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The purpose of this study was to examine the relationship between night-to-night variability and nightly duration of continuous positive airway pressure (CPAP) therapy over the first 9 weeks of treatment and to determine when patients begin to establish a nonadherent pattern of use. Data were analyzed from a study of daily CPAP use covertly monitored in 32 diagnosed patients with obstructive sleep apnea (OSA) using a microprocessor monitor encased in a CPAP machine. Patterns of CPAP use were bimodal, based on the frequency of nightly use. Approximately half the subjects were consistent users of CPAP, applying it > 90% of the nights for an average of 6.22 +/- 1.21 hours per night, while the other half comprised intermittent users who had a wide range of daily use averaging 3.45 +/- 1.94 hours per night on the nights CPAP was used. The percent of days skipped was significantly correlated with decreased nightly duration (rho = -0.73, p < 0.0001). Analysis of the night-to-night pattern of use revealed that the two groups differed significantly in the nightly duration of CPAP use by the fourth day of treatment (p = 0.001). Exploration of factors that potentially differentiate the two groups revealed no reliable predictors. However, intermittent users continued to report significantly greater OSA symptoms (snoring, snorting, and apnea) posttreatment, suggesting that they continued to experience sleep disordered breathing.

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Questionnaire data from patients presenting at three sleep disorders centers were used to develop and assess a screening tool for sleep apnea based on the reporting of the frequency of various symptoms of sleep apnea and other sleep disorders plus age, body mass index (BMI) and gender. Patients were not specifically referred for suspicion of sleep apnea. Separate factor analyses of survey responses from 658, 193 and 77 respondents from the first, second and third sites, respectively, each yielded four orthogonal factors, one of which accounted for all the questions concerned with the frequency of disordered breathing during sleep. The survey was shown to be reliable in a subset of patients from one of the sites (test-retest correlation = 0.92). Survey data were then compared to a clinical measure of sleep apnea (respiratory disturbance index) obtained from polysomnography. A multivariable apnea risk index including survey responses, age, gender and BMI was estimated using multiple logistic regression in a total sample of 427 respondents from two of the sites. Predictive ability was assessed using receiver operating characteristic (ROC) curves. The area under the ROC curve was 0.79 (p < 0.0001). For BMI alone, it was 0.73, and for an index measuring the self-report of the frequency of apnea symptoms, it was 0.70. The multivariable apnea risk index has potential utility in clinical settings.

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Recently, investigators demonstrated that acute sleep deprivation in healthy subjects results in significant periodic decrements in ventilation during recovery rapid-eye-movement (REM) sleep. The neural bases of such phenomena are unknown. The decrements in ventilation coincide with REM sleep-associated phasic activities, such as bursts of eye movements. The purpose of this study was to determine the effects of acute sleep deprivation on control of diaphragm activity during recovery REM sleep. In chronically implanted, naturally sleeping, unrestrained cats, we recorded the electroencephalogram, electrooculogram, pontogeniculooccipital waves, neck and diaphragmatic electromyograms, and the computed moving average of the diaphragm. Acute sleep deprivation resulted in an increase in REM sleep-associated phasic alterations in diaphragmatic control during recovery REM sleep. There was an increase in the percentage of bursts during recovery REM sleep with reduced inspiratory drive. Acute sleep deprivation resulted in a substantial increase in the number of brief pauses (fractionations) in diaphragmatic activity during recovery REM sleep. Respiratory timing was also affected by sleep deprivation, with a reduced expiratory time resulting in an increased duty cycle ratio. There was a significant increase in the percentage of bursts with decremented peak amplitude of the moving average of the diaphragm, a measure that correlates with tidal volume. Despite significant increases in respiratory-related phasic alterations, there were no parallel increases in excitatory phenomena, i.e., eye movements or pontogeniculooccipital waves. These results imply that respiratory control mechanisms in REM sleep are sensitive to the effects of prior sleep deprivation.

