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the rst, evolving insidiously over many years or decades Constituting this second group are mainly the heredodegenerative diseases of the peripheral nervous system

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Polyneuropathy Associated with Paraproteinemia The occurrence of a chronic sensorimotor polyneuropathy in association with an abnormality of serum immunoglobulins is recognized with increasing frequency but its boundaries are still not well established as will be apparent in the following discussion The excess blood protein, called a paraprotein, or an M-spike is usually in the form of a monoclonal immunoglobulin It may be an isolated abnormality or a by-product of a plasma cell malignancy, speci cally multiple myeloma, plasmacytoma, or Waldenstrom macroglobulinemia Several lines of evidence suggest that a pathogenetically active antibody against components of myelin or axon is present in at least some of these diseases Special forms of neuropathy are also associated with amyloidosis Both the acquired and genetic forms of amyloidosis are discussed further on Monoclonal Gammopathy of Undetermined Signi cance (MGUS, Benign Monoclonal Gammopathy) The association of a nonneoplastic IgM monoclonal protein and a neuropathy was rst described by Forssman and colleagues and was treated as coincidental until Kahn established a compelling statistical association between them A more direct relationship was established by the nding of antiperipheral nerve antibodies in some patients who had such a protein in their blood This important category of polyneuropathy is associated with a nonneoplastic monoclonal or polyclonal excess of immunoglobulin (IgG, IgM, or IgA, rarely others; see reviews of Kyle and Dyck and of Thomas and Willison) These cases are far more common than those with malignant plasma cell disorders In our experience, monoclonal proteins underlie the largest group of otherwise unexplained neuropathies in adults The polyneuropathy associated with monoclonal gammopathy affects mainly, but not exclusively, males in the sixth and seventh decades of life The onset is insidious over weeks or months with numbness and paresthesias of the feet and then of the hands, followed by a relatively symmetrical weakness and slight wasting of these muscles over a year or so In some patients sensory signs predominate The tendon re exes, eventually lost or diminished, may be preserved in the early phases of the illness The course is usually slowly progressive, sometimes static after a year or so and rarely remitting and relapsing The CSF typically shows an elevation of the protein in the range of 50 to 100 mg/ dL and this is not due to passive diffusion of the excess paraprotein into the CSF The majority of cases of polyneuropathy with monoclonal gammopathy have a demyelinating or mixed axonal-demyelinating pattern in the EMG, but once the illness is well established most will have predominantly axonal features With the exception of somewhat less sensory loss and preserved or reduced tendon re exes (the latter in some axonal cases) we have been unable to distinguish the axonal and demyelinating groups on clinical grounds or by their response to therapy (Gorson, Ropper, et al) Sural nerve biopsies show a loss of myelinated bers of all sizes; unmyelinated bers are mostly spared; hypertrophic changes, re ecting cycles of demyelination and remyelination with brosis are present in about half the cases according to Smith et al They found the monoclonal IgM antibody bound to surviving myelin sheaths,.

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assigned and one data provider Start by choosing the correct BI pattern Small Web Template with Chart Web Item and 1 DP Please refer to Figure 2-1 for this initial screen Like the template presented in the preceding section, this template has only two steps to complete In fact, the first step has the same options as the previous template, as shown in the following illustration The Title Settings and General Template Settings work the same in this template as they do in the previous template, as described in Table 2-1