AJR:184, May 2005 1679

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 Lymphoma
H. Wayne Slone
1
, Joseph J. Blake, Rajul Shah, Sangeeta Guttikonda, Eric C. Bourekas
Slone HW, Blake JJ, Shah R, Guttikonda S, Bourekas EC
rimary CNS lymphoma is the con-
finement of extranodal lymphoma
to 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 all
lymphomas and as many as 16% of all pri-
mary brain tumors [1]. This amplified preva-
lence makes primary CNS lymphoma an
important consideration in the differential di-
agnosis of brain lesions. This pictorial essay
will review the varied CT and MRI appear-
ances of intracranial lymphomas.
Primary CNS Lymphoma in the
Immunocompetent
Most primary CNS lymphomas are of the
non-Hodgkins B-cell type [1]. B-cell primary
CNS lymphoma typically presents when the pa-
tient is approximately 50 years old and is more
frequent in men. The most common presenting
symptom is a change in mental status followed
by nausea, headache, hemiparesis, cerebellar
signs, cranial nerve palsies, and visual distur-
bances [1, 2]. Cerebrospinal fluid analysis
yields a cytologic diagnosis in fewer than half of
patients with B-cell primary CNS lymphoma.
Neuroimaging reveals solitary lesions that are
most commonly located supratentorially in the
white matter of the frontal or parietal lobes or in
the subependymal regions, but the lesions may
also involve the deep gray matter (Figs. 1 and 2).
In 12% of B-cell primary CNS lymphomas, the
leptomeninges are involved [1]. CT scans usu-
ally show high attenuation, probably because of
high cellularity, and virtually all lesions show
homogeneous contrast enhancement (Fig. 1A).
On MRI, B-cell primary CNS lymphoma le-
sions are clearly delineated masses that appear
isointense to hypointense on T1-weighted im-
ages and mostly hypointense on T2-weighted
images [1, 2] (Fig. 1B). Nearly all lesions show
homogeneous enhancement with contrast mate-
rial (Fig. 1C). A classic presentation is the lesion
that crosses the corpus callosum in a butterfly
pattern (Fig. 3). Rarely, necrosis, cyst forma-
tion, calcification, and hemorrhage can be seen.
If steroids are administered, the tumor may
shrink and vanish, compromising the ability
to obtain a histologic diagnosis (Fig. 4).
Primary CNS Lymphoma in the
Immunocompromised
Immunocompromised patients are at in-
creased risk for developing primary CNS lym-
phoma. In fact, estimates indicate that nearly
6% of the AIDS population will be afflicted
with an intracranial lymphoma [3]. Indeed, pri-
mary CNS lymphoma in an HIV-seropositive
patient is an AIDS-defining condition. The age
at presentation is earlier (fourth decade) in im-
munocompromised patients than in the immu-
nocompetent, but the cell type (B cell) and
presenting 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 the
immunocompromised population, an impor-
tant dilemma is the difficulty in distinguishing
primary CNS lymphoma from the more com-
mon cerebral toxoplasmosis using CT and
MRI, because both entities can present with
multiple ring-enhancing lesions. Thallium
SPECT or PET can aid in this setting, although
frequently the patient is treated for presumed
toxoplasmosis, and if the patient responds the
diagnosis is established.
Primary Leptomeningeal Lymphoma
Although 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.
1
All 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 Dr.,
Columbus, OH 43210. Address correspondence to H. W. Slone (slone-1@medctr.osu.edu).
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Slone et al.
1680 AJR:184, May 2005
nosis is often elusive because clinical findings are
often suggestive of meningoencephalitis or com-
mon conditions that cause increased intracranial
pressure. Analysis of the cerebrospinal fluid of
patients with primary leptomeningeal lym-
phoma has failed to show a consistent presence
of malignant cells. Neuroimaging is often unre-
markable or may show nonspecific findings
such as hydrocephalus. On occasion, significant
imaging findings may include widespread
meningeal 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 presence
of high signal intensity in the subarachnoid
space may support a diagnosis of primary lep-
tomeningeal lymphoma.
Metastatic CNS Lymphoma, B-Cell Type
In 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 perivascular
spaces (Fig. 9).
