Citation

Shimosegawa E, Hatazawa J, Nagata K, Okudera T, Inugami A, Ogawa T, Fujita H, Itoh H, Kanno I, Uemura K. J. Nucl. Med. 1992; 33(9): 1696-1698.

Affiliation

Department of Radiology and Nuclear Medicine, Research Institute of Brain and Blood Vessels, Akita, Japan.

Copyright

(Copyright © 1992, S.N. Turiel and Association)

DOI

unavailable

PMID

1517846

Abstract

A 29-yr-old woman was studied for 1 yr after acute carbon monoxide intoxication following an attempted suicide by inhalation of automobile exhaust fumes. The patient demonstrated impaired responsiveness to stimuli without any specific neurological deficits for 1 yr after carbon monoxide intoxication. Repeated brain magnetic resonance imaging consistently displayed only bilateral globus pallidus lesions, but no lesions in either deep white matter or cerebral cortex. Position emission tomography measurements of regional cerebral blood flow, and glucose utilization rate were made in this patient at 6 mo and 1 yr following carbon monoxide intoxication. Impairment of both blood flow and glucose metabolism were found not only in the basal ganglia but also in morphologically normal frontal cortex. The decrease in glucose utilization in the frontal cortex was greater than that in the basal ganglia. During the period of 6 mo to 1 yr, blood flow and glucose metabolism in the basal ganglia recovered to the normal range. In the frontal cortex, however, blood flow and glucose metabolism remained approximately 20% lower than the normal mean values. This prolonged dysfunction in the frontal cortex may therefore be responsible for the impaired responsiveness of the subject.

Language: en