Subfalcine Herniation

Article Author:
Kassie Kostecki
Article Editor:
Anthony Pearson-Shaver
12/28/2019 3:07:22 PM
PubMed Link:
Subfalcine Herniation


Once the fontanels close in infancy, the cranium becomes a rigid structure with a fixed volume containing three components the brain, the cerebrospinal fluid (CSF), and blood. The Monroe-Kellie Doctrine states that intracranial volume is constant and an increase in the volume of one component will cause a decrease in the volume of one or both of the others. Within a rigid structure, this change can have significant effects, such as decreased cerebral blood flow or herniation of brain tissue. When herniation occurs, the location of the herniation affects the presenting symptoms and the clinical outcomes.

Herniation occurs when brain tissue is displaced across a structure within the cranium. The most common form of intracranial herniation occurs when brain tissue is displaced under the falx cerebri and is aptly named a subfalcine herniation. The falx cerebri is the sickle-shaped dura mater that spans the length of the cerebral hemispheres and extends downward into the longitudinal fissure, separating the cerebral hemispheres and leaving a free edge inferiorly.  The cingulate gyrus is herniated, and if progression occurs, the frontal lobe becomes involved.


Subfalcine herniation is a secondary intracranial injury that caused by several primary injuries. The list below represents a sample of lesions associated with subfalcine hernias. In each case, a change in volume in one compartment precedes herniation.[1][2]

  • Increased brain volume
    • Traumatic brain injury (TBI)
    • Hemorrhage (epidural, subdural, subarachnoid)
    • Hematoma (epidural, subdural, intraparenchymal)
    • Ischemia due to stroke
    • Tumor
    • Cytotoxic/Vasogenic/Osmotic edema
      • Status epilepticus[3]
      • Hyperosmolality (hyponatremia[4])
      • Diabetic ketoacidosis/diabetes insipidus[5] (hyperammonemia[6])
  • Change in CSF volume
    • Increase
      • Increased production
      • Choroid plexus tumor
      • Obstructive hydrocephalus
      • Non-obstructive hydrocephalus
      • Pseudotumor cerebri
      • Meningeal inflammation or granulomas
    • Decrease
      • CSF leak[7]
      • CSF shunt over-drainage[8]
  • Change in blood volume
    • Increase
      • Loss of autoregulation due to TBI
      • Increased cerebral blood flow (aneurysm, hypercapnia, hypoxia)
      • Hemorrhage (epidural, subdural, subarachnoid, aneurysmal)
      • Dural sinus tear
      • Venous sinus thrombosis
      • Elevated right atrial pressure (heart failure)
      • Acidosis
    • Decrease
      • Rapid decompression of a hematoma[9]


While many sources state subfalcine herniations are the most common type of intracranial herniation, not all agree.  It is difficult to assess this claim because the prevalence (existing cases at any given time) and incidence (the number of new cases in a year) of subfalcine herniation are not well documented. This is likely because many patients have symptoms too benign to require neuroimaging (headache), or the patient's condition progressed rapidly, and the patient develops an uncal herniation. The neuroimaging, in this case, would not identify a subfalcine hernia, only the more pressing uncal herniation. 

Though reports describing the epidemiology of subfalcine herniation are lacking, the epidemiology of subfalcine hernias is likely reflected in the epidemiology of those conditions noted to cause subfalcine herniation and ischemic events that might result from subfalcine hernias. Of those lesions, traumatic brain injury and strokes are important causes. According to the Centers for Disease Control and Prevention, traumatic brain injury is a leading cause of death and disability in the United States among all races, ethnicities, social, economic levels, and age groups.[10]

During the period between 2002 and 2006, about 1.7 million US civilians sustained a TBI annually. Of these, approximately 1.4 million were treated and released from emergency departments (EDs), 275,000 were hospitalized and discharged alive, and 52,000 died. TBI-related deaths represent approximately one-third of injury-related deaths. These data are exclusive of members of the United States military who sustained a traumatic brain injury while serving abroad and those patients who did not seek medical care. An estimated 25% of patients who sustain traumatic brain injury do not seek medical care. As a result, the reported incidence of traumatic brain injury is likely less than the true occurrence of TBI. Similarly, one might speculate that the true incidence of subfalcine herniation is less than reports of clinical data would suggest.[11]

