Radiation plexopathy …

Neuro-Oncology

Updated 10.17.2023
Released 04.26.1996
Expires For CME 10.17.2026

Radiation plexopathy

Authors: Muzamil Arshad MD, Steven J Chmura MD

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Editor: Deric M Park MD FACP

Radiation plexopathy

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Introduction

Overview

Brachial plexopathy is the most common complication of therapeutic irradiation affecting the peripheral nervous system. Patients treated for breast carcinoma are most often affected; radiation brachial plexopathy is a significant source of morbidity. Lumbosacral plexopathy is also an increasingly recognized complication of radiation therapy for a number of neoplasms. Radiation techniques such as stereotactic body irradiation and intensity-modulated radiotherapy also carry a risk of plexus injury. It is important for neurologists to diagnose radiation-induced plexopathies early and to differentiate them from plexus metastases or other causes of plexopathy. The authors discuss the clinical presentations, diagnostic issues, and management of patients with radiation plexopathies.

Key points

	• Radiation injury to the brachial plexus most often occurs after treatment for breast cancer, whereas lumbosacral plexopathy occurs after treatment of a number of primary or metastatic pelvic tumors.
	• Radiation plexopathy generally presents with painless numbness and sensory symptoms in the affected limb, with variable weakness. Pain may occur but is usually not early or prominent.
	• The most frequent differential diagnosis distinguishes radiation plexopathy from metastases to the brachial or lumbosacral plexus.
	• The clinical course of radiation plexopathy is variable, though most patients suffer from progressive sensory and motor deficits. Therapy options are very limited.

Historical note and terminology

The first reports of radiation-induced brachial plexopathy appeared in the early 1960s, shortly after the widespread introduction of modern megavoltage radiotherapy for treatment of breast carcinoma. Radiation brachial plexopathy is the most frequent complication of radiotherapy affecting the peripheral nervous system. Lumbosacral plexopathy is less common and has been clearly recognized only during the past 20 years.

Clinical manifestations

Presentation and course

Radiation-induced brachial plexopathy can be divided into two categories: (1) relatively rare instances occurring during or shortly after completion of radiotherapy and (2) the more common "delayed progressive" cases. Acute brachial plexopathy may occur during the course of axillary and supraclavicular irradiation for Hodgkin disease (87; 76). Severe unilateral or bilateral shoulder pain is followed by weakness involving mainly the deltoid and supraspinatus muscles, with partial recovery. The acute onset of symptoms and the distribution of weakness in these patients closely resemble "cryptogenic" brachial plexopathy or "neuralgic amyotrophy."

A syndrome of "early delayed" radiation, brachial plexopathy occurs in approximately 1% of women treated for breast carcinoma (95; 88). Onset of neurologic symptoms occurs within the first 6 months after completion of radiotherapy. Paresthesias of the hand and forearm are the presenting symptoms in 90% of patients, with shoulder and axillary pain in some patients; the pain and sensory symptoms improve over several months. During this time, some patients develop mild weakness, which resolves almost completely.

The latent interval for delayed radiation brachial plexopathy is generally at least 12 months, with a broad peak of onset of neurologic symptoms from 1.5 to 4 years after radiotherapy (08; 65; 37; 20; 15). Patients may continue to develop brachial plexopathy 10 years or more after radiation therapy (59). There is no obvious relationship between the latent period and the radiation dose, except for shorter latencies in patients who receive a second course of irradiation to the plexus.

The most common presenting symptoms of radiation brachial plexus injury are numbness and paresthesias of the hand and fingers, with weakness tending to develop later in the course (109; 65; 69; 53; 37; 15). Most patients do not have pain at the outset, and approximately one third of patients have minimal or no pain throughout their entire course (109; 65).

Acute lumbosacral plexopathy may occur during or shortly after radiation therapy for pelvic tumors (44); in some of these patients, pain is intractable and out of proportion to motor or sensory symptoms. A subacute lumbosacral plexopathy has been reported in 3% of young men treated with radiation for testicular seminoma (13). Patients develop some combination of pain, weakness, and sensory symptoms after a postradiation latency of 2 to 6 months; the symptoms generally resolve over several weeks to months. The latent interval between irradiation and the onset of neurologic symptoms in patients with "delayed" lumbosacral plexopathy varies from 3 months to 30 years, with a median interval of approximately 5 years (86; 108). There is not a clear correlation between the radiation dose and the duration of the latent interval. Radiation-induced lumbosacral plexopathy usually presents as bilateral but asymmetric leg weakness (108). The weakness may involve any muscles innervated by L2 through S1, but it often has an L5-S1 predominance. Atrophy, fasciculations, and loss of tendon reflexes accompany the weakness. Pain eventually occurs in approximately one half of patients, but it is usually not early or severe. Approximately one third of patients have early and prominent numbness and paresthesias (05). Bladder or bowel symptoms are unusual, and if present, they are often attributable to radiation-induced proctitis or bladder fibrosis (108).

Prognosis and complications

Radiation brachial plexopathy generally takes one of two courses (109; 08; 65; 37). In at least two thirds of patients, the motor and sensory deficits gradually worsen over several years to a level of severe neurologic disability. The remaining patients spontaneously cease progression after 1 to 3 years (109; 53; 61). Spontaneous recovery of neurologic function is highly unusual. In some patients, the dysesthesias and pain diminish concurrently with worsening weakness, whereas other patients suffer from persistent or even increasing pain with progressive motor and sensory loss.

Patients with a syndrome suggestive of lumbosacral plexopathy occurring shortly after radiation often show neurologic improvement (13). The most frequent course of “delayed” radiation lumbosacral plexopathy is a slow progression over months to years (108). A few patients have a more rapid progression or alternatively show stabilization of neurologic deficits after a period of progression (48). Exceptional patients eventually have significant resolution of weakness and sensory symptoms (34; 24).

Clinical vignette

A 56-year-old woman underwent right modified radical mastectomy and axillary lymph node dissection for breast carcinoma followed by radiotherapy (55 Gy) encompassing the supraclavicular and axillary areas. She remained well until 50 months after completion of radiation, when she developed painless numbness and paresthesias of the first three digits of the right hand, extending along the dorsum of the hand and forearm. Over the subsequent 3 months she noted decreased grip strength and dexterity of the right hand. Examination revealed postradiation skin changes and lymphedema of the right arm. There was no Horner syndrome. Motor examination showed 4+/5 weakness of the right triceps, wrist dorsiflexors, wrist pronation, and supination. Muscle stretch reflexes were 2+ and symmetric except for decreased right triceps jerk. There was patchy decrease in pinprick sensation over the dorsum of the hand and first two digits. Chest x-ray and MR scans of the cervical spine and brachial plexus were all unremarkable. Electrophysiologic studies showed normal nerve conduction velocities but low amplitude median and ulnar sensory nerve action potentials. Needle EMG showed large amplitude motor units, fibrillations, and positive sharp waves in the triceps and first dorsal interosseous, and myokymic discharges in the first dorsal interosseous. A 2-week tapering course of dexamethasone had no effect on her symptoms. Over the next 4 months, she noted further decrease in grip strength. A 3-month trial of warfarin did not produce any improvement in symptoms, neurologic examination, or electrophysiologic findings. Eighteen months after the onset of neurologic symptoms, she remained without evidence for recurrent tumor.

Biological basis

Etiology and pathogenesis

The restricted occurrence of acute brachial plexopathy during radiotherapy for Hodgkin disease, but not for other tumors (87; 76), argues against direct radiation damage to the plexus and in favor of an inflammatory or immune process specifically related to the Hodgkin disease. Early delayed reversible brachial plexopathy reported within several months of treatment for breast carcinoma is most likely due to reversible damage to axons or myelin (95).

