INTRODUCTION — Sleep-related breathing disorders, including obstructive sleep apnea (OSA), central sleep apnea (CSA), and Cheyne-Stokes breathing, are common in patients with stroke or transient ischemic attack (TIA) and have been associated with adverse outcomes both in the general population and in patients with stroke. In addition, OSA may itself be an independent risk factor for stroke.
OSA is characterized by the intermittent cessation or reduction of airflow during sleep due to complete or partial upper airway obstruction, while CSA is characterized by the intermittent absence of airflow and ventilatory effort. Cheyne-Stokes breathing refers to cyclic crescendo-decrescendo airflow and respiratory effort during wakefulness or sleep, without upper airway obstruction, lasting at least 40 seconds. Cheyne-Stokes breathing is considered a type of CSA when the decrescendo effort is accompanied by apnea during sleep. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults".)
Clinical signs and symptoms of sleep-related breathing disorders are not reliable in patients with stroke, and diagnostic sleep testing with polysomnography or home sleep apnea testing (HSAT) is required to make the diagnosis. While clinical trials in the general population have demonstrated that treatment of OSA with continuous positive airway pressure (CPAP) or other therapies significantly reduces apneas and oxygen desaturation during sleep and other outcomes, data in stroke patients are more limited.
The association between OSA and stroke as well as the epidemiology, clinical features, diagnosis, and management of sleep-related breathing disorders following stroke or TIA are discussed here. Other cardiovascular complications of OSA and other respiratory abnormalities that can occur after a stroke are described separately. (See "Obstructive sleep apnea and cardiovascular disease in adults" and "Complications of stroke: An overview", section on 'Pulmonary complications'.)
SLEEP APNEA AS A RISK FACTOR FOR STROKE — Obstructive sleep apnea (OSA) has been associated with an increased risk for ischemic stroke, independent of vascular risk factors [1]. The risk of stroke in patients with other sleep-related breathing disorders, including central sleep apnea syndrome, is not well studied.
Clinical evidence — Accumulating evidence from prospective cohort studies suggests that OSA increases the risk for stroke [2-8]. Confidence in the evidence is increased by the findings of a large effect [3] and a dose-response gradient (ie, correlation between the severity of OSA and the risk for stroke) [2,3].
Several large observational studies demonstrate this effect:
●A prospective cohort study followed 5422 individuals without a history of stroke for a median of 8.7 years [5]. Men whose obstructive apnea-hypopnea index (AHI) was in the highest quartile were more likely to have an ischemic stroke than men whose AHI was in the lowest quartile, even after adjustment for potential confounders (adjusted hazard ratio [HR] 2.86, 95% CI 1.10-7.39). The highest AHI quartile included patients who had >19.1 respiratory events per hour of sleep, whereas the lowest AHI quartile included patients who had <4.1 respiratory events per hour of sleep.
●In a prospective cohort study of nearly 1000 women with possible OSA who were free of stroke or coronary heart disease at baseline and were followed for a median of 6.8 years, those with untreated OSA had a significantly increased risk of incident stroke compared with those without OSA (adjusted HR 6.4, 95% CI 1.5-28.3) [9]. Women with treated OSA did not have an increased risk of stroke (HR 0.9, 95% CI 0.4-2.0).
●In another large observational study using a universal insurance claims database in Taiwan, women with sleep apnea were at higher risk than men, and younger women were at higher risk than older women [10]. The incidence of stroke in patients with sleep apnea by polysomnography (n = 29,961) was 52 per 10,000 person-years for males and 62 per 10,000 person-years for females; in controls, the incidence was 41 per 10,000 person-years for males and 37 per 10,000 person-years for females. In women with sleep apnea, the magnitude of the risk of stroke decreased with age (adjusted HR 4.9 for subgroup aged 20 to 35 years; HR 1.6 for subgroup aged 36 to 50 years; HR 1.4 for subgroup aged 51 to 65 years). While the pathophysiology behind this finding could not be determined by the study, the higher risk in women of childbearing age provides support for the recognition and treatment of OSA during pregnancy [11]. (See "Obstructive sleep apnea in pregnancy".)
Effect of treatment — Since elevated blood pressure is a known risk factor for stroke, and the treatment of OSA has been associated with decreased blood pressure, it is reasonable to expect that the treatment of OSA may reduce the incidence of stroke among patients who have OSA. In addition, some of the observational studies described above have found a lower stroke risk in patients with treated versus untreated OSA.
