This copy is for personal use only. To order printed copies, contact reprints@rsna.

org
1686
NEUROLOGIC/HEAD AND NECK IMAGING

Anatomy, Imaging, and Pathologic

Conditions of the Brachial Plexus
Brian M. Gilcrease-Garcia, MD
Swati D. Deshmukh, MD
Matthew S. Parsons, MD
Abbreviations: CIDP = chronic inflammatory
demyelinating polyneuropathy, DRG = dorsal
root ganglion, FDG = fluorine 18 fluorodeoxy-
glucose, MIP = maximum intensity projection,
MPNST = malignant PNST, PNST = periph-
eral nerve sheath tumor, SCM = sternocleido-
mastoid muscle, SNAP = sensory nerve action
potential, STIR = short π inversion recovery,
TOS = thoracic outlet syndrome, 3D = three
dimensional
RadioGraphics 2020; 40:1686–1714
https://doi.org/10.1148/rg.2020200012
Content Codes:
From the Department of Radiology, Feinberg
School of Medicine, Northwestern University,
Chicago, Ill (B.M.G., S.D.D.); and Mallinckrodt
Institute of Radiology, Washington University
School of Medicine, 510 S Kingshighway Blvd,
Box 8131, St Louis, MO 63110 (M.S.P.). Recip-
ient of a Certificate of Merit award for an educa-
tion exhibit at the 2019 RSNA Annual Meeting.
Received February 20, 2020; revision requested
March 19 and received April 13; accepted April
15. For this journal-based SA-CME activity, the
author S.D.D. has provided disclosures (see end
of article); all other authors, the editor, and the
reviewers have disclosed no relevant relation-
ships. Address correspondence to M.S.P. (e-
mail: parsonsms@wustl.edu).
© ©
RSNA, 2020
The brachial plexus is an intricate anatomic structure with an
important function: providing innervation to the upper extrem-
ity, shoulder, and upper chest. Owing to its complex form and
longitudinal course, the brachial plexus can be challenging to con-
ceptualize in three dimensions, which complicates evaluations in
standard orthogonal imaging planes. The components of the bra-
chial plexus can be determined by using key anatomic landmarks.
Applying this anatomic knowledge, a radiologist should then be
able to identify pathologic appearances of the brachial plexus by
using imaging modalities such as MRI, CT, and US. Brachial
plexopathies can be divided into two broad categories that are
based on disease origin: traumatic and nontraumatic. In the trau-
matic plexopathy group, there are distinct imaging findings and
management methods for pre- versus postganglionic injuries. For
nontraumatic plexopathies, having access to an accurate patient
history is often crucial. Knowledge of the timing of radiation
therapy is critical to diagnosing post–radiation therapy brachial
plexopathy. In acute brachial neuritis, antecedent stressors occur
within a specific time frame. Primary and secondary tumors of
the brachial plexus are not uncommon, with the most common
primary tumors being peripheral nerve sheath tumors. Direct ex-
tension and metastasis from primary malignancies such as breast
and lung cancer can occur. Although diagnosing a brachial plexus
anomaly is potentially perplexing, it can be straightforward if it is
based on foundational knowledge of anatomy, imaging findings,
and pathologic features.
RSNA, 2020 • radiographics.rsna.org

SA-CME LEARNING OBJECTIVES

After completing this journal-based SA-CME
activity, participants will be able to:
„ Recognize the various components of
the brachial plexus by using anatomic
landmarks.
Describe the distinguishing imaging
„ the patient history and performing a physical examination and electro-
features of pre- and postganglionic trau-
matic brachial plexus injuries.
Identify key features of various non-
„
traumatic brachial plexopathies.
See rsna.org/learning-center-rg.
Introduction
The brachial plexus is an intricate neural network that provides motor
and somatosensory innervation of the arm, shoulder, and upper chest.
Evaluation of brachial plexus disease typically begins with obtaining
physiologic testing. In many cases, imaging has an important role in
lesion localization and characterization and affects the management of
traumatic and nontraumatic brachial plexopathies.
Although the brachial plexus is commonly included in the field of
view at nondedicated imaging, it can be challenging for the radiolo-
gist to assess owing to its convoluted course, portions of which can
be obscured. Even with use of dedicated advanced imaging, the
findings can be difficult to correlate to traditional anatomic and
diagrammatic representations. Effective reporting of brachial plexus
imaging findings requires familiarity with the brachial plexus anat-
omy and relevant landmarks, the spectrum and categories of brachial
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1687
TEACHING POINTS
„ Various muscles, vessels, and osseous structures can be used
as landmarks for identifying the various subdivisions of the
brachial plexus on imaging studies.
„ CT myelography performed 3–4 weeks after injury is recom-
mended, as this allows any potential hemorrhagic material at
the site of injury that might displace the contrast material to
disappear. Pseudomeningoceles, which are strongly associ-
ated with root avulsion, may take 3–4 weeks to develop after
injury as well. MRI should be performed 3–4 weeks after injury
for similar reasons and to allow improvement in adjacent soft-
tissue edema.
„ Traumatic plexopathies are generally classified according to
the degree, location, and mechanism of injury. The goal is
to estimate the likelihood of spontaneous recovery and help
identify cases that would benefit from surgical management.
„ Patients with a history of breast cancer who are found to have
ulnar neuropathy at presentation should have the medial cord
interrogated carefully. For similar reasons, particular attention
should be paid to the lower trunk in patients with lung cancer
who are found to have ulnar neuropathy.
„ Thoracic outlet syndrome (TOS) refers to neurovascular im-
pingement within the thoracic outlet, resulting in significant
disability. It remains controversial because of a lack of widely
accepted diagnostic criteria and limited data regarding surgi-
cal treatment.
plexopathies, and the associated clinically rel-
evant terminology. A structured report template
used to report brachial plexus imaging findings is
available at https://radreport.org/home/RPT50822. It
is critical to review the clinical data in each case
to understand how imaging may affect patient
care. This article is intended to serve as an image-
rich review of the brachial plexus, with emphasis
on multimodality comparison of US, CT, and
MRI techniques and findings.
Brachial Plexus Anatomy
To interpret imaging studies of the brachial
plexus accurately, one must have a firm grasp of
the anatomy of this complex network of periph-
eral nerves. This knowledge extends beyond
recalling the customary mnemonic “Radiology
Techs Drink Cold Beverages” to remember the
order of the brachial subdivisions (roots, trunks,
divisions, cords, and branches) or recognizing
that the number of components in the brachial
plexus forms a palindrome (five roots, three
trunks, six divisions, three cords, five branches
[5-3-2-3-5]). Various muscles, vessels, and osse-
ous structures can be used as landmarks for iden-
tifying the various subdivisions of the brachial
plexus on imaging studies.
Classically, the brachial plexus is formed
from the ventral rami of the C5–T1 spinal
nerves. These ventral rami are the roots of the
brachial plexus. However, variant anatomy of
the brachial plexus is present in approximately
50% of the population (1). Occasionally, six or
seven roots may be found within the brachial
plexus when the C4 or T2 spinal nerve or both
these nerves contribute to the brachial plexus.
When the C4 nerve supplies the brachial plexus
without significant involvement from the T1
nerve, this process is termed a prefixed brachial
plexus, while a postfixed brachial plexus refers to
a T2 nerve contribution without a significant
contribution from the C5 nerve. Furthermore,
some subdivisions of the brachial plexus, such as
the trunks, divisions, and cords, may be spo-
radically absent. The most common anatomic
variant of brachial plexus nerves is the passage
of the C5-C6 root anterior to or through the
anterior scalene muscle (2). In this article, a
normal brachial plexus anatomy is assumed for
five anatomic landmarks: the neural foramen,
interscalene triangle, lateral border of the first
rib, medial border of the coracoid process, and
lateral border of the pectoralis minor muscle.
The first key anatomic landmark, the neural
foramen, corresponds to the origin of the bra-
chial plexus and is well demonstrated on axial
(Fig 1a, 1b) and sagittal views. Within the spinal
canal, the ventral and dorsal nerve roots exit
the spinal cord laterally; the ventral roots carry
motor fibers, while the dorsal roots carry sen-
sory fibers. The ventral and dorsal roots course
into the neural foramen, where they merge to
form the spinal nerve. The neural foramen also
approximates the location of the dorsal root
ganglion (DRG), a bulbous structure along the
dorsal root located just proximal to the union of
the ventral and dorsal roots, which contains the
first-order sensory nerve cell bodies. The DRG
serves as an important landmark for pre- versus
postganglionic injuries. Distal to the neural fora-
men, the spinal nerve divides into ventral and
dorsal rami. The dorsal rami extend posteriorly
to innervate the paraspinal muscles. The ven-
tral rami are known as the roots of the brachial
plexus and course slightly anteriorly toward the
interscalene triangle. The roots appear as five
stacked points on sagittal images, and the proxi-
mal aspect of the first rib is a useful landmark
for locating the roots of the brachial plexus in
the sagittal plane, as the T1 root is below the
rib, while the C8 root is above the rib (Fig 1c).
The interscalene triangle, the second key ana-
tomic landmark, is formed by the anterior and
middle scalene muscles. These muscles originate
from the anterior and posterior tubercles of the
cervical spine transverse processes and insert
onto the first rib. The anterior scalene muscle
originates from the C3–C6 processes, while the
middle scalene muscle originates from the C2–
C6 processes. The anterior scalene muscle inserts
1688  October Special Issue 2020 radiographics.rsna.org

Figure 1.  Drawings and MR image depict brachial plexus anatomy in axial (a, b) and sagittal (c–g) planes, with
key landmarks shown. (a, b) At the spine, the neural foramen (bisected by the dotted line in a) is an important spinal
landmark for approximating the location of the dorsal root ganglion (DRG) (* in b) and distinguishing the pre- versus
postganglionic plexus. Axial oblique T2-weighted MR image (b) at the C3-C4 spinal level shows ventral (long arrow)
and dorsal (short arrow) spinal roots coursing toward the neural foramen. The DRG appears as a slight swelling along
the dorsal nerve root within the foramen. (c) The spinal roots can be appreciated just beyond the neural foramen.
The first rib is a useful marker for identifying the C8 and T1 roots above and below the first rib, respectively. (d) The
interscalene triangle contains the trunks and subclavian artery (red circle) and is always found above the first rib.
(e) Beyond the lateral margin of the first rib and posterior to the clavicle, the three anterior and three posterior divi-
sions have a “piled” appearance and remain superior to the axillary artery (red circle). (f) At the coracoid process, the
sagittal appearance of the cords and adjacent axillary artery (red circle) resembles a paw print. (g) The main terminal
branches have a typical relationship with the axillary artery (red circle), and the identity of each nerve can be confirmed
by following the branches distally. MCN = musculocutaneous nerve.
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1689
onto the first rib anteriorly, while the middle sca-
lene muscle inserts onto it posterolaterally. The
subclavian artery ascends into the interscalene
triangle, coursing posterior to the anterior scalene
muscle. Within the medial aspect of the triangle,
the C5–C7 roots are superior to the artery, while
the C8 and T1 roots are posterior to the artery.
Along the lateral border of the middle scalene
muscle within the lateral aspect of the intersca-
lene triangle, the three trunks (upper, middle,
and lower) can be detected. The upper trunk is
formed by the union of the C5 and C6 roots,
while the lower trunk represents the union of the
C8 and T1 roots. The middle trunk is a continua-
tion of the C7 root. Like the roots, the upper and
middle trunks are superior to the artery, while
the lower trunk is posterior to the subclavian
artery. The trunks appear as three stacked points
on sagittal images (Fig 1d).
The lateral border of the first rib is the third
key anatomic landmark. As the trunks continue in-
ferolaterally, each trunk separates into an anterior
and posterior division at or near the lateral border
of the first rib. At this same location, the subcla-
vian artery becomes the axillary artery. Together,
the three anterior and posterior divisions form a
triangular cluster of six points just superior to the
artery and posterior to the midclavicle (Fig 1e).
The divisions of the brachial plexus are functional:
the anterior divisions innervate the flexor muscles
of the upper limb, and the posterior divisions in-
nervate the extensor muscles of the upper limb.
The medial border of the coracoid process, the
fourth key landmark, serves as the landmark for
the cords. As the divisions continue inferolater-
ally, they form three cords: the lateral, posterior,
and medial cords. These cords are named for
their relation to the axillary artery, with the pos-
terior cord located between the lateral and medial
cords. These three cords, along with the axillary
artery, form a three-toed “paw-print” configu-
ration on sagittal images (Fig 1f). The flexor mus-
cles of the upper limb are innervated by branches
of the lateral and medial cords, while the extensor
posterior muscles are innervated by branches of
the posterior cord.
The fifth and last anatomic landmark is the lat-
eral border of the pectoralis minor muscle, where
the cords separate into the five terminal branches.
As the posterior cord travels inferolaterally, it gives
off a branch posteriorly, looping under the scapu-
lar neck to become the axillary nerve. The remain-
ing four branches are centered around the axillary
or brachial artery (depending on the location). The
position of these branches can be approximated
into quadrants. The median nerve is located within
the anterior superior quadrant; the musculocuta-
neous nerve, in the posterior superior quadrant;
the radial nerve, in the posterior inferior quadrant;
and the ulnar nerve, in the anterior inferior quad-
rant (Fig 1g). In unclear situations, the identity of
each terminal branch can be confirmed by tracing
the branch distally.
In addition to the major components of the
brachial plexus, several additional important
branches originate or receive contributions from
the proximal plexus. These include the phrenic,
long thoracic, dorsal scapular, and suprascapular
nerves. The phrenic nerve originates from the
C3–C5 roots and turns anteriorly to pass through
or around the anterior scalene muscle, cours-
ing between the subclavian vein and artery as it
passes inferiorly into the middle region of the
mediastinum. The long thoracic nerve originates
from the C5–C6 roots and turns posteriorly to
pass through or around the middle scalene mus-
cle before descending posterior to the brachial
plexus along the surface of the serratus anterior
muscle. The dorsal scapular nerve originates from
the C5 root and turns posteriorly to pass through
the middle scalene muscle before continuing
inferiorly deep to the levator scapulae.
Last, the suprascapular nerve branches from
the upper trunk of the brachial plexus (derived
from C5–C6 roots) at a location known as Erb
point and travels laterally along the posterior
border of the clavicle, turning posteriorly at the
superior margin of the scapula to pass through the
suprascapular notch before continuing into the
supraspinatus fossa. Although all of these terminal
branches potentially have clinical significance, they
are often difficult to visualize at imaging. In this
article, we focus on the larger components of the
brachial plexus.
Peripheral Nerve Structure
The nerves of the brachial plexus are similar in
composition to other peripheral nerves throughout
the body. Although the spatial resolution of fine
microscopic anatomy is at the limit of conven-
tional imaging spatial resolution, it is helpful to
comprehend the composition of peripheral nerves
to interpret their imaging appearances and better
understand normal nerve function versus patho-
logic nerve entities.
Each peripheral nerve is composed of grouped
nerve fibers, or fascicles, surrounded by an
intricate arrangement of connective tissues that
protect the nerve and support nerve function
and metabolism. The fundamental conducting
unit is the neuronal axon, also known as a nerve
fiber. Schwann cells envelop and provide support
to every neuron, although they produce only a
conductive lipoprotein layer around certain larger
nerves. This process, known as myelination, en-
ables faster conduction. The surrounding layers
1690  October Special Issue 2020 radiographics.rsna.org

