A text-book of pathology in relation to mental diseases / by W. Ford Robertson.

  • Robertson, W. Ford (William Ford), 1867-
Date:
1900
    may be few in number or numerous. The second variety is wliat I term the concentric body of the starch grain form (fig. 55). It is much smaller than the typical hyaline concentric body, though it like- wise varies considerably in size. It has usually an oval shape, which is also assumed by the one or two concentric markings that it com- monly shows. In hsematoxylin and eosin preparations concentric bodies of this kind stain of a violet colour, and liave an opaque appearance. Very rarely, however, a portion of their structure may be seen to have hyaline characters. Their general appearance sug- gests at once the simile of a starch grain. They are, as a rule, accompanied by much granular debris. Concentric bodies of the large hyaline form are much the more common. I have found them in 41 out of 60 duras examined microscopically. In some cases they are present in very large numbers. They may occur in groups or singly. They are by no means confined to the insane, though they certainly occur in such patients in far greater numbers than in the mentally sound, so far as I have seen. They may be found in duras that show practically no other morbid change. They are certainly most common in old people, but probably may form at any age. It is in senile insanity that they are found in greatest numbers. They occur chiefly at the inner surface, but also sometimes in the spaces that exist between the dura and the cranium. I have observed them only very occasionally in the deeper tissues of the dura. They occur also, and often in very large numbers, on the surface of the pia-arachnoid (especially in association with the milky change that is so common in this membrane in the insane), in the Pacchionian granulations, choroid plexuses, and endotheliomata of the dura, as well as in psammomata. Their occurrence has long been recognised by pathologists, but the earlier observers misunderstood their essential nature and origin. The following are some of their reactions:—They stain deeply with eosin and haematoxylin, generally showing a much greater affinity for the former when double staining with these dyes is employed. They also stain deeply with carmine and many of the aniline dyes. They are slightly darkened but not blackened by osmic acid, although occasionally this reagent may demonstrate the presence of a few fatty granules in them. They have a dark brown colour in silver preparations, exactly resembling that assumed by portions of the endothelial cell-plate. As they occur in the dura they are seldom affected by the action of mineral acids, but in some situa- tions, as in the choroid plexuses, they commonly contain carbonate of lime, on account of the presence of which an evolution of gas occurs. Findlay (56), who has recently given an excellent account of these formations as they occur in the choroid plexuses, states that
    it is necessary to use strong hydrochloric acid in order to obtain effervescence. Most of the older writers on the subject, including Obersteiner, have described concentric bodies as being composed essentially of carbonate and phosphate of lime, but it is now certain that calcareous infiltration is merely a secondary and comparatively unusual occur- rence. They essentially consist of hyaline degenerative material. Concentric bodies of the starch-grain form can be clearly traced from the nucleus of a single endothelial cell. They do not develop only from the surface cells, though these are probably their most common source. I have frequently observed them in the perivascular canals deep in the substance of the dura. The process of the development of hyaline concentric bodies is much more easily followed on the surface of the pia-arachnoid than on that of the dura, as in the former situation there are no rods of hyaline material to complicate the appearances. They develop on the surface of the pia-arachnoid as the result of a coalescence of certain of the endothelial cells that have undergone hyaline degenerative change, which is specially prone to occur in the proliferated cells that constitute granulations. The cell-plate becomes first affected, assuming a homogeneous appearance, and generally a slightly increased affinity for eosin in hsematoxylin and eosin preparations. The nucleus has at first an increased affinity for hsematoxylin, but as the morbid change advances it gradually loses this affinity, becoming homogeneous, and staining with eosin in the same way as the degenerated cell-plate, with which it ultimately blends. A homo- geneous globule is thus developed from a single endothelial cell. This may become a small concentric body, but more commonly, owing to the circumstance that several endothelial cells in a granulation are usually affected simultaneously, the hyaline globules developed from several adjacent endothelial cells coalesce into one large mass. This being apparently of a semi-fluid consistence assumes a spherical form. Concentric rings appear subsequently, evidently owing to shrinkage. In many developmental forms there is an irregular central mass which stains more deeply with eosin than the peripheral portion. It may be that this central mass corresponds to the nuclei of the degenerated cells, but the point is doubtful. This deeper staining of the central portion, as already indicated, is often maintained in the fully developed concentric body. It may be fairly conclusively demonstrated, and it may indeed be accepted as certain, that hyaline concentric bodies develop in the same way from the surface endothelial cells of the dura, and also occasionally from those of the perivascular canals (fig. 41). As in the pia-arachnoid, they develop specially from the localised aggregations of proliferated endothelial cells that form granu-
