Imaging Spectrum of Pediatric Corpus Callosal Pathology: A Pictorial Review

Views and Reviews

Imaging Spectrum of Pediatric Corpus Callosal Pathology:A Pictorial Review

Jeong Hyun Yoo, MD, PhD, Jill Hunter, MDMokdong Hospital, Ewha Womans University, School of Medicine, Radiology, Seoul, Republic of Korea (JHY); Texas Children’s Hospital, Division of Neuroradiology, DiagnosticImaging, Houston, Texas (JH).

Keywords: Corpus callosum, MR imag-ing, pediatric.

Acceptance: Received February 15,2011, and in revised form August 1, 2011.Accepted for publication September 16,2011.

Correspondence: Address correspon-dence to Jeong Hyun Yoo, MD, PhD,Mokdong Hospital, Ewha WomansUniversity, School of Medicine, 911-1,MokDong, YangcheonKu, Seoul, Korea,158-710. E-mail: [email protected].

Conflict of Interest: None.

J Neuroimaging 2012;XX:1–15.DOI: 10.1111/j.1552-6569.2011.00681.x

A B S T R A C TA wide spectrum of pediatric corpus callosal diseases can occur in the pediatric age group.Cross-sectional magnetic resonance imaging plays an important role in the diagnosis ofthese patients. We reviewed our imaging record and collected cases of corpus callosalpathology. The purpose of this review is to illustrate the imaging features of variouscorpus callosal lesions encountered in children.

IntroductionThe corpus callosum is a large dense white matter tract con-necting the two cerebral hemispheres. Disease of the corpuscallosum in children is different from that of adults, includinga large number of congenital diseases. In order to understandthese diseases, it is essential to understand the basic conceptsof commissural development. It is not a common site for theacquired disease because dense compact white matter can bea barrier to the disease process. We retrograde reviewed thecorpus callosal lesions diagnosed on magnetic resonance imag-ing (MRI) during the last 5 years using a word engine searchin our PACS at the large tertiary referral pediatric center in theUnited States, and collected cases of corpus callosal pathology.The purpose of this review is to illustrate various imaging fea-tures of many congenital and acquired corpus callosal diseasesencountered in children with short reviews.

Embryology Overview

Embryologically, the corpus callosum begins to develop atabout 7 weeks of gestation, the callosal plate is detected by14 weeks, and the adult form is virtually complete by 20weeks of gestational age. It gradually increases thickeningand length during the first year, reaching adult thickness bythe sixth or ninth year (Fig 1). It is composed of four por-tions: rostrum, genu, body, and splenium. There has been

a lot of debate over the sequence and timing of the devel-opment of the corpus callosum. In general, it was acceptedthat the corpus callosum starts with the development of thegenu; the body and splenium develop later. The rostrum wasthought to be the last part to develop.1 However, recent stud-ies based on diffusion tensor imaging (DTI) have demonstratedthat the rostrum was already present at around 15 weeks ofgestational age, along with the genu and anterior part of thebody.2

Classification of Corpus Callosal AnomalyAgenesis of the corpus callosum (ACC) is a relatively frequentmalformation. If the normal developmental process of the cor-pus callosum is disturbed, it may be completely absent (agen-esis) or partial (hypogenesis). Two types of ACC can be dis-tinguished morphologically: Type 1 ACC, in which axons arepresent but are unable to cross the midline; they form largeaberrant longitudinal fiber bundles (Probst bundles) (Fig 2).Type 2 ACC, apparently less frequent, in which axons fail toform; therefore, no Probst bundles are found.3 For understand-ing the hypogenesis of corpus callosum, the basic knowledgeof the developmental sequence is absolutely required. Whenthe corpus is hypogenetic, the earlier formed genu and anteriorbody will be formed; however, the later formed posterior body

