May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Oculomotor Fixation and Its Rehabilitation in Acquired Brain Injury
Author Affiliations & Notes
  • K.J. Ciuffreda
    Vision Sciences,
    SUNY College of Optometry, New York, NY
  • Y. Han
    Vision Sciences,
    SUNY College of Optometry, New York, NY
  • N. Kapoor
    Clinical Science,
    SUNY College of Optometry, New York, NY
  • Footnotes
    Commercial Relationships  K.J. Ciuffreda, None; Y. Han, None; N. Kapoor, None.
  • Footnotes
    Support  Langeloth Foundation
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2325. doi:
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      K.J. Ciuffreda, Y. Han, N. Kapoor; Oculomotor Fixation and Its Rehabilitation in Acquired Brain Injury . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2325.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To assess two–dimensional fixational oculomotor deficits and their rehabilitation in individuals with acquired brain injury (ABI). Methods: Adults with ABI comprising either stroke (S) with hemianopia (n=5; 3 with hemi–inattention) or traumatic brain injury (TBI) (n=9) participated in the laboratory–based, computer–controlled training at least 1 year following their brain injury. Training included fixation in different directions of gaze (center, 10degL, 10degR, 10degU, and 10degD), as well as saccades, pursuit, and simulated reading paradigms for 1 hour twice weekly for 8 weeks. Training modes included normal internal visual feedback, at times in conjunction with external oculomotor auditory feedback. Two–dimensional (horizontal and vertical) fixational behavior before and after training was assessed objectively using an infrared eye movement system (OBER2; 120 Hz sampling) with corrective lenses in place. Horizontal, vertical, and radial (frequency of each sampled error magnitude summed across all meridians) errors were quantified. Results: In all 13 subjects prior to training, fixational errors for all 3 parameters were abnormally large. This primarily reflected increased drift, with some saccadic intrusions and at times jerk nystagmus present. The group mean eye positional error across the 3 parameters was 1 degree, with individual means ranging from 0.3–3.5 degs. This error was twice as large in S versus TBI. In both subgroups, the positional error was largest in the radial dimension. Following training, mean fixational error across the 3 parameters decreased by 50% (60% in S and 45% in TBI). Improvement was greatest in the horizontal dimension in S (65%) and in the vertical dimension in TBI (60%). Fixational error for all 3 parameters regressed moderately at the 3–month, post–training follow–up. Conclusions: Fixational deficits were consistently found in individuals with ABI. However, these were significantly reduced by formal oculomotor training. This improvement is believed to reflect considerable residual oculomotor plasticity/rapid motor learning, despite the pervasive brain insult. In addition, enhancement of visual attentional mechanisms is believed to play a prominent role, especially in stroke (i.e., reduced hemi–inattention). The regression of fixational improvement at follow–up suggests that more intensive and longer training may be necessary to physiologically reinstate and maintain the affected neural pathways.

Keywords: eye movements • plasticity • ocular motor control 
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