CLINICAL IMAGING OF THE BRACHIAL PLEXUS:

Himadri S. Das, N. Medhi, P. K. Sharma, P. Goswami, P. Hazarika, B. J. Sharma

Primus Imaging, Guwahati
The Brachial Plexus (BP) is comprised of the roots, trunks, divisions, cords, and branches.
ANATOMY
The brachial plexus originates from the anterior divisions of the spinal nerve roots of C5-T1.
Variations in innervation are occasionally present. A pre-fixed BP occurs when C4 replaces
T1 as a dominant contributor. A post-fixed plexus is present when BP receives contributions
from C6 T2. These variations appear to have little clinical significance.
The BP is formed in the majority by the anterior divisions of the spinal nerves of C5 T1 that
forms its roots. The roots of the BP then combine to form the 3 trunks (upper, middle, lower).
The roots of C5 and C6 combine to form the upper trunk, while the roots of C8 / T1 combine to
form the lower trunk. The C7 root is the sole contributor of the middle trunk.
The trunks of the BP then split into anterior and posterior divisions. These divisions combine to
form the cords of the BP. The cords of the BP are named (posterior, lateral, medial) according
to their relationship with the adjacent subclavian artery. The posterior divisions of the upper,
middle and lower trunk combine to form the posterior cord. The anterior divisions of the upper
and middle trunks combine to form the lateral cord, and the anterior division of the lower trunk
continues to form the medial cord.
The BP terminates in various branches, which supply motor sensory innervation to the upper
extremity. The suprascapular nerve is the only terminal branch that originates from a trunk of
the BP.

FIG1: ANATOMY OF THE BP

PERIPHERAL NERVES THAT ORIGINATE FROM CORDS OF THE BRACHIAL PLEXUS

Branches from the lateral cord
Lateral pectoral nerve
Musculocutaneous never
Lateral head of the median nerve
Branches from the median cord
Medial pectoral nerve
Medial cutaneous nerve of the upper arm
Medial cutaneous nerve of the forearm
Medial root of the median nerve
Branches from the posterior cord
Upper subscapular nerve
Thoracodorsal nerve
Lower subscapular nerve
Axillary nerve
Radial nerve
SURGICAL ANATOMY
The surgical classification is based on the relationship of the BP to the clavicle and divides it
into supraclavicular, retroclavicular, and infraclavicular segments. The supraclavicular BP
contains the roots and trunks and is situated in the posterior triangle between the anterior and
middle scalene muscles.
The retroclavicular plexus contains the divisions and is located posterior to the clavicle
adjacent to the subclavian artery. The infraclavicular plexus also courses adjacent to the
subclavian artery and contains the cords and portions of the distal branches of the BP.
RADIOGRAPHIC ANATOMY
The radiologist can identify specific portions of the BP based on certain anatomic structures,
which are easily seen on imaging studies. The fascial plane between the anterior and middle
scalene muscles contains the roots and cords of the BP. The divisions and cords course
adjacent to the subclavian artery. Thus, any mass that is adjacent to the subclavian artery is in
close proximity to the divisions and cords of the BP. The branches of the BP are difficult to
identify individually on imaging studies. However, it may be safely assumed that a mass in the
axillary region is likely to involve the terminal branches of the cords.

