CPD - optometry, Uncategorized

Traumatic brain injury: diagnosis and management of vision impairment

At the completion of this article, the reader should be able to improve their management of patients with traumatic brain injury (TBI), including: 

  • Recognise the ocular conditions related to TBIs
  • Review assessment measures available to classify the level of TBI 
  • Be aware of the symptoms in patients suffering mild,  moderate and severe TBI.

Sight begins with the eyes, but the vision process takes place in the brain. In this overview of traumatic brain injury, DR SULTAN ALOTAIBI AND A/PROF MARIA MARKOULLI show that even a mild injury to the brain can have a significant impact on the processes involved in vision.

Sultan Alotaibi
School of Optometry and Vision Science, University of New South
Wales, Sydney, Australia
Optometry Department at the College of Applied Medical Science, King Saud University, Saudi Arabia

Maria Markoulli
PhD MOptom GradCertOcTher FBCLA FAAO
Associate Professor, Director of Learning & Teaching, and Academic
Lead, UNSW Dry Eye Clinic, School of Optometry and Vision Science
Deputy Editor, Clinical and Experimental Optometry
Board Member, The Optical Foundation
TFOS Ambassador

In the last months of 2022, a large portion of the planet was transfixed by the FIFA World Cup in Qatar. The skill shown by the players was nothing short of impressive, but one skill that impresses particularly is the ability to use one’s head to change the trajectory of the ball. As eyecare practitioners, it is natural to question whether the impact to the head, with force, on a regular basis, could have long-term consequences to vision and eye health, let alone general health. This is a question that is particularly pertinent for athletes playing higher-impact sports such as Australian and American football, rugby, boxing, cycling and even horseback riding.1 

When a sudden external force hurts the head, it can induce structural damage to the brain and cranial nerves, causing a change in brain function, and leading to immediate and long-term complications.2 This is traumatic brain injury (TBI). 

The complications associated with TBI include physical, behavioural, perceptual and cognitive problems, memory loss, gut dysmotility, and visual disorders.3,4,5 Management of TBI symptoms and complications requires collaboration between a team of medical specialists, including neurologists, physiotherapists, psychiatrists, endocrinologists and optometrists. For optometrists, awareness of TBI and its associated complications is necessary as they may play a vital role in not only managing visual symptoms, but also in improving the patient’s quality-of-life.

Definition and prevalence 

Several TBI definitions have been proposed.6 The most commonly used was proposed by the Centers for Disease Control and Prevention in the US, which define TBI as a “bump, blow or jolt to the head, or penetrating head injury, that results in disruption of the normal function of the brain”.7 TBI can occur as the result of falls, sports-related injuries, car accidents, assaults and blasts in war zones.7 The problem is widespread and increasing, with an estimated 70 million cases occurring annually around the globe, affecting different age groups.8,9 TBI produces a financial burden to the health system, patients, families and society, estimated to be around $AU530 billion annually.10 


Damage to brain tissue occurs in two stages, categorised as ‘primary’ and ‘secondary’ TBI. Primary TBI can be due to focal or diffuse injury,11 and takes place during the initial assault.12 Secondary TBI follows the primary TBI, when the patient’s status deteriorates over time as a result of cellular degeneration, axonal-cell body separation and biochemical cascade,13 leading to cerebral hypoxia, increased intracranial pressure and brain oedema.13,14 Focal injury refers to condensed damage due to either contusion or laceration in a single location, which also can be in multiple areas in the brain.12 Diffuse injury refers to scattered, or widespread, damage of axons, accompanied by diffuse vascular injury and brain swelling.12,13 Diffuse brain injury occurs as a result of the movement of the head during the insult, so specific parts of the brain move faster than others which causes tearing, stretching and induced compressive forces within the brain tissues.12 


Diagnosis of TBI is one of its challenges, especially in those with no visible head injury.15,16 It is primarily diagnosed in the emergency department by a combination of measures, including assessment of neurological function, body movement, consciousness and memory. Its severity can be determined using the Glasgow Coma Scale (Table 1),9 which assesses three aspects: eye-opening, best motor response and best verbal response. 

