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PubMed1985

Abnormal breathing in the Rett syndrome.

Four girls affected with the Rett syndrome showed stereotyped hand movements and psychomotor regression beginning in the first or second year of life after initially normal development, with total loss of language, a severe gait, and chewing and swallowing disturbances. Breathing during active wakefulness was abnormal, with clusters of arrhythmic, tachypneic and irregular respiratory acts, intermixed with prolonged apneic episodes causing cyanosis and even fainting. On the other hand, breathing was regular during both NREM and REM sleep stages. Breathing impairment in the Rett syndrome is characterized by an inability to maintain normal respiratory patterns during wakefulness, and represents a functional disturbance of the behavioral control of breathing, which occurs during active wakefulness.

Adolescent↗
PubMed2004

Effects of three hypnotics on the sleep-wakefulness cycle in sleep-disturbed rats.

RATIONALE: New sleep disturbance model in rats is useful for estimating the characteristics of some hypnotics. OBJECTIVES: The present study was undertaken to investigate the utility of a sleep disturbance model by placing rats on a grid suspended over water using three kinds of hypnotics, that is, short-acting benzodiazepine (triazolam), intermediate-acting benzodiazepine (flunitrazepam) and long-acting barbiturate (phenobarbital). METHODS: Electrodes for measurement of EEG and EMG were implanted into the frontal cortex and the dorsal neck muscle of rats. EEG and EMG were recorded with an electroencephalogram. SleepSign ver.2.0 was used for EEG and EMG analysis. Total times of wakefulness, non-REM and REM sleep were measured from 0900 to 1500 hours. RESULTS: In rats placed on the grid suspended over water up to 1 cm under the grid surface, not only triazolam but also flunitrazepam and phenobarbital caused a shortening of sleep latency. Both flunitrazepam and phenobarbital were effective in increasing of total non-REM sleep time in rats placed on sawdust or the grid, and the effects of both drugs in rats placed on the grid were larger than those in rats placed on sawdust. Measurement of the hourly non-REM sleep time was useful for investigating the peak time and duration of effect of the three hypnotics. Phenobarbital showed a decrease in total REM sleep time in rats placed on the grid, although both triazolam and flunitrazepam were without effect. CONCLUSIONS: The present insomnia model can be used as a sleep disturbance model for testing not only the sleep-inducing effects but also the sleep-maintaining effects including non-REM sleep and REM sleep of hypnotics.

Analysis of Variance↗
PubMed2005

Increased delta power and discrepancies in objective and subjective sleep measurements in borderline personality disorder.

BACKGROUND: Previous studies have shown depression-like sleep abnormalities in borderline personality disorder (BPD). However, findings in BPD are not unequivocal for REM dysregulation, as well as for a decrement of slow wave sleep and sleep continuity disturbances. Earlier findings in sleep EEG abnormalities in BPD may have been confounded by concomitant depressive symptoms. METHODS: Twenty unmedicated female BPD patients without current comorbid major depression and 20 sex- and age-matched control subjects entered the study. Conventional polysomnographic parameters and for the first time sleep EEG spectral power analysis was performed on two sleep laboratory nights. Subjective sleep parameters were collected by sleep questionnaires in order to assess the relationship between objective and subjective sleep measurements. RESULTS: BPD patients showed a tendency for shortened REM latency and significantly decreased NonREM sleep (stage 2). Spectral EEG analysis showed increased delta power in total NREM sleep as well as in REM sleep in BPD patients. Subjective ratings documented drastically impaired sleep quality in BPD patients for the two weeks before the study and during the two laboratory nights. CONCLUSION: Not-depressed BPD patients only showed tendencies for depression-like REM sleep abnormalities. Surprisingly, BPD patients displayed higher levels of delta power in the sleep EEG in NREM sleep than healthy control subjects. There was a marked discrepancy between objective and subjective sleep measurements, which indicates an altered perception of sleep in BPD. The underlying psychological and neurobiological mechanisms of these alterations are still unclear and need to be clarified in future studies including interventions on a pharmacological and cognitive-behavioral level.

