This is a topic of current interest and various guidelines regarding return to play have been published. A summary from the American Academy of Neurology can be consulted (authored by Giza and colleagues) and as can an often cited consensus statement of the International Conference on Concussion (McCrory et al, 2009). The later-life development of dementia and other neurodegenerative conditions in professional athletes is also discussed further on. Many useful observations have emerged from study of athletes after head injury. Foremost among these observations is that athletes who have had concussion are more likely than other players to have another concussion in the same playing season (Guskiewicz et al); whether this is a reflection of incoordination or the person’s style of play, or another factor, is not known. Second, most prospective studies show a decline in reaction time and in other neuropsychologic tests after concussion, which returns to baseline over several days or weeks. Third, there is an indication from several series of concussions in National Collegiate Athletic Association and National Football League players that the number of recollected concussions is proportional to the degree of impairment on neuropsychologic tests (McCrea et al, 2003). Similar results have been found in other pursuits such as jockeying (Wall et al), but there are few adequate prospective studies.
The appropriate duration of removal from play has been the subject of numerous and largely arbitrary systems. The duration of loss of the initial symptoms of concussion and of amnesia was formerly a major component of the decision about return to play. Current guidelines focus instead on slowness in answering questions, uncertainty about plays or game assignments, slowed motor skills, and clumsiness, with or without loss of consciousness or amnesia. All such players are removed from the game. The basis of most rules has been an appropriate conservatism that requires the absence of cerebral symptoms both at rest and under graduated increased physical stress testing such as running or repetitive squatting. After medical evaluation, which may include imaging and neuropsychologic testing, a program of physical and cognitive “rest” is followed by graduated physical and mental activity under observation and a return to a lower level if symptoms occur (McCrory et al, 2003). Specifically, light aerobic exercise is followed by sport-specific training and noncontact, then contact, drills.
In contrast to concussion, in cases of traumatic brain injury that are fatal or very serious, the brain is contused, swollen, or lacerated, and there are hemorrhages, both meningeal and intracerebral, as well as hypoxic-ischemic lesions. A majority of patients who remain in a coma for more than 24 h after a head injury are found to have intracerebral hematomas and contusions. Of these lesions, the most frequent are contusions of the surface of the brain beneath the point of impact (coup lesion) and the sometimes more extensive lacerations and contusions on the side opposite the site of impact (contrecoup lesion), as shown in
Fig. 34-4. Blows to the front of the head may produce mainly coup lesions, whereas blows to the back of the head may cause mainly contrecoup lesions. Blows to the side of the head produce either coup or contrecoup lesions, or both. Irrespective of the site of the impact, the common sites of cerebral contusions are in the frontal and temporal lobes, as illustrated in Figs. 34-4 and 34-5. The inertia of the malleable brain—which causes it to be flung against the side of the skull that is struck, to be pulled away from the contralateral side, and to be impelled against bony promontories within the cranial cavity, explains these coup–contrecoup patterns. Relative sparing of the occipital lobes in coup–contrecoup injury has been explained by the smooth inner surface of the occipital bones and subadjacent tentorium, as pointed out by Courville.