Case Report Paraneoplastic Brachial Plexopathy in a Patient With Hodgkin's Disease
DANIEL H. LACHANCE, M.D.,* Department ofNeurology; BRIAN P. O'NEILL, M.D., Department ofNeurology and Comprehensive Cancer Center; C. MICHEL HARPER, Jr., M.D., Department ofNeurology; PETER M. BANKS, M.D.,t Division ofPathology and Comprehensive Cancer Center; TERRENCE L. CASCINO, M.D., Department ofNeurology and Comprehensive Cancer Center
We describe a case of inflammatory brachial plexopathy that occurred in the context of a mild, diffuse sensorimotor peripheral neuropathy associated with Hodgkin's disease. Clinical, electrophysiologic, and pathologic studies helped distinguish this disorder from other causes ofbrachial plexopathy in patients with cancer. Treatment with corticosteroids seemed beneficial in this patient. We suggest that this may be another type of paraneoplastic condition associated with Hodgkin's disease.
Paraneoplastic neurologic syndromes are disorders that are associated with a systemic malignant process but are not caused by direct tumor invasion, infection, usual metabolic derangements, or antineoplastic therapy.' The cause of these paraneoplastic syndromes is unknown, but immunologic mechanisms are strongly suspected." The immune pathophysiologic features may be attributable to several factors that relate directly or indirectly to the presence of a neoplasm. Disorders of the brachial plexus are infrequently found in patients with Hodgkin's disease; tumor infiltration and radiation damage are the most common causes." In comparison, paraneoplastic conditions are only slightly more common in patients with Hodgkin's disease, but
a well-substantiated case of paraneoplastic brachial plexopathy has not been reported." Herein we describe a case of inflammatory brachial plexopathy in a patient with a mild, diffuse sensorimotor peripheral neuropathy associated with Hodgkin's disease.
REPORT OF CASE A 36-year-old man noted paresthesias of the radial aspect of the right forearm in March 1985. Biopsy of an enlarged left supraclavicular lymph node revealed nodular sclerosing Hodgkin's disease. Staging laparotomy revealed no evidence of disease, and he received 3,600 cGy of mantle irradiation for stage IIA disease. The paresthesias remitted. Two months later, however, he noted the gradual onset of mild asymmetric weakness and paresthesias of both upper extremities. During the next 2 months, his *Current address: Duke University Medical Center, Dursymptoms progressed to the point that he could ham, North Carolina. tCurrent address: University of Texas Health Science no longer lift his 9-kg child. Center, San Antonio, Texas. The patient was referred to our institution in November 1985. The initial neurologic examiAddress reprint requests to Dr. B. P. O'Neill, Department nation showed diffuse, asymmetric (right greater of Neurology, Mayo Clinic, Rochester, MN 55905. Mayo Clin Proc 66:97-101,1991
97
98
PARANEOPLASTIC BRACHIAL PLEXOPATHY
than left and proximal greater than distal) moderate arm weakness; upper limb areflexia; and an increase in all sensory thresholds in the upper extremities. In addition, the patient had a slight reduction in perception of pain on the toes and dorsal aspect of the feet. The results of nerve conduction studies are summarized in Table 1. Motor nerve conduction studies showed block of ulnar and musculocutaneous conduction across the brachial plexus bilaterally. Median and ulnar conduction velocities were reduced, in conjunction with mild dispersion compound motor action potential amplitudes, prolonged distal latencies, and prolonged or absent F responses. Sensory nerve action potentials of ulnar, median, and radial nerves were reduced in amplitude or absent bilaterally. The right peroneal conduction velocity was mildly reduced, and F waves were absent. Needle
Mayo CUn Proc, January 1991, Vol 66
examination revealed fibrillation potentials and high-amplitude, long-duration, poorly recruited motor unit potentials in muscles innervated by the upper and middle trunks of the brachial plexus bilaterally, in association with milder changes in motor unit potentials in distal muscles of the upper and lower extremities. No myokymic discharges were observed. The right tibial somatosensory evoked potential was normal. Median and radial somatosensory evoked potentials showed a substantial reduction in amplitude ofthe brachial plexus potential and normal central conduction times bilaterally. The findings on electrophysiologic studies indicated the presence of bilateral severe brachial plexopathies superimposed on a mild diffuse sensorimotor peripheral neuropathy. Computed tomography and magnetic resonance imaging scans of the chest (including the brachial plexus), com-
Table I.-Results of Nerve Conduction Studies in 36-Year-Old Man With Hodgkin's Disease and Brachial Plexopathy*
Nerve Motor Ulnar
Musculocutaneous Median Peroneal
Sensory Ulnar Median Radial Sural
Site Stimulation Recording] Wrist Elbow Upper arm Erb's point Upper arm Erb's point Wrist Elbow
ADM
Ankle Knee
EDB
Wrist Elbow Wrist Elbow Forearm Calf
Digit 5
Biceps APB
Digit 2 Wrist Ankle
Rightlleft measurements Amplitude CV§ Latency (m/s) (ms) (mV or IlV):j: 10.0/9.5 9.0/7.5 9.0/7.0 0.5/0.2 4.2/4.7 0.5/2.6 8.5/... 7.5/ ... 0.5/... 0.5/ ... 10.0/12.0 4.0/ ... 0/10.0 .. ./0 23.0/... 7.0/...
