Figure 33-39. Venous sinus thrombosis. Coronal (left) and sagittal (center) magnetic resonance venogram demonstrating absence of flow in the superior sagittal and left transverse sinuses (arrows). Note that the straight sinus and right transverse sinuses remain patent. Axial T2-FLAIR MRI shows left otomastoiditis, which was the cause of the extensive thrombosis. The clot can be seen in the MRI (right) (arrow).
Among the vast array of neurologic diseases, cerebral trauma ranks high in order of frequency and gravity. In the United States, trauma is the leading cause of death in persons younger than 45 years of age and more than half of these deaths are a result of head injuries. According to the American Trauma Society, an estimated 500,000 Americans are admitted to hospitals yearly following cerebral trauma; of these, 75,000 to 90,000 die and even larger numbers, most of them young and otherwise healthy, are left permanently disabled. Among adults over age 40, approximately 20 percent recall having had a head injury of any severity in their lifetimes (NHANES-Schneider A).
The basic problem in craniocerebral trauma is at once both simple and complex: simple because there is usually no difficulty in determining causation, namely, a blow to the head or in some cases a percussion wave from explosion, and complex because of a number of immediate and delayed effects to the brain and cranium that complicate the injury. As for the trauma itself, little can be done, for it is finished before the physician or others arrive on the scene. At most there can be an assessment of the full extent of the immediate cerebral injury, an evaluation of factors conducive to complications and further lesions, and the institution of measures to avoid additional problems. Specifically, the neck can be stabilized and adequate perfusion and particularly, oxygenation can be secured. New techniques of cellular biology are exposing phenomena that are set in motion by traumatic injury of nerve cells and glia. Some of these changes may be reversible, but at the moment, despite a large body of animal experimentation such knowledge is limited.
It is a common misconception that craniocerebral injuries are matters that concern only the neurosurgeon and not the general physician or neurologist. Actually, 80 percent of head injuries are first seen by a physician in an emergency department, and fewer than 20 percent ever require neurosurgical intervention of any kind, and even this number is decreasing. The neurologist must be familiar with the clinical manifestations and the natural course of primary brain injury and its complications and have a grasp of the underlying physiologic mechanisms. Such knowledge must also relate to the interpretation of CT and MRI, both of which have enhanced our ability to deal with traumatic brain injury. The present chapter reviews the salient facts concerning craniocerebral injuries and outlines a clinical approach that the authors have found useful over the years. Matters pertaining to spinal injuries, often coexistent with head trauma, are considered in Chap. 42.
The very language that one uses to discuss certain types of head injuries divulges a number of misconceptions inherited from previous generations of physicians. Certain terms have crept into the medical vocabulary and have been retained long after the ideas for which they stood have been refuted, attesting to the disadvantage of premature adoption of explanatory terms rather than descriptive ones. The word concussion, for example, implies a violent shaking or jarring of the brain and a resulting transient functional impairment. Yet despite numerous postulates of physical changes within nerve cells, axons, or myelin sheaths (vibration effects, formation of intracellular vacuoles) that putatively occur with concussion, confirmation of their existence has proved difficult in humans and experimental animals.