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Home , Lumbosacral plexus, Lumbosacral trunk, Plexopathy, Radiculopathy

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Plexopathies

KURT A. JAECKLE

Tumors may invade the cervical, brachial, and lum- dysfunction due to epidural compression by tumor, bosacral plexus by direct extension from primary neoplastic meningitis, and other disorders of pe- tumors in regional organs or by secondary invasion ripheral . In clinical practice, physicians following metastases to regional lymph nodes. Oc- usually encounter patients with brachial or lum- casionally, tumor tracks along the epineurium sur- bosacral . Cervical plexopathy is also rounding the trunks of the plexuses. In the discussed as its clinical presentation, tumor his- previously treated patient, the major differ- tologies, and therapeutic implications differ some- ential diagnostic consideration is radiation-induced what, although there is considerable overlap with plexopathy. Less frequently, the plexopathy results brachial plexopathy. Finally, one must be able to as a complication of regional (usually intra-arter- distinguish between those patients with plex- ial) chemotherapy or is due to fibrosis following opathies due to radiation or other causes, which is surgical resection of primary tumor within the re- discussed separately. gion. Tumor plexopathy is a symptomatic complication in approximately 1 of 100 patients with cancer. In CERVICAL PLEXOPATHY two retrospective reviews from cancer hospitals, based on 12,000 patient visits per year, the preva- Anatomy lence of brachial plexopathy resulting from tumor in- vasion was 0.43%, and the prevalence of lumbosacral The is formed from the ventral rami plexopathy was 0.71% (Kori et al., 1981; Jaeckle et of the four upper cervical nerve roots (C1–C4). Af- al., 1985). The actual prevalence may be higher, as ferent sensory fibers from the skin and soft tissues of not all patients with plexopathy accompanying termi- the travel via the greater and lesser occipital nal malignancy are reported. The best estimates have nerves (posterior occiput and postauricular area); been obtained from breast cancer patients treated the great auricular and transverse cervical nerves with conventional radiotherapy in whom the preva- (preauricular area, mandibular angle, anterosupe- lence of brachial plexopathy at 5 years was 1.8% to rior neck, and submandibular area); and the medial 4.9%; however, this study likely included some pa- and lateral supraclavicular nerves (inferior antero- tients with radiation-induced plexopathy (discussed lateral neck) through the cervical plexus. The cervi- below) (Pierce et al., 1992; Powell et al., 1990; Shel- cal plexus supplies motor innervation to the di- don et al., 1987). aphragm and, deep cervical and hyoid muscles and Familiarity with plexus neuroanatomy is neces- via the spinal accessory nerve to the sternocleido- sary to correctly interpret the clinical findings and mastoid and trapezius muscles (Truex and Carpen- to distinguish between plexopathies and neurologic ter, 1969).

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414 SYMPTOMS SECONDARY TO CANCER AND ITS TREATMENT

Pathophysiology terior cervical chain or supraclavicular nodes are present. Local sensory loss may be demonstrable, but The cervical plexus is usually invaded by tumor from is often incomplete due to overlap of root zones. Of- neighboring soft tissue or bony structures (Fig. ten, one must distinguish postsurgical sensory loss 18–1). The may invade the plexus directly from that due to tumor recurrence. The timing and or indirectly by metastatic spread to regional lymph location of sensory loss are useful points of distinc- nodes, ribs, or vertebral bodies. The most commonly tion. Most commonly, surgical dissection transects associated tumors of the cervical plexus include squa- superficial branches of the greater auricular nerve mous cell carcinoma of the head and neck, lym- over the preauricular area and mandibular angle, or phoma, and adenocarcinomas of the lung and breast. the transverse cervical branches, producing numb- ness in the skin of the upper anterior neck and sub- mandibular area. Clinical Presentation Tumor may involve the phrenic nerve producing a Patients with cervical plexopathy usually present with paralyzed hemidiaphragm, which can be confirmed located in the neck, shoulder, or throat, which by chest radiograph or fluoroscopy. Patients may have is often exacerbated by neck movement, swallowing, dyspnea and paradoxical diaphragmatic excursions. and coughing. The pain is often deep, boring, and Motor dysfunction of branches to the deep cervical constant, but may have intermittent sharp compo- and hyoid muscles are usually asymptomatic. In- nents or caulsalgic features. On examination, the cer- volvement of the spinal accessory XIth cranial nerve vical musculature may be tender to palpation. One may produce shoulder weakness and instability. Ster- should suspect tumor plexopathy from tumor inva- nocleidomastoid weakness may produce head devia- sion if large palpable tumors or firm anterior or pos- tion or tilt. Head and neck tumors and lymphomas

