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he corpus callosum is made up ofdense myelinated fibers that usu-ally interconnect homologous ter-

ritories of the two cerebral hemispheres. Thedense compact nature of the white mattertracts, relative to the adjacent hemisphericwhite matter, makes it a barrier to the flow ofinterstitial edema and tumor spread. Thus onlyaggressive tumors, such as glioblastoma multi-forme and lymphoma, typically cross or in-volve the corpus callosum. This denselycompact nature of the white matter tracts alsomakes it more susceptible to shear injury in theevent of trauma. Because it is composed pre-dominantly of myelinated axons, demyelinat-ing processes can affect the corpus callosum.Our pictorial essay shows 11 classic and un-common lesions of the corpus callosum.

Tumors

Lipoma

Intracranial lipomas are rare developmen-tal lesions of the central nervous system,which are usually asymptomatic and discov-ered incidentally. They mainly occur in theregion of the corpus callosum and the peri-callosal cistern, accounting for up to 65% ofall intracranial lipomas and frequently asso-ciated with callosal dysgenesis. The diagno-sis of intracranial lipoma can easily be made

on MR imaging, which shows a homoge-neous well-circumscribed lesion displayingthe characteristic short-T1 and T2 signal offat [1] (Fig. 1).

Glioblastoma Multiforme

Glioblastoma multiforme is an extremelyaggressive diffuse astrocytic tumor commonlyfound in the supratentorial white matter of thecerebral hemispheres. It is the most commonprimary brain tumor in adults, accounting for25% of all cases. Glioblastomas most com-monly spread via direct extension along whitematter tracts, including the corpus callosum,although hematogenous, subependymal, andcerebrospinal fluid spread can also be seen.When the corpus callosum is affected, glio-blastoma multiformes commonly display acharacteristic bihemispheric involvement, re-sulting in a classic butterfly pattern. On MRimaging, these tumors typically enhance sol-idly and intensely in the corpus callosum, al-though occasionally no enhancement is seen.Because the corpus callosum is relatively re-sistant to infiltration, glioblastoma multiformeshould be considered for any lesion crossingthe corpus callosum [2] (Fig. 2).

Lymphoma

Primary central nervous system lympho-mas are rare aggressive neoplasms of the

brain, accounting for less than 2% of malig-nant primary brain tumors. They are almostalways of the B-cell non-Hodgkins type.Common locations include the corpus callo-sum, deep gray matter structures, and theperiventricular region. Lymphomas differfrom glioblastoma multiformes because theyusually have less peritumoral edema, aremore commonly multiple, are less commonlynecrotic, are highly radiosensitive, and fre-

Lesions of the Corpus Callosum:

MR Imaging andDifferential Considerations in Adults and Children

Eric C. Bourekas

1

, Kaliope Varakis, Douglas Bruns, Gregory A. Christoforidis, Melissa Baujan, H. Wayne Slone, Dimitris Kehagias

Received March 14, 2001; accepted after revision January 11, 2002.

1

All authors: Department of Radiology, Section of Neuroradiology, The Ohio State University, 160 Means Hall, 1654 Upham Dr., Columbus, OH 43210-1250. Address correspondence to E. C. Bourekas.

AJR

2002;179:251257 0361803X/02/1791251 American Roentgen Ray Society

Pictorial Essay

T

Fig. 1.2-year-old boy with lipoma of corpus callosum.Coronal T1-weighted MR image shows large well-de-fined homogeneous midline mass lesion in region of cor-pus callosum with characteristic bright signal of lipoma.Note associated dysgenesis of corpus callosum.

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quently temporarily respond dramatically tosteroid administration producing vanishinglesions. These lesions are usually iso- or hy-pointense on T1-weighted images and hyper-intense on T2-weighted images, with 91%showing contrast enhancement [3] (Fig. 3).