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Nasal continuous positive airway pressure (CPAP) has become the nonsurgical treatment of choice for obstructive sleep apnea syndrome (OSAS). Recent evidence suggests that intermittent use of CPAP by patients is more common than nightly compliance. To determine the consequences of intermittent CPAP use, in terms of a return of sleep-disordered breathing and daytime hypersomnolence, 15 OSAS subjects were evaluated at three times: (1) before CPAP treatment (pretreatment), (2) after 30 to 237 days posttreatment during a night of CPAP use (on CPAP), and (3) during a night without CPAP (off CPAP). Evaluations of sleep-disordered breathing and three domains of hypersomnolence, physiologic sleep tendency, subjective sleepiness, and performance, were accomplished with the respiratory disturbance index (RDI), multiple sleep latency test (MSLT), Stanford sleepiness scale (SSS), and psychomotor vigilance task (PVT), respectively. CPAP use was encouraged and monitored from pretreatment to post-treatment by daily diaries for most subjects and an electronic device for a subset of subjects. As expected, CPAP eliminated apneas and hypopneas, and following the on CPAP night, there were statistically significant improvements in objective measures of sleepiness (MSLT and PVT). Subjective measures of sleepiness and fatigue also showed improvement. Sleeping without CPAP for one night reversed virtually all of the sleep and daytime alertness gains derived from sleeping with CPAP. This occurred despite a statistically significant reduction in the RDI on the night off CPAP (M = 36.8, SD = 28.0 events/h) relative to the pretreatment night (M = 56.6, SD = 24.8 events/h), which may be due to a lessening of the edema of the upper airway following CPAP use.(ABSTRACT TRUNCATED AT 250 WORDS)

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Obstruction of the upper airway during sleep (OSAS) is widely treated by having patients self-administer nasal continuous positive airway pressure (CPAP). To obtain objective evidence of the patterns of CPAP use, information was gathered from two urban sites on 35 OSAS patients who were prescribed CPAP for a total of 3,743 days. Patients were given CPAP machines that contained a microprocessor and monitor that measured actual pressure at the mask for every minute of each 24-h day for an average of 106 days per patient. They were not aware of the monitor inside the CPAP machines. Monitor output was compared with patients' diagnostic status, pretreatment clinical and demographic characteristics, and follow-up self-reports of CPAP use, problems, side effects, and aspects of daytime fatigue and sleepiness. Patients attempted to use CPAP an average of 66 +/- 37% of the days monitored. When CPAP was used, the mean duration of use was 4.88 +/- 1.97 h. However, patients' reports of the duration of CPAP use overestimated actual use by 69 +/- 110 min (p < 0.002). Both frequency and duration of CPAP use in the first month reliably predicted use in the third month (p < 0.0001). Although the majority (60%) of patients claimed to use CPAP nightly, only 16 of 35 (46%) met criteria for regular use, defined by at least 4 h of CPAP administered on 70% of the days monitored. Relative to less regular users, these 16 patients had more years of education (p = 0.05), and were more likely to work in professional occupations.(ABSTRACT TRUNCATED AT 250 WORDS)

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Night-to-night variability of apneas on overnight polymnography exists in patients with documented obstructive sleep apnea (OSA). In this study, we evaluated the possibility that this variability may be severe enough to miss the diagnosis of OSA in patients clinically at risk for the disease. We prospectively studied 11 patients who were deemed on clinical grounds to have probable OSA, but had a negative result on overnight polysomnography. Six of the 11 patients were found to have a positive second study with a significant rise in the apnea/hypopnea index (AHI) from 3.1 +/- 1.0 to 19.8 +/- 4.7 (mean +/- SEM, p < 0.01). The cause of the negative first study in these patients is unclear, but it does not seem related to risk factor pattern, sleep architecture, or test interval. The change in AHI was not found to be rapid eye movement (REM)-dependent. This study demonstrates that a negative first-night study is insufficient to exclude OSA in patients with one or more clinical markers of the disease.

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Basic mechanisms of sleep-disordered breathing (SDB) during rapid-eye-movement sleep (REMS) have been little investigated, despite the fact that events are often more prolonged and SaO2 nadirs lower during REMS. We predicted that the mechanisms of SDB in REMS would be related to the normal phasic changes in respiratory control in that state, rather than to cyclic arousals or responses to hypoxia as postulated for non-REMS SDB. Recordings of the EMG of the diaphragm (DIA) and the sternohyoid (SH), an upper airway dilating muscle, were made in five English bulldogs during sleep. We found that, as predicted, SDB events were associated with phasic influences rather than with arousals or response to hypoxia. The onset of SDB was significantly related to suppression of drive to both the DIA (p less than 0.01) and the SH (p less than 0.01). The mean drive of the DIA was suppressed to 42% of normal and of the SH to 17% of normal; the suppression of the SH was significantly greater than that of the DIA (p less than 0.05). Events were associated with changes in respiratory muscle EMG patterns typical of phasic REMS (p less than 0.01 for each muscle). The occurrence and duration of events exhibited no clear pattern or relationship to arousal or SaO2. Rather, as would be expected of phenomena associated with phasic REMS, the onset and termination of events were unpredictable. The association of SDB in REMS with phasic REMS influences rather than arousal or hypoxia suggests new directions for therapeutic approaches.

