Magnetic Resonance Imaging of Brachial Plexus Pathologies: A Pictorial Essay

Hong Kong J Radiol 2025 Mar;28(1):e55-65 | Epub 19 March 2025

 

 

Department of Diagnostic and Interventional Radiology, Queen Elizabeth Hospital, Hong Kong SAR, China

 

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Magnetic resonance imaging (MRI) is the imaging modality of choice to assess the brachial plexus given its superb soft tissue contrast and lack of radiation.[1] It can detect certain brachial plexus pathologies such as neural and muscle oedema that computed tomography cannot.

 

Thorough anatomical knowledge is essential for interpretation of brachial plexus–related diseases. In this article, the anatomy of the brachial plexus and some of its disease entities are reviewed and illustrated with relevant MRI images.

 

Figure 1 shows the normal anatomy of the brachial plexus. The brachial plexus is divided into five main regions, namely, roots, trunks, divisions, cords, and terminal branches. Some anatomical landmarks, such as the interscalene triangle, clavicle, and subclavian artery, serve as important reference points in image interpretation.

 

Figure 1. Normal sagittal anatomy of the brachial plexus. (a) At the level just lateral to the neural foramina, the C5 to T1 nerves roots are seen. The C8 and T1 nerve roots are separated by the first rib (R). (b) The C5 to T1 nerve roots are seen at the medial aspect of the interscalene triangle formed by the anterior scalene muscle (AS) and the middle scalene muscle (MS). The subclavian artery (SA) is seen in the anterior aspect of the interscalene triangle. (c) The superior trunk (ST), middle trunk (MT) and inferior trunk (IT) are seen just lateral to the interscalene triangle. (d) Divisions (D) are seen at the retroclavicular region above the SA. The subclavian vein (SV) is anteroinferior to the SA. (e) The lateral cord (LC), posterior cord (PC) and middle cord (MC) are seen around the axillary artery (AA) in the infraclavicular region, forming a ‘paw-print’ configuration. The axillary vein (AV) is inferior to the AA. (f) The median nerve (MN), mucocutaneous nerve (MCN), ulnar nerve (UN) and radial nerve (RN) are seen around the AA near the lateral border of the pectoralis minor muscle.

 

The brachial plexus typically originates from the ventral rami of spinal nerves C5 through T1. In the sagittal plane, the first rib can help identify the C8 and T1 nerve roots, with the C8 nerve root above it and the T1 nerve root below it (Figure 1a). The roots, along with the subclavian artery, course towards the interscalene triangle formed by the anterior and middle scalene muscles. The C5 to C7 nerve roots are superior to the artery, while the C8 and T1 nerve roots are posterior to the artery (Figure 1b). The roots merge to form three trunks: the superior (formed by the C5 and C6 roots), middle (the continuation of the C7 root), and inferior trunks (formed by the C8 and T1 roots). These trunks are seen at the lateral aspect of the interscalene triangle (Figure 1c). The upper and middle trunks are superior to the subclavian artery, while the lower trunk is posterior to the subclavian artery. Each trunk divides into anterior and posterior divisions at the lateral border of the first rib, where the subclavian artery becomes the axillary artery. The divisions can be identified superior to the axillary artery in the retroclavicular region (Figure 1d). The six divisions intermingle to form the three cords: the lateral, posterior, and medial cords. They are found inferior to the clavicle at the medial border of the coracoid process with a ‘paw-print’ configuration on sagittal images along with the axillary artery. The cords are named according to their position relative to the axillary artery. On sagittal MRI, the lateral cord is located most anteriorly, the posterior cord most superiorly, and the medial cord most posteriorly (Figure 1e). The cords give rise to the terminal branches, which include the axillary, musculocutaneous, median, ulnar, and radial nerves at the lateral border of the pectoralis minor muscle. The latter four terminal branches surround the axillary artery at this location (Figure 1f).[2] [3] [4]

 

