For patients with mild to moderate CTS who opt for conservative treatment, corticosteroids are of greater benefit.

Background The mechanisms contributing to worsening of obstructive sleep apnea (OSA) during rapid eye movement (REM) sleep have been minimally studied. Reduced upper-airway muscle tone may be an important contributor. Because respiratory events and the associated blood gas changes can influence genioglossus (GG) activity, we compared GG activity between OSA patients and control subjects during REM sleep using continuous positive airway pressure (CPAP) to minimize the influences of upper-airway resistance (RUA) and blood gas disturbances on GG activity. Methods Twenty subjects (10 female subjects), 12 healthy individuals, and 8 OSA patients, were studied overnight. Sleep staging, epiglottic pressure, minute ventilation, and GG electromyogram (GGEMG) were recorded. GGEMG was compared between REM sleep with (phasic REM) and without (tonic REM) eye movements, non-REM (NREM) sleep, and wakefulness. Results Breathing frequency increased from stable NREM, to tonic REM to phasic REM sleep, whereas tidal volume and GGEMG decreased (ie, peak GGEMG: 3.0 ± 0.7 vs 1.7 ± 0.4 vs 1.2 ± 0.3% max, respectively; p < 0.001). Reductions in GGEMG during REM sleep were not different between OSA patients and control subjects or between genders. Conclusions When RUA and blood gas disturbances are minimized by CPAP, genioglossal activity is reduced in a stepwise manner from stable NREM, to tonic REM to phasic REM sleep to a similar extent in OSA and healthy individuals of both genders. Thus, an inherent abnormality in GG neural control in OSA patients during REM sleep is unlikely to explain the increased upper-airway collapse in this sleep stage. Rather, a generalized reduction in GG activity during REM likely renders individuals who are highly reliant on upper-airway dilator muscles vulnerable to pharyngeal collapse during REM sleep.

Numerous studies have demonstrated upper-airway neuromuscular abnormalities during wakefulness in snorers and obstructive sleep apnea (OSA) patients. However, the functional role of sensorimotor impairment in OSA pathogenesis/disease progression and its potential effects on protective upper-airway reflexes, measures of respiratory sensory processing, and force characteristics remain unclear. This study aimed to gain physiological insight into the potential role of sensorimotor impairment in OSA pathogenesis/disease progression by comparing sensory processing properties (respiratory-related evoked potentials; RREP), functionally important protective reflexes (genioglossus and tensor palatini) across a range of negative pressures (brief pulses and entrained iron lung ventilation), and tongue force and time to task failure characteristics between 12 untreated OSA patients and 13 controls. We hypothesized that abnormalities in these measures would be present in OSA patients. Upper-airway reflexes (e.g., genioglossus onset latency, 20 ± 1 vs. 19 ± 2 ms, P = 0.82), early RREP components (e.g., P1 latency 25 ± 2 vs. 25 ± 1 ms, P = 0.78), and the slope of epiglottic pressure vs. genioglossus activity during iron lung ventilation (-0.68 ± 1.0 vs. -0.80 ± 2.0 cmH(2)O/%max, P = 0.59) were not different between patients and controls. Maximal tongue protrusion force was greater in OSA patients vs. controls (35 ± 2 vs. 27 ± 2 N, P < 0.01), but task failure occurred more rapidly (149 ± 24 vs. 254 ± 23 s, P < 0.01). Upper-airway protective reflexes across a range of negative pressures as measured by electromyography and the early P1 component of the RREP are preserved in OSA patients during wakefulness. Consistent with an adaptive training effect, tongue protrusion force is increased, not decreased, in untreated OSA patients. However, OSA patients may be vulnerable to fatigue of upper-airway dilator muscles, which could contribute to disease progression.

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