Brain Herniation

Overview

Brain herniation is the displacement of brain tissue through the rigid dural folds (i.e., falx and tentorium) or skull openings (e.g., foramen magnum). Although patients with chronic brain herniation associated with developmental defects, such as Arnold–Chiari malformation, may remain asymptomatic for many years, acute brain herniation following neurosurgery is a catastrophic event that results in mechanical and vascular damage of the brain. In many circumstances, brain herniation is often regarded as a terminal event.

Mechanism of Brain Herniation

From a mechanistic point of view, brain herniation is the result of a pressure gradient that squeezes the vulnerable brain matter from one compartment in the brain to another through various anatomical channels. In general, any pathologic process that increases intracranial pressure provides the driving pressure for brain herniation. It should be clear that the pressure gradient appears to be the most important factor, and brain herniation may occur regardless of the size of the opening. In the perioperative setting, hemorrhage, cerebral swelling associated with perioperative stroke, and hydrocephalus are the common causes for intracranial hypertension after neurosurgery ( Table 1 ). In a systematic review of patients with clinical deterioration following intracranial surgery, 0.8–6.9% of cases were thought to be due to postoperative hemorrhage. In patients who received regular imaging surveillance, up to 50% of cases had evidence of significant intracranial hemorrhage following neurosurgery. It is reassuring that few patients with postoperative intracranial hematoma actually end up with brain herniation. However, even a small amount of blood may produce sufficient pressure to produce significant brain herniation. This is especially important in patients who already have limited intracranial compliance.

It should be noted that not all cases of brain herniation are related to intracranial hypertension. In patients who had decompressive craniectomy, acute drainage of cerebrospinal fluid, upright posture, or hyperventilation may produce a transient negative pressure gradient between the atmosphere and intracranial compartments. This extra intracranial pressure gradient across the skull defect may be large enough to push the brain matter down into the tentorial notch or the foramen magnum, resulting in a rare phenomenon known as paradoxical brain herniation.

Classification of Brain Herniation

The brain can be broadly divided into a number of compartments, with boundaries formed by the falx, the tentorium, and the foramen magnum. When the pressure within a compartment is increased, its contents will be pushed toward the adjacent compartments. The directions of displacements are shown in Figure 1 . Briefly, the inner part of the temporal lobe (uncal herniation), the entire diencephalon (central/downward transtentorial herniation), and the frontal lobe (cingulate or subfalcine herniation) are common areas for herniation within the supratentorial compartment. In the infratentorial compartment, cerebellar tonsils may be squeezed down through the foramen magnum (tonsillar herniation or coning). In contrast, the cerebellum in the posterior fossa may also be pushed upward when the infratentorial pressure exceeds that in the supratentorial compartment (reverse transtentorial herniation). Finally, the part of brain matter that is adjacent to a craniectomy wound or site of fracture may be herniated out of the skull (transcalvarial herniation).

Clinical Features of Brain Herniation

The clinical presentation of brain herniation depends largely on the underlying lesion in the brain, the manifestations of intracranial hypertension, and the function of specific part of the brain that is being compressed. Table 2 summarizes the mechanisms and common clinical signs associated with different forms of brain herniations.