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LETTER TO THE EDITOR
Midlatency respiratory-related evoked potentials were measured during wakefulness by using a 60-electrode array placed over the cortical region of the scalp. We studied the responses evoked by 200-ms pressure pulses at -5 and -10 cmH2O applied at inspiratory onset and during control tests (no pressure applied) in 14 subjects with obstructive sleep apnea syndrome (OSAS) and 18 normal subjects. Wavelet decomposition was used to smooth and dissect the respiratory-related evoked potentials in frequency and time in eight frequency bands. After denoising, selected wavelet scales were used to reconstruct the respiratory-related evoked potentials, which were quantified by using global field power estimates. The time course of the global field power activity in OSAS subjects compared with normal subjects was significantly depressed in the period 55-70 ms poststimulus onset, a time when afferent traffic from upper airway receptors arrives in normal subjects. The reduced evoked response in subjects with OSAS suggests that these subjects receive less afferent input from upper airway mechanoreceptors. This may reflect reduced sensitivity of mechanoreceptors or reduced mechanoreceptor stimulation due to decreased upper airway compliance during wakefulness in OSAS.
To the Editor: Akay and colleagues (1) studied respiratory-related evoked potential (RREP) elicited by applying brief negative pressure pulses at the mouth in obstructive sleep apnea syndrome (OSAS) and normal subjects while awake. The evoked activity was quantified by using the global field power. The normalized global field power responses of 55-70 ms poststimulus, reflecting supralaryngeal mechanoreceptors activation, are significantly less in OSAS subjects. Supported by the evidence that OSAS subjects, also while awake, have a augmentated genioglossal activity (4) and related stiffening of the upper airway (UA), the authors suggest that decreased compliance of the UA accounts for the reduced output of supralaryngeal mechanoreceptors to a given pressure pulse. Although the results are original and interesting, we have some major remarks to address to the authors. All but one of the OSAS patients underwent nasal continous positive airway pressure (CPAP) treatment for varying lengths of time. CPAP treatment significantly improves both sleepiness and neurocognitive performance in compliant OSAS patients (3, 5). The possible roles of sleep, sleepiness, and sleep deprivation in the observed cortical activity have been largely discussed in the paper. However, any data about compliance to CPAP treatment, macro- and microstructure of sleep the night before the experimental session, or subjective sleepiness (i.e., Epworth score) at the time of RREP study have been shown. Therefore, all these potential confounding factors in the interpretation of the results were not taken in to account. It has been shown that CPAP treatment normalizes structural and functional characteristics of genioglossal activity in awake OSAS subjects (2). According to Carrera et al. (2), it is unlikely that compliance of the UA can be decreased, as suggested by Akay et al. (1), thus accounting for reduced mechanoreceptor stimulation. Furthermore, Akay et al. regressed weight, apnea-hypopnea index, and sleepiness measured at the time of polysomnographic diagnosis of OSAS against the normalized global field power responses of 55-70 ms obtained at many days to weeks after CPAP treatment had been started. Once again, the effect of CPAP treatment was not considered. Consistent with everything above, clinical and anatomofunctional findings of OSAS patients are completely different before and after a CPAP treatment. Although Akay and colleagues studied cortical activity by using a very elegant technique, they did not consider the relevant effect of CPAP treatment as a confounding factor. In conclusion, Akay et al. did not study RREP in OSAS patients but in CPAP-treated OSAS patients. Thus, if any physiopathological interpretations can be done of RREP changes in OSAS patients, "naif" (pretreatment) patients should be studied.
REFERENCES
A. Grippo
Unità di Neurofisiologia
Università di Firenze
Firenze 50134, Italy
E-mail: Agrippo{at}unifit.it
Drs. Sanna and Grippo noted that we studied patients suffering from OSAS only after they had been treated with CPAP for weeks to months. They felt that this would have allowed disease-related changes in airway compliance to revert to normal. This is possible. We stated that there were at least two possible reasons for the reduced afferent activity that we observed in these patients, and it is possible that another option, perhaps the one we suggested (reduced sensitivity of airway mechanoreceptors), is the basis for our observations.
Drs. Sanna and Grippo suggested that untreated OSAS subjects ought to be used for such experiments to permit cleaner pathophysiological interpretations of the results. In an ideal world, this would of course be desirable. Unfortunately, untreated OSAS patients are sleep deprived, and this would influence their very ability to perform the experiment without falling asleep. Surely, this would confound interpretation of the physiological findings. In an imperfect world, one is confronted with imperfect options and makes the best of them. So it is here: We are left knowing that upper airway (UA) afferent information available to our OSAS subjects is deficient, but we cannot discern exactly why, although we did conclude that reduced mechanoreceptor sensitivity seemed a more likely basis than reduced airway compliance for this finding. Whether these studies had been done in naive or treated OSAS patients is not likely to change the essential finding that OSAS subjects get deficient information about the state of their UA.
REFERENCES
James C. Leiter
Department of Physiology
Dartmouth Medical School
Lebanon, New Hampshire 03756
Metin Akay
Department of Physiology
Dartmouth Medical School
Lebanon, New Hampshire 03756
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