口內負壓睡眠裝置對於睡眠呼吸中止病人的轉譯研究- 針對解剖結構治療療效及策略探討

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陳嘉琪(Chia-Chi Chen) 查詢紙本館藏

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跨領域轉譯醫學研究所

論文名稱

口內負壓睡眠裝置對於睡眠呼吸中止病人的轉譯研究- 針對解剖結構治療療效及策略探討
(Translational Research on Intraoral Negative Pressure Sleep Devices for Sleep Apnea Patients: Exploring Therapeutic Efficacy and Strategies Based on Anatomical Structures)

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★ 體外加強反搏治療裝置開發	★ 自12導程心電圖擷取P波特徵辨識竇性心律下之心房顫動高風險病患

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摘要(中)

引言
阻塞性睡眠呼吸暫停症（OSA）是一種常見且嚴重的睡眠障礙，特徵是在睡眠期間上呼吸道反覆塌陷，導致呼吸中止或顯著減少。OSA的高發病率及其潛在的嚴重併發症，如心血管疾病、高血壓、代謝紊亂和神經精神疾病，使得尋找有效的治療方法變得至關重要。

研究背景與目的
傳統的OSA治療方法主要包括持續正壓呼吸器（CPAP）、口內裝置（Oral Appliance）和手術等。然而，這些方法存在一定的局限性，如CPAP治療的耐受性問題，口內裝置對部分患者的有效性不足，以及手術的侵入性和風險。本研究旨在評估口內負壓裝置（iNAP）在治療OSA患者中的效果和安全性，並探索其作為OSA替代治療方案的潛力。

MRI研究方法
所有MRI影像均使用3.0 Tesla掃描器，採用32通道頭部線圈進行掃描。採用二維單鏡頭渦輪場回波進行區域分析和三維體積計算，以減少吞咽運動偽影。受試者在MRI檢查過程中裝置了MRI相容的EEG電極和鼻氣流監測導管，確保受試者正確使用iNAP。
療效研究方法
療效研究是一項前瞻性、自我對照、盲性樞紐試驗，涉及32名OSA患者，其中包括28名男性和4名女性，平均年齡為47.4歲，平均體重指數（BMI）為26.59 kg/m² 。研究使用多導睡眠監測（PSG）技術記錄受試者的睡眠狀況，並在治療前後比較主要終點變數，包括呼吸暫停低通氣指數（AHI）、血氧飽和度（SpO2）和睡眠結構參數。

研究結果
MRI影像分析
MRI影像顯示，使用iNAP裝置後，上呼吸道的整體容積和顎後及舌後區域的最大面積和體積均顯著增加。尤其在清醒和睡眠狀態下，這些變化尤為明顯。根據基線特性數據，治療反應組（Responder）和無反應組（Non-responder）在使用iNAP前後的變化均有顯著差異。
PSG數據分析
研究結果顯示，iNAP裝置顯著降低了OSA患者的AHI，從基線值32.04次/小時降至治療後的8.79次/小時。此外，患者的最低SpO2從80.0%提高到85.5%。PSG數據顯示，iNAP治療顯著改善了患者的睡眠結構，增加了N3階段（深睡眠）百分比，減少了覺醒指數。
結論
iNAP裝置是一種安全且有效的OSA治療選擇，能顯著改善患者的AHI、SpO2和睡眠結構。治療結果顯示，使用iNAP裝置後，總睡眠時間、睡眠效率、N1階段和N2階段的百分比沒有顯著變化，但N3階段、REM階段和覺醒指數顯著改善。這表明iNAP裝置能夠有效改善睡眠呼吸暫停，特別是在深睡眠和快速眼動睡眠階段的質量上。研究表明，iNAP裝置作為一種非侵入性的OSA治療方法，具有顯著的療效和良好的安全性，為OSA患者提供了一種有效的替代治療選擇。
未來研究方向
研究建議未來應進行更多的隨機對照試驗，以進一步驗證iNAP裝置的治療效果。還建議探索iNAP與其他治療方法的結合使用，例如牙套和CPAP，以提供更多樣化的治療選擇。此外，增加樣本量和延長研究時間，可以更全面地了解iNAP在不同OSA患者群體中的長期效果和耐受性。

摘要(英)

Introduction
Obstructive Sleep Apnea (OSA) is a common and severe sleep disorder characterized by repeated collapse of the upper airway during sleep, leading to cessation or significant reduction in breathing. The high prevalence of OSA and its potential severe complications, such as cardiovascular diseases, hypertension, metabolic disorders, and neuropsychiatric illnesses, underscore the critical need for effective treatment modalities.