CDC reports suggest that children younger than 5 years of age have the highest rates of traumatic brain injury as evidenced by emergency department visits, hospital visits and death secondary to traumatic brain injury. [11] The next most frequently affected groups are adolescents aged 15 to 19 years followed by adults 75 years of age or older. Older adults have the highest rates of TBI hospitalizations and deaths in all 3 age groups. During the time reviewed, the leading causes of traumatic brain injury in the United States civilian population were falls, motor vehicle injuries, a blow to the head and assaults.

Reported incidence rates of ischemic strokes in infants, children, and adults younger than 45 years of age range from 0.62 to 7.9 per 100,000 children per year and 3.4 to 11.3 per 100,000 people per year for adults younger than 45 years old. The incidence rates noted were in primarily white populations. Studies report the incidence rate of ischemic stroke in young black adults to be as high as 22.8 per 100,000 people per year.[12]

If one accepts that the incidence rates of traumatic brain injury and ischemic strokes reflects the incidence rate of a subfalcine hernia, healthcare personnel, treating patients with traumatic brain injury or stroke due to any of the causes listed above should maintain a high index of suspicion or the occurrence of subfalcine hernias in patients who present following brain injury or symptoms of ischemic stroke.


Herniation occurs when a pressure difference is created on either side of a fixed intracranial structure — the pressure differential results from increases in brain volume as seen with tumors or localized hemorrhage. Changes in CSF volume cause herniation when a collection of CSF increases pressures on one side of a fixed structure; however, a sudden decrease in CSF volume causes herniation by lowering the pressure on one side of a fixed structure. Similar to the effects noted with CSF, either increases or rapid decreases in blood volume cause herniation.

Compensatory mechanisms (autoregulation, CSF shift, and shifts in blood volume) allow for the constant maintenance of intracranial pressure (ICP). When intracranial lesions exceed the capacity of native compensatory mechanisms, pressure increases occur, and herniation becomes possible. The true measure of intracranial pressure is the pressure of CSF within the cerebral ventricles. CSF opening pressures are used as surrogates for ICP though patient variables (position, sedation, level of activity) likely affect the accuracy of the measurement. As reflected by opening pressures, intracranial pressure in children normally ranges from 8 to  28 cm H20 pressure.[13][14] The probability of herniation occurs when intracranial pressures exceed 28 cm H2O for more than 5 minutes.[15]

For example, a hematoma can cause a mass effect and CSF volume and venous blood volume within the brain are decreased to maintain a normal ICP. As the lesion's volume increased and overwhelms the compensatory mechanisms’ ability to maintain a normal ICP, the ICP increases and the probability of herniation increases.

History and Physical

A subfalcine herniation may not initially cause severe clinical symptoms. The initial presentation can be as benign as a headache. When patients develop a subfalcine hernia, the cingulate gyrus is forced under the falx cerebri and decreased blood flow caused by compression of the ipsilateral anterior cerebral artery (ACA) results in contralateral leg weakness.[5] If the herniation affects the dominant hemisphere and injures the contralateral arcuate fasciculus.  Wernicke and Broca’s areas are affected[16] and patients present with conduction aphasia, receptive/sensory aphasia or expressive/motor aphasia.

If the primary lesion becomes large enough, uncal or central herniation may develop. As the lesion grows and herniation becomes prominent, symptoms progress and patients may develop anisocoria, a decreased level of consciousness, changes in respiratory pattern, changes in muscle tone and posturing.