Copyright ◦C 2012 by the American Society of Neuroimaging 1

Fig 1. Schema explaining corpus callosal development, and congenital hypogenesis, hypoplasia, and acquired defects of corpus callosum.Normal corpus callosal development (a-d); corpus callosum begins to develop from the genu (a), the body (b) and splenium later, and therostrum is the last part, the adult form of corpus callosum is virtually complete by 20 weeks of gestational age (c). But, it gradually increasesthickening and length during the 1st year reaching adult thickness by the 6th-9th year (d). Congenital hypogenesis of corpus callosum (e-g);Based on the developmental sequence of corpus callosum, as earlier corpus callosal development is arrested, as smaller dot-like genu oranterior body is formed. Distal part developed later period is terminated (e-g). Hypoplasia refers to diffuse thinning of corpus callosum withpreserving shape, which can be in prematurity (h). Acquired defects of corpus callosum (i-l); in contrast with sequential arrest of corpus callosalgrowth in the congenital hypogenesis, defects can be anywhere of corpus callosum. Although there is focal defect of anterior body (i) or diffusethinning genu and anterior body (j), other parts of corpus callosum already formed are intact. Focal or multifocal defects of corpus callosumresulted after corpus callosum completed show full length and thickness of corpus callosum (k, l).

and splenium will not4 (Figs 1 and 3). Hypogenesis of corpuscallosum can also be linked to a clastic lesion and can be asso-ciated with metabolic disease. In contrast, the term hypoplasiais nonspecific, and refers to a thin corpus callosum preservingits shape, which may be in prematurity without full maturation.

Callosal dysgenesis is defined as the malformation of the cor-pus callosum as a result of an injury during the formation ofits precursors, rather than from an injury to the corpus itself.This failure may result from extrinsic causes (lipoma, interhemi-spheric cyst [IHC], etc.), from disorders in neuronal migration,

2 Journal of Neuroimaging Vol XX No X 2012

Fig 2. Agenesis of the corpus callosum. Typical radiating medial sulci into the third ventricle (a), everted cingulated gyrus enable crossing ofthe midline to form the Probst bundle (b), and colpocephaly (c).

Fig 3. Various hypogenesis of the corpus callosum. A small dot of the corpus callosal genu only (a), thin hypoplastic genu and anterior bodyformation (b), and partial agenesis of splenium and rostrum with the genu and major portion of the body remaining (c).

Yoo and Hunter: Imaging Spectrum of Pediatric Corpus Callosal Pathology 3

Fig 4. Acquired dysplasia of the corpus callosum. Focal defect of the anterior body of the corpus callosum with only small islands of a genuand mid body formed in static encephalopathy (a), diffuse thinning genu, and anterior body of the corpus callosum in sequellae of perinatalischemic insult; however, a relatively intact posterior body and splenium can be embryologic differential points from congenital dysgenesis(b), diffuse thinning of the posterior body and splenium of the corpus callosum due to corticospinal tract injury in spastic diplegia (c), diffuseatrophy of the corpus callosum in nonaccidental injury (NAI).

or an intracortical disposition linked with a gyral anomaly. Theknowledge of the developmental sequence of the corpus callo-sum is helpful in the differentiation of congenital hypogenesisor dysgenesis versus acquired dysplasia or destruction (Figs 1and 4). Focal defect or thinning genu and anterior body of thecorpus callosum but intact posterior body and splenium aretypical findings of acquired dysplasia or destruction of corpuscallosum, which can be embryologic differential points fromcongenital hypogenesis or dysgenesis. If the corpus callosum isarrested at the level of genu and anterior body, posterior bodyand splenium is terminated without formation.

Congenital Diseases Associated with CorpusCallosal AbnormalityFormation of most of the cerebrum and cerebellum occurs atthe same time as that of the corpus callosum, between 8 and 20weeks of gestational age. Therefore, anomalies in the corpus cal-losum are often associated with other anomalies in the cerebrumand cerebellum, including occasionally holoprosencephaly, en-cephalocele, and posterior fossa anomalies (Fig 5). Holopros-encephaly shows variable callosal anomalies from the ACCto the dysgenesis associated with lobal types, and it is knownto be the only brain malformation in which the posterior cor-pus callosum can be formed in the absence of anterior callosalformation3,4 (Fig 6). The corpus callosum is already formed

in the migration stage and then migration anomaly shows anintact or mild dysgenetic appearance (Fig 7). IHC is new clas-sified by subtypes based on morphology and clinical featuresby Barkovich and colleagues.5 Loculated cyst without ventric-ular continuation, known as a Type II cyst, has frequently beenassociated with brain anomalies, including those of the cor-pus callosum5-9 (Fig 8). Nowadays, intracranial lipomas arethought to be congenital malformation resulting from abnor-mal, persistent maldifferentiation of meninx primitive, the for-mal primordium of the meninges during subarachnoid cisternsdevelopment; therefore, it is not surprising that intracranial lipo-mas are associated with up to 40% to 50% of callosal anoma-lies10,11. Pericallosal area is the most frequent site, and ante-rior pericallosal lipomas are commonly associated with severecorpus callosal anomalies than posterior pericallosal lipomas(Fig 9).

