The autonomic nervous system (ANS) plays a vital role in maintaining and regulating homeostatic processes. ANS dysfunction has been reported in patients with moderate to severe traumatic brain injury (TBI), but its role in mild TBI (mTBI) is understudied. The objective of this review is to elucidate the role of ANS dysfunction following mTBI and the underlying pathophysiology specifically neuroinflammation, neurodegeneration, oxidative stress, and altered cerebral blood flow. ANS dysfunction is thought to be one of the many factors contributing to clinical features following mTBI including headache, anxiety, cognitive impairment, mood disorders, and sleep disturbances. The ANS has been shown to play a role in the production and regulation of pro-inflammatory molecules. ANS dysfunction most often results in exaggerated sympathetic neural activation (SNA) which contributes to neuroinflammation and oxidative stress. SNA is associated with the production of reactive oxygen species and subsequent neurodegeneration following mTBI. Additionally, changes in cerebral blood flow can be seen in patients with mTBI showing evidence of ANS dysfunction. No Level I studies have explored the relationship between mTBI and ANS dysfunction. Better understanding of the role of the ANS in mTBI will improve the evaluation and clinical management of mTBI by offering additional diagnostic and novel treatment strategies.