MRI of the brachial plexus employs a series of sequences to provide detailed visualisation of the complex network of nerves. These sequences include T1-weighted imaging (T1WI), T2-weighted imaging (T2WI), and fat-suppressed fluid-sensitive sequences such as short-tau inversion recovery (STIR) and the Dixon sequences. T1WI offers excellent anatomical detail for assessing the nerves which appear hypointense against the hyperintense fat. It is also useful in detecting masses and assessing their relationship to adjacent structures. Contrast-enhanced fat-suppressed T1WI sequence is helpful in characterisation of pathologies in the brachial plexus. T2WI, particularly when combined with fat suppression techniques such as STIR, accentuates the signals of the nerves, allowing for better identification of pathological changes such as oedema, inflammation, or infiltration by tumours. In our department, the Dixon technique used in our standard protocol has the advantage of more robust fat suppression, improving the quality of fat-suppressed T2WI.[5] It also enables simultaneous acquisition of fat-suppressed (water-only) and non–fat-suppressed images. Three-dimensional sequences such as T1W magnetisation-prepared rapid gradient-echo or T2W sampling perfection with application-optimised contrasts using different flip angle evolution provide high spatial resolution and multiplanar reconstruction capabilities to visualise the complex anatomy of the brachial plexus.

 

Diffusion-weighted imaging (DWI) and diffusion tensor imaging (DTI) are often incorporated in the protocols of brachial plexus MR neurography by analysing the movement of water molecules. DWI effectively suppresses background signals using techniques such as STIR and heavy diffusion gradients, resulting in high-contrast nerve images. This makes it particularly suitable for identifying demyelinating diseases and neuropathies throughout the body. DTI builds upon DWI by measuring the direction of water movement, providing parameters such as fractional anisotropy (FA) and radial diffusivity. FA reflects the degree of organisation within nerve fibres, while radial diffusivity indicates the integrity of the nerves’ myelin sheaths, offering advantages over traditional nerve conduction studies for diagnosing and monitoring nerve degeneration and regeneration, especially in cases of mild neuropathy. DTI also allows for three-dimensional visualisation of the nerve fibre tracts through tractography, which employs mathematical constructions based on eigenvectors and FA.[6]

 

Axial and coronal images allow comparison with the contralateral side if it is included in the field of view. Sagittal images clearly demonstrate the anatomy of the brachial plexus and its relationships to the surrounding structures. Given the fact that the brachial plexus runs obliquely from superomedial to inferolateral in the coronal plane, alternative imaging planes such as axial oblique, coronal oblique, and sagittal oblique images can be used to visualise the brachial plexus along its true short and long axes. The oblique sagittal images facilitate the assessment of the fascicular structures of the nerves, as the cross-sectional architecture is better depicted.[6]

 

In trauma, MRI is useful in localising nerve involvement as well as determining the degree of chronicity of the injury. In acute denervation, the denervated muscles exhibit T2W hyperintense signals within days after the injury. Chronic denervation results in loss of muscle bulk and fatty infiltration. Within the first 4 weeks after injury, the muscles may show increased signals on contrast-enhanced sequence, possibly due to sympathetic vascular tone alteration.[4]

 

According to Seddon’s classification, there are three types of nerve injury.[4] First-degree injury, also known as neuropraxia, is the lowest grade and corresponds to localised demyelination that does not disrupt the axon. A more severe nerve injury is known as axonotmesis or second-degree injury (Figure 2), which involves the axon. Neurotmesis, or third-degree injury, is nerve transection and is the most serious injury where no axonal regeneration is possible. Generally, lower-grade injuries are treated conservatively to encourage spontaneous healing, while higher-grade injuries require surgical intervention, including primary repair, nerve graft placement, and nerve or myotendinous transfer.[4]

 

Figure 2. Axonotmesis of the left supraclavicular nerve and the posterior cord of the left brachial plexus secondary to clavicular fracture. (a) Anterior posterior radiograph of the left shoulder shows a displaced clavicular fracture with callus formation (arrow). Fractures of the left second through the fifth ribs are also seen (dotted arrows). (b) Coronal T1-weighted image shows the proximal left suprascapular nerve to be focally oedematous just posteromedial to the clavicular fracture, suggestive of neuroma-in-continuity (arrow). (c) Sagittal T2-weighted image (T2WI) shows thickening with mild hyperintense signal and adjacent scarring of the posterior cord of the left brachial plexus inferior to the clavicular fracture (arrow). (d) Fat-suppressed T2WI shows denervation oedema in the left supraspinatus (S), infraspinatus (I), teres minor (T) and deltoid muscles (De). Normal signals can be appreciated in the subscapularis muscle (Sub).

