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Cannabis, Cannabinoids, and Sleep: a Review of the Literature.
PURPOSE OF REVIEW:
The current review aims to summarize the state of research on cannabis and sleep up to 2014 and to review in detail the literature on cannabis and specific sleep disorders from 2014 to the time of publication.
Preliminary research into cannabis and insomnia suggests that cannabidiol (CBD) may have therapeutic potential for the treatment of insomnia. Delta-9 tetrahydrocannabinol (THC) may decrease sleep latency but could impair sleep quality long-term. Novel studies investigating cannabinoids and obstructive sleep apnea suggest that synthetic cannabinoids such as nabilone and dronabinol may have short-term benefit for sleep apnea due to their modulatory effects on serotonin-mediated apneas. CBD may hold promise for REM sleep behavior disorder and excessive daytime sleepiness, while nabilone may reduce nightmares associated with PTSD and may improve sleep among patients with chronic pain. Research on cannabis and sleep is in its infancy and has yielded mixed results. Additional controlled and longitudinal research is critical to advance our understanding of research and clinical implications.
Obstructive sleep apnea: focus on myofunctional therapy
Orofacial myofunctional therapy (OMT) is a modality of treatment for children and adults with obstructive sleep apnea (OSA) to promote changes in the musculature of the upper airways. This review summarizes and discusses the effects of OMT on OSA, the therapeutic programs employed, and their possible mechanisms of action.
We conducted an online literature search using the databases MEDLINE/PubMed, EMBASE, and Web of Science. Search terms were “obstructive sleep apnea” in combination with “myofunctional therapy” OR “oropharyngeal exercises” OR “speech therapy”. We considered original articles in English and Portuguese containing a diagnosis of OSA based on polysomnography (PSG). The primary outcomes of interest for this review were objective measurement derived from PSG and subjective sleep symptoms. The secondary outcome was the evaluation of orofacial myofunctional status.
Eleven studies were included in this review. The studies reviewed reveal that several benefits of OMT were demonstrated in adults, which include significant decrease of apnea-hypopnea index (AHI), reduced arousal index, improvement in subjective symptoms of daytime sleepiness, sleep quality, and life quality. In children with residual apnea, OMT promoted a decrease of AHI, increase in oxygen saturation, and improvement of orofacial myofunctional status. Few of the studies reviewed reported the effects of OMT on the musculature.
The present review showed that OMT is effective for the treatment of adults in reducing the severity of OSA and snoring, and improving the quality of life. OMT is also successful for the treatment of children with residual apnea. In addition, OMT favors the adherence to continuous positive airway pressure. However, randomized and high-quality studies are still rare, and the effects of treatment should also be analyzed on a long-term basis, including measures showing if changes occurred in the musculature.
Obstructive sleep apnea: Who should be tested, and how?
Patients who have risk factors for obstructive sleep apnea (OSA) or who report symptoms of OSA should be screened for it, first with a complete sleep history and standardized questionnaire, and then by objective testing if indicated. The gold standard test for OSA is polysomnography performed overnight in a sleep laboratory. Home testing is an option in certain instances.
Common risk factors include obesity, resistant hypertension, retrognathia, large neck circumference (> 17 inches in men, > 16 inches in women), and history of stroke, atrial fibrillation, nocturnal arrhythmias, heart failure, and pulmonary hypertension. Screening is also recommended for any patient who is found on physical examination to have upper-airway narrowing or who reports symptoms such as loud snoring, observed episodes of apnea, gasping or choking at night, unrefreshing sleep, morning headaches, unexplained fatigue, and excessive tiredness during the day.
The American Academy of Sleep Medicine suggests three opportunities to screen for OSA1:
- At routine health maintenance visits
- If the patient reports clinical symptoms of OSA
- If the patient has risk factors.
A DISMAL STATISTIC
The prevalence of OSA in the United States is high, estimated to be 2% in women and 4% in men in the middle-aged work force,2 and even more in blacks, Asians, and older adults.3 Yet only 10% of people with OSA are diagnosed4—a dismal statistic considering the association of OSA with resistant hypertension5 and with a greater risk of stroke,6cardiovascular disease, and death.7
CONSEQUENCES OF UNTREATED OSA
Untreated OSA is associated with a number of conditions7:
- Hypertension. OSA is one of the most common conditions associated with resistant hypertension. Patients with severe OSA and resistant hypertension who comply with continuous positive airway pressure (CPAP) treatment have significant reductions in blood pressure.
- Coronary artery disease. OSA is twice as common in people with coronary artery disease as in those with no coronary artery disease. In patients with coronary artery disease and OSA, CPAP may reduce the rate of nonfatal and fatal cardiovascular events.