Juvenile Pilocytic Astrocytoma

Juvenile pilocytic astrocytomas are a dis-tinct low-grade variant of astrocytoma. Theyare usually well-circumscribed unencapsulatedmasses, with frequent cyst formation, eithermicroscopic or macroscopic. Most lesions

commonly involve the cerebellar vermis, cere-bellar hemispheres, optic chiasm, hypothala-mus, or floor of the third ventricle. The corpuscallosum is an uncommon location. On MRimaging, pilocytic astrocytomas are hypo- orisointense on T1-weighted images and hyper-

A B C

Fig. 2.46-year-old woman with glioblastoma multiforme. A, Axial T1-weighted MR image shows hypointensity (arrow) of left parietal white matter extending across corpus callosum.B, Axial T2-weighted MR image shows hyperintensity (arrow) in left parietal white matter extending across corpus callosum with mass effect on lateral ventricle.C, Enhanced axial T1-weighted MR image shows glioblastoma (arrow) of left parietal white matter that extends across corpus callosum, classic for glioblastoma multi-forme or lymphoma. Lack of enhancement, however, is unusual for glioblastoma.

A B C

Fig. 3.79-year-old nonimmunocompromised woman with primary central nervous system lymphoma who presented with disorientation.A, Axial T1-weighted MR image shows hypointense lesion (arrow) in deep left parietooccipital white matter extending into splenium of corpus callosum. B, Axial T2-weighted MR image shows hyperintense lesion involving corpus callosum surrounded by high-signal-intensity edema.C, Enhanced axial T1-weighted MR image shows markedly enhancing lesion (arrow) of left parietooccipital white matter, crossing corpus callosum in classic butterfly pattern.

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intense on T2-weighted images relative to graymatter. The solid portion of the tumor usuallyenhances, in contrast to most low-grade infil-trative astrocytomas, which tend not to en-hance [4] (Fig. 4).

Demyelinating Diseases

Multiple Sclerosis

Multiple sclerosis is a demyelinating diseaseof unknown cause that more commonly affects

young women. Lesions characteristically in-volve the periventricular white matter, internalcapsule, corpus callosum, and pons, althoughplaques can be found anywhere in the whitematter and less commonly even in gray matter.

A B C

Fig. 4.4-year-old girl with pilocytic astrocytoma.A, Sagittal T1-weighted MR image shows well-circumscribed hypointense lesion in body of corpus callosum.B, Axial T2-weighted MR image shows that lesion is hyperintense.C, Enhanced coronal T1-weighted MR image shows marked contrast enhancement of lesion. This figure and Figure 2 show that intense contrast enhancement is not nec-essarily indicative of high-grade glioma, just as lack of contrast enhancement is not necessarily indicative of low-grade lesion.

A B C

Fig. 5.24-year-old woman with multiple sclerosis who presented with visual complaints. A, Axial T2-weighted MR image shows multiple hyperintense somewhat ovoid lesions of corpus callosum and periventricular white matter, classic for multiple sclerosis.B, Sagittal T2-weighted MR image shows multiple hyperintense lesions (arrows) in corpus callosum.C, Sagittal fluid-attenuated inversion recovery paramedian image obtained through corpus callosum shows multiple ovoid hyperintense lesions (arrow).

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A B

Fig. 6.44-year-old man with HIV presented with be-havioral changes and facial droop caused by progres-sive multifocal leukoencephalopathy.A, T2-weighted axial MR image shows asymmetricwhite matter lesion of frontal lobes with involvementof corpus callosum.B, Enhanced axial T1-weighted MR image shows no en-hancement of lesion. Biopsy of lesion (not shown) con-firmed progressive multifocal leukoencephalopathy.

A B

Fig. 7.54-year-old man with Marchiafava-Bignamidisease and 30-year history of heavy alcohol use. (Re-printed with permission from [7])A, Axial T2-weighted MR image shows signal abnormal-ity of corpus callosum and periventricular white matter. B, Sagittal T1-weighted MR image shows corpus cal-losum atrophy (short arrow), which is characteristicof chronic form. Involvement of central layers of cor-pus callosum, indicated by hypointensity, with sparingof dorsal and ventral layers results in the sandwichsign (long arrow).

