Cerebral metabolic rate

Relatively few human imaging studies have evaluated the effects of marijuana or THC on metabolism or blood flow. Acute intravenous THC in both normal controls and habitual marijuana users led to increased an increased regional cerebral metabolic rate (CMR) in the cerebellum. This increase is positively correlated both with concentrations of THC in the plasma and with the intensity of the subjective sense of intoxication [5]. In a 1997 PET/[lsO]water study with 32 abusers [6], THC dose-depend-ently increased cerebral blood flow (CBF) in the frontal regions, insula... 

Kennedy, C. Sokoloff, L. (1957). An adaptation of the nitrous oxide method to the study of the cerebral circulation in children normal values for cerebral blood flow and cerebral metabolic rate during childhood. J. Clin. Invest. 36, 1130-7. 

Cerebral metabolic rate increases during early development 535... 

Cerebral metabolic rate declines from developmental levels and plateaus after maturation 535... 

TABLE 31-2 Cerebral metabolic rates (CMR) are regionally and activity-dependent... 

The rate of blood flow in different structures of the brain reaches peak levels at different developmental stages, depending on the maturation rate of the particular structure. In structures that consist predominantly of white matter, the peaks coincide roughly with maximal rates of myelination. From these peaks, blood flow and, probably, cerebral metabolic rate decline to the levels characteristic of adulthood [2,39,44],... 

Cerebral metabolic rate declines from developmental levels and plateaus after maturation. Reliable quantitative data on the changes in cerebral circulation and metabolism in humans from the middle of the first decade of life to old age have been reported [2,39,44]. By 6 years of age, cerebral blood flow and oxygen consumption already have attained high rates, and they decline thereafter to the rates of normal young adulthood [45]. Oxygen is utilized in the brain almost entirely for the oxidation of carbohydrates [46]. The equation for the complete oxidation of glucose is ... 

Kinnala, A., Suhonen-Polvi, H., Aarimaa, T. etal. Cerebral metabolic rate for glucose during the first six months of life an FDG positron emission tomography study. Arch. Dis. Child. Fetal Neonat. Ed. 74 F153-F157,1996. 

Heiss, W. D., Pawlik, G., Herholz, K. etal. Regional kinetic constants and cerebral metabolic rate for glucose in normal human volunteers determined by dynamic positron... 

Ammonia concentrations in arterial blood of patients with liver failure rise to 0.5-1 mmol/1, in contrast to the normal range of 0.01-0.02 mmol/1. Using positron emission tomography (PET see Ch. 58), increases of the cerebral metabolic rate for ammonia (CMRA), i.e. the rate at which ammonia is taken up and metabolized by the brain, have been reported in chronic liver failure [9]. Increased CMRA in chronic liver failure is accompanied... 

ATF activating transcription factor CMR cerebral metabolic rate... 

ATP adenosine 5 -triphosphate CMRglc cerebral metabolic rate for glucose... 

AZM active zone material CMRA cerebral metabolic rate for ammonia... 

BBB blood-brain barrier cmro2 cerebral metabolic rate for oxygen... 

Baxter, L.R., Phelps, M.E., Mazziotta, J.C., Schwartz, J.M., Gerner, R.H., Selin, C.E., and Sumida, R.M. (1985) Cerebral metabolic rates for glucose in mood disorders. Studies with positron emission tomography and fluorodeoxyglucose F 18. Arch Gen Psychiatry, 42 441-447. 

Nonetheless, there is considerable cause for concern about the use of psychotropic medication in preschool-age children during a period of continued rapid neural maturation (including synaptic remodeling and construction). The cortical synaptic density reaches its maximum at the age of 3 years and is substantially modified by the pruning process during the next 7 years (Huttenlocher, 1990). At the same time, the cerebral metabolic rate peaks between 3 and 4 years of... 

