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Journal articles on the topic 'Sleep apnea, obstructive'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Sisniega, Carlos, and Umakanth Katwa. "Children with Upper Airway Dysfunction: At Risk of Obstructive Sleep Apnea." Journal of Child Science 09, no. 01 (January 2019): e59-e67. http://dx.doi.org/10.1055/s-0039-1688956.

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AbstractObstructive sleep apnea is characterized by prolonged partial upper airway obstruction or intermittent complete obstruction that disrupts normal ventilation during sleep and alters normal sleep patterns. Patients with obstructive sleep apnea tend to develop neurocognitive, cardiovascular, behavioral, attention issues, and poor academic performance. Therefore, it is essential to diagnose and treat obstructive sleep apnea early and avoid significant and long-lasting adverse outcomes. Most commonly, upper airway obstruction is caused by enlarged lymphoid tissues within the upper airway, and therefore adenotonsillectomy is considered as the first-line treatment of obstructive sleep apnea in children. Fifty to 70% of patients who have obstructive sleep apnea and treated by surgery are not entirely cured on follow-up polysomnography. In light of this, it is recommended that patients with suspected obstructive sleep apnea undergo a thorough evaluation, and all potential risk factors are identified and treated. The purpose of this review is to familiarize pediatricians with developmental, anatomical, and physiological risk factors involved in the development of obstructive sleep apnea. Additionally, we will present an array of evaluation techniques that can offer adequate assessment of the patient's upper airway anatomy and physiology.

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2

Khan, Muhammad Talha, and Rose Amy Franco. "Complex Sleep Apnea Syndrome." Sleep Disorders 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/798487.

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Complex sleep apnea is the term used to describe a form of sleep disordered breathing in which repeated central apneas (>5/hour) persist or emerge when obstructive events are extinguished with positive airway pressure (PAP) and for which there is not a clear cause for the central apneas such as narcotics or systolic heart failure. The driving forces in the pathophysiology are felt to be ventilator instability associated oscillation in PaCO2arterial partial pressure of Carbon Dioxide, continuous cositive airway pressure (CPAP) related increased CO2carbon dioxide elimination, and activation of airway and pulmonary stretch receptors triggering these central apneas. The prevalence ranges from 0.56% to 18% with no clear predictive characteristics as compared to simple obstructive sleep apnea. Prognosis is similar to obstructive sleep apnea. The central apnea component in most patients on followup using CPAP therap, has resolved. For those with continued central apneas on simple CPAP therapy, other treatment options include bilevel PAP, adaptive servoventilation, permissive flow limitation and/or drugs.

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3

McGinley, Brian M., Alan R. Schwartz, Hartmut Schneider, Jason P. Kirkness, Philip L. Smith, and Susheel P. Patil. "Upper airway neuromuscular compensation during sleep is defective in obstructive sleep apnea." Journal of Applied Physiology 105, no. 1 (July 2008): 197–205. http://dx.doi.org/10.1152/japplphysiol.01214.2007.

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Obstructive sleep apnea is the result of repeated episodes of upper airway obstruction during sleep. Recent evidence indicates that alterations in upper airway anatomy and disturbances in neuromuscular control both play a role in the pathogenesis of obstructive sleep apnea. We hypothesized that subjects without sleep apnea are more capable of mounting vigorous neuromuscular responses to upper airway obstruction than subjects with sleep apnea. To address this hypothesis we lowered nasal pressure to induce upper airway obstruction to the verge of periodic obstructive hypopneas (cycling threshold). Ten patients with obstructive sleep apnea and nine weight-, age-, and sex-matched controls were studied during sleep. Responses in genioglossal electromyography (EMGGG) activity (tonic, peak phasic, and phasic EMGGG), maximal inspiratory airflow (VImax), and pharyngeal transmural pressure (PTM) were assessed during similar degrees of sustained conditions of upper airway obstruction and compared with those obtained at a similar nasal pressure under transient conditions. Control compared with sleep apnea subjects demonstrated greater EMGGG, VImax, and PTM responses at comparable levels of mechanical and ventilatory stimuli at the cycling threshold, during sustained compared with transient periods of upper airway obstruction. Furthermore, the increases in EMGGG activity in control compared with sleep apnea subjects were observed in the tonic but not the phasic component of the EMG response. We conclude that sustained periods of upper airway obstruction induce greater increases in tonic EMGGG, VImax, and PTM in control subjects. Our findings suggest that neuromuscular responses protect individuals without sleep apnea from developing upper airway obstruction during sleep.

