AJR 2002; 179:251-257
© American Roentgen Ray Society
Lesions of the Corpus Callosum: MR Imaging and Differential Considerations in Adults and Children
Eric C. Bourekas1,
Kaliope Varakis,
Douglas Bruns,
Gregory A. Christoforidis,
Melissa Baujan,
H. Wayne Slone and
Dimitris Kehagias
1 All authors: Department of Radiology, Section of Neuroradiology, The Ohio
State University, 160 Means Hall, 1654 Upham Dr., Columbus, OH
43210-1250.
Received March 14, 2001;
accepted after revision January 11, 2002.
Address correspondence to E. C. Bourekas.
Introduction
The corpus callosum is made up of dense myelinated fibers that usually
interconnect homologous territories of the two cerebral hemispheres. The dense
compact nature of the white matter tracts, relative to the adjacent
hemispheric white matter, makes it a barrier to the flow of interstitial edema
and tumor spread. Thus only aggressive tumors, such as glioblastoma multiforme
and lymphoma, typically cross or involve the corpus callosum. This densely
compact nature of the white matter tracts also makes it more susceptible to
shear injury in the event of trauma. Because it is composed predominantly of
myelinated axons, demyelinating processes can affect the corpus callosum. Our
pictorial essay shows 11 classic and uncommon lesions of the corpus
callosum.
Tumors
Lipoma
Intracranial lipomas are rare developmental lesions of the central nervous
system, which are usually asymptomatic and discovered incidentally. They
mainly occur in the region of the corpus callosum and the pericallosal
cistern, accounting for up to 65% of all intracranial lipomas and frequently
associated with callosal dysgenesis. The diagnosis of intracranial lipoma can
easily be made on MR imaging, which shows a homogeneous well-circumscribed
lesion displaying the characteristic short-T1 and T2 signal of fat
[1]
(Fig. 1).
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Fig. 1. —2-year-old boy with lipoma of corpus callosum. Coronal
T1-weighted MR image shows large well-defined homogeneous midline mass lesion
in region of corpus callosum with characteristic bright signal of lipoma. Note
associated dysgenesis of corpus callosum.
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Glioblastoma Multiforme
Glioblastoma multiforme is an extremely aggressive diffuse astrocytic tumor
commonly found in the supratentorial white matter of the cerebral hemispheres.
It is the most common primary brain tumor in adults, accounting for 25% of all
cases. Glioblastomas most commonly spread via direct extension along white
matter tracts, including the corpus callosum, although hematogenous,
subependymal, and cerebrospinal fluid spread can also be seen. When the corpus
callosum is affected, glioblastoma multiformes commonly display a
characteristic bihemispheric involvement, resulting in a classic butterfly
pattern. On MR imaging, these tumors typically enhance solidly and intensely
in the corpus callosum, although occasionally no enhancement is seen. Because
the corpus callosum is relatively resistant to infiltration, glioblastoma
multiforme should be considered for any lesion crossing the corpus callosum
[2] (Fig.
2A,2B,2C).
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Fig. 2B. —46-year-old woman with glioblastoma multiforme. Axial
T2-weighted MR image shows hyperintensity (arrow) in left parietal
white matter extending across corpus callosum with mass effect on lateral
ventricle.
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Fig. 2C. —46-year-old woman with glioblastoma multiforme. Enhanced
axial T1-weighted MR image shows glioblastoma (arrow) of left
parietal white matter that extends across corpus callosum, classic for
glioblastoma multiforme or lymphoma. Lack of enhancement, however, is unusual
for glioblastoma.
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Lymphoma
Primary central nervous system lymphomas are rare aggressive neoplasms of
the brain, accounting for less than 2% of malignant primary brain tumors. They
are almost always of the B-cell non-Hodgkin's type. Common locations include
the corpus callosum, deep gray matter structures, and the periventricular
region. Lymphomas differ from glioblastoma multiformes because they usually
have less peritumoral edema, are more commonly multiple, are less commonly
necrotic, are highly radiosensitive, and frequently temporarily respond
dramatically to steroid administration producing "vanishing
lesions." These lesions are usually iso- or hypointense on T1-weighted
images and hyper-intense on T2-weighted images, with 91% showing contrast
enhancement [3] (Fig.
