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Twenty consecutive patients (16 women and 4 men), with a mean age of 40 years, who were diagnosed and treated for myasthenia gravis were enrolled in a prospective investigation aimed at determining the amount of respiratory disturbance occurring during sleep while they received treatment. Patients were clinically evaluated to determine body mass index, presence of upper airway anatomical abnormalities, level of functional capacity and activity scored from 1 to 5, and presence of sleep-related complaints. They underwent daytime pulmonary function tests, determination of maximal static inspiratory pressure, measurement of transdiaphragmatic pressure, and measurement of arterial blood gas levels. Polygraphic monitoring during sleep, evaluating respiration and oxygen saturation, was also performed. Results indicated that in the studied population, all subjects had evidence of daytime diaphragmatic weakness as demonstrated by transdiaphragmatic pressure measurements, independent of the degree of autonomy and functional capacity and activity level reached. Older patients with moderately increased body mass index, abnormal total lung capacity, and abnormal daytime blood gas concentrations were the primary candidates for development of diaphragmatic sleep apneas and hypopneas, and oxygen desaturation of less than 90% during sleep. However, these clear indicators were not found in all subjects with sleep-related disordered breathing. Rapid-eye-movement sleep was the time of highest breathing vulnerability during sleep. Sleep-related complaints may also help identify subjects at risk for abnormal breathing during sleep, even when daytime functional activity is judged normal.

The hypothesis that, in neuromuscular and chest wall diseases, improvement in central respiratory drive explains the effects of night-time ventilation on diurnal gas exchanges was tested.The effects at 6 months, 1, 2 and 3 yrs of intermittent positive pressure ventilation (IPPV) on arterial blood gas tension, pulmonary function, muscle strength, sleep parameters, respiratory parameters during sleep and ventilatory response to CO 2 were evaluated in 16 consecutive patients with neuromuscular or chest wall disorders.As compared with baseline, after IPPV daytime arterial oxygen tension (Pa,O 2 ) increased (+2.3 kPa at peak effect) and arterial carbon dioxide tension (Pa,CO 2 ) and total bicarbonate decreased (-1.8 kPa and -5 mmol . L -1 , respectively) significantly; vital capacity, total lung capacity, maximal inspiratory and expiratory pressures and alveolar-arterial oxygen gradient did not change; the apnoea±hypopnoea index and the time spent with an arterial oxygen saturation (Sa,O 2 ) value <90% decreased (-24 and -101 min, respectively), sleep efficiency and mean Sa,O 2 increased (+16% and +5%, respectively); and ventilatory response to CO 2 increased (+4.56 L . min -1 . kPa -1 ) significantly. The reduction in Pa,CO 2 observed after IPPV correlated solely with the increase in the slope of ventilatory response to the CO 2 curve (r=-0.68, p=0.008).In neuromuscular or chest wall diseases, improvement of daytime hypoventilation with nocturnal intermittent positive pressure ventilation may represent an adaptation of the central chemoreceptors to the reduction of profound hypercapnia during sleep or reflect change in the quality of sleep. Eur Respir J 1999; 13: 157±162. Nocturnal intermittent positive pressure ventilation (IPPV) results in improved chronic hypoventilation during daytime spontaneous ventilation in patients with neuromuscular or chest-wall diseases [1±6] and chronic obstructive pulmonary disease (COPD) [7]. In COPD, this improvement has usually been attributed to improved respiratory muscle strength [8±11] (see however, ELLIOTT et al. [12]), rather than to an increase in ventilatory response to CO 2 [12]. Because numerous studies [1,6,13] provided evidence that in neuromuscular diseases nocturnal IPPV did not affect respiratory muscle strength, it appears that mechanisms for the improvement of diurnal arterial blood gases with nocturnal IPPV are different in these patients than in COPD patients. Therefore, an improvement in lung mechanics with IPPV in neuromuscular or chest wall diseases could account for an improvement in arterial blood gases. However, although slight increases in lung volumes have been reported [1,14], it seems more likely that nighttime IPPV has no significant effect on lung compliance [6,15]. The last possible mechanism may be an improvement in central respiratory drive. The explanation could be a reduction of an exposure of the central chemoreceptors to profound hypercapnia during sleep and a possible relief of sleep deprivation with nocturnal IPPV, which both would ...