Thesis (Ph. D.)--University of Chicago, 1911. / "Private edition, distributed by the University of Chicago Libraries, Chicago, Illinois, 1911." Includes bibliographical references.

Thesis--Bryn Mawr College, 1926. / Vita. Published also as Psychological review publications, Psychological monographs, vol. XXXVIII, no. 1 ; whole no. 173. Bibliography: p. 85-87.

Thesis (Ed.D.)--Fairleigh Dickinson University, 1988. / Source: Dissertation Abstracts International, Volume: 49-05, Section: B, page: 1983. Adviser: Leonard Grob.

No description available.

No description available.

Three experiments were run in order to determine the antecedents and consequences of the evoked K-Complex. In all three experiments, a train of auditory stimuli was presented during stages 2, 3 and 4 of sleep. In experiment 1, the intensity of the stimulus (80 and 60 dB SPL), its rise-and-fall time (2 and 20 ms) and its tonal frequency (500, 1000 and 2000 Hz) were manipulated. The evoked K-Complex consisted of two different negative components peaking at approximately 350 ("N350") and 550 ("N550") ms, respectively, and followed by a positive component peaking at approximately 900 ("P900") ms. K-Complexes occurred more often with high intensity, fast rise-and-fall time stimuli. When a K-Complex was evoked, the amplitude and latency of the different components remained invariant regardless of the intensity, rise-and-fall or tonal frequency of the stimulus. The K-Complex therefore appears to be an all-or-none phenomenon. On trials on which a K-Complex could not be on elicited, N350 was still visible although much attenuated. On these trials, its amplitude was further reduced when stimulus intensity was lowered. N350 might need to reach a certain critical threshold before the much larger N550-P900 complex is elicited. Experiment 2 examined the effects of rate of presentation on the evoked K-Complex. In different conditions, brief duration tone pips were presented every 5, 10 or 30 sec. K-Complexes were elicited most often when the rate of stimulus presentation was slowest (i.e., every 30 sec) compared to when it was faster (i.e., every 5 or 10 sec). When a K-Complex was evoked, the amplitudes of N350 and N550 were greater with the 30 than the 10 or 5 sec rate of stimulus presentation. A micro-analysis was carried out when 3 consecutive K-Complexes were elicited. With the faster rates of presentation, N350 and N550 following the second and third occurrence of the K-Complex were significantly attenuated compared to the first occurrence. There was no difference in N350 and N550 amplitudes among the 3 consecutive occurrences during the Slow condition. The decay in amplitude over consecutive occurrences of the K-Complex was interpreted as due to either habituation or refractory processes. Experiment 3 was designed to determine the function of the K-Complex. It has been considered to reflect either an arousal or a sleep protector mechanism. A spectral analysis of the EEG prior to and following the presentation of a stimulus was compared on trials on which a K-Complex was and was not elicited. Tone pips were presented every 20 sec during non-REM sleep. FFTs were computed on the EEG prior to and following stimulus onset. In the absence of a K-Complex, a small but significant power elevation following stimulus onset was apparent during Slow Wave Sleep. There were no changes in EEG activity when a K-Complex was elicited. The K-Complex therefore appears to prevent arousal that might otherwise occur to external stimuli.

In the present study, sleep characteristics in reading disabled (RD) children were recorded to examine suggested relationships among sleep, maturational and cognitive processes. Subjects were thirty-nine 8-10 year old boys (15 controls (Cs), M = 9.2, SD = 0.6 yrs; 24 RD, M = 9.0, SD = 0.5 yrs, (Boder criteria)). Reading disabled children were classified as: (a) dysphonetic (N = 8; (auditory-sequential processing deficits)); (b) dyseidetic (N = 8; (visual-simultaneous processing deficits)); or (c) nonspecific (N = 8; (absence of cognitive impairments)). Sleep was recorded in the laboratory for four consecutive nights (2 adaptation, 2 baseline) using standard polysomnography. All groups exhibited variations across nights reflecting adaptation to the sleep laboratory, although these seemed attenuated in the RD subtypes relative to the Cs. Group comparisons (with nights 3-4 collapsed) were undertaken between Cs and: (1) RD children pooled into one group; and, (2) the three RD subtypes. Relative to the Cs, RD children showed: (1) more stage 4 sleep (p .009); (2) less REM sleep (p .02); (3) an extended initial NREM cycle (p .009), composed of greater absolute amounts of stages 2 (p .03) and 4 (p .005); and, (4) a longer REM onset latency (p .009), also composed of more minutes of stages 2 (p .05) and 4 (p .003). Subtype analyses revealed that differences in REM sleep, initial NREM cycle duration and REM onset latency were largest among Cs and nonspecifics (p .05; p .05; p .01, respectively). Eye movement density (EMD) analyses revealed that, with the exception of the initial REM period, in which the RD children (pooled) exhibited higher mean values than the Cs (p .05), no significant group differences were noted over all REM periods, across the first 4 REM periods or for each individual REM period. The sleep profile observed in RD children, (the nonspecifics in particular), was characterized by a significantly extended initial NREM cycle with increased amounts of stage 4 sleep. This may reflect the influence of an underlying maturational delay, which decreases the functional quality of stage 4 sleep, resulting in a decelerated restitution process in RD children. The overall absence of differences between groups in EMD suggest that the presence or nature of its relationship to information processing in RD children remains unclear. The subtype differences observed were not expected, given Boder's description of the nonspecific subtype and suggest that her interpretation of the behavioral profile of these children may need revision.

