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Brain Herniation
Jointly Produced by:
Greg Petermann, M.D.
Chief, Neuroradiology
James G. Smirniotopoulos, M.D.
Professor and Chair
Department of Radiology
Tripler Army Medical Center
Honolulu, HI
Department of Radiology and Radiological Sciences
Uniformed Services University
Bethesda, MD
Peer Review:  Bahman Jabbari, COL, MC, Professor and Chair, Department of Neurology
Uniformed Services University
Bethesda, MD
Video Channel-MedPix® Video

Table of Contents
Transtentorial Table 1 Descending
Table 2 Ascending
Alar/Sphenoid Table 3 Alar
Subfalcine Table 4  Subfalcine
Foramen Magnum Table 5 F. Magnum


Brain herniations represent shift of the normal brain through or across regions to another site due to mass effect. These are generally complications of mass effect whether from tumor, trauma, or infection. Herniations of the brain can be divided into four large categories. These include transtentorial, subfalcine, foramen magnum, and alar or sphenoid herniation. We will discuss the imaging findings, clinical characteristics and possible complications involved in the four main types of brain herniations. (Fig A) The key to recognizing all herniations of the brain is evaluation of the cisterns.


Transtentorial herniations occur when the brain traverses across the tentorium at the level of the incisura. These can be divided into ascending and descending transtentorial herniations. Descending transtentorial herniations are a larger category caused by mass effect in the cerebrum which pushes the supratentorial brain through the incisura to the posterior fossa. Ascending transtentorial herniation is caused by mass effect in the posterior fossa which leads to brain extending through the incisura in an upward.

Clinical presentation of descending transtentorial herniation includes an , oculomotor (CNN III) paresis (ipsilateral dilated pupil, abnormal EOM's), contralateral hemiparesis, and at times ipsilateral hemiparesis (Table 1). These may be isolated or occur together. Ipsilateral pupil dilatation occurs as the parasympathetic fibers, which are located around the outer aspect of the third nerve, are compressed by the uncus. This leads to dysfunction of the parasympathetic fibers with subsequent unopposed sympathetic responds. This will dilate the ipsilateral pupil. Contralateral hemiparesis occurs with compression of the ipsilateral cerebral peduncle. Since the cortical spinal tracts decussate (cross over) below the mid brain in the level of pons, the hemiparesis is contralateral. In some cases, an ipsilateral hemiparesis can occur with a contralateral dilated pupil or oculomotor paresis.  This occurs when the lateral translation of the brainstem is so great as to push the midbrain and cerebral peduncles all the way across the perimesencephalic cistern, so that the opposite (contralateral) third nerve and peduncle are pressed against the opposite tentorial edge.  This phenomenon is called a Kernohan’s notch - a hemorrhage that occurs in the contralateral cerebral peduncle (image shows damage of the right peduncle with hemorrhage centrally from Durette hemorrhage). Thus causing ipsilateral hemiparesis. This neurologic sign can be termed a "false localizer", since it can be confusing or misleading for lateralization of the inciting lesion's location.  Durette hemorrhages in the brainstem have several causes including kinking or stretching of the penetrating arterioles and kinking of venules (causing hemorrhagic infarction).

Imaging findings of descending transtentorial herniations include ipsilateral ambient cistern widening and ipsilateral prepontine cistern widening. A contralateral temporal horn is also widened. These findings occur as the ipsilateral, lateral ventricle is compressed with subsequent dilatation of the contralateral ventricle to maintain the same volume. The ipsilateral cistern is widened because of the fact that the brain stem is inferiorly contiguous with the spinal cord leading to a long rigid structure as shown in the coronal CT image. Note the mass on the right with widening of the ipsilateral, right ambient cistern. As the supratentorial brain shifts say to the right, the superior aspect of this long column of mid brain and cord also shifts to the right. This will narrow the contralateral cistern and widen the ipsilateral cistern at the anterolateral aspects of the brain stem.