The quality of such data is limited, however, and few controlled trials have directly measured the impact of treating OSA on the incidence of stroke. Two trials have reported no difference in the rate of stroke or other cardiovascular events in patients treated with continuous positive airway pressure (CPAP) compared with controls [12,13]. However, treatment of sleep apnea may have been insufficient [14]. (See "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Cardiovascular events'.)
In patients with established cerebrovascular disease, limited data suggest that treatment of sleep-disordered breathing may improve stroke-related outcomes, particularly in the early post-stroke setting. (See 'Management' below.)
Mechanisms — There are several mechanisms by which OSA may increase the risk of stroke.
One possibility is that cerebral blood flow velocity is decreased by the negative intrathoracic pressure that is typically generated during an obstructive apnea. Alternatively, cerebrovascular dilatory responses to hypoxia in patients with OSA may be decreased due to intermittent hypoxia, oxidant-mediated endothelial dysfunction, increased sympathetic activity, and impaired cerebral vasomotor response to carbon dioxide [15]. Recurrent reductions of cerebral blood flow velocity then precipitate ischemic changes in patients with poor hemodynamic reserve (eg, intracranial arterial stenosis), particularly in border-zone areas and terminal artery territories [16]. Permanent structural changes in the white matter of the hemispheres may result [17].
OSA may exacerbate cerebrovascular abnormalities or other risk factors for stroke. Supporting this hypothesis, patients with OSA have an increased prevalence of systemic hypertension, heart disease, impaired vascular endothelial function, accelerated atherogenesis, diabetes, atrial fibrillation, prothrombotic coagulation shifts, proinflammatory states, and increased platelet aggregation [18]. In patients with atrial fibrillation, OSA has been independently associated with recurrent atrial fibrillation after cardioversion or ablation as well as stroke [19,20]. (See "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Atrial fibrillation'.)
Patent foramen ovale (PFO) has also been suggested as a possible mechanism for increased stroke risk. Retrospective studies have found that patients with OSA are about twice as likely as controls to have evidence of a PFO by transcranial Doppler with agitated saline [21,22]. In patients with a PFO, nocturnal apneas and pulmonary hypertension associated with OSA could increase right-to-left shunting, thereby increasing the risk of paradoxical embolism and stroke.
The potential role of vibratory trauma on carotid endothelial function due to snoring is discussed separately. (See "Snoring in adults", section on 'Potential consequences'.)
PREVALENCE AFTER STROKE — Both obstructive and central respiratory events (apneas and hypopneas) occur with increased frequency in patients with stroke compared with the general population [1]. Similar to the general population, obstructive sleep apnea (OSA) is more common than central sleep apnea (CSA) in patients with stroke.
In a meta-analysis of 132 studies that included over 14,000 patients who had a stroke or transient ischemic attack, the pooled prevalence of a sleep-related breathing disorder in the acute phase was 67, 50, and 32 percent for mild (apnea-hypopnea index [AHI] ≥5), moderate (AHI ≥15), and severe (AHI ≥30) sleep apnea, respectively [23]. The prevalence of mild sleep-related breathing disorders remained stable in the subacute and chronic phases after stroke, whereas the prevalence of moderate and severe disease gradually decreased over time. In the chronic phase after stroke or transient ischemic attack, the pooled prevalence of severe sleep apnea in seven studies was 25 percent.
In a separate analysis of 17 studies that distinguished central from obstructive respiratory events, OSA was the most common type of sleep-related breathing disorder [24]. Only 7 percent of patients had CSA or Cheyne-Stokes breathing as their predominant respiratory abnormality.
Sleep-related breathing disorders are often detectable within 24 hours after the stroke and tend to be more severe if the stroke began while the patient was asleep [25-27]. They are particularly prominent among older male patients whose stroke was caused by diabetes and macroangiopathy and whose stroke began at night [28]. There is some evidence that CSA is more prevalent during the first five days after acute stroke, declining later [29].
CONTRIBUTING FACTORS — In some cases, sleep-disordered breathing is a direct consequence of central nervous system injury. A wide variety of central nervous system locations can manifest obstructive sleep apnea (OSA) and/or central sleep apnea (CSA), and the type of sleep-disordered breathing is not helpful in localizing stroke:
●Vascular injury to the respiratory centers in the medulla (eg, lateral medullary syndrome) can cause OSA, CSA, or both [30].
