Ophthalmic Manifestations, Evaluation, and Guidelines for Testing of Concussion

Ophthalmic Manifestations, Evaluation, and Guidelines for Testing of Concussion

The Open Ophthalmology Journal 10 Feb 2023 REVIEW ARTICLE DOI: 10.2174/18743641-v17-e230111-2022-43


Early detection and treatment of concussions is crucial to preventing further brain damage. Current subjective standard-of-care tests used to diagnose concussions, such as symptom reporting and standardized concussion checklists, can often underdiagnose patients with concussions. This review will cover novel biomarkers of concussions related to concussion-associated visual deficits and how they can be used to more accurately monitor patient concussion symptom improvement. Visual deficits are seen in up to 90% of patients within hours after a concussion-inducing trauma and can serve as objective biomarkers in diagnosing and monitoring concussions. Some of the key visual deficits that are seen in patients with concussions include convergence insufficiency, problems with accommodation and smooth pursuit of eye movements, saccade dysfunction, and decreased optokinetic nystagmus gain. Patients frequently report blurred vision, difficulty reading, double vision and eyestrain, dizziness, visual field defects, and light sensitivity related to concussions. Promising eye tests to detect and track concussions include pupillary light reflexes, the circle test, and the Samandarani group’s non-spatially calibrated binocular motility test/algorithm in conjunction with video oculography and eye tracking equipment. The EYE-SYNC eye-tracking device allows for portable and accurate detection of eye movements in the field and is a promising tool for detecting concussions both in the field and clinic. Optical coherence tomography and other retinal imaging modalities also represent a promising method of identifying individuals who have sustained a concussion.

Keywords: Concussion, Traumatic brain injury, Visual symptoms, Accommodation, Nystagmus, Convergence insufficiency, Saccades, Smooth pursuit movements, Concussion evaluation testing.


A concussion is a mild traumatic brain injury (mTBI) and results from trauma to the head or body, leading to either a loss of consciousness, memory, altered mental status, or neurological signs [1]. Concussions typically resolve within several weeks of the injury [2-5]. More serious sequelae can occur when the diagnosis is missed, and a second head injury occurs.

Several estimates based on emergency room admissions have shown that the incidence of concussions is about 3.8 million annually in the US [6-8]. However, the true concussion incidence is likely much higher than what is reported since many athletes continue to compete after sustaining a concussion and do not realize the extent of their injury [9]. Many sports-related concussions are diagnosed subjectively utilizing symptom checklists, standardized assessments of balance, sports concussion assessment tools, and the King-Devick test [10]. It is critical, however, to provide objective and accurate methods of detection of concussions to prevent the potentially serious complications of repeated concussions, including second impact syndrome, which can lead to life-threatening brain swelling [11]. In addition, repeated mTBI acutely can lead to longer recovery times and more severe physiological effects and neurocognitive outcomes [12, 13]. Chronic repeated concussions may result in cognitive dysfunction and even neurodegeneration [14].

In addition to neurological dysfunction, concussions, especially when repeated, can result in visual dysfunction. Even five years after experiencing mild TBI (concussion), veterans from the wars in Iraq and Afghanistan reported visual symptoms associated with the initial concussion [15]. In fact, between 40% and 90% of individuals with acquired brain injuries have eye movement deficits [16-18]. Visual symptoms are frequently seen in patients with concussions because over half of all brain circuits involve vision and eye movement [19]. Brain areas that regulate proper eye movement, such as the frontal lobe, parietal cortices, and subcortical nuclei, are particularly susceptible to damage from concussions [20, 21].

Due to the clinical relevance of eye findings in concussions, ophthalmic screening is an effective method for diagnosing and evaluating the progression and severity of patients presenting with concussions, due to their objective nature and potential ability to serve as concussion biomarkers. This paper describes the ophthalmic symptoms and signs associated with mild traumatic brain injuries (TBIs). Ophthalmologic testing and devices used to diagnose concussion are reviewed and evaluated for effectiveness and accuracy. Future modalities to identify early mTBI are reviewed.


A PubMed and Google Scholar search was done to find recent experimental research studies, case reports, and review papers on the topics of concussion, ophthalmic manifestations, and new technologies and screening methods. First, a search was done for current methods of concussion screening to evaluate the efficacy and accuracy of current tests, as well as to summarize the standard of care practices being used both in the clinic and on sports fields. Then, further searches were done to evaluate the most objective and accurate ophthalmic tests for concussion screening, with particular emphasis on new methods and screening techniques that have been used within the past five years. To evaluate the references, further searches were done on the techniques and devices reported to evaluate responses and criticisms, and the efficacy values of contrasting methods. Then based on those findings, more literature review was done showing links between concussion manifestations and optical coherence tomography, retinal imaging, as well as EYE SYNC, to further evaluate new approaches to accurately diagnosing concussions both in sports/field settings and in clinic settings that are not currently implemented but hold promise as diagnostic methods for the future.


