Restless legs syndrome: From clinic to personalized medicine.

Restless legs syndrome (RLS) is a common neurological sensorimotor disorder that impairs sleep, mood and quality of life. RLS is defined by an urge to move the legs at rest that increases in the evening and at night, and is frequently associated with metabolic and cardiovascular diseases. Symptoms frequency, age at RLS onset, severity, familial history and consequences of RLS vary widely between patients. A genetic susceptibility, iron deficiency, dopamine deregulation, and possible hypo-adenosinergic state may play a role in the pathophysiology of RLS. Polysomnographic recordings found often periodic leg movements during sleep and wakefulness in patients with RLS. RLS can be classified as primary or comorbid with major diseases: iron deficiency, renal, neurological, rheumatological and lung diseases. First-line treatments are low-dose dopamine agonists, and alpha-2-delta ligands depending on the clinical context, and second/third line opiates for pharmacoresistant forms of RLS. Augmentation syndrome is a serious complication of dopamine agonists and should be prevented by using the recommended low dose. Despite an increase in knowledge, RLS is still underdiagnosed, poorly recognized, resulting in substantial individual health burden and socioeconomic coast, and education is urgently needed to increase awareness of this disabling disorder.

Narcolepsies, update in 2023.

Narcolepsy type 1 (NT1) and type 2 (NT2), also known as narcolepsy with and without cataplexy, are sleep disorders that benefited from major scientific advances over the last two decades. NT1 is caused by the loss of hypothalamic neurons producing orexin/hypocretin, a neurotransmitter regulating sleep and wake, which can be measured in the cerebrospinal fluid (CSF). A low CSF level of hypocretin-1/orexin-A is a highly specific and sensitive biomarker, sufficient to diagnose NT1. Orexin-deficiency is responsible for the main NT1 symptoms: sleepiness, cataplexy, disrupted nocturnal sleep, sleep-related hallucinations, and sleep paralysis. In the absence of a lumbar puncture, the diagnosis is based on neurophysiological tests (nocturnal and diurnal) and the presence of the pathognomonic symptom cataplexy. In the revised version of the International Classification of sleep Disorders, 3rd edition (ICSD-3-TR), a sleep onset rapid eye movement sleep (REM) period (SOREMP) (i.e. rapid occurrence of REM sleep) during the previous polysomnography may replace the diurnal multiple sleep latency test, when clear-cut cataplexy is present. A nocturnal SOREMP is very specific but not sensitive enough, and the diagnosis of cataplexy is usually based on clinical interview. It is thus of crucial importance to define typical versus atypical cataplectic attacks, and a list of clinical features and related degrees of certainty is proposed in this paper (expert opinion). The time frame of at least three months of evolution of sleepiness to diagnose NT1 was removed in the ICSD-3-TR, when clear-cut cataplexy or orexin-deficiency are established. However, it was kept for NT2 diagnosis, a less well-characterized disorder with unknown clinical course and absence of biolo biomarkers; sleep deprivation, shift working and substances intake being major differential diagnoses. Treatment of narcolepsy is nowadays only symptomatic, but the upcoming arrival of non-peptide orexin receptor-2 agonists should be a revolution in the management of these rare sleep diseases.

Nocturnal agitation: From sleep state dissociation to sleep-related dissociative state.

Nocturnal agitation refers to a broad spectrum of symptoms from simple movements to aggressive behaviors with partial or complete loss of awareness. An accurate identification of its etiology is critical for appropriate therapeutic intervention. In children and young adults, distinguishing between non-rapid eye movement (NREM) sleep parasomnias and psychogenic non-parasomniac manifestations, a condition known as sleep-related dissociative disorder (SRDD), can be challenging. This review aims to summarize current clinical, neurophysiological, and epidemiological knowledge on NREM parasomnia and SRDD, and to present the pathophysiological hypotheses underlying these nocturnal manifestations. Sleepwalking, sleep terror and confusional arousals are the three main presentations of NREM parasomnias and share common clinical characteristics. Parasomniac episodes generally occur 30minutes to three hours after sleep-onset, they are usually short, lasting no more than few minutes and involve non-stereotyped, clumsy behaviors with frequent amnesia. The prevalence of NREM parasomnia decreases from 15-30% in children to 2-4% in adults. Parasomniac episodes are incomplete awakening from the deepest NREM sleep and are characterized by a dissociated brain activity, with a wake-like activation in motor and limbic structures and a preserved sleep in the fronto-parietal regions. SRDD is a less known condition characterized by dramatic, often very long episodes with frequent aggressive and potentially dangerous behaviors. SRDD episodes frequently occur in quiet wakefulness before falling asleep. These dissociative manifestations are frequently observed in the context of psychological trauma. The pathophysiology of SRDD is poorly understood but could involve transient changes in brain connectivity due to labile sleep-wake boundaries in predisposed individuals. We hypothesize that SRDD and NREM parasomnia are forms of sleep-related dissociative states favored by a sleep-wake state dissociation during sleep-onset and awakening process, respectively.

