Older Age is Associated With Positional Obstructive Sleep Apnea.

OBJECTIVES: Untreated obstructive sleep apnea (OSA) is associated with cognitive dysfunction; however studies report low adherence rates to standard continuous positive airway pressure (CPAP) treatment in the elderly. Positional OSA (p-OSA) is a subset that can be cured by positional therapy of avoiding supine sleep. However, there is no well-established criteria to identify patients who could benefit from positional therapy as an alternative or adjunct to CPAP. This study investigates if older age is related to p-OSA using different diagnostic criteria. DESIGN: Cross-sectional study. PARTICIPANTS: Participants aged 18 years old or more who underwent polysomnography for clinical reasons at University of Iowa Hospitals and Clinics over a 1-year period from July 2011 to June 2012 were enrolled retrospectively. MEASUREMENT: P-OSA was defined as a high supine-position dependency of obstructive breathing events with potential resolution of OSA in nonsupine positions [high apnea-hypopnea index on supine positions (s-AHI)/ AHI on nonsupine positions (ns0AHI) combined with ns-AHI < 5/hour]. Different cutoff points (2, 3, 5, 10, 15, 20) were applied to determine a meaningful ratio of supine-position dependency of obstructions [s-AHI/ns-AHI]. We compared the proportion of patients with p-OSA between the older age group (≥65 years old) and the propensity score (PS)-matched (upto 1:4) younger age group (<65 years old) using logistic regression analyses. RESULTS: In total, 346 participants were included. The older age group had a higher s-AHI/ns-AHI ratio than the younger age group (mean 31.6 [SD 66.2] versus 9.3 [SD 17.4], median 7.3 [interquartile range [IQR], 3.0-29.6) versus 4.1 (IQR, 1.9-8.7). After PS-matching, the older age group (n = 44) had higher proportion of those with a high s-AHI/ns-AHI ratio and ns-AHI< 5/hour compared with the younger age group (n = 164). (s-AHI/ns-AHI≥10: 54.6% versus 31.7%, OR 2.44 (95% CI, 1.22-4.90); s-AHI/ns-AHI≥15: 47.7% versus 26.2%, OR 2.24 (95% CI, 1.14-4.37); s-AHI/ns-AHI≥20: 40.9% versus 19.5%, OR 2.52 (95% CI, 1.22-5.20)) CONCLUSION: Older patients with OSA are more likely to have severe position dependent OSA, that is potentially more treatable with positional therapy. Thus, clinicians treating older, cognitively impaired geriatric patients unable to tolerate CPAP therapy should consider positional therapy as an adjunct or alternative.

Acute inorganic nitrate supplementation and the hypoxic ventilatory response in patients with obstructive sleep apnea.

Patients with obstructive sleep apnea (OSA) have increased cardiovascular disease risk largely attributable to hypertension. Heightened peripheral chemoreflex sensitivity (i.e., exaggerated responsiveness to hypoxia) facilitates hypertension in these patients. Nitric oxide blunts the peripheral chemoreflex, and patients with OSA have reduced nitric oxide bioavailability. We therefore investigated the dose-dependent effects of acute inorganic nitrate supplementation (beetroot juice), an exogenous nitric oxide source, on blood pressure and cardiopulmonary responses to hypoxia in patients with OSA using a randomized, double-blind, placebo-controlled crossover design. Fourteen patients with OSA (53 ± 10 yr, 29.2 ± 5.8 kg/m2, apnea-hypopnea index = 17.8 ± 8.1, 43%F) completed three visits. Resting brachial blood pressure and cardiopulmonary responses to inspiratory hypoxia were measured before, and 2 h after, acute inorganic nitrate supplementation [∼0.10 mmol (placebo), 4.03 mmol (low dose), and 8.06 mmol (high dose)]. Placebo increased neither plasma [nitrate] (30 ± 52 to 52 ± 23 µM, P = 0.26) nor [nitrite] (266 ± 153 to 277 ± 164 nM, P = 0.21); however, both increased following low (29 ± 17 to 175 ± 42 µM, 220 ± 137 to 514 ± 352 nM) and high doses (26 ± 11 to 292 ± 90 µM, 248 ± 155 to 738 ± 427 nM, respectively, P < 0.01 for all). Following placebo, systolic blood pressure increased (120 ± 9 to 128 ± 10 mmHg, P < 0.05), whereas no changes were observed following low (121 ± 11 to 123 ± 8 mmHg, P = 0.19) or high doses (124 ± 13 to 124 ± 9 mmHg, P = 0.96). The peak ventilatory response to hypoxia increased following placebo (3.1 ± 1.2 to 4.4 ± 2.6 L/min, P < 0.01) but not low (4.4 ± 2.4 to 5.4 ± 3.4 L/min, P = 0.11) or high doses (4.3 ± 2.3 to 4.8 ± 2.7 L/min, P = 0.42). Inorganic nitrate did not change the heart rate responses to hypoxia (beverage-by-time P = 0.64). Acute inorganic nitrate supplementation appears to blunt an early-morning rise in systolic blood pressure potentially through suppression of peripheral chemoreflex sensitivity in patients with OSA.NEW & NOTEWORTHY The present study is the first to examine the acute effects of inorganic nitrate supplementation on resting blood pressure and cardiopulmonary responses to hypoxia (e.g., peripheral chemoreflex sensitivity) in patients with obstructive sleep apnea (OSA). Our data indicate inorganic nitrate supplementation attenuates an early-morning rise in systolic blood pressure potentially attributable to blunted peripheral chemoreflex sensitivity. These data show proof-of-concept that inorganic nitrate supplementation could reduce the risk of cardiovascular disease in patients with OSA.