Research Background and Objectives
Traditional OSA treatment methods include Continuous Positive Airway Pressure (CPAP), oral appliances, and surgery. However, these methods have limitations such as tolerance issues with CPAP, insufficient effectiveness of oral appliances for some patients, and the invasiveness and risks associated with surgery. This study aims to evaluate the effectiveness and safety of intraoral negative pressure devices (iNAP) in treating OSA patients and to explore their potential as an alternative treatment option.

MRI Study Methods
All MRI images were acquired using a 3.0 Tesla scanner with a 32-channel head coil. Two-dimensional single-shot turbo spin-echo imaging for regional analysis and three-dimensional volumetric calculations were utilized to minimize swallowing artifacts. During the MRI examinations, participants were equipped with MRI-compatible EEG electrodes and nasal airflow monitoring tubes to ensure proper use of iNAP.

Efficacy Study Methods
The efficacy study was a prospective, self-controlled, blind pivotal trial involving 32 OSA patients, including 28 males and 4 females, with an average age of 47.4 years and a mean Body Mass Index (BMI) of 26.59 kg/m². The study employed polysomnography (PSG) to record participants’ sleep conditions and compared primary endpoint variables before and after treatment, including the Apnea-Hypopnea Index (AHI), oxygen saturation (SpO2), and sleep architecture parameters.

Study Results
MRI Imaging Analysis
MRI imaging revealed significant increases in overall upper airway volume and the maximum area and volume in the retroglossal and retropharyngeal regions after using the iNAP device. These changes were particularly notable during both wakefulness and sleep states. According to baseline characteristics, significant differences were observed between the responder and non-responder groups before and after using iNAP.

PSG Data Analysis
The results indicated that the iNAP device significantly reduced AHI in OSA patients, from a baseline of 32.04 events/hour to 8.79 events/hour post-treatment. Furthermore, the minimum SpO2 improved from 80.0% to 85.5%. PSG data demonstrated that iNAP treatment significantly enhanced sleep architecture, increasing the percentage of N3 stage (deep sleep) and reducing the arousal index.

Conclusion
The iNAP device is a safe and effective treatment option for OSA, significantly improving AHI, SpO2, and sleep structure. Treatment outcomes showed that while total sleep time, sleep efficiency, and the percentages of N1 and N2 stages did not change significantly, there were significant improvements in the N3 stage, REM stage, and arousal index. This indicates that the iNAP device effectively improves sleep apnea, particularly the quality of deep and rapid eye movement sleep stages. The study demonstrates that iNAP, as a non-invasive treatment method for OSA, offers significant therapeutic efficacy and safety, providing an effective alternative treatment option for OSA patients.

Discussion
The study suggests further randomized controlled trials to validate the therapeutic effects of the iNAP device. It is also recommended to explore the combination use of iNAP with other treatment modalities such as dental appliances and CPAP to provide more diverse treatment options. Additionally, increasing the sample size and extending study durations would enable a more comprehensive understanding of the long-term effects and tolerability of iNAP across different OSA patient groups.

關鍵字(中)

★ 睡眠呼吸中止症
★ 口內負壓治療
★ 持續正壓呼吸器
★ CPAP 替代治療

關鍵字(英)

★ Obstructive Sleep Apnea
★ Intraoral Negative Pressure Therapy
★ Continuous Positive Airway Pressure (CPAP)
★ CPAP alternative treatment option.