Figure 2.  Overview of peripheral nerve microstructure. (a) Drawing depicts a nerve cell axon. Each
axon is enveloped by a glial Schwann cell, which myelinates larger nerve fibers to accelerate transmission.
These axon–Schwann cell units course within a collagen matrix of the endoneurium, which is surrounded
by a tough layer of perineurium, to form a fascicle. The blood-nerve barrier exists at the level of the
perineurium and its penetrating endoneurial microvessels. The most peripheral enveloping layer of con-
nective tissue surrounding the peripheral nerve is the epineurium (3,4). (b) Coronal oblique T1-weighted
MR image at the axilla shows the normal fascicular appearance of the posterior cord as it branches into
the radial nerve (white arrowhead) and axillary nerve (black arrowhead). The nerve fascicles, which have
T1 intermediate signal intensity, are outlined by T1-hyperintense fat-equivalent connective tissue and
perineural fat and usually are more difficult to appreciate in smaller nerves.

of the endoneurium, perineurium, and epineu- Imaging Modalities and Techniques

rium structurally organize each nerve into a fas-
cicular structure (Fig 2) (3,4). It is important that
the epineurium and interfascicular tissues serve
as a “gliding layer” that allows the nerve trunk to
mechanically adapt to deformation from joint mo-
tion and enables interfascicular rearrangement in
the setting of focal compression (5). The integrity
of the neuron and supportive connective tissue is
important for normal nerve function (3,4).
The nerve fiber network within a peripheral
nerve is tremendously complex, and the fascicular
organization changes rapidly along the longitudi-
nal course of the nerve. Larger nerves carry more
fascicles and have thicker connective tissue layers
owing to their more complex cellularity. Each
nerve fascicle may contain a combination of nerve
types (sensory, motor, and/or autonomic) and a
combination of myelinated and nonmyelinated
fibers. Motor and sensory neurons are chemically
and structurally distinct. The cell bodies of motor
neurons are located within the anterior horn of the
spinal cord gray matter, while the cell bodies of
first-level sensory nerves are extramedullary and
located within the DRG.
The vascular supply to peripheral nerves is
made up of an intricate network of vessels, featur-
ing parent vessels running longitudinally along the
epineurium and perineurium and connected by
tiny penetrating vessels that extend inward into the
endoneurial space. A blood-nerve barrier at the
level of the perineurium and endoneurial capillar-
ies limits the passage of plasma constituents into
the endoneurial space containing nerve axons and
Schwann cells (4).
Radiography
An initial radiographic evaluation of the cervical
spine, shoulder, or chest may be performed in
the setting of trauma or pain. Although radio-
graphs may show normal findings in the clinical
setting of brachial plexopathy, pertinent findings
may be seen occasionally. For instance, relevant
findings may include musculoskeletal disease
that can cause compressive neuropathy, such as a
cervical rib, an anomalous first rib (a hypoplastic
rib forming pseudoarthrosis to the second rib),
an elongated C7 transverse process, or other
structural lesions between the clavicle and first
rib, such as hypertrophic callus formation from
clavicular fracture.
Tumors involving the thoracic apex, such as a
Pancoast tumor, may be detected first as a pulmo-
nary mass or osseous erosion. Symptoms of bra-
chial plexopathy, together with radiographic find-
ings of diaphragmatic elevation, suggest phrenic
nerve palsy, implicating a serious preganglionic
injury including the C4–C5 nerve roots. Gleno-
humeral arthropathy may be seen on radiographs,
with chronic brachial plexopathy due to shoulder
dysfunction related to denervation of the rotator
cuff musculature. Findings of cervical spondylosis
may suggest an alternative cause of the pain.
Ultrasonography
Overview.—US is a noninvasive, low-cost, and
well-tolerated imaging modality that can supple-
ment clinical evaluation, electrodiagnostic testing,
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1691
and cross-sectional imaging of the postganglionic
brachial plexus. A unique advantage of sono-
graphic assessment of the brachial plexus is the
ease with which dynamic imaging across a spec-
trum of neck and shoulder movements can be
performed. Furthermore, US can be used with
local anesthetics to guide peripheral nerve or intra-
muscular blocks (6–11).
Technique.—Optimal patient and sonographer
positioning is crucial for performing brachial
plexus US. The patient may be examined while
in a seated position or supine, with the head
inclined to approximately 30°–45°. The sonogra-
pher should be situated on the side of the bra-
chial plexus that is being scanned, with a clear
view of the patient’s ipsilateral neck and shoulder
and the screen. The patient should slightly extend
his or her neck and turn to the contralateral side
(6). US of the infraclavicular brachial plexus is
facilitated with the ipsilateral arm in the abducted
and externally rotated (ABER) position (7).
Since the brachial plexus is a relatively su-
perficial structure for the majority of its course
that is visualized at US, a high-frequency probe
should be used (6,7). In our practice, we typi-
cally use a 14- or 18-MHz linear-array trans-
ducer (Canon Aplio i-series; Canon Medical,
Tustin, Calif). Ultra-high-spatial-resolution
probes (with 22-MHz hockey-stick and 24-
MHz linear-array transducers) may be used for
small superficial nerves such as the long thoracic
and suprascapular nerves. To distinguish small
nerves from the vasculature, Doppler US inter-
rogation and compression are helpful (7).
The US scanning technique often begins with
placement of the probe in a transverse orientation
along the anterolateral neck. This enables iden-
tification of the nerve roots lateral to the carotid
artery and jugular vein and emerging superficial
to the transverse processes of the cervical spine
(Fig 3a–3d). While the C5–C7 roots are read-
ily visualized, the C8 and T1 nerve roots can be
difficult to identify in some individuals. Slightly
distally and with the probe in an oblique trans-
verse orientation, the distal roots and proximal
trunks are identified between the anterior and
middle scalene muscles (Fig 3e, 3f). Superficial
to the scalene muscles is the sternocleidomastoid
muscle (SCM). The subclavian artery serves as
a useful anatomic landmark, as it passes be-
tween the anterior and middle scalene muscles
and separates the C5–C7 nerve roots (above the
artery) from the C8 and T1 nerve roots (below
the artery).
Further laterally, the brachial plexus divisions
are identified adjacent to the subclavian ar-
tery; however, they typically are not completely
visualized owing to the overlying clavicle and
first rib (Fig 3g, 3h). Infraclavicular assessment
of the brachial plexus allows visualization of the
cords, with the probe in a longitudinal orienta-
tion and medial to the coracoid process (Fig
3i, 3j). Using the axillary artery as an anatomic
reference, the lateral cord is superficial and
slightly lateral to the artery, the posterior cord
is deep and lateral to the artery, and the medial
cord is deep and typically medial to the artery.
US assessment of the main terminal branches
requires imaging from an axillary window with
use of the axillary-brachial artery as an anatomic
landmark. The median nerve is lateral to the
artery, the ulnar nerve is medial to the artery,
and the radial nerve is posterior to the artery. Of
note, because the brachial plexus anatomy can
be variable, it is best to rely on known anatomic
landmarks to guide image acquisition. Compari-
son with the contralateral side can be easily per-
formed with US and is often helpful in complex
cases (6,8,10–12).
Conventional CT
CT historically has been regarded as a subop-
timal modality for assessment of the brachial
plexus relative to MRI owing to lower soft-tissue
contrast resolution and less flexible multiplanar
acquisition. However, because CT is ubiquitous,
it may be the initial cross-sectional imaging study
performed, particularly in emergency and spinal
imaging. With the improved spatial resolution
and multiplanar reconstructive capabilities of
modern multidetector CT units, portions of the
brachial plexus are evident, even at routine CT of
the neck, chest, and shoulder. CT-based contour-
ing atlases have been created and sanctioned by
the Radiation Therapy Oncology Group to help
radiation oncologists identify the brachial plexus
on CT images and avoid administering toxic
radiation doses during radiation therapy (13,14).
Although evaluation of individual nerves and
microstructural nerve abnormalities is not pos-
sible, gross abnormalities such as hematoma,
perineural scarring, and tumor involvement can
often be identified. CT is also excellent for as-
sessment of osseous anatomy, such as rib and
vertebral body erosion in the setting of malig-
nancy. In addition, CT angiography and venogra-
phy protocols involving arms-up and arms-down
patient positioning may be tailored for assess-
ment of vascular thoracic outlet syndrome (15).
CT Myelography
CT myelography involves the injection of nonionic
water-soluble iodinated contrast material into the
subarachnoid space to outline the spinal cord and
exiting nerve rootlets. It has traditionally been
1692  October Special Issue 2020 radiographics.rsna.org

Figure 3.  Drawings and US images depict the brachial plexus. (a–d) The roots of the brachial plexus can be found
deep to the SCM, posterolateral to the carotid artery, and within the interscalene triangle on transverse (b, c) and
longitudinal (d) US views. AS = anterior scalene muscle, MS = middle scalene muscle, vert = vertebral artery. (e, f) The
three trunks are resolved by scanning in a transverse orientation along the lateral aspect of the interscalene triangle,
deep to the lateral margin of the SCM. (Figure 3 continues)

the imaging examination for evaluating possible
preganglionic brachial plexus injury. There remain
limited data on the accuracy of CT myelography,
as compared to that of MRI. However, CT my-
elography may still be preferred by some surgeons
or for troubleshooting indeterminate MRI findings
(16). It may also be reasonable to use this exami-
nation for assessment of suspected brachial plexus
injury in neonates, as evaluation of such small
structures may be limited with MRI.
The diagnosis of root avulsion hinges on
findings of spinal nerve discontinuity near the
rootlet-cord interface or the presence of a pseu-
domeningocele, implying meningeal rupture. CT
myelography performed 3–4 weeks after injury
is recommended, as this allows any potential
hemorrhagic material at the site of injury that
might displace the contrast material to disappear
(17). Pseudomeningoceles, which are strongly
associated with root avulsion (18), may take 3–4
weeks to develop after injury as well. MRI should
be performed 3–4 weeks after injury for similar
reasons and to allow improvement in adjacent
soft-tissue edema. Drawbacks of CT myelogra-
phy include the invasive nature of the examina-
tion, as well as exposure to iodinated contrast
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1693

Figure 3.  (Continued) (g, h) The divisions are often difficult to visualize because the neurovascular bun-
dle has a retroclavicular course at this level. subclav = subclavian artery. (i, j) In thin patients, the terminal
branches may be visualized surrounding the axillary-brachial artery. The musculocutaneous nerve (MCN)
may not be evident and usually penetrates the coracobrachialis (originating from the coracoid process)
between its two heads, but the median, ulnar, and radial nerves are easily followed distally along the arm.