The multifaceted aspects of sleep and sleep-wake disorders following stroke.

Sleep-wake disorders (SWD) are acknowledged risk factors for both ischemic stroke and poor cardiovascular and functional outcome after stroke. SWD are frequent following stroke, with sleep apnea (SA) being the most frequent SWD affecting more than half of stroke survivors. While sleep disturbances and SWD are frequently reported in the acute phase, they may persist in the chronic phase after an ischemic stroke. Despite the frequency and risk associated with SWD following stroke, screening for SWD remains rare in the clinical setting, due to challenges in the assessment of post-stroke SWD, uncertainty regarding the optimal timing for their diagnosis, and a lack of clear treatment guidelines (i.e., when to treat and the optimal treatment strategy). However, little evidence support the feasibility of SWD treatment even in the acute phase of stroke and its favorable effect on long-term cardiovascular and functional outcomes. Thus, sleep health recommendations and SWD treatment should be systematically embedded in secondary stroke prevention strategy. We therefore propose that the management of SWD associated with stroke should rely on a multidisciplinary approach, with an integrated diagnostic, treatment, and follow-up strategy. The challenges in the field are to improve post-stroke SWD diagnosis, prognosis and treatment, through a better appraisal of their pathophysiology and temporal evolution.

Socioeconomic impact of restless legs syndrome and inadequate restless legs syndrome management across European settings.

Restless legs syndrome (RLS) is one of the most common neurological disorders. It describes an irresistible urge to move the legs, mostly manifested in the evening and at night, which can lead to severe sleep disturbance. As part of the European Brain Council (EBC)-led Value-of-Treatment project, this study aimed at capturing the socioeconomic impact of RLS related to the inadequate diagnosis and treatment across different European healthcare settings. The economic burden of RLS was estimated using the published EBC framework of analysis in three separate European Union healthcare systems (France, Germany, and Italy). The RLS care pathway was mapped to identify the unmet needs of patients. Based on specific patient stories, the economic impact of correctly diagnosing RLS and changing between inadequate and target treatment was calculated using appropriate scenario analysis. RLS proved to be a significant personal and social burden, when epidemiological data, high prevalence of RLS, and its need for treatment are combined. By looking at the savings emerging from the provision of optimal care management (timely and correct diagnosis, evidence-based therapy, avoidance of therapy-related complications such as augmentation), the authors foresee substantial economic savings with the achievement of adequate diagnosis and treatment of RLS. Education about RLS is urgently needed for all subspecialties involved in RLS patient care as well as the general public. Equally important, the search for new causal treatment strategies should be intensified to reduce suffering and substantial societal cost.

French consensus: Augmentation syndrome in restless legs syndrome.

Augmentation syndrome is one of the most severe complications of RLS. It is characterised by a worsening of treated symptoms; principally an increase in the severity of symptoms and an earlier onset time. Augmentation syndrome occurs primarily with dopaminergic treatments. It is crucial for the patient to be sufficiently well informed to prevent its occurrence and the prescription of too high doses of dopaminergic agonists avoided. In the presence of augmentation syndrome confirmed using the diagnostic criteria, the specialist treating the restless legs syndrome should quickly modify the patient's treatment. In this article, our expert group proposes a practical strategy for the diagnosis, prevention and treatment of augmentation syndrome.

French consensus. Hypersomnolence: Evaluation and diagnosis.