Table 1: Glasgow Coma Scale. 9 scores between 13 -15 are classified as ‘mild,’ between 9-12 are considered as ‘moderate’ and ≤ 8 is considered as ‘severe’ TBI.

Neuroimaging currently plays a major role, particularly in identifying those who require urgent intervention, despite the fact that it has the limitation of giving false results.17 TBI also can be classified based on the time of injury.18 Cases who had TBI within one month or less are classified as acute, while more than three months are considered chronic.18 

Symptoms and complications

Patients with TBI may suffer from various symptoms, including visual disorders. Awareness of these symptoms is essential. Those who have had mild TBI are usually misdiagnosed as there is often no apparent head injury.15 They may lose consciousness for a few seconds or minutes during the incident and may suffer from photophobia, headache, dizziness, confusion, fatigue, sleep disorders, tinnitus, depression and mood changes,19 cognitive impairment, and trouble with concentration, memory and thinking.6 

Patients with moderate and severe TBI may have the same symptoms with a higher degree of severity.6 In addition, they may also experience repeated vomiting, nausea, muscle spasm, pupil dilation, slurred speech, sleep paralysis, loss of sensation, sensitivity to light and sound and fluid leakage from the nose or the ear.6 These symptoms may resolve within 12 weeks after the injury, or persist for months or years.18 

Complications associated with TBI

Patients with TBI are also vulnerable to further complications, including strokes and neurodegenerative disease. Those with severe TBI have a higher mortality rate of 30 to 35% during the period of six months post-injury.20 Individuals who are exposed to multiple mild TBIs, such as sports players, may develop chronic traumatic encephalopathy.21 This term is used to describe brain degradation; there is no cure for chronic traumatic encephalopathy, it can only be diagnosed at autopsy by analysing brain sections. A separation of the brain and dura mater may also develop, leading to a breaking of bridging veins and causing an acute subdural hematoma.1 

As a third of the brain is involved in vision and visual perception,22 75% of patients with TBI have been reported to suffer from a wide range of visual and ocular complications, including visual acuity loss, visual field loss, photophobia, accommodative dysfunction, convergence insufficiency, nystagmus, abnormalities in eye movement, asthenopia and headache, diplopia, strabismus and cranial nerve palsies,23,24,25,26,27 in addition to ocular complications such as optic neuropathy or orbital trauma.28,29 

Visual acuity

Visual acuity loss is common after a head injury, and reports suggest that patients return to normal or close to normal vision after a few weeks.15,30 A study on those with differing severities of TBI found that the majority of patients maintained visual acuities of 6/18 or better.30 In the same report, those with
moderate-to-severe TBI were more likely to experience visual acuity loss,30 while in a separate large cohort study of individuals with TBI, a lack of association between severe visual acuity loss and severe TBI was reported.31 No light perception or total blindness is not common and is only found in those with more significant head injuries, such as blast injuries.15,30 

Visual field 

Visual field loss is a common issue in TBI, as patients usually have multiple intracranial lesions along the visual pathways resulting in various visual field defects.27 Patients with moderate-to-
severe TBI demonstrate a higher rate of visual field loss compared to those with mild TBI.27 Types of reported visual field loss include homonymous or nonhomonymous hemianopia, quadrantanopia, tunnel vision and central and paracentral scotoma.27 Management of visual field loss includes using optical aids such as prisms, visual restoration training and compensatory training.32 


Photophobia is a common sensory symptom accompanying TBI.33,34 Its prevalence is highest within the first week of the injury and declines to a steady level after three months.35 The pathophysiological reason is not understood, but recent work has linked photophobia to inflammation of the trigeminothalamic pathways.36 

To mitigate photophobia-related discomfort, test the patient’s response to light with different coloured glasses, then prescribe that colour for indoor tasks and dark glasses for outdoor activities.37 Also, dimming the light of electronic devices while using computers and electronic devices might help to minimise the symptoms.37 

