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Keywords:

  • anomalies;
  • corpus callosum;
  • corpus callosum agenesis, magnetic resonance imaging (MRI);
  • variation

Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. Normal imaging appearance
  5. Lesions of the CC
  6. Conclusion
  7. References

Various types of lesions can occur within the corpus callosum (CC) which is a white matter tract communicating corresponding regions of the cerebral hemispheres. Magnetic resonance imaging is the modality of choice for the evaluation of the CC. In addition, diffusion weighted imaging and diffusion tensor imaging can provide additional information about the CC. The aim of this study is to illustrate the imaging features of the corpus callosum and its pathologies.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. Normal imaging appearance
  5. Lesions of the CC
  6. Conclusion
  7. References

The corpus callosum (CC) is the largest white matter tract that crosses the two cerebral hemispheres.1–3 Various types of lesions can occur within this structure such as congenital anomalies with or without various associated abnormalities, toxic and metabolic diseases, ischemic-hypoxic disease, demyelinating diseases, tumours, trauma and transient signal changes.1–14 Ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI) can be used in the assessment of CC. However, MRI is the modality of choice for the evaluation of this structure.1,2,6,7

The aims of this article are to discuss the role of state-of-the-art imaging tools and techniques in the imaging evaluation of CC, to describe the classification of CC pathologies and to recognize the patterns and imaging features of diseases that may involve the CC.

Normal imaging appearance

  1. Top of page
  2. Summary
  3. Introduction
  4. Normal imaging appearance
  5. Lesions of the CC
  6. Conclusion
  7. References

The CC is divided into four sections: the rostrum, genu, body and splenium. Magnetic resonance images in the three planes (especially in sagittal plane) can be used in detecting normal appearance and developmental and acquired lesions of the CC (Fig. 1).

image

Figure 1. Normal appearance of the corpus callosum (CC) in 6-year-old boy. Sagittal T1-weighted (a) and axial diffusion tensor (DT) (b) MR images show the normal CC (R = rostrum, G = genu, C = corpus, S = splenium).

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Lesions of the CC

  1. Top of page
  2. Summary
  3. Introduction
  4. Normal imaging appearance
  5. Lesions of the CC
  6. Conclusion
  7. References

Congenital anomalies

Agenesis

Agenesis of the CC is one of the common central nervous system malformations. This condition may be encountered as an isolated lesion or, more commonly, in association with a wide variety of other malformations of the central nervous system or other organ systems. The main feature of this entity is the lack of commissural fibers crossing the midline. These fibers instead migrate ipsilaterally and course along the superomedial region of the lateral ventricles and form a structure known as Probst bundles (Fig. 2).1,2

image

Figure 2. Agenesis of the CC. Sagittal T1-weighted (a) and axial DT (b) MR images show complete absence of the CC accompanied by the presence of Probst bundles (arrows).

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Dysgenesis

Growth of the CC is primarily from anterior to posterior with the genu forming first, then the anterior body, posterior body and splenium. The exception to this orderly anterior–posterior development is the rostrum. As a consequence of the order of formation, in dysgenesis, the splenium and rostrum are always missing (Fig. 3).1–3

image

Figure 3. 2-year-old boy with dysgenesis of the CC. Sagittal T1-weighted image shows absence of the entire CC, but the genu (arrow).

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Associated abnormalities

Interhemispheric cyst

Interhemispheric cysts occur in fewer than 7% of the patients with agenesis of the CC. The Barkovich classification divides cases of interhemispheric cysts associated with agenesis of the CC into two groups. The type 1 cysts are diverticula of the lateral or third ventricles, unilocular and isointense to cerebrospinal fluid (CSF). The type 2 cysts do not communicate with the ventricular system and have four subgroups (2a–d). Type 2a, 2b and 2c cysts are multilocular, whereas type 2d cysts are unilocular. When compared to CSF, type 2b cysts are hyperintense on the T1-weighted images, whereas other three subgroups are isointense (Fig. 4).4

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Figure 4. 2-year old boy with type 2b interhemispheric cyst. Axial (a) and sagittal (b) T1- weighted images demonstrate absence of the posterior body, splenium and rostrum of the CC, and loculated interhemispheric cyst (white arrows) with higher signal intensity in the posterior portion. Right posterior and periventricular gray matter heterotopia areas can be also seen (black arrows).

