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Drs. Guilleminault and Davé are affiliated with the Stanford University Sleep Disorders Clinic.
Correspondence to: Christian Guilleminault, MD, BiolD, Stanford Sleep Clinic, Suite 3301, 401 Quarry Rd, Stanford, CA 94305; e-mail: cguil{at}stanford.edu
Snoring is probably the main reason that patients with sleep-disordered breathing (SDB) have been referred. Otolaryngologists often see these patients. Internists and pulmonary specialists have recognized an association between SDB and obesity. Historically, the first sleep and breathing studies were performed on very obese patients ("pickwickians") who had developed multiple cardiovascular complications.1 The majority of these patients were men. The presence of nonobese male SDB patients was emphasized thereafter, and the term obstructive sleep apnea syndrome (OSAS) was coined. The associated cardiovascular risks and repetitive episodes of nocturnal hypoxemia attracted widespread medical attention. Decreases in daytime performance and professional competence, mostly due to sleepiness, led these patients to accept unattractive treatments such as permanent tracheostomy and nasal continuous positive airway pressure. Not all subjects with SDB had the above-mentioned profile. By 1972, the association between SDB and chronic insomnia was recognized.2 But further studies of SDB have revealed different clinical presentations.
At birth, infants are obligatory nose breathers, and thus choanal atresia can be fatal. However, little attention has been given to chronic mouth breathing by adults. By the early 20th century, psychiatrists associated chronic abnormal nasal breathing with anxiety. However, psychiatrists today do not check nasal turbinates or the oropharyngeal anatomy of patients referred for mild or moderate anxiety trait or "functional somatic syndromes." Family practitioners often diagnose chronic fatigue syndrome before investigating an individual’s breathing during sleep.
Since its description, upper airway resistance syndrome (UARS) in adults should have attracted more attention. Several studies revealed that many patients who experienced UARS, including a large proportion of women, were unrecognized and untreated.3 The lack of recognition was in part related to the nonspecific complaints, the technology used in the sleep studies, and the erroneous idea that sleep apnea/hypopnea were only a health risk if the patient presented with hypoxemic events.
SDB affects an individual in many ways in addition to cardiovascular functioning, which is probably a symptom of the late stages of the disease. The astute clinician should be able to recognize the presence of abnormal breathing during sleep before the development of local, pharyngeal lesions that lead to repetitive airway obstruction during sleep.
Why some subjects present with UARS while others present with obstructive sleep apnea (OSA) is not yet completely understood. Histologic and electron microscopy investigations of patients with OSA show local pharyngeal lesions with evidence of polyneuropathy.4 5 Two-point discrimination tests show clear sensory defects in patients with OSA6 7 and no deficits in those with UARS.7 The results of the 2-point discrimination studies indicate that peripheral input, particularly from the oropharynx, is not transmitted to the CNS in the same way in OSA patients as in UARS patients and healthy individuals. In addition, OSA patients present significantly reduced vasodilation (monitored by laser Doppler perfusion) with electrical stimulation of peripheral nerve endings in the mucosa of the soft palate.5 Cortical response during wakefulness and non-rapid eye movement sleep has been measured with the rapid application of loads that are resistant to breathing. Awake OSAS patients present with a normal auditory evoked response and respiratory-related evoked potential (with reduced amplitude of only one of the respiratory-related evoked potential waves [N550]). However, during non-rapid eye movement sleep, despite a perfectly normal auditory evoked response, inspiratory occlusions led to a blunted cortical response.8
In agreement with the above findings, spectral analyses of the sleep EEG of healthy individuals, patients with UARS, and patients with OSAS have shown a similar dichotomy of results.9
Central leads on OSAS patients, compared to control subjects, present an important anomaly. They show a complete destructuring of sleep with a significant decrease in 
power, which often is considered an index of sleep homeostasis. Impairment is seen in other EEG bands without significant increases in the 
and ß bands.9
In opposition, UARS patients present a comparatively high continuous power in the and EEG bands. This increase in absolute power is seen in successive sleep cycles throughout the night. power, which may be related to the "need (or pressure) to sleep," does not seem to decline throughout the night as in healthy subjects. The pressure still exists at the end of the night in UARS subjects, despite a substantial amount of power in the sleep cycles during the night, which is a major difference compared to OSAS patients. The significant increase in power in UARS patients, which is not present in OSAS patients, suggests that the cortex is continuously challenged and is in an arousal status.
