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Biomedical subjects

John Trinder

Publications and source records attributed to John Trinder.

At least 19 recordsLinked to original sources
PubMed2006

The impact of slow wave sleep proximity on evoked K-complex generation.

During human stage 2 non-rapid eye movement (NREM) sleep, spontaneous K-complexes are more likely to occur prior to transitions to stage 3 or stage 4 sleep (referred to as slow wave sleep or SWS) compared to transitions to REM sleep, suggesting that the K-complex may be the 'forerunner' of SWS. The present study investigated the impact of SWS or REM sleep proximity on the probability of evoking a K-complex (pKC) during stage 2 and on components of the NREM sleep averaged evoked potential. Ten subjects spent three nights in the laboratory. On either the second or third night tones were presented continuously during sleep. Evoked K-complexes and sleep-evoked potentials were assessed for the 10 min of stage 2 prior to SWS (SWS-10) or REM (REM-10) sleep episodes as well as for all of SWS. pKC did not differ between SWS-10 (0.88) and SWS (0.91) but was significantly larger in SWS-10 than REM-10 (0.63). Amplitude effects were seen for the P2, N350, P900 NREM sleep-evoked potential components but not for the K-complex related N550. In each case where amplitude effects were found, SWS-10 was larger than REM-10. No latency differences were seen between conditions for the earlier components (P2, N350) however, both N550 and P900 were significantly shorter during SWS-10 compared to REM-10. These results are consistent with previous spontaneous K-complex studies and are supportive of a relationship between the K-complex and delta activity. They also indicate that stage 2 may consist of a continuum of microstates between SWS and REM sleep that are indicative of different brain stem, diecephalic and cortical patterns of activation.

Acoustic Stimulation↗
PubMed2006

The cardiorespiratory activation response at an arousal from sleep is independent of the level of CO(2).

Arousal from sleep is associated with transient cardiorespiratory activation. Traditionally, this response has been understood to be a consequence of state-dependent changes in the homeostatic control of ventilation. The hypothesis predicts that the magnitude of ventilatory and cardiac responses at an arousal will be a function of the intensity of concurrent respiratory stimuli (primarily PCO(2)). Alternatively, it has been proposed that increased cardiorespiratory activity is due to reflex activation. This hypothesis predicts that the magnitude of the cardiorespiratory response will be independent of respiratory stimuli. To compare these hypotheses we measured minute ventilation (V(i)), heart rate (HR) and blood pressure (BP) during wakefulness and stage 2 sleep, while manipulating P(et)CO(2). Further, we assessed the magnitude of the response of these variables to an arousal from sleep at the various levels of P(et)CO(2). The subjects were male aged 18-25 years. P(et)CO(2) was manipulated by clamping it at four levels during wakefulness [wake eucapnic, sleep eucapnic (Low), and sleep eucapnic +3 mmHg (Medium) and +6 mmHg (High)] and three levels during sleep (Low, Medium and High). The average number of determinations for each subject at each level was 14 during wakefulness and 25 during sleep. Arousals were required to meet American Sleep Disorders Association criteria and were without body movement. The results indicated that average increases in V(i), HR and BP at arousal from sleep did not significantly differ as a function of the level of P(et)CO(2) present at the time of the arousal (all P > 0.05). Further, the magnitude of the ventilatory response to an arousal was significantly less than the values predicted by the homeostatic hypothesis (P < 0.05). We conclude that, in normal subjects, the cardiorespiratory response to an arousal from sleep is not because of a homeostatic response, but of a reflex activation.

Adolescent↗
PubMed2005

Subjective and predicted sleepiness while driving in young adults.