Oculomotor dysfunction 

The oculomotor system comprises the eye muscles, their innervation by the 3rd, 4th and 6th cranial nerves and the pre-oculomotor centres in the brainstem with their tectal, neocortical and cerebellar afferent paths.38 The system stabilises eye position and controls its movement in order to preserve the image on the fovea at the highest resolution.39 

The oculomotor system stabilises eye position and controls its movement in order to preserve the image on the fovea at the highest resolution.(39)

Disruption to neuronal integrity due to TBI leads to oculomotor dysfunction13 as reported in 90% of TBI cases.40 This manifests as abnormalities in eye movement (saccades, pursuit, vergence, and vestibulo-ocular reflex). Oculomotor dysfunction can be assessed using The Craig Hospital Eye Evaluation Rating Scale (CHEERS).41 This is a grading scale that examines smooth pursuit, saccades, vestibular ocular reflex, vergence, fixation and nystagmus. A high score indicates significant impairment.42 Other tests such as vestibular/ocular motor screening can be applied as well, in addition to near-point convergence and visual motion sensitivity.43 

Saccades and pursuit

Saccades and pursuit eye movements are part of cognitive and motor processes and are commonly impaired following head injury.18,44 Symptoms include losing lines while reading and being unable to change fixation from one object to another or track moving objects.45 Saccades can be assessed by instructing the patient to fixate alternately on two objects.46 Pursuit accuracy is usually evaluated by moving an object manually in nine directions.47 

Saccade and pursuit measurements have been included in a proposed model of optometric vision care for those with TBI,48 and evaluation of their subtypes has been reported to may reflect different brain and cognitive functions.18,45 The antisaccade task, which is a saccadic eye movement away from a target, has been shown to correlate with the loss of the white matter in the splenium of the corpus callosum in acute mild TBI.49 

Another study examined six oculomotor tasks in asymptomatic participants, including eye fixation, reflexive saccades, antisaccades, memory-guided saccades, self-paced saccades, and circular and sinusoidal smooth pursuit, in conjunction with brain neuroimaging, and found a significant difference in three measures (antisaccade, self-paced saccade, and memory-guided saccade) between normal individuals and concussed participants, corresponding with neuroimaging findings.50 

Saccades and pursuit eye movement can be improved in those with TBI by applying occupational therapy using eye exercise protocols, such as The Six Eye Exercise protocol and Standard of Care protocol.42 These protocols use a remedial approach to improve the fixation, tracking, gaze stabilisation, spatial localisation, saccades, and vergence.42

Nystagmus and vestibular dysfunction

Nystagmus and symptoms of vestibular dysfunction,51 such as vertigo, feeling dizzy and unbalanced, were also reported in 50% of acute TBI cases.51,52 The function of the vestibulo-ocular system is to coordinate the head and eye movement. Assessment of that can be done using dynamic visual acuity. In this test, the best-corrected vision, with and without head movement, is compared. Losing more than two lines indicates vestibulo-ocular dysfunction.43 

Symptoms of vestibular dysfunction may resolve within 21 days in teenage years,43 and those with persistent symptoms may require further management. Vestibular rehabilitation therapy, provided by a vestibular physiotherapist, is recommended to enhance gaze and postural stability,53 mediate vertigo symptoms and to hasten patient recovery.52,53 

A ‘return to activity’ rehabilitation plan also can be developed in conjunction with other healthcare providers, involving continuous assessment of the condition, using a graded symptom checklist scale, a review of past medical history to identify risk factors associated with a prolonged recovery, cognitive testing, cranial nerve assessment, cervical range of motion, balance, gait, and vestibular testing.43 

Convergence insufficiency and accommodation dysfunction

Convergence insufficiency and accommodation dysfunction are also common manifestations of oculomotor dysfunction and have also been reported in mild TBI injury in 43.2% and 37.2%, respectively.27 Patients may experience difficulties in maintaining normal binocular vision and suffer from eye strain, fatigue and diplopia, accommodative spasm, unable to change their fixation from far to near, and blurred vision after changing their focus point, which affects their performance when doing regular daily life tasks, such as reading and driving.54 

Management involves using optical devices, including prisms, binocular occlusion, and computer gaming glasses. In addition, training and vision therapy with and without optical devices may also enhance the functionality and may improve the quality-of-life of the TBI patients.40 


Patients with TBI may be frequently encountered in optometric clinical practice. Their presentation may include visual and ocular symptoms. Optometrists play an important role as part of the team of medical specialists co-managing these patients. 

