The neuropathies of Waldenström's Macroglobulinemia (WM) and IgM-MGUS

Christopher Jon Klein, Joon Shik Moon, Michelle M Mauermann, Steven R. Zeldenrust, Yanhong Wu, Angela Dispenzieri, Peter J Dyck

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Background: Neuropathy is common in Waldenström's macroglobulinemia (WM, an IgM-associated lymphoplasmacytic lymphoma) and in IgM-monoclonal gammopathy of undetermined significance (IgM-MGUS). Paraneoplastic or paraimmune mechanisms are thought to be involved in the pathogenesis of these neuropathies. Attempts at distinguishing WM and IgM-MGUS neuropathies are lacking especially among bone marrow (BM) confirmed patients. Methods: Retrospective analyses were performed on BM confirmed WM (N=30) and IgM-MGUS (N=73) neuropathy patients with neurologic assessments and hematologic features. Results: The presence of anemia and quantity of IgM monoclonal protein were significantly greater in WM. Based on multiple neurologic assessments differences were not found for: 1) length of time from neurologic symptom onset to evaluation; 2) chief complaint of painless loss of feeling in the feet, Romberg's sign and tremor; and 3) clinical motor, sensory and reflex abnormalities. Autonomic testing was normal in both diseases. Using nerve conduction (NCS) criteria for demyelination, 62% of IgM-MGUS and 27% of WM met this criteria (p=0.013). IgM MGUS patients had greater terminal conduction slowing by ulnar residual latency calculation (<0.01). The degree of axonal loss as measured by summated compound muscle action potentials and available nerve biopsy was not significantly different between diseases. Conclusion: Although WM and IgM-MGUS must be distinguished for hematologic prognosis and treatment, clinical neuropathy presentations of WM and IgM-MGUS are similar and likely related to comparable axonal loss in both conditions. Despite these similarities, evidence of demyelination was found by electrophysiologic studies much more commonly in IgM-MGUS. This difference may reflect varied immune mechanism(s) in the two disorders.

Original languageEnglish (US)
Pages (from-to)289-295
Number of pages7
JournalCanadian Journal of Neurological Sciences
Volume38
Issue number2
StatePublished - Mar 1 2011

Fingerprint

Monoclonal Gammopathy of Undetermined Significance
Waldenstrom Macroglobulinemia
Immunoglobulin M
Demyelinating Diseases
Nervous System
Bone Marrow
Neural Conduction
Tremor
Neurologic Manifestations
Action Potentials
Reflex
Foot
Anemia
Lymphoma
Emotions

ASJC Scopus subject areas

  • Clinical Neurology
  • Neurology

Cite this

The neuropathies of Waldenström's Macroglobulinemia (WM) and IgM-MGUS. / Klein, Christopher Jon; Moon, Joon Shik; Mauermann, Michelle M; Zeldenrust, Steven R.; Wu, Yanhong; Dispenzieri, Angela; Dyck, Peter J.

In: Canadian Journal of Neurological Sciences, Vol. 38, No. 2, 01.03.2011, p. 289-295.

Research output: Contribution to journalArticle

@article{4e28593b440e4f2fa0b11fdf5e34a7bc,
title = "The neuropathies of Waldenstr{\"o}m's Macroglobulinemia (WM) and IgM-MGUS",
abstract = "Background: Neuropathy is common in Waldenstr{\"o}m's macroglobulinemia (WM, an IgM-associated lymphoplasmacytic lymphoma) and in IgM-monoclonal gammopathy of undetermined significance (IgM-MGUS). Paraneoplastic or paraimmune mechanisms are thought to be involved in the pathogenesis of these neuropathies. Attempts at distinguishing WM and IgM-MGUS neuropathies are lacking especially among bone marrow (BM) confirmed patients. Methods: Retrospective analyses were performed on BM confirmed WM (N=30) and IgM-MGUS (N=73) neuropathy patients with neurologic assessments and hematologic features. Results: The presence of anemia and quantity of IgM monoclonal protein were significantly greater in WM. Based on multiple neurologic assessments differences were not found for: 1) length of time from neurologic symptom onset to evaluation; 2) chief complaint of painless loss of feeling in the feet, Romberg's sign and tremor; and 3) clinical motor, sensory and reflex abnormalities. Autonomic testing was normal in both diseases. Using nerve conduction (NCS) criteria for demyelination, 62{\%} of IgM-MGUS and 27{\%} of WM met this criteria (p=0.013). IgM MGUS patients had greater terminal conduction slowing by ulnar residual latency calculation (<0.01). The degree of axonal loss as measured by summated compound muscle action potentials and available nerve biopsy was not significantly different between diseases. Conclusion: Although WM and IgM-MGUS must be distinguished for hematologic prognosis and treatment, clinical neuropathy presentations of WM and IgM-MGUS are similar and likely related to comparable axonal loss in both conditions. Despite these similarities, evidence of demyelination was found by electrophysiologic studies much more commonly in IgM-MGUS. This difference may reflect varied immune mechanism(s) in the two disorders.",
author = "Klein, {Christopher Jon} and Moon, {Joon Shik} and Mauermann, {Michelle M} and Zeldenrust, {Steven R.} and Yanhong Wu and Angela Dispenzieri and Dyck, {Peter J}",
year = "2011",
month = "3",
day = "1",
language = "English (US)",
volume = "38",
pages = "289--295",
journal = "Canadian Journal of Neurological Sciences",
issn = "0317-1671",
publisher = "Canadian Journal of Neurological Sciences",
number = "2",

