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DOI: 10.1055/s-0044-1791664
Brachial and Lumbosacral Plexopathies
- Abstract
- Brachial Plexopathies
- Lumbosacral Plexopathies
- Conclusion
- References
Abstract
The brachial and lumbosacral plexuses are complex neural structures that transmit sensory, motor, and autonomic information between the spinal cord and the extremities. Plexus disorders can be particularly disabling because lesions in the plexus usually affect large groups of nerve fibers originating from several spinal levels. Electrodiagnostic studies are often required to confirm a plexus lesion and determine the extent of injury and prognosis. Magnetic resonance is the imaging modality of choice for detecting intrinsic nerve abnormalities; recently, high-resolution ultrasound has emerged as an alternative method for dynamic evaluation and visualization of internal nerve architecture. Once a plexopathy is confirmed, the list of possible etiologies is relatively limited and includes traumatic and nontraumatic causes. Treatment relies on symptom management and physical rehabilitation unless a treatable underlying condition is found. Surgical approaches, including nerve grafts or tendon transfers, may improve limb function when spontaneous recovery is suboptimal.
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Keywords
plexopathies - brachial plexus - lumbosacral plexus - radiculoplexus neuropathy - electrodiagnostic studiesDisorders of the brachial and lumbosacral plexuses can be complex and difficult to diagnose. Due to some clinical and electrodiagnostic overlap, brachial and lumbosacral plexopathies may be difficult to distinguish from other peripheral nerve disorders, including mononeuropathies and radiculopathies. A plexopathy should be considered in any patient presenting with diffuse or patchy motor and sensory deficits in the affected limb, often associated with neuropathic pain and reduced tone and reflexes that do not localize to a single peripheral nerve or nerve root distribution.
It is important to note that injury to the brachial or lumbosacral plexus may be isolated to the plexus itself (pure plexopathy) or may extend from the plexus proximally into the nerve roots and distally into the peripheral nerves arising from it, the latter commonly referred to as cervical or lumbosacral radiculoplexus neuropathy (RPN).[1] RPN may be more common than a pure plexopathy, particularly in the lower limbs, and is typically associated with metabolic, inflammatory, or infiltrative mechanisms ([Table 1]).[2] [3] [4]
Abbreviation: HIV, human immunodeficiency virus.
This article provides a review of brachial and lumbosacral plexopathies, including important anatomical considerations, clinical features, and diagnostic evaluation. The most clinically relevant syndromes and their specific treatment and prognosis are briefly discussed.
Brachial Plexopathies
Anatomical Considerations
The brachial plexus is a complex network of nerves that originate from the anterior rami of the C5 through T1 nerve roots and provide sensory and motor innervation to the arm, shoulder, and upper chest. In some individuals, the C4 or T2 nerve roots also contribute to the plexus, leading to prefixed and postfixed anatomical variations, respectively. The brachial plexus courses inferolaterally from the lateral neck towards the axilla and it is classically divided into five anatomical segments, from proximal to distal: roots, trunks (upper, middle, and lower), divisions (three anterior and three posterior), cords (lateral, posterior, and medial), and five major terminal branches (musculocutaneous, axillary, radial, median, and ulnar nerves; [Fig. 1]). The clavicle is an important anatomical landmark and further subdivides the brachial plexus into supraclavicular (roots and trunks), retroclavicular (divisions) and infraclavicular (cords and terminal nerves) segments.[5] Given the characteristic segmental arrangement of nerve fibers in the trunks, supraclavicular plexopathies present with deficits in a myotomal and dermatomal pattern, while infraclavicular plexopathies present in a pattern that resembles single or multiple mononeuropathies. Supraclavicular plexopathies are more common and severe than infraclavicular plexopathies and are less likely to have complete recovery. A solid understanding of the anatomy of the brachial plexus and the corresponding muscle and skin innervation of its different components ([Table 2]) is important for lesion localization, as well as for planning and interpretation of electrodiagnostic studies, which are often required to confirm a plexus lesion.
Upper trunk (C5–C6) |
Middle trunk (C7) |
Lower trunk (C8–T1) |
||
---|---|---|---|---|
MOTOR[a] |
Supraspinatus (Ssc) (Infraspinatus (Ssc) |
– |
– |
|
Lateral cord |
Biceps (Mc) Brachialis (Mc) |
Pronator teres (Med) Flexor carpi radialis (Med) |
– |
|
Posterior cord |
Deltoid (Ax) Teres minor (Ax) Brachioradialis (Rad) Supinator (Rad) |
Triceps (Rad) Anconeus (Rad) Extensor carpi radialis (Rad) Extensor digitorum communis (Rad) Extensor carpi ulnaris (Rad) |
Extensor indicis proprius (Rad) Extensor carpi ulnaris (Rad) |
|
Medial cord |
Abductor pollicis brevis (Med) Flexor pollicis longus (Med) Flexor carpi ulnaris (Uln) Flexor digitorum profundus (Uln) First dorsal interosseous (Uln) Abductor digiti minimi (Uln) |
|||
SENSORY |
Lateral cord |
Lateral aspect of the forearm (Labc) Thumb and second digit (Med) |
– |
– |
Posterior cord |
Lateral aspect of the upper arm (Ax) |
Posterior aspect of the upper arm, forearm and third digit (Rad) |
– |
|
Medial cord |
– |
Medial aspect of the forearm (Mabc) Medial aspect of the hand, and fourth and fifth digits (Uln) |
Abbreviations: Ax, axillary nerve; Labc, lateral antebrachial cutaneous nerve; Mabc, medial antebrachial cutaneous nerve; Mc, musculocutaneous nerve; Med, median nerve; Rad, radial nerve; Ssc, suprascapular nerve; Uln: ulnar nerve.
a Only muscles typically assessed with needle electromyography are listed.


The following are important anatomical considerations when evaluating brachial plexus disorders:
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Some peripheral nerves arise directly from the cervical roots, including the phrenic nerve (C3–5) to the diaphragm, the dorsal scapular nerve (C4–5) to the rhomboids and levator scapula, and the long thoracic nerve (C5–C7) to the serratus anterior muscle. Clinical involvement of any of these nerves indicates the lesion is proximal to the formation of the trunks.
