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At least 19 recordsLinked to original sources
PubMed2002

Circadian rhythm sleep disorders (CRSD).

Circadian Rhythm Sleep Disorders (CRSD) are a group of sleep disorders characterized by a malsynchronization between a person's biological clock and the environmental 24-h schedule. These disorders can lead to harmful psychological and functional difficulties and are often misdiagnosed and incorrectly treated due to the fact that doctors are unaware of their existence. In the following review we describe the characteristics of CRSD, diagnosis, treatment as well as their relationship to psychopathology, psychotropic drugs and head trauma.

Antipsychotic Agents↗
PubMed2005

Idiopathic chronic sleep onset insomnia in attention-deficit/hyperactivity disorder: a circadian rhythm sleep disorder.

To investigate whether ADHD-related sleep-onset insomnia (SOI) is a circadian rhythm disorder, we compared actigraphic sleep estimates, the circadian rest-activity rhythm, and dim light melatonin onset (DLMO) in ADHD children having chronic idiopathic SOI with that in ADHD children without sleep problems. Participants were 87 psychotropic-medication-naïve children, aged 6 to 12 yrs, with rigorously diagnosed ADHD and SOI (ADHD-SOI) and 33 children with ADHD without SOI (ADHD-noSOI) referred from community mental health institutions and pediatric departments of non-academic hospitals in The Netherlands. Measurements were 1 wk, 24 h actigraphy recordings and salivary DLMO. The mean (+/-SD) sleep onset time was 21:38 +/- 0:54 h in ADHD-SOI, which was significantly (p < 0.001) later than that of 20:49 +/- 0:49 h in ADHD-noSOI. DLMO was significantly later in ADHD-SOI (20:32 +/- 0:55 h), compared with ADHD-noSOI (19:47 +/- 0:49 h; p < 0.001). Wake-up time in ADHD-SOI was later than in ADHD-noSOI (p = 0.002). There were no significant between-group differences in sleep maintenance, as estimated by number of wake bouts and activity level in the least active 5 h period, or inter- and intradaily rhythm variability. We conclude that children with ADHD and chronic idiopathic sleep-onset insomnia show a delayed sleep phase and delayed DLMO, compared with ADHD children without SOI.

Attention Deficit Disorder with Hyperactivity↗
PubMed2006

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↗
PubMed2006

Circadian rhythm sleep disorders.

Humans exhibit endogenous circadian rhythms that are regulated by the master circadian clock of the body, the suprachiasmatic nucleus. These endogenous circadian rhythms are aligned to the outside world by social and environmental cues. Circadian rhythm sleep disorders (CRSD) occur when there is an alteration of the internal timing mechanism or a misalignment between sleep and the 24-h social and physical environment. CRSD are often underrecognized yet should be considered in the differential of patients presenting with symptoms of insomnia and/or hypersomnia. Because behavioral and environmental factors often are involved in the development and maintenance of these conditions, a multimodal treatment approach of behavioral and/or pharmacologic approaches is usually required to synchronize a patient's circadian rhythm to the 24-h environment, consolidate sleep, and improve alertness. Rapid advances in our understanding of the physiologic, cellular, and molecular basis of circadian rhythm and sleep regulation will likely lead to improved diagnostic tools and treatments for CRSD.

Circadian Rhythm↗
PubMed2005

Diagnosis and assessment of sleep and circadian rhythm disorders.

Sleep and wakefulness are fundamental behavioral and neurobiological states that characterize all higher animals, including human beings. This article presents an overview of the current state of our knowledge concerning the function of sleep and sleep-wake rhythms, the neurobiology of circadian rhythms, how wakefulness and sleep are studied, and the clinical assessment and diagnosis of sleep and circadian rhythm disorders. Major theories of the function of sleep and sleep-wake rhythms are reviewed, including ecological or environmental advantage, physical restoration, optimizing waking function, learning and integration of experience, and survival. The author then reviews what is known about the neurobiology of endogenous circadian rhythms and how they are affected by environmental time cues. How sleep is studied using polysomnography (PSG) is explained, and the PSG characteristics of the three major neurobehavioral states, wakefulness, rapid eye movement (REM) sleep, and non-rapid eye movement (NREM) sleep, are described. Systems of classifying sleep disorders are reviewed, including those of the DSM-IV-TR, the International Classification of Sleep Disorders, and the ICD-10. Methods of assessing sleep complaints are then described, including taking an accurate history from the patient and bed partner, use of sleep history questionnaires and sleep-wake diaries, use of actigraphy, and use of PSG.

Adult↗
PubMed2005

Daily expression of clock genes in whole blood cells in healthy subjects and a patient with circadian rhythm sleep disorder.

