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

  • Robertson, W. Ford (William Ford), 1867-
Date:
1900
    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
    ■1 MOEBID CONDITIONS OF THE DUKA MATEE 101 diameter of a red blood corpuscle. Each group usually has a com- paratively faintly-stained gelatinous capsule. Isolated cells with a similar capsule may occasionally be seen, but the mulberry form is the typical one. Eindlay (56) has traced these bodies in the choroid plexuses from single endothelial cells, and believes that the pathological alteration giving rise to them is one closely allied to hyaline degeneration. He further maintains that they develop into hyaline concentric bodies. {g) Granular patches in the fibrous tissue.—In superficial horizontal sections stained with haematoxylin and eosin there may frequently be seen, scattered over the surface, numerous small irregular patches which stain deeply with both dyes, and have an opaque and faintly granular appearance (fig. 11). They usually occur in the centre of the inter- vascular areas, suggesting that they result from imperfect nutrition. They are generally quite easily recognised under the low power. The connective tissue corpuscles of the part are fattily degenerated, and stain very faintly. Most of the granules outside of the cells do not, however, give a fatty reaction. Many of them stain deeply with eosin. The endothelial cells are generally denuded over these areas. "When present they usually show advanced vitreous degeneration. Similar patches may frequently be observed at a deeper level in horizontal or transverse sections. They are exceedingly common at the inner sur- face of duras from general hospital patients, as well as in those from the insane. A gross lesion, representing a further stage in this granular change, has been described by Dr Middlemass and myself (48). An example is shown in fig. 10, in which part of the degenerative material has undergone a hyaline change. These larger patches, which, however, are somewhat rare, are readily recognisable with the unaided eye, appearing as dark, opaque, slightly depressed spots, when the membrane is held up to the light. 3. The Morbid Processes concerned in Subdural False Membrane Formation. As already indicated, I maintain that in considering the morbid processes concerned in the formation of subdural false membranes, it is necessary at the outset to distinguish between two classes of cases that occur. In the first place, there is a class in which false membranes develop as the direct outcome of a widespread morbid process in the tissues of the dura itself; and, in the second place, there is a class in which they are formed as a result of a hemorrhage mto the subdural space, which takes place quite independently of this morbid process in the dura. In the first class we have a morbid
    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-
    arachnoid, from which it also tends to become separated as pre- viously described. The cerebral aspect of the clot becomes covered over with endothelial cells, continuous with those of the surface of the dura or pia-arachuoid at its margin. Thus the false membrane does not lead to the obliteration of any portion of the subdural cavity, but forms for it a new outer wall. The subsequent stages are practically identical with those of organisation of a thrombus in a vein, the clot, if vital processes continue, in time becoming entirely replaced by granulation tissue. In very large h£emorrhages the red clot in the centre is apt to break down before the process of organisation has reached it, and in this way a typical " arachnoid cyst" is produced. After false membranes formed by comparatively small haemorrhages have become vascularised, they closely resemble those that are pro- duced by the other morbid process presently to be described, and the further changes that may occur in them are also probably very similar. Coming now to what I regard as the special subdural false membrane formation of the insane, we have a process to consider which is in certain respects essentially the same as the preceding, but in others entirely different. It is the same, in that a part of it consists in the occurrence of haemorrhage into the subdural space, and all its consequences. It is different, in that it generally consists in the occurrence of multiple haemorrhages, in that these are due to definite morbid changes in the tissues of the dura (from which the blood is always effused), and in that it may result in the formation of a thin false membrane even without the occurrence of hemorrhage. It is to be understood, however, that no sharp distinction can be made between the two classes. They merge into one another, and there are many cases which cannot properly be wholly assigned to either group. Yet I think it will be evident presently that the classification is a scientific and necessary one. Before sketching this process, however, I must diverge for a moment to direct attention to a matter which, to my view, has very important bearings upon the pathology of subdural false membrane formation in the insane, but which does not seem to have been grasped by previous writers on the subject. I think that it can be shown that, with very few exceptions, all the false membranes found ill the subdural space of the insane are the development of a few days preceding death. Of the 18 subdural membranes from the insane examined microscopically in the course of a systematic research upon this subject, only 3 showed a structure of fully-developed granula- tion tissue. All the others showed a basis of fibrin threads, which pointed to a very recent origin. To these 15 cases there have to be added 13 others in which there was microscopic evidence of the
    presence of false membranes of a fibrinous structure, giving a total of 28 cases out of 31 in which the false membrane was undoubtedly of recent development. The appearances presented by the other 28 subdural membranes that occurred in my cases, but which were not examined microscopically, were such as to warrant, when taken in conjunction with the results of the microscopic examination of similar false membranes, the conclusion that they also were, with only one or two exceptions, of very recent growth. Many of them, as already stated, were simply recent blood-clots. Moreover, the accounts given of the naked-eye appearances of subdural membranes by various writers, e.g. Wiglesworth (40 and 41), are in most instances clearly descriptions of membranes mainly of a fibrinous character. Numerous more recent occasional observations of my own have tended to confirm the opinion that these formations are mostly of a fibrinous nature. It seems to me, therefore, that the great majority of the false mem- branes that occur in the subdural space of the insane are formed in the course of a few days or a few hours preceding death. In the general hospital cases examined (putting aside 5 in which there was head injury), it was found that in 9 out of 15 there was either naked-eye or microscopic evidence of haemorrhage (often ex- ceedingly slight) having occurred from the vessels of the dura very shortly before death. Now, since in several cases new capillaries had begun to shoot into these recent effusions, they cannot be entirely attributed to the severe congestion attending an asphyxial mode of death. Therefore I think we must further recognise that there are certain factors furnished by the moribund condition which predispose to haemorrhage from the dura in all patients. These factors are, I believe, merely the fatty and other molecular changes that occur in the walls of the dural vessels in common with many other tissues of the body, to some extent in the last stages of practically all diseases not resulting in sudden death, but especially in acute illnesses attended with high temperatures, and in the last stages of chronic diseases, towards the termination of which there is prolonged and great bodily enfeeblement. At the same time, we have to account for the undoubted fact that subdural false membranes appreciable to the unaided eye are far more frequently met with at post-mortem examinations upon the insane than at those upon general hospital patients. Erom the investigations I have made, I conclude that this is due to the circumstance that the insane are specially prone to a chronic morbid condition of the dura mater, on account of which these same pathological factors which cause htemorrhages from the dural vessels in the mentally sound shortly before death, make their influence felt in them at a much earlier sta^e and to a much more marked degree. This chronic