Vascular LesionsVascular Anomalies

Vascular anomalies involving the corpus callosum are not com-mon; however, several diseases such as arteriovenous malfor-mation (AVM), cavernous angioma, the Osler-Rendu-Webersyndrome, and the Sturge-Weber syndrome can involve thecorpus callosum.12-15 Corpus callosal AVM, about 10% of allcerebral AVM, shows typical MR finding with signal voided


Fig 5. Posterior fossa anomalies associated with the corpus callosum. Dysplastic corpus callosum with thin body and splenium in Chiary IImalformation (a), unusual beaked shape of the corpus callosum in the posterior fossa anomaly with a mesencephalic cleft (b,c), hypogeneticcorpus callosum in the Dandy-Walker malformation with inferior vermian hypoplasia and a large posterior fossa cyst (d), dysgenesis of thecorpus callosum with rhombencephalonsynapsis (e).

Fig 6. Holoprosencephaly with ACC. Absence of the corpus callosum of the genu, but presence of the posterior body and splenium.

malformed vessel commonly presented with intraventricu-lar hemorrhage. About 5% to 10% of patients with Osler-Rendu-Weber syndrome, also known as hereditary hemor-rhagic telangiectasia, have cerebral AVMs. The most strikingfeature is their multiplicity in comparison with other AVMs.In the Sturge-Weber syndrome, dilated deep medullary veinsdeveloped as a compensatory mechanism can extend to thecorpus callosum (Fig 10).

Hemorrhage and Infarct

The corpus callosum has a rich blood supply from pericallosaland penetrating arteries and from the anterior and posteriorcerebral arteries; therefore, ischemic injury of the corpus callo-sum is not common. The most common site of callosal infarct,

if it occurs, is the splenium followed by the body and genu.In pediatrics, cardiac surgery for the congenital heart diseasecan be associated with callosal ischemic change. Acute infarctshave the same characteristics as strokes occurring elsewherewith diffusion restriction on MR.

Nontraumatic hemorrhage may occur with underlying vas-cular lesions such as AVM or pericallosal aneurysm rup-ture.16-20 Traumatic injury commonly occurs in head traumabecause compact white matter tracts make it more suscepti-ble to shear injury. The splenium is the mostly commonly in-volved eccentric focal or full thickness. Acute hemorrhagic ax-onal injury shows signal intensities similar to those of the typicalhemorrhage on T1- and T2-weighted scan; however, gradient-echo sequences are superior in detection of microbleed and


Fig 7. Corpus callosal anomaly associated with migration anomaly. Diffuse smoothness of the corpus callosum in the thick band of graymatter throughout the subcortical white matter (a,b). Focal thinning of corpus callosal body in the bilateral schizencephaly (c,d)

chronic hemosiderin deposits due to the susceptibility effects(Fig 11). Pediatric nonaccidental injury can result in corpus cal-losal injury when the brain is shaken (Fig 12). DTI can easilydemonstrate fiber tract disconnection in corpus callosal injury(Fig 13).

Infection and InflammationAlthough the dense compact fiber tracts of corpus callosum canact as a barrier to disease process, corpus callosum is rarely af-fected by infection and inflammation related to the rich bloodsupplies. In children with chronic immune compromised con-ditions such as leukemia, fungal, and unusual bacterial infec-tion rarely involve the corpus callosum. Extension from theadjacent ventriculitis is the usual pattern (Fig 14) with focal ordiffuse enhancing foci or abscess. Uncommonly, nonenhancinghigh-signal intensity lesions involving the splenium with AIDShave been reported.21

