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PubMed1988

Perception of waking and sleeping: possible implications for the evaluation of insomnia.

Perception of awakening, its connection to electroencephalogram (EEG), and its significance for morning recall were studied in insomniacs and normals. Fourteen insomniacs and 14 age- and sex-matched controls kept a sleep log for 1 week and slept once in the laboratory (standard polygraphy). In addition, actual perception of awakening was measured by a behavioral device. Results suggest that physiological arousal is necessary, but not sufficient, for perception of awakening. Many arousals that are not perceived occur during the first REM-NREM cycle. Insomniacs nearly exclusively perceive those arousals occurring after consolidated sleep (at least 15 min) and at the beginning of interrupted sleep intervals. It is suggested that insomniacs perceive these intervals as continuous wakefulness and have difficulty in perceiving short-lasting sleep, whereas controls often do not perceive wakefulness at all. The latter may be a sleep-protecting mechanism. Number and correlation suggest that recalled awakenings are exactly those perceived. The connection between physiological and experimental subjective data is discussed.

Adult↗
PubMed1999

Efficiency of continuous positive airway pressure versus theophylline therapy in sleep apnea: comparative sleep laboratory studies on objective and subjective sleep and awakening quality.

Sleep apnea is the most common sleep-related breathing disorder characterized by repetitive episodes of hypoxemia. Therapies include behavioral, surgical, orthodontic, pneumological, and pharmacological interventions. The aim of the present study was to compare the efficiency of pneumological therapy by nasal continuous positive airway pressure (CPAP) versus a pharmacological approach with theophylline (Respicur retard(R) 400 mg) on respiratory variables as well as objective and subjective sleep and awakening quality in patients with moderate sleep apnea measured by polysomnography and psychometry. Under CPAP therapy all respiratory variables improved and normalized, while under theophylline only the apnea-hypopnea index and the desaturation index improved but still did not return to normal values. Regarding sleep initiation and maintenance, CPAP therapy prolonged sleep latency and reduced movement time, while patients treated with theophylline showed reduced total sleep period, total sleep time and sleep efficiency. Sleep architecture demonstrated an increase in deep sleep and REM stages under CPAP therapy, and remained unchanged under theophylline. Concerning subjective sleep and awakening quality, both treatments improved well-being in the morning. Regarding objective awakening quality, reaction time performance was improved in both groups. In conclusion, CPAP treatment is more effective than theophylline regarding respiratory variables as well as the normalization of sleep maintenance and sleep architecture in sleep apnea patients.

Bronchodilator Agents↗
PubMed1999

Effective treatments for age-related sleep disturbances.

Fundamental changes in sleep patterns are associated with normal aging, but disturbed sleep with resultant daytime sleepiness and fatigue is an extremely common occurrence among older persons and a frequent catalyst for physician visits. Sleep disorders result from multiple factors--including pharmacologic, physiologic, biologic, and behavioral--and can be mildly debilitating or life-threatening. Diagnosis includes consideration of the presence of physical or mental illness, drug and/or alcohol use or abuse, a primary sleep disorder such as sleep-disordered breathing or periodic limb movements during sleep, changes in circadian rhythms, or poor sleep hygiene. Despite a high rate of use, hypnotics are best suited for periodic rather than chronic sleep disorder symptoms and, in general, should be used only after adjustments in sleep hygiene prove unsuccessful as first-line therapy.

Age Factors↗
PubMed1992

Ambulatory polysomnography: technical aspects and normative values.

Ambulatory polysomnographic (APSG) assessment of sleep disorders is now possible, but the technique of APSG is sufficiently different from in-laboratory PSG that normative data from in-laboratory PSG may not apply to APSG. This paper reviews the technical aspects of APSG and presents normative APSG data from 20 older healthy males. Subjects underwent medical and psychiatric screening before completing APSG in their homes. Total sleep time and the rapid-eye-movement sleep latency (RL) were both shorter than those reported by others using traditional in-laboratory techniques. The shorter total sleep may be related to behaviors at home that impinge upon sleep. The shorter RL may be related to differences in calculation methods. Periodic limb movements were common in our subjects but did not contribute to sleep disturbance. We conclude that APSG is sufficiently different from traditional PSG as to warrant collection of a large normative data base.

