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Background: The obesity-hypoventilation syndrome (OHS), commonly defined as a combination of obesity and diurnal hypercapnia, is efficiently treated using nasal positive pressure ventilation (NPPV). The present study aimed to determine whether nocturnal polysomnography allows detection of respiratory disturbances occurring in patients with OHS treated with NPPV that may interfere with the quality of sleep and of ventilatory support, and are not detected by nocturnal pulse oximetry and capnography., Methods: Twenty OHS patients in stable clinical condition treated by NPPV for at least 3 months with a bilevel pressure support ventilator were studied. All patients underwent single-night polysomnography under NPPV including transcutaneous measurement of Pco(2) (TcPco(2)). Four types of respiratory events were defined and quantified: patient/ventilator desynchronization, periodic breathing (PB), autotriggering, and apnea-hypopneas., Results: Eleven patients (55%) exhibited desynchronization occurring mostly in slow-wave sleep and rapid eye movement sleep and associated with arousals but not inducing significant changes in TcPco(2) or oxygen saturation using pulse oximetry (Spo(2)). Eight patients (40%) showed a high index of PB, mostly occurring in light sleep and associated with more severe nocturnal hypoxemia. Autotriggering was sporadic and usually limited to one or two breaths, although prolonged and asymptomatic autotriggering occurred in one patient during 10.6% of total sleep time., Conclusions: Patient/ventilatory asynchrony and PB are respiratory patterns occurring frequently in OHS patients treated using NPPV. Nocturnal monitoring of Spo(2) and TcPco(2), commonly used to assess the efficacy of ventilatory support, do not adequately explore this aspect of therapy that might influence its efficacy as well as sleep quality.

Study Objectives: The relationship between event-related potentials (ERPs) and sleep alterations in patients with sleep disorders is still controversial. Whether the ERP alterations are affected by sleep loss and sleep discontinuity can be addressed by studying presleep-to-postsleep changes in ERPs. We investigated if presleep-to-postsleep ERP latencies and amplitudes differ in patients with insomnia and sleep-related breathing disorders and whether these changes are affected by the degree of subjective and objective sleep alterations., Methods: Fifteen patients with a diagnosis of insomnia, 45 patients with sleep-related breathing disorders, and 13 healthy controls were examined. Auditory ERPs were measured in the evening before sleep and in the morning after polysomnography. Subjective sleepiness and sleep quality were assessed by the Epworth Sleepiness Scale and the Saint Mary's Hospital Quality of Sleep Questionnaire., Results: Analysis of evening-to-morning ERP variations did not reveal significant between-group differences in N100 latency and amplitude or in P200 and P300 amplitudes. Patients with sleep-related breathing disorders had a significant lengthening of P200 and P300 latencies in the morning, compared with controls and insomniacs. A trend to delayed morning P300 was present in patients with insomnia but did not reach statistical significance. The evening-to-morning ERP differences were not significantly related to subjective sleep quality, indexes of sleep fragmentation, or total sleep time., Conclusions: ERPs are sufficiently sensitive to assess attention dysfunction in patients with sleep disorders when presleep-to-postsleep changes are considered. The lack of relationship between indexes of sleep loss and sleep fragmentation and presleep-to-postsleep ERP changes might suggest that other factors outside sleep alterations affect ERP deterioration in patients with sleep disorders.

Background and Purpose: Although a night-to-night variability in periodic leg movements (PLM) occurrence has been described in patients with primary PLM disorder and sleep apnea syndrome, no study has apparently considered the inter-night effect on PLM index during wakefulness and sleep in patients with Restless Legs Syndrome (RLS). Moreover, no study has examined the night-to-night variability in PLM index according to sleep stage and time of night. We therefore examined changes in PLM index during wakefulness and sleep during two consecutive nights in a group of untreated RLS patients., Patients and Methods: Twenty-eight drug-free RLS patients, aged 53.4+/-2.3 yr, with a mean International Restless Legs Syndrome Study Group (IRLSSG) severity score of 20.2+/-1.6, were studied during two consecutive nights. PLM duration and interval, PLM index during wakefulness (PLMWI), during total sleep time (PLMSI), as well as during each sleep stage were measured. Analysis was also extended to examine PLM occurrence during sleep cycles., Results: In the group of patients as a whole, the PLMW and PLMS index, duration and interval did not show significant difference between nights, these measures being consistently similar for both nights. Comparison of PLMS index between different sleep stages did not reveal inter-night differences. Nocturnal variation in PLM number, duration and interval for total recording time and sleep period revealed a progressive decline across the night for PLM index (P

It has recently been described that the maximal respiratory effort developed at the end of an apnea (Pesmax)--which is regarded as an index of arousal threshold in patients with obstructive sleep apnea syndrome (OSA)--increases progressively during the night, probably as a consequence of associated sleep fragmentation. In order to find out whether the nocturnal trend of Pesmax may be more influenced by a sleep-dependent circadian rhythm than by sleep fragmentation, we revised the polygraphic recordings of 37 patients in whom obstructive apneas were recorded for at least 7 hours. In 15 of these patients, analysis was made for eight hours of the night. During each hour we analyzed at least 7 obstructive apneas, in which we measured the minimal esophageal pressure at the start of the apnea, the maximum value recorded at the end of the apnea (Pesmax), the difference from the minimum to the maximum (delta Pes), and the rate of increase in esophageal pressure (RPes). As indices of sleep fragmentation, we defined the number of arousals, awakenings and sleep state transitions. In the group of patients as a whole, we found a trend toward a gradual increase for apnea duration (F = 98.8, p < 0.001) and Pesmax F = 31.6, p < 0.001) which was significant from the first to the last hour. The time-dependent evolution of apnea duration and Pesmax showed that the rise in these two variables peaked during the first 3 hours of sleep, followed by a plateau and a decrease in the last hour of the night. This temporal profile was more evident when the analysis was available for 8 hours. No significant changes across the night were found for nocturnal hypoxemia and number of arousals. Considering the slope of Pesmax changes across the night, we saw that neither the apnea+hypopnea index nor the indices of sleep fragmentation affected the nocturnal trend. The present data demonstrate the presence of a nocturnal trend in arousal threshold in OSA patients independent of sleep fragmentation. The biphasic evolution of the arousal threshold may be caused by factors that influence the circadian and homeostatic processes.

