Brain herniation, the displacement of brain from one cranial compartment to another, is an important complication of intracranial lesions. The key to determining herniations and their sequelae is a complete anatomical knowledge of the brain, skull, and dural reflections. It is a thorough understanding of this anatomic relationship which can help define the cause, appearance, and complications of the various herniations.
Everyday, a variety of intracranial lesions are evaluated and
abnormal imaging characteristics, including location, size,
enhancement, associated hemorrhage and mass effect, are described.
One important complication of mass effect is brain herniation,
which is the displacement of brain from one cranial compartment to
another. The most common causes of brain herniation are tumors,
intraparenchymal hematomas, cerebral infarctions and subdural or
The effects of brain herniations are most severe in children and
adults of less than 50 years of age. Patients over 50 usually have
more cerebrospinal fluid (CSF) both surrounding the brain and
within the ventricular system due to atrophy, and this increased
CSF content, in combination with larger ventricles, allows for
greater insult from mass effect and less compression of brain
tissue. Younger individuals have small, closely apposed basilar
cisterns and ventricles, allowing less compensation for increasing
intracranial pressure and mass effect. Herniation can occur slowly
from non-acute pathology such as tumors, or may occur rapidly due
to acute events like traumatic hemorrhage.1
Many aspects contribute to the formation of mass effect with
subsequent herniation. Mass effect is produced when there is
alteration of the normal equilibrium between blood flow, CSF
production, and existing brain tissue. The arteries provide a
constant supply of fluid with oxygen and nutrients to the neural
tissue, while veins simultaneously remove the fluid. CSF is
produced in the choroid plexuses of the ventricles and then travels
into the subarachnoid space where it is eventually resorbed by the
arachnoid villi. Any insult involving the vascular supply or the
ventricular system can result in mass effect.
The fact that the brain is confined to the skull makes the
problem worse, as there is no room for expansion. Venous occlusion,
either due to thrombosis or compression, will compromise the
removal of fluid that is constantly reintroduced by the arteries.
Elevated production or the inadequate resorption of CSF causes
increased fluid within the intracranial cavity. The increase in
fluid volume within the CNS is effectively increased "mass", with
associated "mass effect" upon adjacent structures.
There are four major types of cerebral herniations: subfalcine,
transtentorial, uncal, and tonsillar (figures 1,2).2-4 A fifth
type, transphenoidal herniation, will be discussed briefly, but is
less frequently seen than the other types. The key to understanding
herniations and their sequelae is a complete anatomical knowledge
of the brain, skull, and dural reflections. It is a thorough
understanding of this anatomic relationship which can help define
the cause, appearance, and complications of the various
Anatomy of the falx cerebri and tentorium
The skull is a fixed structure that allows no compensation for
expansion of brain tissue. The cranial cavity within the skull is
functionally divided into compartments by combinations of bony
ridges and dural folds (figure 3). The base of the skull provides a
floor for the frontal and temporal lobes to rest on, as well as to
allow passage of peripheral neural structures. Inward reflections
of the dura mater are present which stabilize and protect the brain
against excessive movement. These dural reflections are formed by
the visceral layer of the dura mater and divide the intracranial
cavity into various compartments, known as the falx cerebri, the
tentorium cerebelli, and the falx cerebelli.
Anteriorly, the falx cerebri is attached to the crista galli,
from where it extends midline along the skull's inner table to the
confluence of sinuses (torcular herophili) posteriorly. It is
narrow anteriorly and broad posteriorly, where it connects with the
upper surface of the tentorium cerebelli.5 The falx cerebri
contains the superior sagittal sinus along its upper margin and the
inferior sagittal sinus along its inferior margin.5 The superior
sagittal sinus drains directly into the sinus confluence, the
inferior sagittal sinus drains into the straight sinus. As the falx
cerebri courses posteriorly, it elongates in its craniocaudad
dimension and forms a larger barrier between the hemispheres
(figure 3). The increased size of the posterior portion of the falx
cerebri makes it more resistant to movement than the anterior falx
cerebri. It is for this reason that subfalcine herniations more
commonly occur anteriorly.
