[How should sleep apnea syndrome be differentiated from other causes of sleepiness?].
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Diagnosis, Differential↗
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Obstructive sleep apnoea and depression--diagnostic and treatment implications.
Sleep apnoea (OSA), a common sleep disorder, is well recognised as a cause of morbidity including psychiatric disorders. There is increasing recognition of the link between OSA and depression. Sleep changes are intrinsic to depressive disorders, most notably disturbances of REM sleep; OSA causes predominantly REM sleep disturbances. The neuro-vegetative features of depression are similar or identical to the symptoms of OSA-an issue which has not achieved wide clinical recognition. A growing number of studies confirm the statistical link between the two conditions. The implications are twofold: OSA needs to be excluded in cases of chronic or resistant depression and treatment of OSA will make it easier to treat the primary depressive disorder. A new method of treatment for OSA, the Sullivan continuous positive airway pump (CPAP), raises the theoretical possibility of treating depression by this means as well.
Adult↗
Dyssomnias, parasomnias, and sleep disorders associated with medical and psychiatric diseases.
Sleep disorders can be intrinsic, as are insomnia or narcolepsy, or can be accounted for by external factors, such as noise, altitude, drug or alcohol abuse, or shift work. The arousal disorders, common in children, are usually benign and disappear by puberty. Sleep-wake transition disorders such as sleep starts are benign as well, and may occur at any age. The parasomnias comprise different entities such as nightmares, REM-sleep behavior disorder, sleep enuresis, and bruxism. Diagnosis and treatment often require a multidisciplinary approach. Virtually every psychiatric, neurologic, or medical disease, when of sufficient severity, leaves its specific fingerprint on sleep; some disorders, such as peptic ulcer disease, gastroesophageal reflux, or epilepsy, tend to be exacerbated during sleep. Fortunately, most sleep disorders are amenable to therapy, which can include counseling, sleep hygiene, withholding of an offending agent, behavioral therapy, light therapy, or cautious drug therapy.
Humans↗
[Cyclic alternating pattern. A new approach to the pharmacology of sleep disorders].
The Cyclic Alternating Pattern (CAP) is an intrinsic component of normal NREM sleep. This periodic activity is organized in biphasic 40-sec cycles clustered in sequences. CAP sequences are functionally correlated to long lasting arousal instability. CAP is induced by endogenous stimuli (change in sleep stage, body movements) but it is considerably increased by exogenous impulses (noise). CAP rate (CAPR) is a novel polysomnographic variable that measures the amount of CAP during sleep, and it may be calculated for total sleep time and total NREM sleep. We demonstrated that all-night exposure to a 45 dB(A) white noise induced a significant CAPR increase, correlated with impaired sleep quality, even without changes in sleep architecture. We hypothesized that administration of an hypnotic should attenuate this CAPR rise. This hypothesis was verified in a double-blind placebo study, in which 12 healthy young adults received zolpidem, a new imidazopyridine hypnotic. During the noise perturbed nights, zolpidem clearly demonstrated a protective effect on CAPR (mainly during slow wave sleep) and on sleep quality. CAPR appears to be a sensitive indicator of sleep quality, and the cumulative distribution of CAPR throughout the night represents a new method to evaluate the effects of an hypnotic in sleep.
Adult↗
Circadian rhythm sleep disorders: pathophysiology and potential approaches to management.
