C H A P T E R

1
Brain Herniation
Patricia K.Y. Kan1, Mandy H.M. Chu2,
Emily G.Y. Koo2, Matthew T.V. Chan3
1Department of Anaesthesia and Intensive Care, Prince of Wales Hospital,
Hong Kong Special Administrative Region, China; 2Department
of Anaesthesia, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong
Kong Special Administrative Region, China; 3Department of Anaesthesia
and Intensive Care, The Chinese University of Hong Kong, Hong Kong
Special Administrative Region, China

O U T L I N E

Overview4
Mechanism of Brain Herniation 4
Classification of Brain Herniation 5
Clinical Features of Brain Herniation 6
Uncal (Transtentorial) Herniation 7
Subfalcine/Cingulate Herniation 7
Transcalvarial Herniation 8
Reverse Transtentorial Herniation 8
Tonsillar Herniation 11
Prevention of Brain Herniation 11
Treatment of Brain Herniation 11
Conclusions12
References13

Complications in Neuroanesthesia 3
http://dx.doi.org/10.1016/B978-0-12-804075-1.00001-8 © 2016 Elsevier Inc. All rights reserved.
4 1.  BRAIN HERNIATION

OVERVIEW

Brain herniation is the displacement of brain tissue through the rigid

dural folds (i.e., falx and tentorium) or skull openings (e.g., foramen mag-
num).1 Although patients with chronic brain herniation associated with
developmental defects, such as Arnold–Chiari malformation, may remain
asymptomatic for many years,2 acute brain herniation following neuro-
surgery is a catastrophic event that results in mechanical and vascular
damage of the brain. In many circumstances, brain herniation is often
regarded as a terminal event.

MECHANISM OF BRAIN HERNIATION

From a mechanistic point of view, brain herniation is the result of a pres-

sure gradient that squeezes the vulnerable brain matter from one com-
partment in the brain to another through various anatomical ­channels. In
general, any pathologic process that increases intracranial pressure pro-
vides the driving pressure for brain herniation.1 It should be clear that
the pressure gradient appears to be the most important factor, and brain
­herniation may occur regardless of the size of the opening.3 In the periop-
erative setting, hemorrhage, cerebral swelling associated with perioperative
stroke, and hydrocephalus are the common causes for intracranial hyper-
tension after neurosurgery (Table 1). In a systematic review of patients with
clinical deterioration following intracranial surgery, 0.8–6.9% of cases were
thought to be due to postoperative hemorrhage.4 In patients who received
regular imaging surveillance, up to 50% of cases had evidence of significant
intracranial hemorrhage following neurosurgery.4,5 It is reassuring that few
patients with postoperative intracranial hematoma actually end up with
brain herniation. However, even a small amount of blood may produce

TABLE 1  Common Causes of Intracranial Hypertension Following Neurosurgery that

May Lead to Brain Herniation

1. Postoperative intracranial hemorrhage (extradural, subdural, intracerebral, or

intraventricular hematoma) due to surgical bleeding or patients with bleeding tendency.
2. Brain contusion related to primary traumatic brain injury or instrumental damage
(e.g., brain retraction injury).
3. Cerebral swelling due to:
a. Perioperative stroke
b. Exacerbation of peritumor or periabscess edema
c. Cerebral venous thrombosis
d. Hyperemia (e.g., hyperperfusion syndrome following carotid endarterectomy)
e. Metabolic causes (e.g., diabetic ketoacidosis, hyponatremia, liver failure)
4. Hydrocephalus

I.  COMPLICATIONS RELATED TO THE BRAIN

 Classification of Brain Herniation 5

sufficient pressure to produce significant brain herniation. This is especially

important in patients who already have limited intracranial compliance.
It should be noted that not all cases of brain herniation are related to
intracranial hypertension. In patients who had decompressive craniec-
tomy, acute drainage of cerebrospinal fluid, upright posture, or hyper-
ventilation may produce a transient negative pressure gradient between
the atmosphere and intracranial compartments. This extra intracranial
pressure gradient across the skull defect may be large enough to push
the brain matter down into the tentorial notch or the foramen magnum,
resulting in a rare phenomenon known as paradoxical brain herniation.6,7

CLASSIFICATION OF BRAIN HERNIATION

The brain can be broadly divided into a number of compartments, with

boundaries formed by the falx, the tentorium, and the foramen magnum.
When the pressure within a compartment is increased, its contents will
be pushed toward the adjacent compartments. The directions of displace-
ments are shown in Figure 1.1 Briefly, the inner part of the temporal lobe
(uncal herniation), the entire diencephalon (central/downward transten-
torial herniation), and the frontal lobe (cingulate or subfalcine herniation)
are common areas for herniation within the supratentorial compartment.

