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2 to 10 min Hypertonic saline solutions (3 or 15%) are equally effective Urea is used less often and glycerol is not much favored in the United States because of its high caloric content, but it is used in Europe, largely because it can be taken orally on an outpatient basis A single administration of these solutes has only a short-lived effect, a matter of several hours or less as the brain extracellular space reaches an equilibrium concentration, but repeated use on a regular schedule can lead to a reduction in headache and stabilization of some of the deleterious effects of a mass Certain diuretic drugs, notably acetazolamide and furosemide, are said to be helpful in special instances (interstitial edema, pseudotumor cerebri) by virtue of creating a hyperosmolar state and by reducing the formation of CSF However, their effects are usually transient Aside from a diuresis, which may raise serum osmolality, highly permeable solutes such as glucose do little to reduce brain volume, since they do not create an osmolar gradient that moves 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; these agents are therefore 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 re ected 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 brain trauma with high ICP (see Chap 55), 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 Brain Displacements and Herniations (See also Chap 17) The problem of brain displacements and herniations is of vital importance in all mass lesions, and the underlying principles are particularly relevant to enlarging brain tumors The main aspects of this problem, particularly the coma-producing mechanisms, have been considered on page 310 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 wellknown herniations are: subfalcial, transtentorial, and cerebellar foramen magnum (see Fig 17-1), and there are several less familiar ones (upward cerebellar-tentorial, diencephalic sella turcica, and orbital frontal middle cranial fossa) Herniation of swollen brain through an opening in the calvarium, in relation to craniocerebral injury or operation, is yet another (transcalvarial) type As mentioned, the transtentorial herniations relating primarily to coma were discussed in Chap 17 Here, those that are often seen in cases of brain tumor are emphasized The writings of Meyer, Jefferson, and Kernohan may be consulted for the early descriptions of the herniations 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 is often occlusion of an anterior cerebral artery and frontal lobe infarction The cerebellar foramen magnum herniation or pressure cone, described by Cushing in 1917, consists of downward displacement of the inferior medial parts of the cerebellar hemispheres (mainly the ventral para occuli or tonsillae) through the foramen magnum, behind the cervical cord The displacement may be bilateral or, in the case of a onesided cerebellar lesion, ipsilateral Bilateral displacement may re-.

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sult from a centrally placed callosal-frontal tumor or from general swelling of the brain and is accompanied by downward displacement of the brainstem It may also be accompanied by bilateral temporal lobe tentorial herniations The clinical manifestations of downward cerebellar herniation 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 Other signs with subacutely evolving masses in the posterior fossa include pain in the neck, stiff neck, head tilt, and paresthesias in the shoulders, dysphagia, and loss of tendon re exes in the arms It is dif cult to determine which signs are due to the cerebellar herniation per se and which to the attendant effects of ICP and hydrocephalus We would suggest that head tilt, stiff neck, arching of the neck, and paresthesias over the shoulders are attributable to the herniation and that tonic extensor spasms of the limbs and body (so-called cerebellar ts) and coma are due to the compressive effects of the cerebellar lesion on medullary structures or of hydrocephalus on upper brainstem structures In any case, respiratory arrest is the most feared and often a fatal effect of medullary compression It may occur suddenly, without the additional aforementioned signs The herniated parts of the inferior cerebellum may undergo infarct necrosis and swelling, adding to the medullary compression With cerebellar mass lesions there may also be upward herniation of the cerebellum through the notch of the tentorium The clinical effects have not been clearly determined, but Cuneo and colleagues have attributed decerebrate posturing and pupillary changes initially both pupils are miotic but still reactive, progressing to anisocoria and enlargement to this type of brain displacement 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.

Now we ll step back into the 70 WAD to demonstrate the migration process Before we start, we need to look and make sure we don t see the 3x WAD template in the list of the 70 WAD templates The following illustrations show the process of logging onto the 70 WAD and then doing a search for the 3x version template within the 70 environment

of a certain type and is located in a particular region These localized growths create certain characteristic syndromes seldom caused by any other disease In the further exposition of this subject, intracranial tumors are considered in relation to these common modes of clinical presentation: Patients who present with focal cerebral signs and general impairment of cerebral function, headaches, or seizures 2 Patients who present with evidence of increased intracranial pressure 3 Patients who present with speci c intracranial tumor syndromes 1

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