No description available.

The Mismatch Negativity (MMN), an auditory event-related potential (ERPs) reflecting the detection of stimulus change, was recorded during wakefulness and sleep onset. In Experiment l, a 1000 Hz standard stimulus was presented every 600 ms. On 20% of the trials, the standard was changed randomly to either a large 2000 Hz (p = .10) or a small 1100 Hz (p = .10) deviant. During alert wakefulness (reading a book), a long-lasting MMN was elicited by presentation of both the small and the large deviant. During relaxed wakefulness (when the subject was asked to fall asleep) and Stage 2 sleep, the MMN to the large deviant, albeit attenuated, remained statistically significant. To test the hypothesis that sensory memory fades rapidly during sleep, Experiment 3 employed a very rapid rate of stimulus presentation. Experiment 2 was used to identify the optimal stimulus parameters for that test by examining the interactive effects of stimulus probability and stimulus presentation rate on the MMN during wakefulness. Auditory stimuli were 1000 Hz standard and 1100 Hz deviant. Stimulus probability was varied across stimulus-onset asynchronies (SOAs) of 150, 600, and 2400 ms. A long-lasting MMN was evident in all conditions except at the longest SOA (2400 ms). When the SOA was 150 ms, the largest MMN was elicited to the lowest deviant probability. In Experiment 3, a long-lasting MMN was elicited in alert wakefulness to either a small deviation (1100 Hz, p = .033) or a large deviation (2000 Hz, p = .033) from the standard (1000 Hz) in auditory frequency. SOA was 150 ms. A long-lasting MMN to the large deviant was observed during relaxed wakefulness, Stage 1 sleep, and non-REM sleep. The results of these experiments support the hypothesis that the MMN comparison system is at least partially automatic. It can be elicited during non-REM sleep, at least to large deviations in auditory frequency. The MMN following a small deviant is, however, difficult to observe during Stage 1 sleep or even as soon as relaxed wakefulness. It is possible that, during sleep onset, cortical encoding of both standard and deviant stimuli is weakened because of prior thalamic inhibition of sensory input.

An occasional "deviant" stimulus presented in a train of frequent homogeneous "standard" stimuli elicits a negativity, called the "mismatch negativity" (MMN), in the human auditory evoked potential (AEP). The MMN occurs at approximately 100-300 ms after stimulus onset. In awake and alert subjects, the MMN appears to be elicited regardless of the level of attention, conscious awareness, or task demands. The purpose of the present thesis was to examine the attentional independence of the MMN by recording event-related potentials (ERP) to different types of stimulus change or "deviance" during natural sleep. In three separate experiments, stimulus deviations involving frequency, duration, and intensity were examined. In experiment 1, two "oddball" stimulus conditions involving auditory frequency deviance were presented to eight subjects. In the "large deviance" condition, 2000 Hz "deviant" tones were presented with 1000 Hz "standard" tones. In the "small deviance" condition, 1050 Hz deviants were used. Both stimulus conditions were presented during wakefulness, as subjects read a book, and during Stage 2, REM, and slow wave sleep (SWS). In experiment 2, two stimulus conditions involving deviations in stimulus duration were presented to eight subjects. In the "increment deviance" condition, 150 ms deviant tones were presented with 100 ms standards. In the "decrement deviance" condition, 50 ms deviant tones were used. Both conditions were presented during wakefulness (reading), and sleep stages 2, REM and SWS. In experiment 3, stimuli involving changes in auditory intensity were presented to seven subjects during a waking reading condition, Stage 2 and REM sleep. Within the same stimulus block, 80 dB "increment deviants" and 60 dB "decrement deviants" were presented with 70 dB standard tones. The results of the three studies indicated that the MMN to frequency deviance is preserved during REM sleep, and, the MMN to duration deviance may also be present in REM sleep, but is much attenuated relative to wakefulness. The detection of intensity deviance persists in REM sleep, but it is uncertain whether this is due to a true mismatch process or a deviant-related negativity specific to the REM sleep state. No MMN-like activity could be recorded to any type of stimulus deviance during NREM sleep. (Abstract shortened by UMI.)