FIG 2(a): CORONAL T1 WEIGHTED MR SEQUENCE

FIG 2(b): AXIAL T1 WEIGHTED MR SEQUENCE

Abbreviations: Clavicles (C), subclavius muscles (SUB), external jugular vein (XJ), internal
jugular vein (J), subclavian veins (SV), axillosubclavian veins (AXV), coracoid processes (CP),
brachiocephalic artery (BR), first ribs (FR), trachea (T), right lung (RL), and left lung (LL) are
labelled for reference. The aorta (A) and pulmonary artery (P) are labeled to identify the heart.
CLINICAL SCENARIO:
Clinical features of a brachial plexopathies are often vague and non-specific. Symptoms
include motor, sensory and sometimes, autonomic disturbances of the supraclavicular region,
shoulder, and upper extremity. Motor weakness is primarily seen in those patients with
obstetric-related palsies and avulsions of anterior roots. Sensory deficits are more often related
to those patients with neoplastic and/or radiation induced plexopathies. Neoplastic
plexopathies tend to be more painful and progress more rapidly than radiation-induced ones.
Long-term complications resulting from brachial plexopathies include muscle wasting, upper
extremity edema, osteoporosis, joint contractures, complex regional pain syndromes and/or
sympathetically mediated pain, and joint degeneration.
There are certain clinical findings that help to localize the inciting lesion and thus permit
radiologists to focus their diagnostic evaluation. The phrenic nerve receives contributions from
C3 C5. Because of this overlap in innervation with the upper roots of the BP, a plexopathy
associated with a paralyzed diaphragm indicates involvement of the upper plexus. The
rhomboid and serratus anterior muscles are innervated by proximal branches of the BP (C5
C7). Thus, rhomboid muscle paralysis or winging of the scapula is indicative of a proximal
injury.
The Erb-Duchene palsy is most often a consequence of birth injury which results from shoulder
dystocia during a vertex vaginal delivery. Obstetrical palsies tend to occur more often in larger
babies, breech or forceps deliveries, and after prolonged labors. The right shoulder is more
commonly affected because the head is usually in a left occiput anterior position. Excessive
traction on the head and neck results in an injury limited to the C5 and C6 nerve roots. Patients
with an Erbs palsy have characteristic physical findings which consist of adduction and internal
rotation of the arm with pronation of the forearm.
Several associated clinical findings implicate a lower BP lesion. The stellate ganglion receives
contributions from C8-T1. Thus, a brachial plexopathy associated with an ipsilateral Horners
syndrome is indicative of a lesion involving the lower BP. The classic Dejerine-Klumpke palsy is
due to a failure to deliver the upper extremities before the head during a breech vaginal
delivery. Forcible abduction of the arms causes excessive stretching and results in an injury to
the nerve roots of C7-T1. This injury involves the lower intrinsic hand muscles, and the radial
innervated extensors. Such an injury characteristically results in a paralysed (claw) hand.

Because of the overlap in innervation with the stellate ganglion, Klumpkes palsy may also be
associated with ipsilateral Horners syndrome.
Several findings may be indicative of a more severe injury to the BP. A plexopathy associated
findings similar to a Brown-Sequard syndrome may suggest a proximal nerve root avulsion and
spinal cord injury. A nail limb with complete absence of deep tendon reflexes is indicative of a
complete disruption of the BP.
INDICATIONS OF MR IMAGING:
1. Are symptoms unilateral or bilateral? The presence of bilateral brachial plexopathies is
usually associated with a lesion in the epidural space or neural foramina, and these
patients should be evaluated initially with a dedicated imaging study of the cervical
spine.
2. Is there a history of trauma? These patients often require dedicated sectional imaging
studies of the cervical spine to supplement the evaluation of the peripheral components
of the plexus.
3. Is there an associated mass in the neck, supraclavicular fossa or axilla?
Characterization of a palpable mass may require the use of double-echo-T2-weighted
rather than SE-T2 weighted sequence and the administration of intravenous contrast.
4. Are the symptoms produced by a particular arm position? Hand pain with arm elevation
of a common finding with thoracic outlet syndrome secondary to a cervical rib, and
identification of a cervical rib on a frontal radiograph should prompt further evaluation of
the subclavian and axillary arteries rather than the soft-tissue components of the
brachial plexus.
5. Does the patient have a prior history of carcinoma? Studies of patients with a history of
malignancy require a careful search for abnormal signal within the trabecular bone of
the cervical spine, clavicle, scapula, and shoulder as well as the soft tissues adjacent to
the nerves. This is especially important if pain is the only presenting symptom.
6. Is there a history os surgery or radiation therapy to the affected axilla, neck or
supraclavicular fossa? Images of the affected side in these patient are often confusing
and oblique coronal and sagittal imaging of the opposite brachial plexus is often useful
for comparison and identification of subtle changes.
IMAGING IN VARIOUS PATHOLOGIES OF THE BRACHIAL PLEXUS:
TRAUMA
The initial imaging evaluation in patients with a post-traumatic brachial plexopathy should
consist of plain films of the cervical spine, shoulder, clavicle and chest. These plain films
should be assesses for fractures of subluxations which could account for the acute
neurological deficit.
Posttraumatic nerve root avulsion of the BP results from forcible trauma which separates the
arm from the shoulder. This may result in stretching and tearing of fibrous attachments which
extends from the nerves to their respective transverse processes. Pseudomeningoceles arise
from tears of the dura and arachnoid membranes caused by the root sleeves being pulled out
into the intervertebral foramen. Nerve root avulsion results if the traction force exceeds the
elastic tolerance of the root. Spinal cord injury may occur from direct contusion or by avulsion
of the nerve root. Thus, it is possible to have post-traumatic Pseudomeningoceles without a
coexistent nerve root avulsion. Conversely, approximately 20% of clinical nerve root avulsions
are not associated with a pseudomeningocele.
Both CT Myelography and MR imaging may be used to evaluate patients with post-traumatic
brachial plexopathies. The characteristic findings in a posttraumatic BP stretch injury are
Pseudomeningoceles which may be detected by both CT Myelography and MR imaging. Thin