Ambulatory Care↗
PubMed2000

NREM parasomnias: arousal disorders and differentiation from nocturnal frontal lobe epilepsy.

Parasomnias emerging from NREM sleep such as sleep walking, sleep terrors and confusional arousals are considered arousal disorders. Nocturnal video-polysomnography is the gold standard to diagnosing and differentiating parasomnias from other arousals with atypical motor behaviors such as nocturnal frontal lobe epilepsy (NFLE). This form of nocturnal seizures with prominent dystonic-dyskinetic components, in some cases genetic, has been recently identified by means of detailed video-analysis of movements during sleep. The clinical picture of parasomnias (with onset in early childhood, rare episodes of long duration, absence of stereotypy, general disappearance after puberty) is different from that of NFLE (which first occurs between the age of 10 and 20, manifests frequent complex and repetitive behaviors of short duration excluding rare prolonged seizures, nocturnal agitation, some daytime complaints such as fatigue or sleepiness, persistence into adulthood). Patients show no difference from classical sleep parameters whilst microstructure analysis shows sleep instability and arousal fluctuations in parasomnias and NFLE. In children as well, at least in our experience, the differential diagnosis between the two disorders is difficult and requires one or more complete nocturnal video-polygraphic recording. In any case the diagnosis of NFLE should be considered in children with nocturnal motor episodes or nocturnal motor agitation, when the attacks persist; this diagnosis is probably more frequent than expected.

Child↗
PubMed2001

Self-reported nap behavior and polysomnography at home in midlife women with and without insomnia.

STUDY OBJECTIVES: To describe self-reported nap behavior and relationships among nap history, nap behavior during the study, indicators of subjective and objective insomnia, and self-reported daytime sleepiness from data previously obtained in a week-long field study of sleep in midlife women with and without insomnia. DESIGN: Descriptive/comparative secondary analysis. SETTING: Individual homes of the participants. PARTICIPANTS: Midlife women (mean age 46+/-4 years) with self-reported insomnia (n=101) and women with adequate sleep (n=30). INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Sleep patterns were assessed by polysomnography (PSG), daily diaries, and a sleep history form. Although all women were requested not to nap, 47% of the women reported nap behavior during the study. Strong relationships were observed between a history of daytime naps and nap behavior (chi2 = 25.63, p < or = .001), and a history of feeling sleepy or struggling to stay awake during the daytime (i.e., sleepiness) and nap behavior (chi2 = 18.05, p < or = .001) during the study. There was also a modest significant (p < or = .05) correlation (r = .25) between tiredness and nap duration during the study. There were no statistical differences in sleep variables between the napping and non-napping groups. In the napping group, there were no differences between women with sleep efficiency < 85% (objective insomnia) and those with sleep efficiency > 85%. CONCLUSIONS: Habitual nap behavior may be indicative of daytime sleepiness in women with insomnia, but it is not necessarily related to subjective or objective measures of insomnia. Women who routinely nap may be unable to refrain from napping during the daytime in long-term research studies.

Adult↗
PubMed1989

Movement disorders during sleep in cats and dogs.

Spontaneous sleep movement disorders in 5 cats and 3 dogs were studied. Objective abnormalities during sleep were confirmed by electrographic or behavioral monitoring techniques in all animals. The cause of the disorder was CNS disease in 3 animals. A cause was not discovered in the other 5 animals, although at necropsy, 2 were found to have thyroid tumors. Many pharmacologic treatments were ineffectual, but trials with the benzodiazepine tranquilizer, clonazepam, suggested it will prove useful in controlling violent movements during rapid-eye-movement sleep.

