fig. 33.3  A 62-year-old woman presented with ulnar nerve dysfunction. After an
extended period of hand-intensive activity, she noted the onset of ulnar nerve
distribution numbness and pain. She had subsequent weakness of extrinsic and
absent intrinsic ulnar motor function. Electrodiagnostic testing revealed complete
denervation without evidence of reinnervation at the intrinsic muscles. Nerve
decompression and transposition at the elbow and decompression at the wrist was
performed. Due to the significant distal abnormalities without evidence of recovery
(at 3 months after onset of symptoms), side-to-side transfers were performed to
restore and/or augment both motor and sensory function. This image depicts the
intraoperative dissection of the distal median and ulnar nerves. The recipient ulnar
nerve has been decompressed at Guyon’s canal and is in continuity. The donor
median nerve has been exposed at the upper aspect of the photo. Bridging
acellularized allograft material is inlaid to provide side-to-side or “cross-grafting”
reinnervation from the donor functional median nerve to the recipient non-functional
sensory ulnar nerve branches. An additional coaptation of the pronator quadratus
branch of the anterior interosseous nerve to the deep motor branch of the ulnar
nerve in supercharge end-to-side fashion was also completed. This will provide an
additional modicum of reinnervation as the ulnar nerve proper also, hopefully,
recovers. (© 2015 nervesurgery.wustl.edu.)
Hints and tips
The end-to-side transfer can be considered as the recipient
nerve “pulling” regenerating axons out of the intact donor,
whereas the reverse end-to-side “supercharge” transfer can
be considered as the donor nerve “pushing” regenerating
axons out into the intact recipient.11
Text continued on p. 747

743
Diagnosis and patient presentation
Pain Questionnaire
Name:
Date:
Age:
1. Pain is difficult to describe. Circle the words that best describe your symptoms:
No pain
Most severe pain
2. Mark your average level of pain in the last month
0%
Very little
100%
A large amount
Mark on this scale how your pain has affected your quality of life:
0%
Not at all
100%
A large amount
Mark on this scale how depressed you currently feel:
4. Where is your pain? (Draw on diagram)
R
R
L
L
No pain
Most severe pain
3. Mark your worst level of pain in the last week
Right
No pain
Left
Most severe pain
Level of symptoms: place a mark through the line to indicate the level of your pain, if zero is no pain
and the end of the line is the most severe pain you can imagine having.
Burning
Cramping
Pulling
Throbbing
Cutting
Smarting
Aching
Shooting
Pressure
Stabbing
Numbing
Coldness
Tingling
Vague
Dull
Twisting
Stinging
Other:
Squeezing
Indescribable
Diagnosis:
Right
Left
Dominant Hand:
Male
Female
Sex:
A
Fig. 33.4  The pain questionnaire is a valuable tool for qualifying and quantifying patient pain and the impact their injury is having on their life. This has uses both in
obtaining baseline information, and also in tracking progress as patients recover. This questionnaire is filled out by every nerve patient at each office visit.
Continued

744
SECTION V
CHAPTER 33 • Nerve transfers
0
At home
10
0
At work
10
5. Mark your average level of stress in the last month?
Very well
At home
Not at all
Very well
At work
Not at all
6. How well are you able to cope with that stress?
7. How did the pain that you are now experiencing occur?

a. Sudden onset with accident or definable event

b. Slow progressive onset

c. Slow progressive onset with acute exacerbation without an accident or definable event

d. A sudden onset without an accident or definable event
9. Does movement have any effect on your pain?

a. The pain is always worsened by use or movement

b. The pain is usually worsened by use and movement

c. The pain is not altered by use and movement
10. Does weather have any effect on your pain?

a. The pain is usually worse with damp or cold weather

b. The pain is occasionally worse with damp or cold weather

c. Damp or coId weather have no effect on the pain
8. How many surgical procedures have you had in order to try to eliminate the cause of your pain?

a. None or one

b. Two surgical procedures

c. Three or four surgical procedures

d. Greater than four surgical procedures
B
Fig. 33.4, cont’d

745
Diagnosis and patient presentation
11. Do you ever have trouble falling asleep or awakening from sleep?

a. No – Proceed to Question 12
b. Yes – Proceed to 11A & 11B
11A. How often do you have trouble falling asleep?

a. Trouble falling asleep every night due to pain

b. Trouble falling asleep due to pain most nights of the week

c. Occasionally having difficulty falling asleep due to pain

d. No trouble falling asleep due to pain

e. Trouble falling asleep which is not related to pain
12. Has your pain affected your intimate personal relationships?

