REBUTTAL FROM DRS. GUILLEMINAULT AND CHOWDHURI

	ARTICLE

TOP ARTICLE REFERENCES

Undoubtedly, there are misquotations of our published work in the outline presented by our colleague. The complete absence of publications on Medline until 1993, relating to nonsnoring, chronically tired individuals, underscores the heuristic value of our description of the syndrome. To date, patients with these symptoms have been dismissed as having major depression, idiopathic hypersomnolence, chronic fatigue syndrome, etc., clearly with important treatment ramifications.

Unfortunately, many have failed to pursue our lead of identifying the temporal relationship between a carefully defined respiratory event and a cortical response based on central EEG leads and more sophisticated techniques (1, 2). We now know that there exists a complex hierarchy of central nervous system responses, from the trigger of brainstem autonomic reflexes to the passage of the thalamic gate, to the reinforcement of sleep patterns before a cortical activation and arousal. However, many have focused, unnecessarily, on the task of merely counting the number of visually defined arousal patterns.

More importantly, instead of dwelling on semantics and dissecting out the diagnostic criteria, one must ask the right questions. The key questions are as follows:

• How does the central nervous system continuously adjust to changes in upper airway patency during different sleep stages?
• Is this adjustment an inherent attempt to overcome the negative consequences?
• Are there specific preconditions that will lead to an abnormal response during sleep? If so, how can these be preconditions be identified and the abnormal pathways be delineated?
• Finally, do the individual responses vary according to the genetic make-up?

To respond to these questions and to decipher the genotypical associations of sleep-disordered breathing we must first accurately identify the clinical variants. For example, we have identified craniofacial dysmorphia, related to a small jaw, in the family members of infants classified as having experienced an ALTE (acute life-threatening event), i.e., obstructed breathing during sleep, and have noted its possible association to a specific gene (3); hence, the importance of differentiating UARS from OSAS. We envision that the progressive subdivision of the different phenotypes will ultimately lead to the identification of the specific genotypes of sleep-disordered breathing.

	References

TOP ARTICLE REFERENCES

1. Guilleminault, C., Y. D. Kim, M. Horita, M. Tsutum, and R. Pelayo. 1999. Power spectral EEG findings in patients with obstructive sleep apnea and upper airway resistance syndromes. Electroencephalogr. Clin. Neurol 50(Suppl.): 109-112 .

2. Black, J., C. Guilleminault, I. Colrain, and O. Carillo. 2000. Upper airway resistance syndrome: Central EEG power and changes in breathing effort. Am. J. Respir. Crit. Care Med. (In press)

3. Guilleminault, C., R. Pelayo, D. Leger, and D. Philip. 1999. First degree relatives of ALTE children (abstract). Pediatr. Res 45: 1A .