material and ionizing radiation. Owing to the
overlapping anatomy at the level of the shoulders,
streak artifact may limit evaluation of the lower
(C8–T1) root levels (19).
MRI Evaluation
MRI is a powerful tool for evaluation of nerve
anomalies and is useful for comprehensive imag-
ing evaluation of the brachial plexus from the
spinal cord to the terminal branches. Newer MRI
techniques enable visualization of the major com-
ponents of the brachial plexus and identification
of both structural and microscopic changes such
as nerve edema, degeneration, and inflammation,
which manifest as T2 signal intensity change or
abnormal enhancement.
In addition to depicting direct nerve injury,
MRI is useful for evaluating end-organ skeletal
muscle denervation. Acute denervation results in
muscular edema within days after an injury, faster
than it leads to electromyographic changes, which
may take weeks to develop. Chronic denervation
manifests as loss of muscle bulk and fatty change.
Within the first 4 weeks after injury, there may be
muscle hyperenhancement, which is possibly due
to alteration in sympathetic vascular tone (20).
Thus, MRI may help localize nerve involvement
and characterize the chronicity of injury.
MRI can be used in the setting of traumatic,
compressive, or nontraumatic brachial plexopa-
thy. In the setting of trauma, MRI is an alter-
native to CT myelography for assessment of
preganglionic nerve root avulsions, with sen-
sitivity and specificity of up to 93% and 72%,
respectively (21,22). Postganglionic lesions are
detected with similar sensitivity and specific-
ity (91% and 60%, respectively) (21). In the
nontraumatic setting, MRI may help identify
neuropathy in the setting of nonspecific shoul-
der or upper extremity symptoms. MRI findings
are included as diagnostic criteria in the diag-
nosis of inflammatory demyelinating disorders
such as chronic inflammatory demyelinating
polyneuropathy (CIDP) and multifocal motor
neuropathy (23). It is also particularly useful
in the evaluation of tumor involvement of the
brachial plexus.
There are limited data on the accuracy of
MRI for the diagnosis of peripheral neuropathy.
A 2014 systematic review (24) in which MRI
results were compared with clinical examination
and electrodiagnostic testing results revealed a
1694  October Special Issue 2020 radiographics.rsna.org
small number of studies with few patients, and
estimations calculated with pooled statistical
analysis showed hyperintensity at T2-weighted
short π inversion-recovery (STIR) MRI to have
moderate sensitivity and low specificity overall
(77% and 67%, respectively; area under receiver
operating characteristic curve [AUC], 0.85) and
nerve enlargement to have low sensitivity and
moderate specificity (63% and 84%, respectively;
AUC, 0.88).
Primary Sequences.—The major challenge in
performing MRI of the brachial plexus is obtain-
ing high-spatial-resolution images of small target
structures on the order of millimeters in the head
and neck region, where air-tissue interfaces cause
significant magnetic susceptibility. A dedicated
brachial plexus MRI examination typically
involves a combination of two-dimensional and
three-dimensional (3D) acquisitions. The two-
dimensional sequences yield better in-plane
spatial resolution and faster acquisition time.
Ideally, coronal and sagittal acquisition planes are
oriented orthogonal to the neurovascular bundles
to profile the plexus.
A T1-weighted non–fat-suppressed sequence
is useful for outlining the nerves against peri-
neural fat and fat-equivalent nerve tissue, assess-
ing fatty muscle atrophy, and outlining anatomic
relationships. A T2-weighted fat-suppressed
sequence is useful for assessing neurovascular
signal abnormality, nerve rootlets against bright
cerebrospinal fluid, soft tissue, and muscular
edema, and for identifying tumors or alternative
pathologic entities.
Although 3D acquisitions, as compared with
two-dimensional acquisitions, tend to yield
slightly lower spatial resolution owing to the
longer imaging time required to achieve an
equivalent signal-to-noise ratio, the isotropic data
enable more accurate multiplanar, thin maximum
intensity projection (MIP), and curvilinear re-
constructions, which are useful for outlining the
course of the nerves (25). The ideal 3D isotropic
acquisition is designed to augment nerve conspi-
cuity with use of heavy T2 weighting, fat suppres-
sion, and often vascular suppression techniques.
The heavy T2 weighting highlights neurovascular
structures against adjacent musculature.
Fat suppression can be achieved by using
chemical suppression, Dixon, or inversion-
recovery techniques. Suppression of the vascular
signal related to slower-moving (usually venous)
blood helps to isolate the nerve signal and is
useful for differentiating nerves from vessels.
Non–contrast material–enhanced vascular sup-
pression techniques have been described and
include the use of flow-sensitized 3D fast spin-
echo, motion-sensitized driven equilibrium, and
low b-value diffusion weighting in gradient-echo
sequences (ie, diffusion-weighted reversed fast
imaging with steady-state precession) (26–29).
Contrast material–enhanced 3D STIR MRI is a
straightforward and effective method of achiev-
ing vascular suppression at brachial plexus
imaging, as it exploits the nulling mechanism on
the basis of the T1 relaxation time (25). Intrave-
nously administered gadolinium-based contrast
material causes T1 shortening of the intravas-
cular signal such that the T1 relaxation time ap-
proaches that of fat; thus, use of a contrast-en-
hanced STIR sequence results in simultaneous
fat and vascular suppression. Therefore, despite
ongoing debate regarding the necessity of intra-
venous gadolinium-based contrast material for
brachial plexus MRI, the usefulness of this agent
for vascular suppression and characterization of
inflammatory and neoplastic processes makes
it a reasonable component of “default” imaging
protocols (30). The parameters used in a typical
MRI protocol at our institution are presented in
Table 1.
Adjunctive Sequences.—Adjunctive sequences
have been described for specific aspects of bra-
chial plexus evaluation. For example, dedicated
high-spatial-resolution 3D fluid-sensitive MRI
centered on the spinal canal, such as that involv-
ing a SPACE (sampling perfection with applica-
tion optimized contrasts using different flip angle
evolution)-T2 or constructive interference in
steady-state sequence, may be used to assess spe-
cifically for preganglionic nerve root avulsion (31).
Diffusion imaging, including both neu-
rography-specific diffusion-weighted imaging
and diffusion tractographic imaging, has been
described for the evaluation of peripheral nerve
tumors and traumatic injury. It may be help-
ful for the detection of subtle neuropathy that
is otherwise below the threshold for imaging
detection and can be used for surgical planning
(32). Diffusion imaging of peripheral nerves re-
lies on the anisotropic motion of water along the
nerve’s longitudinal axis, whereby normal nerves
exhibit diffusion restriction along their cross-
sectional plane. Various measures of diffusivity—
for example, fractional anisotropy and radial
diffusivity—may be calculated on the basis of
diffusion tractographic image acquisition and
used to estimate the degree of fiber organization
and myelin–connective tissue integrity, although
data on the clinical value of these parameters are
limited (33).
Coils.—The coil selection for MRI of the
brachial plexus affects the signal-to-noise ratio
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1695

Table 1: Sample Protocol for MRI of the Brachial Plexus

Section Thick- Intersection Echo Train

MRI Sequence ness (mm) Gap (mm) TR/TE Length Flip Angle Matrix
Scout imaging
  Sagittal T1-weighted TSE (affected side) 4 5 700/10 3 180 320 3 240
  Sagittal T2-weighted fat-suppressed 4 5 3000/50 15 180 320 3 224
TSE (affected side)
  Coronal T1-weighted TSE (midclavicle 2 2.5 790/10 4 150 320 3 376
to midclavicle)
  Coronal STIR 2 2.5 4700/55 15 150 320 3 315
(shoulder-to-shoulder FOV)
  Coronal T1-weighted fat-suppressed 2 2.5 670/10 3 150 320 3 315
Dixon FSE (shoulder-to-shoulder
FOV)
  Sagittal T1-weighted fat-suppressed 4 5 700/10 3 180 320 3 240
Dixon FSE (affected side)
Contrast-enhanced imaging
  Axial T1-weighted fat-suppressed 4 5 900/10 3 150 320 3 224
Dixon FSE (affected side)
  Coronal T1-weighted fat-suppressed 2 2.5 670/10 3 150 320 3 315
FSE (shoulder-to-shoulder FOV)
  Sagittal T1-weighted fat-suppressed 4 5 700/10 3 180 320 3 244
Dixon FSE (affected side)
  Coronal 3D STIR (shoulder-to-shoul- 1.2 NA 2600/250 145 120 448 3 120
der FOV)
  Three-plane thin MIP* 5–8 NA NA NA NA NA
Note.—FOV = field of view, FSE = fast spin echo, NA = not applicable, TR/TE = repetition time (msec)/echo
time (msec), TSE = turbo spin echo.
*For three-plane thin maximum intensity projection (MIP) MRI, 1–3-mm intersection spacing was used.

throughout the relevant field of view. Although
imaging can be performed by using a rigid
neurovascular coil, such as that used for carotid
angiography, this coil offers limited coverage
of the infraclavicular plexus. Combinations of
posterior embedded, head and neck, body, and
flexible surface coils or custom coil arrays pro-
vide the best coverage (25,34). Use of a tissue
susceptibility matching pillow and image-based
shimming may reduce B0 field inhomogeneity
and improve image quality. Using the minimal
field of view at unilateral imaging results in
better image quality; however, this must be bal-
anced against the benefit of having symmetry
for comparison with bilateral coverage. Motion
artifact related to respiration can be signifi-
cantly limiting, but it can be mitigated by using
respiratory-gating techniques in select circum-
stances (25,34).
Field Strength.—In general, high-field-strength
MRI of the brachial plexus with use of 3-T units
is considered optimal because of the higher
signal-to-noise and contrast-to-noise ratios,
which enable higher spatial resolution. High-
quality 3-T imaging more clearly depicts nerve
fascicular architecture, potentially improving
diagnostic accuracy (24). However, there are
limited data to show the diagnostic superiority
of 3.0-T versus 1.5-T MRI in the clinical setting
(22,35). In addition, high-field-strength units
exaggerate artifacts related to B0 and B1 field in-
homogeneity, for example in the setting of blood
products, metallic foreign bodies, or orthopedic
instrumentation, and 3-T imaging may not be
available in all settings. Therefore, MRI at 1.5-T
field strength may be a better examination in
select situations (33).
Normal Imaging Findings
The imaging appearance of the brachial plexus
reflects the composition of its peripheral nerve
constituents. Normal nerve trunks are longitudi-
nally uniform in size, with very gradual changes
in caliber along their length. They tend to follow
the course of adjacent vessels and are similar in
caliber. Thus, the nerve trunks may be confused
with these vessels. The internal fascicular archi-
tecture of larger nerves appears striated longi-
tudinally and has a honeycomb appearance on
cross-sectional views. Normal nerves are sharply
outlined against the surrounding perineural fat,
1696  October Special Issue 2020 radiographics.rsna.org
which may even outline the nerve through an in-
tramuscular course. The normal blood-nerve bar-
rier prevents intrinsic nerve enhancement except
at specific locations such as the DRG (36).
On US images, the normal brachial plexus
roots, trunks, and cords are visualized as dis-
crete homogeneous hypoechoic structures with a
round-ovoid shape on cross-section and a tubular
appearance in the longitudinal orientation.
There should be no evidence of focal narrowing,
disproportionate enlargement, mass lesion, or
discontinuity. The branches of the brachial plexus
demonstrate the typical US appearance of normal
peripheral nerves, with a honeycomb fascicular
architecture on cross-section and a surrounding
hyperechoic epineurium (Fig 3d) (8).
On CT images, the supraclavicular plexus can
often be visualized within the fat of the inter-
scalene triangle (Fig 4b). In the axial view, the
roots and trunks appear as an ill-defined linear
structure exiting the neural foramen, between
the origin of the anterior and middle scalene
muscles from the anterior and posterior tuber-
cles of the cervical transverse processes, respec-
tively. In the sagittal view, the roots are outlined
by a small amount of perineural fat as they exit
the neural foramen. Although the upper and
middle roots are usually obscured owing to the
proximity of the scalene muscles, the C8 and T1
roots are often visible above and below the first
rib (Fig 4b).
The retroclavicular plexus is typically obscured
in the axial view, but a sagittal view may show nu-
merous dotlike structures immediately superior
to the subclavian artery corresponding to the bra-
chial plexus divisions. At the level of the coracoid
process, the infraclavicular brachial plexus is usu-
ally evident in the axial view as a wispy striated
structure surrounding the axillary artery. In the
sagittal view, the cords and branches are usually
partially visible, but the spatial relationships rela-
tive to the neurovascular bundle are inconsistent
because of anatomic variation and differences in
upper extremity positioning. For example, shoul-
der flexion with the arms overhead (as at typical
chest CT) tends to rotate the nerves posterior to
the axillary artery.
At MRI, normal nerves are isointense to skel-
etal muscle on T1-weighted images and isoin-
tense to slightly hyperintense to skeletal muscle
on T2-weighted images (Fig 4c). It is important
to be aware that peripheral nerves, like tendons,
are susceptible to a magic angle effect owing to
the longitudinal orientation of collagen fibers
throughout the connective tissue layers surround-
ing the nerve axon. This results in artifactually
increased signal intensity when the longitudinal
course of the nerve approaches a 55° orientation
to the B0 field. Although the effect is more pro-
nounced at T1- and intermediate-weighted MRI
sequences, Chappell et al (37) showed a magic
angle effect involving the brachial plexus, even
with a brachial plexus protocol STIR sequence.
Therefore, the signal intensity of the nerves of the
brachial plexus should be compared with those
on the contralateral side, as the normal plexus
should appear symmetric. A recommended
search pattern is included in Table 2.
Pathologic Imaging Findings
The causes of brachial plexopathy can be divided
into traumatic and nontraumatic causes, as the
indications for imaging, relevant findings, and
management are distinct. Traumatic plexopathy
occurs across a broad spectrum of severities, and
imaging can be used to assess severe injury for
prognostication and to guide potential surgical
intervention. Nontraumatic plexopathy is a broad
category that includes neuritis of various causes
(eg, radiation, inflammation, infection, metabolic
condition, compression or entrapment) and neo-
plasias (benign and malignant).
Traumatic Causes of Brachial Plexopathy
Traumatic brachial plexus injuries can be devas-
tating and may result in life-altering functional
and cosmetic disability, as well as chronic pain.
Injury occurs along a spectrum of severities
and produces certain patterns, depending on
the mechanism of injury. Timely diagnosis and
management of traumatic brachial plexopathy are
essential. Nerve injuries are often overshadowed
in the setting of polytrauma, in which emergent
treatment of other life-threatening injuries takes
precedence. However, even in cases of less severe
trauma, a coexisting musculoskeletal injury may
mask underlying nerve injury and delay the
diagnosis.
Demographics and Mechanisms.—Traumatic
brachial plexus injuries usually occur in new-
borns and young adults. Neonatal brachial
plexus palsy occurs in approximately 0.2% of
live births (similar to the incidence of cerebral
palsy) (38,39). The exact causes are controver-
sial, and traction, compression, vascular disrup-
tion, and inflammatory mechanisms have been
proposed (38). Shoulder dystocia, or failure to
deliver the fetal shoulders after the head has
been delivered, is considered the strongest risk
factor for injury, and it possibly contributes to
increased traction force between the fetal head
and neck during delivery. However, nearly half
of all reported neonatal brachial plexus injuries
are reported in the absence of obstetric com-
plications (38). The point of injury is usually
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1697

