peated measurements with positron emission tomography(PET) of regional cerebral blood flow (rCBF) and glucosemetabolism in a patient at 6 mo and 1 yr following acuteCo intoxication are presented.

CASE REPORT

Materials and MethodRegional CBF measurement was performed following a H2150

bolus injection (30 mCi) into the cubital vein (7) using a HEADTOME IV (Shimadzu Co, Kyoto) positron emission tomograph,which has an effective resolution of 7 mm (8). Arterial bloodsampling to estimate the arterial input function ofthe radiotracerinto the brain wasdone by continuouswithdrawalthrougha betascintillation detector. After allowing for the decay of 150 in thebrain, 8 mCi of ‘8F-2-fluoro-2-deoxy-D-glucose(FDG) were administered. Sequential PET scanning was started at the beginningof administration, after which fourteen 2-mm scans followed byfive 4-mm scans were obtained. Manual arterial plasma sampleswerecollected(every 15secduring the first 2 mm, every 30 secfor the following 3 mm and then at increasing times) to definethe input function. Rate constants defined by SokolofFs model(9) werecalculatedfromthe dynamicimages(10). Regionalcerebral glucose utilization (rCMRG1u) was then estimated byemploying the extension of the Sokoloff's equation (11) andusing the calculated [‘8FJFDGrate constants and a lumpedconstant ofO.52 (12). All emission data were corrected for tissueattenuation using transmission data measured by a 68Ge-68Gaexternalring source.

MR scanswere obtained using a 0.5 tesla superconductiveMRsystem (SMT-50X, Shimadzu, Kyoto) with a quadrature headcoil.All imagesweretaken in the axialprojection,parallelto theanterior commisure-posterior commisure (AC-PC) line, and were6 mm thick covering a 25-cm field of view. The pulse sequencewas 500/35/4 (TR/TE/excitations) by the gradient echo method

for the Ti-weighted image and 3000/35,90/1 by the double-spinecho method for the proton density-weighted and T2-weightedimages.

The PET and MR studies were performed at 6 mo and 1 yrafter CO intoxication, and the same scanning protocols wereemployed each time.

CaseA 29-yr-old woman was admitted following inhalation of

automobile exhaust fumes in a suicide attempt. Although her

A 29-yr-old woman was studiedfor 1 yr after acute carbonmonoxideintoxicationfollowingan attempted suicideby inhalation of automobile exhaust fumes. The patient demonstrated impaired responsiveness to stimuli without any spacific neurological defidts for 1 yr after carbon monoxideintoxication. Repeated braln magnetic resonance imagingconsistently displayed only bilateral globus pallidus lesions,but no lesions in either deep white matter or cerebral cortex.Positronemissiontomographymeasurementsof regionalcarebral blood flow, and glucoseutilizationrate were made inthis patient at 6 mo and 1 yr followingcarbon monoxideintoxication.Impairmentof both bloodflow and glucosemetabolism were found not only in the basal ganglia but also inmorphologicallynormal frontal cortex. The decrease in glucose utilization in the frontal cortex was greater than that inthe basal ganglia. Dunng the period of 6 mo to 1 yr, bloodflow and glucosemetabolismin the basalgangliarecoveredto the normal range. In the frontal cortex, however, bloodflow and glucose metabolism remained approximately 20%lower than the normal mean values. This prolonged dysfunction in the frontal cortex may therefore be responsible for theimpaired responsiveness of the subject.

J NucIMed1992;33:1696—1698

arbon monoxide (CO) intoxication produces profound anemic hypoxia due to its 250 fold higher affinityfor the ferrous haem of hemoglobin than oxygen (1-3).Survivors of acute CO intoxication often suffer from impaired responsiveness to stimuli, pyramidal and extrapyramidal deficits and other focal neurological disturbances(4). Bilaterallesionsofthe globuspallidusand hemisphericdeep white matter are frequently observed on both computed tomographic (CT) and magnetic resonance (MR)images (4-6). The abnormalities in perfusion and metabolism in the brains of survivors of acute CO intoxication,however, have not been documented. In this report, re

ReceivedDec.24,1991; revisionacceptedApr.21, 1992.For repdnts contact: Eku Shimosegawa, MD, Department of RadkIOgy and

Nuclear Medicine, 6-10 Senshu-Kubota Machi, Akita 010, Japan.

1696 The Journal of Nuclear Medicine •Vol. 33 •No. 9 •September 1992

CerebralBlood Flow and Glucose MetabolismMeasurements in a Patient Surviving One YearAfter Carbon Monoxide IntoxicationEku Shimosegawa, Jun Hatazawa, Ken Nagata, Toshio Okudera, Atsushi Inugami, Toshihide Ogawa,Hideaki Fujita, Hiroshi Itoh, Iwao Kanno, and Kazuo Uemura

Department ofRadiology and Nuclear Medicine and Department ofNeurology, Research Institute ofBrain and BloodVessels-Akita, Akita, Japan

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CBF(ml/100mI/mm)CMRGIu(mg/100mI/mm)Normal6

mo1 2 moNormal6 mo12moCortex

mean52.2 ±9.940.650.46.19 ±0.655.685.81Frontalcortex48.6 ±8.033.139.16.40 ±0.704.505.02Basal

ganglia59.3 ±12.935.053.76.20 ±0.615.095.46Centrumsemiovale26.4 ±5.323.424.33.22 ±0.283.142.63

