Bursts Of Rapid Eye Movements Research Articles

Eye movement patterns correlate with overt emotional behaviours in rapid eye movement sleep

Growing evidence suggests that sleep plays a key role in regulating emotions. Rapid eye movements (REMs) in REM sleep could be associated with dreams emotions, but supporting evidence is indirect. To highlight this association, we studied the REM sleep during video-polysomnography of 20 subjects with REM sleep behaviour disorder (RBD), a model of enacted dreams offering direct access to the emotional content of the sleeper (face expression, speeches, behaviour). Video and the electro-oculography recordings were divided into 3 s time intervals and classified as non-behavioural, or behavioural (neutral, positive or negative emotions), and as containing no eye movements (EMs), slow eye movements (SEMs) or REMs (isolated or bursts). Compared to the absence of EMs, neutral behaviours successively increased in the presence of SEMs (odd ratio, OR = 1.4), then isolated REMs (OR = 2.8) and then REM bursts (OR = 4.6). Positive behaviours increased with SEMs (OR = 2.8) but did not increase further with isolated REMs (OR = 2.8) and REM bursts (OR = 3). Negative behaviours were absent with SEMs, increased with isolated REMs (OR = 2.6) and further with REM bursts (OR = 10.1). These results support an association between REMs and SEMs, and dream emotions.

Twitches emerge postnatally during quiet sleep in human infants and are synchronized with sleep spindles

In humans and other mammals, the stillness of sleep is punctuated by bursts of rapid eye movements (REMs) and myoclonic twitches of the limbs.1 Like the spontaneous activity that arises from the sensory periphery in other modalities (e.g., retinal waves),2 sensory feedback arising from twitches is well suited to drive activity-dependent development of the sensorimotor system.3 It is partly because of the behavioral activation of REM sleep that this state is also called active sleep (AS), in contrast with the behavioral quiescence that gives quiet sleep (QS)-the second major stage of sleep-its name. In human infants, for which AS occupies 8h of each day,4 twitching helps to identify the state;5-8 nonetheless, we know little about the structure and functions of twitching across development. Recently, in sleeping infants,9 we documented a shift in the temporal expression of twitching beginning around 3months of age that suggested a qualitative change in how twitches are produced. Here, we combine behavioral analysis with high-density electroencephalography (EEG) to demonstrate that this shift reflects the emergence of limb twitches during QS. Twitches during QS are not only unaccompanied by REMs, but they also occur synchronously with sleep spindles, a hallmark of QS. As QS-related twitching increases with age, sleep spindle rate also increases along the sensorimotor strip. The emerging synchrony between subcortically generated twitches and cortical oscillations suggests the development of functional connectivity among distant sensorimotor structures, with potential implications for detecting and explaining atypical developmental trajectories.

Rapid eye movements during sleep in mice: High trait-like stability qualifies rapid eye movement density for characterization of phenotypic variation in sleep patterns of rodents

BackgroundIn humans, rapid eye movements (REM) density during REM sleep plays a prominent role in psychiatric diseases. Especially in depression, an increased REM density is a vulnerability marker for depression. In clinical practice and research measurement of REM density is highly standardized. In basic animal research, almost no tools are available to obtain and systematically evaluate eye movement data, although, this would create increased comparability between human and animal sleep studies.MethodsWe obtained standardized electroencephalographic (EEG), electromyographic (EMG) and electrooculographic (EOG) signals from freely behaving mice. EOG electrodes were bilaterally and chronically implanted with placement of the electrodes directly between the musculus rectus superior and musculus rectus lateralis. After recovery, EEG, EMG and EOG signals were obtained for four days. Subsequent to the implantation process, we developed and validated an Eye Movement scoring in Mice Algorithm (EMMA) to detect REM as singularities of the EOG signal, based on wavelet methodology.ResultsThe distribution of wakefulness, non-REM (NREM) sleep and rapid eye movement (REM) sleep was typical of nocturnal rodents with small amounts of wakefulness and large amounts of NREM sleep during the light period and reversed proportions during the dark period. REM sleep was distributed correspondingly. REM density was significantly higher during REM sleep than NREM sleep. REM bursts were detected more often at the end of the dark period than the beginning of the light period. During REM sleep REM density showed an ultradian course, and during NREM sleep REM density peaked at the beginning of the dark period. Concerning individual eye movements, REM duration was longer and amplitude was lower during REM sleep than NREM sleep. The majority of single REM and REM bursts were associated with micro-arousals during NREM sleep, but not during REM sleep.ConclusionsSleep-stage specific distributions of REM in mice correspond to human REM density during sleep. REM density, now also assessable in animal models through our approach, is increased in humans after acute stress, during PTSD and in depression. This relationship can now be exploited to match animal models more closely to clinical situations, especially in animal models of depression.