Animals↗
PubMed1998

[Alertness disorders and parasomnias of the wakefulness-sleep transition].

INTRODUCTION: Disorders of arousal and parasomnias of sleep-wake transition are revisited. Disorders of arousal are: Sleepwalking (SW), confusional arousals (CA) and sleep terrors (ST). SW, CA and ST are different clinical manifestations of the same disorder being ST the most severe and SW the mildest manifestation. Disorders of arousal are typical parasomnias of NREM sleep, mainly slow wave sleep. Pathophysiological mechanism of these disorders is the state's dissociation of wakefulness and sleep. The conjunction of the constitutional factors (genetic, age, sleep privation, drugs, psychological, etc.), and precipitant factors (light, sound, temperature, touch, apnea, gastroesophageal reflux, seizure, fever, psychological, etc.) permit three possible arousal behavioral response: A full awakening, a shift stage of sleep or a partial arousal. Clinical significance of arousal parasomnias depend on the age. In children are caused by developmental and genetic factors and usually are autolimited. In adults usually are caused by psychopathology. In the elderly are often caused by organic brain syndromes. Parasomnias of sleep-wake transition are: Rhythmic movements of sleep, sleeptalking, starts and the nocturnal cramp. Most of them are mild disorders, almost physiological phenomena that usually don't need any treatment.

Adult↗
PubMed1979

Hypersomnia with simultaneous waking and sleep patterns in the electroencephalogram. A case report with neurotransmitter studies.

A mildly dyslexic boy of 11 years, with no neurological deficit or history of epileptic seizures, had marked hypersomnia for 2 years, which was most pronounced in the morning hours. Repeated EEG studies and power spectral analysis revealed simultaneous posterior alpha rhythm and sleep patterns (spindles, vertex waves, K complexes) over vertex and frontocentral regions, while the patient was behaviorally awake. Bilateral synchronous anterior spikes were frequently noted in association with sleep patterns. A polysomnogram over 24 h confirmed excessive sleep, night and day (especially morning hours) and there was evidence of a large REM sleep percentage (on EMG and EOG basis) while the EEG had predominantly non-REM sleep patterns. Special neurotransmitter studies were performed in view of a presumed disturbance affecting the neurobiochemical sleep regulation. These studies were based on CSF metabolite levels and provided evidence for a high serotonin metabolite (5HIAA) level. It is tempting to hypothesize that the biochemical disturbance has led to encroachment of non-REM sleep patterns on both wakefulness and REM sleep. Further discussion deals with the bilateral-synchronous spike activity and its relationship to arousal patterns in sleep.

Child↗
PubMed1993

Sleep problems in childhood.

Sleep, like eating and toileting, is an individual physical requirement that changes with time as the child matures. Although much about a child's sleep is biologically determined, extrinsic factors, usually through the parents, also mold the child's sleep behavior. Normal sleep for a child is restful to the child and not excessively disruptive to others. Sleep problems interfere with the quality of the child's sleep and frustrate or frighten caretakers. Several sleep problems have their origins in normal sleep behavior from an earlier age. Some, the parasomnias, are caused by self-limited biologic diatheses. Many sleep problems have psychosocial triggers. Sleep disorders only rarely are a primary medical problem that is adequately treated with medication (e.g., narcolepsy). Good history-taking, often accompanied by diary-keeping, will usually identify the problem--the first step in effective treatment. Treatment of a sleep disorder in the pediatrician's office can start with educating caretakers about normative sleep for the age of the child and providing information regarding the cause and natural course of the problem. Treatment also may involve behavioral or psychological intervention or both, but medication is generally not indicated. When needed for short-term treatment, mild sedatives such as antihistamines are used most often. More serious sleep or behavioral problems should be acknowledged by the primary care pediatrician, followed by referral to an appropriate specialist. Inquiry into a child's sleep habits at each well-child visit, coupled with appropriate anticipatory guidance, could make an important contribution to the child and family by preventing problems with sleep and identifying sleep problems early in their evolution. Pediatricians and parents can work together to help children develop good sleep habits that fulfill the child's evolving sleep requirements within the context of the family's needs and expectations.

