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Objective Recent studies have suggested that patients with obstructive sleep apnea (OSA) might be affected by olfactory impairment. However, more evidence is needed on the effect that OSA has on the chemical senses (olfaction and gustatory) of these patients, and whether continuous positive airway pressure (CPAP) treatment might help to reverse possible impairment. Methods A prospective study was conducted with 44 OSA patients (17 female and 27 male, mean age 54 ± 9.9 years) who were diagnosed via polysomnography and eligible for CPAP treatment. Orthonasal olfactory and gustatory function was measured with the extended Sniffin' Sticks test battery and "taste strips," respectively, before and after CPAP treatment. Results Baseline olfaction was decreased in OSA patients and after CPAP therapy olfactory scores (odor threshold-discrimination-identification score [TDI]: baseline 29.4 ± 4.11 after CPAP 32.3 ± 4.82; p = 0.001; odor threshold [THR]: baseline 5.28 ± 1.69 after CPAP 6.78 ± 2.61; p = 0.000; odor identification [ID]: baseline 12.9 ± 1.95 after CPAP 13.6 ± 1.33; p = 0.013) improved significantly. In contrast, neither baseline taste function in OSA patients nor gustatory function after treatment seemed to be affected. Conclusion Orthonasal olfactory function in patients with OSA improves under CPAP therapy; however, gustatory function is not impaired in OSA patients.

Objective A new and unique methodology was developed to evaluate the association between periodic limb movements (PLMs) and nocturnal blood pressure (BP) excursions in patients with restless legs syndrome (RLS). Methods All data were collected at baseline of the ENCORE (Effects of Neupro on Cardiovascular Observations in Patients with Restless Legs Syndrome) study, a placebo-controlled polysomnographic study of rotigotine in patients with idiopathic RLS. Continuous beat-by-beat BP and heart rate assessments were performed during a full night of polysomnography. All BP elevations occurring with and without PLMs were systematically identified and analyzed. Results Patients ( n = 89) had a mean total of 508.9 ± 405.7 PLMs, 788.4 ± 261.9 systolic BP elevations, and 349.7 ± 242.9 diastolic BP elevations during the night. Higher time-adjusted frequencies of systolic BP elevations [mean difference (95% confidence interval, CI): 543.0 (487.2, I); p 0.0001] and diastolic BP elevations (205.8 (169.3, I); p 0.0001) were observed with PLMs than without PLMs. A peak in the frequency of PLM onset coincided with BP elevation onset. Conclusion Our methodology allowed the first evaluation of the total number of nocturnal PLM-associated BP elevations occurring in patients with RLS. Our data clearly indicate an interdependence between BP elevations and PLMs, and they have clinical relevance as BP variability is a potential cardiovascular risk factor.

This review article discusses various forms of sleep disorders associated with musculoskeletal diseases (MD). It presents the pathophysiology and interaction of sleep-related disorders and MD and summarizes clinical symptoms and therapies from a somnological perspective. BACKGROUND: A large number of patients suffering from MD report fragmented sleep with poor overall sleep quality. Sleep disorders often lead to increased symptoms such as daytime fatigue, depression, or increased pain intensity. In contrast, the perception of pain worsens the quality of sleep. Sleep is a complex regulation of hormonal and neuromodulatory influences to maintain regenerative processes and signal processing. Furthermore, interleukins (e.g., IL-6 and TNFα), messenger substances, or inflammatory markers (e.g., CRP) may have a regulatory influence on sleep. THERAPY: Sleep disorders in MD can often be treated with behavioral therapies or drug approaches. Another and very important influence is physical activity. In combination with training, regular physical activity can lead, for instance, to improved sleep quality, endurance performance, and reduced inflammation values. The change of lifestyle with regard to activity and nutrition is another key concept in the optimal therapy of patients with MD.

We performed a double-blind single-dose placebo/hypnotics crossover study randomized within groups to test the potential problems that a group of normal subjects, including subjects who snore, may face using hypnotic medications. Two benzodiazepine hypnotics--triazolam, 0.25 mg, and flunitrazepam, 2 mg tablets--were considered. Subjects were monitored with nocturnal polysomnography, including esophageal pressure (Pes) monitoring as a measure of respiratory efforts, and were given daytime performance tests. Results were analyzed for the total nocturnal sleep period and also by thirds of the night in consideration of the different half-lives of the studied drugs. Three specific respiratory variables were evaluated: mean breathing frequency for selected unit of time, "Delta Pes" (esophageal pressure at peak end-expiration minus Pes at peak end-inspiration) expressed in cm H2O, and the ratio of Delta Pes/Delta TI (inspiratory time), taken as an index of respiratory drive calculated for each respiratory cycle. There was no significant increase in either the respiratory disturbance index or the oxygen desaturation index (number of drops in arterial oxygen saturation of 4% or more per hour of sleep, as measured by pulse oximetry). There was a significant increase in mean breathing frequency with flunitrazepam compared with placebo, as well as a significantly larger percentage of time during sleep with Delta Pes above 10 cm H2O (taken as a cutoff point for normal respiratory effort) with both triazolam and flunitrazepam compared with placebo. These respiratory changes, even if significant, were minor but may become a liability in association with specific abnormalities.