●Infratentorial lesions can cause OSA, CSA, or both [31].
●Bilateral hemispheric lesions typically cause Cheyne-Stokes breathing.
More commonly, patients have preexisting OSA or CSA, often undiagnosed. In such cases, the sleep-related breathing disorder may be exacerbated after stroke, particularly when level of consciousness is impaired by the stroke itself or sedating medications. The most important risk factors for OSA in the general population are advancing age, male sex, obesity, and craniofacial or upper airway soft tissue abnormalities.
Limited data also suggest that hypoglossal nerve dysfunction is common in patients after acute stroke, although it is not clear whether this finding is a cause or consequence of sleep-disordered breathing [32].
CLINICAL FEATURES — In the general population, the most common clinical features of obstructive sleep apnea (OSA) are daytime sleepiness and loud snoring. Additional symptoms include waking up gasping or choking, morning headaches, nocturia, moodiness or irritability, lack of concentration, and memory impairment (table 1). On physical examination, patients are often obese and may have evidence of a crowded oropharynx and increased neck circumference. Clinical features of central sleep apnea are similar, except that obesity is less likely to be present. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features' and "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Clinical findings'.)
In patients with stroke, typical clinical features may be less reliable indicators of sleep-disordered breathing [4,24,33-39]. In one or more studies, the following clinical features have been associated with an increased likelihood of sleep-disordered breathing in post-stroke patients [24,25,34,35,40,41]:
●Increased body mass index
●Male sex
●Systolic hypertension
●Early neurologic deterioration
●Nocturnal oxygen desaturations
●Increased stroke severity
●Hemorrhagic stroke
●History of prior stroke
●Atrial fibrillation
In two studies, the Berlin questionnaire, a tool that has been used in community-based populations to estimate the likelihood of OSA, had only moderate diagnostic utility in post-stroke patients, with a sensitivity of 60 to 70 percent and specificity of 15 to 55 percent [36,37]. Other studies have found that a modified version of the STOP-Bang questionnaire (table 2) without the neck circumference variable ("STOP-Bag") has better sensitivity (91 to 93 percent using a cutpoint of less than 2 or 3 for low risk) but low specificity (<30 percent) [41,42]. Even in a community-based population, however, screening questionnaires are of limited value in identifying patients with a high likelihood of sleep apnea. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Screening questionnaires'.)
DIAGNOSIS — The diagnosis of a sleep-related breathing disorder in patients with stroke requires a high index of suspicion and formal sleep testing with either polysomnography or home sleep apnea testing (HSAT) type III or IV, since clinical features and questionnaires lack high predictive value in patients with stroke.
Obstructive sleep apnea (OSA) is defined by the presence of ≥5 predominantly obstructive respiratory events (ie, obstructive and mixed apneas, hypopneas, or respiratory effort-related arousals) per hour of sleep (for in-laboratory polysomnography) or per hour of recording time (for HSAT) [43]. Patients with stroke need not have additional symptoms to fulfill the diagnostic criteria. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnosis'.)
Central sleep apnea (CSA) is defined by the presence of ≥5 central apneas and/or hypopneas per hour of sleep plus a requirement that more than 50 percent of the total number of apneas and hypopneas are central [43]. In addition, patients must have one or more symptoms related to the disorder. (See "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Diagnostic criteria'.)
Screening in post-stroke patients — Clinically significant sleep apnea is highly prevalent in patients with acute stroke and has the potential to cause neurologic deterioration during the acute stage. In addition, moderate to severe apnea is associated with adverse rehabilitation outcomes in the post-stroke setting. Clinicians should therefore maintain a high state of awareness in post-stroke patients and at the very least review overnight oximetry during the first five days post stroke. (See "Obstructive sleep apnea and other sleep disorders in hospitalized adults", section on 'Evaluation and diagnosis in the inpatient setting'.)
Frequent nocturnal oxygen desaturations (eg, 15 or more episodes per hour of a ≥3 percent decrease in oxygen saturation for ≥10 seconds) are highly suggestive of moderate to severe sleep apnea [44]. Sleep apnea is also highly prevalent in acute stroke patients with dysphagia or dysphonia, since the same dysfunctional oropharyngeal muscles involved in swallowing and phonation are involved in sleep inspiration.
