Cerebral herniations - Applied Radiology Online

E veryday, 

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 

Dr. Coburn and Dr. Rodriguez are in 

the Department of Radiology at the 

University of Missouri Hospital and 

Clinics in Columbia, MO. 

Cerebral herniations 

Mark W. Coburn, MD and Fabio J. Rodriguez, MD 

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, 

10 APPLIED RADIOLOGY, May 1998

FIGURE 1. Patterns of brain herniation, 

coronal drawing. (1) Subfalcine herniation 

of the cingulate gyrus beneath the falx 

cerebri; (2) compression of ipsilateral lateral 

ventricle due to subfalcine herniation; 

(3) dilatation of the contralateral ventricle 

due to obstruction of the foramen of Monro; 

(4) uncal herniation through the tentorial 

notch; (5) tentorium cerebelli; (6) tonsillar 

herniation through the foramen magnum; 

(7) transverse sinus within the tentorium 

cerebelli; (8) superior sagittal sinus within 

the falx cerebri. (Adapted from Bassett DL: 

A Stereoscopic Atlas of Human Anatomy.) 

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. 

APPLIED RADIOLOGY, May 1998 

FIGURE 2. Patterns of brain herniation, sagittal drawing. (1) Ascending transtentorial herniation; 

(2) associated obstruction of the cerebral aqueduct; (3) tentorium cerebelli; (4) fourth 

ventricle; (5) tonsillar herniation through the foramen magnum. 

FIGURE 3. Dural reflections. (1) Falx cerebri; (2) tentorium cerebelli; (3) superior sagittal 

sinus within the falx cerebri; (4) inferior sagittal sinus within the falx cerebri; (5) straight sinus 

within the tentorium cerebelli; (6) transverse sinus within the tentorium cerebelli; (7) confluence 

of sinuses (torcular herophili); (8) anterior attachment of falx cerebri to the crista galli; 

(9) black arrows demonstrate the free edges of the tentorial notch; (10) anterior clinoid 

process. (Adapted from Wilkins RH, Rengachery SS: Neurosurgery, ed 2, pp 349-350. New 

York, McGraw-Hill, 1989.) 

11

FIGURE 4. Subfalcine herniation. Note 

extensive midline shift due to the acute and 

chronic subdural hematoma. There is compression 

of the ipsilateral ventricle due to 

mass effect. The frontal and temporal horns 

of the contralateral ventricle are dilated due 

to foramen of Monro obstruction and continued 

CSF production. Also note the compression 

upon the quadrigeminal cistern 

causing a “crooked smile.” 

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. 

A 

FIGURE 5. Unilateral descending transtentorial herniation due to a right-sided glioblastoma. 

Image A is approximately 1 cm inferior to B. (A) The inferior tip of the herniated right parahippocampal 

gyrus with mild mass effect upon the brainstem is demonstrated. (B) Also demonstrated 

is herniation of the right parahippocampal gyrus t through the tentorial notch, with 

displacement of the brainstem to the left and obliteration of the perimesencephalic cisterns. 

Notice that the inferior aspect of the third ventricle can be seen immediately superior to the 

midline of the midbrain. Dilatation of the contralateral lateral ventricle is present due to the 

concomitant subfalcine herniation. 

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 move- 

B 

ment, 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 


FIGURE 6. Bilateral descending transtentorial 

herniation in a 12-year-old who was hit 

by a car and died shortly after the CT scan 

was performed. Both parahippocampal gyri 

have herniated downward through the 

transtentorial notch. The perimesencephalic 

cisterns are obliterated and the brainstem is 

elongated. Note the ischemic “reversal sign” 

manifested by higher density in the cerebellum 

than the cerebral hemispheres, due to 

massive supratentorial edema. 

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 


FIGURE 7. Midbrain/parahippocampus. Cerebral peduncles and adjacent structures. 

(1) Uncus of parahippocampal gyrus; (2) parahippocampal gyrus; (3) ambient cistern; 

(4) quadrigeminal cistern; (5) posterior cerebral artery in the ambient cistern; (6) middle cerebral 

artery; (7) anterior cerebral artery; (8) posterior communicating artery; (9) oculomotor 

nerve (CN3). 

