Psychophysical Investigation of Cognitive Processes behind Oculomotor Deficits associated with Traumatic Brain Injury

Purpose: People with Traumatic brain injury (TBI) manifest deficits in oculomotor functions such as antisaccades and memory-guided prosaccades. Generation of these voluntary saccades are influenced by high-level cognitive processes. To dissociate the cognitive processes associated with oculomotor deficits in TBI, a delayed paradigm was used and the temporal characteristics of saccade generation, response inhibition and working memory processes were investigated. Methods: Twenty-six adults with TBI with mean age of 22+/-7, 14 females and thirty-three controls with mean age of 23+/-7, 19 females without TBI participated in the study. Three saccade paradigms, specifically delayed antisaccades, delayed memory-guided prosaccades and delayed memory-guided antisaccades were investigated. For each task, the participants fixated a central target and made a pro- or antisaccade to/from the stimulus after a visual-cue which appeared after one of six variable delays (delay for delayed antisaccades: 0, 0.0625, 0.125, 0.250, 0.500 and 1s and for memory-guided prosaccades: 0, 0.125, 0.250, 0.500, 1 and 2 s). The task for delayed and memory-guided antisaccades was to look exactly opposite to the stimulus location while for memory-guided prosaccades was to look at the remembered stimulus location. In the delayed antisaccade task, the stimulus remained visible throughout the trial while in the memory-guided tasks, the stimulus was flashed for a brief period. The GazepointGP3 eye tracker was used to record eye movements. Saccade latency, disinhibition errors (incorrect saccades made before cue) and directional errors (incorrect saccades made after cue) were determined. Results: Participants with TBI demonstrated significantly longer latency (F(1, 57) = 4, p = 0.04) for delayed antisaccades, increased directional errors (delayed antisaccades: F (1, 57) = 4.4, p = 0.04); memory-guided prosaccades F(1, 57) = 23.03, p < 0.0001) and memory-guided antisaccades (F (1, 57) = 15.56, p = 0.0002) and disinhibition prosaccade errors (delayed antisaccades: F(1, 56) = 8.297, p = 0.005), memory-guided prosaccades (F (1, 57) = 4.8, p = 0.03) and memory-guided antisaccades (F(1, 54) = 9.225, p = 0.004), for all three tasks, and increased disinhibition antisaccade errors for memory-guided antisaccades (F(1, 54) = 9.225, p = 0.004) compared to controls. With increased delay duration, the latency and directional errors decreased while the disinhibition errors increased for all three tasks for both groups. Across saccade tasks, participants with TBI showed longer latency for delayed antisaccades (471ms) than memory-guided prosaccade (426ms) and antisaccade (456ms) tasks, initial increased directional errors for delayed antisaccade (25%) and memory-guided antisaccade (19%) tasks than for the memory-guided prosaccade task (8%) at 0 delay, increased premature incorrect disinhibition errors for delayed antisaccades (18%) compared to the memory-guided antisaccade tasks (25%) and increased premature correct disinhibition errors for memory-guided prosaccades (45%) compared to the delayed antisaccade tasks (18%) at 1s delay. Conclusions: With delay, both TBI and control group demonstrated similar descending trend for latency and directional errors while ascending trend for disinhibition pro- and antisaccade errors. However, the trend for latency, disinhibition incorrect prosaccades and directional errors for the delayed antisaccades and disinhibition correct prosaccades for memory-guided prosaccades were higher for the TBI group with delay period compared to controls suggesting a baseline saccade generation deficit. However, these deficits in generating a voluntary saccade eye movement may be caused by the underlying cognitive deficit from the impact of head injury and may not primarily be an oculomotor defect alone. This was evident by the fact that the latency for memory-guided pro- and antisaccade and gain parameters of memory guided anti saccades were unaffected in the TBI group compared to controls. This study suggests evidence for saccadic eye-movement deficits being associated with increased problems in impulsivity and response inhibition which could be due to difficulty in inhibiting the response to a visual stimulus or memory of that stimulus in participants with TBI