47/43 48/44 43/42 36/44 48/... 35/... 50/...
3.2/3.4
3.0/3.4 5.0/... 4.0/ ... 3.1/2.7 .. ./3.7
39/ ...
2.3/... 4.0/ ...
*F waves not shown. tADM = abductor digiti minimi manus; APB = abductor pollicis brevis; EDB = extensor digitorum brevis. :j:Millivoltsfor amplitude in motor nerve conduction studies and microvolts for amplitude in sensory nerve conduction studies. §CV = conduction velocity.
Mayo cue Proc, January 1991, Vol 66
puted tomography of the abdomen, contrastenhanced myelography, and cerebrospinal fluid analysis yielded normal findings. On surgical exploration, the right brachial plexus appeared normal, but a discrete firmness of the upper trunk was noted on palpation. Three fascicles were excised from this region for pathologic examination (Fig. 1 and 2). The density of the myelinated fibers was slightly decreased. In longitudinal sections, single or small groups of mononuclear cells were distributed between nerve bundles, and conspicuous subperineurial edema was noted. Paraffin section immunostaining demonstrated that most mononuclear cells reacted for UCHL1 antigen, indicative of a T-cell nature." In the teased fiber preparation, the length and thickness of internodal myelin varied considerably. Many regions were devoid of myelin, whereas others exhibited typical findings ofremyelination. No histologic evidence of Hodgkin's disease was found. The presumptive diagnosis of paraneoplastic inflammatory demyelinating plexopathy (and peripheral neuropathy) was made, a regimen of orally administered prednisone (80 mg/day) was prescribed, and the patient was dismissed. Within 1 month, the patient noted a vast improvement in strength. Nerve conduction studies showed improvement in the conduction block across the brachial plexus and higher amplitude sensory nerve action potentials. Needle examination disclosed fewer fibrillation potentials and widespread variation in amplitude of motor unit potentials, an indication of ongoing renervation. The prednisone regimen was gradually tapered. By August 1986, the patient was taking 50 mg of prednisone on alternate days. On examination, the strength and reflexes of the upper extremities were almost normaL Nerve conduction studies showed only mild slowing of conduction velocities and a slight reduction in the amplitude of sensory nerve action potentials in the upper extremities. Needle examination revealed long-duration, polyphasic, varied motor unit potentials in muscles of the upper extremities. During the subsequent year, the
PARANEOPLASTIC BRACHIAL PLEXOPATHY
99
Fig. 1. Longitudinal plane histologic section from biopsy specimen of right brachial plexus, showing dispersed mononuclear infiltrate and perineurial edema (top offield), (Hematoxylin-eosin; x160.)