Whether all patients with stroke should undergo diagnostic sleep testing is debated, since widespread testing would require significant resources. Decisions must be individualized and take into account patient preferences, expected ability to adhere to positive airway pressure (PAP) therapy, overall functional status, quality of life, and goals of care. Patients with normal overnight oximetry and no clinical signs of sleep apnea (eg, loud snoring, excessive daytime sleepiness, nocturnal restlessness) probably do not need formal sleep testing.
Clinical practice guidelines from different organizations reflect a lack of consensus. The 2019 American Heart Association/American Stroke Association (AHA/ASA) guidelines for the early management of acute ischemic stroke recommend against routine screening for OSA in patients with recent stroke [45]. This recommendation is based largely on the SAVE RCT trial, which found no benefit of CPAP on vascular events, including stroke, in patients with moderate to severe OSA and established cardiovascular or cerebrovascular disease [13]. The 2021 AHA/ASA guidelines for secondary stroke prevention suggest that screening may be considered, based on other non-stroke benefits of CPAP [46]. Canadian Stroke Best Practice Recommendations endorse screening for OSA in all patients with stroke or transient ischemic attack (TIA), and the American Academy of Sleep Medicine clinical practice guidelines include a recommendation that patients with stroke or TIA and symptoms of OSA undergo polysomnography [47,48].
Ongoing clinical trials will likely provide further clinical guidance. As an example, the phase III Sleep for Stroke Management and Recovery Trial (Sleep SMART; NCT03812653) is examining whether management of sleep-disordered breathing with PAP devices shortly after ischemic stroke or TIA reduces recurrent stroke and improves stroke outcomes after three months [49].
Timing and modality of diagnostic testing — Sleep-related breathing disorders are often present on polysomnography within 24 hours after stroke, and in many cases the breathing disorder probably preceded the stroke. The timing of diagnostic testing must take into account the stability of the patient and their ability to comply with testing.
In-laboratory full-night or split-night polysomnography has traditionally been the gold standard diagnostic test for sleep-related breathing disorders. HSAT is an alternative in many patients, which may be preferred by patients and more cost effective than in-laboratory testing [50]. Sleep studies may be unavailable or impractical in the inpatient setting in many institutions but can be arranged at the time of discharge. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnostic tests'.)
Continuous registration of overnight oximetry may reveal intermittent hypoxia highly suggestive of moderate to severe sleep apnea in the post-stroke setting [44]. If frequent oxygen desaturations occur (<90 percent oxygen saturation over >5 minutes of sleep time), patients can be treated with continuous positive airway pressure (CPAP) therapy, bilevel positive airway pressure (BPAP), or supplemental oxygen while hospitalized. In-laboratory polysomnography should then be performed after discharge, as overnight oximetry is not considered an adequate diagnostic test by most, if not all, insurers in order to obtain a prescription for PAP therapy. (See "Obstructive sleep apnea and other sleep disorders in hospitalized adults", section on 'Post-discharge follow-up'.)
In addition to these modalities, limited data suggest that auto-titrating CPAP has acceptable validity in post-stroke patients and may be feasible in patients with non-severe stroke or TIA [36,51-53]. This modality is particularly relevant in the acute stroke population, since it can be applied in the inpatient or rehabilitation settings and provides immediate PAP therapy without delaying to conduct formal polysomnography [46]. However, as discussed below, auto-titrating CPAP may be poorly tolerated if central apneas are prevalent.
MANAGEMENT — Positive airway pressure (PAP) therapy and behavioral modifications are the mainstays of treatment for patients diagnosed with sleep-related breathing disorders. In patients with acute stroke, treatment decisions must be tailored to the clinical status of the patient and their perceived ability to adhere to PAP therapy.
Initial treatment typically involves avoiding factors that may exacerbate sleep-disordered breathing, in particular hypnotics and benzodiazepine derivatives, and PAP therapy, with the type of positive airway therapy determined by the predominant type of sleep-related breathing disorder. The efficacy of other therapies (eg, oral appliances) in patients who have obstructive sleep apnea (OSA) following a stroke has not been studied. The treatment of OSA and central sleep apnea (CSA) is reviewed in greater detail elsewhere. (See "Management of obstructive sleep apnea in adults" and "Central sleep apnea: Treatment".)
