Comparison of rhythmic masticatory muscle activity during non‐rapid eye movement sleep in guinea pigs and humans

Rhythmic masticatory muscle activity can be a normal variant of oromotor activity, which can be exaggerated in patients with sleep bruxism. However, few studies have tested the possibility in naturally sleeping animals to study the neurophysiological mechanisms of rhythmic masticatory muscle activity. This study aimed to investigate the similarity of cortical, cardiac and electromyographic manifestations of rhythmic masticatory muscle activity occurring during non‐rapid eye movement sleep between guinea pigs and human subjects. Polysomnographic recordings were made in 30 freely moving guinea pigs and in eight healthy human subjects. Burst cycle length, duration and activity of rhythmic masticatory muscle activity were compared with those for chewing. The time between R‐waves in the electrocardiogram (RR interval) and electroencephalogram power spectrum were calculated to assess time‐course changes in cardiac and cortical activities in relation to rhythmic masticatory muscle activity. In animals, in comparison with chewing, rhythmic masticatory muscle activity had a lower burst activity, longer burst duration and longer cycle length (P < 0.05), and greater variabilities were observed (P < 0.05). Rhythmic masticatory muscle activity occurring during non‐rapid eye movement sleep [median (interquartile range): 5.2 (2.6–8.9) times per h] was preceded by a transient decrease in RR intervals, and was accompanied by a transient decrease in delta elelctroencephalogram power. In humans, masseter bursts of rhythmic masticatory muscle activity were characterized by a lower activity, longer duration and longer cycle length than those of chewing (P < 0.05). Rhythmic masticatory muscle activity during non‐rapid eye movement sleep [1.4 (1.18–2.11) times per h] was preceded by a transient decrease in RR intervals and an increase in cortical activity. Rhythmic masticatory muscle activity in animals had common physiological components representing transient arousal‐related rhythmic jaw motor activation in comparison to human subjects.     

Decline in hippocampal theta activity during cessation of locomotor approach sequences: amplitude leads frequency and relates to instrumental behavior

Hippocampal theta frequency and amplitude decrease as locomotor approach slows and the goal is reached. This study compared the declines of these theta parameters and related them to behavioral events. Theta activity was recorded with bipolar electrodes spanning cornu Ammon, sector 1 or cornu Ammon, sectors 2/3 cell layers of the dorsal hippocampus in 12 rats trained to approach and depress a treadle which exposed a milk dipper. Behavioral events were identified using a video capture system (20-ms sampling) synchronized to the hippocampal recording system (10-ms sampling). Peri-event averages of theta activity were made around the initial paw contact with the treadle, the presentation of the dipper, and the first lick at the dipper. Phase relationships between averaged hippocampal slow wave activity and behavioral events occasionally were found but they were inconsistent. In averages of both amplitude and frequency, times of minimum were less variable around paw contact indicating that compared with reward presentation and consummatory behavior, it more closely related to the processes determining the declines. Theta amplitude declined more rapidly than frequency and reached an earlier minimum in averages around initial paw contact and dipper presentation. Mean amplitude minimum occurred after the paw contact at 159 ms but the decline of frequency continued into the licking bout with its minimum occurring at 343 ms. The findings indicate that during the termination of approach locomotion, the amplitude of hippocampal theta activity is closely related to specific expected sensorimotor events.     

Fragments of wake-like activity frame down-states of sleep slow oscillations in humans: New vistas for studying homeostatic processes during sleep

During NREM sleep cortical activity corresponding to EEG fast rhythms (FRs > 10 Hz) is interrupted by fragments of neural stillness (down-states), responsible for the negative peak within sleep slow oscillation (SSO). Researchers still debate whether the down-states spontaneously occur or need an initial overshoot in fluctuating activity. Herein, we studied temporally-isolated SSO in healthy subjects in order to identify two distinct EEG markers defining a putative initial up-state: i) a significant positive deflection and ii) an associated FR increase, before the negative peak.     

Slow wave activity and slow oscillations in sleepwalkers and controls: effects of 38 h of sleep deprivation

Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non‐rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto‐central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.     