a. No


b. Yes
16. Have you ever thought of suicide?

a. No


b. Yes
c. Previous suicide attempts
17. Have you been a victim of emotional abuse?

a. No


b. Yes
c. No comment
18. Have you been a victim of physical abuse?

a. No


b. Yes
c. No comment
19. Have you been a victim of sexual abuse?

a. No


b. Yes
c. No comment
20. Are you presently a victim of abuse?

a. No


b. Yes
c. No comment
13. Are you involved in any legal action regarding your physical complaint?

a. No


b. Yes
14. Is this a Workers' Compensation case?

a. No


b. Yes
15. Are you receiving or have you ever received psychiatric/psychological treatment?

a. No

b. Presently receiving psychiatric treatment
c. Previous psychiatric treatment
11B. How often do you awaken from sleep?

a. Awakened by pain every night

b. Awakened from sleep by pain more than 3 times per week

c. Not usually awakened from sleep by pain

d. Restless sleep or early morning awakening with or without being able to

return to sleep, both unrelated to pain
C
Fig. 33.4, cont’d
Continued

746
SECTION V
CHAPTER 33 • Nerve transfers
21. If you are retired, a student or homemaker, proceed to Question 21B
21A. Are you still working?

a. Work every day at the same pre-pain job

b. Work every day but the job is not the same as the pre-pain job, with reduced responsibility or physical activity

c. Work occasionally

d. Not presently working
21B. Are you able to do your household chores?

a. Do same level of household activities without discomfort

b. Do same level of household chores with discomfort

c. Do a reduced amount of household chores

d. Most household chores are now performed by others
22. What medications have you used in the past month?

a. No medications

b. List medications:
23. If you had three wishes for anything in the world, what would you wish for?
a.
b.
c.
D
Fig. 33.4, cont’d