Sleepiness is a significant contributor to car crashes and sleepiness related crashes have higher mortality and morbidity than other crashes. Young adult drivers are at particular risk for sleepiness related car crashes. It has been suggested that this is because young adults are typically sleepier than older adults because of chronic sleep loss, and more often drive at times of increased risk of acute sleepiness. This prospective study aimed to determine the relationship between predicted and perceived sleepiness while driving in 47 young-adult drivers over a 4-week period. Sleepiness levels were predicted by a model incorporating known circadian and sleep factors influencing alertness, and compared to subjective ratings of sleepiness during 2518 driving episodes. Results suggested that young drivers frequently drive while at risk of crashing, at times of predicted sleepiness (>7% of episodes) and at times they felt themselves to be sleepy (>23% of episodes). A significant relationship was found between perceived and predicted estimates of sleepiness. However, the participants nonetheless drove at these times. The results of this study may help preventative programs to specifically target factors leading to increased sleepiness when driving (particularly time of day), and to focus interventions to stop young adults from driving when they feel sleepy.

Accidents, Traffic↗
PubMed2005

The effect of sleep onset on upper airway muscle activity in patients with sleep apnoea versus controls.

Pharyngeal dilator muscles are important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that during wakefulness, the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) is greater in patients with OSA compared with controls. Further, EMG activity decreases at sleep onset, and the decrement is greater in apnoea patients than in healthy controls. In addition, it is known that the prevalence of OSA is greater in middle-aged compared with younger men. Thus, we had two goals in this study. First we compared upper airway muscle activity between young and middle-aged healthy men compared with men with OSA. We also explored the mechanisms responsible for the decrement in muscle activity at sleep onset in these groups. We investigated muscle activity, ventilation , and upper airway resistance (UAR) during wakefulness and sleep onset (transition from alpha to EEG activity) in all three groups. Measurements were obtained during basal breathing (BB) and nasal continuous positive airway pressure (CPAP) was applied to reduce negative pressure-mediated muscle activation). We found that during wakefulness there was a gradation of GGEMG and UAR (younger < older < OSA) and that muscle activity was reduced by the application of nasal CPAP (to a greater degree in the OSA patients). Although CPAP eliminated differences in UAR during wakefulness and sleep, GGEMG remained greater in the OSA patients. During sleep onset, a greater initial fall in GGEMG was seen in the OSA patients followed by subsequent muscle recruitment in the third to fifth breaths following the alpha to transition. On the CPAP night, and GGEMG still fell further in the OSA patients compared with control subjects. CPAP prevented the rise in UAR at sleep onset along with the associated recruitment in GGEMG. Differences in TPEMG among the groups were not significant. These data suggest that the middle-aged men had upper airway function midway between that of young normal men and the abnormal airway of those with OSA. Furthermore it suggests that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefulness' stimulus, rather than to loss of responsiveness to negative pressure, and that this wakefulness stimulus may be greater in the OSA patient than in healthy controls.

Adolescent↗
PubMed2004

Postural effects on pharyngeal protective reflex mechanisms.

STUDY OBJECTIVES: Pharyngeal muscle dilators are important in obstructive sleep apnea pathogenesis because the failure of protective reflexes involving these muscles yields pharyngeal collapse. Conflicting results exist in the literature regarding the responsiveness of these muscles during stable non-rapid eye movement sleep. However, variations in posture in previous studies may have influenced these findings. We hypothesized that tongue protruder muscles are maximally responsive to negative pressure pulses during supine sleep, when posterior tongue displacement yields pharyngeal occlusion. DESIGN: We studied all subjects in the supine and lateral postures during wakefulness and stable non-rapid eye movement sleep by measuring genioglossus and tensor palatini electromyograms during basal breathing and following negative pressure pulses. SETTING: Upper-airway physiology laboratory of Sleep Medicine Division, Brigham and Women's Hospital. SUBJECTS/PARTICIPANTS: 17 normal subjects. MEASUREMENTS AND RESULTS: We observed an increase in genioglossal responsiveness to negative pressure pulses in sleep as compared to wakefulness in supine subjects (3.9 percentage of maximum [%max] +/- 1.1 vs 4.4 %max +/- 1.0) but a decrease in the lateral decubitus position (4.1 %max +/- 1.0 vs 1.5 %max +/- 0.4), the interaction effect being significant. Despite this augmented reflex, collapsibility, as measured during negative pressure pulses, increased more while subjects were in the supine position as compared with the lateral decubitus position. While the interaction between wake-sleep state and position was also significant for the tensor palatini, the effect was weaker than for genioglossus, although, for tensor palatini, baseline activity was markedly reduced during non-rapid eye movement sleep as compared with wakefulness. CONCLUSION: We conclude that body posture does have an important impact on genioglossal responsiveness to negative pressure pulses during non-rapid eye movement sleep. We speculate that this mechanism works to prevent pharyngeal occlusion when the upper airway is most vulnerable to collapse eg, during supine sleep.

