To define the roles of circadian rhythmicity (intrinsic effects of time of day independent of the sleep or wake condition) and sleep (intrinsic effects of the sleep condition, irrespective of the time of day) on the 24-h variation in glucose tolerance, eight normal men were studied during constant glucose infusion for a total of 53 h. The period of study included 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h ofdaytime sleep. Blood samples for the measurement of glucose, insulin, C-peptide, cortisol, and growth hormone were collected at 20-min intervals throughout the entire study. Insulin secretion rates were derived from C-peptide levels by deconvolution. Sleep was polygraphically monitored.During nocturnal sleep, levels of glucose and insulin secretion increased by 31±5% and 60±11%, respectively, and returned to baseline in the morning. During sleep deprivation, glucose levels and insulin secretion rose again to reach a maximum at a time corresponding to the beginning of the habitual sleep period. The magnitude of the rise above morning levels averaged 17±5% for glucose and 49±8% for calculated insulin secretion. Serum insulin levels did not parallel the circadian variation in insulin secretion, indicating the existence of an approximate 40% increase in insulin clearance during the night.Daytime sleep was associated with a 16±3% rise in glucose levels, a 55±7% rise in insulin secretion, and a 39±5% rise in serum insulin.The diurnal-variation in insulin secretion was inversely related to the cortisol rhythm, with a significant correlation of the magnitudes of their morning to evening excursions. Sleep-associated rises in glucose correlated with the amount of concomitant growth hormone secreted. These studies demonstrate previously underappreciated effects of circadian rhythmicity and sleep on glucose levels, insulin secretion, and insulin clearance, and suggest that these effects could be partially mediated by cortisol and growth hormone. (J. Clin. Invest. 1991. 88:934-942.)

Electrocorticographic (ECoG) spectral patterns obtained during language tasks from 12 epilepsy patients (age: 12-44 years) were analysed in order to identify and characterize cortical language areas. ECoG from 63 subdural electrodes (500 Hz/channel) chronically implanted over frontal, parietal and temporal lobes were examined. Two language tasks were performed. During the first language task, patients listened to a series of 50 words preceded by warning tones, and were asked to repeat each word. During a second memory task, subjects heard the 50 words from the first task randomly mixed with 50 new words and were asked to repeat the word only if it was a new word. Increases in ECoG gamma power (70-100 Hz) were observed in response to hearing tones (primary auditory cortex), hearing words (posterior temporal and parietal cortex) and repeating words (lateral frontal and anterior parietal cortex). These findings were compared to direct electrical stimulation and separate analysis of ECoG gamma changes during spontaneous inter-personal conversations. The results indicate that high-frequency ECoG reliably differentiates cortical areas associated with receptive and expressive speech processes for individual patients. Compared to listening to words, greater frontal lobe and decreased temporal lobe gamma activity was observed while speaking. The data support the concept of distributed functionally specific language modules interacting to serve receptive and expressive speech, with frontal lobe 'corollary discharges' suppressing low-level receptive cortical language areas in the temporal lobe during speaking.

No abstract

✓ The authors describe their criteria for evaluating brain-tumor patients, and present a numerical rating scale devised to designate response to testing. They discuss the reliability of test combinations that permit accurate prediction of response or deterioration during therapy in their experience with 100 patients treated on the Chemotherapy Service at the Brain Tumor Research Center, University of California, San Francisco School of Medicine. Specifically, the paper summarizes the predictive value of the neurological examination, radionuclide scintiscan, computerized tomographic brain scan (CT scan), and electroencephalogram (EEG), in the determination of response (tumor regression) or deterioration (tumor growth) during brain-tumor chemotherapy and chemotherapy-radiotherapy. By retrospective analysis, the neurological examination, radionuclide scintiscan, and CT scan were of equal value individually as tests to predict response to therapy. However, the prognostic values of the neurological examination or the radionuclide scintiscan proved moderately superior to the CT scan in predicting deterioration during therapy. Under circumstances whereby a neurological examination, radionuclide scintiscan, and CT scan were all performed during the same testing session, and steroid dosage was carefully monitored, two of the three tests accurately predicted deterioration in 65% of patients, and response to therapy in 82% of patients. Two of the three tests correctly established deterioration in the remaining 35% of patients, and response in the remaining 18% of patients, when the two positively correlated tests had occurred within a mean period of 7 weeks.