 

The distinction between preganglionic injury and postganglionic injury is vital because preganglionic injuries are deemed to be permanent, while postganglionic injuries have a better chance of being surgically treated or grafted.

 

Root avulsion may be clearly visible on MRI as disconnection of the ventral or dorsal nerve roots from the spinal cord (Figure 3). The roots can retract over the neural foramen and into the supraclavicular fossa, which is more prevalent in high-energy traction injury.

 

Figure 3. Preganglionic injury of the left C8 and T1 nerve roots. (a) Sagittal T2-weighted image (T2WI) shows small cerebrospinal fluid–filled structures near the left C7/T1 and T1/T2 intervertebral foramina in a trauma patient, compatible with pseudomeningoceles (arrows). (b) A torn C8 nerve root (dotted arrow) at the lateral aspect of the C7/T1 pseudomeningocele (arrow) is identified on axial fat-suppressed T2WI.

 

Imaging of suspected preganglionic damage is best performed at least 3 to 4 weeks after injury since this allows for resolution of acute oedema and subarachnoid haemorrhage as well as detection of any development of pseudomeningocele caused by a leak of cerebrospinal fluid through a meningeal tear, one of the most significant secondary findings of root avulsion. Pseudomeningocele may present as a massive cystic collection extending through a neural foramen and communicating with the subarachnoid space. It develops upon root avulsion because the nerve epineurium and outer perineurium are continuous with the dura mater and arachnoid mater.[4]

 

Postganglionic traumatic brachial plexopathy may manifest as focal calibre change or discontinuity of the nerve, loss of fascicular architecture, neuroma formation, perineural fibrosis, or abnormal nerve signal intensity on MRI. The area of nerve discontinuity is typically best seen on coronal or axial views, with abnormal hyperintensity and contour irregularities on T2WI. The distance between the discontinuous proximal and distal nerve extremities (nerve gap) in cases of neurotmesis should be reported because it may influence the planning of surgical repair.[4]

 

More than 90% of primary brachial plexus tumours are benign nerve sheath tumours. Schwannomas make up approximately 90% of benign brachial plexus nerve sheath tumours, while neurofibromas constitute the remaining 10%.[7] Schwannomas are characterised by being outside the nerve fascicles. They have a well-defined capsule and are essentially eccentric nerve sheath tumours. They cause displacement of the nerve fascicles, allowing resection without injuring the nerve. Cystic components are occasionally be seen in schwannomas. Neurofibromas, however, lack a capsule and invade the nerve fascicles, making resection of the tumour without damaging the nerves challenging.[7]

 

Schwannomas and neurofibromas appear homogeneously hyperintense on T2WI. They are oval lesions with smooth, circumscribed margins along the longitudinal axis of the nerve on MRI (Figure 4).[3] Neurofibromas are more likely to show the ‘target sign’ of central T2WI hypointensity and peripheral T2WI hyperintensity. The ‘reverse target sign’ may be demonstrated on T1WI following gadolinium contrast administration, in which there is enhancement of the central collagenous component with relative hypoenhancement of the peripheral myxoid component. This correlates histologically to a core region of collagen surrounded by myxomatous tissue. The ‘target sign’, however, is present in just a portion of neurofibromas and malignant peripheral nerve sheath tumours (MPNSTs).[8]

 

Figure 4. Schwannoma of the right brachial plexus. (a) Coronal fat-suppressed T2-weighted image (T2WI) shows the tumour along the right C8 nerve root in the right interscalene triangle (arrow). Medially the tumour extends into the right C7/T1 intervertebral foramen which is expanded. (b) Axial fat-suppressed T2WI illustrates the ‘target sign’ of the tumour with peripheral high signal intensity (arrow) and central low signal intensity (dotted arrow). (c) On axial contrast-enhanced fat-suppressed T1-weighted imaging, the mass shows reversal of the ‘target sign’ with peripheral low signal intensity (arrow) and central high signal intensity (dotted arrow).

