Absence Of Slow Wave Sleep Research Articles

Characterization of sleep in six patients with pantothenate kinase-associated neurodegeneration

BackgroundPantothenate kinase-associated neurodegeneration (PKAN) is a rare neurologic disorder included in the group of neurodegeneration with brain iron accumulation diseases (NBIA). Information regarding sleep in patients with PKAN is limited. ObjectivesTo describe the clinical and polysomnographic characteristics of sleep in six patients with genetically confirmed PKAN. MethodsThe evaluation included a clinical interview, sleep questionnaires -Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI) and Hospital Anxiety and Depression Scale (HADS)- and a video-polysomnography (VPSG). In addition to standard sleep measures we manually quantified sleep spindle density in stage N2 and rapid eye movements in REM sleep comparing the results with matched controls. Quantification of EMG activity in REM sleep was performed following standard criteria. ResultsAll the patients reported at least one sleep complaint, most commonly sleep fragmentation (4/6) and sleep onset insomnia (3/6). ESS and PSQI were abnormal in 3/6 and 4/6, respectively. VPSG showed in 4/6 decreased ocular movements during REM sleep, an increase in sleep spindles in 3/6 (all of them with deep brain pallidal stimulation), an absence of slow wave sleep in 2 and undifferentiated NREM sleep and delayed sleep phase in one. Three patients had an abnormal sleep apnea/hypopnea index, and 2 periodic limb movements of sleep. REM sleep muscular atonia was preserved in all. ConclusionsSleep disorders are common in patients with PKAN. Although our sample is small and heterogeneous, with different symptomatic treatments possibly influencing the results, it suggests that evaluation of sleep should be considered in their management.

1250 Agrypnia Excitata in a Patient with Paraneoplastic Autoimmune Encephalitis

Abstract Introduction Agrypnia Excitata (AE) is a syndrome characterized by loss of sleep with permanent motor and autonomic hyper activation. This case describes this peculiar syndrome in a patient with paraneoplastic autoimmune encephalitis. Report of Case DG is a 35 yr old male with a history of anti-Ma2 limbic encephalitis secondary to cystic teratoma of the left testis diagnosed 6 months prior to presenting in Sleep Clinic. His parents described significant sleep disturbances including short sleep and wake periods throughout the day and night with no apparent pattern, acting out dreams, motor activity during sleep including pulling at his clothes or using his hands to manipulate invisible objects. Additionally they described low-grade fevers, and severe hyperphagia. Polysomnogram showed absence of slow-wave sleep and what appeared to be an admixture of stage 1 non-rapid eye movement (NREM) with rapid-eye movement (REM) sleep. Multiple sleep-latency testing (MSLT) demonstrated a mean sleep latency of 5.2 minutes and four sleep-onset REM periods (SOREMPs). Magnetic resonance imaging of the brain revealed persistent inflammation of the mesial temporal lobes and hippocampal region. Cerebral spinal fluid testing showed persistent anti-Ma2 antibodies. Based on this clinical presentation we made a diagnosis of Agrypnia Excitata. Conclusion Agrypnia Excitata is a syndrome characterized by loss of the normal sleep-wake rhythm. Sleep consists of the disappearance of spindle-delta activities, and persistent stage 1 NREM sleep mixed with recurrent episodes of REM sleep. The second hallmark of AE is persistent motor and autonomic hyperactivity observed during wake and sleep. AE has been described in three distinct clinical syndromes: Morvan Syndrome (autoimmune encephalitis), Fatal Familial Insomnia, and Delirium tremens. The pathogenesis of AE consists of intra-limbic disconnection releasing the hypothalamus and brainstem reticular formation from cortico-limbic inhibitory control. In autoimmune encephalitis, antibodies that act on voltage-gated potassium channels within the limbic system have been implicated in the pathophysiology.

