Search

It is well accepted that obstructive sleep apnea (OSA) is not merely a simplistic anatomical imbalance of a small box (jaw) versus the over-crowding of tissue contents (namely the tonsils, tongue, palate, and lateral pharyngeal walls) within this container. Most sleep specialists agree that there is a strong complex neuro-physiological interconnected web of neurological and proprioceptor mechanism ongoing in this sleep disorder, perhaps simplified phenotypically as the PALM scale (Pcrit, arousal threshold, loop gain, and muscle responsiveness). What determines which patient would sleep through a prolonged and profound apneic event with a high arousal threshold and low muscle responsiveness versus another patient who would be easily aroused (low arousal threshold) and have frequent sleep fragmentations, no one has the answer. It has been shown that there is a complex relationship and physiological feedback mechanisms in the pathophysiology of upper airway collapse, cortical arousals, and teeth clenching in order to maintain airway patency. We are fairly clear that upper airway resistance syndrome (UARS) is the non-hypoxic sleep-disordered breathing that is closely related to cortical arousals, sleep fragmentation, psycho-somatic issues, excessive daytime sleepiness, neckaches, headaches, bruxism, and almost invariably nasal congestion.

In a large clinical sample, we tested the hypothesis that levels of sleepiness and fatigue among upper airway resistance syndrome (UARS) patients are correlated with levels of somatic arousal (SA; reflecting the sympathetic nervous system component of the stress response). We also tested the correlations of post-treatment change in these three parameters, and we extended the investigation to obstructive sleep apnea/hypopnea (OSA/H) patients. From 5 years of patient data, we obtained scores on the body sensation questionnaire (BSQ), measuring the level of SA, the fatigue severity scale (FSS), and Epworth sleepiness scale (ESS) for 152 consecutive UARS patients and 150 consecutive OSA/H patients. For each group, we correlated the FSS and ESS scores with the BSQ scores. Among the 45 UARS patients and 49 OSA/H patients treated with nasal CPAP who provided post-treatment data, we correlated change in FSS and ESS scores with change in BSQ scores. Scores on the BSQ, FSS, and ESS for UARS patients and OSA/H patients were comparable. In both UARS and OSA/H patients, both the FSS and ESS scores were positively correlated with the BSQ score. Nasal CPAP use decreased all three questionnaire scores in both patient groups. In the pooled data, changes in FSS were significantly correlated with changes in BSQ. Our findings confirm our preliminary observations that sleepiness and fatigue among UARS patients are correlated with their level of SA and suggest that the same is true for OSA/H patients. The decrease of SA following treatment suggests that SDB is a cause of SA among patients with UARS and OSA/H.

The purposes of this study are to investigate the usefulness of polygraphy (PG) in diagnosing obstructive sleep apnea (OSA) in sleepy/tired snorers compared to polysomnography (PSG) and, further, to search for suspected respiratory arousals in the PG. One hundred eighty-seven adults suffering from sleepiness/tiredness and snoring had undergone ambulant PG and were considered to be normal, using American Academy of Sleep Medicine’s 2007 hypopnea criteria A. After approximately 7 months, in-lab PSG was performed using hypopnea criteria B, where arousals are also recognized. Validated questionnaires (Hospital Anxiety and Depression Scale, self-rated general health) were answered. In a subgroup, the sensitivity and specificity were calculated for flow limitation index (FLI) and flattening index (FlatI) in PG compared with the respiratory distress index (RDI) in PSG. Despite the normal PG, at PSG, the median RDI was 11.0 (range, 0–89.1). One hundred sixty-eight out of one hundred seventy-eight (90 %) were found to have at least mild OSA and 119/187 (64 %) with moderate–severe OSA according to the RDI values. The sensitivity and specificity were low (

