Origin of dreams: Anticipation of modern theories in the philosophy and physiology of the eighteenth and nineteenth centuries.

Notes that the concept of dreaming as an endogenous product of brain activity appears to be a 20th-century development linked to the discovery of REM sleep. A review of the 17th, 18th, and 19th centuries' philosophical and physiological literature, however, reveals specific anticipations of this idea and of some of the prevailing views of the sleep process. These early writings have been scarcely mentioned in modern literature on sleep and dreaming and were completely overlooked in Freud's (translated by A. A. Brill, 1913) influential review of the pre-20th-century scientific literature on dreams. The development of this idea is traced from the 17th-century writings of G. W. Leibnitz (translated by A. G. Langley, 1896) until the birth of psychophysiology in the 2nd half of the 19th century. It is argued that Leibnitz's ideas of petites perceptiones allowed his successors to explain dreaming as an endogenous product of the brain. For the 18th and 19th centuries' physiologists, petites perceptiones were engendered by a specific type of brain reflex in which neither the stimulus nor the response reached awareness. (62 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of systemic atropine sulfate administration on the frequency content of the cat sensorimotor EEG during sleep and waking.

Sensorimotor electroencephalogram (EEG) frequencies in cats were evaluated with power spectral analysis before and after 3 doses of atropine sulfate. All doses of atropine tested caused enhanced EEG slow waves (0–7 Hz) and spindles (8–25 Hz) during waking immobility, and postdrug frequency profiles during slow-wave sleep and waking immobility were identical. With 0.75 mg/kg atropine, movement (head movement, locomotion) resulted in EEG desynchronization and reduced power in all frequencies less than 24 Hz. After 1.5 or 3.0 mg/kg atropine, power in low frequencies remained elevated during movement, but power in spindle frequencies was significantly reduced compared with other states. During active REM sleep after 1.5 mg/kg atropine, power in spindle frequencies was significantly lower than that during quiet REM sleep. These results indicate that the sensorimotor cortical EEG in cats is under the control of multiple systems. At least 1 of these systems is active during movement, and its actions are resistant to muscarinic receptor blockade. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sleep architecture in a canine model of obstructive sleep apnea

Obstructive sleep apnea (OSA) causes recurrent sleep disruption that is thought to contribute to excessive daytime sleepiness in patients with this disorder. The purpose of this study was to determine the specific effects of OSA on overall sleep architecture in a canine model of OSA. The advantage of this model is that sleep during long-term OSA can be compared to both normal sleep before OSA and recovery sleep after OSA. Studies were performed in four dogs in which sleep-wake state was monitored continuously by a computer that received telemetered EEG and EMG signals. Whenever sleep was detected, the computer sent a signal to close a valve through which the dog breathed; when the dog awoke the occlusion was released. In each dog, data were analyzed from 4 consecutive nights in three phases: a control phase before induction of OSA, a phase during long-term OSA (mean = 85 days, apnea index = 59/hour), and a recovery phase after cessation of OSA. During recovery there was a significant increase in the amount of rapid-eye-movement (REM) sleep compared to the OSA phase (p < 0.01), as well as significant increases in sleep efficiency and decreases in wakefulness (p < 0.01), similar to that reported in OSA patients. The REM rebound during recovery, however, could not be attributed to overall REM deprivation since the amount of REM sleep during the OSA phase was not different from the control phase (p = 0.708). This finding suggests that REM rebound during recovery from OSA is not the result of an overall REM sleep deficit per se. Rather, repeated sleep disruption due to the effects of repetitive apneas and hypoxia may lead to an increased REM sleep drive that manifests itself as a REM sleep rebound during recovery sleep after OSA.     

REM suppression induced by digital mobile radio telephones

In the present study we investigated the effects of pulsed high-frequency electromagnetic fields irradiated by digital mobile radio telephones on sleep in healthy humans. Besides a hypnotic effect with shortening of sleep onset latency, a REM suppressive effect with reduction of duration and percentage of REM sleep was found under exposure to the field. Moreover, spectral analysis revealed an increased spectral power density of the EEG signal during REM sleep, especially in the alpha frequency band. These results emphasise the necessity to carry out further investigations on the interaction of this type of electromagnetic fields and the human organism.     

