|Title||CARBON MONOXIDE POISONING: ACQUIRED BRAIN INJURY AND FUNCTIONAL BINOCULAR VISION DEFECTITS|
|Author, Co-Author||Cynthia Zara, Neera Kapoor|
|Abstract|| BACKGROUND: It has been reported in the literature that carbon monoxide poisoning has resulted in decreased visual sensitivity and visual tracking facility, as well as reduced performance with repetitive tasks. Carbon monoxide poisoning has also been linked to color vision disturbances in the central field of vision and perceptive agnosia. More severe cases are associated with optic atrophy; VEP and ERG deficits may be noted.
CASE REPORT(S): A 57-year-old female with a history of acquired brain injury resulting from carbon monoxide poisoning presented with complaints of poor visual focusing, difficulty with reading eye movements, and an inability to maintain prolonged fixation. During testing, fixation targets did not appear clear along the midline. Signs of inattention to her right field of vision were also noted. Binocular testing revealed a significant convergence insufficiency with reduced compensatory fusional ability. Although her eyes were aligned and motilities were full and comitant, she was only able to perceive the Randot global stereopsis target at 250 seconds of arc when the target was held just off her central visual axis. The Developmental Eye Movement test score was significantly reduced relative to age related normative data. The response time during the Humphrey 76 point 3-zone visual field testing was consistently delayed in her right field OS, however there were no neurological deficits. Pupillary responses were normal, and the dilated fundus examination revealed no evidence of optic atrophy or other pathology.
CONCLUSIONS: Right visual neglect and central visual agnosia are suspected. When acquired brain injury results from carbon monoxide poisoning, such visual sequelae may be permanent, while others temporary. This poster presents the diagnosis and management of multiple visual and ocular problems sustained as a result of carbon monoxide poisoning and associated acquired brain injury. The pathophysiologic basis of this patient’s clinical presentation as it relates to carbon monoxide poisoning are discussed.
|Affiliation of Co-Authors||State University of New York, College of Optometry|