DIAGNOSTIC NEURORADIOLOGY

Intracranial involvement in plasmacytomas and multiplemyeloma: a pictorial essay

Alfonso Cerase & Annachiara Tarantino &

Alessandro Gozzetti & Carmine Franco Muccio &

Paola Gennari & Lucia Monti & Arturo Di Blasi &Carlo Venturi

Received: 8 February 2008 /Accepted: 19 March 2008 /Published online: 31 May 2008# Springer-Verlag 2008

AbstractIntroduction The purpose of this pictorial essay is toincrease awareness of the clinical presentation, neuroradio-logical findings, treatment options, and neuroradiologicalfollow-up of plasmacytomas and multiple myeloma withintracranial growth.Methods This pictorial essay reviews the clinical features andneuroradiological findings in seven patients (four women, three

men; age range at diagnosis 62–82 years) followed in twoinstitutions. Six patients, one with IgG-k plasmacytoma, andfive with IgG-k (n=3), IgG-l (n=1), and nonsecretory (n=1)multiple myeloma, had been seen over a period of 9 years inone institution, and the other patient with IgG-k plasmacy-toma had been seen over a period of 3.5 years in the other.Results Intracranial involvement is rare, most frequentlyresulting from osseous lesions in the cranial vault, skullbase, nose, or paranasal sinuses. Primary dural or leptome-ningeal involvement is rarer. Some typical findings of adural and/or osseous plasmacytoma include iso- to hyper-density on CT scan, T1 equal to high signal intensity andT2 markedly hypointense signal on MRI, and highvascularity possibly documented on intraarterial digitalsubtraction angiography. However, the neuroradiologicalfindings generally lack specificity, since they are generallyno different from those of meningioma, metastasis, lym-phoma, dural sarcoma, plasma cell granuloma, infectiousmeningitis, and leptomeningeal carcinomatosis.Conclusion The spectrum of clinical and neuroradiologicalevaluation shows that intracranial involvement from plasma-cytoma and multiple myeloma must be taken into account inthe differential diagnosis of cranial osseous and meningealdisease.

Keywords Digital subtraction . Angiography . CT.MRI .

Multiple myeloma . Plasmacytoma

Introduction

Plasma cell tumors [1–4] include solitary plasmacytoma,multiple solitary plasmacytomas, and multiple myeloma(MM) which is also known as myeloma, plasma cell

Neuroradiology (2008) 50:665–674DOI 10.1007/s00234-008-0390-x

This paper was presented as a Scientific Poster at the 23rd Congress ofthe Associazione Italiana di Neuroradiologia 2007, the 32nd Congressof the European Society of Neuroradiology 2007, and the AnnualConference of the British Society of Neuroradiologists 2007.

A. Cerase (*) : P. Gennari : L. Monti :C. VenturiUnit of Diagnostic and Therapeutic Neuroradiology,and InterDepartmental Center of Nuclear Magnetic Resonance,Policlinico “Santa Maria alle Scotte”,Azienda Ospedaliera Universitaria Senese,Viale Mario Bracci,53100 Siena, Italye-mail: alfonsocerase@interfree.it

A. Tarantino : C. F. MuccioUnit of Neuroradiology, Department of Neurosciences,Azienda Ospedaliera “G. Rummo”,Via dell’Angelo, 1,82100 Benevento, Italy

A. GozzettiUnit of Hematology and Transplants,Policlinico “Santa Maria alle Scotte”, University of Siena,Viale Mario Bracci,53100 Siena, Italy

A. Di BlasiUnit of Pathology, Department of Oncology,Azienda Ospedaliera “G. Rummo”,Via dell’Angelo, 1,82100 Benevento, Italy

myeloma, or Kahler’s disease [5], although MM wasdescribed for the first time by MacIntyre in 1850 [6].These tumors show different clinical courses and prognosis,leading some authors to consider them as separate diseasesrather than a spectrum of the same disease [1, 2, 4].Plasmacytomas may arise from osseous (intramedullary) or

nonosseous (extramedullary) sites, may be solitary ormultiple, and may be associated with or progress to MM.Solitary extramedullary plasmacytomas occur in 2% to 10%of newly diagnosed patients with MM. Primary extrame-dullary plasmacytomas are uncommon, accounting for 4%of all plasma cell tumors, mainly arising in the head and