Neuroimaging techniques assessing cerebral blood flow (CBF] and cerebral metabolic rate provide powerful windows onto the effects of ECT. Nobler et al. [1994] assessed cortical CBE using the planar xenon-133 inhalation technique in 54 patients. The patients were studied just before and 50 minutes after the sixth ECT treatment. At this acute time point, unilateral ECT led to postictal reductions of CBF in the stimulated hemisphere, whereas bilateral ECT led to symmetric anterior frontal CBE reductions. Regardless of electrode placement and stimulus intensity, patients who went on to respond to a course of ECT manifested anterior frontal CBE reductions in this acute postictal period, whereas nonresponders failed to show CBF reductions. Such frontal CBF reductions may reflect functional neural inhibition and may index anticonvulsant properties of ECT. A predictive discriminant function analysis revealed that the CBF changes were sufficiently robust to correctly classify both responders (68% accuracy] and nonresponders (85% accuracy]. More powerful measures of CBF and/or cerebral metabolic rate, as can be obtained with positron-emission tomography, may provide even more sensitive markers of optimal ECT administration. 

HI based on their findings of incomplete recovery of NTP. However, as the cerebral metabolic rate of oxygen did not correlate with any metabolic changes, they concluded impaired mitochondrial function could not be the only factor. 

Sevoflurane has a dose-dependent effect on cerebral blood flow and intracranial pressure cerebral autoregulation is preserved (this is not the case with isoflurane). During hypocarbia, in the absence of nitrous oxide, 1 MAC does not increase intracranial pressure (ICP). It reduces the cerebral metabolic rate for oxygen (CMR02) by approximately 50% at concentrations approaching 2 MAC. This is similar to the reduction observed during isoflurane anaesthesia. 

Desflurane reduces cerebral metabolic rate for oxygen (CMR02) to a similar extent as isoflurane. Cerebral vascular resistance is reduced and is accompanied by an increase in cerebral blood flow (0.5-2.0 MAC). It suppresses EEC activity and there is no evidence of epileptiform activity. Somatosensory evoked potentials are preserved at clinical concentrations. 

Ethosuximide has an important effect on Ca2+ currents, reducing the low-threshold (T-type) current. This effect is seen at therapeutically relevant concentrations in thalamic neurons. The T-type calcium currents are thought to provide a pacemaker current in thalamic neurons responsible for generating the rhythmic cortical discharge of an absence attack. Inhibition of this current could therefore account for the specific therapeutic action of ethosuximide. Ethosuximide also inhibits Na+/K+ ATPase, depresses the cerebral metabolic rate, and inhibits GABA aminotransferase. However, none of these actions are seen at therapeutic concentrations. 

Fig. 4.4. Bar graph of viability thresholds of cerebral blood flow for a variety of functions and metabolites. Note that selective neuronal loss occurs at consistently higher flow values than overt infarction. CMRG, cerebral metabolic rate of glucose PCr, phosphocreatine ATP, adenosine triphosphate. [Adapted and reproduced with permission from Hossmann (1994)]...

When mild hypothermia was first shown to be beneficial, the assumption was that a substantial portion of its neuroprotective effect stemmed from a reduction in cerebral metabolism. However, studies on cerebral metabolic rate (CMR) made it clear that the degree of neuro-pathological injury following ischemia with mild hypothermic treatment did not correlate with the magnitude of metabolic depression observed (42). A reduction in temperature from 37°C to 34°C produces a 15-20% reduction in cerebral metabolism (approx 5-7% per °C), which is far less than the 50% decrease seen with electroencephalogram (EEG) silence. Furthermore, reductions in metabolism produced by anesthetics vs hypothermia are not equally neuroprotective (43). Thus, hypothermic neuroprotection cannot be explained by alterations in metabolic rate alone. 

Nakashima K., Todd M. M., and Warner D. S. (1995) The relation between cerebral metabolic rate and ischemic depolarization. A comparison of the effects of hypothermia, pentobarbital, and isoflurane. Anesthesiology 82, 1199-1208. 

CBF, Cerebral blood flow CMR02, cerebral metabolic rate for oxygen ICP, intracranial pressure CPP, cerebral perfusion pressure. 

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