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The C5 and C6 nerve roots merge to form the upper trunk, the C7 nerve root contributes to the middle trunk, and the C8 and T1 nerve roots merge to form the lower trunk. A lesion in one of the trunks presents with sensory and motor deficits in the spinal segments that contribute to that trunk and will spare other segments. Of note, the suprascapular nerve branches off directly from the upper trunk to innervate the supraspinatus and infraspinatus muscles and may be affected in upper trunk plexopathies.
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As they course beneath the clavicle, each of the trunks divides into two primary divisions: one anterior and one posterior. The anterior divisions of the upper and middle trunks form the lateral cord, the anterior division of the lower trunk forms the medial cord, and the posterior divisions of all the trunks form the posterior cord. Since it is extremely rare for a process to solely affect the divisions and spare the trunks and cords, the divisions have no clinical relevance.
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The cords terminate into five major terminal branches: musculocutaneous (lateral cord), axillary and radial (posterior cord), median (combination of the medial and lateral cords), and ulnar (medial cord). A lesion in one of the cords presents with deficits isolated to the peripheral nerves arising from that cord.
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The lateral and medial antebrachial cutaneous nerves contain sensory fibers that travel along the upper trunk/lateral cord and lower trunk/medial cord, respectively, before leaving the plexus to provide sensory innervation to the lateral and medial forearm. Clinical and/or electrodiagnostic abnormalities in one of these nerves may help localize the lesion to a particular trunk (upper or lower) or cord (lateral or medial).
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Etiology
Brachial plexopathies can be broadly classified as traumatic and nontraumatic depending on the etiology. Trauma is the most common cause of brachial plexus lesions in both children and adults. Traumatic mechanisms of nerve damage include compression, traction or stretch, and transection. While transection usually implies complete disruption of the entire nerve, including the myelin sheath, the axon and surrounding connective tissue (neurotmesis), compression and stretch cause various degrees of demyelination (neurapraxia) and/or axonal damage (axonotmesis) depending on the type of insult and severity.[6] Of note, severe traction may be accompanied by concomitant nerve root avulsion (complete separation of the cervical roots from the spinal cord). Nontraumatic causes of brachial plexus injury include metabolic, inflammatory, infiltrative, neoplastic, delayed damage from radiation, and, rarely, ischemia. Common etiologies of brachial plexopathies are summarized in [Table 3].
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Clinical Features and Diagnosis
Clinical and Examination Features
Clinical symptoms and signs of a brachial plexopathy include those expected in other peripheral nerve lesions, such as sensory disturbances, neuropathic pain, motor deficits, reduced muscle tone, and hyporeflexia in the affected arm, in a distribution that depends on the segments involved.
Upper trunk (C5–6) plexopathies present with weakness in shoulder abduction, external rotation, and elbow flexion, and sensory deficits extending from the lateral aspect of the upper arm and forearm into the thumb and second finger. Middle trunk (C7) plexopathies demonstrate weakness in elbow, wrist and finger extension, and sensory deficits in the posterior aspect of the arm and forearm. In lower trunk (C8–T1) plexopathies, the weakness predominantly affects intrinsic hand muscles and finger and wrist flexors, and sensory deficits involve the medial aspect of the forearm and fourth and fifth digits. The biceps and brachioradialis tendon reflexes may be affected in upper trunk plexopathies, while the triceps reflex is affected in middle trunk plexopathies.
Pain is a common symptom but may be absent in compressive and radiation-induced lesions. When present, the pain is described as aching, shock-like, burning, or throbbing and frequently radiates from the lateral neck, clavicular region, or shoulder, into the arm and hand following a dermatomal pattern. The location and radiating nature of the pain may contribute to the diagnostic confusion between plexopathies and radiculopathies or orthopedic problems of the shoulder joint.[7] Pain that is exacerbated by swallowing, coughing, or neck movements is more suggestive of nerve root than plexus pathology. Other associated clinical manifestations, such as the presence of Horner's syndrome (due to disruption of postganglionic sympathetic T1 fibers) or a palpable mass or Tinel's sign in the supraclavicular region, may provide additional clues to brachial plexus localization. Autonomic features, such as cutaneous trophic changes and vasomotor or sudomotor abnormalities, may also be noted.
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Electrodiagnostic Evaluation
Because of the complex organization of the brachial plexus, extensive nerve conduction studies (NCSs) and needle electromyography (EMG) of several muscles are required for precise anatomical localization and exclusion of mimickers.[8] Most brachial plexopathies do not involve the entire plexus (panplexopathy), but they are rather partial or patchy, which complicates the electrodiagnostic evaluation.
Sensory NCSs show abnormalities early in the course of plexopathies and have important localizing value. On one hand, abnormalities on sensory responses indicate the lesion is at or distal to the dorsal root ganglion (postganglionic) and help exclude nerve root (preganglionic) pathology. On the other hand, while routine motor NCSs (median, ulnar, and radial) assess predominantly the lower and middle trunks, sensory NCSs evaluate all segments of the plexus. The median (second digit), superficial radial, and ulnar (fifth digit) sensory NCSs assess the upper trunk/lateral cord, middle trunk/posterior cord, and lower trunk/medial cord, respectively.[8] In addition, the lateral and medial antebrachial cutaneous sensory responses are highly sensitive to detect upper and lower trunk lesions, respectively, even when median and ulnar sensory studies are normal. Motor NCSs provide information regarding the severity of axonal loss and can also detect focal demyelination within the plexus. Less commonly performed motor NCSs, such as axillary, suprascapular, or musculocutaneous, may be required to assess upper trunk lesions and stimulation at proximal nerve sites (e.g., Erb's point, direct root stimulation), may help detect the presence of conduction block or temporal dispersion across the plexus, indicative of demyelination. It is important to note that sensory and motor responses that fall within reference values may still be considered abnormal if the side-to-side amplitude difference is >50%. Therefore, comparison of NCSs with the unaffected side is recommended. Sensory and motor NCSs commonly obtained in brachial plexus evaluation are listed in [Table 4].
Abbreviations: ADM, abductor digiti minimi; APB, abductor pollicis brevis; FDI, first dorsal interosseous.