- Heart failure. OSA is common in patients with systolic dysfunction (11% to 37%). OSA also has been detected in more than 50% of patients with heart failure with preserved systolic function. CPAP treatment can improve ejection fraction in patients with systolic dysfunction.
- Arrythmias. Atrial fibrillation, nonsustained ventricular tachycardia, and complex ventricular ectopy have been reported to be significantly more common in people with OSA.8 If the underlying cardiac conduction system is normal and there is no significant thyroid dysfunction, bradyarrhythmias and heart block may be treated effectively with CPAP.7 Treatment of OSA may decrease the incidence and severity of ventricular arrhythmias.7
- Sudden cardiac death. OSA was independently associated with sudden cardiac death in a longitudinal study.9
- Stroke. The Sleep Heart Health Study6 showed that OSA is 30% more common in patients who developed ischemic stroke. Long-term CPAP treatment in moderate to severe OSA and ischemic stroke is associated with a reduction in the mortality rate.10
- Diabetes. The Sleep Heart Health Study showed that OSA is independently associated with glucose intolerance and insulin resistance and may lead to type 2 diabetes mellitus.11
A QUESTIONNAIRE HELPS IDENTIFY WHO NEEDS TESTING
If you suspect OSA, consider administering a sleep disorder questionnaire such as the Berlin,12 the Epworth Sleepiness Scale, or the STOP-Bang questionnaire (Table 1). The STOP-Bang questionnaire is an easy-to-use tool that expands on the STOP questionnaire (snoring, tiredness, observed apnea, high blood pressure) with the addition of body mass index, age, neck size, and gender. The Berlin questionnaire has been validated in the primary care setting.12 The STOP-Bang questionnaire has been validated in preoperative settings13 but not in the primary care setting (although it has been commonly used in primary care).
WHICH TEST TO ORDER?
If the score on the questionnaire indicates a moderate or high risk of OSA, the patient should undergo objective testing with polysomnography or, in certain instances, home testing.1Polysomnography is the gold standard. Home testing costs less and is easier to arrange, but the American Academy of Sleep Medicine recommends it as an alternative to polysomnography, in conjunction with a comprehensive sleep evaluation, only in the following situations14:
- If the patient has a high pretest probability of moderate to severe OSA
- If immobility or critical illness makes polysomnography unfeasible
- If direct monitoring of the response to non-CPAP treatments for sleep apnea is needed.
Home testing for OSA should not be used in the following situations:
- If the patient has significant morbidity such as moderate to severe pulmonary disease, neuromuscular disease, or congestive heart failure
- In evaluating a patient suspected of having comorbid sleep disorders such as central sleep apnea, periodic limb movement disorder, insomnia, parasomnias, circadian rhythm disorder, or narcolepsy
- In screening of asymptomatic patients.
Home testing has important drawbacks. It may underestimate the severity of sleep apnea. The rate of false-negative results may be as high as 17%. If the home test was thought to be technically inadequate or the results were inconsistent with those that were expected—ie, if the patient has a high pretest probability of OSA based on risk factors or symptoms but negative results on home testing—then the patient should undergo polysomnography.14
The diagnosis of OSA is confirmed if the number of apnea events per hour (ie, the apnea-hypopnea index) on polysomnography or home testing is more than 15, regardless of symptoms, or more than 5 in a patient who reports OSA symptoms. An apnea-hypopnea index of 5 to 14 indicates mild OSA, 15 to 30 indicates moderate OSA, and greater than 30 indicates severe OSA.