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Fig. 2 A 79-year-old man with persistent headache, and subtle rightexophthalmos. a–d, g, h Unenhanced T2-weighted axial (a) andcoronal (b), T1-weighted axial (c) and sagittal (d), and gadolinium-enhanced T1-weighted axial (g) and sagittal (h) MR images show amarkedly contrast-enhancing expansile lesion arising in the rightzygomaticosphenotemporal buttress, with ipsilateral intracranial andintraorbital extension. e, f, i The lesion shows slight high signal intensityon the diffusion-weighted image (b=1,000) (e), 590.00×10−6 mm2/s on

the apparent diffusion coefficient map (f ), and a marked increase inregional blood volume (rCBV) on the perfusion-weighted image (i),with a lesion/contralateral normal-appearing white matter rCBV ratio of5.7. After surgical resection, histology and immunohistochemistryshowed a monomorphic population of small cells with a plasmacytoidcytological appearance, and intense cytoplasmic reactivity to antibody tok light chains, resulting in the diagnosis of plasmacytoma. A 12-monthdiagnostic work-up ruled out MM

Fig. 1 A 67-year-old woman with an enlarging mass in the rightfrontal region and weakness. a–c Scout view (a) and axial bonewindow (b left image), unenhanced soft-tissue window (b middleimage), and contrast-enhanced soft-tissue window (b right image) CTimages show a large osteolytic mass lesion (arrows), with highattenuation density (b middle image), and intense contrast-enhancement(c right image), arising from the right frontal bone. The lesion is iso- tohypointense on T2-weighted (c left image), hyperintense on unenhancedT1-weighted (c middle image), and markedly contrast-enhancing ongadolinium-enhanced T1-weighted (c right image) coronal MR images.Some flow voids are evident within the lesion, consistent with feedingvessels. d Early (left image) and middle (middle image) arterial phase

films from angiography of the left internal carotid artery, lateral view,and middle (right image) arterial phase film from angiography of theright external carotid artery show marked tumor staining by accessorymeningeal branches from the left ophthalmic artery and right superficialtemporal artery. The lesion is fed also by the left superficial temporalartery (not shown). Complete surgical removal of the lesion resulted in ahistopathological diagnosis of IgG-k monoclonal plasma cell neoplasm.Diagnostic work-up ruled out MM. A 45-month clinical and neurora-diological follow-up including gadolinium-enhanced T1-weighted coro-nal MR image (e) shows no local relapse or clinical progression to MM

R

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neck, particularly the upper aerodigestive tract. Conversionto MM has been reported to occur in about 50% ofplasmacytomas, more frequently if plasmacytoma is intra-medullary. MM usually affects the axial skeleton. In MM,the intramedullary neoplastic cells may extend toward thebone cortex, resulting in extramedullary tumor masses.

Plasmacytomas generally present as bone or soft-tissuetumors with a variable mass effect, pain, and infiltrativebehavior. The typical clinical features of MM are bone pain,weakness, fatigue, fever and infection. From a classical pointof view, cranial and intracranial plasmacytomas and MMmayinvolve (1) the cranial vault and/or the skull base only, (2) thebrain parenchyma, arising in the cranial vault and/or the skullbase or not, and (3) the orbit [7]. However, intracranialinvolvement in plasmacytomas and MM is rare [2, 8–10].

The purpose of this pictorial essay is to increaseawareness of the clinical presentation, neuroradiologicalfindings, treatment options, and neuroradiological follow-up of plasmacytomas and MM with intracranial growth.