An intrinsic body clock residing in the suprachiasmatic nucleus (SCN) within the brain regulates a complex series of rhythms in humans, including sleep/wakefulness. The individual period of the endogenous clock is usually >24 hours and is normally entrained to match the environmental rhythm. Misalignment of the circadian clock with the environmental cycle may result in sleep disorders. Among these are chronic insomnias associated with an endogenous clock which runs slower or faster than the norm [delayed (DSPS) or advanced (ASPS) sleep phase syndrome, or irregular sleep-wake cycle], periodic insomnias due to disturbances in light perception (non-24-hour sleep-wake syndrome and sleep disturbances in blind individuals) and temporary insomnias due to social circumstances (jet lag and shift-work sleep disorder). Synthesis of melatonin (N-acetyl-5-methoxytryptamine) within the pineal gland is induced at night, directly regulated by the SCN. Melatonin can relay time-of-day information (signal of darkness) to various organs, including the SCN itself. The phase-shifting effects of melatonin are essentially opposite to those of light. In addition, melatonin facilitates sleep in humans. In the absence of a light-dark cycle, the timing of the circadian clock, including the timing of melatonin production in the pineal gland, may to some extent be adjusted with properly timed physical exercise. Bright light exposure has been demonstrated as an effective treatment for circadian rhythm sleep disorders. Under conditions of entrainment to the 24-hour cycle, bright light in the early morning and avoidance of light in the evening should produce a phase advance (for treatment of DSPS), whereas bright light in the evening may be effective in delaying the clock (ASPS). Melatonin, given several hours before its endogenous peak at night, effectively advances sleep time in DSPS and adjusts the sleep-wake cycle to 24 hours in blind individuals. In some blind individuals, melatonin appears to fully entrain the clock. Melatonin and light, when properly timed, may also alleviate jet lag. Because of its sleep-promoting effect, melatonin may improve sleep in night-shift workers trying to sleep during the daytime. Melatonin replacement therapy may also provide a rational approach to the treatment of age-related insomnia in the elderly. However, there is currently no melatonin formulation approved for clinical use, neither are there consensus protocols for light or melatonin therapies. The use of bright light or melatonin for circadian rhythm sleep disorders is thus considered exploratory at this stage.
Animals↗
A review of common sleep disorders.
What should clinicians know about sleep disorders? This article briefly introduces the reader to sleep medicine and succinctly reviews common sleep disorders. First, the authors describe the diagnostic tools unique to sleep medicine: the over-night polysomnogram and the multiple sleep latency test. Next, the authors review essential features of a subset of the sleep, described in the International Classification of Sleep Disorders-Revised, that sleep disorder specialists commonly evaluate, diagnose, and treat. The disorders reviewed include the intrinsic and circadian rhythm subsets of the dyssomnias group and the parasomnia group of sleep disorders. The authors identify the core signs and symptoms, polysomnogram findings, multiple sleep latency test findings, and treatment of these disorders.
Diagnosis, Differential↗
Disorders of the sleep-wake cycle in adults.
Adults have an intrinsic body clock which regulates a complex series of rhythms including sleep and wakefulness, fatigue and cognitive ability. This endogenous clock naturally runs more slowly than the solar day and is entrained to a 24-h rhythm primarily by the alternation of light and darkness. Jet lag, shift-work sleep disorder, and some of the chronic insomnias are caused by a temporal discrepancy of the body clock relative to the surrounding environment and social network. The underlying mechanisms and general management are described. Both bright light and melatonin therapy have potential in the management of these disorders. Traditionally, bright light therapy has been used to alleviate the depression associated with seasonal affective disorder. Melatonin has received much ill-formed publicity, it being claimed that it is a panacea and an 'antiageing' treatment. Both of these treatment approaches are reviewed.
Adult↗
Circadian rhythm sleep disorders and phototherapy.
Circadian rhythm sleep disorders are characterized by a desynchronization between the timing of the intrinsic circadian clock and the extrinsic light-dark and social/activity cycles resulting in symptoms of excessive sleepiness and insomnia. This article explores the six recognized circadian rhythm sleep disorders: delayed sleep phase syndrome, advanced sleep phase syndrome, non-24-hour sleep-wake syndrome, irregular sleep-wake pattern, shift work sleep syndrome, and time zone change syndrome. Additionally discussed are the therapeutic roles of synchronizing agents, such as light and melatonin.
Humans↗
Disturbed sleep in children with Tourette syndrome: a polysomnographic study.
