What is brain herniation

Brain herniation is also called cerebral herniation, acquired intracranial herniation or brain herniation syndrome, is a condition in which a portion of the brain, cerebrospinal fluid (CSF) and blood vessels is displaced because of increased pressure inside the skull. Increase in pressure results in progressive damage to brain tissue that may include life-threatening damage to the brainstem.

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 ¹. Within a rigid structure, this change can have significant effects, such as decreased cerebral blood flow or herniation of brain tissue. When brain herniation occurs, the location of the herniation affects the presenting symptoms and the clinical outcomes.

Brain herniation can occur:

• Between areas inside the skull, such as those separated by a rigid membrane like the tentorium cerebelli or falx cerebri
• Through a natural opening at the base of the skull called the foramen magnum
• Through openings created during brain surgery

Meninges

The meninges are membranes that envelop the brain and spinal cord. The meninges consist of three layers: the dura mater, the arachnoid mater (membrane), and the pia mater.

The dura mater is a thick, tough, and durable membrane composed of dense fibrous connective tissue. The dura mater of the brain is composed of two layers, an outer periosteal layer that connects to the inside of the skull, and a deep meningeal layer. In certain areas these two layers separate and the meningeal layer forms folds that extend into the brain forming physical partitions in the brain. The Falx cerebri separates the two cerebral hemispheres, the tentorium cerebelli separates the occipital lobes of the cerebrum from the cerebellum; and the falx cerebelli separates the two cerebellar hemispheres.

The arachnoid mater or arachnoid membrane is directly under the dura mater. These two membranes are not physically connected and there is a space (more like a virtual space) between the dura mater and the arachnoid mater. The arachnoid mater is a very thin and transparent membrane that lies on top of a fluid filled space directly inferior to the membrane. This space, the subarachnoid space, is filled with cerebropinal fluid. The arachnoid membrane together with the cerebral spinal fluid helps to cushion the central nervous system and fits like a loose sac over it.

Figure 1. Brain meninges

Brain herniation types

The tentorium is an extension of the dura mater that separates the cerebellum from the cerebrum. There are two major classes of herniation: supratentorial and infratentorial. Supratentorial refers to herniation of structures normally found above the tentorial notch, and infratentorial refers to structures normally found below it.

Supratentorial herniation

• Uncal (transtentorial)
• Central
• Cingulate (subfalcine/transfalcine herniation)
• Transcalvarial
• Tectal (posterior)

Infratentorial herniation

• Upward (upward cerebellar or upward transtentorial)
• Tonsillar (downward cerebellar)

Figure 2. Brain herniation types

Subfalcine herniation

Subfalcine herniation or cingulate herniation, the most common brain herniation pattern, is characterized by displacement of the brain (typically the cingulate gyrus) beneath the free edge of the falx cerebri due to raised intracranial pressure.

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 (see Figure 1 above). The cingulate gyrus is herniated, and if progression occurs, the frontal lobe becomes involved.

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 ².

During the period between 2002 and 2006, about 1.7 million US civilians sustained a traumatic brain injury 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. Traumatic brain injury-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 traumatic brain injury. Similarly, one might speculate that the true incidence of subfalcine herniation is less than reports of clinical data would suggest ³.

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 ³. 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 traumatic brain injury 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 ⁴.

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.

Subfalcine herniation key facts

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

Subfalcine herniation causes

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 ⁵.

• Increased brain volume
  • Traumatic brain injury (traumatic brain injury)
  • Hemorrhage (epidural, subdural, subarachnoid)
  • Hematoma (epidural, subdural, intraparenchymal)
  • Ischemia due to stroke
  • Tumor
  • Cytotoxic/Vasogenic/Osmotic edema
    • Status epilepticus ⁶
    • Hyperosmolality e.g., hypernatremia ⁷
    • Diabetic ketoacidosis/diabetes insipidus ⁸ or hyperammonemia ⁹
• Change in CSF volume
  • Increase
    • Increased production
    • Choroid plexus tumor
    • Obstructive hydrocephalus
    • Non-obstructive hydrocephalus
    • Pseudotumor cerebri
    • Meningeal inflammation or granulomas
  • Decrease
    • CSF leak ¹⁰
    • CSF shunt over-drainage ¹¹
• Change in blood volume
  • Increase
    • Loss of autoregulation due to traumatic brain injury
    • 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 ¹²

Subfalcine herniation signs and symptoms

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 results in contralateral leg weakness ⁸ If the herniation affects the dominant hemisphere and injures the contralateral arcuate fasciculus. Wernicke and Broca’s areas are affected ¹³ 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.