The aim of this study is to describe a distinctive respiratory pattern seen in subjects with inferior turbinate hypertrophy, nasal obstruction, and a polysomnogram-proven diagnosis of primary snoring or mild obstructive sleep apnea. These subjects demonstrated increased snoring with purely nasal breathing and alleviation of snoring with oral breathing. The study design is case series with chart review. The setting was a university-based tertiary care hospital.A retrospective chart review was performed for patients with complaints of nasal obstruction with associated inferior turbinate hypertrophy and a polysomnogram-proven diagnosis of mild obstructive sleep apnea or primary snoring. Demographic and polysomnography information were collected and analyzed. Snoring and airflow patterns were reviewed.Twenty-five subjects were identified as having met the inclusion and exclusion criteria on polysomnography for either primary snoring or mild obstructive sleep apnea with inferior turbinate hypertrophy and no other significant nasal deformity or abnormality. Seventeen (68 %) of these patients had polysomnograms which demonstrated snoring during nasal breathing and alleviation of snoring with oral breathing. Of the 17 who snored during nasal breathing, ten of the subjects were female and seven of the subjects were male. The mean age was 27 years (range 18 to 68 years). The mean apnea-hypopnea index was 2.3 events/h (range 0 to 9.7 events/h). The mean body mass index was 25 kg/m(2) (range 20 to 43 kg/m(2)).Our study describes a newly recognized pattern of snoring in patients with a polysomnogram-proven diagnosis of either primary snoring or mild obstructive sleep apnea. This pattern of breathing demonstrates patients who snore during nasal breathing even with known nasal obstruction present and subsequently have resolution or improvement of the snoring with oral breathing.

A test of the hypothesis that upper airway resistance syndrome (UARS) patients have an increased prevalence of inspiratory airflow limitation (IFL) during sleep compared to healthy controls. We compared inspiratory airflow dynamics during sleep between 12 UARS patients (nine females and three males) and 12 healthy controls matched for age, gender and obesity with maximal age limited at 45 years. A standard clinical polysomnogram (airflow measured with a nasal/oral pressure catheter) was performed to assess the impact of SDB on the participants’ natural sleep. A second full-night polysomnogram with a pneumotachograph and a supraglottic pressure catheter to measure airflow and effort was performed to compare the maximal inspiratory airflow and effort and the percentage of flow-limited breaths during supine, continuous stage 2 sleep between groups. During clinical polysomnography, UARS participants did not differ significantly from controls in sleep architecture or fragmentation. We observed a small difference in apnea hypopnea index between UARS participants and controls (1.6 ± 1.9 vs. 0.4 ± 0.3, respectively; p = 0.035). During supine, continuous stage 2 sleep, 64.2 % (35.8; mean (SD)) of UARS participants’ breaths were flow-limited compared with 34.0 % (39.3) of controls’ breaths (p = 0.06). The groups did not differ in maximal inspiratory airflow or inspiratory effort. Our findings indicate a less-than-robust difference in respiratory parameters during sleep between UARS patients and healthy controls and no difference in standard sleep parameters or sleep fragmentation. We consider a pathophysiology of UARS that incorporates these findings.

The objective of the study was to formulate a statistical model for postoperative apnea-hypopnea index (AHI) 3 and 12 months after multilevel surgery using the predictors preoperative AHI, body mass index (BMI) and age. The study design was a prospective cohort study. Data of 144 patients were collected prospectively 3 and 12 months after multilevel surgery for obstructive sleep apnea syndrome (OSAS) or upper airway resistance syndrome with excessive daytime sleepiness. The primary endpoint postoperative AHI and the secondary endpoint success according to the Sher criteria (postoperative AHI20 h and50% reduction of preoperative AHI) were modeled with multiple linear and logistic regression using the predictors preoperative AHI, BMI, age and the indicator whether the patient had undergone a tonsillectomy. Preoperative AHI and tonsillectomy had a highly significant positive influence on postoperative AHI after 3 months, whereas the influence of preoperative BMI was only marginally significant but numerically rather large. Age was not a significant decisive factor. The success according to the Sher criteria was highly significantly determined by the circumstance whether the patient had undergone a tonsillectomy, but not by the other predictors preoperative BMI or age. The responder rate with and without tonsillectomy was 58 and 19%, respectively. The odds ratio to be a responder if a tonsillectomy was conducted was 5.7. This study provides statistical models predicting postoperative AHI and success according to the Sher criteria after multilevel surgery for OSAS.

We aimed to investigate the prevalence of primary snoring (PS) and its association with neurocognitive impairments.Data from a community-based study in 1,114 primary school children were used to identify children who never (N = 410) or habitually snored (N = 114). In order to separate children with PS from those with upper airway resistance syndrome (UARS) or obstructive sleep apnoea (OSA), home polysomnography was conducted in all habitually snoring children. Neurocognitive impairments and poor school performance were compared between children who never snored, PS, and UARS/OSA.Polysomnography was successfully conducted in 92 habitual snorers. Of these, 69 and 23 had PS and UARS/OSA, respectively. Prevalence [95% confidence interval (95% CI)] of PS was 6.1% (4.5-7.7). Compared to children who had never snored, children with PS had more hyperactive (39% vs. 20%) and inattentive behaviour (33% vs. 11%), as well as poor school performance in mathematics (29% vs. 16%), science (23% vs. 12%), and spelling (33% vs. 20%; all P values0.05). PS was a significant risk factor (odds ratio; 95% CI) for hyperactive behaviour (2.8; 1.6-4.8), inattentive behaviour (4.4; 2.4-8.1), as well as daytime sleepiness (10.7; 4.0-28.4). PS was also an independent risk factor for poor school performance in mathematics (2.6; 1.2-5.8), science (3.3; 1.2-8.8), and spelling (2.5; 1.1-5.5). Odds ratios throughout were similar to the UARS/OSA group.Children with non-hypoxic, non-apnoeic PS may exhibit significant neurocognitive impairments. Consequences may be similar to those associated with UARS or OSA. If confirmed, PS is not "benign" and may require treatment.

