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Neuroradiology(1982)23 : 4547

© Springer-Verlag 1982

Demonstration of Decreased Functional Activity of Visual Cortex
by [11C]Methylglucose and Positron Emission Tomography
W.-D. Heiss 1, K. Vyska 2, G. Kloster 3, H. Traupe 1, C. Freundlieb 2, A. Hoeck 2, L. E. Feinendegen 2
and G. Stoecklin 3
~MaxPlanck Institute for Brain Research, Cologne; 2MedicalInstitute and
3Institute of Chemistry I (Nuclear Chemistry), Nuclear ResearchCenter, Jfilich, FR G

Summary. A hemorrhagic infarction which caused
left hemiparesis and homonymous hemianopia was
demonstrated as a hypodense lesion on the first CT; 2
weeks later it was hyperdense and enhanced after injecting meglumine. Positron emission tomography
with [11C]methyl_D_glucose also revealed the ischemic lesion, but also marked decrease of glucose uptake
in the visual cortex, which indicated decreased functional activity.

Key words: Positron

emission tomography [11C]methyl-D-glucose - Functional activity, decreased - Visual pathway, interruption

The coupling of functional activity and metabolism in
centers of the brain was demonstrated by []4C]deoxyglucose autoradiography in animal experiments
[1] and by [iSF]deoxyglucose positron emission tomography (PET) in humans [24]. The lack of activation due to interruption of visual pathways was repeatedly shown in animal experiments [5, 6], but reports on such phenomena in patients with focal brain
damage are still scarce [4]. The following case demonstrates an ischemic lesion causing interruption of a
sensory pathway leading to inactivation of visual cortex.

Case Report
A 29-year-old man suddenly developed left hemiparesis at 10 pm on 28 December 1980. On the next
morning he was admitted to hospital, alert, with left
hemiparesis, deviation of the head to the right, and
left homonymous hemianopia. There was no sensory
disturbance.

Electroencephalogram showed a theta-delta focus over the fight anterior half of the head. Doppler
sonography indicated a high grade stenosis of the internal carotid artery at the bifurcation, which was
proved by carotid angiography.
Computed tomography (CT) (30 December 1980)
revealed a large hypodense lesion on the right, which
compressed the lateral ventricle and shifted the midline to the left (Fig. 1). CT on 13 January 1981 revealed
a hyperdense mass 2-3cm in size in the temporal
operculum, but the ventricle was not compressed and
the midline not shifted. EnhanCement was visible in
the caudate nucleus and parietal lobe after an injection of meglumine (Fig. 2). This CT was interpreted as
an infarction with secondary hemorrhage.
The patient's condition improved slightly. He was
able to walk with help, to raise his left arm at the
shoulder and to move his fingers, but the homonymous hemianopia did not change.
Positron emission tomography (PET) was performed on 20 January 1981 after injecting 3 mCi
3 [11C]methyl-D-glucose [HCMG] utilizing
an
ECAT II (EG & G Ortec) with medium resolution
shadow shield and high resolution data collection
mode. I~CMG has been previously shown to be a suitable agent for scanning the glucose transmembrane
transport [7, 8]. From twenty 2-min scans starting 40 s
after tracer injection accumulation curves were calculated in selected regions of interest corresponding to
the superior longitudinal sinus as an internal blood
standard and to various areas in the gray and white
matter of infarcted and normal brain. Regional perfusion and glucose transport rates were calculated from
these accumulation curves [9]. Distribution of 11CMG
was studied in integral images from several single
scans taken at a time when the isotope was accumulated in the brain tissue, and a five point smoothing and
color coding of accumulated regional ~ C M G activity

0028-3940/82/0023/0045/$01.00

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Fig. 1. CT at OM + 6 cm 2 days after
stroke shows large hypodense lesion
on fight
Fig.2. CTs at OM + 5.5 and OR +
6.5 cm after contrast injection 15 days
after stroke show hyperdense mass in
temporal operculum and enhancement within previously hypodense
lesion

in normal cortex) [9], and the perfusion to 0.68
ml/g min (0.8-0.98 ml/g rain in normal cortex) [9].

Discussion

Fig.3. Positron emission tomographic image at OM + 5-6 cm of
I~CMG distribution showing large right frontotemporal and occipital (visual cortex) defects. The figure is a black and white reproduction of a color image where highest activity in the cortex is represented as dark red; this red appears as black in the black and white
print

was used to improve the quality of the image. The image taken 5-6 cm above the orbitomeatal line (Fig. 3)
clearly showed, as did CT, the large frontotemporal
ischemic area extending from the surface of the brain
to the depth. The rate of accumulation in this area was
very low (more than 20 min compared to 2-3 min in
normal gray matter), indicating necrosis of the tissue.
An area with markedly decreased 11CMG uptake was
also visible in the visual cortex of the occipital lobe,
where CT did not show any abnormality. The glucose transport of this area w a s decreased to
0.35 l.tmol/g min (compared to 0.43-0.6 .umol/g min

1 1 C M G c a n be used for imaging the distribution of
glucose in the brain [10], but the formulation of an appropriate model and the quantification of transfer
and perfusion values [9] are complicated by back diffusion of the tracer which cannot be further metabolized [11]. However, the distribution of the tracer is dependent on the flow and the metabolism of cerebral
tissue; this is well demonstrated by the lack of uptake
in the ischemic area. The markedly decreased uptake
in an area with intact structure but impaired function,
as is the visual cortex in our case, also stresses the usability of this tracer for metabolic studies. The metabolic response of the primary and associative visual
cortex to stimulation with simple or complex visual
scenes was demonstrated with [18F]deoxyglucose [3]
and was also observed with 11CMG [10]. This report
stresses the usefulness of 11CMG as a tracer for depressed cortical activity due to deafferentiation; the
results are comparable to the data obtained with
[18F]deoxyglucose [4]. However, with an appropriate
model [9] 11CMG as a single tracer may be suitable to
demonstrate perfusion and transfer of glucose in normal and ischemic brain, which, until now, could be
achieved only by a double tracer technique as applied
by Kuhl et al. [12] for the investigation of stroke patients.

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47
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Received: 4 November 1981
Dr. W.-D. Heiss
Max-Planck-Institut ffir Hirnforschung
Forschungsstelle ftir Hirnkreislaufforschung
Ostmerheimer Strage 200
D-5000 K61n91
Federal Republic of Germany