The corpus callosum is the principal supratentorial cerebral commissure (white matter tract) connecting symmetrical areas of cerebral hemispheres (between the parietal lobes,
posterior frontal and superior temporal regions).
It is divided in four segments: rostrum,
genu,
body and splenium.
It forms during embryogenesis,
between the 8th and 20th week of life.
It develops in an anterior-posterior direction except for the rostrum,
which is the last to form.
It contains very compacted myelinated axonal fibres,
which hinder the diffusion of interstitial oedema and tumour extension.
However,
its high density also makes it more susceptible to shear injuries in a traumatic context.
Magnetic resonance imaging (MRI) is the most sensitive technique for the detection of lesions in the corpus callosum,
considering both conventional and advanced techniques.
This exhibit describes the radiological MRI findings of a variety of pathologies affecting the corpus callosum,
including tumoural diseases,
inflammatory-demyelinising events,
vascular processes,
traumatic injuries,
endocrine and metabolic causes,
infectious agents and toxic insults,
among others.
1.
CONGENITAL DISORDERS
1a) Agenesis and dysgenesis
There is a complete (agenesia) or partial (dysgenesia) absence of the corpus callosum (Fig.
1).
• 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.
Congenital malformations of the corpus callosum may occur in isolation although although are frequently associated to other brain abnormalities,
such as:
- Interhemispheric cyst: in 7% of patients with agenesis of the corpus callosum.
It appears as a thin walled-unilocular cyst,
usually hyperintense on T2W images and isointense on T1W images,
although it varies depending on its protein content.
- Lipoma: 50% of lipomas are associated with different degrees of dysgenesis of the corpus callosum.
It displays the characteristic short-T1 and T2 signal of fat (Fig.
2).
- Dandy-Walker malformation: agenesis or hypoplasia of the cerebellar vermis,
cystic dilatation of the fourth ventricle and enlargement of the posterior fossa.
It may be accompanied by supratentorial abnormalities such as agenesis or dysgenesis of the corpus callosum,
polymicrogyria,
cortical heterotopias and hydrocephalus (Fig 3).
- Septo optic dysplasia (Morsier Syndrome): partial or total absence of the septum pellucidum and hypoplasia of the optic nerves.
50% have schizencephaly or heterotopias and 66% have hypothalamic-pituitary dysfunction (Fig 4).
-Holoprosencephaly: incomplete or absent division of the embryonic forebrain (prosencephalon) into distinct lateral cerebral hemispheres.
Distinctive midline facial malformations occur in most cases.
It is categorized into three types:
• A-lobar: is the most severe.
There is a complete absence of midline forebrain division,
resulting in a monoventricle and fused cerebral hemispheres.
There are remnants of normal cortical tissue in the anterior zone (horseshoe aspect) without identifying the falx cerebri,
the corpus callosum and the olfactory nerves.
The roof of the third ventricle can dilate and result in a large dorsal cyst.
• Semi-lobar: there is an incomplete division of the cerebral hemispheres with H-shaped single ventricle with rudimentary occipital and temporal horns and a partial separation of the thalamus.
• Lobar: is the least severe.
It is not accompanied by craniofacial abnormalities.
There is complete ventricular separation with focal areas of incomplete cortical division.
Absent posterior falx cerebri and septum pellucidum with fusion of thalami.
The corpus callosum is often incomplete or dysplastic (Fig 5).
- Chiari II malformation: more common in females (2:1).
Downward displacement through the foramen magnum of the cerebellum,
tonsils,
brainstem and fourth ventricle into the posterior cervical canal.
This condition is associated with a variety of findings:
Infratentorial malformations:
.
Posterior fossa hypoplasia with a low tentorial attachment and elongation of the fourth ventricle.
.
Tethered cord mielocele with lumbar or sacral myelomeningocele,
possibly associated with a lipoma of the filum terminale.
Supratentorial malformations:
.
Hydrocephalus due to obstruction in the IV ventricle pathway.
.
Agenesis or dysgenesis of the corpus callosum (in 75-90% of cases) and distortion due to hydrocephalus.
.
Enlargement of he heads of caudate nuclei and intermediate mass.
.
Interdigitation of gyri across the interhemispheric fissure by a fenestrated falx.
.