Subfalcine herniation complications

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 herniation can occur coincident to other cerebral herniation syndromes, subfalcine hernias are not the cause of other herniation syndromes.

• Contralateral hydrocephalus due to obstruction of the foramen of Monro
• Anterior cerebral artery (ACA) territory infarct due to compression of anterior cerebral artery branches. Anterior cerebral artery infarction occurs as the cingulate sulcus extends under the falx dragging the ipsilateral anterior cerebral artery with it. If this becomes compressed against the falx occlusion can lead to a distal anterior cerebral artery infarction and thus the clinical symptom of contralateral leg weakness.

Uncal herniation

Uncal herniation is a subtype of transtentorial downward brain herniation, usually related to cerebral mass effect increasing the intracranial pressure.

In uncal herniation, the uncus and the adjacent part of the temporal lobe glide downward across the tentorial incisura compressing the brainstem and the posterior cerebral arteries in the ambient cistern. Uncal herniation may be unilateral or bilateral ¹⁴.

Uncal herniation carries a bad prognosis due to the direct compression of the vital midbrain centers. They often require emergency neurosurgical decompression.

Uncal herniation causes

Uncal herniation occurs secondary to large mass effect (that can occur from traumatic or non-traumatic hemorrhage, malignancy, etc.) that will lead to increased intracranial pressure and herniation.

Uncal herniation signs and symptoms

• pupils and globe clinical features ¹⁵
  • initially, an ipsilateral dilated pupil that is unresponsive to light, signifying ipsilateral oculomotor nerve compression
  • may develop into bilaterally blown pupils due to compression of the mesencephalon and its parasympathetic nuclei
  • rarely, an isolated contralateral dilated pupil that is unresponsive to light may develop, signifying contralateral oculomotor nerve compression from midline shift
  • tonic lateral deviation may occur due to unopposed abducens nerve activity
  • ptosis may occur due to oculomotor nerve palsy (not paralysis of Müller’s muscle)
  • vertical gaze palsy may occur after compression of the rostral interstitial nucleus of the medial longitudinal fasciculus
• altered mental state ¹⁵
  • compression of the reticular activating system of the mesencephalon leads to alteration in conscious state
• motor deficits ¹⁵
  • usually contralateral hemiparesis
  • in ~25% ipsilateral hemiparesis due to Kernohan phenomenon

Uncal herniation complications

• extensive brainstem ischemia
• Duret hemorrhage. Duret hemorrhage is a small hemorrhage (or multiple hemorrhages) seen in the medulla or pons of patients who are rapidly herniating.
• contralateral midbrain compressed against the tentorium may cause Kernohan phenomenon
• compression of the ipsilateral posterior cerebral artery will result in ischemia of the visual cortex with resultant homonymous hemianopsia

Transtentorial herniation

Transtentorial herniation is a type of cerebral herniation. There are two types:

1. Descending transtentorial herniation, more frequently known as uncal herniation (see above)
2. Ascending transtentorial herniation, which is less common than uncal herniation

Ascending transtentorial herniation is a situation where space-occupying lesions in the posterior cranial fossa cause superior displacement of superior parts of the cerebellum through the tentorial notch.

Ascending transtentorial herniation signs and symptoms

• nausea and/or vomiting
• rapid progression toward a decreased level of consciousness and, eventually, death

Transalar herniation

Transalar (transsphenoidal) herniation describes herniation of brain matter in and around the middle cranial fossa across the greater sphenoid wing and can be ascending or descending. Compression of structures against the sphenoid bone results in symptoms.

Transalar herniation is not as common as the other types of brain herniation. It often occurs in combination with subfalcine and transtentorial herniation.

Descending transalar herniation

Descending transalar herniation occurs as a result of frontal lobe mass effect. There is posterior and inferior displacement of the posterior aspect of the frontal lobe orbital surface over the sphenoid wing. Small herniations involve only the orbital gyri, while larger herniations may include the gyrus rectus.

