All Title Author
Keywords Abstract


Mood Predicts Response to Placebo CPAP

DOI: 10.1155/2012/404196

Full-Text   Cite this paper   Add to My Lib

Abstract:

Study Objectives. Continuous positive airway pressure (CPAP) therapy is efficacious for treating obstructive sleep apnea (OSA), but recent studies with placebo CPAP (CPAP administered at subtherapeutic pressure) have revealed nonspecific (or placebo) responses to CPAP treatment. This study examined baseline psychological factors associated with beneficial effects from placebo CPAP treatment. Participants. Twenty-five participants were studied with polysomnography at baseline and after treatment with placebo CPAP. Design. Participants were randomized to either CPAP treatment or placebo CPAP. Baseline mood was assessed with the Profile of Mood States (POMS). Total mood disturbance (POMS-Total) was obtained by summing the six POMS subscale scores, with Vigor weighted negatively. The dependent variable was changed in apnea-hypopnea index (ΔAHI), calculated by subtracting pre- from post-CPAP AHI. Negative values implied improvement. Hierarchical regression analysis was performed, with pre-CPAP AHI added as a covariate to control for baseline OSA severity. Results. Baseline emotional distress predicted the drop in AHI in response to placebo CPAP. Highly distressed patients showed greater placebo response, with a 34% drop (i.e., improvement) in AHI. Conclusion. These findings underscore the importance of placebo-controlled studies of CPAP treatment. Whereas such trials are routinely included in drug trials, this paper argues for their importance even in mechanical-oriented sleep interventions. 1. Introduction Placebo responses remain one of the great mysteries of medicine. While a clinical benefit of treatment (any treatment) is always a “plus” for the patient, such placebo responses can complicate clinical trials. This paper examines some placebo response characteristics in patients being treated with continuous positive airway pressure (CPAP) for obstructive sleep apnea (OSA). OSA is a potentially devastating illness that involves sleep fragmentation and associated hypoxia, affecting up to 9% of middle-aged adults and higher percentages in the elderly [1–3]. The pathological consequences of upper airway obstruction during sleep may lead to cardiovascular complications, marked psychological distress, and impairment in daytime performance and cognitive functioning [4–9]. The most commonly used treatment is nasal CPAP [10, 11]. CPAP has been efficacious in improving many outcome measurements, especially in patients with severe OSA [12–15]. However, some researchers have reported inconsistencies in improvement, for example, a nonspecific (or placebo) effect of