Patients who receive therapy for their sleep-related breathing disorder should be frequently reassessed for its ongoing need. Repeat testing can be performed in the laboratory or with home sleep apnea testing (HSAT). Sleep-disordered breathing can improve as the stroke improves and therapy may not be required indefinitely [29,54], although it is generally required into the rehabilitative phase of the stroke. Auto-titrating continuous positive airway pressure (CPAP) may be considered if changing CPAP pressure requirements are anticipated as the stroke condition evolves [55]. However, CSA may be prevalent during the first five days of acute stroke, and auto-titrating CPAP may not be tolerated [56].
CSA in the context of Cheyne-Stokes breathing is more likely to be self-limited than OSA in the post-stroke setting [26,52,57]. Of note, ticagrelor, a P2Y12 receptor antagonist used in secondary stroke prevention, has been associated with a shift from OSA to CSA [58,59]. If auto-titrating CPAP is being considered in a patient who has been started on ticagrelor, clinicians should be aware of the potential for increasing intolerance to auto-titrating CPAP due to central apneas. Mode selection and titration of PAP therapy for OSA and CSA are discussed in detail separately. (See "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea" and "Mode selection for positive airway pressure titration in adult patients with central sleep apnea syndromes".)
The rationale for treating sleep-disordered breathing in patients with stroke is primarily extrapolated from patients with sleep-related breathing disorders that are unrelated to a stroke. In such patients, PAP therapy reduces the frequency of respiratory events and oxygen desaturation during sleep and improves daytime sleepiness, quality of life, cognitive function, and hypertension [60-64]. (See "Management of obstructive sleep apnea in adults".)
Evidence that treatment of sleep-related breathing disorders improves stroke-specific outcomes such as stroke severity, functional status, and recurrent vascular events is more limited, consisting of several small randomized trials and prospective cohort studies [1,65,66]. Trials of early CPAP therapy in the acute stroke setting have had mixed results:
●In a randomized trial of 55 patients with acute stroke, patients assigned to early auto-titrating CPAP therapy (median time from symptom onset to CPAP initiation, 39 hours) had greater improvement in stroke severity scores at one month compared with those who received usual care [55]. Similar results were reported in a study of comparable size and design, but the benefit was only significant in patients with high levels of CPAP adherence [67].
●A trial that randomly assigned 140 older adults with an ischemic stroke and an apnea-hypopnea index (AHI) of ≥20 events per hour (primarily obstructive events) to either auto-titrated CPAP or no CPAP three to six days after the stroke, found that CPAP increased the proportion of patients with neurological improvement after one month, although the improvements were no longer statistically significant after three months [68]. At two years, the rate of recurrent stroke was similar in patients randomized to CPAP versus usual care (5 versus 4 percent). With longer follow-up, cardiovascular event-free survival was better in the CPAP group, although the event rate in both arms was small and there was no difference in overall mortality [69].
●Several other smaller randomized trials have found no significant difference in short-term functional outcomes or rate of recurrent stroke when CPAP is administered in the post-stroke setting [68,70,71] as well as difficulties with tolerance and adherence [71].
Most of these trials measured short-term endpoints, and long-term follow-up data are lacking. One observational study of 96 patients with an ischemic stroke and an AHI of ≥20 events per hour found lower mortality at five years [72] and fewer nonfatal cardiovascular events at seven years [73] among patients who tolerated CPAP therapy than among those who did not. A large trial in patients with established cardiovascular disease (44 percent with a history of stroke) found no difference in the rate of stroke or other cardiovascular events in patients treated with CPAP compared with controls [13].
Poor adherence with positive airway therapy among patients who have had a stroke has been attributed to difficulty tolerating the PAP, poor motivation, cognitive deficits, age, and neglect [67,70,74]. Frequent reassessment is necessary for patients who receive a trial of PAP therapy, due to the theoretical potential for a reduction in blood pressure induced by PAP to impair cerebral perfusion [75] and worsen physical function [70]. (See "Management of obstructive sleep apnea in adults", section on 'Follow-up' and "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)
COMPLICATIONS — Patients with sleep-related breathing disorders after stroke are at increased risk for both early and delayed complications and worse outcomes [76,77].