Ascending transalar herniation

Ascending transalar herniation is produced by middle cranial fossa or temporal lobe mass effect. There is displacement of the temporal lobe superiorly and anteriorly across the sphenoid ridge.

Posterior displacement of the frontal lobe can cause compression of the middle cerebral artery against the sphenoid ridge, resulting in middle cerebral artery territory infarction.

Superior displacement of the temporal lobe can compress the supraclinoid internal carotid artery against the anterior clinoid process and result in infarction of the anterior and middle cerebral artery territories.

Tonsillar herniation

Tonsillar herniation is also called downward cerebellar herniation, is a type of cerebral herniation characterized by the inferior descent of the cerebellar tonsils below the foramen magnum.

Tonsillar herniation is a secondary sign of significant intracranial mass effect. Any intra-axial or extra-axial lesion (e.g. tumor, hemorrhage, stroke, abscess) exerting mass effect on the brain parenchyma can displace the posterior cranial fossa structures inferiorly. In doing so the brainstem is compressed against the clivus thereby altering the vital life-sustaining functions of the pons and medulla, such as the respiratory and cardiac centers.

Tonsillar herniation of the cerebellum is also known as a Chiari malformation (CM), or previously an Arnold-Chiari malformation (ACM). There are four types of Chiari malformation, and they represent very different disease processes with different symptoms and prognosis. These conditions can be found in asymptomatic patients as an incidental finding, or can be so severe as to be life-threatening. This condition is now being diagnosed more frequently by radiologists, as more patients undergo MRI scans of their heads, especially upright MRI, which is more than twice as sensitive for detecting this condition.[13] Cerebellar tonsillar ectopia (CTE) is a term used by radiologists to describe cerebellar tonsils that are “low lying” but that do not meet the radiographic criteria for definition as a Chiari malformation. The currently accepted radiographic definition for a Chiari malformation is that cerebellar tonsils lie at least 5mm below the level of the foramen magnum. Some clinicians have reported that some patients appear to experience symptoms consistent with a Chiari malformation without radiographic evidence of tonsillar herniation. Sometimes these patients are described as having a ‘Chiari [type] 0’.

There are many suspected causes of tonsillar herniation including: decreased or malformed posterior fossa (the lower, back part of the skull) not providing enough room for the cerebellum; hydrocephalus or abnormal CSF volume pushing the tonsils out; or dural tension pulling the brain caudally. Connective tissue disorders, such as Ehlers Danlos Syndrome, can be associated.

For further evaluation of tonsillar herniation, CINE flow studies are used. This type of MRI examines flow of CSF at the cranio-cervical joint. For persons experiencing symptoms but without clear MRI evidence, especially if the symptoms are better in the supine position and worse upon standing/upright, an upright MRI may be useful ¹⁶.

Extracranial brain herniation

Extracranial brain herniation refers to herniation of brain tissue external to the calvaria through a skull bone defect, which may be post-traumatic or post-surgical. Unlike encephaloceles, brain herniation is not surrounded by the meninges.

The herniated brain tissue requires surgical reduction as it is at risk of ischemia and venous infarction from occluded cortical veins.

Brain herniation causes

Brain herniation occurs when something inside the skull produces pressure that moves brain tissues. This is most often the result of brain swelling from a head injury, stroke, or brain tumor.

Brain 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 H2O pressure ¹⁷. The probability of brain herniation occurs when intracranial pressures exceed 28 cm H2O for more than 5 minutes ¹⁸.

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 intracranial pressure (ICP), the ICP increases and the probability of herniation increases.

Brain herniation can be a side effect of tumors in the brain, including:

• Metastatic brain tumor
• Primary brain tumor, meningioma, base of skull tumors and suprasellar tumors

Brain herniation can also be caused by other factors that lead to increased pressure inside the skull, including:

• Brain abscess – a collection of pus and other material in the brain, usually from a bacterial or fungal infection
• Bleeding in the brain (hemorrhage) or intracranial hemorrhage:
  • extradural hemorrhage
  • subdural hemorrhage
  • intracerebral hemorrhage
• Buildup of fluid inside the skull that leads to brain swelling (hydrocephalus)
• Strokes that cause brain swelling
• Swelling after radiation therapy
• Defect in brain structure, such as a condition called Chiari malformation

