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Journal of Clinical Oncology, Vol 23, No 1 (January 1), 2005: pp. 233-235 © 2005 American Society of Clinical Oncology. DOI: 10.1200/JCO.2005.01.103
Unusual Cases in Multiple Myeloma and a Dramatic Response in Metastatic Lung CancerCASE 3. Intracranial Plasmacytoma With Cranial Nerve Neuropathy in Multiple MyelomaDepartment of Internal Medicine, Hospital Ramó n y Cajal, Madrid, Spain
Department of Neuroradiology, Hospital Ramó n y Cajal, Madrid, Spain
Department of Pathology, Hospital Ramó n y Cajal, Madrid, Spain
A 54-year-old man complained of intense lower back lasting for 6 months. In the 2 weeks preceding admission, he developed diplopia. Physical examination revealed a large mass in the vertex of the skull and an incomplete palsy of right III and IV cranial nerves. Laboratory tests revealed anemia (hemoglobin 11 g/dL), an erythrocyte sedimentation rate of 127, urea 66 mg/dL, serum calcium 9.4 mg/dL, and a monoclonal immunoglobulin (Ig) G-
The most common neurologic complications of MM are spinal cord compression due to epidural plasmacytomas or vertebral fractures and peripheral polyneuropathy due to the presence of antibodies directed against myelin structures or due to amyloid deposits. However, neurologic symptoms due to plasmacytomas located either in the base of the skull or at intracranial locations are extremely rare. In a MEDLINE search between 1995 and 2003, we found less than 30 cases in the English, French, and Spanish literature, and a few more cases in the Japanese literature that were not available to us. Two series referred to eight and nine patients, respectively, with intracranial plasmacytomas who had had surgery,1,2 and the rest of the publications referred only to isolated cases.3-8 There have been published cases of the involvement of almost all cranial nerves (III to XII), as well as different syndromes with involvement of different cranial nerve groups, such as Collet-Sicard syndrome affecting the IX, X, XI, and XII cranial nerves,6 lateral-wall cavernous sinus involvement affecting the V and VI cranial nerves (and occasionally also III and IV),7 and other combinations. The cause of the neuropathy is the direct compression of nerves or nerve groups either in their intracranial course, especially when there is involvement of the body of the sphenoid or the apex of the petrous bone, or at the cranial outlets in the base of the skull. Computed tomography scan or MRI show destructive masses involving osseous structures (sella turcica, clival bone, petrous bone, occipital foramen). Plasmacytomas located at the base of the skull usually occur in the context of pre-existing MM. If not, MM tends to develop rapidly.1,2 Both circumstances therefore carry a worse prognosis. In most of these plasmacytomas, plasma cells express the neural cell adhesion molecule NCAM/CD56,2 which is also associated with the occurrence of lytic bone lesions.9 In our case study, we have no histologic or cytologic data of the plasmacytoma tissue, but plasma cells in the bone marrow expressed CD56. On the other hand, solitary plasmacytomas affecting calvarium do not usually progress to MM. In most published cases, the diagnosis was made after finding criteria for MM in bone marrow, or when the masses appeared in the context of a previously diagnosed MM. In some other cases, mostly described by neurosurgical departments, the diagnosis was obtained after surgical biopsy or surgery of an intracranial mass or at postmortem examination.6 Occasionally, the diagnosis was made after finding plasma-cell infiltration of CSF fluid.7 When plasmacytomas appear in the context of MM, as occurred in our case, a histologic diagnosis of these lesions is not needed. The reduction of the intracranial masses (as in our case) along with that occurring in other locations after treatment for MM, further supports the diagnosis. Authors' Disclosures of Potential Conflicts of Interest The authors indicated no potential conflicts of interest.
REFERENCES 1. Bindal AK, Bindal RK, van Loveren H, et al: Management of intracranial plasmacytoma. J Neurosurg 83:218-221, 1995[Medline] 2. Schwartz TH, Rhiew R, Isaacson SR, et al: Association between intracranial plasmacytoma and multiple myeloma: Clinicopathological outcome study. Neurosurgery 49:1039-1045, 2001[CrossRef][Medline] 3. Giraldo MP, Sánchez Jacob M, Rubio Félix D, et al: Myeloma without a monoclonal component with tumor and neurologic manifestations. Sangre (Barc) 32:517-518, 1987 4. Delgado Lamas JL, Vazquez Villegas V, Galvan Villegas F: Multiple myeloma and destruction of the sella turcica. Sangre (Barc) 35:237-238, 1990 5. Forrett-Kaminsky MC, Scherer C, Platini C, et al: Isolated paralysis of the great hypoglossal nerve disclosing multiple myeloma. Rev Neurol (Paris) 147:238-239, 1991[Medline]
6. Tappin JA, Satchi G, Corless JA, et al: Multiple myeloma presenting as the Collet-Sicard syndrome. J Neurol Neurosurg Psychiatry 60:14, 1996
7. Cockerell OC, Kapoor R: Cranial neuropathy. Postgrad Med J 73:441-442, 1997
8. Weihrauch MR, Diehi V: Retrobulbar, intracranial, and cutaneous secondary plasmacytomas in a patient with atypical multiple myeloma. N Engl J Med 345:1917, 2001
9. Scott A, Knowles E, Knowles D: Expression of CD56/neural cell adhesion molecule correlates with the presence of lytic bone lesions in multiple myeloma and distinguishes myeloma from monoclonal gammopathy of undetermined significance and lymphomas with plasmacytoid differentiation. Am J Pathol 160:1293-1299, 2002
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Copyright © 2005 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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with a total IgG of 6,050 mg/dL. Monoclonal 
