[Sleep disorders in patients with a neurocognitive disorder]. / Les troubles du sommeil chez les patients atteints d'un trouble neurocognitif.

INTRODUCTION: Sleep disorders are prevalent in patients with a neurocognitive disorder, and diagnosis and treatment in these patients remain challenging in clinical practice. METHODS: This narrative review offers a systematic approach to diagnose and treat sleep disorders in neurocognitive disorders. RESULTS: Alzheimer's disease is often associated with circadian rhythm disorders, chronic insomnia, and sleep apnea-hypopnea syndrome. Alpha-synucleinopathies (e.g., Parkinson's disease and Lewy body dementia) are often associated with a rapid eye movement sleep behavior disorder, restless legs syndrome, chronic insomnia, and sleep apnea-hypopnea syndrome. A focused history allows to diagnose most sleep disorders. Clinicians should ensure to gather the following information in all patients with a neurocognitive disorder: (1) the presence of difficulties falling asleep or staying asleep, (2) the impact of sleep disturbances on daily functioning (fatigue, sleepiness and other daytime consequences), and (3) abnormal movements in sleep. Sleep diaries and questionnaires can assist clinicians in screening for specific sleep disorders. Polysomnography is recommended if a rapid eye movement sleep behavior disorder or a sleep apnea-hypopnea syndrome are suspected. Sleep complaints should prompt clinicians to ensure that comorbidities interfering with sleep are properly managed. The main treatment for moderate to severe obstructive sleep apnea-hypopnea syndrome remains continuous positive airway pressure, as its efficacy has been demonstrated in patients with neurocognitive disorders. Medications should also be reviewed, and time of administration should be optimized (diuretics and stimulating medications in the morning, sedating medications in the evening). Importantly, cholinesterase inhibitors (especially donepezil) may trigger insomnia. Switching to morning dosing or to an alternative drug may help. Cognitive-behavioral therapy for insomnia is indicated to treat chronic insomnia in neurocognitive disorders. False beliefs regarding sleep should be addressed with the patient and their caregiver. The sleep environment should be optimized (decrease light exposure at night, minimize noise, avoid taking vital signs, etc.). Sleep restriction can be considered as patients with a neurocognitive disorder often spend too much time in bed. The need for naps should be assessed case by case as naps may contribute to insomnia in some patients but allow others to complete their diurnal activities. Trazodone (50mg) may also be used under certain circumstances in chronic insomnia. Recent evidence does not support a role for exogenous melatonin in patients with a neucognitive disorder and insomnia. Patients in long-term care facilities are often deprived of an adequate diurnal exposure to light. Increasing daytime exposure to light may improve sleep and mood. Patients with circadian rhythm disorders can also benefit from light therapy (morning bright light therapy in case of phase delay and evening bright light therapy in case of phase advance). Rapid eye movement sleep behavior disorder can lead to violent behaviors, and the sleeping environment should be secured (e.g., mattress on the floor, remove surrounding objects). Medication exacerbating this disorder should be stopped if possible. High dose melatonin (6 to 18mg) or low dose clonazepam (0.125-0.25mg) at bedtime may be used to reduce symptoms. Melatonin is preferred in first-line as it is generally well tolerated with few side effects. Patients with restless legs syndrome should be investigated for iron deficiency. Medication decreasing dopaminergic activity should be reduced or stopped if possible. Behavioral strategies such as exercise and leg massages may be beneficial. Low-dose dopamine agonists (such as pramipexole 0.125mg two hours before bedtime) can be used to treat the condition, but a prolonged treatment may paradoxically worsen the symptoms. Alpha-2-delta calcium channel ligands can also be used while monitoring for the risk of falls. CONCLUSION: Multiple and sustained nonpharmacological approaches are recommended for the treatment of sleep disturbances in patients with neurocognitive disorder. Pharmacological indications remain limited, and further randomized clinical trials integrating a multimodal approach are warranted to evaluate the treatment of sleep disorders in specific neurocognitive disorders.

The association of coffee consumption and oxygen desaturation index during sleep among Japanese male workers.

