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UNLABELLED: Twenty children, aged 4-9 years, underwent adeno/tonsillectomy because of unequivocal anamnestic nocturnal obstructive breathing. Preoperatively, apnea-hypopnea index was > 5 in 10 cases only, AI > 1 in 17. Nineteen children had signs of increased respiratory labour in movement recordings and inspiratory EMG-activity. Oxygen desaturation index was 0 in 7 children, and nadir SaO2 was > or = 90% in 10. Cephalometry and dentition study models initially revealed significant changes, chiefly lateral cross-bite (n = 11) and vertical growth direction of the mandible. Tonsillar size or duration of disease was not correlated with the severity of polysomnographic findings, nor were orthodontic variables. Symptoms disappeared promptly postoperatively. After one year, respiratory recordings were normalized or improved in the majority of children, and orthodontic variables normalized or improved in all children. CONCLUSION: Oximetry and airflow recordings may be normal in children who benefit from treatment of anamnestic nocturnal obstruction. Craniofacial deformities are common and improve significantly with surgical treatment of the airway obstruction.

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A local disturbance in the afferent nerves involved in the reflexogenic dilation of the upper airways (UAs) could contribute to the increased collapsibility seen in patients with obstructive sleep apnea (OSA). Laser Doppler perfusion monitoring, combined with electrical stimulation, is a method for investigating the afferent nerve regulation of the microcirculation. It was used in the mucosa of the soft palate in 35 patients with various degrees of UA obstruction and in 13 control subjects, all nonsmoking men. In a majority of snorers and patients with mild OSA, stimulation induced an exaggerated vasodilation, compared with controls. In contrast, in patients with severe OSA, the vasodilation was significantly reduced, compared with controls. These signs of disturbances in the microcirculation support the hypothesis of a local progressive afferent nerve lesion in heavy snorers with or without OSA.

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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.

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Habitual snoring precedes obstructive sleep apnea (OSA), but the pathophysiological mechanisms behind progression are still unclear. The patency of upper airways depends on a reflexogen mechanism reacting on negative intrapharyngeal pressure at inspiration, probably mediated by mucosal receptors, i.e., via afferent nerve endings. Such nerves contain a specific nerve protein, protein-gene product 9.5 (PGP 9.5) and in some cases substance P (SP) and calcitonin gene-related (CGRP). Biopsies of the soft palatial mucosa were obtained from non-smoking men ten OSA patients, 11 habitual snorers and 11 non-snoring controls. The specimens were immunohistochemically analyzed for PGP 9.5, SP and CGRP. As compared to controls, an increased number of PGP-, SP- and CGRP-immunoreactive nerves were demonstrated in the mucosa in 9/10 OSA patients and 4/11 snorers, in addition to varicose nerve endings in the papillae and epithelium. Using double staining methodology, it could be shown that SP- and CGRP-like immunoreactivities (LIs) often coexisted in these fibres, as did CGRP- and PGP 9.5-LIs. The increased density in sensory nerve terminals are interpreted to indicate an afferent nerve lesion. Our results support the hypothesis of a progressive neurogenic lesion as a contributory factor to the collapse of upper airways during sleep in OSA patients.

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The localization and production at the single cell level of 19 different human cytokines, IL-1 alpha, IL-1 beta, IL-1ra, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, TNF alpha, TNF beta, IFN gamma, GM-CSF, G-CSF, and TGF beta 1-3, were studied in cryopreserved tonsillar tissue using immunohistochemical staining. The cytokine producing cells, with the exception of IL-1 expressing cells, had a characteristic morphology due to the accumulation of cytokine onto the Golgi organelle. The production of each cytokine was localized to specific compartments in tonsillar tissue sections from children with tonsillar hypertrophy or recurrent tonsillitis in the resting state. Immunoregulatory cytokines such as IL-2, IL-3, IL-4, G-CSF, GM-CSF and TGF beta were produced in the extrafollicular area and entrapped on the cell membranes as well as in pudels in the extracellular matrix surrounding the producer cells. The dominating cytokines both in tissues from recurrent tonsillitis and tonsillar hypertrophy were GM-CSF, G-CSF, and TGF beta 1-3 which were synthezised predominantly in the reticular crypt site. IL-1 alpha, beta and IL-1ra, on the other hand, were localized to the surface and crypt epithelium and to scattered regions in the extrafollicular area. IL-2, IL-6, IFN gamma and IL-10 were found much more often in sections obtained from recurrent tonsillitis tissue compared with those from tonsillar hypertrophy. Reversely, an excessive production of IL-4 was noted in tonsillar hypertrophy compared with that in recurrent tonsillitis. Thus, concomitant production of multiple cytokines was evident with similarities but also differences in cytokine pattern between the two groups studied. The data suggest that T-cell mediated B-cell activation and differentiation take place in the extrafollicular area. Children with recurrent tonsillitis had a higher amount of B-cells and monocytes compared with children with tonsillar hypertrophy. However, the number of CD3, CD4, CD8 or cytoplasmic Ig-positive cells did not differ between the two groups.

