ntroduction

The uncus is a structure at the anterior medial aspect of the parahippocampal gyrus in the
medial temporal region of the brain. The medial temporal region is within the supratentorial
compartment of the cranium connected to the subtentorial compartment via the tentorium
cerebelli through the tentorial notch. The structures in the tentorial notch include the
midbrain, third cranial nerve, posterior cerebral arteries, and superior cerebellar arteries. The
cerebellum occupies the posterior portion of the tentorial notch. Uncal herniation occurs
when rising intracranial pressure causes portions of the brain to flow from one intracranial
compartment to another; this is a life-threatening neurological emergency and indicates the
failure of all adaptive mechanisms for intracranial compliance.[1]
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Etiology
The causes of uncal herniation include any situations which will cause a significant rise in
intracranial pressure. Any expanding space-occupying lesion within the cranium can subject a
patient to be at risk for uncal herniation. Uncal herniation can occur following severe head
trauma which may lead to a rapidly expanding subdural or epidural hematoma. In uncal
herniation, there is usually some supratentorial driving force occurring with a raised ICP
causing the uncus to slide over the supratentorial notch.[2]
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Epidemiology
The actual incidence of uncal herniation is poorly understood. Since uncal herniation can
occur secondary to traumatic brain injury, it is essential to understand the occurrence of TBI
to highlight an at-risk population. According to the CDC's 2015 Report to Congress on
Traumatic Brain Injury, there are approximately 30 million injury-associated emergency
department visits, hospitalizations, and deaths every year in the United States. TBI accounts
for 16% of injury-related hospitalizations and one-third of injury-related deaths. Specifically,
in 2010, the CDC estimated that TBIs accounted for about 2.5 million ED visits,
hospitalizations, and deaths in the United States, either isolated or in combination with other
injuries.
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Pathophysiology
The three components which make up the intracranial compartment are brain tissue, arterial
or venous blood, and cerebrospinal fluid. According to the Monro-Kellie principle, any
increase in one of these components will come at the expense of another
component.[3][4] For example, a mass present in the supratentorial compartment will reduce
CSF and venous blood volume first, followed by reductions in arterial blood flow and volume
and herniation of brain tissue through existing cranial openings.[3] The uncus herniates over
the tentorial notch and pushes against the brainstem and corresponding cranial nerves,
compressing the third cranial nerve located just medial to the uncus.
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History and Physical
A patient with impending uncal herniation will initially present with symptoms of increased
intracranial pressure. These symptoms include headache, nausea, vomiting, and altered
mental status. Physical exam in increased ICP will reveal Cushing's triad of hypertension,
bradycardia, and irregular respirations or apnea.[1] A late finding on an ophthalmologic exam
in a patient with increased ICP is papilledema, which presents with a blurring of the optic
disc margin and decreased venous pulsations. The cardinal signs of uncal herniation are an
acute loss of consciousness associated with ipsilateral pupillary dilation and contralateral
hemiparesis. These symptoms are due to compression or displacement of ascending arousal
pathways, the oculomotor nerve (CN III), and corticospinal tract.[1] The hallmark unilateral
dilated pupil can be the first symptom to appear without severe impairment in the level of
consciousness or contralateral hemiparesis. In patients who present with isolated anisocoria,
this could be a sign that there is impending uncal herniation.[5] Over time, the patient may
develop impaired ocular motility which will give the eye a classic down-and-out appearance.
Further compression of the midbrain due to uncal herniation can then progress to lethargy,
coma, or death. Ultimately if untreated, uncal herniation progresses to central herniation.
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Evaluation
Uncal herniation diagnosis is by its characteristic physical exam findings and confirmed with
brain imaging. Any patient who presents with Cushing's triad warrants immediate CT scan to
rule out life-threatening hemorrhage, herniation, or mass lesion.[6] A cranial CT scan is the
preferred imaging technique over magnetic resonance imaging (MRI) in the emergent setting;
it can be completed quickly, and CT imaging technology is more available.[1]
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Treatment / Management
When the signs of uncal herniation are present, the physician must act rapidly to reduce
intracranial pressure by adjusting the volume of one component of the intracranial
compartment, either brain, blood, or cerebrospinal fluid.[4] Management strategies to achieve
this include:
 Elevating the head of the bed thirty degrees
 Keeping the head midline
 Hyperventilation
 Hyperosmolar therapy with either mannitol or hypertonic saline
Hyperventilation works to reduce the intracranial pressure by decreasing arterial carbon
dioxide levels which will induce vasoconstriction to reduce the cerebral blood volume; this is
achievable by increasing tidal volume or respiratory rate with a target PaCO2 of 30-35
mmHg. Hyperventilation is typically reserved for situations where there is life-threatening
intracranial hypertension, such as in uncal herniation.[3]
Hyperosmolar therapy with mannitol or 3% hypertonic saline is administered to patients with
intracranial pressure elevations above 20 mmHg or when there is suspected brain herniation.
Mannitol is given as a bolus dose of 0.5-1 g/kg and can be administered every four hours as
needed for intracranial pressures above 20 mmHg, maintaining the osmolar gap less than 20
mOsm. 3% hypertonic saline is given as a bolus dose of 5-10 mL/kg in patients with acute
elevations of intracranial pressure or with signs of brain herniation. Hypertonic saline can be
administered as a continuous infusion at 0.5-1.5 mL/kg/hr.[1]
The next step for management of uncal herniation if clinical signs do not resolve with
interventions to reduce intracranial pressure is to consider decompressive surgical
options.[1] These include:
 Placement of a ventricular drain
 Evacuation of an extra-axial lesion such as epidural hematoma
 Resection of an intracerebral lesion
 Removal of brain parenchyma
 Uni- or bilateral craniectomies
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Differential Diagnosis
Since uncal herniation occurs after a significant elevation in intracranial pressure, the
differential diagnosis would include any conditions with symptoms of a headache, nausea,
vomiting, or altered mental status. Some possible differentials for uncal herniation could
include:
 Meningitis
 Encephalitis
 Sepsis
 TBI/concussion syndrome
 Ischemic stroke
 Intracranial hemorrhage
 Subdural/epidural hematoma
 Neoplasm
 Toxins exposure
 Diabetic ketoacidosis
 Systemic lupus erythematosus
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Prognosis
An important factor for a better neurosurgical outcome in patients with uncal herniation is
early diagnosis and timely management of the condition.[5] The degree of herniation will
also affect the prognosis of patients with uncal herniation. The reversibility of the herniation
becomes more difficult in patients with multiple traumas or when new complications arise as
herniation increases. Reversal of uncal herniation can be achieved, however, if
the interventions commence rapidly.[7] Reversal of uncal herniation is known to occur in 50–
75% of adult patients with either traumatic brain injury or with supratentorial mass
lesions.[1] Long-term outcomes after successful treatment for herniation may be more
favorable in children than in adults.[1]
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Complications
The most severe complications seen in uncal herniation are coma or death due to the failure
of management strategies to reverse the herniation syndrome. Depending on the amount of
tissue involved in the herniation, the patient is also at risk for development of brainstem or
cortical ischemia because of the anatomical proximity of major blood vessels. There are few
cases of a rare complication of chronic uncal herniation seen mostly in children with Dandy-
Walker syndrome or other cystic cavities in communication with the fourth ventricle because
of posterior fossa shunting.[2]
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Consultations
A team familiar with the signs and symptoms of herniation syndromes should monitor
patients presenting with TBI. Neurointensivists, neurosurgeons and support staff with
experience caring for patients with significant neuro injury will be crucial members of the
team.
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Deterrence and Patient Education

