A traumatic brain injury (TBI) refers to a brain injury caused by an external force. This may occur due to a forceful bump or blow to the head. TBI can be categorized as mild, moderate, or severe, with 80% of cases categorized as mild.1 The Centers for Disease Control and Prevention (CDC) estimates 2.5 million people sustain a traumatic brain injury annually.2
A TBI is composed of primary and secondary injuries. Primary injury is a mechanical event causing vascular structural and neural damage. This injury triggers a cascade of cellular events, including neuroinflammation, oxygen free radical generation, and raised intracranial pressure. These events are referred to as secondary injury.3 Primary injury is irreversible, while secondary injury prevention can improve outcomes.4,5
Presentation of traumatic brain injury
A TBI can present with a combination of signs and symptoms, such as confusion, headaches, memory loss, seizures, and vision changes (ex: diplopia, intermittent blurred vision).6
TBI patients may also experience visual-vestibular dysfunction such as:6
- Dizziness
- Vertigo
- Nausea
- Balance problems
- Increased motion sensitivity
This occurs due to abnormal function of the vestibular-ocular reflex (VOR) that controls gaze stabilization. The VOR stabilizes images on the retina during head movements by producing eye movements that are opposite to the direction of head movement.6
Dysfunction of the VOR may occur with damage to the semicircular canals in the ears, cranial nerves III, IV, VI, or VII.6 For these patients, a consultation for an ear, nose, and throat specialist may be warranted to rule out any additional or underlying pathology. An evaluation with a vestibular rehabilitation therapist may benefit patients to help improve balance or any dizziness.
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Acute TBI in Optometry Cheat Sheet
Use this cheat sheet to screen patients for traumatic brain injury with a red flags checklist and diagnostic testing scales.
A closer look at ocular manifestations of TBI
Vision changes may include blurry vision, photophobia, reading difficulties/eyestrain, diplopia, visual field defects, color vision changes, and vestibular dysfunction.6 TBI-related damage to the afferent pathway may include the optic nerve, optic tract, optic chiasm, optic radiation, or occipital cortex. Damage to any part of this pathway may result in decreased visual acuity.6
Photophobia
Photophobia is one of the most common complaints elicited in a TBI population.6,7 It may be more pronounced under specific conditions, such as indoor fluorescent lighting or present at all times. The underlying cause of photophobia remains unclear, but it is thought to occur due to alterations in the visual system’s ability to adapt to prolonged light or darkness.7
Abnormal critical flicker fusion frequency, the minimum light flicker frequency for an individual to perceive a steady presentation of light, may also be related to discomfort with fluorescent lighting in some patients.6 Management includes filters and tints.
Contrast sensitivity
A decrease in contrast sensitivity has also been found in those with a mild TBI but may improve months after injury.8 Contrast sensitivity charts such as the Pelli-Robson chart may help determine contrast sensitivity thresholds.
TBI may affect color perception by damaging the retina, optic nerve, and the parvocellular pathway through the optic tract and radiations.9 Treatments may include tints, filters and vision therapy.
Pupillary abnormality
Patients with a TBI are more likely to have a pupillary abnormality or reduced response compared to a normal population.10,11 This may occur due to elevated intracranial pressure.12
In addition, damage to the oculomotor nerve may present with pupillary dilation, the eye appearing down and out due to impairment in extraocular movement, and lid ptosis.13,14 This may occur due to a posterior communicating aneurysm or subdural hematoma.15 Non-reactive pupils are associated with poor prognosis.16
Other frequent ocular findings in TBI
- Blurry or decreased vision may occur following a TBI due to structural ocular changes or refractive error changes.6
- Altered tear film compositions may cause dry eye symptoms.
- Refractive changes may occur due to trauma to the cornea and crystalline lens, which may also contribute to accommodative dysfunction.
