Article Text

An MRI review of acquired corpus callosum lesions
  1. Dimitri Renard,
  2. Giovanni Castelnovo,
  3. Chantal Campello,
  4. Stephane Bouly,
  5. Anne Le Floch,
  6. Eric Thouvenot,
  7. Anne Waconge,
  8. Guillaume Taieb
  1. Department of Neurology, CHU Nîmes, Hôpital Caremeau, Nîmes, France
  1. Correspondence to Dr Dimitri Renard, Department of Neurology, CHU Nîmes, Hôpital Caremeau, Place du Pr Debré, 30029 Nîmes Cedex 4, France; dimitrirenard{at}


Lesions of the corpus callosum (CC) are seen in a multitude of disorders including vascular diseases, metabolic disorders, tumours, demyelinating diseases, trauma and infections. In some diseases, CC involvement is typical and sometimes isolated, while in other diseases CC lesions are seen only occasionally in the presence of other typical extra-callosal abnormalities. In this review, we will mainly discuss the MRI characteristics of acquired lesions involving the CC. Identification of the origin of the CC lesion depends on the exact localisation of the lesion(s) inside the CC, presence of other lesions seen outside the CC, signal changes on different MRI sequences, evolution over time of the radiological abnormalities, history and clinical state of the patient, and other radiological and non-radiological examinations.

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The corpus callosum (CC) is a large, densely packed, white matter tract that connects both cerebral hemispheres, explaining the multitude of possible clinical signs and symptoms seen in CC involvement. Absence of a clear neurological deficit can be seen when the CC lesion is solitary and small, in contrast to large, diffuse or multifocal CC lesions often leading to severe neurological deficit. Alien limb syndrome is typically seen with anterior CC lesions, left agraphia, right constructional apraxia and left tactile anomia in case of injury to the body of the CC, and left hemialexia when the splenium is involved.1–5 Briefly, the aetiology of CC lesions can be divided into disorders typically affecting the CC (often in an isolated manner; eg, Marchiafava–Bignami disease (MBD), mild encephalitis/encephalopathy with a reversible splenial lesion (MERS)), disorders where the coexistence of callosal and extra-callosal lesions is often present (eg, multiple sclerosis (MS), trauma, leucodystrophy), and disorders where CC involvement is only seen occasionally together with typical extra-callosal abnormalities (eg, Wernicke encephalopathy (WE)). MRI is a powerful tool to analyse CC lesions. Because of the anterior–posterior orientation of the CC, sagittal MRI imaging is of special interest in patients with CC abnormalities. T1-, T2-, T2*-weighted imaging, fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI)/apparent diffusion coefficient (ADC) sequences together with gadolinium-enhanced T1-weighted images are essential to analyse CC lesions. Axial, sagittal and coronal images give information of the precise localisation of the CC lesion.

Additional imaging techniques including magnetic resonance spectroscopy, perfusion-weighted MRI, positron emission tomography and single-photon emission CT can sometimes be useful in the diagnosis of these CC lesions.

Vascular lesions


The large anterior part of the CC is supplied by the pericallosal artery, a branch of the anterior cerebral artery, while the splenium is supplied by the posterior pericallosal artery, a branch of the posterior cerebral artery. The most common location of CC infarction is the splenium (see online supplementary figure S1). Infarctions are most often central (ie, respecting the upper and lower margins) in the CC and accompanied by infarction in other brain areas supplied by the same artery. Because of the bilateral arterial supply, most ischaemic CC lesions are confined to one side although they may cross the midline. Rare midline CC lesions are seen in case of watershed infarction between both anterior (eg, in case of occlusion of a common anterior cerebral artery) or both posterior (eg, in case of top-of-the-basilar infarction) cerebral arteries, or in case of occlusion of a third small artery originating from the anterior communicating artery as seen in the majority of postmortem angiograms (see online supplementary figure S2). Signal intensities and radiological evolution are like those seen in classical brain infarction. Gadolinium enhancement, often peripheral, can be seen in the subacute phase of ischaemic lesions. Lesions may become necrotic, seen as a central FLAIR hypointensity surrounded by FLAIR hyperintensity.