Needle EMG is very sensitive to detect changes related to axonal loss (denervation and reinnervation), and is arguably the most efficient method to evaluate the different components of the brachial plexus, as abnormalities in a particular muscle can be easily tracked to its root, trunk, cord, and terminal branch innervation. The presence of unusual spontaneous discharges may point toward a specific etiology, such as the presence of myokymia in patients with radiation-induced plexopathy.[9] Cervical paraspinal muscles are spared in pure brachial plexopathies, but may show abnormalities in cervical RPN due to concomitant nerve root involvement.[10]
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Imaging Studies
If a brachial plexopathy is suspected or confirmed by clinical and/or electrodiagnostic evaluation, imaging studies are warranted to better assess for possible etiologies. Routine chest and spine films can identify a cervical rib in suspected thoracic outlet syndrome (TOS) or a Pancoast tumor in patients with associated Horner's syndrome.[11] [12] Computed tomography (CT) is useful to detect extrinsic compression due to vascular abnormalities (e.g., hematoma, pseudoaneurysm) or soft tissue masses.
Conventional magnetic resonance (MR) is the imaging modality of choice to identify intrinsic nerve abnormalities, such as increased T2 signal, variations in nerve caliber, enhancement post-gadolinium administration, and nodularity or fascicular disorganization, the latter typical of aggressive tumors.[13] [14] Indirect signs of nerve injury, such as muscle denervation (increased T2 signal) and muscle atrophy or fatty replacement (increased T1 signal), may also be observed.[13] [14] MR neurography is an advanced MR modality that facilitates visualization of neural elements by using special suppression techniques to minimize the signal from surrounding tissues (fat, muscles, vessels) and three-dimensional reconstruction images.[15] High-resolution ultrasound (US) is noninvasive and can be performed at bedside but requires special expertise and it is still not widely available. US can distinguish preganglionic from postganglionic traumatic lesions, evaluate nerve continuity in the axial and longitudinal axis, and detect scarring and neuroma formation; it also allows for dynamic evaluation and may be helpful to identify compression of plexus structures with various positions and maneuvers.[16] [17]
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Laboratory Studies
Laboratory testing has a limited role in the evaluation of brachial plexopathies. In the absence of structural causes or direct trauma, screening for inflammatory and metabolic conditions, such as connective tissue disorders, vasculitis, and diabetes or impaired glucose metabolism, may be useful. Cerebrospinal fluid (CSF) analysis is rarely required. However, if infiltration of nerve roots and proximal plexus segments by lymphoma or other cancer is suspected, cytology and flow cytometry may be diagnostic; serial lumbar punctures may be needed to increase diagnostic sensitivity.[18] CSF is often normal in inflammatory brachial plexopathies.
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Common Disorders of the Brachial Plexus
Neonatal Brachial Plexopathies
In the pediatric population, brachial plexopathies occur more often in the perinatal period with an incidence of 1.74 per 1,000 live births.[19] They are caused by stretch or compression of the C5–6 roots/upper trunk (Erb's palsy) or the C8–T1 roots/lower trunk (Klumpke's palsy) during a complicated vaginal delivery or intrauterus. Risk factors in descending order of frequency are shoulder dystocia, macrosomia, breech presentation, and instrumented vaginal delivery.[20] Newborns present with a flail and hypotonic arm. When the upper trunk is involved in isolation, motor deficits result in the classic “waiter's tip” posture with arm adducted, shoulder internally rotated, elbow extended, and forearm pronated. With more severe traction injuries, middle and lower trunks may become involved, the latter resulting in impairment in hand function and a “claw hand.” A surgical approach, including nerve grafting or transfers, is considered if there is no spontaneous recovery in the first 3 to 4 months, preferably performed within the first year of life.[21] Deficits that persist into adulthood are seen in 20 to 30% of patients.
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Other Traumatic Brachial Plexopathies
Brachial plexopathies due to direct trauma affect predominantly young and middle-aged adults involved in high-speed vehicular accidents, fall from a height, or assaults using firearms or sharp objects. Given the strong forces involved, concomitant injury to the head, spine, or vascular structures is possible, which may delay the recognition of a plexus injury.[22] Traumatic brachial plexopathies often cause severe neurological deficits and, if nerve root avulsion is present, complete paralysis and profound sensory loss of the entire arm are expected. In the presence of nerve root avulsion, sensory NCSs are typically normal and paraspinal muscles show abnormalities on EMG, indicative of a preganglionic lesion; however, it is important to note that root avulsion and plexus injury often coexist, and mixed electrodiagnostic findings are possible.[5] CT myelogram or MR of the cervical spine can identify the absence of rootlets in the spinal canal, or a spinal cord tear or pseudomeningocele formation as surrogate markers of root avulsion.[23] The prognosis of traumatic brachial plexopathy depends on the severity and extent of the initial insult. Most patients require prolonged rehabilitation and endorse severe residual deficits. Surgical management includes nerve reconstruction (direct repair, neurolysis, nerve grafting, or nerve transfers) and/or soft tissue procedures (tendon transfer) to improve arm and hand function. Ideally, nerve reconstruction should not be delayed for more than 6 months after trauma.[24]
A milder type of direct trauma to the brachial plexus is the so-called burners and stingers syndrome.[25] This term refers to the transient neurological symptoms (painful paresthesias, numbness with or without weakness) typically experienced by athletes after traction injury to the brachial plexus during participation in contact sport activities. The mechanism of injury is usually a forceful blow to the shoulder or head. While symptoms are typically brief and self-limited, they can persist for several weeks or months depending on severity. Recurrent injuries may lead to permanent neurological deficits.
Rucksack palsy results from traction or direct compression of the upper trunk in individuals carrying a heavy load over the shoulders (e.g., backpack, child-carrying harness).[26] Although rapid improvement is expected after the load is removed from the shoulders, recovery may be slower or incomplete if axonal damage is present.
Finally, iatrogenic injury to the brachial plexus can occur during surgery and other medical procedures, including median sternotomy or regional anesthetic blocks.[5] Traction damage of the lower trunk during sternotomy should be distinguished from ulnar compression at the elbow related to positioning during surgery in order to avoid unnecessary ulnar release procedures. Weakness of muscles supplied by C8 via the median nerve (e.g., flexor pollicis longus) and radial nerve (e.g., extensor digitorum communis) favors a lower trunk plexopathy over an ulnar neuropathy.