747
Diagnosis and patient presentation
Hints and tips
Remember to check not only for what muscles have lost
function, but also for potential nerve transfer donors.
Hints and tips
Order baseline electrodiagnostic studies at 6–8 weeks and
subsequent testing as indicated by the injury:
• Electromyography (EMG) showing fibrillations (fibs) and
positive sharp waves (PSW) suggest denervation. Motor
unit potentials (MUP) and nascent units suggest
reinnervation.
• Do not be confused by automated EMG reporting errors
– “normal” may appear in some reports by default. If a
muscle has fibs and PSWs but the MUP column says
“normal” this may be a machine printout error – consult
with your electrodiagnostician as it more likely that there are
absent MUPS (not “normal” MUPS).
• When assessing for recovery over time, ask to check
proximal muscles first (example flexor carpi ulnaris not first
dorsal interosseous, when evaluating ulnar nerve recovery).
• Remember, the EMG provides qualitative information only
(not quantitative).
• Above all, careful communication with the
electrodiagnostician and correlation to clinical exam
findings are imperative when interpreting these test results.
the level and degree of injury and the availability of branches
(flexor carpi ulnaris, flexor carpi palmaris, palmaris longus)
for use as donor nerves. In the hand, a complete examination
of extrinsic and intrinsic function again helps to delineate the
level of injury.
Assessment of muscles and grouping the exam by periph­
eral nerve branch and/or by cervical root level pattern may
be helpful, depending on the appropriate clinical scenario.
Sensation should be examined by both dermatome and
peripheral nerve distribution, and can be helpful in distin­
guishing these injuries. The authors advocate the use of both
two-point discrimination and the ten-test to evaluate sensory
loss in the hand.14 A Tinel’s sign, the tingling sensation elicited
with percussion over a regenerating nerve, will help to local­
ize the level of nerve injury, and may also be followed on
serial clinical examination to check for signs of advancement,
indicating spontaneous recovery. An advancing Tinel’s sign
distal to the site of injury quite often precedes clinical motor
recovery.
For completeness, the presence of Horner’s syndrome and
dysfunction of nerve branches that come off the proximal
brachial plexus (dorsal scapular nerve to rhomboids, long
thoracic nerve to serratus anterior) indicate a very proximal
level of injury.
One of the most important components of the physical
examination is the simple determination of what is function­
ing, and what function has been lost. Not only does this help
to determine the level of injury, it can guide future surgical
planning. In the presence of an injury requiring surgical
intervention, it is important to examine the patient for puta­
tive nerve donors, both intraplexal and extraplexal (spinal
accessory, medial pectoral, and thoracodorsal).
Imaging
Imaging is primarily useful for confirming level of injury in
more complex closed-mechanism nerve injury patients. For
example, imaging such as computed tomography myelogram
and magnetic resonance imaging provides additional confir­
mation of a nerve root avulsion pattern. Additional X-rays,
such as shoulder films that demonstrate scapular notch-level
trauma, may provide information of localized trauma that
would make proximal transfer to the suprascapular nerve
ineffective due to the extensive zone of injury. Other plain
films such as chest X-ray might be used to evaluate pathology
such as rib fractures or diaphragm dysfunction that might
make the use of intercostal and phrenic nerves as donor
nerves less palatable, although the former is debatable.15
Electrodiagnostic testing
Electrodiagnostic testing, performed by an experienced
person, can be a useful adjunct to physical examination for
serial assessment of reinnervation in closed nerve injuries.
Electromyography records the electrical activity of muscle
fibers, tested both at rest and activity, by the insertion
of needles into the muscle. Denervated muscles will
demonstrated fibrillations and positive sharp waves on needle
insertion; however, the findings are not reliable until approxi­
mately 4 weeks after injury.16 Initial electrodiagnostic testing
should be deferred until a minimum of 6–8 weeks post-injury
to assess for signs of both axonal injury and root-level avul­
sion. Serial testing will reveal signs of reinnervation with
nascent potential and motor unit potentials in the affected
muscle groups, often prior to clinical evidence of recovery.
Detailed testing of both putative functioning donors and
non-functioning recipient muscles is important to confirm
physical exam findings. This is particularly important because
subtle abnormalities in donor muscles correlate with subse­
quent clinical results. In fact, abnormalities seen in the puta­
tive donor muscles may dictate a change to a different donor,
if available, or an understanding that results may be detri­
mentally affected.
Conduction velocity is used to measure the integrity of a
peripheral nerve (sensory nerve action potentials [SNAP] or
compound motor action potentials [CMAP]).16 A severed
nerve will lose the ability to conduct a signal as Wallerian
degeneration occurs; however, if measured too early, the
distal aspect of the nerve will still conduct, leading to an
inaccurate assessment. This is another reason for delaying
initial electrodiagnostic studies. Preganglionic injuries will be
associated with a loss of sensation but an intact SNAP and an
absent CMAP.16 Thus the level of injury can be confirmed with
electrodiagnostic studies.
In patients with no evidence of recovery 3 months after a
closed nerve injury, the balance should tilt towards consider­
ation of surgical intervention.
Overall, the complete picture, including history, physical
examination, and adjunct testing, should facilitate surgical
decision-making. Appropriate treatment for open injuries
with nerve dysfunction begs for timely management with
surgery on an urgent or semi-urgent basis. For these injuries,
direct exploration and repair have historically been the

