Circadian Temperature and Activity Rhythms in Unmedicated Narcoleptic Patients

Mayer, G; F, Hellmann; Leonhard, E; Meier-Ewert, K.

doi:10.1016/s0091-3057(97)00241-4

Cited by 32 publications

(12 citation statements)

References 10 publications

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“…Evidence has accumulated showing that REM sleep propensity follows an endogenous circadian rhythm, which is closely coupled to the BcT rhythm (Czeisler et al, 1980), raising the possibility that the wake-sleep disturbance of narcolepsy might be associated with an impaired BcT modulation (Mayer et al, 1997;Mosko et al, 1983). This hypothesis was not confirmed by our results that showed a normal statedependent BcT modulation in NC patients during the D period, despite their higher sleep fragmentation and their enhanced REM sleep propensity.…”

Section: Discussioncontrasting

confidence: 68%

“…These results are in contrast with the previous findings of Mosko et al (1983), who reported higher mesor values in narcoleptic subjects compared to controls when studied during their daily routine, but it is in agreement with Mayer et al (1997), who also evaluated narcoleptic subjects during the daily routine, and with Pollack et al (1994), who studied narcoleptics in a time-isolation condition. The different investigative approaches used by the previous authors make our results obtained in controlled conditions hardly comparable.…”

Section: Discussionsupporting

confidence: 68%

“…Nevertheless, the NC group was characterized by an increased sleep fragmentation throughout the 24 h, being more evident during the L period. Despite these differences, the analysis of the time-course changes of BcT during the 44-h period revealed an overlapping course of the two groups that was confirmed also by the analysis of the 2-min changes of BcT aligned with the sleep onset; this result is in contrast with previous findings that showed in narcoleptic subjects a dampened BcT amplitude (Mayer et al, 1997) and a reduced increase of BcT following nocturnal sleep, hypothetically caused by their reduced motor activity (Mayer et al, 1997;Pollak et al, 1994).…”

Section: Discussionsupporting

confidence: 49%

“…The idea that NC might be associated with an altered BcT modulation, either as a direct consequence of the hypocretin deficiency or as a consequence of the disrupted wakesleep pattern, has been poorly investigated until now. Three studies have been performed to evaluate the BcT circadian and time-dependent pattern in narcoleptic patients with and without cataplexy under uncontrolled conditions, and they led to inconclusive results (Mayer et al, 1997;Mosko et al, 1983;Pollak et al, 1994). The aim of this study was to determine whether in NC patients without therapy and under controlled conditions the deficiency of the hypocretin system is associated with an altered circadian control of BcT and whether the fragmentation of the wake-sleep cycle results in an altered time-and state-dependent BcT modulation.…”

Section: Introductionmentioning

confidence: 99%

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Hypocretin Deficiency in Narcolepsy With Cataplexy Is Associated With a Normal Body Core Temperature Modulation

Grimaldi¹,

Agati

Pierangeli³

et al. 2010

Chronobiology International

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Narcolepsy with cataplexy (NC) is a sleep disorder caused by the loss of the hypothalamic neurons producing hypocretin. The clinical hallmarks of the disease are excessive daytime sleepiness, cataplexy, other rapid eye movement (REM) sleep phenomena, and a fragmented wake-sleep cycle. Experimental data suggest that the hypocretin system is involved primarily in the circadian timing of sleep and wakefulness but also in the control of other biological functions such as thermoregulation. The object of this study was to determine the effects of the hypocretin deficit and of the wake-sleep cycle fragmentation on body core temperature (BcT) modulation in a sample of drug-free NC patients under controlled conditions. Ten adult NC patients with low cerebrospinal fluid (CSF) hypocretin levels (9 men; age: 38 ± 12 yrs) were compared with 10 healthy control subjects (7 men; age: 44.9 ± 12 yrs). BcT and sleep-wake cycle were continuously monitored for 44 h from 12:00 h. During the study, subjects were allowed to sleep ad libitum, living in a temperature- and humidity-controlled room, lying in bed except when eating, in a light-dark schedule (dark [D] period: 23:00-07:00 h). Sleep structure was analyzed over the 24-h period, the light (L) and the D periods. The wake-sleep cycle fragmentation was determined by calculating the frame-shift index (number of 30-s sleep stage shifts occurring every 15 min) throughout the 44-h study. The analysis of BcT circadian rhythmicity was performed according to the single cosinor method. The time-course changes in BcT and in frame-shift index were compared between narcoleptics and controls by testing the time × group (controls versus NC subjects) interaction effect. The state-dependent analysis of BcT during D was performed by fitting a mixed model where the factors were wake-sleep phases (wake, NREM stages 1 and 2, slow-wave sleep, and REM sleep) and group. The results showed that NC patients slept significantly more than controls during the 24 h due to a higher representation of any sleep stage (p < .001) during L, whereas the total amount of night sleep and its architecture were comparable in the two groups. Wake-sleep fragmentation was higher (p < .001) in NC subjects especially during L. Despite these differences, mesor (24-h mean), amplitude, and acrophase (peak time) of BcT circadian rhythm were comparable in narcoleptics and controls, and no between-group differences were detected in the time-course changes and in the state-dependent modulation at night of BcT. These data indicate that the hypocretin deficit in drug-free NC patients and their altered wake-sleep cycle couple with an intact modulation of BcT.