Patterns of intracranial spread and clinical presentation

Intracranial involvement generally results from extramedul-lary tumor masses arising from bone lesions in the cranialvault, skull base, nose, or paranasal sinuses [2, 11, 12].Notably, plasma cell tumor dural deposits usually resultfrom direct spread from contiguous bone lesions (Figs. 1, 2,3, 4, and 5), since the dura mater is a relatively avascularstructure. Neoplastic cells usually reach the subdural space

Fig. 3 A 72-year-old man with weakness and dizziness. Consecutivebone window (a), unenhanced soft-tissue window (b), and contrast-enhanced soft-tissue window (c) axial CT images show a largeexpansile osteolytic mass lesion arising in the left condylar occipitalbone, involving the posterior lacerum foramen, and mastoid (not

shown). The lesion shows a high attenuation density, and slightcontrast enhancement. Surgery resulted in a histopathological diagno-sis of IgG-k monoclonal plasma cell neoplasm. Diagnostic work-upshowed an IgG-k MM, stage IIIA

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by breaching the skull inner table and fibrous dura.Myelomatous deposits in dural reflections distant from thebony skull, i.e. tentorium and falx, are rarer, and probablyresult from dissection along layers of meninges [13].Primary dural involvement (Fig. 6) is rare [12–20]. Thefrequency of leptomeningeal involvement (Fig. 7) is about1% [9, 10, 21–23]. Leptomeningeal spread of MM isthought to be hematogenous, following a mechanismcomparable to that of leukemic meningitis. Notably,autopsy studies in patients with leptomeningeal MM havedemonstrated circulating myeloma cells diffusely infiltratingarachnoid veins, resulting in destruction of arachnoidtrabeculae, and myeloma cells able to spill over into thecerebrospinal fluid [13]. Intraaxial brain lesions withoutosseous or dural contact have been reported sporadically, andmay be associated with tumoral bleeding [10, 24–26].

Osseous and pachymeningeal masses in the cranial vaultor in the skull base (Figs. 1, 2, 3, 4, 5, and 6) may result in

tumefaction, pain, headache, single or multiple cranialnerve palsies, or seizure [10, 20]. Involvement of the orbitsmay result in orbital pain, and exophthalmos. Diplopia mayresult from both the direct effect of an orbital plasmacytomaor from ophthalmoplegia caused by cranial nerve involve-ment, possibly in the cavernous sinus (Figs. 4, 5, and 6)[10, 12]. The more relevant presenting features of leptome-ningeal MM include paraparesis, symptoms from increasedintracranial pressure, cranial nerve palsies (particularlynerves V and IV), convulsions, and confusion [10, 20].Furthermore, encephalopathy, and cranial nerve palsiesmay also result from metabolic derangements such ashypercalcemia and uremia, antibodies directed againstmyelin structures, amyloid deposits, and hyperviscositysyndrome, in addition to treatment-related toxicity andcomplications [27, 28]. Clinical symptoms and signs ofMM with intracranial growth are rare, but they may bepresent at disease presentation [10, 12].

Fig. 4 A 62-year-old womanwith left diplopia, exophthal-mia, ptosis and orbital pain,resulting from ipsilateral thirdcranial nerve palsy on neuro-logical examination, occurring9 months after near completeremission of IgG-k MM, stageIIIA, following chemotherapyand autologous stem cell trans-plantation [12]. Consecutiveunenhanced T1-weighted(a, b), T2-weighted (c), andgadolinium-enhanced T1-weighted (d) coronal MRimages show a lesion infiltratingthe left cavernous sinus(arrowheads), resulting frombony involvement of theipsilateral clival bone (openarrow). Note also involvementof the right parietal vault(confined to the bone), C-1 andC-2 vertebrae (arrows)

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Neuroradiology of intracranial plasmacytomasand multiple myeloma

Most commonly, CT and MRI show well-defined destruc-tive masses arising from osseous structures in the cranialvault (Fig. 1), orbit (Fig. 2), or skull base with possibleinvolvement of neural foramina (Figs. 3, 4, and 5).Parenchymal edema may be present (Fig. 2). Cranial bonelesions are not seen in primary pachymeningeal disease(Fig. 6) or leptomeningeal MM (Fig. 7). [4, 9, 28].