Eye Movements and Abducens Motoneuron Behavior after Cholinergic Activation of the Nucleus Reticularis Pontis Caudalis

the aim of this work was to characterize eye movements and abducens (ABD) motoneuron behavior after cholinergic activation of the nucleus reticularis pontis caudalis (NRPC). six female adult cats were prepared for chronic recording of eye movements (using the scleral search-coil technique), electroencephalography, electromyography, ponto-geniculo-occipital (PGO) waves in the lateral geniculate nucleus, and ABD motoneuron activities after microinjections of the cholinergic agonist carbachol into the NRPC. unilateral microinjections of carbachol in the NRPC induced tonic and phasic phenomena in the oculomotor system. Tonic effects consisted of ipsiversive rotation to the injected side, convergence, and downward rotation of the eyes. Phasic effects consisted of bursts of rhythmic rapid eye movements directed contralaterally to the injected side along with PGO-like waves in the lateral geniculate and ABD nuclei. Although tonic effects were dependent on the level of drowsiness, phasic effects were always present and appeared along with normal saccades when the animal was vigilant. ABD motoneurons showed phasic activities associated with ABD PGO-like waves during bursts of rapid eye movements, and tonic and phasic activities related to eye position and velocity during alertness. the cholinergic activation of the NRPC induces oculomotor phenomena that are somewhat similar to those described during REM sleep. A precise comparison of the dynamics and timing of the eye movements further suggests that a temporal organization of both NRPCs is needed to reproduce the complexity of the oculomotor behavior during REM sleep.

Behavioural and neurophysiological correlates of human cataplexy: A video-polygraphic study

To investigate the behavioural and neurophysiological pattern of cataplexy. Seven narcolepsy with cataplexy patients underwent daytime videopolygraphy using humorous movies or/and jokes to trigger cataplectic attacks. During segmental cataplectic attacks, EMG showed brief and irregular periods of silencing focally involving facial, neck, axial or limb muscles, sometimes coinciding with bursts of rapid eye movements. All patients enacted intentional movements in response to these segmental postural lapses. During global cataplectic attacks, EMG showed suppression of activity alternated with patterned enhancement, enhanced EMG activity in neck muscles preceding that of other cranial, axial and lower limb muscles. This waxing and waning EMG pattern ended with a complete body collapse and persistent muscle atonia. Breathing irregularities, heart rate (HR) instability and EEG desynchronization were observed during global cataplectic attacks without any appreciable blood pressure changes, but with HR deceleration and silencing of sympathetic skin response while in complete atonia. Patients subjectively perceived the involuntary postural lapses as startling and alarming. Cataplexy in our patients showed many of the features of tonic REM sleep. Cataplexy can be construed as a "freezing-like" perturbation of the orienting response with transient impairment of posture and movements resulting in a "patchwork-compromise-behaviour".

Evidence of subthalamic PGO-like waves during REM sleep in humans: a deep brain polysomnographic study.