Adolescent↗
PubMed2005

Acute tryptophan depletion. Part II: clinical effects and implications.

OBJECTIVE: This is the second of two articles reviewing the modern dietary technique of acute tryptophan depletion (ATD), a method of transiently reducing central serotonin levels in both healthy volunteers and clinical populations. This article details the clinical studies to date and discusses the implications of this research methodology. METHOD: The authors present a review of clinical ATD studies collated from a MEDLINE search, unpublished communications and the authors' considerable experience with this paradigm. RESULTS: Following from the initial use of ATD in subjects with depressive illness, studies of anxiety disorders and other psychiatric illnesses have been reported. Sleep, aggressive and cognitive effects are also active areas of research and are reviewed here. CONCLUSIONS: Acute tryptophan depletion remains a useful psychiatric research tool. The findings from the clinical studies reviewed here are summarized and implications for future research detailed.

Alleles↗
PubMed1992

Polysomnography in the Rett syndrome.

The features of sleep parameters in the Rett syndrome were compared with those in early infantile autism (EIA) and hereditary progressive dystonia with marked diurnal fluctuation (HPD). The sleep-wakefulness cycle and the tonic and phasic components of sleep were evaluated in each disorder, the former was estimated by the day-by-day plot method and the latter two by polysomnography (PSG) following our method. Abnormalities of the sleep-wakefulness cycle were observed in the Rett syndrome and EIA, but in the latter these abnormalities became inapparent with age and improved markedly by correcting the environmental condition and completely by 5-hydroxytriptophan. The latter, if treated early, was followed by improvement of behavior. In the Rett syndrome, however, the abnormalities continued into late childhood to adolescence. In HPD, PSG abnormalities were restricted to the phasic component, which improved completely after levodopa in accordance with the clinical improvement. On the other hand, in the Rett syndrome as well as in EIA both the phasic and tonic components were involved and also the leakage of the components of REM stage into NREM stage was observed. In the Rett syndrome, these abnormalities aggravated with age, with disturbances in % sleep stage, nocturnal variation of tonic and phasic components of sleep and REM-NREM cycles, while in EIA the results of PSGs revealed no such progressions but showed an increase in twitch movement and a lack of normal increase in the number of REMs occurring in short intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Historical note on sleep and eye movements.

Involuntary eye movements at the onset of sleep are mentioned in Virgil's Aeneid (19 BC). "Nystagmus" in relation to states of lowered consciousness was painstakingly catalogued by Sauvages (1768). Sporadic studies of eye behavior during sleep were recorded during the 19th century and were associated with disorders of brainstem physiology, culminating in von Economo's observations during the encephalitis lethargica epidemic of the 1920s.

England↗
PubMed2005

Power and coherent oscillations distinguish REM sleep, stage 1 and wakefulness.

The objective of this work is to determine differences in spectral power and coherent activity between stage 1 (S1) and REM sleep. The EEG activity of the two sleep stages is almost indistinguishable by visual inspection. Although many efforts have been directed toward understanding the process of falling asleep, little is known about differences in EEG activity between stage 1 (S1) and REM sleep. Polysomnography of 8 healthy young adults from S1, REM sleep and wakefulness was recorded. Spectral power and spectral correlation were obtained for 1-50 Hz. Stage 1 was distinguished (ANOVAs) from REM sleep by lower power in 1-9 Hz, higher power in alpha, beta and gamma, lower interhemispheric correlation in 1-8 Hz and gamma, and higher right correlation in 30-50 Hz. It differed from wakefulness by lower power in 9-50 Hz, but not in 1-8 Hz, or in inter- and intrahemispheric correlation. EEG differences between S1 and REM sleep reside not only in changes in power but also in coherent activity. The different behavior of slow and fast frequencies suggests two different mechanisms involved in the gate into sleep, one implicated in promoting sleep, the thalamo-cortical oscillator mode and the other in reducing alertness involving activation mechanisms. Stage 1 is a mixed state, alertness is already reduced but sleep-promoting mechanisms are not yet fully installed. The EEG differences between these two sleep stages contribute to the understanding of REM sleep and S1 physiology and may be relevant for understanding disorders in falling asleep.