The best deterrence and prevention is appropriate precautions when operating motor vehicles
or using firearms as these are common causes of traumatic brain injury. Most medical causes
of space-occupying brain lesions are difficult if not impossible to prevent.
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Pearls and Other Issues

 Uncal herniation occurs because of a lesion that overwhelms the ability of the three
components in the cranium to compensate for pressure increases.
 The cardinal signs of uncal herniation are an acute loss of consciousness associated
with ipsilateral pupillary dilation and contralateral hemiparesis.
 Anisocoria is a cause for concern, and its cause should be sought.
 CT scan is the preferred imaging technique over magnetic resonance imaging (MRI)
in the emergent setting as it can be completed quickly and CT imaging technology is
more available
 Uncal herniation can is reversible if recognized early and treated aggressively.
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Enhancing Healthcare Team Outcomes
Neurological resuscitation is a true team sport requiring close communication between
disciplines. Nurses are the ultimate patient monitors and recognition of subtle changes may
make the difference in outcomes. Respiratory therapists, like nurses, should be
keenly attuned to subtle changes in the patient's respiratory status as changes in pulmonary
compliance may affect ICP by increasing venous pressure and increasing PCO2. Care will
require a team of physicians and their ability to communicate freely will be essential to
improving outcomes. All members of the team should be empowered to contribute freely and
encouraged to report subtle changes that can affect the patient's outcome. The most effective
teams will find a method of discussing the patient's care at least twice and developing a plan
that addresses the patient's needs.