Altered local cerebral glucose utilization by unilateral frontal cortical ablations in rats

Alterations in local cerebral glucose utilization (LCGU) following ablations of the unilateral frontal cortex in rats were studied to elucidate the effect of the lesion on the functional activity in the related cerebral structures. Frontal cortical ablations (areas 2, 4, 6 and 10) were made by aspiration on the left side, and LCGU was evaluated at 7 days after the operation, using the [14C]deoxyglucose method. Significant decreases in LCGU in rats with unilateral frontal cortical ablations, were observed in the ipsilateral thalamic nuclei (ventroanterior-ventrolateral (VAL), ventrobasal (VB), reticular), red nucleus and pontine nucleus. The ipsilateral globus pallidus showed a significant LCGU increase. The contralateral cerebellar cortex showed a tendency toward a decrease in LCGU. The striatum, which receives direct projections from the frontal cortex, showed no LCGU change. These results indicated that ablations of unilateral frontal cortex in rats produced LCGU changes in the cerebral structures which have direct or indirect neuronal connections with the ablated area. These LCGU changes were, for the most part, brought about by alteration in the neuronal activity. Particularly, the LCGU increase in the globus pallidus which receives transsynaptic neuronal input from the frontal cortex, without changes in the striatum, which receives direct projection, was attributed to the functional alteration of the globus pallidus produced by the cortical ablation. Destructive lesion of a cerebral structure, therefore, does not necessarily cause functional depressions in the pertinent structures, but it may enhance the function of some structures, depending on the functional characteristics of each neuronal connection and functional organization of those structures.     

Alterations in local cerebral glucose utilization during electrical stimulation of the striatum and globus pallidus in rats

Alterations in local cerebral glucose utilization (LCGU) in conscious rats during electrical stimulation of the striatum and the globus pallidus were investigated using the [14C]deoxyglucose method. Stimulation of the globus pallidus produced a marked contraversive circling behavior, while stimulation of the striatum led only to contraversive head turning. Unilateral stimulation of the striatum increased LCGU bilaterally in the globus pallidus and substantia nigra pars compacta, but only ipsilaterally in the entopeduncular nucleus, substantia nigra pars reticulata and subthalamic nucleus. Similar stimulation of the globus pallidus increased LGCU in the globus pallidus, substantia nigra pars reticulata and compacta, entopeduncular nucleus, subthalamic nucleus, lateral habenular nucleus, parafascicular nucleus of the thalamus, deep layers of the superior colliculus and pedunculopontine nucleus, exclusively on the ipsilateral side. These results indicate that the electrical stimulation induces LCGU changes in the respective structures having both monosynaptic and transsynaptic neuronal inputs. Some changes may also be mediated by antidromic activation. They also suggest that activation of a synaptic process whether excitatory or inhibitory results in increases in LCGU. The bilateral modulatory effects of striatal stimulation may cancel out the circling behavior seen during pallidal stimulation, and cause only head turning.     

Effects of the self-administration of ethanol and ethanol/sucrose on rates of local cerebral glucose utilization in rats

In a previous study, the voluntary ingestion of ethanol by rats was found to be associated with a discrete pattern of changes in functional activity that included the nucleus accumbens, medial prefrontal cortex, basolateral and central nuclei of the amygdala, as well as the ventral midbrain. Rats in this study, however, consumed a combination of ethanol in a sucrose vehicle. The purpose of the present experiment was to characterize the role of sucrose in determining the effects of orally self-administered ethanol using the quantitative autoradiographic 2-[¹⁴C]deoxyglucose (2DG) method for measurement of rates of local cerebral glucose utilization. A modified sucrose-substitution procedure was employed to train three groups of Wistar rats to self-administer either water, 10% ethanol (10E), or a 10% ethanol/2% sucrose solution (10E/2S) in daily sessions. An additional group of rats was trained using a modified acclimation procedure (home cage) in order to determine if any exposure to sucrose would alter rates of glucose utilization. Once stable rates of consumption were established, the 2DG method was applied immediately following completion of the final test session. Rats received a dose of ethanol equivalent to 0.5 g kg⁻¹ on the day of the procedure or a comparable volume of water. Rates of energy metabolism were significantly increased in all three groups of rats that consumed ethanol (10E/2S, 10E, and home cage), as compared to rates in rats that consumed water. The areas of significant change included the rostral pole and posterior shell of the nucleus accumbens, medial prefrontal cortex, the basolateral and central nuclei of the amygdala, the ventral tegmental area, and the substantia nigra pars compacta. Thus, the pattern of changes in functional brain activity that accompanies voluntary ingestion of ethanol is independent of the vehicle in which the ethanol is presented or the procedures used to initiate consumption. Furthermore, these data demonstrate that it is the simultaneous activation of an interrelated network of limbic brain regions that serves as the substrate of the effects of ethanol self-administration.     