The aim of this study was to examine whether the subthalamic nucleus (STN) plays a role in the transmission of PGO-like waves during REM sleep in humans. Simultaneous recordings from deep brain electrodes to record local field potentials (LFPs), and standard polysomnography to ascertain sleep/wake states. Main Hospital, department of clinical neurophysiology sleep laboratory. 12 individuals with Parkinson's disease, with electrodes implanted in the STN; and, as a control for localization purposes, 4 cluster headache patients with electrodes implanted in the posterior hypothalamus. All subjects underwent functional neurosurgery for implantation of deep brain stimulation electrodes. Sharp, polarity-reversed LFPs were recorded within the STN during REM sleep in humans. These subthalamic PGO-like waves (2-3 Hz, 80-200 pV, and 300-500 msec) appeared during REM epochs as singlets or in clusters of 3-13 waves. During the pre-REM period, subthalamic PGO-like waves were temporally related to drops in the submental electromyogram and/or onset of muscular atonia. Clusters of PGO-like waves occurred typically before and during the bursts of rapid eye movements and were associated with an enhancement in fast (15-35 Hz) subthalamic oscillatory activity. Subthalamic PGO-like waves can be recorded during pre-REM and REM sleep in humans. Our data suggest that the STN may play an active role in an ascending activating network implicated in the transmission of PGO waves during REM sleep in humans.

In the flicker of an eye

In the flicker of an eye

REM sleep-related brady-arrhythmia syndrome

Rapid eye movement (REM) sleep-related brady-arrhythmia syndrome is a cardiac rhythm disorder characterised by asystoles lasting several seconds during REM sleep in otherwise healthy individuals. In contrast to arrhythmias associated with obstructive sleep apnea, REM sleep-related sinus arrests and atrioventricular (AV) blocks are not associated with episodes of apnea or hypopnea. In literature, only few cases have been published, suggesting that the prevalence of this nighttime rhythm disorder is very rare. In this paper, we report two new cases of REM sleep-related sinus arrests and one case of REM sleep-related total AV block. To explore the underlying mechanism, an analysis of heart rate variability was performed. In a matched control population, we observed a significant lower low-to-high frequency (LF/HF) ratio in slow wave sleep as compared to REM sleep (2.04 +/- 1.2 vs 4.55 +/- 1.82, respectively [Mann-Whitney U test p < 0.01]), demonstrating a global increase in sympathetic activity during REM. When using the same technique in two of three patients with REM-related arrhythmias, the shift to an increased LF/HF ratio from slow wave sleep to REM sleep tended to be lower. This may reflect an increased vagal activity (HF component) during REM sleep in these subjects. We, therefore, hypothesise that, in our patients with REM sleep-related arrhythmias, the overall dominance of sympathetic activity during REM is present but to a lesser extent and temporarily switches into vagal dominance when the bursts of REMs occur. As it was still unclear whether these REM sleep-related asystoles needed to be paced, we compared our treatment and these of previously reported cases with the current American College of Cardiology/American Heart Association guidelines for implantation of cardiac pacemakers.

Sibling cases of Vici syndrome: Sleep abnormalities and complications of renal tubular acidosis

Vici syndrome is a rare congenital disorder characterized by albinism, agenesis of the corpus callosum, and developmental delays. Cardiac complications usually cause poor prognosis. We report sibling cases of Vici syndrome, and address complications of renal tubular acidosis. We also demonstrate the significance of serial examinations of brain natriuretic peptides, and discuss the possible early use of a beta-blocker to control cardiomyopathy. A sleep study including polysomnography indicated functional brainstem involvement, in which muscle atonia during non-rapid sleeping eye movements, and bursts of rapid eye movements increased. These findings provide new clues for medical care of patients with Vici syndrome.

Detection of Rapid-Eye Movements in Sleep Studies

One of the key features of rapid-eye movement (REM) sleep is the presence of bursts of REMs. Sleep studies routinely use REMs to classify sleep stages. Moreover, REM count or density has been used in studies involving learning and various psychiatric disorders. Most of these studies have been based on the visual identification of REMs, which is generally a very time-consuming task. This and the varying definitions of REMs across scorers have warranted the development of automatic REM detection methodologies. In this paper, we present a new detection scheme that combines many of the intrinsic properties of REMs and requires minimal parameter adjustments. In the proposed method, a single parameter can be used to control the REM detection sensitivity and specificity tradeoff. Manually scored training data are used to develop the method. We assess the performance of the method against manual scoring of individual REM events and present validation results using a separate data set. The ability of the method to discriminate fast horizontal ocular movement in REM sleep from other types of events is highlighted. A key advantage of the presented method is the minimal a priori information requirement. The results of training data (recordings from five subjects) show an overall sensitivity of 78.8% and specificity of 81.6%. The performance on the testing data (recording from five subjects different from the training data) showed overall sensitivity of 67.2% and specificity of 77.5%.