Figure 4.  Normal sagittal appearance of the brachial plexus. Drawing (a) illustrates the roots, trunks, divisions, cords, and termi-
nal branches of the brachial plexus, which grossly appear on CT images (b) but are much better seen on MR images (c) obtained
with T2-weighted fat-suppressed (top row in c) and T1-weighted (bottom row in c) sequences. The roots (yellow circles in far left
drawing in a, arrows in far left images in b and c) are easily identified relative to the first rib (* in b and c) as they exit the neural
foramen (C8 root above the rib, T1 root below the rib). The three trunks (yellow circles in second drawing from left in a, black
brackets in b and c) within the interscalene triangle are superior to the subclavian artery (red circle in second drawing from left in a;
black arrowheads in second images from left in b and c). The divisions (yellow circles in third drawing from left in a, white brackets
in b and c) are usually retroclavicular and always superior to the axillary artery (red circles in third, fourth, and fifth drawings from
left in a; black arrowheads in third, fourth, and fifth images from left in b and c). The cords (yellow circles in fourth drawing from
left in a, arrows in fourth image from left in b and c) and axillary artery together form a paw print at the medial border of the
coracoid process. The main terminal branches (yellow circles in far right drawing in a, white arrowheads in b and c) surround the
axillary artery lateral to the coracoid process.
1698  October Special Issue 2020 radiographics.rsna.org
supraclavicular, at the level of the spinal nerves,
roots, or trunks (40).
The two most common clinical syndromes
are upper brachial plexus palsy (Duchenne-Erb
palsy) and lower brachial plexus palsy (Klumpke
palsy). The upper C5–C7 roots are more sus-
ceptible to postganglionic injury (rupture at an
extraforaminal location), whereas the lower C8–
T1 roots more commonly manifest with pre-
ganglionic injury (root avulsion) (41). Although
most cases resolve spontaneously, permanent
injury is not uncommon. Injuries involving the
lower trunk are more likely to result in perma-
nent deficits (38).
In adults, traumatic brachial plexus injury oc-
curs most commonly in the setting of high-energy
blunt trauma and less commonly with penetrat-
ing trauma (Fig 5). Owing to the combination
of high kinetic energy and projectile motion,
motorcycle collisions are notoriously associated
with brachial plexus injury. Surgical complica-
tions include iatrogenic lacerations (Fig 6) and
compression injuries. Gunshot injuries may result
in direct penetrating nerve injury and/or second-
ary blast injury from the shock wave.
Classifications.—Traumatic plexopathies are gen-
erally classified according to the degree, location,
and mechanism of injury. The goal is to estimate
the likelihood of spontaneous recovery and help
identify cases that would benefit from surgical
management. It is useful to understand key con-
cepts and the terminology used to describe nerve
injury to better communicate with referring clini-
cians and understand the potential alterations to
surgical management.
Lesion severity is important because it cor-
relates with the potential for recovery. Peripheral
nerves have a remarkable capacity for repair and
regeneration. If the cell body remains viable,
disrupted nerve axons can regenerate from the
proximal axonal stump in a process known as
axonal sprouting. The trajectory of sprouting
axons depends on delicate contact guidance and
chemical coordination with the surrounding
supportive tissue; therefore, the integrity of the
nerve connective tissue is instrumental to re-
covery (42). Incremental damage at the cellular
level results in increasing fibrosis, a histologi-
cally disorganized response that impairs nerve
regeneration (3). For this reason, lesion severity
is usually graded on the basis of the estimated
damage to the various layers of connective tissue
surrounding the nerve (Fig 7) (42,43).
The mildest grade of injury is neuropraxia,
or first-degree injury, which corresponds to fo-
cal demyelination without compromise of the
associated neuronal axon. Clinically, this injury
Table 2: Structures to Assess at MRI of the
Brachial Plexus
Coronal view
 Lungs
  Clavicle and ribs
  Muscles innervated by brachial plexus
  Trunks through branches of plexus
  Subclavian and axillary arteries
Sagittal view
  Cervical spine and spinal cord
  Muscles innervated by brachial plexus
  Interscalene triangle, divisions, cords
  Subclavian and axillary arteries
Axial view
  Spinal cord
  Extradural space
manifests as a transient conduction abnormality,
with the return to mostly normal function within
weeks. Axonotmesis, or second-degree injury, is
a more advanced nerve injury that disrupts the
axon itself. Axonotmesis triggers an advancing
reparative degeneration of the distal nerve known
as wallerian degeneration and is followed by ante-
grade regeneration from the proximal stump due
to axonal sprouting.
Lesions are progressively graded as second-
to fifth-degree injuries on the basis of the num-
ber of compromised supportive layers, which
corresponds to the likelihood of functional
recovery. The most severe injury is a disruption
of all layers, known as neurotmesis or nerve
transection. A sixth-degree injury indicates a
lesion comprising multiple second- to fifth-
degree injuries (Table 3) (42,43). In general,
lower-grade injuries are managed conservatively
to allow spontaneous healing, while surgical
intervention is reserved for high-grade (fourth
degree and higher) injuries.
The location of an injury also is important for
injury classification. Pre- versus postganglionic
injury is a major distinction, as preganglionic
lesions are devastating injuries that are generally
considered to be irreparable at the site of injury. In
contrast, postganglionic injuries potentially can be
repaired or treated with graft placement surgically
and portend a better prognosis. Because of the
limited time frame of muscle viability following
denervation, the level of injury also aids in deter-
mining what surgical treatment may be feasible.
Even with timely and technically perfect direct
nerve repair, the slow axonal regrowth to the end-
organ muscle may delay reinnervation beyond the
point of functional recovery. Thus, supraclavicular
lesions are often treated with alternative measures
such as nerve transfer.
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1699

Figure 5.  Complete rupture of the entire left

brachial plexus at the level of the trunks after a
fall, representing neurotmesis with fifth-degree
injury. (a) Axial nonenhanced CT image of the
cervical spine shows a hematoma (long arrow)
obliterating the fat within the left interscalene
triangle, compared with a normal-appearing
right interscalene triangle (short arrow); this
finding is highly suggestive of neurovascular in-
jury. (b) Coronal CT angiogram (MIP rendering)
of the left upper extremity shows cutoff of the
left axillary artery (arrow), consistent with arte-
rial transection, which was confirmed surgically.
(c) Coronal oblique 3D T2-weighted fat-sup-
pressed MR image obtained several weeks later
shows pan-plexus rupture at the level of the
roots (short arrow), with retraction of the distal
nerves (long arrow) and irregular thickening of
the nerve ends.

Figure 6.  Laceration of the axillary nerve during surgical excision of a shoulder lipoma. (a) Axial T1-
weighted MR image shows fatty atrophy of the teres minor (white *) and middle-posterior deltoid (black
*) muscles. (b) Coronal contrast-enhanced 3D STIR (thin MIP rendering) MR image shows thickening
and T2 hyperintensity of the axillary nerve (large arrow) with end-bulb neuroma (small arrow), consistent
with complete transection.
1700  October Special Issue 2020 radiographics.rsna.org

Figure 7.  Diagram illustrates the grading of classic traumatic peripheral nerve injury based on an “inside-out” model derived from
the Seddon and Sunderland classifications. Conduction block or demyelination represents the mildest form of injury, while axonal
discontinuity results in wallerian degeneration of the distal nerve, with the potential for regrowth. Higher-grade injury causes damage
to the surrounding supportive connective tissue, limiting regeneration (42,43).

Table 3: Classification of Traumatic Brachial Plexopathy

Seddon Sunderland and MacKin-

Classification non Classifications Description Natural History Management
Neuropraxia First degree Impaired nerve conduction Recovery is likely, Conservative
(ie, axonal demyelin- mediated by glial
ation), with intact axons cell repair
and connective tissue
layers
Axonotmesis Second degree Axonal disruption, with Recovery is likely Conservative
intact endoneurium, peri- but prolonged
neurium, and epineurium owing to wallerian
degeneration
Third degree Axonal and endoneurial Regeneration is Conservative
disruption, with intact hindered by mild
perineurium and epineu- fibrosis; recovery
rium is likely with mild
deficits
Fourth degree Axonal, endoneurial, and Regeneration is Surgery may be
perineurial disruption, hindered by mod- considered
with intact epineurium erate to severe
fibrosis; recovery
is unlikely, with
serious deficits
Neurotmesis Fifth degree Complete nerve disruption No chance of spon- Surgery may be
(ie, complete rupture or taneous recovery; considered
laceration) neuroma forma-
tion
Sixth degree Any combination of first- to Surgery may be
fifth-degree injuries considered
Note.—Data are based on the Seddon, Sunderland, and MacKinnon classifications (43).

Last, the mechanism of injury is an important Preganglionic Injury.—A preganglionic injury

consideration. Penetrating trauma resulting in
focal nerve laceration, which often involves less
wound contamination, is associated with a bet-
ter prognosis and may be repaired expediently.
Blunt trauma is often more difficult to assess, with
high-grade lesions manifesting as either continuity
or discontinuity (“rupture”), and distinguishing
viable from nonviable tissue can be challenging.
usually consists of an avulsion of the nerve rootlets
from the spinal cord. A diagnosis of root avulsion
is important because it directly affects treatment
and portends a worsened prognosis, as an injury at
the root-cord interface cannot be directly repaired.
Although imaging may be used for preoperative
planning and patient counseling, surgical explora-
tion remains the reference standard for diagnosis
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1701
of nerve root avulsion. Investigators in a recent
systematic review of MRI for presurgical assess-
ment of preganglionic injury (22) estimated a
mean sensitivity of 93% and a mean specificity of
72%. Ideally, imaging of suspected preganglionic
injury is performed at least 3–4 weeks after the
injury, as this allows resolution of acute edema
and subarachnoid hemorrhage and formation of a
pseudomeningocele (17).
CT myelography or MRI may show discon-
tinuity of the ventral or dorsal nerve roots from
the spinal cord as a direct sign of root avulsion.
This occurs more often with high-energy traction
injury, in which the roots can be retracted beyond
the neural foramen and into the supraclavicular
fossa. In advanced cases, root avulsion can be
visualized at US as discontinuity of the affected
nerve root (7). However, data in the surgical
literature (44) suggest that subtle root avulsion
in which the root remains fixed within the neural
foramen comprises a significant number of pre-
ganglionic injuries.
One of the most important secondary find-
ings of root avulsion is a pseudomeningocele, a
leakage of cerebrospinal fluid through a menin-
geal tear. A pseudomeningocele may appear as
an expanded appearance of the nerve root sleeve
or a cystic collection that can track through
the neural foramen and communicate with the
subarachnoid space at CT myelography (Fig
8a, 8b). Pseudomeningocele occurs with root
avulsion because the dura mater and arachnoid
mater are continuous with the nerve epineurium
and outer perineurium at the subarachnoid
angle within the neural foramen (5). Although
a pseudomeningocele is a useful indicator of
preganglionic injury, it is important to recog-
nize that up to 23% of root avulsions do not
have an associated pseudomeningocele, and
pseudomeningocele-like lesions are identified
in the absence of root avulsion in up to 24% of
cases (22,45). The differential diagnosis should
include nontraumatic extradural meningeal cyst,
although this is uncommon at the cervicotho-
racic junction.
Other signs of preganglionic injury include
spinal cord edema near the level of a root avul-
sion. The cord itself may be lateralized within the
spinal canal, either away from the site of injury
(contralateral) acutely or toward the side of the
injury (ipsilateral) following the development
of scar tissue. (44). Denervation change of the
ipsilateral paraspinal muscles, which are supplied
by the dorsal branch of the spinal nerve, also sug-
gests a preganglionic injury (Fig 9) (46).
Postganglionic Injury.—Traumatic brachial
plexopathy may manifest as a focal caliber change
of the nerve trunk, loss of fascicular architecture,
nerve trunk or fascicular discontinuity, neuroma
formation, perineural scarring, or nerve signal
intensity abnormality at MRI (Fig 10). Although
imaging findings of traumatic neuropathy do not
directly correlate with the classic injury grading
schemes, the more important distinction of low-
grade (nonsurgical) versus high-grade lesions can
often be made. For example, neurophysiologic
testing may yield evidence of axonal injury, but
imaging can help differentiate a low-grade injury
from nerve discontinuity (47).
In addition, imaging may be useful for sur-
gical planning. US has been shown to affect
disease management in up to 58% of traumatic
nerve lesions, although it has limited sensitiv-
ity for C8 and T1 nerve injuries (48,49). Al-
though there are limited data on the accuracy of
MRI for distinguishing low- versus high-grade
injuries, this modality was shown to have 75%
sensitivity and 83% specificity in a small study
(50) involving 24 patients with posttraumatic
sciatic neuropathy.
Imaging manifestations parallel the histo-
pathologic changes observed after peripheral
nerve injury. Following traumatic injury, nerve
repair commences in a predictable sequence of
reparative degeneration and subsequent regen-
eration and is mediated by complex intracellular
and paracrine molecular signaling. Soon after the
injury, reactive Schwann cells and macrophages
within the endoneurium begin breaking down
damaged myelin and axons, and subsequent
extracellular fluid shifts result in endoneurial
edema after several days (4,42,51,52). If there
is an axonal disruption (axonotmesis or second-
degree injury), the degeneration and regeneration
advance distally (in wallerian degeneration). In
animal models, this acute inflammatory response
has been shown to correspond to abnormal T2
hyperintensity within the nerves as early as 24–48
hours after the injury. The endoneurial edema is
responsible for macroscopic and fascicular nerve
enlargement, and probably also contributes to T2
signal intensity alteration (51). Given that these
findings represent a generalized reparative re-
sponse, it is not surprising that T2 signal intensity
and nerve enlargement are nonspecific and may
be seen in both low- and high-grade traumatic
injuries (50).
Nerve trunk or fascicular discontinuity is a di-
rect sign of high-grade injury (neurotmesis) and
may occur with blunt (rupture) or penetrating
(laceration) trauma. On US scans, partial tran-
section of a nerve is best visualized in the longitu-
dinal orientation, which demonstrates a partial-
thickness cleft through the nerve, with disruption
of the fascicular architecture and an associated
1702  October Special Issue 2020 radiographics.rsna.org

Figure 8.  Pseudomeningocele in a 31-year-old man who presented with right upper extremity weakness 3 months after a motor-
cycle collision. Axial (a–c) and oblique sagittal (d) CT myelographic images demonstrate a pseudomeningocele (arrow in a and b,
small arrow in c, * in d) originating from the level of the right C5–T1 neural foramen, with discontinuity of the C8 nerve rootlets (large
arrow in c), as well as a contralateral shift of the spinal cord.

