Brain Herniation: Types and Pathology

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

Brain herniation is the displacement of brain tissue across a dural reflection or through a skull opening because of raised intracranial pressure. It is a mechanical event with a vascular and metabolic consequence, because displaced tissue compresses the vessels and cranial nerves that share its pathway.

Herniation is the final common pathway of many intracranial diseases. A tumor, hematoma, abscess, or edema fluid all raise intracranial pressure inside a rigid skull, and once compensatory mechanisms are exhausted, brain tissue moves along the path of least resistance. The movement itself injures tissue, but the more serious damage is compression of the brainstem, which contains the respiratory and cardiovascular centers. Recognizing the type of herniation and its clinical correlate lets a clinician anticipate deterioration before it becomes irreversible.

The Mechanical Basis of Herniation

The skull is a closed box with three contents: brain parenchyma, cerebrospinal fluid (CSF), and blood. The Monro-Kellie doctrine states that the total volume of these three components is fixed, so an increase in one must be offset by a decrease in another. Early compensation works through displacement of CSF into the spinal subarachnoid space and reduction of cerebral blood volume. When those reserves are exhausted, the pressure-volume curve becomes steep, and small additional volumes produce large pressure increases.

Once intracranial pressure rises above the pressure in the compartment next door, tissue moves. The direction of movement is determined by anatomy. The falx cerebri separates the cerebral hemispheres, the tentorium cerebelli separates the cerebrum from the cerebellum and brainstem, and the foramen magnum is the opening at the base of the skull. Each of these structures creates an edge against which herniating tissue can be compressed.

A 2026 conceptual model proposed that supratentorial herniation follows a vertical compaction gradient rather than a simple mechanical shift [1]. In that prospective study of 287 patients with traumatic supratentorial herniation, five stages of deterioration were identified, progressing from the diencephalon downward to the medulla. The authors described a demarcation line of tissue compaction, a boundary between viable and irreversibly failing neural tissue. This model helps explain why clinical decline in herniation is stepwise rather than smooth, and why the level of brainstem dysfunction visible on examination predicts outcome.

Types of Herniation of Brain

Herniation syndromes are classified by the anatomy they cross. The five classical types are subfalcine, transtentorial (uncal), central, tonsillar, and transcalvarial. Ascending transtentorial herniation is a sixth, less common pattern seen with posterior fossa lesions.

Subfalcine Herniation

Subfalcine herniation, also called cingulate herniation, occurs when unilateral hemispheric swelling pushes the cingulate gyrus under the free edge of the falx cerebri. The falx is a sickle-shaped dural fold in the longitudinal fissure. The herniating brain is the cingulate gyrus and adjacent medial frontal lobe.

The main structure at risk is the anterior cerebral artery, which runs along the medial surface of the hemisphere and can be compressed against the falx, producing infarction in its territory. Midline shift is the imaging hallmark. In dogs with prosencephalic brain tumors and epileptic seizures, subfalcine herniation was present in over 75 percent of cases in a multicenter retrospective study of 80 dogs, making it the most common herniation type identified on MRI in that population [2].

Subfalcine herniation is often clinically silent on its own. Its importance is as a marker of mass effect and as a precursor to more dangerous downward herniation.

Transtentorial (Uncal) Herniation

Transtentorial herniation occurs when the medial temporal lobe, specifically the uncus and hippocampal gyrus, moves through the tentorial incisura, the opening in the tentorium cerebelli through which the midbrain passes. This is the classic uncal herniation.

The uncus is the anteromedial part of the parahippocampal gyrus. As it descends, it compresses the ipsilateral oculomotor nerve (cranial nerve III), which runs along the edge of the tentorium. The first sign is often ipsilateral pupillary dilation because the parasympathetic fibers on the surface of the nerve are affected first. As compression continues, the pupil becomes fixed. Contralateral hemiparesis follows as the cerebral peduncle is compressed against the opposite tentorial edge, and the patient may develop a decreased level of consciousness.

In a series of 24 patients with intracerebral hemorrhage, uncal herniation was the second most common type after subfalcine herniation and correlated with pupillary abnormalities and lower Glasgow Coma Scale scores [3]. In a neurosurgical series of 239 patients who underwent craniotomy with lumbar spinal drainage, uncal herniation was the most frequent postoperative herniation, occurring in 18 of 24 affected patients [4]. That study found that brain herniation occurred in 24 patients with lumbar drainage versus 8 without, an odds ratio of 3.21, though favorable outcomes were more common in the drainage group [4].

Central Herniation

Central herniation is a symmetric, downward displacement of the diencephalon and brainstem through the tentorial incisura. It typically results from bilateral hemispheric swelling or from a centrally located mass. Because the displacement is symmetric, the early clinical picture differs from uncal herniation.

