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Brain Herniation Syndromes - 2 Nursing CEs
Brain Herniation Syndromes - 2 Nursing CEs
Author: Kristi Hudson RN MSN CCRN
Course Objectives
Upon completion of this course, the student will be able to:
  • Discuss the major components of the brain
  • Describe how the different compartments of the brain are separated
  • Explain the theory behind the Monroe-Kellie Doctrine
  • List the three types of Supratentorial Herniation
  • Describe 3 early symptoms of Uncal herniation and 3 late stage symptoms of Uncal herniation
  • Discuss nursing care and management of the patient with increased intracranial pressure
  • List the 3 goals of therapy for increased intracranial pressure
Definition of Herniation
The definition of brain herniation is the protrusion of the brain tissue from one compartment (of higher pressure) to a compartment of lower pressure. With this shift of brain tissue, blood and oxygen supplies are diminished causing herniating tissue to suffer from ischemia, hypoxia and finally cell death. To better understand the different herniation syndromes, lets take a look at what the brain is comprised of and how it is divided. The components of the brain include:
  • Parenchyma - The essential tissue (Brain in this case) of an organ distinct from its surrounding connective tissue. This is the largest intracranial volume (80%).
  • Blood vessel - The volume of blood in the cerebral arteries is an important determinant of intracranial pressure (10%).
  • Cerebral Spinal Fluid - CSF is comprised of fluid in the ventricles and subarachnoid spaces and is produced by the choroid plexus.  Approximately 500 cc is produced daily (10%).
The Monroe-Kellie Doctrine simply states that in a non-expandable, non-contractable, freely communicating space, the pressure of the fluid contents and the brain itself, must be directly porportional to eachother in order to maintain a constant pressure. If one of these pressures increases, another must decrease in order to compensate.
In addition to the parenchyma, blood vessels and CSF, the brain is also comprised of several individual compartments that are separated by folds of fibrous and relatively rigid dura mater. Two of the major dura folds include:
Falx Cerebri – which is a double fold of dura mater that drops into the longitudinal fissure and partially, divides the supratentorial space into the left and right side.
Tentoruim Cerebelli – this is also a double fold of the dura mater that forms a tent like partition (higher in the middle), between the cerebrum and cerebellum. (The area above the tentorium is the supratentorium space and the area below is known as the infratentorial space).

 Note: Because it is surrounded by strong bone and it is comprised of several small compartments divided by dura mater, the brain is at greater risk then other body organs for herniation.
Types and Location of Herniation Syndromes
Supratentorial Herniation (descending) – There are three major types of herniation that are caused by expanding supratentorial lesions, these include:
Cingulate Herniation – This occurs when the cingulated gyrus is forced under the falx cerebri, displacing it to the opposite side. Cingulate herniation alone is not considered to be life threatening, but because it displaces the falx cerebri and can cause compression and/or loss to local blood supply and surrounding cerebral tissue, it can lead to increases in ICP, which can contribute other and more devastating forms of herniation.
Signs and symptoms from Cingulate Herniation are not well defined, but thought to include:
  • Increased ICP
  • Cerebral Edema
  • Altered LOC
  • Change in Neuro Exam
Note: Though Cingulate Herniation is without defined symptomatology; it is often thought to be a precursor to other more serious herniation syndromes.
Central Transtentorial Herniation (Central Syndrome) – This occurs when a downward shift or displacement, pushes the cerebral hemispheres, basal ganglia, diencephalons, mid-brain and finally the medulla through the tentorial incisura (notch). Progression of signs and symptoms vary depending on whether herniation is in the early (reversible) or late (irreversible) stage. These include:
Early herniation to the diencephalons region (reversible):
  • Change in LOC (decreased alertness, agitation, drowsiness)
  • Pupils are small (1-3mm) but reactive
  • Conjugate or slightly disconjugate pupils at rest
  • Early hemiparesis or hemiplegia develop bilateral signs
  • Purposeful to painful stimuli
  • Babinski’s sign absent
  • Respiratory will show deep sigh, yawns and occasional pauses
Herniation to the Midbrain/Upper Pons (Middle phase of Central Herniation):
  • Deep Coma
  • Pupils midpoint (3-5mm) and non-reactive
  • Disconjugate pupils with limited horizontal movement
  • Decorticate posturing changes to decerebrate posturing
  • Babinski’s sign present
  • Gradual respiratory change to sustained hyperventilation
  • Diabetes Insipidus (not seen early)
  • Hyperthermia (not seen early)
Herniation to the Medulla (Late phase of Central Herniation and irreversible):
  • Deep Coma
  • Pupils dilated and non-reactive
  • Absent pupil movement
  • Flaccid extremities at rest, occasional flexor response to deep pain
  • Slow irregular respiratory rate, ataxia and periods of apnea
  • Cushing’s Triad (Hypertension, Bradycardia, Irregular Respirations)
Note: The underlying pathophysiology is that in the early phase of Central Transtentorial Herniation, ischemia and compression, which are, both thought to be reversible conditions, are the basis for signs and symptoms of diencephalic involvement. In the later phase after the midbrain becomes involved, it is thought that infarction of brain tissue has begun and it is at this point that the damage is irreversible.