References

[1]  S. Ancoli-Israel, D. F. Kripke, M. R. Klauber, W. J. Mason, R. Fell, and O. Kaplan, “Sleep-disordered breathing in community-dwelling elderly,” Sleep, vol. 14, no. 6, pp. 486–495, 1991.
[2]  T. Young, M. Palta, J. Dempsey, J. Skatrud, S. Weber, and S. Badr, “The occurrence of sleep-disordered breathing among middle-aged adults,” New England Journal of Medicine, vol. 328, no. 17, pp. 1230–1235, 1993.
[3]  W. C. Orr, “Sleep apnea, hypoxemia, and cardiac arrhythmias,” Chest, vol. 89, no. 1, pp. 1–2, 1986.
[4]  P. Lanfranchi and V. K. Somers, “Obstructive sleep apnea and vascular disease,” Respiratory Research, vol. 2, no. 6, pp. 315–319, 2001.
[5]  H. Kraiczi, Y. Peker, K. Caidahl, A. Samuelsson, and J. Hedner, “Blood pressure, cardiac structure and severity of obstructive sleep apnea in a sleep clinic population,” Journal of Hypertension, vol. 19, no. 11, pp. 2071–2078, 2001.
[6]  H. M. Engleman, R. N. Kingshott, S. E. Martin, and N. J. Douglas, “Cognitive function in the sleep apnea/hypopnea syndrome (SAHS),” Sleep, vol. 23, supplement 4, pp. S102–S108, 2000.
[7]  R. Day, R. Gerhardstein, A. Lumley, T. Roth, and L. Rosenthal, “The behavioral morbidity of obstructive sleep apnea,” Progress in Cardiovascular Diseases, vol. 41, no. 5, pp. 341–354, 1999.
[8]  T. Akashiba, S. Kawahara, N. Kosaka et al., “Determinants of chronic hypercapnia in Japanese men with obstructive sleep apnea syndrome,” Chest, vol. 121, no. 2, pp. 415–421, 2002.
[9]  D. E. Green and D. A. Schulman, “Obstructive sleep apnea and cardiovascular disease,” Current Treatment Options in Cardiovascular Medicine, vol. 12, no. 4, pp. 342–354, 2010.
[10]  C. E. Sullivan, F. G. Issa, M. Berthon-Jones, and L. Eves, “Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares,” The Lancet, vol. 1, no. 8225, pp. 862–865, 1981.
[11]  L. J. Epstein, D. Kristo, P. J. Strollo et al., “Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults,” Journal of Clinical Sleep Medicine, vol. 5, no. 3, pp. 263–276, 2009.
[12]  N. McArdle and N. J. Douglas, “Effect of continuous positive airway pressure on sleep architecture in the sleep apnea-hypopnea syndrome: a randomized controlled trial,” American Journal of Respiratory and Critical Care Medicine, vol. 164, no. 8, part 1, pp. 1459–1463, 2001.
[13]  F. Barbé, L. R. Mayoralas, J. Duran et al., “Treatment with continuous positive airway pressure is not effective in patients with sleep apnea but no daytime sleepiness: a randomized, controlled trial,” Annals of Internal Medicine, vol. 134, no. 11, pp. 1015–1023, 2001.
[14]  C. Jenkinson, R. J. O. Davies, R. Mullins, and J. R. Stradling, “Comparison of therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised prospective parallel trial,” The Lancet, vol. 353, no. 9170, pp. 2100–2105, 1999.
[15]  T. A. McFadyen, C. A. Espie, N. McArdle, N. J. Douglas, and H. M. Engleman, “Controlled, prospective trial of psychosocial function before and after continuous positive airway pressure therapy,” European Respiratory Journal, vol. 18, no. 6, pp. 996–1002, 2001.
[16]  M. Barnes, D. Houston, C. J. Worsnop et al., “A randomized controlled trial of continuous positive airway pressure in mild obstructive sleep apnea,” American Journal of Respiratory and Critical Care Medicine, vol. 165, no. 6, pp. 773–780, 2002.
[17]  H. M. Engleman, S. E. Martin, I. J. Deary, and N. J. Douglas, “Effect of CPAP therapy on daytime function in patients with mild sleep apnoea/hypopnoea syndrome,” Thorax, vol. 52, no. 2, pp. 114–119, 1997.
[18]  H. M. Engleman, R. N. Kingshott, P. K. Wraith, T. W. Mackay, I. J. Deary, and N. J. Douglas, “Randomized placebo-controlled crossover trial of continuous positive airway pressure for mild sleep apnea/hypopnea syndrome,” American Journal of Respiratory and Critical Care Medicine, vol. 159, no. 2, pp. 461–467, 1999.
[19]  J. E. Dimsdale, J. S. Loredo, and J. Profant, “Effect of continuous positive airway pressure on blood pressure: a placebo trial,” Hypertension, vol. 35, no. 1, part 1, pp. 144–147, 2000.
[20]  K. G. Henke, J. J. Grady, and S. T. Kuna, “Effect of nasal continuous positive airway pressure on neuropsychological function in sleep apnea-hypopnea syndrome: a randomized, placebo-controlled trial,” American Journal of Respiratory and Critical Care Medicine, vol. 163, no. 4, pp. 911–917, 2001.