Sleep and quantitative EEG in patients with progressive supranuclear palsy

Sleep architecture and quantitative EEG from wakefulness and REM sleep were studied in six patients (mean age, 70.5 years) with progressive supranuclear palsy (PSP) and compared with that of six control subjects (mean age, 69.8 years). Particular attention was given to quantifying REM sleep variables because of the known PSP-associated degeneration of the pedunculopontine tegmentum (PPT)--a critical structure in REM sleep generation. Patients with PSP had a shorter total sleep time, a lower sleep efficiency, a drastic reduction in sleep spindles, an atonic slow-wave sleep, and a lower percentage of REM sleep. The lower percentage of REM sleep was the result of both a reduction in the number of REM periods and a reduction in mean period of duration. REM density was also reduced while REM efficiency, atonia, and phasic EMG were similar to control values. REM sleep findings are consistent with the known role of the PPT in REM sleep induction. A slowing of the awake EEG was found for the six frontal leads and for C4, P4, and T4 in PSP patients. The frontal EEG slowing found in wakefulness is in accord with imaging and neuropsychological studies showing impairment of the frontal lobes in these patients. REM sleep EEG was not significantly slower in any regions. Because all previous studies on PSP have relied on visual inspection of the EEG tracings, the present finding of EEG slowing in the frontal lobes (rather than in the temporal regions or diffusely) suggests that our quantitative EEG approach may be more useful in determining specific regions of impaired cortical activity.     

Manic-depressive psychosis and electroencephalogram

The literature dealing with electroencephalogram (EEG) in manic-depressive psychosis is reviewed. It is concluded that although there are no specific EEG patterns in the psychosis, some reports suggest a predominance of the alpha activity and a heightened arousal response. From many studies on sleep and depression, it appears that the EEG sleep architecture in depression is characterized by reduced total sleep time, intermittent awakenings, decreased slow-wave sleep and shortened REM latency. In particular, shortened REM latency is important for diagnosis of primary depression. Furthermore, the meaning of abnormal EEGs reported in the psychosis is worth investigating. In order to make the pathophysiology of manic-depressive psychosis clearer, it is important to carry out a comprehensive research, including clinical, physiological, biochemical and molecular biological study.     

Respiratory responses to tracheobronchial stimulation during sleep and wakefulness in the adult cat

The response to tracheal stimulation (50 microliters of tap water) during wakefulness, non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep was investigated in adult cats. In wakefulness, repetitive coughing occurred on 80% of the trials. In NREM and REM sleep, the most frequent response (approximately 69% and 58% of the trials, respectively) was arousal, followed by coughing. Apneas occurred following the stimulus and before arousal in 11% and 24% of the trials in NREM and REM sleep, respectively. In NREM sleep, the tracheal stimulus sometimes evoked expiratory efforts following a normal inspiratory effort (11% of the trials). These were much weaker than the expiratory efforts during coughing in wakefulness. In REM sleep, stimulation in 11% of the trials elicited increased inspiratory efforts. Although these may have been diminutive preparatory inspirations for coughing, they were much smaller than preparatory inspirations associated with coughing in wakefulness, and they were never followed by active expiratory efforts. Arousal from either NREM or REM sleep in response to tracheal stimulation was sometimes associated with an augmented breath. This response, which is common upon spontaneous arousal, may lead to deeper aspiration of the tracheal fluid. We conclude that in cats coughing requires wakefulness and that airway stimuli in sleep cause a variety of respiratory responses, some of which may be maladaptive.     