Space-occupying lesion

FIGURE 1  Coronal view of brain herniations. (1) uncal herniation, (2) central transtentorial
herniation, (3) subfalcine/cingulate herniation, (4) transcalvarial herniation, (5) reverse transtento-
rial herniation, and (6) tonsillar herniation. Red arrows indicate the direction of brain displacement.
Noted that reverse transtentorial herniation is due to the effect of infratentorial lesion and not related
to the space occupying lesion shown (red).

I.  COMPLICATIONS RELATED TO THE BRAIN

6 1.  BRAIN HERNIATION

In the infratentorial compartment, cerebellar tonsils may be squeezed

down through the foramen magnum (tonsillar herniation or coning). In
contrast, the cerebellum in the posterior fossa may also be pushed upward
when the infratentorial pressure exceeds that in the supratentorial com-
partment (reverse transtentorial herniation). Finally, the part of brain
matter that is adjacent to a craniectomy wound or site of fracture may be
herniated out of the skull (transcalvarial herniation).

CLINICAL FEATURES OF BRAIN HERNIATION

The clinical presentation of brain herniation depends largely on the

underlying lesion in the brain, the manifestations of intracranial hyperten-
sion, and the function of specific part of the brain that is being ­compressed.
Table 2 summarizes the mechanisms and common clinical signs associ-
ated with different forms of brain herniations.

TABLE 2  Clinical Presentations of Brain Herniation

Type of herniation Mechanisms Clinical presentations

Uncal herniation 1. Compression on 1. Dilated pupils, ptosis, and

parasympathetic followed “down and out position” of
by somatic component of the ipsilateral eye
oculomotor nerve 2. Contralateral homonymous
2. Infarction of ipsilateral visual hemianopia
cortex 3. Ipsilateral hemiparesis or
3. Lateral displacement of hemiplegia
brain stem to compress the 4. Unconsciousness
contralateral corticospinal 5. Decorticate posture,
tract respiratory depression, and
4. Distortion of the ascending death
arousal system
5. Duret hemorrhage

Central 1. Early stage 1. Agitation and drowsiness;

transtentorial 2. Late stage pupils are small but reactive
herniation 3. Compression of pituitary 2. Decorticate, decerebrate
stalk posture
3. Diabetes insipidus

Subfalcine Compression of cingulate gyrus Nonspecific signs

herniation and intracranial hypertension

Transcalvarial Compression against external Physical sign depends on

herniation wound the part and extent of brain
herniation
Tonsillar herniation Brain stem compression 1. Unconsciousness
2. Respiratory depression and
cardiovascular instability

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 Clinical Features of Brain Herniation 7

Uncal (Transtentorial) Herniation

The uncus is the most medial part of the temporal lobe. When it is
squeezed against the tentorium, it exerts pressure on the third cranial
(oculomotor) nerve as it leaves the midbrain and travels along the free
edge of the tentorium. In addition, there is pressure against the ipsilat-
eral brain stem. Not surprisingly, the earliest clinical signs associated
with an uncal herniation are those due to ipsilateral third nerve palsy. It
is often suggested that the parasympathetic input to the eye, lying in the
outermost part of the nerve, is first affected. This will result in an ipsilat-
eral fixed and dilated pupil. As the pressure on the third cranial nerve
is further increased, the somatic component is also affected, leading to
complete ptosis and deviation of the eye to a “down and out” position.
However, the motor functions of the eye cannot be easily tested in an
unconscious patient. Therefore, a fixed and dilated pupil may become the
only physical sign of an uncal herniation. As lateral displacement becomes
more severe, the brain stem is being compressed against the c­ ontralateral
tentorium leading to injury of the contralateral corticospinal tract with
ipsilateral hemiparesis.8 This is obviously a false localizing sign. In
addition, the contralateral posterior cerebral artery may be compressed
leading to ipsilateral visual cortex infarction and giving rise to contralat-
eral homonymous hemianopia.
When both hemispheres are under pressure, the diencephalon and parts
of the temporal lobes are squeezed through the tentorial notch, resulting
in central transtentorial herniation. In the early stage, the pupils are small
and reactive. Interestingly, they dilate briskly in response to pinching of
the neck (ciliospinal reflex). Oculocephalic reflexes and plantar responses
are intact. In patients who are breathing spontaneously, yawning with
occasional pauses are often observed. This may progress to Cheyne–
Stokes breathing in the later stage. Further compression on the brain stem
will result in decorticate posture, respiratory depression, and death.
Radiologically, one should observe the general features of intracranial
hypertension in the computed tomography (CT) scans. These include
midline shift, obliteration of ventricles, and effacement of sulci and cis-
terns. Specifically, uncal herniation produces a duret hemorrhage that
appears as flame or linear-shaped hyperintensities in the brain stem. This
is due to tearing of small vessels. In addition, notching of the contralateral
midbrain (Kernohan’s notch)8 indicates severe lateral displacement of the
brain stem (Figure 2).