BENEFITS OF TREATMENT
Treatment of OSA with CPAP reduces the 10-year risk of fatal and nonfatal motor vehicle accidents by 52%, the 10-year expected number of myocardial infarctions by 49%, and the 10-year risk of stroke by 31%.7 It has also been found to be cost-effective, for men and women of all ages with moderate to severe OSA.15
Obstructive sleep apnea (OSA) is common in morbidly obese patients, with a reported prevalence as high as 45% in obese subjects.1 In fact, according to one study presented at the American Society of Metabolic and Bariatric Surgery, of 359 patients who had preoperative polysomnography, 86% had positive tests, which showed severe OSA in half of the cases.2
Obesity predisposes to and potentiates OSA, which demonstrates the need to diagnose OSA through polysomnography testing as part of the preoperative evaluation for bariatric surgery. Preoperative diagnosis of OSA is important for both perioperative airway management and the prevention of postoperative pulmonary complications.3
Assessment of OSA
Polysomnography remains the gold standard for diagnosis and assessment of OSA. Assessing a patient’s BMI is not a fully diagnostic indicator for OSA. In one study, 40 patients being evaluated for bariatric surgery underwent a polysomnography regardless of symptoms. OSA was present in 71% of patients. The majority of the patients were women whose patient characteristics failed to predict the severity of OSA. For that reason, providers should have a low threshold for ordering a polysomnography as part of the preoperative evaluation for bariatric surgery.4
Preoperative Treatment for OSA
CPAP is the mainstay treatment for moderate to severe OSA and has been shown to improve objective and subjective measures of OSA. Appropriate therapy with CPAP perioperatively would theoretically prevent hypoxic complications associated with OSA.5
CPAP has been shown to be a highly effective treatment if appropriately used. Medical literature demonstrates that CPAP can also lead to an improvement in hypertension, especially for patients with moderate to severe OSA.4
Postoperative Treatment for OSA
Data in the literature demonstrates subjective improvement in symptoms of OSA after bariatric surgery, including improvement in self-reported postoperative sleep quality and the reduction in daytime sleepiness. Improvement in validated quality of life scores was shown after bariatric surgery.7
Continuous pulse oximetry (in a critical care or step-down unit or by a dedicated, appropriately trained professional observer in the patient’s room) is felt to reduce the likelihood of complications among patients with OSA.8
Another report recommends continuous monitoring should be maintained for as long as patients remain at increased risk and for at least 3 hours beyond the standard observation time of their non-OSA counterparts.9
Postoperative use of CPAP should not be viewed as potentially adverse to outcomes following bariatric surgery due to any such concerns, and its use should be employed by bariatric surgeons based on the patient’s pulmonary status postoperatively. The risk of anastomotic complications is not increased by CPAP use in the immediate postoperative period following routine gastric bypass based on the existing literature.10 In fact, the risk for prolonged or repeat hospital stays is reduced with CPAP treatment.
Untreated OSA is a comorbidity observed with high prevalence in the bariatric patient population that leads to increased mortality and increased medical disability from several cardiovascular diseases.
Polysomnography is recommended prior to bariatric surgery to determine the if OSA is present and manage symptoms prior to surgery.
Appropriate follow up with a sleep medicine physician is needed to ensure postoperative compliance with CPAP treatment. Management of OSA after bariatric surgery can help aid in postoperative weight loss in the long term.
Click here to download a PDF of this case study.
1Young T, Palta M, Dempsey J, Skatrud J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230–1235.
2Bangura AS, Gibbs KE. Is routine preoperative polysomnography necessary in patients having bariatric surgery. ASMBS 2011; Abstract P-77.
3O’Keeffe T, Patterson EJ. Evidence supporting routine polysomnography before bariatric surgery. Obes Surg. 2004 Jan;14(1):23-6.
4Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006;18(4):CD005308.
5Frey WC, Pilcher J. Obstructive sleep-related breathing disorders in patients evaluated for bariatric surgery. Obes Surg. 2003 Oct;13(5):676-83.
6Lettieri CJ, Eliasson AH, Greenburg DL. Persistence of obstructive sleep apnea after surgical weight loss. J Clin Sleep Med. 2008;4(4):333-8.
7Dixon JB, Schachter LM, O’Brien PE. Polysomnography before and after weight loss in obese patients with severe sleep apnea. Int J Obes (Lond). 2005;29(9):1048-54.
8Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: A report by the american society of anesthesiologists task force on perioperative management of patients with obstructive sleep apnea. Anesthesiology. 2006;104(5):1081-93.
9Schumann R, Jones SB, Cooper B, Kelley SD, Bosch MV, Ortiz VE, et al. Update on best practice recommendations for anesthetic perioperative care and pain management in weight loss surgery, 2004-2007. Obesity (Silver Spring). 2009;17(5):889-94.
10Ramirez A, Lalor PF, Szomstein S, Rosenthal RJ. Continuous positive airway pressure in immediate postoperative period after laparoscopic roux-en Y gastric bypass: Is it safe? Surg Obes Relat Dis. 2009;5(5):544-6.
Obstructive Sleep Apnea and Cardiovascular Disease
Sleep-related breathing disorders are highly prevalent in patients with established cardiovascular disease. Obstructive sleep apnea (OSA) affects an estimated 22 million adult Americans1 and is present in a large proportion of patients with hypertension and in those with other cardiovascular disorders, including coronary artery disease, stroke, tachycardia, cardiac arrhythmias, congestive heart failure and atrial fibrillation.2
Quantity and quality of sleep show secular trends alongside changes in modern society, reducing the average duration of sleep across westernized populations with increased reporting of fatigue, tiredness, and excessive daytime sleepiness. Too little or too much sleep are associated with adverse health outcomes, including hypertension and other cardiovascular disorders.3
Obstructive Sleep Apnea (OSA) and Cardiovascular Disease Correlation
Obstructive sleep apnea (OSA) is characterized by repetitive interruption of ventilation during sleep caused by collapse of the pharyngeal airway. A diagnosis of OSA is accepted when a patient has an apnea-hypopnea index (AHI; number of apneas and hypopneas per hour of sleep) >5 and symptoms of excessive daytime sleepiness.