OBJECTIVE: To evaluate objective data on sleep quantity/quality and motor activity during night sleep in children with Tourette syndrome (TS). METHOD: Polysomnography of 17 unmedicated TS children (ages: 7;11-15;5, mean: 11;10 years) without comorbid attention-deficit hyperactivity disorder (ADHD) was compared with 16 age-, sex- and IQ-matched healthy controls. Sleep analyses according to the procedure of Rechtschaffen and Kales were supplemented by counting epochs with short arousal-related movements (<or=15 s), thus allowing to calculate correlations between motor activity and sleep parameters. RESULTS: Children with TS demonstrated changes in sleep parameters, including longer sleep period time, longer sleep latency, reduced sleep efficiency, and prolonged wakefulness after sleep onset. Their sleep profiles showed significantly more time awake and less sleep stage II. However, REM sleep variables, slow-wave sleep, and number of sleep stage changes were unaffected. Movement time was similar in both groups, but epochs with short arousal-related movements were increased in TS. Further analyses showed no significant correlations between sleep parameters and nighttime nontic movements, level of psychopathology or tic severity during daytime. Periodic limb movements during sleep (PLMS) were only seen in one TS patient (low PLMS index of 7.8/h). CONCLUSIONS: Children with TS have disturbed sleep quality with increased arousal phenomena, which both may be intrinsic to the disorder and might trigger tics and other behavioral problems during daytime. This indicates the need for sleep evaluation in patients with TS.
Adolescent↗
[Periodic movements of the limbs during sleep in childhood].
INTRODUCTION: Periodic movements of the limbs (PML) whilst sleeping is a disorder included in the group of intrinsic dysomnias which cause problems of insomnia and somnolence during the day. It is usually associated with the restless legs syndrome (it occurs in 80% of the patients with this syndrome) although PML may occasionally be an isolated finding. The prevalence of the disease is of 11%. It usually occurs in patients aged over 50 years, and the frequency increase with age. It is uncommon in persons aged under 30 years. In children it is almost unknown. When it does occur in this age group it is usually associated with the restless legs syndrome. OBJECTIVE: To obtain data regarding this disorder in childhood, in view of the scarcity of information available in the literature and the importance of the neuropsychological problems and difficulty with learning that affected children have. CLINICAL CASES: We report two cases of PML occurring in girls of under 7 years of age. They had severe associated neuropsychological disorders (disorders of behavior and feeding, psychotic episodes, etc.). The effect on performance at school led to complete failure in one case. We describe the clinical course of the two girls, emphasizing the variability, and both diagnostic and therapeutic difficulties. CONCLUSIONS: Although this condition is uncommon in childhood, it should always be borne in mind in cases of children with sleep disorders, since early diagnosis will prevent major behavior and learning problems.
Anticonvulsants↗
Prevalence of sleep disorders in childhood and adolescence with headache: a case-control study.
Although a relationship between headache and sleep disturbances has been reported in adults, only few data have been available in children. Accordingly, we performed a survey to determine the prevalence of sleep disturbances in children with migraine and tension-type headache. A questionnaire of history and clinical data and of sleep disturbances was given to parents of 283 headache subjects (164 with migraine and 119 with tension-type headache). Results were compared to a normative group comparable for age and sex of 893 normal healthy subjects. Migraine subjects showed a higher prevalence of sleep disturbances during infancy as well as 3-month colic. In both headache groups, more parents had sleep disturbances and there was a higher occurrence of co-sleeping and napping. A high frequency of sleep disturbances involving sleep quality, night awakenings, nocturnal symptoms and daytime sleepiness was reported in headache children. No statistical differences were found in the prevalence of sleep disturbances between migraine and tension-type headache. However, the migraine group tended to have "disturbed sleep" more often with increased prevalence of nocturnal symptoms such as sleep breathing disorders and parasomnias. Our results give further support to an association between sleep and migraine that may have a common intrinsic origin.
Adolescent↗
[Circadian rhythm in normal and pathological sleep].