Rapid eye movement activity before spontaneous awakening in elderly subjects.

Previous research in young subjects found that rapid eye movement (REM) density is higher in those REM phases which are followed by an awakening (REM-W) than in those preceding NREM (REM-N), suggesting a 'gating role' of REM sleep toward the awakening. It is not yet known whether this evidence is maintained in elderly subjects, who display, relative to young subjects, more awakenings, different sleep states from which the awakenings come (NREM in a high proportion of cases) and a general impairment of rapid eye movement activity (REMA). To investigate this issue, we have compared in three different age groups (young, old and 'old old' subjects) the features of REMA, including REM density and the amount and duration of REM bursts, between REM-W and REM-N. Whereas in the young REM density is higher in REM-W than in REM-N, this difference is already reduced in the old group and fully cancelled in the old old subjects. The evidence that old individuals spontaneously wake up despite the absence of an increase of REMA could imply that in the aged awakening is not preceded by an increase of the arousal level (expressed in REM sleep by the REMA). The similar duration of REM bursts for REM-W and REM-N in both groups of old subjects suggests that with age a marked impairment occurs in the organizational aspects of REMs, independently from the following state.

Rapid-eye-movement sleep in jittery infants

The pathogenesis of neonatal jitteriness (JT) remains unknown. Neonatal JT could be one of the symptoms associated with drug withdrawal syndrome due to maternal medication. To study the influence of chemicals and environment on brain development in the fetal period, Swaab and Mirmiran proposed "behavioral teratology". JT could be one of the targets for this concept. Swaab and Mirmiran postulated that rapid-eye-movement sleep (REM sleep) is useful for studying behavioral teratology. We aimed to determine the neurophysiological alterations in infants with JT by investigating REM sleep. Sleep records were obtained three times for each of six jittery infants. The mothers of three infants had been on medication (either alpha-methyl dopa, reserpine or haloperidol) during pregnancy, whereas the mothers of the other three infants took no medication during pregnancy. REM sleep parameters (the amount of REM sleep against the total sleep time, newly designated indices-tonic inhibition index (TII) and phasic inhibition index--, and the incidences of gross movements, phasic chin muscle activity (PCMA), and bursts of rapid eye movements) in the six jittery infants were compared with those in age-matched controls. Regardless of maternal medication, TIIs, which represent the shortening of PCMA during REM sleep, were higher in the jittery infants than in the controls. No other REM sleep parameters showed constant differences between the patients and controls. Release of the blockade of dopamine D2 receptors in the fetal brain is considered to be critical for the occurrence of neonatal JT with elevation of TII. Since the abnormal elevation of TII continued after 6 months of age when our patients did not show JT anymore, we have to keep monitoring jittery infants from the standpoint of "behavioral teratology".