On unenhanced CT scans, the extraaxial mass generallyappears hyperdense with respect to brain tissue (Figs. 1, 3,and 6), possibly mimicking meningioma [15, 18], orsubdural hematoma [22]. CT is better than MRI indelineating subtle bone erosions, but the best assessmentis achieved by MRI due to its superiority in the study ofboth bone marrow and meninges. On MRI, neoplastictissue generally shows iso- to hyperintense signal on T1-weighted images, and iso- to hypointense signal on T2-

weighted images, relative to muscle and gray matter (Figs. 1and 6). Contrast enhancement is mild to marked on both CTand MR images. Diffusion-weighted imaging and apparentdiffusion coefficient maps may show restricted diffusion inplasmacytomas (Fig. 2), and increased diffusion in MM(Fig. 7), depending on the entity of cellularity andnucleocytoplasmic ratio. Notably, high density on CTimages, T1 high signal intensity and T2 low signal intensityon MR images, and restricted diffusion are consistent withlesions with high cellularity and low nucleocytoplasmicratio.

Plasmacytoma may be a highly vascular tumor [30–34],and this may be confirmed on perfusion-weighted MRimages (Fig. 2), or possibly on perfusion CT images.Notably, if a surgical approach is required, the preoperativemanagement of plasmacytomas should include intraarterialdigital subtraction angiography (DSA). Intraarterial DSA(Fig. 1) may show a blush mainly supplied by branchesarising from the external carotid artery system [30, 32–34].

Fig. 5 An 80-year-old woman with nonsecretory MM (stage IIIA)who had been treated with a standard melphalan-prednisone regimenevery 28 days for 6 months. She remained well for 8 months untilsystemic disease relapse (bone marrow involvement) and unilateraldiplopia, ptosis and orbital pain in the right side, resulting fromipsilateral third cranial nerve palsy on neurological examination.Unenhanced T1-weighted sagittal (a), consecutive T2-weighted axial(b), and T2-weighted coronal (c) MR images show diffuse bony

involvement of the clivus as low signal intensity, with extension of thepathological tissue into the right cavernous sinus region (arrows). Ongadolinium-enhanced T1-weighted images (not shown), the lesionexhibited slight contrast enhancement. Note also the diffuse low signalintensity of the cervical spine bodies included in the sagittal images.The patient received palliative radiotherapy treatment plus high-dosedexamethasone but without efficacy and died soon after [12]

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Meningeal branches arising from the ophthalmic arteriesare rare embryonic variants which may contribute (Fig. 1),such those occurring in meningiomas of the cranialconvexity [35].

Leptomeningeal MM may be focal, multifocal (Fig. 7),or diffuse. MRI findings may be similar to those ofinfectious leptomeningitis and neoplastic leptomeningealspreading [29]. Neuroradiological findings generally lackspecificity, since they generally are no different from metas-tasis, lymphoma, meningioma, dural sarcoma, plasma cell

granuloma, infectious meningitis, or leptomeningeal carcino-matosis. The diagnosis is usually made when the lesionsappear in the context of a previously diagnosed MM (Figs. 4,5, and 7), or after finding criteria for MM (Figs. 3 and 6).

Pathological tissue may be obtained at surgery (Figs. 1, 2,and 3). Cerebrospinal fluid examination remains the defin-itive test for diagnosing leptomeningeal myelomatosis.However, in daily clinical practice surgical resection andcerebrospinal fluid examination are reserved for selectedpatients [9, 10].