Uncal herniation is a subset of descending transtentorial herniations. The uncus is displaced into the suprasellar cistern. The usual six pointed star appearance of the suprasellar cistern then becomes truncated on the ipsilateral side of the herniation. Coronal imaging can also demonstrate uncal herniation either by CT or MRI. Coronal gross image in a patient with a right sided mass effect demonstrates shift of the uncus into the suprasellar cistern as well (there is also a subfalcine shift to the right). A gross image of descending transtentorial herniation can demonstrate the cleft or crease on the parahippocampal gyrus as the brain herniates through the incisura. This CT scan demonstrates a Durette hemorrhage, descending transtentorial shift to the left, widening of the contralateral, right temporal horn and a residual ipsilateral ambient cistern (left) still remaining. The uncus is also filling the left aspect of the suprasellar cistern.

Complications of descending transtentorial herniations include occipital infarction. The posterior cerebral artery becomes compressed as the ipsilateral uncus and parahippocampal gyrus compresses the artery against the ipsilateral cerebral peduncle. The gross specimen associated with the CT of occipital infarcts demonstrates the excellent correlation. This can occur unilaterally or bilaterally depending on the extent of injury and amount of mass effect. Generally, an ipsilateral occipital infarct will appear first followed by contralateral infarction.

Another complication of descending transtentorial herniation includes Durette hemorrhage. This is due to pontine perforators which are displaced downward by mass effect. The basilar artery sends these perforators posteriorly into the pons. As the pons shifts inferiorly, these perforators are stretch and can cause hemorrhage within the brain stem or pons. Sagittal and axial MRI demonstrates the hemorrhage in the dorsal lateral pons.

Kernohan’s notch is another type of hemorrhagic damage caused by transtentorial herniation. This is due to compression of the contralateral cerebral peduncle against the incisura. If this occurs, it leads to ipsilateral hemiparesis since the cortical spinal tracts become damaged. The gross specimen demonstrates hemorrhage in the left central midbrain from Durette hemorrhage and cortical damage with some hemorrhage at the right cerebral peduncle consistent with Kernohan’s notch. There is also a left uncal herniation.

Ascending transtentorial herniation is less common then descending transtentorial herniation. Perhaps this is due to the much larger area of the supratentorial brain leading to complications with the transtentorial herniation. This type of herniation is usually caused by a slowly growing cerebellar or brainstem process, such as a diffusely infiltrating astrocytoma.  Due to the symmetric cistern findings and the different appearances of the quadrigeminal plate cistern depending on the angle of the CT scan, ascending transtentorial herniation can often be more difficult to evaluate on imaging studies. The clinical presentation includes nausea and vomiting followed by obtundation (Table 2). With these few clinical signs, this can at times be considered emergency since patients can progress from nausea and vomiting to obtundation and coma rapidly depending on the length of time the mass effect has been present in the posterior fossa. Long term, slow growing metastatic disease in the posterior fossa may not present as an emergency as an acute posterior fossa hemorrhage from hypertension due to the brain's ability to adjust to the herniation.

Imaging characteristics of ascending transtentorial herniation include a "spinning top" appearance of the midbrain. This is due to compression bilaterally on the posterolateral aspects of the midbrain as the posterior fossa squeezes through the incisura from below. There is subsequent narrowing of the bilateral ambient cisterns again as the cerebellar tissue extends through the ambient cisterns. Finally, there is filling of the quadrigeminal plate cistern as the cerebellum again persistently extends upward through the incisura. These findings may be difficult to visualize if one is not searching for them specifically. This may be due to the bilateral nature of the findings or merely absence of the cisterns themselves. Angling of the CT gantry can also lead to different appearances of the quadrigeminal plate cistern and should be compared to other scans depending on the angle in question.

As the brain herniates superiorly through the incisura, it compresses the midbrain from a bilateral location and not only narrows both ambient cisterns but also can cause flattening at the quadrigeminal plate cistern. This had been termed previously as the "crooked smile or toothless smile". The previous smile like shape of the quadrigeminal plate cistern and ambient cisterns are transformed first to a straight line and then finally to a "frown". It may be easier to demonstrate ascending herniation over a period of time, especially if there is a previous scan. For example, here is a CT from day 1 and day 2. On day 1, the ambient cisterns and quadrigeminal plate cisterns are present. Note the loss of ambient cisterns and quadrigeminal plate cisterns on the day 2 study. At times, the cerebellum can be seen actually protruding through the quadrigeminal plate cistern while demonstrating the "spinning top" appearance of the midbrain.