Adult↗
PubMed2004

Evoked K-complex generation: the impact of sleep spindles and age.

OBJECTIVE: It has been proposed that spindles and spontaneous K-complexes reflect two sides of a coin, with the spindle reflecting an inhibitory microstate and the K-complex reflecting an excitatory or aroused microstate [Physiol Behav 1993;54(4):795]. This hypothesis predicts that the presence of a sleep spindle at the time of stimulus presentation would decrease the likelihood of a K-complex being elicited by that stimulus. The present study sought to test this hypothesis in young and elderly subjects. METHODS: Ten young and 7 elderly adults who were neurologically healthy and free from medications spent one night in the sleep laboratory. EEG was recorded from 6 gold plate electrodes (Fz, FCz, Cz, CPz, Pz and O2) referenced to A1+A2. Tone clicks (1000 Hz) at 80 dB above measured awake detection thresholds were presented binaurally either during a spindle (SP+) or in the absence of a spindle (SP-). This was achieved by viewing a central EEG channel filtered to pass only the frequencies between 12 and 14 Hz. Trials were further classified based on whether (KC+) or not (KC-) they produced a K-complex. K-Complex probability and the amplitude and latency of the N550 component of the averaged evoked potential for KC+ trials were assessed using a two-way analysis of variance with main effects of age and spindle presence/absence. RESULTS: There were significant reductions in K-complex probability and N550 amplitude and a significant increase in N550 latency, as a function of age. However, no variable displayed a significant effect of spindle presence/absence, or an age x spindle interaction effect. CONCLUSIONS: The data failed to support the hypothesis that sleep spindles are antagonistic to the production of K-complexes, both in terms of the likelihood of K-complexes being elicited or in their amplitude when elicited (N550). The absence of spindle effects on K-complex generation argues against them being two sides of a coin and supports the notion of K-complexes having an extra-thalamic or non-specific generation mechanism.

Acoustic Stimulation↗
PubMed2004

The impact of smoking cessation on objective and subjective markers of sleep: review, synthesis, and recommendations.

Sleep disturbance is commonly reported as a prominent subjective symptom by quitting smokers. However, little research on this issue has used objective measures of sleep quality. Previous research has relied mainly on retrospective report of sleep disturbance, with few studies investigating sleep during the initial period after quitting tobacco use. Studies that have used objective measurements suggest that sleep fragmentation is a common occurrence during the withdrawal period. In sleep medicine, sleep disturbance is viewed as a consequence of frequent arousals and is now considered to have particularly deleterious daytime consequences, including sleepiness and dysphoric mood. Recent work also indicates that such awakenings affect the cardiovascular system by providing repetitive bursts of sympathetic nervous system activation, possibly contributing to elevated levels of cardiovascular and cerebrovascular morbidity. Pharmacological treatments designed to facilitate smoking cessation are ineffective for sustained abstinence in many smokers, which may be related to sleep disturbance. Indeed, preliminary evidence suggests that the administration of nicotine replacement therapy (NRT) or bupropion can result in disrupted sleep, particularly in women. However, to better understand the role that nicotine withdrawal and bupropion or NRT treatment, independently and in combination, might play in sleep disturbance, it is necessary to develop a better understanding of the nature of the sleep disturbance than can be provided by self-report. This is particularly important for the development of treatment approaches targeted to ameliorate sleep disruption as part of an overall smoking cessation strategy. The present review seeks to report the current state of knowledge based on extant findings and argues for the need to conduct more detailed polysomnographic investigations of the potentially vicious cycle of smoking cessation leading to sleep disturbances that may prove iatrogenic to sustained cessation.

