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 epidural hemorrhages.

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 herniations.

Anatomy of the falx cerebri and tentorium cerebelli

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 axis and

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 complications

may result from compression upon adjacent arteries, veins, nerves and brain parenchyma.

Subfalcine herniation

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 1).

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 necrosis.1

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 present.11

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

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 fatal.

Descending

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 lesion.

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 cerebral artery.

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

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

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 and the

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

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.

Summary

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 intervention. AR

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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, MO.