Stenogyria: brain sulcation disorder with packaging of small gyri with shallow sulci and preservation of the general sulcal pattern.
.Variable degrees of fusion of the colliculi and tectum resulting in prominent breaking and inferior displacement of the tectal plate.
- Chiari III malformation: is the most serious and relatively uncommon.
It consists of a posterior cervico-occipital encephalocele containing cerebellar dysplastic tissue,
fourth ventricle and sometimes brainstem.
1b) Atrophy due to perinatal brain injury:
It is related to agenesis,
dysgenesis or hypoplaisa of the corpus callosum caused by an injury to the grey or white matter when it is not fully formed,
that is,
in the weeks 18 to 20 of gestation.
Disorders that could lead to a damage include a viral infection,
maternal drug or alcohol use during pregnancy or for example a hypoplasia of the corpus callosum due to severe anoxia (Fig 6),
or hypoplasia secondary to hydrocephalus caused by Silvi’s aqueduct stenosis (Fig 7).
2.
TUMOURAL DISEASES
2a) Glioma
Glioblastoma multiforme (GBM) are the most common primary brain tumours in adults.
They are the 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.
Hematogenous,
subependymal and cerebrospinal fluid spread can also be seen.
On MR imaging are characterized by being poorly demarcated and infiltrative lesions,
with intratumoural necrosis and intense enhancement of the solid portion,
although occasionally no enhancement is seen.
Diffusion-weighted imaging shows restriction (lowest ADC) within the solid tumour component.
There may be intratumoural bleeding including the development of pathologically deformed vessels (neoangiogenesis),
fast tumour growth and direct invasion of the vessel wall.
This explains the increase of relative cerebral blood volume (rCBV) values in dynamic T2*-weighted perfusion MR imaging.
GBM associate a moderate peritumoral oedema contributing to mass effect (Fig.
8).
The MR spectroscopy study highlights higher levels in Cho/Cr and NAA/Cho ratios and the presence of lactate and lipids.
2b) Lymphoma
Primary central nervous system lymphomas are rare aggressive neoplasms of the brain,
accounting for less than 2% of malignant primary brain tumours.
They are almost always of the B-cell non-Hodgkin's type.
Common locations include the corpus callosum,
deep gray matter structures,
and the periventricular region.
Lymphomas differ from glioblastoma multiformes because they usually have less peritumoral oedema,
are more commonly multiple,
are less commonly necrotic,
are highly radiosensitive,
and frequently temporarily respond dramatically to steroid administration producing “vanishing lesions.” These lesions are usually iso- or hypointense on T1W images and iso or hyperintense on T2W images.
Lymphomas occur commonly in immunocompromised patients,
showing a ring-shaped pattern contrast enhancement,
whereas it is usually homogeneous and intense in immunocompetent patients.
Diffusion-weighted imaging shows restriction within the tumour given its high cellularity (Fig.
9). The MR spectroscopy study includes elevated signal of lipid,
lactate,
and choline and reduced NAA,
which cannot be differentiated from GBM.
2c) Juvenile pilocytic astrocytoma
They are a low-grade variant of astrocytoma.
They are usually a well-defined unencapsulated mixed cystic-solid appearance mass.
They are usually well-circumscribed unencapsulated masses,
with frequent cyst formation,
either microscopic or macroscopic.
Most lesions commonly involve the cerebellar vermis,
cerebellar hemispheres,
optic chiasm,
hypothalamus,
or floor of the third ventricle.
The corpus callosum is an uncommon location.
On MR imaging they are hypo or isointense on T1W images and hyperintense on T2W images,
in contrast to most low-grade infiltrative astrocytomas,
which tend not to enhance.
2d) Intraventricular tumours with extension to the corpus callosum
2e) Metastasis (affected directly / indirectly by oedema)
Intracraneal metastases represent the most common brain tumours in adults,
occurring in 25-50% of all cancer patients.
They are often supratentorial and multiple.
In adults,
lung cancer is the main cause of BMs (50-60%),
followed by breast cancer (15-20%) and melanoma (5-10%) respectively,
while tumours of the gastrointestinal tract and renal cell carcinomas are less common origins of metastases to the brain.
They are usually well-defined,
in contrast to gliomas,
with disproportionate vasogenic oedema relative to the size of metastases.
