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Normal circadian rhythms are synchronized to a regular 24 h environmental light-dark cycle, and the suprachiasmatic nucleus and the hormone melatonin have important roles in this process. Desynchronization of circadian rhythms, as occurs in chronobiological disorders, can produce severe disturbances in sleep patterns. According to the International Classification of Sleep Disorders, circadian rhythm sleep disorders (CRSDs) include delayed sleep phase syndrome, advanced sleep phase syndrome, non-24 h sleep-wake disorder, jet lag and shift-work sleep disorder. Disturbances in the circadian phase position of plasma melatonin levels have been documented in all of these disorders. There is compelling evidence to implicate endogenous melatonin as an important mediator in CRSD pathophysiology, although further research involving large numbers of patients will be required to clarify whether the disruption of melatonin secretion is a causal factor in CRSDs. In this Review, we focus on the use of exogenous melatonin and light therapy to treat the disturbed sleep-wake rhythms seen in CRSDs.

This retrospective study describes the effects of long-term treatment with melatonin in 33 adolescents (age range, 10-18 years) with delayed sleep phase syndrome (DSPS). Patients were treated with oral melatonin, 3 to 5 mg/day for an average period of 6 months. During the treatment, sleep onset was advanced and sleep duration was longer. Treatment was also associated with a decrease in the proportion of patients reporting school difficulties. No adverse effects of melatonin were noted. This study indicates that long-term treatment with melatonin can be beneficial for adolescents with DSPS in terms of sleep-wake schedule and school performance.

This case study describes a 14-year-old male suffering from significant academic and personal difficulties, who has been diagnosed with depression, schizotypal personality disorder, and learning disabilities. Because of excessive sleepiness, assessment for a potential sleep disorder was performed. An overnight polysomnographic study revealed no primary sleep disorders. Wrist actigraphy revealed a non-24-hour sleep-wake pattern. Delay in temperature rhythm and dissociation with melatonin rhythms were also noted. Treatment with oral melatonin restored normal sleep-wake schedule. In a follow-up psychiatric evaluation, none of the above diagnoses were present. Greater awareness of sleep disorders may prevent psychiatric misdiagnosis of treatable sleep-wake schedule disorders.

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.

The last several decades have been characterized by the widespread usage of digital devices, especially smartphones. At the same time, there have been reports of both decline in sleep duration and quality and male fertility decline. The aim of this study was to assess the relationship between evening exposure to the light-emitting screens of digital media devices and measures of both sleep and sperm quality. Semen samples were obtained from 116 men undergoing fertility evaluation for the following sperm variables: volume (mL), pH, sperm concentration (million/mL), motility percentage (progressive% + non-progressive motility%), and total sperm count. Exposure to the screens of electronic devices and sleep habits was obtained by means of a questionnaire. Smartphone and tablet usage in the evening and after bedtime was negatively correlated with sperm motility (−0.392; −0.369; p <.05), sperm progressive motility (−0.322; −0.299; p <.05), and sperm concentration (−0.169; p <.05), and positively correlated with the percentage of immotile sperm (0.382; 0.344; p <.05). In addition, sleep duration was positively correlated with sperm total and progressive motility (0.249; 0.233; p <.05) and negatively correlated with semen pH (−0.349; p <.05). A significant negative correlation was observed between subjective sleepiness and total and progressive motility (−0.264; p <.05) as well as total motile sperm number (−0.173; p <.05). The results of this study support a link between evening and post-bedtime exposure to light-emitting digital media screens and sperm quality. Further research is required to establish the proposed causative link and may lead to the future development of relevant therapeutic and lifestyle interventions. [ABSTRACT FROM AUTHOR]

A patient who developed an irregular sleep-wake pattern following prolactin-secreting pituitary microadenoma is described. The patient reported difficulties in sleep onset and awakening at the desired time, which caused major dysfunction in his daily life activities. Despite these difficulties, the sleep-related complaints of the patient remained unrecognized for as long as three yrs. Statistical analyses of the patient's rest-activity patterns revealed that the disruption of the sleep-wake circadian rhythm originated from a disharmony between ultradian (semicircadian) and circadian components. The circadian component displayed shorter than 24 h periodicity most of the time, but the semicircadian component fluctuated between longer and shorter than 12 h periods. Additionally, desynchrony in terms of period length was found in the tentative analyses of the rest-activity pattern, salivary melatonin, and oral temperature. While the salivary melatonin time series data could be characterized by a best-fit cosine curve of 24 h, the time series data of oral temperature was more compatible with 28 h best-fit curve. The rest-activity cycle during the simultaneous measurements, however, was best approximated by a best-fit curve of 21h. The dysregulation of circadian rhythms occurred concomitantly, but not beforehand, with the onset of pituitary disease, thus suggesting an association between the two phenomena. This association may have interesting implications to the modeling of the circadian time-keeping system. This case also highlights the need to raise the awareness to circadian rhythm sleep disorders and to consider disruptions of sleep-wake cycle in patients with pituitary adenoma. [ABSTRACT FROM AUTHOR]

Certain sleep-wake schedule disorders (SWSDs) cannot be successfully managed clinically using conventional methods of sleep therapy. We describe two cases of SWSD, the first following head trauma and the second originating during childhood, that had been misdiagnosed by physicians for many years. After conventional treatment for SWSD with light therapy and melatonin failed to bring about substantial improvement, it was determined that they were suffering from an incurable disability. Hence, we propose new medical terminology for such cases—SWSD disability. SWSD disability is an untreatable pathology of the circadian time structure. Patients suffering from SWSD disability should be encouraged to accept the fact that they suffer from a permanent disability, and that their quality of life can only be improved if they are willing to undergo rehabilitation. It is imperative that physicians recognize the medical condition of SWSD disability in their patients and bring it to the notice of the public institutions responsible for vocational and social rehabilitation. (Chronobiology International, 18(6), 1019–1027, 2001) [ABSTRACT FROM AUTHOR]

Background: In this study we examined the effects of caffeine on sleep quality and melatonin secretion. Melatonin is the principal hormone responsible for synchronization of sleep. Melatonin secretion is controlled by neurotransmitters that can be affected by caffeine.Methods: In the first part of the study, six volunteers drank either decaffeinated or regular coffee in a double-blind fashion on one day, and the alternate beverage 7 days later. Sleep parameters were assessed by actigraphy. In the second part of the study, the subjects again drank either decaffeinated or regular coffee, and they then collected urine every 3 h for quantitation of 6-sulphoxymelatonin (6-SMT), the main metabolite of melatonin in the urine.Results: We found that drinking regular caffeinated coffee, compared to decaffeinated coffee, caused a decrease in the total amount of sleep and quality of sleep, and an increase in the length of time of sleep induction. Caffeinated coffee caused a decrease in 6-SMT excretion throughout the following night.Conclusions: The results of our study confirm the widely held belief that coffee consumption interferes with sleep quantity and quality. In addition, we found that the consumption of caffeine decreases 6-SMT excretion. Individuals who suffer from sleep abnormalities should avoid caffeinated coffee during the evening hours. [Copyright &y& Elsevier]