1. The corpus callosum is commonly involved by lesions from various etiologies including congenital abnormalities, demyelination, infection, leukodystrophy, neoplasms, trauma, and vascular causes. 2. Transient lesions of the splenium are often seen in association with epilepsy, antiepileptic drug changes, infections, electrolyte imbalances, and PRES. They typically appear hyperintense on T2/FLAIR and DWI with restricted diffusion resolving within 1 month. 3. Common neoplasms involving the corpus callosum include glioblastoma, which may appear as a "butterfly" lesion crossing the genu, and primary CNS lymphoma presenting with a similar pattern

1. Radiological Imaging of Corpus Callosum lesions.
Dr/ ABD ALLAH NAZEER. MD.

2. Normal anatomy of the corpus callosum. T1-weighted
(left), T2-weighted (middle), and FLAIR (right) MR
images show the corpus callosum (CC). The splenium
is the most posterior and thickest portion of the CC.

3. Lesions of the corpus callosum are uncommon and arise from
multiple different etiologies. The lesions can be classified according
to underlying Pathophysiology .
Congenital
agenesis of the corpus callosum
enlarged perivascular spaces
tubonodular pericallosal lipoma: associated with dysgenesis
of the corpus callosum.
Demyelination
acute disseminated encephalomyelitis
Marchiafava-Bignami disease: demyelination and necrosis, can
appear as cystic lesions
multiple sclerosis
neuromyelitis optica
progressive multifocal leukoencephalopathy
Susac syndrome
wallerian degeneratio

4. Infection
aspergillosis: can involve corpus callosum
transient lesions of the splenium: many underlying etiologies including infectious agents
subacute sclerosing panencephalitis: can involve the corpus callosum in advanced stages
tuberculosis: callosal tuberculomas have been reported, although rare
Leukodystrophy
Krabbe disease
metachromatic leukodystrophy
Susac syndrome
X-Linked adrenoleukodystrophy
Neoplasm
Typically, amongst neoplasms, only aggressive lesions can invade the corpus callosum as
it is composed of very dense white matter tracts which act as a barrier to tumour
spreading.
anaplastic astrocytoma
callosal oligodendroglioma
glioblastoma (butterfly glioma)
gliomatosis cerebri
meningioma: secondary involvement from primary falx lesion
metastasis: rare, mainly from contiguous extension of lesion adjacent to corpus callosum
primary CNS lymphoma

5. Other
corpus callosum impingement syndrome
transient lesion of the splenium: many underlying aetiologies
post shunt decompression: after placement of ventriculostomy in patients with
chronic hydrocephalus
Trauma
diffuse axonal injury
Vascular
aneurysm: can occasionally rupture into the corpus callosum
arteriovenous malformation: arising around the corpus callosum
cavernous malformation (cavernoma)
gliosis: secondary to small vessel chronic ischemia, subcortical arteriosclerotic
encephalopathy and radiation therapy; histologically corresponds to
subependymal gliosis
hypoxic-ischemic encephalopathy: corpus callosum only involved in severe or
advanced case
infarction: rare because of extensive collateral vascular supply, most often seen
with emboli, major ischaemic stroke, subfalcine herniation with mass effect and
vasculitides.

6. Transient lesions of the splenium of the corpus
callosum, also known as mild
encephalitis/encephalopathy with a reversible
isolated SCC lesion (MERS), are occasionally encountered
on MRI studies and may be due to a number of underlying
etiologies.
Clinical presentation
Unlike other causes of splenium of corpus callosum (SCC)
lesions, the small transient lesions of the splenium seen in
epilepsy and antiepileptic drug cessation use do not
demonstrate convincing signs or symptoms of hemispheric
disconnection, such as pseudo-neglect, alien hand
syndrome, apraxia of the left hand, agraphia, alexia,
and visual apraxias.