Cortical thinning and sleep slow wave activity reductions mediate age-related improvements in cognition during mid-late adolescence

Study ObjectivesGains in cognitive test performance that occur during adolescence are associated with brain maturation. Cortical thinning and reduced sleep slow wave activity (SWA) are markers of such developmental changes. Here we investigate whether they mediate age-related improvements in cognition.Methods109 adolescents aged 15–19 years (49 males) underwent magnetic resonance imaging, polysomnography (PSG), and a battery of cognitive tasks within a 2-month time window. Cognitive tasks assessed nonverbal intelligence, sustained attention, speed of processing and working memory and executive function. To minimize the effect of sleep history on SWA and cognitive performance, PSG and test batteries were administered only after at least 8 nights of 9-h time-in-bed (TIB) sleep opportunity.ResultsAge-related improvements in speed of processing (r = 0.33, p = 0.001) and nonverbal intelligence (r = 0.24, p = 0.01) domains were observed. These cognitive changes were associated with reduced cortical thickness, particularly in bilateral temporoparietal regions (rs = −0.21 to −0.45, ps < 0.05), as well as SWA (r = −0.35, p < 0.001). Serial mediation models found that ROIs in the middle/superior temporal cortices, together with SWA mediated the age-related improvement observed on cognition.ConclusionsDuring adolescence, age-related improvements in cognition are mediated by reductions in cortical thickness and sleep SWA.     

Changes in oscillatory activity of neurons in the medial septal area in animals with a model of chronic temporal epilepsy

Comparative studies of the activity of extracellularly recorded neurons in living slices of the medial septal area of healthy guinea pigs and animals with a model of chronic temporal epilepsy demonstrated differences between them in terms of the frequency and pattern of cell discharges. The brains of animals with experimental epilepsy showed a doubling of the total level of activity as compared with controls, due to increases in the discharge frequencies of irregular and regular non-volleying neurons. There was a sharp (three-fold) increase in the number of cells with rhythmic discharge volleys, along with changes in the parameters of volley activity — both in neurons with the endogenous (pacemaker) pattern and in cells with secondary involvement in rhythmic activity. The possible mechanisms for these changes are discussed. These data widen our understanding of the processes forming pathological synchronization in epilepsy and may assist in the creation of new approaches to the treatment of this disease. __________ Translated from Zhurnal Vysshei Nervnoi Deyatel'nosti imeni I. P. Pavlova, Vol. 57, No. 5, pp. 618–623, September–October, 2007.     

Topographic sleep EEG changes in the acute and chronic stage of hemispheric stroke

After stroke, the injured brain undergoes extensive reorganization and reconnection. Sleep may play a role in synaptic plasticity underlying stroke recovery. To test this hypothesis, we investigated topographic sleep electroencephalographic characteristics, as a measure of brain reorganization, in the acute and chronic stages after hemispheric stroke. We studied eight patients with unilateral stroke in the supply territory of the middle cerebral artery and eight matched controls. All subjects underwent a detailed clinical examination including assessment of stroke severity, sleep habits and disturbances, anxiety and depression, and high‐density electroencephalogram examination with 128 electrodes during sleep. The recordings were performed within 10 days after stroke in all patients, and in six patients also 3 months later. During sleep, we found higher slow‐wave and theta activity over the affected hemisphere in the infarct area in the acute and chronic stage of stroke. Slow‐wave, theta activity and spindle frequency range power over the affected hemisphere were lower in comparison to the non‐affected side in a peri‐infarct area in the patients’ group, which persisted over time. Conversely, in wakefulness, only an increase of delta, theta activity and a slowing of alpha activity over the infarct area were found. Sleep slow‐wave activity correlated with stroke severity and outcome. Stroke might have differential effects on the generation of delta activity in wakefulness and sleep slow waves (1–8 Hz). Sleep electroencephalogram changes over both the affected and non‐affected hemispheres reflect the acute dysfunction caused by stroke and the plastic changes underlying its recovery. Moreover, these changes correlate with stroke severity and outcome.     

