OBJECTIVE: This study evaluated the utility of ocular motor measures in characterizing subtle cognitive changes after carbon monoxide (CO) poisoning. BACKGROUND: Delayed onset of neurologic and psychiatric symptoms occurs in a number of patients with no apparent deficit immediately after CO poisoning. Although historically attributed to necrosis of the globus pallidus (GP), subsequent demyelination of the cerebral white matter has been proposed as the principal driver of these deficits. Here, we evaluate cognitive changes in a patient with structural deficits largely confined to the globus pallidus at 3 years post-CO poisoning, using ocular motor measures. METHOD: A battery of ocular motor tasks evaluated the basic metrics of movements, and the higher-order cognitive control processes governing movement. RESULTS: Abnormalities were revealed across a broad range of saccadic measures, including latency, accuracy, and error rate, reflected impaired response inhibition, working memory, and attentional processes. CONCLUSIONS: These observations suggest subclinical deficits potentially reflecting damage to the GP. Furthermore, we have shown that ocular motor measures sensitively characterize cognitive deficits that may otherwise be overlooked after CO poisoning, and that may benefit from intervention.
OBJECTIVE: This study evaluated the utility of ocular motor measures in characterizing subtle cognitive changes after carbon monoxide (CO) poisoning. BACKGROUND: Delayed onset of neurologic and psychiatric symptoms occurs in a number of patients with no apparent deficit immediately after COpoisoning. Although historically attributed to necrosis of the globus pallidus (GP), subsequent demyelination of the cerebral white matter has been proposed as the principal driver of these deficits. Here, we evaluate cognitive changes in a patient with structural deficits largely confined to the globus pallidus at 3 years post-COpoisoning, using ocular motor measures. METHOD: A battery of ocular motor tasks evaluated the basic metrics of movements, and the higher-order cognitive control processes governing movement. RESULTS: Abnormalities were revealed across a broad range of saccadic measures, including latency, accuracy, and error rate, reflected impaired response inhibition, working memory, and attentional processes. CONCLUSIONS: These observations suggest subclinical deficits potentially reflecting damage to the GP. Furthermore, we have shown that ocular motor measures sensitively characterize cognitive deficits that may otherwise be overlooked after COpoisoning, and that may benefit from intervention.