Respiratory arousal from sleep: mechanisms and significance

The mechanisms by which respiratory stimuli induce arousal from sleep and the clinical significance of these arousals have been explored by numerous studies in the last two decades. Evidence to date suggests that the arousal stimulus in nonrapid eye movement sleep (NREM) is related to the level of inspiratory effort rather than the individual stimuli that contribute to ventilatory drive. A component of the arousal stimulus proportional to the level of inspiratory effort may originate in mechanoreceptors either in the upper airway or respiratory pump. Medullary centers responsible for ventilatory drive may also send a signal proportionate to the level of drive to higher centers in the brain which are responsible for arousal. Thus, the arousal stimulus may consist of multiple components, each increasing as inspiratory effort increases. The level of effort triggering arousal is an index of the arousability of the brain (arousal threshold). A deeper stage of sleep, central nervous system depressants, prior sleep fragmentation, and the presence of obstructive sleep apnea (OSA) have been observed to increase the arousal threshold to airway occlusion. Less information is available concerning the mechanisms of arousal from rapid eye movement (REM) sleep. While REM sleep is associated with the longest obstructive apneas in patients with OSA, normal human subjects appear to have a similar or lower arousal threshold to respiratory stimuli in REM compared to NREM sleep. Recent studies have challenged the assumption that the termination of all obstructive apnea is dependent on arousal from sleep. Improvements in methods to detect and quantitate changes in the cortical electroencephalogram (EEG) may better define the relationship between arousal and apnea termination. This may result in improved criteria for identifying EEG changes of clinical significance. While little is known concerning the mechanisms of arousal in central sleep apnea, arousal may play an important role in inducing this type of apnea in some patients.     

Stimulus-elicited behavior in rapid eye movement sleep without atonia.

Alert wakefulness (W) and rapid eye movement sleep (REM) are remarkably similar on several measures of brain activity, but 2 differences in REM are reduced sensory responsiveness and atonia in postural muscles. Pontine tegmental lesions create REM without atonia (REM-A), releasing motor behavior. In 9 cats, we studied the acoustic startle reflex (ASR), orienting (OR), and ponto-geniculo-occipital waves (PGOE) elicited by tones during W, REM, REM-A, and non-REM (NREM). OR occurred in W and REM-A, being most complete in cats with the most elaborate spontaneous behavior. ASR occurred in W, NREM, and REM-A in lesioned cats. In normal cats, ASR rarely appeared in NREM and REM. PGOE had similar characteristics in both groups. The similarity of REM to W is particularly obvious when cats lack motoneuronal inhibition. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Monotremes and the evolution of rapid eye movement sleep

Early studies of the echidna led to the conclusion that this monotreme did not have rapid eye movement (REM) sleep. Because the monotremes had diverged from the placental and marsupial lines very early in mammalian evolution, this finding was used to support the hypothesis that REM sleep evolved after the start of the mammalian line. The current paper summarizes our recent work on sleep in the echidna and platypus and leads to a very different interpretation. By using neuronal recording from mesopontine regions in the echidna, we found that despite the presence of a high-voltage cortical electroencephalogram (EEG), brainstem units fire in irregular bursts intermediate in intensity between the regular non-REM sleep pattern and the highly irregular REM sleep pattern seen in placentals. Thus the echidna displays brainstem activation during sleep with high-voltage cortical EEG. This work encouraged us to do the first study of sleep, to our knowledge, in the platypus. In the platypus we saw sleep with vigorous rapid eye, bill and head twitching, identical in behaviour to that which defines REM sleep in placental mammals. Recording of the EEG in the platypus during natural sleep and waking states revealed that it had moderate and high-voltage cortical EEGs during this REM sleep state. The platypus not only has REM sleep, but it had more of it than any other animal. The lack of EEG voltage reduction during REM sleep in the platypus, and during the REM sleep-like state of the echidna, has some similarity to the sleep seen in neonatal sleep in placentals. The very high amounts of REM sleep seen in the platypus also fit with the increased REM sleep duration seen in altricial mammals. Our findings suggest that REM sleep originated earlier in mammalian evolution than had previously been thought and is consistent with the hypothesis that REM sleep, or a precursor state with aspects of REM sleep, may have had its origin in reptilian species.     