Adult↗
PubMed1996

Sleep in psychiatric disorders.

Psychiatric disorders are some of the most common causes of sleep-related complaints, particularly insomnia. Sleep abnormalities may be caused by CNS abnormalities associated with psychiatric illnesses as well as by accompanying behavioral disturbances. Although sleep patterns are not necessarily diagnostic of particular psychiatric disorders, there are relationships between certain sleep abnormalities and categories of psychiatric disorders. Sleep disturbances associated with psychiatric disorders and general approaches to treatment are reviewed.

Anxiety Disorders↗
PubMed1993

Biochemistry and pharmacology of reversible inhibitors of MAO-A agents: focus on moclobemide.

Moclobemide, p-chloro-N-[morpholinoethyl]benzamide, is a prototype of RIMA (reversible inhibitor of MAO-A) agents. The compound possesses antidepressant efficacy that is comparable to that of tricyclic and polycyclic antidepressants. In humans, moclobemide is rapidly absorbed after a single oral administration and maximum concentration in plasma is reached within an hour. It is moderately to markedly bound to plasma proteins. MAO-A inhibition rises to 80% within two hours; the duration of MAO inhibition is usually between eight and ten hours. The activity of MAO is completely reestablished within 24 hours of the last dose, so that a quick switch to another antidepressant can be safely undertaken if clinical circumstances demand. RIMAs are potent inhibitors of MAO-A in the brain; they increase the free cytosolic concentrations of norepinephrine, serotonin and dopamine in neuronal cells and in synaptic vesicles. Extracellular concentrations of these monoamines also increase. In the case of moclobemide, increase in the level of serotonin is the most pronounced. Moclobemide administration also leads to increased monoamine receptor stimulation, reversal of reserpine induced behavioral effects, selective depression of REM sleep, down regulation of beta-adrenoceptors and increases in plasma prolactin and growth hormone levels. It reduces scopolamine-induced performance decrement and alcohol induced performance deficit which suggest a neuroprotective role. Tyramine potentiation with moclobemide and most other RIMA agents is negligible.

Benzamides↗
PubMed2003

Genetic aspects and genetic epidemiology of parasomnias.

Parasomnias are undesirable phenomena associated with sleep. Many of them run in families, and genetic factors have been long suggested to be involved in their occurrence. This article reviews the present knowledge of the genetics of the major classical behavioral parasomnias as well as present results from genetic epidemiological studies. The level and type of evidence for genetic effects varies much from parasomnia to parasomnia. The genetic factors are best established in enuresis, with several linkages to chromosomal loci, but their functions are not so far known. Environmental causes and gene-environment interactions are most probably also of great importance in the origin of complex traits or disorders such as parasomnias.

Arousal↗
PubMedDate not supplied

Do patients with "pure" chronic fatigue syndrome (neurasthenia) have abnormal sleep?

OBJECTIVE: To determine whether patients with "pure" chronic fatigue syndrome (neurasthenia) have sleep abnormalities which may contribute to subjective measures of daytime fatigue. METHOD: Sleep characteristics of 20 patients meeting research criteria for chronic fatigue syndrome (CFS) but not depression, anxiety, or sleep disorder were compared with sleep characteristics of 20 healthy subjects matched for age and sex. Measures of sleep included a) subjective interview reports and sleep diaries and b) home-based polysomnography. RESULTS: Patients with CFS complained of poor quality unrefreshing sleep. They also napped during the day. Polysomnograph data showed no difference in actual nocturnal sleep time between the two groups although patients with CFS spent significantly longer in bed (p < .01), slept less efficiently (p < .03), and spent longer awake after sleep onset (p < .05). The polysomnographs of seven patients with CFS and one healthy subject were regarded as significantly abnormal. Five patients and one healthy subject had difficulty maintaining sleep. One patient had a disorder of both initiating and maintaining sleep and one patient woke early. CONCLUSIONS: Patients with "pure" CFS complain of unrefreshing sleep but only a minority have a clearly abnormal polysomnograph. The most common abnormality is of long periods spent awake after initial sleep onset. Although sleep abnormalities may play a role in the etiology of CFS, they seem to be unlikely to be an important cause of daytime fatigue in the majority of patients. However, pharmacological and behavioral methods that improve sleep quality may be an important component of a pragmatically based treatment package for patients who do have abnormal sleep.