論文目次

目錄
1. 引言 6
1.1 睡眠呼吸中止的臨床挑戰 6
1.1.1 睡眠呼吸障礙研究的歷史 6
1.1.2 OSA的高盛行率和潛在嚴重併發症 9
1.2 阻塞性睡眠呼吸中止併發症 11
1.2.1 阻塞性睡眠呼吸中止症 (OSA) 對心血管併發症的關係與影響： 11
1.2.2 阻塞性睡眠呼吸中止症 (OSA) 對高血壓的關係與影響 12
1.2.3 阻塞性睡眠呼吸中止症對代謝併發症的關係與影響 13
1.2.4 阻塞性睡眠呼吸中止症 (OSA) 對慢性呼吸疾病的關係與影響： 14
1.2.5 阻塞性睡眠呼吸中止（OSA）與神經及精神併發症的關聯與影響： 15
1.3 阻塞性睡眠呼吸中止（OSA）疾病的治療 17
1.3.1 持續正壓呼吸器（CPAP）: 17
1.3.2 口內裝置(Oral Appliance): 19
1.3.3 OSA手術 20
1.3.4 其他OSA替代治療： 22
2. 口內負壓治療理論背景 26
2.1 口內負壓睡眠裝置的先前研究和結果 26
2.1.1 WINX 睡眠治療系統 26
2.1.2 安鎂睡眠呼吸治療裝置 (iNAP Sleep Therapy System) 28
2.2 口內負壓技術的原理 31
2.2.1 壓力梯度療法 31
2.2.2 吸力、壓力和口內空間的關係 33
變化後的原理和公式 36
2.2.3 iNAP治療壓力範圍的安全性： 37
2.3 口內負壓治療睡眠呼吸中止的生理機轉 39
2.3.1 增加上呼吸道的通暢性 39
2.3.2 提高上呼吸道軟組織的穩定性 42
2.3.3 幫助閉口鼻呼吸： 43
3. 口內負壓睡眠治療影像研究 45
3.1 研究目的 45
3.2 研究方法 46
3.2.1 影像參數設置： 47
3.2.2 MRI 影像資料分析 49
3.3 結果 51
3.4 研究討論 55
3.4.1 口內負壓對於呼吸道軟組織的影響 55
3.4.2 MRI 個案研究 56
3.5 結論 57
4. 口內負壓睡眠裝置療效研究 58
4.1 研究目的 58
4.2 研究方法 58
4.2.1 研究設備 58
4.2.2 試驗設計 59
4.3 研究結果 63
4.3.1 研究族群特性 63
4.4 治療結果 64
4.4.1 主要終點 64
4.4.2 PSG變數 65
4.4.3 問卷調查 67
4.4.4 不良事件 67
4.5 討論 68
4.5.1 治療效果 68
4.5.2 研究限制 70
4.6 結論 71
5. 口內負壓睡眠裝置壓力滴定研究 73
5.1 .導言 73
5.2 方法 75
5.2.1 研究參與者: 75
5.2.2 研究設計 75
5.3 結果 78
5.4 結論： 81
6. 討論 85
6.1 解剖結構對口內負壓治療效果的影響 85
6.2 口內負壓治療的建議族群 87
6.2.1 無法使用與耐受CPAP的患者 87
6.2.2 女性族群 88
6.2.3 中重度OSA族群 88
6.3 口內負壓作為OSA替代治療的角色 88
7. 結論與未來研究方向 91
7.1 總結發現 91
7.2 建議未來研究方向 93
8. 參考文獻 95

