Biomedical subjects
Publications and source records attributed to L C Johnson.
A 61-hear-old man was followed up for more than 17 years with what was thought to be fibrous dysplasia of the frontal bone. Postmortem microscopic examination of the lesion showed an intraosseous lipoma with myxomatous foci and bony metaplasia involving the frontal and orbital portions of the frontal bone.
Two experiments examined the relation of prestimulus electroencephalographic (EEG) frequency to choice RT. Based on previous studies, initial analysis was concerned with 3--7 c/sec activity. In well-rested subjects (Exp. 1), trial-by-trial analyses indicated large variations in prestimulus EEG activity which were unrelated to RT and large variations in RT which were unrelated to prestimulus EEG. In Exp. 2, subjects were deprived of sleep for 1 night and within-subject comparisons made between RT and EEG activity immediately preceding the 10 shortest and 10 longest RT trials, and 10 trials where the subject failed to respond. Significant univariate correlations were found, largely between RT and the frequencies in the 15--20 c/sec range of EEG activity and not in the 3--7 c/sec activity. A multiple regression analysis using up to 5 EEG frequencies indicated significant correlations of prestimulus EEG activity with RT; but with considerable subject-to-subject variability in the EEG frequencies contributing to the multiple R. The overall results suggest that there can be considerable variation in EEG activity which is unrelated to performance, except when the EEG fluctuations are secondary to changes in arousal which, in turn, effect performance.
To further evaluate the effects of flurazepam on EEG during sleep, following 7 nights of placebo baseline, flurazepam (30 mg) was administered to 6 young adult poor sleepers for 10 additional nights while 6 other young adult poor sleepers continued to receive placebo capsules in a double-blind paradigm. Three placebo follow-up nights were recorded 2--3 weeks post-treatment. Twelve good sleepers received only placebo capsules for the first 7 nights. Delta waves, 0.5--2 c/sec, and sleep spindles were counted on-line by a phasic detector. Delta activity was also analyzed off-line by PDP-12 computer for only the first 4 h of sleep and involved a comparison over stages of sleep. Click-evoked K-complexes during NREM sleep were analyzed for 6 good sleepers and 11 poor sleepers. Repeated use of flurazepam caused a gradual decrease in delta amplitude and count, and a gradual increase in sleep spindle rate. The decrease in delta amplitude was seen in all sleep stages, but the decrease was significant only during SWS and stage 2. The decrease in delta amplitude was significant by the 3rd drug night, but the rate of amplitude decrease tended to slow with continued treatment. The decrease in delta count was less pronounced and more gradual over drug nights than the rate of decrease in amplitude. Flurazepam also significantly reduced evoked K-complex amplitude but did not affect latency. Sleep spindle rate was significantly increased by drug night 5. Results of this study indicate that the reduction of SWS with flurazepam during the initial drug nights is due primarily to the decrease in delta amplitude, but, with continued use, the decrease in delta count also contributes to the decrease in stage 4 sleep.
Auditory arousal thresholds of good (N = 12) and poor (N = 12) sleepers (sleep onset insomniacs) were obtained during stage 2, stage 4, and REM sleep at various times of the night. Despite claims of being "light" sleepers who are easily awakened by noise, poor sleeper auditory arousal thresholds were the same as those of good sleepers. Flurazepam (30 mg) increased the auditory arousal thresholds of poor sleepers (N = 6), but the increase was statistically significant only during the period of peak effect which occurred 1--2 hr after ingestion. Consistent with poor sleeper complaints of trouble falling asleep, the return to sleep (i.e., sleep latency) was significantly longer for poor than for good sleepers following stimulus arousals during the first stage 2 and first stage 4 periods of the night. Sleep latencies for good and poor sleepers did not differ significantly following subsequent arousals. The sleep latency following the first stage 2 stimulus arousal was significantly reduced in poor sleepers during flurazepam-induced sleep.
The hypothesis that the functional role of the sleep spindle is to preserve sleep by inhibiting sensory input (Yamadori 1971) was examined. Series of 44 dB, 10 msec, 1000 c/sec 'clicks' were presented to 12 subjects at a 30-sec ISI during stage 2 sleep either during spindle bursts (i.e. spindle-synchronous clicks) or during interburst periods (i.e. spindle-asynchronous clicks). Contrary to the spindle inhibitory hypothesis, cortical EEG and cardiovascular responses showed no evidence of spindle 'suppression'. Evoked K-complexes were potentiated by the spindle-synchronous stimulation. A second study with 7 subjects replicated this result and extended the finding to include stage 3--4 sleep. It was suggested that the potentiation of evoked K-complexes was due to phasic reductions in inhibitory action during sleep spindles resulting in increased transmission of sensory events or, perhaps, an increase in the lability of certain EEG response systems.
