Test refraction, balance, contrast sensitivity in suspected mTBI

Issue: January 2018

Mild traumatic brain injury is, by definition, a complex pathophysiologic process affecting the brain, induced by biomechanical forces, according to McCrory.

It must be taken seriously, because it is an injury to the brain resulting in three categories of symptoms: physical/somatic (eg, headache, vision, gastrointestinal disturbance), cognitive (eg, attention, memory) and psychiatric (eg, mood swing, personality changes). Most of these symptoms should get better within 2 to 3 weeks of total rest (sometimes more) barring any second-impact syndrome.

The Glasgow Coma Scale (GCS) is based on objective observation gauging the initial and subsequent level of consciousness after brain injury. Three functions – eye, verbal and motor responses – are assessed, with a numerical value assigned to them and then added for a total score. The lower the score, the more severe the condition. GCS 13 to 15 can result from a concussion lasting less than 30 minutes and will identify the patient as having a mild traumatic brain injury (mTBI).

Neuro-imaging tests such as CT scan or MRI may or may not show evidence of any damage. A modified GCS for pediatric patients has been devised.

According to the Brain Injury Research Institute, high school football accounts for 47% of all reported sports concussions, followed by ice hockey and soccer. An estimated 1.6 million to 3.8 million sports- and recreation-related concussions occur in the U.S. each year.

The prevalence of TBI in the U.S. military between 2000 and 2010 was reported to be 202,281 with 67% classified as mTBI secondary to blast events, according to the Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury. A more recent survey by the U.S. Department of Defense statistics reported 340,000 cases of TBI clinically confirmed from 2000 to 2015, with 82.5% consisting of mTBI.

Military personnel

Goodrich and colleagues at the Palo Alto Veterans Affairs Polytrauma Rehabilitation Center were the first to report the prevalence of visual dysfunction/impairment in mTBI. Seventy-four percent of the subjects self-reported visual complaints, and half had a visual impairment.

Capó-Aponte was the first to study blast-induced mTBI in active duty military 15 to 45 days after the blast event, taking into account various confounders and comorbid injuries as well as medications. In the absence of ocular injuries, the authors identified oculomotor dysfunctions at near as biomarkers of mTBI severely affecting reading and comprehension. Light sensitivity and vestibular symptoms such as tinnitus and balance issues were manifest. Of note is that the authors did not find large disagreement with the many retrospective general studies of mTBI. They also reported recently similar high rates of visual dysfunction between blast and non-blast induced mTBI with tentative extrapolation to civilian population.

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Clinical pearls

Small refractive errors are significant in the mTBI patient and need to be corrected.

Pay attention to vertical imbalance as well as head posture. A large prevalence of hyperphoria was first reported by Capó-Aponte; the researchers postulated that the mTBI patient may tilt the head as a compensatory mechanism, which, in turn, may cause the inner ear fluid to shift, causing dizziness and balance disorders. Therefore, a vertical prism is judiciously used and recommended.

Contrast sensitivity and use of filters should be considered. Subclinical deficit in the flicker fusion threshold function could be the cause of light sensitivity, especially with fluorescent lights. A blue or yellow filter should be used, depending on which optic tract bundle is affected, magno vs. parvo cells. Magno cells in the lateral geniculate body are thought to respond to gross peripheral movement and flicker frequency threshold, while the parvo cells deal with foveal details and color. Filter choice is decided by trial and error.

No correlation was found between the much-discussed intrinsically photosensitive retinal ganglion cells implicated in migraine sufferers and the much-discussed blue light sensitivity stemming from cell phone and tablet users. Yuhas and colleagues then set out to study pupillary responses to blue and red light in mTBI; they established no correlation.

Recently, Poltavski and colleagues administered a specially designed visual evoked potential test to two groups of patients diagnosed with convergence insufficiency, where one group had a history of concussion. They found slower processing of the magnocellular pathway in the concussed group, which correlates with the increased visual sensitivity to motion, crowding, photophobia and certain lighting fixtures, such as fluorescent.

Accommodative facility in the younger mTBI population must be addressed. It is important to measure the accommodative ranges monocularly as well as binocularly. Inconsistent values may indicate localized pathology with symptoms of fatigue and asthenopia.

Vergences, saccades and fusional ranges should be assessed as well as accommodative facility. The superior colliculus plays a role in eye movements. Armstrong and colleagues reported neuronal loss in this area of the brain in chronic traumatic encephalopathy, which is a sequela of multiple mTBI temporaneous successive events.

Repetitive injuries

It is important to mention that mTBI and concussions are not isolated events, especially in sports-related injuries such as boxing, football and hockey. Years later these repetitive injuries result in taupathy, which is the accumulation of Tau protein in various forms of dementia and Alzheimer’s disease. In addition, pTau, a hyperphosphorylated Tau protein, forms neurofibrillary tangles around blood vessels of the cortex in an irregular and patchy distribution within neurons and glia. The concussive force leads to changes in neuronal cell wall permeability followed by cellular damage and ultimately cell death. That, in turn, engenders release of cytokines and inflammatory response with subsequent injury cascade leading to chronic traumatic encephalopathy.

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Brain function, even though highly specialized and somewhat compartmentalized, shows a high degree of redundancy. In many cases, a deficit in one area is mitigated by another pathway to allow functioning, albeit not at the same efficiency and high degree of performance as before the loss.

An amblyopic eye regains a few lines of visual acuity after the loss of vision in the nonamblyopic and dominant eye. Some patients show miraculous recovery after cerebrovascular accident (CVA); that so-called spontaneous recovery occurs usually within 3 months post-CVA. The term “neuro-plasticity” was coined in the last decades to account for the various unconventional recoveries after specific rehabilitation program and techniques. Despite various reports of nerve regeneration (Rakic et al., Porter), neuro-plasticity is a more appropriate term than regeneration or restoration for highly specialized and intricate neuro functions.

It is important to note that a primary condition for the rehabilitation techniques to be successful is to assure that the target activity is integrated and internalized in one’s self. It also follows that younger patients are more successful in their rehabilitation efforts because they are more amenable to a process of reorganization and integration and should have more flexibility in their system.

MTBI is a serious concussive injury induced by biomechanical forces and not easily detectable by neuro-imaging. It results in various visual, perceptual, oculomotor and oculo-vestibular dysfunctions interfering with numerous and important activities of daily living. – by Joseph Hallak, PhD, OD, FAAO, and Jeffrey Becker, OD

References:
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Capó-Aponte JE, et al. Mil Med. 2012;177(7):804.
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For more information:
Joseph Hallak, OD, PhD, FAAO, is in private practice in Syosset, N.Y. He can be reached at drjhallak@aol.com.
Jeffrey Becker, OD, is director of vision rehabilitation at the Neurosensory Center of Eastern Pennsylvania and a consultant to many rehabilitation hospitals. He can be reached at jeffreyb20@aol.com.

Disclosures: Becker and Hallak report no relevant financial disclosures.