Cortical functional connectivity indexes arousal state during sleep and anesthesia.

Disruption of cortical connectivity likely contributes to loss of consciousness (LOC) during both sleep and general anesthesia, but the degree of overlap in the underlying mechanisms is unclear. Both sleep and anesthesia comprise states of varying levels of arousal and consciousness, including states of largely maintained conscious experience (sleep: N1, REM; anesthesia: sedated but responsive) as well as states of substantially reduced conscious experience (sleep: N2/N3; anesthesia: unresponsive). Here, we tested the hypotheses that (1) cortical connectivity will exhibit clear changes when transitioning into states of reduced consciousness, and (2) these changes will be similar for arousal states of comparable levels of consciousness during sleep and anesthesia. Using intracranial recordings from five adult neurosurgical patients, we compared resting state cortical functional connectivity (as measured by weighted phase lag index, wPLI) in the same subjects across arousal states during natural sleep [wake (WS), N1, N2, N3, REM] and propofol anesthesia [pre-drug wake (WA), sedated/responsive (S), and unresponsive (U)]. Analysis of alpha-band connectivity indicated a transition boundary distinguishing states of maintained and reduced conscious experience in both sleep and anesthesia. In wake states WS and WA, alpha-band wPLI within the temporal lobe was dominant. This pattern was largely unchanged in N1, REM, and S. Transitions into states of reduced consciousness N2, N3, and U were characterized by dramatic changes in connectivity, with dominant connections shifting to prefrontal cortex. Secondary analyses indicated similarities in reorganization of cortical connectivity in sleep and anesthesia. Shifts from temporal to frontal cortical connectivity may reflect impaired sensory processing in states of reduced consciousness. The data indicate that functional connectivity can serve as a biomarker of arousal state and suggest common mechanisms of LOC in sleep and anesthesia.

Driving Safety and Fitness to Drive in Sleep Disorders.

Driving an automobile while sleepy increases the risk of crash-related injury and death. Neurologists see patients with sleepiness due to obstructive sleep apnea, narcolepsy, and a wide variety of neurologic disorders. When addressing fitness to drive, the physician must weigh patient and societal health risks and regional legal mandates. The Driver Fitness Medical Guidelines published by the National Highway Traffic Safety Administration (NHTSA) and the American Association of Motor Vehicle Administrators (AAMVA) provide assistance to clinicians. Drivers with obstructive sleep apnea may continue to drive if they have no excessive daytime sleepiness and their apnea-hypopnea index is less than 20 per hour. Those with excessive daytime sleepiness or an apnea-hypopnea index of 20 per hour or more may not drive until their condition is effectively treated. Drivers with sleep disorders amenable to pharmaceutical treatment (eg, narcolepsy) may resume driving as long as the therapy has eliminated excessive daytime sleepiness. Following these guidelines, documenting compliance to recommended therapy, and using the Epworth Sleepiness Scale to assess subjective sleepiness can be helpful in determining patients' fitness to drive.