Figure 18–1. Cervical plexopathy. Magnetic resonance imaging scan of metastatic adenocarcinoma from submandibular primary tumor to lower left cervical plexus (arrows), producing C4–C5 pain, tingling, hoarseness, and Horner’s syndrome. 3601_e18_p413-422 2/19/02 8:58 AM Page 415

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involving the anterior cervical lymphatic chain may Pathophysiology grow inferiorly, producing additional involvement of More than two-thirds of tumors involving the bra- the upper . chial plexus originate from the lung or breast and By definition, involvement of the cervical plexus generally spread to the plexus directly from the lung implies a close proximity of the tumor to the cervi- or from regional metastases to the axillary lymph cal spine. If sharp and severe pain occurs with neck nodes or lung apex (Kori et al., 1981) (Fig. 18–2). movements, or pain is elicited with percussion over Early in the disease process, the tumor often invades the spine, there may be associated involvement of the the lower plexus, particularly the inferior trunk and cervical spine or impending epidural extension. medial cord, a pattern that was part of the original description of the superior sulcus syndrome (Pan- coast, 1932). Conversely, tumors of the head and BRACHIAL PLEXOPATHY neck usually invade the superior trunk or posterior cord from above. Often, the clinical pattern of Anatomy plexus involvement is patchy, due to irregular in- volvement of the plexus by growth from the rela- The brachial plexus originates from ventral rami of tively random arrangement of lymph node metas- the lower four cervical (C5–C8) and the first tho- tases. Patchy involvement is most commonly racic roots and forms three trunks: a superior trunk identified when formal electrophysiologic investiga- (C5–C6); a medial trunk (C7); and an inferior trunk tions are performed. (C8–T1). These trunks each divide into dorsal and ventral divisions. The three dorsal divisions join together to form the posterior cord, which then Clinical Presentation splits into (1) the thoracodorsal nerve, to the latis- simus dorsi; (2) the subscapular nerve, which in- In a large series of patients with cancer and brachial nervates the subscapularis; (3) the axillary nerve, plexopathy, pain was the most common presenting which supplies the deltoid; and (4) the , symptom (75%), followed by dysesthesias (25%) which innervates the triceps, brachioradialis, wrist, (Kori et al., 1981). The pain was typically located in and finger extensors and provides sensory supply to the shoulder and axilla and often radiated along the the posterior arm and forearm. The ventral division medial aspect of the arm and forearm into the fourth forms two cords: the lateral cord, which receives and fifth fingers. Initially, pain was often incorrectly contributions from the superior and medial trunks, attributed to other potential causes, such as arthritis and the medial cord, which is a direct continuation and fibromyalgia. Pain, reflex changes, and of the inferior trunk. The lateral cord then divides were concentrated in the lower plexus (C8–T1) dis- into two branches: one becomes the musculocuta- tribution in 75% of patients, whereas the remaining neous nerve (C5–C7, motor to biceps, brachialis, 25% of patients had global signs of involvement of the coracobrachialis and sensory innervation of the ra- entire (C5–T1) plexus. dial forearm); and the other joins a similar branch When brachial plexopathy is due to tumor, lymph- from the medial cord to form the edema is relatively infrequent (15%). It is most often (C8–T1, forearm flexors and pronators, medial seen in the setting of prior radiotherapy or axillary hand flexor, and lumbrical muscles; and sensation lymph node dissection. Involvement of the sympa- to medial palm, first three fingers, and radial one- thetic trunk or ganglia near the upper thoracic (par- half of the fourth finger). The remaining portion of ticularly T1) vertebrae may produce unilateral the medial cord forms (1) the medial brachial cu- Horner’s syndrome, which has been identified in ap- taneous nerve (T1, sensory to medial arm); (2) the proximately 23% of patients. When Horner’s syn- medial antebrachial cutaneous nerve (C8–T1, drome is present, concomitant epidural disease can sensory to medial forearm) and; (3) the ulnar be identified in 32% of patients. In general, the pres- nerve (C8–T1, ulnar forearm flexor muscles, in- ence of Horner’s syndrome, serratus anterior or terossei, and lumbricals; and sensation to the ulnar rhomboid muscle weakness, or pain consistent with aspect of hand the hand and fifth finger) (Truex and vertebral involvement should raise the clinical suspi- Carpenter, 1969). cion of epidural extension. 3601_e18_p413-422 2/19/02 8:58 AM Page 416

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Figure 18–2. Brachial plexopathy. Computed tomography scan of patient with non-Hodgkin’s lymphoma showing a huge shoul- der and chest wall mass displacing mediastinal structures and invading the left brachial plexus (arrows).