Sleep homeostasis and cortical synchronization: III. A high-density EEG study of sleep slow waves in humans

STUDY OBJECTIVES: The mechanisms responsible for the homeostatic decrease of slow-wave activity (SWA, defined in this study as electroencephalogram [EEG] power between 0.5 and 4.0 Hz) during sleep are unknown. In agreement with a recent hypothesis, in the first of 3 companion papers, large-scale computer simulations of the sleeping thalamocortical system showed that a decrease in cortical synaptic strength is sufficient to account for the decline in SWA. In the model, the reduction in SWA was accompanied by decreased incidence of high-amplitude slow waves, decreased wave slopes, and increased number of waves with multiple peaks. In a second companion paper in the rat, local field potential recordings during early and late sleep confirmed the predictions of the model. Here, we investigated the model's predictions in humans by using all-night high-density (hd)-EEG recordings to explore slow-wave parameters over the entire cortical mantle. DESIGN: 256-channel EEG recordings in humans over the course of an entire night's sleep. SETTING: Sound-attenuated sleep research room PATIENTS OR PARTICIPANTS: Seven healthy male subjects INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: During late sleep (non-rapid eye movement [NREM] episodes 3 and 4, toward morning), when compared with early sleep (NREM sleep episodes 1 and 2, at the beginning of the night), the analysis revealed (1) reduced SWA, (2) fewer large-amplitude slow waves, (3) decreased wave slopes, (4) more frequent multipeak waves. The decrease in slope between early and late sleep was present even when waves were directly matched by wave amplitude and slow-wave power in the background EEG. Finally, hd-EEG showed that multipeak waves have multiple cortical origins. CONCLUSIONS: In the human EEG, the decline of SWA during sleep is accompanied by changes in slow-wave parameters that were predicted by a computer model simulating a homeostatic reduction of cortical synaptic strength.     

Skin sympathetic nerve activity and effector function during sleep in humans

Multi-unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep-deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5-min periods as the area-under-curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3–4 by nine and rapid eye movement (REM) sleep by six subjects. Non-REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293±48 vs. 175±4% of awake control level, n= 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397±79% of the awake control level (n= 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non-REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K-complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin. Therefore the unchanged strength of multiunit SSA during non-REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.     

The microstructure of active and quiet sleep as cortical delta activity emerges in infant rats

STUDY OBJECTIVES: Previous investigators have suggested that quiet sleep (QS) in rats develops rapidly upon the emergence of cortical delta activity around postnatal day (P)11 and that the presence of "half-activated" active sleep (AS) suggests that infant sleep is initially disorganized. To address these issues, we examined the temporal organization of sleep states during the second postnatal week in rats as delta activity emerges. DESIGN: Subjects were P9, P11, and P13 Sprague-Dawley rats. Electroencephalogram and nuchal electromyogram electrodes were implanted, and data were recorded at thermoneutrality for 2 hours. RESULTS: At all ages, using electromyogram and behavioral criteria, QS (defined as nuchal atonia and behavioral quiescence) dominated the first third of each sleep period, whereas AS (defined as nuchal atonia accompanied by myoclonic twitching) dominated the last third. When delta activity, which was first detected at P11, could be added to the definition of QS, gross assessments of sleep-state organization were not altered, although it was now possible to identify brief periods of QS interposed between periods of AS. No evidence of "half-activated" AS was found. Finally, "slow activity transients" were detected and were primarily associated with QS; their rate of occurrence declined as delta activity emerged. CONCLUSIONS: When delta activity emerges at P11, it integrates smoothly with periods of QS, as defined using electromyogram and behavioral criteria alone. Delta activity helps to refine estimates of QS duration but does not reflect a significant alteration of sleep-state organization. Rather, this organization is expressed much earlier in ontogeny as fluctuations in muscle tone and associated phasic motor activity.     