748
SECTION V
CHAPTER 33 • Nerve transfers
avoid doing a complex nerve exploration in the setting of
dense fibrotic scar is particularly advantageous.
Nerve transfers allow for a very targeted intervention in
cases of partial nerve injury such as in treatment of a sixth-
degree or neuroma-in-continuity injury, where transfer can
be done distal to the site of injury specifically to the non-
functioning nerve branch. This allows for preservation of all
intact function and restoration of only missing function. In
addition, the ability to “supercharge” a recovering nerve is
invaluable when it is unclear whether the nerve transfer or
intrinsic recovery will be more beneficial.
Unlike tendon transfers, nerve transfers typically do not
require immobilization, which is especially valuable in
patients presenting with significant baseline stiffness. Nerve
transfers also preserve the biomechanical properties of the
musculotendinous unit, such as end organ origin, insertion,
excursion, and length–tension relationships. Finally, nerve
transfers can restore unique function such as pronation,
which is incredibly difficult to restore by traditional surgical
techniques.17
Thus nerve transfers are indicated in a number of situations
(Table 33.2), for example, in proximal brachial plexus injury
where grafting is not possible or the required distance for
reinnervation will not allow motor axons to reach the target
motor before denervation and fibrosis have occurred. In situ­
ations of extreme scarring, or major upper extremity trauma,
a nerve transfer is preferable to risking damage to critical
structures within the scarred region. Nerve transfers are also
indicated in segmental nerve loss, and in partial nerve injury
patterns with functional loss. Patients presenting in a delayed
manner with inadequate time to reinnervate the distal targets
are good candidates for distal nerve transfers. Also, patients
with sensory nerve deficits in critical regions should be con­
sidered for nerve transfer to restore sensation.
The main reason a nerve transfer should not be performed
is similar to the contraindication for any other traditional
nerve repair/graft intervention, namely end organ unrespon­
siveness. An old peripheral nerve injury will not respond to
the new “magic” of nerve transfers. Muscle that is in complete
discontinuity with the nerve for greater than 1 year will not
be reinnervated, no matter how elaborate the reinnervation
strategy employed.
More relative contraindications for nerve transfer include
issues such as the time required for regeneration, challenges
of the surgery, the anatomic knowledge required, and prob­
lems of postoperative retraining and therapy, as these tech­
niques are less familiar to hand therapists. There are some
patients, such as the young manual laborer with a radial nerve
treatment of choice, but in very proximal injuries, distal nerve
transfer can allow for more timely and successful reinnerva­
tion. In closed nerve injuries or in gunshot wounds, appropri­
ate management demands a more measured approach and
surgery should be delayed to allow for spontaneous recovery,
which is often superior to that seen in patients treated with
hasty surgery. These patients in particular may benefit from
“supercharging” with reverse end-to-side nerve transfer
procedures, which can more quickly deliver regenerating
axons to the appropriate end organ, while still allowing
slower spontaneous recovery.10
Patient selection
Hints and tips
When considering nerve transfers, be aware of the various
advantages, disadvantages, and limitations:
• Nerve transfers may allow for an unprecedented level of
timely and biomechanically appropriate return of function.
• A single donor nerve (from one muscle) can provide
individual and isolated muscle function to more than one
recipient through motor re-education and cortical
adaptation.
• It will take months to years for maximal function to be
achieved after nerve transfer (time for regeneration,
relearning and strengthening) but function can continue to
improve over years post-surgery.
• A distal nerve transfer will not directly address pain from a
proximal neuroma or neuroma-in-continuity.
• No transfer, no matter how close to the target, can restore
function after terminal muscle denervation has occurred
(that deadline occurs somewhere between 12–18 months
after nerve injury).
Nerve transfers have become increasingly popular for a
number of reasons, the most compelling of which is the “time
is muscle” issue. The biggest challenge facing peripheral
nerve surgeons is that with increasing time since injury, the
ability to achieve good motor function becomes increasingly
limited. In fact, for any nerve injury where there is complete
discontinuity with the motor end organ, no reinnervation
procedure will be able to restore muscle once denervation and
fibrosis have occurred, a process which occurs as early as 1
year. Nerve transfers, by bringing the regenerating motor
fibers closer to the target end organ more rapidly, essentially
convert a more proximal-level injury to a more distal-level
injury, thus increasing the chance of achieving meaningful
muscle function.
Another advantage of nerve transfers is that they enable
surgical reconstruction outside the zone of the original injury,
avoiding complex dissections and limiting injury to critical
neurovascular structures. In patients with brachial plexus
trauma, the proximity of vital structures (great vessels, tho­
racic duct, lung) makes the occurrence of potentially life-
threatening complications a real possibility. In other cases,
such as concomitant vascular injury, previous blast injury, or
soft-tissue deficits requiring flap reconstruction, the ability to
Table 33.2  Indications for nerve transfer
• Proximal brachial plexus injuries where grafting is not possible
• Proximal peripheral nerve injuries requiring long distance for
reinnervation of distal targets
• Severely scarred areas with risk of damage to critical structures
• Segmental nerve loss
• Major upper extremity trauma4dc
• Partial nerve injuries with functional loss
• Delayed presentation with inadequate time for reinnervation of
distal targets with grafting
• Sensory nerve deficits in critical regions