3A,3B,3C).
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Fig. 3A. —79-year-old nonimmunocompromised woman with primary central
nervous system lymphoma who presented with disorientation. Axial T1-weighted
MR image shows hypointense lesion (arrow) in deep left
parieto—occipital white matter extending into splenium of corpus
callosum.
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Fig. 3B. —79-year-old nonimmunocompromised woman with primary central
nervous system lymphoma who presented with disorientation. Axial T2-weighted
MR image shows hyperintense lesion involving corpus callosum surrounded by
high-signal-intensity edema.
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Fig. 3C. —79-year-old nonimmunocompromised woman with primary central
nervous system lymphoma who presented with disorientation. Enhanced axial
T1-weighted MR image shows markedly enhancing lesion (arrow) of left
parieto—occipital white matter, crossing corpus callosum in classic
butterfly pattern.
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Juvenile Pilocytic Astrocytoma
Juvenile pilocytic astrocytomas are a distinct low-grade variant of
astrocytoma. They are usually well-circumscribed unencapsulated masses, with
frequent cyst formation, either microscopic or macroscopic. Most lesions
commonly involve the cerebellar vermis, cerebellar hemispheres, optic chiasm,
hypothalamus, or floor of the third ventricle. The corpus callosum is an
uncommon location. On MR imaging, pilocytic astrocytomas are hypo- or
isointense on T1-weighted images and hyperintense on T2-weighted images
relative to gray matter. The solid portion of the tumor usually enhances, in
contrast to most low-grade infiltrative astrocytomas, which tend not to
enhance [4] (Fig.
4A,4B,4C).
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Fig. 4C. —4-year-old girl with pilocytic astrocytoma. Enhanced coronal
T1-weighted MR image shows marked contrast enhancement of lesion. This figure
and Figure
2A,2B,2C
show that intense contrast enhancement is not necessarily indicative of
high-grade glioma, just as lack of contrast enhancement is not necessarily
indicative of low-grade lesion.
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Demyelinating Diseases
Multiple Sclerosis
Multiple sclerosis is a demyelinating disease of unknown cause that more
commonly affects young women. Lesions characteristically involve the
periventricular white matter, internal capsule, corpus callosum, and pons,
although plaques can be found anywhere in the white matter and less commonly
even in gray matter. The lesions of the corpus callosum can be focal or
confluent nodular lesions and tend to affect the callosal—septal
interface, which is the central inferior aspect of the corpus callosum. On MR
imaging, the prevalence of lesions in the corpus callosum has been reported to
be up to 93% in the radiology literature. Atrophy of the corpus callosum can
coexist in long-standing multiple sclerosis, making the diagnosis of corpus
callosum lesions difficult. The lesions are hyperintense on long-TR sequences
and can best be seen with proton-density and fluid-attenuated inversion
recovery (FLAIR) sequences. Enhancement is common in the acute stage.
Differentiation should be made from ischemia, trauma, and other demyelinating
processes on the basis of morphology, location, and the presence of concurrent
multiple sclerosis plaques in the periventricular region
[5] (Fig.
5A,5B,5C).
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Fig. 5A. —24-year-old woman with multiple sclerosis who presented with
visual complaints. Axial T2-weighted MR image shows multiple hyperintense
somewhat ovoid lesions of corpus callosum and periventricular white matter,
classic for multiple sclerosis.
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Fig. 5C. —24-year-old woman with multiple sclerosis who presented with
visual complaints. Sagittal fluid-attenuated inversion recovery paramedian
image obtained through corpus callosum shows multiple ovoid hyperintense
lesions (arrow).