}

TY - JOUR

T1 - The neuropathies of Waldenström's Macroglobulinemia (WM) and IgM-MGUS

AU - Klein, Christopher Jon

AU - Moon, Joon Shik

AU - Mauermann, Michelle M

AU - Zeldenrust, Steven R.

AU - Wu, Yanhong

AU - Dispenzieri, Angela

AU - Dyck, Peter J

PY - 2011/3/1

Y1 - 2011/3/1

N2 - Background: Neuropathy is common in Waldenström's macroglobulinemia (WM, an IgM-associated lymphoplasmacytic lymphoma) and in IgM-monoclonal gammopathy of undetermined significance (IgM-MGUS). Paraneoplastic or paraimmune mechanisms are thought to be involved in the pathogenesis of these neuropathies. Attempts at distinguishing WM and IgM-MGUS neuropathies are lacking especially among bone marrow (BM) confirmed patients. Methods: Retrospective analyses were performed on BM confirmed WM (N=30) and IgM-MGUS (N=73) neuropathy patients with neurologic assessments and hematologic features. Results: The presence of anemia and quantity of IgM monoclonal protein were significantly greater in WM. Based on multiple neurologic assessments differences were not found for: 1) length of time from neurologic symptom onset to evaluation; 2) chief complaint of painless loss of feeling in the feet, Romberg's sign and tremor; and 3) clinical motor, sensory and reflex abnormalities. Autonomic testing was normal in both diseases. Using nerve conduction (NCS) criteria for demyelination, 62% of IgM-MGUS and 27% of WM met this criteria (p=0.013). IgM MGUS patients had greater terminal conduction slowing by ulnar residual latency calculation (<0.01). The degree of axonal loss as measured by summated compound muscle action potentials and available nerve biopsy was not significantly different between diseases. Conclusion: Although WM and IgM-MGUS must be distinguished for hematologic prognosis and treatment, clinical neuropathy presentations of WM and IgM-MGUS are similar and likely related to comparable axonal loss in both conditions. Despite these similarities, evidence of demyelination was found by electrophysiologic studies much more commonly in IgM-MGUS. This difference may reflect varied immune mechanism(s) in the two disorders.

AB - Background: Neuropathy is common in Waldenström's macroglobulinemia (WM, an IgM-associated lymphoplasmacytic lymphoma) and in IgM-monoclonal gammopathy of undetermined significance (IgM-MGUS). Paraneoplastic or paraimmune mechanisms are thought to be involved in the pathogenesis of these neuropathies. Attempts at distinguishing WM and IgM-MGUS neuropathies are lacking especially among bone marrow (BM) confirmed patients. Methods: Retrospective analyses were performed on BM confirmed WM (N=30) and IgM-MGUS (N=73) neuropathy patients with neurologic assessments and hematologic features. Results: The presence of anemia and quantity of IgM monoclonal protein were significantly greater in WM. Based on multiple neurologic assessments differences were not found for: 1) length of time from neurologic symptom onset to evaluation; 2) chief complaint of painless loss of feeling in the feet, Romberg's sign and tremor; and 3) clinical motor, sensory and reflex abnormalities. Autonomic testing was normal in both diseases. Using nerve conduction (NCS) criteria for demyelination, 62% of IgM-MGUS and 27% of WM met this criteria (p=0.013). IgM MGUS patients had greater terminal conduction slowing by ulnar residual latency calculation (<0.01). The degree of axonal loss as measured by summated compound muscle action potentials and available nerve biopsy was not significantly different between diseases. Conclusion: Although WM and IgM-MGUS must be distinguished for hematologic prognosis and treatment, clinical neuropathy presentations of WM and IgM-MGUS are similar and likely related to comparable axonal loss in both conditions. Despite these similarities, evidence of demyelination was found by electrophysiologic studies much more commonly in IgM-MGUS. This difference may reflect varied immune mechanism(s) in the two disorders.

UR - http://www.scopus.com/inward/record.url?scp=79951745066&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79951745066&partnerID=8YFLogxK

M3 - Article

VL - 38

SP - 289

EP - 295

JO - Canadian Journal of Neurological Sciences

JF - Canadian Journal of Neurological Sciences

SN - 0317-1671

IS - 2

ER -