The lesions of the corpus callosum can be focalor confluent nodular lesions and tend to affectthe callosalseptal interface, which is the centralinferior aspect of the corpus callosum. On MRimaging, the prevalence of lesions in the corpuscallosum has been reported to be up to 93% inthe radiology literature. Atrophy of the corpuscallosum can coexist in long-standing multiplesclerosis, making the diagnosis of corpus callo-sum lesions difficult. The lesions are hyperin-tense on long-TR sequences and can best beseen with proton-density and fluid-attenuatedinversion recovery (FLAIR) sequences. En-hancement is common in the acute stage. Dif-ferentiation should be made from ischemia,trauma, and other demyelinating processes onthe basis of morphology, location, and the pres-ence of concurrent multiple sclerosis plaques inthe periventricular region [5] (Fig. 5).

Progressive Multifocal Leukoencephalopathy

Progressive multifocal leukoencephalopathyis an uncommon progressive fatal demyelinat-ing disease that affects immunocompromisedpatients. The cause is a papovavirustheCreutzfeldt-Jakob virus. The lesions are usuallymultifocal and asymmetric, most commonly af-fecting the subcortical white matter and corpuscallosum. In the corpus callosum, focal lesionscan occur that enlarge and become confluent asthe disease progresses. The lesions are hyperin-tense on long-TR sequences and hypointenseon short-TR/TE sequences. The lesions usuallydo not enhance, although they may enhancefaintly at the periphery. Progressive multifocalleukoencephalopathy should be considered inthe differential diagnosis of space-occupying le-sions in HIV patients. The lack of enhancementand mass effect can act as features differentiat-

ing this entity from others such as lymphoma orglioblastoma [6] (Fig. 6).

Marchiafava-Bignami Disease

Marchiafava-Bignami disease is a rare demy-elinating neurologic disorder, primarily affect-ing the corpus callosum. It was first described inItalian wine drinkers and is thought to be due tochronic and massive alcohol use. The centrallayers of the corpus callosum are affected, withsparing of the dorsal and ventral layers (sand-wich sign). The disease can follow one of threeclinical courses, a fulminate acute form or sub-acute and chronic forms. The acute form affectsthe genu and splenium, whereas the chronicform most commonly affects the body. In theacute form, the central corpus callosum en-larges, presumably because of edema. The cor-pus callosum is of low signal on T1-weighted

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images and high signal on T2-weighted imagesand often enhances. In the subacute and chronicforms, the lesions involve the central part of thebody most commonly and are hypointense onT1-weighted images and hyper- or hypointense(hemosiderin deposits) on T2-weighted images[7] (Fig. 7).

Vascular Processes

Infarction

Infarcts involving the corpus callosum arerare, in part because the corpus callosum is adense white matter tract and therefore is lesssensitive to ischemic injury than gray matter.

The anterior and posterior cerebral arteriesprovide the major blood supply of the corpuscallosum via the pericallosal artery and smallpenetrating vessels that run perpendicular tothe parent artery. On MR imaging, infarctshave the same characteristics as strokes else-where, with similar enhancement patterns.Differentiation of lacunar infarcts from otherentities such as trauma and demyelinating pro-cesses can be made by the presence of concur-rent infarcts in characteristic sites (centrumsemiovale, basal ganglia). With large-vessel is-chemic events, the corpus callosum is usuallyinvolved as part of a large vascular distribution[8] (Fig. 8).

Arteriovenous Malformations

Arteriovenous malformations of the corpuscallosum comprise 911% of all cerebral ar-teriovenous malformations. Clinically, 84%of patients with these malformations presentwith intracranial hemorrhage, most with in-traventricular hemorrhage. Most are suppliedby both the anterior and posterior cerebral ar-teries, and many have a bilateral blood sup-ply. Drainage is mainly into the internalcerebral vein or interhemispheric superficialveins. The MR imaging characteristics arethose of arteriovenous malformations else-where, with serpentine flow voids notedthrough the corpus callosum and the ventricle

A B

Fig. 8.59-year-old man with infarct who presentedwith confusion.A, Axial T2-weighted MR image shows well-definedlesion of corpus callosum genu.B, Axial T2-weighted image obtained 2 weeks after A showsthat lesion (arrow) is smaller and has decreased in signal. C, Enhanced axial T1-weighted MR image obtained 2weeks after B shows enhancement of lesion (arrow).D, Axial T2-weighted MR image 6 weeks after initialpresentation shows that lesion (arrow) is smaller. E, Enhanced axial T1-weighted MR image 6 weeks af-ter initial presentation shows enhancement has es-sentially resolved, typical of evolution of infarct.