Changes to sleep patterns in young migrants at high altitude

Objective: To explore the relationship between the level of acclimatization and the changes to sleep architecture in migrants at high altitude. Methods: Nocturnal sleep recordings of 50 subjects aged between 18 and 25 years [mean age (20.9±2.0) years] were analyzed. Those young volunteers were divided into 3 700 m-3 m group(n=10, migrated to an altitude of 3 700 metres for 3 months), 3 700 m-1 y group(n=10, for 1 year) , 5 380 m-3 m group(n=8), 5 380 m-1 y group(n=9), and compared with a control group(n=13, at 1 400 m altitude). Results: When the migrants stayed at 5 380 m for 3 months or 1 year, the wake time increased significantly during sleep[(81.81±59.80)min vs(47.19±24.98) min, P=0.026; (77.94±25.64)min vs(47.19±24.98)min, P=0.040]. Concerning the percentage of total sleep time(TST) in each stage, participants in the 5 380 m-3 m group had a shift in sleep stage distribution with near absence of slow wave sleep(SWS) and a significant increase of N1 , but N2 and rapid eye movement(REM) did not differ. Interestingly, there were entirely concordant changes among the other 3 groups of results, decreased N2 and increased REM. Conclusions: The migrants' abilities to acclimatize themselves to plateau were varied according to the arrived altitude and the length of stay. The sleep of short- time migrants was characterized by increased N1 and decreased SWS, whereas that of well acclimatized migrants was characterized by less N2 and more REM. The efficient recovery in SWS may be an objective reference in high altitude acclimatization.

A theoretical protocol of all-night EEG in polysomnography (PSG) as a preparation and precaution for repetitive transcranial magnetic stimulation (rTMS) in the elderly subjects aged 65 years and over

Objectives: A brief introduction focusing on slow wave sleep (SWS), slow wave activity (SWA), and others was presented. A hypothesis was set then proved: there were 48 among total 117 subjects, aged at least 65 years, had apnea-hypopnea index (AHI) no more than ten. Among those 48, the presence or absence of SWS had made no difference in 12 sleep parameters. The latter were gender, age, BMI, neck circumference, stage 1 sleep duration in minutes, stage 1 sleep percentage, total sleep time, rapid eye movement in minutes, rapid eye movement percentage, sleep latency, snoring, and AHI. A protocol was then reported. It was with all-night EEG/polysomnography (PSG) in an effort as a supplementary preparation of next-day rTMS in the elderly subjects/patients at least 65 years of age. Methods: A design of retrospective sequential collection of clinical data was used. Results: The data in this study, hence, were able to reach a protocol. Conclusion: This study provides reasonable baseline information of an all-night EEG/PSG prior to a next-day rTMS for the elder subject aged 65 or over.

Effects of selective slow-wave sleep deprivation on nocturnal blood pressure dipping and daytime blood pressure regulation

Nocturnal blood pressure (BP) decline or "dipping" is an active, central, nervously governed process, which is important for BP regulation during daytime. It is, however, not known whether the sleep process itself or, more specifically, slow-wave sleep (SWS) is important for normal dipping. Therefore, in the present study, healthy subjects (6 females, 5 males) were selectively deprived of SWS by EEG-guided acoustic arousals. BP and heart rate (HR) were monitored during experimental nights and the following day. Additionally, nocturnal catecholamine excretion was determined, and morning baroreflex function was assessed by microneurographic measurements of muscle sympathetic nerve activity (MSNA) and heart rate variability (HRV). Data were compared with a crossover condition of undisturbed sleep. SWS was successfully deprived leading to significantly attenuated mean arterial BP dipping during the first half (P < 0.05), but not during the rapid-eye-movement-dominated second half of total sleep; however, dipping still evolved even in the absence of SWS. No differences were found for nighttime catecholamine excretion. Moreover, daytime resting and ambulatory BP and HR were not altered, and morning MSNA and HRV did not differ significantly, indicating that baroreflex-mediated sympathoneural BP regulation was not affected by the preceding SWS deprivation. We conclude that in healthy humans the magnitude of nocturnal BP dipping is significantly affected by sleep depth. Deprivation of SWS during one night does not modulate the morning threshold and sensitivity of the vascular and cardiac baroreflex and does not alter ambulatory BP during daytime.

The effects of repeated audiogenic convulsions on the organization of sleep in rats