Typical eye findings associated with concussions include convergence insufficiency, accommodation deficits, smooth pursuit abnormalities, saccadic dysfunction, and decreased optokinetic nystagmus gain [8, 10, 20, 22-25]. These deficits often result in symptoms of diplopia, decreased visual attention, blurred vision, asthenopia, ocular pain, and difficulty with accommodation, photophobia, abnormalities of color perception, pupillary abnormalities, abnormal eye tracking movements, and potential visual field defects [20, 26-28]. Despite large variability in the causes and degrees of traumatic brain injury, the incidence of visual symptoms in patients with concussions remains consistent and trackable over time [20, 26]. Examination of an acutely concussed patient should include near and distance acuity, identification of anisocoria, vestibulo-ocular reflex defects, slowed and reduced eye movement, convergence and/or accommodation defects, and assessment of peripheral visual fields [20, 29].

Accommodation involves focusing the eyes on a near object. This mechanism requires neural input from the visual cortex, brainstem, and ciliary muscles, and due to the large number of complex pathways involved, accommodation is highly susceptible to damage from trauma [20]. Clinical features of problems with accommodation include blurred vision, asthenopia, and difficulty seeing small print [28]. Across pediatric and adult populations, individuals with concussions had a significantly reduced capacity for accommodation [30]. A confounding factor for errors with accommodation is myopia, since there is commonly an accommodative lag with these patients [20].

Convergence is the inward movement of the eyes to maintain a binocular fixation on an object. This ability involves the visual cortex, parietal lobe, frontal eye fields, supra-oculomotor area and cerebellum [20]. The clinical manifestations of convergence dysfunction in patients with a concussion include double or blurred vision with prolonged close-up tasks [27, 31, 32]. 14-55% of patients with concussions have convergence abnormalities for at least a month after a mTBI [15, 27, 31-36].

Saccades are rapid eye movements between two fixation points, and abnormalities in saccadic eye movements may be the result of damage to the parietal, frontal, temporal, and caudate brain regions [37]. Up to 30% of patients that have concussions have saccadic dysfunction [27, 30, 33]. Compared to healthy controls, patients with concussions make more saccadic eye movements to complete number-naming tasks [38]. Furthermore, patients had impairments related to cortical saccadic tasks, particularly with memory-guided saccades and anti-saccades [39, 40]. Patients with a longer recovery time had greater saccadic dysfunction and made significantly more errors performing memory-guided saccades and anti-saccades that require high cognitive function [8, 41-43]. Patients with concussions also made significantly more position errors during memory-guided saccade tests [42, 43]. Some clinical manifestations of saccadic dysfunction include the increased time between target presentation and the start of the saccade, as well as dysmetria, resulting in difficulties reading and driving [20, 39, 40].

Smooth pursuit movements are used to keep an image steadily on the fovea [20]. Because this is another ocular movement that integrates many different regions of the brain, it is also susceptible to dysfunction from concussion. Patients with concussion experience difficulty following moving objects [29, 30]. In particular, patients have decreased target position, eye position errors, and low velocity gains, and their gaze trajectory is uneven when moving to a target. Visual tracking, which is the combination of smooth pursuit and saccadic eye movement that gives rise to visual stability and continuous observation of targets, is also impaired in patients with concussions [10].

Chronic mild traumatic brain injury has been demonstrated to lead to progressive neural degeneration demonstrated by retinal nerve fiber layer (RNFL) loss on Optical Coherence Tomography (OCT) in athletes and veterans [44, 45]. Mice with repeated mTBI exhibited decreased optic nerve diameter, and increased cellularity and demyelination compared to healthy controls [46]. Additionally, there were regions of decreased retinal ganglion cell layer and thinning of the inner retina [46].

In a study done of Division I football players that had sustained previous concussions, the retinal nerve fiber layer (RNFL) and the ganglion cell complex (GCC) both thickened, possibly as a result of immunological response and gliotic scarring [47, 48]. On the other hand, other studies have demonstrated RNFL thinning in athletes playing contact sports, as well as patients with Alzheimer’s Disease, suggesting RNFL damage [49, 50]. A study of retired Australian professional rugby league players demonstrated RNFL changes correlated with cerebral white matter loss and neurodegeneration [49]. Additionally, a study of Olympic boxers demonstrated RNFL thinning as compared to healthy controls [51].

