jurnal radiologi mri brain lymphoma

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AJR 2005;184:16791685 0361803X/05/18451679 American Roentgen Ray Society

Neuroradiology -

Slone et al.CT and MRI of Intracranial Lymphoma

Pictorial Essay

CT and MRI Findings of Intracranial LymphomaH. Wayne Slone1, Joseph J. Blake, Rajul Shah, Sangeeta Guttikonda, Eric C. Bourekas

Slone HW, Blake JJ,Shah R,Guttikonda S,BourekasEC

rimary CNS lymphoma is the con-finement of extranodal lymphomato the CNS. Classically, lympho-mas are divided into Hodgkins

lymphoma and non-Hodgkins lymphoma,with a primary extranodal presentation in 5%and 30% of cases, respectively. With an in-creasing incidence in both the immunocompe-tent and immunocompromised populations,primary CNS lymphoma represents 1% of alllymphomas and as many as 16% of all pri-mary brain tumors [1]. This amplified preva-lence makes primary CNS lymphoma animportant consideration in the differential di-agnosis of brain lesions. This pictorial essaywill review the varied CT and MRI appear-ances of intracranial lymphomas.

Primary CNS Lymphoma in theImmunocompetent

Most primary CNS lymphomas are of thenon-Hodgkins B-cell type [1]. B-cell primaryCNS lymphoma typically presents when the pa-tient is approximately 50 years old and is morefrequent in men. The most common presentingsymptom is a change in mental status followedby nausea, headache, hemiparesis, cerebellarsigns, cranial nerve palsies, and visual distur-

bances [1, 2]. Cerebrospinal fluid analysisyields a cytologic diagnosis in fewer than half of patients with B-cell primary CNS lymphoma.

Neuroimaging reveals solitary lesions that aremost commonly located supratentorially in thewhite matter of the frontal or parietal lobes or inthe subependymal regions, but the lesions mayalso involve the deep gray matter (Figs. 1 and 2).In 12% of B-cell primary CNS lymphomas, theleptomeninges are involved [1]. CT scans usu-ally show high attenuation, probably because of high cellularity, and virtually all lesions showhomogeneous contrast enhancement (Fig. 1A).On MRI, B-cell primary CNS lymphoma le-sions are clearly delineated masses that appearisointense to hypointense on T1-weighted im-ages and mostly hypointense on T2-weightedimages [1, 2] (Fig. 1B). Nearly all lesions showhomogeneous enhancement with contrast mate-rial (Fig. 1C). A classic presentation is the lesionthat crosses the corpus callosum in a butterflypattern (Fig. 3). Rarely, necrosis, cyst forma-tion, calcification, and hemorrhage can be seen.If steroids are administered, the tumor mayshrink and vanish, compromising the abilityto obtain a histologic diagnosis (Fig. 4).

Primary CNS Lymphoma in theImmunocompromised

Immunocompromised patients are at in-creased risk for developing primary CNS lym-

phoma. In fact, estimates indicate that nearly6% of the AIDS population will be afflictedwith an intracranial lymphoma [3]. Indeed, pri-

mary CNS lymphoma in an HIV-seropositivepatient is an AIDS-defining condition. The ageat presentation is earlier (fourth decade) in im-munocompromised patients than in the immu-nocompetent, but the cell type (B cell) andpresenting signs and symptoms are similar.Neuroimaging reveals a higher frequency of multiple lesions and more often displays ir-regular margins, heterogeneity, and ring en-hancement [1, 3] (Figs. 5 and 6). In theimmunocompromised population, an impor-tant dilemma is the difficulty in distinguishingprimary CNS lymphoma from the more com-mon cerebral toxoplasmosis using CT andMRI, because both entities can present withmultiple ring-enhancing lesions. ThalliumSPECT or PET can aid in this setting, althoughfrequently the patient is treated for presumedtoxoplasmosis, and if the patient responds thediagnosis is established.

Primary Leptomeningeal LymphomaAlthough extension of primary CNS lym-

phoma into the leptomeninges is common, pri-mary leptomeningeal lymphoma is rare,constituting fewer than 8% of all cases of pri-mary CNS lymphoma [4]. The clinical presen-tation of primary leptomeningeal lymphoma is

similar to that of B-cell primary CNS lym-phoma but may also include dizziness, tinnitus,spinal neuropathies, and meningismus. The diag-

Received July 26, 2004; accepted after revision November 8, 2004.

Presented at the 2004 annual meeting of the American Roentgen Ray Society, Miami Beach, FL.

1All authors: Department of Radiology, The Ohio State University Medical Center and The Ohio State University College of Medicine and Public Health, 629 Means Hall, 1654 Upham DColumbus, OH 43210. Address correspondence to H. W. Slone ([email protected]).