The progression follows a rostrocaudal pattern. Early signs include drowsiness and a reduced level of consciousness. As the diencephalon is compressed, small pupils that remain reactive may be seen. With further descent, the midbrain is involved, and pupils become midposition and fixed. Respiratory patterns change from Cheyne-Stokes to central neurogenic hyperventilation. In the lumbar drainage study, central herniation accounted for 5 of 24 postoperative herniations [4].

The 2026 compaction model identified a hyperthermia, hypertonia, and hypertension cluster, termed the Hyper-H triad, that often preceded further deterioration in patients with progressive herniation [1]. This triad reflects loss of hypothalamic and brainstem autonomic control.

Tonsillar Herniation

Tonsillar herniation, also called foramen magnum herniation, occurs when the cerebellar tonsils descend through the foramen magnum. The foramen magnum is the large opening at the base of the skull through which the medulla oblongata and spinal cord pass. Because the medulla contains the respiratory and cardiac centers, tonsillar herniation is the most immediately life-threatening type.

In dogs and cats, cerebellar tonsillar herniation through the foramen magnum is common with space-occupying lesions. A retrospective study of 32 cats with brain herniation diagnosed on MRI found that cats with intracranial neoplasia had 4.8 times the odds of herniation compared with cats with other diagnoses, and the odds increased with age [5]. Cats with herniation had significantly lower levels of consciousness on the Modified Glasgow Coma Scale [5]. In dogs, a study of 54 cases found that herniated dogs had significantly higher systolic blood pressure, a greater difference between systolic blood pressure and heart rate, and lower Modified Glasgow Coma Scale scores compared with controls [6]. In a study of 77 dogs with structural brain lesions, midline shift, which often accompanies or precedes foramen magnum herniation, was associated with a median survival time of 34.5 days versus 241 days in dogs without midline shift [7].

A case report described a 2-year-old cat with occipital bone angiomatosis and a chronic subdural hematoma that caused severe cerebellar and brainstem compression, foramen magnum herniation, and obstructive hydrocephalus [8]. This illustrates how a mass lesion in the posterior fossa can force the cerebellar tonsils through the foramen magnum.

Transcalvarial Herniation

Transcalvarial herniation occurs when brain tissue extrudes through a defect in the skull. The defect may be traumatic, surgical, or congenital. In veterinary medicine, open fontanelles in young animals and skull fractures are the usual causes.

A 2024 case report described a 1-year-old female Chihuahua with traumatic skull injury in which CT revealed brain herniation through the bregmatic fontanelle [9]. The hernia was manually reduced and the defect repaired with polypropylene mesh. This was the first reported case of brain herniation through the bregmatic fontanelle in a dog [9]. Transcalvarial herniation is the only type in which the herniating tissue is visible externally or through a palpable skull defect.

Ascending Transtentorial Herniation

Ascending transtentorial herniation is the upward movement of cerebellar tissue through the tentorial incisura. It is a rare complication of posterior fossa lesions, particularly those associated with obstructive hydrocephalus. A case report described a 3-year-old boy with a cerebellar anaplastic ependymoma and obstructive hydrocephalus who developed ascending transtentorial herniation after ventriculoperitoneal shunt placement [10]. The authors noted that in patients with posterior fossa tumors and hydrocephalus, upfront tumor excision may be preferable to preoperative CSF diversion because rapid decompression of the supratentorial compartment can create a pressure gradient that pulls cerebellar tissue upward [10].

Summary Table: Herniation Types, Anatomy, Imaging, and Clinical Correlate

Pathology of the Herniating Brain

The pathology of herniation has two components: the direct mechanical injury to displaced tissue and the secondary vascular and metabolic consequences.

Vascular Injury

Displaced brain tissue compresses arteries and veins. The anterior cerebral artery is at risk in subfalcine herniation. The posterior cerebral artery can be compressed against the tentorial edge in transtentorial herniation, producing occipital infarction. The most feared vascular consequence is Duret hemorrhage, a secondary brainstem hemorrhage that results from downward displacement of midline structures. A case report described a 22-year-old man with traumatic brain injury who developed a Duret hemorrhage that evolved from initial interpeduncular subarachnoid bleeding to a focal upper brainstem parenchymal hemorrhage and then resorbed [11]. The patient recovered well after decompressive craniectomy, suggesting that Duret hemorrhage does not always indicate a poor prognosis, particularly in young patients treated promptly [11].

Brainstem Compression

The brainstem is the target of the most dangerous herniation syndromes. Compression of the midbrain and medulla disrupts the reticular activating system, producing loss of consciousness. It also disrupts cranial nerve nuclei and long tracts, producing pupillary abnormalities, motor deficits, and respiratory pattern changes. Traumatic brainstem injury can occur as a primary injury or as a secondary hemorrhagic or ischemic complication of brain herniation and intracranial hypertension [12].