 

Myxoma is a mesenchymal neoplasm characterised by undifferentiated stellate cells within a myxoid stroma. The majority of myxomas are intramuscular; intermuscular, subcutaneous, and juxta-articular myxomas are uncommon. Myxomas show low-to-intermediate signals on T1WI and hyperintense signals on unenhanced T2WI (Figure 5). They are usually well-defined and homogeneous to mildly heterogeneous. A thin rim of fat that indicates atrophy of the nearby muscle is commonly seen in intramuscular myxomas, most prominently at the superior and inferior aspects of the lesion. Perilesional high signal on fluid-sensitive sequences can be seen in most of the myxomas due to leakage of the myxomatous materials into surrounding muscle resulting in oedema. Myxomas can exhibit mild to moderate contrast enhancement in a homogeneous pattern or a thick rim and septal pattern. Cystic regions are present in slightly more than half of all myxomas.[8]

 

Figure 5. Myxoma in the left interscalene triangle. (a) Axial contrast-enhanced fat-suppressed T1-weighted image (T1WI) and (b) coronal fat-suppressed T2-weighted image (T2WI) show an intermuscular myxoma (T) in the left interscalene triangle. It is hypointense on T1WI and hyperintense with mild heterogeneity on T2WI. The lesion slightly displaces the adjacent brachial plexus (dotted arrow).

 

Fibromatoses are made up of spindle-shaped fibrous cells that are separated and surrounded by an abundance of collagen material with rare mitoses. Their aggressiveness is intermediate between that of benign fibrous lesions and fibrosarcomas. Fibromatoses are divided into two main groups, namely, superficial (fascial) and deep (musculoaponeurotic). Superficial fibromatoses are typically small, slow-growing lesions that originate in the fascia and aponeurosis. Deep fibromatoses commonly originate in the deep fascia surrounding muscle and aponeurotic tissue, and are more extensive and aggressive. It can be challenging to entirely resect the tumour, which has a propensity to recur.

 

MRI of deep fibromatosis typically shows hypointense signals on T1WI and T2WI if the lesion has abundant collagen with hypocellularity (Figure 6). The lesion shows hyperintensity on T2WI if the lesion is highly cellular. Deep fibromatoses typically demonstrate moderate to marked contrast enhancement, particularly in collagen-deficient and cellular regions. Only 10% of lesions lack significant enhancement.[9]

 

Figure 6. Fibromatosis involving the right brachial plexus. (a) Coronal T1-weighted image (T1WI), (b) contrast-enhanced fat-suppressed T1WI and (c) fat-suppressed T2-weighted image (T2WI) show the fibromatosis (arrows) encasing the brachial plexus (dotted arrows) and subclavian vessels (arrowheads). It is hypointense on T1WI and T2WI with patchy contrast enhancement.

 

MPNSTs are the most common malignant tumour in the brachial plexus. Approximately 50% of MPNSTs are associated with neurofibromatosis type 1, while the other half are sporadic.[10] A small proportion of MPNST cases are associated with a history of prior radiotherapy with the field covering the brachial plexus, with an average latency period of 15 years.[10]

 

Imaging cannot reliably distinguish between benign and malignant peripheral nerve sheath tumours but is useful in detecting suspicious features that can aid direct biopsy or resection.[3] Suspicious features of MPNST include large size, a perilesional oedema-like zone, a peripheral enhancement pattern, and intratumoural cystic lesion as a result of haemorrhage or necrosis (Figure 7). The presence of two to four of these features is suggestive of malignancy with high specificity (90%) but limited sensitivity (61%). Heterogeneity on T1WI is an additional suspicious feature for those MPNST cases associated with neurofibromatosis type 1.[11] Significant diffusion restriction, particularly at a minimal apparent diffusion coefficient <1.0 mm²/s, also suggests malignancy.[4]