Available data indicate that OSA prevalence is 2 to 3 times higher in patients with cardiovascular disease.4 Obstructive apneas may induce severe intermittent hypoxemia and CO2 retention during sleep, with oxygen saturation sometimes dropping to ≤60%, disrupting the normal structured autonomic and hemodynamic responses to sleep.5
The relationship between duration of sleep and vascular events is U-shaped, suggesting that different mechanisms may operate at either end of the distribution of sleep duration.6
In a systematic review of prospective population-based studies from 1966–2009, one study aimed to assess the relationship between duration of sleep and morbidity and mortality from coronary heart disease (CHD), stroke, and total cardiovascular disease (CVD).
This study showed an increased risk of developing or dying from CHD and stroke on either end of the distribution of sleep duration. Pooled analyses indicate that short sleepers have a greater risk of CHD and stroke than those sleeping 7–8 hours per night. Furthermore, long sleepers also show an increased risk for these events, confirming the presence of a U-shape association, with some heterogeneity among studies for CHD and CVD outcomes, no presence of publication bias, high statistical power, no difference between men and women, or by the duration of follow-up.7
Another respective study explored the incidence of CVD in a consecutive sleep clinic cohort of 182 middle-aged men (mean age, 46.8 ± 9.3; range, 30–69 years in 1991) with or without obstructive sleep apnea (OSA) throughout a period of seven years. The study concluded that the risk of developing CVD is increased in middle-aged OSA subjects independently of other risk factors like age, BMI, and smoking. Furthermore, the study concluded that efficient treatment of OSA reduces the excess CVD risk and may be considered also in relatively mild OSA without regard to daytime sleepiness.8
A systematic review of literature published in the Annals of Thoracic Medicine aimed to summarize a broad array of the pathophysiological mechanisms underlying the relationship between OSA and cardiac arrhythmias to assess the effects of OSA treatment on the presence of cardiac arrhythmias. The association between OSA and arrhythmias was first documented over 30 years ago. Since then, the literature has concluded that individuals with severe OSA were found to have two-to-fourfold higher odds of complex arrhythmias than those without OSA.9
Special emphasis should be given to recognizing the patient with cardiovascular disease who has coexisting sleep apnea to identifying strategies for co-management to best serve the patients needs. A board certified sleep medicine physician is best suited to work with you and your patients to determine an appropriate treatment plan.
SOMNAS and Allergy Sleep & Lung Care are dedicated to improving and maintaining the health status of our patients by providing compassionate, top-quality care. A patient’s special needs, concerns, and lifestyle, and those of their family, will guide our treatment planning. The care our patients receive with us will be on par with the highest national standards.
SOMNAS Sleep and wake disorders center offers state-of-the-art diagnostic options to identify specific sleep disorders and manage them using the latest treatments and therapies in an individualized treatment plan. Our office will work with your patients, communicating every step of the way for the overall health and wellbeing of your patients.
Click here to download a PDF of this case study.
1American Sleep Apnea Association.
2Caples S.M., Garcia-Touchard A., Somers V.K. (2007) Sleep-disordered breathing and cardiovascular risk. Sleep 30:291–303.
3Gangwisch JE, Heymsfield SB, Boden-Albala B, et al. Short sleep duration as a risk factor for hypertension: analyses of the first National Health and Nutrition Examination Survey. Hypertension 2006;47:833-839.
4Wolk R., Kara T., Somers V.K. (2003) Sleep-disordered breathing and cardiovascular disease. Circulation 108:9–12.
5Somers V.K., Dyken M.E., Mark A.L., Abboud F.M. (1993) Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med 328:303–307.
6Knutson KL, Turek FW. The U-shaped association between sleep and health: the 2 peaks do not mean the same thing. Sleep 2006;29:878-879.
7Francesco CP, Daniel C, Lanfranco D, et al. Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies. European Heart Journal 2001;1484-1492.
8Peker Y, Hedner J, Norum, J, et al. Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med 2002;166:159–165.
9Ahmad Salah Hersi. Obstructive sleep apnea and cardiac arrhythmias. Ann Thorac Med. 2010 Jan-Mar; 5(1): 10–17.