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4

Fairbanks, David W., and David N. F. Fairbanks. "Neurostimulation for Obstructive Sleep Apnea: Investigations." Ear, Nose & Throat Journal 72, no. 1 (January 1993): 52–57. http://dx.doi.org/10.1177/014556139307200111.

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Neurostimulation of the upper airway muscles (accessory muscles of respiration) was accomplished in anesthetized dogs and sleeping humans by electrical stimulation of the hypoglossal nerves. Such stimulations relieved partial airway obstructions in dogs. They also aborted (shortened) obstructive sleep apnea events in humans who suffer with obstructive sleep apnea syndrome. In one subject, stimulations delivered in advance of apneic events (by automatic cycling) prevented apneas. Neurostimulation for obstructive sleep apnea may be an important concept for future research and development.

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Basner, R. C., E. Onal, D. W. Carley, E. J. Stepanski, and M. Lopata. "Effect of induced transient arousal on obstructive apnea duration." Journal of Applied Physiology 78, no. 4 (April 1, 1995): 1469–76. http://dx.doi.org/10.1152/jappl.1995.78.4.1469.

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Six untreated male patients (age 19–55 yr) with obstructive sleep apnea underwent nocturnal polysomnography with acoustic stimulation to determine the effect of transient arousal on obstructive apneas during sleep. Binaural tone bursts (25–95 dB) were delivered in late expiration during the second obstructive apnea of a cycle consisting of four consecutive apneas. For the group, stimulated apneas were significantly shorter (P < 0.05, Fisher's protected least significant difference test) than were the unstimulated apneas when transient electrocortical arousal was elicited in both non-rapid-eye-movement (non-REM) sleep [mean 17 +/- 7 (SD) vs. 26 +/- 9, 23 +/- 10, and 26 +/- 12 s for 2nd vs. 1st, 3rd, and 4th apnea, respectively, of each cycle] and REM sleep (mean 19 +/- 10 vs. 35 +/- 15, 45 +/- 18, and 39 +/- 20 s). Without electrocortical arousal, the stimulated apnea was significantly shortened in non-REM (23 +/- 9 vs. 25 +/- 7, 24 +/- 8, and 26 +/- 8 s) but not in REM (32 +/- 16 vs. 37 +/- 12, 32 +/- 15, and 30 +/- 16 s). Tones delivered relatively early and late in the apnea were equally likely to be associated with resolution of the apnea. The nadir of arterial oxygen saturation of hemoglobin was inversely proportional to apnea length, with higher saturation nadirs associated with the stimulated apneas. These data indicate that transient arousal, induced by nonrespiratory stimulation, influences the resolution of obstructive apneas during sleep.

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6

Durgan, David J., Randy F. Crossland, and Robert M. Bryan. "The rat cerebral vasculature exhibits time-of-day-dependent oscillations in circadian clock genes and vascular function that are attenuated following obstructive sleep apnea." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (January 1, 2016): 2806–19. http://dx.doi.org/10.1177/0271678x16675879.

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Circadian clock components oscillate in cells of the cardiovascular system. Disruption of these oscillations has been observed in cardiovascular diseases. We hypothesized that obstructive sleep apnea, which is associated with cerebrovascular diseases, disrupts the cerebrovascular circadian clock and rhythms in vascular function. Apneas were produced in rats during sleep. Following two weeks of sham or obstructive sleep apnea, cerebral arteries were isolated over 24 h for mRNA and functional analysis. mRNA expression of clock genes exhibited 24-h rhythms in cerebral arteries of sham rats (p < 0.05). Interestingly, peak expression of clock genes was significantly lower following obstructive sleep apnea (p < 0.05). Obstructive sleep apnea did not alter clock genes in the heart, or rhythms in locomotor activity. Isolated posterior cerebral arteries from sham rats exhibited a diurnal rhythm in sensitivity to luminally applied ATP, being most responsive at the beginning of the active phase (p < 0.05). This rhythm was absent in arteries from obstructive sleep apnea rats (p < 0.05). Rhythms in ATP sensitivity in sham vessels were absent, and not different from obstructive sleep apnea, following treatment with L-NAME and indomethacin. We conclude that cerebral arteries possess a functional circadian clock and exhibit a diurnal rhythm in vasoreactivity to ATP. Obstructive sleep apnea attenuates these rhythms in cerebral arteries, potentially contributing to obstructive sleep apnea-associated cerebrovascular disease.