The exact pathogenesis of delayed radiation injury to the brachial or lumbosacral plexus remains unclear. The bulk of experimental animal data support vascular injury as the key event (56); however, peripheral axons and myelin sheaths are also clearly susceptible to direct damage by irradiation (110).

Radiation plexopathy is characterized by extensive fibrosis within and surrounding nerve trunks of the brachial or lumbosacral plexus with demyelination and loss of axons (109; 108). It is difficult, however, to reconstruct the pathophysiology based on this end-stage appearance. The occasional finding of hyalinized and obliterated vessels supports the hypothesis that vascular damage is an important, if not the primary, cause of plexopathy.

There is a correlation between the risk of radiation brachial plexopathy and the total dose of radiation administered to the plexus. The risk of brachial plexopathy is generally considered to be 5% or less within 5 years after 60 to 62 Gy given in daily fractions of 2 Gy or less (33). At doses above 70 Gy the risk of brachial plexopathy rises sharply, to as high as 50% after 75 to 77 Gy (20; 32). There is some evidence for increased risk of plexopathy when patients receive daily dose fractions of more than 2 Gy (“hypofractionation”) (45; 43). However, newer data may suggest that hypofractionated radiation results are similar compared to conventional fractionated courses (99; 09; 75; 113) and possibly have decreased rates of plexopathy (22). Plexopathy occurs more frequently when a larger volume of the plexus is irradiated (32; 21), which may be more pronounced in thin and younger patients as they typically receive a higher dose of radiation during breast treatment (118). It also occurs when patients receive two separate courses of "subthreshold" irradiation, and some evidence suggests a higher risk of plexopathy if patients receive concurrent radiation and chemotherapy, though this remains unclear (88; 84).

Changes in clinical practice and the development of new radiotherapy technologies have increased concern for radiation brachial plexopathy. The recommended radiation dose for non-small-cell lung carcinoma has increased, leading to an increased incidence of brachial plexopathy after treatment of apical tumors (04; 32). Stereotactic body radiation therapy (SBRT), which delivers an extremely conformal treatment course in less than five fractions, for apical lung carcinoma results in conflicting amounts of plexopathy (41; 100), with the risk from stereotactic body radiation therapy being low when the maximum dose to the brachial plexus is less than 30 Gy in three fractions (72). Moreover, stereotactic body radiation therapy to the cervical/thoracic spine is being used to provide durable control of painful metastases but also poses a risk for brachial plexopathy (127). Other forms of radiation, specifically for patients with head and neck cancer, can exceed 70 Gy (21). In one modern series, 20% of 5-year survivors had symptoms of brachial plexopathy (20). Intensity-modulated radiation therapy (IMRT) for head and neck cancer may increase exposure of the plexus compared to historical conventional radiation therapy (19). However, intensity-modulated radiation therapy may also allow a higher dose of radiation delivered to the adjacent tumors while avoiding the brachial plexus (111; 81) and may still be safe when delivered at high doses to the brachial plexus (90). So, these modern treatments allow improved dose delivery to tumors near adjacent critical structures but they may place patients at increased risk for plexopathy.

There are several formulas for computing a dose equivalent to allow comparison of the radiobiological effect (and risk of delayed tissue injury) for different radiation fractionation schedules. As of 2021, the most frequently used formula is the linear-quadratic model (42; 119), and most recently a log-linear model demonstrating a low rate of plexopathy when the conventionally fractionated dose is less than 60-66 Gy (120). Although these models are reassuring, there is no absolute safety threshold for radiation brachial plexopathy, as there are reports of a higher-than-expected incidence after relatively low radiation doses (82; 84). Whereas other series report a low incidence of brachial plexopathy despite radiation schedules delivering a high dose equivalent (07).

The relationship between radiation dose and the occurrence of lumbosacral plexopathy is more complicated than for brachial plexopathy. With standard once-daily external beam radiotherapy, lumbosacral plexopathy has occurred after doses ranging from 30 Gy to 67.5 Gy (05; 108). Many patients with radiation lumbosacral plexopathy received two courses of external beam irradiation (05), a combination of external beam treatment plus intracavitary radiation implants (86; 48), or combined photon and proton beam radiation (89). The radiation exposure to the lumbosacral plexus and cauda equina in these patients may be 80 “Gy equivalents" or more. Another factor is that irradiation of the para-aortic region or pelvis exposes the nerves over long distances. Irradiation injury to peripheral nerves becomes more likely as the radiation field size increases, but this factor is difficult to quantify (110). Intensity-modulated radiation therapy (IMRT) is increasingly used to treat several pelvic neoplasms, including carcinomas of the cervix, rectum, and prostate. Pre-treatment delineation of the lumbosacral plexus is important to avoid inadvertent over-exposure to the plexus (122), with dose constraints being proposed for cervical cancer treatments (115). Lumbosacral plexopathy has been reported following re-irradiation of spinal and pelvic metastases with stereotactic body radiation (47; 12; 127).

Differential diagnosis

The major issue in differential diagnosis is distinguishing brachial or lumbosacral radiation plexopathy from tumor metastasis to the plexus. Carcinomas of the breast and lung together account for an overwhelming majority of brachial plexus metastases. Symptomatic brachial plexus metastases have been estimated to occur in approximately 4% of patients with lung cancer and 2% of patients with breast cancer. Among other primary tumors, only lymphomas metastasize to the brachial plexus with any appreciable frequency (71). There are scattered reports of brachial plexus metastases from various other tumors (65; 16). In most cases, metastatic tumors reach the plexus by extension from axillary or supraclavicular lymph nodes, whereas superior sulcus (Pancoast) bronchogenic carcinomas spread directly to the adjacent plexus. Rarely, tumors may spread hematogenously into the nerve trunks in the absence of tumor in the adjacent soft tissues or lymph nodes (80).

The diagnosis of radiation brachial plexopathy in the literature is often made inferentially because of the limitations of imaging studies (especially in the pre-MR era) and the fact that few patients undergo surgical exploration. Patients were, therefore, presumed to have radiation brachial plexopathy if they had not concurrently developed systemic metastases; if there was no evident tumor in bone, lymph nodes, or soft tissue adjacent to the plexus; and if follow-up over a certain period did not reveal evidence for brachial plexus metastases. These criteria clearly have exceptions because brachial plexus metastases may occur as an isolated site of tumor spread, and some patients have no other evidence for metastatic tumor for several years or more after the onset of metastatic plexopathy (109; 65; 78).

The latent period between the completion of irradiation and the onset of neurologic symptoms for patients with metastatic versus radiation brachial plexopathy can be as short as several months or longer than 5 years following irradiation. Median latent intervals were shorter for metastatic than for radiation plexopathy patients in some series (65; 69), but the two groups overlap considerably, and a shorter interval for metastatic disease has not been observed universally (109; 06).

Radiation-induced skin changes, lymphedema, and soft-tissue induration of the axilla and supraclavicular fossa are each present in 30% to 75% of patients with radiation brachial plexopathy (109; 06; 65; 69). These changes are also present in a lower, but still sizable, proportion of patients with brachial plexus metastases. Horner syndrome is present in up to one half of patients with metastatic plexopathy and is virtually never seen in patients with radiation brachial plexopathy (65; 69; 82).