Sleepiness is one of the most frequently reported complaints in adults and children during specialised sleep consultations. It is responsible for an alteration that can be severe in quality of life, a lowering of academic or professional performance, and domestic or work accidents. Hypersomnolence is the first cause of road accidents on the highway, responsible for a third of fatal accidents. Furthermore its presence is associated with an increased risk of morbi-mortality related to cardiovascular and neurodegenerative pathologies. Hence, its represents a real public health issue. Recent revisions in international classifications have clarified confusing terminology, and the complaint of hypersomnia has now been replaced by the terms hypersomnolence or excessive sleepiness. It is clinically defined as an excessive quantity of sleep over 24hours, and/or by an alteration in the quality of arousal defined as incapacity to maintain a satisfactory level of vigilance during the day or in the morning on awakening (defined as sleep inertia). The evaluation of sleepiness requires a rigorous clinical approach, completed by subjective and objective measurements. The Epworth Sleep Scale, Multiple Sleep Latency Tests and the Maintenance of Wakefulness Test are the most studied and used in clinical practice. However, to date, no gold standard measurement of excessive sleepiness exists, and there are no quantifiable biological markers. It is therefore important to optimise our evaluation tools, improve our pathophysiological understanding of sleepiness, and define genetic and environmental risk factors.

French consensus. Idiopathic hypersomnia: Investigations and follow-up.

Idiopathic hypersomnia is a rare, central hypersomnia, recently identified and to date of unknown physiopathology. It is characterised by a more or less permanent, excessive daytime sleepiness, associated with long and unrefreshing naps. Night-time sleep is of good quality, excessive in quantity, associated with sleep inertia in the subtype previously described as "with long sleep time". Diagnosis of idiopathic hypersomnia is complex due to the absence of a quantifiable biomarker, the heterogeneous symptoms, which overlap with the clinical picture of type 2 narcolepsy, and its variable evolution over time. Detailed evaluation enables other frequent causes of somnolence, such as depression or sleep deprivation, to be eliminated. Polysomnography and multiple sleep latency tests (MSLT) are essential to rule out other sleep pathologies and to objectify excessive daytime sleepiness. Sometimes the MSLT do not show excessive sleepiness, hence a continued sleep recording of at least 24hours is necessary to show prolonged sleep (>11h/24h). In this article, we propose recommendations for the work-up to be carried out during diagnosis and follow-up for patients suffering from idiopathic hypersomnia.

French consensus. Type 1 and type 2 Narcolepsy: Investigations and follow-up.

In the new international classification of sleep disorders (ICSD-3), narcolepsy is differentiated into two distinct pathologies: type 1 narcolepsy (NT1) and type 2 narcolepsy (NT2). NT1 is characterised by periods of an irrepressible need to sleep, cataplexy (a sudden loss of muscle tone triggered by emotion) and in some cases the presence of symptoms such as hypnagogic hallucinations, sleep paralysis and disturbed night-time sleep. Its physiopathology is based on the loss of hypocretin neurons in the hypothalamus, seemingly connected to an auto-immune process. By definition, cataplexy is absent and the hypocretin levels in the CSF are normal in NT2. Confirming the diagnosis requires polysomnography and multiple sleep latency tests. The choice of further investigations is based on the presence or absence of typical cataplexy. Further investigations include HLA typing, lumbar puncture to measure the hypocretin level in the CSF, or even brain imagery in the case of narcolepsy suspected to be secondary to an underlying pathology. In this consensus we propose recommendations for the work-up to be carried out during diagnosis and follow-up for patients suffering from narcolepsy.

French consensus. Management of patients with hypersomnia: Which strategy?

Central hypersomnias principally involves type 1 narcolepsy (NT1), type 2 narcolepsy (NT2) and idiopathic hypersomnia (IH). Despite great progress made in understanding the physiopathology of NT1 with low cerebrospinal fluid hypocretin-1 levels, current treatment remains symptomatic. The same applies to NT2 and IH, for which the physiopathology is still largely unknown. Controlling excessive daytime sleepiness (EDS), cataplexy, hypnagogic hallucinations, sleep paralysis and disturbed night-time sleep are key therapeutic targets in NT1. For IH and NT2, reducing EDS is the main objective. Based on European and American directives for the treatment of narcolepsy, we propose French recommendations for managing central hypersomnias as well as strategies in the case of drug-resistance. Stimulating treatments target EDS, and Modafinil is the first-line treatment. Other stimulants such as methylphenidate, pitolisant, and exceptionally dextro-amphetamine can be prescribed. Selective serotonin and noradrenaline reuptake inhibitor antidepressants are effective for the management of cataplexy in NT1. Sodium oxybate is an effective treatment for several symptoms, including EDS, cataplexy and disturbed night-time sleep. Treatment of central hypersomnia must also take into consideration frequent cardiovascular, metabolic and psychiatric comorbidities, particularly in NT1. New therapies are currently under study with the development of new stimulants and anti-cataplectics. The next few years will see innovative emerging therapies, based on a physiopathological approach, aiming to restore hypocretinergic transmission or to interrupt the autoimmune processes causing the loss of hypocretin neurons.