Ischaemic CC involvement can also be seen in small vessel disease including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), small vessel vasculitis, Susac syndrome, and autosomal dominant hereditary cerebrovascular disease due to COL4A1 point mutations (figure 1, and see online supplementary figures S3 and S4). In CADASIL, diffuse bilateral (T2 and FLAIR hyperintense) leucoencephalopathy is usually observed, sometimes associated with cerebral microbleeds.6 ,7 When CADASIL-related leucoencephalopathy is less severe, the external capsula and anterior part of the temporal lobes are the most frequently involved structures. Susac syndrome is a rare disorder affecting the precapillary arterioles of the brain, retina and cochlea leading to cerebral symptoms, branch retinal artery occlusions, and visual and hearing loss.8 The CC is almost always involved in Susac syndrome, typically affecting the central CC portion (with microinfarctions that are typically small), together with ischaemic involvement of the periventricular areas and often also the posterior fossa structures. When CC infarctions are larger, the so-called ‘snowball’ appearance can be seen. Sometimes, linear defects (‘spokes’) are observed from the callosal–septal surface extending to the superior margin of the CC or wedge-shaped lesions extending from the roof of the CC (the so-called ‘icicles’). In the chronic phase, lesions appear as holes (ie, as hypointensity on T1 and FLAIR sequences), together with CC atrophy. COL4A1 point mutations have been recently identified as a rare cause of an autosomal dominant hereditary cerebrovascular disease, often associated with systemic injury affecting eyes, kidney and muscles.9 Other COL4A1-related cerebral manifestations include asymptomatic porencephaly, diffuse white matter lesions, intracerebral haemorrhage, transient ischaemic attack, brain infarction, dilated perivascular spaces, silent microbleeds, mental retardation, epilepsy, migraine with aura, dolichoid carotid siphons and intracranial aneurysms.

Figure 1

DWI sequences (A–C) showing multifocal lateralised corpus callosum (CC) involvement in a Susac patient. On sagittal FLAIR imaging (D), a typical wedge-shaped lesion in the splenium extending from the roof of the CC (the so-called ‘icicle’) can be observed.

Delayed posthypoxic leucoencephalopathy

Delayed posthypoxic leucoencephalopathy (DPL) has been reported in patients with carbon monoxide poisoning, narcotic overdose, myocardial infarction and other global cerebral hypoxic events. DPL is often associated with other manifestations of posthypoxic brain injury including acute haemorrhagic necrosis of the pallidum, arterial borderzone infarction or late laminar necrosis.10 The proposed pathophysiological mechanism postulates that prolonged moderate hypo-oxygenation in white matter disrupts adenosine triphosphate-dependent enzymatic pathways involved in myelin turnover which would result in delayed demyelination. Another possible explanation is that oligaemia restricted to white matter may result in delayed apoptosis of the oligodendrocytes.

The most frequent involved areas are the frontal and the parietal white matter and the CC. Lesions in these areas are seen as hyperintensity on T2 and FLAIR sequences, together with transient (lasting for up to several weeks) reduced diffusion on DWI and ADC map, and usually without contrast enhancement (see online supplementary figure S5). DPL lesions are transitory in a portion of patients.


Rare cases of bleeding in the CC have been reported due to anterior communicating artery or distal anterior cerebral artery aneurysm, arteriovenous malformation or cavernoma (see online supplementary figure S6). These, usually large, haemorrhagic lesions are often associated with intraventricular haemorrhage. Cavernous malformations often show calcification. Susceptibility-weighted imaging (SWI) is more sensitive than T2*-weighted imaging in detecting cavernous malformations, especially in multifocal/familial cases.11 Cavernous malformations are typically not enhanced on gadolinium-injected T1-imaging, although minimal enhancement may be present.

Haemorrhagic CC lesions, most often small, can also be seen secondary to trauma, haemorrhagic small vessel disease, infarction and brain tumour.