prednisone dosage was tapered and then discontinued, and the patient's condition remained stable without treatment. Results of the latest neurologic examination, in April 1990, were normaL
DISCUSSION We believe that our patient's condition represents an example of paraneoplastic inflammatory brachial plexopathy associated with Hodgkin's disease. This condition had to be distinguished from direct invasion of the plexus by tumor," radiation-induced plexopathy,"-" and idiopathic acute inflammatory brachial plexopathy (Parsonage-Turner syndrome)." The absence of tumor in a biopsy specimen of the brachial plexus and progression of plexopathy despite radiographic evidence of tumor
100
Mayo Clin Proc, January 1991, Vol 66
PARANEOPLASTIC BRACHIAL PLEXOPATHY
Fig. 2. High magnification from same field as shown in Figure 1, demonstrating perivascular mononuclear infiltrate. By immunostaining, mononuclear cells were phenotyped as ofT-cell nature. (Hematoxylin-eosin; x640.)
remission after the radiotherapy excluded neoplastic plexopathy with reasonable certainty. The onset of neuropathic symptoms before irradiation of the plexus and the absence of myokymic discharges on electromyography'? similarly excluded the diagnosis ofradiation-induced plexopathy with reasonable certainty. In contrast to cases of a reversible brachial plexopathy after radiation therapy described by Salner and associates," our patient did not receive adjuvant chemotherapy and had evidence of neurologic disease outside the field of irradiation. The distinction between paraneoplastic brachial plexopathy and Parsonage-Turner syndrome may be a semantic one, inasmuch as both disorders may be mediated by similar immunologic mechanisms. Although pain is an early and prominent feature of most cases of Parsonage-
Turner syndrome," its absence is not of itself sufficient to separate these two disorders." In our patient, the collective picture of the absence of pain, the associated malignant lesion, and the evidence of a diffuse underlying peripheral neuropathy on nerve conduction studies and electromyography favors the diagnosis of a paraneoplastic plexopathy over acute idiopathic inflammatory plexopathy. Pezzimenti and colleagues-" described two patients with painful progressive brachial plexopathies in the setting of Hodgkin's disease. In both patients, symptoms began during the early stage of radiation therapy and eventually regressed. Although the possibility of inflammatory plexopathy was raised, each patient had adjacent adenopathy, and neither underwent surgical exploration of the plexus. Williams and co-workers" described 12 patients with brachial plexopathy in a series of 1,583 patients with Hodgkin's disease; however, all 12 patients had pathologic or radiographic evidence of neoplastic disease in the region of the brachial plexusmost likely, examples of neoplastic plexopathy. Paraneoplastic syndromes occur in an estimated 2.5% of patients with Hodgkin's disease." Paraneoplastic disorders of the peripheral nervous system that have previously been associated with Hodgkin's disease include subacute sensory neuropathy.!' subacute motor neuronopathy.!" and both acute and chronic inflammatory polyradiculoneuropathy.P-" Recognition of paraneoplastic neurologic syndromes is important because they may precede or herald the onset of a malignant process, or they may occur when the disease is quiescent, as a symptom of recurrence of cancer. The presence of such disorders should alert the physician to search carefully for the cancer and, if not found, to maintain close surveillance of the patient.
REFERENCES 1.
Henson RA, Urich H: The concept of paraneoplastic disorders. In Cancer and the Nervous System: The Neurological Manifestations of Systemic Malignant Disease. Edited by RA Henson, H Urich. Oxford, England, Blackwell Scientific Publications, 1982, pp 311-313
PARANEOPLASTIC BRACHIAL PLEXOPATHY
Mayo Clrn Proc, January 1991, Vol 66
2.
3.
4.
5.
6. 7. 8. 9.
Jaeckle KA, Graus F, Houghton A, Cardon-Cardo C, Nielsen SL, Posner JB: Autoimmune response of patients with paraneoplastic cerebellar degeneration to a Purkinje cell cytoplasmic protein antigen. Ann Neurol 18:592-600, 1985 Williams HM, Diamond HD, Craver LF, Parsons H: Neurological Complications of Lymphomas and Leukemias. Springfield, Illinois, Charles C Thomas, Publisher, 1959 Currie S, Henson RA, Morgan HG, Poole AJ: The incidence of the non-metastatic neurological syndromes of obscure origin in the reticuloses. Brain 93:629-640, 1970 Norton AJ, Ramsay AD, Smith SH, Beverley PCL, Isaacson PG: Monoclonal antibody (UCHL1) that recognises normal and neoplastic T cells in routinely fixed tissues. J Clin Pathol 39:399-405, 1986 Thomas JE, Colby MY Jr: Radiation-induced or metastatic brachial plexopathy? A diagnostic dilemma. JAMA 222:1392-1395,1972 Westling P, Svensson H, Hele P: Cervical plexus lesions following post-operative radiation therapy of mammary carcinoma. Arch Radiol 11:209-216, 1972 Cascino TL, Kori S, Krol G, Foley KM: CT of the brachial plexus in patients with cancer. Neurology 33:1553-1557,1983 Tsairis P, Dyck PJ, Mulder DW: Natural history of brachial plexus neuropathy. Arch Neurol 27:109117,1972
10. 11.