Sleep apnea is associated with early neurologic deterioration after stroke in some patients. In one study in which 50 patients with acute stroke underwent polysomnography within 24 hours of stroke, sleep apnea (defined as an apnea-hypopnea index [AHI] >10 events per hour) and hyperglycemia were independent predictors of early neurologic worsening [25].
Longer-term outcomes may also be worse in patients with sleep-related breathing disorders [73,78-80]. In a large prospective population-based cohort of adults with an ischemic stroke within the previous 30 to 45 days, the prevalence of sleep apnea (respiratory event index ≥10) on home sleep apnea testing (HSAT) was 63 percent [79]. Sleep apnea was associated with worse 90-day cognitive and functional outcomes, independent of age, vascular risk factors, and other comorbidities.
Increasing data also suggest that intermittent nocturnal hypoxia associated with clinically significant obstructive sleep apnea (OSA) may increase the risk of vascular cognitive impairment and other forms of dementia, possibly by contributing to cerebral subcortical small vessel disease [81,82]. (See "Risk factors for cognitive decline and dementia", section on 'Obstructive sleep apnea'.)
Other complications of obstructive sleep apnea in the general population, including decreased daytime function, risk of motor vehicle accidents and workplace errors, and increased risk for a range of cardiovascular morbidities, are discussed separately. (See "Obstructive sleep apnea and cardiovascular disease in adults".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders in adults".)
SUMMARY AND RECOMMENDATIONS
●Sleep-related breathing disorders, including obstructive sleep apnea (OSA), central sleep apnea (CSA), and Cheyne-Stokes breathing, are common in patients with stroke or transient ischemic attack (TIA) and have been associated with adverse outcomes both in the general population and in patients with stroke. (See 'Introduction' above.)
●OSA has been associated with an increased risk for stroke, independent of vascular risk factors. The risk of stroke in patients with other sleep-related breathing disorders, including CSA syndrome, is not well studied. (See 'Sleep apnea as a risk factor for stroke' above.)
●Sleep-related breathing disorders are common in patients with stroke, occurring in up to 70 percent of patients when defined by an apnea-hypopnea index (AHI) ≥5 events per hour. (See 'Prevalence after stroke' above.)
●In some cases, sleep-related breathing disorders occur as a consequence of acute central nervous system injury; more commonly, patients have preexisting OSA or more rarely CSA, often undiagnosed. In such cases, the sleep-related breathing disorder may be exacerbated after stroke, particularly when level of consciousness is impaired by the stroke itself or sedating medications. (See 'Contributing factors' above.)
●Typical clinical features of sleep-disordered breathing, such as daytime sleepiness and snoring, may be lacking in patients with stroke. Clinical features that have been associated with an increased risk for sleep-disordered breathing in patients with stroke include obesity, systolic hypertension, nocturnal oxygen desaturations, and increased stroke severity. (See 'Clinical features' above and 'Diagnosis' above.)
●Diagnostic sleep testing is recommended in stroke patients with one or more physical signs or symptoms of sleep-disordered breathing (table 1). Post-stroke patients with nocturnal desaturations, dysphagia, or dysphonia are particularly likely to have sleep apnea. Diagnostic testing can take the form of in-laboratory polysomnography or home sleep apnea testing (HSAT) type III or type IV. In addition, emerging data suggest that auto-titrating continuous positive airway pressure (CPAP) therapy may be useful as a treatment tool in stroke patients and feasible to initiate in the acute setting if CSA has been ruled out. (See 'Screening in post-stroke patients' above and 'Timing and modality of diagnostic testing' above.)
●Positive airway pressure (PAP) therapy and behavioral modifications are the mainstays of treatment for patients diagnosed with sleep-related breathing disorders. In patients with acute stroke, treatment decisions must be tailored to the clinical status of the patient and their perceived ability to adhere to PAP therapy. The type of positive airway therapy is determined by the predominant type of sleep-disordered breathing. The efficacy of other therapies (eg, oral appliances) in patients who have OSA following a stroke has not been studied. (See 'Management' above.)
●Sleep-related breathing disorders are associated with early neurologic worsening after stroke and may also be associated with poorer long-term outcomes and increased risk for cognitive impairment and dementia among adults with and without cerebrovascular disease. (See 'Complications' above.)