Signs and symptoms of brain herniation

Signs and symptoms of brain herniation may include:

• High blood pressure
• Irregular or slow pulse
• Headache
• Weakness
• Cardiac arrest (no pulse)
• Loss of consciousness, coma
• Loss of all brainstem reflexes (blinking, gagging, and pupils reacting to light)
• Respiratory arrest (no breathing)
• Wide (dilated) pupils and no movement in one or both eyes

Signs of impending brain herniation

Cushing triad is a clinical syndrome consisting of hypertension, bradycardia and irregular respiration and is a sign of impending brain herniation ¹⁹. This occurs when the increased intracranial pressure is too high the elevation of blood pressure is a reflex mechanism to maintain cerebral perfusion pressure (CPP). High blood pressure causes reflex bradycardia and brain stem compromise affecting respiration.

Cerebral perfusion pressure (CPP) is the pressure gradient between mean arterial pressure (MAP) and intracranial pressure (CPP = MAP – ICP). CPP = MAP – CVP (central venous pressure) if central venous pressure is higher than intracranial pressure. Cerebral perfusion pressure (CPP) targets for adults following severe traumatic brain injury is recommended at greater than 60 to 70 mm Hg, and a minimum cerebral perfusion pressure (CPP) greater than 40 mm Hg is recommended for infants, with very limited data on normal CPP targets for children in between ¹⁹.

Cerebral autoregulation is the process by which cerebral blood flow varies to maintain adequate cerebral perfusion. When the mean arterial pressure (MAP) is elevated, vasoconstriction occurs to limit blood flow and maintain cerebral perfusion. However, if a patient is hypotensive, cerebral vasculature can dilate to increase blood flow and maintain CPP ¹⁹.

Brain herniation complications

Brain herniation complications may include:

• Brain death
• Permanent and significant neurologic problems

Prompt treatment of increased intracranial pressure and related disorders may reduce the risk for brain herniation.

Brain herniation diagnosis

A brain and nervous system (neurological) exam shows changes in alertness (consciousness). Depending on the severity of the herniation and the part of the brain that is being pressed on, there will be problems with one or more brain-related reflexes and nerve functions.

Tests may include:

• X-ray of the skull and neck
• CT scan of the head
• MRI scan of the head
• Blood tests if an abscess is suspected

Brain herniation treatment

Brain herniation is a medical emergency. The goal of treatment is to save the person’s life.

To help reverse or prevent a brain herniation, the medical team will treat increased swelling and pressure in the brain. Treatment may involve:

• Placing a drain into the brain to help remove cerebrospinal fluid (CSF)
• Medicines to reduce swelling, especially if there is a brain tumor
• Medicines that remove fluid from the body, such as mannitol or other diuretics, which reduce pressure inside the skull
• Placing a tube in the airway (endotracheal intubation) and increasing the breathing rate to reduce the levels of carbon dioxide (CO2) in the blood
• Removing blood or blood clots if they are raising pressure inside the skull and causing herniation
• Removing part of the skull to give the brain more room

Long term effects of brain herniation

People who have a brain herniation have a serious brain injury. They may already have a low chance of recovery due to the brain injury that caused the herniation. When brain herniation occurs, it further lowers the chance of recovery.

The outlook varies depending on where in the brain the herniation occurs. Without treatment, death is likely.

There can be damage to parts of the brain that control breathing and blood flow. This can rapidly lead to death or brain death.

Damage to the midbrain, which contains the reticular activating network which regulates consciousness, will result in coma ²⁰. Damage to the cardio-respiratory centers in the medulla oblongata will cause respiratory arrest and (secondarily) cardiac arrest ²⁰. Investigation is underway regarding the use of neuroprotective agents during the prolonged post-traumatic period of brain hypersensitivity associated with the brain herniation syndrome ²¹.

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 ²² and 60% in patients who suffered transtentorial herniation ²³. Overall, mortality rates from traumatic brain injury have been decreasing in recent years ³ and a 2003 CDC surveillance report noted that 73% of patients discharged following traumatic brain injury had a good functional recovery. Sixteen percent of traumatic brain injury patients had poor outcomes: persistent coma, severe disability, and moderate disability ²⁴.

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