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Pericallosal lipoma

Approximately one-third of all intracranial lipomas arise in the pericallosal region. Depending on their size, either partial or complete agenesis of the CC is present in over 50% of cases with pericallosal lipoma.5 Lipomas of the CC are classically seen as well-marginated masses showing same signal intensities with fat tissue in all MR sequences (Fig. 5).

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Figure 5. 27-year-old woman with pericallosal lipoma. Sagittal T1-weighted image demonstrates a high intensity, linear mass (arrows), adjacent to the CC.

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Dandy–Walker complex

In Dandy–Walker complex, associated supratentorial anomalies such as callosal dysgenesis and neuronal migration anomalies may be present.6

Syntelencephaly

Syntelencephaly, also known as middle interhemispheric holoprosencephaly, was originally thought to be a semilobar holoprosencephaly type. However, it has been determined to be a unique malformation characterized by failure of cleavage of the dorsal regions of the brain. MRI reveals fusion of cerebral hemispheres in the dorsal region of the brain along with various degree of partial agenesis of the CC (Fig. 6).

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Figure 6. 2-year-old girl with syntelencephaly. Sagittal (a) and coronal (b) T1-weighted MR images demonstrate fusion of the cerebral hemispheres across the midline and partial agenesis of the CC.

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Toxic and metabolic diseases

Adrenoleukodystrophy

Adrenoleukodystrophy is a sex-linked metabolic encephalopathy of the childhood in which the basic defect is an impaired capacity to degrade very long chain fatty acids, caused by a peroxisomal enzyme defect in beta-oxidation, leading to the demyelination of the central nervous system. Involvement of the peritrigonal white matter and white matter tracts follows the involvement of the splenium of the CC which is usually the first affected site. Enhancing peritrigonal demyelination is the most important imaging feature (Fig. 7).7

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Figure 7. Biochemically and genetically proven adrenoleukodystrophy in an 11-year-old boy. Sagittal T1-weighted image (a) demonstrates low signal intensity in the splenium of the CC (arrow). Axial T2-weighted image (b) shows very intense signals within the entire white matter of both parieto-occipital lobes extending into the posterior part of internal capsules, thalamus and splenium of the CC (arrow).

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Mucopolysaccharidosis

The mucopolysaccharidoses lead to the accumulation of glycosaminoglycans in many tissues, such as brain parenchyma. Enlarged perivascular spaces can be prominent in healthy individuals. However, during the natural course of mucopolysaccharidoses, the formation of the enlarged perivascular spaces is usually followed by white matter changes and atrophy (Fig. 8).8

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Figure 8. 1-year old boy with mucopolysaccharidosis (Hurler syndrome) proven by clinical examination, urine tests and enzyme assays. Sagittal (a) and axial (b) T1-weighted images demonstrate involvement of the CC and periventricular white matter by dilated perivascular spaces.

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Ischemic-hypoxic disease (periventricular leukomalacia)

Periventricular leukomalacia (PVL) is the most common ischemic brain injury in premature infants. The ischemia occurs in the border zone of the arterial territories. This process typically involves the white matter surrounding the lateral ventricles. Direct corpus callosal involvement in PVL is extremely rare. However, atrophied and irregular CC may be seen in advanced PVL (Fig. 9).9

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Figure 9. 2-year old boy with periventricular leucomalacia. Axial fluid attenuated inversion recovery (FLAIR) image (a) shows bilateral symmetrical periventricular hyperintensities consistent with periventricular leucomalacia. Sagittal T1-weighted image (b) shows gross atrophy of the CC (arrows).

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Demyelinating diseases

Multiple sclerosis

Multiple sclerosis is a demyelinating disease that commonly affects young women. Although plaques can be found anywhere in the white matter, lesions of the multiple sclerosis characteristically involve the periventricular white matter, internal capsule, CC and pons. The CC lesions that occur along the ventricular margin and callosal-septal interface are considered to be very sensitive and specific for multiple sclerosis (Fig. 10).1

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Figure 10. 33-year-old woman with clinically and radiologically proven multiple sclerosis. Sagittal FLAIR image shows multiple hyperintense lesions in the CC and callosal-septal interface.

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Acute disseminated encephalomyelitis

Acute disseminated encephalomyelitis (ADEM) is an uncommon immune-mediated inflammatory demyelinating disease of the central nervous system. Usually, it is a monophasic illness, which may occur after viral infection or vaccination, in association with rheumatic fever, or without any recognized antecedent disease. Patients with ADEM and multiple sclerosis have a similar pattern of abnormalities on conventional MR images (Fig. 11).10

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Figure 11. 21-year-old man with clinically and radiologically proven acute disseminated encephalomyelitis. Sagittal FLAIR image shows focal hyperintense areas in rostrum, genu and anterior body, and diffuse hyperintensity in posterior body and splenium of the CC.

