to support vision therapy in mTBI; examination of these patients is often normal, other than a high prevalence of convergence insufficiency; visual symptoms are common in patients with normal ocular… Click to show full abstract
to support vision therapy in mTBI; examination of these patients is often normal, other than a high prevalence of convergence insufficiency; visual symptoms are common in patients with normal ocular motility; eye-tracking studies have shown that simple saccades (ie, visually guided prosaccades) are often spared and cognitively demanding saccades (ie, memory-guided and anti-saccades) are often abnormal after mTBI. We would like to provide additional perspective on the authors’ references to our articles. There is no question that ocular motor networks are widely distributed in the brain, including the frontal lobes, which are prone to traumatic brain injury. Although abnormalities of memory-guided and anti-saccades do, indeed, rely upon attention and executive function, behavioral changes are detected through ocular motor measurements and are thus referred to as ocular motor research in the literature. Furthermore, deficits represent dysfunction of specific frontal neuronal populations involved in saccade control, regions in which pathologic changes are reported on autopsy in athletes after suicide in the acute– subacute period after mTBI. Most of our work relates to validation of rapid automatized naming tests (numbers in the King-Devick test or pictures in Mobile Universal Lexicon Evaluation System (MULES)), which demonstrate high sensitivity for mTBI detection. Eye movement behavior is altered during these tasks in mTBI, with prolonged inter-saccadic intervals and increased numbers of saccades. Such findings do not automatically imply abnormal core ocular motor structures, but might reflect an inseparable network responsible for attention, cognition, language retrieval, and eye movements. Nonetheless, ocular motor pathways do deviate from cognitive circuits as they descend towards the brainstem and cerebellum and can be injured selectively by trauma. Focal rostral brainstem injury is the likely cause of convergence deficits, and theoretical support for asymmetric frontal eye field injury is provided in a neuromimetic model by Dr Lance Optican and our team. There are many unanswered questions in the nascent field of mTBI; however, we maintain that convergence, cognitively demanding saccades, and saccades and fixations during rapid automatized naming tests deserve further study as potential biomarkers and hold promise as objective clinical trial outcome measures. Well-designed prospective trials of vision therapy are necessary, but we should not reject scientific progress because of this need.
               
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