Introduction

Brachial and lumbosacral plexopathies are among some of the most complicated and challenging conditions to diagnose. The peripheral nerves are susceptible to various traumatic, inflammatory, metabolic, and neoplastic processes often resulting in multiple sites of injury. A meticulous evaluation for accurate identification of plexopathy traditionally relies on patients’ medical history, clinical examination, and electrodiagnostic tests. Magnetic resonance (MR) imaging plays an increasing role in characterization, location and extent of plexus involvement and is developing into a useful diagnostic tool that substantially affects disease management.

All upper limb motor functions are provided by the brachial plexus, with the exception of the levator scapula and trapezius muscles. The brachial plexus also provides all of the cutaneous sensation for the upper limb, with the exception of the axilla, which is innervated by the intercostobrachial nerve. The brachial plexus consists of 5 segments: roots, trunks, cords, divisions, and branches. The brachial plexus is derived from the C5, C6, C7, C8, and T1 roots. The roots converge after exiting the neural foramina to form trunks in the supraclavicular interscalene space between the anterior and middle scalene muscles. The C5 and C6 roots form the superior trunk, the C7 root continues on as the middle trunk, and the C8 and T1 roots form the inferior trunk.

The terminal innervations that emerge directly from the upper trunk include the suprascapular nerve (C5, C6 to the supraspinatus and infraspinatus) and the subclavian nerve (C5, C6 to the subclavius. The 3 trunks split into anterior and posterior divisions. The anterior divisions, in general, supply flexor muscles, and the posterior divisions supply extensor muscles. The anterior divisions of the superior and middle trunks converge to create the lateral cord. The anterior division of the inferior trunk continues on as the medial cord. The 3 posterior divisions from all 3 trunks unite to create the posterior cord. The cords are named according to their position in relation to the axillary artery.

Terminal nerves branch from the cords: the pectoral nerve (C5, C6, C7 to the pectoralis major) from the lateral cord; from the posterior cord emerges the upper subscapular nerve (C5, C6 to the subscapularis), the thoracodorsal nerve (or middle subscap- ular) (C6, C7, C8 to the latissmus dorsi), and the lower subscapular nerve (C5, C6 to a portion of the subscapularis and teres major); the medial pectoral nerve emerges from the medial cord (C8, T1 to pectoralis major and pectoralis mi- nor), as do the sensory branches of the medial cutaneous nerve of the arm (medial cord, T1) and medial cutaneous nerve of the forearm [2]. The musculocutaneous, axillary, radial, median, and ulnar nerves are the terminal branches of the brachial plexus.

Lumbosacral Plexus

The lumbosacral plexus comprises a network of nerves that provide motor and sensory innervation to most structures of the pelvis and lower extremities. The lumbosacral plexus can be functionally divided into the lumbar plexus and the sacral plexus. The lumbar plexus is formed from the ventral rami of the L1 through L4 nerve roots. These rami cluster within or posterior to the body of the psoas major anterior to the L2 through L5 transverse processes and then exit into the pelvis. The sacral plexus is formed by the combination of the lumbosacral trunk with the ventral rami of S1-S4 and contributions from the first coccygeal nerve. The sacral plexus arises on the anterior surface of the piriformis. The lumbar plexus gives off the terminal branches of the iliohypogastric, ilioinguinal, genitofemoral, femoral, and obturator nerves. The sacral plexus gives off the terminal branches of the superior and inferior gluteal nerves and the sciatic nerve, which comprises the peroneal, tibial, and sural sensory distributions.

Imaging

Conventional imaging techniques adapted for optimal peripheral nerve visualization include multi-planar high resolution T1 and heavily T2-weighted fat suppressed sequences. Normal peripheral nerves demonstrate isointense T1 and isointense to slightly hyperintense T2 signal. T1-weighted sequences with 2-4mm slice thickness and high resolution (< 1 mm2 pixel size) demonstrate the fascicular pattern of the normal nerve, outlining the epineurial fat plane, and delineating the anatomic structures surrounding the nerve. Fat-suppressed T2-weighted imaging enables sensitive detection of water content alterations in a variety of nerve pathologies. Because the intrinsic T2 hyperintense signal of fat surrounding a nerve may mask the T2 prolongation effect of nerve pathology, fat suppression techniques are routinely utilized with T2 imaging.

