Almost 10 million head injuries occur annually in the United States, about 20% of which are serious enough to cause brain damage. Among men <35 years, accidents, usually motor vehicle collisions, are the chief cause of death and >70% of these involve head injury. Furthermore, minor head injuries are so common that almost all physicians will be called upon to provide immediate care or to see patients who are suffering from various sequelae.
Medical personnel caring for head injury patients should be aware that (1) spinal injury often accompanies head injury, and care must be taken in handling the patient to prevent compression of the spinal cord due to instability of the spinal column; (2) intoxication is a common accompaniment of traumatic brain injury and, when appropriate, testing should be carried out for drugs and alcohol; and (3) additional injuries, including rupture of abdominal organs, may produce vascular collapse or respiratory distress that requires immediate attention.
This form of minor head injury refers to an immediate and transient loss of consciousness that is associated with a short period of amnesia. Many patients do not lose consciousness after a minor head injury but instead are dazed or confused, or feel stunned or “star struck.” Severe concussion may precipitate a brief convulsion or autonomic signs such as facial pallor, bradycardia, faintness with mild hypotension, or sluggish pupillary reaction, but most patients are quickly neurologically normal.
The mechanics of a typical concussion involve sudden deceleration of the head when hitting a blunt object. This creates an anterior-posterior movement of the brain within the skull due to inertia and rotation of the cerebral hemispheres on the relatively fixed upper brainstem. Loss of consciousness in concussion is believed to result from a transient electrophysiologic dysfunction of the reticular activating system in the upper midbrain that is at the site of rotation (Chap. 274).
Gross and light-microscopic changes in the brain are usually absent following concussion but biochemical and ultrastructural changes, such as mitochondrial ATP depletion and local disruption of the blood-brain barrier, are transient abnormalities. CT and MRI scans are usually normal; however, a small number of patients will be found to have a skull fracture, an intracranial hemorrhage, or brain contusion.
A brief period of both retrograde and anterograde amnesia is characteristic of concussion and it recedes rapidly in alert patients. Memory loss spans the moments before impact but may encompass the previous days or weeks (rarely months). With severe injuries, the extent of retrograde amnesia roughly correlates with the severity of injury. Memory is regained from the most distant to more recent memories, with islands of amnesia occasionally remaining. The mechanism of amnesia is not known. Hysterical posttraumatic amnesia is not uncommon after head injury and should be suspected when inexplicable behavioral abnormalities occur, such as recounting events that cannot be recalled on later testing, a bizarre affect, forgetting one's own name, or a persistent anterograde deficit that is excessive in comparison ...