The tentorium cerebelli creates a compartment between the
posterior fossa and the cerebral hemispheres. It is attached to the
occipital bone posteriorly, the petrous portions of the temporal
bones laterally, and the clinoid processes anteriorly; it courses
superomedially from its bony attachments to join the falx cerebri.
The tentorium cerebelli contains the transverse sinuses, which
eventually course through the skull base, and the straight sinus,
which empties into the sinus confluence.5
The tentorium cerebelli contains an opening anteriorly that
allows passage of the brain stem and cerebral peduncles (figure 3).
This opening is known as the tentorial hiatus, tentorial notch, or
incisura and measures approximately 5.5 cm in the fronto-occipital
3 cm in the interparietal axis.6 The tentorial notch is
semiovular in shape and its only bony attachment is at the clinoid
processes anteriorly.5 The remaining lateral and posterior borders
of the tentorial notch are the "free edges." These are without
direct attachment, but are taut and firm nonetheless.
Obviously, a herniation is a critical finding that reflects
evidence of a pathologic process and the need for possible emergent
intervention. It is imperative to not only report the presence of a
herniation, but to also evaluate for possible complications. Such
may result from compression upon adjacent arteries, veins,
nerves and brain parenchyma.
A subfalcine herniation, or midline shift, occurs when mass
effect causes displacement of the falx cerebri laterally (figure
4). It is the most common type of brain herniation and is often
associated with herniation of the cingulate gyrus below the falx
cerebri. The cingulate gyrus of each cerebral hemisphere normally
lies medial to the inferior aspect of the falx cerebri (figure
The degree of herniation can be mild with minimal midline shift
or can be severe, exhibiting complete herniation of the cingulate
gyrus and adjacent white matter. Due to the tough fibrous structure
of the falx and its resistance to movement, a few millimeters of
midline shift is considered significant. With increasing mass
effect, the ipsilateral lateral ventricle and both foramina of
Monro become compressed. This compression results in a slit-like
appearance of the ipsilateral ventricle and an enlarged
contralateral ventricle. This enlargement is due to continued
production of CSF that cannot escape into the third ventricle.7
Chronic compression upon the cingulate gyrus may cause
The anterior cerebral arteries and their branches (the
callosomarginal, pericallosal, and frontopolar arteries) are
located between the falx cerebri and the adjacent gyri of the
frontal and parietal lobes. When subfalcine herniation is
present there is the possibility of anterior cerebral artery
compression,8,9 especially when an anterior lesion also is present.
If these vessels become trapped against the falx, the patient may
be at risk of infarction.10 Formation of an aneurysm due to
vascular damage is another unusual complication of compression of
the anterior cerebral arteries by the falx cerebri that may be
When the lesion is located posteriorly in the hemisphere, there
may be compression of the internal cerebral veins,9 vein of Galen,
or the deep subependymal veins. Compression of these veins raises
the pressure of the entire deep venous system, which further
aggravates parenchymal congestion and increases intracranial
pressure (ICP).12 When a subfalcine herniation is present, the
concomitant presence of a transtentorial or uncal herniation also
should be evaluated.1
Transtentorial herniation is due to mass effect that causes
shift of neural components into the tentorial notch. There are
three separate types of herniations which cross the tentorium
cerebelli. Descending and ascending transtentorial herniation
will be discussed here, and uncal herniation, a subtype of a
transtentorial herniation, will be discussed separately.
There is limited space within the tentorial notch, which
contains the brain stem and its surrounding subarachnoid cisterns.
Only a few millimeters of space are present between the midbrain
and the rigid tentorial edge.13 Therefore, much lateral
displacement of the brainstem cannot be tolerated, and a shift from
the midline of a few millimeters will result in compression.14-16
Both ascending and descending herniation can produce enough
pressure on the brainstem to produce cerebral aqueduct occlusion
(figure 2).1 When this occurs, it results in obstructive
hydrocephalus supratentorially, which compounds the problem by
increasing ICP.14 Eventually, the increasing compression upon the
brainstem compromises the cardiorespiratory centers, which can be
Descending transtentorial herniation occurs when mass effect
displaces the medial part of the temporal lobe through the
tentorial notch. Specifically, it is the middle and posterior
portions of the parahippocampal gyrus that herniate and compress
the brainstem.17 Descending transtentorial herniation is commonly
seen with masses involving the inferior portion of a hemisphere.