They are located in the gray and white matter junction,
following a vascular distribution.
They also appear in the basal ganglia,
the cerebellum,
and are rarely involve the corpus callosum.
On MRI lesions are isointense to mildly hypointense on T1W images and hyperintense on T2W images.
However,
hemorrhagic metastases or melanoma lesions may be hypointense on T1W and hyperintense on T2W images,
owing to the chronic breakdown of blood products.
Following administering of intravenous contrast agent,
different enhancement patterns may be seen: solid,
ring-pattern,
irregular,
homogeneous or heterogeneous (Fig 10).
3.
INFLAMMATORY-DEMYELINISING EVENTS
3a) Multiple Sclerosis (MS)
MS is an acquired demyelinising disease that affects young women more than men.
Although MS plaques can be found in any region of the brain parenchyma,
typical locations are the periventricular region,
corpus callosum,
centrum semiovale,
and deep white matter structures and basal ganglia.
According to the literature,
93% of MS patients show lesions in the corpus callosum,
characteristically involving the callososeptal surface (Fig.
11).
Eventually lesions may coexist with corpus callosum atrophy.
These plaques typically are hyperintense on the proton density,
T2,
and fluid-attenuated inversion recovery (FLAIR) sequences of MRI.
They appear hypointense on T1 weighted images without gadolinium and show enhancement during the acute phase.
Plaques may also exhibit a reversible restriction of diffusion due to exocytotoxic intramyelinic oedema.
Diffusion tensor imaging can demonstrate and measure lesional damage in white matter tracts and gray matter and in areas of normal-appearing white matter (Fig 12.).
3b) Susac Syndrome
Susac syndrome is a rare disease attributed to a microangiopathy affecting the arterioles of the brain,
retina,
and cochlea,
characterized by mono-phase fluctuating episodes of the classic clinical triad of subacute encephalopathy,
visual loss secondary to retinal branch occlusions,
and sensorineural hearing loss.
MRI demonstrates multiple white matter lesions,
usually smaller than the MS lesions,
and more prone to affect basal ganglia and thalamus.
There may also be enhancement of leptomeninges,
better shown in postcontrast fluid-attenuated inversion recovery sequences (Fig.
13).
3c) Acute disseminated encephalomyelitis (ADEM)
ADEM is an autoimmune disease with demyelisation of the CNS,
which usually occurs after a viral infection,
a vaccine,
or less frequently associated with rheumatic fever or idiopathic form.
The MRI shows multiple large T2W-hyperintenses lesions,
located in the periventricular white matter,
cerebral cortex,
brainstem,
cerebellum,
spinal cord and optic nerves.
Lesions may show nodular or ring enhancement (Fig 14).
Differential diagnosis between ADEM and MS may be difficult although ADEM has usually a monophasic clinical course and no new lesions usually appear after 6 months from the onset.
3d) Progressive multifocal leukoencephalopathy (PML)
It is a rare AIDS-related demyelinising disease of the brain resulting from opportunistic infection with the JC virus.
It only causes disease in immunocompromised conditions.
MRI shows multifocal and asymmetric lesions that may coalesce into large lesions.
They may occur anywhere although injuries predominate in subcortical white matter (especially with parieto-occipital and frontal lobes U-fibres involvement) and in the corpus callosum.
This predilection accounts for the scalloped margins of the lesions.
The lesions are typically hypointenses on T1W images and hyperintenses on T2W images.
They are not usually associated with mass effect or enhancement after administration of intravenous contrast,
although in some cases a slight enhancement of the periphery of the lesion and mass effect can be seen.
These characteristics allow differentiation of PML from lesions such as GBM and lymphoma.
4.
VASCULAR PROCESSES
4a) Infarcts
Isolated Ischemic lesions of the corpus callosum are rare so it is usually involved as a part of a large vascular distribution in a large-vessel ischemic event.
Vascularisation of the corpus callosum is assured by the anterior communicating and pericallosal arteries for the rostrum and genu,
the anterior cerebral arteries for the body and the posterior cerebral arteries for the splenium.
Imaging characteristics of infarcts are the same as strokes in other locations.
Ischemic lesions usually affect the splenium,
followed by the body and genu,
with preservation of the dorsal and ventral surface.