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nosis is often elusive because clinical findings areoften suggestive of meningoencephalitis or com-mon conditions that cause increased intracranialpressure. Analysis of the cerebrospinal fluid of patients with primary leptomeningeal lym-phoma has failed to show a consistent presenceof malignant cells. Neuroimaging is often unre-markable or may show nonspecific findingssuch as hydrocephalus. On occasion, significantimaging findings may include widespreadmeningeal calcification, discrete masses or den-sities, and faint meningeal enhancement (Figs. 7

and 8). In the absence of other findings, proton-

density or FLAIR MRI revealing the presenceof high signal intensity in the subarachnoidspace may support a diagnosis of primary lep-tomeningeal lymphoma.

Metastatic CNS Lymphoma, B-Cell TypeIn 59% of systemic non-Hodgkins lym-

phoma, secondary spread involves the CNS[5], usually in the form of leptomeningeal in-filtrates, and has a poor prognosis. Parenchy-mal lesions, when present, typically result

from secondary involvement from the lep-

tomeninges via infiltration of the perivascularspaces (Fig. 9).

Intravascular LymphomatosisWith fewer than 50 reported cases, intra-

vascular lymphomatosis is an extraordinarilyrare form of large B-cell non-Hodgkins lym-phoma that is characterized by aggressive, in-travascular proliferation of lymphoid cells.Proclivity for involvement and subsequentocclusion of CNS vessels often leads to non-localizing neurologic deficits and changes in

mental status. Because no specific clinical or

A B C

Fig. 1.72-year-old immunocompetent woman with primary CNS non-Hodgkins B-cell lymphoma who presented with progressive motor weakness.A, Unenhanced CT image shows classic hyperdense masses involving deep white and gray matter.B, Axial FLAIR MR image shows isointensity of lesions to brain parenchyma and surrounding edema.C, Axial contrast-enhanced T1-weighted MR image shows homogeneous enhancement of multiple bilateral tumors.

A B

Fig. 2.62-year-old immunocompetent woman with primary CNS non-Hodgkins B-cell lymphoma with leptomeningeal spread who presented with left hemiparesis, severeheadache, and confusion. Systemic workup was negative. Cerebrospinal fluid cytology was positive for leptomeningeal spread.A, Axial FLAIR MR image shows high-signal-intensity edema in white matter around trigone of left lateral ventricle.B, Contrast-enhanced coronal T1-weighted MR image shows focal enhancing lesion in deep white matter of left parietal and posterior temporal regions with enhancementof adjacent subependyma ( arrow ).


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CT and MRI of Intracranial Lymphoma

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A B

Fig. 4.61-year-old immunocompetent man wi th primary CNSnon-Hodgkins B-cell lymphoma and vanishing hyperdensemasses when treated with steroids. Systemic workup wasnegative.A, Initial axial CT image shows hyperdense masses in basalganglia bilaterally.

B, On follow-up CT image obtained 10 days after initiation ofsteroids, lesions have nearly resolved, consistent with van-ishing tumor.

A B C

Fig. 5.44-year-old HIV-positive woman with primary CNS non-Hodgkins B-cell lymphoma. She presented with changes in mental status and CD-4 count of 0.A, Contrast-enhanced CT image shows low-density infiltrating butterfly lesion crossing corpus callosum with ring of enhancement ( arrows ).B, Axial FLAIR MR image shows lesion isointense to gray matter ( arrows ).C, Contrast-enhanced T1-weighted axial MR image shows ring of enhancement ( arrows ).

A B

Fig. 3.50-year-old immunocompetent man with pri-mary CNS non-Hodgkins B-cell lymphoma.A, Axial T2-weighted MR image shows infiltrativehyperintense mass expanding genu and splenium ofcorpus callosum in butterfly pattern.B, Contrast-enhanced axial T1-weighted MR imageshows homogeneous enhancement of lesion.


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A B

C

Fig. 6.42-year-old HIV-positive man with primary CNS non-Hodgkins B-cell lymphoma. Presenting signs were third andfourth cranial nerve palsies. Patient underwent irradiation 1 year

earlier for stage I palate cancer.A, Axial FLAIR MR image shows lesion involving left cerebralpeduncle.B, Contrast-enhanced coronal T1-weighted MR image showsmasslike enhancement.C, Contrast-enhanced coronal T1-weighted MR image showsenhancement along third and fourth cranial nerves ( arrow ).

A B C

Fig. 7.63-year-old woman with primary meningeal lymphoma who presented with frequent falls and vertigo. CT scan from outside institution ( not shown ) showed hyerden-sity along surface of parietotemporal covexity that was incorrectly interpreted as subdural hemorrhage. Systemic workup was negative.A, Axial FLAIR image shows hyperintensity (arrow ) involving sulci and leptomeninges of parietotemporal convexity.B and C, Contrast-enhanced T1-weighted axial ( B) and coronal ( C) MR images show focal thickening and homogeneous enhancement of leptomeninges of parietotemporalconvexity (arrows ).