This increase in mass effect forces the diencephalon and midbrain
inferiorly through the tentorial notch (figure 5).3 The herniated
parahippocampal gyrus generally is unilateral, but has also been
found to be bilateral.1 Bilateral herniation is commonly produced
by a midline mass, bilateral mass, or supratentorial hydrocephalus
whose vector forces are directed inferiorly and medially (figure
6).18 Transtentorial herniation commonly is associated with a
concomitant subfalcine herniation.1
In severe cases of descending transtentorial herniation, there
is obliteration of all basilar cisterns. When displaced inferiorly,
the parahippocampal gyrus compresses regions of the midbrain,
including the cerebral aqueduct. Increasing herniation will then
sequentially compress the pons and, subsequently, the medulla.19
Often, acute compression of the entire brain stem occurs
simultaneously due to the acute and catastrophic nature of the
The midbrain is surrounded laterally by the ambient cisterns,
posteriorly by the quadrigeminal cistern, and anteriorly by the
interpeduncular and suprasellar cisterns (figure 7). These cisterns
serve as corridors for the passage of the posterior cerebral
arteries and the third cranial nerves. Each third cranial nerve
courses through the interpeduncular cistern below the posterior
To a variable extent, the herniated temporal lobe can compress
the oculomotor nerve, the posterior cerebral artery, the anterior
choroidal artery, and the superior cerebellar artery.20 Compression
of the oculomotor nerve produces ipsilateral pupillary dilatation.
Compression of the posterior cerebral artery between the temporal
lobe and tentorial edge results in infarction. Both posterior
cerebral arteries may become compressed if bilateral herniation is
present.21 Occlusion of the anterior choroidal artery results in
infarction of the structures in its vascular supply, which include
the optic tract, temporal lobe, basal ganglia, cerebral peduncles,
and midbrain.22 Cerebellar infarction will occur if the superior
cerebellar artery is compressed.
In severe cases of transtentorial herniation, a Duret hemorrhage
may occur. This is a brainstem hemorrhage caused by mechanical
shearing of the pontine and mesencephalic perforating vessels,
especially the arterials, by the herniating tissue.23,24
Compression related to Duret hemorrhage may compromise the
cardiorespiratory centers, resulting in death.3,25
Transtentorial herniation is a grim finding as it usually is an
acute process which is lethal in a very short time. In unilateral
descending transtentorial herniation, the brainstem is shifted away
from the herniating temporal lobe, resulting in enlargement of the
ipsilateral cerebellopontine angle cistern.7 In this instance, the
brainstem will appear flattened and elongated, with compressed or
obliterated perimesencephalic cisterns.
Ascending transtentorial herniation is due to increased pressure
in the posterior fossa. This increase in pressure projects the
central lobule, culmen, and superior surface of the cerebellum
upward through the tentorial notch, resulting in compression of the
brain stem (figure 2).7 This brainstem displacement is well
visualized on multiplanar magnetic resonance images.
In ascending transtentorial herniation, the superior vermian
cistern is effaced and the fourth ventricle is compressed and
displaced anteriorly (figures 8,9).7 With increasing upward
herniation, the quadrigeminal cistern becomes effaced and the
midbrain displaced anteriorly against the clivus.26,27 Increasing
mass effect may occlude the cerebral aqueduct, resulting in
increased intracranial pressure.14 An ascending transtentorial
herniation also is likely to obstruct venous outflow through direct
compression of the vein of Galen and the basal vein of Rosenthal,
which further aggravates parenchymal congestion and increases the
ICP.12 Midbrain compression also may be complicated by
periaqueductal necrosis of the brain stem.
Uncal herniation occurs when the uncus is displaced medially and
inferiorly over the free edge of the tentorium cerebelli.2 The
uncus is the hooked, anterior extension of the parahippocampal
formation of the medial temporal lobe (figure 7). Normally it is
located 3 to 4 mm medial to the free edge of the tentorium, which
is adjacent to the suprasellar cistern.28 In herniation, the uncal
gyrus is displaced into the suprasellar cistern between the free
edge of the tentorium and the anterior edge of the midbrain
(figures 10,11,12).14 This type of herniation usually is secondary
to a mass located more inferiorly in the cerebral hemisphere, such
as in the temporal lobe.
