Common Pathophysiologic Complications

The enclosure of the brain and its coverings in the rigid box of the skull limit the potential for alterations of its volume. This renders the brain susceptible to interrelated pathophysiologic complications that occur in many different pathologic processes.

Any space-occupying lesion that is able to increase the volume of the intracranial contents is also able to produce increased intracranial pressure—for example, hemorrhage, infarct, tumor, cerebral abscess, cerebral diffuse or focal edema, and hydrocephalus.

The edema is either a correlate of the primary brain lesion, such as diffuse swelling due to cerebral hypoxia or due to severe head trauma, or it develops as a secondary perifocal edema surrounding focal brain lesions (e.g., due to hematoma, tumor, abscess, or filiae). The underlying mechanisms of cerebral edema can be divided into a cytotoxic and a vasogenic component. The most common form is the vasogenic edema. This results in an accumulation of a protein containing filtrate of plasma in the extracellular space that settles either on damaged capillaries that have lost their barrier function (infarcts and contusions) or on newly formed capillaries that have not yet established a barrier (primary or metastatic tumors). Predominantly the white matter is affected.

Cytotoxic edema is the accumulation of excess intracellular water that occurs in processes resulting in a breakdown of cerebral energy metabolism. Since the sodium/potassium pumps are altered in their function, this leads to a passive influx of sodium and water into the cells. This type of edema is more pronounced in the gray matter than in the white matter.

An internal hydrocephalus often occurs as a consequence of a focal brain edema with compression of the aqueduct (e.g., due to a cerebellar swelling caused by a "malignant" cerebellar infarction) or as a consequence of a blockage of the foramen of Monroi (e.g., due to compression of the third ventricle caused by a hemispherical swelling with a "midline shift'').

The interaction among the three processes of primary brain lesions, the (focal or diffuse) edema, and the potential development of a secondary hydro-cephalus is one of the most frequently encountered and potentially dangerous complications of CNS afflictions.

Depending on the size of the lesion and the acuity of expansion, there are initially three ways to compensate a potential increase in intracranial pressure. The volumes of CSF are reduced by enlarged resorption and reduced production, and the volumes of blood are reduced by vasoconstriction. These compensatory mechanisms allow the brain to expand without serious effects. Pressure-induced atrophy occurs most commonly with slow-growing extrinsic lesions.

After this phase, a critical period occurs in which a further increase in the intracranial contents will cause an abrupt increase in intracranial pressure. Further expansions lead to a shift of intracranial tissue, evident in the shift of midline structures, which is followed by herniation. Depending on the site of the space-occupying lesion, herniations occur mainly at characteristic sites (transtentorial, cerebellar tonsillar, and below the falx cerebri). Since vital respiratory centers in the medulla are compressed, transtentorial hernia-tions are a frequent cause of death.

The impact of brain lesions varies depending on different degrees of size, site, subcortical extent, and temporal evolution. Apart from the functional deficits within the lesion area, local brain lesions involve corticocortical connections as well as afferent and efferent cortical projections. They also affect functionally connected but structurally intact brain regions (diaschisis).

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