SDMRad

INTRODUCTION

• The corpus callosum is the largest white matter structure in the brain, consisting of millions of contralateral axonal projections and the major commissural pathway connecting the hemispheres of the human brain.

• The pathology of the corpus callosum includes a wide variety of entities that arise from different causes.

NORMAL ANATOMY

• —The CC is visualised with a high signal in T1WI  and a low signal in T2 images.

• —Four regions: Anterior to posterior they are the rostrum, the genu, the body and the splenium

A. CONGENITAL DISORDERS

    Complete or partial absence of the corpus callosum

• The white matter tracts, which usually cross the midline, migrate ipsilaterally and go over the supero-internal region of the lateral ventricles forming the so called Probst bundles

• Radial guidance and racing car sign configuration of the gyri.

• Parallel lateral ventricles and high-riding third ventricle adjoining the interhemispheric fissure

• Colpocephaly: dilatation of the trigone and posterior and occipital temporal horns of the lateral ventricles

• Associated to other brain abnormalities, such as Lipoma, holoprosencephaly.

    Complete Agenesis of corpus callosum with lipoma

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B. ATROPHY DUE TO PERINATAL BRAIN INJURY

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• —Related to agenesis, dysgenesis or hypoplasia of the corpus callosum caused by an injury to the grey or white matter when it is not fully formed, in the weeks 18 to 20 of gestation approximately.

• Disorders that could lead to a damage include a viral infection or  hypoplasia of the corpus callosum due to severe anoxia.

 

 Hypoplasia of corpus callosum

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 C. TUMORAL DISEASES

• —Glioblastoma multiforme (GBM) are the most common primary brain tumors in adults.

• Most aggressive type of glioma, usually supratentorial, which usually spread via direct extension along the white matter tracts, including the corpus callosum, resulting in a "butterfly pattern" by bihemispheric involvement

 GBM involving corpus callosum

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 D. INFLAMMATORY-DEMYELINISING EVENTS

—Multiple Sclerosis (MS)

• MS is an acquired demyelinising disease

• MS plaques can be found in any region of the brain parenchyma- periventricular region, corpus callosum, centrum semiovale, and deepwhite matter structures and basal ganglia

• 93% of MS patients show lesions in the corpus callosum, characteristically involving the callososeptal surface.

• —Plaques are typically hyperintense on the proton density, T2, and FLAIR sequences and hypointense on T1 and show enhancement during the acute phase.

• Plaques may also exhibit a reversible restriction of diffusion due to exocytotoxic intramyelinic edema.

 MS Plaque invloving the Splenium

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 E. VASCULAR PROCESSES

 Infarcts

• Isolated Ischemic lesions of the corpus callosum are rare.

• Rostrum and genu- Anterior communicating and Pericallosal arteries

• Body - Anterior cerebral arteries

• Splenium –Posterior cerebral arteries

• Ischemic lesions usually affect the splenium, followed by the body and genu, with preservation of the dorsal and ventral surface.

 Arterial and venous infarcts involving the Splenium

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—Periventricular leukomalacia

• Most common ischemic brain injury in premature infants.

• —Characteristically occurs in the periventricular white matter adjacent to the lateral ventricles.

• —Atrophy and irregularity of the corpus callosum in advanced stages

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Periventricular leukomalacia with interhemispheric cyst and 

atrophy of corpus callosum

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 F.INFECTIOUS AGENTS

• —Viral infections( HSV -6,Influenza, JC ,EBV) cause reversible lesions of the CC splenium .

• —MRI  - high T2 signal,  low on T1 imaging, with restricted diffusion and a decreased ADC.

• —Dissapears after 48-72 hrs 

 

 Encephalitis involving the splenium 

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 G. TRANSIENT LESIONS

 

• —Associated with oedematous and  or inflammatory changes.

• —Risk  factors -Acute withdrawal of antiepileptics , epileptic status, Wernicke, or virus infections.

• MRI  reveals an oval-shaped lesion of 1-2cm in the corpus callosum splenium, hypointense on T1W images and hyperintense on T2W images and show restriction of Diffusion(boomerang sign ), which is usually reversible due to exocitotoxic edema.

• Lesions usually disappear withina few weeks following adequate therapy

 

 Transient splenic lesion ( Boomerang sign )

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 H. MISCELLANEOUS

—CC atrophy can be the result of cortical and subcortical hemispheric lesions due to ischaemic parenchymal destruction, degenerative diseases.

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Focal Atrophy of corpus callosum

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 CONCLUSION

• —MRI is the modality of choice for the study of the CC.

• —The CC remains a relatively unexplored region of the brain, somewhat of a “terra incognita’’ for the radiologist

• —Familiarity with its anatomy and pathology is important to the radiologist in order to recognise its disease at an early stage and help the clinician establish the optimal therapeutic approach.

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 References

• — Masot VL,  Blasco G , Alcántara JP et al Lesions of the corpus callosum: MRI findings anddifferential diagnosis. ECR 2013

• —BourekasCE , Varakis K  Bruns D et al, Lesions of the Corpus Callosum:MR Imaging and Differential Considerations in Adults and ChildrenAJR 2002;179:251–257

• —A Fitsiori , Ngyuen , Karentzos  et al,The corpus callosum: white matter or terra incognita. BJR, Jan 2011;84 :5–18.

• — Hetts WS, SherrHE, Chao S et al .Anomalies of the Corpus Callosum:An MR Analysis of the Phenotypic Spectrum of Associated Malformations. AJR 2006; 187:1343–1348.

• —Malhotra HS ,Garg RK,Vidhate RM et al .Boomerang sign clinical significance of  transient lesion in corpus callosum .An Indian Acad Neurol,2012;15:151-7

• —N. Bulakbasi ,M. Kocaoglu ,C. Tayfunet al Transient Splenial Lesion of the Corpus Callosum in Clinically Mild Influenza-AssociatedEncephalitis /Encephalopathy. Am J Neuroradiol  2006 oct ;27:1983– 86 

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