參考文獻

[1] J. A. Dempsey, S. C. Veasey, B. J. Morgan, and C. P. O’Donnell, “Pathophysiology of Sleep Apnea,” Physiol Rev, vol. 90, no. 1, pp. 47–112, Jan. 2010, doi: 10.1152/physrev.00043.2008.
[2] C. Guilleminault, A. Tilkian, and W. C. Dement, “The Sleep Apnea Syndromes,” Annu Rev Med, vol. 27, no. 1, pp. 465–484, Feb. 1976, doi: 10.1146/annurev.me.27.020176.002341.
[3] C. V. Senaratna et al., “Prevalence of obstructive sleep apnea in the general population: A systematic review,” Sleep Med Rev, vol. 34, pp. 70–81, Aug. 2017, doi: 10.1016/j.smrv.2016.07.002.
[4] R. Heinzer, H. Marti-Soler, and J. Haba-Rubio, “Prevalence of sleep apnoea syndrome in the middle to old age general population,” The Lancet Respiratory Medicine, vol. 4, no. 2. Lancet Publishing Group, pp. e5–e6, Feb. 01, 2016. doi: 10.1016/S2213-2600(16)00006-0.
[5] D. J. Gottlieb and N. M. Punjabi, “Diagnosis and Management of Obstructive Sleep Apnea,” JAMA, vol. 323, no. 14, p. 1389, Apr. 2020, doi: 10.1001/jama.2020.3514.
[6] J.-S. Sunwoo, Y. Hwangbo, W.-J. Kim, M. K. Chu, C.-H. Yun, and K. I. Yang, “Prevalence, sleep characteristics, and comorbidities in a population at high risk for obstructive sleep apnea: A nationwide questionnaire study in South Korea,” PLoS One, vol. 13, no. 2, p. e0193549, Feb. 2018, doi: 10.1371/journal.pone.0193549.
[7] X. Soler et al., “High Prevalence of Obstructive Sleep Apnea in Patients with Moderate to Severe COPD,” Ann Am Thorac Soc, p. 150414075541005, Apr. 2015, doi: 10.1513/AnnalsATS.201407-336OC.
[8] M. Gleeson and W. T. McNicholas, “Bidirectional relationships of comorbidity with obstructive sleep apnoea,” European Respiratory Review, vol. 31, no. 164. European Respiratory Society, Jun. 30, 2022. doi: 10.1183/16000617.0256-2021.
[9] M. Butt, G. Dwivedi, O. Khair, and G. Y. H. Lip, “Obstructive sleep apnea and cardiovascular disease,” Int J Cardiol, vol. 139, no. 1, pp. 7–16, doi: 10.1016/j.ijcard.2009.05.021.
[10] T. Menon and D. K. Kalra, “Sleep Apnea and Heart Failure—Current State-of-The-Art,” Int J Mol Sci, vol. 25, no. 10, p. 5251, May 2024, doi: 10.3390/ijms25105251.
[11] X. Wang et al., “Association of obstructive sleep apnoea with cardiovascular events in women and men with acute coronary syndrome,” European Respiratory Journal, vol. 61, no. 1, Jan. 2023, doi: 10.1183/13993003.01110-2022.
[12] M. Marin-Oto, E. E. Vicente, and J. M. Marin, “Long term management of obstructive sleep apnea and its comorbidities,” Multidisciplinary Respiratory Medicine, vol. 14, no. 1. BioMed Central Ltd., Jul. 04, 2019. doi: 10.1186/s40248-019-0186-3.
[13] C. C. Gonzaga, A. Bertolami, M. Bertolami, C. Amodeo, and D. A. Calhoun, “Obstructive sleep apnea, hypertension and cardiovascular diseases,” J Hum Hypertens, vol. 29, pp. 705–712, 2015, doi: 10.1038/jhh.2015.15.
[14] T. Konečný, T. Kara, and V. Somers, “Obstructive Sleep Apnea and Hypertension: An Update,” Hypertension, vol. 63, pp. 203–209, 2014, doi: 10.1161/HYPERTENSIONAHA.113.00613.
[15] A. Cai, L. Wang, and Y. Zhou, “Hypertension and obstructive sleep apnea,” Hypertension Research, vol. 39, pp. 391–395, 2016, doi: 10.1038/hr.2016.11.
[16] A. M. Das and R. Khayat, “Hypertension in obstructive sleep apnea: risk and therapy,” Expert Rev Cardiovasc Ther, vol. 7, pp. 619–626, 2009, doi: 10.1586/erc.09.25.
[17] H. Becker et al., “Effect of Nasal Continuous Positive Airway Pressure Treatment on Blood Pressure in Patients With Obstructive Sleep Apnea,” Circulation: Journal of the American Heart Association, vol. 107, pp. 68–73, 2003, doi: 10.1161/01.CIR.0000042706.47107.7A.
[18] J. Börgel et al., “Obstructive sleep apnea and blood pressure. Interaction between the blood pressure-lowering effects of positive airway pressure therapy and antihypertensive drugs.,” Am J Hypertens, vol. 17, pp. 1081–1087, 2004, doi: 10.1016/J.AMJHYPER.2004.06.026.