FIGURE 1. T2-walghted axial MRimages obtained at45 (upperIeft)and80mm (upper right)aboveand paralleltoorbitomeatallineat 6mo after Co exposure. High intensityinthebilateralglobuspalliduswas evident.No detectable deepwhite matter demyelination was found.At 12 mo after COintoxication, therewere no remarkablechanges in correspondingMRimages(lower left and lowerright).

arterial carboxy hemoglobin concentration was not measured,she was diagnosed as suffering from CO intoxication circumstantially.On admission,she showedsymptomsof impairedresponsiveness, but showed no focal neurological deficits. Systemicarterial blood pressure, electrocardiographic and hematologicalexaminationswere normal. Althoughshe was under psychiatrictherapy, antidepressanttherapy and hyperbaricoxygentherapyfor 5 mo after the suicide attempt, her low spontaneity and slowresponsiveness did not change during that period.

Brain MR at 6 mo after the intoxication indicated symmetricalhigh intensity only in the bilateral globus pallidus on the T2-weighted image. No signal changes in deep white matter, corticalgray matter or the hippocampus were seen. The repeat MR studyat 12 mo after the intoxication showed no remarkable changes(Fig. 1).

RegionalCBF and glucoseutilization rates in the serial PETstudies are summarized in Table 1. Mean values from nine agematched normals (one female, eight males) obtained using thesame PET protocol are also listed in Table 1. The first PETexamination revealed 41% and 32% decreases in rCBF in thebasal ganglia, including the globus pallidus and frontal cortex,respectively, compared to normal mean. In the follow-up study,blood flow in the basal ganglia recovered to a value 10% lowerthan the normal, but frontal cortex blood flow was still 20%lower than the normal value. Glucose utilization rates in thefrontal cortex were most severelydecreasedamong brain structures in the repeated examination although morphological lesionswere detected only in the globus pallidus and not in the frontalcortex. No decrease in rCBF or rCMRG1u was evident in centrum

p; rr.r@t@-@3-f+@r 1h@ :r@e+

12 mor,tI-,@ •3-t@t@r@ .:r@@+

{-@T@'

FIGURE 2. PETrCBFandrCMRGIuimagescorrespondingtoMR imagesat 6 mo (upperraw)and 12 mo (bottomraw)afterCO intoxication.DecreasedCBF inthe bilateralbasalgangliaat6 mo (smallarrow)recoveredto normalrangeat 12 mo afterintoxication. The most severe decline in rCBF was found inbilateralfrontal cortex at 12 mo after CO exposure(arrowhead).Temporal and occipital cortex as well as thalamus showed nosignificantchangesduring this period (left column).Hypometabolism of glucose was found predominanfly In bilateral basalganglia and frontal cortex. In the follow-up study, no significantchanges of rCMRGIuwere evident. Glucose utilization in thefrontal cortex was still 22% lower than the normalmean.

semiovale in the repeatPET study. Figure2 illustratesTCBFandrCMRG1u images obtained at 6 and 12 mo after CO intoxication.

DISCUSSION

After exposure to CO, various levels of impaired consciousness and subsequent slow responsiveness to stimuliare characteristics of CO encephalopathy. Many patientssuffer from longstanding neuropsychiatric deficits and occasionally relapse to severe mental deterioration and fatalcoma (4). Neuropathologic studies have revealed that lesions in the globus pallidus and deep white matter are

TABLE 1Values of rCBF and rCMRGIu at 6 and 12 Months After Carbon Monoxide Intoxication

Carbon Monoxide Intoxication •Shimosegawa at al 1697

6iiionths after the onz•tCBF CMRG1u

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l2months after the onsetCBF CMRG1@

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frequently found in an autopsied brain ofCO encephalopathy (1). With the use ofCT (5) and, more recently, MRI(6), thesemorphologicalchangesarewelldocumented.Inparticular, MRI detected lesions in the spongy cerebralcortex, necrotic lesions in the hippocampus and globuspallidus, as well as demyeination in white matter (6).

To date, only a preliminary study of rCMRG1u in sixsurvivors of CO intoxication has been reported (13).Global cortical hypometabolism ofglucose utilization witha 15%-30% decrease was reported. This case also showedregional decreases in rCBF and rCMRG1u, predominantlyin the frontal cortex. Although the pathogenesis of COencephalopathy is not clearly established, flow-metabolismdisturbances detected in the PET measurements definitelyextended beyond the morphological lesions observed inthe MR images. Prolonged slow response and impairedspontaneity observed in the present case might be inducedby dysfunction of the frontal cortex. The measurement offlow and metabolism in patients with various severities ofCO encephalopathy may provide prognostic informationas well as improve the understanding of CO encephalopathy.

ACKNOWLEDGMENTS

We thank our staff for their generoushelp in completingthiswork. The present study was supported by grant 2A-l0 from theNational Center of Neurologyand Psychiatryand a grant forcardiovascular diseases (2A-2) from the Ministry of Health andWelfare.

1698 The Journal of Nuclear Medicine•Vol.33 •No. 9 •September1992

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1992;33:1696-1698.J Nucl Med.   Hiroshi Itoh, Iwao Kanno and Kazuo UemuraEku Shimosegawa, Jun Hatazawa, Ken Nagata, Toshio Okudera, Atsushi Inugami, Toshihide Ogawa, Hideaki Fujita,  One Year After Carbon Monoxide IntoxicationCerebral Blood Flow and Glucose Metabolism Measurements in a Patient Surviving

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