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7

Mattiuzzi, Camilla, Massimo Franchini, and Giuseppe Lippi. "Sleep apnea and venous thromboembolism." Thrombosis and Haemostasis 114, no. 11 (2015): 958–63. http://dx.doi.org/10.1160/th15-03-0188.

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SummaryRecent evidence suggests that obstructive sleep apnea is a significant and independent risk factor for a number of cardiovascular disorders. Since the association between obstructive sleep apnea and cardiovascular disease is mediated by endothelial dysfunction, hypercoagulability and platelet abnormalities, we sought to investigate whether sleep apnea may also be considered a risk factor for venous thromboembolism (VTE). We carried out an electronic search in Medline and Scopus using the keywords “apnea” OR “apnoea” AND “venous thromboembolism” OR “deep vein thrombosis” OR “pulmonary embolism” in “Title/Abstract/Keywords”, with no language or date restriction. Fifteen studies (8 case-control, 4 retrospective observational, 2 prospective case-control and 1 prospective observational) were finally selected for this systematic review. In all studies except one (14/15; 93%), obstructive sleep apnea was found to be an independent risk factor for VTE, either deep-vein thrombosis (DVT) or pulmonary embolism (PE). In the two prospective case-control studies the risk of DVT or PE was found to be two-to three-fold higher in patients with obstructive sleep apnea than in those without. In conclusion, the current epidemiological evidence supports the hypothesis that obstructive sleep apnea may be an independent risk factor for VTE.

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8

Bhandarkar, Dr Ajay M., Dr Rukma Bhandary, and Dr Suraj S. Nair. "Clinical Indicators of Obstructive Sleep Apnea Syndrome." International Journal of Scientific Research 2, no. 12 (June 1, 2012): 399–400. http://dx.doi.org/10.15373/22778179/dec2013/120.

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9

Bilińska, Małgorzata, and Kazimierz Niemczyk. "Hypoglossal nerve stimulation [HGNS] for Obstructive Sleep Apnea [OSA] treatment – a review." Polski Przegląd Otorynolaryngologiczny 6, no. 3 (September 30, 2017): 66–71. http://dx.doi.org/10.5604/01.3001.0010.5196.

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Obstructive sleep apnea (OSA) is characterized by recurrent periods of upper airway obstruction (hypopneas and apneas) during sleep. It leads to repeated oxyhemoglobin desaturations, nocturnal hypercapnia, and arousals. Common symptoms include loud snoring with breathing interruptions. Excessive daytime sleepiness and cognitive impairment occur. Obstructive sleep apnea is a major cause of morbidity and mortality in Western society. Its association with an increased risk of development and progression of neurocognitive, metabolic, cardiovascular and oncologic diseases and complications is well described. The significant factor in OSA pathogenesis is reduced muscle tone in the tongue and upper airway. In the recent years, devices providing neurostimulation of the hypoglossal nerve (HGNS) were developed as an alternative for noncompliant CPAP (continuous positive airway pressure) patients. Clinical trials suggest that electrical stimulation of the hypoglossal nerve is effective. This is considered to be one of the targets of neurostimulation in the treatment of obstructive sleep apnea (OSA).

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10

Hanly, Patrick J., and David Ford. "Sleep Apnea and Aortic Dissection." Canadian Respiratory Journal 2, no. 1 (1995): 69–73. http://dx.doi.org/10.1155/1995/254831.

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A 62-year-old man presented with obstructive sleep apnea, congestive heart failure and Cheyne-Stokes respiration. Further evaluation revealed a chronic dissecting aneurysm of the aorta causing vena caval obstruction. Surgical correction or the aneurysm dramatically improved ventricular function with resolution of Cheyne-Stokes respiration. Nasal continuous positive airway pressure corrected the obstructive sleep apnea and associated clinical features. The cardiopulmonary interactions between sleep apnea and aortic dissection are discussed.

