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Edema

Local edema may be induced directly by cortical hemorrhage. Experimentally it could be shown that an impact load creates an immediate increase in the cerebral blood supply, followed a few minutes later by a drop in cerebral blood flow to one-third of its normal volume; normalization begins after 40 min (Nils-son and Nordstrom 1977). During the brief initial increase in cerebral blood flow the oxygen supply to the brain increases; but this does not compensate for the subsequent drop in blood flow however. Among the sequelae is a disturbance of the blood-brain barrier, attributable in part to vasomotor paralysis leading to vasodilatation and vasogenic edema.

The presence of edema (Richard 1991) can be easily detected by computed tomography as early as 20 min after an external traumatic event (Kobrine et al. 1977). The pathogenesis of trauma-induced cerebral edema is poorly understood, but microthrom-bosis and chemokine influences may play a role. Depending upon how severely the blood-brain barrier is disrupted and the extent of tissue destruction, elevated enzyme activity can be demonstrated in the cerebrospinal fluid (Liu et al. 1979). Likewise, the severity of injury determines the amount of increase in plasma catecholamine levels (Nayak et al. 1980). Like

Fig. 9.23a-d. Brain stem hemorrhage. a Primary brain stem ventricular tissue associated with intraventricular hemorrhage;

hemorrhage which is associated with fracture of the right part of d cystic alteration in a case with secondary midbrain hemorrhage the basal skull (primary contact injury); b acute secondary brain which was survived for several years stem hemorrhage in the center of the pons, as well as c in the peri-

Fig. 9.23a-d. Brain stem hemorrhage. a Primary brain stem ventricular tissue associated with intraventricular hemorrhage;

hemorrhage which is associated with fracture of the right part of d cystic alteration in a case with secondary midbrain hemorrhage the basal skull (primary contact injury); b acute secondary brain which was survived for several years stem hemorrhage in the center of the pons, as well as c in the peri-

hyperglycemia, glycosuria, and increased amino acid secretion, they can be attributed to mechanical loading of the hypothalamic region and brain stem.

There exists a close association between edema of one cerebral hemisphere and ipsilateral SDH. Diffuse edema of both central hemispheres tends to occur only in children and adolescents (Graham et al. 1989a). It is not known why some patients exhibit increased intracranial pressure due more to the congestion created by the paralysis-induced vasodila-

tation than to disturbance of barrier function (see Chap. 4, pp. 42 ff).

Secondary changes caused by edema can be more important for understanding the development of clinical signs, especially the psychopathology of the post-contusional syndrome (see p. 105) and of the fatal process, than the primary injury. Morphologically, secondary sequelae of edema are found in the following regions of the brain (see also pp. 51 ff):

Fig. 9.24a, b. Bilateral secondary hemorrhagic infarct of the pratentorial mechanically induced brain swelling, which causes a base of the temporal and occipital lobe caused by massive su- compression of the occipital cerebral artery

— In the mediobasal cortical areas of the temporal lobes ("Liebermeister's furrow," which is caused by a rise in supratentorial pressure).

— In the contralateral margins of the base of the cerebral peduncles due to supratentorial pressure on the tentorial notch produced by unilateral displacement; the localization is diagnosed clinically by the presence of homolateral pyramidal signs.

— At the top of the corpus callosum, notched by the free edge of the falx cerebri and - with lateral displacement - notching of the cingulate convolution, sometimes combined with hemorrhage in the crest of the cingulate gyrus.

— In the basal cortex of the temporal and/or occipital lobes (uni- or bilateral), with possible extension to all associated cortical areas of these two brain lobes as a hemorrhagic infarct attributable to transient (or incomplete) compression of the occipital cerebral artery (Fig. 9.24, see also Fig. 8.10).

— In the case of infratentorial pressure, on the dorsal surfaces of the cerebellar hemispheres notched by the free edges of the cerebellar tentorium.

— In the midbrain, necrosis and bleeding caused chiefly by venous congestion in the medial sections of the pons.

— On the cerebellar tonsils resulting from a rise in supra- and/or infratentorial pressure with necroses; the tonsils may be hemorrhagically infarcted or exhibit necrotic changes due to herniation (Oehmichen 1994).

— A special type of late white matter alteration is a demyelination (Fig. 9.25) which is caused by perifocal or traumatic edema. The edema may be associated with a mechanically caused hemorrhage.

9.4.2 Ischemia

MBI gives rise to neuronal loss in the hippocampus, cortex, thalamus, and cerebellum independent of the sites of hemorrhages (Kotapka et al. 1992; Ross et al. 1993). A bilateral loss of hippocampal neurons, for example, was observed in 85% (Kotapka et al. 1992) or 90% (Graham et al. 1978) of fatal head injury cases as early as 48 h post-wounding.

Morphological signs of ischemia are more common in the basal ganglia and hippocampal area than in the cerebellar or cerebral cortexes. In a significant proportion of cases the ischemia is due to poor post-accident management, i.e., impossibility of an adequate stabilization of circulation or delayed re

Fig. 9.25a-d. Demyelination caused by mechanical brain injury. a Close to the injury site there are schizogyric alterations, which are remnants of cortical hemorrhages in the frontobasal brain surface; b the demyelination is histologically seen, caused by

perifocal edema; c, d moreover a demyelinating process also occurs without a primary hemorrhage as a result of edema necrosis (b van Gieson stain, magnification x5)

Fig. 9.26a, b. Diffuse axonal injury as demonstrated by axonal swelling and axonal bulbs in the corpus callosum (a) and midbrain (b) (P-APP reactivity; magnification a x100, b x1,000)

lease of cerebral compression from intracerebral hematomas and/or failure to properly treat respiratory disturbances, cardiac arrest, status epilepticus (Graham et al. 1989b) or hypotonia. The main predictors of mortality 12 months post impact are the duration of hypotension, pyrexia, and hypoxia (Jones et al. 1994).

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