Figure 9.  Axial-view drawing of the cervical spine at the level of the
neural foramina illustrates imaging findings of preganglionic avulsion
injury: avulsion or discontinuity of the ventral and/or dorsal roots; local
spinal cord edema; an expanded appearance of the ipsilateral nerve root
sleeve; pseudomeningocele, which may extend through the neural fora-
men; and denervation change of the ipsilateral paraspinal musculature in
the setting of anterior root injury. Avulsion may occur at multiple levels,
and the postganglionic nerves must be scrutinized for preganglionic and
postganglionic injuries.

overlying soft-tissue abnormality corresponding Traumatic neuroma is generally considered a

to the site of penetrating trauma.
At MRI, the area of nerve discontinuity may
be best appreciated on coronal or axial views,
and there is usually abnormal T2 hyperintensity
and irregular morphology of the surrounding
nerve. The distance between the discontinu-
ous proximal and distal nerve ends (nerve gap)
should be reported, as this may affect the plan
for surgical repair.
finding of high-grade injury because it represents
the sequela of irremediable connective tissue
damage and failed regeneration (Sunderland
fourth- to fifth-degree injury). Histologically,
traumatic neuroma is a disorganized nonencap-
sulated proliferation of axons and additional cells
within a densely fibrotic matrix. This prolifera-
tion, the result of haphazard axon sprouting,
occurs at the proximal stump of a complete nerve
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1703
Figure 10.  Drawing illustrates imaging findings of postganglionic nerve injury, which include fascicular or gross nerve trunk enlarge-
ment, loss of fascicular architecture, and intrinsic MRI signal intensity alteration, which is seen in neuritis of any cause. Perineural scar-
ring appears as ill-defined soft tissue disrupting the smooth perineural fat planes. Partial or complete nerve disruption and neuroma
(in-continuity or end-bulb neuroma) are indicators of high-grade injury.
transection (end-bulb neuroma). However, it also
occurs with incomplete disruptions (neuroma in-
continuity), and the conduction of adjacent intact
fibers may be maintained. Neuromas tend to be
small, usually less than 2 cm (53).
At US, a neuroma is visualized as a focal thick-
ening of the affected nerve with loss of fascicular
definition (7,12). At MRI, neuromas appear as
T1-isointense, T2-hyperintense oval lesions with
ill-defined margins in continuity with the par-
ent nerve. The T2 appearance may be heteroge-
neous, and there is usually avid enhancement.
Although a neuroma may resemble a peripheral
nerve sheath tumor, discontinuity of the parent
nerve and a history of trauma are helpful for the
diagnosis of end-bulb neuroma. All end-bulb
neuromas and many neuromas in-continuity are
associated with muscle denervation change (53).
Soft-tissue abnormalities may provide im-
portant information about a neurologic injury.
Although skeletal muscle denervation change at
MRI implies at least axonotmesis (second-degree
injury), it is not specific for low- versus high-
grade injury (47). The full extent of muscular
denervation may not be appreciated if the af-
fected end-organ musculature is distal to the field
of view. Posttraumatic or surgical fluid collections
may be evident at US, CT, or MRI, and hema-
toma within the interscalene triangle or coursing
along the neurovascular bundle is suggestive of
brachial plexus injury.
In the late posttraumatic injury setting, peri-
neural fibrosis and scar encasement of the bra-
chial plexus may occur and are believed to cor-
relate with the grade of injury and likelihood of
recovery (4,42). At imaging, perineural scarring
appears as the loss of the distinct uniform plane
between the nerve fascicles and the fatty perineu-
rial tissue. US can be helpful for the detection of
perineural fibrosis and scar encasement along the
superficial portions of the brachial plexus (8,12).
At MRI, perineural fibrosis is best appreciated on
T1-weighted or proton-density–weighted images
without fat suppression (Table 4).
Management.—The management of traumatic
brachial plexopathy requires a multidisciplinary
approach, beginning with a meticulous diagnos-
tic evaluation, because accurate diagnosis and
classification of injury are important for deter-
mining the appropriate treatment (43,54). The
radiologist should be familiar with the general
tenets of management. The majority of traumatic
brachial plexopathies are low-grade (first- and
second-degree) injuries and recover with conser-
vative management. Intermediate-grade (third-
degree) injuries heal with mild fibrosis and mild
functional deficits. High-grade (fourth- and
fifth-degree) injuries have low or no potential for
recovery and are generally considered to require
surgery. Preganglionic lesions (root avulsion) can-
not be repaired at the site of injury, although they
may be managed with use of a more distal nerve
or myotendinous transfer to preserve function.
Obtaining the medical history and perform-
ing a physical examination, including a detailed
sensory and motor function assessment, are
critical for identifying neuromuscular deficits
and determining the chronicity of injury (43).
Electrophysiologic testing and imaging are
considered adjunctive examinations, and their
usefulness depends on the clinical scenario. For
example, for high-grade traumatic plexopathy,
preoperative imaging of the brachial plexus
may help to reduce the surgical time and extent
of surgical dissection (41). Electrophysiologic
testing, including nerve conduction and electro-
myographic studies, is helpful for confirming a
diagnosis, localizing the level of the lesion, and
estimating the severity of axon loss. It also helps
in distinguishing preganglionic from postgangli-
onic lesions.
1704  October Special Issue 2020 radiographics.rsna.org

Table 4: Features of Preganglionic and Postganglionic Injuries

Feature Preganglionic Injury Postganglionic Injury

Direct sign of T2 hyperintensity of spinal cord at level of injury Nerve T2 hyperintensity at site of injury
injury Discontinuity of anterior and posterior nerve Discontinuity distal to neural foramen
rootlets Nerve thickening or loss of fascicular
Expanded appearance of nerve root sleeve architecture
Indirect sign of Pseudomeningocele Denervation changes limited to distal
injury Denervation changes involving ipsilateral paraspi- end-organ musculature
nal musculature
Sign of repara- … Nerve T2 hyperintensity and/or thicken-
tive response ing distal to injury due to wallerian
degeneration
Perineural scarring
In-continuity or end-bulb neuroma
Electrodiagnos- Normal SNAP maintained in insensate nerve Decreased amplitude or absence of SNAP
tic findings distribution in second-degree or higher injury
Management Primary repair at cord–spinal nerve interface not First- to third-degree injuries managed
possible conservatively
Nerve or myotendinous transfer Fourth- to fifth-degree injuries managed
with primary repair, nerve graft place-
ment, nerve or myotendinous transfer
Note.—SNAP = sensory nerve action potential.

The sensory nerve action potential (SNAP) is
important specifically for localizing the lesion as
pre- or postganglionic. The cell body of the sen-
sory neuron is located within the DRG; therefore,
the SNAP is preserved in lesions proximal to the
DRG owing to ongoing postganglionic electrical
activity. In patients with a preganglionic lesion,
the SNAP is maintained despite the extremity be-
ing insensate in the dermatomal distribution. The
SNAP is not present in postganglionic or com-
bined pre- and postganglionic lesions (18).
For high-grade lesions, the timing of repair
usually depends on the mechanism of injury.
Penetrating trauma with minimal contamination
may be managed by means of surgical explora-
tion, with the potential for primary repair within
72 hours. In contrast, blunt trauma is often ob-
served for at least 3 months to allow the injury to
“declare itself” (ie, fully manifest) and to assess
for evidence of any spontaneous recovery (42).
Similarly, infants with neonatal brachial plexus
palsy are typically given 3 months to demonstrate
evidence of spontaneous recovery or are evalu-
ated more expediently in the setting of pan–bra-
chial plexus deficit (40,41).
The basic types of microreconstructive nerve
surgery include direct nerve repair, nerve graft
placement, and nerve transfer. Nerve repair
involves suturing discontinuous injured nerves
together, with tension-free apposition and care-
ful realignment of the fascicles. When tension-free
apposition is not possible—for example, after
débridement of nonviable tissue—the severed
nerve may be reconnected by using an autograft
or allograft to bridge the gap and reconnect the
nerves at two separate suture points. Lysis of
perineural or interfascicular adhesions (neurolysis)
may be necessary. Nerve transfer involves resecting
a normal peripheral nerve segment and connecting
it to a functionally significant denervated nerve.
For example, an intercostal donor nerve may be
used to reconnect a denervated musculocutaneous
nerve to restore elbow flexion (19).
Preganglionic (root avulsion) injuries are not
directly repaired, and functional deficits of the
upper extremity may be managed with distal nerve
or myotendinous transfer. Postganglionic injuries
may be treated by means of primary nerve repair,
nerve graft placement, or distal nerve or tendon
transfer (43). Even in patients with severe injury,
surgical nerve repair often enables restoration to a
functional useful limb, even if only to provide sup-
port to the uninjured side (55). In general, restora-
tion of some elbow flexion and shoulder abduction
is the priority (19,55).
Nontraumatic Causes of Brachial
Plexopathy
Nontraumatic brachial plexopathy includes
inflammatory and compressive processes. These
abnormalities also include tumors that primarily
or secondarily involve the brachial plexus.
Postirradiation Brachial Plexopathy
Lower neck, upper chest, and breast malignan-
cies are commonly treated with radiation therapy
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1705
Figure 11.  Radiation neuritis in a 65-year-old man who
presented with left upper extremity pain and weakness
7 years after undergoing radiation therapy for left tonsil-
lar carcinoma. Coronal contrast-enhanced 3D STIR MR
image (thin MIP rendering) of the left brachial plexus
shows longitudinal extension of fusiform thickening and
T2 hyperintensity of the roots to the divisions (arrows),
compatible with classic delayed radiation neuritis.
in the suprascapular and/or axillary regions.
Radiation-induced brachial plexopathy (RIBP) in
patients with breast cancer was first reported in
1966, when patients received relatively high doses
of radiation to the brachial plexus owing to the
use of older treatment techniques and a lack of
awareness of the radiosensitivity of nerve tissue.
RIBP has also been identified in patients who
were treated with radiation therapy for apical
lung cancer and head and neck cancers (56,57).
Consequently, the brachial plexus has been
identified as an organ at risk, with specific dose
constraints and contouring guidelines sanctioned
by the Radiation Therapy Oncology Group to
prevent neurotoxicity (13,58).
Two main clinical syndromes of RIBP,
corresponding to distinct pathophysiologic
mechanisms, are described: early transient
radiation-induced plexopathy and classic pro-
gressive radiation plexopathy (59,60). Radiation
exposure leads to immediate lethal and sub-
lethal oxidative molecular damage of connec-
tive tissues, setting off a complex biochemical
cascade of events (60). Early transient radiation-
induced plexopathy most commonly manifests
3–10 months following radiation therapy and is
believed to be secondary to an acute inflamma-
tory response and small-vessel ischemia related
to endothelial cell damage (58,60). Symptoms
tend to be mild and include distal upper extrem-
ity paresthesia with variable pain (58).
In contrast, classic progressive radiation
plexopathy has a widely reported latency period
for symptom onset of between 6 months and 30
years following radiation treatment. It is caused
by progressive fibrosis of the perineural con-
nective tissues, with or without associated acute
inflammation, which results in entrapment of
nerve fibers, thickening of the endoneurium,
demyelination, and damage to small vessels of
the epineurial plexus (60–62). Symptoms of
classic progressive RIBP are variable but tend to
manifest as insidious upper extremity dysesthe-
sia that progresses to pain and worsening motor
dysfunction. Rarely, acute brachial plexopathy in
the setting of postradiation subclavian vascular
occlusion has been reported (63).
In patients who are found to have new bra-
chial plexopathy and a history of malignancy
treated with local radiation therapy, US and
MRI can be used to help distinguish RIBP from
recurrent or metastatic cancer. RIBP is visual-
ized at US as a hyperechoic thickening of the
brachial plexus and surrounding fat (8,12). MRI
findings of radiation neuritis include smooth
longitudinal thickening of the nerves, often with
increased T2 signal intensity and longitudinal
thin enhancement (Fig 11) (61,64). Associated
perineural fibrosis appears as ill-defined tissue
that effaces the normal perineural fat planes
on T1-weighted MR images and has a variable
T2 appearance, hypointense or hyperintense,
with the latter believed to represent vascularized
scar tissue. In comparison, tumor or perineural
metastasis may have similar signal characteris-
tics, T1 hypointense and T2 hyperintense, but
is more likely to appear as a nodular discretely
enhancing lesion (59,64).
It has been suggested that lesion morphology
may be more helpful than signal intensity charac-
teristics for distinguishing neoplastic involvement
(59). When the diagnosis remains uncertain, fluo-
rine-18 fluorodeoxyglucose (FDG) PET can be
helpful, as RIBP manifests with minimal or mild
avidity, while a tumor is more likely to be frankly
hypermetabolic (64).
Acute Brachial Neuritis
Acute brachial neuritis, also known as Parson-
age-Turner syndrome or idiopathic neuralgia
amyotrophy, classically manifests as acute-onset
pain of the upper extremity that lasts for hours
to several weeks and gives way to numbness and
weakness within hours to weeks after the initial
pain. It is more common in males and more
often unilateral. Symptoms characteristically
occur in a patchy distribution, affecting multiple
peripheral nerves. There is a predilection for in-
volvement of the upper and middle trunks of the
brachial plexus, although extrabrachial nerves
such as the phrenic nerve and even the lumbo-
sacral plexus can be involved. Medial scapular
winging is a classic physical examination finding
(65). Autonomic symptoms are less common,
1706  October Special Issue 2020 radiographics.rsna.org
Figure 12.  Acute brachial neuritis in a 35-year-old man with spontaneous acute arm pain and weakness. Sagit-
tal T1-weighted (a) and STIR (b) MR images show edema and fatty atrophy of the supraspinatus (short arrow)
and infraspinatus (long arrow) muscles, compatible with subacute denervation change. The patient was clini-
cally diagnosed with acute brachial neuritis.
and the presence of Horner syndrome should
prompt further imaging to assess for a structural
lesion (66).
The cause of acute brachial neuritis is not
known. However, various antecedent stressors,
including infection, minor trauma, unaccustomed
strenuous exercise, childbirth, and surgery occur-
ring within 24 hours to 1–2 weeks before symp-
tom onset have been suggested (66). Symptoms
are managed conservatively with steroids, and
pharmacologic analgesia is used for pain man-
agement (65). Although most symptoms tend to
slowly improve within 3 years, some degree of
chronic pain and functional deficit persisting be-
yond 3 years after onset has been reported (65).
The diagnosis of acute brachial neuritis is
usually made clinically on the basis of the typi-
cal manifestation and distribution of symptoms
of this disease. Adjunctive electromyographic
testing has been advocated to confirm the dis-
tribution of nerve involvement and help assess
improvement over time. Electromyographic
testing most commonly reveals single or mul-
tiple mononeuropathies. Although basic imaging
such as chest radiography may be performed to
exclude alternative pathologic entities, includ-
ing cervical rib or apical lung cancer, dedicated
MRI of the cervical spine or brachial plexus
is usually reserved for atypical or progressive
cases. Findings of brachial neuritis may also be
discovered during evaluation for other suspected
causes of shoulder pain (eg, rotator cuff tear).
Although the early literature on imaging of
acute brachial neuritis was focused on findings
related to muscular denervation, more recent
studies using MR neurography techniques
(66,67) have shown that intrinsic nerve abnor-
mality involving one or multiple levels of the
plexus may be detected. An abnormal appearance
of the brachial plexus is most often localized to
the level of the roots to cords. The C5 root is the
most common nerve root involved, and the lateral
cord is the most common cord involved (66).
Muscular denervation changes in acute bra-
chial neuritis are typical and usually involve two
or more muscles, most commonly the supra-
spinatus muscle followed by the infraspinatus
muscle (Fig 12) (66). The most common dener-
vation pattern is acute or subacute, with muscle
edema and varying degrees of fatty atrophy noted
in up to two-thirds of cases. Although chronic de-
nervation (ie, isolated atrophy) is described in up
to one-third of cases, it is less common (66,68).
Although imaging findings are not commonly
followed up, the resolution of muscular changes
with symptom improvement has been seen in a
few cases (68).
Although MRI is currently the standard modal-
ity for imaging acute brachial neuritis owing to
capability to depict early denervation changes,
US with ultra–high-resolution probes also can be
performed. US findings of Parsonage-Turner syn-
drome may include segmental nerve enlargement
or focal nerve constriction, with the suprascapular
nerve most commonly affected (7). Assessment of
the spinoglenoid notch should be included in the
US protocol, given that the differential diagnosis
for suprascapular nerve pathologic entities in-
cludes spinoglenoid notch cyst (8).
Brachial Plexus Tumors
The brachial plexus may be affected by primary
or secondary neoplasms. Primary tumors of the
brachial plexus are considered rare, but the true
incidence is unknown because most of these
neoplasms are benign and asymptomatic. It is
important to consider benign primary tumors,
as they may be misdiagnosed as metastasis in
the setting of another malignancy. Imaging may
help with the initial diagnosis, tumor character-
ization, and localization to direct surgical biopsy
in the setting of suspected malignancy. It is
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1707
important to provide a precise description of the
suspected benign or malignant brachial plexus
tumor, including lesion size, nerve(s) involved,
nerve location, and soft-tissue involvement, to
guide the surgical approach and assess resect-
ability. The boundaries of tumor involvement
should be carefully corroborated by using all
available imaging sequences, keeping in mind
that some T2 hyperintensity of the nerve adja-
cent to the lesion may be reactive. Any uncer-
tainty should be explicitly communicated to the
surgeon (34).
Benign Primary Tumors.—Peripheral nerve sheath
tumors (PNSTs) are the most common primary
tumors of the brachial plexus. In the body, benign
PNST is by far the most common and represents
a subset of nonaggressive neuroepithelial tumors
that include schwannoma and neurofibroma.
Schwannoma is a slow-growing tumor comprised
of differentiated Schwann cells. Although it
mainly occurs sporadically, it can manifest with
neurofibromatosis type 1 (NF1) and neurofi-
bromatosis type 2. Schwannoma is one of only
a few truly encapsulated tumors, as it remains
contained within the parent nerve epineurium as
it grows (69). This explains why larger schwan-
noma tumors have a typical eccentric appearance
in relation to the peripheral nerve, closely joined
to the nerve fibers and yet surgically separable
(70). Microscopically, schwannoma characteristi-
cally has distinct zones of hypercellularity and
hypocellularity known as Antoni A and Antoni B
zones, respectively (69).
Most schwannomas are asymptomatic or mini-
mally symptomatic, while those causing pain or
progressive neurologic symptoms are considered
for surgical resection (70). Surgical studies (70)
have shown that most symptomatic schwannoma
lesions involve the supraclavicular plexus. Malig-
nant transformation of schwannoma is exceed-
ingly rare, with only a few case reports (71,72)
describing transformation to malignant PNST
(MPNST) or angiosarcoma.
Neurofibroma is a more variable tumor that
has localized, diffuse, or plexiform variants. The
localized form is most common and may oc-
cur along peripheral nerves in the superficial or
deep soft tissues. It mainly occurs sporadically,
although there is a strong association with NF1.
Microscopically, the tumor comprises a vari-
ety of proliferating peripheral nerve cells, pre-
dominantly Schwann cells in combination with
fibroblasts, nerve axons, and sometimes perineu-
rium-like cells. In contrast to schwannoma, neu-
rofibroma infiltrates the adjacent nerve fascicles
as it grows, making it difficult to fully resect (73).
Malignant transformation of neurofibroma is rare
but more common than malignant transforma-
tion of schwannoma.
Plexiform neurofibroma is a rare subtype of
neurofibroma that is believed to be congenital
and manifests as a tortuous and multinodular
expansion of a nerve. Plexiform neurofibroma oc-
curs mainly with NF1 or neurofibromatosis type
3 (schwannomatosis). Plexiform neurofibroma
is notably recognized as having a higher risk of
malignant transformation (6%–10%) (74).
Benign PNST has a characteristic imaging ap-
pearance and can be diagnosed with reasonable
confidence in the absence of atypical findings. At
US, schwannoma and neurofibroma appear as
oval homogeneous hypoechoic masses involving
multiple fascicles of a nerve, with limited flow on
Doppler US images (8,10). At CT, they appear
as low-attenuation (15–30-HU) masses owing
to a mucinous matrix with lipid components.
At MRI, schwannoma and neurofibroma are
T2-hyperintense homogeneously enhancing oval
lesions with smooth circumscribed margins that
follow the longitudinal axis of the nerve (34). The
parent nerve often can be seen entering and exit-
ing the lesion, although this may not be evident
in small tumors (75). Most PNSTs are solitary,
but neurofibromas may be complex and feature
plexiform components, as suggested by a partial
fusiform component or fascicular nerve enlarge-
ment (34). Schwannomas and neurofibromas
are often indistinguishable with use of imaging
alone, although schwannomas are more likely to
be eccentric to the parent nerve owing to their
histologic growth pattern.
A “target sign” of central T2 hypointensity and
peripheral T2 hyperintensity, with reversal of the
target sign following contrast material adminis-
tration, is more common with neurofibroma and
corresponds histologically to a central area of col-
lagen surrounded by myxomatous tissue. How-
ever, the target sign is present in only a subset of
neurofibromas, and a similar pattern has been
observed less commonly in both schwannoma
(likely corresponding to Antoni A and B zones
of varying cellularity) and MPNST and thus
has limited utility (34,76,77). In larger benign
PNSTs, modest internal fatty or cystic change
is common (for example, in so-called “ancient
schwannomas”), although more extensive areas
of cystic change or heterogeneous enhancement
should raise suspicion for malignant degenera-
tion (34,75). Muscular denervation change in the
distribution of the parent nerve may occur in up
to 33% of cases and is more common with larger
tumors (75).
Malignant Primary Tumors.—MPNST is rare, but
it is the most common primary malignant tumor
1708  October Special Issue 2020 radiographics.rsna.org