Subfalcine/Cingulate Herniation
Subfalcine herniation is the displacement of the medial frontal lobe
(cingulate gyrus) underneath the free edge of the falx cerebri. Symptoms

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8 1.  BRAIN HERNIATION

Midline shi

Space-occupying lesion

Kernohan’s notch
with PCA
compression

Uncus

Midbrain
compression
with inferior
Duret hemorrhage
displacement

FIGURE 2  Important radiological features seen in uncal and central transtentorial herniation.
Red arrows indicate the direction of brain displacement.

are generally nonspecific. On the axial image of a CT scan, subfalcine shift

can be demonstrated by drawing a straight line from the anterior to the
posterior aspect of the falx, highlighting the deviation of the septum pel-
lucidum from its expected midline position (Figure 3). This may result
in cerebral infarction over the ipsilateral anterior cerebral artery territory.
One may also note the dilatation of the contralateral ventricle due to the
obstruction of the foramen of Monro.

Transcalvarial Herniation
This is also known as “external herniation,” where part of the brain is dis-
placed out of the cranium because intracranial pressure is much larger than
that of the atmosphere (Figure 4). Obviously, clinical presentation depends on
the part and extent of brain matter that is herniated through the skull defect.

Reverse Transtentorial Herniation

Reverse transtentorial herniation occurs when pressure in the poste-
rior fossa exceeds that of the supratentorial compartment. The cerebellum
is therefore pushed superiorly between the free edges of the tentorium
(Figure 5). Clinically, bilateral fixed dilated pupils may be the only physical
sign that can be elicited. This is due to injury to the third cranial nerves as
the midbrain is being compressed and the tentorium is stretched. Reverse
transtentorial herniation should be suspected when there is rapid postop-
erative deterioration in patients with unrelieved pressure in the posterior
I.  COMPLICATIONS RELATED TO THE BRAIN
 Clinical Features of Brain Herniation 9

Ipsilateral
Falx cerebri
ACA infarcon

Space-occupying lesion

Dilataon of
contralateral
ventricle

Compression and
displacement of
ipsilateral ventricle

Expected posion of
septum pallucidum

FIGURE 3  Subfalcine/cingulate herniation. Dotted line indicate the expected position of septum
pellucidum. Red arrow indicates the direction of brain displacement. ACA, anterior cerebral artery.

Extension of
brain ma er
beyond cranium

Gross cerebral edema

Acquired skull defect

FIGURE 4  Transcalvarial herniation through acquired skull defect. Red arrow indicates the
direction of brain displacement.

fossa (e.g., residual cerebellar tumor). In this setting, acute drainage of

hydrocephalus produces sufficient negative pressure gradient from infra-
to supratentorial compartments for brain herniation.
I.  COMPLICATIONS RELATED TO THE BRAIN
10 1.  BRAIN HERNIATION

PCA infarcon
Hydrocephalus

Midbrain Quadrigeminal
Tentorium cistern
compression

Foramen
Superior mangum
cerebellar artery
infarcon

FIGURE 5  Reverse transtentorial herniation. Sagittal view (left) showing upward displacement
of cerebellum toward supratentorial compartment. Transverse view (right) showing reverse and flat-
tening of quadrigeminal cistern (frown-shaped appearance). Red arrow indicates the direction of
brain displacement. PCA, posterior cerebral artery.