A 2026 review of brain death and the brainstem noted that a primary supratentorial lesion usually provokes a rostrocaudal transtentorial herniation syndrome, resulting in impairment of both cerebral hemispheres and the brainstem [13]. This progression is why herniation is a neurologic emergency.

Edema and the Vicious Cycle

Herniation and edema reinforce each other. As tissue is compressed, local ischemia develops, which increases blood-brain barrier permeability and worsens vasogenic edema. In high altitude cerebral edema, a condition in which death occurs from brain herniation, MRI studies suggest a predominantly vasogenic mechanism, with protein and water leaking through a disrupted blood-brain barrier [14]. Once vasogenic edema develops, cytotoxic edema generally follows [14]. The same principle applies in any condition that raises intracranial pressure: edema begets more edema, which begets more herniation.

Clinical Signs of Brain Herniation

The signs of herniation reflect the level of the neuroaxis that is failing. They progress in a rostrocaudal sequence in most cases.

Altered Mentation

A decreasing level of consciousness is the earliest and most consistent sign. In dogs with brain herniation, the Modified Glasgow Coma Scale score was significantly lower than in dogs without herniation, with a cutoff of 14 or less providing high specificity [6]. In cats, herniation was also associated with significantly lower levels of consciousness [5]. The Modified Glasgow Coma Scale assesses motor activity, brainstem reflexes, and level of consciousness, and a falling score is a warning sign.

Pupillary Abnormalities

Pupillary changes are a direct reflection of oculomotor nerve or midbrain compression. In uncal herniation, the ipsilateral pupil dilates first because the parasympathetic fibers on the surface of cranial nerve III are compressed against the tentorial edge. As compression progresses, the pupil becomes fixed. In central herniation, pupils are initially small and reactive, then become midposition and fixed as the midbrain is involved. A case report of a patient who received bilateral stellate ganglion block noted that the block may have hidden clinical signs of the Cushing triad by producing bilateral areflexic mydriasis, which delayed diagnosis of intracranial hypertension and brainstem herniation [15]. This is a reminder that pupillary findings must be interpreted in context.

Respiratory Pattern Changes

Respiratory patterns change as the brainstem is compressed. Cheyne-Stokes respiration, characterized by alternating periods of hyperventilation and apnea, reflects diencephalic or early midbrain dysfunction. Central neurogenic hyperventilation reflects midbrain involvement. Ataxic or irregular breathing reflects medullary compression and is a preterminal sign. In patients with intracerebral hemorrhage, hyperventilation was one of the features of raised intracranial pressure recorded alongside extensor rigidity and pupillary asymmetry [3].

The Cushing Reflex

The Cushing reflex is a triad of hypertension, bradycardia, and irregular respiration that occurs when intracranial pressure rises enough to compress the brainstem and impair cerebral perfusion. The body responds by raising systemic blood pressure to maintain cerebral blood flow, and the heart rate falls reflexively. In dogs with brain herniation, a systolic blood pressure of 178 mm Hg or higher, a systolic blood pressure minus heart rate difference of 60 or greater, and a Modified Glasgow Coma Scale score of 14 or less each provided 90 to 98 percent specificity for herniation [6]. A combination of systolic blood pressure greater than 140 mm Hg and heart rate less than 80 per minute provided 24 percent sensitivity and 100 percent specificity [6]. A retrospective study of dogs under general anesthesia for MRI found that the Cushing reflex was suspected in a subset of dogs with intracranial hypertension based on blood pressure and heart rate changes [16].

How Herniation Is Identified in Practice

Herniation is identified through a combination of clinical examination and advanced imaging. MRI is the preferred modality because it shows soft tissue detail and can demonstrate the position of the cerebellar tonsils relative to the foramen magnum, the position of the uncus relative to the tentorial incisura, and the presence of midline shift.

In a study of 80 dogs with prosencephalic brain tumors and epileptic seizures, MRI features reflecting mass effect were highly prevalent. Peritumoral edema was observed in 85 percent of cases, lateral ventricular compression in 77.5 percent, midline shift in 87.5 percent, subfalcine herniation in over 75 percent, caudal transtentorial herniation in over 31 percent, and displacement of the quadrigeminal lamina in 57 percent [2]. Larger lesions were positively correlated with edema, ventricular compression, and laminar displacement [2].

CT is faster and more available in emergency settings. It can show midline shift, effaced cisterns, and transcalvarial herniation. A case report of a puppy with a cerebral vascular hamartoma described CT findings of transtentorial herniation and an intra-axial mass with dystrophic mineralization [17].

Clinical scoring systems help quantify the level of consciousness. The Modified Glasgow Coma Scale is used in veterinary medicine and has been shown to correlate with herniation in both dogs and cats [5][6].

