Navigating the Link Between Concussions and Glaucoma

A concussion, also known as a mild traumatic brain injury (mTBI), occurs when a plausible mechanism of injury results in an external force that induces a physiological disruption of brain function. The mechanism may be direct trauma from the head being hit by or striking an object or indirect trauma from the brain undergoing an acceleration/deceleration movement without direct contact between the head and an object, such as in the case of whiplash or forces generated from a blast or explosion.¹

The most common visual deficits and dysfunctions in mTBI are due to oculomotor dysfunction(s), including convergence and accommodative insufficiency.² Emerging research suggests the effects of concussions may extend beyond immediate, short-term symptoms and oculomotor findings and could have potential implications for conditions such as glaucoma, particularly traumatic glaucoma. This article explores the potential relationship between these two conditions.

MECHANISMS OF TRAUMATIC GLAUCOMA

Traumatic glaucoma is a secondary type of glaucoma that can occur after blunt or penetrating trauma, chemical or thermal burns, and/or radiation. Increased IOP can occur due to multiple pathophysiologic mechanisms causing either an early-onset acute spike in IOP or a later-onset chronic, gradual increase in IOP, both of which can increase the risk of glaucoma.

Early-Onset Traumatic Glaucoma

This form of glaucoma can occur after an eye injury. Acutely, if the trauma causes tearing of the blood vessels of the iris or ciliary body, a resultant hyphema can obstruct the trabecular meshwork, leading to a sudden rise in IOP, which can be worse in patients on blood thinners or those who have clotting disorders and/or sickle cell disease.³Coup-contrecoup injury, which is common in head/brain trauma (Figure 1), can occur to the eye and cause sheering forces on the trabecular meshwork/iris, leading to angle recession, ciliary body clefts, and, in extreme cases, iridodialysis and/or cyclodialysis, which can also cause an acute rise in IOP.

Post-traumatic iris and/or trabecular meshwork inflammation (traumatic iritis or trabeculitis) can compromise the blood-aqueous barrier, causing leakage of blood cells into the anterior chamber that can lead to an acute increase in trabecular meshwork resistance and a subsequent increase in IOP. Chemical injuries and thermal burns can damage the corneal epithelium and limbal stem cells, causing scarring and inflammation of the cornea, conjunctiva, and trabecular meshwork and leading to impeded aqueous outflow and increased glaucoma risk. Liberated pigment from the iris rubbing on the lens during the trauma can have similar effects.

Late-Onset Traumatic Glaucoma

This form of glaucoma occurs years after an eye injury and can be caused by a number of mechanisms. The most common cause of late-onset traumatic glaucoma is angle recession, which occurs when there is a tear in the ciliary muscles, indicating damage to the trabecular meshwork.^4,5 Increased angle recession (> 180°) and pigmentation have been associated with a higher risk of subsequent glaucoma.^4,5 Keep in mind that a lack of angle recession on gonioscopy does not mean the injury did not cause damage to the trabecular meshwork.

Other less common mechanisms for late-onset traumatic glaucoma include complications from vitreous hemorrhage (hemolytic glaucoma) and lens dislocation/subluxation.⁶

OTHER ASSOCIATIONS BETWEEN CONCUSSION AND GLAUCOMA

Although concussions without orbital trauma do not directly cause elevated IOP, they may create conditions that make the eye more vulnerable to pressure fluctuations. There have been an increasing number of studies showing retinal nerve fiber layer and ganglion cell layer thinning in patients with mTBI.^7-9

Patients with mTBI and more moderate to severe TBI are also at higher risk of chronic cardiovascular, endocrine, and neurologic comorbidities, which can affect ocular blood flow and oxidative stress over time.¹⁰ Traumatic optic neuropathy/maculopathy, reduced blood flow, and increased oxidative stress may make the eye more susceptible to injury and stressors, leading to increased risk of glaucomatous damage later in life. In addition, these patients may experience comorbidities, including post-traumatic migraine, sleep issues, and psychiatric and pain disorders, that cause them to be placed on medications, such as topiramate and anticholinergics, which can induce angle-closure glaucoma.

ASSESSING AND MANAGING CONCUSSION-RELATED GLAUCOMA RISK

Given the potential connection between concussions and glaucoma, optometrists should inquire about any history of head trauma or concussions in all patients with glaucoma, including suspects, even if the injury occurred years earlier. In the case of a head or brain injury, it is important to ask if the patient experienced any direct trauma to the orbit and/or eye. If they cannot recall, which is not uncommon in patients with post-traumatic amnesia, ask whether they experienced any bruising under or around their eyes. Some patients may even develop periorbital ecchymosis due to facial or skull fractures from the trauma (Figure 2).

IOP should be taken at every visit. Baseline OCT imaging of the optic nerve and macula, including ganglion cell layer and retinal nerve fiber layer analysis, is important to monitor for progression. Gonioscopy and anterior segment OCT can be beneficial diagnostics to evaluate for any anterior segment trauma.

Optometrists should inform patients who have a history of head trauma about the importance of regular eye examinations and the possible risks associated with their injury. Additionally, educating non-eye care providers on the importance of referral for routine eye care and evaluation for glaucoma in patients with a history of head/orbital trauma is also critical for the continued care of these patients.