The influence of alcohol on genioglossus single motor units in men and women during wakefulness.

NEW FINDINGS: What is the central question of this study? How does alcohol intake, which worsens obstructive sleep apnoea, alter motor control of the genioglossus muscle, an upper airway dilator, in healthy awake human volunteers, and does alcohol alter genioglossus muscle afterdischarge? What is the main finding and its importance? Alcohol consumption had a very minor effect on the activity of the genioglossus in healthy young individuals studied during wakefulness and did not alter afterdischarge, leaving open the possibility that alcohol worsens obstructive sleep apnoea via other mechanisms. ABSTRACT: Alcohol worsens obstructive sleep apnoea (OSA). This effect is thought to be due to alcohol's depressant effect on upper airway dilator muscles such as the genioglossus, but how alcohol reduces genioglossal activity is unknown. The aim of this study was to investigate the effect of alcohol consumption on genioglossus muscle single motor units (MUs). Sixteen healthy individuals were studied on two occasions (alcohol: breath alcohol concentration ∼0.07% and placebo). They were instrumented with a nasal mask, four intramuscular genioglossal EMG electrodes, and an ear oximeter. They were exposed to 8-12 hypoxia trials (45-60 s of 10% O2 followed by one breath of 100% O2 ) while awake. MUs were sorted according to their firing patterns and quantified during baseline, hypoxia and recovery. For the alcohol and placebo conditions, global muscle activity (mean ± SD peak inspiratory EMG = 119.3 ± 44.1 and 126.5 ± 51.9 µV, respectively, P = 0.53) and total number of MUs recorded at baseline (68 and 67, respectively) were similar. Likewise, the peak discharge frequency did not differ between conditions (21.2 ± 4.28 vs. 22.4 ± 4.08 Hz, P = 0.09). There was no difference between conditions in the number (101 vs. 88, respectively) and distribution of MU classes during hypoxia, and afterdischarge duration was also similar. In this study, alcohol had a very minor effect on genioglossal activity and afterdischarge in these otherwise healthy young individuals studied while awake. If similar effects are observed during sleep, it would suggest that the worsening of OSA following alcohol may be related to increased upper airway resistance/nasal congestion or arousal threshold changes.

Sleep-disordered breathing was associated with lower health-related quality of life and cognitive function in a cross-sectional study of older adults.

BACKGROUND AND OBJECTIVE: The clinical significance of sleep-disordered breathing (SDB) in older age is uncertain. This study determined the prevalence and associations of SDB with mood, daytime sleepiness, quality of life (QOL) and cognition in a relatively healthy older Australian cohort. METHODS: A cross-sectional analysis was conducted from the Study of Neurocognitive Outcomes, Radiological and retinal Effects of Aspirin in Sleep Apnoea. Participants completed an unattended limited channel sleep study to measure the oxygen desaturation index (ODI) to define mild (ODI 5-15) and moderate/severe (ODI ≥ 15) SDB, the Centre for Epidemiological Studies Scale, the Epworth Sleepiness Scale, the 12-item Short-Form for QOL and neuropsychological tests. RESULTS: Of the 1399 participants (mean age 74.0 years), 36% (273 of 753) of men and 25% (164 of 646) of women had moderate/severe SDB. SDB was associated with lower physical health-related QOL (mild SDB: beta coefficient [ß] -2.5, 95% CI -3.6 to -1.3, p < 0.001; moderate/severe SDB: ß -1.8, 95% CI -3.0 to -0.6, p = 0.005) and with lower global composite cognition (mild SDB: ß -0.1, 95% CI -0.2 to 0.0, p = 0.022; moderate/severe SDB: ß -0.1, 95% CI -0.2 to 0.0, p = 0.032) compared to no SDB. SDB was not associated with daytime sleepiness nor depression. CONCLUSION: SDB was associated with lower physical health-related quality of life and cognitive function. Given the high prevalence of SDB in older age, assessing QOL and cognition may better delineate subgroups requiring further management, and provide useful treatment target measures for this age group.

Randomised controlled trial of polysomnographic titration of noninvasive ventilation.