The analysis of snoring sounds has been in focus for the past two decades. Conventional approaches by fast Fourier transformation face various limitations and demonstrate the necessity for alternative methods of investigation. Psychoacoustic analyses which are common for environmental noise analyses propose a potential approach. The present study investigates the psychoacoustic qualities (loudness, sharpness, roughness) of three different real snoring sounds (primary snoring, PS; Upper airway resistance syndrome, UARS; obstructive sleep apnea syndrome, OSAS) and their alterations under increasing, artificially created sound pressure levels (SPL) from 60-85 dB. PS and UARS were detected to obtain a greater loudness as well as a higher increase under increasing SPL than OSAS. The sharpness was higher in PS and UARS, remaining stable under rising SPL compared to OSAS. The intensities of roughness were at higher levels for PS compared to URAS and OSAS, with an increase of all snoring sounds under rising SPL. By merging the psychoacoustic qualities, an individual acoustic fingerprint can be created to differentiate the three types of snoring. A potential application is proposed for the analysis of snoring sounds during polysomnography as well as for an adequate evaluation of the annoyance by snoring sounds.

We report a young female with snoring and daytime sleepiness who exhibited frequent premature ventricular complexes (PVCs) primarily during non-rapid eye movement sleep. She was underweight and suspected to have respiratory effort-related arousal (RERA) based on polysomnographic data. The presence of autonomic instability and alternating conducting system provoked by repetitive markedly negative intrathoracic pressure was assumed to be precipitating PVCs. Follow-up polysomnography after oral appliance therapy showed reduced PVCs. The results suggest that a careful evaluation of polysomonographic data is warranted when RERA is suspected as an underlying mechanism for nocturnal PVCs even in non-obese patients.

Sleep-disordered breathing (SDB) and the associated symptom of excessive daytime sleepiness (EDS) in military personnel has influential consequences in both the garrison and the deployed environments. The maintenance of wakefulness test (MWT) is a daytime study used to evaluate the tendency to stay awake. We evaluated consecutive patients diagnosed with mild to moderate obstructive sleep apnea (OSA) and upper airway resistance syndrome (UARS) to provide an objective measure of their EDS using the MWT.All military personnel referred between February 2004 and March 2005 with a clinical evaluation suspicious for SDB were evaluated with an overnight polysomnography (PSG). After overnight PSG, military personnel with mild to moderate OSA and UARS were evaluated with a 40-min protocol MWT. Abnormal MWT was defined as sleep onset latency mean below 19.4 min (2 SD below the mean).Sixty-two military personnel met entry criteria. Fifty-nine were men. Nineteen patients (32%) were diagnosed with UARS with a mean respiratory disturbance index of 11/h (5-20/h). Forty-one (68%) of the military personnel had OSA with a mean apnea-hypopnea index of 12/h (5-29/h). As a collective group, the mean Epworth Sleepiness Scale was elevated at 13/24 (1-24). This subjective excessive sleepiness was assessed with the MWT test, which resulted in a group mean MWT sleep onset latency of 27 min (5-40 min). Eighteen soldiers (30% of the total patients) had abnormal MWTs [six patients (33.3%) with UARS and 12 (67%) with OSA].Military personnel with mild to moderate OSA and UARS often have abnormal MWTs and therefore have a pathological tendency to fall asleep. This EDS could pose a safety hazard in those personnel, military or civilian, who operate dangerous vehicles, machinery, or carry a firearm. Military personnel with untreated SDB are also at risk for the consequences of decreased mental alertness and decreased cognitive functioning due to daytime sleepiness.

