Info

Space-Occupying Effects

Brain swelling is one of a wide variety of neurological conditions, among them tumors, hemorrhages, and ischemia/hypoxia, that can induce an increase in ICP. A rise in ICP leads not only to compression of the brain, but to diminished CSF volume, shifting, and herniation, as well as to secondary complications such as ischemia and hemorrhage. If not treated, ICP can rapidly progress to death due to brain stem compression secondary to cerebellar or uncal herniation (Meyer 1920). Focal expanding mass lesions must be distinguished from diffuse space-occupying processes.

— Diffuse brain lesions such as inflammation, bilateral intracranial hemorrhage, total brain ischemia (cardiac arrest) or intoxication are macro-scopically characterized (Fig. 4.2) by a tension of

Fig. 4.7a-d. Cell response to edema and beginning edema- astrocytic reaction whereby the sessile astrocytes contain al-

tous necrosis. a The first stage is characterized by a leuko- bumin (c), and the astrocytes increased in number upregulate cyte infiltration, the second stage (b) by an increase of mac- GFAP and vimentin (d) (a N-AS-DClAE, b, c albumin reactivity, rophages ingesting albumin and red cells in the case of a si- d GFAP reactivity; magnification a, d X300, b Xl,000, c X500) multaneous hemorrhage; c, d the last stage is marked by an

Fig. 4.7a-d. Cell response to edema and beginning edema- astrocytic reaction whereby the sessile astrocytes contain al-

tous necrosis. a The first stage is characterized by a leuko- bumin (c), and the astrocytes increased in number upregulate cyte infiltration, the second stage (b) by an increase of mac- GFAP and vimentin (d) (a N-AS-DClAE, b, c albumin reactivity, rophages ingesting albumin and red cells in the case of a si- d GFAP reactivity; magnification a, d X300, b Xl,000, c X500) multaneous hemorrhage; c, d the last stage is marked by an the dura, gyral flattening, and by narrow ventricles that are symmetrically compressed. No lateral shift of midline structures is seen, but rather central herniation of the diencephalon (centren-cephalic herniation) and by cerebellar tonsil-lar herniation and compression of the medulla oblongata. Bilateral herniation may occur and various types of herniation result from caudal displacement of the brain parenchyma (for types of herniation, see below).

— Focal intracranial processes such as abscess, tumor, infarction or subdural hemorrhage (Fig. 4.8a, b) are also capable of inducing a life-threatening homolateral rise in ICP. Because they allow time for intrinsic compensatory mechanisms to operate, particularly reduced CSF volume, slowly expanding focal lesions are less likely to cause an early increase in ICP and brain shift. However, the distortion and herniation of the brain in such cases can be considerable. Rapidly expanding focal lesions, by contrast, are more likely to produce an immediately elevated ICP. Brain death often supervenes in such cases before much distortion or herniation can occur.

Distortion of the brain results from compressive forces exerted by adjacent structures, which leads to overall expansion of the hemispheres. The dura mater may become so tense as to compress the terminal branches of the cerebral arteries, with consequent ischemic or hemorrhagic necrosis of cortical structures (Lindenberg 1955) or impairment of perfusion (Janzer and Friede 1979) accompanied by perisulcal infarcts.

Continued expansion of the mass may provoke contralateral displacement of the midline structures (see Chap. 7 and Fig. 4.8a). If the contralateral foramen of Monro is obliterated, the contralateral lateral ventricle may become enlarged, triggering a further rise in ICP. A lesion that expands in the frontal lobe may displace the free margin of the anterior part of the falx cerebri (Fig. 4.8a, d). If a lesion expands in the temporal lobe, a disproportionately pronounced shift of the third ventricle will occur (Fig. 4.8a), with upward displacement of the Sylvian fissure and neighboring branches of the middle cerebral artery.

Fig. 4.8a-e. Unilateral intracranial pressures. a Subdural hemorrhage on the left parietal lobe leads to a distinct shift (upper arrow) of the midline structures from left to right, which may be associated with a hemorrhage in the left cingulate gyrus and a left midbrain hemorrhage (lower arrow), b a hippocam-pal hemorrhage (arrows), as well as (c) a pontine hemorrhage;

d a hemorrhage in the upper frontal lobe may lead to a notch, a hemorrhage or a softening of the corpus callosum; e a rare tentorial displacement caused by an infratentorial space-occupying process is demonstrated by notches on the upper cerebellar surface (arrows)

Fig. 4.8a-e. Unilateral intracranial pressures. a Subdural hemorrhage on the left parietal lobe leads to a distinct shift (upper arrow) of the midline structures from left to right, which may be associated with a hemorrhage in the left cingulate gyrus and a left midbrain hemorrhage (lower arrow), b a hippocam-pal hemorrhage (arrows), as well as (c) a pontine hemorrhage;

d a hemorrhage in the upper frontal lobe may lead to a notch, a hemorrhage or a softening of the corpus callosum; e a rare tentorial displacement caused by an infratentorial space-occupying process is demonstrated by notches on the upper cerebellar surface (arrows)

Was this article helpful?

0 0
Booze Basher

Booze Basher

Get All The Support And Guidance You Need To Permanently STOP The Battle With Alcohol Once And For All. This Book Is One Of The Most Valuable Resources In The World When It Comes To Transformational Tools For Battling Booze Binges And Staying Alcohol-Free.

Get My Free Ebook


Post a comment