Some rare and more serious visual disturbances related to traumatic brain injury include visual field anomalies such as homonymous hemianopia and quadrantanopia or cranial nerve palsy which could present as frank strabismus or more subtle diplopia in different fields of gaze [20, 26].


There are some currently established eye tests that are used in diagnosing concussions, such as the King-Devick test (K-D test). Other tests and diagnostic tools that are in development and are showing promise include video oculography and eye tracking.

The King-Devick (K-D) test evaluates eye movements while subjects have to read a series of numbers on scorecards as quickly as possible, minimizing the number of errors that they make [52]. The K-D test has high test-retest reliability and has been shown to accurately identify concussions in boxers and mixed martial arts fighters [52, 53]. For this test, patients read single-digit numbers aloud on test cards, and the time it takes to read all the numbers and the number of errors is recorded. When performing this test on the sidelines for football players before the season and after the season, individuals with no concussion had a 0.72 second improvement while subjects with concussions had a 5.9 second increase in their K-D time [52]. Individuals with concussions showed improvements in their K-D time score immediately after a two-hour scrimmage which suggests that this test is situationally-dependent to a degree [52]. The advantage of this test is its portability and adaptability for use in any environment. The disadvantage of this test is that it has approximately 75% sensitivity in detecting concussions, so it cannot be used alone to diagnose the condition [10, 53] or relied upon to determine if a player should be allowed to continue to participate in the athletic event.

Video oculography is a non-invasive technique that typically uses infrared cameras on a head mount to measure horizontal, vertical, and torsional eye movements, and can track pupils and corneal reflection [54]. This has proven to be an effective method for tracking visual symptoms associated with concussion, such as smooth pursuit and saccade deficiencies. Simultaneous measurements of pupils and corneal reflection have been validated as a biomarker for anticipatory neural activity, and can be useful in measuring visual tracking ability in patients with concussions [10, 55, 56]. This can be done by having patients look at a circular trajectory because of its predictable path while tracking their eye behavior [10]. This test is able to show concussion-associated defects in smooth pursuit tracking, increased reaction times and lower saccade velocities, decreased optokinetic nystagmus gain, phase error, root-mean-square error, as well as the variability in gaze position [23, 57, 58]. Visual tracking metrics had correlations up to 0.68 with concussion survey metrics that are the current standard of diagnosis for up to two weeks after the initial mTBI [59].

Video oculography is also used to track disconjugate gaze, as individuals with chronic symptoms of concussion have a significant decline in visual tracking abilities [55, 57]. The dysfunctions seen using video oculography were correlated with diffusion tensor imaging that showed white matter tract damage in the corona radiata and genu of the corpus callosum, which further correlated with attentional and working memory problems [10, 58].

The EYE-SYNC device has been commercialized for concussion detection, and it is able to quantify the dynamic visuomotor synchrony (DVS) of individuals’ gaze with the target during the predictive circular tracking task [55, 57]. Simultaneous measurements of pupils and corneal reflection have been validated as a biomarker for anticipatory neural activity, and can also prove to be useful in measuring visual tracking ability in patients with concussions [10, 55, 56] After developing the standard values and tracking longitudinal data for individuals for the EYE-SYNC, the Maruta group also showed a significant decline in DVS in patients that had concussions within two weeks of testing, and these DVS scores returned to normal values as patients recovered [56, 59]. However, studies with larger sample sizes will help to fully validate this technique.

Eye tracking helps detect saccadic and pursuit deficits that are often missed during complete eye examinations. Eye tracking can detect abnormal eye movements within several hours after a concussion and shows a worsening deficit for 1-2 weeks after injury but then an improvement and a gradual recovery over approximately one month [43, 60, 61]. However, some studies suggest that even six months after a concussion, individuals may have some saccadic and visual pursuit deficits [8, 42].

The Samandani group developed a non-spatially calibrated binocular motility test/algorithm that is able to detect disconjugate gaze in patients with concussions [60]. This new algorithm minimizes the limitations seen from previous eye tracking tests that were spatially calibrated, such as subject fatigue, misleading results due to visual and attentional deficits, and distraction [60, 61]. Patient levels of horizontal dysconjugacy correlated well with standard concussion metrics such as SCAT-3 and SAC scores, and went back to baseline after patients recovered [60]. In follow-up studies, this algorithm was shown to have 88% sensitivity and 87% specificity for identifying concussion [62]. However, there are criticisms from other groups that ocular disconjugacy is difficult to measure with spatially calibrated eye tracking equipment [63].