 

Figure 7. Malignant peripheral nerve sheath tumour involving the left brachial plexus. (a, b) Axial contrast-enhanced fat-suppressed T1-weighted images (T1WI) show that the heterogeneously enhancing tumour (arrowheads in [a]) with necrotic areas extends through the left C7/T1 neural foramen into the spinal canal. The left vertebral artery (VA), the left subclavian artery (SA) and the left proximal common carotid artery (CCA) are encased. (c) Coronal contrast-enhanced fat-suppressed T1WI image and (d) T2-weighted image show that the tumour extends into the spinal canal (arrows) and involves the left lung apex (arrowheads) as well as the left upper mediastinum (dotted arrow in [c]).

 

The term ‘superior pulmonary sulcus tumour’ is typically applied to all non–small cell lung carcinomas that originate from the lung apex and invade the chest wall or soft tissues of the thoracic inlet, regardless of the symptom complex. It accounts for 3% of all lung malignancies and is associated with poor prognosis in the majority of cases.[12]

 

Since the brachial plexus is surrounded by connective tissue, a tumour can indent the brachial plexus and displace the nerve roots or trunks superiorly without actually invading them, which is shown as loss of the intervening fat plane separating the apical pleura from the T1 nerve root and subclavian artery on MRI (Figure 8). Loss of sensory function may be the result of extrinsic nerve compression, whereas loss of motor function is more likely due to nerve invasion. To avoid overestimating brachial plexus involvement when evaluating the local extent of a tumour, it is crucial to correlate imaging findings with the patient’s symptoms.[11] Notably, invasion of the brachial plexus roots or trunks at a level above T1 is an absolute contraindication to surgery.

 

Figure 8. Left lung superior sulcus tumour (arrowheads). (a-c) Coronal contrast-enhanced fat-suppressed T1-weighted images show that the tumour abuts the left brachial plexus (dotted arrows in [b] and [c]) and subclavian artery (arrows in [a] and [c]) superiorly. (d) Coronal T2-weighted image shows hyperintense signal in the tumour centre, suggestive of necrosis (arrow).

 

Primary malignant tumours arising from the surrounding structures, such as soft tissue sarcoma and primary bone tumours, can involve the brachial plexus, resulting in neurological impairment (Figures 9 and 10). Certain tumours may have more specific MRI features. For instance, tail-like tapering enhancement along the adjacent fascial plane of the tumour (‘tail sign’) is a common MRI feature of myxofibrosarcoma and undifferentiated pleomorphic sarcoma.[13]

 

Figure 9. Myxofibrosarcoma in the right supraclavicular fossa (arrowheads). (a) Coronal contrast-enhanced fat-suppressed T1-weighted image and (b) fat-suppressed T2-weighted (T2W) image show an irregular T2W hyperintense tumour with peripheral enhancement in the right supraclavicular fossa. Inferiorly, the mass indents the right brachial plexus (arrows).

 

Figure 10. Post-irradiation malignant spindle cell carcinoma. (a) Coronal T1-weighted image (T1WI) and (b) contrast-enhanced fat-suppressed T1WI show the enhancing tumour (dotted arrows) in the left supraclavicular fossa (arrowheads). (c) Sagittal T1WI and (d) contrast-enhanced fat-suppressed T1WI show that the branches and divisions of the left brachial plexus (arrowheads), which are normally seen posterior to the subclavian artery (SA) in the interscalene triangle and the retroclavicular area, are invaded by the tumour (dotted arrows). The subclavian vein (SV) is not invaded.

 

Metastatic involvement of the brachial plexus occurs mainly with breast, lung, and, less commonly, head and neck cancers.[3] The plexopathy may be the result of mass effect from adjacent tumour or direct nerve infiltration. The medial cord is frequently involved in metastatic breast cancer given its proximity to the axillary venolymphatic drainage pathway. On MRI, metastasis manifests as irregular or nodular enlargement and T2 hyperintensity of the affected nerves, which is typically accompanied by enhancement (Figure 11).