749
Examples of nerve transfer procedures for specific injury patterns
Upper plexus injury
Specific patient exam findings
Patients with upper plexus injuries present with glenohumeral
joint subluxation, loss of shoulder abduction and external
rotation, and absent elbow flexion. When C7 is also involved,
additional deficits in function may include loss of elbow
extension and weakness of wrist and digit extension. Numb­
ness over the corresponding dermatomes is noted.
Reconstruction techniques
injury, who may prefer the more rapid recovery associated
with tendon transfer at the expense of the independent fine
motor control that could be achieved through the use of nerve
transfers. The surgery itself is challenging because of the
detailed knowledge of internal nerve topography required.
Most surgeons are not formally trained in the intraneural
dissection techniques required to perform nerve transfers and
the results are not apparent until months down the line. This
requires a significant leap of faith for surgeons who are more
used to immediate gratification and a clear result in weeks,
not months or years!
Direct nerve repair and nerve grafting also remain valu­
able tools for the peripheral nerve surgeon and should
continue to be the treatment of choice in a variety of sce­
narios. These include cases of multiple nerve injuries where
there is a paucity of nerve donor material for nerve transfer.
Also, in distal single-function nerve injuries, direct or graft
repair is preferable to nerve transfer because one-to-one
function is preserved, no retraining is necessary, no donor
function is sacrificed, and the distance to the end target
is short.
Patient general health, comorbidities, and associated
injuries factor into the decision to perform nerve transfers.
These procedures can be lengthy, and are not without sig­
nificant risk from anesthesia in the fragile patient. In addi­
tion, patient compliance is an integral part of the recovery
process, and patients require education preoperatively about
the prolonged recovery and therapy times associated with
nerve transfer.
Examples of nerve transfer procedures
for specific injury patterns
Hints and tips
• Avoid paralytics, or use only short-term paralytics
with anesthesia induction to allow for nerve
stimulation.
• Minimize or avoid tourniquet time to avoid interference with
nerve stimulation.
• Use plain epinephrine in proximal incisions to minimize
blood loss without lidocaine paralysis.
• Obtain wide surgical exposure to identify nerves and
appropriate branches.
• Choice of optimal nerve donor is based on quantity of
motor axons, proximity to target muscles, synergy of
muscle function, and donor expendability.
• Conduct neurolysis with your “eyes”, except at the site of
actual transfer, to avoid prolonged dissection and increased
trauma to nerve branches.
• Confirm no intraoperative stimulation in putative recipient
before dividing donor.
• Divide donor nerve distally and recipient nerve
proximally.
• Use 9-0 nylon and the operating microscope to perform
tension-free epineurial repair.
• Use bupivacaine block at end of case for postoperative
pain control.
Hints and tips
Priorities for upper plexus injuries include restoration of
shoulder external rotation and abduction, as well as elbow
flexion. Standard transfers include: (1) spinal accessory to
suprascapular nerve; (2) medial triceps to axillary nerve; and
(3) double fascicular nerve transfer.
Use of spinal accessory nerve (cranial nerve XI) to
suprascapular nerve transfer (motor)
Restoration of shoulder stability and external rotation are
facilitated by transferring the spinal accessory nerve (cranial
nerve XI) to the suprascapular nerve. This transfer can be
conducted by either an anterior or a posterior approach. In
the posterior approach, the patient is positioned prone and
surface landmarks are used to approximate the position of
the nerves (Fig. 33.5A–D). The spinal accessory nerve runs
parallel to the border of the trapezius and is localized 44%
of the way along a line connecting the acromion to the dorsal
midline at the level of the superior border of the scapula
(Fig. 33.6). The suprascapular nerve is located midway
between the medial border of the scapula and the acromion
as it runs through the suprascapular notch.18 Dissection is
carried through the trapezius in a muscle-splitting fashion
and an end-to-end coaptation, sparing the upper trapezius
nerve branches.
For the anterior approach, a supraclavicular incision is
made; the lateral aspect of the trapezius is released off of the
clavicle and the spinal accessory nerve is identified on its
anterior surface (Fig. 33.7). The suprascapular nerve sits at the
superolateral aspect of the upper trunk, which is identified
between the anterior and middle scalene muscles. An end-to-
side approach with a partial neurectomy of the donor acces­
sory nerve is preferred as this preserves some donor function.
A short interpositional graft from the recipient suprascapular
nerve to the donor spinal accessory nerve is required to avoid
tension. A proximal crush injury to the donor nerve encour­
ages axonal sprouting such that regeneration into the recipient
suprascapular nerve occurs without loss of significant donor
nerve trapezius function.19
Use of triceps to axillary nerve transfer
(motor component)
Additional abduction of the shoulder is provided by transfer­
ring a branch of the triceps, usually from the medial head, to