section CT Myelography (1mm-3mm thick sections) allows for consistent visualization of the
ventral and dorsal nerve roots within the spinal canal and is therefore the preferred imaging
modality.
Absence of a nerve root shadow on CT Myelography is indicative of nerve root avulsion. Nerve
root or dural thickening seen on MR imaging is suggestive of nerve root avulsion or edema.
Recent technical advances in MR imaging permit improved visualization of the nerve roots
within the spinal canal in normal patients, however, these advanced techniques are mostly
limited to tertiary institutions and are not currently in general use. MR imaging does allow
visualization of Pseudomeningoceles , which do not fit with contrast on CT Myelography. The
role of MR Myelography for evaluating BP injuries is currently being evaluated.
Other post-traumatic lesions which may result in a brachial plexopathy include hematomas,
vascular compression from pseudoaneurysm formation, and complete disruption of the
brachial plexus. The presence of intramedullary or extramedullary haematoma may be
detected with MR imaging. MR imaging is superior to CT for evaluating for the presence and
extent of soft tissue injuries.

FIG 3: CORONAL T2 W IMAGE SHOWING POST TRAUMATIC PSEUDOMENINGOCELE

TRAUMATIC CAUSES OF BRACHIAL PLEXOPATHY

Fractures of the cervical spine or clavicle
Nerve root avulsion with or without an associated pseudomeningocele
Soft tissue edema
Hematoma
NONTRAUMATIC CAUSES OF BRACHIAL PLEXOPATHY
Primary neural tumors such as meningioma and schwannomas
Metastatic disease
Pan coast tumor
Post irradiation injury
Radiculopathy secondary to disk disease
Bony abnormalities such as cervical rib.
NEOPLASMS
A variety of neoplasms may involve the BP. These lesions may be classified as tumours of
neural (primary) and of non-neural origin (secondary). Primary BP tumors most commonly