 

Figure 11. Metastatic carcinoma of the breast. (a, b) Coronal contrast-enhanced fat suppressed T1-weighted images show heterogeneously enhancing soft tissue thickening along the right brachial plexus (dotted arrows). Medially, it reaches the right C6/7 neural foramen (arrowhead in [b]). A right axillary metastatic lymph node with central necrosis (N) is present. (c) Axial T2-weighted image shows denervation oedema and atrophy of the right upper limb muscles (arrows) supplied by the right brachial plexus.

 

Radiation-induced brachial plexopathy usually manifests between 6 months and 20 years after treatment. On MRI, post-radiation plexopathy is characterised by smooth longitudinal thickening of the nerves, frequently accompanied by T2W hyperintense signals and longitudinal thin enhancement (Figure 12). Associated perineural fibrosis appears as ill-defined tissue that effaces the normal perineural fat planes on T1WI. It is usually isointense to hypointense on T2WI but can be hyperintense in the presence of vascularised scar tissue. In comparison, tumour or perineural metastasis may have similar signal characteristics on T1WI and T2WI but is more likely to appear as a nodular, discrete enhancing lesion.[4]

 

Figure 12. Post-irradiation bilateral brachial plexopathy. (a) Coronal fat-suppressed T2-weighted image (T2WI) and (b) contrast-enhanced fat-suppressed T1-weighted image show symmetric thickening of the bilateral C5 to C8 nerve roots with hyperintense signals on T2WI and mild contrast enhancement, extending from the intervertebral foramina to the trunks and divisions of the brachial plexuses (arrows). The features are suggestive of bilateral brachial plexopathy secondary to prior radiotherapy for nasopharyngeal carcinoma.

 

Acute brachial neuritis, also known as Parsonage-Turner syndrome or idiopathic neuralgia amyotrophy, classically manifests as acute onset of pain of the upper extremity lasting for hours to weeks, followed by numbness and weakness. The cause of this condition is not known but predisposing factors include infection, minor trauma, unaccustomed strenuous exercise, childbirth, and surgery. The diagnosis is usually made clinically with electromyographic testing and imaging as adjuncts. On MRI, the involved plexus shows hyperintense signals with or without mild thickening on T2WI (Figure 13). Roots are the most common site of involvement, followed by trunks and cords.[14] The C5 root is the most common nerve root involved while the lateral cord is the most common cord involved.[3] The most frequently affected nerve is the suprascapular nerve, followed by the axillary nerve.[15] Muscular denervation changes with intramuscular oedema and various degrees of fatty atrophy are typical, most commonly affecting the supraspinatus and infraspinatus muscles.[16]

 

Figure 13. Acute left brachial neuritis. (a) Coronal fat-suppressed T2-weighted image (T2WI) and (b) contrast-enhanced fat-suppressed T1-weighted image (T1WI) show oedema of the left brachial plexus with diffuse hyperintense signals from the roots down to the terminal branches on T2WI (arrows). There is no significant contrast enhancement on T1WI. Features are supportive of the clinical suspicion of acute brachial neuritis.

 

Apart from the general limitations of the MRI scan, such as patients with metallic implants or claustrophobia, a comprehensive MR neurography protocol often involves multiple sequences in different planes to fully assess the plexus, further extending the overall scan duration.

 

Motion artifacts present a significant hurdle in achieving clear and diagnostic images of the brachial plexus. Even slight patient movements during the scan, whether voluntary or involuntary, can obscure subtle findings and compromise image quality. Respiratory motion, particularly affecting the infraclavicular region, can significantly degrade image quality. While techniques such as respiratory triggering can help mitigate this issue, they may not eliminate it entirely and can further lengthen scan times.

 

This article provides an overview of the basic anatomy and common pathologies of the brachial plexus, highlighting salient MRI findings to aid radiologists in formulating accurate differential diagnoses and guiding appropriate management.