NeoplasmThe corpus callosum is relatively resistant to the passage ofedematous fluid; therefore unless the lesion primarily invadesthe corpus callosum, it is unusual to meet a bilateral pattern ofhemispheres. Most common primary corpus callosal tumors of

glioblastoma multiforme (GM) and lymphoma in adults are notuncommon in pediatrics. The commonly characteristic butter-fly pattern of GM (Fig 15) differs from that of lymphoma. Lym-phoma shows homogeneous enhancement, less central necro-sis, less peritumoral edema, and more commonly multiple, andshows low signal intensity on T2WI reflecting dense cellularity.Lymphomas also differ from GM in being highly radiosensitiveand temporarily respond dramatically to steroid therapy. Othersupratentorial tumor can involve the corpus callosum when itis aggressive or diffuse infiltrative (Fig 15). Atypical or malig-nant extra-axial tumor can also invade and spread through-out the brain parenchyma and corpus callosum (Fig 16). Germcell tumors commonly found in pineal and suprasellar regionsare involved in the corpus callosum through ependymal andsubependymal spreading of the tumor (Fig 17). Medulloblas-toma can also spread into the corpus callosum, including lep-tomeningeal spread in pediatric patients (Fig 18).

White Matter Diseases Affecting the CorpusCallosumDemyelinating Diseases

The corpus callosum is the thickest bundle of the white mattertract; therefore, the involvement of the corpus callosum in white


Fig 8. IHC with a corpus callosal anomaly. Huge IHC communicating with the bilateral ventricle (type I) with a superiorly elevated hypoplasticthin corpus callosum (a,b). Large round IHC without ventricular communication (type II) with ACC associated with both frontal and perisylvianpolymicrogyria and subependymal heterotopia in the right frontal and left atrium (c,d).

Fig 9. Intracranial lipoma associated with corpus callosal anomaly. Severe hypogenesis of the corpus callosum with anterior pericallosallipoma (a). Posterior pericallosal lipoma around the relatively well developed corpus callosum (c,d).


Fig 10. Congenital vascular lesions of the corpus callosum. Cavernous angioma with typical popcorn-like hemorrhage (a). Osler-Rendu-Weber syndrome with massive arteriovenous malformation of the left cerebral hemisphere with ipsilateral brain atrophy (b). Sturge-Webersyndrome with a large draining deep medullary vein (c).

Fig 11. Traumatic hemorrhage of the corpus callosum. Swelling and hemorrhage of the corpus callosal splenium (a,b), hemorrhage wellvisualized on the gradient-echo sequence (c).

Fig 12. Corpus callosum injuries associated with nonaccidental injury (NAI). Cystic defect of the genu and anterior body with bilateralsubdural collection (a,b), high signal intensity in the diffusion weighted image along the right parietal white matter and corpus callosalsplenium (c).

Fig 13. Diffusion tensor image (DTI) of traumatic axonal injury. (a) A posttraumatic cyst following traumatic birth injury, diffusion tractographysuperimposed on B0 and without B0 image demonstrating paucity of fibers (b, c). Red = R-L, Green = A-P, Blue = I-S.


Fig 14. Fungal infections in different acute leukemia patients. Thick band-like enhancement along the ventricles and choroids plexus in ALL(a), focal enhancement of the left corpus callosal splenium in AML (b).

Fig 15. Neoplasm involving corpus callosum. Glioblastoma multiforme crossing corpus callosum with typical butterfly pattern and intenseenhancement (a,b), anaplastic ependymoma with irregular huge solid and cystic mass invading corpus callosal body complicated obstructivehydrocephalus (c,d).


Fig 16. Choroid plexus carcinoma with irregular enhancing mass of right lateral ventricle direct invading brain parenchyma and splenium(a,b), atypical meningioma with huge bifrontal extraxial mass involving corpus callosum (c,d)

Fig 17. Germinoma direct spreading into the corpus callosum. Intensely enhancing mass involving the pineal and suprasellar regions withextensive genu and minimal left splenium enhancing extension with surrounded white matter edema.


Fig 18. Metastasis of medulloblastoma. Diffuse swelling and patch enhancement of the corpus callosum and pachymeningeal involvement,indicative of tumor spreading.