Acute administration of high doses of estrogen increases glucose utilization throughout brain

The effects of high intravenous doses of estradiol benzoate on local cerebral glucose utilization were studied by the [14C]2-deoxyglucose method in conscious ovariectomized adult rats. Statistically significant increases in glucose utilization averaging 20% were observed in 42 of 60 anatomically discrete regions of the estrogen-treated animals. The possible role of catechol estrogen, a potent inhibitor of catechol-O-methyltransferase, in these effects is considered.     

Effects of lateral habenular lesions on local cerebral glucose utilization in the rat

The autoradiographic 2-[14C]deoxyglucose method was employed to map the distribution of the changes in local cerebral glucose utilization following unilateral and bilateral electrolytic lesions of the lateral habenula nucleus. Local cerebral glucose utilization was measured one week after the placement of the lesions. Unilateral lesions of the nucleus had no effect on the rates of glucose utilization in the 79 brain structures examined. Bilateral lesions, however, produced selective reductions in glucose utilization in several structures compared to the results in sham-operated animals. Reductions were found in the dorsal and median raphe nuclei and the ventral and dorsal tegmental nuclei which receive projecting fibers mainly from the medial part of the lateral habenula nucleus. The rates of glucose metabolism in the interpeduncular nucleus and mamillary body were also reduced by the bilateral habenular lesions. No anatomic structures rostral to the lesions were metabolically affected.     

Effects of dopaminergic agonists and antagonists on [H]apomorphine binding to striatal membranes: sulpiride lack of interactions with positive cooperative [H]apomorphine binding

Effects of dopaminergic agonists and antagonists on [³H]apomorphine binding to striatal membranes of rat brain was examined. Haloperidol and spiroperidol exhibited biphasic inhibition of [³H]apomorphine binding; one of which had the Hill coefficient of 0.9, whereas the other had that of 0.4. The former accounted for 65% of [³H]apomorphine binding while the latter consisted of 35% of the binding. Furthermore, the latter disappeared after kainic acid lesions. On the other hand, sulpiride and metoclopramide reduced [³H]apomorphine binding to 31% with the Hill coefficient of 0.9. The inhibition of [³H]apomorphine binding with the Hill coefficient of 0.4 which was shown by haloperidol and spiroperidol was not observed for sulpiride and metoclopramide.Previously, we demonstrated non- and positive-cooperative [³H]apomorphine binding to striatal membranes. In the present study, it has been also shown that sulpiride inhibits non-cooperative [³H]apomorphine binding leaving that with allosteric properties unaffected. No inhibition of dopamine-sensitive adenylate cyclase was observed by 10⁻⁴ M sulpiride while 90% inhibition was obtained with 10⁻⁵ M haloperidol. From those results, it is suggested that non-cooperative [³H]apomorphine binding is not coupled with dopamine-sensitive adenylate cyclase.     

Olfactory bulbectomy reduces cerebral glucose utilization: 2-[14C]deoxyglucose autoradiographic study

The olfactory bulbectomized (OBX) rat is an extensively investigated animal model of depression. In the present study the effects of olfactory bulbectomy in drug-naive adult male Sprague–Dawley rats (200–240 g) on global (gCGU) and regional cerebral glucose (rCGU) utilization was evaluated. Two weeks following surgery, the autoradiographic measurement of CGU using [¹⁴C]-2-deoxyglucose was employed. The levels of CGU in the OBX and sham-operated rats were compared in 40 brain regions. Statistical methods indicate significantly lower levels of global (overall) CGU in the OBX group than in the sham group. Discriminant analysis was done on the z-scores to remove animal to animal variability. The following thirteen regions were identified by the stepwise discriminant analysis of the z-scores as significantly contributing to the differences between the sham and OBX: amygdala, cingulate cortex, caudate putamen at the level of globus pallidus, caudate putamen-lateral part, dorsal subiculum, dorsal thalamus, hypothalamus, median raphe, somatosensory cortex, substantia nigra, ventral hippocampus, ventral tegmental area and the ventral thalamus. The pattern of changes in the rCGU following OBX does not completely correlate with the pattern of connectivity of the olfactory bulbs, however, many regions with direct connection to the olfactory bulbs (e.g., amygdala, hypothalamus, ventral hippocampus, and ventral tegmental area) were found to be important for differentiation. No left to right asymmetries in the rCGU were found. The data suggest that there are very important regional differences in glucose utilization between the OBX and sham operated rats, which points to the need to study antidepressants in an animal model of depression rather than in normal animals.     