3 Tesla scanning and accelerated acquisition schemes allow 3-dimensional (3D) sequences, thinner slices (less than 1 mm), approximating in-plane matrix dimensions. The resulting isotropic voxel size also allows for maximum intensity projection (MIP), multi-planar, and curved-planar reformations, thereby increasing signal-to-noise ratio and better delineating complex anatomy.

Intravenous MRI contrast agents are particularly helpful when there is loss of integrity of the blood-nerve barrier (BNB), such as in trauma (neuromas), inflammatory or neoplastic neuropathies. Fat suppression is usually applied with post-contrast imaging so that enhancement is not masked by the intrinsic T1 shortening effect of adjacent fat.

Diffusion weighted imaging (DWI) with high diffusion sensitizing gradient moments (i.e. b-value ≥ 500 s/mm2) takes advantage of the anisotropic diffusion of water within nerve fibers preferentially paralleling the course of axonal bundles. DWI enhances nerve contrast, increasing sensitivity to pathologic alterations in nerve internal architecture. DWI with acquisition of at least six non-collinear diffusion gradient directions allows tensor modelling and diffusion tensor tractography.

Imaging Patterns

General imaging patterns suggest abnormalities of the peripheral nerves and plexus. Normally their course should be smooth without abrupt kinking. Individual fascicles of the nerves may be visible in nerves greater than approximately 3mm in diameter. Normal nerves have a clear fat plane around them defined by the epineurium. Size discrepancy between corresponding nerves suggests either chronic atrophy of the smaller nerve or pathologic enlargement of the larger nerve. Abrupt kinking of a nerve suggests nerve entrapment. Obvious discontinuity is strongly suggestive of nerve transection.

Normal nerve T1 signal is intermediate, typically isointense to muscle. Adjacent fat in and around the fascicles of the larger nerves will have characteristic fat signal. Normal nerve T2 signal is slightly hyperintense compared to muscle due to endoneurial fluid. Asymmetric or focal increased T2 signal might suggest increased interstitial fluid, which can be seem in variety of pathologies. Focal areas of enhancement are due to breakdown of the blood nerve barrier and may be due to tumor infiltration or by an adjacent/intrinsic inflammatory process.

Muscle signal characteristics will vary based on the length of time of denervation. The acute phase of denervation is within the first 4 weeks and will feature homogenously increased signal on fluid sensitive sequences and enhancement on post-gadolinium sequences. The subacute phase is between 4 weeks and 3 months. During this time the involved muscles will continue to feature homogenously increased signal on fluid sensitive sequences and will also develop increased T1 signal intensity due to the infiltration of fat and connective tissue. The chronic phase is beyond 12 weeks and involved muscles will continue to have increased T1 signal intensity as more muscle is replaced by fat.

Conditions Affecting Peripheral Nerves

Infection

Infectious processes can affect the plexus, typically due to direct extension of a primary infectious source which may include septic arthritis, myositis, osteomyelitis, and abscesses. Infections are rare causes of plexopathy/neuropathy. Varicella zoster plexopathy and mononeuropathy as well as hepatitis C and HIV associated plexopathy have been demonstrated. Clinical findings include pain and sensory deficits in the context of fever and leukocytosis. MRI features include long segment diffuse enlargement of the involved nerves or plexuses. T2 hyperintensity related to edema will be present and contrast enhancement of the involved nerves which is often heterogeneous.

Ischemic Injury

Inflammation and dysfunction of peripheral nerves can occur due to both local or global ischemia. Global ischemia occurs in states of shock due to sepsis, exsanguination, or other causes. When global ischemia occurs injury tends to be symmetric and occur in multiple nerves. Findings include long segment diffuse nerve thickening, prominence of the fascicular pattern of the nerves, diffusely increased T2 hyperintensity, and possible diffuse enhancement due to breakdown of the blood-nerve barrier. Local ischemia can occur in numerous conditions including compartment syndrome, direct trauma, or infarction of the capillaries within the perineurium. Infarction most commonly occurs in patients with trauma, diabetes, vasculitidies, or other rheumatologic conditions. Similar to global ischemia, an ischemic nerve demonstrates long segment diffuse nerve thickening, fasicular prominence, diffusely increased T2 hyperintensity, and possible enhancement.