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11

Wetmore, Stephen J., Lawrence Scrima, and F. Charles Hiller. "Sleep Apnea in Epistaxis Patients Treated with Nasal Packs." Otolaryngology–Head and Neck Surgery 98, no. 6 (June 1988): 596–99. http://dx.doi.org/10.1177/019459988809800611.

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The presence of anterior and posterior nasal packs in patients with epistaxis is known to be associated with cardiorespiratory problems and sometimes death, although the mechanism has not been well understood. To determine the incidence and severity of obstructive sleep apnea in patients with epistaxis treated with both anterior and posterior nasal packs, we obtained polysomnograms on twelve patients while the packs were in place. Ten of these patients demonstrated obstructive sleep apnea. The apnea index (apneas/hour sleep) ranged from 1 to 83, with a mean of 29; the hypopnea index (hypopneas/hour sleep) ranged from 9 to 33, with a mean of 20; and the lowest oxygen saturation (SaO2) ranged from 17% to 91%, with a mean of 77%. Ten patients returned for another polysomnogram after removal of the packs. These baseline studies showed improvement in the apnea index and in the lowest SaO2 in all patients, although four patients still demonstrated at least mild obstructive sleep apnea. This study demonstrates that nasal packs used for the treatment of epistaxis may induce obstructive sleep apnea or markedly exacerbate underlying obstructive sleep apnea and, therefore, contribute to the sudden deaths that have been reported in epistaxis patients.

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12

Davis, Eric M., Landon W. Locke, Angela L. McDowell, Patrick J. Strollo, and Christopher P. O'Donnell. "Obesity accentuates circadian variability in breathing during sleep in mice but does not predispose to apnea." Journal of Applied Physiology 115, no. 4 (August 15, 2013): 474–82. http://dx.doi.org/10.1152/japplphysiol.00330.2013.

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Obesity is a primary risk factor for the development of obstructive sleep apnea in humans, but the impact of obesity on central sleep apnea is less clear. Given the comorbidities associated with obesity in humans, we developed techniques for long-term recording of diaphragmatic EMG activity and polysomnography in obese mice to assess breathing patterns during sleep and to determine the effect of obesity on apnea generation. We hypothesized that genetically obese ob/ob mice would exhibit less variability in breathing across the 24-h circadian cycle, be more prone to central apneas, and be more likely to exhibit patterns of increased diaphragm muscle activity consistent with obstructive apneas compared with lean mice. Unexpectedly, we found that obese mice exhibited a greater circadian impact on respiratory rate and diaphragmatic burst amplitude than lean mice, particularly during rapid eye movement (REM) sleep. Central apneas were more common in REM sleep (42 ± 17 h−1) than non-REM (NREM) sleep (14 ± 5 h−1) in obese mice ( P < 0.05), but rates were not different between lean and obese mice in either sleep state. Even after experimentally enhancing central apnea generation by acute withdrawal of hypoxic chemoreceptor activation during sleep, central apnea rates remained comparable between lean and obese mice. Last, we were unable to detect patterns of diaphragmatic burst activity suggestive of obstructive apnea events in obese mice. In summary, obesity does not predispose mice to increased occurrence of central or obstructive apneas during sleep, but does lead to a more pronounced circadian variability in respiration.

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13

TOADER, Corneliu, Mioriţa TOADER, Andreea ŞERBĂNICĂ, Mircea DRĂGHICI, Alina OPREA, and Iolanda Cristina VIVISENCO. "Pediatric obstructive sleep apneea – surgical treatment." Romanian Journal of Medical Practice 10, no. 2 (June 30, 2015): 182–86. http://dx.doi.org/10.37897/rjmp.2015.2.16.

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Obstructive sleep apnea is characterized by recurrent episodes of partial or complete obstruction of upper respiratory airways which appear during sleep and lead to the decrease of oxygen saturation and numerous awakenings. The symptomatology in pediatric obstructive sleep apnea is very different from the adult type in many aspects. The gold standard examination for diagnosis and evaluation of severity is polysomnography. The authors present their experience in the surgical tratament of children with obstructive sleep apnea. It is outlined a group of patient enrolled during a period of 5 years (2010-2014) who had their tonsils reduced through coblation and radiofrequency techniques.