Daytime sleepiness is one of the major symptoms of obstructive sleep apnea. However, its definition raises problems, since it may be based on either subjective feeling (evaluated by means of questionnaires or analog visual scales), physiological drive or need (inferred by a sleep latency) or on the concept of sleep propensity defined as the probability of falling asleep (measured by the occurrence of sleep in various circumstances of daily life). Data from the literature suggest that sleep fragmentation and hypoxemia, both related to sleep apneas, cause daytime sleepiness. Our own data show that sleep propensity in a group of 44 patients with obstructive sleep apnea was correlated with the increase in esophageal pressure swings during obstructive apneas. This result suggests that the increased respiratory effort against occluded upper airways also contributes to daytime sleepiness in patients with obstructive sleep apnea.

To investigate the factors responsible for the morning rise in blood pressure (BP) in obstructive sleep apnea syndrome (OSAS) we examined a group of 253 consecutive snorers or OSAS patients. On the basis of their AHI the patients were classified in four groups. BP was measured on the evening before sleep onset and on the following morning after 15 min of rest by a finger arterial pressure device (Finapres). In 150 subjects BP was monitored during the night by a Finapres device. In the morning BP increased in the patient group with an average difference of 9.9 +/- 0.5 mmHg for systolic (SBP) and 9.9 +/- 0.4 mmHg for diastolic pressure (DBP). The increase was significant in snorers and OSAS patients without differences between groups. The morning rise in SBP was related to diurnal values of SBP, age and AHI whereas the time spent in apnea and the diurnal values of DBP significantly contributed to the DBP increase. In the subgroup of 150 patients in whom BP was analyzed during sleep, the awakening increase was related to the absolute BP value during sleep and to the BP changes from wakefulness to sleep. The magnitude of the BP changes from evening to morning was not dependent on the degree of BP variability during sleep. We conclude that the awakening increase in BP in patients with snoring or OSAS may be mediated by the setting of pressure response to apnea or to mechanical effort during sleep. Anthropometric variables and diurnal cardiovascular setting may play an additional role in modulating the final pressure response to upper airway obstruction.

Fatal familial insomnia is a prion disease in which a selective thalamic degeneration leads to total sleep deprivation, hypertension, dysautonomia, adrenal overactivity, and impaired motor functions. With patients under continuous recumbency and polysomnographic control, we assessed the changes in the 24-hour patterns of blood pressure, heart rate, plasma catecholamines, corticotropin, and serum cortisol in three patients at different stages of the disease. Six healthy volunteers were used as control subjects. A dominant 24-hour component was detected at rhythm analysis of all variables, both in patients and control subjects. In the patients, the amplitudes gradually decreased as the disease progressed, leading to the obliteration of any significant dirunal variation only in the preterminal stage. A shift in phase corresponded to the loss of the nocturnal fall in blood pressure in an early stage of the disease, when nocturnal bradycardia was still preserved. Plasma cortisol was high and became increasingly elevated, whereas corticotropin remained within normal levels; abnormal nocturnal peaks appeared in their circadian patterns. The disrupted patterns of cortisol and blood pressure preceded the development of hypertension and severe dysautonomia, which in turn were paralleled by increasing catecholamine and heart rate levels. Our data demonstrate that in patients with fatal familial insomnia the changes detectable in the rhythmic component of diurnal blood pressure variability result in a pattern of secondary hypertension. Disturbances in thalamic, pituitary-adrenal, and autonomic functions seem to be involved in mediating these changes.

Fatal familial insomnia (FFI) is a disease characterized by loss of sleep activity due to selective thalamic degeneration. To assess the secretory pattern of melatonin (MT) in FFI, we studied two cases of overt disease under standardized conditions and polysomnographic control. Each patient underwent repeated 24-h study sessions, and MT was assayed at 30-min intervals. Six healthy volunteers were used as controls. Slow wave sleep was never recorded, whereas occasional episodes of enacted dreaming accompanied by rapid ocular movements and complex muscular activities were documented, with no detectable rhythm. Plasma MT concentrations gradually decreased as the disease progressed. A significant circadian rhythm was detected in the earlier recordings, with decreasing amplitudes with disease progression. Complete rhythm obliteration was achieved in the most advanced stage. Normally placed nocturnal acrophases were detected in the earlier stages, but then a shift toward the daytime hours was observed. Thalamic lesions of FFI appear to determine a progressive disruption of the sleep/wake cycle accompanied by decreased circulating levels of MT, with progressive alterations in the circadian rhythm of this hormone. On the other hand, decreased secretion of MT may contribute to the sleep disturbances of FFI.

We used a chronobiological inferential statistical method to investigate circadian rhythms of hypophyseal hormones, cortisol, melatonin and catecholamines in two females of the same family affected by fatal familial insomnia. Case 1 (confirmed at autopsy) presented an absent or progressive loss of circadian rhythms of all hormones. In case 2 there was a loss of GH circadian rhythm and a less significant rhythm for melatonin, catecholamines and gonadotropins. These results confirm the role of the thalamus in regulating hormonal circadian rhythm.