Visual dysfunction following traumatic brain injury

Traumatic brain injury (TBI) is a common cause of death and disability worldwide. Those who sustain TBI commonly experience visual dysfunction, which can vary significantly in type and intensity. Current research suggests that variations in TBI-related vision problems are likely associated with the mechanism of injury and with injury severity.

The most common visual complaint following TBI is photophobia, or sensitivity to light, which is often accompanied by a headache or migraine. Other frequently reported vision problems include:

  • Loss of visual acuity, or the ability to see clearly and sharply
  • Color discrimination
  • Brightness detection
  • Contrast sensitivity
  • Nystagmus, a condition which causes uncontrolled movements of the eyes
  • Visual midline shift syndrome, a condition which causes a movement of the perceived midline of the field of vision, leading to disorientation and balance impairment

Causes of vision problems

Current research suggests that a primary cause of TBI-related visual dysfunction isretinal thinning. The retina, which is the photosensitive tissue that lines the back of the eye, is responsible for receiving, processing, and transmitting visual information. Retinal thinning occurs primarily in the ganglion cell layer, formed by the retinal neurons that project visual information to the brain. However, it can also affect the retinal nerve fiber layer, the area of the retina from which the optic nerve projects. Researchers have found that mice exposed to simulated blast trauma have fewer cells in the retinal nerve fiber and ganglion cell layer three months following injury. Importantly, the researchers also discovered that these mice demonstrate decreased pupillary light response; in other words, the mice’s pupils failed to expand and contract in response to the absence or presence of light. As a result, the researchers suggest that pupillary light response may function as a diagnostic tool for identifying visual problems following TBI.

Human clinical research studies have also found evidence of retinal thinning following TBI. A recent case study describes a 25-year old man with severe TBI who experienced progressive thinning of the ganglion cell and retinal nerve fiber layers in the 10 months following his injury. Additionally, a study of veterans with and without a history of TBI found that brain-injured veterans displayed thinning in both the ganglion cell layer and the retinal nerve fiber layer. Their ganglion cell layers were significantly thinner than their non-injured colleagues’.

Diagnosis of TBI-related vision problems

Despite reports of visual dysfunction, most patients present with normal exams and radiological findings. Additionally, symptoms that are not apparent at the time of injury may instead manifest during or after the recovery period. To address these limitations, researchers and clinicians seek to identify accurate diagnostic metrics to identify and characterize visual dysfunction in TBI patients. Vision experts at the Department of Veterans Affairs have developed guidelines to aid clinicians in the screening process for visual dysfunction following TBI. The screening protocol includes a series of functional visual questions that allow the clinician to understand specific details about the nature of patients’ visual concerns. Clinicians can also use the guidelines to mark symptoms that may indicate red-flag (immediately urgent) or yellow-flag (referral and follow-up needed) conditions.

Treatment

Visual symptoms often resolve on their own over time. However, people with TBI can take charge of mitigating their symptoms by engaging in recommended behaviors and taking certain precautions. For example, an individual suffering from photophobia can wear sunglasses to reduce the amount of light entering the eye, reducing discomfort and headaches. Corrective or specialized glasses, which can alter the way that light typically enters the eye, may help patients adapt to changes in the visual field. Experts recommend regular follow-up appointments with an ophthalmologist and/or neurologist, particularly for those who experience TBI-related persistent headaches. And, of course, they emphasize the most common treatment recommendation following a TBI: plenty of rest.

Kardon R, Garvin M, Wang JK, et al. Prevalence of structural abnormalities of the retinal nerve fiber layer (RNFL) and ganglion cell layer complex (GCLC) by OCT in veterans with traumatic brain injury (TBI). Investigative Ophthalmology & Visual Science, 54(15): 2360-2360. (2013).

Mohan K, Kecova H, Hernandez-Merino E, et al. Retinal ganglion cell damage in an experimental rodent model of blast-mediated traumatic brain injury. Investigative Ophthalmology & Visual Science, 54(5): 3440-3450. (2013).

Richman E. Traumatic brain injury and visual disorders: What every ophthalmologist should know. American Academy of Ophthalmology Clinical Update. (May 2014).

Singman EL. Automating the assessment of visual dysfunction after traumatic brain injury. Medical Instrumentation, 1(1): 3. (2013).

Vien L, DalPorto C, & Yang D. Retrograde degeneration of retinal ganglion cells secondary to head trauma. Optometry and Vision Science, 94(1): 125-134. (2017).

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