Fig 19. Multiple sclerosis. Multifocal high signals along the callososeptal interface (a), and multiple ovoid-shaped high signals in the bilateralparietal region, corpus callosum, and midbrain (b) in different patients.

matter disease is possible. Corpus callosum is one of the com-monly involving sites of the multiple sclerosis (MS) includingperiventricular white matter, interval capsule, and pons. Cal-lososeptal interface is the most characteristic sites. MS plaquesinvolving the corpus callosum show similar signal findings suchas usual MS plaques in T2-weighted and FLAIR sequences(Fig 19). Enhancement is common in the active stage, and dif-fusion restriction can occur in the acute stage. Atrophy of thecorpus callosum coexists in long-standing chronic MS as wellas an extensive white matter change, which can be a surrogatemarker of disease worsening with significant correlation of mor-phological and functional impairment.20,22-26 Acute dissemi-nated encephalomyelitis (ADEM) is often very similar to MSin MR imaging, although clinically monophasic symptoms withcomplete recovery is typical that can be a differential point withMS. It can be helpful in differential diagnosis of preferentiallydeep gray matter, and subcortical white matter is more com-monly involved in ADEM than periventricular white matter inMS (Fig 20).

Vanishing White Matter Disease

Vanishing white matter disease, also called childhood ataxiawith diffuse CNS hypomyelination, is one of the most

Fig 20. Acute disseminated encephalitis. Bilateral symmetric highsignal intensities of genu of the corpus callosum and subcortical whitematter.


Fig 21. Vanishing white matter disease. Extensive cystic necrosis of the entire corpus callosum especially center, with extensive white matterencephalopathy (a,b).

Fig 22. Adrenoleukodystrophy. Bilateral symmetric high signal intensities of periventricular and subcortical white matter, posterior thalami,and the corpus callosal splenium (a), marginal enhancement of the affected region, characteristic and helpful in differential diagnosis (b).

Fig 23. Type II mucopolysaccharidosis (Hunter disease). Multiple cystic change and atrophy of the corpus callosum combined with extensivewhite matter high signal intensities.


Fig 24. Traumatic sharing injury induces posttraumatic cysts of the corpus callosum.

Fig 25. Morphologic change of the corpus callosum after VPS with irregular contracted contour and high signal intensities of the corpuscallosum.

prevalent inherited childhood white matter disorders. It is anautosomal recessive inheritance related to mutation in any ofthe five genes (EFI2B1–5) with progressive leukodystrophy witha relapsing-remitting course. The typical finding of corpus cal-losum is extensive rarefaction with central cystic degenerationsparing peripheral portion of corpus callosum. There is no con-trast enhancement27 (Fig 21).

Metabolic Diseases Affecting the Corpus Callosum

Adrenoleukodystrophy is a rare inherited disorder involvingbreakdown of very long chain fatty acid metabolism resultingin progressive damage to the myelin and bran and even-tually death. The most common X-linked form shows sym-metric peri-trigonal white matter and splenium involve-ment with characteristic marginal contrast enhancement(Fig 22).

Mucopolysacharidosis (MPS) is a part of the lysosomal stor-age disease family caused by the absence of lysosomal enzymes.Among the 11 enzymes, type II MPS, called Hunter, shows typ-ical brain MR findings involving white matter changes. Corpuscallosum and white matter show multiple but typical round cys-tic lesions, which are known to be filled not with CSF but withmucopolysacharide infiltration (Fig 23).

Secondary Changes of the Corpus CallosumCystic Lesions

Cystic lesions of the corpus callosum can be the results oftrauma such as axonal injury or nonaccidental injury in pe-diatrics, and can be a finding of such as Hunter syndrome orchronic disease (Fig 23 and 24).18,28-30

Morphologic Change After Ventriculo-Peritoneal Shunt (VPS)

Secondary change of the corpus callosum has been describedin patients with long-standing hydrocephalus after VPS. Sev-eral causes have been suggested including edema, ischemia,demyelination due to by prolonged severe stretching of thecorpus callosum from ventriculomegaly, and subsequent rapidventricular decompression after VPS. Most authors have in-dicated the long-standing compression of the corpus callosumagainst the rigid falx as the causative agent, more common inthe obstructive hydrocephalus. Scalloping of the dorsal surfaceof corpus callosum was attributed to ventral collapse of the cor-pus callosum after shunt placement with segmental tethering ofthe dorsal surface. After shunt removal, this callosal change canbe reversible; however, changes reported in the literature maybe irreversible. Although the changes may persist on imaging,they appear to be clinically silent31-33 (Fig 25).


Fig 26. Transient signal change of the corpus callosal splenium in a diffusion weighted image in an epileptic patient.