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Thoracic Outlet Syndrome
TOS is a condition caused by dynamic compression of neurovascular structures—the brachial plexus and/or the subclavian artery or vein—as they course between the clavicle, the scalene muscles, and the first rib in the base of the neck, an anatomical passage known as the thoracic outlet. TOS is more common in young females (3:1) between the ages of 20 and 40 years; some cases are bilateral.[27] The presence of a cervical rib, a fibrous band extending from the first rib, or an elongated C7 transverse process has been described. Other factors, such as hypertrophic neck musculature, repetitive activities performed overhead, or abnormally inserted ligaments may contribute to the problem.[11] There seems to be a link between some cases of TOS and hypermobility syndromes.[28] In neurogenic TOS, the compression affects the lower trunk of the brachial plexus, particularly the fibers derived from the T1 root, causing discomfort, pain, and numbness or paresthesias extending from the clavicular region into the medial aspect of the forearm, exacerbated by shoulder or neck movements. Weakness and atrophy affecting thenar muscles is rare. In vascular TOS, arm swelling, pallor, skin discoloration, and rarely ischemia or deep venous thrombosis may occur due to compression of the subclavian artery and/or vein.[11] Electrodiagnostic findings in neurogenic TOS are those of a lower trunk plexopathy; an abnormal medial antebrachial cutaneous sensory response may be the only finding in milder cases. Dynamic nerve US and CT or MR angiogram of the chest with provocative maneuvers (outstretching of the arms overhead) can help identify the compressed neurovascular elements ([Fig. 2]).[29] [30] The treatment of TOS is challenging. Conservative management focused on physical rehabilitation, posture correction, and lifestyle modifications is initially attempted.[28] If there is no improvement, scalene muscle blocks or exploratory decompressive surgery is considered. Resection of the first rib or distal scalenectomy may improve symptoms, although recovery is often incomplete in severe cases.[11] Recurrence rate after surgery ranges between 5 and 30%.[31] [32]


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Neuralgic Amyotrophy
Also known as inflammatory brachial plexopathy or Parsonage–Turner syndrome, neuralgic amyotrophy is one of the most common forms of brachial plexopathy, with an incidence that ranges between 3 and 100/100,000 persons per year.[33] The pathophysiology is not entirely understood, but inflammatory and immune-mediated mechanisms are likely implicated, as suggested by targeted nerve biopsies showing perivascular inflammatory infiltrates in these patients. A precipitating event or immune trigger, such as infection, immunization, minor trauma, pregnancy, or surgery, have been described in almost 50% of cases. Recently, checkpoint inhibitor therapies and coronavirus-2019 infection and vaccination have been associated with attacks.[34]
Neuralgic amyotrophy is a motor predominant disorder that affects the brachial plexus and/or nerves derived from it, although it can also be extraplexal (e.g., involvement of the phrenic or recurrent laryngeal nerves).[34] [35] Most patients present with rapid onset of severe, radicular-like pain, localized to the base of the neck, shoulder, and/or upper arm, followed by ipsilateral and disabling arm weakness and atrophy. Sensory disturbances in the form of paresthesias and/or sensory loss are often overshadowed by pain and weakness. The upper and middle trunks and motor-predominant nerves (e.g., suprascapular, long thoracic, axillary, and musculocutaneous) are more commonly affected.[36] Winged scapula is reported in 30 to 70% of attacks. Coexisting or isolated lower trunk involvement affecting hand and forearm muscles is less common (<10% of cases).[36] Involvement of peripheral nerves in isolation, such as the suprascapular, posterior interosseous, or phrenic nerves, is also seen.[35] Despite having a monophasic and self-limited course, some patients experience prolonged recovery and continue to suffer from musculoskeletal pain, weakness, and functional disability beyond 2 to 3 years.
Recurrent attacks of inflammatory brachial plexopathy should raise the possibility of a hereditary disorder, known as hereditary neuralgic amyotrophy.[34] SEPT9 gene mutations (duplications and point mutations) have been described in familial cases associated with short stature, hypotelorism (close-set eyes), increased frequency of brachial plexopathy attacks brought on by similar immune triggers, and earlier age at onset.
The diagnosis of neuralgic amyotrophy relies mainly on clinical features and electrodiagnostic testing. Abnormalities on needle EMG are often patchy and more severe and widespread than clinically suspected. In fact, patchy and nonuniform denervation of arm and shoulder muscles in patients without a history of trauma or obvious structural lesion should raise the possibility of an inflammatory brachial plexopathy. Recent studies of neuralgic amyotrophy using MR and high-resolution US describe the presence of swelling and hourglass constrictions in proximal and distal upper limb nerves in some cases.[37] However, most patients have normal imaging and findings of nerve inflammation, such as nerve enlargement or increased T2 signal, are rarely seen.[38]
Early treatment with high-dose oral or intravenous steroids (1 gram of intravenous methylprednisolone per day for 3 to 5 days, followed by repeated infusions every 1 to 2 weeks for 12 weeks) may be efficacious for pain control; however, strong evidence that steroids hasten recovery or improve neurological outcomes is lacking.[39]
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Diabetes-Related Brachial Plexopathy
Plexopathies related to diabetes mellitus typically affect nerve roots and terminal nerves beyond the plexus and are considered within the spectrum of RPN. Although lumbosacral plexopathies are more common, cervical RPN has been described, either in isolation or in combination with lumbosacral RPN.[10] Diabetic cervical RPN presents with acute onset of severe pain and paresthesias followed by weakness and atrophy in the affected arm, and it may be clinically indistinguishable from neuralgic amyotrophy. Compared to neuralgic amyotrophy, diabetic cervical RPN more commonly presents with associated weight loss, diffuse autonomic features, lower trunk involvement, and bilateral disease.[10] The lumbosacral form, which is far more common, will be discussed in greater detail in the next section.
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Neoplastic and Radiation-Induced Brachial Plexopathies
The brachial plexus may be affected by primary or secondary neoplasms. Primary tumors of the brachial plexus are rare and can be classified into benign tumors typically arising from the neural sheath, such as schwannomas and neurofibromas, and malignant tumors, such as primary malignant peripheral nerve sheath tumor. The former are observed in the context of neurocutaneous disorders (neurofibromatosis and schwannomatosis), and the latter may develop spontaneously, as a malignant transformation of a benign tumor, or as a late complication of radiotherapy.[40] [41]
Secondary neoplasms occur due to local infiltration or metastatic disease. Lung and breast cancers, lymphoma, and sarcoma account for nearly 80% of secondary neoplasms.[42] The most common sites of involvement are the lower trunk followed by the entire plexus. Direct tumor infiltration of the lower trunk from a mass in the lung apex (Pancoast tumor) results in Horner's syndrome and weakness and sensory loss in the C8–T1 distribution.[12] Mass effect or local invasion from head and neck tumors may occur due to the proximity of these structures to the upper plexus.[43]
Radiation-induced brachial plexopathies occur in 2 to 5% of patients treated with radiation therapy.[44] The most frequently radiated areas are the supraclavicular/infraclavicular and axillary regions and the chest wall for treatment of breast cancer, lung cancer, and lymphoma. Several factors increase the risk of developing radiation plexopathy, including radiation dose (greater risk for each 1,000 cGy of radiation greater than 6,000 cGY), number of ports of radiation administration, adjuvant chemotherapy, and the extent of axillary node dissection.[45] Compared to neoplastic plexopathies, radiation-induced plexopathies are typically painless. Neurological symptoms may appear from a few months to years following radiation exposure.
