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.

Fifty unselected consecutive patients with obstructive sleep apnea syndrome (OSAS) diagnosed by nocturnal recordings of respiration movements by a static charge sensitive bed (SCSB) and oximetry, alone or combined with polysomnography, were studied. Renewed SCSB-oximetry recordings evaluated treatment. Six months after surgery, 30 of 50 were classified as responders. Twenty-one months after surgery, 19 of 49 were responders. Patients who relapsed showed a significant increase in mean body mass index (BMI). Four years after surgery, 24 of 48 patients were responders. Preoperative BMI was significantly lower in the responder group. Subsequent treatment was required in 15 nonresponders. There was no correlation between patients' subjective improvement and objective results. The study resulted in the following conclusions: 1. The responder rate to UPPP in unselected patients is low. 2. Obesity and high indices of nocturnal respiratory disturbance are negative predictors. 3. The patients' subjective recovery alone must not be used for postoperative evaluation. 4. With regular follow-up and the use of the treatment alternatives available today, the majority of OSAS patients can receive effective treatment.

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The temperature thresholds for warmth and cold were determined on the oropharyngeal mucosa of 15 patients with obstructive sleep apnea syndrome (OSAS) and 15 age-matched nonsnoring control subjects. We found that six of the patients with OSAS were not able to detect either the upper (50 degrees C) or lower (25 degrees C) temperature limits of the test when recording from the tonsillar pillar, whereas all control subjects detected the temperature change within the measuring range. The OSAS patients showed a statistically significant higher threshold for warmth on the anterior tonsillar pillar, 46.8 degrees C (95% confidence interval 45.2-48.4) versus 42.5 degrees C (41.3-43.8) for the control subjects (p = 0.0006). The same was found on the tip of the tongue-40.1 degrees C (38.7-41.6) for OSAS patients and 38.2 degrees C (37.1-39.4) for the control subjects (p = 0.036). Determination of temperature thresholds on the skin is an established method of detecting a neuropathy. We speculate that patients with OSAS suffer from a neuropathy in the pharynx caused by prolonged and progressive trauma to the pharyngeal structures from vibration induced by snoring and/or stretching of the structures during apneas. A neuropathy may interfere with the normal stabilizing function of the pharyngeal muscles and with the local reflex mechanism preventing the upper airway from collapsing during inspiration. It is thus possible that snoring itself, by inducing a neuropathy in the pharynx, may contribute to the sequence of events that transform a snorer into a patient suffering from OSAS.

Fifty-six men who underwent uvulopalatopharyngoplasty (UPPP) because of habitual snoring without preoperative obstructive sleep apnea (OSA), according to respiratory sleep recordings, were interviewed concerning persistent snoring and excessive daytime sleepiness (EDS). Renewed recordings were made in 53 of them at a median time of 63 months postoperatively. Median preoperative oxygen desaturation index (ODI) was 0; the median postoperative index was 1. Median duration of the preoperative obstructive respiratory pattern was 8% of total sleeping time, and the median duration postoperatively was 17%. (Significant individual increases were P = .0005 and P = .004, respectively.) Six patients answered to OSA criteria postoperatively. Weight increases were significantly correlated to increases in both ODI and obstructive respiratory pattern and to persistent snoring. Preoperatively 51 of 56 patients reported EDS, and 73% of the patients were improved or cured. From snoring, 87% reported improvement or cure. No patient had any serious sequelae of UPPP. Uvulopalatopharyngoplasty is a safe and effective treatment for habitual snoring, but it does not give absolute protection from development of OSA.