Noninvasive ventilation (NIV) settings determined during wakefulness may produce patient-ventilator asynchrony (PVA) during sleep, causing sleep disruption and limiting tolerance. This study investigated whether NIV titrated with polysomnography (PSG) is associated with less PVA and sleep disruption than therapy titrated during daytime alone.Treatment-naive individuals referred for NIV were randomised to control (daytime titration followed by sham polysomnographic titration) or PSG (daytime titration followed by polysomnographic titration) groups. Primary outcomes were PVA and arousal indices on PSG at 10 weeks. Secondary outcomes included adherence, gas exchange, symptoms and health-related quality of life (HRQoL).In total, 60 participants were randomised. Most (88.3%) had a neuromuscular disorder and respiratory muscle weakness but minor derangements in daytime arterial blood gases. PVA events were less frequent in those undergoing polysomnographic titration (median (interquartile range (IQR)): PSG 25.7 (12-68) events·h-1 versus control 41.0 (28-182) events·h-1; p=0.046), but arousals were not significantly different (median (IQR): PSG 11.4 (9-19) arousals·h-1 versus control 14.6 (11-19) arousals·h-1; p=0.258). Overall adherence was not different except in those with poor early adherence (<4 h·day-1) who increased their use after polysomnographic titration (mean difference: PSG 95 (95% CI 29-161) min·day-1 versus control -23 (95% CI -86-39) min·day-1; p=0.01). Arterial carbon dioxide tension, somnolence and sleep quality improved in both groups. There were no differences in nocturnal gas exchange or overall measures of HRQoL.NIV titrated with PSG is associated with less PVA but not less sleep disruption when compared with therapy titrated during daytime alone.

Genioglossus reflex responses to negative upper airway pressure are altered in people with tetraplegia and obstructive sleep apnoea.

KEY POINTS: Protective reflexes in the throat area (upper airway) are crucial for breathing. Impairment of these reflexes can cause breathing problems during sleep such as obstructive sleep apnoea (OSA). OSA is very common in people with spinal cord injury for unknown reasons. This study shows major changes in protective reflexes that serve to keep the upper airway open in response to suction pressures in people with tetraplegia and OSA. These results help us understand why OSA is so common in people with tetraplegia and provide new insight into how protective upper airway reflexes work more broadly. ABSTRACT: More than 60% of people with tetraplegia have obstructive sleep apnoea (OSA). However, the specific causes are unknown. Genioglossus, the largest upper-airway dilator muscle, is important in maintaining upper-airway patency. Impaired genioglossus muscle function following spinal cord injury may contribute to OSA. This study aimed to determine if genioglossus reflex responses to negative upper-airway pressure are altered in people with OSA and tetraplegia compared to non-neurologically impaired able-bodied individuals with OSA. Genioglossus reflex responses measured via intramuscular electrodes to ∼60 brief (250 ms) pulses of negative upper-airway pressure (∼-15 cmH2 O at the mask) were compared between 13 participants (2 females) with tetraplegia plus OSA and 9 able-bodied controls (2 females) matched for age and OSA severity. The initial short-latency excitatory reflex response was absent in 6/13 people with tetraplegia and 1/9 controls. Genioglossus reflex inhibition in the absence of excitation was observed in three people with tetraplegia and none of the controls. When the excitatory response was present, it was significantly delayed in the tetraplegia group compared to able-bodied controls: excitation onset latency (mean ± SD) was 32 ± 16 vs. 18 ± 9 ms, P = 0.045; peak excitation latency was 48 ± 17 vs. 33 ± 8 ms, P = 0.038. However, when present, amplitude of the excitation response was not different between groups, 195 ± 26 vs. 219 ± 98% at baseline, P = 0.55. There are major differences in genioglossus reflex morphology and timing in response to rapid changes in airway pressure in people with tetraplegia and OSA. Altered genioglossus function may contribute to the increased risk of OSA in people with tetraplegia. The precise mechanisms mediating these differences are unknown.

Sleep-disordered breathing in hypertensive disorders of pregnancy: a BMI-matched study.