MR of the brachial plexus with contrast is the most useful study for characterization of plexus tumors and masses. Benign tumors present as well-circumscribed, round-shaped, and homogeneously enhancing soft tissue lesions in continuity with the plexus. Poorly defined margins, T2 hyperintense signal, fascicular disorganization, and nodular or heterogeneous enhancement suggest malignancy.[46] Malignant lesions also show marked uptake on fluorodeoxyglucose positron emission tomography (FDG-PET), allowing for their differentiation from radiation changes ([Fig. 3]).[47]


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Lumbosacral Plexopathies
Anatomical Considerations
The lumbosacral plexus originates from the anterior rami of the L1 through S4 nerve roots, with a small contribution from T12, and supplies sensory and motor innervation to the leg and pelvic structures. The lumbosacral plexus can be divided into two adjacent plexuses: the upper lumbar (L1–L4) and the lower lumbosacral (L5–S4), each of them terminating into several nerve branches ([Fig. 4]). Given that the lumbosacral plexus has fewer connections between its components, it lacks the anatomical complexity of the brachial plexus. Some individuals have prefixed or postfixed anatomical variations.


The upper lumbar plexus innervates muscles responsible for hip flexion, hip adduction, and knee extension (L2–4), and provides sensory innervation to the groin, the genital region (L1–2), and the thigh and medial aspect of the lower leg (L2–4). The major branches of the upper lumbar plexus are the obturator and femoral nerves; the lateral femoral cutaneous nerve arises directly from the L2 and L3 nerve roots and travels independently from other plexus structures. The lower lumbosacral plexus innervates muscles responsible for hip abduction and extension, knee flexion, and all movements at the ankle joint (L5–S2). Motor innervation of the urinary and anal sphincters (S2–4) and sensory innervation to the buttocks, perineal region, posterior thigh, and the entire lower leg below the knee, with the exception of its medial aspect (L5–S2), are also provided by the lower lumbosacral plexus. The major branches of the lower lumbosacral plexus are the superior gluteal, the inferior gluteal, the sciatic, the posterior femoral cutaneous, and the pudendal nerves ([Table 5]).
Nerve |
Motor[a] |
Sensory |
|
---|---|---|---|
Upper lumbar plexus (L2–L4) |
Iliohypogastric (L1–2) |
– |
Inferior abdominal wall |
Ilioinguinal (L1–2) |
– |
Medial groin |
|
Genitofemoral (L1–2) |
– |
Groin and genitalia |
|
Lateral femoral cutaneous [b] (L3–4) |
– |
Anterolateral thigh |
|
Obturator (L2–4) |
Adductor magnus Adductor longus Gracilis |
Medial thigh |
|
Femoral (L2–4) Saphenous (L2–4) |
Iliopsoas Quadriceps |
Medial leg and foot |
|
Lower lumbosacral plexus (L5–S4) |
Superior gluteal (L4–5) |
Gluteus medius Tensor fascia lata |
– |
Inferior gluteal (L4–S1) |
Gluteus maximus |
– |
|
Sciatic, tibial division (L5–S2) |
Semitendinosus Gastrocnemius Tibialis posterior |
Posterior thigh and lower leg, sole of the foot |
|
Sciatic, peroneal division (L4–S1) |
Tibialis anterior Peroneus longus |
Lateral lower leg and dorsum of the foot |
|
Pudendal (S2–4) |
Anal sphincter |
Perineum |
a Only muscles typically assessed with needle electromyography are listed.
b The lateral femoral cutaneous nerve arises from L2 and L3 nerve roots and does not join other plexus structures.
As previously discussed, some conditions affecting the lumbosacral plexus cause more extensive damage to nerves proximal and distal to the plexus and are better classified within the group of lumbosacral RPN.
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Etiology
Lumbosacral plexopathies are probably more common than usually recognized, and their etiology can be traumatic or nontraumatic. Given its location deep within the pelvis surrounded by bone structures, the lumbosacral plexus is relatively protected against direct trauma but, in turn, it is more vulnerable to conditions arising from abdominopelvic organs and tissues, including malignant infiltration, infection, or mass compression.[2] Among nontraumatic causes of lumbosacral plexopathy, neoplastic infiltration has been classically considered one of the most common; however, diabetes-related plexopathies are increasingly recognized.[48] [Table 6] includes a list of common etiologies of lumbosacral plexopathies.
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Clinical Features and Diagnosis
Clinical and Examination Findings
The array of symptoms and signs associated with a lumbosacral plexopathy varies depending on what portion of the plexus is involved. Damage to the upper lumbar plexus results in proximal leg weakness (hip flexion, hip adduction, and/or knee extension), sensory deficits in the medial and anterolateral thigh, and an absent or reduced patellar reflex. Involvement of the lower lumbosacral plexus presents with distal leg weakness and sensory loss, often associated with foot drop and an absent or reduced Achilles reflex. Diffuse rather than partial plexus lesions are more common and cause extensive motor and sensory deficits in the entire leg; however, patchy involvement affecting nonconsecutive myotomes (e.g., hip flexion weakness with a foot drop) and/or dermatomes (e.g., numbness in the medial thigh and foot) is often seen.
Pain in lumbosacral plexopathies localizes to the lower back and/or proximal leg (hip, groin, or knee), and is one of the great mimickers of radicular pain. Contact allodynia and/or hyperalgesia on examination point toward inflammatory and metabolic etiologies, as small fibers may be particularly susceptible to these types of insults. The presence of enlarged inguinal lymph nodes and systemic symptoms, such as fever or night sweats, may suggest a neoplastic etiology, and a pulsatile inguinal mass raises the possibility of aneurysm in the femoral artery. Saddle anesthesia and sphincter dysfunction are seen with bilateral plexus involvement and require exclusion of cauda equina syndrome.