The smooth pursuit test and reflexive saccade tests were commonly used to evaluate concussions through eye-tracking equipment [43]. Areas of the brain that are involved in attention and executive function help regulate both of these types of movements. Additionally, the proportion of position errors an individual makes during a memory-guided saccade test is a sensitive enough measure to distinguish between patients who were suspected to have a concussion from healthy controls [42, 43]. This test involves the hippocampus and cerebellum as well as the ventral visual pathway, and it is possible that these eye findings occur due to individuals being unable to maintain a high cognitive load due to errors in encoding and retrieving information [43, 64].

Pupillometry can be effective in measuring both accommodation and convergence deficits in patients with mTBI. Pupil constriction percentage, constriction and dilation velocity, and peak dilation and constriction velocity were all significantly altered in patients exhibiting concussions [65, 66].

Accommodation can be tested both with specialized ophthalmic equipment such as the RAF Rule (for values of amplitude of accommodation) and by bringing text closer to the subject until it becomes blurry, and comparing that distance with healthy age-matched metrics [20]. Current clinical tools to measure accommodation, however, have several confounding errors related to reaction times, instrument design, refractive errors, and psychological factors [67]. Convergence is often tested by bringing an object closer to a patient’s eye, and clinicians will look for breaks in binocular fusion as seen as a divergence of an eye from the target or from a patient reporting diplopia [20]. It is possible to test saccadic eye movements by having patients move their eyes between two close targets, and a secondary eye movement adjustment suggests saccadic dysfunction [20]. However, saccades can be further evaluated using eye tracking equipment [66, 67], head-mounted saccadometers [68], or electrooculography, although this test has, for the most part, been replaced by video oculography [69-71]. The K-D test can also measure saccades, cognition, and attention abilities, and is typically used on the sidelines in sports. Smooth pursuit movement can be evaluated by having patients track an object across vertical and horizontal planes and measure the presence of any jerky movements or failures to follow the target.


Future modalities to detect traumatic brain injury include retinal imaging techniques. Retinal OCT may serve a useful purpose in the evaluation of concussions, both acute and chronic. Overall retinal nerve fiber layer loss is evident in veterans who have undergone traumatic brain injury [44]. OCT abnormalities are detectable in up to 53% of patients with mTBI that do not have any other visual deficits [45, 48]. Furthermore, since there is a correlation between retinal nerve fiber layer thinning shown on OCT with cerebral white matter loss on MRI, it is possible that OCT can be useful for monitoring the severity of a patients’ neurodegeneration as a result of repeated TBIs [49, 72, 73]. Veterans with chronic mTBI showed peripapillary retinal nerve fiber layer thinning related to traumatic optic neuropathy, as well as subfoveal choroidal thinning and retinal nerve fiber layer thinning [45]. More objective studies tracking patient concussion recovery course with OCT imaging is needed to evaluate more precise tissue changes using this modality, though.

Electroretinography of mice with repeated mTBI models has also shown a decrease in photopic negative response amplitude with no changes in timing or a and b wave amplitude [46]. Patients with mTBI and sports concussions show abnormal findings in the acute and nonacute injury stages [74]. In another study, there was a decrease in the OP3 component of ERG in a mouse model of repeated TBI which is possibly due to optic tract damage, though no other ERG changes were apparent in the mTBI mouse model [75]. Patients with mTBIs lacked photopic negative responses that were seen in ERGs from control patients, which suggests reduced plexiform layer function [76]. Furthermore, patients showing light sensitivity as a result of concussions showed shifted rod b-wave latency [76].

Additionally, retinal vessels serve as a marker of cerebral vascular changes, and there is evidence of an association between head injury and wider mean retinal venular caliber, as measured with Fundus photographs and computer-assisted techniques [77]. However, more studies are needed to validate these findings. Other modalities to evaluate the retinal vasculature may also be a future consideration, as studies have demonstrated TBI to be associated with quantifiable changes in the retinal vessels, including increased arterial and venous tortuosity [78].