A key take-home message for optometrists is to enquire about patients’ hobbies and careers at every consultation. If the patient is at risk of TBI due to these activities, extra attention can be paid for any signs or symptoms. And if a patient presents with a pattern of symptoms suggestive of TBI, the optometrist can provide the needed eyecare, deliver vital information to the patient and refer them to TBI rehabilitation and other medical specialists. This will improve their care and treatment and provide higher-quality outcomes.  

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1.Mizobuchi Y, Nagahiro S. A Review of Sport-Related Head Injuries. Korean Journal of Neurotrauma. 2016; 12 (1): 1.

2. Bramlett HM, Dietrich WD. Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes. J Neurotrauma. 2015; 32 (23): 1834-48.

3. Marszał J, Bartochowska A, Gawęcki W, Wierzbicka M. Efficacy of surgical treatment in patients with post-traumatic facial nerve palsy. Otolaryngol Pol. 2021; 75 (4): 1-6.

4. Atkins EJ, Newman NJ, Biousse V. Post-traumatic visual loss. Rev Neurol Dis. 2008; 5 (2): 73-81.

5. Hanscom M, Loane DJ, Shea-Donohue T. Brain-gut axis dysfunction in the pathogenesis of traumatic brain injury. Journal of Clinical Investigation. 2021; 131 (12).

6. Injury. CotRotDoVAEfTB. Evaluation of the Disability Determination Process for Traumatic Brain Injury in Veterans.: national academics press; 2019.

7. Douglas DB, Ro T, Toffoli T, Krawchuk B, Muldermans J, Gullo J, et al. Neuroimaging of Traumatic Brain Injury. Med Sci (Basel). 2018; 7 (1).

8. Dewan MC, Rattani A, Gupta S, Baticulon RE, Hung Y-C, Punchak M, et al. Estimating the global incidence of traumatic brain injury. Journal of Neurosurgery. 2019; 130 (4): 1080-97.

9. Teasdale G, Jennett B. ASSESSMENT OF COMA AND IMPAIRED CONSCIOUSNESS: A Practical Scale. The Lancet. 1974; 304 (7872): 81-4.

10. Howe EI, Andelic N, Fure SCR, Røe C, Søberg HL, Hellstrøm T, et al. Cost-effectiveness analysis of combined cognitive and vocational rehabilitation in patients with mild-to-moderate TBI: results from a randomised controlled trial. BMC Health Services Research. 2022; 22 (1).

11. Huffman JC, Brennan MM, Smith FA, Stern TA. 19 – Patients with Neurologic Conditions I. Seizure Disorders (Including Nonepileptic Seizures), Cerebrovascular Disease, and Traumatic Brain Injury. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JF, editors. Massachusetts General Hospital Handbook of General Hospital Psychiatry (Sixth Edition). Saint Louis: W.B. Saunders; 2010. p. 237-53.

12. Andriessen TMJC, Jacobs B, Vos PE. Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury. Journal of Cellular and Molecular Medicine. 2010; 14 (10): 2381-92.

13. Armstrong RA. Visual problems associated with traumatic brain injury. Clinical and Experimental Optometry. 2018; 101 (6): 716-26.

14. Gabrielian L, Willshire LW, Helps SC, van den Heuvel C, Mathias J, Vink R. Intracranial pressure changes following traumatic brain injury in rats: lack of significant change in the absence of mass lesions or hypoxia. J Neurotrauma. 2011; 28 (10): 2103-11.

15. Hussain SF, Raza Z, Cash ATG, Zampieri T, Mazzoli RA, Kardon RH, et al. Traumatic brain injury and sight loss in military and veteran populations– a review. Military Medical Research. 2021; 8 (1).