Obstructive sleep apnea and risk for late-life depression.

BACKGROUND: Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by repetitive pharyngeal collapse. Because of the association between OSA, ischemia, and late-life depression, we hypothesized that older patients with OSA would have a higher prevalence of depression relative to their younger counterparts. METHODS: We retrospectively reviewed charts of patients evaluated at the Sleep Disorders Center (SDC) at University of Iowa Hospitals and Clinics. A total of 617 patients age≥18 seen at SDC for diagnostic and therapeutic sleep studies were identified. Patients with a chart diagnosis of depressive disorder or treatment with antidepressants were identified as having a depressive disorder. Patients with an Apnea/Hypopnea Index≥5 were identified as having OSA. RESULTS: No evidence of an escalating prevalence of depression with age was found in patients with OSA relative to those without the disorder. Prevalence of depression was similar in the OSA and the nonapnea groups (40.9% vs 40.3%, respectively; χ2=0.02; df=1; P=.89). Individuals with OSA had a significantly higher body mass index and greater number of chart diagnoses of hypertension, diabetes mellitus, and coronary artery disease compared with the nonapnea group. CONCLUSIONS: The prevalence of depression among individuals with OSA does not appear to be moderated by age. Similarly high rates of depression were observed across the population of individuals referred for sleep studies, whether or not they were diagnosed with OSA.

Sleep-related problems in neurologic diseases.

There is a strong association between sleep-related problems and neurologic diseases. Neurologic diseases of the CNS can directly cause sleep problems when sleep-wake mechanisms associated with the ascending reticular activating system are involved. The major sleep disorders associated with neurologic problems are outlined in the International Classification of Sleep Disorders, 2nd edition, as hypersomnias of central origin, sleep-related breathing disorders, the insomnias, circadian rhythm sleep disorders, sleep-related movement disorders, parasomnias, and sleep-related epilepsy. In a patient with CNS disease and excessive sleepiness, sleep-related breathing disorders should be a first concern, given the known association between obstructive sleep apnea (OSA) and cerebrovascular disease and the potential confounding effects that OSA might have on an otherwise compromised ischemic CNS penumbra. A basic knowledge of the anatomy and physiology of the sleep-wake mechanisms provides a rationale for pharmacologic intervention. Nonpharmacologic treatments are also important, especially when sleep-related breathing disorders are a concern. In addition, as patients with neurologic diseases are often prone to the adverse effects of many medications, the specific treatment regimen for any given individual should always include good sleep hygiene practices that use cognitive behavioral therapy.

The impact of atypical antipsychotic use on obstructive sleep apnea: a pilot study and literature review.

BACKGROUND: Limited evidence links atypical antipsychotics (AAs) use to sleep related respiratory dysfunction and greater severity of obstructive sleep apnea (OSA). The present paper reviews the published evidence and examines the impact of AA use on the presence and severity of OSA among subjects with clinically suspected OSA after adjusting for several confounds. METHODS: Archives of the University of Iowa Sleep Laboratory from 2005 to 2009 were searched for patients using AAs at the time of diagnostic polysomnogram (PSG). PSG data of the 84 AA users with heterogeneous psychiatric disorders (of these 20 diagnosed only with depression) were subsequently compared to PSG data of two randomly selected, non-AA user groups from the same patient pool: (i) 200 subjects with a depressive disorder as the only psychiatric diagnosis, and (ii) 331 mentally healthy controls. PSG data were analyzed adjusting for known demographic, medical, and psychiatric risk factors for OSA. RESULTS: Prevalence and severity of OSA did not differ significantly across three groups. Sex, age, body mass index (BMI), and neck circumference (NC) independently predicted OSA. Odds ratio for OSA in the subset of AA users carrying the diagnosis of depression (n=20) compared with subjects without mental illness was 4.53 (p<.05). By contrast, AA users without depression or those with multiple psychiatric diagnoses including depression did not show a statistically significantly elevated OSA risk. CONCLUSIONS: AA use in subjects with depression appears to increase the risk of OSA after controlling for known predisposing factors.

Management of sleep disorders in stroke.

