Brain herniation occurs when brain tissue shifts or is displaced from its normal anatomical compartment within the skull. This displacement is caused by high pressure inside the rigid cranial vault, a condition known as intracranial hypertension. The brain is squeezed across the fibrous partitions that separate its sections, such as the falx cerebri or the tentorium cerebelli. This shifting is a neurological emergency requiring immediate intervention to prevent irreversible damage to the brainstem, which controls basic life functions. Untreated herniation can rapidly lead to coma, brain death, or respiratory arrest.
The Mechanism of Pressure Buildup
The physical process leading to brain herniation is governed by the Monro-Kellie doctrine. This doctrine states that the skull is a fixed container holding three components: brain tissue, blood, and cerebrospinal fluid (CSF). To maintain normal intracranial pressure (ICP), an increase in the volume of one component must be compensated by a decrease in the others. For instance, the body can temporarily compensate for minor swelling by reducing blood volume or shifting CSF into the spinal canal.
When a new or expanding mass appears, these compensatory mechanisms are rapidly overwhelmed, causing ICP to rise sharply. Common causes of this volume increase include hematomas (epidural or subdural), large brain tumors, or abscesses. A blockage in CSF flow, known as hydrocephalus, also causes fluid buildup and contributes to pressure. When the brain’s ability to buffer this rising pressure is exhausted, the tissue begins to squeeze past the internal partitions, initiating herniation.
Anatomical Classifications of Herniation
Brain herniation is classified based on the specific direction of brain tissue displacement and the anatomical boundaries it crosses.
Uncal Herniation
This type, also known as descending transtentorial herniation, occurs when the uncus (innermost part of the temporal lobe) is pushed downward and inward over the tentorium cerebelli. This movement compresses the oculomotor nerve (Cranial Nerve III), leading to classic signs like pupil dilation on the same side as the lesion. The downward pressure also affects the midbrain, quickly reducing the level of consciousness.
Tonsillar Herniation
Tonsillar herniation, sometimes called coning, involves the cerebellar tonsils being forced downward through the foramen magnum. This action directly compresses the medulla oblongata, the lowest part of the brainstem, which controls respiration and heart rate. Compression of these centers can cause immediate respiratory arrest and subsequent cardiac arrest, making it a rapidly fatal event.
Central Herniation
Central herniation involves the downward movement of the brain’s central structures, including the diencephalon, through the tentorial notch. This shift is often caused by diffuse swelling in both hemispheres or masses located more centrally. This type of herniation typically progresses through a series of neurological changes as the brainstem is sequentially affected.
Subfalcine Herniation
This is the most common type, occurring when the cingulate gyrus shifts under the falx cerebri, the membrane separating the two cerebral hemispheres. This usually results in a midline shift visible on imaging.
Emergency Diagnosis and Intervention
Recognizing brain herniation is a time-sensitive process relying on specific clinical signs of high ICP. A rapidly deteriorating level of consciousness is a primary concern, often accompanied by abnormal posturing of the limbs. Clinicians look for Cushing’s triad, which indicates intracranial hypertension: high blood pressure, a slow heart rate (bradycardia), and an irregular breathing pattern. Pupillary changes, particularly a fixed and dilated pupil on one side, are a cardinal sign of Uncal herniation.
Diagnosis is confirmed immediately with neuroimaging, typically a rapid Computed Tomography (CT) scan. The CT scan visualizes the anatomical shift and the underlying cause, such as a hematoma or tumor. Intervention begins immediately with medical management to reduce ICP.
Medical interventions include:
- Osmotic diuretics (Mannitol or hypertonic saline) administered intravenously to draw excess fluid out of the brain tissue.
- Temporary controlled hyperventilation to decrease carbon dioxide levels, causing cerebral blood vessels to constrict and reducing intracranial blood volume.
Surgical interventions are often necessary to remove the source of pressure or create space for the swollen brain. Emergency surgery may be performed to evacuate a large blood clot, such as an epidural hematoma. For diffuse brain swelling, a Decompressive Craniectomy involves removing a section of the skull bone to allow the brain to expand outward. Shunt placement may also be used to drain excess cerebrospinal fluid if hydrocephalus is a contributing factor.
Outcomes and Recovery
The prognosis following brain herniation is guarded, with mortality rates sometimes reaching 60% even with aggressive treatment. The outcome for survivors depends on the severity of the initial injury and the specific brain structures compressed. Damage to the brainstem can result in long-term consequences, ranging from minor neurological deficits to profound cognitive impairment or a persistent vegetative state. Survivors typically require intensive long-term rehabilitation to address physical, cognitive, and emotional changes.