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A concussion is a type of mild traumatic brain injury that is now at the forefront of both the academic literature and the lay media, with an ever-growing demand for more effective evaluation and treatment service systems, particularly in youth.1
Return-to-school after a concussion is a significant aspect of concussion management and, ultimately, requires an evidence-based, practical set of guidelines. This article addresses the foundation of the concept of "cognitive rest," the common treatment prescription. Understanding the injury's underlying pathophysiology sets the stage for an informed individualized treatment approach.
Although physical and cognitive "rest" have been recommended in the sports concussion literature for the past 10 years, more recently, cognitive rest has generated considerable confusion in terms of its rationale and its practical application.
During the past 10 years, animal models and human data in concussion have helped develop a better understanding of the reach of concussion and its metabolic and functional effects. The Centers for Disease Control and Prevention (CDC) defines a concussion as "a complex pathophysiologic process affecting the brain, induced by traumatic biomechanical forces secondary to direct or indirect forces to the head."
The blow to the head or body results in significant movement of the brain with shear strain disrupting its function due to changes in neurometabolism and neurotransmission. This disturbance of brain function is typically associated with normal head CT and MRI findings, as concussion does not typically result in structural damage to the brain tissue or blood vessels.
A constellation of physical, cognitive, emotional, and sleep symptoms ensues, infrequently involving loss of consciousness (less than 10% to 20%). The duration of these symptoms can vary widely from minutes to months, and even longer in a small number of cases.2
Fundamentally, an acute concussion can be viewed as a metabolic problem. After an acute injury, the metabolic needs of the neurons and axons are very high. Under normal conditions, mitochondria up-regulate production of adenosine triphosphate (ATP) to meet those metabolic demands. However, the concussion injury produces a neurometabolic cascade that results in impaired mitochondrial function.
In addition, fuel sources that generate ATP, such as glucose and, to a lesser degree, selected amino acids, are less bioavailable after a concussion, further compounding the problem. Shortly after a concussion, the...