LUMBOSACRAL PLEXOPATHY The arises from the ventral rami of S1–S4 and runs lateral to the border of the , penetrating the sciatic notch. A portion of the lower Anatomy plexus (L4–L5) connects to the sacral plexus The forms from the ventral rami via the , which runs over the sacral of the L1–S2 nerve roots and is anatomically divided ala to join the upper sacral plexus within the true into lumbar and sacral portions. The pelvis. The anterior division of the sacral plexus pro- forms within the iliacus muscle lateral to the L1–L4 vides motor supply to the gemelli, quadratus femoris, vertebrae and then courses posterolaterally, just an- obturator internus, and hamstrings; the remaining terior to the iliac wing. components continue as the (L4–S3), The lumbar plexus consists of anterior and pos- which provides motor supply to the foot plantar flex- terior divisions. The anterior division gives rise to ors and intrinsic muscles and sensation to the heel the iliohypogastric, ilioinguinal, and genitofemoral and sole. The posterior division continues as the nerves (L1–L2), which carry sensory fibers from the (L4–S2) to the peroneal skin of the lower abdomen, upper thigh, and lateral muscles, the tibialis anterior, extensor digitorum, and genitalia, and the (L2–L4), which extensor hallucis muscles and carries sensory fingers provides motor supply to the adductors and gracilis from the lateral leg and dorsal foot and toes. The pos- muscles. The posterior division of the lumbar plexus terior division also gives rise to the superior (L4–S1) divides into the iliohypogastric and lateral femoral and inferior (L5–S2) gluteal nerves, which supply cutaneous nerves (L2–L3), which provide sensation the gluteus muscles. The , which con- to the lateral hip and thigh, and to the tains components of the common peroneal and tib- (L2–L3), which carries motor fibers to the psoas, il- ial nerves, is part of the posterior division; the pos- iacus, sartorius, and quadriceps muscles and pro- terior femoral cutaneous nerve (S1–S3), which vides sensory fibers to the skin of the anterior thigh follows the course of the sciatic nerve as a separate and medial upper leg. bundle, carries sensory fibers from skin of the pos- 3601_e18_p413-422 2/19/02 8:58 AM Page 417

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terior thigh from the buttock to the knee. The puden- sions and why in some circumstances the location of dal nerve (S2–S4), along with many smaller nerve the pelvic tumor seems unrelated to the principal site bundles, supplies the pelvic floor and genital muscu- of neurologic involvement. lature, as well as the external anal and urethral sphinc- ters. This nerve also carries afferent sensory fibers Clinical Presentation from the perineum (Truex and Carpenter, 1969). Tumors invading the lumbosacral plexus typically produce clinical syndromes based on their level of Pathophysiology involvement. Clinical patterns of plexus involvement Tumors commonly invade the lumbosacral plexus by include the upper plexus (L1–L4), the lumbosacral direct extension from pelvic primary and trunk (L4–L5), and the lower plexus (S1–S4). Plex- less frequently by secondary extension from metas- opathy is usually unilateral, although bilateral find- tases to regional pelvic lymph nodes, the sacrum or ings are present in 25% of patients. Patients typically iliac wings, or (Fig. 18–3). The present with leg pain, which is often followed weeks most commonly reported tumors producing lum- to months later by progressive leg numbness and bosacral plexopathy include carcinomas of the colon weakness. The pain is typically severe, constant, dull, and rectosigmoid, gynecologic malignancies, retro- and aching and may have sharp or cramping super- peritoneal sarcomas, and lymphomas (Jaeckle et al., imposed local, referred, or radicular components. 1985; Pettigrew et al., 1984). Plexopathy is part of Pain is often worse when the patient becomes supine; the original tumor presentation in approximately 15% usually the patient has difficulty finding a comfortable of patients. In general, bulky tumors within the pelvis position. Additional pain that worsens with movement compress and invade the plexus directly. On occa- or weight bearing generally implies nearby bony in- sion, tumor tracks along the connective tissue and vasion. Involvement of the iliopsoas muscle may force epineurium of the nerve trunks (Ebner et al., 1990). the patient to assume a position in bed with the hips This tendency to infiltrate along the nerve may explain and knees flexed, similar to that seen with meningeal why some patients with findings of diffuse plexopathy inflammation. The pain may worsen following a bowel do not have radiographically demonstrable mass le- movement or be exacerbated by a rigorous neuro-