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Electrodiagnostic Evaluation
Electrodiagnostic studies are often required to confirm a lumbosacral plexopathy and evaluate the extent of nerve injury. As with brachial plexopathies, comparison of NCS and needle EMG with the unaffected side may be useful to look for asymmetric findings.
It is important to recognize that electrodiagnostic confirmation of a lumbosacral plexopathy will most likely be accomplished if it is first suspected clinically, particularly when the upper lumbar plexus is predominantly affected.[49] [50] Upper lumbar segments are not adequately assessed by routine NCSs of the lower limb (peroneal, tibial, sural, and superficial peroneal) which primarily assess lower lumbosacral segments, or commonly examined leg muscles. Therefore, the electromyographer should obtain additional information from lateral femoral cutaneous, saphenous, and femoral motor NCS and needle examination of hip girdle muscles, including the iliopsoas, tensor fascia lata, and adductor magnus or adductor longus, to increase the yield of finding abnormalities. Useful sensory and motor NCS for the evaluation of lumbosacral plexopathies are listed in [Table 7].
Abbreviations: AH, abductor hallucis; AT, anterior tibialis; EDB, extensor digitorum brevis; NCS, nerve conduction studies.
Confirmation of a lumbosacral plexopathy requires the presence of abnormalities in “at least two peripheral nerves from at least two different nerve root distributions,” along with normal needle examination of paraspinal muscles and abnormal sensory responses to support a postganglionic process.[51] In lumbosacral RPN, findings of denervation and/or reinnervation (depending on the time of the study) are extensive and can be observed from paraspinals to distal leg muscles involving multiple myotomes in a patchy fashion.[52] Some patients, particularly those with diabetes, may have an underlying polyneuropathy with symmetrically reduced responses on NCS, which complicates the interpretation of the study.[2] In the presence of polyneuropathy and abnormal sensory NCS, it may also be difficult to distinguish a lumbosacral plexopathy from multilevel radiculopathies; clinical judgement and imaging are important in those cases. Extensive denervation in multiple lumbosacral myotomes without imaging correlation (e.g., no abnormal root enhancement or structural explanation on lumbar spine MR) favors a priori a lumbosacral plexopathy. In addition, L2–3 innervated muscles (iliopsoas, hip adductors) are more commonly affected in plexopathies than radiculopathies. A proposed electrodiagnostic approach to lumbosacral plexopathy is presented in [Fig. 5].


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Imaging Studies
MR is superior to other imaging modalities to evaluate the lumbosacral plexus and surrounding pelvic structures. The role of MR is similar in both brachial and lumbosacral plexopathies. MR allows for detection of abnormalities in nerve signal and caliber, root avulsion, muscle changes suggestive of denervation or fatty replacement, and extrinsic compression by pelvic mass, retroperitoneal hematoma, or abscess. It is important to note that some conditions affecting the plexus may not demonstrate imaging abnormalities; therefore, a normal MR of the lumbosacral plexus does not completely exclude the possibility of a plexopathy.[53] High-resolution US is not effective to visualize deep nerves within the pelvis, and its role in lumbosacral plexus evaluation is currently limited.
Some patients with lumbosacral plexopathy may undergo MR of the lumbar spine to rule out radiculopathy, even before electrodiagnostic evaluation is obtained. Spondylitic changes and disc disease are common in the general population and these findings should not be overestimated as they often fail to explain the severity and distribution of deficits in patients with plexopathy.
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Laboratory Studies
Laboratory testing may be considered if the etiology of a lumbosacral plexopathy remains uncertain despite other investigations. Blood tests are useful to screen for conditions that may affect the plexus, including lymphoma and other hematologic disorders (e.g., complete blood count, serum protein electrophoresis with immunofixation, serum-free light chains), diabetes (e.g., glycated hemoglobin), inflammatory and rheumatologic disorders (e.g., sedimentation rate, C-reactive protein, connective tissue screening, antineutrophilic cytoplasmic antibodies), and infection (e.g., serologies for human immunodeficiency virus, Epstein–Barr virus, Lyme disease, and syphilis). CSF cell count, protein, and cytology can also be helpful to look for occult infection or malignancy.[2]
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Common Disorders of The Lumbosacral Plexus
Traumatic Lumbosacral Plexopathies
Direct trauma accounts for only a small proportion of lumbosacral plexopathies. Most common injuries occur after high-speed collisions or gunshot wounds. In a series of trauma patients, those involved in motor vehicle accidents had more frequent damage to the lower lumbosacral plexus, particularly if a sacral fracture and/or sacroiliac joint dislocation were present. In patients suffering from gunshot wounds, because most occurred in the abdomen, the upper plexus was preferentially involved.[54] The prognosis of traumatic lumbosacral plexopathies is usually poor given the presence of severe nerve disruption. Surgical reconstruction is less efficacious than in brachial plexopathies.[55]
The lumbosacral plexus may be rarely compressed by a retroperitoneal hematoma in patients with history of anticoagulation or bleeding disorders, an aneurysm of the common iliac or femoral arteries, or by the fetal head during vaginal delivery.
Iatrogenic injury can occur following vascular procedures (e.g., canulation of femoral artery, aortic aneurysm repair) and abdominopelvic or orthopedic surgeries.[55] It is important to recognize that not all perioperative plexopathies are iatrogenic and inflammatory cases exist. Postsurgical inflammatory plexopathies present with leg pain and weakness within 1 month after surgery, often not adequately explained by intraoperative factors, such as patient positioning, direct surgical trauma, or regional anesthesia. Clinical features such as spatio-temporal separation from the site and time of surgery, prolonged course with lack of improvement or clinical worsening beyond the first postoperative month, and disproportionate/intractable neuropathic pain should prompt the consideration of an inflammatory etiology; early recognition and initiation of corticosteroids may improve outcomes in these patients.[3]
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Diabetes-Related Lumbosacral Plexopathies
Diabetes is the most common risk factor associated with development of lumbosacral plexopathy in clinical practice.[56] Lumbosacral plexus injury linked to diabetes is the most frequently reported cause of lumbosacral RPN.[52] Additional risk factors for lumbosacral RPN have been recently proposed and include immune dysfunction and components of the metabolic syndrome, such as obesity, or hypertension.[56] Although the pathophysiology is not entirely understood, rapid glycemic changes or relative hypoglycemia, similar to what occurs in treatment-induced neuropathy of diabetes, have been proposed as potential triggers of an inflammatory reaction that targets the lumbosacral plexus. Energy restriction mechanisms caused by glucose deprivation in plexus nerve fibers may be implicated.[56] [57] The incidence of this condition may be increasing due to the high prevalence of diabetes and the use of potent glucose-lowering medications.