    lations. But there are other morbid appearances in the dura, evidently associated with the formation of concentric bodies, which cannot be explained so simply. Many of the hyaline rods already described show what appear to be transition forms in the development of concentric bodies. They evidently split across, the segments contracting into rounded masses. Some of the appearances presented are exceedingly difficult to interpret, and I am still uncertain as to the explanation of many of them. I think there can be little doubt that most of the hyaline rods that develop into concentric bodies, though in appearance identical with others that may often be traced into continuity with vessels, with dense strands of fibrous tissue, and even with fibrinous films on the surface, are those having their origin either (1) from a vitreous degeneration of the endothelial cells of a perivascular canal, as already described (a process which I have been able to trace clearly in one case); or (2) from the surface endothelial cells, the hyaline material developed from them having run together in the form of a rod instead of collecting into globular masses. The latter is the only explanation I could offer of such appearances in subdural false membranes as that shown in fig. 54. Histological evidence is, I think, strongly against their development in any instance from contracting fibrinous films and the obliterated new vessels that these often contain. From our early studies of the pathology of the dura, Dr Middlemass and I were led to maintain that these concentric bodies develop from dural capillaries that have undergone hyaline degeneration. While there is no doubt that we were wrong in regarding this as their typical mode of develop- ment, and although my own later observations led me to conclude that the opinion we had expressed was entirely erroneous, the recent obser- vations of Findlay (56) upon the changes in the tissues of the choroid plexuses, seem to prove that concentric bodies are capable of forming from vessels that have undergone hyaline degeneration. Therefore it cannot be excluded that hyaline concentric bodies occasionally develop from hyaline capillaries in the dura. I have never seen any evidence of retrogressive or disintegrative changes in these bodies. When once formed they seem to remain indefinitely. It may be, however, that some of the hyaline material is removed by leucocyte action. After a time a distinct fibrous cap- sule develops round them. (/) Mulberry bodies.—I have applied this name to certain curious structures that may occasionally be seen on the surface of the dura in superficial horizontal sections (fig. 56). They consist of groups of rounded or oval cells of a homogeneous appearance, which stain of a deep purple colour in hsemotoxylin and eosin preparations. The individual cells are pretty uniform in size, being about twice the
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    condition which, while it is very common in the insane, is com- paratively rare in the mentally sound. In the second class we have one that is probably almost as common in the mentally sound as in the insane. It will be most convenient to consider first the development of false membranes that are to be included in the latter class. The causes of the hfumorrhage are merely those that give rise to intra- cranial haemorrhage in general. Many of the larger effusions, which, however, are comparatively rare, have their source in a pial vein. The cases of this kind that I have seen have distinctly suggested that an important factor in leading to the rupture of the vessel was its partial obstruction by fibrous overgrowth of the tissues of the pia-arachnoid, where they join the dura at the side of the superior longitudinal sinus. As this condition of the pia-arachnoid is in its extreme degrees practically confined to the insane, haemorrhage from this cause may be almost special to them. The blood may also escape from a pial artery, an artery at the base, a venous sinus, an intra-cerebral vessel, or one near the inner surface of the dura. To take, for example, a fairly large haemorrhage, one of the first effects of the presence of the blood in the subdural space is to set up very active proliferation of the cells of the en- dothelium lining the subdural cavity. Many of the proliferated cells are shed and pass into the effusion, in which they may be afterwards recognised in large numbers. After a certain interval coagulation of the blood takes place. This commences on the walls of the subdural space, so that a white clot forms at the periphery and envelops the red clot which forms later. The peripheral white clot, probably mainly owing to the effects of pressure, often forms quite a dense membrane. In the case of small hsemorrhages the clot is spread out as a thin layer, the red portion occupying the central area, and the white appearing as a delicate surrounding film which gradually becomes more and more attenuated until it is lost to view on an apparently normal surface. The microscope reveals the fact that it extends much further than the unaided eye can trace it. If, as occasionally occurs, especially in chronic insanity, there is marked excess of fluid in the subdural space, the eff'used blood becomes mixed with it, and after a time its fibrin coagulates out upon the walls of the cavity, often forming a film which extends over the entire surface, including that of the spinal dura. At first the clot is not adherent to either wall. Very soon, however, new capillaries shoot out into it from the dura, so that vascular connections are formed by which it adheres to the outer wall of the space. Vessels very seldom penetrate it from the inner wall, for the reason that there are practically no capillaries near the outer surface of the pia-