Split-night polysomnography can both establish the diagnosis and titrate continuous positive airway pressure (CPAP) during a single study in patients with sleep-disordered breathing. We sought to determine if split-night polysomnography could be effectively used in upper airway resistance syndrome (UARS) without diminishing diagnostic accuracy or success of CPAP titration.Consecutive patients diagnosed with UARS were included. Split-night studies were performed in patients meeting predefined criteria. We compared data between those undergoing traditional and split-night polysomnography.We included 100 consecutive patients (41.2 +/- 7.4 years, 54% men). Forty-six underwent split-night polysomnography. Groups were similar at baseline. There were no differences in polysomnography or success rate of CPAP titration. Among those not undergoing split-night studies, the mean time between diagnostic polysomnography and CPAP titration was 71.9 +/- 49.0 days.Split-night polysomnography can be effectively utilized to diagnose UARS and initiate CPAP therapy. This practice can reduce the number of studies needed and obviate the inherent delay in initiating CPAP therapy.

To determine the effects of a nasal dilation appliance on 3-D nasopharyngeal airway patency. The sample comprised 187 adults (98 males, 89 females) with a history of sleep-disordered breathing. Acoustic rhinometry readings were taken from all patients before and after the intra-oral placement of a nasal dilation appliance (OASYS®). The mean left and right nasopharyngeal airways were reconstructed in 3-D, and the data from the right and left nostrils were subjected to principal components analysis (PCA) and finite-element scaling analysis (FESA). Comparing the pre- and post-treatment 3-D mean, left nasopharyngeal airways using PCA, the first two eigenvalues accounted for 96% of the total shape change, and statistical differences were found (p

The importance of quantitative changes in respiratory effort during routine polysomnographic investigation has been recognized since the description of the upper airway resistance syndrome. In clinical settings, oesophageal manometry is rerely conducted on a routine basis. We therefore developed a new technique for semiquantitative assessment of respiratory effort using diaphragmatic EMG (EMGdi) monitoring and tested its efficacy. Five patients with obstructive sleep apnoea syndrome and five subjects without sleep-disordered breathing were investigated in a private sleep disorders laboratory. EMGdi was sampled at 0.25 kHz and processed to a moving average. For each inspiratory effort during apnoea/hypopnoea and unobstructed breathing, we calculated maximum EMGdi and Pes. Data were normalized calculating the percentage difference between the first obstructed and each subsequent inspiratory effort during respiratory events and control periods. A total of 583 periods with unobstructed breathing and 477 apnoeas and hypopnoeas were scored to compare the evolution between Pes and EMGdi. There was a significant difference in the evolution of both respiratory parameters in unobstructed breathing versus apnoeas and hypopnoeas. EMGdi and Pes evolution corresponded in each condition investigated. In unobstructed periods, the increase of Pes averaged +2.6±24.1% versus −1.1±37.4% for EMGdi (P=0.616). In apnoeas and hypopnoeas, the respective values were +90.2±38.0% for Pes and +82.4±31.6% for EMGdi (P=0.7330). EMGdi can be used in lieu of oesophageal manometry to describe relative changes in respiratory effort under conditions of normal and obstructed breathing during sleep.

Obstructive sleep apnea (OSA) is a major public health problem in the US that afflicts at least 2% to 4% of middle-aged Americans and incurs an estimated annual cost of 3.4 billion dollars. At Stanford, we utilize a multispecialty team approach combining the expertise of sleep medicine specialists (adult and pediatric), maxillofacial and ear, nose, and throat surgeons, and orthodontists to determine the most appropriate therapy for complicated OSA patients. The major treatment modality for children with OSA is tonsillectomy and adenoidectomy with or without radiofrequency treatment of the nasal inferior turbinate. Children with craniofacial anomalies resulting in maxillary or mandibular insufficiency may benefit from palatal expansion or more invasive maxillary/mandibular surgery. Continuous positive airway pressure (PAP) therapy is used in children with OSA who are not surgical candidates or have failed surgery. As a last resort, tracheotomy may be used in patients with persistent or severe OSA who do not respond to other measures. The cornerstone of treatment in adults utilizes PAP: continuous PAP, bilevel PAP, or auto PAP. Treatment of nasal obstruction, appropriate titration, attention to mask-fit issues, desensitization for claustrophobia, use of heated humidification for nasal dryness and nasal pain with continuous PAP, patient education, regular follow-up, use of compliance software (in selected individuals), and referral to support groups (AWAKE) are measures that can improve patient compliance. Adjunctive treatment modalities include lifestyle/behavioral/pharmacologic measures. Oral appliances can be used in patients with symptomatic mild sleep apnea or upper airway resistance syndrome. Patients who are unwilling or unable to tolerate continuous PAP or who have obvious upper airway obstruction may benefit from surgery. Surgical success depends on appropriate patient selection, the procedure performed, and the experience of the surgeon. Phase I surgeries have a success rate of 50% to 60%, whereas phase II surgeries have a success rate greater than 90%.