[Role and actions of the orphan rare diseases reference center for central hypersomnias in France]. / Quel apport des centres de référence maladies rares dans la prise en charge des hypersomnies rares?

Narcolepsy (with or without cataplexy), idiopathic hypersomnia (with or without long sleep duration) and Kleine - Levin syndrome are the main central rare hypersomnias. They may be considered models to help us to better understand the mechanisms controlling sleep and waking regulation in humans. When creating the national centers for rare hypersomnias, the aims were: 1) screening and earlier treatment of patients with hypersomnia; 2) improving patient care with guidelines, a specific patient's card, coordination of treatments between centers and professionals, and the development of new treatments; 3) encouraging research studies into the epidemiology, pathophysiology and genotype/phenotype through the creation of clinical, DNA, sera and cerebrospinal fluid banks; 4) increasing public awareness among patients and their relatives, the general public and in the mass media of rare hypersomnias; and 5) regular evaluation of our activities. These goals appear to have been achieved over the past 5 years. However, there are now financial difficulties to be faced, given the increasing demands of patients and professionals while having to stay within the same limited budgets.

[Potential teratogenicity of modafinil - Conflicting evidence, need for research]. / Tératogénicité potentielle du modafinil ­ des données contradictoires, un besoin de recherche.

Central disorders of hypersomnolence include narcolepsy type 1, narcolepsy type 2, idiopathic hypersomnia and hypersomnia associated with medical or mental disorders. Treatment is both non-pharmacological and pharmacological, including wake enhancing drugs and stimulants. One of the first-line treatment (modafinil, MODIODAL®) was the subject of a health authority alert in 2019 concerning a risk of major congenital malformations when taken during organogenesis. Since this date, three epidemiological studies have presented contradictory results. Given their methodological weaknesses, it is not possible at this stage to confirm or deny such a risk for the embryo and its nature if there is one. In clinical practice, because of these uncertainties, it is preferable if possible to suspend the treatment of a pregnant woman during the first 10 weeks from last menstrual period (organogenesis). There is an unmet clinical need for research to clarify the potential teratogenic impact of modafinil.

[How to manage daytime sleepiness associated with Parkinson's disease]. / Comment prendre en charge la somnolence associée à la maladie de Parkinson ?

Excessive daytime sleepiness (EDS) is frequent in Parkinson's disease. It should be explored by an Epworth sleepiness scale, a nighttime sleep recording and multiple sleep latency tests. EDS can be secondary to disturbed nighttime sleep that should be explored first. The main reasons for nighttime sleep disturbances are pain, nocturia, restless legs syndrome, obstructive sleep apnea syndrome and depression. They should be treated step by step. EDS can also be secondary to antiparkinsonian dopaminergic treatments that can induce nighttime insomnia and/or daytime sleepiness sometimes with sleep attacks. Treatment modifications and, when indicated, deep brain stimulation can improve these symptoms. Furthermore, EDS can be secondary to the disease itself modifying the sleep wake regulation systems. When the treatment of disturbed nighttime sleep and adjustments of the dopaminergic treatments are not sufficient to improve EDS, wake promoting treatments can be used. Their efficacy is variable but new hopeful drugs are coming soon.

Natural history of excessive daytime sleepiness: a population-based 5-year longitudinal study.