To diagnose a concussion in the clinic, key recommendations include oculomotor, neurocognitive, pupillometry, and tracking retinal manifestations of concussions. A non-spatially calibrated binocular motility test to detect disconjugate gaze developed from the Samandani group can help track oculomotor dysfunction. Smooth pursuit and reflexive saccade tests using eye tracking equipment can measure simultaneous pupil and corneal reflection to detect delays with anticipatory activity and neurocognitive activity. The EYE-SYNC device, which is practical for use outside the clinic, can also help detect neurocognitive changes correlated with anticipatory activity. Video oculography and pupillometry can aid in detecting accommodation and convergence deficits, as well as smooth pursuit tracking errors, increased reaction times, lower saccade velocities, decreased optokinetic nystagmus gain, phase error, and root-mean-square error that are all associated with concussion-related defects. Additionally, ERG testing is an effective way of detecting functional deficits in retinal activity associated with concussions, such as decreases in the OP3 component of ERGs.

This article evaluated the current diagnostic knowledge in the field related to ophthalmic manifestations of concussions and synthesized recent findings in the field to develop guidelines for the most accurate and efficient ophthalmic testing both in the clinic and outside of the clinic. This review also emphasized novel approaches that can more objectively track ophthalmic and neurological changes related to concussions. This review synthesized previous findings to more accurately diagnose concussions and create a new set of recommendations for methods to best evaluate concussions. This paper was a review and synthesis of literature and did not include any retrospective or prospective experimentation in relation to the new set of diagnostic criteria for concussions and how it differs from current standard-of-care methods. The literature reviews and methodologies in this paper solely relied on the data reported from a conglomeration of studies related to the ophthalmic manifestations of concussions.


Concussions are a frequent result of head trauma and are particularly common with sports related activities that involve direct blows to the head. Although most signs and symptoms of concussions resolve in several weeks, a second concussion in the early phase can lead to a serious condition such as second impact syndrome, which can lead to life-threatening brain swelling, brain herniation, and death [79, 80]. In addition, repeated concussions can result in chronic neurodegenerative disease.

Thus, in a setting where a person experiencing head trauma may be exposed to a further head injury (especially in the setting of an athletic event), there is a need for methods to quickly, accurately, and correctly identify those individuals who have sustained a concussion. In such a manner, the risk of second impact syndrome can be reduced by quick identification of a concussion and proper restriction of further impact to the head.

This paper has demonstrated that ophthalmic presentations of signs of concussion are frequently present, including convergence insufficiency, accommodative defects, smooth pursuit abnormalities, and saccade dysfunction. We have also reviewed some of the current methods to detect ophthalmic signs of concussion, including examination by a trained professional, the King-Devick test, video oculography, the EYE-SYNC device, pupillometry, and the Sanaandani group binocular motility test. Future possibilities of retinal OCT, ERG, and retinal vascular imaging are being studied. It is important to be able to perform this testing on the field and off the field to correctly identify individuals who should immediately refrain from the possibility of a second impact along with its potential devastating consequences.


mTBI = mild Traumatic Brain Injury
RNFL = Retinal Nerve Fiber Layer
GCC = Ganglion Cell Complex
DVS = Dynamic Visuomotor Synchrony
K-D test = King-Devick test
OCT = Optical Coherence Tomography


Not applicable.




The authors declare no conflict of interest, financial or otherwise.


Declared none.