Administration, Cutaneous↗
PubMed2004

Protocolized weaning from mechanical ventilation: ICU physicians' views.

BACKGROUND: The use of protocols during weaning from mechanical ventilation is uncommon in the UK, despite research pointing to their potential benefits. This may be because the research evidence is considered not to apply in different settings. Intensive care unit consultant physicians are the major decision-makers in weaning in the UK and any attempt to introduce protocolized weaning will require consideration of their views. AIM: The aim of this paper is to report a study exploring intensive care physicians' views on (i) weaning from mechanical ventilation, (ii) the utility of weaning protocols and (iii) nurses' roles in the weaning process. A specific goal was to identify potential aids and barriers to developing weaning protocols and their introduction into clinical practice. METHODS: Qualitative interviews were conducted with a purposive sample of 10 consultant physicians in two intensive care units in Northern Ireland and subjected to content analysis. FINDINGS: The primary themes identified were (i) information required for weaning decisions and clinical judgement, (ii) professional boundaries, (iii) protocol issues and (iv) timing of weaning. Three types of information were deemed to be required for weaning decisions - empirical objective, empirical subjective and abstract - and interviewees considered that it would be challenging to incorporate all into a protocol. They were divided on whether protocols were useful when nursing experience was limited. Some groups of patients were thought more suitable than others for protocolized weaning. CONCLUSIONS: Although local physicians were supportive in theory, introduction of protocolized weaning is likely to be difficult because of the breadth of information required for successful decision-making. Consultant views in this study were not consistent with American findings that physicians' caution may unnecessarily prolong weaning.

Attitude of Health Personnel↗
PubMed2003

The influence of lung volume on pharyngeal mechanics, collapsibility, and genioglossus muscle activation during sleep.

STUDY OBJECTIVES: Previous studies in both awake and sleeping humans have demonstrated that lung-volume changes substantially affect upper-airway size and pharyngeal resistance and, thus, may influence pharyngeal patency. We sought to systematically investigate the isolated effects of lung-volume changes on pharyngeal collapsibility and mechanics and genioglossus muscle activation during stable non-rapid eye movement sleep. We hypothesized that lower lung volumes would lead to increased pharyngeal collapsibility, airflow resistance, and, in compensation, augmented genioglossus muscle activation. DESIGN: Nineteen normal individuals (age, 30.4 +/- 0.5 years; body mass index: 24.5 +/- 0.4 kg/m2) were studied during stable non-rapid eye movement sleep in a rigid head-out shell equipped with a variable positive/negative pressure attachment for manipulations of extrathoracic pressure and, thus, lung volume. SETTING: Sleep physiology laboratory. PARTICIPANTS: Normal healthy volunteers. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: We measured change in end-expiratory lung volume (EELV) (magnetometers), genioglossus electromyogram (GGEMG) (intramuscular electrodes), pharyngeal pressure, and collapsibility of the pharynx in response to a brief pulse of negative pressure (-8 to -15 cm H2O) under the following conditions: (1) baseline, (2) increased EELV (+1 liter), and (3) decreased EELV (-0.6 liter). Reduced lung volumes led to increased inspiratory airflow resistance (7.54 +/- 2.80 cm H2O x L(-1) x s(-1) vs 4.53 +/- 1.05 cm H2O x L(-1) x s(-1), mean +/- SEM, P = 0.02) and increased genioglossus muscle activation (GGEMG peak 14.6% +/- 1.5% of maximum vs 8.6% +/- 1.5% of maximum, maximum P = 0.001) compared to baseline. The pharynx was also more collapsible at low lung volumes (4.3 +/- 0.5 cm H2O vs 5.4 +/- 0.6 cm H2O, P = 0.04). CONCLUSIONS: We conclude that upper-airway muscles respond to changes in lung volumes but not adequately to prevent increased collapsibility. These results suggest that lung volume has an important influence on pharyngeal patency during non-rapid eye movement sleep in normal individuals.