Sleep-disordered breathing is more common in hypertensive disorders during pregnancy; however, most studies have not adequately accounted for the potential confounding impact of obesity. This study evaluated the frequency of sleep-disordered breathing in women with gestational hypertension and pre-eclampsia compared with body mass index- and gestation-matched normotensive pregnant women. Women diagnosed with gestational hypertension or pre-eclampsia underwent polysomnography shortly after diagnosis. Normotensive controls body mass index-matched within ±4 kg m-2 underwent polysomnography within ±4 weeks of gestational age of their matched case. The mean body mass index and gestational age at polysomnography were successfully matched for 40 women with gestational hypertension/pre-eclampsia and 40 controls. The frequency of sleep-disordered breathing in the cases was 52.5% compared with 37.5% in the control group (P = 0.18), and the respiratory disturbance index overall did not differ (P = 0.20). However, more severe sleep-disordered breathing was more than twice as common in women with gestational hypertension or pre-eclampsia (35% versus 15%, P = 0.039). While more than half of women with a hypertensive disorder of pregnancy meet the clinical criteria for sleep-disordered breathing, it is also very common in normotensive women of similar body mass index. This underscores the importance of adjusting for obesity when exploring the relationship between sleep-disordered breathing and hypertension in pregnancy. More severe degrees of sleep-disordered breathing are significantly associated with gestational hypertension and pre-eclampsia, and sleep-disordered breathing may plausibly play a role in the pathophysiology of pregnancy hypertension in these women. This suggests that more severe sleep-disordered breathing is a potential therapeutic target for reducing the prevalence or severity of hypertensive disorders in pregnancy.

Magnetic resonance imaging of the upper airway in patients with quadriplegia and obstructive sleep apnea.

The aim of this study was to investigate upper airway anatomy in quadriplegics with obstructive sleep apnea. Fifty subjects were recruited from three hospitals in Australia: people with quadriplegia due to spinal cord injury and obstructive sleep apnea (n = 11), able-bodied people with obstructive sleep apnea (n = 18), and healthy, able-bodied controls (n = 19). All underwent 3-Tesla magnetic resonance imaging of their upper airway. A subgroup (n = 34) received a topical vasoconstrictor, phenylephrine and post-phenylephrine magnetic resonance imaging. Mixed-model analysis indicated no significant differences in total airway lumen volume between the three groups (P = 0.086). Spinal cord injury-obstructive sleep apnea subjects had a significantly larger volume of soft palate (P = 0.020) and retroglossal lateral pharyngeal walls (P = 0.043) than able-bodied controls. Able-bodied-obstructive sleep apnea subjects had a smaller mandible volume than spinal cord injury-obstructive sleep apnea subjects and able-bodied control subjects (P = 0.036). No differences were seen in airway length between groups when controlling for height (P = 0.055). There was a marginal increase in velopharyngeal volume across groups post-phenylephrine (P = 0.050), and post hoc testing indicated the difference was confined to the able-bodied-obstructive sleep apnea group (P < 0.001). No other upper airway structures showed significant changes with phenylephrine administration. In conclusion, people with obstructive sleep apnea and quadriplegia do not have a structurally smaller airway than able-bodied subjects. They did, however, have greater volumes of soft palate and lateral pharyngeal walls, possibly due to greater neck fat deposition. The acute response to upper airway topical vasoconstriction was not enhanced in those with obstructive sleep apnea and quadriplegia. Changes in upper airway anatomy likely contribute to the high incidence in obstructive sleep apnea in quadriplegic subjects.

Effects of 1-month withdrawal of ventilatory support in hypercapnic myotonic dystrophy type 1.

BACKGROUND AND OBJECTIVE: The benefits of domiciliary non-invasive ventilation (NIV) in myotonic dystrophy type 1 (DM1) are unclear. We sought to determine the effects of elective discontinuation of ventilatory support for 1 month in DM1 patients receiving NIV for chronic hypercapnic respiratory failure. METHODS: At baseline, 12 patients underwent polysomnography, and assessment of subjective (Epworth Sleepiness Scale) and objective (Oxford Sleep Resistance Test) sleepiness, fatigue (Fatigue Severity Scale), respiratory function including muscle strength, arterial blood gas (ABG), hypercapnic ventilatory response (HCVR), Blood Pressure, peripheral arterial tonometry (PAT) and pulse wave velocity (PWV). They also completed the SF36. Testing was repeated (Visit 2) 1 month after elective cessation of NIV and again (Visit 3) 1 month after NIV reintroduction. RESULTS: No changes were seen in SF36, sleepiness or fatigue, respiratory function, muscle strength nor HCVR. Likewise, there were no changes in Blood Pressure, PAT or PWV. Mean nocturnal SpO2 deteriorated off NIV and improved on resumption (mean ± SD = 95.02 ± 1.90%, 92.23 ± 3.61% and 95.08 ± 2.28%, P = 0.006 change Visit 1 to Visit 2, 0.009 Visit 2 to Visit 3). Daytime PaCO2 (arterial partial pressure of carbon dioxide) was 43.13 ± 4.20 mm Hg, 46.28 ± 2.25 mm Hg and 43.87 ± 2.85 mm Hg, P = 0.056 and 0.017 over the same intervals. CONCLUSION: DM1 patients derive little benefit in symptoms or quality of life from NIV. Nocturnal and diurnal ventilatory functions deteriorate slightly off NIV for 1 month, but this does not appear to be due to changes in HCVR or respiratory function. HCVR changes may be of primary CNS origin given stability on or off NIV.

