The etiology of upper airway collapsibility in patients with snoring and obstructive sleep apnea (OSA) remains unclear. Local muscular abnormalities, including neurogenic lesions, could be a contributory factor. The aim of this study was to histologically evaluate the hypothesis of a progressive snorers disease. Biopsies of palatopharyngeal muscle were obtained from 21 patients with habitual snoring and different degrees of upper airway obstruction (10 patients with OSA) and 10 nonsnoring control subjects. Morphological abnormalities, including neurogenic signs (e.g., type grouping), were blindly quantified. The degree of abnormality was significantly increased in patients compared with control subjects. The individual score of abnormalities was significantly correlated to the percentage periodic obstructive breathing but not to oxygen desaturation index. Analyses of the individual fiber-size spectra demonstrated a significantly increased number of hypertrophied and/or atrophied fibers in patients compared with controls. The subjects were also divided into three groups according to their type of nocturnal breathing, i.e., nonsnorers, patients with < 20%, and patients with > or = 45% obstructive breathing. These groups correlated significantly with the degree of abnormality and pathological fiber-size spectra. In conclusion, these results support the hypothesis of a progressive local neurogenic lesion, caused by the trauma of snoring, as a possible contributory factor to upper airway collapsibility.
The results of this study provide insight into a number of concerns that stand in the way of success when it comes to the implementation and use of digital technology. If nurses are to adapt to the new policies and practices that accompany the current digitalised development in Swedish primary health care, the concept of a nurse's traditional work role needs to be amended in terms of the scope of work tasks and established views of traditional nursing. The study also highlights the need for more research to enable eHealth systems/services to be designed to fulfil multiple requirements. The digitised systems should be a tool for achieving good quality self-management support as well as giving the primary healthcare nurses adequate resources to support patients' self-management while still maintaining the values associated with person-centred care.
Muscle biopsies from the palatopharyngeal muscle of eight patients with obstructive sleep apnoea were performed during uvulopalatopharyngoplasty. Control biopsies were performed during tonsillectomy in seven control patients with no history of symptoms suggesting obstructive sleep apnoea. The diagnosis was based on the patient's history and a whole night recording of arterial oxygen saturation and respiration movements. The mean number of oxygen desaturations > 4% per sleeping hour was 39 (range 7-80) in patients with obstructive sleep apnoea. In the control patients the occurrence of muscle fibre type and size relation between type I and type II fibres were comparable to what is found in the quadriceps femoris muscle, but the mean size of the fibres was < 25% of what is found in limb muscles.All biopsies from patients with obstructive sleep apnoea showed abnormalities. Atrophy with a fascicular distribution, increased number of angulated atrophic fibres, a twin or multiple peak distribution of the fibre size spectra, and an abnormal distribution of fibre types in many muscle fascicles corresponding to "type grouping" all points to a neurogenic alteration. This neurogenic lesion may be a primary phenomenon or secondary to the trauma of repetitive and prolonged stretching of the pharyngeal structures during apnoeas. A disturbance of the function of the dilating muscles of the upper airway may be important in causing the abnormal airway collapse seen in obstructive sleep apnoea. The pathogenesis of obstructive sleep apnoea still remains obscure, and only fragmentary knowledge exists concerning the pathophysiology underlying the closure of the upper airway.' In normal subjects the activity of the dilating muscles of the upper airway is coordinated with the activity of the inspiratory muscles. This activity of the dilating muscles is considered vitally important in maintaining the patency of the airway during inspiration, and a dysfunction of these muscles may be of pathogenetic imortance in obstructive sleep apnoea.Some information is available on the macromorphology of the uvular muscle in patients with obstructive sleep apnoea2 but there has been no structural evaluation at the cellular or subcellular level.To determine whether histopathological changes were present in the pharyngeal muscles in patients with obstructive sleep apnoea, muscle biopsy specimens from the palatopharyngeal muscle were obtained in eight patients with obstructive sleep apnoea undergoing uvulopalatopharyngoplasty3 and in seven control patients undergoing tonsillectomy.
Material and methods
PATIENTSEight patients with obstructive sleep apnoea, all male and with a mean age of 43 (range 28-54) years, were examined. One patient had arterial hypertension and one had had a minor cerebral infarction but with no remaining symptoms. The diagnosis of obstructive sleep apnoea was based on the patient's history, clinical examination, and a whole night recording of arterial oxygen saturation (Biox 3700, earprobe) and of respiration and body mov...
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