The Apoplectic Cavity

The Apoplectic Cavity is, in general capable of a still further reparative change, or decay (involution): viz., gradual contraction and finally closure - wasting of the apoplectic cyst.

This result ensues when the lining of the cyst is sufficiently penetrable to admit of the absorption of its fluid contents. The cyst becomes gradually smaller, especially in the diameter corresponding to the course of the fibres in its neighborhood: and its walls approach one another, and finally unite. The spot where the cyst has existed, is then generally marked by an elongated callus (apoplectic cicatrix), containing frequently, though, as I have already said, not constantly, a streak of pigment in its centre.

The period occupied by these different changes, up to the complete healing of the apoplectic cell, cannot be accurately determined. In general, it may perhaps be said, that the apoplectic cyst is formed within two or three months, but nothing is certain with reference to its subsequent changes and closure. These depend mostly on the size of the cyst.

I proceed to mention the most important of the conditions under which the shrinking and closure of the apoplectic cyst are impeded and entirely prevented.

a. Large cysts generally do not cicatrize; their size certainly diminishes more or less; but after this they generally remain permanently: there is, however, an occasional exception in the case of considerable contraction, and almost, and even quite, complete closure of very large cells.

b. Vascularity of the lining membrane of the apoplectic cyst appears to present an obstacle to this result, as it is not unlikely that a secretion of serous fluid may coexist with absorption.

It is, indeed, not improbable, that under such a condition the cyst may even become enlarged, as a consequence of the atrophy of the brain which follows an attack of apoplexy, and the congestion and increased secretion of the vascular lining resulting from the atrophy.

c. An especial and a permanent obstacle to the contraction and closure of the apoplectic cyst, is found in the fibrin being separated, while the extravasation is recent, in the form of a peripheral, or of a central, clot.

In the former case, the extravasation lies enclosed in a capsule of coagulated fibrin, colored red from admixture with the coloring matter of the blood, just as in the extravasations into the sac of the arachnoid. The changes already described go on in its interior; while externally, in the contiguous cerebral substance, the reactionary process advances to the formation of a callous wall. But the compactness of this capsule of fibrin renders absorption of its contents impossible, or, at least, very difficult; and the cavity is scarcely capable of any reduction in size. In the second case, the fibrin of the extravasation is coagulated into a solid, and generally rounded, mass. It is true, that a certain diminution in the size of the mass is then possible, partly by solution in the serous fluid surrounding it, and partly by the shrinking that attends its conversion into a fibrous tissue: the diminution, however, is not considerable, and occurs but very slowly, and the mass of fibrin offers a permanent obstacle to the complete closure of the cavity.

Such a separation of the fibrin could be expected only in an extravasation which is of large size and rapidly formed; and it is, in fact, only in large cavities that I have observed it. In the so-called capillary apoplexy, the clots are formed by repeated small hemorrhages occurring in different points, and gradually coalescing in a single cavity, and in it these unfavorable modes of separation of the fibrin into large coherent masses, are not likely to occur.

d. Apoplexy occurring at the surface of the brain (peripheral apoplexy), especially when extensive, scarcely ever terminates by a complete closure of the cavity.

The healing process, in these forms of apoplexy, is essentially the same as that already explained. Some differences arise simply from the locality: the walls of the cavity are, cerebral substance on one side, and pia mater on the other; and the callous induration also occupies both the pia mater and the cerebral wall. When the cortical substance is destroyed in its whole thickness by the hemorrhage, the white matter of the convolutions and that forming the grooves, partake of the induration. The lining of pigment also adheres both to the membranous and to the cerebral walls of the cavity. It is generally of greater thickness on the latter, and constitutes, as I believe, the "yellow plates of the convolutions" spoken of by Durand-Fardel. This observer attributes the disease in question to chronic softening (inflammation); and in a monograph which he has issued, he has unduly extended the sphere of inflammatory softening of the brain, and seems, moreover, to have altogether misunderstood peripheral hemorrhages of the brain and their results. In cavities of small extent, complete closure, by cohesion of their two walls, is not unfrequent; but larger ones, as has been already remarked, not only continue for a long time, or permanently, in the condition of the apoplectic cyst, but they become manifestly larger, and give rise at the same time to considerable atrophy of the brain. The cause of this unquestionably is, that the vascular structure composing the outer wall of the cavity, viz., the pia mater, becomes congested in consequence of the vacuum existing within the cranium, and serum exudes from its vessels into the cavity. In the situation of such cavities the membranous wall is seen projecting, in the form of pendent, fluctuating bags.