OPINION STATEMENT: Scientific studies have proven a very strong association between stroke and obstructive sleep apnea (OSA). The prevalence of OSA is very high in patients with acute stroke, and untreated OSA is a stroke risk factor. In the stroke patient population, symptoms of OSA may atypically appear as isolated insomnia, hypersomnia, a dysfunction of circadian rhythm, a parasomnia, or a sleep-related movement disorder. Thus, we believe that in patients with acute stroke, OSA should be addressed first, using full in-laboratory, attended polysomnography (PSG), before other specific sleep disorders are aggressively addressed with specific therapeutic interventions. When OSA is diagnosed, supportive techniques including the application of continuous positive airway pressure (CPAP) therapy, positional therapies, or both should be considered first-line treatments. If OSA is ruled out by PSG, the therapeutic emphasis for sleep-related complaints is routinely based on instituting good sleep hygiene practices and using cognitive behavioral techniques (cognitive therapies, sleep restriction, stimulus control, and progressive relaxation therapies) because patients with stroke may be prone to the adverse effects of many of the medications that are otherwise routinely prescribed for a variety of specific sleep disorders.

Obstructive sleep apnea and stroke.

Obstructive sleep apnea (OSA) and stroke are frequent, multifactorial entities that share risk factors, and for which case-control and cross-sectional studies have shown a strong association. Stroke of respiratory centers can lead to apnea. Snoring preceding stroke, documentation of apneas immediately prior to transient ischemic attacks, the results of autonomic studies, and the circadian pattern of stroke, suggest that untreated OSA can contribute to stroke. Although cohort studies indicate that OSA is a stroke risk factor, controversy surrounds the cost-effectiveness of the screening for and treatment of OSA once stroke has occurred.

REM alpha rhythm: diagnostic for narcolepsy?

SUMMARY: A young man, in whom narcolepsy was subsequently diagnosed, had the simultaneous onset of quadriparesis and a rapid eye movement (REM)-sleep polysomnographic pattern. During this REM-sleep pattern, a waking alpha EEG rhythm, appearing when he was asked to close his eyes, immediately attenuated when he was instructed to open his eyes, after which the REM-sleep pattern persisted. The juxtaposition of REM sleep patterns and reactive alpha rhythms are likely unique to sleep paralysis and may prove valuable in diagnosing narcolepsy.

Obstructive sleep apnea associated with cerebral hypoxemia and death.

An increase in the arousal threshold may predispose critically ill patients with obstructive sleep apnea (OSA) to prolonged apneas and death during sleep. We report two cases in whom polysomnographically documented OSA resulted in EEG changes compatible with cerebral hypoxemia with subsequent respective transient encephalopathy in one instance and death in the other.

Prospective polysomnographic analysis of obstructive sleep apnea in down syndrome.

OBJECTIVES: To investigate obstructive sleep apnea (OSA) in a consecutively encountered, nonselected population of young patients with Down syndrome using standard overnight polysomnography and to determine the effects of therapy. METHODS: In a population of patients seen for routine developmental evaluations, 9 boys and 10 girls were studied using standard overnight polysomnography. RESULTS: Using pediatric standards, OSA was found in 79% of the subjects (95% confidence interval, 54%-94%), with a median apnea index of 3 events per hour (interquartile range, 2-5), a median apnea-hypopnea index of 6 events per hour (interquartile range, 3-8), and a median arterial oxygen saturation (SaO2) low point of 88% (interquartile range, 84%-90%). Higher body mass index was significantly associated with a higher apnea index and a lower SaO2 level, and there was a significant inverse relationship between age and the lowest SaO2 value as well as a possible association between sleep-related symptoms at the time of diagnosis and the lowest SaO2 value. In addition, patients with OSA had a significantly higher movement arousal index than those without OSA. CONCLUSIONS: Using rigid polysomnographic standards, this pilot study revealed OSA in a high percentage of young subjects with Down syndrome and an association between OSA and obesity, age, and poor sleep quality. These findings justify larger and more detailed population studies to further define clinical factors that are concomitant with OSA in Down syndrome and to improve therapy.

Transient obstructive sleep apnea and asystole in association with presumed viral encephalopathy.

Evidence suggests that untreated obstructive sleep apnea (OSA) can lead to hypertension, cardiovascular disease, and stroke. Conversely, the systemic effects of a wide variety of critical illnesses can lead to CNS dysfunction, which can precipitate respiratory failure. Reported is a patient in whom an acute encephalopathy may have been responsible for transient OSA.