7. Aetiology
epilepsy
classic presentation is seen in patients with sudden cessation of antiepileptic
drugs
seizures: focal lesions have been described after focal status epilepticus and
unusually after single seizures and were explained as focal brain edema.
electrolyte imbalance
including extrapontine myelinolysis
demyelination
multiple sclerosis (MS)
acute disseminated encephalomyelitis (ADEM)
posterior reversible encephalopathy syndrome (PRES)
Marchiafava-Bignami disease
diffuse axonal injury (DAI)
AIDS dementia complex
infections
viral: influenza, measles, herpes, mumps, adenovirus, varicella zoster, rotavirus
and HIV
bacterial: salmonella, Legionnaires' disease
mycobacterial: tuberculous meningitis
hypoglycemia
hemolytic-uremic syndrome with encephalopathy.

8. Radiographic features
Transient lesions of the splenium are only really appreciable on MRI where they
have two distinct patterns:
well circumscribed, small, oval lesions in the midline within the substance of
the corpus callosum
more extensive ill-defined irregular lesions extending throughout the splenium
and into the adjacent hemispheres (boomerang sign)
The smaller well-circumscribed lesions are the typical lesion seen in the setting of
seizures/cessation of antiepileptic medication, whereas the larger lesion is more
typical of other etiologies.
MRI
These lesions tend to demonstrate the following signal characteristics:
T1: hypointense
T2: hyperintense
DWI/ADC: restricted diffusion
T1 C+: no enhancement
Studies have shown that patients recover completely on MRI studies within
1 month, mostly within 1 week following the neurologic recovery .

9. A 1-year-old female patient with complete corpus callosal
agenesis. T1-weigted axial image (left) shows parallel
configuration of both lateral ventricles. T1-weighted sagittal
image (right) reveals complete agenesis of the corpus callosum.

10. Agenesis of corpus
callosum.
A, Sagittal midline
T1-weighted
image shows
complete absence
of corpus callosum
(arrows).
Axial T2-weighted image
shows colpocephalic
configuration with dilated
occipital horns, right greater
than left (asterisks), and
parallel (racecar) orientation
of lateral ventricles. Third
ventricle (arrow) is high riding
and forms interhemispheric
arachnoid cyst.
Axial T2-weighted
image at higher
level illustrates
crescentic
(teardrop)
morphology of
frontal horns
(arrows).

11. 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.
Corpus callosal
Agenesis with Lipoma.

12. A 70-year-old male patient with a pericallosal lipoma and partial corpus callosal agenesis.
Axial CT image (left) shows a lipoma in frontal interhemispheric fissure. There is a linear
calcification at left side of the lesion. Sagittal T1-weighted MR image (right) reveals partial
agenesis of the corpus callosum and a hyperintense pericallosal lipoma.

13. A 64-year-old male patient with a pericallosal lipoma and partial corpus
callosal agenesis. T1-weighted axial (left) and sagittal (right) images show
a hyperintense lipoma superior and posterior to the corpus callosum (CC).
The CC shows partial agenesis. The splenial portion is not fully developed.

14. Callosal infarcts. A, Left anterior cerebral artery infarct (thick arrow) with extension
into genu (thin arrow) is seen on diffusion-weighted (left) and apparent diffusion
coefficient (ADC) (right) images, which confirm reduced diffusivity in these areas.

15. A 62-year-old male patient with acute splenial infarction. Axial FLAIR image (left)
and DWI (middle) show multiple hyperintense lesions in bilateral basal ganglia,
left thalamus, the splenium of the corpus callosum, and left occipital lobe. The
lesions are more conspicuously demonstrated on DWI than on FLAIR image. ADC
map image (right) reveals restricted water diffusion of the lesions.

16. A 70-year old female patient with chronic splenial infarction. Axial FLAIR (left) and
sagittal T2-weighted (middle) images show a hyperintense lesion in the splenium
of the corpus callosum. On DWI (right), the lesion is seen as isointensity.

17. Traumatic brain injury. A, Unenhanced
CT images at level of lateral (A) and
third (B) ventricles show hyperdense
areas of acute hemorrhage in
splenium (S) and genu (G).
T2* gradient recalled-echo MR images at same
levels confirm magnetic susceptibility in these
areas. There are multiple additional foci of
microhemorrhage throughout gray-white matter
junction and basal ganglia (arrows).

