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Borreliosis is known to be a common cause of peripheral facial palsy in Stockholm and its vicinity. The aim of the present study was to investigate the frequency and characteristics of borreliosis among patients with peripheral facial palsy in different parts of Sweden. All serological tests were performed in one laboratory. Ten Swedish Ear Nose and Throat clinics participated in a prospective 1-year study of patients seeking medical attention for acute peripheral facial palsy. Twenty-eight (6%) out of totally 446 patients fulfilled the criteria for the diagnosis of borreliosis. The frequency varied between 1 and 16% and was highest along the southeast coast of Sweden whereas no case was reported from the northern part of the country. Borreliosis was more common among children with facial palsy than among adults. The infection occurred during all seasons although it appears to be less frequent during the spring months. Only a minority of the borrelial patients had a history of a preceding tick bite or erythema migrans. The fairly low overall frequency of this secondary stage of borreliosis in the study may be a result of better knowledge of the disease and earlier treatment of its early manifestations. In Sweden's endemic areas borreliosis is a common cause of peripheral facial palsy, and therefore all patients with facial palsy in these regions should be examined for borrelial infection.

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.

Patients with a peripheral facial palsy due to an underlying Ixodes-borne borreliosis often have cerebrospinal fluid findings indicating meningeal involvement. The aim of the present study was to identify signs of CNS involvement by means of brain-stem evoked response audiometry (BSER) in patients with a facial palsy due to borreliosis, as well as in patients with a facial palsy of unknown aetiology. Bell's palsy. Abnormalities in BSER were found to be significantly more common along the borrelial patients. Furthermore, a reversal of these abnormalities following treatment with benzyl-penicillin was found in the majority of patients with borreliosis. The results of the present study emphasize the importance of diagnosing and treating an underlying borreliosis in patients with a peripheral facial palsy.

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 with20%, and patients withor = 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.

Ten patients with obstructive sleep apnoea syndrome cured by uvulopalatopharyngoplasty were compared to nine patients considered as surgical failures, using cardiovascular reflex tests--Valsalva manoeuvre, respiratory sinus arrhythmia, isometric handgrip and head-up tilt. Two patients had signs of moderate vagal dysfunction, but no case of definite autonomic nervous dysfunction was diagnosed. The overall results indicated sympathetic overreactivity, positively correlated to oxygen desaturation indices and remaining after successful treatment. Four patients did not exhibit bradycardia during sleep apnoea. Two of them had decreased respiratory sinus arrhythmia when awake, but two had normal values. This implies a difference in vagal responsiveness between the awake and sleeping states, or that other factors besides vagus function influence the bradycardia response to apnoea. The group mean values were all within normal limits. There was no significant difference between the two groups in any test. Autonomic nervous dysfunction therefore does not seem to contribute to surgical failure, nor to occur with increased incidence among patients with primary obstructive sleep apnoea syndrome.