jueves, 9 de abril de 2009
- BMC Neurol. 2007 Dec 5;7:40.
- Perception versus polysomnographic assessment of sleep in CFS and non-fatigued control subjects: results from a population-based study.
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, USA. firstname.lastname@example.org
BACKGROUND: Complaints of unrefreshing sleep are a prominent component of chronic fatigue syndrome (CFS); yet, polysomnographic studies have not consistently documented sleep abnormalities in CFS patients. We conducted this study to determine whether alterations in objective sleep characteristics are associated with subjective measures of poor sleep quality in persons with CFS. METHODS: We examined the relationship between perceived sleep quality and polysomnographic measures of nighttime and daytime sleep in 35 people with CFS and 40 non-fatigued control subjects, identified from the general population of Wichita, Kansas and defined by empiric criteria. Perceived sleep quality and daytime sleepiness were assessed using clinical sleep questionnaires. Objective sleep characteristics were assessed by nocturnal polysomnography and daytime multiple sleep latency testing. RESULTS: Participants with CFS reported unrefreshing sleep and problems sleeping during the preceding month significantly more often than did non-fatigued controls. Participants with CFS also rated their quality of sleep during the overnight sleep study as significantly worse than did control subjects. Control subjects reported significantly longer sleep onset latency than latency to fall asleep as measured by PSG and MSLT. There were no significant differences in sleep pathology or architecture between subjects with CFS and control subjects. CONCLUSION: People with CFS reported sleep problems significantly more often than control subjects. Yet, when measured these parameters and sleep architecture did not differ between the two subject groups. A unique finding requiring further study is that control, but not CFS subjects, significantly over reported sleep latency suggesting CFS subjects may have an increased appreciation of sleep behaviour that may contribute to their perception of sleep problems.
- Fuente: Pubmed
- Neurosci Lett. 1991 Jan 28;122(2):195-8.
Adaptation of the melatonin rhythm in human subjects following night-shift work in Antarctica.
British Antarctic Survey Medical Unit, RGIT Survival Centre Ltd., Aberdeen, Scotland, U.K.
Different environmental conditions, particularly daylength and intensity of natural light, may influence the ability of shiftworkers to adapt to the abrupt phase-shifts of 24 h time cues imposed by the nature of their work. We have investigated this problem in terms of the circadian rhythm of the pineal hormone melatonin in nightshift workers on the British Antarctic Survey Base at Halley (75 degrees South). Melatonin production was assessed by measurement of its major urinary metabolite 6-sulphatoxymelatonin (aMT6s) by radio-immunoassay in sequential urine samples collected for 48 h at weekly intervals. The acrophase of the melatonin rhythm was significantly delayed from 5.22 h. min to 14.54 h. min (summer) and 8.73 h.min to 13.23 h.min (winter) during a week of night-shift work. Readaptation of the rhythm following night-shift work was markedly slower during the Antarctic winter taking 3 weeks compared to summer where the baseline phase position was re-established after 1 week. Morning and evening treatment (08.00-09.00 h, 16.00-17.00 h) with bright (greater than 2500 lux) full spectrum white light did not significantly modify this phenomenon in summer, but a trend to faster adaptation with light treatment was seen in winter. These observations are likely to be of importance to shift-workers in temperate zones. Further investigations of phase-shifting techniques, such as appropriately timed bright light and administration of melatonin itself, are indicated, particularly in relation to performance at work.
En el caso del sueño, se han descubierto dos genes implicados en su regulación y que se activan/desactivan con los cambios lumínicos: los genes per y tim, que sintetizan unas proteínas que también se llaman per y tim.
Concretamente estos genes se activan con la luz y sintetizan estas proteínas, que se quedan en el citoplasma de las células. Durante la oscuridad, las proteínas per y tim se unen y entran en el núcleo de las células, donde está el ADN, y bloquean la actividad de los genes ger y tim.
Cuando vuelve a aparecer la luz, las dos proteínas desaparecen y así los genes per y tim se activan otra vez.
Estas activaciones/inactivaciones se van repitiendo cíclicamente.