Foramen mangum
Cerebellar tonsil and
brainstem descent

FIGURE 6  Tonsillar herniation—descent of cerebellar tonsils and brain stem beyond foramen
magnum. Red arrow indicates the direction of brain displacement.

In the CT scans, flattening of the superior cerebellar cistern may be

observed. The usual “smile-shaped” quadrigeminal cistern is reversed to
produce a “frown-shaped” appearance (Figure 5). One should also look
for infarction in areas supplied by the posterior cerebral and superior
cerebellar arteries. Obstructive hydrocephalus due to compression of the
cerebral aqueduct may also occur.

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 Treatment of Brain Herniation 11

Tonsillar Herniation
This is commonly known as coning, when the cerebellar tonsils move
downward through the foramen magnum (Figure 6). Tonsillar herniation
exerts pressure over the lower brain stem and the upper cervical spinal
cord against the narrow foramen magnum. In the postoperative setting,
brain stem compression results in unconsciousness, flaccid paralysis, and
respiratory and cardiac depression.
In sagittal scans, an inferior descent of the cerebellar tonsils, >5 mm in
adults and >7 mm in children, below the foramen magnum is considered
significant. The cerebrospinal fluid cisterns around the brain stem may
become effaced as well.

PREVENTION OF BRAIN HERNIATION

Little is known about prevention of brain herniation after neurosur-

gery. Nevertheless, appropriate preoperative preparation for patients
with a bleeding diathesis (e.g., desmopressin administration for von
Willebrand’s disease), stopping aspirin, other antiplatelets, and antico-
agulants ahead of scheduled surgery or prior embolization of a vascu-
lar tumor may avoid massive bleeding during surgery and may prevent
postoperative hematoma.9 Meticulous surgery to avoid retraction injury
and inappropriate coagulation of perforators will prevent postoperative
ischemic brain swelling. Other maneuvers include administration of cor-
ticosteroid for brain tumor and p­ rophylactic anticonvulsant therapy may
also decrease the risk of postoperative malignant brain swelling. Despite
success of endovascular treatment for acute stroke in the general popula-
tion,10 it is unclear whether the treatment for perioperative stroke could
produce a similar benefit after neurosurgery.

TREATMENT OF BRAIN HERNIATION

Brain herniation following neurosurgery is a life-threatening neu-

rosurgical emergency and requires immediate resuscitation to prevent
­irreversible injury and death. Treatment strategies should be directed
to control intracranial pressure, so that an intracranial pressure ≤20 mm
Hg and a cerebral perfusion pressure ≥70 mm Hg are the therapeu-
tic ­targets. General ­measures include maneuvers to ensure good oxy-
genation, ­ appropriate head positioning to facilitate cerebral venous
drainage, osmotherapy, sedation to decrease cerebral metabolic rate,
and h ­ yperventilation to reduce cerebral blood volume (Table 3).11,12 In
addition, it is important to correct any underlying pathology. This may

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12 1.  BRAIN HERNIATION

TABLE 3  General Management for Control of Intracranial Pressure

1. Ensure airway patency, adequate breathing, and circulation.

a. Tracheal intubation for airway protection and invasive mechanical ventilation.
b. Ensure oxygenation with hemoglobin saturation ≥92%.
c. Limit positive end-expiratory pressure <12 cm H2O.
d. Maintain cerebral perfusion pressure (50–70 mm Hg).
2. Positioning to facilitate cerebral venous drainage with head of bed elevated to 30°–45°
in neutral position.
3. Hyperventilation to maintain arterial carbon dioxide tension of 30–35 mm Hg.
4. Correct hyponatremia and maintain normoglycemia.
5. Antipyretics for fever.
6. Use of prophylactic anticonvulsants and treat seizure promptly.
7. Administer sedation and analgesia, when appropriate.
8. Administer dexamethasone for brain tumor–related vasogenic edema.
9. Osmotherapy using mannitol (0.25–2 g/kg over 10–15 min) or hypertonic salinea (but
keeping plasma sodium <160 mmol/L).
10. Careful drainage of cerebrospinal fluid if an external ventricular drainage device is
available.
a Common regimens include 3% solution at 5 ml/kg over 15 min; 7.5% solution at 2.5 ml/kg over 15 min; 23.4%
solution at 30 ml over 20–30 min.

