Sleep Breath 2002; 06(3): 152-154
DOI: 10.1055/s-2002-34316-2
Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Author's Response

Riccardo A. Stoohs[1].
  • Sleep Disorders Clinic and Research Center, Dortmund, Germany
Further Information

Publication History

Publication Date:
02 June 2004 (online)

The main purpose of our case report was to express the need for recording of leg movements for the appropriate diagnosis and differential diagnosis of PLMD (periodic limb movement disorder) and sleep-disordered breathing. We are reiterating this view especially in light of the letter of Dr. Eliasson and colleagues.

We acknowledge the fact that there are a number of patients with daytime symptoms presenting with the upper airway resistance syndrome, where leg movements are part of the respiratory activation as a result of flow limitation during sleep. In those cases, flow limitation can be diagnosed from pressure sensors as shown in Figure [1].

Our example of central hypoventilation following transient event from sleep is not in error, as suggested by Dr. Eliasson and colleagues. Commonly used recording techniques of respiratory activity during sleep are mostly qualitative in nature, and subtle changes will not be reflected. This was the reason why the pathophysiologic mechanisms of UARS (upper airway resistance syndrome) were not identified until the description of its mechanisms.[1] If quantitative or semiquantitative methods such as pneumotachogram or pressure recordings are used, this central hypoventilation in the absence of flow limitation, such as presented in our case report, can be noted in the absence of changes in qualitative respiratory effort. See Figure [3].

In the recording in Figure [3], flow measurements were made using semi-quantitative oro-nasal prong pressure recording. It can also be noted that no audible snoring is present in this case.

Thus, the example in our original case report was not in error, as qualitative effort signals will not appropriately reflect the subtle changes in flow amplitude. We maintain that in the case we presented, central hypoventilation was caused by periodic movements during sleep leading to transient events during sleep.

REFERENCE

  • 1a Stoohs R A, Guilleminault C. Snoring during NREM sleep: respiratory timing, esophageal pressure and EEG arousal.  Respir Physiol . 1991;  85 151-167