Different challenges, constraints for quality of sleep and wakefulness, sleep in extreme conditions, search for a better identification of disorders of sleep and wakefulness, spur researches on the circadian rhythm of sleep and on its disorders. Any advance in that field rests on the understanding of different physiologic phenomena: the intrinsic period of our internal clock is not 24-hours but a little less than 25-hours and it must be reset daily by the Zeitgebers. A sudden phase shift provokes an external desynchronisation. In addition not all rhythms resynchronize together resulting in an internal desyncronization. There is a close relationship between quantities of total sleep and REM sleep and the time of sleep onset within the 24-hours. The propensity to sleep follows a circasemidian rhythm with a major peak during the night and a secondary peak in the midafternoon. Disorders of the circadian rhythm of sleep are of two types: related to the misalignment of the sleep-wake schedule and the synchronizer-controlled rest-activity rhythm (shift work sleep disorder and time zone change syndrome) or related to an abnormal escape of the individual rest-activity rhythm from synchronizer control (delayed sleep phase syndrome, advanced sleep phase syndrome and non 24-hour sleep-wake syndrome.
Biological Clocks↗
The brain's master circadian clock: implications and opportunities for therapy of sleep disorders.
The suprachiasmatic nuclei (SCN) residing in the anterior hypothalamus maintains a near-24-h rhythm of electrical activity, even in the absence of environmental cues. This circadian rhythm is generated by intrinsic molecular mechanisms in the neurons of the SCN; however, the circadian clock is modulated by a wide variety of influences, including glutamate and pituitary adenylate cyclase-activating peptide (PACAP) from the retinohypothalamic tract, melatonin from the pineal gland, and neuropeptide Y from the intergeniculate leaflet. By virtue of these and other inputs, the SCN responds to environmental cues such as light, social and physical activities. In turn, the SCN controls or influences a wide variety of physiologic and behavioral functions, including attention, endocrine cycles, body temperature, melatonin secretion, and the sleep-wake cycle. Regulation of the sleep-wake cycle by the SCN has important implications for development of therapies for sleep disorders, including those involving desynchronization of circadian rhythms and insomnia.
Antioxidants↗
Cardiac autonomic function during sleep in several neuropsychiatric disorders.
Cardiac autonomic activity during sleep is only very slightly influenced by the emotional state of the patient and, unlike some of the traditional tests of autonomic function, may be studied in all patients. In an attempt to evaluate autonomic function in patients with different neuropsychiatric disorders, two different methods of quantifying the changes in sympathetic and parasympathetic cardiac control during sleep were used: (1) the ratios of consecutive R-wave (R-R) intervals before and after spontaneous body movements; (2) spectral analysis of R-R intervals. It was found that more than one third of patients with presenile Alzheimer's disease had defective cardiac sympathetic control. Untreated parkinsonian patients showed predominantly defective parasympathetic, and to a lesser extent sympathetic, function during sleep. In these patients, as well as in patients with multiple sclerosis, autonomic evaluation during sleep led to earlier detection of impairment than the traditional tests during wakefulness. Narcoleptic patients and patients with panic disorder showed normal autonomic function during sleep, but had altered control levels during the wakeful period before sleep. The findings in these narcoleptic patients were probably related to the impairment of their sleep-wake cycle. The sympathetic overactivity found in patients with panic disorder was probably a result of cognitive activity, as the nocturnal data excluded an intrinsic defect in autonomic regulation.
Alzheimer Disease↗
Autonomic blockade and sick sinus syndrome. New concept in the interpretation of electrophysiological and Holter data.