Complications of ascending transtentorial herniations include hydrocephalus. The dilatation of the bilateral temporal horns and the third ventricle are the easiest method of determining the presence of hydrocephalus. Rapid onset of coma and death can occur given the small space of the posterior fossa and rapid progression in an acute process such as large hypertensive hemorrhage. This patient demonstrates hydrocephalus with brain herniating through the quadrigeminal plate cistern and causing mass effect on the posterior midbrain. The ambient cisterns are also compressed.


Alar brain herniations are often not discussed much due to the relative absence of clinical symptomatology. These can also be difficult to demonstrate on imaging studies if one is not attentive to the subtle findings and changes. Clinical symptoms are generally minimal. In general, this type of herniation is associated with other herniations such as subfalcine or transtentorial herniations which are more clinically apparent. (Table 3)

Alar herniations can be divided into posterior and anterior herniations. These occur over the sphenoid wing itself. Frontal lobe masses will cause a posterior alar herniation as the frontal lobe extends posterior and inferiorly over the sphenoid ridge. Temporal lobe lesions or lesions of the insula can cause anterior alar herniations. This occurs as the temporal lobe extends superiorly and anteriorly over the sphenoid bone. This is often difficult to image well.

The imaging findings of alar herniation are best demonstrated utilizing the middle cerebral artery. Contrast enhanced studies or MRI can demonstrate anterior or posterior displacement of the middle cerebral artery in alar herniation. Here a CT scan demonstrates anterior left alar herniation. Notice also the cerebellum filling the quadrigeminal plate cistern and ambient cisterns from an ascending transtentorial herniation. Similarly, anterior displacement of the middle cerebral artery occurs in anterior alar herniation. A sagittal MRI can also demonstrate anterior or posterior displacement over the sphenoid bone.

Clinical complications of alar herniations have not been discussed extensively most likely due to the association of other herniations and their clinical complications. Although there can be shift in this location, it may be more academic especially in the presence of other herniations.


Subfalcine herniations occur as the brain extends under the falx in the supratentorial cerebrum. This may be the most common form of herniation although many authors in the past suggest transtentorial herniation is the most common. Perhaps this is due to the multitude of clinical symptomatology and urgency involved in transtentorial herniations. While subfalcine herniations often occur in conjunction with transtentorial herniation or in isolation. Presence however, does not necessarily lead to severe clinical symptomatology or alarm.

Subfalcine herniations can present clinically as headache. Later on as the herniation progresses, contralateral leg weakness can occur. (Table 4)

The imaging signs of subfalcine herniations include amputation of the ipsilateral anterior aspect to the frontal horn. This occurs as the mass effect truncates the anterior aspect of the frontal horn and widens the contralateral frontal horn. There is asymmetry at the anterior falx with a widened CSF space on the contralateral anterior falx . This image also demonstrates ipsilateral lateral ventricle compression with contralateral lateral ventricle and atria dilation.

Probably the easiest method of evaluating for subfalcine shift is a straight line drawn in the expected location of the septum pellucidum from the posterior most aspects to the falx on axial images. Shift of the septum pellucidum from this midline can be measured in millimeters and compared over time to determine any change.

Gross photo demonstrates shift to the cingulate sulcus under the falx. This corresponds well to the coronal CT examination again showing the ipsilateral frontal horn narrowing, contralateral cistern widening, and shift of the cingulate gyrus under the falx. The falx itself has an arch like configuration with the anterior aspect of the falx higher than the more posterior aspect. This allows a space for the cingulate sulcus to extend through. This can cause a crease on the ipsilateral cingulate gyrus as on this gross photo.