STUDY OBJECTIVES: To document the rates of persistent, remitted, and intermittent excessive daytime sleepiness (EDS) in a longitudinal 5-year community study of adults and to assess how changes in risk factors over time can predict improvement of daytime sleepiness (DS). METHODS: Participants were recruited in 2007-2008 as part of a population-based epidemiological study implemented in Canada. They completed postal assessments at baseline and at each yearly follow-up. An Epworth Sleepiness Scale total score >10 indicated clinically significant EDS; a 4-point reduction between two consecutive evaluations defined DS improvement. Socio-demographic, lifestyle, health characteristics, and sleep-related measures (e.g. insomnia symptoms, sleep duration, sleep medication) were self-reported at each time point. Cox proportional-hazard models were used to predict EDS and DS remissions over 5 years. RESULTS: Among the 2167 participants, 33% (n = 714) met criteria for EDS at baseline, of whom 33% had persistent EDS, 44% intermittent EDS, and 23% remitted EDS over the follow-up. Furthermore, 61.4% of 2167 initial participants had stable DS, 27.1% sustained DS improvement and 8.5% transient improvement over the follow-up. The main predictors of EDS remission or DS improvement were normal weight, taking less hypnotics, having hypertension, increased nighttime sleep duration, and decreased insomnia, and depressive symptoms. CONCLUSIONS: EDS waxes and wanes over time with frequent periods of remission and is influenced by behavioral characteristics and changes in psychological, metabolic, and nighttime sleep patterns. Targeting these predictors in future interventions is crucial to reduce DS in the general adult population.

Effects of an individualized exercise training program on severity markers of obstructive sleep apnea syndrome: a randomised controlled trial.

OBJECTIVE: Obstructive sleep apnea (OSA) is a high prevalent disorder with severe consequences including sleepiness, metabolic, and cardiovascular disorders. The aim of this study was to assess the effect of an individualized exercise-training (IET) program with educational sessions vs educational sessions alone on severity markers of OSA over an eight-week duration. METHODS: This was a randomised, controlled, parallel-design study. In sum, 64 patients with moderate-to-severe OSA (apnea-hypopnea index AHI 15-45/hour), low physical activity level (Voorrips<9), body-mass index (BMI) <40 kg/m2 were included in intervention group (IG) or control group (CG), and 54 patients finished the study. All underwent polysomnography (PSG), multiple sleep latency test (MSLT), constant workload exercise test, blood samples and fulfilled questionnaires twice. The primary endpoint was the change in apnea-hypopnea (AHI) at eight weeks from baseline. Main secondary endpoints were daytime sleepiness assessed by questionnaire and objective tests. RESULTS: No significant between-group differences were found for changes in AHI. A reduction in AHI was found in IG only (p = 0.005). Compared to CG, exercise training leads to a greater decrease in AHI during REM sleep (p = 0.0004), with a significant increase in mean daytime sleep latency (p = 0.02). Between-group differences were significant for weight reduction, severity of fatigue, insomnia and depressive symptoms with trend for sleepiness symptoms. CONCLUSIONS: In adult patients with moderate-to-severe OSA, IET did not decrease AHI compared to the control group but improved markers of severity of OSA, in particular AHI in rapid eye movement (REM) sleep and objective daytime sleepiness. Adding personalized exercise training to the management of patients with OSA should be considered. CLINICALTRIALS. GOV IDENTIFIER: NCT01256307.

A polysomnographic study of daytime sleepiness in myotonic dystrophy type 1.

OBJECTIVES: To assess contributors to excessive daytime sleepiness (EDS) in myotonic dystrophy type 1 (DM1), to characterise subjects with sleep-onset REM periods (SOREMPs), and to verify whether self-reported instruments and respiratory function tests can predict multiple sleep latency test (MSLT) and sleep-disordered breathing. METHODS: A sample of 43 DM1 patients without selection bias underwent polysomnography (PSG) for two consecutive nights and MSLT, completed a sleep diary and Epworth Sleepiness Scale (ESS), and were assessed for respiratory function and narcolepsy symptoms. RESULTS: ESS scores (ES) > or =11 and MSLT mean sleep latency (MSL) < or =8 min were found in 21 (50.0%) and 19 (44.2%) subjects, and either in 30 (69.8%) subjects. ES did not relate to MSL. Subjects with subjective sleepiness (ES> or =11) reported more cataplexy-like and sleep paralysis symptoms, longer habitual sleep times, and higher sleep efficiency and REM sleep per cent than those without. Subjects with objective sleepiness (MSL< or =8 min) had a higher stage 4 sleep per cent. Subjects with > or =2 SOREMPs (25.6%) showed higher muscular impairment, lower MSL, higher ES, and more cataplexy-like symptoms than those with < or =1 SOREMP. Apnoea-hypopnoea index (AHI) > or =5, predominantly obstructive, was found in 37 (86.0%) subjects, and AHI >30 in 12 (27.9%). Neither subjective nor objective sleepiness could be explained by AHI, nor satisfactorily predicted by daytime respiratory abnormalities. CONCLUSIONS: DM1 entails frequent EDS but with different phenotypes and distinct mechanisms involved. The high prevalence of daytime sleepiness and severe sleep apnoeas found in this study supports the routine use of clinical sleep interviews, PSG and MSLT in DM1, and emphasises the need for more randomised trials of psychostimulants.

