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Dating of Cortical Hemorrhages

Forensic practice often requires dating of contusional (and intracerebral) hemorrhages (cf. Müller 1930; Lindenberg and Freytag 1957; Krauland 1973;

Fig. 9.10a-d. Scar formation process. The end phase of reactiv- enous fibers (a, b van Gieson, c H&E, d Prussian blue reaction; ity is characterized by a cystic scar produced by glial and collag- magnification a-d x10)

Oehmichen and Raff 1980; Oehmichen et al. 1981; Oehmichen 1990; Hausmann 2002). A temporal classification is possible within certain limits based on neuronal degeneration and the leukocyte, glial cell, and mesenchymal reactions.

Analysis of more than 300 cases of mechanically induced cortical hemorrhage produced detailed statistical data regarding the individual phenomena, which will only be dealt with briefly here (cf. Oehmichen et al. 2003). The results may be transferred to timing problems in instances of intracerebral hemorrhages - within certain limitations. The temporal course is given in Table 9.4 and the following observations were made.

Primary mechanically induced hemorrhage is followed by three phenomena that occur simultaneously: (1) red blood cell flooding, (2) degeneration of neurons, axons, and white matter, and (3) emigration of leukocytes.

Red blood cells (Fig. 9.6) are the hallmarks of a vessel tear caused by mechanical injury. The degradation of the erythrocytes takes time and depends on the extent of the bleeding. Because of spontaneous rebleeding, which cannot be definitively ruled out, intact red blood cells are present for nearly 5 months after the initial blunt impact, but only in very rare cases.

The changes in the degenerating neurons (Fig. 9.14) consist of a cloudy swelling and/or a shrinkage and nuclear pyknosis. They become visible within the first few minutes after external violence to the brain. Ischemic nerve cell injury is uncommon. Over the ensuing hours and days, the neurons disappear, in part without a reaction, in part in the form of a satellitosis (after 4 h and 45 min at the earliest). Sometimes, however, they remain in loco and are mineralized in situ (ferruginated) for 6 days to several years.

Between 10 and 70 min after wounding, extravasal polymorphonuclear leukocytes (neutrophils) (Fig. 9.7) may appear within and around the hemorrhage. This phenomenon is especially conspicuous if perivascu-lar bleeding is accompanied by neuropil destruction, i.e., if the hemorrhages are associated with destruction of brain tissue at the site of impact. The earliest neutrophilic emigration is seen as a reactive process in contusion injuries associated with subarachnoid hemorrhage. The number of neutrophils decreases during the first 3 days after wounding.

Macrophages and/or activated microglia (Fig. 9.8) are seen within 11-12 h (Oehmichen 1978). Their number increases during the ensuing 7-14 days, then their numbers decline again. In many instances, macrophages can still be demonstrated in the vicinity of the scar tissue years later.

Fig. 9.11a-f. Scar formation process. a, b Endothelial proliferation associated with macrophages; c-f different stages of an in-

The behavior of lipid-containing macrophages over time is a function of the type of fat they contain (Oehmichen et al. 1986). The lipid within the macrophages is the result of myelin degradation. Using a myelin stain such as Luxol fast blue (Fig. 9.15) myelin-containing macrophages (Fig. 9.15b) are demonstrated. Intracellular neutral fat first appears 17 h post impact (Fig. 9.16a). Immunohistochemical demonstration of myelin debris (Lassmann 1997) can provide further information regarding the temporal course of the phagocytic process in brain macrophages.

1. In the acute phase of myelin breakdown, as a result of the traumatic event, the presence of im-munoreactivity for both myelin oligodendrocyte

crease of glial and collagenous fibers (a, d, e, f van Gieson stain; b, c Gomori stain; magnification a, b, d X500, c, e, f X100)

glycoprotein (MOG) and myelin-associated gly-coprotein (MAG) within macrophages is a reliable marker.

2. During the further digestion of myelin within macrophages the minor myelin proteins, such as MOG and MAG, are lost. The macrophages contain degradation products reactive for myelin basic protein (MBP) and proteolipid protein.

3. After 1-2 weeks, all myelin proteins have been degraded and macrophages contain only neutral lipids (Oil Red O). This stage may last up to 6 months. Other markers of early macrophage activation are the antigens 27E10 and MRP14 (Brück et al. 1995).

Fig. 9.12a-d. Macroscopic aspect of the final stages of cortical hemorrhages. a Cystic alteration of the left frontal pole with rust-colored mesenchymal tissue; b schizogyric alteration of the lateral parts of the right occipital, parietal, and temporal lobe; c cystic defect of the crest of the inferior temporal gyrus; d discrete color alteration at the crests of both the rectal and pararectal gyri as an indication of an old mechanically caused cortical hemorrhage

Fig. 9.12a-d. Macroscopic aspect of the final stages of cortical hemorrhages. a Cystic alteration of the left frontal pole with rust-colored mesenchymal tissue; b schizogyric alteration of the lateral parts of the right occipital, parietal, and temporal lobe; c cystic defect of the crest of the inferior temporal gyrus; d discrete color alteration at the crests of both the rectal and pararectal gyri as an indication of an old mechanically caused cortical hemorrhage

Hemosiderin-containing macrophages (Fig. 9.17) are easy to date since they almost always appear after 4-5 days, in rare cases after 3 days (Oehmichen 1976). Hematoidin as well as hematoidin-containing macrophages (Fig. 9.18) also follow a regular temporal course, becoming evident in frozen sections within 3-4 days, in paraffin sections after 12 days (Laiho 1995).

Some of the first signs of vital phenomena are alterations caused by axonal injury (Fig. 9.19), which can be demonstrated in single cases as early as 105 min after impact (Blumbergs et al. 1995) by expression of P-amyloid precursor protein (P-APP) by injured axons, and regularly after 3 h (in our own material after 2.75 h). The reperfusion during resuscitation may succeed in extraordinary cases to make axonal flow possible: in one case, a 20-min survival time was followed by a 90-min resuscitation attempt, which led to the incipient expression of P-APP in axons (personal observations; see also Gorrie et al. 2002).

As described by Zhao et al. (2003) astrocytes are marked by a loss of GFAP immunohistochemistry in rat ipsilateral hippocampal CA3 neurons within 30 min to 4 h after a traumatic event. Reactive astrocytes (Fig. 9.9) express GFAP and sometimes vimen-tin after only a 7-h survival time (Chen and Swanson 2003). Hypertrophic astrocytes can be demonstrated in the early days after wounding of the brain, in H&E-stained slides after several days. Primarily activated GFAP-expressing astrocytes evolve into fibrocytic astrocytes beginning on the sixth day post-impact, and by the conclusion of the degradation process they have formed a glial-mesenchymal scar.

Endothelial proliferation (Fig. 9.11) first becomes evident through the expression of proliferation markers on the third day after wounding. Collag-enous fibers and fibrosis (Fig. 9.10) appear during the first 5 days and increase over the ensuing weeks. They constitute the end product of the healing process, namely a cystic scar.

Fig. 9.13a-d. Mineralized astrocytes (a, b) and neurons (c, d) at the marginal zone of old brain wounds after MBI (a-d Prussian blue reaction; magnification a X200, b, c X500, d Xl,000)

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