12. 13. 14. 15. 16.
17. 18.
101
Albers JW, Allen AA II, Bastron JA, Daube JR: Limb myokymia. Muscle Nerve 4:494-504,1981 Salner AL, Botnick LE, Herzog AG, Goldstein MA, Harris JR, Levene MB, Hellmann S: Reversible brachial plexopathy following primary radiation therapy for breast cancer. Cancer Treat Rep 65:797802, 1981 Weikers NJ, Mattson RH: Acute paralytic brachial neuritis: a clinical and electrodiagnostic study. Neurology 19:1153-1158, 1969 PezzimentiJF, Bruckner HW, DeContiRC: Paralytic brachial neuritis in Hodgkin's disease. Cancer 31:626629, 1973 Horwich MS, Cho L, Porro RS, Posner JB: Subacute sensory neuropathy: a remote effect of carcinoma. Ann Neurol 2:7-19, 1977 Schold SC, Cho E-S, Somasundaram M, Posner JB: Subacute motor neuronopathy: a remote effect of lymphoma. Ann Neurol 5:271-287,1979 Cameron DG, Howell DA, Hutchison JL: Acute peripheral neuropathy in Hodgkin's disease: report of a fatal case with histologic features of allergic neuritis. Neurology 8:575-577,1958 Julien J, Vital CI, Aupy G, Lagueny A, Darriet D, Brechenmacher C: Guillain-Barre syndrome and Hodgkin's disease. J Neurol Sci 45:23-27,1980 Klingon GH: The Guillain-Barre syndrome associated with cancer. Cancer 18:157-163, 1965
DANIEL H. LACHANCE, M.D.,* Department ofNeurology; BRIAN P. O'NEILL, M.D., Department ofNeurology and Comprehensive Cancer Center; C. MICHEL HARPER, Jr., M.D., Department ofNeurology; PETER M. BANKS, M.D.,t Division ofPathology and Comprehensive Cancer Center; TERRENCE L. CASCINO, M.D., Department ofNeurology and Comprehensive Cancer Center
We describe a case of inflammatory brachial plexopathy that occurred in the context of a mild, diffuse sensorimotor peripheral neuropathy associated with Hodgkin's disease. Clinical, electrophysiologic, and pathologic studies helped distinguish this disorder from other causes ofbrachial plexopathy in patients with cancer. Treatment with corticosteroids seemed beneficial in this patient. We suggest that this may be another type of paraneoplastic condition associated with Hodgkin's disease.
Paraneoplastic neurologic syndromes are disorders that are associated with a systemic malignant process but are not caused by direct tumor invasion, infection, usual metabolic derangements, or antineoplastic therapy.' The cause of these paraneoplastic syndromes is unknown, but immunologic mechanisms are strongly suspected." The immune pathophysiologic features may be attributable to several factors that relate directly or indirectly to the presence of a neoplasm. Disorders of the brachial plexus are infrequently found in patients with Hodgkin's disease; tumor infiltration and radiation damage are the most common causes." In comparison, paraneoplastic conditions are only slightly more common in patients with Hodgkin's disease, but
a well-substantiated case of paraneoplastic brachial plexopathy has not been reported." Herein we describe a case of inflammatory brachial plexopathy in a patient with a mild, diffuse sensorimotor peripheral neuropathy associated with Hodgkin's disease.