18. 9-year-old female patient with Wallerian degeneration due to intracerebral hematomas.
A, B. Axial T2 (A) and T1-weighted (B) images show two hyperintense hematomas in right
occipital lobe (thick arrows) and left temporooccipital lobes (asterisks). There is moderate
amount of surrounding brain edema. Splenium also shows mild swelling and increased
signal intensity (thin arrows). C. Follow-up T2-weighted image obtained 20 months later
reveals atrophic change and increased signal intensity of splenium (thin arrows).

19. A 29-year-old female patient with diffuse axonal injury lesion. She had a
motor vehicle accident 9 days age. Axial FLAIR (left) and DWI (middle) images
show a hyperintense lesion in the splenial portion of the corpus callosum. The
lesion is more conspicuously demonstrated on DWI than on FLAIR image. ADC
map image (right) reveals restricted water diffusion of the lesion.

20. A 29-year-old female patient with diffuse axonal injury
lesion. Follow-up MR images were obtained 17 months
later. On axial T2 (left), FLAIR (middle) and DWI (right)
images, the splenial lesion has disappeared.

21. A 27-year-old male patient with diffuse axonal injury lesion. He had a motor
vehicle accident 2 days age. Axial FLAIR (left) and DWI (middle) images show
a focal hyperintense lesion in the splenial portion of the corpus callosum. The
lesion is more conspicuously demonstrated on DWI than on FLAIR image. ADC
map image (right) reveals restricted water diffusion of the lesion.

22. A 56-year-old male patient with diffuse axonal injury lesions. He had a motor
vehicle accident 4 months age. Axial FLAIR image (left) shows a hyperintense
lesion in the splenial portion of the corpus callosum. On DWI (middle), the
lesion is seen as hypointensity. GE T2*-weighted image (right) reveals tiny
hemorrhagic foci in the splenial lesion. There are also multiple tiny
hemorrhage in right thalamus and left frontal white matter.

23. A 2-month-old female patient with hypoxic-ischemic encephalopathy.
She had hypoxic insult 3 days ago. Axial DWI (left) shows diffuse
hyperintense lesions in the bilateral cerebral cortices and white
matter including the genu and splenium of the corpus callosum. ADC
map image (right) reveals restricted water diffusion of the lesions

24. 2-month-old female patient with hypoxic-ischemic encephalopathy. Follow-up MR images
were obtained 9 days later (12th day from hypoxic insult). On axial T2-weighted image
(left) and DWI (middle left), the bilateral basal ganglia and thalami are newly involved and
the corpus callosal (CC) lesions show more prominent hyperintensities compared to on
initial DWI. Both cerebral cortices and white matter lesions are decreased in their signal
intensities. ADC map image (middle right) reveals restricted water diffusion of the CC
lesions. On contrast-enhanced T1-weighted image, there is strong contrast enhancement
along the cortices and subcortical white matter of both cerebral hemispheres.

25. 2-day-old female with hypoglycemic encephalopathy. Glucose level was 2 mg/dL at
presentation. A. On FLAIR axial image, there is no definite lesion. B. Axial DWI shows
hyperintense lesions in both occipital lobes and splenium (arrows). C. ADC map image
reveals restricted water diffusion of lesions (arrows). ADC = apparent diffusion coefficient,
DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery

26. 8-year-old female patient with CO-intoxication. Axial FLAIR image (A) and DWI (B)
show multiple hyperintense lesions in bilateral globus pallidus (arrowheads) and
cerebral white matter (thin arrows) including splenium of corpus callosum (thick
arrows). DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery

27. 59-year-old male patient with chronic alcoholism. A, B. FLAIR (A) and T2-weighted (B)
images show hyperintense lesions in body (thin arrows) and splenial portion (thick
arrows) of corpus callosum. C. There is focal contrast enhancement of lesions (arrows)
on post-contrast T1-weighted image. FLAIR = fluid-attenuated inversion recovery

28. 5-day-old male with rotavirus-related white matter injury. A, B. Initial axial DWI (A) and ADC
map (B) demonstrate extensive areas of restricted diffusion in periventricular white matter,
deep white matter, corpus callosum, internal capsule, and posterior thalami. C. Follow-up
FLAIR image obtained five years later shows residual ischemic lesions due to previous white
matter injury in both periventricular white matters (arrows). ADC = apparent diffusion
coefficient, DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery

29. Multiple sclerosis who presented with visual complaints. Sagittal MR
image shows multiple hyperintense lesions (arrows) in corpus callosum.