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 

13

FIGURE 8. Ascending transtentorial and 

tonsillar herniations due to medulloblastoma. 

Gadolinium-enhanced T1weighted 

image demonstrates that the 

superior portions of the cerebellum have 

herniated through the tentorial notch. The 

brainstem is compressed, showing displacement 

both superiorly and anteriorly. 

Supratentorial hydrocephalus is present 

due to cerebral aqueduct compression. The 

cerebellar tonsils have herniated below the 

foramen magnum and also exhibit compression 

of the medulla. There is near obliteration 

of the fourth ventricle. 

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 compres- 

FIGURE 9. Ascending transtentorial herniation 

in the same patient as figure 8. This 

gadolinium-enhanced T1-weighted axial 

image is at the level of the cerebral peduncles. 

The cerebellum is enlarged and demonstrates 

compression of the quadrigeminal 

plate. The quadrigeminal cistern and posterior 

ambient cisterns are obliterated. The 

third and lateral ventricles are enlarged due 

to cerebral aqueduct compression. 

sion 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 


FIGURE 10. Unilateral uncal herniation due 

to an intraparenchymal hematoma. The left 

uncus has herniated through the tentorial 

notch, evidenced by distortion of the 

suprasellar cistern. The normal “star” configuration 

has been disrupted. There is mild 

compression upon the ipsilateral cerebral 

peduncle, with associated tilting and displacement 

of the brainstem to the right. The 

right perimesencephalic cisterns are obliterated 

due to the brainstem displacement. 

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 


FIGURE 11. Unilateral uncal herniation. 

This axial CT image through the level of the 

4th ventricle demonstrates widening of the 

left cerebellopontine angle due to a left unilateral 

uncal herniation. The inferior tip of 

the left uncus can be seen anterolateral to 

the brainstem. 

peduncle causes a recognizable clinical 

syndrome, characterized by a blown 

pupil with contralateral hemiparesis. 10 

Alternatively, the uncus can displace the 

A 

B 

FIGURE 13. Tonsillar herniation. (A) An axial CT of a patient with a large cerebellar metastasis. 

(B) An axial T1-weighted image of the same patient with medulloblastoma in figure 8. 

Image shows that the foramen magnum is nearly completely filled with brain tissue, and virtually 

no CSF is seen. The brainstem is elongated and compressed bilaterally by the herniating 

cerebellar tonsils. This image demonstrates the similar findings, with an abnormally low 

position of the cerebellar tonsils and very little surrounding CSF. 

FIGURE 12. Bilateral uncal herniation due 

to traumatic injury. The normal “star” configuration 

is disrupted with inferomedial displacement 

of the uncus bilaterally. 

Associated cerebellar infarctions are seen 

due to compression of both superior cerebellar 

arteries. 

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 cerebel- 

15

lopontine 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 

REFERENCES 

1. Taveras JM: Neuroradiology, ed 3, pp 111-115. 

Baltimore, Williams & Wilkins, 1996. 

2. Meyer A: Herniation of the brain. Arch Neurol 

Psychiatr 4:387-400, 1920. 

3. Scheinker IM: Transtentorial herniation of the 

brainstem; A characteristic clinicopathologic syndrome; 

Pathogenesis of hemorrhages in the brainstem. 

Arch Neurol Psychiatr 53:289-298, 1945. 

4. Reich JB, Sierra J, Camp W, et al: Magnetic resonance 

imaging measurements and clinical changes 

accompanying transtentorial and foramen magnum 

brain herniation. Ann Neurol 33:159-170, 1993. 

5. Gray H: Gray’s Anatomy, pp 512-523. Philadelphia, 

Running Press, 1974. 

6. Sunderland S: The tentorial notch and complications 

produced by herniations of the brain through 

that aperture. Br J Surg 455:422-438, 1958. 

7. Osborn AG: Handbook of Neuroradiology: 

Brain and Skull, ed 2, pp 222-230. St. Louis, 

Mosby, 1996. 

8. Hassler O: Arterial pattern of human brainstem: 

Normal appearance and deformation in expanding 

supratentorial conditions. Neurology 17:1-6, 1967. 

