According to VisionAware’s Gregory L. Goodrich, Ph.D., writing about combat-related traumatic brain injury (TBI) and its effect on vision:
“… It can be argued that … it took the wars in Afghanistan and Iraq to highlight the fact that head injury often leads to visual loss and/or visual dysfunctions. These wars have resulted in over 253,000 traumatic brain injuries (TBI). How many of these TBIs resulted in vision loss or dysfunction is not known.”
“Kevin Fricke has estimated that between the years 2000 and 2011, over 54,000 U.S. troops experienced an eye injury or visual loss/dysfunction. He estimated the direct medical cost for these troops to be $2.82 billion dollars. The projected cost to the economy over the lifetime of these individuals, including rehabilitation, lost wages, and other costs is estimated to be an additional $24.286 billion.”
Source: K. Fricke (2012). Costs of Military Eye Injury, Vision Impairment, and Related Blindness and Vision Dysfunction Associated with Traumatic Brain Injury (TBI) without Eye Injury. Report prepared for the National Alliance for Eye and Vision Research.
Blast Exposure and the Retina
wounded by a roadside bomb
in Baghdad, Iraq
Most recently, a research group from Iowa State University and the National Animal Disease Center, United States Department of Agriculture has built upon this prior research, reporting that combat-related blast exposure which does not cause detectable changes in the brain can result in long-term retinal injury.
Co-author M. Heather West Greenlee, Ph.D. states that “In this model, the retina may serve as an area of the central nervous system that is more vulnerable than the brain and, therefore, may be an effective and more sensitive indicator of low-level injury due to blast-wave pressure. We believe that eventually examination of the retina may help to assess the magnitude of exposure and identify individuals who may need or benefit from proactive treatments as they become available.”
From the American Journal of Pathology
This new traumatic brain injury and retinal injury research, titled Lasting Retinal Injury in a Mouse Model of Blast-Induced Trauma, has been published in the July 2017 edition of the American Journal of Pathology, the official journal of the American Society for Investigative Pathology.
The authors are Najiba Mammadova, Shivani Ghaisas, Gary Zenitsky, Donald S. Sakaguchi, Anumantha G. Kanthasamy, Justin J. Greenlee, and M. Heather West Greenlee, from Iowa State University and the National Animal Disease Center, US Department of Agriculture, Agricultural Research Service, Ames, Iowa.
About the Research
Excerpted from Retina may be sensitive gauge of blast-wave pressure injury, via Medical Xpress:
There is a lack of validated biomarkers, as well as limited understanding of the underlying mechanisms of retinal injury due to blast exposure.
[Editor’s note: A biomarker is a substance in the body that can be measured and whose presence indicates disease, infection, or environmental exposure. Biomarkers are measured and evaluated to examine normal body processes, disease processes, or responses to drugs used in a therapeutic intervention.
Currently, diagnosis and measurement of progression of disease rely upon clinical observation, and despite a “normal” [eye] examination, some patients present with chronic visual complaints. Combat veterans show a high percentage of visual field defects, light sensitivity (photophobia), eye movement problems, and decreased contrast sensitivity.
“Our results may explain symptoms of visual dysfunction reported by combat veterans who have experienced traumatic brain injury,” explained lead investigator Heather West Greenlee, PhD. “These results are not surprising, since the retina is the most accessible part of the central nervous system; as such, it is particularly vulnerable to injuries similar to those that affect the brain.”
Investigators used a compressed air-driven shock tube system to expose mice to blast wave pressure of 300 kPa (equivalent to three times atmospheric pressure) per day for three days. After 30 days, the mice were subjected to a variety of tests to probe for cognition or motor function deficits and subsequently underwent analyses of the retina and brain.
Retinas of blast-pressure-exposed animals displayed several pathological changes, including activation of [retinal glial cells], microglial activation, inflammation, and photoreceptor cell death. Eyes on the same side as the blast showed greater abnormalities than eyes on the other side. Interestingly, researchers also found accumulation of tau, the protein associated with pathologies of the central nervous system including Alzheimer’s disease, Parkinson’s disease, and chronic traumatic encephalopathy [i.e., inflammation of the brain or abnormal brain function].
[Editor’s note: Glial cells surround neurons, or nerve cells, and provide support for, and insulation between, them. Microglia are a type of glial cell located throughout the brain and spinal cord. They act as the primary form of immune defense in the central nervous system.]
These findings showed the prolonged impact of blast injury on the retina, as well as the vulnerability of particular retinal cell types to blast injury. Despite the effects in the retina, there were no detectable cognitive or motor deficits and no evidence of injury in the striatum or pre-frontal cortex, areas of the brain responsible for motor function. Executive decision making and memory remained unaffected.
More about the Retina and Its Function
The retina is the light-sensitive tissue that lines the inside surface of the eye, much like wallpaper. The macula is the small sensitive area in the center of the retina that provides clear central vision. The fovea is located in the center of the macula and provides the sharpest detail vision.
The retina contains photoreceptor cells that convert (or process) incoming light into electrical impulses. These electrical impulses are carried by the optic nerve (which resembles your television cable) to the brain, which finally interprets them as visual images.
There are two types of photoreceptors: rods and cones, which are the light-processing cells responsible for peripheral (side) and central (straight-ahead) vision.
Rods
- The specialized, highly light-sensitive retinal processing cells that are able to function in low light levels. They provide peripheral (or side) vision, are responsible for dark adaptation, and are most sensitive to movement/motion. They are less sensitive to color perception.
- A normal retina contains approximately 120-150 million rods, primarily in the peripheral, or outer, retina.
- Rods provide scotopic vision which refers to eyesight in low light conditions.
Cones
- The specialized retinal processing cells that function in bright light levels and provide central (or straight-ahead) vision, along with sharp visual acuity, detail, and color vision. They require bright light to function and are not sensitive to lower light levels.
- A normal retina contains approximately 6-7 million cones, primarily in the macula, the small area in the center of the retina that provides clear central vision. Cones are the most concentrated in the fovea, which is located in the center of the macula and provides the sharpest detail vision.
- Cones provide photopic vision, which refers to eyesight in daylight conditions.
More About the Study from the American Journal of Pathology
Excerpted from the study Abstract:
Traumatic brain injury due to blast exposure is currently the most prevalent of war injuries. Although secondary ocular blast injuries due to flying debris are more common, primary ocular blast exposure resulting from blast wave pressure has been reported among survivors of explosions, but with limited understanding of the resulting retinal pathologies.
Using a compressed air-driven shock tube system, adult male and female C57BL/6 mice [i.e., a common inbred strain of laboratory mice] were exposed to blast wave pressure of 300 kPa (43.5 psi) per day for 3 successive days, and euthanized 30 days after injury…. Primary blast wave pressure resulted in activation of Müller glia, loss of photoreceptor cells, and an increase in phosphorylated tau in retinal neurons and glia.
We found that 300-kPa blasts yielded no detectable cognitive or motor deficits, and no neurochemical or biochemical evidence of injury in the striatum or prefrontal cortex, respectively. These changes were detected 30 days after blast exposure, suggesting the possibility of long-lasting retinal injury and neuronal inflammation after primary blast exposure.
VisionAware will continue report on this research as results become available.