Patients commonly have a history of hypertension,
diabetes or other cardiovascular risk factors (Fig 15). Diffusion tensor imaging can evaluate the anisotropic changes of cerebral white matter tracks in patients with ischemic stroke (Fig.16).
4b) Periventricular leukomalacia
Periventricular leukomalacia is the most common ischemic brain injury in premature infants.
The ischemia occurs in the border zone at the end of arterial vascular distributions.
Characteristically occurs in the periventricular white matter adjacent to the lateral ventricles.
There is atrophy and irregularity of the corpus callosum in advanced stages (Fig.
17).
4c) Arteriovenous malformation,
aneurysm rupture or cavernoma
Vascular malformations may occur elsewhere in the brain parenchyma including to the corpus callosum.
They are prone to bleed,
causing a bruise or intraventricular haemorrhage.
Most receive blood supply from anterior and posterior cerebral arteries,
possibly bilateral,
and drain into the internal cerebral vein or superficial interhemispherical veins.
4d) Traumatic injuries
- Callosotomia: in cases of refractory generalized epilepsy.
- Diffuse axonal injury (DAI): is a frequent result of traumatic acceleration/deceleration or rotational injuries that causes a loss of consciousness.
DAI typically consists of several focal white-matter lesions measuring 1-15 mm.
MRI demonstrates more lesions than CT-scan,
especially magnetic susceptibility techniques,
which are superior in detecting chronic haemoglobin degradation products because of the susceptibility effects of hemosiderin.
Keeping in mind that these lesions may be non-bleeding,
they are best visualized on sagittal T2W-FLAIR sequences.
Otherwise,
for the detection of hemorrhagic lesions in the acute phase T2W images are recommended,
while after the third day stands on the usefulness of the T1W images for the detection of subacute-chronic microhaemorrhages.
(Fig 18)
Grading is described according to the anatomic distribution of injury,
which correlates with outcome:
- Grade I : involves grey-white matter interfaces
- most commonly : parasagittal regions of frontal lobes,
periventricular temporal lobes
- less commonly : parietal and occipital lobes,
internal and external capsules,
and cerebellum
- Grade II : involves corpus callosum(frequently unilateral) in addition to stage I locations
- most commonly : eccentric,
posterior body and splenium but does advance anteriorly with increasing severity of injury
- Grade III : involves brainstemin addition to stage I and II locations
- most commonly : rostral midbrain,
superior cerebellar peduncles,
medial lemnisci and corticospinal tracts
5.
ENDOCRINE AND METABOLIC CAUSES
5a) Metachromatic leukodystrophy
It is an autosomal recessive familial disorder with an enzymatic defect that causes demyelination.
At T2-weighted MR imaging,
metachromatic leukodystrophy manifests as symmetric confluent areas of high signal intensity on T2W images in the periventricular white matter with sparing of the subcortical U-fibers.
The cerebellar white matter may appear hyperintense at T2W imaging.
No enhancement is evident at MR imaging.
The corpus callosum,
internal capsule,
and corticospinal tracts are also frequently involved.
In the later stage of metachromatic leukodystrophy,
corticosubcortical atrophy often occurs,
particularly when the subcortical white matter is involved.
5b) Adrenoleukodystrophy
It is an autosomal recessive X-linked chromosomal disorder of childhood characterized by an enzymatic defect of peroxisome that produces demyelination of the CNS,
adrenal cortex and testes.
In the early stages symmetric white matter demyelination occurs in the parietooccipital (peritrogonal),
sparing the subcortical U fibers and extending across the corpus callosum splenium.
The affected cerebral white matter typically has three different zones.
The inner zone appears moderately hypointense on T1W images and markedly hyperintense on T2W images,
corresponding to irreversible gliosis.
The intermediate zone represents active inflammation and breakdown in the blood-brain barrier.
On T2W images it appears isointense or slightly hypointense and readily enhances after intravenous administration of contrast material.
The outer zone represents the leading edge of active demyelination and it appears moderately hyperintense on T2W images and demonstrates no enhancement.
Symmetrical abnormal areas of hyperintensity along the descending pyramidal tract are common at T2W imaging.
There may also be calcifications in trigones and around the frontal horns of the lateral ventricles.