The distribution of neurologic signs and symptoms varies somewhat between patients with metastatic versus radiation brachial plexopathy, but the degree of overlap does not permit an absolute distinction to be made on these grounds alone. In some series, patients with plexus metastases had predominant involvement of C8-T1 roots or of the lower trunk (65; 69). Of the patients with signs and symptoms of "diffuse" metastatic brachial plexopathy, many were found to have epidural tumor extension to account for the "upper trunk" deficits (65). In contrast, patients with radiation brachial plexopathy reported paresthesias of the first two digits as the earliest symptom, and most patients had weakness restricted to muscles innervated by the C5 to C6 roots (65). The differential localization of radiation versus metastatic plexopathy was thought to be due to the close proximity of the lower trunk of the plexus to the lateral group of axillary lymph nodes (which drains the breast) and to the upper lobe of the lung, enabling breast and lung tumors to reach the plexus by direct extension. The relative sparing of the lower plexus in radiation injury was believed to be due to partial shielding of these elements by the clavicle.

In several other series, however, there was a much less clear-cut clinical distinction between radiation and metastatic brachial plexopathy. Many patients with radiation brachial plexopathy in these series had weakness involving mainly the muscles innervated by the C8-T1 roots or lower trunk (69; 53). Conversely, "diffuse" involvement of the plexus was equally common among patients with metastases and patients with radiation damage (109; 112; 37).

The most reliable clinical feature to distinguish radiation brachial plexopathy from plexus metastases is pain. Metastatic brachial plexopathy is characterized by early, severe, and unrelenting pain in more than 80% of patients (109; 65; 69; 53). Pain often precedes numbness or weakness by up to several months (65). Pain is generally, but not always, most severe in a C8-T1 dermatomal distribution (65). In contrast, fewer than 20% of patients with radiation brachial plexopathy report pain at the outset, and approximately one third of patients have minimal or no pain throughout their entire course (109; 65). Exceptional patients with radiation plexopathy do have early and severe pain.

Metastases to the lumbosacral plexus most often arise from colorectal carcinomas, breast carcinoma, gynecologic carcinomas, retroperitoneal or pelvic sarcomas, or lymphoma (58; 108). In most patients, tumors invade the plexus by direct extension from pelvic tumor or from metastases to nearby lymph nodes. At least 75% of patients with lumbosacral plexus metastases present with pain, usually unilateral and affecting the low back, hip, and thigh (86; 58; 108). Nearly all patients eventually develop local or radicular pain that is characteristically worse at night and is usually unrelenting despite narcotics. Most patients subsequently develop weakness and sensory symptoms after a lag period of weeks to months. Bladder dysfunction is uncommon. The tempo of progression of symptoms is usually faster in patients with metastases than with radiation plexopathy. Some patients with lumbosacral plexus metastases show clinical improvement with dexamethasone; this does not occur with radiation plexopathy (86).

The brachial plexus may rarely be the site of primary benign or malignant nerve sheath tumors. Schwannomas and neurofibromas are the most common benign tumors arising in the brachial plexus (62; 26). Approximately one third of reported patients have type 1 neurofibromatosis. Nearly all patients with brachial plexus schwannomas have a palpable mass. Slightly fewer than half the patients have local or radiating pain at the time of diagnosis; pain is more frequent with neurofibromas than with schwannomas. Paresthesias or sensory loss are less common, and fewer than 20% of patients have weakness at presentation. There is no particular predilection for involvement of specific segments of the plexus. Some neurofibromas are "dumbbell tumors," which extend into the spinal epidural space.

Malignant nerve sheath tumors (including malignant schwannomas and neurofibrosarcomas) arising in the brachial plexus are much less common than benign tumors. Malignant nerve sheath tumors of the plexus occasionally arise from malignant degeneration of preexisting benign tumors, particularly in the setting of neurofibromatosis. Malignant nerve sheath tumors of the brachial plexus typically present as a painful mass with a relatively short duration of symptoms (30; 62).

Neurofibroma, schwannoma, or malignant nerve sheath tumors may arise in the brachial plexus as a sequel to prior irradiation. These nerve sheath tumors may occur from 2 years to more than 30 years following irradiation to the region for Hodgkin lymphoma, breast cancer, or other tumors (40; 114; 29; 125). Postirradiation malignant fibrous histiocytoma or other sarcomas in the brachial or lumbosacral plexus have also been reported (86; 51; 112).

There are anecdotal reports of plexopathy occurring as a complication of cancer treatment other than radiation, including acute brachial plexopathy occurring after high-dose cytarabine (96) or after infusion of cisplatin into the axillary artery (60). Reversible unilateral or bilateral brachial plexopathy has occurred within 1 week of interleukin-2 treatment for renal carcinoma or melanoma (74).

Bilateral "demyelinating" brachial plexopathy has been reported in a patient with syngeneic graft-versus-host disease (124). Lumbosacral plexopathy with acute onset and permanent neurologic deficit may occur after infusion of cisplatin, doxorubicin, 5-fluorouracil, or other chemotherapy agents into the internal iliac artery (86; 17). Lumbosacral polyradiculopathy can occur acutely after intrathecal methotrexate administration (85).

Brachial plexopathy may rarely occur as a paraneoplastic syndrome in patients with Hodgkin lymphoma (67), manifesting as painless, bilateral asymmetric weakness and sensory symptoms that may improve with prednisone. Involvement of the anterior horns of the cervical spinal cord in patients with paraneoplastic encephalomyelitis and small-cell lung carcinoma may produce bilateral upper extremity weakness mimicking brachial plexopathy (79).

Delayed injury to the cauda equina after radiation can mimic lumbosacral radiation plexopathy. Patients develop asymmetric bilateral leg weakness and less often pain or sensory loss more than 10 years after radiation for lymphoma, seminoma, or other abdominal or pelvic tumors (57; 89; 31). MRI scans show patchy or multinodular enhancement along the conus medullaris and cauda equina. CSF protein is elevated but cytology is negative. The neurologic deficits eventually stabilize or may continue to worsen slowly over years.

Radiation injury to the cauda equina may overlap with what was previously described as a selective lower motor neuron syndrome following periaortic lymph node radiotherapy for testicular tumors or lymphoma or following spinal axis radiation for medulloblastoma (66; 46; 68; 11). Patients develop subacute, unilateral, or asymmetric bilateral leg weakness beginning 6 to 24 months after completion of irradiation with no pain or sensory symptoms. Examination shows muscle atrophy, fasciculations, normal or decreased muscle stretch reflexes, flexor plantar responses, and no sensory or sphincter involvement. Nerve conduction over sensory pathways is usually normal, but some patients have prolonged somatosensory evoked potentials (38). Needle EMG shows denervation changes. MR scanning was unremarkable in the few cases published. In most patients, the syndrome progresses slowly over several months and then stabilizes but does not improve. In one autopsied patient, microvascular changes were present in the cauda equina, whereas the spinal cord was normal (11). It is believed that nerve roots are the primary site of injury in these patients; the selective involvement of motor fibers is unexplained.

A syndrome termed "subacute motor neuronopathy" occurs as a paraneoplastic syndrome in patients with lymphomas or thymoma (97). Patients develop subacute, progressive weakness, often asymmetric or patchy and predominantly involving the legs, without pain or significant sensory loss. Examination reveals a pure lower motor neuron picture with moderate to severe weakness, fasciculations, atrophy, and diminished deep tendon reflexes. The syndrome has occurred before the discovery of a neoplasm as well as after complete remission. The neurologic deficits eventually stabilize spontaneously or partially improve in most patients after a period of months to years.