Figure 13.  MPNST in a 21-year-old woman with

NF1 and known neurofibromas who presented with
left upper extremity pain and paresthesia. (a) Pos-
teroanterior chest radiograph shows a soft-tissue
mass (arrow) at the left thoracic apex. (b, c) Sagittal
STIR (b) and contrast-enhanced T1-weighted fat-
suppressed (c) MR images show a homogeneous
hyperintense enhancing mass (small arrow) ex-
panding the interscalene triangle near the first rib,
displacing the scalene muscles (black arrowheads)
superiorly, the subclavian artery (white arrowhead
in b) anteriorly, and the apical lung (large arrow)
inferiorly. Comparison with prior imaging find-
ings (not shown) revealed significant enlargement,
and subsequent FDG PET/CT images (not shown)
showed avidity, with a maximal standardized up-
take value greater than 3.5 (not shown). These find-
ings are consistent with the development of MPNST
from known neurofibroma.

of the brachial plexus. It exists as a spectrum
of disease that ranges from neurofibroma with
atypia to high-grade MPNST. Approximately
half of MPNSTs are associated with NF1, and
half occur sporadically. Although prior radiation
therapy is considered a risk factor, it is believed
to be responsible for only a small percentage of
MPNST cases, with an average latency period
following radiation treatment of 15 years (78).
Typical manifestations are new pain and neu-
ropathy in patients with known neurofibroma, es-
pecially those with NF1. Standard treatment for
localized lesions includes surgical resection with
wide margins and adjuvant radiation therapy,
and neoadjuvant chemoradiation may be con-
sidered to downstage borderline resectable cases
(78). High-grade MPNST is associated with a
poor prognosis, as it is highly aggressive, tends to
invade adjacent structures, and has a high rate of
recurrence and metastasis. In contrast, atypical
neurofibroma and low-grade MPNST are associ-
ated with a better prognosis, even after incom-
plete surgical resection (73).
Imaging is useful for identifying suspicious
features that may help direct biopsy or resection;
however, benign PNST versus MPNST cannot
be reliably differentiated with imaging alone. In
patients with NF1, plexiform neurofibroma and
MPNST often have overlapping features, includ-
ing heterogeneous composition and associated os-
seous erosion. US features suggestive of MPNST
include lesion heterogeneity and increased Dop-
pler flow. At CT and MRI, suspicious features
include large size or significant enlargement,
ill-defined margins, a perilesional edema-like zone,
and heterogeneous composition and enhancement
due to necrosis caused by uncontrolled growth
(Fig 13) (34,79). The presence of two or more of
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1709

Figure 14.  Neurolymphomatosis in a 65-year-old man with dif-

fuse large B-cell lymphoma but no known active disease who
presented with right upper extremity pain. (a, b) Axial contrast-
enhanced T1-weighted fat-suppressed (a) and coronal STIR (b)
MR images show massive fusiform enlargement of the upper
and middle components of the supra- and infraclavicular bra-
chial plexus (long arrow in a, arrows in b) and small and adja-
cent lymphadenopathy (short arrows in a). (c) Coronal MIP FDG
PET/CT image shows marked hypermetabolism associated with
the enlarged brachial plexus, as well as some adjacent supracla-
vicular lymphadenopathy, consistent with lymphoma recurrence
manifesting as neurolymphomatosis.

cranial nerves directly, and this unique subtype

these features is up to 90% specific for MPNST
but has limited sensitivity (61%) (79).
MPNSTs are, on average, larger than benign
neurofibromas (mean diameter ± standard devia-
tion, 7.4 cm ± 4.1 vs 4.8 cm ± 2.7, respectively),
but there is significant overlap (78). Significant
diffusion restriction, particularly at a minimal ap-
parent diffusion coefficient lower than 1.0 mm2/
sec, suggests malignancy (77). T1-weighted MRI
sequences are useful for assessing invasion across
tissue planes. FDG PET may be helpful as an
adjunctive imaging examination, as a maximal
standardized uptake value greater than 5.4–7.0 g/
mL is more suggestive of malignancy (78,80).
Extremely rare tumors arising from the
brachial plexus have been reported and include
malignant granular cell tumor, synovial sar-
coma, and peripheral primitive neuroectodermal
tumor (73). Sarcomas may appear as enhancing
T2-hyperintense oval tumors resembling benign
PNST, but they are more likely to demonstrate
irregular margins (34). Rarely, non-Hodgkin
lymphoma may involve the peripheral and
of extranodal disease is known as neurolympho-
matosis (Fig 14) (81). Leukemic involvement of
the peripheral nerves also occurs but rarely. The
typical clinical manifestation is painful, rapidly
progressive neuropathy in a patient with known
lymphoma, although lymphoma may involve
primarily the peripheral nerves in up to 26%
of cases. Imaging is particularly important for
assessing the extent of disease, because lym-
phomatous involvement of the central nervous
system (CNS) may require intrathecal chemo-
therapy and potentially radiation therapy (81).
Thus, although FDG PET/CT is the standard
examination for staging disease and evaluating
treatment response, contrast-enhanced MRI of
the CNS also is commonly used to assess for
neurolymphomatosis or leptomeningeal disease.
MRI features of brachial plexus neurolympho-
matosis include nerve enlargement and nodular-
ity, with variable T2 hyperintensity and dif-
fuse enhancement of the entire affected nerve.
Muscle denervation change is common (34).
Malignant Secondary Tumors.—Secondary malig-
nancy or metastasis involving the brachial plexus
occurs mainly with breast, lung, and less com-
monly head and neck cancers. The plexopathy
may be due to mass effect from adjacent tumor
or direct infiltration of the nerves. The anatomy
of the brachial plexus explains some of the most
common clinical manifestations. For example,
1710  October Special Issue 2020 radiographics.rsna.org
the medial cord is a common site for brachial
plexus involvement in metastatic breast cancer,
likely due to its relative proximity to the path of
axillary venolymphatic drainage. The ulnar nerve
is derived entirely from the medial cord, receiv-
ing major contributions from the lower trunk
(C8 and T1 roots). Thus, patients with a history
of breast cancer who are found to have ulnar neu-
ropathy at presentation should have the medial
cord interrogated carefully. For similar reasons,
particular attention should be paid to the lower
trunk in patients with lung cancer who are found
to have ulnar neuropathy (82).
Although US cannot be used to stage invasive
tumors, it can accurately depict mass effect on
or encasement of the brachial plexus by a mass
lesion. It can also depict regional lymph node
enlargement and be used to guide needle biopsy
(8). At MRI, metastasis appears as irregular or
nodular enlargement and T2 hyperintensity of the
affected nerves, usually with associated patho-
logic enhancement.
Other Tumors.—Other tumor masses that are
recognized to involve or impinge on the brachial
plexus include extra-abdominal desmoid tumor,
pleomorphic undifferentiated sarcoma (for-
merly known as malignant fibrous histiocytoma),
hemangioma, and intra- or extraneural lipoma.
Desmoid tumors are fibrous T1-hypointense,
variably T2-hypointense enhancing masses that
have an infiltrative appearance and encase nerves
as they grow.
Polyneuropathy
Polyneuropathies are diseases that affect mul-
tiple peripheral nerves, may have symmetric or
asymmetric distribution, and have varied causes,
including metabolic, infectious, autoimmune, and
genetic mechanisms. The most common poly-
neuropathies are diabetic peripheral neuropathy,
alcohol-related neuropathy, CIDP, and Guillain-
Barré syndrome with acute inflammatory demy-
elinating polyneuropathy. Hereditary motor and
sensory neuropathies, including Charcot-Marie-
Tooth disease, are uncommon and are caused
by any one of several monogenic mutations that
affect myelination or axonal integrity. The imag-
ing manifestations of polyneuropathy are non-
specific and include T2 hyperintensity and nerve
enlargement. However, compared with acquired
polyneuropathies, hereditary conditions such as
demyelinating-type Charcot-Marie-Tooth disease
are more likely to manifest with symmetric nerve
changes (36).
The imaging findings of CIDP are notable in
that they may resemble a nerve tumor. CIDP is
a type of inflammatory demyelinating neuropa-
thy that characteristically manifests as smooth
fascicular or fusiform nerve enlargement with
marked T2 hyperintensity and minimal periph-
eral enhancement at MRI (34). Involvement may
include few or many nerves in any distribution
across the body. Although the masslike nerve en-
largement may resemble plexiform neurofibroma,
it can be distinguished by the relative lack of en-
hancement (34). Muscle denervation changes are
rarely evident in CIDP (34). It is interesting that
the nerves have been shown to remain morpho-
logically abnormal despite clinical improvement.
Thoracic Outlet Syndrome
Thoracic outlet syndrome (TOS) refers to neuro-
vascular impingement within the thoracic out-
let, resulting in significant disability. It remains
controversial because of a lack of widely accepted
diagnostic criteria and limited data regarding
surgical treatment. TOS is believed to result
from chronic mechanical injury to the neuro-
vascular structures that occurs at the narrowest
points of enclosure within the thoracic outlet.
There are three spaces that most often constrain
the neurovascular bundle through the shoulder’s
broad range of motion: the interscalene triangle,
costoclavicular space, and pectoralis minor or
retropectoral space (Fig 15) (83). Various struc-
tural aberrations (eg, variant rib anatomy, muscle
scarring and/or hypertrophy, posttraumatic bone
callus) can further narrow these spaces and pre-
dispose the affected person to neurovascular in-
jury from even a relatively minor incident trauma
or repetitive stress injury.
TOS is classified as neurogenic, venous, or
arterial according to the neurovascular structure
involved. Each TOS type is associated with a
distinct clinical syndrome that necessitates dif-
ferent diagnostic and management approaches.
The interscalene triangle may be implicated in
either neurogenic or arterial TOS, as it contains
the roots and trunks of the brachial plexus and
the subclavian artery. The costoclavicular space
is mainly implicated in venous TOS. The pecto-
ralis minor space may contribute to neurogenic
TOS and less commonly to venous TOS; either
of these types is known as pectoralis minor syn-
drome (83,84).
Neurogenic TOS is considered by far the
most common type and is a compressive brachial
plexopathy within the interscalene triangle or
pectoralis minor space. The classic manifesta-
tion is pain or paresthesia of the upper extremity
exacerbated by provocative shoulder movements
such as abduction and external rotation. Weak-
ness and/or muscular atrophy can occur, but they
are late signs. In contrast, venous TOS is throm-
bosis or intermittent positional obstruction of the
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1711