The upper airway resistance syndrome (UARS) is associated with neurobehavioral morbidity in children. The diagnostic gold standard for UARS is esophageal manometry. However, this is invasive. Furthermore, upper airway obstructive events in sleeping children frequently terminate without visible electrocortical (EEG) arousal. The pulse transit time (PTT) is a noninvasive marker of blood pressure and, therefore, subcortical arousal. Blood pressure elevation, associated with respiratory arousal from sleep, results in a drop in the PTT. We hypothesized that: 1) the PTT is a more sensitive measure of respiratory arousal than EEG; and 2) the PTT arousal index can distinguish children with UARS from those with primary snoring. Polysomnography, including esophageal manometry and PTT, was measured prospectively in 24 symptomatic children and 10 normal controls. Apnea, hypopnea, and respiratory effort-related arousal events terminated in a PTT arousal 91%, 83%, and 80% of the time, and in an EEG arousal in 55%, 51%, and 43% (all p < 0.05), respectively. The PTT arousal index was significantly greater in children with UARS (6.8 events/h) than primary snoring (2.2 events/h) (p < 0.05). We conclude that, in children, PTT arousals are a more sensitive measure of obstructive events than visible EEG arousals.

Question of the Study This review focuses on nasal/oronasal cannulas (NOCs) used as flow sensors and their advantages and disadvantages especially in comparison with oronasal thermistors for diagnostics in sleep medicine. The significance of NOCs in the detection of the upper airway resistance syndrome (UARS) is discussed in comparison with other methods of measurement.

151 Sleep and Breathing, volume 6, number 3, 2002. Address for correspondence and reprint requests: Arn H. Eliasson, M.D., Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC 20307. 1Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC. Published by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. 1520-9512,p;2002,06,03,151,151,ftx,en;sbr00214x. In the case report by Dr. Stoohs and colleagues,1 the authors make the main point that recording and scoring of leg movements must be an integral part of polysomnogram evaluations. They reason that arousals and sleep fragmentation may be improperly assigned to respiratory events and periodic limb movement (PLM) would be missed all together. However, in Figure 2, their representative example appears to be in error. The authors denote central hypopnea following PLM associated with electroencephalogram (EEG) arousal, but there is no decrease in respiratory effort during the periods of hypopnea. The portions of two events recorded in Figure 2 are most appropriately interpreted as obstructive hypopneas followed by PLM and arousals. This is a pattern of sleep-disordered breathing commonly seen in our sleep center. We also see PLM caused by the sleep-disordered breathing termed upper airway resistance syndrome (UARS).2 We have discovered patients previously diagnosed with periodic limb movement disorder (PLMD), and ineffectively treated with medication for PLMD, who in fact have UARS verified by esophageal catheter manometry during overnight polysomnogram. Arousals, PLM, and sleep fragmentation have been clearly associated with UARS events.3 As shown in Figure 2 of Dr. Stoohs et al, some hypopneas do not produce desaturations as is also the case with respiratory events in UARS.4 Either Figure 2 is confirmatory of sleepdisordered breathing in Mr. M. W. or this recording was not a representative choice for demonstrating primary PLMD. A second issue in the case report involves the extensive neurological evaluation afforded this patient, including physical examination, daytime EEG, computed tomographic scan of the head, and nerve conduction studies. It is unclear why these studies followed an unrevealing neurologic exam in a man whose chief complaints were snoring, witnessed apneas, and intolerance to CPAP. We agree with the decision to discontinue both drug treatment and nasal CPAP. Dr. Stoohs and associates summarize their rationale very effectively by noting the patient’s lack of cardiovascular risk factors and normal subjective alertness. Is it possible that Mr. M. W. does have mild sleep-disordered breathing and UARS events that cause his PLM?

Custom-made mandibular advancement devices are an effective treatment option for snoring, upper airway resistance syndrome, and obstructive sleep apnea (OSA). Evidence-based data indicates their efficacy, and international sleep societies recommend oral appliance (OA) therapy for patients with sleep-related breathing disorders. The following position paper by the German Society of Dental Sleep Medicine (DGZS) is to guide the interdisciplinary team (sleep physician and sleep disorder dentist) in detail when to prescribe oral appliances. This position paper supports the responsible use of OA as an effective treatment option for patients with sleep-related breathing disorders. The paper advises of proper indication regarding OSA severity, body mass index (BMI), and dentition. It emphasizes the interdisciplinary approach of oral appliance therapy and suggests treatment under the guidance of dentists trained in dental sleep medicine.