The clinical presentation in patients with diabetic lumbosacral RPN, also known as diabetic amyotrophy, is quite stereotypical. It begins with severe burning or achy pain in the back, hip, groin, or thigh, followed days or weeks later by disabling weakness and atrophy involving predominantly proximal leg muscles.[58] Progression to foot drop or involvement of the contralateral limb may occur over time, with a median time to bilateral disease of 3 months.[59] Some patients have no pain or experience bilateral leg involvement at onset. Interestingly, a clinically indistinguishable syndrome has been described in people without known history of diabetes or altered glucose metabolism (nondiabetic lumbosacral RPN).[52]
The following accompanying manifestations over the course of the disease may provide important clues to the diagnosis: significant weight loss (>10 lb), autonomic manifestations (orthostatic intolerance, gastrointestinal dysmotility, and urinary or erectile dysfunction), and involvement of nerves in other body regions (thoracic radiculopathy and/or cervical RPN).[58]
MR neurography has anecdotally demonstrated thickening and increased T2 signal in the plexus or individual nerves, such as the femoral, sciatic, or obturator, but it can also be normal.[60] A Cochrane systematic review about treatment of this condition did not find evidence that corticosteroids or intravenous immunoglobulins alter the disease course.[61] However, treatment with corticosteroids may provide pain relief and should be offered to these patients. Diabetic lumbosacral RPN is considered a monophasic but disabling illness associated with significant gait and functional impairment; recovery is usually slow, and many patients require gait aids (cane, walker, or knee/ankle orthotics) at some stage in the disease course.[59]
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Neoplastic and Radiation-induced Lumbosacral Plexopathies
As with brachial plexopathies, cancer-related lumbosacral plexopathies can occur due to neoplasm or as a result of the treatment received for cancer. Primary neoplasms include benign and malignant tumors similar to those observed in the brachial plexus.
Lumbosacral plexus involvement occurs in less than 1% of all cancers.[62] It is usually a late complication when the tumor has locally or regionally spread; however, it can also be the initial manifestation in 15% of patients.[63] The following pathophysiologic mechanisms have been reported: direct tumoral invasion and perineural spread from neighboring pelvic organs (colon, rectum, uterus, ovaries, and prostate), distant metastasis (lung, breast), compression from enlarged metastatic lymph nodes, and intraneural lymphomatosis.[64] [65] [66] It is important to distinguish plexus involvement from epidural cord compression or leptomeningeal carcinomatosis as they can have a similar presentation or develop simultaneously.[64] In a case series of 85 patients with neoplastic lumbosacral plexopathy, the lower plexus was involved in approximately half of the patients, the upper plexus in a third of the patients, and the entire plexus in less than 20%.[66] Pain is a prominent symptom at onset; leg weakness and sensory loss develop gradually in most patients.
Perineural spread demonstrates irregular and nodular thickening on T1-weighted images, increased signal on T2-weighted images, and perifascicular and irregular enhancement with gadolinium, while direct tumor invasion appears as a growing mass infiltrating the plexus ([Fig. 6]).[64] Neurolymphomatosis can have variable appearances on neuroimaging; contrast enhancement is usually prominent but can also be absent.[65] In general, it is difficult to determine the specific etiology of nerve infiltration based solely on imaging. Histopathologic confirmation with targeted fascicular nerve biopsy is rarely required but may be necessary if there are no other tissues amenable for biopsy.[67] Treatment is focused on pain management and treatment of the underlying neoplasm with surgical debulking, localized radiation, and/or chemotherapy.


Radiation-induced lumbosacral plexopathy results from radiotherapy directed to the pelvis to treat testicular and prostate cancer in men, gynecologic cancers in women, and lymphoma or bladder cancer in both genders. The presence of myokymic discharges on EMG or lack of hypermetabolic activity on FDG-PET favors radiation-induced injury over cancer recurrence.[68]
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Conclusion
Brachial and lumbosacral plexopathies are relatively common disorders, often associated with significant functional disability and neuropathic pain in the affected limb. A high index of clinical suspicion and a comprehensive and individualized electrodiagnostic approach to each case help increase diagnostic accuracy and avoid misdiagnosis. In the absence of trauma, history of cancer or radiation, or obvious structural lesion, metabolic and inflammatory etiologies need to be considered. The last two can be particularly difficult to diagnose as imaging and laboratory testing may not demonstrate abnormalities. Nerve reconstruction or tendon transfer procedures may improve functional outcomes in patients who endorse severe residual neurologic deficits.
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Conflict of Interest
None declared.
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Publication History
Article published online:
17 October 2024
© 2024. Thieme. All rights reserved.
