Luigi Mansi

Positron emission tomography in generalized seizures.

We used 1BF-fluorodeoxyglucose (FDG) positron emission tomography (PET) to study nine patients with clinical absence or generalized seizures. One patient had only absence seizures, two had only generalized tonic-clonic seizures, and six had both seizure types. Interictal scans in eight failed to reveal focal or lateralized hypometabolism. No apparent abnormalities were noted. Two patients had PET scans after isotope injection during hyperventilation-induced generalized spike-wave discharges. Diffusely increased metabolic rates were found in one compared with an interictal scan, and in another compared with control values. Another patient had FDG injected during absence status: EEG showed generalized spike-wave discharges (during which she was unresponsive) intermixed with slow activity accompanied by confusion. Metabolic rates were decreased, compared with the interictal scan, throughout both cortical and subcortical structures. Interictal PET did not detect specific anatomic regions responsible for absence seizure onset in any patient, but the results of the ictal scans did suggest that pathophysiologic differences exist between absence status and single absence attacks.

Cortical motor-sensory hypometabolism in amyotrophic lateral sclerosis: a PET study

We previously reported generalized cerebral glucose hypometabolism in amyotrophic lateral sclerosis (ALS) patients with upper motor neuron disease, using positron emission tomography (PET) with [18F]2-fluoro-2-deoxy-D-glucose. The present article presents a more detailed regional analysis of the hypometabolism, including measurements of the motor-sensory cortex at higher levels than used earlier. The analysis is based on 19 PET studies of 12 patients with ALS, four of whom had only lower motor neuron involvement, and 11 studies of age-matched control subjects. A brain size correction was included to eliminate differences in metabolism related to brain size but not to pathology. The eight ALS patients with both upper and lower motor neuron disease showed generalized hypometabolism, compared with the normal control subjects, that was greatest in the motor-sensory cortex and putamen. The motor-sensory deficit was strongly correlated with length of disease, and a marked sequential reduction was seen in repeat studies on four of the patients. There was also significant right-left asymmetry in these scans. No cerebral hypometabolism was seen in the four ALS patients without upper motor neuron involvement. Although the observed motor-sensory deficit in ALS is consistent with histopathological findings, the more generalized hypometabolism and the asymmetry suggest more widespread effects.

Depressed cerebellar glucose metabolism in supratentorial tumors

Fifty-four patients with supratentorial tumor and one with brainstem tumor were examined with positron 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.

Effect of moderate level x-radiation to brain on cerebral glucose utilization

The effect of x-radiation in doses used in treatment of brain malignancies has previously been established largely by histologic examination of the tissue or by observation of a deficit in function. At moderate dose levels such effects are usually delayed and are vascular in origin. We have used the 2-[14C]deoxyglucose method for the quantitative measurement of local cerebral glucose utilization to learn whether x-radiation administered to rat brain in a dose below that which is known to result in any histologic change may nevertheless affect the brains local rates of glucose utilization. Measurements were made 4 days and 4 weeks after exposure of groups of rats to 1,500 rad. Rates of glucose utilization in 54 gray and eight white matter structures in both groups were compared with rates in sham-irradiated controls. Statistically significantly lower rates were found in 16 structures in rats 4 days after radiation and in 25 structures 4 weeks after radiation exposure. A weighted average rate for the brain as a whole was ~15% below that of the controls for both radiated groups, but this difference was short of being of statistical significance. It is clear from this study that the metabolic rates of some brain structures are reduced following moderate doses of x-radiation.

CORTICAL ABNORMALITIES IN ALZHEIMERʼS DISEASE

Regional cerebral glucose metabolism, an index of neuronal activity, was compared in 20 patients with Alzheimers disease and 8 age-matched normal volunteers by positron emission tomography following [18F]2-fluoro-2-deoxy-D-glucose administration. Overall cortical glucose utilization in the Alzheimers group was 10 to 49% below that of control individuals. The posterior parietal cortex and contiguous portions of posterior temporal and anterior occipital lobes were most severely affected; frontal cortex was relatively spared. This pattern of cortical involvement is consistent with the major clinical features of Alzheimers disease. Comparison of patients with early and more advanced dementia suggested that a substantial decline in glucose metabolism occurs before cognitive impairment becomes evident; once the patient is symptomatic, however, small additional metabolic decrements are associated with a marked deterioration in intellectual function.