The brain and spinal cord are encased within the skull and spinal canal, with nerves and blood vessels passing through specific foramina. The advantage of housing the delicate CNS within hard, rigid structures is obvious, but this arrangement provides little room for expansion of the brain in disease states. As a result, virtually any increase in the volume of the skull contents brings with it an increase in intracranial pressure. Substantial increases in the intracranial pressure compromise the ability of the cardiovascular system to deliver blood to the brain, resulting in decreased brain perfusion, with serious or fatal consequences. Disorders that may cause dangerous increases in the volume of intracranial contents include generalized cerebral edema, hydrocephalus, hemorrhages, ischemia, and mass lesions such as tumors.
Cerebral edema is the accumulation of excess fluid within the brain parenchyma. There are two types, which often occur together, particularly after generalized injury.
Vasogenic edema occurs when the integrity of the normal blood-brain barrier is disrupted, allowing fluid to shift from the vascular compartment into the extracellular spaces of the brain. Vasogenic edema can be localized (e.g., the result of increased vascular permeability due to inflammation or in tumors) or generalized.
Cytotoxic edema is an increase in intracellular fluid secondary to neuronal and glial cell injury, as might follow generalized hypoxic or ischemic insult or exposure to certain toxins.
The edematous brain is softer than normal and often appears to “overfill” the cranial vault. In generalized edema, the gyri are flattened, the intervening sulci are narrowed, and the ventricular cavities are compressed (
Fig. 23.2 http://ebooksmedicine.net
Fig. 23.2 Cerebraledema.Thesurfacesofthegyriareflattenedasaresultofcompressionoftheexpandingbrainbytheduramaterandinnersurfaceoftheskull.Suchchangesareassociatedwithadangerousincreaseinintra-cranialpressure.
After being produced by the choroid plexus within the ventricles, CSF circulates through the ventricular system and flows through the foramina of Luschka and Magendie into the subarachnoid space, where it is absorbed by arachnoid granulations. The balance between rates of generation and resorption regulates CSF volume.
Hydrocephalus refers to an increase in the volume of the CSF within the ventricular system. This disorder most often is a consequence of impaired flow or decreased resorption of CSF. If there is a localized obstacle to CSF flow within the ventricular system, then a portion of the ventricles enlarges while the remainder does not. This pattern is referred to as noncommunicating hydrocephalus and most commonly is caused by masses obstructing the foramen of Monro or compressing the cerebral aqueduct. In communicating hydrocephalus, the entire ventricular system is enlarged; it is usually caused by reduced CSF resorption.
If hydrocephalus develops in infancy before closure of the cranial sutures, the head enlarges. Once the sutures fuse, hydrocephalus causes ventricular expansion and increased intracranial pressure, but no change in head circumference (
Fig. 23.3 ). In contrast to these disorders, in which increased CSF volume is the primary process, a compensatory increase in CSF volume (hydrocephalus ex vacuo) may occur secondary to a loss of brain volume from any underlying cause (e.g., infarction, neurodegenerative disease). In such settings, the hydrocephalus merely reflects the primary disorder and is of no clinical significance.
Herniation is the displacement of brain tissue from one compartment to another in response to increased intra-cranial pressure. The intra-cranial compartment is divided by rigid dural folds (falx and tentorium). If the pressure is sufficiently high, portions of the brain are displaced across these rigid structures. This herniation often leads to compromise of the blood supply to compressed tissue, producing infarction, additional swelling, and further herniation.
There are three main types of herniation (