The organization of sleep in Krushinskii-Molodkina rats, with an inherited predisposition to audiogenic convulsions, was studied during and after repeated audiogenic convulsions consisting of two, three, or five relatively rare (separated by intervals of 90 min) or three, five, or nine relatively frequent (separated by intervals of 45 min) generalized clonic-tonic convulsions. In rats subjected to repeated seizures with rare convulsions, behavior in the periods between individual convulsions was dominated by passive waking (75.2 +/- 4.6% of the time), with a low level (24.8 +/- 4.3%) of slow-wave and a complete absence of fast-wave sleep, i.e., there was selective removal of the fast-wave sleep phase from the sleep-waking cycle of the rats. In rats subjected to frequent seizures with frequent convulsions, the period between convulsions showed only passive waking, with complete loss of slow-wave and fast-wave sleep, i.e., total sleep deprivation took place. The minimal latent period before the appearance of the first episodes of slow-wave sleep after repeated convulsions was 59.9 +/- 10.8 min; that for fast-wave sleep was 158.2 +/- 13.4 min. However, the first episodes of slow-wave and fast-wave sleep had an essentially normal structure, though episodes shorter than those in controls were seen, albeit more rarely. Despite the prolonged (up to 7 h) absence of slow-wave sleep during seizures and the prolonged (8.5 h) decrease in fast-wave sleep, there was no compensatory increase in the levels of these states in the sleep-waking cycle during the 12 h of recovery after seizures. Overall, the recovery period after repeated seizures was characterized by an increase (compared with controls) in the total proportion of waking in the behavior of the rats, with a decrease in the total duration of slow-wave and fast-wave sleep. It is concluded that the paroxysmal status significantly disorganizes the operation of the sleep-generating structures of the brain. The functioning of the systems responsible for slow-wave sleep is less affected, while impairments of the activity of the systems responsible for the formation of fast-wave sleep are more significant, affecting primarily the mechanisms triggering this sleep phase.

Progressive Dementia and Hypersomnolence With Dream-Enacting Behavior

Sleep disorders are associated with several types of degenerative dementias, including Alzheimer and prion diseases. Animal models have demonstrated abolition of rapid eye movement atonia, resulting in dream-enacting complex movements termed oneiric behavior, and patients with fatal familial insomnia may have vivid dreams that intrude on wakefulness. To describe a new form of progressive dementia with hypersomnia and oneiric behavior. Neuropsychological and polysomnographic studies of a middle-aged woman with a progressive dementia, excessive daytime sleepiness, and a vertical gaze palsy. Neuropsychological testing revealed decreased verbal fluency, impaired attention and working memory, amnesia, poor recall, and bradyphrenia with hypersomnia. Polysomnography revealed a rapid eye movement behavioral disorder with complete absence of slow wave sleep. Prion protein analysis did not reveal the mutation associated with fatal familial insomnia, and other diagnostic test findings were unrevealing. Our patient had a previously unreported syndrome of progressive dementia associated with rapid eye movement behavioral disorder and the absence of slow wave sleep.

Sleep physiological characteristics of exhausted men.

Problems initiating and maintaining sleep, and waking up exhausted have been implicated as precursors of a first nonfatal myocardial infarction. These sleep problems are part of an array of complaints that we have labeled as reflecting a state of 'vital exhaustion.' Excess fatigue, loss of vigor, increased irritability, and feelings of demoralization are also characteristic of this state of vital exhaustion, which has been found to constitute a risk indicator for future myocardial infarction. In the present study, we tested the hypothesis that the sleep of exhausted subjects is characterized by a relative absence of slow wave sleep. To test this hypothesis, all-night recordings of the EEG, EOG, and submental EMG of nine exhausted and eight nonexhausted subjects were made for four nights. Sleep stages were rated according to standard criteria. Because these stages do not adequately reflect the essentially continuous aspect of slow wave sleep (SWS), a more detailed analysis of changes in frequencies of the EEG during sleep was also made, using spectral analysis. It seemed that SWS was significantly diminished in exhausted subjects. This suggests that the normal restoration processes that take place during sleep are impaired in exhausted subjects. Additional studies are required to determine the significance of this finding with respect to cardiovascular control during sleep.

STUDIES ON THE POSTPONED GROWTH HORMONE SECRETION FOLLOWING THE INFUSION OF SOMATOSTATIN

It is well known and also confirmed in this study that somatostatin (growth hormone inhibiting factor, GHIF) prevents the noctural GH secretion, as long as the peptide is infused. Following the infusion a rapid rise in GH levels is seen in sleeping subjects with peak values of 26.8 +/- 9.7 ng/ml compared to 31.7 +/- 4.7 ng/ml (+/- SEM) in control nights. Delayed GH peaks were seen even in the absence of slow wave sleep. No postponed GH rise was observed when subjects fell asleep again. These data demonstrate that the postponed nocturnal GH peak does not represent a rebound phenomenon to a previous trigger mechanism but is acutely sleep induced.