REPORT OF CASE A 36-year-old man noted paresthesias of the radial aspect of the right forearm in March 1985. Biopsy of an enlarged left supraclavicular lymph node revealed nodular sclerosing Hodgkin's disease. Staging laparotomy revealed no evidence of disease, and he received 3,600 cGy of mantle irradiation for stage IIA disease. The paresthesias remitted. Two months later, however, he noted the gradual onset of mild asymmetric weakness and paresthesias of both upper extremities. During the next 2 months, his *Current address: Duke University Medical Center, Dursymptoms progressed to the point that he could ham, North Carolina. tCurrent address: University of Texas Health Science no longer lift his 9-kg child. Center, San Antonio, Texas. The patient was referred to our institution in November 1985. The initial neurologic examiAddress reprint requests to Dr. B. P. O'Neill, Department nation showed diffuse, asymmetric (right greater of Neurology, Mayo Clinic, Rochester, MN 55905. Mayo Clin Proc 66:97-101,1991
97
98
PARANEOPLASTIC BRACHIAL PLEXOPATHY
than left and proximal greater than distal) moderate arm weakness; upper limb areflexia; and an increase in all sensory thresholds in the upper extremities. In addition, the patient had a slight reduction in perception of pain on the toes and dorsal aspect of the feet. The results of nerve conduction studies are summarized in Table 1. Motor nerve conduction studies showed block of ulnar and musculocutaneous conduction across the brachial plexus bilaterally. Median and ulnar conduction velocities were reduced, in conjunction with mild dispersion compound motor action potential amplitudes, prolonged distal latencies, and prolonged or absent F responses. Sensory nerve action potentials of ulnar, median, and radial nerves were reduced in amplitude or absent bilaterally. The right peroneal conduction velocity was mildly reduced, and F waves were absent. Needle
Mayo CUn Proc, January 1991, Vol 66
examination revealed fibrillation potentials and high-amplitude, long-duration, poorly recruited motor unit potentials in muscles innervated by the upper and middle trunks of the brachial plexus bilaterally, in association with milder changes in motor unit potentials in distal muscles of the upper and lower extremities. No myokymic discharges were observed. The right tibial somatosensory evoked potential was normal. Median and radial somatosensory evoked potentials showed a substantial reduction in amplitude ofthe brachial plexus potential and normal central conduction times bilaterally. The findings on electrophysiologic studies indicated the presence of bilateral severe brachial plexopathies superimposed on a mild diffuse sensorimotor peripheral neuropathy. Computed tomography and magnetic resonance imaging scans of the chest (including the brachial plexus), com-
Table I.-Results of Nerve Conduction Studies in 36-Year-Old Man With Hodgkin's Disease and Brachial Plexopathy*
Nerve Motor Ulnar
Musculocutaneous Median Peroneal
Sensory Ulnar Median Radial Sural
Site Stimulation Recording] Wrist Elbow Upper arm Erb's point Upper arm Erb's point Wrist Elbow
ADM
Ankle Knee
EDB
Wrist Elbow Wrist Elbow Forearm Calf
Digit 5
Biceps APB
Digit 2 Wrist Ankle
Rightlleft measurements Amplitude CV§ Latency (m/s) (ms) (mV or IlV):j: 10.0/9.5 9.0/7.5 9.0/7.0 0.5/0.2 4.2/4.7 0.5/2.6 8.5/... 7.5/ ... 0.5/... 0.5/ ... 10.0/12.0 4.0/ ... 0/10.0 .. ./0 23.0/... 7.0/...
47/43 48/44 43/42 36/44 48/... 35/... 50/...
3.2/3.4
3.0/3.4 5.0/... 4.0/ ... 3.1/2.7 .. ./3.7
39/ ...
2.3/... 4.0/ ...
*F waves not shown. tADM = abductor digiti minimi manus; APB = abductor pollicis brevis; EDB = extensor digitorum brevis. :j:Millivoltsfor amplitude in motor nerve conduction studies and microvolts for amplitude in sensory nerve conduction studies. §CV = conduction velocity.