A rare cause of CC (and extra-CC) haemorrhages, most often small and multiple, is extracorporeal membrane oxygenation (ECMO), which occurs usually in association with infarction and involvement of other brain areas (see online supplementary figure S7).12 ECMO is used for severe respiratory or cardiac failure unresponsive to conventional therapy and is associated with a high mortality and morbidity. Neurological complications occur more frequently when venoarterial ECMO is used compared with venovenous ECMO. ECMO therapy may cause hypoxia during cannulation, solid or air emboli during perfusion, haemodynamic instability and bleeding. ECMO-related cerebral haemorrhages may result from continuous heparin infusion during ECMO and/or from haemorrhagic diathesis (an adverse effect of ECMO).

Demyelinating lesions

Multiple sclerosis

The CC is frequently affected in MS, most characteristically involving asymmetrically the inferior part of the CC, radiating from the ventricular surface into the overlying CC, appearing as T2 and FLAIR hyperintensity (figure 2). These so-called callosal–septal interface lesions are highly specific for MS. Therefore, T2/FLAIR-weighted sagittal MRI imaging is essential in the work-up when MS is suspected. Acute lesions are isointense or mildly hypointense on T1 sequences, often with ‘open-ring’ enhancement after gadolinium injection. Rare cases of acute MS lesions with transient reduced diffusion on diffusion-weighted imaging have been described. When T1 hypointensity persists in the chronic stage, these MS lesions are called ‘black hole’ on imaging. Beside the CC, MS lesions commonly affect the periventricular white matter (often presenting as ovoid or linear lesions) and the posterior fossa (especially the cerebellar peduncles) and sometimes also the cerebral cortex. Diffuse brain atrophy, which also affects the CC, is typical in chronic MS, making the T2 hyperintense CC lesions sometimes difficult to interpret, especially since these T2 lesions often become diffuse and confluent in long-standing MS (see online supplementary figure S8).13

Figure 2

Sagittal T2 (A) and FLAIR (B) imaging of two different multiple sclerosis patients showing in the first patient a callosal–septal interface lesion in the anterior part of the corpus callosum (CC) (A) and in the second patient multifocal callosal–septal interface lesions along the entire CC (B).

Acute disseminated encephalomyelitis

In acute disseminated encephalomyelitis (ADEM), radiological features overlapping with MS are often observed although CC and periventricular lesions are less frequent. CC lesions at the callososeptal interface are usually not seen. In contrast, basal ganglia lesions are more frequent in ADEM than in MS. Gadolinium-enhanced T1 imaging typically shows enhancement of all (or near all) lesions in ADEM, whereas in MS enhancement is completely absent or seen in only some of the lesions. Distinction between both entities is important since MS patients seem to benefit from long-term treatment, while ADEM is most often a monophasic postinfectious or postvaccination disorder not requiring long-term treatment.

Neuromyelitis optica

Classically, neuromyeltis optica (NMO) was thought to show any or only discrete brain MRI signal changes. However, recent studies analysing systematically brain lesions in NMO showed that these lesions are extremely frequent, although they present different radiological characteristics (ie, more often diffuse, heterogeneous, cystic and with blurred margins) as compared with MS.14 ,15 When present, the periventricular white matter is the most frequently area involved followed by the CC (see online supplementary figure S9). NMO-related CC lesions are typically diffuse and heterogeneous; they principally involve the splenium (more frequently than in MS), spreading from the lower to the upper edges of the CC.14 ,15 The predominant inferior involvement of the NMO-related CC lesions is probably explained by the high expression of aquaporin-4 protein along the callosal lower surface.

Non-demyelinating inflammatory diseases

In non-demyelinating inflammatory diseases (eg, Sjögren syndrome, lupus erythematosis, sarcoidosis), CC lesions can be often observed together with more frequent periventricular white matter lesions. Both enhancing and non-enhancing lesions have been described in these disorders, sometimes associated with leptomeningeal involvement.

Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a recently described CNS inflammatory syndrome. The most characteristic lesions in CLIPPERS are multiple small, punctuate and curvilinear gadolinium-enhancing lesions peppering the brainstem. Associated lesions in the cerebellum, the spinal cord and the cerebral hemispheres (including the CC) are relatively frequent (see online supplementary figure S10).16 After corticoid treatment, contrast-enhancing lesions typically improve dramatically, at least transitory.


Diffuse axonal injury

Diffuse axonal injury (DAI) typically involves the CC (with the posterior CC part as most frequently involved CC area), midbrain (especially the dorsolateral portion) and the lobar white matter (most often at the grey–white matter junction). When small, CC lesions are often unilateral and slightly eccentric to the midline, whereas large, bilateral and symmetric lesions sometimes involving the entire CC can also be seen (see online supplementary figure S11). DIA is best seen on DWI and FLAIR sequences as hyperintense signal, frequently associated with haemorrhagic hypointense lesions on T2*-weighted images (and even better seen on SWI sequences).17 When present, DAI lesions tend to be multiple. On ADC map, lesions may be hypointense indicating cytotoxic oedema. Traumatic CC lesions are usually focal although diffuse CC lesions are sometimes encountered. Small traumatic CC lesions are often eccentric whereas large lesions most frequently involve the complete extent of the CC in coronal sections. DAI is often associated with other radiological manifestations of head trauma (including epidural, subdural, subarachnoid or intraventricular haemorrhage, contusion). DAI lesions tend to reduce in number and volume over time.18


Glioblastoma multiforme

Glioblastoma multiforme (GBM) commonly affects the CC as the tumour progresses from one cerebral hemisphere to another along the CC, giving sometimes the aspect of an asymmetrical or symmetrical ‘butterfly glioblastoma’ (figure 3). GBM MRI signal is typically heterogeneous, isointense to hypointense (especially when necrosis is present) on T1 sequences, and hyperintense on T2 and FLAIR imaging. Central necrosis, perilesional vasogenic (T2/FLAIR/ADC hyperintense) oedema and strong (solid, nodular, patchy or ‘closed-ring’) enhancement are typical, and sometimes haemorrhage occurs inside the tumour.

Figure 3

Diffuse infiltration of the genu and the anterior part of the body of the corpus callosum is observed on sagittal FLAIR sequences (A) in a patient with a gliobastoma multiforme. On gadolinium-enhanced T1-weighted imaging (sagittal view (B); coronal view (C); and axial view (D)), central hypointense necrosis is seen with strong peripheral contrast enhancement in the callosal and frontal white matter giving an aspect of the so-called ‘butterfly lesion’.

Gliomatosis cerebri

In gliomatosis cerebri, diffuse white matter infiltration (best seen as homogenous T2 and FLAIR hyperintensity, and hypointense on T1) involving two or more lobes is seen with enlargement of the involved structure. Absent (or minimal) enhancement on gadolinium-injected T1-weighted imaging is typically seen. Associated CC, basal ganglia and/or thalamic involvement are often observed (see online supplementary figure S12).


Lymphoma often involves the CC, periventricular white matter and basal ganglia, with homogenous contrast enhancement in absence of central necrosis. They appear isointense or hypointense on unenhanced T1 sequences while hyperintense on T2/FLAIR imaging (see online supplementary figures S13 and S14). In immunocompromised patients and rarely in non-immunocompromised patients, contrast enhancement is rather peripheral than homogeneous, or may be less evident or even absent. Surrounding oedema as well as central necrosis may be seen in HIV-related lymphoma. In contrast to glioblastoma, there is less (or absent) peritumoural oedema, and necrosis and haemorrhage are less common in lymphoma. Reduced diffusion has been reported occasionally. Lymphoma often responds dramatically (and frequently disappear on MRI), but temporarily, to steroid treatment and radiation therapy.

Other primary brain tumours

CC involvement can rarely be seen in other primary brain tumours including pilocytic astrocytoma and germinoma.