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14

Hossain, AKM Mosharraf, and Mostofa Midhat Pasha. "Obstructive sleep apnea and cardiovascular effects-a review." University Heart Journal 4, no. 2 (February 2, 2009): 41–45. http://dx.doi.org/10.3329/uhj.v4i2.2075.

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Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing, affecting 5-15% of the population. It is characterized by intermittent episodes of partial or complete obstruction of the upper airway during sleep that disrupts normal ventilation and sleep architecture, and is typically associated with excessive daytime sleepiness, snoring, and witnessed apneas. Patients with obstructive sleep apnea present risk to the general public safety by causing 8-fold increase in vehicle accidents, and they may themselves also suffer from the physiologic consequences of OSA; these include hypertension, coronary artery disease, stroke, congestive heart failure, pulmonary hypertension, and cardiac arrhythmias. Of these possible cardiovascular consequences, the association between OSA and hypertension has been found to be the most convincing. Although the exact mechanism has not been understood, there is some evidence that OSA is associated with frequent apneas causing mechanical effects on intrathoracic pressure, cardiac function, and intermittent hypoxemia, which may in turn cause endothelial dysfunction and increase in sympathetic drive. Therapy with continuous positive airway pressure has been demonstrated to improve cardiopulmonary hemodynamics in patients with OSA and may reverse the endothelial cell dysfunction. Limited availability of diagnostic measures and unawareness of physicians, many patients with OSA remain undiagnosed. Awareness and timely initiation of an effective treatment may prevent potential deleterious cardiovascular effects of OSA. Key words: Obstructive Sleep apnea, Hypertension, Atherosclerosis, Continuous positive airway pressure. Â doi:10.3329/uhj.v4i2.2075 University Heart Journal Vol. 4 No. 2 July 2008 p.41-45

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15

Nouraddin, Nouraddin, and Louella Amos. "844 Pediatric Vagus Nerve Stimulator-Induced Obstructive Sleep Apnea." Sleep 44, Supplement_2 (May 1, 2021): A328—A329. http://dx.doi.org/10.1093/sleep/zsab072.841.

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Abstract Introduction Vagus nerve stimulation (VNS) is an adjunct treatment for seizures refractory to medications. VNS in children with epilepsy can reduce seizures by up to 90%. VNS settings include stimulation on-time, off-time, frequency and output current. Complications of VNS include sleep-disordered breathing due to laryngopharyngeal dysfunction, which can also cause voice alteration, hoarseness, and cough. Both obstructive apneas (more common) and central apneas can be seen in those patients who have VNS-induced sleep-disordered breathing. Report of case(s) A 14-year-old male with Lennox-Gastaut syndrome treated with multiple antiepileptic drugs and VNS was admitted to the PICU with worsening seizures. He developed acute respiratory failure due to status epilepticus, requiring intubation. After extubation, he was observed to have repetitive respiratory obstruction at regular intervals, occurring throughout the day and night, and associated with mild oxygen desaturations. Polysomnography showed cyclical obstructive respiratory events lasting 30 seconds followed by approximately 2-minute intervals of regular breathing. Interrogation of his VNS device revealed the following settings: output current of 1.75 mA, 30 seconds on, and 1.8 minutes off. CPAP therapy improved his oxygen saturations, but he continued to clinically exhibit the repetitive obstructive apneas even on positive pressure. However, after his VNS device settings were decreased, repeat polysomnography showed resolution of his obstructive breathing. Conclusion This case report demonstrates pediatric VNS-induced obstructive sleep apnea. Activation of the vagus nerve can cause laryngopharyngeal dysfunction, including laryngospasm and vocal cord dysfunction, with subsequent upper airway obstruction, causing obstructive apneas or hypopneas. Treatment options for pediatric VNS-induced OSA include CPAP, decreasing the VNS settings and adenotonsillectomy. Support (if any):

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16

V.G, Hridya, Rani Somani, Shipra Jaidka, Deepti Jawa, Aiswarya Madhu, and Muhamed Sabin. "OBSTRUCTIVE SLEEP APNEA." International Journal of Advanced Research 9, no. 03 (March 31, 2021): 692–712. http://dx.doi.org/10.21474/ijar01/12634.