OSAS subjects do not respond well to occlusive respiratory stimuli during several successive breaths while asleep. This lack of adequate response leads to a decrease in tidal volume and the development of hypoxemia. The repetitive stimulation induced by successive occlusive breaths and the development of abnormal blood gas levels, which is a poor stimulus during sleep, eventually corrects the sleep-related problem. UARS subjects are able to correct their problem much more quickly, probably due to the appropriate processing of local sensory inputs but at the cost of continuous cortical arousal. In this issue of CHEST (see page 87), Gold et al use visual scoring to confirm the power spectrum analysis data reported on UARS. The usage of the cyclical alternating pattern scoring system10
can better confirm the increase in - sleep (which is better labeled - sleep).
A lot of confusion exists when the notion of arousal is discussed. Neurophysiologic studies on arousal should refer to the pioneering and fundamental work of Moruzzi.11 Sensory stimuli during wakefulness or sleep causes monosynaptic and polysynaptic reflexes at many levels of the CNS, including, for example, the spinal cord, medulla, pons, and upper brainstem. The response will differ depending on the recruitment triggered by the stimulation. The most efficient response involves the cortex. During sleep, the continuous good functioning of our vital organs shows that the CNS controls are maintained and that our subcortical structures integrate input. This information then is transmitted to structures that control the autonomic nervous system. A joint motor and autonomic adjustment is needed when polysynaptic reflexes are induced and an appropriate complex subcortical response is requested. Habituation to repetitive auditory stimulation has been demonstrated during sleep with absence of EEG arousal.12 A reinvestigation of the published data on auditory stimuli that did not cause arousals show that they caused autonomic activation and a change in heart rate. An autonomic nervous system response can be observed with or without motor response.
The lack of discrimination between CNS activation and autonomic responses (which are subcortical phenomena)11 and arousal (which is a cortical function) is an issue. Few studies have adequately addressed this physiologic dissociation. This is even more of a problem when devices have been reported to investigate autonomic arousal, which is a misnomer when studying autonomic activation. This also explains the important differences in sensitivity and specificity that are found in devices using autonomic indicators to find arousal.13 Corrections should be made by the analytic systems sold with these devices to try limiting the recognition of autonomic responses to those associated only with arousal.
UARS patients appear to present with a very different ability to respond to certain respiratory stimuli during sleep than OSA patients. The stimuli may lead to CNS activation, but very often it will lead to an EEG arousal. This difference in responses between UARS and OSA patients will lead to different clinical presentations. Gold et al document well that the clinical presentation may be unspecific in UARS patients, but the general practitioner should know the symptoms they outline. This syndrome is not associated with important upper airway histologic lesions and cardiovascular complications. In addition, not all women with UARS are chronic snorers. The method to be used to study these subjects during sleep has not been well-resolved, including Gold et al, who only studied airway collapsibility. And, we still do not know the natural history of UARS.
One may conceive, for example, that the sleep fragmentation induced by UARS may lead to less activity, weight increase, and complications associated with secondary obesity. But a recent randomized study14 on the treatment of insomnia associated with UARS also has indicated that waking up during the night may lead to anxiety that is related to sleep and to conditioned sleep onset and sleep maintenance insomnia. What wakes a person up is different from what keeps the person awake. UARS must be considered as a possible cause of somatic functional syndromes that may be as common in men as in women.15
References
This article has been cited by other articles:
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  M. Ekstedt, T. Akerstedt, and M. Soderstrom Microarousals During Sleep Are Associated With Increased Levels of Lipids, Cortisol, and Blood Pressure Psychosom Med, November 1, 2004; 66(6): 925 - 931. [Abstract] [Full Text] [PDF]
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