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Simultaneous recordings of the diaphragmatic electromyogram (EMG) were made from two separate regions of the costal diaphragm in six normal cats. The diaphragmatic activities were always synchronous and the amplitudes and rates of rise were similar during slow-wave sleep. In contrast, during natural rapid-eye-movement (REM) sleep, different activity was often present in the two leads. These differences were in the time of onset and offset, as well as in the amplitude and spike patterns, and occurred in approximately 5-20% of the diaphragmatic bursts averaged over the entire REM sleep period. With respect to eye movement density, the rate of differential activation was higher during periods of high density (26%) than in the absence of eye movements (1%) in the four animals for which these data were available. Differential activation of portions of the costal diaphragm is apparently a normal event of REM sleep. This could result from descending state-specific phasic neuronal activity that bypasses the medullary respiratory generator. Differential activation of portions of the diaphragm could contribute to disordered ventilation during REM sleep.

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Muscle atonia is a feature of normal rapid-eye-movement sleep (REMS). The suppression of accessory respiratory muscle activity has been investigated and a role for sleep-disordered breathing hypothesized, but the suppression of diaphragmatic activity has rarely been considered. We hypothesized that the activity of the diaphragm was suppressed by an area of the dorsolateral pons during REMS. Lesions in this region have previously been shown to abolish the atonia of REMS. The diaphragmatic electromyogram (EMG) activity was analyzed in five naturally sleeping cats before and after pontine lesions leading to REMS without atonia. Although respiratory timing parameters were not altered by the lesion, the inspiratory rate of rise was significantly increased in all cats, and the brief pauses (40-100 ms) in the diaphragmatic EMG normally seen in REMS were virtually abolished. We conclude that the dorsolateral pons has a role in suppressing diaphragmatic activation during REMS. This suppression affects the average rate of rise of diaphragmatic activity and also leads to brief intermittent complete cessation of ongoing muscle activity. These decrements in diaphragm activity could jeopardize ventilation during REMS.

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Tonic inhibition of some respiratory muscles occurs as part of the generalized muscle atonia of rapid-eye-movement sleep (REMS). A second type of inhibition of the diaphragm during REMS, fractionations, consists of brief pauses in the diaphragmatic electromyogram (DIA EMG) in association with phasic events. Because motor inhibition can occur as part of the startle response, and the brain is highly activated during REMS, we hypothesized that the neural basis of the fractionations might be activation of a startle network. To test this hypothesis, tone bursts (100 dB, 20-ms duration at 15-s intervals) were applied to cats at a fixed inspiratory level in the DIA moving average during REMS, non-rapid-eye-movement sleep (NREMS), and wakefulness. Parallel sham studies (no tone applied) were obtained for each state. The response of the DIA EMG was averaged over 100 ms by using the tone pulse as a trigger, and the following parameters of the DIA EMG were measured: latency to peak and/or nadir, increment or decrement in activity, and duration of peak and/or nadir. After a tone, all five animals studied displayed a profound suppression of DIA activity during REMS (latency to nadir 42.4 +/- 10.0 ms, duration of suppression 35.9 +/- 17.6 ms). Similarly, DIA activity was suppressed in all cats during NREMS (latency to nadir 40.9 +/- 13.3 ms, duration 23.9 +/- 13.4 ms). An excitatory response was observed in only two cats during NREMS and wakefulness. The similarity of startle-induced DIA EMG pauses to spontaneous fractionations of DIA activity during REMS suggests that the latter result from activation of a central startle system.

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The effect of phasic eye movement activity on ventilation during rapid-eye-movement (REM) sleep was studied in seven healthy young adults by use of the respiratory inductive plethysmograph. Mean ventilation (VE) and ventilatory components during REM sleep were not significantly different from that seen in either stages 1-2 or 3-4 sleep. The percent of rib cage contribution to ventilation in REM sleep, 29.3 +/- 5.1%, was reduced compared with 54.4 +/- 5.8% in stage 1-2 and 52.2 +/- 4.3% in stage 3-4 sleep (P less than 0.005). When one separated breaths by the degree of associated phasic eye movement activity, it became apparent that breathing during REM sleep is very heterogeneous. Increasing eye movement activity was associated with inhibition of ventilation with a reduction in VE from 5.1 +/- 0.3 to 3.8 +/- 0.3 l/min. Tidal volume and frequency both fell, whereas inspiratory duration was unchanged. Compartmental ventilation was also affected, with the fall in the rib cage contribution from 37.8 +/- 6.4 to 15.3 +/- 5.6%. Chest wall and abdominal movement became more asynchronous as phasic-eye-movement activity increased and frank paradoxical breathing was seen.