Figure 18–3. Lumbosacral plexopathy. Computed tomography scan showing large left pelvic node metastases from melanoma that caused severe pain and weakness in L4–L5 distribution. 3601_e18_p413-422 2/19/02 8:58 AM Page 418

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logic examination. Pain is so common (98%) that its apex), as determined by clinical examination, mag- absence should raise a red flag regarding this diag- netic resonance imaging (MRI), and/or computed to- nosis. mography imaging (CT) (Thyagarajan et al., 1995). Symptomatic weakness and sensory complaints Radiation plexopathy is implicated if there is evidence eventually develop in 60% of patients. In a series of of radiation-induced changes in skin, bone or soft tis- 85 cancer patients with lumbosacral plexopathy and sues and if myokymic discharges are found on elec- radiographic or surgical evidence of tumor in the re- tromyography (EMG), which are unusual findings in gion of the plexus (Jaeckle et al., 1985), objective leg tumor plexopathy. weakness was identified in 86%, sensory loss in 73%, The syndromes of brachial and lumbosacral plex- focal reflex loss in 64%, and ipsilateral leg edema in opathy due to irradiation have been reasonably well 47% of patients. Patients typically had tenderness over described (Kori et al., 1981; Pierce et al., 1992; Pow- the sciatic notch, and straight leg raising tests often ell et al., 1990; Sheldon et al., 1987; Basso-Ricci et reproduced their pain. Clinical dysfunction of the al., 1980; Bagley et al., 1978; Harper et al., 1989; lower plexus is most common and is most commonly Killer and Hess, 1990; Mondrup et al., 1990; Thomas seen with colorectal tumors. A dysesthetic syndrome et al., 1985; Olsen et al., 1990; Ashenhurst et al., (“hot dry foot”) has been described in as many as 1977). The incidence was probably higher in patients one-third of patients (Dalmau et al., 1989) due to treated in the 1960s with telecobalt therapy. Recently, sympathetic plexus involvement within the pelvis. In- a long-term (34 years) follow-up study of 71 breast continence and impotence are typically absent unless cancer patients who received a calculated dose of 57 bilateral plexopathy is present. Gy in 16 to 17 fractions over 3 to 4 weeks to the ax- Tumors deep in the pelvis, in particular those ac- illa, supraclavicular area, and parasternal lymph companying cervical carcinomas and tumors of the nodes, reported that late-stage progressive plexopa- rectosigmoid region, present with numbness and thy was common. Eleven of the 12 patients alive at dysesthesias in the perianal area and perineum. These the time of follow-up had paralysis of the limb (Jo- patients may have a palpable rectal mass, decreased hansson et al., 2000). anal sphincter tone, and sensory loss of the perineum The frequency of radiation plexopathy in treated from involvement of the lower sacral plexus, located patients is approximately 1.8% to 4.9% (Pierce et al., anterior to the piriformis muscle. The sensory symp- 1992; Powell et al., 1990; Sheldon et al., 1987). Shel- toms often occur early and are followed later by lower don et al. (1987) reported this complication in 2% extremity pain and weakness. of patients with stage III breast cancer treated with 4.5 to 5 Gy to the breast and regional lymphatics at a median follow-up period of 65 months (5 years). DIFFERENTIAL DIAGNOSIS: In other series, the interval between administration PLEXOPATHY IN THE CANCER PATIENT of radiotherapy and the development of plexopathy ranged from 3 months to 14 years, with a median of 1.5 years, and was most frequent at tissue doses Radiation Plexopathy greater than 50 Gy (Kori et al., 1981; Killer and Hess, Because the timing of onset of tumor plexopathy fol- 1990). lowing the original cancer diagnosis overlaps with the Radiation plexopathy probably has a multifactor- typical time frame for radiation plexopathy, the clin- ial etiology. Cavanaugh (1968) studied the effects of ician is often confronted with the difficult task of dis- radiation and crush injury of rat sciatic nerve at doses tinguishing these two entities in previously treated pa- between 200 and 2000 R. At doses above 1000 R, tients. Complicating this issue, these conditions may there was failure of cellular proliferation and devel- coexist simultaneously in a given patient, which opment of pathologic changes in Schwann cells, en- may in part explain why patients whose tumor re- doneurial fibroblasts, and vascular and perineural sponds to treatment may not have clinical improve- cells. In another physiologic study, severe delayed ment. The single most valuable diagnostic clinical pa- damage of the anterior and posterior nerve roots was rameter suggestive of tumor plexopathy is the observed following 35 Gy administered to the lumbar demonstration of persistent or recurrent tumor in the region in rodents (Bradley et al., 1977). In humans, general region of the plexus (e.g., in the axilla or lung radiation plexopathy is presumably caused by tissue 3601_e18_p413-422 2/19/02 8:58 AM Page 419