[21]  S. Redline, N. Adams, M. E. Strauss, T. Roebuck, M. Winters, and C. Rosenberg, “Improvement of mild sleep-disordered breathing with CPAP compared with conservative therapy,” American Journal of Respiratory and Critical Care Medicine, vol. 157, no. 3, part 1, pp. 858–865, 1998.
[22]  J. S. Loredo, S. Ancoli-Israel, and J. E. Dimsdale, “Effect of continuous positive airway pressure vs placebo continuous positive airway pressure on sleep quality in obstructive sleep apnea,” Chest, vol. 116, no. 6, pp. 1545–1549, 1999.
[23]  W. A. Bardwell, S. Ancoli-Israel, C. C. Berry, and J. E. Dimsdale, “Neuropsychological effects of one-week continuous positive airway pressure treatment in patients with obstructive sleep apnea: a placebo-controlled study,” Psychosomatic Medicine, vol. 63, no. 4, pp. 579–584, 2001.
[24]  B. H. Yu, S. Ancoli-Israel, and J. E. Dimsdale, “Effect of CPAP treatment on mood states in patients with sleep apnea,” Journal of Psychiatric Research, vol. 33, no. 5, pp. 427–432, 1999.
[25]  “1983 metropolitan height and weight tables,” Stat Bull Metrop Life Found, vol. 64, no. 1, pp. 3–9, 1983.
[26]  A. Rechstschaffen and A. Kales, Manual of Standardized Terminology, Techniques and Scoring Systems for Sleep Stages of Human Subjects, National Health Institutes, Washington, DC, USA, 1968.
[27]  R. Farré, L. Hernández, J. M. Montserrat, M. Rotger, E. Ballester, and D. Navajas, “Sham continuous positive airway pressure for placebo-controlled studies in sleep apnoea,” The Lancet, vol. 353, no. 9159, p. 1154, 1999.
[28]  D. M. McNair, M. Lorr, and L. F. Droppleman, POMS Manual: Profile of Mood States, Educational and Industrial Testing Service, San Diego, Calif, USA, 1992.
[29]  D. Spiegel, J. R. Bloom, and I. Yalom, “Group support for patients with metastatic cancer. A randomized prospective outcome study,” Archives of General Psychiatry, vol. 38, no. 5, pp. 527–533, 1981.
[30]  S. E. Taylor, R. R. Lichtman, and J. V. Wood, “Attributions, beliefs about control, and adjustment to breast cancer,” Journal of Personality and Social Psychology, vol. 46, no. 3, pp. 489–502, 1984.
[31]  M. J. Dickel and S. S. Mosko, “Morbidity cut-offs for sleep apnea and periodic leg movements in predicting subjective complaints in seniors,” Sleep, vol. 13, no. 2, pp. 155–166, 1990.
[32]  S. Mosko, M. Zetin, S. Glen et al., “Self-reported depressive symptomatology, mood ratings, and treatment outcome in sleep disorders patients,” Journal of Clinical Psychology, vol. 45, no. 1, pp. 51–60, 1989.
[33]  T. J. Kaptchuk, “Powerful placebo: the dark side of the randomised controlled trial,” The Lancet, vol. 351, no. 9117, pp. 1722–1725, 1998.
[34]  A. J. Vickers and A. J. M. de Craen, “Why use placebos in clinical trials? A narrative review of the methodological literature,” Journal of Clinical Epidemiology, vol. 53, no. 2, pp. 157–161, 2000.
[35]  R. B. Berry and A. J. Block, “Positive nasal airway pressure eliminates snoring as well as obstructive sleep apnea,” Chest, vol. 85, no. 1, pp. 15–20, 1984.
[36]  F. G. Issa and C. E. Sullivan, “Upper airway closing pressures in snorers,” Journal of Applied Physiology Respiratory Environmental and Exercise Physiology, vol. 57, no. 2, pp. 528–535, 1984.
[37]  M. Valencia-Flores, D. L. Bliwise, C. Guilleminault, R. Cilveti, and A. Clerk, “Cognitive function in patients with sleep apnea after acute nocturnal nasal continuous positive airway pressure (CPAP) treatment: sleepiness and hypoxemia effects,” Journal of Clinical and Experimental Neuropsychology, vol. 18, no. 2, pp. 197–210, 1996.
[38]  P. Scheltens, F. Visscher, A. R. J. van Keimpema, J. Lindeboom, M. J. B. Taphoorn, and E. C. Wolters, “Sleep apnea syndrome presenting with cognitive impairment,” Neurology, vol. 41, no. 1, pp. 155–156, 1991.
[39]  N. Meslier, T. Lebrun, V. Grillier-Lanoir et al., “A French survey of 3,225 patients treated with CPAP for obstructive sleep apnoea: benefits, tolerance compliance and quality of life,” European Respiratory Journal, vol. 12, no. 1, pp. 185–192, 1998.

Full-Text

comments powered by Disqus