Mayo cue Proc, January 1991, Vol 66
puted tomography of the abdomen, contrastenhanced myelography, and cerebrospinal fluid analysis yielded normal findings. On surgical exploration, the right brachial plexus appeared normal, but a discrete firmness of the upper trunk was noted on palpation. Three fascicles were excised from this region for pathologic examination (Fig. 1 and 2). The density of the myelinated fibers was slightly decreased. In longitudinal sections, single or small groups of mononuclear cells were distributed between nerve bundles, and conspicuous subperineurial edema was noted. Paraffin section immunostaining demonstrated that most mononuclear cells reacted for UCHL1 antigen, indicative of a T-cell nature." In the teased fiber preparation, the length and thickness of internodal myelin varied considerably. Many regions were devoid of myelin, whereas others exhibited typical findings ofremyelination. No histologic evidence of Hodgkin's disease was found. The presumptive diagnosis of paraneoplastic inflammatory demyelinating plexopathy (and peripheral neuropathy) was made, a regimen of orally administered prednisone (80 mg/day) was prescribed, and the patient was dismissed. Within 1 month, the patient noted a vast improvement in strength. Nerve conduction studies showed improvement in the conduction block across the brachial plexus and higher amplitude sensory nerve action potentials. Needle examination disclosed fewer fibrillation potentials and widespread variation in amplitude of motor unit potentials, an indication of ongoing renervation. The prednisone regimen was gradually tapered. By August 1986, the patient was taking 50 mg of prednisone on alternate days. On examination, the strength and reflexes of the upper extremities were almost normaL Nerve conduction studies showed only mild slowing of conduction velocities and a slight reduction in the amplitude of sensory nerve action potentials in the upper extremities. Needle examination revealed long-duration, polyphasic, varied motor unit potentials in muscles of the upper extremities. During the subsequent year, the
PARANEOPLASTIC BRACHIAL PLEXOPATHY
99
Fig. 1. Longitudinal plane histologic section from biopsy specimen of right brachial plexus, showing dispersed mononuclear infiltrate and perineurial edema (top offield), (Hematoxylin-eosin; x160.)
prednisone dosage was tapered and then discontinued, and the patient's condition remained stable without treatment. Results of the latest neurologic examination, in April 1990, were normaL
DISCUSSION We believe that our patient's condition represents an example of paraneoplastic inflammatory brachial plexopathy associated with Hodgkin's disease. This condition had to be distinguished from direct invasion of the plexus by tumor," radiation-induced plexopathy,"-" and idiopathic acute inflammatory brachial plexopathy (Parsonage-Turner syndrome)." The absence of tumor in a biopsy specimen of the brachial plexus and progression of plexopathy despite radiographic evidence of tumor
100
Mayo Clin Proc, January 1991, Vol 66
PARANEOPLASTIC BRACHIAL PLEXOPATHY
Fig. 2. High magnification from same field as shown in Figure 1, demonstrating perivascular mononuclear infiltrate. By immunostaining, mononuclear cells were phenotyped as ofT-cell nature. (Hematoxylin-eosin; x640.)
remission after the radiotherapy excluded neoplastic plexopathy with reasonable certainty. The onset of neuropathic symptoms before irradiation of the plexus and the absence of myokymic discharges on electromyography'? similarly excluded the diagnosis ofradiation-induced plexopathy with reasonable certainty. In contrast to cases of a reversible brachial plexopathy after radiation therapy described by Salner and associates," our patient did not receive adjuvant chemotherapy and had evidence of neurologic disease outside the field of irradiation. The distinction between paraneoplastic brachial plexopathy and Parsonage-Turner syndrome may be a semantic one, inasmuch as both disorders may be mediated by similar immunologic mechanisms. Although pain is an early and prominent feature of most cases of Parsonage-
Turner syndrome," its absence is not of itself sufficient to separate these two disorders." In our patient, the collective picture of the absence of pain, the associated malignant lesion, and the evidence of a diffuse underlying peripheral neuropathy on nerve conduction studies and electromyography favors the diagnosis of a paraneoplastic plexopathy over acute idiopathic inflammatory plexopathy. Pezzimenti and colleagues-" described two patients with painful progressive brachial plexopathies in the setting of Hodgkin's disease. In both patients, symptoms began during the early stage of radiation therapy and eventually regressed. Although the possibility of inflammatory plexopathy was raised, each patient had adjacent adenopathy, and neither underwent surgical exploration of the plexus. Williams and co-workers" described 12 patients with brachial plexopathy in a series of 1,583 patients with Hodgkin's disease; however, all 12 patients had pathologic or radiographic evidence of neoplastic disease in the region of the brachial plexusmost likely, examples of neoplastic plexopathy. Paraneoplastic syndromes occur in an estimated 2.5% of patients with Hodgkin's disease." Paraneoplastic disorders of the peripheral nervous system that have previously been associated with Hodgkin's disease include subacute sensory neuropathy.!' subacute motor neuronopathy.!" and both acute and chronic inflammatory polyradiculoneuropathy.P-" Recognition of paraneoplastic neurologic syndromes is important because they may precede or herald the onset of a malignant process, or they may occur when the disease is quiescent, as a symptom of recurrence of cancer. The presence of such disorders should alert the physician to search carefully for the cancer and, if not found, to maintain close surveillance of the patient.