Complications of subfalcine herniations include ipsilateral anterior cerebral infarction. This occurs as the cingulate sulcus extends under the falx. This drags with it the ipsilateral anterior cerebral artery. If this becomes compressed against the falx and occludes, this can lead to a distal anterior cerebral artery infarction and thus the clinical symptom of contralateral leg weakness. Notice the infarction at the distal anterior cerebral artery surrounding the compressed left atria of the lateral ventricle.


Clinical symptomatology maybe subtle in foramen magnum herniation until the patient becomes obtunded. Patients with a Chiari malformation may have little or no clinical symptomatology or may demonstrate Lhermitte’s phenomenon. This is changed or dysesthesia in the arms or legs with forward bending of the head. This is postulated to occur as the anterior spinal tracts within the ventral spinal cord, become compressed against the bone of the posterior vertebral bodies. Acute foramen magnum herniation clinically can be catastrophic as the brains extrudes through the foramen magnum. Again, this is generally associated with other herniations such as ascending transtentorial herniation depending on the level of the mass. (Table 5)

Imaging findings include on the axial images, cerebellar tonsils at the level of the dens. In Chiari malformations, five millimeters below the foramen magnum in adults or seven millimeters below the foramen magnum in children are considered abnormal. If there is an old film however this makes any change easy to interpret. In general if the tonsils are located at the level of the dens on the axial images, this generally is an indicator of foramen magnum herniation. Excessive cerebellar tissue can be seen at the foramen magnum but it may be best to visualize the dens and cerebellum together since the CT gantry angle can yield different appearances at the foramen magnum. A sagittal MRI is a much easier method of determining if foramen magnum herniation is present as in this patient with a tentorial subdural and shift through the foramen magnum. This is because the association between the inferior aspect of the clivus and inferior aspect of the occipital bone is much easier to demonstrate on the sagittal images. This gross specimen also shows a crease on the cerebellar tonsils as they extend through the foramen magnum. Clinical complications would include obtundation and death as this progresses.

EXTRACRANIAL (Calvarial) HERNIATION     - [back]

Shift of the brain through an extracranial defect can also occur. These are generally post traumatic or post surgical. The brain can become ischemic and infarct. Post trauma patients or patients with significant intracranial mass effect may undergo craniectomy to remove the ipsilateral, overlying bone . This will allow the brain to decompress through the defect. This gross specimen correlates with the CT of the brain shifting through the cranial defect

TABLE 1   - [back]
Descending Transtentorial Herniation
Clinical Findings  Imaging Findings  Complications
Ipsilateral dilated pupil

Contralateral hemiparesis

Ipsilateral hemiparesis if Kernohan’s Notch is present (false localizer)

Contralateral temporal horn widening

Ipsilateral ambient cistern widening

Ipsilateral prepontine cistern widening

Uncus extending into the suprasellar 


Occipital infarct from posterior cerebral artery compression


TABLE 2   - [back]
Ascending Transtentorial Herniation
Clinical Findings Imaging Findings  Complications



Spinning top appearance of midbrain

Narrowing of bilateral ambient cisterns

Filling of the quadrigeminal plate cistern


Rapid onset of obtundation and possibility of death


TABLE 3   - [back]
Alar or Sphenoid Herniation
Clinical Findings Imaging Findings  Complications

Usually associated with other types of herniations

Anterior or posterior displacement of the middle cerebral artery on axial images

Sagittal MRI with distortion of the insular cortex

None but associated with other herniations


TABLE 4   - [back]
Subfalcine Herniation
Clinical Findings Imaging Findings  Complications

Contralateral leg weakness

Amputation of the ipsilateral aspect of the frontal horn

Asymmetric anterior falx

Obliteration of the ipsilateral atrium of the lateral ventricle

Septum pellucidum shift

Ipsilateral anterior cerebral artery (ACA) infarction as ACA is entrapped under the falx

Other associated herniations


TABLE 5   - [back]
Foramen Magnum Herniation
Clinical Findings Imaging Findings  Complications
Bilateral arm dysesthesia


Cerebellar tonsils at the level of the dens on axial images

Cerebellar tonsils on sagittal images 5mm below foramen magnum in adults; 7mm below in children

Obtundation and Death



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