Patients presenting with signs or symptoms of neurologic compromise require a thorough history and physical. The history may raise suspicion of intracranial lesions that night lead to neurologic compromise.  All patients with neurologic injury require frequent re-evaluation. If there is a significant change that raises suspicion of intracranial injury and possible intracranial herniation, a non-contrast computed tomography (CT) brain scan should be ordered immediately as it is the preferred modality of neuroimaging in these patients. The CT scan accurately detects acute hemorrhagic lesions and subtle subsequent midline shifts. Its general availability makes it easily accessible and the rapid results which can improve prognosis and outcome.[17][18]

While CT scans are the gold standard for immediate neuroimaging and evaluation for herniation syndromes, other methods of evaluation are being researched. Non-invasive ICP monitoring and transcranial Doppler ultrasonography[19] are being tested to expose patients to less radiation.

Treatment / Management

Management of herniation syndromes depends on etiology, but all methods of resuscitation focus on support of the patient's respiratory and cardiovascular systems while attempting to decrease intracranial pressure. Patients presenting with evidence of herniation are treated using a tiered emergency neurological life support (ENLS) management protocol.[5] If one tier does not arrest or even reverse the herniation, progress to the next tier sequentially. During the resuscitation, it is crucial to identify and treat the cause. Neurologic resuscitation often requires patience. If resuscitation is successful, clinical and radiological improvement will be noted. When resuscitation is less successful, more invasive therapies are available including decompressive craniectomy, ventriculostomy, and/or removal of space-occupying lesions (hemorrhages, tumors, abscesses).


Prognosis depends on the cause of the herniation, the elevation in intracranial pressure, the presence and duration of resultant ischemia and the intracranial structures affected. While many patients may make a full recovery, many are left with deficits and disability. Old reports suggested mortality rates as high as 33% in children with severe nonpenetrating traumatic brain injuries.[20] and 60% in patients who suffered transtentorial herniation.[21] Overall, mortality rates from traumatic brain injury have been decreasing[11] in recent years, and a 2003 CDC surveillance report noted that 73% of patients discharged following traumatic brain injury had a good functional recovery. Sixteen percent of TBI patients had poor outcomes: persistent coma, severe disability, and moderate disability.[22] 


The primary complication of subfalcine herniation is the compromise of the blood flow through the anterior cerebral artery that results in ischemia in the frontal and parietal lobes. While a subfalcine hernia can occur coincident to other cerebral herniation syndromes, subfalcine hernias are not the cause of other herniation syndromes.

Pearls and Other Issues

  1. Subfalcine herniation is noted in many conditions that cause an increase in one of the three compartments within the skull:
    1. Increased blood volume due to hemorrhage
    2. Increased brain volume due to swelling, edema or tumor
    3. Increased cerebral spinal fluid volume due to hydrocephalus
  2. Subfalcine hernias may present with very subtle clinical symptoms. The hernia may be missed because the symptoms don’t warrant neural imaging.
  3. Subfalcine hernias may present with subtle clinical symptoms that progress to uncal or central herniation syndromes.
  4. If a subfalcine hernia has been noted, patients require close observation and monitoring.
  5. Subtle clinical changes in patients with subfalcine hernias must be taken seriously to prevent significant morbidity and death.

Enhancing Healthcare Team Outcomes

Because symptoms of subfalcine herniation may present subtly or present with rapid deterioration, it is important that the interprofessional healthcare team maintain open and clear lines of communication. It is likely that parents, family members, or nurses caring for patients within the hospital environment will recognize subtle neurologic changes or more problematic neurologic changes in the patient status first. When family members recognize changes, they must report the changes to the patient’s nurse, and the nurse should take the family's concerns seriously. The bedside nurse should examine the patient for the changes reported and contact a physician responsible for the patient’s care. Again, physicians receiving the report must take the report seriously. A thorough evaluation by the physician must follow, and imaging studies ordered immediately. In the event of an active herniation, the team care should immediately start resuscitation to stabilize the airway, maintain adequate cardiovascular perfusion, and decrease the intracranial pressure.

These patients will frequently require neurosurgical consultation and monitoring by critical care physicians in a medical or neurological intensive care unit. The interprofessional team should be prepared to intervene aggressively to prevent progressive herniation, morbidity, and death.

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      Image courtesy S Bhimji MD


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