Herniation occurs when the brain shifts across structures within the skull, from one intracranial compartment to another, as a result of pressure gradients created by high intracranial pressure (ICP). Although the brain has considerable elasticity, the arteries and veins responsible for its blood supply are relatively fixed in space, leading to the risk that a shifting brain will cause moving portions to lose their blood supply. It is essential to be able to recognize the early clinical manifestations of herniation syndromes and to rapidly institute therapies to decrease ICP in order to reverse the process and maintain viability of the patient. Herniation syndromes of the brain can be classified as follows: central, uncal, cerebellar tonsillar, subfalcine, and transcalvarial.

Central (transtentorial) herniation syndrome occurs as a result of diffuse brain swelling due to trauma or a centrally located mass. This causes the diencephalon (thalamus, hypothalamus, epithalamus, subthalamus, and pretectum) to move caudally through the tentorial notch. The resulting alteration of consciousness is thought to be caused by cerebral hypoperfusion secondary to increased ICP as well as dysfunction of the reticular formation. The reticular formation is involved in stereotypical actions such as walking, sleeping, and lying down. It is absolutely essential for the basic functions of life and is evolutionarily one of the oldest portions of the brain. Consequently, an initial presenting sign of potential central herniation is a decreased level of alertness, which later progresses to stupor and coma.

Other key early features of the central herniation syndrome include meiotic but reactive pupils secondary to loss of sympathetic output from the hypothalamus; decorticate or flexor posturing that can be elicited spontaneously or via noxious stimuli; and Cheyne-Stokes respiration, an abnormal pattern of breathing characterized by periods of breathing with gradually increasing and decreasing tidal volumes scattered with periods of apnea. It is crucial to recognize this constellation of symptoms in the face of severe traumatic brain injury or a known central intracranial mass, because at this stage, herniation is potentially reversible.

In addition to these early signs of central herniation, it is crucial to be able to recognize signs and symptoms of Parinaud syndrome. Children with midbrain or pineal tumors, as well as direct or compressive trauma to the midbrain often present with Parinaud syndrome, also known as dorsal midbrain syndrome or pretectal syndrome. This syndrome consists of paralysis of up gaze, Pseudo-Argyll Robertson pupils (light-near dissociation), convergence-retraction nystagmus, and eyelid retraction (Collier sign). If this group of symptoms is present or even just a limitation of upward gaze is present, it behooves the physician to obtain neuroimaging to rule out an intracranial process.