Psychological health in central hypersomnias: the French Harmony study.

BACKGROUND: A large observational French study of central hypersomnia, including narcolepsy with cataplexy (C+), without cataplexy (C-) and idiopathic hypersomnia (IH), was conducted to clarify the relationships between the severity of the condition, psychological health and treatment response. METHODS: 601 consecutive patients over 15 years of age suffering from central hypersomnia were recruited on excessive daytime sleepiness, polysomnography and Multiple Sleep Latency Test (MSLT) results. 517 (47.6% men, 52.4% women) were finally included: 82.0% C+, 13.2% C- and 4.8% IH. Face to face standardised clinical interviews plus questionnaires (Epworth Sleepiness Scale (ESS), short version Beck Depression Inventory (S-BDI), Pittsburgh Sleep Quality Index (PSQI) and 36-item Short Form Health Survey (SF-36)) were performed. Patients affected with a different diagnosis and with and without depressive symptoms were compared. RESULTS: Mean ESS and body mass index were higher in C+ compared with C-/IH patients. Half of the patients (44.9%) had no depressive symptoms while 26.3% had mild, 23.2% moderate and 5.6% severe depressive symptoms. C+ patients had higher S-BDI and PSQI and lower SF-36 scores than C-/IH patients. Depressed patients had higher ESS scores than non-depressed patients, with no difference in age, gender, duration of disease or MSLT parameters. Finally, C+ patients treated with anticataplectic drugs (38.7%) had higher S-BDI and lower SF-36 scores than C+ patients treated with stimulants alone. CONCLUSION: Our data confirmed the high frequency of depressive symptoms and the major impact of central hypersomnias on health related quality of life, especially in patients with cataplexy. We recommend a more thorough assessment of mood impairment in central hypersomnias, especially in narcolepsy-cataplexy.

Sleep disorders and their impacts on healthy, dependent, and frail older adults.

BACKGROUND: Sleep disorders differ widely in the heterogeneous older adult population. Older adults can be classified into three groups based upon their overall level of disability: healthy, dependent, and frail. Frailty is an emerging concept that denotes older persons at increased risk for poor outcomes. OBJECTIVE: The aim of this consensus review is to describe the sleep disorders observed in healthy and dependent older adults and to discuss the potential sleep disorders associated with frailty as well as their potential consequences on this weakened population. METHODS: A review task force was created including neurologists, geriatricians, sleep specialists and geriatric psychiatrists to discuss age related sleep disorders depending on the three categories of older adults. All published studies on sleep in older adults on Ovid Medline were reviewed and 106 articles were selected for the purpose of this consensus. RESULTS: Many healthy older adults have complains about their sleep such as waking not rested and too early, trouble falling asleep, daytime napping, and multiple nocturnal awakenings. Sleep architecture is modified by age with an increased percentage of time spent in stage one and a decreased percentage spent in stages three and four. Insomnia is frequent and its mechanisms include painful medical conditions, psychological distress, loss of physical activity and iatrogenic influences. Treatments are also involved in older adults' somnolence. The prevalence of primary sleep disorders such as restless legs syndrome, periodic limb movements and sleep disordered breathing increases with age. Potential outcomes relevant to these sleep disorders in old age include mortality, cardiovascular and neurobehavioral co-morbidities. Sleep in dependent older adults such as patients with Alzheimer Disease (AD) is disturbed. The sleep patterns observed in these patients are often similar to those observed in non-demented elderly but alterations are more severe. Nocturnal sleep disruption and daytime sleepiness are the main problems. They are the results of Sleep/wake circadian rhythm disorders, environmental, psychological and iatrogenic factors. They are worsened by other sleep disorders such as sleep disordered breathing. Sleep in frail older adults per se has not yet been formally studied but four axes of investigation should be considered: i) sleep architecture abnormalities, ii) insomnia iii) restless legs syndrome (RLS), iv) sleep disordered breathing. CONCLUSION: Our knowledge in the field of sleep disorders in older adults has increased in recent years, yet some groups within this heterogeneous population, such as frail older adults, remain to be more thoroughly studied and characterized.