Global increase in cerebral metabolism and blood flow produced by focal electrical stimulation of dorsal medullary reticular formation in rat

We sought to determine whether the increases in local cerebral blood flow (LBCF) elicited by focal electrical stimulation within the dorsal medullary reticular formation (DMRF), are secondary to or independent of, increased local cerebral glucose utilization (LCGU).Rats were anesthetized (chloralose), paralyzed, artificially ventilated and arterial pressure and blood gases controlled. LCBF and LCGU were determined in two separate groups of animals, using the autoradiographic [¹⁴C]iodoantipyrine and [¹⁴C]2-deoxyglucose methods, respectively. In unstimulated controls, LCBF (n= 5) and LCGU (n= 5) were linearly related (r = 0.780; P < 0.001) in the 27 brain regions studied. During DMRF stimulation LCGU increased significantly in 21 of the 27 regions, including cerebral cortex (up to 168% of control), thalamic nuclei (up to 161%) and selected ponto-medullary regions (e.g. parabrachial complex: 212%; vestibular complex: 147%). Along with LCGU, LCBF rose significantly in 25 regions (sensory motor cortex: 163%; anterior thalamus: 161%; parabrachial complex: 186%). Correlation analysis demonstrated that, during DMRF stimulation, the close relationship between LCBF and LCGU is preserved (r = 0.845; P < 0.001) and that, in addition, the increase in LCBF (δ LCBF) is proportional to the increase in LCGU (δ LCGU) (δLCGU+ 6.92; r = 0.7729; P < 0.001).Excitation of neurons or fibers within DMRF increases brain metabolism globally and blood flow secondarily. The DMRF appears to modulate cerebral metabolism globally, by as yet undefined pathways.     

Rolling mouse Nagoya as a mutant animal model of basal ganglia dysfunction: determination of absolute rates of local cerebral glucose utilization

In order to elucidate the neuronal mechanism of the motor disturbances of the Rolling mouse Nagoya (rolling), a neurological mutant mouse (genotype rol/rol) showing frequent lurching and falling over on walking, we determined absolute rates of local cerebral glucose utilization (LCGU) with the [14C]deoxyglucose method. The rates were compared with those of heterozygote (+/rol) with normal behavior, and of normal mice (+/+) of the same strain (C3Hf/Nga). Rolling showed marked and significant increases in LCGU in the structures of the basal ganglia such as the globus pallidus, entopeduncular nucleus, substantia nigra pars compacta and pars reticulata, and subthalamic nucleus, confirming our previous finding with semiquantitative LCGU determination. Additional significant but much less marked increases in LCGU of rolling were found in some structures of the brainstem and limbic system, such as the pedunculopontine nucleus, red nucleus, ventral tegmental area, lateral habenula, and CA1 and CA3 of the hippocampus. Although rolling has been regarded as an animal model of cerebellar ataxia, rolling showed no alterations of LCGU in the cerebellum. The heterozygote showed intermediate increases in LCGU between rolling and normal mice in the basal ganglia structures such as the globus pallidus, substantia nigra pars reticulata and subthalamic nucleus. Our findings indicate that rolling has a definite, genetically determined dysfunction of the basal ganglia. The primary site of the basal ganglia dysfunction might probably be in the striatum, involving both the neostriatum and limbic striatum, and resulting in secondary dysfunction in their target structures.     

Elevated glucose utilization in subfornical organ and pituitary neural lobe of the Brattleboro rat

Homozygous Brattleboro rats have a genetic inability to synthesize vasopressin and therefore manifest the signs and symptoms of diabetes insipidus. Measurement of local cerebral glucose utilization in these rats has revealed increases specifically localized to the subfornical organ and pituitary neural lobe. Vasopressin replacement reverses the increased glucose utilization only in the subfornical organ. The results suggest that vasopressin regulates the rate of glucose metabolism in the subfornical organ.     

