Cerebral infarction secondary to occlusive arterial disease.

Abstract

The classification adopted to describe the pathologic changes that occur in central nervous system infarction is that used by pathologists for identical lesions in all the organs of the body. Bland infarcts are of two forms. By far the more common in the central nervous system is the anemic type, in which the scant secondary hemorrhage is limited to the periphery of the area of necrosis. In contrast, in the far less common hemorrhagic infarct, the blood fills all or most of the area destroyed. The obstructing or occluding arterial lesions that result in the production of infarcts may be divided generally into three types that exist either singly or in combination. These are atherosclerosis of a significant vessel (usually associated with a drop in blood pressure), thrombosis, and embolism. Other causes of vascular occlusive disease are so rare that they will not be included in this discussion. When an anemic infarct is produced, softening and liquefaction gradually ensue, leading to early and progressive enlargement of the region infarcted. Although the beginnings of these changes are recognizable by the pathologist within six hours, the radiologist is most often confronted with an anemic infarct that is in the second or third week after occurrence. It is at this time that fluid attraction and cell infiltration within the necrotic region can produce a degree of enlargement that may result in the clinical appearance of an expanding mass lesion (Fig. 1). A roentgenogram of the skull taken during this period may disclose a shift of the pineal gland, and pneumoencephalograms a decrease in size of the adjoining arachnoid and ventricular spaces or even displacement of the ventricular system. As is to be expected, these changes are more likely to occur when the area of infarction is large. The diagnostic problems are sometimes compounded by an accompanying papilledema, usually of slight degree, and by signs of temporal lobe herniation (1). The period of progressive enlargement ends when the rate of removal of the necrotic contents exceeds the rate of attraction of fluid and reactive cells. This generally begins toward the end of the third week, although with older individuals there may be a slight shift in time toward the right, while in younger individuals the change may occur slightly earlier. The succeeding interval is characterized by a gradual decrease in the size of the infarct accompanied by a focal ex vacuo enlargement of the adjoining ventricular and subarachnoid spaces. Ordinarily the lining ependyma remains intact, separating the infarct cavity from the ventricle. Should loss of the ependyma occur, however, a localized ventricular dilatation, sometimes referred to as an acquired porencephalic cyst, will follow (Fig. 2). The story of hemorrhagic infarction is very similar to that of the anemic infarct, complicated only by the addition of variable degrees of bleeding.