Adult↗
PubMed2003

Control of upper airway muscle activity in younger versus older men during sleep onset.

Pharyngeal dilator muscles are clearly important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) are decreased at sleep onset, and that this decrement in muscle activity is greater in the apnoea patient than in healthy controls. We have also previously shown this decrement to be greater in older men when compared with younger ones. In order to explore the mechanisms responsible for this decrement in muscle activity nasal continuous positive airway pressure (CPAP) was applied to reduce negative pressure mediated muscle activation. We then investigated the effect of sleep onset (transition from predominantly alpha to predominantly theta EEG activity) on ventilation, upper airway muscle activation and upper airway resistance (UAR) in middle-aged and younger healthy men. We found that both GGEMG and TPEMG were reduced by the application of nasal CPAP during wakefulness, but that CPAP did not alter the decrement in activity in either muscle seen in the first two breaths following an alpha to theta transition. However, CPAP prevented both the rise in UAR at sleep onset that occurred on the control night, and the recruitment in GGEMG seen in the third to fifth breaths following the alpha to theta transition. Further, GGEMG was higher in the middle-aged men than in the younger men during wakefulness and was decreased more in the middle-aged men with the application of nasal CPAP. No differences were seen in TPEMG between the two age groups. These data suggest that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefulness' stimulus, rather than to loss of responsiveness to negative pressure. In addition, it suggests that in older men, higher wakeful muscle activity is due to an anatomically more collapsible upper airway with more negative pressure driven muscle activation. Sleep onset per se does not appear to have a greater effect on upper airway muscle activity as one ages.

Adolescent↗
PubMed2003

On the nature of cardiovascular activation at an arousal from sleep.

STUDY OBJECTIVES: The intent of the study was to explore the nature and function of the cardiovascular activation response that occurs at an arousal from sleep. DESIGN: Four experiments were conducted. The first compared the pattern of physiologic response to orienting and startle stimuli and arousal from sleep. The second and third measured the amplitude of the cardiovascular arousal response as a function of the trait of fearfulness and the threat value of the arousing stimulus, respectively. The final experiment assessed the effect of arousal duration. SETTING: The experiments were conducted in the sleep laboratory of the Department of Psychology, University of Melbourne. PARTICIPANTS: A total of 42 (24 women and 18 men) healthy individuals between the ages of 18 and 24 participated in the experiments. INTERVENTIONS: The experiments manipulated the stimuli to which participants were exposed (orienting and startle stimuli and arousal from sleep), the threat value of stimuli used to arouse participants from sleep, and individual differences in fearfulness. MEASUREMENTS AND RESULTS: The major dependent variables were heart rate, blood pressure, and a measure of peripheral vasoconstriction (digital pulse volume). In addition, in the first study, the galvanic skin response and orbicularis oculi electromyographic activity were measured. Experiment 1 showed that the pattern of physiologic response at an arousal from sleep differed, with a substantially larger cardiovascular component, from responses to orienting and startle stimuli. Experiments 2a and 2b indicated that the magnitude of the cardiovascular response at an arousal was unrelated to either individual differences in fearfulness or differences in the threat value of arousing stimuli. The final experiment showed that the cardiovascular response at an arousal was not a return to waking levels of activity but, rather, was a transient activation response. CONCLUSIONS: The study supported the view that the cardiovascular activation response at an arousal from sleep is a transient, reflex-like response that is different from the response that occurs during normal wakefulness.

Adult↗
PubMed2003

Within-breath control of genioglossal muscle activation in humans: effect of sleep-wake state.