Inflammatory Demyelinating Polyneuropathies

Inflammatory polyneuropathies may be acute or chronic. Acute inflammatory demyelinating polyneuropathy (AIDP or Gullain-Barré syndrome) is a syndrome that can be idiopathic but usually follows a recent viral or bacterial illness. Cross reactivity against gangliosides within myelin form and the host immune system attacks peripheral nerve myelin. The severity of symptoms, as well as the rate of progression, is highly variable. Patients may only have mild peripheral weakness that resolves completely or may have rapid development of permenant neurologic deficits. Symptoms are primarily motor with sensory involvement being much more rare.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is less well understood and can develop from incompletely resolved AIDP or independently. Pathogenesis is similar with formation of auto-antibodies, but why some patients undergo a chronic course isn't well understood. Symptoms are both sensory and motor and improve with corticosteroid therapy, one of the criteria for the diagnosis. Patients with CIDP may completely recover with time, or have a relapsing-remitting pattern, or a slowly progressive course. MRI findings for both AIDP and CIDP can be overlapping, and the distinction is therefore based on clinical features and time course. AIDP usually has smooth, confluent enhancement of nerve roots and peripheral nerves with mild symmetric enlargement. However, CIDP tends to have more nerve root and peripheral nerve enlargement, homogenous and diffuse T2 hyperintensity in addition to diffuse enhancement.

Post-radiation Neuropathy

Typically patients develop symptoms more than 6 months after radiation therapy, and symptoms may even develop more than 20 years later. The degree of symptoms is related to overall radiation dose and proximity to the radiation target. Symptoms most commonly include pain and paresthesias. If severe, patients may have complete paresis and debilitating pain, which may only be cured with symphathetectomy. MRI findings demonstrate confluent enlargement and/or enhancement of multiple nerves, and the pattern of injury will conform to a known radiation field. Typically nearby soft tissue fibrosis and fatty bone marrow changes will be present to suggest prior radiation. Special attention should be paid to the nearby soft tissues - particularly in resection beds of any primary malignancy - as tumor recurrence with plexus invasion is an important differential.

Charcot-Marie-Tooth

Charcot-Marie-Tooth syndrome (CMT) refers to two separate entities related to disordered myelination of peripheral nerves (CMT1) and primary axonal loss without demyelination (CMT2). CMT, within the spectrum of hypertrophic neuropathies, is the most common inherited neurologic disorder and is characterized by distal motor weakness and atrophy, radicular pain, and a variable degree of sensory loss. Patients may present anywhere between infancy and the second decade of life depending on the specific mutation. On MRI there is bilateral, symmetric and confluent enlargement of the nerve roots, dorsal root ganglia, and peripheral nerves. The nerves will be diffusely hyperintense on T2 weighted imaging with disruption of the normal fasicular architecture. Contrast enhancement is variable and depends on both the specific mutation involved as well as the chronicity of demyelination. Acutely demyelinating CMT1 for example will demonstrate mild, diffuse enhancement of the nerves. CMT2 however involves direct axonal degeneration and does not feature contrast enhancement. Changes of the muscles will be prominent and include the typical findings related to denervation depending on the chronicity of denervation. Typically the presentation will be chronic and the muscles will feature relative fatty atrophy.

Trauma

Traumatic peripheral nerve injury ranges from disruption of axonal conduction with preservation of anatomic continuity of the nerve connective tissue sheaths (neurapraxic injury) to transection with complete loss of nerve continuity (neurotmetic injury). Post-traumatic plexopathy may be the sequela of laceration, compression, stretching, perineural fibrosis or nerve root avulsion. Traumatic meningocele, or pseudomeningocele, may occur with or without avulsion. Pseudomeningoceles and fusiform retraction of the distal plexus may suggest avulsion injury. However, simple dural tears or partial avulsion injuries can also result in the presence of pseudomeningoceles.