5c) Inherited metabolic disorders
There is a long list of hereditary metabolic disorders including mucoplisacaridosis and Kearns-Sayre syndrome.
They can be distinguished by the distribution of lesions through the cerebral and cerebellar parenchyma affecting the gray matter (cortex and basal ganglia),
the white matter (periventricular,
deep and subcortical) and the cerebellum (nuclei and white matter).
5d) Wernicke’s encephalopaty
Wernicke's encephalopathy is an acute neurological syndrome resulting from thiamine (vitamin B1) deficiency.
It is characterized by confusion,
ataxia,
abnormal eye movements,
and loss of visual acuity.
Typical MRI findings are represented by symmetric hyperintensity on T2Wimages in the thalami,
mamillary bodies,
tectal plate,
and periaqueductal.
Atrophy of this structures,
the corpus callosum and supratentorial cortex may be found only in alcoholic patients.
These lesions may show a restriction of diffusion because of exocitotoxic oedema that may be reversible if treated appropriately.
6.
INFECTIOUS AGENTS
Viruses are the most common pathogens causing encephalitis,
mainly by the herpes virus infection.
However,
other pathogens such as bacteria (eg tuberculosis,
Whipple's disease (Fig.
19),
Lyme disease),
rickettsia,
fungi or parasites (eg toxoplasmosis,
cysticercosis) may cause encephalitis and involve the corpus callosum.
HIV also affects the corpus callosum splenium and fornix in patients with cognitive impairment,
although there is a more common involvement of the white matter (sparing the subcortical U fibers),
and basal ganglia (usually sparing the cortical gray matter),
without evidence of mass effect or enhancement.
Otherwise,
you should consider the possibility of HIV infection with other pathogens or coexistence of tumours such as lymphoma.
The infection of the brain parenchyma appears as ill-defined large areas of hyperintensity on T2W images predominantly affecting the cortical gray matter,
although it can also affect,
in addition,
the white matter (corpus callosum included) or the deep gray nuclei.
Mottled haemorrhagic areas as well as contrast enhancement may be seen.
Restriction of diffusion may be often found as the unique and earlier finding,
being unapparent on the conventional MRI sequences.
Diffusion tensor imaging can demonstrate and measure lesional damage of the corpus callosum (as well as in the ipsilateral occipital lobe) and white and gray matter tracts in areas of normal-appearing white matter (Fig.
20). MRI findings are not specific and can mimic other diseases,
so it is crucial a good clinical context to establish an accurate diagnosis and an early treatment in order to reduce mortality.
7.
TOXIC INSULTS
7a) Marchiafava-Bignami
Marchiafava-Bignami is a rare disease associated with alcoholism though rarely also seen in patients without alcoholism.
It is characterized by demyelination and necrosis of the corpus callosum with involvement of the central layers with relative sparing of the dorsal and ventral surfaces (which may be seen as a sandwich sign on sagittal MRI imaging). Since clinical symptoms can vary from cognitive impairment,
gait disturbance,
and hemiparesis to stupor,
coma,
and death,
early recognition of neuroimaging characteristics is crucial for diagnosis and treatment.
There are different temporal clinical presentations.
The corpus callosum (mainly the genu and splenium) appears enlarged because of oedema during the acute phase,
demonstrating hyperintensity on T2 and proton density-weighted MR images with possible T2-hyperintense foci in the centrum semiovale,
and hypointense on T1W images.
During the subacute phase,
cystic lesions and small foci of T2 hypointensity can develop mainly in the body of the corpus callosum,
most likely because of hemosiderin,
and often exhibit enhancement (Fig 21).
After a few months,
signal intensity alterations become less evident but residual atrophy of the involved structure (and,
in some cases,
also of the cortex) usually is present.
Diffusion tensor imaging can demonstrate and measure lesional damage of white matter tracts as the corpus callosum (Fig.
22).
7b) Disseminated necrotizing leukoencephalopathy
Disseminated necrotizing leukoencephalopathyis a rare syndrome of progressive neurologic deterioration seen most often in patients who have received central nervous system irradiation combined with intrathecal or systemic chemotherapy in the treatment or prophylaxis of various malignancies.
Diffuse white matter changes are explained because of microvascular occlusion and subsequent ischemia or excititotoxic oedema.