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To establish a natural model of sleep-disordered breathing, we investigated respiration during wakefulness and sleep in the English bulldog. This breed is characterized by an abnormal upper airway anatomy, with enlargement of the soft palate and narrowing of the oropharynx. During sleep, the animals had disordered respiration and episodes of O2 desaturation. These were worst in rapid-eye-movement (REM) sleep, with most bulldogs having O2 saturations of less than 90% for prolonged durations. In contrast, control dogs never desaturated. In REM sleep, the bulldogs had episodes of both central and obstructive apnea, the latter being associated with paradoxical movements of the rib cage and abdomen. During wakefulness, the bulldogs were hypersomnolent as evidenced by a shortened sleep latency (mean of 12 min compared with greater than 150 min for controls). This animal model should facilitate studies of the natural history of the sleep apnea syndrome and its complications.

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While a number of recent reports have documented the changing clinical and radiographic spectrum of parenchymal tuberculosis, relatively little attention has been paid to changes in the patterns of pleural tuberculosis. We therefore reviewed the clinical, laboratory, and radiographic characteristics of 26 adult patients with tuberculous pleural effusions. We found that pleural tuberculosis has become a disease of older adults (median age, 56 years) and that 19 percent (5/26) of the cases were due to postprimary (reactivation) disease. This shift in age led to problems in diagnosis, since many of these older patients had underlying or coexisting disease that could have caused a pleural effusion. Both specimens of pleural fluid and pleural biopsy were useful in establishing the diagnosis. Examination of sputum was less helpful. All patients who were not anergic had positive cutaneous reactions to first-strength purified protein derivative of tuberculin. Lymphocytosis of the pleural fluid was not a uniform finding; only 62 percent of our patients had greater than 50 percent lymphocytes on their initial examinations of pleural fluid, and four patients had greater than 90 percent polymorphonuclear cells. All of the effusions were exudates, and four had glucose levels in the pleural fluid that were less than 30 mg/dl. Pleural tuberculosis is an important diagnostic consideration in adult or elderly patients with exudative pleural effusions.

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Respiration in rapid-eye-movement sleep (REMS) is known to be highly variable. The purpose of this study was to investigate the source of this variability and to determine which ordering principles remained operative in REM sleep. In unrestrained, naturally sleeping cats we recorded the electroencephalogram, electrooculogram, neck electromyogram, and diaphragmatic electromyogram (EMG) and computed its moving average (MAdi). As a reference, we first examined MAdi during "tonic" REMS, since breathing is fairly regular in this state. "Control" ranges for peak amplitude (PEMG), inspiratory time (TI), duration of postinspiratory inspiratory activity, expiratory time, and the calculated inspiratory slope (PEMG/TI) were determined by overlaying individual breath traces of the time course of MAdi during tonic REMS to form a composite tracing. Next, the time course of the EMG during individual breaths in slow-wave sleep (SWS) and a complete period of consecutive breaths in REMS (both tonic and phasic) were compared with this tonic REMS composite. The number of eye movements per breath was tabulated as an index of phasic activity. The inspiratory slopes during SWS and tonic REMS were similar. However, during phasic REMS, many breaths displayed either increases (excitation) or decreases (inhibition) in slope compared with the "typical" breaths seen in tonic REMS. The occurrence of these altered slopes increased with the frequency of phasic events. TI was inversely related to the slope of the EMG, which tended to minimize changes in PEMG.(ABSTRACT TRUNCATED AT 250 WORDS)

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Previously reported cases of pulmonary parenchymal amyloidosis were diagnosed by open lung biopsy or postmortem examination. We describe 3 patients who were found to have amyloid deposits within the lung parenchyma by flexible fiberoptic bronchoscopy. In each case, the diagnosis was suspected when a waxy eosinophilic substance was observed within the alveolar walls of transbronchial biopsy specimens stained with hematoxylin-eosin. When stained with Congo red and examined under polarized light, this amorphous material exhibited the apple-green birefringence characteristic of amyloid fibrils. We suggest that a diagnosis of pulmonary amyloidosis can be made by transbronchial biopsy provided the appropriate histologic stains are employed. Special stains for amyloid should be obtained whenever histologic sections from transbronchial biopsy specimens reveal amorphous eosinophilic material within the alveolar septa or within the walls of small vessels.

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