Activities of Daily Living↗
PubMed1986

Jactatio nocturna after head injury.

Nocturnal head banging or body rocking often occurs in childhood in relation to sleep, and is generally considered a developmental or behavioral disorder. A few cases of jactatio nocturna have been considered manifestations of sleep disorder, and an analogy to somnambulism and pavor nocturnus has been suggested. We observed episodes of jactatio nocturna in a patient with global encephalopathy and frontal lobe dysfunction after closed head injury, and successfully treated these with imipramine. Sleep disorders are increasingly recognized after head injury; jactatio nocturna must be differentiated from post-traumatic seizures, and may represent partial or defective arousal during light non-REM sleep, analogous to the parasomnias of deeper sleep and possibly representing dysfunction of frontal arousal mechanisms.

Adolescent↗
PubMed2004

Psychiatric symptoms in children with insomnia referred to a pediatric sleep medicine center.

BACKGROUND AND PURPOSE: To assess the frequency and nature of clinical and psychiatric symptoms in children referred to a pediatric sleep center for evaluation of insomnia. PATIENTS AND METHODS: A retrospective chart review of all children referred to the pediatric sleep medicine was conducted. Children presenting exclusively with sleep initiation and/or maintenance problems underwent a structured clinical psychiatric interview and their parents completed the behavioral assessment system for children (BASC), pediatric symptom checklist, the clinical attention problem scale and a detailed sleep questionnaire. RESULTS: Twenty-three of 46 children (50%) with persistent insomnia had a professional diagnosis of another psychiatric disorder. In the remaining 50%, although parents denied any previous psychiatric history, 40% displayed psychiatric symptoms as documented by psychometric measures and clinical interview. A significant positive correlation was observed between depressive BASC score and sleep onset latency and an inverse correlation was present with REM sleep latency. CONCLUSION: The vast majority of children presenting with persistent insomnia exhibit clinical symptoms of an accompanying psychiatric disorder, suggesting that comprehensive psychometric assessments are warranted in this population.

Attention Deficit Disorder with Hyperactivity↗
PubMed1993

Sleep-wake disturbances in an animal model of chronic cholinergic insufficiency.

Rats reared on a diet in which choline is replaced with N-aminodeanol (NADE), undergo > 50% replacement of brain acetylcholine with acetylated NADE, a false cholinergic transmitter. We examined amounts of sleep and wakefulness in 7 littermate pairs of rats fed either NADE-substituted, or a choline control diet for > 100 days after weaning. During the lights-on portion of the 12/12 h light/dark cycle, NADE rats spent more time awake, and less time in both non-REM and REM sleep compared to littermate controls. Average durations of waking episodes were significantly increased in NADE rats. During the 12 h dark period, there were no between-group differences in sleep-waking amounts. Behavioral hyper-responsiveness which interferes with sleep onset, combined with reduced activity in brainstem cholinergic mechanisms involved in REM sleep generation may underlie daytime sleep-waking disturbances in NADE rats.

Acetylation↗
PubMed1983

Spectral analysis of neocortical and hippocampal EEG in the protein malnourished rat.