Validation of an EEG-derived spectral frequency index (SFx) for continuous monitoring of sleep depth in humans

Sleep in humans is classically assessed by recording a multichannel electroencephalogram (EEG) in connection with an electrooculogram (EOG) and an electromyogram (EMG). In general, human sleep is manually staged into 6 categories (from awake through REM sleep to stage 4 reflecting deep sleep) on the basis of a visual inspection of EEG periods (epochs) of 20 - 30 s duration. This cumbersome methodology is still used in practice and for reference purposes. - The conversion of EEG-signals by means of Fast Fourier Transformation provides objective and reproducible information reflecting specific communicative features of the central nervous system. A special part of this information based on a specific algorithm is defined by the so-called spectral frequency index (SFx). This SFx-algorithm contains relationships among some particular EEG frequencies and provides objective percentage values about the state of consciousness of a person. In order to validate this new SFx-method, sleep as a physiological state of continuous alterations of consciousness and vigilance was chosen. A total of 36 nights of sleep from 18 healthy volunteers were staged manually by a scientist unaware of the protocol. The volunteers received either placebo or lormetazepam prior to commencement of the nocturnal recordings. The manually staged data were compared with the data obtained by the SFx-analysis. Both data sets SFx values and manually staged data were made comparable by averaging their values to a basic period length of 2 min duration giving 7960 pairs of data. The SFx data for sleep were found within a range from 35% to 100%. The SFx-medians of the manually staged data from "awake" to stage 4 were found in a decending order ("awake": 83% (lower and upper quartile 78% / 87%);"REM": 68% (63%/74%),"stage 1" :63% (57%/70%),"stage 2" :51% (47%/57%), "stage 3" :44% (42%/46%) and "stage 4" :42% (40%/44%). The rank correlation coefficient between the data pairs was calculated to be 0.79 indicating a substantial matching between the manually staged score and the SFx. We therefore conclude that the SFx is a suitable and objective indicator of sleep depth in humans.     

Functional neuroanatomy of human rapid-eye-movement sleep and dreaming

Rapid-eye-movement (REM) sleep is associated with intense neuronal activity, ocular saccades, muscular atonia and dreaming. The function of REM sleep remains elusive and its neural correlates have not been characterized precisely in man. Here we use positron emission tomography and statistical parametric mapping to study the brain state associated with REM sleep in humans. We report a group study of seven subjects who maintained steady REM sleep during brain scanning and recalled dreams upon awakening. The results show that regional cerebral blood flow is positively correlated with REM sleep in pontine tegmentum, left thalamus, both amygdaloid complexes, anterior cingulate cortex and right parietal operculum. Negative correlations between regional cerebral blood flow and REM sleep are observed bilaterally, in a vast area of dorsolateral prefrontal cortex, in parietal cortex (supramarginal gyrus) as well as in posterior cingulate cortex and precuneus. Given the role of the amygdaloid complexes in the acquisition of emotionally influenced memories, the pattern of activation in the amygdala and the cortical areas provides a biological basis for the processing of some types of memory during REM sleep.     

An analysis of the brain's transfer properties in schizophrenia: amplitude frequency characteristics and evoked potentials during sleep

BACKGROUND: Classical analysis of spontaneous sleep electroencephalogram (EEG) in schizophrenia commonly reveals alterations of sleep continuity, number of awakenings, slow-wave sleep (SWS), and REM sleep compared to healthy controls; however, conventional analysis cannot help understand dynamic differences of the sleep EEG during different sleep stages. METHODS: We measured late components of auditory evoked potentials (AEPs) and visual evoked potentials (VEPs) during different sleep stages of 11 schizophrenic inpatients and in a sex- and age-matched control group from scalp positions FZ, CZ, and PZ. According to linear system theory, we then computed the amplitude-frequency characteristic (AFC) from averaged AEPs and VEPs in different sleep stages. These AFCs describe the input-output relation of the system under study, leading to a characterization of the transfer properties of the schizophrenic brain during sleep. RESULTS: Significant differences could be found for the transfer properties during stage II and SWS between schizophrenics and controls. During REM a marked enhancement of theta resonance was seen in schizophrenics. CONCLUSIONS: The results of the present study point to highly different central nervous system transfer properties in schizophrenics and controls. Compared to previous investigations in depression, the results provide additional information for distinguishing schizophrenia and depression in EEG studies.     