Child↗
PubMed1992

[The dynamics of the normalization of the behavioral and neurochemical disorders evoked in rats by deprivation of the paradoxical sleep phase].

The 24-hr deprivation of paradoxical sleep interferes with the passive avoidance response in rats and decreases the absolute amount of proteins in neurons and gliocytes of the raphe nucleus' dorsal portion while increasing the amount of proteins and nucleic acids in the locus coeruleus' cells. The protein metabolism in serotoninergic cells of the raphe nucleus seems to be involved in the processes of memory and behaviour.

Animals↗
PubMed1993

Allergy and depression: a neurochemical threshold model of the relation between the illnesses.

Empirical studies suggest a very high prevalence of atopic disorder in people with depression. Research indicates that individuals with allergy have cholinergic hyperresponsiveness and beta-adrenergic hyporesponsiveness in the autonomic nervous system. Evidence is reviewed that similar imbalances in central nervous system cholinergic-adrenergic activity play a casual role in depression behaviors. It is hypothesized that the allergic state or allergic reactions can accentuate cholinergic-adrenergic activity imbalances in the central nervous system of a small subgroup of people at risk for endogenous depression thereby producing depression symptomatology.

Adrenergic Agonists↗
PubMed1994

Homicidal somnambulism: a case report.

A case of a homicide and an attempted homicide during presumed sleepwalking is reported in which somnambulism was the legal defense and led to an acquittal. Other possible explanations including complex partial seizures, dissociative state, rapid eye movement sleep behavior disorder and volitional waking behavior are discussed. The evidence supporting the probability that this act occurred during an episode of somnambulism and sleep-related confusional arousal is reviewed and weighed. This evidence includes personal and family history of somnambulism and related disorders; neurological, psychiatric and psychological assessments; presence of possible precipitating factors; and polysomnographic data.

Adult↗
PubMed2000

Narcolepsy -- cataplexy and psychoanalytic theory of sleep and dreams.

Narcolepsy had been documented some twenty years before the psychoanalytic movement, emphasizing the central role of sleep and dreams in the understanding of mental health, offered an entirely novel theory of its aetiology. And when the full range of the behavioral aspects of the condition were documented, it was obvious that intense psychoanalytic interest in it was inevitable. Unfortunately, even mainstream neurology, lacking any rival physiological explanation, for a time tended to entertain a definite role for such beliefs, at least in some cases. However, such a theory involving outre concepts of repressed, guilt-ridden sexual drives as an explanation of the behavioral aspects of narcolepsy-cataplexy, of necessity simply added to the burdens of the sufferer. For it became clear that the condition by itself produced enough psycho-social problems without further adding to them. This historical note details the persistence of this misconceived theory up to the later decades of this century, and the burden that it placed upon those who suffered from this condition.

Cataplexy↗
PubMed1991

Dopamine D2 mechanisms in canine narcolepsy.

Narcolepsy is a sleep disorder characterized by abnormal manifestations of rapid-eye-movement (REM) sleep and excessive daytime sleepiness. Using a canine model of the disease, we found that central D2 antagonists suppressed cataplexy, a form of REM-sleep atonia occurring in narcolepsy, whereas this symptom was aggravated by D2 agonists. The effect on cataplexy was stereospecific for the S(-) enantiomer of sulpiride (a D2 antagonist) and the R(+) enantiomer of 3-PPP (a D2 agonist). There was also a significant correlation between the in vivo pharmacological potency and in vitro drug affinity for D2 receptors (but not for D1 and alpha 2 receptors) among the seven central D2 antagonists tested. Selective D1 compounds were also tested; however, the results were inconsistent because both antagonists and agonists generally suppressed cataplexy. Our current results demonstrate that central D2-type receptors are critically involved in the control of cataplexy and REM sleep. Furthermore, the finding that small doses of D2 antagonists suppressed cataplexy and induced behavioral excitation, while small doses of D2 agonists aggravated cataplexy and induced sedation, suggests that this effect is mediated presynaptically. However, considering the fact that selective dopamine reuptake inhibitors did not modify cataplexy and that our previous pharmacological results demonstrated a preferential involvement of the noradrenergic system in the control of cataplexy, we believe that the effect of D2 compounds on cataplexy is mediated secondarily via the noradrenergic systems.

