Cerebral dysfunction from TBI occurs in two categories. The primary effect manifests within minutes to hours and is due to direct trauma to the neurons. This direct trauma causes diffuse axonal injury. The secondary effect, which appears hours to days following the injury, results from nerve edema, inflammation, and/or compression from surrounding swollen areas. The damage from the secondary effect can be more pronounced and long standing than the primary effect and may cause the many symptoms in mTBI [17–19]. The neural injury from mTBI is transient, though recovery from symptoms can take a few days to 6 months, and in some cases, a year or longer [20–22].

The image of the visual world is transmitted from the retina through the optic nerve to the occipital lobe in the cerebral cortex. Most connections are directed toward area V1, which is the primary visual cortex of the brain. Information is then relayed to higher visual cortical pathways ultimately splitting into one directed to the temporal lobe (“what” pathway) and the other directed to the parietal lobe (“where” pathway). The “what” pathway, also called the ventral stream, processes information regarding object recognition (i.e., form, shape, and color). The “where” pathway, also called the dorsal stream, processes information regarding visual action (i.e., motion, eye movements, visual attention, and spatial localization). A separate subcortical pathway communicates information from the eye to the midbrain (superior colliculus), and this processing stream relays information on eye movement, pupil control, and accommodation (eye’s ability to focus). Finally, the frontal cortex integrates information from the superior colliculus as well as the parietal, temporal, and occipital cortices. Visual information is processed by these centers in the human brain, and proper function is critical to integration of information; hence, disturbances across several cortical and subcortical regions lend individuals vulnerable to visual dysfunction after mTBI.

Since the effect of mTBI on the visual system is varied, tests incorporating multiple measures of visual function are necessary. Many of these tests can be excellent predictors of subtle cortical and subcortical changes in the brain from injury. Recently, a test incorporating eye movements, the King–Devick test (K–D), may be useful as a rapid screening tool in determining whether an athlete has suffered a concussion [23].

Visual complaints following concussion include blurry vision, difficulty focusing, light sensitivity, double vision, eyestrain, headache when reading, and difficulty reading. In addition, interactions between the visual and vestibular systems cause dizziness and motion sickness, especially in crowded environments. When these symptoms manifest, daily activities such as performance in sport and in school can be affected.

Early and accurate diagnosis is crucial as one of the current recommendations for concussion management is cognitive rest [3, 47–49]. Patients suspected of having concussion should undergo a standard battery of tests of the visual system, especially those with prolonged visual symptoms after the first 3–6 weeks. This evaluation is necessary as part of the diagnostic work-up but also as part of the approach to treatment. The visual exam needs to include tests that assess eye teaming, eye focusing, and eye tracking skills. Specifically, recent evidence suggests that near point of convergence, accommodative amplitude, and vergence and accommodative peak velocity yield the highest sensitivity in identifying vision-related deficits post-concussion [50]. This diagnostic evaluation needs to be performed by an eye-care provider versed in addressing binocular visual function. Pediatric optometrists and optometrists specializing in binocular vision eye exam are typically the most proficient in performing these exams, and they should be sought out to appropriately diagnose and manage these patients.