Changes in EEG power density during sleep laboratory adaptation

First- and second-night effects on the electroencephalogram (EEG) were investigated by means of polygraphic sleep recordings and all-night spectral analysis. Eighteen normal subjects were studied for three consecutive nights in a hospital sleep laboratory. Visual sleep scoring showed that there was a first-night effect in normal subjects similar to that reported previously [increased wakefulness; decreased total sleep time, sleep efficiency, and rapid eye movement (REM) sleep]. Spectral analysis of the sleep EEG revealed important changes, most of which occurred in REM sleep. Increased delta, theta, and beta1 power densities accompanied by decreased mean frequency were seen in REM sleep in the second night. On the basis of REM sleep deprivation results previously published, our data suggest that the second night could be affected by partial REM sleep deprivation that occurred in the first night. Delta and theta power density values decreased in the first non-rapid eye movement episode of nights 1 and 2; this could result from increased REM sleep pressure. The overall consistency of spectral data in the first and second night with REM sleep findings derived from visual scoring in the first night lends further support to this hypothesis. The sleep disturbance experienced during the first night in a sleep laboratory may be a useful and valid model of transient insomnia. Therefore, we conclude that data from all nights recorded should be included in assessing a subject's sleep.     

Droloxifene does not blunt bone anabolic effects of prostaglandin E2, but maintains prostaglandin E2-restored bone in aged, ovariectomized rats

The authors examined 1) effects of nortriptyline (NT) on electroencephalographic (EEG) sleep measures in elderly patients with bereavement-related depression in remission under randomized, double-blind, placebo-controlled conditions, and 2) the effects of clinical remission on sleep after discontinuation of medication. Subjects were classified as responders to placebo (n = 9) or NT (n = 18) and had EEG sleep studies at three time-points: before treatment (T1), remitted on medication or placebo (T2), and remitted off medication or placebo (T3). As compared with placebo, NT was differentially associated with decreases in REM sleep time and percent and increases in REM sleep density (T2). No changes in EEG sleep measures occurred in placebo responders. REM sleep measures in NT responders reverted to T1 levels after T3, with persistence of robust clinical remission and normal subjective sleep quality. These data suggest that NT alters REM sleep, but that EEG sleep characteristics in bereavement-related depression persist into remission.     

Effects of passive-avoidance training on sleep-wake state-specific activity in the basolateral and central nuclei of the amygdala.

This study examined the effects of intense emotional learning on the sleep-wake state-specific electroencephalographic (EEG) activities of the basolateral (BLA) and central (CeA) nuclei of the amygdala. Rats were trained on a passive-avoidance learning (PAL) protocol that was followed by 6 hrs of undisturbed polygraphic recording and a PAL test. After PAL training, the total amount of REM sleep decreased; high-frequency EEG power decreased in the CeA during REM sleep and increased in the BLA during all sleep-wake stages. These results suggest that there is no homeostatic demand for REM sleep after intense emotional learning. However, the PAL-specific changes in the local EEG suggest that some form of memory processing may occur within the amygdala during REM sleep. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

C-fos expression in the pons and medulla of the cat during carbachol-induced active sleep