750
SECTION V
CHAPTER 33 • Nerve transfers
Use of the double fascicular (ulnar/median redundant
branches to biceps brachii and brachialis branches of the
musculocutaneous) nerve transfer (motor)
Restoration of elbow flexion is achieved with the double
fascicular nerve transfer (Fig. 33.11). This transfer reinner­
vates both the biceps brachii and brachialis muscles using
redundant fascicles from the ulnar and median nerves, if
available.22 However, in cases of limited donor availability,
reinnervation of biceps alone may provide adequate anti­
gravity elbow flexion.23 A medial arm incision allows expo­
sure of the musculocutaneous, median, and ulnar nerves.
Dissection at the underside of the biceps brachii muscle
allows exposure of the proximal biceps and distal brachialis
the axillary nerve (Fig. 33.8).18,20 Better results in upper plexus
injury patients are achieved by reinnervating both the supra­
scapular and axillary nerves.21 A longitudinal incision is made
on the posterior surface of the arm (Fig. 33.9). The axillary
nerve is identified in the quadrangular space and dissected
proximally to include the branch to teres minor, then divided
proximally. The natural cleavage plane between the lateral
and long heads of the triceps muscles is identified and blunt
dissection is conducted to expose the donor radial nerve
running along the humerus. The branch to the medial triceps
sits superficially and medially on the surface of the radial
nerve as a distinct branch. The donor triceps nerve is dissected
as far distally as possible and then coapted to the axillary
nerve (Fig. 33.10).
Fig. 33.5  The posterior approach for spinal accessory to suprascapular nerve transfers. (A) The nerves can be seen in their original orientation. (B) The end-to-end transfer
has been completed. The transfer includes the functional spinal accessory nerve (donor) being transposed and coapted to the non-functional suprascapular nerve
(recipient).
A
B
Spinal accessory nerve
Spinal accessory nerve
Trapezius
Supraspinatus
Infraspinatus
Non-functional musculature
Functional musculature
Suprascapular nerve
Suprascapular nerve
Acromion

751
Examples of nerve transfer procedures for specific injury patterns
to end. Reinnervation occurs at approximately 5–6 months
postoperatively.
Other potential donors (medial pectoral nerve and
thoracodorsal nerve)
Other potential donors that can be used to restore elbow
flexion include the medial pectoral nerves and the thora­
codorsal nerve. The medial pectoral nerves are identified by
making an incision in the deltopectoral groove then dividing
the pectoralis major tendon at the humeral head for exposure;
the tendon can be reinserted using bone anchors or attaching
to the remaining tendon insertion if the tendon is initially
transected. While some advocate elevating the pectoralis
minor to gain access to the nerves, we find that simple transec­
tion of the muscle belly affords the best exposure (Fig. 33.13).
There are several branches to the pectoralis minor and these
can be followed as distally as possible into the muscle to
increase available donor nerve length.24 Often a nerve graft
will be required to reach the musculocutaneous recipient. The
thoracodorsal nerve runs from the axilla along the lateral
chest wall and can be exposed through an incision running
along the free border of latissimus dorsi.
Lower plexus injury
Specific patient exam findings
Lower plexus injuries usually involve damage to C8 and T1
nerve roots. Patients have a resultant loss of the intrinsic hand
function and variable loss of extrinsic hand and wrist func­
tion. Involvement of C7 can dramatically influence available
options for nerve transfer.
Fig. 33.6  Surface markings for posterior approach to spinal accessory to
suprascapular. The spinal accessory nerve is located 44% of the way along a line
connecting the dorsal midline to the acromion. The suprascapular nerve is located
at the halfway point between the medial border of the scapula and the acromion on
an obliquely oriented line at the superior aspect of the scapular spine. It runs in the
suprascapular notch.
Fig. 33.7  In the anterior approach to the spinal accessory to suprascapular nerve transfer, upper trapezius function is preserved by performing the nerve transfer in an
end-to-side manner. (A) To inset this transfer with no tension, an interpositional lateral antebrachial cutaneous nerve (LABC) nerve graft is used. (B) To facilitate
regenerative sprouting, injury to the donor nerve is required proximally. This is accomplished by “crushing” the nerve with a hemostat to cause a second-degree nerve
injury. (C) Wallerian degeneration occurs distal to the site of compression. (D) Axons regenerate from the level of the crush injury, with some axons following the donor
nerve and restoring function to the upper trapezius muscle, and some axons diverting into the distal recipient nerve via the LABC graft.
A
B
C
D
Spinal accessory nerve
Spinal accessory nerve
Suprascapular nerve
Suprascapular nerve
Compression site
Compression site
Epineurotomy
LABC autograft
LABC autograft
LABC autograft
LABC autograft
Proximal
Proximal
Proximal
Proximal
Distal
Distal
Distal
Distal
nerve branches, (Fig. 33.12), which are divided and draped
over to the median and ulnar nerves to determine best
donor–recipient pairings. The ulnar and median nerves are
then neurolyzed at the appropriate level, and expendable
fascicles to the flexor carpi ulnaris (FCU) (ulnar), flexor carpi
radialis (FCR), flexor digitorum superficialis (FDS), or pal­
maris longus (median) are divided distally and coapted end

