In all attempts to analyze the mechanisms of closed, or blunt (nonpenetrating), head injury, one fact is preeminent: there must be the sudden application of a physical force of considerable magnitude to the head. Unless the head is struck, the brain suffers no injury except in the rare instances of violent flexion–extension (whiplash) of the neck and possibly in explosion-blast injury with a sudden extreme increase of atmospheric pressure. In military medical practice, blast injuries assume great importance and in theory, challenge many concepts of loss of consciousness in closed head injury; that is, there is no contact with, or sudden acceleration or deceleration of the cranium. The mechanical factors of importance in brain injury are the differential mobility of the head on the neck, and of the brain within the cranium, the tethering of the upper brainstem that allows movement of the cerebral hemispheres around that vertex, and the striking of parts of the brain on dural septa and bony prominences. As to concussive injuries, it is useful to point out that concussions usually involve a physical force that imparts motion to the stationary head or more commonly, a hard surface that arrests the motion of a moving head, that is, concussion does not occur if the head remains entirely stationary. This sudden deceleration or acceleration of the cranium is the mechanism of most civilian head injuries, and they are notable in two respects: they may induce at least a temporary loss of consciousness, and the brain may suffer gross damage even though the skull is not penetrated, that is, contusion, laceration, hemorrhage, and swelling. In the past few decades, the definition of concussion has been expanded to include any neurological phenomenon that follows a strike to the head, as discussed further on, and there has been renewed interest in the degenerative brain changes that follow especially repeated concussion by years or decades. A theory that brings coherence to all of these physical and gross neuropathologic changes and their relation to concussion and coma has not been formulated. As mentioned in alter parts of the chapter, several degenerative neurological disorders have been attributed to repeated traumatic brain injury, the most prevalent of which seems to be “chronic traumatic encephalopathy” due to deposition of tau in the cortex. However, epidemiologic studies have been conflicting on whether other conditions are associated with prior head injury, for example, the report by Crane et al on 3 large prospective cohorts, in which only Lewy body disease and progression of
Parkinson disease were found to be associated. Other similar surveys came to different conclusions.
In contrast to closed head injury, high-velocity missiles penetrate the skull and cranial cavity, or rarely, the skull may be compressed between two converging forces that crush the brain without causing significant displacement of the head or the brain. In these circumstances, the patient may suffer severe and even fatal injury without preceding loss of consciousness. Hemorrhage, destruction of brain tissue, and, if the patient survives for a time, meningitis or abscess are the principal pathologic changes created by injuries of these types. They offer little difficulty to our understanding. Figure 34-1 illustrates these various types of head injuries.
The relation of skull fracture to brain injury has been viewed in changing perspective throughout the history of the subject. In the first half of the last century, fractures dominated the thinking of the medical profession, and cerebral lesions were regarded as secondary. Later, it became clear that the skull, although rigid, is still flexible enough to yield to a blow that injures the brain without causing fracture. Therefore, the presence of a fracture, although a rough measure of the force to which the brain has been exposed, is not an infallible index of the presence of cerebral injury (see further on in discussion of predictive features for imaging abnormalities with concussion). Even in immediately fatal head injuries, autopsy reveals an intact skull in 20 to 30 percent of cases. Of course, many patients suffer skull fractures without serious or prolonged disorder of cerebral function, partly because the energy of a blow is dissipated in the fracture. Indeed, this diffusion of the impact might be expected to reduce underlying brain damage.