Identifying who will benefit from non-invasive ventilation in amyotrophic lateral sclerosis/motor neurone disease in a clinical cohort.

BACKGROUND: Respiratory failure is associated with significant morbidity and is the predominant cause of death in motor neurone disease/amyotrophic lateral sclerosis (MND/ALS). This study aimed to determine the effect of non-invasive ventilatory (NIV) support on survival and pulmonary function decline across MND/ALS phenotypes. METHODS: Cohort recruited via a specialist, multidisciplinary clinic. Patients were categorised into four clinical phenotypes (ALS, flail arm, flail leg and primary lateral sclerosis) according to site of presenting symptom and the pattern of upper versus lower motor neurone involvement. NIV was initiated according to current consensus practice guidelines. RESULTS: Between 1991 and 2011, 1198 patients diagnosed with ALS/MND were registered. 929 patients (77.5%) fulfilled the selection criteria and their data were analysed. Median tracheostomy free survival from symptom onset was 28 months in NIV-treated patients compared to 15 months in untreated (Univariate Cox regression HR=0.61 (0.51 to 0.73), p<0.001). The positive survival effect of NIV persisted when the model was adjusted for age, gender, riluzole and percutaneous endoscopic gastrostomy use (HR=0.72 (0.60 to 0.88, p=0.001). In contrast with the only randomised controlled trial, NIV statistically significantly increased survival by 19 months in those with ALS-bulbar onset (Univariate HR=0.50 (0.36 to 0.70), multivariate HR=0.59 (0.41 to 0.83)). These data confirm that NIV improves survival in MND/ALS. The overall magnitude of benefit is 13 months and was largest in those with ALS-bulbar disease. Future research should explore the optimal timing of NIV initiation within phenotypes in order to optimise respiratory function, quality of life and survival.

Hypoglossal nerve stimulation improves obstructive sleep apnea: 12-month outcomes.

Reduced upper airway muscle activity during sleep is a key contributor to obstructive sleep apnea pathogenesis. Hypoglossal nerve stimulation activates upper airway dilator muscles, including the genioglossus, and has the potential to reduce obstructive sleep apnea severity. The objective of this study was to examine the safety, feasibility and efficacy of a novel hypoglossal nerve stimulation system (HGNS; Apnex Medical, St Paul, MN, USA) in treating obstructive sleep apnea at 12 months following implantation. Thirty-one subjects (35% female, age 52.4 ± 9.4 years) with moderate to severe obstructive sleep apnea and unable to tolerate positive airway pressure underwent surgical implantation and activation of the hypoglossal nerve stimulation system in a prospective single-arm interventional trial. Primary outcomes were changes in obstructive sleep apnea severity (apnea-hypopnea index, from in-laboratory polysomnogram) and sleep-related quality of life [Functional Outcomes of Sleep Questionnaire (FOSQ)]. Hypoglossal nerve stimulation was used on 86 ± 16% of nights for 5.4 ± 1.4 h per night. There was a significant improvement (P < 0.001) from baseline to 12 months in apnea-hypopnea index (45.4 ± 17.5 to 25.3 ± 20.6 events h(-1) ) and Functional Outcomes of Sleep Questionnaire score (14.2 ± 2.0 to 17.0 ± 2.4), as well as other polysomnogram and symptom measures. Outcomes were stable compared with 6 months following implantation. Three serious device-related adverse events occurred: an infection requiring device removal; and two stimulation lead cuff dislodgements requiring replacement. There were no significant adverse events with onset later than 6 months following implantation. Hypoglossal nerve stimulation demonstrated favourable safety, feasibility and efficacy.

Mechanisms underlying the prolonged activation of the genioglossus following arousal from sleep.