752
SECTION V
CHAPTER 33 • Nerve transfers
Reconstruction techniques
There are few good direct nerve transfer options for lower
plexus injury reconstruction. Strategies include transfer of the
nerve to brachialis (a branch of the musculocutaneous nerve)
to the anterior interosseous nerve (AIN) to regain thumb and
finger flexion. The details of this technique are described
under the median nerve injury section below. The brachiora­
dialis (if function is preserved) may also be used as a donor
to the AIN.25 Additional options include the use of the supina­
tor to the posterior interosseous nerve to restore thumb and
finger extension.26
Fig. 33.8  The triceps to axillary nerve transfer via a posterior approach to the upper arm. (A) The axillary and radial nerves in their normal anatomical position. (B) The
branch to the medial head of the triceps (donor) is transposed to meet the divided end of the axillary nerve (recipient). The branch to the medial head is coapted end to end
to the axillary nerve.
A
B
Teres minor
Teres major
Triceps brachii
Non-functional musculature
Functional musculature
Superior lateral
cutaneous nerve
Nerve to lateral head
Nerve to medial head
Nerve to long head
Nerve to lateral
head
Nerve to medial
head
Nerve to
long head
Axillary nerve
Superior deltoid
motor nerve
Deep deltoid
motor nerve
Superior lateral
cutaneous nerve
Superior deltoid
motor nerve
Deep deltoid
motor nerve
Acromion
Axillary nerve
Fig. 33.9  Set-up and incision for triceps to axillary. The patient is positioned in
the prone position and draped with the entire extremity free and the medial border
of the scapula exposed. A line connecting the olecranon and the acromion is drawn
on the posterior aspect of the arm and then extended in a curvilinear fashion just
above the posterior axillary fold. Positioning is facilitated by placing a “bump”
beneath the anterior shoulder preventing internal rotation and anterior subluxation.
The arm is draped free so that distal function can be assessed with intraoperative
nerve stimulation.
Hints and tips
Priorities for lower plexus injuries include restoration of hand
extrinsic function. Restoration of hand intrinsic function is
virtually unobtainable except in the very young pediatric
patient.

753
Examples of nerve transfer procedures for specific injury patterns
Fig. 33.10  A clinical example of the triceps to axillary nerve transfer. The patient is positioned with the head to the top right. The cross-hatchings of the posterior midline
incision in the upper arm are visible and the quadrangular space is exposed. (A) The intact nerve in situ prior to division. A white vessel loop surrounds the entire nerve at
that level. (B) The divided nerve transposed caudally with the proximal-most aspect held by the forceps. The branches are clearly visible with vessel loops around motor
branches. The superior-most branch is the branch to teres minor. The sensory branch is the most inferior branch (no vessel loop) and can be visualized heading more
superficially than the other branches. (C) The cut end of the recipient axillary nerve is visible on the most proximal blue background. The radial nerve is visualized at the
base of the wound, with vessel loops around branches to the medial, long, and lateral heads of triceps. (D) The divided branch to the medial head (donor) is transposed
proximally and coapted to the recipient axillary nerve.
A
B
C
D
Fig. 33.11  A schematic of the double fascicular nerve
transfer. The divided recipient branches of the
musculocutaneous nerve (biceps brachii laterally and
brachialis medially) are transposed medially to the median
and ulnar nerves. In this example, a redundant fascicle to
flexor digitorum superficialis (median donor) is transferred to
the biceps brachii branch and a redundant fascicle of the
flexor carpi ulnaris (ulnar donor) is transferred to the
brachialis branch.
Posterior cord
Medial cord
Ulnar nerve
Radial nerve
Median nerve
Musculocutaneous nerve
Axillary nerve
Flexor carpi
ulnaris fasicle
Brachialis nerve branch
Biceps brachii
nerve branch
Lateral antebrachial
cutaneous nerve
Flexor carpi radialis fasicle
Lateral cord