Pharyngeal dilator muscles are clearly important in the pathogenesis of obstructive sleep apnoea syndrome. Substantial data support the role of a local negative pressure reflex in modifying genioglossal activation across inspiration during wakefulness. Using a model of passive negative pressure ventilation, we have previously reported a tight relationship between varying intrapharyngeal negative pressures and genioglossal muscle activation (GGEMG) during wakefulness. In this study, we used this model to examine the slope of the relationship between epiglottic pressure (Pepi) and GGEMG, during stable NREM sleep and the transition from wakefulness to sleep. We found that there was a constant relationship between negative epiglottic pressure and GGEMG during both basal breathing (BB) and negative pressure ventilation (NPV) during wakefulness (slope GGEMG/Pepi 1.86+/-0.3 vs. 1.79+/-0.3 arbitrary units (a.u.) cmH2O(-1)). However, while this relationship remained stable during NREM sleep during BB, it was markedly reduced during NPV during sleep (2.27+/-0.4 vs. 0.58+/-0.1 a.u. cmH2O(-1)). This was associated with a markedly higher pharyngeal airflow resistance during sleep during NPV. At the transition from wakefulness to sleep there was also a greater reduction in peak GGEMG seen during NPV than during BB. These data suggest that while the negative pressure reflex is able to maintain GGEMG during passive NPV during wakefulness, this reflex is unable to do so during sleep. The loss of this protective mechanism during sleep suggests that an airway dependent upon such mechanisms (as in the patient with sleep apnoea) will be prone to collapse during sleep.

Adult↗
PubMed2003

Seasonality and circadian phase delay: prospective evidence that winter lowering of mood is associated with a shift towards Eveningness.

BACKGROUND: Lewy's phase shift hypothesis (PSH) of seasonal affective disorder (SAD) asserts that winter depression is caused by an abnormal delay of circadian phase in winter. The aim of this study was to further investigate the PSH by testing the novel hypothesis that winter pattern seasonality of mood in the general population is associated with a phase delay of circadian rhythms in winter. METHODS: Using a random community sample of 244 adults in Melbourne, seasonality of mood was measured prospectively as the within-subject difference between self-reports of behavioural engagement in summer and winter across 3 years. The Horne-Ostberg Morningness-Eveningness questionnaire (MEQ) was used as a self-report estimate of circadian phase. Phase delay in winter was measured as the within-subject difference between summer and winter estimates of circadian phase, with relative shifts towards Eveningness being interpreted as phase delay. RESULTS: As expected, a significant association was found between winter pattern seasonality of mood and within-subject phase delay in winter (r=0.17, P<0.01). LIMITATIONS: Circadian phase was operationalised on the MEQ. While a number of studies have shown the MEQ to correlate with physiological measures of circadian phase, the findings await replication using a more direct measure of the circadian system. CONCLUSIONS: A positive association was found between lowered mood in winter and winter phase delay amongst a random community sample. This provisional finding adds support to Lewy's PSH by demonstrating that phase delay may be causally important not just in clinical cases of SAD, but across the continuum of mood seasonality.

Adult↗
PubMed2003

The influence of sleep onset on the diurnal variation in cardiac activity and cardiac control.

Heart rate (HR), blood pressure (BP) and autonomic nervous system (ANS) activity vary diurnally, with a reduction in HR and BP, and a shift to vagal dominance during the dark phase. However, the cause of these changes, particularly the relative influence of sleep and circadian mechanisms, remains uncertain. The present study assessed the effect of sleep onset on HR, BP, high frequency (HF) component of heart rate variability (HRV), low frequency/high frequency (LF/HF) ratio and pre-ejection period (PEP). Sleep onset was dissociated from circadian influences by having subjects go to sleep at two different circadian phases, their normal time of sleep onset (normal sleep onset, NSO), and after a delay of 3 h (delayed sleep onset, DSO). The assumption was that changes caused by sleep onset would occur in association with sleep onset, irrespective of its timing, while circadian effects would have a consistent circadian phase and be independent of when sleep onset occurred. Thirteen and 17 subjects were run in the NSO and DSO conditions, respectively. Following a 1-h adaptation period, data collection began 2 h before subjects' normal time of sleep onset and continued until morning awakening. The lights were turned out after 2 h in the NSO condition and 5 h in the DSO condition. Subjects were required to maintain a supine position throughout the experimental sessions. The night-time decrease in HR was found to be due to both sleep onset and a circadian influence, with the circadian component being more prominent. In contrast, the fall in BP was largely due to a sleep onset effect. Increased vagal activity, as reflected in the HF component and a shift to vagal dominance in the LF/HF ratio, appeared to be primarily a function of the sleep system, while sympathetic activity, as assessed by PEP, reflected a circadian influence.