Introduction We evaluated polysomnograms of chronic fatigue syndrome (CFS) patients with and without fibromyalgia to determine whether patients in either group had elevated rates of sleep-disturbed breathing (obstructive sleep apnea or upper airway resistance syndrome) or periodic leg movement disorder. We also determined whether feelings of unrefreshing sleep were associated with differences in sleep architecture from normal. Methods We compared sleep structures and subjective scores on visual analog scales for sleepiness and fatigue in CFS patients with or without coexisting fibromyalgia (n = 12 and 14, respectively) with 26 healthy subjects. None had current major depressive disorder, and all were studied at the same menstrual phase. Results CFS patients had significant differences in polysomnograpic findings from healthy controls and felt sleepier and more fatigued than controls after a night's sleep. CFS patients as a group had less total sleep time, lower sleep efficiency, and less rapid eye movement sleep than controls. A possible explanation for the unrefreshing quality of sleep in CFS patients was revealed by stratification of patients into those who reported more or less sleepiness after a night's sleep (a.m. sleepier or a.m. less sleepy, respectively). Those in the sleepier group reported that sleep did not improve their symptoms and had poorer sleep efficiencies and shorter runs of sleep than both controls and patients in the less sleepy group; patients in the less sleepy group reported reduced fatigue and pain after sleep and had relatively normal sleep structures. This difference in sleep effects was due primarily to a decrease in the length of periods of uninterrupted sleep in the a.m. sleepier group. Conclusion CFS patients had significant differences in polysomnographic findings from healthy controls and felt sleepier and more fatigued than controls after a night's sleep. This difference was due neither to diagnosable sleep disorders nor to coexisting fibromyalgia but primarily to a decrease in the length of periods of uninterrupted sleep in the patients with more sleepiness in the morning than on the night before. This sleep disruption may explain the overwhelming fatigue, report of unrefreshing sleep, and pain in this subgroup of patients.

Fibromyalgia pathophysiology is a labyrinth where "our understanding has grown from counting tender points to an evolving concept of subgroups and a countless variety of dysfunctional biochemical and metabolic interactions" [1]. Sleep disorders have been reported in fibromyalgia patients [2], including daytime somnolence and tiredness, and non-restorative and fragmented sleep with higher occurrence of arousals, often associated with breathing-related disturbances. Electroencephalogram findings exhibit alpha-delta sleep and a reduction of slow-wave sleep [2,3]. More sophisticated studies may identify upper airway resistance syndrome or obstructive sleep apnea-hypoapnea syndrome associated with increased risk for cardiovascular events [4]. Conflicting results have been reported on the prevalence of fibromyalgia observed in patients with sleep apnea; it was significantly increased versus a control group according to Germanowicz [4], but was not according to Plantamura and colleagues [3]. It is noteworthy that Moldofsky [5], 30 years ago, demonstrated the induction of a musculoskeletal pain syndrome by selective deep sleep deprivation. These findings allow a better understanding of the subtle mechanisms of fibromyalgia, including decreased levels of serotonin and tryptophan, increased tumor necrosing factor alpha and interleukin 6 [4] or reduced growth hormone secretion. Recently, Martinez and Cassol [2] defined sleep-disordered breathing as a missing link between fibromyalgia, metabolic syndrome and orthostatic intolerance. Rather than a missing link, it could be one of the many links – mainly biological but also biomechanical, such as myofascial trigger points – that probably complicate the diagnosis and management of functional diseases and chronic pain. These fibrolinks were roughly summarized in complex figures presented at the Myopain 2007 congress in Washington DC, and have recently been published [7]. This labyrinth concerns: neurotransmitters or hormones; 'nociceptive' or 'antinociceptive' receptors [7]; inflammatory cytokines and insulin resistance [7]; glucose metabolism and nitric oxide/endothelin imbalance as well as apoptotic pathways or reactive oxygen species; and genetic disorders or neuro-vegetative disturbances [2]. Whatsoever, the rediscovery of the sleep-disordered breathing link deserves further investigation, in order to avoid or limit the eternal return of anti-depressant and anticonvulsivant therapies, which are often deceiving and, with respect to some recent drugs, poorly tolerated by fibromyalgia patients.