Decq P, Brauge D, Calmat A, et al. Diagnosis clinical criteria of sport related concussion: Toward an operational criteria definition in France. Neurochirurgie 2021; 67(3): 222-30.
Collins MW, Grindel SH, Lovell MR, et al. Relationship between concussion and neuropsychological performance in college football players. JAMA 1999; 282(10): 964-70.
Macciocchi SN, Barth JT, Alves W, Rimel RW, Jane JA. Neuropsychological functioning and recovery after mild head injury in collegiate athletes. Neurosurgery 1996; 39(3): 510-4.
McCrea M, Kelly JP, Randolph C, et al. Standardized assessment of concussion (SAC): on-site mental status evaluation of the athlete. J Head Trauma Rehabil 1998; 13(2): 27-35.
McCrea M, Guskiewicz KM, Marshall SW, et al. Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003; 290(19): 2556-63.
Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil 2006; 21(5): 375-8.
Meehan WP III, Micheli LJ. Preface. Clin Sports Med 2011; 30(1): xvii-xviii.
Ventura RE, Balcer LJ, Galetta SL, Rucker JC. Ocular motor assessment in concussion: Current status and future directions. J Neurol Sci 2016; 361: 79-86.
Torres DM, Galetta KM, Phillips HW, et al. Sports-related concussion: Anonymous survey of a collegiate cohort. Neurol Clin Pract 2013; 3(4): 279-87.
Sussman ES, Ho AL, Pendharkar AV, Ghajar J. Clinical evaluation of concussion: the evolving role of oculomotor assessments. Neurosurg Focus 2016; 40(4): E7.
Guskiewicz KM, Weaver NL, Padua DA, Garrett WE Jr. Epidemiology of concussion in collegiate and high school football players. Am J Sports Med 2000; 28(5): 643-50.
Giza CC, Choe MC, Barlow KM. Determining if rest is best after concussion. JAMA Neurol 2018; 75(4): 399-400.
Giza CC, Hovda DA. The new neurometabolic cascade of concussion. Neurosurgery 2014; 75 Suppl 4(0 4): S24-33.
Esopenko C, Levine B. Aging, neurodegenerative disease, and traumatic brain injury: the role of neuroimaging. J Neurotrauma 2015; 32(4): 209-20.
Urosevich TG, Boscarino JJ, Hoffman SN, et al. Visual dysfunction and associated co-morbidities as predictors of mild traumatic brain injury seen among veterans in non-va facilities: Implications for clinical practice. Mil Med 2018; 183(11-12): e564-70.
Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S. Occurrence of oculomotor dysfunctions in acquired brain injury: A retrospective analysis. Optometry 2007; 78(4): 155-61.
Hunt AW, Mah K, Reed N, Engel L, Keightley M. Oculomotor-based vision assessment in mild traumatic brain injury: A systematic review. J Head Trauma Rehabil 2016; 31(4): 252-61.
Kapoor N, Ciuffreda KJ, Han Y. Oculomotor rehabilitation in acquired brain injury: A case series11No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit on the author(s) or on any organization with which the author(s) is/are associated. Arch Phys Med Rehabil 2004; 85(10): 1667-78.
Felleman DJ, Van Essen DC. Distributed hierarchical processing in the primate cerebral cortex. Cereb Cortex 1991; 1(1): 1-47.
Gunasekaran P, Hodge C, Rose K, Fraser C. Persistent visual disturbances after concussion. Aust J Gen Pract 2019; 48(8): 531-6.
Mckee AC, Daneshvar DH. The neuropathology of traumatic brain injury. Handb Clin Neurol 2015; 127: 45-66.
Ellis MJ, Ritchie L, Cordingley D, Essig M, Mansouri B. Traumatic optic neuropathy. Curr Sports Med Rep 2016; 15(1): 27-32.
Kelly KM, Kiderman A, Akhavan S, et al. Oculomotor, vestibular, and reaction time effects of sports-related concussion: Video-oculography in assessing sports-related concussion. J Head Trauma Rehabil 2019; 34(3): 176-88.
Li Y, Singman E, McCulley T, Wu C, Daphalapurkar N. The biomechanics of indirect traumatic optic neuropathy using a computational head model with a biofidelic orbit. Front Neurol 2020; 11: 346.
Merezhinskaya N, Mallia RK, Park D, Bryden DW, Mathur K, Barker FM II. Visual deficits and dysfunctions associated with traumatic brain injury: a systematic review and meta-analysis. Optom Vis Sci 2019; 96(8): 542-55.
Armstrong RA. Visual problems associated with traumatic brain injury. Clin Exp Optom 2018; 101(6): 716-26.
Brahm KD, Wilgenburg HM, Kirby J, Ingalla S, Chang CY, Goodrich GL. Visual impairment and dysfunction in combat-injured servicemembers with traumatic brain injury. Optom Vis Sci 2009; 86(7): 817-25.