Arecoline-induced elevations of regional cerebral metabolism in the conscious rat

Local cerebral glucose utilization (LCGU) was measured, using the quantitative [14C]2-deoxy-D-glucose ([14C]DG) method, at 3 min after administration to 3-month-old, awake Fischer rats of the muscarinic agonist arecoline (AREC) 0.05, 0.5, 5, 15 or 50 mg/kg or saline i.p. Animals were pretreated with methylatropine (a cholinergic antagonist which does not enter the brain and has no effect on cerebral metabolism) 4 mg/kg s.c. to prevent parasympathomimetic side-effects of AREC. Tremor produced by AREC was rated subjectively. Intensity of tremor was dose-related, peaked at 2-5 min after AREC, and abated within 30 min. Elevations in LCGU (measured after [14C]DG injection during peak behavior) in extrapyramidal regions, which mediate tremor, were related to the intensity of tremor. The lowest dose of AREC selectively increased LCGU in the hippocampus and median raphe; higher doses produced more generalized metabolic enhancement. In the hippocampus and cortex, LCGU rose in layers in which cholinoceptive cells are located. Regions of the auditory pathway and superficial neocortical layers (I-III) were generally unaffected by AREC, but LCGU did not decrease in any region. The selective increase in LCGU produced by low doses of AREC in the hippocampus presumably is due to a specific action of AREC, and demonstrates the high sensitivity of this region to cholinomimetic stimulation.     

Effects of MK-801 upon local cerebral glucose utilisation in conscious rats following unilateral lesion of caudal entorhinal cortex

Local cerebral glucose utilisation was examined in 62 discrete regions of conscious rats following unilateral ibotenic acid lesion of the caudal entorhinal cortex, and subsequent pharmacological challenge with (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist. Fourteen days after unilateral lesion of the entorhinal cortex, there were no significant alterations in local cerebral glucose use except within the lesioned entorhinal cortex (reduced by 31% compared to sham-operated control animals). In sham-operated animals, systemic administration of MK-801 (0.5 mg/kg, i.v.) induced anatomically organised alterations in glucose use with increases in olfactory areas, subicular complex and some limbic areas (posterior cingulate cortex, mammillary body and anteroventral thalamic nucleus), and decreases in the inferior colliculus and neocortex (auditory, sensory-motor, somatosensory and frontal cortices). In animals with unilateral entorhinal cortex lesions, the metabolic response to MK-801 differed significantly from the response to the drug in sham-lesioned animals in a number of regions, viz. hippocampus, molecular layer (ipsilateral to lesion), entorhinal cortex (ipsilateral), dentate gyrus (ipsilateral), presubiculum (bilateral), parasubiculum (bilateral) and nucleus accumbens (bilateral). The ability of MK-801 to reduce glucose use in the neocortex was not altered by entorhinal cortex lesion. These data suggest that the functional consequences of non-competitive NMDA receptor blockade are dependent in some areas upon the integrity of the perforant pathway from the entorhinal cortex to the hippocampus.     

Differences in quinpirole-induced local cerebral glucose utilization between naive and sensitized rats

Dopaminergic psychostimulants produce behavioral responses of greater magnitude with repeated, intermittent administration, than a single, acute dose, a phenomenon known as ‘sensitization’. Alterations in regional neuronal activity produced by quinpirole, a D₂/D₃ agonist, in quinpirole-naive and quinpirole-sensitized rats were assessed on the basis of local cerebral glucose utilization (LCGU) using the [¹⁴C]2-deoxyglucose (2-DG) method. Adult, male Long-Evans rats (180–200 g, n=7–9/group) were subjected to ten injections of quinpirole (0.5 mg/kg, s.c.) administered every 3rd day; controls and quinpirole-naive rats received saline. Locomotor activity was quantitated after injections one and ten to confirm sensitization. The 2-DG procedure was initiated 60 min after an 11th injection in freely moving rats. LCGU was determined in 43 brain regions by quantitative autoradiography. In quinpirole-naive rats, quinpirole decreased LCGU in the caudate/putamen (84% of control), lateral habenula (80% of control), and motor cortex (79% of control). In sensitized rats, quinpirole decreased LCGU in the nucleus accumbens core and shell (77 and 83% of control, respectively) and ventral pallidum (82% of control) as well as in the caudate/putamen (86% of control), lateral habenula (77% of control), and motor cortex (79% of control). This suggests that decreased neuronal activity in the nucleus accumbens and ventral pallidum may underlie the augmented behavioral response to quinpirole in sensitized animals.     