Adaptation, Physiological↗
PubMed2002

Evidence of a sleep-specific blunted cortical response to inspiratory occlusions in mild obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome (OSAS) patients have elevated non-rapid eye movement (REM) sleep arousal thresholds to inspiratory loading. To test the hypothesis that this is due to sleep-specific dampening of cortical responses to inspiratory effort, respiratory-related evoked potentials (RREPs) were evaluated in six mild OSAS patients and six age- and body mass index-matched controls during wakefulness and Stage 2 non-REM sleep. Electroencephalogram was recorded from six scalp sites (Fz, FCz, Cz, CPz, Pz, and O(2)). Electrooculogram, electromyogram, and mask pressure signals were also recorded. During sleep, pharyngeal pressure was recorded using a Millar pressure catheter placed 2 cm below the glottis. The RREP waveform was broadly similar in the two groups during wakefulness, but was markedly different during Stage 2 non-REM sleep. During wakefulness, only the N1 component showed reduced amplitude in the OSAS group. During sleep, the occlusion stimulus elicited fewer K-complexes in the OSAS patients. In addition, the N550 component in the average of K-complex responses was smaller in amplitude in the OSAS group. The data suggest that patients with mild OSAS have a "blunted" response to the respiratory occlusion stimulus. This appears not to be related to compromised mechanoreceptor function, as the RREP was normal in the patients when they were awake.

Adult↗
PubMed2002

A randomized controlled trial of continuous positive airway pressure in mild obstructive sleep apnea.

A common clinical dilemma faced by sleep physicians is in deciding the level of severity at which patients with obstructive sleep apnea (OSA) should be treated. There is particular uncertainty about the need for, and the effectiveness of, treatment in mild cases. To help define the role of nasal continuous positive airway pressure (CPAP) treatment in mild OSA we undertook a randomized controlled cross-over trial of CPAP in patients with an apnea- hypopnea index (AHI) of 5 - 30 (mean, 12.9 +/- 6.3 SD). Twenty-four-hour blood pressure and neurobehavioral function were measured at baseline, after 8 wk of treatment with CPAP, and after 8 wk of treatment with an oral placebo tablet. Twenty-eight of 42 patients enrolled in the study completed both treatment arms. Baseline characteristics were not different between those who completed the study and those who did not complete the study. Patients used CPAP for a mean (SD) of 3.53 (2.13) h per night and the mean AHI on the night of CPAP implementation was 4.24 (2.9). Nasal CPAP improved self-reported symptoms of OSA, including snoring, restless sleep, daytime sleepiness, and irritability (in-house questionnaire), more than did placebo, but did not improve objective (Multiple Sleep Latency Test) or subjective (Epworth Sleepiness Scale) measures of daytime sleepiness. We found no benefit of CPAP over placebo in any tests of neurobehavioral function, generic SF-36 (36-item Short Form Medical Outcomes Survey) or sleep-specific (Functional Outcomes of Sleep Questionnaire) quality of life questionnaires, mood score (Profile of Moods States and Beck Depression Index), or 24-h blood pressure. However, the placebo tablet resulted in a significant improvement in a wide range of functional variables compared with baseline. This placebo effect may account for some of the treatment responses to CPAP observed previously in patients with mild OSA.

Adult↗