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laboratory findings are associated with intra-vascular lymphomatosis, the diagnosis is rarelyestablished before histologic examination dur-ing autopsy. MRI findings in intravascular lym-phomatosis include high-signal deep whitematter lesions and infarctlike, high-signal le-sions in vascular territories on T2-weighted im-ages. After the administration of contrastmaterial, enhancement can be masslike [6] (Fig.10). Various patterns of parenchymal andmeningeal enhancement may also be seen.

Primary CNS Lymphoma, T-Cell TypePrimary T-cell lymphoma of the CNS consti-

tutes a small fraction of all primary CNS lym-phomas in the immunocompetent population. Athreefold higher incidence of T-cell primary

CNS lymphoma in Japan compared with the

United States has been reported. In a review of 25 cases of T-cell primary CNS lymphoma, Liuet al. [7] reported that T-cell primary CNS lym-phoma is similar to B-cell primary CNS lym-phoma in clinical presentation and imagingfeatures. Unlike B-cell primary CNS lym-phoma, involvement of the cerebrospinal fluidin T-cell primary CNS lymphoma is uncom-mon. CT and MRI typically show one or morehomogeneous masses that uniformly enhancewith contrast material [7] (Fig. 11). Associationwith AIDS or other types of immunodeficiencyhas only rarely been reported.

Intracranial Hodgkins LymphomaFewer than 0.5% of patients with

Hodgkins lymphoma have CNS involve-

ment, and most of these cases are late mani-

festations of disseminated disease outside theCNS. Primary intracranial Hodgkins lym-phoma, with only a few case reports, is per-haps the rarest of all intracranial lymphomas.In the reported cases, neuroimaging usuallyshows meningeal involvement. IntracranialHodgkins lymphoma may mimic meningi-oma, although parenchymal lesions withoutmeningeal attachment have been reported [8](Figs. 12 and 13).

ConclusionThe CT and MRI findings of intracranial

lymphomas can be nonspecific or share com-mon features with other diseases such as de-myelinating disorders, other neoplasms,sarcoid, tuberculosis, and toxoplasmosis.

Therefore, a definitive diagnosis of primary

Fig. 8.39-year-old man with AIDS and primary CNS non-Hodgkins B-cell lymphoma of leptomeninges who pre-sented with diplopia, facial weakness, and eyelid droop. No parenchymal lesions were identified. Coronal contrast-enhanced T1-weighted MR image shows enhancement of multiple cranial nerves ( arrows ) bilaterally.

A B

Fig. 9.71-year-old woman with metastatic leptomeningeal CNS non-Hodgkins B-cell lymphoma who presented with left facial droop. She was previously diagnosed withsystemic stage IV non-Hodgkins lymphoma (B-cell type).A, Axial contrast-enhanced T1-weighted MR image shows linear l eptomeningeal enhancement ( arrows ). Enhancement of fifth cranial nerve ( arrowhead ) is evident as well.B, Coronal contrast-enhanced T1-weighted MR image shows enhancement of fifth, seventh, and eighth cranial nerves ( arrows ).


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A B

Fig. 11.40-year-old man with primary CNSnon-Hodgkins T-cell lymphoma who pre-sented with seizure.A, Axial FLAIR MR image shows hyperintense signal in tectum and posterior aspectof midbrain (arrow ).B, Axial contrast-enhanced T1-weightedMR image shows leptomeningeal enhance-ment (arrows ).

A B C

Fig. 10.48-year-old man with intravascular non-Hodgkins B-cell lymphoma who presented with left leg weakness for 1 year.A, Axial FLAIR MR image shows hyperintense deep white matter signal.

B, Diffusion-weighted axial MR image shows restricted diffusion of lesion.C, Contrast-enhanced axial T1-weighted MR image shows nodular enhancement.

A B

Fig. 12.48-year-old woman with primaryHodgkins lymphoma who presented with progres-sive left-sided weakness. Systemic workup wasnegative.A, Contrast-enhanced CT image shows enhance-ment along frontoparietal convexity.B, Contrast-enhanced T1-weighted coronal MRimage shows dura-based enhancing lesion withdural tail (arrows ) causing compression of frontal lobe and subfalcine herniation.


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CNS lymphoma requires histologic assess-ment. However, a high index of suspicion andthe presence of features similar to those illus-trated in this article can aid in the diagnosis of intracranial lymphoma.

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Fig. 13.35-year-old HIV-positive man with systemic nodular sclerosing Hodgkins lymphoma who presented with mental status change. Last CD-4 count was more than 1,200per cubic millimeter with undetectable viral load. Patient did not respond to antitoxoplasmosis treatment and underwent biopsy.A, Axial unenhanced CT image shows hypodense vasogenic edema around subtle hyperdense lesion ( arrow ) along medial margin of left parietooccipital lobe.B, Axial T2-weighted MR image shows low signal intensity of lesion ( arrow ).

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