Herniation Syndromes


John M. Barkley
Denise Morales
L. Anne Hayman
Pedro J. Diaz-Marchan


Severe intracranial injuries such as large hematomas or brain swelling, exert mass effect on the pliable brain within the closed-box of the adult cranium. The production of CSF and cerebral blood flow vary inversely with increasing intracranial pressure. Intracranial pressure will change if there are additions or subtractions to the fixed intracranial contents (brain, CSF, blood).

This is called the Monro–Kellie Doctrine (2). Mechanical displacement of the brain, if severe enough, may lead to herniation syndromes. These include subfalcine, transtentorial, tonsillar, transsphenoidal, or external herniation.

Subfalcine herniation

Subfalcine herniation consists of midline shift of the cingulate gyrus under the midline dural reflection of the falx cerebri. This results in effacement of the ipsilateral lateral ventricle and noncommunicating hydrocephalus of the contralateral lateral ventricle (3). Dilation of the contralateral ventricle in subfalcine herniation occurs because of obstruction at the level of the foramen of Monro. If severe enough, cerebral infarction in the anterior cerebral artery distribution may occur because of compression of the vessels under the falx cerebri. Subfalcine herniation is the most common herniation syndrome (4).

Temporal lobe herniates

If the uncal portion of the temporal lobe herniates across the tentorium (Figure 11-6), the midbrain is compressed, leading to injury of the contralateral cerebral peduncle (Kernohan’s notch) or ischemia/infarction in the posterior cerebral artery distribution. Uncal herniation may also cause an ipsilateral cranial nerve III (occulomotor nerve) palsy. Uncal herniation may manifest clinically as ispsilateral dilated pupil and an ipsilateral hemiparesis, the latter due to compression of the contralateral cerebral peduncle.

Transtentorial herniation

Transtentorial herniation occurs in a cranial or caudal direction across the tentorium, that separates the posterior fossa contents from the supratentorial compartment. Descending herniation through the tentorium appears on CT as effacement of the suprasellar and perimesencephalic cisterns. Transtentorial herniation may lead to disruption of brainstem perforating vessels, causing petechial hemorrhages in the midline brainstem, Duret hemorrhages. If the cerebellum herniates upward through the tentorium, the basilar cisterns are effaced. This typically occurs due to a posterior fossa hemorrhage or mass.

Cerebellar tonsillar herniation

Cerebellar tonsillar herniation occurs when the inferior portion of the cerebellum herniates downward through the foramen magnum. Tonsillar herniation may cause infarction in the posterior inferior cerebellar artery territory (PICA). Cerebellar tonsillar herniation occurs due to a posterior fossa mass, hemorrhage or swelling. This is important to distinguish from nontraumatic cerebellar tonsillar herniation of greater than 5 mm through the foramen magnum—Chiari I malformation. Some of these patients with this congenital malformation are subject to trauma; however the herniation in these cases is not due to the trauma itself.

Transsphenoidal herniation

Transsphenoidal herniation occurs when the frontal or temporal lobes are displaced posteriorly or anteriorly across the greater wing of the sphenoid bone respectively. External herniation occurs when brain contents herniate through a bony defect—either fracture or surgical defect, outside of the calvarium. Any of the aforementioned herniation syndromes may occur due to mass effect from trauma, hemorrhage or neoplasm (1, 3). In some patients with severe mass effect, a combination of different herniation syndromes may result (Figure 11-7).

Original: Brain Injury Medicine. Principles and Practice


  1. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology, 2nd edition. Baltimore: Williams & Wilkins, 1999, pp. 25–65.

  2. Noback, CR, Strominger NL, Demarest RJ. The Human Nervous System: Structure and Function. 5th edition. Baltimore: Williams & Wilkins, 1996, pp. 67–82.

  3. WeissLeder R, Rieumont MJ, Wittenberg J: Primer of Diagnostic Imaging, 2nd edition. St. Louis: Mosby, 1997, pp. 465–80.

  4. Lane FJ, Sheden AI, Dunn MM, Ghatak NR. Acquired intracranial herniations: MR imaging findings. AJR 1995; 165: 967–73.