Diagnostic workup

Electrodiagnostic studies are useful in assessing the topography and severity of radiation brachial plexopathy. Characteristic changes include diminished amplitude of sensory nerve action potentials (often the earliest finding), prolongation of F wave latencies, and EMG evidence for chronic partial denervation (117; 82). A motor nerve conduction block across the plexus is present in most patients (53; 35). In many patients, the electromyographic abnormalities are more extensive than would have been predicted by the clinical examination. In agreement with the clinical signs and symptoms, EMG evidence of denervation in many patients with radiation plexopathy is diffuse or is present predominantly in muscles supplied by the upper trunk (117). In some patients, however, the EMG abnormalities are mainly in the distribution of C8 and T1 (36).

The electrophysiologic abnormality that most reliably differentiates radiation from metastatic brachial plexopathy is myokymia, defined as spontaneous, semirhythmic bursts of potentials. Myokymia is present in one or more muscles in 50% to 70% of patients with radiation brachial plexopathy (03; 103; 69; 53). Other abnormal discharges less frequently seen include low-frequency bizarre discharges, "grouped discharges," and "myoclonic" discharges (103). The number of myokymic discharges may vary considerably among muscles innervated by the same trunks and cords of the plexus. Myokymia is rarely present in patients with brachial plexus metastases (03; 69; 53; 112).

Electrophysiologic testing in patients with radiation lumbosacral plexopathy shows reduced amplitude of compound muscle action potentials, abnormal or absent sural nerve potentials, fibrillations, and chronic motor unit changes (108). One half of patients have fibrillations in paraspinal muscles, indicating additional injury to nerve roots. Myokymic discharges are present in approximately 60% of patients, especially in proximal muscles (103; 108). The discharges may be widely scattered and are often present in muscles that are not overly weak. Low-frequency periodic discharges have also been reported (02).

CT or MR scanning is often, but not always, useful in distinguishing between radiation brachial plexopathy and plexus metastases.

MR scanning with and without contrast provides simultaneous multiplanar images and better resolution of soft tissue structures than CT scanning. The sensitivity of MR scanning in detecting metastases in or near the brachial plexus is more than 80% (112). MR appears to be somewhat more sensitive than CT in detecting metastases (112). The presence of a mass in the plexus is the most reliable feature distinguishing metastases from radiation injury. Patients with radiation plexopathy may have low or high signal intensities in the plexus on T2-weighted images, and some patients show gadolinium enhancement (10; 116; 94). Novel qualitative and quantitative MRI methods (magnetic resonance neurography, T2-relaxometry, magnetization transfer contrast imaging) may enable development of imaging biomarkers for earlier diagnosis and study of progression of neuropathies (64). Some patients have no obvious tumor mass on MR scans and have changes consistent with "fibrosis" or radiation injury, but they later turn out to have plexus metastases. MR scanning may identify myositis or unsuspected bone metastases, which may contribute to patients' symptoms (73).

High-quality contrast-enhanced CT scans show a circumscribed soft tissue mass or diffuse soft tissue infiltration in up to 90% of patients with brachial plexus metastases (16). CT scans in patients with radiation plexopathy are either normal or show an ill-defined loss of normal tissue planes without any identifiable mass (16; 07; 53). CT scanning with multiplanar reconstruction probably increases the sensitivity in detecting metastases (39). In patients unable to undergo MRI, CT scanning provides the next best anatomic evaluation of the plexopathy (14).

Positron emission tomography using fluoro-deoxyglucose may be useful in identifying metastatic breast cancer in or near the brachial plexus (01; 55; 102). In some patients, fluoro-deoxyglucose-PET identifies tumors not clearly imaged by CT or MR scanning. Conversely, fluoro-deoxyglucose-PET scans are negative in a few patients believed to have radiation plexopathy. A negative fluoro-deoxyglucose-PET scan may prove useful in diagnosing radiation plexopathy in select cases with positive MR findings (18). However, there is little solid information regarding the reliability with which fluoro-deoxyglucose-PET can differentiate brachial plexus metastases from radiation plexopathy.

CT scans of the abdomen and pelvis are generally normal in patients with radiation lumbosacral plexopathy (86; 108). CT scans of the pelvis or abdomen show lymphadenopathy, tumor masses, or bone erosion in 75% of patients with lumbosacral plexus metastases (58; 108). Tumor cells that spread in a linear fashion along nerve roots may not be apparent on scans; in these patients, the initial scan is normal, but repeat scans usually show a tumor within 6 months (58). MR scanning is somewhat more sensitive than CT in detecting thickening of the lumbosacral plexus or tumor masses that involve the plexus (106). MR "neurography" using high-resolution T1-weighted sequences and fat-suppression T2-weighted sequences probably increases the sensitivity for detecting diffuse tumor infiltration of the lumbosacral plexus (83). Although imaging of plexopathy can be challenging, knowledge of anatomy, pathology, and imaging findings can significantly aid in noninvasive diagnosis (49).

Surgical exploration of the brachial plexus or CT-guided needle biopsy is rarely needed given the advances in diagnostic imaging but may be done as a "last resort" effort in attempting to differentiate metastases from radiation damage, but surgery carries morbidity and may miss metastatic tumor (06; 65; 23).

Management

There are numerous anecdotal reports or uncontrolled studies of surgical attempts to improve neurologic function and relieve pain in patients with radiation-induced brachial plexopathy. The most common procedure is neurolysis (opening the epineural sheath) and removal of scar tissue, with or without placement of an omental flap to "revascularize" the plexus (70). Some patients with severe pain obtained significant pain relief following surgery (63; 61; 28; 52). However, the likelihood of improvement is difficult to glean from the literature, and there are few reports that include long-term follow-ups of patients. Neurolysis rarely relieves motor or sensory deficits, and it is not clear whether surgery can halt the progression of deficits (109; 61). In 20% to 50% of patients, surgery causes a significant deterioration in sensory or motor function (63; 28). Some patients who undergo neurolysis are found to have previously unsuspected plexus metastases (28). Additional surgical options include omentoplasty (77) and adipofascial deltopectoral flap (27), in which 82% of patients reported improved pain symptoms. Both techniques are thought to improve symptoms by promoting revascularization. In a small series of eight patients who underwent segmental nerve resection and autografting, seven of eight regained at-least antigravity elbow flexion at a median follow-up of 33 months (123).

There are anecdotal reports of long-lasting pain relief in patients with radiation brachial plexopathy following dorsal root entry zone lesions (126; 107) or chemical sympathectomy (37). There is a single case report using pulsed radiofrequency ablation showing a decrease in total opiate use; however, this patient passed away in hospice 2 weeks after ablation, and therefore, long-term data are limited (98).

Anticoagulation with intravenous heparin followed by chronic warfarin has been reported to bring about neurologic improvement in a few patients with radiation-induced brachial or lumbosacral plexopathy (50; 101). Based on only a few anecdotal reports, the actual likelihood of neurologic improvement in patients treated with anticoagulants is not known.

Several regimens, including hyperbaric oxygen and vitamin E, have been tried with limited success. In a double-blind randomized trial, hyperbaric oxygen did not produce clear beneficial effects in patients with radiation brachial plexopathy (91). A triplet regimen of pentoxifylline-tocopherol and clodronate was used in a randomized comparison to placebo and failed to show a benefit regarding pain, paresthesia, or motor disability (25). However limited these experiences are, providers still recommend vitamin E and hyperbaric oxygen (104).