Uncal herniation often exhibits compression of one or both of
the cerebral peduncles, as well as the adjacent oculomotor nerve.
The oculomotor nerve is located medial to the uncus and passes
between the superior cerebellar artery and the posterior cerebral
artery.29 Mass effect upon the third cranial nerve and compression
of the ipsilateral cerebral peduncle causes a recognizable clinical
syndrome, characterized by a blown pupil with contralateral
hemiparesis.10 Alternatively, the uncus can displace the brain stem
against the opposite tentorial edge and cause an indentation of the
contralateral cerebral peduncle, known as Kernohan's notch.28,29
This contralateral compression causes ipsilateral hemiparesis,
which falsely localizes the symptoms to the other side.22
Uncal herniation can compress the posterior cerebral artery as
it encircles the cerebral peduncle anterolaterally; however, the
risk of infarction is greater with transtentorial herniation due to
a closer anatomic relationship between the parahippocampal gyrus
posterior cerebral artery (figure 3). Additionally, there also
can be compression upon the anterior choroidal artery and superior
cerebellar artery, with resultant infarction.
Imaging features of uncal herniation include distortion of the
suprasellar cistern due to the medial and inferior position of the
uncus. The normal suprasellar cistern has a "star"" configuration,
but in uncal herniation the lateral aspect of the star is
obliterated by the uncus.30 The cerebral peduncle will appear
flattened and the midbrain can be rotated or tilted.1 The
ipsilateral cerebellopontine angle cistern may be widened due to
shift of the brainstem (figure 11).
Tonsillar herniation occurs when mass effect in the posterior
fossa causes inferior displacement of the cerebellar tonsils into
or beyond the foramen magnum (figures 1,2).31 Two-thirds of
patients with ascending transtentorial and one-half of those with
descending transtentorial shift have concurrent tonsillar
herniation (figures 8,13).4
Tonsillar herniation usually is not fatal; however, in rare
cases, there can be significant compression upon the medulla which
can be fatal.1 Additionally, compression upon the posterior
inferior cerebellar arteries can produce infarction.10 The presence
of a concomitant ascending transtentorial herniation must be
evaluated because of its common association and clinical
importance. Tonsillar herniation can obstruct CSF outflow from the
fourth ventricle, resulting in hydrocephalus.1
Tonsillar herniation is difficult to accurately characterize on
axial CT images. However, the demonstration of brain parenchyma
around the medulla in the foramen magnum and a less than adequate
amount of CSF in the foramen magnum (figure 13) may provide clues
to its presence.22 Although sagittal MR images have been found to
be the best method for evaluating tonsillar herniation, direct or
reconstructed coronal CT images also will demonstrate an abnormal
inferior location of the cerebellar tonsils.
It is important to know not to perform a lumbar puncture in the
presence of significant herniation, especially a transtentorial or
tonsillar herniation. The withdrawal of CSF will decrease the
pressure below the foramen magnum, allowing further herniation
inferiorly. This can increase compression upon the brain stem
suddenly, often resulting
in death due to cardiorespiratory center compromise.32
Transphenoidal (transalar) herniation
Transphenoidal herniation is found when mass effect displaces
brain tissue across the sphenoid wing. There are two types of
transphenoidal herniation, ascending and descending, which involve
the temporal lobe and frontal lobe, respectively. Descending
herniation occurs when the frontal lobe is forced posteriorly over
the greater sphenoid wing, causing backward displacement of the
sylvian fissure, the horizontal middle cerebral artery, and the
temporal lobe. This type of herniation, caused by a lesion in the
anterior frontal lobe, can lead to ischemic changes in the inferior
frontal lobe.1 Ascending herniation occurs when the temporal lobe,
sylvian fissure, and middle cerebral artery are displaced
anterosuperiorly over the sphenoid ridge by all adjacent mass.
Complications due to mass effect are commonly seen. It is
extremely important to not only describe an inciting mass lesion,
but also to comment on any associated complications such as
cerebral herniation. The type of herniation and any associated
complications are important to the clinician to help assess
therapeutic options and the possible need for emergent
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Dr. Coburn and Dr. Rodriguez are in the Department of Radiology
at the University of Missouri Hospital and Clinics in Columbia,