30. Axial brain MRI (fluid-attenuated inversion recovery) with tumefactive lesions
(A) developed exacerbation 67 days after the start of interferon-β-1b (IFNβ-1b)
therapy; MRI showed huge tumefactive lesion in right hemisphere. Case 5 (B)
developed exacerbation 32 days after the start of IFNβ-1b therapy; MRI showed
tumefactive lesions in corpus callosum extending to the right parietal white matter.

31. 4-year-old girl with pilocytic
astrocytoma. Axial T2-
weighted MR image shows
that lesion is hyperintense.
4-year-old girl with pilocytic
astrocytoma. Sagittal T1-
weighted MR image shows
well-circumscribed
hypointense lesion in body
of corpus callosum.
4-year-old girl with
pilocytic astrocytoma.
Enhanced coronal T1-
weighted MR image shows
marked contrast
enhancement of lesion.

32. A 59-year-old female patient with a glioblastoma. Axial T2-weighted image (left)
and DWI (middle left) show a large heterointense mass in right temporoparietal
white matter and adjacent splenium of the corpus callosum. There is large
amount of surrounding brain edema. Perfusion MR image (middle right) reveals
increased perfusion in the peripheral solid portion of the mass. On contrast-
enhanced T1-weighted image, there is peripheral rim enhancement of the mass.

33. Glioblastoma multiforme. A, Unenhanced CT image shows
heterogeneously hypodense mass with surrounding
vasogenic edema. This involves both frontal lobes and
crosses genu (G) of corpus callosum, producing butterfly
appearance. There is compression and distortion of frontal
horns of both lateral ventricles.
Contrast-enhanced T1-weighted MR image
shows involvement of genu (G). Lesion
shows rim enhancement and central
hypointensity, compatible with necrosis.

34. A 46-year-old female patient with gliomatosis cerebri. Axial FLAIR image (left)
show an ill-defined hyperintense lesion involving bilateral posterior cerebral white
matter and the splenium of the corpus callosum. On enhanced T1-weighted axial
image (middle), there is no definite contrast enhancement of the lesion. Single
voxel 1H MR spectroscopy (right) reveals increased choline peak.

35. Nonimmunocompromised woman with primary central nervous system lymphoma
who presented with disorientation. MRI show lesion (arrow) of left parieto—
occipital white matter, crossing corpus callosum in classic butterfly pattern.

36. Primary CNS lymphoma.

37. A 23-year-old male patient with a pineal germinoma. Axial T2 (left) and T1-
weighted (middle) images show a mass in the pineal area. The mass extends into
the 3rd ventricle anteriorly and to the splenium of the corpus callosum
posteriorly. On enhanced T1-weighted image, the mass is strongly enhanced.

38. A 62-year-old male patient with epilepsy. Axial DWI (left) shows a focal
hyperintense lesion in the splenium of the corpus callosum. ADC map
image (middle) reveals restricted water diffusion of the lesion. On follow-
up DWI (right) obtained 14 days later, the splenial lesion has disappeared.

39. A 38-year-old female patient with bacterial meningoencephalitis due to S.
pneumoniae. Axial FLAIR image (left) and DWI (middle) show a hyperintense lesion in
the splenium of the corpus callosum. The lesion is more conspicuously demonstrated
on DWI than on FLAIR image. There is tissue loss in left frontal lobe. ADC map image
(right) reveals markedly restricted water diffusion of the splenial lesion.

40. A 15-year-old male patient with abc meningoencephalitis. Axial FLAIR image (left)
and DWI (middle) shows a focal hyperintense lesion in midline corpus callosum.
The lesion is more conspicuously demonstrated on DWI than on FLAIR image. ADC
map image (right) reveals markedly restricted water diffusion of the lesion.