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-
References
- 1 Collins MP, Hadden RD. The nonsystemic vasculitic neuropathies. Nat Rev Neurol 2017; 13 (05) 302-316
- 2 Dyck PJ, Thaisetthawatkul P. Lumbosacral plexopathy. Continuum (Minneap Minn) 2014; 20 (5 Peripheral Nervous System Disorders): 1343-1358
- 3 Staff NP, Engelstad J, Klein CJ. et al. Post-surgical inflammatory neuropathy. Brain 2010; 133 (10) 2866-2880
- 4 Chahin N, Temesgen Z, Kurtin PJ, Spinner RJ, Dyck PJ. HIV lumbosacral radiculoplexus neuropathy mimicking lymphoma: diffuse infiltrative lymphocytosis syndrome (DILS) restricted to nerve?. Muscle Nerve 2010; 41 (02) 276-282
- 5 Rubin DI. Brachial and lumbosacral plexopathies: a review. Clin Neurophysiol Pract 2020; 5: 173-193
- 6 Sunderland S. The anatomy and physiology of nerve injury. Muscle Nerve 1990; 13 (09) 771-784
- 7 van Alfen N. The trouble with neuralgic amyotrophy. Pract Neurol 2006; 6: 298-307
- 8 Ferrante MA, Wilbourn AJ. Electrodiagnostic approach to the patient with suspected brachial plexopathy. Neurol Clin 2002; 20 (02) 423-450
- 9 Oishi T, Ryan CS, Vazquez Do Campo R, Laughlin RS, Rubin DI. Quantitative analysis of myokymic discharges in radiation versus nonradiation cases. Muscle Nerve 2021; 63 (06) 861-867
- 10 Massie R, Mauermann ML, Staff NP. et al. Diabetic cervical radiculoplexus neuropathy: a distinct syndrome expanding the spectrum of diabetic radiculoplexus neuropathies. Brain 2012; 135 (Pt 10): 3074-3088
- 11 Panther EJ, Reintgen CD, Cueto RJ, Hao KA, Chim H, King JJ. Thoracic outlet syndrome: a review. J Shoulder Elbow Surg 2022; 31 (11) e545-e561
- 12 Davis GA, Knight SR. Pancoast tumors. Neurosurg Clin N Am 2008; 19 (04) 545-557 , v–vi
- 13 Rehman I, Chokshi FH, Khosa F. MR imaging of the brachial plexus. Clin Neuroradiol 2014; 24 (03) 207-216
- 14 Gasparotti R, Shah L. Brachial and lumbosacral plexus and peripheral nerves. In: Hodler J, Kubik-Huch RA. , von Schulthess GK, eds. Diseases of the Brain, Head and Neck, Spine 2020–2023: Diagnostic Imaging [Internet]. Cham (CH): Springer; 2020. . Chapter 20
- 15 Jung JY, Lin Y, Carrino JA. An updated review of magnetic resonance neurography for plexus imaging. Korean J Radiol 2023; 24 (11) 1114-1130
- 16 Griffith JF. Ultrasound of the brachial plexus. Semin Musculoskelet Radiol 2018; 22 (03) 323-333
- 17 Chen DZ, Cong R, Zheng MJ. et al. Differential diagnosis between pre- and postganglionic adult traumatic brachial plexus lesions by ultrasonography. Ultrasound Med Biol 2011; 37 (08) 1196-1203
- 18 van Alfen N, Malessy MJ. Diagnosis of brachial and lumbosacral plexus lesions. Handb Clin Neurol 2013; 115: 293-310
- 19 Chauhan SP, Blackwell SB, Ananth CV. Neonatal brachial plexus palsy: incidence, prevalence, and temporal trends. Semin Perinatol 2014; 38 (04) 210-218
- 20 Van der Looven R, Le Roy L, Tanghe E. et al. Risk factors for neonatal brachial plexus palsy: a systematic review and meta-analysis. Dev Med Child Neurol 2020; 62 (06) 673-683
- 21 Osorio M, Lewis S, Tse RW. Promoting recovery following birth brachial plexus palsy. Pediatr Clin North Am 2023; 70 (03) 517-529
- 22 Tharin BD, Kini JA, York GE, Ritter JL. Brachial plexopathy: a review of traumatic and nontraumatic causes. AJR Am J Roentgenol 2014; 202 (01) W67-75
- 23 Wade RG, Takwoingi Y, Wormald JCR. et al. Magnetic resonance imaging for detecting root avulsions in traumatic adult brachial plexus injuries: protocol for a systematic review of diagnostic accuracy. Syst Rev 2018; 7 (01) 76
- 24 Noland SS, Bishop AT, Spinner RJ, Shin AY. Adult traumatic brachial plexus injuries. J Am Acad Orthop Surg 2019; 27 (19) 705-716
- 25 Feinberg JH. Burners and stingers. Phys Med Rehabil Clin N Am 2000; 11 (04) 771-784
- 26 Fraiman PHA, Papa IMD, Fernandes BM, Santos FTAD, Godeiro-Junior C. Rucksack palsy after military boot camp. Arq Neuropsiquiatr 2022; 80 (06) 658
- 27 Cralle LE, Harris LM, Lum YW, Deery SE, Humphries MD. Thoracic outlet syndrome in females: a systematic review. Semin Vasc Surg 2023; 36 (04) 487-491
- 28 Levine NA, Rigby BR. Thoracic outlet syndrome: biomechanical and exercise considerations. Healthcare (Basel) 2018; 6 (02) 68
- 29 Charon JP, Milne W, Sheppard DG, Houston JG. Evaluation of MR angiographic technique in the assessment of thoracic outlet syndrome. Clin Radiol 2004; 59 (07) 588-595
- 30 Nwawka OK. Ultrasound imaging of the brachial plexus and nerves about the neck. Ultrasound Q 2019; 35 (02) 110-119
- 31 Sanders RJ, Haug CE, Pearce WH. Recurrent thoracic outlet syndrome. J Vasc Surg 1990; 12 (04) 390-398 , discussion 398–400
- 32 Atasoy E. Recurrent thoracic outlet syndrome. Hand Clin 2004; 20 (01) 99-105
- 33 Kim TU, Chang MC. Neuralgic amyotrophy: an underrecognized entity. J Int Med Res 2021; 49 (04) 3000605211006542
- 34 Meiling JB, Boon AJ, Niu Z. et al. Parsonage-Turner syndrome and hereditary brachial plexus neuropathy. Mayo Clin Proc 2024; 99 (01) 124-140
- 35 Ferrante MA. The distribution of neuralgic amyotrophy lesions is overwhelmingly extraplexal. Muscle Nerve 2018; 58 (03) 325-326
- 36 Ferrante MA. Brachial plexopathies: classification, causes, and consequences. Muscle Nerve 2004; 30 (05) 547-568
- 37 Granata G, Tomasello F, Sciarrone MA, Stifano V, Lauretti L, Luigetti M. Neuralgic amyotrophy and hourglass nerve constriction/nerve torsion: two sides of the same coin? A clinical review. Brain Sci 2024; 14 (01) 67
- 38 van Alfen N, van Engelen BG. The clinical spectrum of neuralgic amyotrophy in 246 cases. Brain 2006; 129 (Pt 2): 438-450
- 39 van Alfen N, van Engelen BG, Hughes RA. Treatment for idiopathic and hereditary neuralgic amyotrophy (brachial neuritis). Cochrane Database Syst Rev 2009; 2009 (03) CD006976
- 40 Yamanaka R, Hayano A. Radiation-induced malignant peripheral nerve sheath tumors: a systematic review. World Neurosurg 2017; 105: 961-970.e8
- 41 Rawal A, Yin Q, Roebuck M. et al. Atypical and malignant peripheral nerve-sheath tumors of the brachial plexus: report of three cases and review of the literature. Microsurgery 2006; 26 (02) 80-86
- 42 Kori SH, Foley KM, Posner JB. Brachial plexus lesions in patients with cancer: 100 cases. Neurology 1981; 31 (01) 45-50
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