Autonomic blockade is commonly employed as a test of sinus node dysfunction. We compared primary and secondary atrial postpacing pauses and postextrasystolic sino-atrial responses before and after autonomic blockade in 56 patients with the clinical diagnosis of sick sinus syndrome. Pharmacological autonomic blockade was achieved by atropine 0.04 mg kg-1 and propranolol 0.2 mg kg-1, i.v. In a group of patients with a normal intrinsic heart rate the number of positive electrophysiologic variables associated with sinus node dysfunction declined after autonomic blockade. In 91% of these patients, sinus node function was characterized by a normal intrinsic recovery time, gradual exponential return to the constant sinus cycle length, and biphasic postextrasystolic return responses. Three patients in this group had intrinsic SA-block revealed by atrial pacing and verified by Holter monitoring. Besides normal intrinsic pacemaker properties in 53% of patients, rhythm monitoring revealed severe sinus node dysfunction as manifested by bradycardia and the tachycardia-bradycardia syndrome. SA-block and sinus arrest up to 29120 ms. In the abnormal intrinsic heart rate group, disturbed intrinsic rhythmicity was characterized in all by a prolonged corrected intrinsic recovery time (2320 +/- 2740 ms [+/- SD]), arrhythmia and/or bradycardia in the secondary postpacing cycles, chaotic postextrasystolic patterns, or prolonged sinoatrial conduction times. Significantly slow minimal heart rates during sleep significantly prolonged average sinus cycle lengths and positive ECGs for sinoatrial disorders in the waking period were present on the 24-h rhythm recording. It is concluded that intrinsic heart rate obtained by autonomic blockade is the best and most simple method for the diagnosis of intrinsic sinus node dysfunction. Combined autonomic blockade and electrophysiological tests can be of great value in unmasking the severity and degree of intrinsic dysfunction and analyzing the abnormality of secondary pacemaker function. These investigations, however, are rather insensitive and therefore ineffective in detecting autonomic sinus node dysfunction. To assess the role and significance of the autonomous neurovegetative tone in the genesis of sinoatrial disorders, rhythm monitoring is required.
Adolescent↗
Polysomnographic assessment of spells in sleep: nocturnal seizures versus parasomnias.
A dilemma can arise when attempting to distinguish a nocturnal seizure from a parasomnia because both phenomena can be characterized by a general increase in motor and autonomic activity with a transient reduction in the level of consciousness. An additional problem is that an accurate clinical diagnosis generally relies heavily on a detailed history. As sleep related disorders occur at a time when the patient is not fully cognizant, polysomnographic analysis can on occasion supplement for the intrinsic paucity of detailed history. Simultaneously, correlating the clinical and polysomnographic analysis immediately prior to, during, and following an event of interest, can be helpful in differentiating nocturnal seizures from parasomnias.
Adult↗
Eating and its relationships with subjective alertness and sleep in narcoleptic subjects living without temporal cues.
The sleep and meal patterns of normal subjects appear to be governed by a common timing mechanism. To investigate whether the postulated mechanism may be disordered in narcolepsy, a disorder of sleep timing, we analyzed the sleep, eating, and subjective alertness of six narcoleptic subjects and seven normal controls while they lived in a temporal isolation laboratory. When subjects were free to eat and sleep whenever they chose ("free-running"), the meal patterns and nutrient intakes of the free-running narcoleptic subjects and controls were similar; no evidence of an eating disorder intrinsic to narcolepsy was found. When meals were offered on a 24-h schedule, narcoleptic subjects ate more frequently than did the controls. In two of three narcoleptic subjects whose free-running biological days markedly lengthened, intermeal intervals lengthened proportionately. This was evidence that the timing of sleep (bed-dark) periods and meals was indeed governed by a common mechanism. Meal onsets of narcoleptic subjects were preceded by a 90-min period of decreased napping and, when meals were scheduled, by increased subjective alertness. They were followed by a 150-min period of increased napping and decreased subjective alertness. Postprandial deactivation was not found in controls. The deactivation could not be explained by a post-absorptive effect of food, since the contents of meals that were followed by naps did not differ from those that were not followed by naps. While a preabsorptive effect of meals has not been ruled out, we suggest that postmeal deactivation may be evidence that the mechanism that times sleep periods and meals also modulates the temporal pattern of narcoleptic naps.
Adult↗
Sleep related breathing disorders: the respiratory control system and its instability during sleep.
Respiratory control and instability in the breathing pattern during sleep. Unstable breathing during sleep plays an important role in the development of sleep related breathing disorders (SRBD). Periodic breathing, as a hallmark of this instability, is a common initiator of these disorders. In addition, structure and function of the upper airway are prone to intrinsic and extrinsic, congenital and acquired abnormalities which are as well responsible for the pathogenesis of SRBD.
Body Mass Index↗