Transient Signal Change of the Corpus Callosum

A transient corpus callosal lesion usually involving splenium isoften seen in epilepsy, encephalitis, migraine, and in antiepilep-tic withdrawal. The lesion shows high SI on T2WI with diffu-sion restriction on the diffusion-weighted image, and subsideswithout sequellae. The pathogenesis is still unclear; however,several theories have been proposed, including intramyelinicedema due to diffusion restriction and reversible change,19,28,34

and interstitial edema of tightly packed fibers and transient in-flammatory infiltrate35,36 (Fig 26).

ConclusionThere are many congenital and acquired diseases involving thecorpus callosum with very unique findings. For the differentialcorrect diagnosis of the many congenital and acquired defectsof the corpus callosum, it is helpful to understand the basicconcepts of corpus callosal development. For the correct diag-nosis of acquired corpus callosal disease, it is helpful to haveknowledge based on the many related diseases. MRI is the mostuseful, not only for the diagnosis of corpus callosum lesions, butalso for understanding the underlying pathophysiology madeeasier by the characteristic anatomical location. MR is also use-ful for differentiation of many congenital and acquired diseasesinvolving the corpus callosum.

References1. Kier EL, Truwit CL. The normal and abnormal genu of the cor-

pus callosum: an evolutionary, embryologic, anatomic, and MRanalysis. AJNR Am J Neuroradiol 1996;17(9):1631-1641.

2. Ren T, Anderson A, Shen WB, et al. Imaging, anatomical, andmolecular analysis of callosal formation in the developing humanfetal brain. Anat Rec A Discov Mol Cell Evol Biol 2006;288(2):191-204.

3. Volpe P, Campobasso G, De Robertis V, et al. Disorders of pros-encephalic development. Prenat Diagn 2009;29(4):340-354.

4. Barkovich AJ. Magnetic resonance imaging: role in the under-standing of cerebral malformations. Brain Dev 2002;24(1):2-12.

5. Barkovich AJ, Simon EM, Walsh CA. Callosal agenesis with cyst:a better understanding and new classification. Neurology 2001;56(2):220-227.

6. Barth PG, Uylings HB, Stam FC. Interhemispheral neuroepithe-lial (glio-ependymal) cysts, associated with agenesis of the corpuscallosum and neocortical maldevelopment. A case study. ChildsBrain 1984;11(5):312-319.

7. Lena G, van Calenberg F, Genitori L, et al. Supratentorial inter-hemispheric cysts associated with callosal agenesis: surgical treat-ment and outcome in 16 children. Childs Nerv Syst 1995;11(10):568-573.

8. Pavone P, Barone R, Baieli S, et al. Callosal anomalies withinterhemispheric cyst: expanding the phenotype. Acta Paediatr2005;94(8):1066-1072.

9. Utsunomiya H, Yamashita S, Takano K, et al. Midline cystic mal-formations of the brain: imaging diagnosis and classification basedon embryologic analysis. Radiat Med 2006;24(6):471-481.

10. Truwit C. MRI findings in 32 consecutive lipomas using con-ventional and advanced sequences. J Neuroimaging 2000;10(3):190-191.

11. Truwit CL, Barkovich AJ. Pathogenesis of intracranial lipoma: anMR study in 42 patients. AJR Am J Roentgenol 1990;155(4):855-864[discussion 865].

12. Kikuchi K, Kowada M, Sasajima H. Vascular malformations ofthe brain in hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease). Surg Neurol 1994;41(5):374-380.

13. Kikuchi K, Kowada M, Tomura N, et al. Hereditary hemorrhagictelangiectasia associated with cerebral arteriovenous fistula andmultiple cerebral arteriovenous malformations: case report. NoShinkei Geka 1994;22(1):85-91.

14. Matsubara S, Mandzia JL, ter Brugge K, et al. Angiographic andclinical characteristics of patients with cerebral arteriovenous mal-formations associated with hereditary hemorrhagic telangiectasia.AJNR Am J Neuroradiol 2000;21(6):1016-1020.

15. Ozer E, Yucesoy K, Kalemci O. Demonstrated rapid growth of acorpus callosum cavernous angioma within a short period of time.J Neurosurg Sci 2005;49(4):155-158 [discussion 158].

16. Leiguarda R, Starkstein S, Berthier M. Anterior callosal haemor-rhage. A partial interhemispheric disconnection syndrome. Brain1989;112 (Pt 4):1019-1037.