Fig. 6 An 82-year-old man with a 2-month history of diplopia, rightptosis and orbital pain from right third cranial nerve palsy onneurological examination. a Unenhanced axial bone window (leftimage) and soft tissue window (right image) CT images show anenlarged right cavernous sinus region (arrow), without alterations inthe sphenoid bone. b, c Unenhanced consecutive T1-weighted sagittal(b) and T2-weighted coronal (c) MR images show a dural mass lesionin the right cavernous sinus (arrowhead) hypo- to isointense to graymatter, which showed slight contrast enhancement on gadolinium-

enhanced T1-weighted images (not shown). There were no abnormal-ities in the occipital and sphenoid bone. Diagnostic work-up showed aIgG-k MM, stage IIIA. d Six-month follow-up T2-weighted coronalMR image after chemotherapy with melphalan-prednisone, bortezo-mib-dexamethasone, and thalidomide shows a slight decrease in thevolume of the lesion which shows homogeneous high signal intensity,consistent with colliquative changes. At this time, a partial serumresponse and a clear-cut neurological improvement occurred [12]

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Treatment of intracranial plasmacytomas and multiplemyeloma

If anatomically suitable, the primary therapy mode forplasmacytomas is surgery followed by irradiation, since thetumor is exquisitely radiosensitive. In calvarial lesions, cureis generally achieved by complete surgical resectionfollowed by at least 50 Gy radiotherapy. Lesions at theskull base are treated by biopsy and/or subtotal resectionfollowed by irradiation, or irradiation alone [2, 36]. Radio-surgery with a relatively low dose of 14 Gy has beenreported to be appropriate when the tumor or tumorremnant volume is suitable [37]. Systemic therapy, suchas chemotherapy or autologous stem cell transplantation, isrecommended for refractory, recurrent, and multiple plas-macytomas [1–4].

The survival of patients with MM ranges from severalmonths to more than 10 years, depending on disease stage atdiagnosis, and laboratory prognostic factors. Patients withintracranial MM have been reported to survive for 1 to96 months after diagnosis. Patients with MM at the skull basehave a median life expectancy of 3 years, while leptomeningealmyelomatosis generally has a poor prognosis despite aggressivesystemic and local therapy [9, 10, 21, 22]. High-dosechemotherapy followed by autologous or allogenic stem cellstransplantation has improved prognosis [10, 38]. Novel drugssuch as thalidomide and bortezomib may have differentactivity on extramedullary myeloma due to an antiangio-genic/antiapoptotic effect [10, 12, 39]. Chemotherapy mayresult in reduction in the size of the lesion, as well as in achange in its characteristics on MR images (Fig. 6). Focalirradiation may be performed in selected patients.

Fig. 7 A 74-year-old woman with a 10-month history of IgG-l MMresistant to chemotherapy presented with multiple subcutaneousnodular lesions and confusion. a–d T2-weighted (a), and unenhancedT1-weighted (b) sagittal, and gadolinium-enhanced T1-weightedsagittal (c) and axial (d) MR images show multifocal infiltrativeleptomeningeal disease in the cerebellar folia (white arrows),interpeduncular (black arrows) and opticochiasmatic cisterns withinvolvement of the pituitary stalk (curved arrows), and frontal region

(arrowheads), resulting in triventricular hydrocephalus. The neoplastictissue shows iso- to hypointense signal to gray matter, and intensecontrast enhancement. There is no cranial bony involvement. Note thebony involvement of C3 vertebra (open arrow). e, f The neoplastictissue shows slight high signal intensity on the diffusion-weightedimage (e), and 793.01 to 1191.54×10−6 mm2/s on the apparentdiffusion coefficient map (f). The patient died some days later [39]

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Conclusion

The clinical and neuroradiological spectrum of intracranialplasmacytomas and MM show that they must be taken inaccount in the differential diagnosis of cranial osseous andmeningeal disease.

Acknowledgements We thank Tiziana Caselli of the Unit ofDiagnostic and Therapeutic Neuroradiology, and InterDepartmentalCenter of Nuclear Magnetic Resonance, Azienda Ospedaliera Uni-versitaria Senese, Policlinico “Santa Maria alle Scotte”, Siena, for hertechnical support, and Roberto Faleri of the Central Library, School ofMedicine, University of Siena, Policlinico “Santa Maria alle Scotte”,Siena, for providing references for the preparation of this article.

Conflict of interest statement We declare that we have no conflictof interest.

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