In recent years, circadian rhythm sleep disorders in humans have been increasing. Clinical features characteristic of this disorder are well known, but the specific causes remain unknown. However, various derangements of circadian expression of the clock gene are a probable cause of this disease. We have attempted to elucidate the relationship between the expression of the clock genes in whole blood cells and the clinical features characteristic of this disorder. In this study, we indicate the daily expression of clock genes period (Per) 1, 2, 3, Bmal1, and Clock in whole blood cells in 12 healthy male subjects. The peak phase of Per1, Per2, and Per3 appeared in the early morning, whereas that of Bmal1 and Clock appeared in the midnight hours. Furthermore, in one patient case with circadian rhythm sleep disorder, we observed variations of the peak phase in clock genes by treatments such as light therapy, exercise therapy, and medicinal therapy. This study suggested that the monitoring of human clock genes in whole blood cells, which may be functionally important for the molecular control of the circadian pacemaker as well as in suprachiasmatic nucleus, might be useful to evaluate internal synchronization.

ARNTL Transcription Factors↗
PubMed1996

High prevalence of personality disorders among circadian rhythm sleep disorders (CRSD) patients.

The purpose of this study was to examine systematically our previous clinical impression regarding the prevalence of personality disorders in patients suffering from circadian rhythm sleep disorders (CRSD). We hypothesized that, in a group of patients suffering from CRSD, there would be a higher frequency of personality disorders than in a group of healthy controls. The experimental group consisted of CRSD patients diagnosed according to a clinical interview and actigraphic recordings. The control group consisted of healthy volunteers in whom CRSD had been ruled out by means of a self-administered questionnaire. Both groups were assessed for personality disorders using the MCMI, a diagnostic tool based on Millon's biopsychosocial theory of personality and the PRQ-R, a diagnostic tool based on the DMS-III-R. Both tests provided clear and significant support for the hypothesis that individuals suffering from CRSD are characterized to a greater extent by personality disorders than a control group. No specific characteristic pattern or profile of personality disorders was clearly detected. Correct early diagnosis and treatment of CRSD may improve afflicted individuals' adaptive capabilities and perhaps even prevent the development of a personality disorder. This suggests how important a greater awareness of CRSD on the part of the professional community may be.

Adolescent↗
PubMed2005

Circadian rhythm sleep disorders.

Individuals who have circadian rhythm sleep disorders present with symptoms of insomnia or excessive sleepiness and complain of an inability to sleep at their desired time. Although the primary etiology of these disorders is a misalignment between the endogenous circadian clock and the external environment, social and behavioral factors can also play important roles in perpetuating or exacerbating these disorders. Currently, the management of circadian rhythm disorders is limited to the use of bright light and melatonin to realign the circadian clock with the desired sleep time.However, as the understanding of the physiologic and genetic basis of sleep and circadian rhythm regulation advances, even more practical and effective treatments should become available.

Humans↗
PubMed1998

Clinical characteristics of circadian rhythm sleep disorders.

From our practice at the sleep disorders clinic in Kohnodai Hospital, National Center of Neurology and Psychiatry (NCNP), we report the clinical characteristics of circadian sleep-wake rhythm disorders. Nearly 90% of circadian rhythm sleep disorders were diagnosed as delayed sleep phase syndrome (DSPS) or as non-24 sleep-wake syndrome (non-24). While DSPS was equally common in males and females, non-24 was more frequently seen in men. It was of psychiatric interest that a considerable number of patients had depressive states in the course of their circadian rhythm sleep disorders. Difficulty in adapting to social life was more severe in patients with non-24 than in those with DSPS.

Adult↗
PubMed2004

Assessment of excessive sleepiness and insomnia as they relate to circadian rhythm sleep disorders.

Sleep disturbances are associated with a number of psychiatric disorders, including depression, anxiety disorders, and substance use disorders, and many psychiatric patients report symptoms such as insomnia, tiredness, fatigue, and excessive sleepiness. Despite their known negative impact on daytime functioning and quality of life, less than 10% of individuals with these symptoms visit physicians specifically for their sleeping problems. Although there are many explanations for this lack of reporting, one possibility is that individuals are often unaware of the impact of sleepiness on their daytime functioning. Therefore, the burden of identifying sleepiness and its consequences often resides with physicians and other health care professionals. This process of detection is assisted by rating scales and subjective and objective tests. Although prior discussions on these topics have focused on the understanding and identification of either excessive sleepiness or insomnia, these symptoms often coexist, introducing a clinical challenge in that it becomes unclear which of these two should become the initial focus of clinical attention. When both excessive sleepiness and insomnia coexist, a circadian rhythm sleep disorder may be present, such as jet lag type, delayed and advanced sleep phase types, and shift work type.

Comorbidity↗
PubMed2002

Molecular genetics of timing in intrinsic circadian rhythm sleep disorders.

Recent advances in circadian biology are identifying key genes and the molecular clockworks they command. These biochemical systems provide new tools for evaluating clinically observed, intrinsic circadian rhythm sleep disorders. A striking example was last year's discovery of a point mutation in a human clock gene that produces a sleep phase syndrome. This finding suggested that other intrinsic sleep disorders may have genetic underpinnings, and that less debilitating variations in sleep/wake behavior may be revealed by molecular screening of known clock genes in broader human populations.