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Obstructive sleep apnea is an under recognized and under diagnosed medical condition, with a myriad of negative consequences on patients health and society as a whole. The most acting reason behind Obstructive sleep apnea given as in literature is due to recurrent episodes of upper airway (UA) collapse during sleep. Episodes may last 10 seconds or longer and commonly last 30 seconds or longer. From the mid-1990s to the present, we have seen an explosion of basic, clinical, and population research directed toward the prevalence, causes, consequences, and treatment of this long-standing, although only recently appreciated, problem. Sleep apnea has attracted a myriad of researchers from diverse disciplines and clinical subspecialties. At the same time, sleep apnea as a serious, undefined clinical problem has also given birth to many sleep medicine clinics throughout the western world. Finally, given the relatively high prevalence of this sleep-specific problem with potential carryover to daytime pathology, sleep apnea has provided great impetus to the growth of sleep medicine as a clinical and research specialty. Dentists have been involved in the collaborative evaluation and treatment of patients with OSA using oral appliances from 1980. Importantly, dentists play a crucial role in evaluating patients with OSA for the suitability of appliance therapy, choosing and adjusting the appliance and assessing the patient for adverse effects. To accomplish holistic treatment approach it is essential that dentists and the sleep medicine physician should work collaboratively. When this occurs, patients will have the best opportunity for the effective treatment of their OSA.

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17

Hudgel, D. W. "Variable site of airway narrowing among obstructive sleep apnea patients." Journal of Applied Physiology 61, no. 4 (October 1, 1986): 1403–9. http://dx.doi.org/10.1152/jappl.1986.61.4.1403.

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The purpose of this was to determine whether the site of physiological narrowing within the upper airway was uniform or differed among patients with obstructive sleep apnea. Inspiratory pressures were measured with an esophageal balloon catheter and three catheters located at different sites along the upper airway: supralaryngeal airway, oropharynx, and nasopharynx. Peak inspiratory pressure differences between catheters allowed assessment of pressure gradients across three airway segments: lungs-larynx-retroepiglottal airway (esophageal-supralaryngeal pressure), hypopharynx (supralaryngeal-oropharynx pressure), and transpalatal airway (oropharynx-nasopharynx pressure). In five patients, hypopharyngeal obstruction was present, and in four patients no hypopharyngeal obstruction existed. In these four patients the site of obstruction was located at the level of the palate. In a given subject, the site of obstruction was the same during repeated measurements. The presence or absence of hypopharyngeal narrowing during sleep was not predictable from gradients measured across different segments of the upper airway during wakefulness. We conclude that the site of physiological upper airway obstruction varies among patients with obstructive sleep apnea and is not predictable from pressure measured during wakefulness. We speculate that uvulopalatopharyngoplasty may not relieve obstructive apneas in patients with hypopharyngeal obstruction.

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18

Orr, William C., Monte L. Stahl, James Duke, Mary Anne McCaffree, Paul Toubas, Cynthia Mattice, and Henry F. Krous. "Effect of Sleep State and Position on the Incidence of Obstructive and Central Apnea in Infants." Pediatrics 75, no. 5 (May 1, 1985): 832–35. http://dx.doi.org/10.1542/peds.75.5.832.

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Sixty-four infants with a history of apnea were studied to determine the effects of sleeping position and sleep state (rapid eye movement [REM]) v (nonrapid eye movement [NREM]) on the occurrence of central and obstructive apneas. All-night polysomnographic studies were conducted on each infant, and the spontaneous occurrence of central and obstructive apneic events was determined in the prone, supine, and side positions. Sleeping position did not significantly affect the rate or duration of central or obstructive apneas. Furthermore, neither central nor obstructive apneic episodes were significantly altered by sleep state. These data suggest that, in spite of an ostensible predisposition to upper airway obstruction in the supine position and during rapid eye movement sleep, neither sleeping position nor sleep state appears to affect the rate of duration of apneic events.

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19

Arnold, Joseph, M. Sunilkumar, V. Krishna, SP Yoganand, MSathish Kumar, and D. Shanmugapriyan. "Obstructive sleep apnea." Journal of Pharmacy And Bioallied Sciences 9, no. 5 (2017): 26. http://dx.doi.org/10.4103/jpbs.jpbs_155_17.

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20

Caples, Sean M., Apoor S. Gami, and Virend K. Somers. "Obstructive Sleep Apnea." Annals of Internal Medicine 142, no. 3 (February 1, 2005): 187. http://dx.doi.org/10.7326/0003-4819-142-3-200502010-00010.

