Histopathological studies were carried out on temporal lobe tissue from 25 patients with partial complex seizures who were studied by interictal positron computed tomography (PCT) with 18F-fluorodeoxyglucose and subsequently underwent anterior temporal lobe resection. Abnormalities were identified on x-ray computed tomographic scans in 7 patients, but none indicated the site of a pathologically confirmed structural lesion. Hypometabolic zones were observed on PCT scans of 22 patients and corresponded to focal pathological abnormalities in 19 (15 mesial temporal sclerosis, 2 small neoplasms, 1 angioma, 1 heterotopia). In 1 patient with a focally abnormal PCT scan and no pathological changes, the lesion may have been located posterior to the resection. In the remaining 2 patients, the hypometabolic zones later disappeared and may have represented a transient response induced by depth electrode implantation. Three patients with normal PCT scans had no pathological abnormalities in their resected tissue. The degree of relative hypometabolism measured by PCT correlated well with the severity of the pathological lesion, but the size of the hypometabolic zone was generally much larger than the area of pathological involvement. This discrepancy could not be considered an artifact of technique and must represent either structural abnormalities below the resolution of routine histopathological studies (e.g., loss of synapses) or functional inactivation of neuronal elements associated with the epileptogenic lesion.

Symptomatic patients with Huntington's disease may have reduced glucose metabolism in the caudate nuclei. We used positron emission tomography and [18F]fluorodeoxyglucose to study cerebral glucose metabolism in 95 subjects: 58 clinically asymptomatic (chorea-free) subjects at risk for Huntington's disease, 10 symptomatic patients with the disease, and 27 controls. All the symptomatic patients had marked reductions in caudate glucose metabolism. Despite a normal structural appearance on computed tomography, caudate glucose metabolism was bilaterally reduced in 31 percent of the subjects at risk (18 of 58). Using each at-risk subject's age and the sex of the affected parent, we averaged individual risk estimates for the development of Huntington's disease for this group and predicted that the probability of having the clinically unexpressed Huntington's disease gene should be 33.9 +/- 6.0 percent for the group. Thus, there was excellent agreement between the predicted percentage of carriers of the Huntington's disease gene (33.9 +/- 6.0 percent) and the percentage with metabolic abnormalities of the caudate nuclei (31 percent). These results indicate that the measurement of glucose metabolism may allow the observation of the pathophysiologic effects of the Huntington's disease gene during the natural development of the disease. It may also provide a direct means to monitor the response to experimental treatments during both the clinically asymptomatic and the symptomatic phases of the disorder.

No abstract

Summary:The [IHF]fluorodeoxyglucose (FDG) scan method with positron emission computed tomography was used to determine patterns of local cere bral glucose utilization (LCMRg1u) in 40 normal volunteer subjects aged 18 to 78 years. Throughout all the studies. each subject was quiet, without movement, with eyes open and ears unplugged, exposed only to ambient room light and sound. For the entire group, whole brain mean CMRglu was 26.1 ± 6. I /Lmol 100 g-l min-1 (mean ± SD, n = 40). At age 78, mean CMRglu was, on the average, 26% less than at age 18, an alteration of the same order as the variance among subjects at any age. The gradual decline of mean CMRglu with advancing age occurred at a faster rate than was reported for mean cerebral oxygen utilization, possibly due to increasingly altered pathways for glucose utilization, or to increasing oxidation of ketone bodies or other alternative substrates. Glucose utilization in the hemispheres was symmetrical and mean CMRglU of overall cortex, caudate, and thalamus was equal in individuals at all ages. The slopes of decline with age were similar when LCM Rglu was averaged over zones corresponding to centrum semiovale, caudate, putamen, and fron tal, temporal, parietal, occipital, and primary visual cortex. However, the met abolic ratio of superior frontal cortex to superior parietal cortex declined with age, possibly due to selective degeneration of superior frontal cortex or to differences between age groups in the sensory and cognitive response to the study. These results should be useful in distinguishing age from disease effects when the FDG scan method is used. 163 koloff et aI., 1977) used in animals, but emission computed tomography is substituted for the au toradiography. After intravenous injection, FDG enters the brain, is phosphorylated by brain hexokinase, and the metabolic product, FDG-6-P0 4 , remains fixed with only slow dephosphoryla tion. The time course of specific activity is mea sured in plasma, brain activity is determined by scanning, and with knowledge of predetermined rate constants, an operational equation allows cal culations of LCMRglu that are distributed in a cross-

No abstract