STUDY OBJECTIVES: Transient arousal from sleep has been shown to elicit a prolonged increase in genioglossus muscle activity that persists following the return to sleep and which may protect against subsequent airway collapse. We hypothesized that this increased genioglossal activity following return to sleep after an arousal is due to persistent firing of inspiratory-modulated motor units (MUs) that are recruited during the arousal. METHODS: Thirty-four healthy participants were studied overnight while wearing a nasal mask with pneumotachograph to measure ventilation and with 4 intramuscular genioglossus EMG electrodes. During stable N2 and N3 sleep, auditory tones were played to induce brief (3-15s) AASM arousals. Ventilation and genioglossus MUs were quantified before the tone, during the arousal and for 10 breaths after the return to sleep. RESULTS: A total of 1089 auditory tones were played and gave rise to 239 MUs recorded across arousal and the return to sleep in 20 participants (aged 23 ±â€…4.2 years and BMI 22.5 ±â€…2.2 kg/m2). Ventilation was elevated above baseline during arousal and the first post-arousal breath (p < .001). Genioglossal activity was elevated for five breaths following the return to sleep, due to increased firing rate and recruitment of inspiratory modulated MUs, as well as a small increase in tonic MU firing frequency. CONCLUSIONS: The sustained increase in genioglossal activity that occurs on return to sleep after arousal is primarily a result of persistent activity of inspiratory-modulated MUs, with a slight contribution from tonic units. Harnessing genioglossal activation following arousal may potentially be useful for preventing obstructive respiratory events.

Associations Between Amyloid Burden, Hypoxemia, Sleep Architecture, and Cognition in Obstructive Sleep Apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with an increased risk of amyloid-ß (Aß) burden, the hallmark of Alzheimer's disease, and cognitive decline. OBJECTIVE: To determine the differential impacts of hypoxemia and slow-wave sleep disruption on brain amyloid burden, and to explore the effects of hypoxemia, slow-wave sleep disruption, and amyloid burden on cognition in individuals with and without OSA. METHODS: Thirty-four individuals with confirmed OSA (mean±SD age 57.5±4.1 years; 19 males) and 12 healthy controls (58.5±4.2 years; 6 males) underwent a clinical polysomnogram, a NAV4694 positron emission tomography (PET) scan for Aß burden, assessment of APOEɛ status and cognitive assessments. Linear hierarchical regressions were conducted to determine the contributions of demographic and sleep variables on amyloid burden and cognition. RESULTS: Aß burden was associated with nocturnal hypoxemia, and impaired verbal episodic memory, autobiographical memory and set shifting. Hypoxemia was correlated with impaired autobiographical memory, and only set shifting performance remained significantly associated with Aß burden when controlling for sleep variables. CONCLUSIONS: Nocturnal hypoxemia was related to brain Aß burden in this sample of OSA participants. Aß burden and hypoxemia had differential impacts on cognition. This study reveals aspects of sleep disturbance in OSA that are most strongly associated with brain Aß burden and poor cognition, which are markers of early Alzheimer's disease. These findings add weight to the possibility that hypoxemia may be causally related to the development of dementia; however, whether it may be a therapeutic target for dementia prevention in OSA is yet to be determined.

Exclusion of EEG-based arousals in wake epochs of polysomnography leads to underestimation of the arousal index.

STUDY OBJECTIVES: There is an internal contradiction in current American Academy of Sleep Medicine standards for arousal index (AI) calculation in polysomnography: Arousals in sleep and wake epochs are counted, but only sleep time is used in the denominator. This study aimed to investigate the impact of including arousals scored in wake epochs on the AI. METHODS: We compared AIs including (AIinc) vs excluding (AIexc) awake-epoch arousals from 100 consecutive polysomnograms conducted for investigation of possible obstructive sleep apnea. To determine the AI that most closely approximated "truth," AIinc and AIexc were compared to an AI calculated from continuous sleep analysis (AIcont) in a 20-polysomnogram subgroup of patients. RESULTS: The median (interquartile range) increase in AIinc was 5.2 events/h (3.5-8.1) vs AIexc (AIinc = 28.0 events/h [18.4-38.9] vs AIexc = 22.9 events/ h [13.1-31.3]), equating to an increase of 25.3% (15.6-40.8). As the AI increased, the difference increased (P < .001), with decreasing sleep efficiency and an increasing apnea-hypopnea index as the strongest predictors of the difference between AIexc and AIinc. The absolute AIexc-AIcont difference (7.7 events/h [5.1-13.6]) was significantly greater than the AIinc-AIcont difference (1.2 events/h [0.6-5.7]; z = -3.099; P = .002). CONCLUSIONS: There was a notable increase in AI when we included wake-epoch arousals, particularly in patients with more severe obstructive sleep apnea or reduced sleep efficiency. However, the AI including wake-epoch arousals best matched the "true" continuous sleep-scoring AI. Our study informs clinical and research practice, highlights epoch scoring pitfalls, and supports the current American Academy of Sleep Medicine standard arousal reporting approach for future standards. CITATION: Wilson DL, Tolson J, Churchward TJ, Melehan K, O'Donoghue FJ, Ruehland WR. Exclusion of EEG-based arousals in wake epochs of polysomnography leads to underestimation of the arousal index. J Clin Sleep Med. 2022;18(5):1385-1393.

