This study evaluated the utility of ocular motor measures in characterizing subtle cognitive changes after carbon monoxide (CO) poisoning.
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.
A battery of ocular motor tasks evaluated the basic metrics of movements, and the higher-order cognitive control processes governing movement.
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.
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.
*Centre for Neuroscience, University of Melbourne, Melbourne, Australia
‡Department of Neurology, Royal Melbourne Hospital, Parkville
†Centre for Developmental Psychiatry and Psychology, School of Psychology, Psychiatry, and Psychological Medicine, Monash University, Clayton
§Cabrini Hospital, Malvern, Victoria, Australia
Reprints: Joanne Fielding, PhD, Centre for Neuroscience, University of Melbourne, Grattan St, Parkville, Victoria 3050, Australia (e-mail: email@example.com).
Dr Fielding is funded by a Fellowship awarded by the NHMRC of Australia #454811.
Received March 22, 2009
Accepted October 11, 2009