Although there are conflicting results with the aforementioned methods, conservative measures with occupational and physical therapy may provide some improvement (54). Medical management options include opiates, anticonvulsants, tricyclic antidepressants, and selective serotonin-norepinephrine reuptake inhibitors (98).

Outcomes

The lack of clearly effective treatments for radiation plexopathy underscores the importance of delivering radiation therapy, which is effective yet minimizes the risk of occurrence of plexopathy.

References

01: Ahmad A, Barrington S, Maisey M, Rubens RD. Use of positron emission tomography in evaluation of brachial plexopathy in breast cancer patients. Brit J Cancer 1999;79:478-82. PMID 10027316
02: Aho K, Sainio K. Late irradiation-induced lesions of the lumbosacral plexus. Neurology 1983;33:953-5. PMID 6306507
03: Albers JW, Allen AA, Bastron JA, Daube JR. Limb myokymia. Muscle Nerve 1981;4:494-504. PMID 7311989
04: Amini A, Yang J, Williamson R, et al. Dose constraints to prevent radiation-induced brachial plexopathy in patients treated for lung cancer. Int J Radiat Oncol Biol Phys 2012;82(3):e391-8. PMID 22284035
05: Ashenhurst EM, Quartey GR, Starreveld A. Lumbosacral radiculopathy induced by radiation. Can J Neurol Sci 1977;4:259-63. PMID 597799
06: Bagley FH, Walsh JW, Cady B, Salzman FA, Oberfield RA, Pazianos AG. Carcinomatous versus radiation-induced brachial plexus neuropathy in breast cancer. Cancer 1978;41(6):2154-7. PMID 207407
07: Barr LC, Kissin MW. Radiation-induced brachial plexus neuropathy following breast conservation and radical radiotherapy. Br J Surg 1987;74:855-6. PMID 2822202
08: Basso-Ricci S, della Costa C, Viganotti G, Ventafridda V, Zanolla R. Report on 42 cases of postirradiation lesions of the brachial plexus and their treatment. Tumori 1980;66(1):117-22. PMID 7376261
09: Bellefqih S, Elmajjaoui S, Arab J, et al. Hypofractionated regional nodal irradiation for women with node-positive breast cancer. Int J Radiat Oncol Biol Phys 2017;97(3):563-570. PMID 28126305
10: Bowen BC, Verma A, Brandon AH, Fiedler JA. Radiation-induced brachial plexopathy: MR and clinical findings. Am J Neuroradiol 1996b;17:1932-6. PMID 8933882
11: Bowen J, Gregory R, Squier M, Donaghy M. The post-irradiation lower motor neuron syndrome: neuronopathy or radiculopathy. Brain 1996a;119:1429-39. PMID 8931568
12: Brown LC, Lester RA, Grams MP, et al. Stereotactic body radiotherapy for metastatic and recurrent ewing sarcoma and osteosarcoma. Sarcoma 2014;2014:418270. PMID 25548538
13: Brydoy M, Storstein A, Dahl O. Transient neurological adverse effects following low dose radiation therapy for early stage testicular seminoma. Radiother Oncol 2007;82:137-44. PMID 17189656
14: Bykowski J, Mulino JM, Berger KL, et al. Acr appropriateness criteria plexopathy. J Am Coll Radiol 2017;14(5s)s225-33. PMID 28473078
15: Cai Z, Li Y, Hu Z, et al. Radiation-induced brachial plexopathy in patients with nasopharyngeal carcinoma: a retrospective study. Oncotarger 2016;7(14):18887-95. PMID 26934119
16: Cascino TL, Kori S, Krol G, Foley KM. CT of the brachial plexus in patients with cancer. Neurology 1983;33:1553-7. PMID 6316204
17: Castellanos AM, Glass JP, Yung WK. Regional nerve injury after intra-arterial chemotherapy. Neurology 1987;37:834-7. PMID 3033546
18: Chandra P, Purandare N, Agrawal A, Shah S, Rangarajan V. Clinical utility of (18)f-fdg pet/ct in brachial plexopathy secondary to metastatic breast cancer. Indian J Nucl Med 2016;31(2):123-7. PMID 27095861
19: Chen AM, Hall WH, Li BQ, et al. Intensity-modulated radiotherapy increases dose to the brachial plexus compared with conventional radiotherapy for head and neck cancer. Brit J Radiol 2011;84(997):58-63. PMID 20858665
20: Chen AM, Hall WH, Li J, et al. Brachial plexus-associated neuropathy after high-dose radiation therapy for head and neck cancer. Int J Rad Oncol Biol Phys 2012;84:165-9. PMID 22444998
21: Chen AM, Wang PC, Daly ME, et al. Dose-volume modeling of brachial plexus-associated neuropathy after radiation therapy for head and neck cancer: findings from a prospective screening protocol. Int J Radiat Oncol Biol Phys 2014;88(4):771-7. PMID 24606846
22: Chitapanarux I, Klunklin P, Pinitpatcharalert A, et al. Conventional verses hypo fractionated post mastectomy radiotherapy: a report on long-term outcomes and late toxicity. Radiate Oncol 2019;14(1):175. PMID 31610801
23: Cole JW, Quint DJ, McGillicuddy JE, Murphy KP. CT-guided brachial plexus biopsy. AJNR Am J Neuroradiol 1997;18:1420-2. PMID 9296180
24: Dahele M, Davey P, Reingold S, Wong CS. Radiation-induced lumbosacral plexopathy: an important enigma. Clin Oncol 2006;18:427-8. PMID 16817337
25: Delanian SE, Lenglet T,Maisonobe T, Resche-Rigon M, Pradat PF. Randomized, placebo-controlled clinical trial combining pentoxifylline-tocopherol and clodronate in the treatment of radiation-induced plexopathy. Int J Radiat Oncol Biol Phys 2020;107(1):154-62. PMID 31987975
26: Desai KI. Primary benign brachial plexus tumors: an experience of 115 operated cases. Neurosurgery 2012;70(1):220-33. PMID 21795865
27: Dolan RT, Moosa A, Giele HP. The adipofascial deltopectoral flap to cover the brachial plexus in thoracic outlet syndrome and radiation plexitis. J Plast Reconstr Aesthetician’s Surg 2020;73(8):1465-72. PMID 32467081
28: Dubuisson AS, Kline DG, Weinshel SS. Posterior subscapular approach to the brachial plexus: report of 102 patients. J Neurosurg 1993;79:319-30. PMID 8360726
29: Ducatman BS, Scheithauer BW. Postirradiation neurofibrosarcoma. Cancer 1983;51:1028-33. PMID 6821867
30: Ducatman BS, Scheithauer BW, Piepgras DG, Reiman HM, Ilstrup DM. Malignant peripheral nerve sheath tumors: A clinicopathologic study of 120 cases. Cancer 1986;57:2006-21. PMID 3082508
31: Ducray F, Guillevin R, Psimaras D, et al. Postradiation lumbosacral radiculopathy with spinal root cavernomas mimicking carcinomatous meningitis. Neuro Oncol 2008;10(6):1035-9. PMID 18755918
32: Eblan MJ, Carradetti MN, Lukens JN, et al. Brachial plexopathy in apical non-small cell lung cancer treated with definitive radiation: dosimetric analysis and clinical implications. Int J Rad Oncol Biol Phys 2013;85:175-81. PMID 22658442
33: Emami B, Lyman J, Brown A, et al. Tolerance of normal tissue to therapeutic irradiation. Int J Radiat Oncol Biol Phys 1991;21(1):109-22. PMID 2032882
34: Enevoldson TP, Scadding JW, Rustin GJ, Senanayake LF. Spontaneous resolution of a postirradiation lumbosacral plexopathy. Neurology 1992;42:2224-5. PMID 1331869
35: Esteban A, Traba A. Fasciculation-myokymic activity and prolonged nerve conduction block. A physiological relationship in radiation-induced brachial plexopathy. Electroencephalogr Clin Neurophysiol 1993;89:382-91. PMID 7507424
36: Fardin P, Lelli S, Negrin P, Maluta S. Radiation-induced brachial plexopathy: clinical and electromyographical considerations in 13 cases. Electromyogr Clin Neurophysiol 1990;30:277-82. PMID 2226271
37: Fathers E, Thrush D, Huson SM, Norman A. Radiation-induced brachial plexopathy in women treated for carcinoma of the breast. Clin Rehab 2002;16(2):160-5. PMID 11911514
38: Feistner H, Weissenborn K, Munte TF, Heinze HJ, Malin JP. Post-irradiation lesions of the caudal roots. Acta Neurol Scand 1989;80:277-81. PMID 2554633
39: Fishman EK, Campbell JN, Kuhlman JE, Kawashima AK, Ney DR, Friedman NB. Multiplanar CT evaluation of brachial plexopathy in breast cancer. J Comput Assist Tomogr 1991;15:790-5. PMID 1653281
40: Foley KM, Woodruff JM, Ellis FT, Posner JB. Radiation-induced malignant and atypical peripheral nerve sheath tumors. Ann Neurol 1980;7:311-8. PMID 7377756
41: Forquer JA, Fakiris AJ, Timmerman RD, et al. Brachial plexopathy from stereotactic body radiotherapy in early-stage NSCLC: dose-limiting toxicity in apical tumor sites. Radiother Oncol 2009;93(3):408-13. PMID 19454366