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Progressive Multifocal Leukoencephalopathy
Progressive multifocal leukoencephalopathy is an uncommon progressive fatal
demyelinating disease that affects immunocompromised patients. The cause is a
papovavirus—the Creutzfeldt-Jakob virus. The lesions are usually
multifocal and asymmetric, most commonly affecting the subcortical white
matter and corpus callosum. In the corpus callosum, focal lesions can occur
that enlarge and become confluent as the disease progresses. The lesions are
hyperintense on long-TR sequences and hypointense on short-TR/TE sequences.
The lesions usually do not enhance, although they may enhance faintly at the
periphery. Progressive multifocal leukoencephalopathy should be considered in
the differential diagnosis of space-occupying lesions in HIV patients. The
lack of enhancement and mass effect can act as features differentiating this
entity from others such as lymphoma or glioblastoma
[6] (Fig.
6A,6B).
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Fig. 6A. —44-year-old man with HIV presented with behavioral changes
and facial droop caused by progressive multifocal leukoencephalopathy.
T2-weighted axial MR image shows asymmetric white matter lesion of frontal
lobes with involvement of corpus callosum.
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Fig. 6B. —44-year-old man with HIV presented with behavioral changes
and facial droop caused by progressive multifocal leukoencephalopathy.
Enhanced axial T1-weighted MR image shows no enhancement of lesion. Biopsy of
lesion (not shown) confirmed progressive multifocal leukoencephalopathy.
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Marchiafava-Bignami Disease
Marchiafava-Bignami disease is a rare demyelinating neurologic disorder,
primarily affecting the corpus callosum. It was first described in Italian
wine drinkers and is thought to be due to chronic and massive alcohol use. The
central layers of the corpus callosum are affected, with sparing of the dorsal
and ventral layers (sandwich sign). The disease can follow one of three
clinical courses, a fulminate acute form or subacute and chronic forms. The
acute form affects the genu and splenium, whereas the chronic form most
commonly affects the body. In the acute form, the central corpus callosum
enlarges, presumably because of edema. The corpus callosum is of low signal on
T1-weighted images and high signal on T2-weighted images and often enhances.
In the subacute and chronic forms, the lesions involve the central part of the
body most commonly and are hypointense on T1-weighted images and hyper- or
hypointense (hemosiderin deposits) on T2-weighted images
[7] (Fig.
7A,7B).
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Fig. 7A. —54-year-old man with Marchiafava-Bignami disease and 30-year
history of heavy alcohol use. (Reprinted with permission from
[7]) Axial T2-weighted MR image
shows signal abnormality of corpus callosum and periventricular white
matter.
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Fig. 7B. —54-year-old man with Marchiafava-Bignami disease and 30-year
history of heavy alcohol use. (Reprinted with permission from
[7]) Sagittal T1-weighted MR
image shows corpus callosum atrophy (short arrow), which is
characteristic of chronic form. Involvement of central layers of corpus
callosum, indicated by hypointensity, with sparing of dorsal and ventral
layers results in the sandwich sign (long arrow).
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Vascular Processes
Infarction
Infarcts involving the corpus callosum are rare, in part because the corpus
callosum is a dense white matter tract and therefore is less sensitive to
ischemic injury than gray matter. The anterior and posterior cerebral arteries
provide the major blood supply of the corpus callosum via the pericallosal
artery and small penetrating vessels that run perpendicular to the parent
artery. On MR imaging, infarcts have the same characteristics as strokes
elsewhere, with similar enhancement patterns. Differentiation of lacunar
infarcts from other entities such as trauma and demyelinating processes can be
made by the presence of concurrent infarcts in characteristic sites (centrum
semiovale, basal ganglia). With large-vessel ischemic events, the corpus
callosum is usually involved as part of a large vascular distribution
[8] (Fig.
8A,8B,8C,8D,8E).
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Fig. 8E. —59-year-old man with infarct who presented with confusion.
Enhanced axial T1-weighted MR image 6 weeks after initial presentation shows
enhancement has essentially resolved, typical of evolution of infarct.