Metastatic CC lesions are rare and most often seen in the presence of other metastatic brain lesions. Imaging characteristics depends on the primary malignancy but usually present with mass effect, surrounding oedema and contrast enhancement.


Progressive multifocal leucoencephalopathy

The JC virus-related progressive multifocal leucoencephalopathy (PML) typically occurs in immunocompromised patients and has a high mortality. These T2/FLAIR hyperintense and T1 hypointense lesions can be unifocal (especially in the early stage) or multifocal, and typically involve the subcortical white matter (involving also the CC in 10%–15% of cases) respecting basal ganglia and the cortex.19 ,20 There is usually no mass effect. Although usually absent faint contrast enhancement can be observed at the periphery of the lesions. Patients surviving PML typically show profound atrophy of the involved brain structures (see online supplementary figure S15).


Although not typical, CC involvement can be seen in some cases of infectious (mainly viral) encephalitis. However, in CMV encephalitis (frequently HIV/AIDS-related), periventricular lesions often also involving the CC are seen as T2/FLAIR hyperintensities, frequently with reduced diffusion on diffusion-weighted imaging and enhancement on gadolinium-enhanced T1-weighted imaging.

Haemorrhagic changes can be observed in rare cases of infectious (eg, due to influenza virus, EBV, VZV, HSV-6 or tickborne infection) or postinfectious haemorrhagic encephalitis, sometimes referred to as Hurst leucoencephalitis.21 In the rare cases of autopsy-proven acute haemorrhagic leucoencephalitis, extensive asymmetrical demyelinating lesions are seen together with foci of microhaemorrhages.

Brain abscess

Brain abscesses commonly occur supratentorially at the grey–white matter junction, with radiological characteristics varying with the stage of abscess development. Reduced diffusion (because of a high content of protein) on diffusion-weighted imaging and (most often ring) enhancement on gadolinium-enhanced T1-weighted imaging are typically observed. In some rare cases of brain abscess, the CC is also involved.22

Metabolic diseases

Marchiafava–Bignami disease

MBD is mainly reported in patients with chronic and severe alcoholism and multiple vitamin deficiencies. MBD preferentially affects the central and medial part of the CC, with the splenium as the most frequently CC part involved. Often, the entire CC or a large part of it is involved with a low signal on T1 and high signal on T2/FLAIR, leading to necrosis and cavitary lesions profoundly hypointense on T1 and FLAIR imaging giving a ‘sandwich-like’ appearance (figure 4). In the acute phase, reduced diffusion is often seen on diffusion-weighted imaging. Contrast enhancement can be occasionally seen in the acute phase, and sometimes slight haemorrhage can also occur inside the lesion.23 Less frequently, other brain structures including white matter tracts, cerebral cortex and middle cerebellar peduncles may be involved in MBD.

Figure 4

In a patient with Marchiafava–Bignami disease in the subacute phase, a diffuse symmetrical splenial lesion is present, seen as hypodensity on CT (A), hypointensity on T1 (B) and hyperintensity on FLAIR (axial view (C); sagittal view (D)) sequences, with reduced diffusion (hyperintensity on DWI (E) and hypointensity on ADC map (F)) on diffusion-weighted imaging. In the chronic phase, a central splenial midline corpus callosum (CC) lesion is seen (and to a lesser degree also in the body of the CC) as hypointensity on both axial FLAIR (G) and sagittal T1-weighted (H) imaging.

Wernicke encephalopathy

WE typically affects periaqueductal grey matter, mamillary bodies, hypothalamus, medial thalamus, perirolandic regions, and less frequently cranial nerve nuclei, frontal and parietal lobes and rarely the CC. It is best seen as hyperintensity on T2/FLAIR sequences. Involved structures sometimes show enhancement (especially in alcoholic WE patients) and/or reduced diffusion in the acute phase. Haemorrhagic lesions can be seen in catastrophic WE cases.