Animals↗
PubMed1999

Etiology and treatment of intrinsic circadian rhythm sleep disorders.

Some individuals experience an acute or chronic sleep disturbance, associated with a misalignment between the timing of their sleep and the sleep-wake cycle that is desired, or considered normal by society. It is estimated that 5-10% of insomniacs seeking treatment have this type of disorder, collectively called circadian rhythm sleep disorders. This paper reviews circadian rhythm sleep disorders of the intrinsic type, which include delayed sleep phase syndrome, advanced sleep phase syndrome, non-24-hour sleep-wake syndrome, and irregular sleep-wake pattern. For each disorder, we present data addressing its pathophysiology and potential treatments, including the use of behavioral measures and chronotherapy, bright light treatment and pharmacological treatments such as melatonin. We conclude by addressing some of the limitations and drawbacks of the various treatments.

Journal Article↗
PubMed2002

Circadian Rhythm Sleep Disorders (CRSD) in psychiatry--a review.

Circadian Rhythm Sleep Disorders (CRSD) are a group of sleep disorders characterized by a de-synchronization between a person's biological clock and the environmental 24-hour schedule. There are four main types of CRSD, namely, Delayed Sleep Phase Syndrome (DSPS) (the most common), Advanced Sleep Phase Syndrome (ASWD), Non-24-hour Sleep-Wake Syndrome (Free-Running Pattern) and Irregular (or Disorganized) Sleep Wake Pattern. These disorders lead to harmful psychological and functional difficulties and certain personality disorders may also be related to them. It has been found that psychotropic drugs, SSRI and haloperidol can cause CRSD, and this is also true for some cases of minor head trauma. They are often misdiagnosed and incorrectly treated due to the fact that many doctors are unfamiliar with them. This review describes the disorders, their consequences and available treatment.

Antipsychotic Agents↗
PubMed2001

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↗
PubMed2006

Neurobiology of circadian rhythm sleep disorders.

To adapt to a 24-hour environment, nearly all organisms, from mammals to single-celled organisms, have developed endogenous mechanisms that generate nearly 24-hour (circadian) rhythms in physiology and behavior, the most notable being that of the daily cycles of sleep and wake. Disruption of these circadian rhythms is often accompanied by disorders of sleep and wakefulness. With the recent advances in the molecular biology that underlies the development and maintenance of these rhythms, the pathophysiology behind circadian rhythm sleep disorders is becoming better understood.

Circadian Rhythm↗
PubMed2002

Case study of circadian rhythm sleep disorder following haloperidol treatment: reversal by risperidone and melatonin.

A patient with Gilles de la Tourette syndrome treated with haloperidol, ingested once daily after awakening from sleep, exhibited an irregular sleep-wake pattern with a free-running component of approximately 48 h. Transfer to risperidone, ingested once daily after awakening from sleep, was beneficial resulting in a sleep-wake cycle more synchronized at the appropriate phase to the external zeitgebers, and fewer nocturnal disturbances. The circadian sleep-wake schedule was fully synchronized when the patient had been subsequently treated with melatonin at 21:00h, before intended nocturnal sleep, in addition to risperidone in the morning. Restoration of the sleep-wake circadian pattern was accompanied by the patient's subjective report of significant improvement in his quality of life, social interactions, and occupational status. This observation suggests that circadian rhythm sleep disorders can be related to the typical neuroleptic haloperidol and restored by the atypical neuroleptic risperidone. Similar findings reported in patients suffering from other disorders support the hypothesis that the described disruption of the sleep-wake schedule is medication rather than illness-related. Therefore, it is very important to realize that circadian rhythm sleep disorders may be a side effect of neuroleptics.

Adult↗
PubMed2005

Behavioral and psychiatric consequences of sleep-wake schedule disorders.

Circadian rhythm sleep disorders (CRSDs) arise when an individual's sleep-wake rhythm mismatches the environmental 24-h schedule. Physiological data and genetic studies in patients with CRSDs suggest that these disorders result from abnormal functioning of the circadian timing system. Diagnosis involves recognition of the characteristics of CRSDs, which can be achieved by clinical interview and actigraphic monitoring of rest-activity patterns. Bright-light therapy and melatonin administration have proved to be the most effective treatment modalities of CRSDs. In psychiatric practice, CRSDs can be encountered on various occasions. Some evidence indicates that a deviant sleep-wake schedule might be a predisposing factor to personality disorders. CRSDs can emerge as an iatrogenic effect of certain psychoactive drugs, such as haloperidol and fluvoxamine. It is not uncommon that the daytime functional difficulties that accompany CRSDs are misinterpreted as symptoms of psychopathology. Recognition and awareness of these disorders should prevent years of erroneous diagnosis and treatment in these patients.

Circadian Rhythm↗