42: Fowler JF. The linear-quadratic formula and progress in fractionated radiotherapy. Brit J Radiol 1989;62:679-94. PMID 2670032
43: Friberg S, Ruden B. Hypofractionation in radiotherapy. An investigation of injured Swedish women, treated for cancer of the breast. Acta Oncol 2009;48(6):822-31. PMID 19504371
44: Frykholm GJ, Sintorn K, Montelius A, Jung B, Pahlman L, Glimelius B. Acute lumbosacral plexopathy during and after preoperative radiotherapy of rectal adenocarcinoma. Radiother Oncol 1996;38(2):121-30. PMID 8966224
45: Galecki J, Hicer-Grzenkowicz J, Grudzien-Kowalska M, Michalska T, Zalucki W. Radiation-induced brachial plexopathy and hypofractionated regimens in adjuvant irradiation of patients with breast cancer—a review. Acta Oncol 2006;45(3):280-4. PMID 16644570
46: Gallego J, Delgado G, Tunon T, Villanueva JA. Delayed postirradiation lower motor neuron syndrome. Ann Neurol 1986;19:308-9. PMID 3963778
47: Garg AK, Wang XS, Shiu AS, et al. Prospective evaluation of spinal reirradiation by using stereotactic body radiation therapy: The University of Texas MD Anderson Cancer Center experience. Cancer 2011;117(15):3509-16. PMID 21319143
48: Georgiou A, Grigsby PW, Perez CA. Radiation induced lumbosacral plexopathy in gynecologic tumors: clinical findings and dosimetric analysis. Int J Radiat Oncol Biol Phys 1993;26:479-82. PMID 8514543
49: Gilcrease-Garcia BM, Deshmukh SD, Parsons MS. Anatomy, imaging, and pathologic conditions of the brachial plexus. Radiographics 2020;40(6):1686-1714. PMID 33001787
50: Glantz MJ, Burger PC, Friedman AH, Radke RA, Massey EW, Schold SC. Treatment of radiation-induced nervous system injury with heparin and warfarin. Neurology 1994;44:2020-7. PMID 7969953
51: Gorson KC, Musaphir S, Lathi ES, Wolfe G. Radiation-induced malignant fibrous histiocytoma of the brachial plexus. J Neurooncol 1995;26:73-7. PMID 8583247
52: Gosk J, Rutowski R, Urban M, Wiecek R, Rabczynski J. Brachial plexus injuries after radiotherapy: analysis of 6 cases. Folia Neuropathol 2007;45(1):31-5. PMID 17357009
53: Harper CM, Thomas JE, Cascino TL, Litchy WJ. Distinction between neoplastic and radiation-induced brachial plexopathy, with emphasis on the role of EMG. Neurology 1989;39:502-6. PMID 2538777
54: Harris SR, Tugwell KE. Neurological and dexterity assessments in a woman with radiation-induced brachial plexopathy after breast cancer. Oncologist 2020;25(10):e1583-5. PMID 32525604
55: Hathaway PB, Mankoff DA, Maravilla KR, et al. Value of combined FDG-PET and MR imaging in the evaluation of suspected recurrent local-regional breast cancer: preliminary experience. Radiology 1999;210(3):807-14. PMID 10207485
56: Haymaker W, Lindgren M. Nerve disturbances following exposure to ionizing radiation. In: Vinken PJ, Bruyn GW, editors. Handbook of Clinical Neurology. Amsterdam: Elsevier, 1970:388-401.
57: Hsia AW, Katz JS, Hancock SL, Peterson K. Post-irradiation polyradiculopathy mimics leptomeningeal tumor on MRI. Neurology 2003;60(10):1694-6. PMID 12771271
58: Jaeckle KA, Young DF, Foley KM. The natural history of lumbosacral plexopathy in cancer. Neurology 1985;35:8-15. PMID 2981417
59: Johansson S, Svensson H, Denekamp J. Timescale of evolution of late radiation injury after postoperative radiotherapy of breast cancer patients. Int J Rad Oncol Biol Phys 2000;48:745-0. PMID 11020571
60: Kahn CE, Messersmith RN, Samuels BL. Brachial plexopathy as a complication of intraarterial cisplatin chemotherapy. Cardiovasc Intervent Radiol 1989;12:47-9. PMID 2540910
61: Killer HE, Hess K. Natural history of radiation-induced brachial plexopathy compared with surgically treated patients. J Neurol 1990;237:247-50. PMID 2391547
62: Kim DH, Murovic JA, Tiel RL, Moes G, Kline DG. A series of 397 peripheral nerve sheath tumors: 30-year experience at Louisiana State University. J Neurosurg 2005;102:246-55. PMID 15739552
63: Kline DG. Operative management of selected brachial plexus lesions. J Neurosurg 1983;58:631-49. PMID 6834110
64: Kollmer J, Bendszus M. Magnetic resonance neurography: improved diagnosis of peripheral neuropathies. Neurotherapeutics 2021;18(4):2368-83. PMID 34859380
65: Kori SH, Foley KM, Posner JB. Brachial plexus lesions in patients with cancer: 100 cases. Neurology 1981;31:45-50. PMID 6256684
66: Kristensen O, Melgard B, Schiodt AV. Radiation myelopathy of the lumbosacral spinal cord. Acta Neurol Scand 1977;56:217-22. PMID 906796
67: Lachance DH, O'Neill BP, Harper CM, Banks PM, Cascino TL. Paraneoplastic brachial plexopathy in a patient with Hodgkin's disease. Mayo Clin Proc 1991;66:97-101. PMID 1846435
68: Lamy C, Mas JL, Varet B, Ziegler M, de Recondo J. Postradiation lower motor neuron syndrome presenting as monomelic amyotrophy. J Neurol Neurosurg Psychiatr 1991;54(7):648-9. PMID 1895131
69: Lederman RJ, Wilbourn AJ. Brachial plexopathy: recurrent cancer or radiation. Neurology 1984;34:1331-5. PMID 6090988
70: LeQuang C. Postirradiation lesions of the brachial plexus: results of surgical treatment. Hand Clin 1989;5(1):23-32. PMID 2722964
71: Liang R, Kay R, Maisey MN. Brachial plexus infiltration by non-Hodgkin's lymphoma. Br J Radiol 1985;58:1125-7. PMID 3879866
72: Lindberg K, Grozman V, Lindberg S, et al. Radiation-induced brachial plexus toxicity after SBRT of apically located lung lesions. Acta Oncol 2019;58(8):1178-86. PMID 31066326
73: Lingawi SS, Bilbey JH, Munk PL, et al. MR imaging of brachial plexopathy in breast cancer patients without palpable recurrence. Skeletal Radiol 1999;28(6):318-23. PMID 10450878
74: Loh FL, Herskovitz S, Berger AR, Swerdlow ML. Brachial plexopathy associated with interleukin-2 therapy. Neurology 1992;42:462-5. PMID 1310533
75: Long N, Truong PT, Tankel K, et al. Hypofractionated nodal radiation therapy for breast cancer was not associated with increased patient-reported arm or brachial plexopathy symptoms. Int J Radiat Oncol Biol Phys 2017;99(5):1166-72. PMID 29165285
76: Malow BA, Dawson DM. Neuralgic amyotrophy in association with radiation therapy for Hodgkin's disease. Neurology 1991;41:440-1. PMID 2006016
77: Manuel de Oliveira AJ, Castro JP, Foroni LH, et al. Treatment of radiation-induced brachial plexopathy with omentoplasty. Autops Case Rep 2020;10(3):e2020202. PMID 33344306
78: Marek T, Howe BM, Amrami KK, Spinner RJ. Perineurial spread of melanoma to the brachial plexus: identifying the anatomic pathway(s). World Neurosurg 2018;111:921-6. PMID 29325942
79: Meador KJ, Richards B, Hunter S, Nichols FT, Watson RT. Bibrachial palsy due to paraneoplastic encephalomyelitis. South Med J 1989;82:1053-4. PMID 2548289
80: Meller I, Alkalay D, Mozes M, Geffen DB, Ferit T. Isolated metastases to peripheral nerves: five cases involving the brachial plexus. Cancer 1995;76:1829-32. PMID 8625055
81: Metcalfe E, Etiz D. Early transient radiation-induced brachial plexopathy in locally advanced head and neck cancer. Contempt Oncol (Pozn) 2016;20(1):67-72. PMID 27095943
82: Mondrup K, Olsen NK, Pfeiffer P, Rose C. Clinical and electrodiagnostic findings in breast cancer patients with radiation-induced brachial plexus neuropathy. Acta Neurol Scand 1990;81:153-8. PMID 2327236
83: Moore KR, Blumenthal DT, Smith AG, Ward JH. Neurolymphomatosis of the lumbar plexus: high-resolution MR neurography findings. Neurology 2001;57:740-2. PMID 11524499
84: Olsen NK, Pfeiffer P, Johannsen L, Schroder H, Rose C. Radiation-induced brachial plexopathy: neurological follow-up in 161 recurrence-free breast cancer patients. Int J Radiat Oncol Biol Phys 1993;26:43-9. PMID 8387067
85: Pascual AM, Coret F, Casanova B, Lainez MJ. Anterior lumbosacral polyradiculopathy after intrathecal administration of methotrexate. J Neurol Sci 2008;267(1-2):158-61. PMID 17949753
86: Pettigrew LC, Glass JP, Maor M, Zornoza J. Diagnosis and treatment of lumbosacral plexopathies in patients with cancer. Arch Neurol 1984;41:1282-5. PMID 6093750