include replacement of clotting factors to correct coagulopathy, relief of

hydrocephalus, drainage of intracranial hematoma, and surgical exci-
sion of contused brain tissue. In patients who suffer from hyperperfu-
sion after neurosurgery, aggressive control of arterial pressure using
labetalol or barbiturate infusion to reduce mean flow velocity <120 cm/s
of the proximal cerebral artery on transcranial Doppler monitoring may
be useful.13
In patients with malignant brain swelling following neurosurgery,
either due to infarction or hyperemia, early decompressive craniec-
tomy may be lifesaving. Based on the experience from acute ischemic
stroke, a large hemicraniectomy performed within 48 h after onset of
stroke has been shown to provide survival benefit as well as functional
improvement.14,15

CONCLUSIONS

Brain herniation is a devastating complication after neurosurgery.

Early recognition of brain herniation based on clinical signs, such as
failure to arouse and dilated pupils after surgery, should alert clini-
cians that brain herniation may have occurred. Radiological assess-
ment should be performed to identify the underlying pathology. Timely
resuscitation to decrease intracranial pressure is the key to minimize
damage.

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 References 13

References
1.  Frosch MP, Anthony DC, De Girolami U. The central nervous system. In: Kumar V, Abbas
AK, Aster JC, eds. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Philadelphia, PA:
Elsevier/Saunders; 2015:1251–1318.
2. Meeker J, Amerine J, Kropp D, Chyatte M, Fischbein R. The impact of Chiari malfor-
mation on daily activities: a report from the National Conquer Chiari Patient Registry
Database. Disabil Health J. 2015;8(4):521–526.
3. Battaglia P, Turri-Zanoni M, Castelnuovo P, Prevedello DM, Carrau RL. Brain herniation
after endoscopic transnasal resection of anterior skull base malignancies. Neurosurgery.
2015;11(suppl 3):457–462.
4. Seifman MA, Lewis PM, Rosenfeld JV, Hwang PY. Postoperative intracranial haemor-
rhage: a review. Neurosurg Rev. 2011;34:393–407.
5. Manninen PH, Raman SK, Boyle K, El-Beheiry H. Early postoperative complications fol-
lowing neurosurgical procedures. Can J Anaesth. 1999;46:7–14.
6.  Creutzfeldt CJ, Vilela MD, Longstreth Jr WT. Paradoxical herniation after decompressive
craniectomy provoked by lumbar puncture or ventriculoperitoneal shunting. J Neurosurg.
2015:1–6.
7. Komotar RJ, Mocco J, Ransom ER, et al. Herniation secondary to critical postcraniotomy
cerebrospinal fluid hypovolemia. Neurosurgery. 2005;57:286–292. discussion 286–292.
8. Panikkath R, Panikkath D, Lim SY, Nugent K. Kernohan’s notch: a forgotten cause of
Hemiplegia-CT scans are useful in this diagnosis. Case Rep Med. 2013;2013:296874.
9. Chan MT, Kan PKY. Blood loss during spine surgery. In: Brambrink A, Kirsch JR, eds.
Essentials of Neurosurgical Anesthesia and Critical Care: Strategies for Prevention, Early Detec-
tion, and Successful Management of Perioperative Complications. Springer; 2012:289–298.
10. Pierot L, Derdeyn C. Interventionalist perspective on the new endovascular trials. Stroke.
2015;46:1440–1446.
11. Stocchetti N, Maas AI. Traumatic intracranial hypertension. N Engl J Med. 2014;370:
2121–2130.
12. Stevens RD, Huff JS, Duckworth J, Papangelou A, Weingart SD, Smith WS. Emergency
neurological life support: intracranial hypertension and herniation. Neurocrit Care.
2012;17(suppl 1):S60–S65.
13. van Mook WN, Rennenberg RJ, Schurink GW, van Oostenbrugge RJ, Mess WH, Hofman
PA, et al. Cerebral hyperperfusion syndrome. Lancet Neurol. 2005;4:877–888.
14. Juttler E, Unterberg A, Woitzik J, Bosel J, Amiri H, Sakowitz OW, et al. Hemicraniec-
tomy in older patients with extensive middle-cerebral-artery stroke. N Engl J Med.
2014;370:1091–1100.
15. Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarc-
tion of the middle cerebral artery: a pooled analysis of three randomised controlled tri-
als. Lancet Neurol. 2007;6:215–222.

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