16. Pozzato I, Meares S, Kifley A, Craig A, Gillett M, Vu KV, et al. Challenges in the acute identification of mild traumatic brain injuries: results from an emergency department surveillance study. BMJ Open. 2020; 10 (2):e034494.

17. Hier DB, Obafemi-Ajayi T, Thimgan MS, Olbricht GR, Azizi S, Allen B, et al. Blood biomarkers for mild traumatic brain injury: a selective review of unresolved issues. Biomarker Research. 2021; 9 (1):70.

18. Mani R, Asper L, Khuu SK. Deficits in saccades and smooth-pursuit eye movements in adults with traumatic brain injury: a systematic review and meta-analysis. Brain Injury. 2018; 32 (11): 1315-36.

19. Hellewell SC, Beaton CS, Welton T, Grieve SM. Characterising the Risk of Depression Following Mild Traumatic Brain Injury: A Meta-Analysis of the Literature Comparing Chronic mTBI to Non-mTBI Populations. Frontiers in Neurology. 2020; 11.

20. Baguley IJ, Nott MT, Howle AA, Simpson GK, Browne S, King AC, et al. Late mortality after severe traumatic brain injury in New South Wales: a multicentre study. Medical Journal of Australia. 2012; 196 (1): 40-5.

21. Kelly JP, Priemer DS, Perl DP, Filley CM. Sports Concussion and Chronic Traumatic Encephalopathy: Finding a Path Forward. Annals of Neurology. 2022.

22. Sheth BR, Young R. Two Visual Pathways in Primates Based on Sampling of Space: Exploitation and Exploration of Visual Information. Front Integr Neurosci. 2016; 10: 37.

23. Stelmack JA, Frith T, Van Koevering D, Rinne S, Stelmack TR. Visual function in patients followed at a Veterans Affairs polytrauma network site: an electronic medical record review. Optometry. 2009; 80 (8): 419-24.

24. 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.

25. Sabates NR, Gonce MA, Farris BK. Neuro-ophthalmological findings in closed head trauma. J Clin Neuroophthalmol. 1991;11(4):273-7.

26. Lew HL, Tanaka C, Pogoda TK, Hall JW. 50 – Auditory, Vestibular, and Visual Impairments. In: Cifu DX, editor. Braddom’s Physical Medicine and Rehabilitation (Sixth Edition). Philadelphia: Elsevier; 2021. p. 1101-20.e3.

27. 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. Optometry and Vision Science. 2019; 96 (8).

28. Qiu J, Boucher M, Conley G, Li Y, Zhang J, Morriss N, et al. Traumatic Brain Injury-Related Optic Nerve Damage. Journal of Neuropathology & Experimental Neurology. 2022; 81 (5): 344-55.

29. He C, Wieder M, Hamade M, Parsikia A, Mbekeani J. Ocular and Head Injuries Associated with Orbital Fractures. Investigative Ophthalmology & Visual Science. 2019; 60 (9):2 528-.

30. 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.

31. Flanagan G, Velez T, Gu W, Singman E. The Relationship Between Severe Visual Acuity Loss, Traumatic Brain Injuries, and Ocular Injuries in American Service Members From 2001 to 2015. Military Medicine. 2020; 185 (9-10): e1576-e83.

32. Lane A. Clinical treatment options for patients with homonymous visual field defects. Clinical Ophthalmology. 2008: 93.

33. Hoffman AN, Lam J, Hovda DA, Giza CC, Fanselow MS. Sensory sensitivity as a link between concussive traumatic brain injury and PTSD. Scientific Reports. 2019; 9 (1).

34. Theis J. Differential diagnosis and theories of pathophysiology of post-traumatic photophobia: A review. NeuroRehabilitation. 2022; 50 (3): 309-19.

35. Merezhinskaya N, Mallia RK, Park D, Millian-Morell L, Barker FM, II. Photophobia Associated with Traumatic Brain Injury: A Systematic Review and Meta-analysis. Optometry and Vision Science. 2021; 98 (8).

