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The lumbosacral plexus may be invaded by local extension of intra-abdominal tumors (73%) or metastasis of
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neuropathies and concurrent IgA or IgG monoclonal gammopathy We test all patients with peripheral neuropathies for the presence of monoclonal gammopathies in the serum and urine Serum and urine protein electrophoresis (SPEP and UPEP) are useful screening tests but are not as sensitive as immunoelectrophoresis or immuno xation Therefore, we order serum and urine immunoelectrophoresis or immuno xation in any patient suspected of having a myeloproliferative disorder An aggressive workup for amyloidosis, multiple myeloma, osteosclerotic myeloma, plasmacytoma, Waldenstr m macroglobo ulinemia, lymphoma, leukemia, and cryoglobulinemia should be performed in any patient in whom a monoclonal gammopathy is identi ed67,69 72 We order a radiologic skeletal survey to assess for osteolytic or sclerotic lesions and hematology consultation to consider a bone marrow biopsy Although most patients with monoclonal gammopathies have no underlying (deemed monoclonal gammopathies of undetermined signi cance or MGUS), approximately 20% of MGUS patients subsequently develop lymphoma, leukemia, myeloma, or plasmacytoma67
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of patients with lymphoma73 The neuropathy can be purely sensory76 or motor but most commonly is sensorimotor73 Autonomic neuropathy may also be seen The pattern of involvement may be symmetric, asymmetric, or multifocal; the course may be acute,52,74 subacute,52,75 chronic progressive,73,75 or relapsing and remitting74,75
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CSF may reveal lymphocytic pleocytosis and elevated protein48,73 Motor and sensory NCS reveal reduced amplitudes with preserved conduction velocities suggestive of a generalized axonal sensorimotor neuropathy73 or demonstrate prolonged distal and F-wave latencies, slow conduction velocities, temporal dispersion, and conduction block,52 similar to those observed in acute in ammatory demyelinating polyneuropathy and chronic in ammatory demyelinating polyneuropathy (CIDP)
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Nerve biopsy may demonstrate endoneurial in ammatory cells in both the in ltrative and the presumed paraneoplastic neuropathies complicating lymphoma (Fig 17 3) A monoclonal population of cells would favor lymphomatous invasion73,74
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LYMPHOMA Clinical Features
Lymphoma may cause neuropathy by in ltration or direct compression of nerves,48 but the neuropathies can also be paraneoplastic in nature73 Both Hodgkin disease and non-Hodgkin lymphoma can cause sensorimotor polyneuropathies45,52,74,75 A prospective study reported clinical symptoms or signs of neuropathy in 8% and electrophysiologic evidence of neuropathy in 35%
The paraneoplastic neuropathy associated with lymphomas is presumably autoimmune in nature, but the exact antigen(s) and trigger for the immune attack are not known
Figure 17 3 Lymphoma Sural nerve biopsy demonstrates perivascular and endoneurial in ltration of lymphomatous cells on routine H&E (A) and immunoperoxidase stain using CD3 antibody (B)
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The neuropathy may respond to treatment of the underlying lymphoma or immunomodulating therapies48,52,76
Multiple myeloma usually presents in the fth to seventh decade of life with fatigue, bone pain, anemia, and hypercalcemia Clinical signs and symptoms of peripheral neuropathies develop in 3 13% of patients,66,71,77,78 while NCS demonstrate that as many as 40% of patients have a subclinical peripheral neuropathy78 The most common pattern is that of a distal, axonal, sensory, or sensorimotor polyneuropathy77,78 Less frequently, a chronic demyelinating polyneuropathy may develop77 Multiple myeloma can be complicated by amyloid polyneuropathy and should be considered in patients with painful paresthesias, loss of pinprick and temperature discrimination, and autonomic dysfunction (suggestive of a small ber neuropathy) and carpal tunnel syndrome Expanding plasmacytomas can compress cranial nerves and spinal roots as well
(eg, Bortezomib and thalidomide) commonly are associated with neuropathy A paraneoplastic effect is speculated in demyelinating neuropathies associated with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, skin changes (POEMS) syndrome (discussed next)
Unfortunately, the treatment of the underlying multiple myeloma does not usually affect the course of the neuropathy
Osteosclerotic myeloma is rare and is responsible for less than 3% of myelomas Symptomatic polyneuropathy develops in near 50% of patients with osteosclerotic myeloma and often is the presenting feature79 Systemic manifestations include hepatosplenomegaly, cutaneous pigmentation, hypertrichosis, edema, pericardial and pleural effusions, leukonychia, nger clubbing, gynecomastia, testicular atrophy with impotence in men, amenorrhea in women, diabetes mellitus, and hypothyroidism This complex constitutes the Crow Fukase or POEMS syndrome71,80 84 Importantly, not every patient displays all the features of POEMS syndrome Most individuals with POEMS syndrome have osteosclerotic myeloma, but the syndrome can also occur with Castleman disease (angiofollicular lymphadenopathy), extramedullary plasmacytomas, Waldenstrom macroglobulinemia, and solitary lytic plasmacytoma, and some patients have no identi able malignancy POEMS syndrome usually presents as symmetric tingling, numbness, and weakness that gradually progresses to involve proximal and distal arms and legs similar to CIDP The sensory modalities mediated by large bers are affected most, with decreased but relative sparing of pain and temperature sensation Muscle stretch re exes are reduced or absent The cranial nerves and respiratory muscles can be affected Papilledema is evident in 29 55% of patients,84 a nding that is uncommon in idiopathic CIDP Patients can also develop a myopathy secondary to associated hypothyroidism or rarely an in ammatory myopathy85
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