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fibrosis with retraction of nerve trunks, direct toxic (Pierce et al., 1992). Many patients with radiation- effects on axons, and radiologic effects involving the induced plexopathy also have skin changes, includ- vasa nervorum, producing microinfarction of nerve ing telangiectasia, atrophy, and diffuse induration; ra- axons (Greenfield and Stark, 1948). diographs may show other associated radiation In the clinical setting, several points can help to changes, including typical changes in the apex of the distinguish radiation-induced from tumor-induced lung, radionecrosis of regional bony structures, and plexopathy (Table 18–1). Radiation plexopathy usu- pericardial fibrosis. ally presents with causalgic dysesthesias in the arm, The lumbosacral plexus is also subject to radia- often accompanied by lymphedema. In contrast, only tion-induced injury. The median onset of this com- a small percentage of patients with tumor plexopathy plication is approximately 5 years (range, 1 month to will present with dysesthesias, and lymphedema is less 31 years) (Thomas et al., 1985). Another series found frequent. In tumor plexopathy, the presenting feature an earlier onset of 12 months (range, 1 month to 156 is often severe unrelenting pain; in contrast, pain usu- months) (Ashenhurst et al., 1977). The incidence ap- ally develops late in the course of radiation plexopa- pears to be higher with larger doses of radiation, but thy and is less often the major symptom. These two has been reported at doses as low as 17 Gy. entities can sometimes be distinguished by the level The clinical features of radiation plexopathy overlap of plexus involvement: Radiation plexopathy usually with tumor plexopathy. Patients with radiation plex- affects the upper (77%) or entire (23%) plexus; in opathy usually present with weakness (60%), numb- tumor plexopathy, the lower plexus (75%) or the en- ness, or (50%) (Thomas et al., 1985). As tire plexus (25%) appears to be more frequently af- in radiation brachial plexopathy, pain at presentation is fected (Kori et al., 1981; Mondrup et al., 1990). How- also uncommon (10%) in patients with radiation lum- ever, recent studies have shown that the neurologic bosacral plexopathy and frequent (98%) in patients with level of plexus involvement can be more variable than recurrent tumor. Later in the course of lumbosacral noticed in these earlier reports (Boyaciyan et al., plexopathy due to radiation, pain develops in 50% of 1996). Sparing of the lower plexus from radiation patients. Weakness is often bilateral in radiation plex- damage afforded by intervening bony and soft tissues opathy in contrast to tumor plexopathy, in which more has been postulated as a reason for the more frequent than 75% of patients primarily have unilateral involve- occurrence of upper plexus involvement with radia- ment. The distribution of plexopathy is not as useful a tion, but seems questionable based on studies of tis- distinguishing point as it is in brachial plexopathy; both sue dosimetry and observations of associated ra- conditions most commonly affect the lower (L5–S1) dionecrosis of the clavicle or ribs in these patients portion. The presence of a rectal mass supports tumor

Table 18–1. Differential Diagnosis of Radiation Plexopathy Versus Recurrent Tumor Plexopathy Tumor Radiation Presentation Pain Paresthesias, weakness Pain Common, severe Occasional Edema Occasional Common Plexus involvement Brachial Usually lower plexus Upper or whole plexus Lumbrosacral Lower plexus, unilateral Commonly bilateral Horner’s syndrome Common Infrequent Local tissue necrosis Infrequent Common Rectal mass lumbosacral Common Unusual plexopathy (LSP) Myokymia (EMG) Unusual Common Nerve enhancement (MRI) Common Unusual 3601_e18_p413-422 2/19/02 8:58 AM Page 420