In these studies, power spectral analysis techniques were utilized to quantify changes in the cortical and hippocampal EEG obtained from rats reared on either an 8% or 25% casein diet as they mature from 14 to 22 days of age. Analyses of the power spectral data obtained from the frontal cortex of rats reared on the 25% casein diet during this preweaning period (14-22 days) indicated increases in the power in the 0.5-3.5 c/sec frequency band primarily during slow-wave sleep. Prenatal protein malnutrition (8% casein diet) significantly reduced the low frequency power content in the cortical EEG obtained during slow-wave sleep at 18 and 22 days of age. Analyses of power spectral data obtained from the hippocampal EEG during REM sleep also revealed developmental and diet-related differences. The frequency at which the peak power occurs in the theta band (4-11 c/sec) was found to increase normally in a linear fashion from 14 to 22 days of age (from 4.4 to 5.5 c/sec) in rats reared on the 25% casein diet. In addition, power in the 4-7 c/sec band significantly increased during this preweaning period. Prenatal protein malnutrition significantly slowed the development of theta frequency and produced higher values of power in the component of theta rhythm. Finally, vigilance profiles showed that rats normally progress from 14 days of age when REM sleep dominates their vigilance profile, to 22 days of age when they spend significantly more time in slow-wave sleep. Prenatal protein malnutrition retards this normal developmental sequence by significantly reducing the REM sleep time at 14 and 18 days of age and increasing the time spend in aroused waking at both these ages. However, at the time of weaning, i.e., at 22 days of age, these differences in sleep-waking behavior were no longer observed to be significant.

Animals↗
PubMed2005

Modafinil more effectively induces wakefulness in orexin-null mice than in wild-type littermates.

Narcolepsy-cataplexy, a disorder of excessive sleepiness and abnormalities of rapid eye movement (REM) sleep, results from deficiency of the hypothalamic orexin (hypocretin) neuropeptides. Modafinil, an atypical wakefulness-promoting agent with an unknown mechanism of action, is used to treat hypersomnolence in these patients. Fos protein immunohistochemistry has previously demonstrated that orexin neurons are activated after modafinil administration, and it has been hypothesized that the wakefulness-promoting properties of modafinil might therefore be mediated by the neuropeptide. Here we tested this hypothesis by immunohistochemical, electroencephalographic, and behavioral methods using modafinil at doses of 0, 10, 30 and 100 mg/kg i.p. in orexin-/- mice and their wild-type littermates. We found that modafinil produced similar patterns of neuronal activation, as indicated by Fos immunohistochemistry, in both genotypes. Surprisingly, modafinil more effectively increased wakefulness time in orexin-/- mice than in the wild-type mice. This may reflect compensatory facilitation of components of central arousal in the absence of orexin in the null mice. In contrast, the compound did not suppress direct transitions from wakefulness to REM sleep, a sign of narcolepsy-cataplexy in mice. Spectral analysis of the electroencephalogram in awake orexin-/- mice under baseline conditions revealed reduced power in the theta; band frequencies (8-9 Hz), an index of alertness or attention during wakefulness in the rodent. Modafinil administration only partly compensated for this attention deficit in the orexin null mice. We conclude that the presence of orexin is not required for the wakefulness-prolonging action of modafinil, but orexin may mediate some of the alerting effects of the compound.

Animals↗
PubMed1976

Drug self-administration and sleep-awake activity in rats dependent on morphine, methadone, or l-alpha-acetylmethadol.

Morphine post-dependent rats were prepared with chronic cortical EEG and temporalis muscle EMG electrodes and i.v. jugular cannulae and permitted to self-administer morphine (10 mg/kg/injection) on a fixed-ratio schedule of reinforcement to reestablish and maintain dependence. Morphine was then replaced by methadone or 1-alpha-acetyl-methadol (LAAM) at a dose of 2 and 1 mg/kg, respectively. The rats developed stable patterns of self-administration of each narcotic and maintained the dependent state. The mean (+/- S.E.) interinjection interval was 2.5 +/- 0.1 h for morphine, 1.4 +/- 0.1 h for methadone and 8.8 +- 0.8 H FOR LAAM. The distribution of sleep, REM sleep, and awake within the interinjection interval for the three narcotics was similar. A short phase of behavioral stupor concomitant with EEG slow bursts emerged following the self-injections. This phase was followed by arousal with EEG activation. Sleep and REM sleep then reappeared and predominated before the next injection. LAAM manifested a relatively slow onset of action in comparison with morphine and methadone.

Animals↗