- Damage to the accommodative pathway or oculomotor nerve may also lead to accommodative dysfunction, producing symptoms such as blurry vision, visual fatigue, asthenopia, and headaches.6
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Addressing accommodative insufficiency
The most common TBI-related accommodative disorder is accommodative insufficiency.17 Accommodative insufficiency is found in approximately 40% of patients following traumatic brain injury.17
Other accommodative disorders may include accommodative infacility and pseudomyopia. Accommodative insufficiency may be treated with reading glasses and both accommodative infacility and insufficiency with accommodative rehabilitation.17
Both versional and vergence oculomotor dysfunction can occur in TBI patients. This may cause symptoms such as reduced reading speed and loss of place while reading. The King-Devick test can be administered in-clinic to identify impaired saccadic function.
Vision therapy and/or prism lenses may help patients with versional or oculomotor dysfunction. Vergence disorders may be noncomitant or comitant and may also occur with damage to cranial nerves III, IV, or VI. Symptoms of vergence disorders may include eyestrain, double vision, and headaches.6
The most common vergence dysfunction in TBI patients is convergence insufficiency as result from damage to the oculomotor nerve or medial rectus muscles.18 This can be managed with prism or vision therapy.
Managing visual field defects after a TBI
An array of visual field defects may occur following a TBI as a result of damage to any portion of the visual pathway from the visual cortex of the brain towards the retina.6
Defects may include:6,19
- A generalized decrease in sensitivity
- Isolated or multiple scattered defects
- Tunnel vision
- Central or paracentral scotoma
- Homonymous hemianopia with or without neglect (most common)
Symptoms of visual field defects include mobility issues, such as patients bumping into objects, reading difficulties, and trouble locating items in tasks of daily living. Peripheral prismatic lenses such as Peli lenses can help expand the visual field.
Figure 1: Visual field testing of a 14-year-old girl who sustained a mild TBI after fainting and sustaining trauma to the upper-temporal part of her right eyebrow.
- A: Humphrey visual field (HVF, threshold 24-2) of the right eye (RE) after a mild TBI and before starting visual therapy showing generalized loss of sensitivity.
- B: HVF 24-2 of the left eye (LE) after an mTBI and before starting visual therapy.
- C: HVF 24-2 of the RE after visual therapy showing generalized improvement in sensitivity.
- D: HVF 24-2 of the LE after visual therapy.
Figure 1: Mild TBI Visual Defect©Carmen López-de-la-Fuente et al. Image used under CC BY 4.0.
Rarer forms of visual impairment after TBI
TBI patients may also present with visual snow syndrome. Visual snow syndrome is a rare condition characterized by the appearance of persistent, pixelated flickering dots in front of the visual field.20 The pathophysiology of visual snow syndrome is not well understood.21 Treatment for it includes neuro-optometric rehabilitation therapy, prism, and tints/filters.22-24
It is estimated that the prevalence of traumatic optic neuropathy is 0.5 to 8% in TBI cases.25 A 2020 retrospective study from the Walter Reed Ocular Trauma Database found that optic nerve injury was significantly associated with TBI and poor visual outcome.26
Traumatic optic neuropathy may be classified as direct or indirect, with indirect being the most common.26 Direct is usually associated with direct injury to the optic nerve, causing severe and immediate vision loss, whereas indirect is due to non-penetrating impact trauma, such as concussion and orbital areas.
Conclusion
Patients who have suffered TBI can present with an array of systemic and ocular findings. A thorough patient history and a clinical exam can help identify these signs, allowing proper diagnosis and subsequent management.
Low vision rehabilitation and devices can provide significant benefits for these patients. Devices, such as hand-held magnifiers can enhance activities of daily living, while orientation and mobility training can reduce the risk of falls.
Ultimately, optometrists play a critical role in the interdisciplinary care of patients with TBI, often identifying subtle visual sequelae that significantly impact quality of life. Early recognition and targeted management of oculomotor, accommodative, and sensory deficits can meaningfully improve functional outcomes.
Collaboration with neurology, rehabilitation, and vestibular specialists is essential to ensure comprehensive care. As our understanding of TBI-related visual dysfunction continues to evolve, so too should our clinical approaches to optimize patient recovery and long-term visual performance.