Transcutaneous measurement of carbon dioxide tension during extended monitoring: evaluation of accuracy and stability, and an algorithm for correcting calibration drift.

BACKGROUND: When polysomnography is indicated in a patient with a presumed sleep disorder, continuous monitoring of arterial carbon dioxide tension (P(aCO(2))) is desirable, especially if nocturnal hypoventilation is suspected. Transcutaneous CO(2) monitors (P(tcCO(2))) provide a noninvasive correlate of P(aCO(2)), but their accuracy and stability over extended monitoring have been considered inadequate for the diagnosis of hypoventilation. We examined the stability and accuracy of P(tcCO(2)) measurements and the performance of a previously described linear interpolation technique designed to correct for calibration drift. METHODS: We compared the P(tcCO(2)) values from 2 TINA TCM-3 monitors to P(aCO(2)) values from arterial blood samples obtained at the beginning, every 15 min of the first hour, and then hourly over 8 hours of monitoring in 6 hemodynamically stable, male, intensive care patients (mean age 46 ± 17 y). RESULTS: Time had a significant (P = .002) linear effect on the P(tcCO(2))-P(aCO(2)) difference, suggesting calibration drift over the monitoring period. We found no differences between monitor type or interaction between time and monitor type. For the 2 monitors the uncorrected bias was 3.6 mm Hg and the limits of agreement were -5.1 to 12.3 mm Hg. Our linear interpolation algorithm improved the bias and limits of agreement to 0.4 and -5.5 to 6.4 mm Hg, respectively. CONCLUSIONS: Following stabilization and correction for both offset and drift, P(tcCO(2)) tracks P(aCO(2)) with minimal residual bias over 8 hours of monitoring. Should future research confirm these findings, then interpolated P(tcCO(2)) may have an increased role in detecting sleep hypoventilation and assessing the efficacy of treatment.

Eye blink parameters to indicate drowsiness during naturalistic driving in participants with obstructive sleep apnea: A pilot study.

OBJECTIVES: To determine whether continuous eye blink measures could identify drowsiness in patients with obstructive sleep apnea (OSA) during a week of naturalistic driving. DESIGN: Observational study comparing OSA patients and healthy controls. SETTING: Regular naturalistic driving across one week. PARTICIPANTS: Fifteen untreated moderate to severe OSA patients and 15 age (± 5 years) and sex (female = 6) matched healthy controls. MEASUREMENTS: Participants wore an eye blink drowsiness recording device during their regular driving for one week. RESULTS: During regular driving, the duration of time with no ocular movements (quiescence), was elevated in the OSA group by 43% relative to the control group (mean [95% CI] 0.20[0.17, 0.25] vs 0.14[0.12, 0.18] secs, P = .011). During long drives only, the Johns Drowsiness Scale was also elevated and increased by 62% in the OSA group relative to the control group (1.05 [0.76, 1.33] vs 0.65 [0.36, 0.93], P = .0495). Across all drives, critical drowsiness events (defined by a Johns Drowsiness Scale score ≥2.6) were twice as frequent in the OSA group than the control group (rate ratio [95% CI] =1.93 [1.65, 2.25], P ≤ .001). CONCLUSIONS: OSA patients were drowsier than healthy controls according to some of the continuous real time eye blink drowsiness measures. The findings of this pilot study suggest that there is potential for eye blink measures to be utilized to assess fitness to drive in OSA patients. Future work should assess larger samples, as well as the relationship of eye blink measures to conventional fitness to drive assessments and crash risk.