The Interpretation of Dreams and the Neurosciences

Shortly after Freud's death, the study of dreaming from the perspective of neuroscience began in earnest. Initially, these studies yielded results which were hard to reconcile with the psychological conclusions set out in this book. The first major breakthrough came in 1953, when Aserinsky and Kleitman discovered a physiological state which occurs periodically (in 90 minute cycles) throughout sleep, and occupies approximately 25% of our sleeping hours. This state is characterized, among other things, by heightened brain activation, bursts of rapid eye movement (REM), increased breathing and heart-rate, genital engorgement, and paralysis of bodily movement. It consists, in short, in a paradoxical physiological condition in which one is simultaneously highly aroused and yet fast asleep. Not surprisingly, Aserinsky and Kleitman suspected that this REM state (as it came to be known) was the external manifestation of the subjective dream state. That suspicion was soon confirmed experimentally, by Aserinsky and Kleitman (1955) and Dement and Kleitman (1957a, 1957b). It is know generally accepted that if someone is awakened from REM sleep and asked whether or not they have been dreaming, they will report that they were dreaming in as many as 95% of such awakenings. Non-REM sleep, by contrast, yields dream reports at a rate of only 5-10% of awakenings. These early discoveries generated great excitement in the neuroscientific field; for the first time it appeared to have in its grasp an objective, physical manifestation of dreaming - the most subjective of all mental states. All that remained to be done, it seemed, was to lay bare the brain mechanisms which produced this physiological state; then we would have discovered nothing less than how the brain produces dreams. Since the REM state can be demonstrated in almost all mammals, this research could also be conducted in subhuman species (which has important methodological implications, for brain mechanisms can be manipulated in animal experiments in ways that they cannot in human research.) A sequence of studies followed, in quick succession, in which different parts of the brain were systematically removed (in cats) in order to isolate the precise structures that produced REM sleep. On this basis, Jouvet was able to report in 1962 that REM (and therefore dreaming) was produced by a small region of cells in a part of the brain stem known as the pons. This part of the nervous system is situated at a level only slightly above the spinal cord, near the nape of the neck. The higher levels of the brain, such as the cerebral hemispheres themselves which fill out the great hollow of the human skull, did not appear to play any causal role whatever in the generation of dreaming. REM sleep occurs with monotonous regularity, throughout sleep, so long as the pons is intact - even if the great cerebral hemispheres are removed completely. Neuroscientific research into the mechanism of REM sleep continued along

Is narcolepsy a REM sleep disorder? Analysis of sleep abnormalities in narcoleptic Dobermans.

Narcolepsy is a chronic sleep disorder marked by excessive daytime sleepiness, cataplexy, sleep paralysis, and hypnagogic hallucinations. Since the discovery of sleep onset REM periods (SOREMPs) in narcoleptic patients, narcolepsy has often been regarded as a disorder of REM sleep generation: REM sleep intrudes in active wake or at sleep onset, resulting in cataplexy, sleep paralysis, or hypnagogic hallucinations. However, this hypothesis has not been experimentally verified. In the current study, we characterized the sleep abnormalities of genetically narcoleptic-cataplectic Dobermans, a naturally occurring animal model of narcolepsy, in order to verify this concept. Multiple sleep latency tests during the daytime revealed that narcoleptic Dobermans exhibit a shorter sleep latency and a higher frequency of SOREMPs, compared to control Dobermans. The total amount of time spent in wake and sleep during the daytime is not altered in narcoleptic dogs, but their wake and sleep patterns are fragmented, and state transitions into and from wake and other sleep stages are altered. A clear 30 min REM sleep cyclicity exists in both narcoleptic and control dogs, suggesting that generation of the ultradian rhythm of REM sleep is not altered in narcoleptics. In contrast, cataplexy displays no cyclicity and can be elicited in narcoleptic animals anytime with emotional stimulation and displays no cyclicity. Stimulation of a cholinoceptive site in the basal forebrain induces a long-lasting attack of cataplexy in narcoleptic dogs; however, bursts of rapid eye movements during this state still occur with a 30 min cyclicity. Sites and mechanisms for triggering cataplexy may therefore be different from those for REM sleep. Cataplexy and a dysfunction in the maintenance of vigilance states, but not abnormal REM sleep generation, may therefore be central to narcolepsy.

Development of REM sleep atonia

To study the functional development of neuronal systems that suppress muscle activity, we quantified the chronological change of atonia in rapid-eye-movement sleep (REMS). REMS atonia was quantified by the tonic and phasic inhibition indices (TII and PII). TII indicates the shortness of chin muscle activity, whereas PII standardizes the simultaneous occurrence of chin muscle activity and bursts of rapid eye movements. TII and PII were calculated in REMS of 135 polysomnographical recordings obtained in healthy humans from premature babies to a 77-year-old man. TII increased significantly with age, while PII decreased significantly. TII reached an adult level at preadolescence, while PII at early infancy. Human nervous systems involved in both tonic and phasic inhibition in REMS raise their activities with age. Since TII and PII reach adult levels at different ages, suppression of muscle activity is hypothesized to be mediated through at least 2 independent systems in humans.