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recurrence; sphincteric dysfunction is slightly more anatomic detail and is usually a preferred procedure, common with radiation-induced plexopathy. Leg edema when available. MRI has been shown to be more sen- occurs with approximately equal frequency in the two sitive than CT in the identification of tumor plexopa- conditions. The progression of neurologic dysfunction thy (Taylor et al., 1997; Qayyum et al., 2000; Thya- is generally slower in radiation plexopathy than with tu- garajan et al., 1995). Diagnosis can be difficult if the mor recurrence. scan does not show a mass lesion. In these instances, appears to be helpful in distin- one must maintain a high clinical suspicion of tumor guishing between these two entities. Approximately recurrence and consider repeating the imaging pro- 60% of patients with radiation-induced plexopathy cedures at further neurologic progression. Although will exhibit myokymia, which is rarely seen in meta- CT or MRI scans may identify tumor recurrence, the static plexopathy (Roth et al., 1988). Neuroimaging radiographic appearance can be difficult to interpret. with CT (Moskovic et al., 1992) or with MRI can be Increased T2 intensity within nerve trunks with or of help in distinguishing tumor recurrence from ra- without enhancement has been identified in patients diation injury. Magnetic resonance imaging appears meeting clinical criteria for radiation plexopathy, to be more sensitive than CT in detecting tumor re- findings considered more typical for tumor plexopa- currence (Taylor et al., 1997). thy; and fibrotic masses may also mimic local tumor The treatment of radiation-induced plexopathy is recurrence (Wouter van Es et al., 1997). A careful symptomatic. Most patients have a slow but steady evaluation by an experienced radiologist may be help- progressive loss of motor function and require sup- ful, as detection of a pattern of T2 abnormalities and portive therapy. enhancement and an associated mass effect may pro- vide provisional bias toward one of these diagnoses. The presence of a local or regional tumor recur- Additional Causes of Plexopathy in rence, by clinical examination or imaging, supports the Cancer Patients diagnosis of tumor plexopathy. In one study, the ab- Plexopathy following chemotherapy appears to be as- sence of a palpable axillary mass was inversely diag- sociated primarily with regional intra-arterial ad- nostic as 95% of patients with CT evidence of brachial ministration (Kahn et al., 1989). Although rare, plex- plexus tumor have a palpable axillary mass (Moskovic opathy has been reported as a paraneoplastic disorder et al., 1992). In a recent study, positron emission to- and on occasion may be steroid responsive (Lachance mography (PET) was utilized to evaluate the brachial et al., 1991). When making a diagnosis, the physician plexopathy in 19 breast carcinoma patients with plex- must also consider conditions affecting the plexus opathy; 14 had abnormal 18-fluorodeoxyglucose uptake that occur in noncancer patients, including aortic within the involved plexus. However, the specificity and aneurysms (Chapman et al., 1964); diabetic amyotro- sensitivity of PET for tumor plexopathy have not been phy (Chokroverty et al., 1977), vasculitis, and other elucidated (Ahmad et al., 1999). rare conditions (Chad and Bradley, 1987). Idiopathic Electromyography can be useful in delineating the or postinfectious brachial can produce symp- distribution and extent of denervation. It occasionally toms very similar to those of metastatic plexopathy, al- reveals more extensive findings than would have been though the onset is usually more acute and often fol- predicted clinically. The main clinical usefulness ap- lows a history of viral or immunization. pears to be in distinguishing radiation plexopathy from Because patients with metastatic systemic cancer often neoplastic involvement, as stated above, and occasion- have more than one site of involvement, ally in supplementing the radiographic findings when the possibility of concomitant leptomeningeal or planning treatment fields. Electromyography in experi- epidural metastases must be considered, which can enced hands can be used to differentiate plexopathy have a similar clinical appearance. from other entities, such as neoplastic meningitis, from epidural tumor, and neuropathy.

