Mechanism of concussion The core features of loss of consciousness or confusion are notable for being immediate after trauma (not delayed even by seconds) and for being largely reversible. This is the sense in which concussion was used to mean a reversible traumatic paralysis of nervous function and any physiologic explanation of the syndrome would have to incorporate this temporal sequence. However, the effects of concussion on brain function may last for a variable time (seconds, minutes, hours, or longer) and to set arbitrary limits on the duration of loss of symptoms, that is, to consider a brief loss as indicative of concussion and a prolonged loss as indicative of contusion or other traumatic cerebral lesion, is unsound physiologically. As pointed out by Symonds, any such difference is quantitative, not qualitative. It is true that in the more prolonged states of stupor or coma, there is a far greater chance of finding brain hemorrhage and contusion, which undoubtedly contribute to the persistence of coma and the likelihood of irreversible change. Finally, the optimal condition for the production of concussion, demonstrated originally by Denny-Brown and Russell, is a sudden change in the momentum of the head; that is, either movement is imparted to the stationary head by a blow or movement of the head is arrested by a hard, unyielding surface.
Rotational movements of the brain also provide a reasonable explanation for the occurrence of surface injuries in specific locations, that is, where the swirling brain comes into contact with bony prominences on the inner surface of the skull (petrous and orbital ridges, sphenoid wings), and of injuries to the corpus callosum, which is flung against the falx.
Not well explained by any of these mechanisms are concussions after blast injuries, a serious problem in military medicine. This syndrome possibly resurrects the notion that a shock wave travels through the brain and disrupts neural function throughout the cerebral hemispheres or in the reticular formation of the midbrain.
These views on the site and mechanism of concussion are not fully accepted but have been supported by a number of additional physiologic observations. Foltz and Schmidt, in 1956, suggested that the reticular formation of the upper brainstem was the anatomic site of concussive injury. They showed that in the concussed monkey, lemniscal sensory transmission through the brainstem was unaltered, but its effect in activating the reticular formation was blocked and that the electrical activity of the medial reticular formation was depressed for a longer time and more severely than that of the cerebral cortex.
What was further noteworthy in most of these cases, and in those reported by Jellinger and Seitelberger, was the presence of additional lesions in the region of the reticular activating system and small hemorrhagic softenings in the corpus callosum, superior cerebellar peduncles, and dorsolateral tegmentum of the midbrain. As discussed further on, Strich (1956) interpreted the extensive white matter lesions, both in the hemispheres and in the upper brainstem, to represent a degeneration of nerve fibers that had been stretched or torn by the shear stresses set up during rotational acceleration of the head, as had been postulated earlier by Holbourn. She suggested that if nerve fibers are stretched rather than torn, the lesions may be reversible and may play a part in the mechanism of concussion. Symonds elaborated on this view and saw in the shearing stresses, which are maximal at the point where the cerebral hemispheres rotate on the relatively fixed upper brainstem, the explanation of concussion.
How these mechanical factors relate directly to the transient confusion, ataxia, or visual impairment of concussion or to the later headache and difficulty with concentration that follow some concussions is not clear. Nor is it known how repeated concussion leads in some individuals to the deposition of tau and degenerative changes subsumed under the term “chronic traumatic encephalopathy” (see below).
Clinical Manifestations of Concussion