[19] M. Martínez-García et al., “Beyond Resistant Hypertension: Relationship Between Refractory Hypertension and Obstructive Sleep Apnea,” Hypertension, vol. 72, pp. 618–624, 2018, doi: 10.1161/HYPERTENSIONAHA.118.11170.
[20] J. Floras, “Hypertension and Sleep Apnea,” Can J Cardiol, vol. 31 7, pp. 889–897, 2015, doi: 10.1016/j.cjca.2015.05.003.
[21] J. Lam and M. Ip, “Obstructive sleep apnea and the metabolic syndrome,” Expert Rev Respir Med, vol. 3, pp. 177–186, 2009, doi: 10.1586/ers.09.10.
[22] A. Castaneda, E. Jauregui-Maldonado, I. Ratnani, J. Varon, and S. Surani, “Correlation between metabolic syndrome and sleep apnea,” World J Diabetes, vol. 9, pp. 66–71, 2018, doi: 10.4239/wjd.v9.i4.66.
[23] M. Gleeson and W. McNicholas, “Bidirectional relationships of comorbidity with obstructive sleep apnoea,” European Respiratory Review, vol. 31, p., 2022, doi: 10.1183/16000617.0256-2021.
[24] S. N. Framnes and D. M. Arble, “The Bidirectional Relationship Between Obstructive Sleep Apnea and Metabolic Disease,” Front Endocrinol (Lausanne), vol. 9, p., 2018, doi: 10.3389/fendo.2018.00440.
[25] A. Calvin, F. Albuquerque, F. Lopez‐Jimenez, and V. Somers, “Obstructive sleep apnea, inflammation, and the metabolic syndrome,” Metab Syndr Relat Disord, vol. 7 4, pp. 271–278, 2009, doi: 10.1089/met.2008.0093.
[26] A. Lurie, “Metabolic disorders associated with obstructive sleep apnea in adults,” Adv Cardiol, vol. 46, pp. 67–138, 2011, doi: 10.1159/000325106.
[27] M. Ip, B. Lam, M. Ng, W. Lam, K. Tsang, and K. Lam, “Obstructive sleep apnea is independently associated with insulin resistance,” Am J Respir Crit Care Med, vol. 165 5, pp. 670–676, 2002, doi: 10.1164/AJRCCM.165.5.2103001.
[28] M. Ambrosetti, A. Lucioni, S. Conti, R. Pedretti, and M. Neri, “Metabolic syndrome in obstructive sleep apnea and related cardiovascular risk,” Journal of Cardiovascular Medicine, vol. 7, pp. 826–829, 2006, doi: 10.2459/01.JCM.0000250873.01649.41.
[29] L. Drager, S. Togeiro, V. Polotsky, and G. Lorenzi-Filho, “Obstructive sleep apnea: a cardiometabolic risk in obesity and the metabolic syndrome,” J Am Coll Cardiol, vol. 62 7, pp. 569–576, 2013, doi: 10.1016/j.jacc.2013.05.045.
[30] W. McNicholas, “Chronic obstructive pulmonary disease and obstructive sleep apnea: overlaps in pathophysiology, systemic inflammation, and cardiovascular disease.,” Am J Respir Crit Care Med, vol. 180 8, pp. 692–700, 2009, doi: 10.1164/rccm.200903-0347PP.
[31] C. Shao, H. Qi, Q. Fang, J. Tu, Q. Li, and L. Wang, “Smoking history and its relationship with comorbidities in patients with obstructive sleep apnea,” Tob Induc Dis, vol. 18, p., 2020, doi: 10.18332/tid/123429.
[32] B. Prasad, S. Nyenhuis, and T. Weaver, “Obstructive sleep apnea and asthma: associations and treatment implications.,” Sleep Med Rev, vol. 18 2, pp. 165–171, 2014, doi: 10.1016/j.smrv.2013.04.004.
[33] E. Önal, J. Leech, and M. Lopata, “Relationship between pulmonary function and sleep-induced respiratory abnormalities.,” Chest, vol. 87 4, pp. 437–441, 1985, doi: 10.1378/CHEST.87.4.437.
[34] M. Nácher et al., “Biological consequences of oxygen desaturation and respiratory effort in an acute animal model of obstructive sleep apnea (OSA).,” Sleep Med, vol. 10 8, pp. 892–897, 2009, doi: 10.1016/j.sleep.2008.09.014.
[35] J. V. J. P. S. G. M. O. K. K. M. H. M. Š. V. N. A. K. M. Sova, “Obstructive sleep apnea, depression and cognitive impairment.,” Sleep Med, vol. 72, pp. 50–58, 2020, doi: 10.1016/j.sleep.2020.03.017.
[36] B. S. F. W. K. E. V. E. I. Khawaja, “Obstructive Sleep Apnea in Posttraumatic Stress Disorder Comorbid With Mood Disorder: Significantly Higher Incidence Than in Either Diagnosis Alone.,” Prim Care Companion CNS Disord, vol. 20 4, p. nan, 2018, doi: 10.4088/PCC.18m02281.
[37] W.-C. L. J. Winkelman, “Obstructive Sleep Apnea and Severe Mental Illness: Evolution and Consequences,” Curr Psychiatry Rep, vol. 14, pp. 503–510, 2012, doi: 10.1007/s11920-012-0307-6.
