ABSTRACT
INTRODUCTION Multiple myeloma is a neoplastic disease involving proliferation of a single clone of plasma cells that produce a monoclonal immunoglobulin. It comprises 1% of all neoplasms and approximately 10% of all hematologic malignancies, and has an annual incidence rate of approximately 5 to 10 per 100,000 population (1-4). Although the first reports of this disease appeared in the literature in the 1840s, it was not until the 1920s that neurological complications were described (1,2,4-6). Multiple possible etiologies exist to account for the neurological symptoms and signs common to multiple myeloma patients; no symptoms or signs are exclusive to one etiology. Both the central and peripheral nervous systems can be affected. Mechanisms of neurological dysfunction include direct infiltration of tumor cells, such as in spinal cord compression and leptomeningeal myelomatosis (LMM), dysfunction from the metabolic derangements associated with multiple myeloma, and damage or dysfunction due to an immunological response, such as in some forms of myeloma-associated peripheral neuropathy. Osteosclerotic myeloma and myeloma associated with amyloidosis are unique entities also associated with neurological complications.