Figure 15.  Drawings illustrate the three sites of compression in thoracic outlet syndrome
(TOS). The interscalene triangle contains arteries and nerves and may be implicated in neu-
rogenic or arterial TOS. The costoclavicular space is most associated with venous TOS, as the
subclavian vein is located more anteriorly and medially within this space and is physiologically
compressed between the clavicle-subclavius muscle region, costoclavicular ligament, first rib,
and anterior (Ant) scalene muscle. The pectoralis (Pec) minor (subcoracoid) space may contrib-
ute to neurogenic TOS but less commonly to venous TOS.

axillosubclavian vein within the costoclavicular
space. Primary venous thrombosis in this location
is strongly associated with antecedent strenuous
activity of the upper extremity and thus is also
known as effort thrombosis, or Paget-Schroeder
syndrome. Venous TOS manifests with upper ex-
tremity swelling and variable pain aggravated by
exertion. Physical examination characteristically
reveals dilated superficial collateral veins and a
swollen discolored arm (85).
Arterial TOS is an injury of the subclavian ar-
tery within the interscalene triangle that ultimately
manifests as stenosis or an aneurysm or pseudoa-
neurysm. It is rare and almost always caused by a
structural abnormality of the upper ribs. Arterial
TOS manifests as upper extremity claudication ag-
gravated by exertion, especially with the shoulder
abducted. If early ischemic symptoms go unrecog-
nized, patients can develop acute ischemia of the
hand and fingers owing to arterial emboli originat-
ing from the subclavian arterial lesion (86).
Accurate diagnosis of TOS is notoriously dif-
ficult, particularly because of the nonspecific na-
ture of the symptoms and limited predictive value
of diagnostic tests (87,88). The typical diagnostic
evaluation involves obtaining the medical history
and performing a focused physical examination
with provocative maneuvers, whereby specific
arm and neck positioning is used to narrow the
thoracic outlet or induce traction on the nerves.
Radiography of the chest and cervical spine is
routinely performed to assess for variant anatomy
(cervical or anomalous ribs), an elongated C7
transverse process, and alternative causes such
as cervical disk disease. Some form of additional
cross-sectional imaging is also recommended to
exclude neoplasm (89).
However, the clinical and imaging findings
are often nonspecific, as most people undergo
at least one provocative test that yields positive
results (87). Further investigations are guided by
the type of TOS that is suspected, and they usu-
ally are not entirely diagnostic but may increase
diagnostic confidence. For example, neurogenic
TOS may be assessed with electrophysiologic
testing and US-guided injections in the scalene,
subclavius, or pectoralis minor muscles. Arterial
TOS may be evaluated by performing Doppler
US, hemodynamic testing with finger plethys-
mography, or CT and/or MR angiography with
provocative maneuvers (15,87). Venous TOS is
routinely evaluated by using Doppler US, with
CT and/or MR venography as an alternative
when the US window is limited. Fixed vascular
stenosis and expanded collateral vessels are sup-
portive findings of vascular TOS (15). Diagnostic
catheter venography is reserved for circumstances
in which an endovascular intervention such as
thrombolysis or angioplasty is anticipated, but
surgical decompression is usually necessary in
spite of endovascular intervention.
Dedicated brachial plexus imaging is not
commonly performed for suspected neurogenic
TOS, but there is growing interest in the use of
US and MRI to support the diagnosis and local-
ize sites of compression (8,87). Dynamic high-
frequency US can be used to assess for brachial
plexus compression, with the patient performing
1712  October Special Issue 2020 radiographics.rsna.org
dynamic maneuvers (eg, neck rotation, tilting,
arm abducted and externally rotated) to reproduce
symptoms (7). US may also yield important in-
formation about the course of the supraclavicular
nerves, as it is increasingly being recognized that
variant anatomy is common, particularly at the
level of the interscalene triangle (2). MRI is excel-
lent for evaluating soft-tissue structures that may
contribute to compression, such as fibrous bands,
abnormal scalene muscular attachments, and
supernumerary muscles (eg, scalene minimus).
Dynamic MRI with the arm imaged in a neutral
position and in overhead positions may depict
brachial plexus impingement manifesting as loss of
the normal perineural fat planes, and T2 hyperin-
tensity of the nerves may be evident (15,87,90).
Conclusion
Brachial plexopathy can be challenging to di-
agnose and manage. The medical history and
physical examination findings are the mainstays
for diagnosis, but imaging can be used to con-
firm physical examination and electrodiagnostic
findings, localize sites of involvement to assist in
preoperative planning, and assess for underlying
structural or neoplastic anomalies. US is increas-
ingly being recognized as a valuable tool for evalu-
ating the superficial components of the brachial
plexus. CT images have limited softtissue contrast
resolution, but they may show initial evidence of
disease, and CT angiography or venography may
be performed to evaluate select cases of vascu-
lar TOS. Although CT myelography has largely
been supplanted by MRI, it may still be useful for
assessment of preganglionic injury, particularly
in neonates. MRI is arguably the best modality
overall for assessing the brachial plexus, and there
is increasing interest in the use of this imaging
examination as a biomarker for assessment of de-
myelinating and inflammatory conditions. Famil-
iarity with the anatomy and nerve distributions of
the brachial plexus and the spectrum of associated
imaging appearances is important for radiologic
evaluation of this structure.
Disclosures of Conflicts of Interest.—S.D.D. Activities related to
the present article: disclosed no relevant relationships. Activities
not related to the present article: paid consultant on musculo-
skeletal US for Canon Medical Imaging at RSNA; Northwest-
ern Memorial Hospital Women’s Board and Dixon Transla-
tional research grants. Other activities: disclosed no relevant
relationships.
References
1. Uysal İİ, Şeker M, Karabulut AK, Büyükmumcu M, Ziylan
T. Brachial plexus variations in human fetuses. Neurosurgery
2003;53(3):676–684; discussion 684.
2. Leonhard V, Smith R, Caldwell G, Smith HF. Anatomi-
cal variations in the brachial plexus roots: implications for
diagnosis of neurogenic thoracic outlet syndrome. Ann Anat
2016;206:21–26.
3. Antoniadis G. The Peripheral Nerve: Neuroanatomical
Principles Before and After Injury. In: Haastert-Talini
K, Assmus H, Antoniadis G, eds. Modern Concepts of
Peripheral Nerve Repair. Cham, Switzerland: Springer,
2017; 1–10.
4. Weerasuriya A, Mizisin AP. The Blood-Nerve Barrier:
Structure and Functional Significance. In: Nag S, ed. The
Blood-Brain and Other Neural Barriers, Vol 686. Totowa,
NJ: Humana, 2011; 149–173.
5. Millesi H, Rath T, Reihsner R, Zoch G. Microsurgical
neurolysis: its anatomical and physiological basis and its
classification. Microsurgery 1993;14(7):430–439.
6. Baute V, Strakowski JA, Reynolds JW, et al. Neuromuscular
ultrasound of the brachial plexus: a standardized approach.
Muscle Nerve 2018;58(5):618–624.
7. Nwawka OK. Ultrasound Imaging of the Brachial Plexus and
Nerves About the Neck. Ultrasound Q 2019;35(2):110–119.
8. Lapegue F, Faruch-Bilfeld M, Demondion X, et al.
Ultrasonography of the brachial plexus, normal appear-
ance and practical applications. Diagn Interv Imaging
2014;95(3):259–275.
9. Griffith JF. Ultrasound of the Brachial Plexus. Semin Mus-
culoskelet Radiol 2018;22(3):323–333.
10. Griffith JF, Lalam RK. Top-Ten Tips for Imaging the
Brachial Plexus with Ultrasound and MRI. Semin Muscu-
loskelet Radiol 2019;23(4):405–418.
11. Griffith JF. Ultrasound of the Brachial Plexus. Semin Mus-
culoskelet Radiol 2018;22(3):323–333.
12. Martinoli C, Gandolfo N, Perez MM, et al. Brachial plexus
and nerves about the shoulder. Semin Musculoskelet Radiol
2010;14(5):523–546.
13. Hall WH, Guiou M, Lee NY, et al. Development and valida-
tion of a standardized method for contouring the brachial
plexus: preliminary dosimetric analysis among patients
treated with IMRT for head-and-neck cancer. Int J Radiat
Oncol Biol Phys 2008;72(5):1362–1367.
14. Truong MT, Nadgir RN, Hirsch AE, et al. Brachial
plexus contouring with CT and MR imaging in radiation
therapy planning for head and neck cancer. RadioGraphics
2010;30(4):1095–1103.
15. Raptis CA, Sridhar S, Thompson RW, Fowler KJ, Bhalla
S. Imaging of the Patient with Thoracic Outlet Syndrome.
RadioGraphics 2016;36(4):984–1000.
16. Fuzari HKB, Dornelas de Andrade A, Vilar CF, et al.
Diagnostic accuracy of magnetic resonance imaging in
post-traumatic brachial plexus injuries: asystematic review.
Clin Neurol Neurosurg 2018;164:5–10.
17. Nagano A, Ochiai N, Sugioka H, Hara T, Tsuyama N.
Usefulness of myelography in brachial plexus injuries. J
Hand Surg [Br] 1989;14(1):59–64.
18. Park HR, Lee GS, Kim IS, Chang JC. Brachial Plexus Injury
in Adults. Nerve 2017;3(1):1–11.
19. Yoshikawa T, Hayashi N, Yamamoto S, et al. Brachial
plexus injury: clinical manifestations, conventional imaging
findings, and the latest imaging techniques. RadioGraphics
2006;26(Suppl 1):S133–S143.
20. Qi L, Xu L, Wang WT, et al. Dynamic contrast-
enhanced magnetic resonance imaging in denervated
skeletal muscle: experimental study in rabbits. PLoS One
2019;14(4):e0215069.
21. Zhang L, Xiao T, Yu Q, Li Y, Shen F, Li W. Clinical Value
and Diagnostic Accuracy of 3.0T Multi-Parameter Magnetic
Resonance Imaging in Traumatic Brachial Plexus Injury.
Med Sci Monit 2018;24:7199–7205.
22. Wade RG, Takwoingi Y, Wormald JCR, et al. MRI for
Detecting Root Avulsions in Traumatic Adult Brachial
Plexus Injuries: A Systematic Review and Meta-Analysis
of Diagnostic Accuracy. Radiology 2019;293(1):125–133.
23. Jongbloed BA, Bos JW, Rutgers D, van der Pol WL, van
den Berg LH. Brachial plexus magnetic resonance imaging
differentiates between inflammatory neuropathies and does
not predict disease course. Brain Behav 2017;7(5):e00632.
https://doi.org/10.1002/brb3.632.
24. Kwee RM, Chhabra A, Wang KC, Marker DR, Carrino JA.
Accuracy of MRI in diagnosing peripheral nerve disease: a
systematic review of the literature. AJR Am J Roentgenol
2014;203(6):1303–1309.
RG  •  Volume 40  Number 6 Gilcrease-Garcia et al  1713
25. Sneag DB, Queler S. Technological Advancements in
Magnetic Resonance Neurography. Curr Neurol Neurosci
Rep 2019;19(10):75.
26. Wang X, Harrison C, Mariappan YK, et al. MR Neurogra-
phy of Brachial Plexus at 3.0 T with Robust Fat and Blood
Suppression. Radiology 2017;283(2):538–546.
27. Chhabra A, Subhawong TK, Bizzell C, Flammang A,
Soldatos T. 3T MR neurography using three-dimensional
diffusion-weighted PSIF: technical issues and advantages.
Skeletal Radiol 2011;40(10):1355–1360.
28. Klupp E, Cervantes B, Sollmann N, et al. Improved Brachial
Plexus Visualization Using an Adiabatic iMSDE-Prepared
STIR 3D TSE. Clin Neuroradiol 2019;29(4):631–638.
29. Cervantes B, Kirschke JS, Klupp E, et al. Orthogonally com-
bined motion- and diffusion-sensitized driven equilibrium
(OC-MDSDE) preparation for vessel signal suppression
in 3D turbo spin echo imaging of peripheral nerves in the
extremities. Magn Reson Med 2018;79(1):407–415.