[38] A. G. A. O. B. A. V. R. Osorio, “The Relationship between Obstructive Sleep Apnea and Alzheimer’s Disease.,” J Alzheimers Dis, vol. 64 s1, pp. S255–S270, 2018, doi: 10.3233/JAD-179936.
[39] A. G. S. T. F. K. M. S. D. S. P. Białasiewicz, “Disruption of Circadian Rhythm Genes in Obstructive Sleep Apnea Patients—Possible Mechanisms Involved and Clinical Implication,” Int J Mol Sci, vol. 23, p. nan, 2022, doi: 10.3390/ijms23020709.
[40] Rosenberg, R. & Doghramji, and P, “Optimal treatment of obstructive sleep apnea and excessive sleepiness,” Sleep Med, vol. 10, pp. 101–102, 2009, doi: 10.1016/j.sleep.2009.02.010.
[41] Gleeson, M, McNicholas, and W, “Bidirectional relationships of comorbidity with obstructive sleep apnoea,” European Respiratory Review, vol. 31, p., 2022, doi: 10.1183/16000617.0256-2021.
[42] Ulander et al., “Side effects to continuous positive airway pressure treatment for obstructive sleep apnoea: changes over time and association to adherence,” Sleep and Breathing, vol. 18, pp. 799–807, 2014, doi: 10.1007/s11325-014-0945-5.
[43] Kribbs et al., “Effects of one night without nasal CPAP treatment on sleep and sleepiness in patients with obstructive sleep apnea,” Am Rev Respir Dis, vol. 147 5, pp. 1162–1168, 1993, doi: 10.1164/AJRCCM/147.5.1162.
[44] Nilius et al., “Upper airway complaints of patients with obstructive sleep apnea - effect of CPAP,” Pneumologie, vol. 61 1, pp. 15–19, 2007, doi: 10.1055/S-2006-954966.
[45] Meslier et al., “A French survey of 3,225 patients treated with CPAP for obstructive sleep apnoea: benefits, tolerance, compliance and quality of life,” Eur Respir J, vol. 12 1, pp. 185–192, 1998, doi: 10.1183/09031936.98.12010185.
[46] Broström et al., “The side‐effects to CPAP treatment inventory: the development and initial validation of a new tool for the measurement of side‐effects to CPAP treatment,” J Sleep Res, vol. 19, p., 2010, doi: 10.1111/j.1365-2869.2010.00825.x.
[47] W. Schmidt-Nowara, A. Lowe, L. Wiegand, R. Cartwright, F. Perez-Guerra, and S. Menn, “Oral appliances for the treatment of snoring and obstructive sleep apnea: a review.,” Sleep, vol. 18 6, pp. 501–510, 1995, doi: 10.1093/SLEEP/18.6.501.
[48] K. Ferguson, T. Ono, A. Lowe, S. Al-Majed, L. Love, and J. Fleetham, “A short-term controlled trial of an adjustable oral appliance for the treatment of mild to moderate obstructive sleep apnoea.,” Thorax, vol. 52, pp. 362–368, 1997, doi: 10.1136/thx.52.4.362.
[49] J. Lim, T. Lasserson, J. Fleetham, and J. Wright, “Oral appliances for obstructive sleep apnoea.,” Cochrane Database Syst Rev, vol. 4, pp. CD004435-, 2006, doi: 10.1002/14651858.CD004435.PUB3.
[50] F. R. de Almeida et al., “Long-term compliance and side effects of oral appliances used for the treatment of snoring and obstructive sleep apnea syndrome.,” J Clin Sleep Med, vol. 1 2, pp. 143–152, 2005, doi: 10.5664/jcsm.8978.
[51] K. Fritsch, A. Iseli, E. Russi, and K. Bloch, “Side effects of mandibular advancement devices for sleep apnea treatment.,” Am J Respir Crit Care Med, vol. 164 5, pp. 813–818, 2001, doi: 10.1164/AJRCCM.164.5.2003078.
[52] E. Rose, R. Staats, C. Virchow, and I. Jonas, “Occlusal and skeletal effects of an oral appliance in the treatment of obstructive sleep apnea.,” Chest, vol. 122 3, pp. 871–877, 2002, doi: 10.1378/CHEST.122.3.871.
[53] M. Hamoda, F. Almeida, and B. Pliska, “Long-term side effects of sleep apnea treatment with oral appliances: nature, magnitude and predictors of long-term changes.,” Sleep Med, vol. 56, pp. 184–191, 2019, doi: 10.1016/J.SLEEP.2018.12.012.
[54] K. Franklin et al., “Effects and side-effects of surgery for snoring and obstructive sleep apnea--a systematic review.,” Sleep, vol. 32 1, pp. 27–36, 2009, doi: 10.5665/SLEEP/32.1.27.
[55] J.-E. C. Holty and C. Guilleminault, “Maxillomandibular advancement for the treatment of obstructive sleep apnea: A systematic review and meta-analysis,” Sleep Med Rev, vol. 14, no. 5, pp. 287–297, Oct. 2010, doi: 10.1016/j.smrv.2009.11.003.
