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Pathology and Differentiation

The morphology of intracerebral hemorrhage depends on its localization and extent as well as the specific histological-cytological reaction elicited by it. The localization and extent of the hemorrhage depend on the severity of the effecting violence applied, and the cellular reaction on the survival time (see also pp. 190 ff). The ruptured vessel(s) sometimes can be detected morphologically by careful examination of serial sections. The detailed histological search for ruptured vessels is usually a frustrating process, since the vessels within the hemorrhage can often no longer be traced. If they are found, the rupture in the vessel wall will be associated with fibrin deposits, possibly also aneurismatic dilatation of vessels' walls and reactive cells, such as macrophages and hemosiderin-containing macrophages (cf. Krauland 1982).

Two important sets of criteria for discrimination between different causes of intracerebral hemorrhages bear emphasizing:

1. Primary mechanically caused hemorrhage versus spontaneous hemorrhage.

A primary mechanically caused hemorrhage is characterized by the following:

- The age, since younger patients rarely suffer hypertonic massive hemorrhages or hyalino-sis of the intracerebral vessels.

- Bruising of the scalp, indicating impact.

- The absence of pathological alteration of vascular walls (atherosclerosis, hyalinosis, etc.) and hemorrhagic diathesis.

- The presence of additional, unequivocally mechanically induced hemorrhage, e.g., cortical hemorrhages on gyral crests.

2. Primary mechanically caused hemorrhages versus secondary hemorrhages (i.e., delayed mechanically caused hemorrhage, see Gentleman et al. 1989). Often the primary mechanically induced hemorrhage will overlap with a secondary

Demyelinating Process The Brain

Fig. 9.15a, b. Myelin-containing macrophages (Luxol fast blue). b an increase of macrophages results from demyelination and a As a result of the ischemic process associated with a closed the macrophages will contain intracytoplasmic blue-colored my-brain injury demyelination takes place (magnification X100); elin (magnification Xl,000)

Fig. 9.15a, b. Myelin-containing macrophages (Luxol fast blue). b an increase of macrophages results from demyelination and a As a result of the ischemic process associated with a closed the macrophages will contain intracytoplasmic blue-colored my-brain injury demyelination takes place (magnification X100); elin (magnification Xl,000)

Fig. 9.16a-d. Lipid-containing macrophages (oil red O). The nification X500); c, d a maximum of fat-containing macrophages extent of lipid phagocytosis depends on the survival time after is demonstrated at the border zone of hemorrhagic necrosis the traumatic event. a Single lipophages are seen perivascularly (magnification c X300, d X100) (magnification X1,000); b several macrophages contain fat (mag-

Fig. 9.16a-d. Lipid-containing macrophages (oil red O). The nification X500); c, d a maximum of fat-containing macrophages extent of lipid phagocytosis depends on the survival time after is demonstrated at the border zone of hemorrhagic necrosis the traumatic event. a Single lipophages are seen perivascularly (magnification c X300, d X100) (magnification X1,000); b several macrophages contain fat (mag-

Fig. 9.17a-c. Hemosiderin-containing macrophages (Prussian blue reaction). a Very early ameboid-reactive macrophages containing erythrocytes and hemosiderin are seen (magnification X1000); b hemosiderin-reactive macrophages which are characterized by processes and have the features of resting microglia (magnification X500); c aggregated as well as diffusely distributed siderophages are demonstrated (magnification X50)

Fig. 9.17a-c. Hemosiderin-containing macrophages (Prussian blue reaction). a Very early ameboid-reactive macrophages containing erythrocytes and hemosiderin are seen (magnification X1000); b hemosiderin-reactive macrophages which are characterized by processes and have the features of resting microglia (magnification X500); c aggregated as well as diffusely distributed siderophages are demonstrated (magnification X50)

hemorrhage due to DIC, increased blood pressure, or decreased intracranial pressure resulting from a subsiding posttraumatic brain edema. For a primary mechanically caused hemorrhage the following additional criteria must be considered:

- Clinical observations: disease course free of acute worsening of cerebral symptoms in the absence of other plausible pathophysiological explanations.

- Clinical and pathological symptoms of a primary or secondary coagulopathy have to be ruled out.

- Histological changes on the margin of the hemorrhage as well as at the site of the vessel rupture (if found), which are consistent with the survival time.

3. Mechanically induced delayed apoplexy.

A form of secondary hemorrhage often mentioned in the literature is the so-called Bollinger's Spatapoplexie. If the primary injury is survived for weeks, months or years, hemorrhagic events can occur that obviously are causally linked to the initial trauma. Sometimes the link with the traumatic event must be assumed, although a direct causal connection cannot be confirmed. To do this however the following criteria must be met:

- The hemorrhage must originate from a vessel located near the original site of the injury. The cause can be, for example, a loading-induced aneurysm.

- Vascular disease capable of causing massive bleeding must be ruled out.

- Illness-related or estrogenic coagulation disturbances must also be excluded.

In an individual case, it can be exceedingly difficult to distinguish between a primary injury and delayed apoplexy.

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