The brain is protected from injury by moderate degrees of violence applied to the head, by the dense and mobile scalp, the dome-like shape of the skull, the elasticity of its outer table and the buffer-like sutural membrane between the numerous bones of which it is composed, and the various internal osseous projections with the membranes attached to them, all of which tend to diminish vibrations and to disperse forces so that they expend themselves before they reach the brain. Further protection is provided by the water-bed of cerebro-spinal fluid, and by the external buttresses formed by the zygomatic arch and the thick muscular pads related to it, as well as by the mobility of the skull upon the spine.
In all cases of head injury, the questions that dominate the whole clinical outlook are, whether the brain is directly damaged or not, and whether it is likely to become the seat of infection.
It is impossible to consider separately in their clinical aspects injuries of the cranium and injuries of the brain. It seldom happens that one is seriously damaged without the other suffering to a greater or less extent. Sometimes the skull suffers comparatively little, while the brain is severely damaged, but it is rare for a serious injury to the bone to be unaccompanied by definite brain lesions. In any case it is the damage to the brain, however slight, that gives to the injury its clinical importance. It is an old and a true saying that “no injury of the head is so trivial as to be despised or so serious as to be despaired of.” Injuries at first sight apparently slight may prove fatal from hæmorrhage or infection; on the other hand, recovery has followed injuries of great severity—for example, the famous “American crowbar case,” in which a bar of iron three and a half feet long and one and a half inches thick passed through the head, and yet the patient recovered.
It is convenient to consider the injuries of the brain before those of the skull.
Traumatic Lesions of the Brain
It is probable that in all cases of injury to the head in which a patient loses consciousness, there is some definite damage to the cerebral tissue. This takes the form of a greater or less degree of contusion or laceration, and the lesions are usually most severe and dangerous when the skull is fractured and fragments are driven in upon the brain, but they may exist—indeed they may be very extensive—in the absence of fracture.
Several degrees are recognised.
(1) Numerous minute petechial hæmorrhages may be found widely scattered throughout the brain substance, as a result of a diffused blow on the head, which has shaken up the brain and caused symptoms of cerebral shock or “concussion.” We have found, on microscopic examination in such cases, in addition to these small extravasations, collections of colloid bodies, patches of miliary sclerosis, and chromatolysis and vacuolation of nerve-cells.[3]
[3] Miles, Laboratory Reports, Royal College of Physicians, Edinburgh, vol. iv.
(2) In more severe cases there are often several visible areas of extravasation, most commonly in the grey matter of the cortex ([Fig. 184]). These foci vary in size from a split-pea to a hazel-nut, and consist of a dark central zone of extravasated blood, surrounded by an area of “red softening” of the brain matter, beyond which are numerous minute capillary hæmorrhages. These intra-cerebral lesions may be accompanied by an effusion of blood into the meshes of the arachno-pial membrane, and they may occur either at the part of the head struck, or at the opposite pole of the axis of percussion—the so-called point of contre-coup. The symptoms vary with the size and site of the extravasations. It is probable that the phenomena of “cerebral irritation” are to be explained by the occurrence of such hæmorrhages widely scattered through the cerebral cortex. Effusions into the cortical motor areas give rise to irritation or paralysis of the muscles governed by the affected centres. Different forms of aphasia and interference with vision or with hearing follow implication of the centres governing these functions. In the pre-frontal and in the lower temporal convolutions no special symptoms seem to follow. When the hæmorrhages are extensive and numerous, symptoms of compression may ensue, and these are aggravated when œdema of the brain is superadded.