Manifestation of Pulmonary Hypertension During REM Sleep in Obstructive Sleep Apnea Syndrome

The effect of sleep stage change on pulmonary circulation has not been well documented in patients with obstructive sleep apnea syndrome (OSAS). We investigated whether or not stage-specific change can affect pulmonary artery pressure (Ppa) in patients with OSAS. Thirty-one patients with OSAS underwent right cardiac catheterization in the daytime and the following night, including 19 patients in whom Ppa could be measured throughout non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Ten of the 19 patients had daytime pulmonary hypertension (PH) defined by a mean Ppa (Ppa) >/= 20 mm Hg. Then we analyzed Ppa response to hypoxia spontaneously occurring during the period of sleep apnea. The slopes of the regression lines between arterial oxygen saturation measured by pulse oximeter (SpO2) and Ppa curves were almost the same in both NREM and REM patient groups with or without daytime PH, whereas the response curve was significantly shifted upward in REM compared with NREM patients with daytime PH. Furthermore, Ppa was elevated more markedly in association with REM burst, phasic REM, compared with tonic REM. We conclude that vascular tone of pulmonary artery could be elevated in association with REM sleep which is independent of the degree of hypoxia, and that this state-specific change is manifested in patients with daytime PH.

Polysomnographic studies of Lesch–Nyhan syndrome

Three cases of Lesch–Nyhan syndrome (LNS) were examined by polysomnography to assess the brainstem function, and to determine the causes of the neurological manifestations and sudden death in this syndrome. In the two older cases, the amount of slow wave and rapid eye movement (REM) sleep, the REM density and the frequency of REM bursts were decreased. In the youngest case, symmetrical phasic movements of all four limbs were observed at all sleep stages other than REM sleep. Although movements other than these symmetrical body movements appeared to be normal in this case, the frequency of twitch movements showed an abnormal pattern in each sleep stage in the two older cases. These findings suggest that in the brainstems of younger cases with LNS the REM-non REM generator as well as multiple neurotransmitter systems influencing body movements during sleep remain relatively normal, but become progressively impaired in adult cases. Severe obstructive apnea was observed in one case with hypothyroidism, but there were no respiratory abnormalities in other two cases.