Uncal Transtentorial Herniation (Uncal Syndrome) – This occurs when the uncus or hippocampal gyrus (or both), shift from the middle fossa through the tentorial notch and into the posterior fossa. When this occurs, there is compression of the ipsilateral third cranial nerve, then contralateral third cranial nerve and finally the mesencephalon. When Uncal Herniation occurs, the diencephalons and mid-brain are shifted to the opposite side of the brain. As with Central Transtentorial Herniation, signs and symptoms of Uncal herniation are considered to be reversible in the early stages and irreversible in the late stages. These signs and symptoms include:
Early herniation to the diencephalons region (potentially reversible):
  • LOC may not be impaired initially
  • Unilateral sluggish, dilating pupil (Ipsilateral to primary lesion)
  • Full extraocular movement
  • Pupils react to “Cold Carolics”
  • No motor function abnormality
  • Babinski’s sign absent
  • Normal respiratory pattern and rate
Herniation to the Midbrain/Upper Pons (Middle phase of Uncal Herniation):
  • Deep Coma
  • Pupils contralaterally fixed and either completed dilated or enlarged to 5-6mm
  • No extraocular movement
  • Bilateral decerebration
  • Bilateral positive Babinski’s sign
  • Hyperventilation (usually with rate 20-4- per minute)
Herniation to the Medulla (Late phase of Uncal Herniation and irreversible):
  • Deep Coma
  • Bilateral and fully dilated and fixed pupils
  • No extraocular movement
  • Flaccid extremities with occasional flexor response to deep painful stimuli
  • Slow and irregular respirations with occasional gasps and periods of apnea
  • Hyperthermia
  • Cushing’s Triad (Hypertension, Bradycardia, Irregular Respirations)
Note: The result of continued and unresolved downward displacement from any of the supratentorial herniation syndromes is ultimate brainstem herniation. When the medulla, which controls such vital functions as respiration and cardiac function, herniates into the foramen magnum, death is immediate.
Infratentorial Herniation (ascending) – Lesions of the infratentorial compartment that contribute to herniation are much less frequent then supratentorial herniation syndromes. Included in the infratentorial compartment are the brainstem and the cerebellum. There are three possible effects of an expanding lesion in the infratentorial compartment and they include:
  • Direct compression of the brainstem, cerebellum or the vascular supply to each area
  • Upward transtentorial herniation of the brainstem and cerebellum
  • Downward herniation of one or both cerebellum tonsils through the foramen magnum, to the cervical spine. When this occurs, the medulla is compressed and death is immediate.
The signs and symptoms of an Infratentorial Herniation vary widely depending on the brainstem involvement. In addition to medullary compression, an infratentorial lesion can also encroach on a portion of the ventricular system (3rd and 4th ventricle), which causes acute hydrocephalus.
Nursing Care and Management of Increased Intracranial Pressure:
  • Monitor LOC using Glasgow Coma Scale (or other objective scale)
  • Assess motor response (bilaterally)
  • Check for positive Babinski’s sign
  • Assess sensory responses (place emphasis on side opposite of injury)
  • Include the following in assessment of pupils:
  • Comparing pupil size, shape and equality bilaterally
  • Check pupils with the direct light reflex (check each eye individually)
  • Check that pupils are equal, round reactive to light accommodation (PERRLA)
  • Assess 6 cardinal fields of gaze (Cranial Nerves 3, 4 and 6)
  • Assess for Doll’s eye phenomenon in unconscious patients (indicates brain stem damage)
  • Monitor vital signs (Notify MD for deviation from set parameters)
  • Provide nursing measures r/t respiratory care including:
  • Suctioning
  • ABG’s
  • Providing O2
  • Monitoring O2 saturation
  • Monitoring ventilator settings
  • Position pt to maintain venous outflow from brain
  • Elevate HOB to 30 degrees (except for dural tear)
  • No pillow under head (can interfere with venous flow)
  • Turn by logrolling q 2 hrs
  • Administer prescribed medications
  • Control noise and stimuli
  • Provide rest/activity balance (stagger tasks)
  • Maintain desired temperature range (use antipyretics or hypothermia blanket)
  • Provide nursing care to prevent damage to eyes, skin, oral mucous
  • Provide education and emotional support to family
Nursing Diagnosis
  • Altered tissue perfusion r/t impaired cerebral circulation
  • Altered sensory perception
  • Impaired gas exchange
  • Self-care deficits
  • Altered body image
  • Potential for skin breakdown
  • Potential for injury
  • Ineffective coping (family)
  • Knowledge deficit
  • Anxiety (fear)
  • Altered Nutrition
Major Goals
  • Maintain normal ICP
  • Vital signs and ABG’s normal for patient
  • Improvement in LOC
Marini, J., J. & Wheeler, A., P. (2006). Critical care medicine: the essentials.(3rd ed.). Lippencott, Williams and Wilkes. Philadelphia
Arbour, R., (2004). Intracranial hypertension: Monitoring and nursing assessment. Critical Care Nurse. Oct. 2004.
Hickey, J., V., (2002). The Clinical Practice of Neurological and Neurosurgical Nursing. (5th ed.) Lippencott. Philadelphia S
Peterman, G., M.D., & Smirniotopoulos, J., G., M.D. (2005). Brain herniation. Retrieved on December 5, 2006 at:
Neurological Nursing NU 454. (2000). Retrieved on December 20, 2004 at:

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