arise from the nerve sheaths. The most common benign neural tumors are neurofibromas and
schwannomas. Neurofibromas are the most common neural tumor to involve the BP.
Histologically; these lesions are unencapsulated tumors that are felt to arise from the nerve
fascicles. One-third of these lesions occur in patients with Neurofibromatosis type 1 (NF-1)
while two- thirds of cases are sporadic. Neurofibromas arising in patients with NF 1 occur with
equal incidence in males and females. These tumors are characteristically multiple and
plexiform in appearance with diffuse involvement of the BP. In contrast, sporadic neurofibromas
are more commonly seen in females (2-3:1 female to male ratio). Sporadic neurofibromas are
typically solitary and most likely originate in the supraclavicular BP. Schwannomas are the
second most common neural tumor involving the BP.
The imaging features of solitary neurofibromas are essentially indistinguishable from those of
the schwannomas. On CT, these lesions have similar attenuation to muscle and enhance
variably with contrast. Both tumors may be associated with bony remodeling. On MR imaging,
these two lesions are isointense to muscle on T1W sequences and hyperintense on T2W
sequences. Both tumors typically enhance following intravenous Gadolinium administration.
The diagnosis of neurofibromas may be made with a high degree of confidence if the lesions
have a plexiform appearance or occur in a patient with NF-1.
Malignant neural tumors are very rare and consist mostly of fibro sarcomas and neurogenic
sarcomas (malignant neurofibromas). Secondary neoplasms may extend to involve the
adjacent BP. These lesions may also be either benign or malignant. Benign masses which
involve the BP include: lipoma, lipoblastoma, desmoid, lymphangioma, myoblastoma,
osteochondroma, and ganglioneuroma.
Malignant neoplasms which may involve the BP are commonly due to direct extension from a
Pancoast tumor or metastatic disease. Involvement of the BP by direct extension of a
Pancoast tumor may be suspected in patients who present with supraclavicular pain,
weakness and paresthesias. Imaging findings suggestive of BP invasion by a superior sulcus
tumor are obliteration of the apical fat and proximity of the mass to the BP. Tumors which have
been reported to metastasize to the BP include breast, lymphoma, bladder, gastrointestinal,
testicular, thyroid, lung, melanoma, head and neck, and sarcomas.
The imaging modality of choice in patients with possible neoplastic invasion of the BP is MR
imaging due to its multiplanar capability and high soft tissue characterization. Previous studies
have shown MRI to have a high sensitivity (100%) in detecting neoplastic involvement of the
BP. The extent of disease is also better depicted with MRI than with CT. Coronal T1W images
are especially helpful for assessing the status of the apical fat in patients with Pancoast tumors
and evaluating the relationship of masses to the BP.
INFLAMMATORY
Inflammatory processes may involve the BP include radiation therapy, neuritis, and infections.
Radiation therapy (RT) may injure the BP and cause a plexopathy. Three classical syndromes
of RT induced brachial plexopathy have been described. The most common form is a delayed
progressive radiation fibrosis. The remaining two forms of radiation damage are a reversible or
transient plexopathy and an acute ischemic plexopathy.
Radiation- induced brachial plexopathy is the most common and severe peripheral nervous
system complication of RT. Radiation damage to the BP appears to be dose related and most
likely occurs in patients who have received doses in excess of 6000 cgys. It is most commonly
seen in females who have been treated with RT for breast cancer. The plexopathy tends to be
delayed and progressive with the majority of patients presenting atleast 6 months after the
completion of RT. The initial symptoms include paresthesias, followd by pain and weakness.
These symptoms typically occur in upper trunk distribution with weakness of the arm flexors
and shoulder abduction. Pain can accompany these paresthesias but it usually occurs late in
the course of this syndrome. However, other reports suggest that RT induced plexopathies are
generalized and that the distribution of the deficits is not helpful in separating this variety of

plexopathy from a neoplastic one. Histologically in RT induced plexopathy, there is dense