Osmotic demyelinating syndrome

The osmotic demyelinating syndrome is associated with any kind of osmotic gradient changes (most commonly in rapid iatrogenic correction of hyponatriemia in patients with alcoholism, chronic liver disease or malnutrition). It was formerly called central pontine myelinolysis because of the frequent pontine involvement, or extrapontine myelinolysis when other than pontine lesions are present. Frequent sites of extrapontine localisations are the cerebellum, basal ganglia, thalamus, cerebral white matter, hippocampus and the CC (especially the splenium).24 The lesions are T2/FLAIR hyperintense and T1 hypointense in the acute phase, often resolving after the acute phase. Haemorrhage and contrast enhancement are uncommon. Lesions may occur with a certain delay after the onset of clinical symptoms or may even be seen in absence of clinical abnormalities.

Transient lesion of the splenium

A transient (most often splenial) CC lesion can be seen in the so-called MERS. Frequently, an isolated lesion in the splenium is seen (figure 5). Associated involvement of the entire CC, symmetrical white matter, caudal nucleus, putamen and/or thalami is rarely encountered (see online supplementary figure S16). Possible mechanisms in MERS include intramyelinic oedema, dysfunction of cerebral blood flow autoregulation, and influx of inflammatory cells and macromolecules and related cytotoxic oedema. Risk factors for MERS are antiepileptic drugs, corticoid treatment, immunoglobulin therapy, mild hyponatremia and encephalitis. The transient round or ovoid lesion of the central splenium is typically T2 and FLAIR hyperintense, T1 hypointense, with reduced diffusion on diffusion-weighted imaging, in the absence of contrast enhancement. These reversible splenial lesions, with similar signal abnormalities as seen in MERS, are sometimes also encountered in cases with altitude sickness and hypoglycaemia (see online supplementary figure S17).25 ,26

Figure 5

MRI showing an ovoid symmetrical midline lesion in the central part of the splenium, hyperintense on T2 (B), FLAIR (C) and DWI image (D), and hypointense on T1-weighted images (A) and ADC map (E). Control MRI 6 weeks later shows complete disappearance of the splenial lesion (F–J).

Reversible posterior leucoencephalopathy syndrome

Risk factors for reversible posterior leucoencephalopathy syndrome (RPLS) include immunosuppressive and cytotoxic agents, hypertension, eclampsia and metabolic abnormalities. The common clinical features of RPLS are headache, decreased alertness, vomiting, seizures and visuoperceptual disturbances. Brain imaging typically shows bilateral white matter lesions in the occipital and posterior parietal lobes. Watershed areas between middle and posterior cerebral arteries are frequently involved. However, associated involvement of grey matter and other regions of the brain including frontal and temporal lobes, brainstem, cerebellum, basal ganglia, thalamus, and CC is frequently seen (see online supplementary figure S18).

Characteristics on diffusion-weighted images are indicative for vasogenic oedema. Lesions are isointense or slightly hyperintense on DWI, hyperintense on T2, FLAIR, and ADC sequences, and isointense to hypointense areas on T1-weighted images. Because of the suppression of the subarachnoid CSF signal, FLAIR sequences are of special interest to detect cortical abnormalities. ADC values seem to be more sensitive to show brain abnormalities than conventional T2 and FLAIR images.27

Associated infarction (in areas of massive oedema, elevated tissue perfusion pressure leads to decreased cerebral blood flow and ischaemia), haemorrhage (especially when RPLS is related to hypertension) and/or gadolinium enhancement are sometimes seen and associated with poorer outcome. In case of infarction, affected regions show highly increased signal on DWI, and pseudonormalised or decreased signal on ADC sequences. In uncomplicated patients, regression (at least partially) of radiological abnormalities is typically seen after discontinuation of offending drug and treatment of elevated blood pressure.