Daum KM. Accommodative dysfunction. Doc Ophthalmol 1983; 55(3): 177-98.
Greenwald BD, Kapoor N, Singh AD. Visual impairments in the first year after traumatic brain injury. Brain Inj 2012; 26(11): 1338-59.
Capó-Aponte JE, Urosevich TG, Temme LA, Tarbett AK, Sanghera NK. Visual dysfunctions and symptoms during the subacute stage of blast-induced mild traumatic brain injury. Mil Med 2012; 177(7): 804-13.
Gallaway M, Scheiman M, Mitchell GL. Vision therapy for post-concussion vision disorders. Optom Vis Sci 2017; 94(1): 68-73.
Howell DR, O’Brien MJ, Raghuram A, Shah AS, Meehan WP III. Near point of convergence and gait deficits in adolescents after sport-related concussion. Clin J Sport Med 2018; 28(3): 262-7.
Master CL, Scheiman M, Gallaway M, et al. Vision diagnoses are common after concussion in adolescents. Clin Pediatr (Phila) 2016; 55(3): 260-7.
Pearce KL, Sufrinko A, Lau BC, Henry L, Collins MW, Kontos AP. Near point of convergence after a sport-related concussion. Am J Sports Med 2015; 43(12): 3055-61.
Storey EP, Master SR, Lockyer JE, Podolak OE, Grady MF, Master CL. Near point of convergence after concussion in children. Optom Vis Sci 2017; 94(1): 96-100.
Vernau BT, Grady MF, Goodman A, et al. Oculomotor and neurocognitive assessment of youth ice hockey players: baseline associations and observations after concussion. Dev Neuropsychol 2015; 40(1): 7-11.
Diwakar M, Harrington DL, Maruta J, et al. Filling in the gaps: Anticipatory control of eye movements in chronic mild traumatic brain injury. Neuroimage Clin 2015; 8: 210-23.
Rizzo JR, Hudson TE, Dai W, et al. Rapid number naming in chronic concussion: Eye movements in the King–Devick test. Ann Clin Transl Neurol 2016; 3(10): 801-11.
Heitger MH, Anderson TJ, Jones RD, Dalrymple-Alford JC, Frampton CM, Ardagh MW. Eye movement and visuomotor arm movement deficits following mild closed head injury. Brain 2003; 127(3): 575-90.
Heitger MH, Jones RD, Macleod AD, Snell DL, Frampton CM, Anderson TJ. Impaired eye movements in post-concussion syndrome indicate suboptimal brain function beyond the influence of depression, malingering or intellectual ability. Brain 2009; 132(10): 2850-70.
Johnson B, Hallett M, Slobounov S. Follow-up evaluation of oculomotor performance with fMRI in the subacute phase of concussion. Neurology 2015; 85(13): 1163-6.
Johnson B, Zhang K, Hallett M, Slobounov S. Functional neuroimaging of acute oculomotor deficits in concussed athletes. Brain Imaging Behav 2015; 9(3): 564-73.
Snegireva N, Derman W, Patricios J, Welman KE. Eye tracking technology in sports-related concussion: a systematic review and meta-analysis. Physiol Meas 2018; 39(12): 12TR01.
Gilmore CS, Lim KO, Garvin MK, et al. Association of optical coherence tomography with longitudinal neurodegeneration in veterans with chronic mild traumatic brain injury. JAMA Netw Open 2020; 3(12): e2030824-.
Chan JW, Hills NK, Bakall B, Fernandez B. Indirect traumatic optic neuropathy in mild chronic traumatic brain injury. Invest Ophthalmol Vis Sci 2019; 60(6): 2005-11.
Tzekov R, Quezada A, Gautier M, et al. Repetitive mild traumatic brain injury causes optic nerve and retinal damage in a mouse model. J Neuropathol Exp Neurol 2014; 73(4): 345-61.
Kathryn Bigsby BB, Bigsby K, Hasselfeld K, et al. Retinal and balance changes based on concussion history: a study of division 1 football players. Int J Phys Med Rehabil 2014; 2(6)
Saliman NH, Belli A, Blanch RJ. Afferent visual manifestations of traumatic brain injury. J Neurotrauma 2021; 38(20): 2778-89.
Kelman JC, Hodge C, Stanwell P, Mustafic N, Fraser CL. Retinal nerve fibre changes in sports-related repetitive traumatic brain injury. Clin Exp Ophthalmol 2020; 48(2): 204-11.
Leong D, Morettin C, Messner LV, et al. Visual structure and function in collision sport athletes. J Neuroophthalmol 2018; 38(3): 285-91.
Childs C, Barker LA, Gage AMD, Loosemore M. Investigating possible retinal biomarkers of head trauma in Olympic boxers using optical coherence tomography. Eye Brain 2018; 10: 101-10.
Galetta KM, Brandes LE, Maki K, et al. The King–Devick test and sports-related concussion: Study of a rapid visual screening tool in a collegiate cohort. J Neurol Sci 2011; 309(1-2): 34-9.
Galetta KM, Barrett J, Allen M, et al. The King-Devick test as a determinant of head trauma and concussion in boxers and MMA fighters. Neurology 2011; 76(17): 1456-62.