BACKGROUND AND OBJECTIVE: Coffee is a major caffeine-containing food source that can be used for treatment of apnea in prematurity. However, few studies have examined the association between coffee consumption and sleep-disordered breathing (SDB). We investigated whether coffee consumption is associated with the oxygen desaturation index (ODI) as a marker of SDB among middle-aged Japanese male workers. METHODS: The subjects were 1126 male local government workers aged 22-59 who participated in SDB screening in 2011-2012. Daily coffee consumption was assessed by a self-administered questionnaire. We measured 3% oxygen desaturation (3%ODI) during a night's sleep using a pulse oximeter. A general linear model was used to calculate the multivariate-adjusted means of 3%ODI per quartile of coffee consumption. We further analyzed the data after stratifying by overweight and current smoking status. RESULTS: A inverse association between coffee consumption and 3%ODI was found. The multivariate-adjusted mean of 3%ODI for the lowest and highest coffee consumption groups were 11.9 times/h and 10.6 times/h (p for trend = 0.06), respectively; 14.6 and 11.5 times/h (p for trend = 0.01) in overweight participants; and 12.7 and 11.0 times/h (p for trend = 0.06) in non-smokers. No associations were found in non-overweight and smoking workers. CONCLUSIONS: Our results suggest that higher coffee consumption was associated with lower 3% ODI as a marker of SDB in overweight and non-smoking workers.

Opioids and Sleep-Disordered Breathing.

Opioid use for chronic pain analgesia, particularly chronic noncancer pain, has increased greatly since the late 1990s, resulting in an increase in opioid-associated morbidity and mortality. A clear link between opioid use and sleep-disordered breathing (SDB) has been established, with the majority of chronic opioid users being affected by the condition, and dose-dependent severity apparent for some opioids. More evidence is currently needed on how to effectively manage opioid-induced SDB. This review summarizes the current state of knowledge relating to management of patients undergoing chronic opioid therapy who have SDB. Initial management of these patients requires a thorough biopsychosocial assessment of their need for opioid therapy, consideration of reduction or cessation of the opioid if possible, and analysis of alternative therapies for treatment of their pain. If opioid therapy must be continued, then management of the associated SDB may be important. Several small- to medium-scale studies have examined the efficacy of noninvasive ventilation, particularly adaptive servo-ventilation (ASV) for the treatment of opioid-associated SDB. This research is particularly important because opioids predispose predominantly to central sleep apnea and also, to a lesser extent, OSA. Generally, these studies have found positive results in treating opioid-associated SDB with ASV in terms of improving outcome measures such as central apnea index and the apnea-hypopnea index. Larger studies that measure longer term health outcomes, patient sleepiness, and compliance are needed, however. Registries of health outcomes of ASV-treated patients may assist with future treatment planning.

The effects of nasal anesthesia on breathing during sleep.

Inability to breathe through the nose is an increasingly recognized cause of disordered breathing during sleep. To test the hypothesis that this respiratory dysrhythmia could result from loss of neuronal input to respiration from receptors located in the nose, we anesthetized the nasal passages of 10 normal men during sleep. Each subject spent 4 consecutive nights in the sleep laboratory while sleep stages, breathing patterns, respiratory effort, and arterial oxygen saturation were monitored. Night 1 was for acclimatization with Nights 3 and 4 being randomized to nasal spraying with either 4% lidocaine or placebo. On the lidocaine and placebo nights (Nights 3 and 4) the nasal passages were also sprayed with a decongestant to prevent increased nasal air-flow resistance resulting from mucosal swelling. To control for the possible effects of this decongestant, an additional night (Night 2) was included during which the nasal passages were sprayed with room air. Parallel studies conducted during wakefulness demonstrated low nasal resistance during the lidocaine-decongestant regimen. Because of the short duration of anesthesia with lidocaine, spraying was done at lights out and 2.5 and 5 h later. On the placebo night (decongestant plus saline) there were 6.4 +/- 1.8 (SEM) disordered breathing events (apneas plus hypopneas) per subject, whereas with lidocaine (plus decongestant) this increased fourfold to 25.8 +/- 7.8 events per subject (p less than 0.05). The majority of the disordered breathing events were apneas and were fairly evenly distributed between central and obstructive events. The magnitude of these changes is similar to that previously reported with complete nasal obstruction. These results suggest that nasal receptors sensitive to air flow may be important in maintaining breathing rhythmicity during sleep.