Diffuse white matter abnormalities (including associated CC involvement) is often seen in hereditary leucodystrophies. The part of the CC affected most frequently corresponds to the part of the cerebral white matter involved. Since leucoencephalopathy is usually diffuse, signal abnormalities are often observed along the entire CC. Lesions are typically hypointense on T1 and hyperintense on T2/FLAIR imaging, in the absence of contrast enhancement. Rare cases with contrast enhancement have been described.28

Radiation-induced leucoencephalopathy

Radiation-induced leucoencephalopathy (RIL) is most often a late and delayed effect of radiation therapy, occurring months or years after radiation and frequently leading to irreversible neurological deficit. Neurological and radiological abnormalities depend on different factors including the volume of irradiated brain, cumulative dose of radiation administered, (fractionated) protocol followed and age of the patient. In whole brain radiation in particular, diffuse white matter involvement, which often includes the CC, can be observed with frequently associated cognitive deficit. These white matter lesions are best detected on T2 and FLAIR sequences as hyperintense signal sparing the U-fibres, involving the brain bilaterally and symmetrically in case of whole brain radiation (see online supplementary figure S19). RIL lesions most typically do not show mass effect nor enhance after gadolinium administration (in contrast to what is most often seen in tumour relapse or radiation necrosis), and are permanent.

Toxic leucoencephalopathy

A multitude of agents, including immunosuppressive drugs, antineoplastic agents, antimicrobial medication, drugs of abuse and environmental toxins, may lead to toxic leucoencephalopathy. Since toxic leucoencephalopathy principally involves the white matter of both hemispheres diffusely, the CC is also frequently affected. Lesions are often bilateral and relatively symmetrical, seen as T2 and FLAIR hyperintensity and T1 hypointensity, typically without contrast enhancement or haemorrhage (see online supplementary figure S20).

Wallerian degeneration

Chronic unilateral or bilateral cerebral hemispherical lesion often lead to atrophy or the related part of the CC. MRI typically shows diffuse hyperintensity on T2 and FLAIR sequences, especially of the inferior part of the CC (see online supplementary figures S21 and S22).


In chronic hydrocephalus, CC lesions generated by the disease itself or by its treatment (drainage or overdrainage) can be observed and they usually involve the midline of the superior CC part.

Brain sagging

Brain sagging can be seen in patients with intracranial hypotension, mainly associated with orthostatic headache and pachymeningeal gadolinium enhancement, and sometimes in patients without headache and without pachymeningeal gadolinium enhancement presenting with progressive behaviour and cognitive changes mimicking behavioural variant frontotemporal dementia: the so-called frontotemporal brain sagging syndrome.29 In brain sagging, transtentoral herniation of medial temporal lobe structures and CC (especially the posterior part) are seen together with brainstem swelling and low-lying cerebellar tonsils. Signal changes of the CC are usually absent in brain sagging.

Inborn errors

Although inborn errors (like embryological callosal malformations, dilated perivascular Virchow–Robin spaces and lipoma) are not discussed in this review, we want to mention only lipomas since these lesions are often incidentally encountered. Lipomas are considered as developmental lesions of the CNS, typically asymptomatic, occurring most often in the region of the CC and the pericallosal cistern. Lesions are well circumscribed and homogenous, hyperintense on both T1- and T2-weighted sequences, and disappearing on fat-suppressed sequences (see online supplementary figure S23).


Identification of the origin of the CC lesion depends on their exact localisation within the lesion(s) inside the CC (eg, midline lesion, paramedian–assymetrical lesion, diffuse symmetrical lesion), volume (eg, focal delineated vs diffuse lesions) of the lesions and signal changes they produce on different MRI sequences.

Tables 13 and online supplementary figures S24–S26 show lesion characteristics in different diseases with frequent CC involvement depending on the localisation of the CC lesion, lesion volume and MRI characteristics.

Table 1

List of the most typical localisations of CC lesions in different diseases with frequent CC involvement

Table 2

List of the most typical volumetric characteristics of different corpus callosum lesions

Table 3

List of the most typical signal changes of corpus callosum lesions on different MRI sequences


We would like to thank Dr Mariella Lomma (BESPIM, Nîmes University Hospital) for proofreading the paper.


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