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and frequently with evidence of intraventricu-lar hemorrhage [9] (Fig. 9).

Trauma

Injury to the corpus callosum occurs com-monly with head trauma, being detected on MRimaging in 47% of patients with nonfatal head

injuries. The classic triad of diffuse axonal in-jury is that of diffuse damage to axons located atthe graywhite matter interface of the cerebralhemispheres, the dorsolateral aspect of the ros-tral brainstem, and the corpus callosum. Thecallosal lesions most commonly involve thesplenium, are usually eccentric in location, andcan involve a focal part or the full thickness of

the corpus callosum. On MR imaging, spin-echo T2-weighted images and FLAIR se-quences during the sagittal plane are most sensi-tive in detecting small nonhemorrhagic lesions.Hemorrhagic lesions are best seen on T2-weighted images during the first 4 days after in-jury and, after 4 days, are better seen on T1-weighted images. Furthermore, gradient-echo

A B

Fig. 9.42-year-old man with arteriovenous malfor-mation who presented with intraventricular hemor-rhage.A, Sagittal T1-weighted MR image shows hemor-rhage (arrows) and multiple flow voids in corpus cal-losum. B, Axial T2-weighted MR image shows hyperintenselesion (arrow) with flow voids.

A B

Fig. 10.20-year-old man with diffuse axonal injury 1 week after motor vehicle crash. A, Sagittal T1-weighted MR image shows nonhemorrhagic hypointense lesion (arrow) of corpus callosum. B, Axial proton densityweighted MR image shows hyperintense lesion of corpus callosum. C, Sagittal T1-weighted MR image on follow-up examination 10 days after B shows hemorrhagic lesion of corpus callosum. D, Enhanced coronal T1-weighted MR image on follow-up examination 10 days after B shows hemorrhagic lesionof corpus callosum, with classic shearing-type lesion also seen at graywhite junction, both indicative of diffuseaxonal injury.

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T2-weighted sequences are superior in detect-ing chronic hemoglobin degradation productsbecause of the susceptibility effects of hemosid-erin. Differentiation from other lesions such asischemia should be made on the basis of historyand the location of the lesions in the corpus cal-losum [10] (Fig. 10).

Miscellaneous Lesions

Lesions in the corpus callosum, both dif-fuse and focal, have been described in pa-tients with long-standing hydrocephalus aftershunting. Callosal lesions and tectal neo-plasms producing hydrocephalus have beenseen in patients with aqueductal stenosis. Pa-tients with these lesions were thought to havelong-standing hydrocephalus before ventric-ular decompression. The exact mechanismresponsible for the production of these cal-losal lesions is unknown, although they maybe the result of ischemia with subsequent de-myelination caused by prolonged severestretching of the corpus callosum from ventric-

ulomegaly and subsequent rapid decompres-sion of the ventricles. These lesions appearhypointense on T1-weighted images and hy-perintense on T2-weighted images, withsparing of the splenium. Although thechanges may persist on imaging, they appearclinically silent [11] (Fig. 11).

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A B

Fig. 11.45-year-old man with cystic lesions associ-ated with long-standing hydrocephalus, with multipleprior shunt revisions. Patient is asymptomatic otherthan for headaches, which are probably due to mildhydrocephalus. A, Sagittal T1-weighted MR image shows well-definedcystic lesions (arrows) of corpus callosum. B, Axial T2-weighted MR image shows abnormal sig-nal (arrow) throughout corpus callosum, which haspersisted for many years.

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