9. Sohn D, Levine S: Frontal lobe infarcts caused 

by brain herniation: Compression of anterior cerebral 

artery branches. Arch Pathol Lab Med 84:509- 

512, 1967. 

10. Barr R, Gean AD: Trauma. In: Brandt WE, 

Helms CA: Fundamentals of Diagnostic Radiology, 

pp 65-68. Baltimore, Williams & Wilkins, 1994. 

11. Nakstad P, Nornes H, Hauge HN: Traumatic 

aneurysms of the pericallosal arteries. Neuroradiology 

28:335-338, 1986. 

12. Ecker A: Upward transtentorial herniation of 

the brainstem and cerebellum due to tumor of the 

posterior fossa: With a special note on tumors of 

acoustic nerve. J Neurosurg 5:51-61, 1948. 

13. Elguera M: Transtentorial Herniation, Finney 

LA, Walker AE (eds). Springfield, IL, Charles C. 

Thomas, 1962. 

14. Schwarz GA, Rosner AA: Displacement and 

herniation of the hippocampal gyrus through the 

incisura tentorii. Arch Neurol Psychiatry 46:297- 

321, 1941. 

15. Jefferson G: The tentorial pressure cone. Arch 

Neurol Psychiatr 40:857-876, 1938. 

16. Smyth GE, Henderson WR: Observations on 

the cerebrospinal fluid pressure on simultaneous 

ventricular and lumbar punctures. J Neurol Psychiatr 

1:226-238, 1938. 

17. Stovring J: Descending tentorial herniations: 

Findings on computed tomography. Neuroradiology 

14:101-106, 1977. 

18. Hahn F, Gurney J: CT signs of central 

descending transtentorial herniation. AJNR 6:844- 

845, 1985. 

19. Feldmann E, Gandy SE, Becker R, et al: MRI 

demonstrates descending transtentorial herniation. 

Neurology 38:697-701, 1988. 

20. Blinkov SM, Gabibov GA, Tanyashin SV: 

Variations in location of the arteries coursing 

between the brain stem and the free edge of the 

tentorium. J Neurosurg 76:973-978, 1992. 

21. Komaki S, Handel S: Molding of the posterior 

communicating artery in downward transtentorial 

herniation. Radiology 113:107-119, 1974. 

22. Grossman RI, Yousem DM: Trauma. In: Neuroradiology 

- The Requisites, pp 161-162. St. 

Louis, Mosby-Year Book, Inc., 1994. 

23. Fisher CM: The arterial source of secondary 

brain stem hemorrhages (abstr). J Pathol 66:9a, 

1972. 

24. Thompson RK, Salcman M: Brain stem hemorrhages: 

historical perspective. Neurosurgery 22: 

623-628, 1988. 

25. Howell DA: Longitudinal brain stem compression 

with buckling. Arch Neurol 4:572-579, 1961. 

26. Osborn AG: Secondary effects of intracranial 

trauma. Neurosurg Clin N Am 1:461-474, 1991. 

27. Speigelman R, Hadani M, Ram Z, et al: 

Upward transtentorial herniation: A complication of 

postoperative edema at the cervicomedullary junction. 

Neurosurg 24:284-288, 1989. 

28. Cohen D, Quest D: Increased intracranial 

pressure, brain herniation. In: Wilkins RH, Rengachary 

SS (eds): Neurosurgery, ed 2, pp 349- 

350. New York, McGraw-Hill, 1996. 

29. Kernohan JW, Woltman HW: Incisura of the 

crus due to contralateral brain tumor. Arch Neurol 

Psychiatry 21:274-287, 1929. 

30. Osborn, AG: Diagnosis of descending 

transtentorial herniation by cranial computed 

tomography. Radiology 123:93-96, 1976. 

31. Ishikawa M, Kikuchi H, Fujisawa I, 

Yonekawa Y: Tonsillar herniation on magnetic resonance 

imaging. Neurosurgery 22:77-81, 1988. 

32. Ramsey RG: Disorders of the spine. In: Neuroradiology, 

ed 3, pp 42-43, 496. Philadelphia, WB 

Saunders, 1994.

Cerebral herniations - Applied Radiology Online

Create successful ePaper yourself

Delete template?

Save as template?