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Balachandran, Jay S., and Sanjay R. Patel. "Obstructive Sleep Apnea." Annals of Internal Medicine 161, no. 9 (November 4, 2014): ITC1. http://dx.doi.org/10.7326/0003-4819-161-9-201411040-01005.

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22

Sullivan, Colin E., and Faiq G. Issa. "Obstructive Sleep Apnea." Clinics in Chest Medicine 6, no. 4 (December 1985): 633–50. http://dx.doi.org/10.1016/s0272-5231(21)00401-9.

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Gogoi, Dr Juganta Jyoti, Dr Anshul Singla, Dr Amrita Puri, Dr Rakshita Kathia, and Dr Atika Tulsyan. "Obstructive sleep apnea." International Journal of Applied Dental Sciences 8, no. 2 (April 1, 2022): 467–71. http://dx.doi.org/10.22271/oral.2022.v8.i2g.1544.

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Patel, Sanjay R. "Obstructive Sleep Apnea." Annals of Internal Medicine 171, no. 11 (December 3, 2019): ITC81. http://dx.doi.org/10.7326/aitc201912030.

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Suurna, Maria V., and Ana C. Krieger. "Obstructive Sleep Apnea." Clinics in Geriatric Medicine 37, no. 3 (August 2021): 429–44. http://dx.doi.org/10.1016/j.cger.2021.04.005.

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Feinsilver, Steven H. "Obstructive Sleep Apnea." Clinics in Geriatric Medicine 37, no. 3 (August 2021): 417–27. http://dx.doi.org/10.1016/j.cger.2021.04.004.

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Brodie, Kara D., and Andrew N. Goldberg. "Obstructive Sleep Apnea." Medical Clinics of North America 105, no. 5 (September 2021): 885–900. http://dx.doi.org/10.1016/j.mcna.2021.05.010.

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Patel, Arpan, and Derek J. Chong. "Obstructive Sleep Apnea." Clinics in Geriatric Medicine 37, no. 3 (August 2021): 457–67. http://dx.doi.org/10.1016/j.cger.2021.04.007.

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Natale, Enrico, and Massimo Pistono. "Obstructive sleep apnea." Journal of Cardiovascular Medicine 18 (January 2017): e30-e34. http://dx.doi.org/10.2459/jcm.0000000000000439.

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Ho, Matthew L., and Steven D. Brass. "Obstructive sleep apnea." Neurology International 3, no. 3 (December 2, 2011): 15. http://dx.doi.org/10.4081/ni.2011.e15.

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Obstructive sleep apnea (OSA) affects millions of Americans and is estimated to be as prevalent as asthma and diabetes. Given the fact that obesity is a major risk factor for OSA, and given the current global rise in obesity, the prevalence of OSA will increase in the future. Individuals with sleep apnea are often unaware of their sleep disorder. It is usually first recognized as a problem by family members who witness the apneic episodes or is suspected by their primary care doctor because of the individual’s risk factors and symptoms. The vast majority remain undiagnosed and untreated, despite the fact that this serious disorder can have significant consequences. Individuals with untreated OSA can stop breathing hundreds of times a night during their sleep. These apneic events can lead to fragmented sleep that is of poor quality, as the brain arouses briefly in order for the body to resume breathing. Untreated, sleep apnea can have dire health consequences and can increase the risk of hypertension, diabetes, heart disease, and heart failure. OSA management has also become important in a number of comorbid neurological conditions, including epilepsy, stroke, multiple sclerosis, and headache. Diagnosis typically involves use of screening questionnaires, physical exam, and an overnight polysomnography or a portable home study. Treatment options include changes in lifestyle, positive airway pressure, surgery, and dental appliances.

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Scott, Brian, Romaine F. Johnson, and Ron B. Mitchell MD. "Obstructive Sleep Apnea." Otolaryngology–Head and Neck Surgery 154, no. 5 (March 15, 2016): 936–43. http://dx.doi.org/10.1177/0194599816636626.

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Goodchild, Traci T., and David J. Lefer. "Obstructive Sleep Apnea." Circulation Research 126, no. 2 (January 17, 2020): 229–31. http://dx.doi.org/10.1161/circresaha.119.316359.