87: Pezzimenti JE, Bruckner HW, DeConti RC. Paralytic brachial neuritis in Hodgkin's disease. Cancer 1973;31:626-9. PMID 4693591
88: Pierce SM, Recht A, Lingos TI, et al. Long-term radiation complications following conservative surgery and radiation therapy in patients with early stage breast cancer. Int J Radiat Oncol Biol Phys 1992;23(5):915-23. PMID 1639653
89: Pieters RS, Niemierko A, Fullerton BC, Munzenrider JE. Cauda equina tolerance to high-dose fractionated irradiation. Int J Rad Oncol Biol Phys 2006;64:251-7. PMID 15993548
90: Prakash BB, Yathiraj PH, Sharan TK, et al. Dosimetric analysis and clinical outcomes of brachial plexus as an oran-at-risk in head-and-neck cancer patients treated with intensity-modulated radiotherapy. J Cancer Res Ther 2019;15(3):522-7. PMID 31169214
91: Pritchard J, Anand P, Broome J, et al. Double-blind randomized phase II study of hyperbaric oxygen in patients with radiation-induced brachial plexopathy. Radiother Oncol 2001;58(3):279-86. PMID 11230889
92: Register SP, Zhang X, Mohan R, Chang JY. Proton stereotactic body radiation therapy for clinically challenging cases of centrally and superiorly located stage I non-small-cell lung cancer. Int J Rad Oncol Biol Phys 2011;80(4):1015-22. PMID 20615629
93: Rudra S, Roy A, Brenneman R, et al. Radiation-induced brachial plexopathy in patients with breast cancer treated with comprehensive adjuvant radiation therapy. Adv Radiat Oncol 2020;6(1):100602. PMID 33665488
94: Qayyum A, MacVicar AD, Padhani AR, Revell P, Husband JE. Symptomatic brachial plexopathy following treatment for breast cancer: utility of MR imaging with surface-coil techniques. Radiology 2000;214:837-42. PMID 10715054
95: Salner AL, Botnick LE, Herzog AG, et al. Reversible brachial plexopathy following primary radiation therapy for breast cancer. Cancer Treat Rep 1981;65(9-10):797-802. PMID 6791820
96: Scherokman B, Filling-Katz MR, Tell D. Brachial plexus neuropathy following high-dose cytarabine in acute monoblastic leukemia. Cancer 1985;69:1005-6. PMID 2992782
97: Schold SC, Cho ES, Somasundaram M, Posner JB. Subacute motor neuronopathy: a remote effect of lymphoma. Ann Neurol 1979;5:271-87. PMID 443760
98: Shah N, Engle AM, Raggi E, Alter B, Emerick T. Pulsed radio frequency ablation: An alternative treatment modality for radiation induced brachial plexopathy. Pain Medicine 2021;22(3):749-53. PMID 33164080
99: Shin SM, No HS, Vega RM, et al. Breast, chest wall, and nodal irradiation with prone set-up: Results of a hypofractionated trial with a median follow-up of 35 months. Pract Radiat Oncol 2016;6(4):81-8. PMID 26723552
100: Sood, SS, McClinton C, Badkul R, et al. Brachial plexopathy after stereotactic body radiation therapy for apical lung cancer: dosimetric analysis and preliminary clinical outcomes. Adv Radiat Oncol 2017;3(1):81-6. PMID 29556585
101: Soto O. Radiation-induced conduction block: resolution following anticoagulant therapy. Muscle Nerve 2005;31:642-5. PMID 15635681
102: Soydal C, Akkuş P, Araz M, Utkan G. Intense 18 F-flourodeoxyglucose uptake in brachial plexus of patients with brachial plexopathy. Mol Imaging Radionucl Ther 2020;29(2):79-81. PMID 32368879
103: Stohr M. Special types of spontaneous electrical activity in radiogenic nerve injuries. Muscle Nerve 1982;5:578-83. PMID 7170000
104: Stowe HB, Mullins BT, Chera BS. Hyperbaric oxygen therapy for radiation-induced brachial plexopathy, a case report and literature review. Rep Pract Oncol Radiother 2020;25(1):23-7. PMID 31762694
105: Stryker JA, Sommerville K, Perez R, Velkley DE. Sacral plexus injury after radiotherapy for carcinoma of cervix. Cancer 1990;66:1488-92. PMID 2169990
106: Taylor BV, Kimmel DW, Krecke KN, Cascino TL. Magnetic resonance imaging in cancer-related lumbosacral plexopathy. Mayo Clin Proc 1997;72:823-9. PMID 9294528
107: Teixeira MJ, Fonoff ET, Montenegro MC. Dorsal root entry zone lesions for treatment of pain related to radiation-induced plexopathy. Spine 2007;32(10):E316-9. PMID 17471080
108: Thomas JE, Cascino TL, Earle JD. Differential diagnosis between radiation and tumor plexopathy of the pelvis. Neurology 1985;35:1-7. PMID 2981416
109: Thomas JE, Colby MY. Radiation-induced or metastatic brachial plexopathy. A diagnostic dilemma. JAMA 1972;222:1392-5. PMID 4344104
110: Thomas PK, Holdorff B. Neuropathy due to physical agents. In: Dyck PJ, Thomas PK, Griffin JW, Low PA, Podulso JF, editors. Peripheral Neuropathy. 3rd ed. Philadelphia: WB Saunders, 1993:1000-8.
111: Thomas TO, Refaat T, Choi M, et al. Brachial plexus dose tolerance in head and neck cancer patients treated with sequential intensity modulated radiation therapy. Radiat Oncol 2015;10:94. PMID 25927572
112: Thyagarajan D, Cascino T, Harms G. Magnetic resonance imaging in brachial plexopathy of cancer. Neurology 1995;45:421-7. PMID 7898688
113: Tovanabutra C, Katanyoo K, Uber P, Chomprasert K, Sukauichai S. Comparison of treatment outcome between hypofractionated radiotherapy and conventional radiotherapy in postmastectomy breast cancer. Asian Pac J Cancer Prev 2020;21(1):119-25. PMID 31983173
114: Trojanowski JQ, Kelinman GM, Proppe KH. Malignant tumors of nerve sheath origin. Cancer 1980;46:1202-12. PMID 7214303
115: Tunio M, Amiri MA, Bayoumi Y, et al. Lumbosacral plexus delineation, dose distribution, and its correlation with radiation-induced lumbosacral plexopathy in cervical cancer patients. Onco Targets Ther 2014;8:21-7. PMID 25565862
116: van Es HW, Engelen AM, Witkamp TD, Ramos LM, Feldberg MA. Radiation-induced brachial plexopathy: MR imaging. Skeletal Radiol 1997;26:284-8. PMID 9194228
117: Wilborn AJ. Electrodiagnosis of plexopathies. Neurol Clin 1985;3:511-29. PMID 2328539
118: Wu SG, Huang SJ, Zhou J, et al. Dosimetric analysis of the brachial plexus among patients with breast cancer treated with post-mastectomy radiotherapy to the ipsilateral supraclavicular area: report of 3 cases of radiation-induced brachial plexus neuropathy. Radiate Oncol 2014;9:292. PMID 25499205
119: Yaes RJ, Patel P, Maruyama Y. On using the linear quadratic formula in daily clinical practice. Int J Radiat Oncol Biol Phys 1991;20:1353-62. PMID 2045309
120: Yan M, Kong M, Kerr A, Brundage M. The radiation dose tolerance of the brachial plexus: a systematic review and meta-analysis. Cain Transl Radiat Oncol 2019;18:23-31. PMID 31309161
121: Yi SK, Hall WH, Mathai M, et al. Validating the RTOG-endorsed brachial plexus contouring atlas: an evaluation of reproducibility among patients treated by intensity-modulated radiotherapy for head and neck cancer. Int J Radiat Oncol Biol Phys 2012a;82(3):1060-4. PMID 21536393
122: Yi SK, Mak W, Yang CC, et al. Development of a standardized method for contouring the lumbosacral plexus: a preliminary dosimetric analysis of this organ at risk among 15 patients treated with intensity-modulated radiotherapy for lower gastrointestinal cancers and the incidence of radiation-induced lumbosacral plexopathy. Int J Rad Oncol Biol Phys 2012b;84:376-82. PMID 22342301
123: Yin Y, Xue Y, Yang B, et al. Outcome of nerve grafting for radiation inducted brachial plexopathy. Open Neurosurg 2023;24(1):55-63. PMID 36519879
124: Yoshiyama Y, Nakajima M, Kuwabara S, Kawano E. Demyelinating brachial neuropathy complicating syngeneic graft-versus-host disease. Neurology 1997;48:287-8. PMID 9008540
125: Zadeh G, Buckle C, Shannon P, et al. Radiation induced peripheral nerve tumors: case series and review of the literature. J Neuro-Oncol 2007;83:205-12. PMID 17206473
126: Zeidman SM, Rossitch EJ, Nashold BS. Dorsal root entry zone lesions in the treatment of pain related to radiation-induced brachial plexopathy. J Spinal Disord 1993;6:44-7. PMID 8382542
127: Zeng KL, Myrehaug S, Soliman H, et al. Stereotactic body radiotherapy for spinal metastases at the extreme ends of the spine: imaging-based outcomes for cervical and sacral metastases. Neurosurgery 2019;85(5):605-12. PMID 30169694