DIAGNOSIS TREATMENT The clinical diagnosis of metastatic plexopathy is best confirmed by MRI or CT scanning of the appropriate Treatment of cancer-related plexopathy is largely pal- areas. Magnetic resonance imaging provides the best liative and symptom directed. Treatment generally in- 3601_e18_p413-422 2/19/02 8:58 AM Page 421

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volves radiation to the involved field and pain control a significant impact on preservation of quality of life measures. Consultation with pain management spe- in these patients. cialists is recommended. Studies have shown that pain is often poorly controlled in patients with plexopathy. Proper pain control often requires multimodality ap- REFERENCES proaches, including a clear understanding of the proper use of opiate , continuous infusion Ahmad A, Barrington S, Maisey M, Rubens RD. 1999. Use of pumps, local and regional blocks, sympathectomy, positron emission tomography in evaluation of brachial plex- opathy in breast cancer patients. Br J Cancer 79:478–482. rhizotomy, or other specialized procedures that are Ampil FL. 1986. Palliative irradiation of carcinomatous lum- generally outside the normal experience of radiation bosacral plexus neuropathy. Int J Radiation Oncol Biol Phys and medical oncologists. In appropriate settings, spe- 12:1681–1686. cific chemotherapy for the underlying neoplasm is Ashenhurst EM, Quartey GR, Starreveld A. 1977. Lumbo-sacral warranted, and tumor response may be associated radiculopathy induced by radiation. Can J Neurol Sci 4:259–263. with improvement of pain and other symptoms (par- Basso-Ricci S, della Costa C, Viganotti G, Ventafridda V, Zanolla ticularly in responsive tumors such as lymphomas). R. 1980. Report on 42 cases of postirradiation lesions of the Occasional relief of chronic pain has been achieved brachial plexus and their treatment. Tumori 66:117–122. with plexus dissection and neurolysis (Sundaresan Bagley FH, Walsh JW, Cady B, Salzman FA, Oberfield RA, and DiGiacinto, 1987). Dysesthesias and causalgia Pazianos AG. 1978. Carcinomatous versus radiation-in- duced brachial plexus neuropathy in breast cancer. Cancer are resistant to therapy, but may respond to transcu- 41:2154–2157. taneous nerve stimulation, tricyclic antidepressants, Boyaciyan A, Oge AE, Yazici J, Aslay I, Baslo A. 1996. Elec- anticonvulsants such as gabapentin, carbamazepine trophysiological findings in patients who received radia- or phenytoin, or regional nerve or sympathetic gan- tion therapy over the brachial plexus: a magnetic stimu- glion blocks. Often, opiate analgesics are required. lation study. Electroencephalogr Clin Neurophysiol 101:483–490. Lymphedema may be treated with compressive de- Bradley WG, Fewings JD, Cumming WJ, Harrison RM. 1977. vices and elevation. Delayed myeloradiculopathy produced by spinal X-irradia- Unfortunately, the reported results of treatment are tion in the rat. J Neurol Sci 31:63–82. largely disappointing. In brachial plexopathy, radia- Cavanaugh JB. 1968. Prior X-irradiation and the cellular re- tion therapy to the involved plexus relieved pain in sponse to nerve crush: duration of effect. Exp Neurol 22:253–258. only 46% of cases (Kori et al., 1981). Treatment of Chad DA, Bradley WG. 1987. Lumbosacral plexopathy. Semin tumor in the lumbosacral plexus produced improve- Neurol 7:97–107. ment in pain in only 15% of patients reassessed at 1 Chapman EM, Shaw RS, Kubik CS. 1964. Sciatic pain from ar- month from treatment; objective improvement in terioscleriotic aneurysm of pelvic arteries. N Engl J Med strength occurred in only 17% and objective reduc- 271:1410–1411. Chokroverty S, Reyes MG, Rubino FA, Tonaki H. 1977. The tion in tumor size in only 28% (Jaeckle et al., 1985). syndrome of diabetic amyotrophy. Ann Neurol 2:181–194. In another study of 28 patients with carcinomatous Dalmau J, Graus F, Marco M. 1989. “Hot and dry foot” as ini- lumbosacral plexus neuropathy, radiation produced tial manifestation of neoplastic lumbosacral plexopathy. improvement in 85% but only a 29% objective re- 39:871–872. sponse rate (Ampil, 1986). The best subjective/ob- Ebner I, Anderl H, Mikuz G, Frommhold H. 1990. [Plexus neu- ropathy: tumor infiltration or radiation damage]. ROFO jective treatment result was observed with a total dose Fortschr Geb Rontgenstr Neuen Bildgreb Verfahr 152:662– of at least 30 Gy. In most cases, the duration of re- 666. sponse has been brief, and the relatively short sur- Greenfield MM, Stark FM. 1948. Post-irradiation neuropathy. vival of patients with tumor plexopathy suggests that Am J Roentgen 60:617–619. its occurrence represents a late-stage complication of Harper CM Jr, Thomas JE, Cascino TL, Litchy WJ. 1989. 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