Correlation of age and body weight with local cerebral glucose utilization in 8–14 week-old rats

The regional cerebral metabolic rate for glucose (rCMRgl) in 8–14 week-old, male, albino, Wistar rats, weighing 200–385 g was a autoradiographically measured using the [¹⁴C]2-deoxyglucose (2-DG) technique. Three age-weight groups of rats were tested: (I) 8–9 weeks old (200–250 g, average227 ± 14); (II) 10–11 weeks old (255–300 g, average280 ± 15g); (III) 12–14 weeks old (305–385 g; average331 ± 25g). A gradual reduction in rCMRgl was observed in the older and heavier groups. The reductions were statistically significant in 18/28 investigated structures in group III as compared to group I. Since such significant variation in the investigated age-weight range may affect rCMRgl values obtained in different experiments, it is suggested to use narrow and uniform age-weight groups for experimentation concerning brain metabolic functions.     

Short- and long-term effects of neonatal diazepam exposure on local cerebral glucose utilization in the rat

The short- and long-term consequences of a neonatal exposure to diazepam (DZP) on the postnatal changes in local cerebral metabolic rates for glucose (LCMRglcs) were studied by the quantitative autoradiographic [¹⁴C]2-deoxyglucose method in a total number of 66 brain structures of freely moving rats. Rat pups received a daily subcutaneous injection of 10 mg/kg DZP, of the dissolution vehicle of saline from postnatal day 2 (P2) to 21 (P21). The animals were studied at 4 ages, P10, P14, P21 and P60. DZP induced a decrease in LCMRglcs which was restricted to 13 areas at P10, mainly sensory and limbic regions. At P14, the treatment had significant metabolic effects on 48 structures belonging to all functional systems. By P21, 23 brain areas were still affected by the treatment, mainly sensory, limbic and motor areas. At P60, i.e. at about 40 days after the end of drug exposure, LCMRglcs still decreased in 14 brain regions which were mainly sensory and limbic structures. The structures most sensitive to both short- and long-term consequences of the anticonvulsant treatment are mammillary body, limbic cortices and sensory regions. The dissolution vehicle increased LCMRglcs in a few brain regions at P14 and P60, whereas it decreased metabolic levels in 5 brain regions at P21. The results of the present study show that the brain appears to be particularly vulnerable to the treatment at P14, period of active brain growth, whereas by P21, the drug is more actively metabolized and a tolerance to the treatment may occur. The long-term effects of the treatment are in good accordance with the well-known effects of DZP on anxiety, sedation and memory. The structures most sensitive to early neonatal DZP exposure are the mammillary body, limbic cortices and sensory regions that all contain a high density of benzodiazepine binding sites.     

Chronic escapable footshock causes a reduced response to morphine in rats as assessed by local cerebral metabolic rates

The 2-deoxy-d-[¹⁴C]glucose (2-DG) method was used to examine the effects of morphine sulfate (MS) on local cerebral metabolic rates for glucose (LCMR_glu) in male F-344 rats required to turn a wheel manipulandum in order to escape from nociceptive footshock. This nociceptive stimulus was identical with that utilized in a previous 2-DG study from this laboratory [15] except that animals were exposed to 15 daily 30 min sessions of footshock prior to the 2-DG testing day rather than a single footshock exposure. This allows a direct comparison of the effects of morphine in chronic and acute pain. Unlike the acute footshock study, morphine in chronic footshock rats did not have a significant effect compared with chronic footshock alone in any of the 73 measured brain structures, including limbic and midline thalamic structures previously shown to be important in morphine-induced analgesia during acute pain [15]. Whereas 93% of measured cerebral structures showed decreases in LCMR_glu following morphine administration in the acute footshock rats, morphine given to chronic footshock rats caused decreases in only 56% of the structures as compared with chronic footshock plus saline. It is hypothesized that these differential effects of morphine are due in part to a habituation to the chronic stressor such that chronic footshock rats are less stressed than acute footshock rats. Additionally, it is suggested that chronic exposure to pain produces a constant elevation of opioid peptides leading to opioid receptor downregulation and consequently morphine tolerance. These results demonstrate that, even in the presence of the same nociceptive stimulus, morphine can have widely disparate effects on brain metabolism if there are differences in the pain history of the animal.     