Regional differences in cortical electroencephalogram (EEG) slow wave activity and interhemispheric EEG asymmetry in the fur seal

Slow wave sleep (SWS) in the northern fur seal (Callorhinus ursinus) is characterized by a highly expressed interhemispheric electroencephalogram (EEG) asymmetry, called ‘unihemispheric’ or ‘asymmetrical’ SWS. The aim of this study was to examine the regional differences in slow wave activity (SWA; power in the range of 1.2–4.0 Hz) within one hemisphere and differences in the degree of interhemispheric EEG asymmetry within this species. Three seals were implanted with 10 EEG electrodes, positioned bilaterally (five in each hemisphere) over the frontal, occipital and parietal cortex. The expression of interhemispheric SWA asymmetry between symmetrical monopolar recordings was estimated based on the asymmetry index [AI = (L?R)/(L+R), where L and R are the power in the left and right hemispheres, respectively]. Our findings indicate an anterior–posterior gradient in SWA during asymmetrical SWS in fur seals, which is opposite to that described for other mammals, including humans, with a larger SWA recorded in the parietal and occipital cortex. Interhemispheric EEG asymmetry in fur seals was recorded across the entire dorsal cerebral cortex, including sensory (visual and somatosensory), motor and associative (parietal or suprasylvian) cortical areas. The expression of asymmetry was greatest in occipital–lateral and parietal derivations and smallest in frontal–medial derivations. Regardless of regional differences in SWA, the majority (90%) of SWS episodes with interhemispheric EEG asymmetry meet the criteria for ‘unihemispheric SWS’ (one hemisphere is asleep while the other is awake). The remaining episodes can be described as episodes of bilateral SWS with a local activation in one cerebral hemisphere.     

Associations between objective afternoon and evening physical activity and objective sleep in patients with fibromyalgia and insomnia

Patients with fibromyalgia (FM) suffer from chronic pain, which limits physical activity and is associated with disturbed sleep. However, the relationship between physical activity, pain and sleep is unclear in these patients. This study examined whether actigraphic (Actiwatch‐2, Philips Respironics) afternoon and evening activity and pain are associated with actigraphic sleep. Adults with FM and insomnia complaints (n = 160, mean age [M_age] = 52, SD = 12, 94% female) completed 14 days of actigraphy. Activity levels (i.e., activity counts per minute) were recorded, and average afternoon/evening activity for intervals 12:00–3:00 PM, 3:00–6:00 PM and 6:00–9:00 PM was computed. Multiple linear regressions examined whether afternoon/evening activity, pain (daily evening diaries from 0 [no pain sensation] to 100 [most intense pain imaginable]), or their interaction, predicted sleep onset latency (SOL), wake time after sleep onset (WASO), total sleep time (TST) and sleep efficiency (SE). Greater afternoon activity was independently associated with lower SE (B = ?0.08, p < .001), lower TST (β = ?0.36, standard error [SE] = 0.06, p < .001) and longer WASO (B = 0.34, p < .001). Greater early evening activity was independently associated with lower SE (B = ?0.06, p < .001), lower TST (β = ?0.26, SE = 0.06, p < .001) and longer WASO (B = 0.23, p < .001). Self‐reported pain intensity interacted with afternoon and early evening physical activity, such that associations between higher activity and lower SE were stronger for individuals reporting higher pain. Late evening activity was not associated with sleep outcomes. Results suggest that in FM, increased afternoon and early evening physical activity is associated with sleep disturbance, and this relationship is stronger in individuals with higher pain.     

A complementary relationship between wake and REM sleep in the auditory system: a pre-sleep increase of middle-ear muscle activity (MEMA) causes a decrease of MEMA during sleep

Since some evidence has supported a complementary relationship between waking and REM-sleep eye movement (variations in frequency, amplitude, or direction of waking saccades have been found to inversely affect the corresponding parameters of rapid eye movements), the present study assessed whether this relationship can also be shown for other phasic components of REM sleep, such as middle-ear muscle activity (MEMA), as a consequence of an increase of middle-ear reflex frequency during pre-sleep wake. Ten subjects were studied in three consecutive nights (one adaptation, one baseline, one experimental). In the experimental night, subjects underwent a 2-h pure-tone (1000 Hz, 90 dB SPL) auditory stimulation and MEMA was monitored every 15 min; noise exposure during daytime was also controlled. Results show that MEMA frequency during REM sleep significantly decreased during the experimental nights compared with baseline nights, while each sleep variable as well as mean daily auditory input did not present any significant difference between baseline and experimental nights. Results suggest that the complementary relationship between wake and REM sleep is not bounded to oculomotor activity, but it may also be extended at least to middle-ear muscle phasic activity. Received: 30 April 1999 / Accepted: 14 September 1999