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Tumours

The most common primary tumour of the CC is glioma. Since the dense compact nature of the white matter tracts in CC makes a barrier to the flow of interstitial oedema and tumour spread, only aggressive tumours, such as glioblastoma multiforme and lymphoma typically cross or involve the CC. The diagnosis of callosal tumours can be made on MRI findings (Fig. 12).1

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Figure 12. 68-year old man with histopathologically proven glioblastoma multiforme. Sagittal T1-weighted (a), and axial T2-weighted (b) images demonstrate expansile lesion in the splenium (arrow) of the CC with extension into both cerebral hemispheres and moderate peritumoural oedema.

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Trauma

Surgery

CC may be traumatised by surgical procedures such as tumour surgery or therapeutic callosotomy. In some cases, seizures may spread from one hemisphere to the other through the CC. Corpus callosotomy may be performed in patients with generalized seizures resistant to multiple seizure medications.11 MRI is an effective method for evaluating callosal surgery and postsurgical changes such as oedema, haemorrhage, infarction and gliosis.

Diffuse axonal injury

Diffuse axonal injury (DAI) is a frequent cause of impaired clinical outcome in patients with traumatic brain injury. The location and severity of traumatic axonal injury is related to various factors, and one of the most common sites of DAI is the CC.12 In the acute and subacute phases, T1 or T2-weighted MR images can be used for detecting hemorrhagic lesions as foci of high signal intensity. On the other hand, T2-weighted images are more sensitive than T1-weighted images in detecting non-haemorrhagic DAI lesions. The use of fluid-attenuated inversion recovery (FLAIR) sequences to show acute non-hemorrhagic DAI and gradient echo sequences to show chronic haemorrhagic DAI lesions are helpful in diagnosis (Fig. 13).13

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Figure 13. 30-year-old man with diffuse axonal injury. Axial gradient echo (GE) T2-weighted image shows non-hemorrhagic hyperintense (black arrow) and hemorrhagic hypointense (white arrows) lesions in the CC. Subdural hematoma overlying the left frontal lobe can be also seen (white arrowheads).

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Transient signal changes

Transient lesions of the CC are significant but non-specific findings. They are probably associated with oedematous and/or inflammatory changes of the CC. Acute withdrawal of the Carbamazepine or various infectious agents such as influenza, rotavirus, Escherichia coli, mumps and adenovirus are reported to be related with this entity. MRI usually reveals an oval-shaped lesion in the splenium of the CC that shows low signal intensity on T1-weighted images and apparent diffusion coefficient (ADC) maps, and high signal intensity on T2-weighted, FLAIR- and diffusion-weighted images. These lesions usually disappear within a few weeks following adequate therapy (Fig. 14).14

image

Figure 14. Transient signal changes in a 22-year old man with acute Carbamazepine withdrawal. Axial FLAIR (a), diffusion trace (b = 1000 s/mm2) (b), and corresponding ADC map (c) images show a well-defined circumscribed splenial lesion (arrow), that is hyperintense on FLAIR and diffusion trace images. On ADC map image restricted diffusion is seen in the lesion. Signal changes recovered in three weeks.

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Vascular malformations

Vascular malformations such as cavernomas and arteriovenous malformation (AVMs) may also involve the CC and have the same appearance with the ones located in any part of the central nervous system other than CC (Fig. 15).

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Figure 15. 34-year-old woman with arteriovenous malformation. Coronal T2-weighted (a) and contrast-enhanced T1-weighted (b) MR images show multiple flow voids in the CC.

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Conclusion

  1. Top of page
  2. Summary
  3. Introduction
  4. Normal imaging appearance
  5. Lesions of the CC
  6. Conclusion
  7. References

MRI findings of the CC may provide clues for understanding the patterns and extent of disease processes and to facilitate diagnosis, staging and in determining prognosis. Diffusion-weighted and diffusion tensor imaging of the CC may be useful especially for the disease processes that are less obvious on conventional sequences such as transient lesions of the CC. CT and US are less accurate imaging modalities for depiction of the CC. However, head US is useful in the newborn period.

References

  1. Top of page
  2. Summary
  3. Introduction
  4. Normal imaging appearance
  5. Lesions of the CC
  6. Conclusion
  7. References