REFERENCES 1.
Henson RA, Urich H: The concept of paraneoplastic disorders. In Cancer and the Nervous System: The Neurological Manifestations of Systemic Malignant Disease. Edited by RA Henson, H Urich. Oxford, England, Blackwell Scientific Publications, 1982, pp 311-313
PARANEOPLASTIC BRACHIAL PLEXOPATHY
Mayo Clrn Proc, January 1991, Vol 66
2.
3.
4.
5.
6. 7. 8. 9.
Jaeckle KA, Graus F, Houghton A, Cardon-Cardo C, Nielsen SL, Posner JB: Autoimmune response of patients with paraneoplastic cerebellar degeneration to a Purkinje cell cytoplasmic protein antigen. Ann Neurol 18:592-600, 1985 Williams HM, Diamond HD, Craver LF, Parsons H: Neurological Complications of Lymphomas and Leukemias. Springfield, Illinois, Charles C Thomas, Publisher, 1959 Currie S, Henson RA, Morgan HG, Poole AJ: The incidence of the non-metastatic neurological syndromes of obscure origin in the reticuloses. Brain 93:629-640, 1970 Norton AJ, Ramsay AD, Smith SH, Beverley PCL, Isaacson PG: Monoclonal antibody (UCHL1) that recognises normal and neoplastic T cells in routinely fixed tissues. J Clin Pathol 39:399-405, 1986 Thomas JE, Colby MY Jr: Radiation-induced or metastatic brachial plexopathy? A diagnostic dilemma. JAMA 222:1392-1395,1972 Westling P, Svensson H, Hele P: Cervical plexus lesions following post-operative radiation therapy of mammary carcinoma. Arch Radiol 11:209-216, 1972 Cascino TL, Kori S, Krol G, Foley KM: CT of the brachial plexus in patients with cancer. Neurology 33:1553-1557,1983 Tsairis P, Dyck PJ, Mulder DW: Natural history of brachial plexus neuropathy. Arch Neurol 27:109117,1972
10. 11.
12. 13. 14. 15. 16.
17. 18.
101
Albers JW, Allen AA II, Bastron JA, Daube JR: Limb myokymia. Muscle Nerve 4:494-504,1981 Salner AL, Botnick LE, Herzog AG, Goldstein MA, Harris JR, Levene MB, Hellmann S: Reversible brachial plexopathy following primary radiation therapy for breast cancer. Cancer Treat Rep 65:797802, 1981 Weikers NJ, Mattson RH: Acute paralytic brachial neuritis: a clinical and electrodiagnostic study. Neurology 19:1153-1158, 1969 PezzimentiJF, Bruckner HW, DeContiRC: Paralytic brachial neuritis in Hodgkin's disease. Cancer 31:626629, 1973 Horwich MS, Cho L, Porro RS, Posner JB: Subacute sensory neuropathy: a remote effect of carcinoma. Ann Neurol 2:7-19, 1977 Schold SC, Cho E-S, Somasundaram M, Posner JB: Subacute motor neuronopathy: a remote effect of lymphoma. Ann Neurol 5:271-287,1979 Cameron DG, Howell DA, Hutchison JL: Acute peripheral neuropathy in Hodgkin's disease: report of a fatal case with histologic features of allergic neuritis. Neurology 8:575-577,1958 Julien J, Vital CI, Aupy G, Lagueny A, Darriet D, Brechenmacher C: Guillain-Barre syndrome and Hodgkin's disease. J Neurol Sci 45:23-27,1980 Klingon GH: The Guillain-Barre syndrome associated with cancer. Cancer 18:157-163, 1965