Leukoencephalopathy is seen as diffuse or multifocal white matter hyperintensities on T2-weighted MR imaging,
predominantly in periventricular regions with sparing of the subcortical U-fibers.
However,
these injuries can be demonstrated in the early stage only in the diffusion sequences,
showing restriction.
Although most signal changes are subclinical and usually transient,
some rare patients have extensive signal changes and contrast-enhancing lesions accompanying rapid neurological deterioration after treatment with MTX,
a condition known as disseminated necrotizing leukoencephalopathy.
Other drugs,
such as BCNU,
melphalan,
fludarabine,
cytarabine,
5-fluorouracil,
levamisole and cisplatin,
have also been implicated.
7c) Changes in radiation therapy
MRI can detect demyelination associated with radiotherapy,
which is called radionecrosis.
As expected,
radiation necrosis occurs most commonly at the site of maximum radiation delivery.
It manifests as hyperintense areas on T2W images and can closely resemble recurrent tumour at imaging because of the following shared characteristics: origin at or close to the original tumour site,
contrast enhancement,
growth over time,
oedema,
and exertion of mass effect.
With respect to the MR imaging characteristics of radiation necrosis,
most lesions consist of an enhancing mass with a central area of necrosis.
The contrast enhancement of these lesions is secondary to radiation-induced endothelial damage,
which leads to the breakdown of the blood-brain barrier.
On T2-weighted images,
the solid portion of the radiation-induced necrotic mass has low signal intensity,
and the central necrotic component shows increased signal intensity.
These changes can occur in the early phase (during treatment),
in the early delayed phase (in the first 3 months) or in the late delayed phase (starting from 3 months).
It is also in this last phase where calcifications and microhaemorrhages are commonly found (because of vasculitis,
formation of telangiectasia or other vascular malformations) in basal ganglia,
dentate nuclei of the cerebellum.
These microhaemorrhages are better depicted in magnetic susceptibility sequences (T2*W GRE sequence).
The use of platinum-based chemotherapy drugs,
such as cisplatin and carboplatin,
combined with radiation therapy may contribute to the development of radiation-induced necrosis.
8.
TRANSIENT LESIONS
Transient lesions of the corpus callosum are probably associated with oedematous and / or inflammatory changes.
Acute withdrawal of antiepilectis (carbamazepine,
phenytoin,
vigabatrina),
a state of hypoglycemia (Fig.
23),
epileptic status (Fig.24),
Wernicke,
Marchiafava-Bignami,
the use of sympathomimetics drugs (cocaine,
fenilciclidina,
hidroclorat,
amphetamines),
or virus infection (such as influenza,
rotavirus,
E.
Coli,
adenovirus and mumps),
hemolytic uremic syndrome,
syndrome of brain damage associated with the altitude are reported as risky factors related to this entity.
MRI usually reveals an oval-shaped lesion of 1-2cm in the corpus callosum splenium,
hypointense on T1W images and hyperintense on T2W images.
These injuries show restriction of diffusion,
which is usually reversible due to exocitotoxic oedema.
These lesions usually disappear within a few weeks following adequate therapy.
9.
MISCELLANEOUS
9a) After drainage cystic lesions of the adult chronic hydrocephalus
In patients with long-standing hydrocephalus after shunting,
focal and diffuse lesions have been described in the corpus callosum,
being hypointense on T1W images and hyperintense on T2W images,
with sparing of the splenium.
The mechanism responsible for the production of these lesions is unknown although it is postulated that may be the result of ischemia with subsequent demyelination caused by prolonged sever stretching of the corpus callosum from ventriculomegalia,
followed by a rapid decompression of the ventricles.
9b) Chronic adult hydrocephalus
It is characterized by the following radiological findings (Fig 25):
- Enlargement of the temporal horns of the lateral ventricles > 2mm.
- Enlargement of both the Silvi’s fissures and convexity sulci,
which helps differentiation from other causes of hydrocephalus.
- Rounding of the frontal horns of the lateral ventricles and third ventricle (biconvex morphology),
with a measured Evans index of more than 0:33.
- “CSF Flow void sign” at the Aqueduct of Sylvius caused by an increase of cerebrospinal fluid peak velocity.
- Increased curvature of the corpus callosum.