Effects of electrolytic and 6-hydroxydopamine lesions of the lateral hypothalamus on rotation evoked by electrical stimulation of the substantia nigra in rats

Contralateral rotation evoked by electrical stimulation of the left substantia nigra was studied in rats before and after electrolytic or 6-hydroxydopamine (6-OHDA) lesions of the lateral hypothalamus. Electrolytic lesions (2 mA DC, 15 sec) which produced mean ipsilateral striatal dopamine depletion of 58% significantly reduced the rotation at 2 h to 14 days postlesion. 6-OHDA (8 μg in 4 μl) which produced mean ipsilateral striatal dopamine depletion of 93% significantly increased the rotation at 3 to 14 days postlesion. Haloperidol 0.1 and 0.5 mg/kg i.p. partially reduced rotation in both control and lesioned rats in a dose-related manner. Control and lesioned rats showed no sognificant differences in haloperidol sensitivity. If stimulus induced rotation were mediated by activation of dopaminergic neurons, one would have expected lesion effects in the present experiments to parallel those on rotation caused by pharmacologically evoked release of dopamine. The lesion effects we obtained on stimulus induced rotation, however, parallel those on rotation evoked by the predominantly directly acting dopamine agonist, apomorphine, rather than those on rotation evoked by the indirect (presynaptic) action of amphetamine. We suggest that contralateral rotation evoked by electrical stimulation of the substantia nigra may reflect direct activation of neurons postsynaptic to the dopaminergic nigrostriatal neurons.     

Double-tracer autoradiographic study of protein synthesis and glucose consumption in rats with focal cerebral ischemia

Abstract

A double-tracer autoradiographic method for simultaneous measurement of regional glucose utilization (rCMR_glc) and regional protein synthesis (PS) in consecutive brain sections is described and applied to study the metabolism of the ischemic penumbra 2 h after occlusion of the middle cerebral artery (MCAO) in rats. In halothane anesthesia, the left middle cerebral artery was permanently occluded. Two hours after MCAO an i.v. bolus injection of ¹⁴C-deoxyglucose and ³H-leucine was given and circulated for 45 min. Two sets of brain sections were processed for quantitative autoradiography. Neighboring brain sections exposed an X-ray film (3 H-insensitive), and a ³H-sensitive for determination of rCMR_glc and PS, respectively. Sections for PS determination were washed in trichloroacetic acid (TCA) prior to film exposure in order to remove ¹⁴C-deoxyglucose and unincorporated ³H-leucine. Regional rates of PS and glucose utilization were measured by densitometric image analysis. Normal rates of metabolism were defined as mean ± 2 SD of values in the non-ischemic cortex. The volumes of ischemic cortex displaying normal rates of PS and glucose utilization, respectively, were measured. The cortical volume with normal PS was significantly less than that of normal rCMR_glc: 142 (127-147) mm³ vs. 203 (184-206) mm³. Treatment with the glutamate antagonists MK-801 (1 mgkg^–1) and NBQX (30 mg kg^–1 x 2) did not significantly change this, although MK-801 tended to reduce the size of the metabolic penumbra calculated as the difference between ischemic cortex with reduced PS and ischemic cortex with reduced rCMReic. [Neurol Res 1991; 21: 687–694]     

Depressed cerebellar glucose metabolism in supratentorial tumors

Fifty-four patients with supratentorial tumor and one with brainstem tumor were examined with emission tomography (PET) using [¹⁸F]fluoro-deoxyglucose (FDG). Twenty-one of these cases had satisfactory studies of the cerebellum. Of these, 12 showed significant metabolic asymmetry between the two cerebellar hemispheres, with the rate of glucose utilization in the hemisphere contralateral to the cerebral tumor being 8–34% lower than on the ipsilateral side, as compared with a right-left asymmetry of only— 1.6% ± 2.1% standard deviation for a group of 5 normal subjects. In these 12 cases the tumor involved the sensorimotor cortex and/or the thalamus with varying degrees of hemiparesis being present. For the remaining 9 patients with no significant cerebellar metabolic asymmetry, the tumor involved regions other than the sensorimotor cortex, and unilateral motor dysfunction was not a prominent clinical feature.The correlation between cerebellar metabolic suppression and unilateral motor dysfunction observed in our cases appears to be due to impairment or interruption of the cortico-thalamo-ponto-olivo-cerebellar circuitry by either the tumor itself or by edema. These results illustrate the ability of FDG-PET scans to detect metabolic changes, not apparent on CT scans, in areas of the brain remote from the primary lesion.