Highly permeable solutes such as glucose do little to reduce brain volume, as they do not create an osmolar gradient that shifts water from the brain to the vasculature. Furthermore, with repeated administration of hyperosmolar solutions such as mannitol or with diuretics, the brain gradually increases its osmolality—the result of added intracellular solute; thus these agents are not suitable for long-term use. The notion that hyperosmolar agents might exaggerate tissue shifts by shrinking normal brain tissue has not been substantiated. The net effect of hyperosmolar therapy is reflected roughly by the degree of hyperosmolarity and hypernatremia that is attained.
Controlled hyperventilation is another method of rapidly reducing brain volume by producing respiratory alkalosis and cerebral vasoconstriction; it is used mainly in cases of brain trauma with high ICP (see Chap. 34), during intracranial surgery, and in the management of patients who have become acutely comatose from the mass effect of a tumor, but its effect is brief.
Chap. 16)
An understanding of the effects of elevated intracranial pressure, localized vasogenic edema, and displacements of tissue and herniations are absolutely essential to understanding the clinical behavior of intracranial tumors and mass lesions of any type. Often the symptoms of intracranial tumors are related more to these effects than to invasion or destruction of neurologic structures by the tumor. The several “false localizing” signs (coma, unilateral or bilateral abducens palsy, pupillary changes, ipsilateral or bilateral corticospinal tract signs, etc.) are also attributable to these mechanical changes and tissue displacements. The main aspects of this problem, particularly the coma-producing mechanisms, were considered in Chap. 16. The pressure from a mass within any one dural compartment causes shifts or herniations of brain tissue to an adjacent compartment where the pressure is lower. The three well-known herniations are subfalcial, transtentorial, and cerebellar–foramen magnum (see Fig. 16-1), and there are several less familiar ones (upward cerebellar-tentorial, diencephalic–sella turcica, and orbital frontal–middle cranial fossa [transalar]). Herniation of swollen brain through an acquired defect in the calvarium, in relation to craniocerebral trauma or surgical craniotomy, is yet another (transcalvarial) type.
Subfalcial herniation, in which the cingulate gyrus is pushed under the falx, occurs frequently, but little is known of its clinical manifestations except that there may be occlusion of an anterior cerebral artery and resultant frontal lobe infarction. The cerebellar–foramen magnum herniation or pressure cone described by Cushing in 1917 consists of downward displacement of the inferomedial parts of the cerebellar hemispheres (mainly the ventral paraflocculi or tonsillae) through the foramen magnum, dorsolateral to the cervical cord. The clinical manifestations are less well delineated than those of the temporal lobe–tentorial herniation. Cushing considered the typical signs of cerebellar herniation to be episodic tonic extension and arching of the neck and back and extension and internal rotation of the limbs, with respiratory disturbances, cardiac irregularity (bradycardia or tachycardia), and loss of consciousness.