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Section: Discussioncontrasting

confidence: 68%

Section: Discussionsupporting

confidence: 68%

Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hypocretin Deficiency in Narcolepsy With Cataplexy Is Associated With a Normal Body Core Temperature Modulation

Grimaldi¹,

Agati

Pierangeli³

et al. 2010

Chronobiology International

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“…It should be noted that narcolepsy was reported to be associated with changes in energy homeostasis several decades ago 67 . Narcolepsy patients are frequently: (i) obese, (ii) have insulin‐resistant diabetes mellitus; 67 (iii) exhibit reduced food intake; 68 and (iv) have lower blood pressure and temperature 69,70 . These findings, however, have not received much attention because they could be secondary to sleepiness or inactivity during the daytime.…”

Section: Hypocretins/orexins and Food Intake Revisitedmentioning

confidence: 99%

History and perspectives of hypocretin/orexin research in sleep medicine

Nishino

Yoshida

2003

Sleep and Biological Rhythms

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By using forward and reverse genetics, genes involved in the pathogenesis of narcolepsy (hypocretin/orexin ligand and its receptor) in animals have been identified. Mutations in hypocretin‐related genes are extremely rare in humans, but hypocretin ligand deficiency is found in many cases. A series of these discoveries are representing the most striking progress in narcolepsy research in the last 100 years, and should continue to contribute to the development of new diagnostic tests and treatments. Impacts of the hypocretin system on sleep physiology have also rapidly increased. Hypocretins/orexins are novel hypothalamic neuropetides discovered outside the sleep research field by using subtractive polymerase chain reaction/reverse pharmacology techniques. Hypocretins are involved in various fundamental hypothalamic functions such as feeding, energy homeostasis and neuroendocrine regulation. Hypocretin neurons project to most ascending arousal systems (including monoaminergic and cholinergic systems), and generally exhibit excitatory inputs. Together with the recent finding of the sleep promoting system in the hypothalamus, especially in the γ‐amynobutyric acid (GABA)/Galanin ventrolateral preoptic area, which exhibits inhibitory inputs to these ascending systems, the hypothalamus is now recognized as the most important brain site for the sleep switch. Meanwhile, narcolepsy now appears to be a more complex condition than previously thought. The pathophysiology of the disease is involved in the abnormalities of sleep and various hypothalamic functions caused by the hypocretin deficiency, such as the changes in energy homeostasis. Narcolepsy is thus an important model to study the fundamental hypothalamic function and the links between sleep regulation, energy homeostasis and/or feeding.

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The neurobiology, diagnosis, and treatment of narcolepsy

Scammell

2003

Annals of Neurology

230

113

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Narcolepsy is a common cause of chronic sleepiness distinguished by intrusions into wakefulness of physiological aspects of rapid eye movement sleep such as cataplexy and hallucinations. Recent advances provide compelling evidence that narcolepsy may be a neurodegenerative or autoimmune disorder resulting in a loss of hypothalamic neurons containing the neuropeptide orexin (also known as hypocretin). Because orexin promotes wakefulness and inhibits rapid eye movement sleep, its absence may permit inappropriate transitions between wakefulness and sleep. These discoveries have considerably improved our understanding of the neurobiology of sleep and should foster the development of rational treatments for a variety of sleep disorders.

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Circadian Temperature and Activity Rhythms in Unmedicated Narcoleptic Patients

Cited by 32 publications

References 10 publications

Hypocretin Deficiency in Narcolepsy With Cataplexy Is Associated With a Normal Body Core Temperature Modulation

Hypocretin Deficiency in Narcolepsy With Cataplexy Is Associated With a Normal Body Core Temperature Modulation

History and perspectives of hypocretin/orexin research in sleep medicine

The neurobiology, diagnosis, and treatment of narcolepsy

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