Intravascular Lymphomatosis
With fewer than 50 reported cases, intra-
vascular lymphomatosis is an extraordinarily
rare form of large B-cell non-Hodgkins lym-
phoma that is characterized by aggressive, in-
travascular proliferation of lymphoid cells.
Proclivity for involvement and subsequent
occlusion 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, severe
headache, 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 enhancement
of adjacent subependyma (arrow).
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CT and MRI of Intracranial Lymphoma
AJR:184, May 2005 1681
A B
Fig. 4.61-year-old immunocompetent man with primary CNS
non-Hodgkins B-cell lymphoma and vanishing hyperdense
masses when treated with steroids. Systemic workup was
negative.
A, Initial axial CT image shows hyperdense masses in basal
ganglia bilaterally.
B, On follow-up CT image obtained 10 days after initiation of
steroids, 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 infiltrative
hyperintense mass expanding genu and splenium of
corpus callosum in butterfly pattern.
B, Contrast-enhanced axial T1-weighted MR image
shows homogeneous enhancement of lesion.
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Slone et al.
1682 AJR:184, May 2005
A B
C
Fig. 6.42-year-old HIV-positive man with primary CNS non-
Hodgkins B-cell lymphoma. Presenting signs were third and
fourth cranial nerve palsies. Patient underwent irradiation 1 year
earlier for stage I palate cancer.
A, Axial FLAIR MR image shows lesion involving left cerebral
peduncle.
B, Contrast-enhanced coronal T1-weighted MR image shows
masslike enhancement.
C, Contrast-enhanced coronal T1-weighted MR image shows
enhancement 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 parietotemporal
convexity (arrows).
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CT and MRI of Intracranial Lymphoma
AJR:184, May 2005 1683
laboratory findings are associated with intra-
vascular lymphomatosis, the diagnosis is rarely
established before histologic examination dur-
ing autopsy. MRI findings in intravascular lym-
phomatosis include high-signal deep white
matter lesions and infarctlike, high-signal le-
sions in vascular territories on T2-weighted im-
ages. After the administration of contrast
material, enhancement can be masslike [6] (Fig.
10). Various patterns of parenchymal and
meningeal enhancement may also be seen.
Primary CNS Lymphoma, T-Cell Type
Primary T-cell lymphoma of the CNS consti-
tutes a small fraction of all primary CNS lym-
phomas in the immunocompetent population. A
threefold 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, Liu
et al. [7] reported that T-cell primary CNS lym-
phoma is similar to B-cell primary CNS lym-
phoma in clinical presentation and imaging
features. Unlike B-cell primary CNS lym-
phoma, involvement of the cerebrospinal fluid
in T-cell primary CNS lymphoma is uncom-
mon. CT and MRI typically show one or more
homogeneous masses that uniformly enhance
with contrast material [7] (Fig. 11). Association
with AIDS or other types of immunodeficiency
has only rarely been reported.
Intracranial Hodgkins Lymphoma
Fewer 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 the
CNS. 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 usually
shows meningeal involvement. Intracranial
Hodgkins lymphoma may mimic meningi-
oma, although parenchymal lesions without
meningeal attachment have been reported [8]
(Figs. 12 and 13).
Conclusion
The 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 con-
trast-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 with
systemic stage IV non-Hodgkins lymphoma (B-cell type).
A, Axial contrast-enhanced T1-weighted MR image shows linear leptomeningeal 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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Slone et al.
1684 AJR:184, May 2005
A B
Fig. 11.40-year-old man with primary CNS
non-Hodgkins T-cell lymphoma who pre-
sented with seizure.
A, Axial FLAIR MR image shows hyperin-
tense signal in tectum and posterior aspect
of midbrain (arrow).
B, Axial contrast-enhanced T1-weighted
MR 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 primary
Hodgkins lymphoma who presented with progres-
sive left-sided weakness. Systemic workup was
negative.
A, Contrast-enhanced CT image shows enhance-
ment along frontoparietal convexity.
B, Contrast-enhanced T1-weighted coronal MR
image shows dura-based enhancing lesion with
dural tail (arrows) causing compression of fron-
tal lobe and subfalcine herniation.
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CT and MRI of Intracranial Lymphoma
AJR:184, May 2005 1685
CNS lymphoma requires histologic assess-
ment. However, a high index of suspicion and
the 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 1,200
per 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.
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