Galetta KM, Morganroth J, Moehringer N, et al. Adding vision to concussion testing. J Neuroophthalmol 2015; 35(3): 235-41.
Debacker J, Ventura R, Galetta SL, Balcer LJ, Rucker JC. Neuro-ophthalmologic disorders following concussion. In: Hainline B, Stern RA, Eds. Handbook of Clinical Neurology. Elsevier 2018; Vol. 158: pp. 145-52.
Maruta J, Suh M, Niogi SN, Mukherjee P, Ghajar J. Visual tracking synchronization as a metric for concussion screening. J Head Trauma Rehabil 2010; 25(4): 293-305.
Maruta J, Heaton KJ, Kryskow EM, Maule AL, Ghajar J. Dynamic visuomotor synchronization: Quantification of predictive timing. Behav Res Methods 2013; 45(1): 289-300.
Maruta J, Ghajar J. Detecting eye movement abnormalities from concussion. Prog Neurol Surg 2014; 28: 226-33.
Maruta J, Spielman LA, Rajashekar U, Ghajar J. Association of visual tracking metrics with post-concussion symptomatology. Front Neurol 2018; 9: 611.
Sundaram V, Ding VY, Desai M, Lumba-Brown A, Little J. Reliable sideline ocular-motor assessment following exercise in healthy student athletes. J Sci Med Sport 2019; 22(12): 1287-91.
Samadani U, Ritlop R, Reyes M, et al. Eye tracking detects disconjugate eye movements associated with structural traumatic brain injury and concussion. J Neurotrauma 2015; 32(8): 548-56.
Samadani U. A new tool for monitoring brain function: eye tracking goes beyond assessing attention to measuring central nervous system physiology. Neural Regen Res 2015; 10(8): 1231-3.
Samadani U, Li M, Qian M, et al. Sensitivity and specificity of an eye movement tracking-based biomarker for concussion. Concussion 2016; 1(1): cnc.15.3.
Maruta J. Ocular disconjugacy cannot be measured without establishing a solid spatial reference. F1000 Res 2015; 4: 71-1.
Massendari D, Lisi M, Collins T, Cavanagh P. Memory-guided saccades show effect of a perceptual illusion whereas visually guided saccades do not. J Neurophysiol 2018; 119(1): 62-72.
Master CL, Podolak OE, Ciuffreda KJ, et al. Utility of pupillary light reflex metrics as a physiologic biomarker for adolescent sport-related concussion. JAMA Ophthalmol 2020; 138(11): 1135-41.
Burns DH, Allen PM, Edgar DF, Evans BJW. Sources of error in clinical measurement of the amplitude of accommodation. J Optom 2020; 13(1): 3-14.
Cifu DX, Wares JR, Hoke KW, Wetzel PA, Gitchel G, Carne W. Differential eye movements in mild traumatic brain injury versus normal controls. J Head Trauma Rehabil 2015; 30(1): 21-8.
Crevits L, Hanse MC, Tummers P, Van Maele G. Antisaccades and remembered saccades in mild traumatic brain injury. J Neurol 2000; 247(3): 179-82.
Mullen SJ, Yücel YH, Cusimano M, Schweizer TA, Oentoro A, Gupta N. Saccadic eye movements in mild traumatic brain injury: a pilot study. Can J Neurol Sci 2014; 41(1): 58-65.
Kraus MF, Little DM, Donnell AJ, Reilly JL, Simonian N, Sweeney JA. Oculomotor function in chronic traumatic brain injury. Cogn Behav Neurol 2007; 20(3): 170-8.
Mutlu U, Bonnemaijer PWM, Ikram MA, et al. Retinal neurodegeneration and brain MRI markers: the Rotterdam Study. Neurobiol Aging 2017; 60: 183-91.
Shi Z, Zheng H, Hu J, et al. Retinal nerve fiber layer thinning is associated with brain atrophy: A longitudinal study in nondemented older adults. Front Aging Neurosci 2019; 11: 69-9.
Gosselin N, Bottari C, Chen JK, et al. Evaluating the cognitive consequences of mild traumatic brain injury and concussion by using electrophysiology. Neurosurg Focus 2012; 33(6): E7-, 1-7.
Morriss NJ, Conley GM, Hodgson N, et al. Visual dysfunction after repetitive mild traumatic brain injury in a mouse model and ramifications on behavioral metrics. J Neurotrauma 2021; 38(20): 2881-95.
Tyler C, Likova L. Release of cone-rod suppression as a key mechanism for concussion-induced light sensitivity. Invest Ophthalmol Vis Sci 2018; 59(9): 4444-4.
Gopinath B, Liew G, Craig A, et al. Association between head injury and concussion with retinal vessel caliber. PLoS One 2018; 13(7): e0200441-.
Childs C, Ong YT, Zu MM, Aung PW, Cheung CY, Kuan WS. Retinal imaging. Eur J Emerg Med 2014; 21(5): 388-9.
Saunders RL, Harbaugh RE. The second impact in catastrophic contact-sports head trauma. JAMA 1984; 252(4): 538-9.
Bey T, Ostick B. Second impact syndrome. West J Emerg Med 2009; 10(1): 6-10.