Polysomnographic Study in Patients with Severe Myoclonic Epilepsy During Infancy

Purpose: Patients with severe myoclonic epilepsy in infancy (SMEI) exhibit frequent febrile seizures before age 2 years when they show no neurologic deficits. They subsequently develop intractable nonfebrile myoclonic and generalized tonic‐clonic seizures with the appearance of ataxia, developmental delay, and mental retardation. Although its cause remains obscure, the progressive involvement of the cortical as well as subcortical structures has been described. Recently we introduced two indices (tonic inhibition index, TII; and phasic inhibition index, PII) that quantify outputs implicated in motor suppression. These indices were calculated through the standard sleep recording by making use of phasic chin‐muscle activity (PCMA) during rapid‐eye‐movement sleep (REMS). To assess the brainstem involvement in SMEI, these indices were examined in patients with SMEI. Methods: Five polysomnograms obtained from three patients aged from 9 to 25 months were examined. Each polygram consisted of electroencephalography, bipolar horizontal electrooculography, and surface electromyography including the chin muscle. In addition to the proportion of sleep stages in the total sleep time, the TII and PII were calculated. These parameters were compared with those obtained from the age‐matched controls (n = 12). PCMA was defined as a phasic chin‐muscle activity that lasted ≥ 2 s, with a peak amplitude of ≤ 50% above the baseline. TII is the rate of a short PCMA during REMS among the total numbers of PCMA during REMS. The short and long PCMA were separated at a duration of 0.5 s. TII expresses the degree of shortness of PCMA during REMS. PII is a geometric means of the following two values in REMS: (a) the percentage of PCMA that occurs with bursts of rapid eye movements (RBs) in relation to the total number of PCMA, and (b) the percentage of RBs that appear with PCMA in relation to the total number of RBs. As long as rapid eye movement‐related phasic inhibition acts on the chin muscle, PCMA is unlikely to appear in association with RBs. PII expresses the rate of the simultaneous occurrence of PCMA and RBs. Results: With the progression of age, the proportion of REMS and of slow‐wave sleep stages in patients gradually showed values lower than those in controls. The mean TII value in patients (0.66; SD, 0.08) did not differ significantly from that in controls (0.63; SD, 0.05). After 100 weeks of postconceptional age, the mean PII value in patients (7.83; SD, 2.11) was significantly higher than that in controls (4.52; SD, 2.32), whereas there was no difference between the patients (5.8) and controls (5.30; SD, 2.75) at earlier ages. Moreover, in contrast to the controls, PII increased with age in the patients. Conclusions: Although the decrease in the amount of REMS and slow‐wave sleep stages might reflect subcortical impairments, the responsible regions for these findings are uncertain. Because PII decreases during infancy in controls, an increase of PII with age in patients with SMEI suggests a progressive involvement of the neuronal systems. The mesopontine tegmentum plays key roles in the occurrence of rapid eye movement‐related phasic motor reduction, which is responsible for determining the PII value. The pontine as well as rostra1 and caudal medullary atonia zones are crucial for determining the TII value; however, an impairment of these brainstem atonia zones might also affect the PII value. Because TII values remain unaffected in our patients, we conclude that the mesopontine tegmentum is progressively disturbed in patients with SMEI.

A quantitative assessment of the maturation of phasic motor inhibition during REM sleep

During rapid eye movement (REM) sleep, phasic and further motor inhibition occurs during clusters of REMs besides tonic motor inhibition. We describe the age-related quantitative change of the activity of this REM-related phasic motor inhibition. For this purpose, we introduced the phasic inhibition index (PII). PII is the rate of simultaneous occurrence of bursts of horizontal REMs and phasic mentalis muscle activity during REM sleep. We examined these phasic REM sleep parameters in 87 healthy children from premature babies to preadolescents. The incidence of bursts of REMs showed no age-related change, while that of the phasic mentalis muscle activity increased with age. The simple ratio between the incidence of bursts of REMs and that of phasic mentalis muscle activity showed no significant age-related change, whereas PII decreased rapidly during infancy and reached low constant values thereafter. We concluded that this age-related PII decline reflected the maturation of REM-related phasic motor inhibition. This is the first quantitative description on the development of human motor inhibition. Taken with the neuronal basis underlying REM-related phasic motor inhibition, we hypothesize that a PII value is within the normal low range as far as both the rostral pontine tegmentum and the brainstem inhibitory pathways are functionally intact.

Disturbances of the rapid eye movements (REMs) of REM sleep in patients with unilateral attentional neglect: clue for the understanding of the functional meaning of REMs

Horizontal saccades during wakefulness and horizontal rapid eye movements (REMs) during REM sleep were recorded in 6 unilateral brain damaged patients suffering from attentional neglect and 6 unilateral brain damaged control patients. During REM sleep, patients with neglect showed a nearly total suppression of REMs directed away from the side of the lesion; controls had a significantly milder frequency reduction of the same movements. In all patients the frequency reduction of REMs contralateral to the lesion equally affected isolated REMs (i.e., REMs preceded by intervals of oculomotor quiescence longer than 2 sec) and REM bursts (i.e., REMs preceded by intervals shorter than 2 sec). During voluntary inspection in waking, saccades directed ipsilaterally and contralaterally to the lesion were present in both groups of patients, although patients with neglect confined their inspection to the hemispace ipsilateral to the lesion. Results are discussed in terms of their implications for the understanding of the neurophysiological basis of REM sleep oculomotor activity and dream production, as well as for the neurophysiopathological basis of the neglect syndrome. It is proposed that REMs are functionally equivalent to waking reflex orienting saccades generated by a neural network including the relevant modulatory action of the parietal lobes and the superior colliculi.