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Arteriovenous Malformations
Arteriovenous malformations of the corpus callosum comprise 9-11% of all
cerebral arteriovenous malformations. Clinically, 84% of patients with these
malformations present with intracranial hemorrhage, most with intraventricular
hemorrhage. Most are supplied by both the anterior and posterior cerebral
arteries, and many have a bilateral blood supply. Drainage is mainly into the
internal cerebral vein or interhemispheric superficial veins. The MR imaging
characteristics are those of arteriovenous malformations elsewhere, with
serpentine flow voids noted through the corpus callosum and the ventricle and
frequently with evidence of intraventricular hemorrhage
[9] (Fig.
9A,9B).
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Fig. 9A. —42-year-old man with arteriovenous malformation who presented
with intraventricular hemorrhage. Sagittal T1-weighted MR image shows
hemorrhage (arrows) and multiple flow voids in corpus callosum.
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Trauma
Injury to the corpus callosum occurs commonly with head trauma, being
detected on MR imaging in 47% of patients with nonfatal head injuries. The
classic triad of diffuse axonal injury is that of diffuse damage to axons
located at the gray—white matter interface of the cerebral hemispheres,
the dorsolateral aspect of the rostral brainstem, and the corpus callosum. The
callosal lesions most commonly involve the splenium, are usually eccentric in
location, and can involve a focal part or the full thickness of the corpus
callosum. On MR imaging, spinecho T2-weighted images and FLAIR sequences
during the sagittal plane are most sensitive in detecting small nonhemorrhagic
lesions. Hemorrhagic lesions are best seen on T2-weighted images during the
first 4 days after injury and, after 4 days, are better seen on T1-weighted
images. Furthermore, gradient-echo T2-weighted sequences are superior in
detecting chronic hemoglobin degradation products because of the
susceptibility effects of hemosiderin. Differentiation from other lesions such
as ischemia should be made on the basis of history and the location of the
lesions in the corpus callosum
[10] (Fig.
10A,10B,10C,10D).
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Fig. 10C. —20-year-old man with diffuse axonal injury 1 week after motor
vehicle crash. Sagittal T1-weighted MR image on follow-up examination 10 days
after B shows hemorrhagic lesion of corpus callosum.
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Fig. 10D. —20-year-old man with diffuse axonal injury 1 week after motor
vehicle crash. Enhanced coronal T1-weighted MR image on follow-up examination
10 days after B shows hemorrhagic lesion of corpus callosum, with
classic shearing-type lesion also seen at gray—white junction, both
indicative of diffuse axonal injury.
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Miscellaneous Lesions
Lesions in the corpus callosum, both diffuse and focal, have been described
in patients with long-standing hydrocephalus after shunting. Callosal lesions
and tectal neoplasms producing hydrocephalus have been seen in patients with
aqueductal stenosis. Patients with these lesions were thought to have
long-standing hydrocephalus before ventricular decompression. The exact
mechanism responsible for the production of these callosal lesions is unknown,
although they may be the result of ischemia with subsequent demyelination
caused by prolonged severe stretching of the corpus callosum from
ventriculomegaly and subsequent rapid decompression of the ventricles. These
lesions appear hypointense on T1-weighted images and hyperintense on
T2-weighted images, with sparing of the splenium. Although the changes may
persist on imaging, they appear clinically silent
[11] (Fig.
11A,11B).
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Fig. 11A. —45-year-old man with cystic lesions associated with
long-standing hydrocephalus, with multiple prior shunt revisions. Patient is
asymptomatic other than for headaches, which are probably due to mild
hydrocephalus. Sagittal T1-weighted MR image shows well-defined cystic lesions
(arrows) of corpus callosum.
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Fig. 11B. —45-year-old man with cystic lesions associated with
long-standing hydrocephalus, with multiple prior shunt revisions. Patient is
asymptomatic other than for headaches, which are probably due to mild
hydrocephalus. Axial T2-weighted MR image shows abnormal signal
(arrow) throughout corpus callosum, which has persisted for many
years.
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Introduction
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