Rory Fleming Richardson, Ph.D., ABMP, TEP
The Emergence of TBI-Related Vision Distortions
Rory Fleming Richardson, Ph.D., FICPPM, ABMP
The tracking of visual problems following a head injury can be traced for hundreds of years but it was not until 1987 that the term “post-concussive vision syndrome” was coined by S.H. Auerbach in his article, “The post-concussive syndrome: Formulating the problem.” Due to the subtleties of symptoms and normal lab and imaging finding (i.e., CT scans, MRI, EEG and routine neurological evaluations showing normal results), those having complaints have had their symptoms mistakenly perceived as being of a psychiatric origin. In 1993, the American Congress of Rehabilitation Medicine provided a standardized definition for mild traumatic brain injury. As the number of individual, suffering from Post Concussive Vision Syndrome who reported symptoms has increased, the number of professionals questioning patients who have had head injuries about visual distortions has improved, although the practice is still too rare. Research has shown that most mild traumatic brain injuries result in multiple lesion rather than single lesion events.
Despite this, most neuropsychologists still fail to include the necessary screening for visual and auditory processing impairments necessary to see if the individual being examined has any distortions. Missing this basic screening places the validity of standardized tests in question, especially since there is the assumption that the examinee has an acceptable level of vision and hearing.
With the increased report of symptoms by military personnel who have served in the Gulf War, research as to the cause of Post-Concussive Vision Syndrome has led to significant research. What has been found is that a TBI is a complex event with the primary insult and secondary pathogenic events. Although the sequence of events may vary, the first phase, the primary insult, of damage is made up of (1) the rupture of cellular and vascular membranes, (2) release of intracellular contents, and (3) cessation of blood flow (McIntosh, 1994; Werner and Engelhard, 2007).
With the reduction of oxygen to the area, anaerobic glycolysis results with the build up of lactic acid (Werner and Engel hard, 2007). The specifics of damage is related directly to the type of impact and the areas involved. The second phase, the beginning of secondary pathogenic events, is made up of biochemical and molecular events leading to the necrotic and apoptotic death of cells (Graham et al., 2002; Thompson et al., 2005). There is an increased release of glutamate and aspartate, excitatory neurotransmitters, which lead to increased excitation of glutamate receptor, an influx of calcium, release of calcium from intracellular stores, generation of free-radicals, and inflamation (Graham et al., 2002; Thompson et al., 2005; Werner and Engelhard, 2007). There is an increase in glutamate which results in overstimulation of ion-channel–linked which result in prolonged depolarization and ionic imbalance and overstimulation of G-protein–linked glutamate receptors. This results in ATP supplies being depleted and the increase in intracellular free calcium. This can result in numerous pathogenic events which result in cellular death (Yi and Hazell, 2006). With the increased Glutamate, ion-channel-linked and G-protein-linked glutamate receptors are overstimulated prolonging depolarization, creating an ionic imbalance, ATP depletion, increase of free intercellular calcium, activation of intercellular proteases, phospholipases and endonucleases. This results in damage to the cellular structure, promotion of free-radicals and cellular injury or death (Marklund et al., 2006; Werner and Engelhard, 2007). As this cascade progresses and there is increase of intracellular calcium, mitochondria become a source of reactive oxygen species (ROS’s) (Bayir and Kagan, 2008; Sullivan et al., 2005). The neuroprotective systems of the brain become overwhelmed resulting in cellular damage. Injured axons in the white matter can also separate from the cells resulting in cellular death. The complexity of residual damage from mild traumatic brain injuries (mTBI) is only partially known. One of the mechanism which is still unclear is the biochemical and neurophysiological process that result in the visual distortions experienced as a result of mTBI patients. Symptoms which are associated with Post-Concussion Vision
Syndrome (or Post-Traumatic Vision Syndrome) include the following:
• Blurred or Double Vision
• Eyes Not Being Able to Focus on One Location
• Spatial Disorientation
• Extreme Light Sensitivity & Photophobia
• Loss of Place While Reading,
• Skipping or Re-reading Words
• Reduced, Inefficient Reading Speed
• Double Vision
• Letter and Line Movement
• Headaches or Migraines
• Sensitivity to Glare
• Impaired Depth Perception
• Slowed Visual Recovery When Changing Focus or Changing One’s Focus
• Motion Sensitivity
• "Shimmering Vision”
• Spatial Perceptual Deficits
• Spatial Awareness Deficits
• Visual Field Deficits (With or Without Inattention)
• Poor Visual Memory
• Visual Hallucinations
• Waviness of Vision
• Graininess of Vision
This list of symptoms are identical to those described as Irlen Syndrome.
Treatment options including various vision therapy approaches which are continuously being developed. One method which has provided significant hope is the use of Irlen Filters which are currently being used by some veterans returning from Iraq. Irlen filters were invented by Helen Irlen, M.A., a school psychologist in Long Beach, California.
While in training at the Irlen Institute in Long Beach, I had the opportunity to observe an examination of a Marine who suffered from Post-Trauma Vision Syndrome. Initially, the Marine bein examined could hardly tolerate opening his eyes in the sunlight without sunglasses. After the proper filter combination was found, he was able to function without any significant discomfort or symptoms of visual distortion.
Over the years, Irlen Syndrome has been a point of debate. Although there continues to be debate over the level of impact that the filtered lenses have, the reality is that they are being used worldwide and in addition to Helen Irlen’s organization, Dr. Arnold Wilkes of the University of Essex has established a separate diagnostic method and utilizes similar filtered lenses to correct this visual distortion. One of the early controversy was if the Meares-Irlen Syndrome was discovered in the 1980s or if it had been identified under other names previously by various vision specialists. Dr. Wilkes’ interest in this visual distortion was fueled by his work in visually induced seizure disorders. The question as to if the symptoms described are real appear to be less of a controversy except for the name being used to describe them.
To determine which combination of filters are needed, an individual is assessed by a Certified Irlen Diagnostician who systematically identifies the combination of filters necessary to correct the distortion. There can be six layers of filters or more for each eye to accomplish this. After the combination is identified, the lense are tinted to duplicate that combination. With the new lenses, improvement is often dramatic and the individual is able to function without the limitations which have been impacting their lives.