[56] A. Sher, K. Schechtman, and J. Piccirillo, “The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome.,” Sleep, vol. 19 2, pp. 156–177, 1996, doi: 10.1093/SLEEP/19.2.156.
[57] E. Y. Kim, M. Courey, and E. Kezirian, “Treatment of Trigger-Point Hypersensitivity of Gag Reflex following Surgical Treatment of Obstructive Sleep Apnea,” Otolaryngology–Head and Neck Surgery, vol. 145, pp. 1055–1056, 2011, doi: 10.1177/0194599811408243.
[58] C. Budin et al., “Therapeutic alternatives with CPAP in obstructive sleep apnea,” Journal of Mind and Medical Sciences, p., 2019, doi: 10.22543/7674.62.p181189.
[59] M. Cao, J. M. Sternbach, and C. Guilleminault, “Continuous positive airway pressure therapy in obstructive sleep apnea: benefits and alternatives,” Expert Rev Respir Med, vol. 11, pp. 259–272, 2017, doi: 10.1080/17476348.2017.1305893.
[60] J. G. Park, T. I. Morgenthaler, and P. Gay, “Novel and emerging nonpositive airway pressure therapies for sleep apnea,” Chest, vol. 144 6, pp. 1946–1952, 2013, doi: 10.1378/chest.13-0273.
[61] M. Ghadiri and R. R. Grunstein, “Clinical side effects of continuous positive airway pressure in patients with obstructive sleep apnoea,” Respirology, vol. 25, no. 6, pp. 593–602, Jun. 2020, doi: 10.1111/resp.13808.
[62] M. Rana, J. August, J. Levi, G. Parsi, M. Motro, and W. DeBassio, “Alternative Approaches to Adenotonsillectomy and Continuous Positive Airway Pressure (CPAP) for the Management of Pediatric Obstructive Sleep Apnea (OSA): A Review,” Sleep Disord, vol. 2020, pp. 1–11, Jul. 2020, doi: 10.1155/2020/7987208.
[63] I. M. Colrain et al., “A multicenter evaluation of oral pressure therapy for the treatment of obstructive sleep apnea,” Sleep Med, vol. 14, no. 9, pp. 830–837, Sep. 2013, doi: 10.1016/j.sleep.2013.05.009.
[64] C.-Y. Cheng, C.-C. Chen, M.-T. Lo, C. Guilleminault, and C.-M. Lin, “Evaluation of efficacy and safety of intraoral negative air pressure device in adults with obstructive sleep apnea in Taiwan,” Sleep Med, vol. 81, pp. 163–168, May 2021, doi: 10.1016/j.sleep.2021.02.013.
[65] T.-C. Hung et al., “Building a model to precisely target the responders of a novel intermittent negative air pressure device-with mechanism definition,” Sleep Med, vol. 72, pp. 20–27, Aug. 2020, doi: 10.1016/j.sleep.2020.03.014.
[66] T.-C. Hung et al., “A novel intermittent negative air pressure device ameliorates obstructive sleep apnea syndrome in adults,” Sleep and Breathing, vol. 23, no. 3, pp. 849–856, Sep. 2019, doi: 10.1007/s11325-018-01778-z.
[67] E. T. Chang et al., “Tongue retaining devices for obstructive sleep apnea: A systematic review and meta-analysis,” Am J Otolaryngol, vol. 38, no. 3, pp. 272–278, May 2017, doi: 10.1016/j.amjoto.2017.01.006.
[68] R. J. Schwab et al., “Examining the Mechanism of Action of a New Device Using Oral Pressure Therapy for the Treatment of Obstructive Sleep Apnea,” Sleep, vol. 37, no. 7, pp. 1237–1247, 2014, doi: 10.5665/sleep.3846.
[69] Y.-H. Kuo et al., “Novel Intraoral Negative Airway Pressure in Drug-Induced Sleep Endoscopy with Target-Controlled Infusion,” Nat Sci Sleep, vol. Volume 13, pp. 2087–2099, Nov. 2021, doi: 10.2147/NSS.S327770.
[70] R. D. Cartwright, “Predicting Response to the Tongue Retaining Device for Sleep Apnea Syndrome,” Archives of Otolaryngology - Head and Neck Surgery, vol. 111, no. 6, pp. 385–388, Jun. 1985, doi: 10.1001/archotol.1985.00800080071008.
[71] W. G. H. Engelke, M. Mendoza, and G. Repetto, “Preliminary radiographic observations of the tongue-repositioning manoeuvre,” The European Journal of Orthodontics, vol. 28, no. 6, pp. 618–623, Dec. 2006, doi: 10.1093/ejo/cjl051.
[72] W. Engelke, W. Engelhardt, M. Mendoza-Gartner, O. Decco, J. Barrirero, and M. Knosel, “Functional treatment of snoring based on the tongue-repositioning manoeuvre,” The European Journal of Orthodontics, vol. 32, no. 5, pp. 490–495, Oct. 2010, doi: 10.1093/ejo/cjp135.