The effect of an altered sleep-wake schedule on the interrelation of oral temperature, performance, and sleepiness was studied in 38 male Naval volunteers who maintained a 60 min treatment--160 min testing schedule for 40 consecutive hrs. During the 60 min treatment portion of each epoch, 8 subjected napped, 10 subjects exercised, and 20 subjects rested in bed. Sleep measures (for the nap subjects), oral temperature, performance on several tests, and Stanford Sleepiness Scale ratings were obtained at 10 equidistant intervals throughout the 40-hr period. Within-subject correlations showed that minimum oral temperature was significantly associated with maximum nap sleep time, errors on a vigilance task, and sleepiness ratings. In the nap subjects, errors and sleepiness ratings were highest following naps with high total sleep time, suggesting that sleep was detrimental to immediately subsequent performance and alertness. The distribution and interrelation of temperature, errors, and sleepiness, however, was similar in the three groups; this indicated that the synchronous circadian variation in these measures was responsible for the apparent detrimental effect of sleep in the nap subjects. When the diurnal effect was removed by holding time of day constant, the correlations among the variables fell to near-zero, indicating no causal relationship among the variables independent of the circadian rhythm.
The relationship of arousal threshold, amounts of various sleep stages, and subjective rating of sleep was studied in two separate experiments involving 7 and 26 young adult subjects, respectively. Electroencephalographic sleep stage data, subjective response data, and arousal threshold data were collected over a series of nights in the sleep laboratory. Only nonsignificant relationships were found between magnitude of arousal threshold and amounts of various sleep stages or subjective rating of sleep quality in between-subjects analyses. However, when the nights representing extremes in arousal threshold were examined within-subject, it was found that nights of high threshold were accompanied by subjective reports of significantly better sleep in both studies and by a significant decrease in the amount of stage W in one study. Arousal threshold was not related to subjective depth of sleep in either study. Rather, subjective ratings of depth of sleep were significantly related to the amount of EEG-defined wakefulness and stage 1.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In this research, a quantitative study of the EEG from 5 subjects permitted a detailed analysis of the effect of 30 mg of flurazepam administered over 7 nights. Four placebo baseline nights and 3 placebo withdrawal nights were also recorded. For 4 of the subjects, a nondrug and nonplacebo follow-up record was obtained 4 to 6 weeks later. The subjects were 4 females, 1 male, age range 23-42. All complained of either sleep onset greater than 45 min, sleep length of less than 6 h, or two or more sleep awakenings. Compressed spectral analysis yielded a computer-generated somnogram on each of the 15 nights of sleep, and an automated spindle detector was used to count and measure the duration of spindle bursts with frequencies of 12.25-15.5 c/sec on baseline nights 3 and 4, drug nights 1, 2, 3 and 7, on the 3rd withdrawal night, and on the 4-6 week followup record. K-complexes were scored visually on the 4th baseline and 7th drug nights. There were no significant differences in spindle rate per minute among baseline nights and the follow-up record. By the 2nd drug night, spindle rate had significantly increased over the baseline rate. Linear contrast analysis indicated there was a significant increase of spindle rate over drug nights. All 5 subjects showed this pattern of increase. In contrast to the increase in spindle activity, the rate per minute of K-complexes significantly decreased during drug administration.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Following 1 baseline night, the sleep of 8 adult males in equally space 1 h naps during a 40 h period was examined. Ten additional subjects were sleep-deprived for 40 h with 1 h periods of exercise given in place of naps. One recovery night followed the 40 h period for both groups. Total sleep time and the amount of stage REM during the naps were negatively related to the circadian-temperature cycle. Stage REM frequently appeared within 10 min of stage 1 onset and the normal sequence of stages REM and 4 were altered, demonstrating that the organization of sleep within a nap is quite different from that in monophasic nocturnal sleep. Auto-correlation and cross-correlation analyses showed that the relation of sleep stages from hour to hour in normal continuous baseline sleep was altered in nap-to-nap comparison. The timing of REM onset may be controlled by a sleep-dependent ultradian clock; the clock may stop upon awakening and resume at the next sleep onset. Naps had recuperative value in terms of maintaining the normal amounts of sleep stages on the recovery night; recovery sleep for the exercise group showed typical sleep-loss effects.
The primary purpose of this experiment was to study classically conditioned autonomic responses of alert versus drowsy subjects. Sixty-nine subjects in conditioning and pseudo-conditioning groups were subdivided into alert and drowsy groups on the basis of EEG recordings during conditioning trials, giving a total of four groups: conditioning-alert, conditioning-drowsy, pseudoconditioning-alert and pseudoconditioning-drowsy. Using the latency criterion to define responses, significant conditioning occurred only in the conditioning-alert group for the following measures: skin resistance anticipatory and UCS-omission responses, and finger plethysmograph anticipatory response. Both conditioning groups showed evidence of conditioned UCS-omission plethysmograph responses. Discussion centered primarily on (1) the implications of the results on the question of the feasibility of learning during sleep; and (2) the importance of including EEG recordings in studies of classically conditioned autonomic responses. The relationship between the various responses was also evaluated.