Animals↗
PubMed1977

The effects of gamma-hydroxybutyrate on sleep.

Sodium gamma-hydroxybutyrate (GHB) is a remarkably safe and nontoxic hypnotic agent which is reported to be free of addicting properties. It is also a normal metabolite of the mammalian nervous system. We examined its effects on the sleep-EEG of eight patients with histories of impaired sleep, as a prelude to a more detailed study of its clinical potential. Sleep induced with GHB was indistinguishable subjectively from natural sleep as well as by behavioral and electroencephalographic criteria. Unlike most synthetic hypnotics, GHB increased delta sleep and did not suppress REM sleep. It shortened the REM sleep latency and shifted REM sleep into the first third of the night. On one occasion it induced a sleep onset REM period which was experienced as an attack of sleep paralysis. Withdrawal was simple; there was no REM sleep rebound and sleep patterns immediately returned to their pre-drug form. Its major clinical drawback was its short duration of action: its hypnotic effect lasting only 2 to 3 hr. We suggest that GHB may serve as the prototype for a new class of hypnotic compounds derived from natural sources and capable of activating the neurological mechanisms of normal human sleep.

Adult↗
PubMed1990

Things that go bump in the night: the parasomnias revisited.

The parasomnias have been identified as a major category of sleep disorders and represent a group of physiologic and behavioral phenomena that occur exclusively during, or are augmented by, the sleeping state. They are commonly encountered in clinical practice and are typically dismissed as "bumps in the night" or attributed to psychiatric disease. Despite their often bizarre nature, most are readily explainable, diagnosable, and treatable. Some have formed the basis for art, literature, and folklore. Pertinent references from a wide variety of disciplines have been collected, and a clinical classification of the parasomnias is proposed to assist in the understanding, diagnosis, and management of these fascinating disorders.

Arousal↗
PubMed2005

Timing and consolidation of human sleep, wakefulness, and performance by a symphony of oscillators.

Daily rhythms in sleep and waking performance are generated by the interplay of multiple external and internal oscillators. These include the light-dark and social cycles, a circadian hypothalamic oscillator oscillating virtually independently of behavior, and a homeostatic oscillator driven primarily by sleep-wake behavior. Both internal oscillators contribute to variation in many aspects of sleep and wakefulness (e.g., sleep timing and duration, REM sleep, non-REM sleep, REM density, sleep spindles, slow-wave sleep, electroencephalographic oscillations during wakefulness and sleep, and performance parameters, including attention and memory). The relative contribution of the oscillators varies greatly between these variables. Sleep and performance cannot be predicted by either oscillator independently but critically depend on their phase relationship and amplitude. The homeostatic oscillator feeds back onto the central pacemaker or its outputs. Thus, the amplitude of observed circadian variation in sleep and performance depends on how long we have been asleep or awake. During entrainment to external 24-h cycles, the opposing interplay between circadian and homeostatic changes in sleep propensity consolidates sleep and wakefulness. Some physiological correlates and mediators of both the circadian process (e.g., melatonin and hypocretin rhythms) and the homeostat (e.g., EEG, slow-wave activity, and adenosine release) have been established, offering targets for the development of countermeasures for circadian sleep and performance disorders. Interindividual differences in sleep timing, duration, and morning or evening preference are associated with changes of circadian or sleep homeostatic processes or both. Molecular genetic correlates, including polymorphisms in clock genes, of some of these interindividual differences are emerging.

Circadian Rhythm↗