[73] E. J. Kim et al., “The impacts of open-mouth breathing on upper airway space in obstructive sleep apnea: 3-D MDCT analysis,” European Archives of Oto-Rhino-Laryngology, vol. 268, pp. 533–539, 2011, doi: 10.1007/s00405-010-1397-6.
[74] M. Suzuki and T. Tanuma, “The effect of nasal and oral breathing on airway collapsibility in patients with obstructive sleep apnea: Computational fluid dynamics analyses,” PLoS One, vol. 15, 2020, doi: 10.1371/journal.pone.0231262.
[75] L. Ueno et al., “Effects of exercise training in patients with chronic heart failure and sleep apnea,” Sleep, vol. 32, pp. 637–647, 2009, doi: 10.1093/SLEEP/32.5.637.
[76] A. M. Kim et al., “Tongue fat and its relationship to obstructive sleep apnea.,” Sleep, vol. 37, no. 10, pp. 1639–1648, Oct. 2014, doi: 10.5665/sleep.4072.
[77] Ryan et al., “Magnetic resonance imaging of the upper airway in obstructive sleep apnea before and after chronic nasal continuous positive airway pressure therapy.,” Am Rev Respir Dis, vol. 144, pp. 939–944, 1991, doi: 10.1164/ajrccm/144.4.939.
[78] W. Chen, E. Gillett, M. C. K. Khoo, S. L. Davidson Ward, and K. S. Nayak, “Real‐time multislice MRI during continuous positive airway pressure reveals upper airway response to pressure change,” Journal of Magnetic Resonance Imaging, vol. 46, no. 5, pp. 1400–1408, Nov. 2017, doi: 10.1002/jmri.25675.
[79] Schwab et al., “Upper airway and soft tissue structural changes induced by CPAP in normal subjects.,” Am J Respir Crit Care Med, vol. 154, pp. 1106–1116, 1996, doi: 10.1164/ajrccm.154.4.8887600.
[80] Mortimore, I, Kochhar, P, & Douglas, and N, “Effect of chronic continuous positive airway pressure (CPAP) therapy on upper airway size in patients with sleep apnoea/hypopnoea syndrome.,” Thorax, vol. 51, pp. 190–192, 1996, doi: 10.1136/thx.51.2.190.
[81] Jung et al., “Upper airway structural changes induced by CPAP in OSAS patients: a study using drug-induced sleep endoscopy.,” European Archives of Oto-Rhino-Laryngology, vol. 274, pp. 247–252, 2016, doi: 10.1007/s00405-016-4110-7.
[82] S. P. Patil, I. A. Ayappa, S. M. Caples, R. J. Kimoff, S. R. Patel, and C. G. Harrod, “Treatment of Adult Obstructive Sleep Apnea with Positive Airway Pressure: An American Academy of Sleep Medicine Clinical Practice Guideline,” Journal of Clinical Sleep Medicine, vol. 15, no. 02, pp. 335–343, Feb. 2019, doi: 10.5664/jcsm.7640.
[83] R. Lauder and Z. F. Muhl, “Estimation of tongue volume from magnetic resonance imaging.,” Angle Orthod, vol. 61, no. 3, pp. 175–84, 1991, doi: 10.1043/0003-3219(1991)061<0175:EOTVFM>2.0.CO;2.
[84] S. S. Rana, O. P. Kharbanda, and B. Agarwal, “Influence of tongue volume, oral cavity volume and their ratio on upper airway: A cone beam computed tomography study,” J Oral Biol Craniofac Res, vol. 10, no. 2, pp. 110–117, Apr. 2020, doi: 10.1016/j.jobcr.2020.03.006.
[85] K. Tamari, K. Shimizu, M. Ichinose, S. Nakata, and Y. Takahama, “Relationship between tongue volume and lower dental arch sizes.,” Am J Orthod Dentofacial Orthop, vol. 100, no. 5, pp. 453–8, Nov. 1991, doi: 10.1016/0889-5406(91)70085-B.
[86] A. Azarbarzin et al., “Palatal prolapse as a signature of expiratory flow limitation and inspiratory palatal collapse in patients with obstructive sleep apnoea,” European Respiratory Journal, vol. 51, no. 2, p. 1701419, Feb. 2018, doi: 10.1183/13993003.01419-2017.
[87] Y. Shigeta, T. Ogawa, I. Tomoko, G. T. Clark, and R. Enciso, “Soft palate length and upper airway relationship in OSA and non-OSA subjects,” Sleep and Breathing, vol. 14, no. 4, pp. 353–358, Dec. 2010, doi: 10.1007/s11325-009-0318-7.
[88] B. C. Neelapu et al., “Craniofacial and upper airway morphology in adult obstructive sleep apnea patients: A systematic review and meta-analysis of cephalometric studies,” Sleep Med Rev, vol. 31, pp. 79–90, Feb. 2017, doi: 10.1016/j.smrv.2016.01.007.

指導教授

羅孟宗(Men-Tzung Lo)

審核日期

2024-7-29

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