fibrous tissue encasing the BP with Wallerian degeneration. On physical examination,
radiation- induced brachial plexopathy may result in reflex abnormalities, intrinsic muscle
weakness, muscle atrophy and lymphedema.
MRI is the modality of choice for evaluating patients previously treated with RT to the
supraclavicular region. The imaging findings of RT induced brachial plexopathy are diffuse
thickening and enhancement of the BP without a focal mass. The presence of a focal mass in a
patient treated with RT is suspicious for recurrent tumor and requires further evaluation,
especially in patients treated with doses less than 6000 cgys. Horners syndrome is rarely
caused by RT alone and, when present, is also strongly suggestive of recurrent tumor.
Active inflammation of the BP is termed brachial neuritis (BN). Its etiology may be due to a
primary viral infection (cytomegalovirus, coxsackie), or complication from prior infection. BN
may also result as a complication of previous serum vaccine, antibiotic, or other drug
administration. Idiopathic and heredofamilial forms of BN have also been described. Patients
with BN typically present between the third to seventh decades of life. The condition is slightly
more common in males than in females (2.4::1). Clinically, these patients present with an ache
in the supraclavicular region and shoulder. The pain often worsens over a 3-10 day period and
may be followed by weakness and sensory and reflex impairment. In most cases, the disease
is self limited and subsides over a 6 to 12 week period. However, residual deficits occur in
some patients. MRI is the modality of choice in patients suspected of having BN. The MRI
findings are diffuse thickening, abnormal T2W signal intensity, and abnormal enhancement of
the BP on the gadolinium enhanced images.
Infectious processes involving the BP most commonly involve its supraganglionic portion and
are most likely due to discitis with associated epidural abscesses. Involvement of the more
distal components of the BP is unusual and may be due to extension from and adjacent
infection.
MISCELLANEOUS
The clinical symptoms of degenerative cervical disc disease may mimic those of a brachial
plexopathy; therefore, evaluation of the cervical spine should be included in imaging studies of
the BP. Eighty to ninety percent of cervical radiculopathies involve the C6 (C5/C6 disc) and C7
(C6/C7 disc) roots. Patients may present with numbness, pain, sensory loss, and diminished
reflexes at the affected levels. These symptoms may be exacerbated by coughing, sneezing,
or lateral head movements.
Brachial plexopathy may also be caused by cervical ribs. Cervical ribs are present in
approximately 1% of the population and are symptomatic in 10% of affected individuals. They
are more common in females than in males (2:1) and are unilateral in 50% - 80% of
individuals. Occasionally, a cervical rib may be attached to the first rib by a fibrous band. The
BP may be affected by cervical ribs in one of two ways. The cervical rib may be positioned so
that the BP must cross over it to enter the axilla, thereby stretching the lower trunk. Secondly,
the cervical rib may narrow the space between the posterior aspect of the first rib and the
anterior scalene muscle reducing the area through which the BP and subclavian artery course.
The cervical rib syndrome is felt to result from compression of the lower trunk of the BP as it
crosses over the cervical rib or by compression of the lower trunk by a fibrous band that
attaches to the first rib. The symptoms consist of pain and /or paresthesias along the ulnar
border of the forearm and hand and motor weakness in a similar distribution. Continued
compression may result in muscle wasting which initially involves the thenar eminence but may
also spread to involve the small muscles of the hand.
REFERENCES :
1. Som P.M, Curtin H. Head & Neck Imaging, 4th edition, 1998, Mosby Inc, Volume-II,
Mosby Inc, page no 22217-2225

2. Mukherji SK, Castillo M, Wagle A. Brachial Plexus. Seminars in CT, US and MR imaging
1996; 17:519
3. Posniak HV, Olson MC, Dudiak CM, Wisniewski R, OMalley C. MR imaging of the
Brachial Plexus. AJR 1993; 161:373-379
4. Guha A, Graham B, Kline DG, Hudson AR. Brachial Plexus injuries. In: Wilkins RH,
Rengachary SS, Eds. Neurosurgery 2nd ed. New York, NY: McGraw-Hill 1996:3121-3134
5. England JD, Summer AJ. Nontraumatic Brachial plexopathy. In: Wilkins RH,
Rengachary SS, eds. Neurosurgery 2nd ed. New York, NY: McGraw-Hill 1996:3245-3250
6. Davies ER, Sutton D, Bligh AS. Myelography in brachial plexus injury. Br J Radiol 1966;
362-371
7. El-Gammel T, Brooks BS, Freedy RM, Crews CC. MR Myelography: imaging findings.
AJR 1995; 164:173-177
8. Bowen BC, Verma A, Brandon AH, Fiedler JA. Radiation induced brachial plexopathy:
MR imaging with clinical correlation AJNR 1996; 17:1932-1936