41. Transient splenial intensity changes.
A, Example images in migraine and visual
scotomas (A), adenovirus encephalitis (B),
and metronidazole toxicity (C) show FLAIR
hyperintensity and reduced diffusivity in
splenium (arrows), which resolved on
follow-up imaging.

42. A 59-year old male patient with chronic alcoholics. FLAIR (left) and
T2-weighted (middle) images show hyperintense lesions in the body
and splenial portion of the CC. There is focal contrast enhancement
of the lesions on post-contrast T1-weighted image (right).

43. 2-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.
2-year-old man with arteriovenous
malformation who presented with
intraventricular hemorrhage. Axial T2-
weighted MR image shows hyperintense
lesion (arrow) with flow voids.

44. Unenhanced CT and Gradient MR image in different patient
who had ruptured anterior communicating artery aneurysm.
Right pericallosal artery aneurysm (arrow).
Aneurysm.

45. Unenhanced CT image shows round well-
circumscribed hyperdense mass (asterisk) centered
in falx cerebri (arrow) and extending across midline.
There is subtle surrounding edema that involves
bilateral temporo-occipital regions
T1-weighted contrast-enhanced MR image
shows relatively homogeneous contrast
enhancement within mass, which deviates
surrounding pial vessels (arrows).

46. Contrast-enhanced CT (A) and contrast-
enhanced T1-weighted MR (B) images show
heterogeneously enhancing dominant
metastasis in left frontal lobe (asterisk).
Additional enhancing foci are noted in
splenium (S), genu (G), and periventricular
regions (arrows).
Contrast-enhanced CT (A) and contrast-enhanced
T1-weighted MR (B) images show
heterogeneously enhancing dominant metastasis
in left frontal lobe (asterisk). Additional
enhancing foci are noted in splenium (S), genu
(G), and periventricular regions (arrows).

47. Hereditary leukoencephalopathies. A, FLAIR MR images show signal abnormalities
in bilateral parietal lobes and intervening splenium of corpus callosum (arrows):
metachromatic leukodystrophy (A) and adrenoleukodystrophy (B)

48. Periventricular leukomalacia. A, T2-weighted MR image
shows periventricular white matter abnormalities, with
increased signal in both frontal and parietal lobes as
well as genu (G) and splenium (S) of corpus callosum.
Susceptibility artifact within choroid plexus of occipital
horns (asterisks) confirms presence of hemorrhage.
Diffusion-weighted MR image identifies
reduced diffusivity within splenium
(arrows) and multiple other areas.

49. Virchow-Robin spaces in Hunter syndrome
(mucopolysaccharidosis type 2). Axial FLAIR
image shows diffusely enlarged perivascular
spaces, which are isointense to CSF and involve
body of corpus callosum (arrows).
Sagittal T1 FLAIR contrast-enhanced
image shows large Virchow-Robin
spaces within corpus callosum
(arrow) and brain parenchyma.

50. Marchiafava-Bignami disease.
(Courtesy of Ginat DT,
Massachusetts General Hospital,
Boston, MA)A, FLAIR MR image
shows increased signal in
splenium (arrow).
Marchiafava-Bignami disease.
(Courtesy of Ginat DT, Massachusetts
General Hospital, Boston,
MA)B, Apparent diffusion coefficient
map confirms reduced diffusivity in
this region (arrow).

51. Susac's syndrome:(a-d) Magnetic resonance imaging FLAIR T2 image showing multiple
well-defined hyperintense lesions in periventricular and callosal area. Magnetic resonance
imaging T1 image showing hypointense lesions in center of corpus callosum. Magnetic
resonance imaging, 4 weeks later showing almost complete disappearance of lesions

53. Magnetic resonance imaging of the brain: Diffusion-weighted sequences during 2010 episode (a-d) showing
restricting lesions in left posterior limb of internal capsule and splenium of the corpus callosum. Lesions
involving bilateral subcortical white matter and centrum semi ovale (e-h) during July 2013 episode. Resolution
of the changes (i-l) in the repeat imaging done after 1.5 months. Arrows showing abnormalities.

54. Callosal thickening of neurofibromatosis type 1. A midsagittal T1W
MR image shows diffuse thickening of the corpus callosum (arrows).

55. Thank You.