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Muzamil Arshad MD

Dr. Arshad of the University of Chicago has no relevant financial relationships to disclose.
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Steven J Chmura MD

Dr. Chmura of the University of Chicago received research support from BMS, EMD Serono, Merck, and Takeda as principal investigator and an honorarium from Reflexion Medical as a consultant.
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Editor

Deric M Park MD FACP

Dr. Park of the University of Chicago has no relevant financial relationships to disclose.
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Former Authors

Benjamin E Onderdonk MD
Rimas V Lukas MD
Edward J Dropcho MD (original author)

Patient Profile

Age range of presentation: 19 to 65+ years
Sex preponderance: female>male, >2:1
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-9: Brachial plexopathy: 353.0

Lumbosacral plexopathy: 353.1
ICD-10: Brachial plexus disorders: G54.0

Lumbosacral plexus disorders: G54.1

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Radiation plexopathy

Associated Disorders

Breast carcinoma
Bronchogenic carcinoma
Head and Neck carcinoma
Hodgkin disease
Lymphoma
- Radiation brachial plexopathy
- Radiation-induced lumbosacral plexopathy

Differential Diagnosis

brachial plexus metastasis
lumbosacral plexus metastasis
nerve sheath tumors of the brachial plexus
brachial plexopathy from chemotherapy
brachial plexopathy from Hodgkin lymphoma
- lumbosacral plexopathy from chemotherapy
- postirradiation lower motor neuron syndrome
- subacute motor neuronopathy

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Radiation plexopathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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Radiation plexopathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neuropathies associated with cytomegalovirus infection

Overview of neuropathology updates for infiltrating gliomas

Anti-LGI1 encephalitis

CNS germinoma

Vestibular schwannoma

Circumscribed astrocytic gliomas [Brief]

Pediatric-type diffuse high-grade gliomas [Brief]

Mesenchymal non-meningothelial tumors [Brief]

This is an article preview.
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