30. Harrell AD, Johnson D, Samet J, Omar IM, Deshmukh
S. With or without? a retrospective analysis of intravenous
contrast utility in magnetic resonance neurography. Skeletal
Radiol 2020;49(4):577–584.
31. Li Z, Chen YA, Chow D, Talbott J, Glastonbury C, Shah
V. Practical applications of CISS MRI in spine imaging.
Eur J Radiol Open 2019;6:231–242.
32. Oudeman J, Verhamme C, Engbersen MP, et al. Diffu-
sion tensor MRI of the healthy brachial plexus. PLoS One
2018;13(5):e0196975.
33. Martín Noguerol T, Barousse R, Gómez Cabrera M,
Socolovsky M, Bencardino JT, Luna A. Functional
MR Neurography in Evaluation of Peripheral Nerve
Trauma and Postsurgical Assessment. RadioGraphics
2019;39(2):427–446.
34. Amrami KK, Felmlee JP, Spinner RJ. MRI of peripheral
nerves. Neurosurg Clin N Am 2008;19(4):559–572, vi.
35. Tagliafico A, Succio G, Emanuele Neumaier C, et al. MR
imaging of the brachial plexus: comparison between 1.5-T
and 3-T MR imaging: preliminary experience. Skeletal
Radiol 2011;40(6):717–724.
36. Chhabra A. MR neurography. Neuroimaging Clin N Am
2014;24(1):xvii.
37. Chappell KE, Robson MD, Stonebridge-Foster A, et al.
Magic angle effects in MR neurography. AJNR Am J Neu-
roradiol 2004;25(3):431–440.
38. Gonik B. Neonatal brachial plexus palsy: antecedent obstet-
rical factors. In: Chung KC, Yang LJS, McGillicuddy JE,
eds. Practical management of pediatric and adult brachial
plexus palsies. Philadelphia, Pa: Elsevier, 2012; 46–53.
39. Mollberg M, Hagberg H, Bager B, Lilja H, Ladfors L.
High birthweight and shoulder dystocia: the strongest
risk factors for obstetrical brachial plexus palsy in a Swed-
ish population-based study. Acta Obstet Gynecol Scand
2005;84(7):654–659.
40. van Ouwerkerk WJR, van der Sluijs JA. Radiographic as-
sessment in pediatric brachial plexus palsies. In: Chung KC,
Yang LJS, McGillicuddy JE, eds. Practical management of
pediatric and adult brachial plexus palsies. Philadelphia, Pa:
Elsevier, 2012; 75–85.
41. Somashekar DK, Di Pietro MA, Joseph JR, Yang LJ, Par-
mar HA. Utility of ultrasound in noninvasive preoperative
workup of neonatal brachial plexus palsy. Pediatr Radiol
2016;46(5):695–703. [Published correction appears in
Pediatr Radiol 2016;46(4):583.].
42. Andrei M, Ioana MR, Mircea ED. Underlying histopathol-
ogy of peripheral nerve injury and the classical nerve repair
techniques. Rom Neurosurg 2019;33(1):17–22.
43. Fox IK, Mackinnon SE. Adult peripheral nerve disorders:
nerve entrapment, repair, transfer, and brachial plexus
disorders. Plast Reconstr Surg 2011;127(5):105e–118e.
44. Yang J, Qin B, Fu G, et al. Modified pathological clas-
sification of brachial plexus root injury and its MR im-
aging characteristics. J Reconstr Microsurg 2014;30(3):
171–178.
45. Wade RG, Itte V, Rankine JJ, Ridgway JP, Bourke G. The
diagnostic accuracy of 1.5T magnetic resonance imaging
for detecting root avulsions in traumatic adult brachial
plexus injuries. J Hand Surg Eur Vol 2018;43(3):250–258.
46. Hayashi N, Masumoto T, Abe O, Aoki S, Ohtomo K,
Tajiri Y. Accuracy of abnormal paraspinal muscle find-
ings on contrast-enhanced MR images as indirect signs
of unilateral cervical root-avulsion injury. Radiology
2002;223(2):397–402.
47. Bischoff C, Kollmer J, Schulte-Mattler W. State-of-the-Art
Diagnosis of Peripheral Nerve Trauma: Clinical Examina-
tion, Electrodiagnostic, and Imaging. In: Haastert-Talini
K, Assmus H, Antoniadis G, eds. Modern Concepts of
Peripheral Nerve Repair. Cham, Switzerland: Springer
International, 2017; 11–25.
48. Padua L, Di Pasquale A, Liotta G, et al. Ultrasound as
a useful tool in the diagnosis and management of trau-
matic nerve lesions. Clin Neurophysiol 2013;124(6):
1237–1243.
49. Chin B, Ramji M, Farrokhyar F, Bain JR. Efficient Imag-
ing: Examining the Value of Ultrasound in the Diagnosis
of Traumatic Adult Brachial Plexus Injuries—A Systematic
Review. Neurosurgery 2018;83(3):323–332.
50. Ahlawat S, Belzberg AJ, Fayad LM. Utility of Magnetic
Resonance Imaging for Predicting Severity of Sciatic Nerve
Injury. J Comput Assist Tomogr 2018;42(4):580–587.
51. Bendszus M, Wessig C, Solymosi L, Reiners K, Koltzenburg
M. MRI of peripheral nerve degeneration and regeneration:
correlation with electrophysiology and histology. Exp Neurol
2004;188(1):171–177.
52. Giorgetti E, Obrecht M, Ronco M, et al. Magnetic Reso-
nance Imaging as a Biomarker in Rodent Peripheral Nerve
Injury Models Reveals an Age-Related Impairment of Nerve
Regeneration. Sci Rep 2019;9(1):13508.
53. Ahlawat S, Belzberg AJ, Montgomery EA, Fayad LM.
MRI features of peripheral traumatic neuromas. Eur Radiol
2016;26(4):1204–1212.
54. Singer AD, Meals C, Kesner V, et al. The Multidisciplinary
Approach to the Diagnosis and Management of Nonobstetric
Traumatic Brachial Plexus Injuries. AJR Am J Roentgenol
2018;211(6):1319–1331.
55. Belzberg AJ, Dorsi MJ, Storm PB, Moriarity JL. Surgical
repair of brachial plexus injury: a multinational survey
of experienced peripheral nerve surgeons. J Neurosurg
2004;101(3):365–376.
56. Chen AM, Hall WH, Li J, et al. Brachial plexus-asso-
ciated neuropathy after high-dose radiation therapy for
head-and-neck cancer. Int J Radiat Oncol Biol Phys
2012;84(1):165–169.
57. Bruzzi JF, Komaki R, Walsh GL, et al. Imaging of non-small
cell lung cancer of the superior sulcus: part 2: initial staging
and assessment of resectability and therapeutic response.
RadioGraphics 2008;28(2):561–572.
58. Metcalfe E, Etiz D. Early transient radiation-induced bra-
chial plexopathy in locally advanced head and neck cancer.
Contemp Oncol (Pozn) 2016;20(1):67–72.
59. Bowen BC, Verma A, Brandon AH, Fiedler JA. Radiation-
induced brachial plexopathy: MR and clinical findings. AJNR
Am J Neuroradiol 1996;17(10):1932–1936.
60. Yarnold J, Brotons MC. Pathogenetic mechanisms in
radiation fibrosis. Radiother Oncol 2010;97(1):149–161.
61. Schierle C, Winograd JM. Radiation-induced brachial
plexopathy: review—complication without a cure. J Reconstr
Microsurg 2004;20(2):149–152.
62. Johansson S, Svensson H, Larsson LG, Denekamp J.
Brachial plexopathy after postoperative radiotherapy of
breast cancer patients--a long-term follow-up. Acta Oncol
2000;39(3):373–382.
63. Gerard JM, Franck N, Moussa Z, Hildebrand J. Acute
ischemic brachial plexus neuropathy following radiation
therapy. Neurology 1989;39(3):450–451.
64. Crush AB, Howe BM, Spinner RJ, et al. Malignant involve-
ment of the peripheral nervous system in patients with
cancer: multimodality imaging and pathologic correlation.
RadioGraphics 2014;34(7):1987–2007.
65. van Alfen N, van Engelen BGM. The clinical spectrum
of neuralgic amyotrophy in 246 cases. Brain 2006;129(Pt
2):438–450.
66. Upadhyaya V, Upadhyaya DN, Bansal R, Pandey T, Pan-
dey AK. MR neurography in Parsonage-Turner syndrome.
Indian J Radiol Imaging 2019;29(3):264–270.
1714  October Special Issue 2020 radiographics.rsna.org
67. Luigetti M, Pravatà E, Colosimo C, et al. MRI neurography
findings in patients with idiopathic brachial plexopathy:
correlations with clinical-neurophysiological data in eight
consecutive cases. Intern Med 2013;52(18):2031–2039.
68. Scalf RE, Wenger DE, Frick MA, Mandrekar JN, Adkins
MC. MRI findings of 26 patients with Parsonage-Turner
syndrome. AJR Am J Roentgenol 2007;189(1):W39–W44.
69. Goldblum J. Soft Tissues. In: Goldblum J, Lamps L, McKen-
ney J, Myers J, eds. Rosai and Ackerman’s Surgical Pathol-
ogy. 11th ed. Philadelphia, Pa: Elsevier, 2018; 1810–1914.
70. Desai KI. The Surgical Management of Symptomatic
Benign Peripheral Nerve Sheath Tumors of the Neck and
Extremities: An Experience of 442 Cases. Neurosurgery
2017;81(4):568–580.
71. Rückert RI, Fleige B, Rogalla P, Woodruff JM. Schwan-
noma with angiosarcoma: report of a case and comparison
with other types of nerve tumors with angiosarcoma. Cancer
2000;89(7):1577–1585.
72. Woodruff JM, Selig AM, Crowley K, Allen PW. Schwan-
noma (neurilemoma) with malignant transformation: a
rare, distinctive peripheral nerve tumor. Am J Surg Pathol
1994;18(9):882–895.
73. Jia X, Yang J, Chen L, Yu C, Kondo T. Primary Brachial
Plexus Tumors: Clinical Experiences of 143 Cases. Clin
Neurol Neurosurg 2016;148:91–95.
74. Khajavi M, Khoshsirat S, Ahangarnazari L, Majdinasab
N. A brief report of plexiform neurofibroma. Curr Probl
Cancer 2018;42(2):256–260.
75. Lee SK, Kim JY, Lee YS, Jeong HS. Intramuscular peripheral
nerve sheath tumors: schwannoma, ancient schwannoma,
and neurofibroma. Skeletal Radiol 2020 Jan 13 [Epub
ahead of print].
76. Jee WH, Oh SN, McCauley T, et al. Extraaxial neurofibromas
versus neurilemmomas: discrimination with MRI. AJR Am
J Roentgenol 2004;183(3):629–633.
77. Demehri S, Belzberg A, Blakeley J, Fayad LM. Conven-
tional and functional MR imaging of peripheral nerve
sheath tumors: initial experience. AJNR Am J Neuroradiol
2014;35(8):1615–1620.
78. James AW, Shurell E, Singh A, Dry SM, Eilber FC. Ma-
lignant Peripheral Nerve Sheath Tumor. Surg Oncol Clin
N Am 2016;25(4):789–802.
79. Wasa J, Nishida Y, Tsukushi S, et al. MRI features in
the differentiation of malignant peripheral nerve sheath
This journal-based SA-CME activity has been approved for AMA PRA Category 1 Credit . See rsna.org/learning-center-rg.
tumors and neurofibromas. AJR Am J Roentgenol
2010;194(6):1568–1574.
80. Meany H, Dombi E, Reynolds J, et al. 18-fluorodeoxyglu-
cose-positron emission tomography (FDG-PET) evaluation
of nodular lesions in patients with neurofibromatosis type 1
and plexiform neurofibromas (PN) or malignant peripheral
nerve sheath tumors (MPNST). Pediatr Blood Cancer
2013;60(1):59–64.
81. Siegal T, Grisariu S, Avni B, Baehring J. Neurolympho-
matosis. In: Batchelor T, DeAngelis L, eds. Lymphoma
and Leukemia of the Nervous System. New York, NY:
Springer, 2012; 219–229.
82. Bowen BC, Pattany PM, Saraf-Lavi E, Maravilla KR. The
brachial plexus: normal anatomy, pathology, and MR imag-
ing. Neuroimaging Clin N Am 2004;14(1):59–85, vii–viii.
83. Sanders R. Anatomy of the Thoracic Outlet and Related
Structures. In: Illig K, Thompson R, Freischlag J, Donahue
D, Jordan S, Edgelow P, eds. Thoracic Outlet Syndrome.
London, England: Springer, 2013; 17–24.
84. Illig KA, Donahue D, Duncan A, et al. Reporting standards
of the Society for Vascular Surgery for thoracic outlet syn-
drome. J Vasc Surg 2016;64(3):e23–e35.
85. Feinberg R. Clinical Presentation and Patient Evaluation
in VTOS. In: Illig K, Thompson R, Freischlag J, Donahue
D, Jordan S, Edgelow P, eds. Thoracic Outlet Syndrome.
London, England: Springer, 2013; 345–353.
86. Azizzadeh A, Thompson R. Clinical Presentation and Patient
Evaluation in ATOS. In: Illig K, Thompson R, Freischlag
J, Donahue D, Jordan S, Edgelow P, eds. Thoracic Outlet
Syndrome. London, England: Springer, 2013; 551–556.
87. Povlsen S, Povlsen B. Diagnosing Thoracic Outlet Syn-
drome: Current Approaches and Future Directions. Diag-
nostics (Basel) 2018;8(1):E21.
88. Dessureault-Dober I, Bronchti G, Bussières A. Diagnostic
Accuracy of Clinical Tests for Neurogenic and Vascular
Thoracic Outlet Syndrome: A Systematic Review. J Ma-
nipulative Physiol Ther 2018;41(9):789–799.
89. Zurkiya O, Ganguli S, Kalva S, et al. American College
of Radiology ACR Appropriateness Criteria Thoracic
Outlet Syndrome. Reston, Va: American College of
Radiology, 2019.
90. Werden S. Radiographic Imaging in Diagnosis and As-
sessment of NTOS. In: Illig K, Thompson R, Freischlag
J, Donahue D, Jordan S, Edgelow P, eds. Thoracic Outlet
Syndrome. London, England: Springer, 2013; 111–125.
TM