Clinical Relevance, Limitations and Common Mistakes

Herniation is not a diagnosis in itself. It is a complication of an underlying disease, and treatment must address both the herniation and the cause. In dogs and cats, the most common underlying causes are intracranial neoplasia, traumatic brain injury, and inflammatory or infectious masses. The presence of herniation on imaging is a negative prognostic factor. In dogs with structural brain lesions, midline shift was associated with a hazard ratio of 3.6 for death compared with dogs without midline shift, and shorter survival times remained significant across etiologic diagnoses [7].

A common mistake is to assume that a normal pupillary light reflex excludes herniation. Early central herniation can present with small reactive pupils. Another mistake is to rely on a single vital sign. The Cushing reflex is a triad, and individual components can be blunted by drugs or anesthesia. A case report described how bilateral stellate ganglion block produced bilateral areflexic mydriasis that may have hidden signs of the Cushing triad and delayed diagnosis [15].

A third mistake is to perform lumbar puncture or lumbar spinal drainage in a patient with suspected raised intracranial pressure without considering the risk of herniation. A propensity score analysis found that brain herniation occurred in 24 of 239 patients who underwent craniotomy with lumbar spinal drainage versus 8 of 239 matched patients who did not, an odds ratio of 3.21 [4]. The authors noted that favorable outcomes were more common in the drainage group, suggesting that the relationship is complex and depends on patient selection and timing [4].

In posterior fossa lesions with obstructive hydrocephalus, rapid CSF diversion can precipitate ascending transtentorial herniation. A case report recommended upfront tumor excision rather than preoperative CSF diversion in such cases [10].

This article is educational and is not a substitute for veterinary diagnosis or treatment.

Quick Review

1. Brain herniation is displacement of brain tissue across a dural reflection or skull opening due to raised intracranial pressure.
2. The five classical types are subfalcine, transtentorial (uncal), central, tonsillar, and transcalvarial. Ascending transtentorial herniation is a sixth, less common type.
3. Subfalcine herniation is the most common type in dogs with prosencephalic tumors and is often clinically silent.
4. Tonsillar herniation through the foramen magnum is common in dogs and cats with space-occupying lesions and is the most immediately life-threatening type.
5. Clinical signs of herniation include altered mentation, pupillary abnormalities, respiratory pattern changes, and the Cushing reflex.
6. In dogs, systolic blood pressure of 178 mm Hg or higher, a systolic blood pressure minus heart rate difference of 60 or greater, and a Modified Glasgow Coma Scale score of 14 or less are specific for herniation.
7. Midline shift on MRI is a negative prognostic factor in dogs with structural brain disease.

Frequently Asked Questions

What is brain herniation?

Brain herniation is the displacement of brain tissue across a dural reflection or through a skull opening because of raised intracranial pressure. It is a mechanical complication of many intracranial diseases.

What are the types of herniation of brain?

The main types are subfalcine, transtentorial (uncal), central, tonsillar, and transcalvarial. Ascending transtentorial herniation is a rare additional type seen with posterior fossa lesions.

What are the signs of brain herniation in dogs and cats?

Signs include a decreasing level of consciousness, pupillary dilation or asymmetry, respiratory pattern changes, and the Cushing reflex of high blood pressure with a low heart rate. A low Modified Glasgow Coma Scale score is also associated with herniation.

Is tonsillar herniation common in dogs and cats?

Yes. Cerebellar tonsillar herniation through the foramen magnum is common in dogs and cats with space-occupying brain lesions, especially intracranial neoplasia.

Can brain herniation be treated?

Treatment depends on the underlying cause and the type of herniation. It may include surgery to remove a mass or relieve pressure, medical management to reduce edema, and supportive care. The prognosis depends on how quickly the herniation is recognized and how much brainstem damage has occurred.

What is the Cushing reflex?

The Cushing reflex is a response to raised intracranial pressure that combines high blood pressure, a slow heart rate, and irregular breathing. It occurs when brainstem compression impairs cerebral perfusion and the body tries to maintain blood flow to the brain.

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Sources

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4. Risk of brain herniation after craniotomy with lumbar spinal drainage: a propensity score analysis.
5. Relationship between admission vitals and brain herniation in 32 cats: a retrospective study.
6. Retrospective evaluation of the relationship between admission variables and brain herniation in dogs (2010-2019): 54 cases.
7. The effect of midline shift on survival time in dogs with structural brain disease diagnosed on MRI.
8. Occipital Bone Angiomatosis and Chronic Subdural Hematoma Causing Severe Cerebellar and Brainstem Compression and Obstructive Hydrocephalus in a Young Adult Cat.
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17. CSF from a puppy with a cerebral vascular hamartoma.