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Post Trauma Vision Syndrome


Post Trauma Vision Syndrome

by Dr. April Eryou

Post Trauma Vision Syndrome (PTVS) occurs when an internal or external insult to the brain negatively affects the ambient part of the visual process. The visual process is made up of two parts, focal and ambient. The focal process provides information about “what” an object is in the visual field. It is generally associated with the function of the macula, which is the part of the eye that allows humans to see small details. The focal process is conscious and attention driven. The ambient process provides information about “where” a person is in space and “where” objects in space are relative to them. Information from the ambient process is required for balance, movement, coordination, perception of space and binocularity. Neurologically, at the level of the retina, information is acquired via rods and cones. Rods exist more in the periphery and respond to low light conditions. Cones are more concentrated in the macula and respond to different colours of light. The signals from the photoreceptors are then combined in one of three ganglion cells: Parvocellular (P-cells), Magnocellular (M-cells) or Koniocellular (K-cells). It is the P cells the mediate most of the focal vision. They provide information about detail and are slower to process information. They travel along with a few M cells from the retina to the Lateral Geniculate Body to the visual cortex and comprise of the focal visual process. The M-cells provide information about shape and movement and are fast to process information. The majority of them make up the retinal-lateral geniculate-midbrain pathway which is the ambient visual process. In the midbrain, the ambient visual information becomes part of a sensorimotor feedback loop as its information is related to concurrent kinesthetic, proprioceptive, vestibular and tactile information. The ambient visual process is thought to be more susceptible to dysfunction because the M-cells are larger in diameter compared to the P-cells and thus mores likely to damage.

The ambient visual process provides information that aids with binocularity, it helps with the anticipation needed for eye movements, it helps with the overall balance of an individual in the visual environment and it helps with interpretation of visual information. Thus, post trauma vision syndrome can manifest as many types of visual problems. Because PTVS can manifest as a multitude of visual, motor and vestibular system dysfunctions, it is hard to determine the exact prevalence of PTVS. A study by Ciuffreda et al. found ocular motor dysfunction in 90% of acquired brain injury (ABI) patients1, suggesting the prevalence is extremely high.

Assessment of a neuro-optometric patient begins with a thorough history. Symptoms that PTVS patients may complain of can include: blurry vision, diplopia, mobility difficulties, bumping into objects, photophobia, headaches, vertigo/motion sensitivity, dry eye, challenges in busy environments, sensations of movement when it isn’t happening and tunneling of vision.

PTVS can have some of the following signs: poor binocularity (impaired vergence ranges, high phorias, strabismus- commonly exotropia, convergence insufficiency), accommodative dysfunctions, poor pursuits/saccades, difficulties fixating, challenges with spatial perception, difficulties with eye-hand coordination, poor attention, difficulties with visual perception (discrimination, figure-ground, visual memory), changes in refractive error, poor repeatability of test results and reduced blink rate.

During the neuro-optometric examination, you would look for the following:

  1. Acuity testing: you would look for fixation instability when doing monocular acuity testing and binocular instability when doing binocular acuity testing. If the patient reported challenges seeing or letters moving when testing binocularity you could then re-test with bi-nasals or base in prisms. Significant improving both numerically and subjectively to either of these probes would suggest an ambient system dysfunction.
  2. Cover test: you would look for high phorias/strabismus, in particular exo-deviations.
  3. Ocular motor testing: you would look for jerky pursuits and challenges disengaging from the target when doing saccades.
  4. Near Point of Convergence (NPC): You would look for a possible remote NPC.
  5. Refraction: The patient may also have a significant change in refractive error (more likely a myopic shift) following the insult.
  6. Perceptual testing: the patient may have trouble with figure-ground activities.

For patients who during the neuro-optometric examination show signs of PTVS, it is suggested that Visually Evoked Potential (VEP) testing be done. PTVS patients tested binocularly with cross-pattern reversal stimuli show reduced amplitudes. When testing is then repeated with either bi-nasal occlusion or base in prism there will be either a significant increase in these amplitudes or a concurrent decrease in both the NI and PI potentials, these findings are characteristic of patients with PTVS. Treatment options may include, optimizing refractive error correction with the goal of promoting balance in the visual system, tinted lenses, binasal occlusion, low power yoked prisms, low powered Base In prisms, sectoral occlusion on lenses, syntonics and neuro-optometric rehabilitation. Neuro-optometric rehabilitation would be unique to the patient depending on how their PTVS presented. Generally, work would be done to help bring awareness to the ambient vision process and to promote change in the ambient visual process and how it integrates with the focal visual process and sensorimotor systems. Techniques to enhance peripheral vision awareness and prevent overfocalizing would be used. Yoked prisms combined with visual-motor tasks would be used in the rehabilitation to promote change and re-structuring of the visual system and how it interacts with the sensorimotor system. Then work would be done to integrate and balance the ambient and focal vision processes.

1. Riestra AR, Barrett AM. Rehabilitation of spatial neglect. Handb Clin Neurol. 2013; 110: 347-355.