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Chua, Willy, and Alejandro D. Chediak. "Obstructive sleep apnea." Postgraduate Medicine 95, no. 2 (February 1994): 123–38. http://dx.doi.org/10.1080/00325481.1994.11945797.

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Aboussouan, Loutfi S., Joseph A. Golish, and Benjamin G. Wood. "Obstructive sleep apnea." Postgraduate Medicine 96, no. 3 (September 1994): 115–23. http://dx.doi.org/10.1080/00325481.1994.11945896.

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Lazor, John B., Jeffrey S. Orringer, and Marvin P. Fried. "Obstructive sleep apnea." Current Opinion in Otolaryngology & Head and Neck Surgery 2 (June 1994): 262–70. http://dx.doi.org/10.1097/00020840-199406000-00009.

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Flemons, W. Ward. "Obstructive Sleep Apnea." New England Journal of Medicine 347, no. 7 (August 15, 2002): 498–504. http://dx.doi.org/10.1056/nejmcp012849.

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Kirsch, Douglas B. "Obstructive Sleep Apnea." CONTINUUM: Lifelong Learning in Neurology 26, no. 4 (August 2020): 908–28. http://dx.doi.org/10.1212/con.0000000000000885.

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Cassiere, Hugh A., Lloyd Blake, and Hugh A. Cassiere. "Obstructive Sleep Apnea." Clinical Pulmonary Medicine 5, no. 3 (May 1998): 195–99. http://dx.doi.org/10.1097/00045413-199805000-00008.

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Blake, Lloyd, and Hugh A. Cassiere. "OBSTRUCTIVE SLEEP APNEA." Clinical Pulmonary Medicine 5, no. 4 (July 1998): 267–70. http://dx.doi.org/10.1097/00045413-199807000-00008.

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&NA;. "Obstructive Sleep Apnea." Clinical Pulmonary Medicine 2, no. 5 (September 1995): 312. http://dx.doi.org/10.1097/00045413-199509000-00010.

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Keller, Stephen. "OBSTRUCTIVE SLEEP APNEA." Journal of the American Dental Association 140, no. 5 (May 2009): 515. http://dx.doi.org/10.14219/jada.archive.2009.0202.

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Martin, Linda L. "Obstructive Sleep Apnea." Dimensions Of Critical Care Nursing 8, no. 2 (March 1989): 83–91. http://dx.doi.org/10.1097/00003465-198903000-00004.

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&NA;. "Obstructive Sleep Apnea." Neurology Now 3, no. 3 (May 2007): 46–47. http://dx.doi.org/10.1097/01.nnn.0000279085.30196.ce.

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Strollo, Patrick J., and Robert M. Rogers. "Obstructive Sleep Apnea." New England Journal of Medicine 334, no. 2 (January 11, 1996): 99–104. http://dx.doi.org/10.1056/nejm199601113340207.

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Khairallah, Alexandre. "Obstructive Sleep Apnea." Smile Dental Journal 12, no. 4 (December 2017): 4–7. http://dx.doi.org/10.12816/0049359.

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Caples, Sean M., Apoor S. Gami, and Virend K. Somers. "Obstructive Sleep Apnea." FOCUS 3, no. 4 (October 2005): 557–67. http://dx.doi.org/10.1176/foc.3.4.557.

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Corbridge, Susan J., and Danielle Richlin. "Obstructive Sleep Apnea." AAOHN Journal 50, no. 11 (November 2002): 494–95. http://dx.doi.org/10.1177/216507990205001103.

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Reishtein, Judith L. "Obstructive Sleep Apnea." Journal of Cardiovascular Nursing 26, no. 2 (March 2011): 106–16. http://dx.doi.org/10.1097/jcn.0b013e3181e3d724.

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Dobrowolska-Zarzycka, Magdalena, and Jolanta Szymańska. "Obstructive sleep apnea." Zdrowie Publiczne 122, no. 4 (October 1, 2012): 430–33. http://dx.doi.org/10.12923/j.0044-2011/122-4/a.18.

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Potsic, William P. "Obstructive Sleep Apnea." Pediatric Clinics of North America 36, no. 6 (December 1989): 1435–42. http://dx.doi.org/10.1016/s0031-3955(16)36798-0.

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