James M. Noble

John F. Crary


Concussion is a mild traumatic brain injury that has been recognized for centuries as an entity in accidents, battle, and sport. The visibility of higher profile cases of recurrent concussion in contact sports and growing concern of the potentially long-term impact of concussion, particularly among potentially vulnerable youth with developing brains, have brought concussion to the fore in recent years and perhaps rightfully so. In reflection of increasing concern, awareness, and research in the field, this chapter is the first version to appear into this established textbook.


The lifetime incidence of single and repeat concussion is not well known but is thought to occur in several million individuals annually in the United States alone. The epidemiology follows a trimodal pattern over lifetime with peaks in the first few months of life, followed by adolescence, and followed by a third peak in the elderly. Contributions to concussion etiology among the very young and very old likely principally relate to accidental falls, whereas concussions in adolescents may relate to risk-taking behaviors involving driving, exposure to violence, as well as exposure to increasingly competitive athletics. The annual incidence of SRC is at least 300,000 in the United States alone, although this is likely an underestimate given poor recognition by affected players. The epidemiology of recurrent concussion is not well described but is thought to happen in a small proportion of players previously affected by SRC.


Given that concussion patients generally have no evidence of structural brain injury using conventional neuroimaging with MRI or CT, concussion has historically been considered a physiologic alteration, but this has become a matter of some debate. Concussion may reflect substantial physiologic disturbance with significant microstructural axonal disruption, which remains difficult to detect but nonetheless occurs. These injuries may be widespread or alternatively relatively focal but involving pathways with major widespread clinical implications. Experimental models suggest metabolic changes including elevated tissue lactate, which peaks over the course of several days followed by gradual recovery of cerebral blood flow within the affected tissues, with most demonstrable changes resolving by 7 to 10 days. In response to rotational or translational shear physical stress, animal histopathologic models of concussion demonstrate disruption of the viscoelastic properties of axons with rare disruption or lysis of axons themselves (Fig. 45.1).

When considering an individual experiencing a single concussion, injury thresholds required to cause concussion are not well understood but are thought to occur following at least 60 g of
linear acceleration or at least 2,000 to 4,000 rad/s2 rotational acceleration; these forces are seldom if ever experienced in the course of normal daily life outside of recognized physically traumatic events experienced by the affected individuals. At present, risks for concussion occurrence, severity, and recurrence are not well understood but suggest prior traumatic brain injury raises the risk of subsequent concussion. The highly variable nature of concussion expression and recovery raises the possibility of an unrecognized gene-environment risk profile.

FIGURE 45.1 A: Conceptualized diagram of a human brain in coronal plane demonstrating brain inertia and distortion typical of rotational forces applied to the brain here during blunt impact to the lateral head causing rightward translational and rotational movement (curved arrowheads depict rotational force applied to the brain). Among myriad circumstances of brain injury, this example could occur during a hit to the left side of the head in the course of contact sports play. B: Physical simulations of intracranial brain deformation in response to linear versus rotational accelerations using 1% gelatin as a brain simulant, which has similar mechanical properties as brain. Linear accelerations cause very little deformation, whereas rotational accelerations induce marked central distortion. (Courtesy of Barclay Morrison, Associate Professor of Biomedical Engineering, Columbia University.)

Jul 27, 2016 | Posted by in NEUROLOGY | Comments Off on Concussion

Full access? Get Clinical Tree

Get Clinical Tree app for offline access