OBJETIVE: To evaluate the effectiveness of adenotonsillectomy for the treatment of obstructive sleep apnea hypopnea syndrome (OSAHS) in children by respiratory polygraphy (RP). MATERIAL AND METHODS: Prospective study was conducted on children referred with clinical suspicion of OSAHS. A clinical history was taken and a general physical and ENT examination was performed on all patients. RP was performed before adenotonsillectomy and six months afterwards. Patients with craniofacial syndromes, neuromuscular disorders, and severe concomitant disease were excluded. RESULTS: We studied 150 children (67. 8% male), with a mean age of 3.74±1.80 years and a BMI of 41.70±31.75. A diagnosis of OSAHS was made if the total number of respiratory events, apneas and hypopneas, divided by the total study time (RDI) was > 4.6, using RP before undergoing adenotonsillectomy. The mean respiratory disturbance index (RDI) was 15.18±11.11, with 58.7% (88) of with severe OSAHS (RDI>10). There was a significant improvement in all clinical and polygraphic variables six months after adenotonsillectomy. The residual OSAHS was 14%. The preoperative RDI was significantly associated with persistent disease (P=.042). CONCLUSIONS: Respiratory polygraphy is useful for monitoring the efficacy of surgical treatment by adenotonsillectomy in children with OSAHS.
The exact underlying pathomechanism of central sleep apnea with Cheyne-Stokes respiration (CSA-CSR) is still unclear. Recent studies have demonstrated an association between cerebral white matter changes and CSA. A dysfunction of central respiratory control centers in the brainstem was suggested by some authors. Novel MR-imaging analysis tools now allow far more subtle assessment of microstructural cerebral changes. The aim of this study was to investigate whether and what severity of subtle structural cerebral changes could lead to CSA-CSR, and whether there is a specific pattern of neurodegenerative changes that cause CSR. Therefore, we examined patients with Fabry disease (FD), an inherited, lysosomal storage disease. White matter lesions are early and frequent findings in FD. Thus, FD can serve as a “model disease” of cerebral microangiopathy to study in more detail the impact of cerebral lesions on central sleep apnea.
- American journal of physiology. Regulatory, integrative and comparative physiology
- Published about 6 years ago
Unilateral sleep in marine mammals has been considered as a defence against airway obstruction, as a sentinel for pod maintenance, and as a thermoregulatory mechanism. Birds also show asymmetric sleep, probably to avoid predation. The variable function of asymmetric sleep suggests a general capability for independence between brain hemispheres. Patients with obstructive sleep apnea share similar problems with diving mammals, but their eventual sleep asymmetry received little attention. The present report shows that human sleep apnea patients also present temporary interhemispheric variations in dominance during sleep, with significant differences when comparing periods of open and closed airways. The Magnitude of Squared Coherence, an index of interhemispheric EEG interdependence in phase and amplitude rises in the delta EEG range during apneic episodes, while the Phase Lag Index, a measure of linear and non-linear interhemispheric phase synchrony, drops to zero. The L index, which measures generalized nonlinear EEG interhemispheric synchronization, increases during apneic events. Thus, the three indexes show significant and congruent changes in interhemispheric symmetry depending on the state of the airways. In conclusion, when confronted with a respiratory challenge, sleeping humans undergo small but significant breathing-related oscillations in interhemispheric dominance, similar to those observed in marine mammals. The evidence points to a relation between cetacean unihemispheric sleep and their respiratory challenges.
This paper reviews our current understanding of the long-term effects of obstructive sleep apnea (OSA) on cardiovascular autonomic function in humans, focusing directly on the knowledge derived from noninvasive measurements of heart rate, beat-to-beat blood pressure (BP), and respiration during wakefulness and sleep. While heart rate variability (HRV) as a means of autonomic assessment has become ubiquitous, there are serious limitations with the conventional time-domain and spectral methods of analysis. These shortcomings can be overcome with the application of a multivariate mathematical model that incorporates BP, respiration and other external factors as physiological sources of HRV. Using this approach, we have found that: (a) both respiratory-cardiac coupling and baroreflex dynamics are impaired in OSA; (b) continuous positive airway pressure therapy partially restores autonomic function; © baroreflex gain, which increases during sleep in normals, remains unchanged or decreases in OSA subjects; and (d) the autonomic changes that accompany transient arousal from NREM sleep in normals are largely absent in patients with OSA.
Upper airway stimulation (UAS) is a new approach to treat moderate-to-severe obstructive sleep apnea. Recently, 12-month data from the Stimulation Treatment for Apnea Reduction (STAR) trial were reported, evaluating the effectiveness of UAS in patients intolerant or non-adherent to continuous positive airway pressure therapy. Our objective was to assess the cost-effectiveness of UAS from a U.S. payer perspective.
Obstructive sleep apnea is associated with considerable health risks. Although continuous positive airway pressure (CPAP) can mitigate these risks, effectiveness can be reduced by inadequate adherence to treatment. We evaluated the clinical safety and effectiveness of upper-airway stimulation at 12 months for the treatment of moderate-to-severe obstructive sleep apnea.
To investigate the association of musculoskeletal pain with objectively-determined obstructive sleep apnea (OSA) and subjective sleep measures in a population-based sample.
Central sleep apnea occurring within the cyclic breathing pattern of Cheyne-Stokes respiration has been reported to be common in patients with heart failure.(1) During sleep, episodes of hyperventilation followed by a complete cessation (apnea) or decrease (hypopnea) in breathing are associated with oxyhemoglobin desaturations, arousals, and sympathetic nervous system activation that could be deleterious to the failing heart. Thus, suppression of central sleep apneas and hypopneas seemed to be a reasonable target in the treatment of patients with heart failure. Cowie et al.(2) now describe in the Journal the results of the SERVE-HF (Treatment of Sleep-Disordered Breathing with Predominant Central . . .
The objective of this study is to determine whether obstructive sleep apnea (OSA) is associated with reduced fetal growth, and whether nocturnal oxygen desaturation precipitates acute fetal heart rate changes.
Obstructive sleep apnea (OSA) is the most common clinically significant breathing abnormality during sleep. It is highly prevalent among patients with atrial fibrillation (AF), and it promotes arrhythmogenesis and impairs treatment efficacy.