17. Riedy G, Melhem ER. Acute infarct of the corpus callosum:appearance on diffusion-weighted MR imaging and MR spec-troscopy. J Magn Reson Imaging 2003;18(2):255-259.

18. Rubens AB, Geschwind N, Mahowald MW, et al. Posttrau-matic cerebral hemispheric disconnection syndrome. Arch Neurol1977;34(12):750-755.

19. Takayama H, Kobayashi M, Sugishita M, et al. Diffusion-weightedimaging demonstrates transient cytotoxic edema involving the


corpus callosum in a patient with diffuse brain injury. Clin Neu-rol Neurosurg 2000;102(3):135-139.

20. Uchino A, Takase Y, Nomiyama K, et al. Acquired lesions of thecorpus callosum: MR imaging. Eur Radiol 2006;16(4):905-914.

21. Georgy BA, Hesselink JR, Jernigan TL. MR imaging of the corpuscallosum. AJR Am J Roentgenol 1993;160(5):949-955.

22. Straus Farber R, Devilliers L, Miller A, et al. Differentiating mul-tiple sclerosis from other causes of demyelination using diffusionweighted imaging of the corpus callosum. J Magn Reson Imaging2009;30(4):732-736.

23. Forrester MB, Coleman L, Kornberg AJ. Multiple sclerosisin childhood: clinical and radiological features. J Child Neurol2009;24(1):56-62.

24. Balassy C, Bernert G, Wober-Bingol C, et al. Long-term MRIobservations of childhood-onset relapsing-remitting multiple scle-rosis. Neuropediatrics 2001;32(1):28-37.

25. Pelletier J, Suchet L, Witjas T, et al. A longitudinal study of callosalatrophy and interhemispheric dysfunction in relapsing-remittingmultiple sclerosis. Arch Neurol 2001;58(1):105-111.

26. Gean-Marton AD, Vezina LG, Marton KI, et al. Abnormal corpuscallosum: a sensitive and specific indicator of multiple sclerosis.Radiology 1991;180(1):215-221.

27. Pineda M, A RP, Baquero M, O’Callaghan M, et al. Vanishingwhite matter disease associated with progressive macrocephaly.Neuropediatrics 2008;39(1):29-32.

28. Rutgers DR, Toulgoat F, Cazejust J, et al. White matter abnor-malities in mild traumatic brain injury: a diffusion tensor imagingstudy. AJNR Am J Neuroradiol 2008;29(3):514-519.

29. Le TH, Mukherjee P, Henry RG, et al. Diffusion tensor imag-ing with three-dimensional fiber tractography of traumatic axonalshearing injury: an imaging correlate for the posterior callosal“disconnection” syndrome: case report. Neurosurgery 2005;56(1):189.

30. Vuilleumier P, Assal G. Lesions of the corpus callosum and syn-dromes of interhemispheric disconnection of traumatic origin. Neu-rochirurgie 1995;41(2):98-107.

31. Mataro M, Matarin M, Poca MA, et al. Functional and magneticresonance imaging correlates of corpus callosum in normal pres-sure hydrocephalus before and after shunting. J Neurol NeurosurgPsychiatry 2007;78(4):395-398.

32. Constantinescu CS, McConachie NS, White BD. Corpus callo-sum changes following shunting for hydrocephalus: case reportand review of the literature. Clin Neurol Neurosurg 2005;107(4):351-354.

33. Lane JI, Luetmer PH, Atkinson JL. Corpus callosal signalchanges in patients with obstructive hydrocephalus after ven-triculoperitoneal shunting. AJNR Am J Neuroradiol 2001;22(1):158-162.

34. Takeuchi S, Takasato Y, Masaoka H, et al. Transient lesion in thesplenium of the corpus callosum caused by diffuse axonal injury.Brain Nerve 2008;60(9):1078-1079.

35. Takanashi J. Two newly proposed infectious encephalitis/encephalopathy syndromes. Brain Dev 2009;31(7):521-528.

36. Gurtler S, Ebner A, Tuxhorn I, et al. Transient lesion in the sple-nium of the corpus callosum and antiepileptic drug withdrawal.Neurology 2005;65(7):1032-1036.


Imaging Spectrum of Pediatric Corpus Callosal Pathology: A Pictorial Review

Documents

Transcript of Imaging Spectrum of Pediatric Corpus Callosal Pathology: A Pictorial Review