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In children with recurrent tonsillitis there may be persistent antigen deposition in tonsil tissue. even between exacerbations. If so, upregulation of immunocompetent cells should occur continuously, in contrast to tonsil tissue from children with tonsillar hypertrophy. The cytokine pattern was studied in cell suspensions prepared from tonsils obtained from 12 children undergoing tonsillectomy. The study group comprised 6 children with recurrent tonsillitis and 6 who had a history of tonsillar hypertrophy causing sleep apnea. Cytokine-producing cells (IL-1alpha, IL-1beta, TNFalpha, IL-6, IL-8, IL-2, IFNgamma, TNFbeta, IL-10 and IL-4) were characterized at the single-cell level by use of cytokine-specific monoclonal antibodies and indirect immunofluorescence technique. A constitutive production of IL-1alpha, IL-1beta, TNFalpha, and IL-8 was found in both groups (10-300/10(5) cells). However, the frequency of spontaneous IL-2, IFNgamma, TNFalpha, IL-6 and IL-10 was consistently low (10 +/- 10 cells) in both groups. Following restimulation by T-cell receptor ligation, using immobilized anti-CD3 mAb, with concentrations chosen so that it did not activate resting cells, increased frequencies of TNFalpha, IL-6, IL-8, IL-2, IFNgamma, IL-4 and 1L-10 synthesizing cells were induced in the recurrent tonsillitis group. Significantly higher incidences of IL-1beta, IL-6 and IL-2 producing cells were found in the recurrent tonsillitis group (60-200/10(5) cells, p <0.05). Microbiological evaluation in the tonsil tissue could not reveal tiny differences between the studied groups regarding bacterial or viral pathogens. However, this does not exclude persistent increased intracellular deposition of microbial antigens as a possible explanation for the elevated incidence of IL-1beta, TNF-alpha, IL-6, IL-8, IL-2, IFNgamma, IL-10 and IL-4 expressing cells noticed in patients with recurrent tonsillitis.

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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.

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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.

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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.

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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.

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Fifty unselected consecutive patients with obstructive sleep apnea syndrome (OSAS) underwent uvulopalatopharyngoplasty (UPPP). The diagnosis was based on the patient's history and recording of respiration movements (Static Charge Sensitive Bed. SCSB) and oximetry, alone or combined with polysomnography. Renewed SCSB oximetry recordings were used to evaluate the success of the treatment. Six months postoperatively 40% of the patients were classified as non-responders, i.e. their oxygen desaturation indices (ODI) were reduced by less than 50% or were still above 20. The mean body mass index (BMI) was significantly higher in the non-responder group. A second recording with complete data was obtained in 45 patients after an average of 21 months. It was found that 9 patients who had been responders in the first postoperative recording had become non-responders. Only 18 of the patients with complete data could be verified as responders after 2 years. The patients who relapsed showed a significant increase in mean BMI between the first and second postoperative recordings compared to the patients who remained responders. There were no significant differences between responders and non-responders concerning age or preoperative severity of OSAS expressed as ODI, nadir SaO2 and percentage of obstructive periodic breathing. Of the non-responders, 47% in the first postoperative recording and 52% in the second reported complete recovery from excessive daytime sleepiness. This subjective improvement was not correlated to the objective results. The conclusions of this study are thus that one postoperative recording is not enough to estimate the outcome of UPPP and that statements of the patient's subjective recovery alone must not be used for this purpose.

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A simplified sleep apnea investigation consisting of combined oximetry and respiration movement monitoring was compared with conventional polysomnography. These two types of recordings were performed simultaneously during one night in 77 patients with suspected obstructive sleep apnea syndrome (OSAS). A static charge sensitive bed (SCSB) was used in the simplified recording because it provides a comfortable and reliable means of recording respiration movements. Periods of obstructive apneas gave a diamond-shaped periodic respiration movement pattern in the SCSB, usually accompanied by repetitive oxygen desaturations. The average number of desaturations greater than or equal to 4 percent per sleeping hour was termed the oxygen desaturation index (ODI) and compared with the apnea index (AI). In the whole population they were well correlated (p less than 0.0001, R2 = 0.41), but in individual cases there were considerable discrepancies. Patients with periodic respiration movements less than 18 percent of total sleeping time and ODI less than 2 never had AI greater than or equal to 5, whereas patients with periodic respiration greater than 45 percent and ODI greater than 6 always had AI greater than or equal to 5. Fifty-one of the 77 patients fulfilled these criteria. A bradycardia response to apneas was absent in 29 percent of patients with AI greater than or equal to 5. A combination of respiration movement and oximetry recording thus seems to give sufficient information to confirm or negate a diagnosis of OSAS in a majority of patients with clinical symptoms. In borderline patients, further investigations should be performed.

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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.

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During a one-year period, 82 consecutive patients seeking medical attention for facial palsy primarily of unknown etiology were examined for underlying Ixodes ricinus-borne borreliosis. Evidence of the infection was found in 16 (20%) of the patients, most of whom had cerebrospinal fluid findings indicating meningeal involvement. Among 9 children included in the study, borreliosis was found in 6 cases. Bilateral facial palsy occurred in 3 of the borrelia-infected patients, as compared with none of the patients without borreliosis. It is suggested that, in areas where the tick vector is present, borreliosis should be regularly sought in patients with facial palsy of otherwise unknown etiology. As regards the serological diagnosis, it is emphasized that normal borrelia antibody titres in serum and cerebrospinal fluid at the time of the first consultation do not exclude the infection. A careful serological follow-up of patients with facial palsy is therefore recommended in order not to miss an underlying borreliosis which, if allowed to go untreated, implies a risk of other organ involvement and a protracted course.

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