A system of practical medicine. By American authors. Vol. 5

by Unknown

The various subjects embraced in this article are so closely united to each other, both in a clinical and in a pathological point of view, that they must be considered to a certain extent in common. It is of course more systematic to group them entirely according to the obvious and final lesion, as hemorrhage, thrombosis, or embolism; but when it is considered how very closely the symptoms of one affection may counterfeit those of another—so closely, in fact, that a diagnosis with absolute certainty is not only difficult, but often impossible—and also that similar conditions of the vessels may give rise either to rupture or occlusion, so that not infrequently two sets of lesions may be found in the same brain, and, finally, that the basis of prognosis and of the later treatment is not unlike in different lesions,—we are surely justified in bringing them, at least in the beginning, under a common head.

Intracranial hemorrhage, and especially cerebral hemorrhage, is the lesion which more frequently than any other gives rise to the group of symptoms known as apoplexy, and from this fact has arisen the frequent incorrect application of the word apoplexy, in a pathological as well as a clinical sense, to indicate an extravasation of blood, as in the so-called pulmonary apoplexy, where the anatomical lesion, being an extensive effusion of blood into the tissues of the lung, bears an apparent resemblance to the state of the brain often found in apoplexy primarily and properly so called, the symptoms, however, being entirely different. This error receives additional support from the fact that in some injuries to the brain, especially to the base, pulmonary hemorrhage may secondarily take place. Apoplexy, however, is not always the result of hemorrhage, but occurs with many cases of embolism and of thrombosis, and is sometimes, so far as we can tell, dependent upon neither of these conditions, recovery in one set of cases taking place so rapidly as to preclude the supposition of a considerable organic lesion, and in others, which are fatal, nothing being found beyond an excess of serum or of vascularity, and sometimes not even that. The first of these conditions has been called simple apoplexy, but with our present knowledge its simplicity seems to border closely on ignorance, or at any rate is not of a character to satisfy the inquiring mind. It is therefore better to retain the term apoplexy strictly as a convenient term for a certain set of symptoms, but, whenever possible to substitute for it an anatomical description of the lesion found post-mortem or diagnosticated with reasonable probability during life.

The practitioner may very properly, and without laying himself open to criticism of his diagnostic accuracy, return the cause of death in a case of sudden death, or where his opportunity for observation has been limited, or where no post-mortem examination has been held, as being apoplexy; but in others, where the symptoms were decisive or a post-mortem has disclosed the exact lesion, the condition of the cranial contents should be stated. It is also a not uncommon mistake—or rather piece of carelessness—to speak of small hemorrhages in the brain as small apoplexies. A small extravasation may give rise to slight symptoms or next to none, but a real apoplexy can hardly be small, although it may be short.

The root from which the word apoplexy is derived seems to have been used by the classic writers in something like its present clinical signification (Απορληκτος, seized with (apoplexy or) stupor—Aristophanes; mad—Demosthenes; Αποπλησσομαι, to be struck with amazement—Sophocles). Morbus attonitus, another of its names, expresses a somewhat similar idea.

Morgagni was familiar with cerebral hemorrhage, and Bonetus in the Sepulchretum gives several cases. The allusions of Galen and Hippocrates supposed to refer to this lesion are not unequivocal, although the Father of medicine could hardly have helped being familiar with the symptoms of so striking a form of disease.

Cerebral softening has been recognized since the early part of the present century, and in some of the cases thirty years ago an efficient cause, in the form of arterial disease, assigned to it; but the complete theory of its causation forms a part of the general doctrine of embolism and thrombosis which was so largely developed and systematized by Virchow. Andral and Durand-Fardel had apparently no idea of the exact mechanism of its origin, the latter supposing it to depend upon inflammation, while Todd mentions a case where softening giving rise to paralysis depended upon a dissecting aneurism of the carotid. He seems to have generalized so far as to say that white softening is atrophic, but the precise way in which this localized atrophy was usually brought about evidently escaped him. According to him, the suddenness of the attack was owing to a gradual disorganization of the brain-substance with few or no symptoms, and then a sudden rupture of diseased fibres by some accidental cause or by their having reached the extreme limit of cohesion.

Intracranial hemorrhage may be situated outside of the dura mater, separating this membrane from the bones of the skull and producing more or less compression of the brain. It is usually the result of a blow, but not necessarily of a fracture of the skull. When a fracture is present, blood may pass through it from the interior and give rise to an external extravasation in addition to that which is likely to be the direct result of the blow upon the skin and subjacent soft parts. The middle meningeal artery is a frequent source of this hemorrhage. Hemorrhage in this position will naturally give rise to symptoms of compression, and, if the fact of the blow be not known or the fracture manifest, may be mistaken for some of the deeper-seated forms.

Blood may be effused upon the surface of the brain in the so-called cavity of the arachnoid—that is, outside of the pia mater—or in the meshes of this membrane, following its course along the sulci. This also is not infrequently the result of violence either with or without fracture of the bone. Its source is likely to be found in the veins which empty into the longitudinal sinus from the surface of the brain. Rupture of a lateral sinus from a not very severe blow has been the source of large and fatal hemorrhage.¹ Blows upon the head, with or without fracture of the cranial bones, are likely to cause rupture of the cerebral substance with hemorrhage, and this may find its way to the outside and cover more or less of the surface. Such injuries to the brain, it is important to note, do not necessarily correspond immediately to the place of the blow or to the external ecchymoses. Meningeal hemorrhage in this region may, however, be observed when no injury has been received, or at least when there is neither history nor external traces of any.

¹ Cincinnati Clinic, p. 135, 1874.