In the adult, brachial plexus injuries can be caused by various mechanisms including penetrating injuries, falls, and most commonly motor vehicle trauma (up to 70% involving motorcycles or bicycles). Often the diagnosis can be delayed or ignored as the clinician may wait for signs of clinical recovery. 3D volumetric acquired sequences allow reformations which can demonstrate peripheral nerve continuity or disruption which is important in determining whether surgical treatment is required. 3D volumetric acquired sequences and diffusion sequences can also aid in identifying pre and post-ganglionic injury which is also important for prognosis and appropriateness of surgical repair. Post-ganglionic injuries are located distal to the dorsal root ganglion (DRG) compared to pre-ganglionic lesions which are located proximal to the DRG. In pre-ganglionic injuries, the nerve has been avulsed from the spinal cord and repair would require a neurotization procedure compared to post-ganglionic injuries which may be surgically repaired or grafted. The ganglia and proximal peripheral nerves can be demonstrated with diffusion imaging and may prove to be useful for distinguishing preganglionic from postganglionic avulsion.

An infrequent injury to the brachial plexus can occur in newborn infants manifest by inability to actively move one upper extremity. When the C5 and C6 cervical roots are involved, it is called Erb’s palsy and there is an associated flaccid upper arm with a lower arm that is extended and internally rotated. An important concept is to detect not only abnormal increased signal on T2 sequences within the nerve, but also to look for an abnormal course of the nerves which may be present as a sequela of traction injury. The loss of the normal oblique orientation of the cervical plexus in the absence of a pseudomeningocele is an important indicator of severe traction injury without avulsion and can result in a relatively lax appearance of the cervical roots. Post-traumatic neuroma formation may interfere with nerve recovery and its presence can be suggested on MR by focal expansion, increased signal and the presence of enhancement with gadolinium. Normal ganglion enhance with gadolinium. Normal nerve-blood barrier results in no appreciable enhancement of the peripheral nerves. Disruption of this normal barrier allows gadolinium to leak into the epineural tissues with resultant enhancement that can be homogeneous, and in the correct clinical setting, suggest the presence of neuroma formation which is important for surgical planning in patients who no longer demonstrate clinical recovery.

Entrapment

MR can localize the site of nerve entrapment by demonstrating abnormal caliber, course and signal at the site of entrapment. Common locations include the lower trunk of the brachial plexus within the thoracic outlet, and the sciatic nerve at the greater sciatic foramen.

There are three potential sites of compression along the course of the brachial plexus or the subclavian /axillary artery or vein; the interscalene triangle, the costoclavicular space between the first thoracic rib and the clavicle, and the retropectoralis minor space posterior to the pectoralis minor muscle. Clinical symptoms of entrapment or compression (“thoracic outlet syndromes”) may be due to venous or arterial compression, brachial plexus compression, or a combined neurovascular compression. Classic neurologic thoracic outlet syndrome usually manifests as a chronic lower trunk plexopathy with paresthesias and atrophy affecting arm, forearm and hand. Compression or entrapment is usually the result of a congenital fibrous band extending from an elongated transverse process or rudimentary cervical rib to the first thoracic rib with resultant stretching, angulation and distortion of the usual course and orientation of the brachial plexus. MR is useful in demonstrating the distortion of the course of the brachial plexus, and in cases of significant compression, the associated intraneural edema along with the osseous and fibrous anomalies. Traumatic thoracic outlet syndrome results from clavicular injury, usually a midshaft fracture with resultant injury to the subjacent blood vessels and brachial plexus. There may be compression by displaced fracture fragments, hematoma or pseudoaneurysm formation. Symptoms may frequently present in a relatively delayed fashion, days to even years after the initial injury due to hypertrophic callus and fracture non-union. The cords of the brachial plexus and portions of the subclavian artery and vein may be damaged alone or in various combinations.

In some patients with leg pain resembling lumbosacral radicular sciatica and normal routine lumbar MRIs, symptoms may be attributable to extraforaminal sciatic nerve injury or compression. In such patients, the symptoms have often been attributed to entrapment of the sciatic nerve in the buttock by the overlying piriformis muscle or by an adjacent band of fascia. MR may reveal abnormal sciatic nerve morphology, course and signal along with denervation and atrophy. The bifid piriformis is a congenital variant with an additional fibrous fasicle of the piriformis inserting onto the trochanteric fossa following the course of the obturator internus and the superior and inferior gemelli. The tibial and peroneal divisions of the sciatic nerve divide around the fasicle and reform before exiting through the greater sciatic foramen. There are case reports of patients who develop piriformis syndrome in association with a bifid piriformis.