36. Diel RJ, Mehra D, Kardon R, Buse DC, Moulton E, Galor A. Photophobia: shared pathophysiology underlying dry eye disease, migraine and traumatic brain injury leading to central neuroplasticity of the trigeminothalamic pathway. Br J Ophthalmol. 2021; 105 (6): 751-60.

37. Clark J, Hasselfeld K, Bigsby K, Divine J. Colored Glasses to Mitigate Photophobia Symptoms Posttraumatic Brain Injury. Journal of Athletic Training. 2017; 52 (8): 725-9.

38. Voogd J. Anatomy of the oculomotor system. In: Sanders EACM, De Keizer RJW, Zee DS, editors. Eye Movement Disorders. Dordrecht: Springer Netherlands; 1987. p. 3-17.

39. Optican LM. Oculomotor System: Models. In: Squire LR, editor. Encyclopedia of Neuroscience. Oxford: Academic Press; 2009. p. 25-34.

40. Simpson-Jones ME, Hunt AW. Vision rehabilitation interventions following mild traumatic brain injury: a scoping review. Disability and Rehabilitation. 2019; 41 (18): 2206-22.

41. Politzer T, Berryman A, Rasavage K, Snell L, Weintraub A, Gerber DJ. The Craig Hospital Eye Evaluation Rating Scale (CHEERS). Pm r. 2017; 9 (5): 477-82.

42. Berryman A, Rasavage K, Politzer T, Gerber D. Oculomotor Treatment in Traumatic Brain Injury Rehabilitation: A Randomized Controlled Pilot Trial. The American Journal of Occupational Therapy. 2020; 74 (1): 7401185050p1-74.

43. Wallace B, Lifshitz J. Traumatic brain injury and vestibulo-ocular function: current challenges and future prospects. Eye and Brain. 2016; 8: 153-64.

44. Murray NG, Szekely B, Islas A, Munkasy B, Gore R, Berryhill M, et al. Smooth Pursuit and Saccades after Sport-Related Concussion. Journal of Neurotrauma. 2020; 37  (2):340-6.

45. Kapoor N, Ciuffreda KJ. Vision disturbances following traumatic brain injury. Current Treatment Options in Neurology. 2002; 4 (4): 271-80.

46. Ling MLH, Tynan D, Ruan CW, Lau FS, Spencer SKR, Agar A, et al. Assessment of Saccadic Velocity at the Bedside. Neuro-Ophthalmology. 2020; 44(2): 71-5.

47. Hirota M, Kato K, Fukushima M, Ikeda Y, Hayashi T, Mizota A. Analysis of smooth pursuit eye movements in a clinical context by tracking the target and eyes. Scientific Reports. 2022; 12 (1).

48. Ciuffreda K, Diana O, Ludlam D. Conceptual Model of Optometric Vision Care in Mild Traumatic Brain Injury. The Journal of Behavioral Optometry. 2011; 22.

49. Ting WK-C, Schweizer TA, Topolovec-Vranic J, Cusimano MD. Antisaccadic Eye Movements Are Correlated with Corpus Callosum White Matter Mean Diffusivity, Stroop Performance, and Symptom Burden in Mild Traumatic Brain Injury and Concussion. Frontiers in Neurology. 2016;6.

50. 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.

51. Marcus HJ, Paine H, Sargeant M, Wolstenholme S, Collins K, Marroney N, et al. Vestibular dysfunction in acute traumatic brain injury. Journal of Neurology. 2019; 266 (10): 2430-3.

52. Gurley JM, Hujsak BD, Kelly JL. Vestibular rehabilitation following mild traumatic brain injury. NeuroRehabilitation. 2013; 32 (3): 519-28.

53. Han BI, Song HS, Kim JS. Vestibular Rehabilitation Therapy: Review of Indications, Mechanisms, and Key Exercises. Journal of Clinical Neurology. 2011; 7 (4):184.

54. Schultheis MT, Whipple EK. Driving After Traumatic Brain Injury: Evaluation and Rehabilitation Interventions. Current Physical Medicine and Rehabilitation Reports. 2014; 2 (3): 176-83.

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