Mild traumatic brain injury, especially sport-related concussion, is common among young persons. Consequences of transient pathophysiologic dysfunction must be considered in the context of a developing or immature brain, as must the potential for an accumulation of damage with repeated exposure. This review summarizes the underlying neurometabolic cascade of concussion, with emphasis on the young brain in terms of acute pathophysiology, vulnerability, alterations in plasticity and activation, axonal injury, and cumulative risk from chronic, repetitive damage, and discusses their implications in the context of clinical care for the concussed youth, highlighting areas for future investigation.