Microinjection of carbachol into the rostral pontine tegmentum of the cat induces a state that is comparable to naturally occurring active (REM, rapid eye movement) sleep. We sought to determine, during this pharmacologically induced behavioral state, which we refer to as active sleep-carbachol, the distribution of activated neuron within the pons and medulla using c-fos immunocytochemistry as a functional marker. Compared with control cats, which were injected with saline, active sleep-carbachol cats exhibited higher numbers of c-fos-expressing neurons in (1) the medial and portions of the lateral reticular formation of the pons and medulla, (2) nuclei in the dorsolateral rostral pons, (3) various raphe nuclei, including the dorsal, central superior, magnus, pallidus, and obscurus, (4) the medial and lateral vestibular, prepositus hypoglossi, and intercalatus nuclei, and (5) the abducens nuclei. On the other hand, the mean number of c-fos-expressing neurons found in the masseter, facial, and hypoglossal nuclei was lower in carbachol-injected than in control cats. The data indicate that c-fos expression can be employed as a marker of state-dependent neuronal activity. The specific sites in which there were greater numbers of c-fos-expressing neurons during active sleep-carbachol are discussed in relation to the state of active sleep, as well as the functional role that these sites play in generating the various physiological patterns of activity that occur during this state.     

Role strain in couples with and without a child with a chronic illness: associations with marital satisfaction, intimacy, and daily mood

The tryptophan depletion test is a research strategy to investigate the functional consequences of decreasing the brain serotonin metabolism. Because serotonin is involved in sleep regulation and the regulation of affective states, we studied the acute polysomnographic effects of tryptophan depletion and expected to induce similar changes of sleep EEG as observed in depressed patients. A total of 12 healthy subjects (mean age 34 +/- 3 years) had eight polysomnograms, divided in two blocks of 4 consecutive nights. After one adaptation and 1 baseline night, subjects received a low-protein diet on day 3 and 4 until midday. On day 4 at 18.00 h, they drank an amino acid mixture either devoid of tryptophan or containing 2.3 g of tryptophan (placebo control) in randomized and double-blind order, resulting in an 85% decrease (tryptophan depletion) and a 144% increase (placebo control) of serum tryptophan at 22.00 h. After tryptophan depletion but not placebo, significant effects on sleep EEG were observed in terms of decreased non-rapid eye movement (non-REM) stage 2, increase of wake %, and of rapid eye movement (REM) density compared with baseline. REM latency was not altered, however the first and second REM period interval were significantly shorter after tryptophan depletion. This study underlines the impact of the serotonergic system on sleep maintenance and on REM sleep.     

Effects of antipsychotic treatment on polysomnographic measures in schizophrenia: a replication and extension

OBJECTIVE: The authors sought to replicate and extend previous observations of improvement in some EEG sleep measures during the course of antipsychotic treatment in schizophrenia patients. METHOD: Fourteen medication-free patients with schizophrenia underwent 2 nights of sleep EEG monitoring before and after 3-4 weeks of treatment with clinically determined doses of haloperidol or thiothixene. RESULTS: Measures of sleep continuity improved consistently. REM latency increased, although five of 14 patients continued to exhibit short REM latencies (less than 60 minutes). Stage 3 sleep increased during neuroleptic treatment, while stage 4 sleep did not change. CONCLUSIONS: These data demonstrate partial improvement of some but not all EEG sleep measures in schizophrenic patients through the course of neuroleptic treatment. They suggest that shortened REM latency and disturbed sleep continuity might represent reversible state abnormalities, while reduced slow-wave sleep may represent a more persistent trait abnormality in schizophrenia.     

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation.

Recent evidence suggests that the human sleep electroencephalogram (EEG) shows regional differences over both the sagittal and coronal planes. In the present study, in a group of 10 right-handers, the authors investigated the presence of hemispheric asymmetries in the homeostatic regulation of human sleep EEG power during and after selective slow-wave sleep (SWS) deprivation. The SWS deprivation was slightly more effective over the right hemisphere, but the left hemisphere showed a markedly larger increase of EEG power in the 1.00-24.75 Hz range during recovery-night non-REM sleep, and a larger increase of EEG power during both deprivation-night and recovery-night REM sleep. These results support the greater need for sleep recuperative processes of the left hemisphere, suggesting that local sleep regulation processes may also act during REM sleep. (PsycINFO Database Record (c) 2010 APA, all rights reserved)