Sleep-Disordered Breathing in the Acute Phase After Stroke and Neuropsychiatric Outcomes

Stroke is the second leading cause of death and a common cause of acquired disability worldwide, and the burden of the disease at the societal level is expected to increase in the coming decades. Stroke can result in various long-term consequences, both neurological (such as aphasia, paresis, sensory or visual disturbances, and coordination and balance disorders) and neuropsychiatric (such as cognitive impairment, depression, and fatigue). These consequences, in turn, affect stroke survivors' physical functions, activity levels, and ability to participate in daily activities.

Post-stroke fatigue is common, with prevalence estimates ranging between 25-85%, and 40% of stroke survivors have reported it as one of their worst symptoms. Recent Swedish studies have estimated the long-term prevalence 3-5 years after stroke to be between 24-52%. Post-stroke fatigue partially overlaps with post-stroke depression, but approximately 70% of individuals with significant fatigue do not exhibit concurrent depressive symptoms . The condition is associated with poorer performance in daily activities and lower health-related quality of life. Currently, there are no specific treatments for post-stroke fatigue. Due to its high prevalence and consequences, it has recently been identified as one of the top ten priority research questions in stroke rehabilitation by the UK National Institute for Health and Care Research.

There are conflicting reports on whether traditional vascular risk factors such as hypertension, hyperlipidemia, heart disease (including atrial fibrillation), and smoking contribute to post-stroke fatigue. Obesity is associated with post-stroke fatigue, and sleep-disordered breathing (SDB) has also emerged as a potential risk factor.

Sleep-disordered breathing is prevalent after stroke, occurring in 50-70% of some populations. The dominant condition is obstructive sleep apnea syndrome (OSAS), followed by central sleep apnea. Established treatments for OSAS include continuous positive airway pressure (CPAP), mandibular advancement devices, surgical interventions, and weight loss, which can reduce daytime sleepiness. Research is ongoing regarding the extent to which treated OSAS can contribute to secondary prevention in stroke. Current American guidelines for secondary prevention provide a class 2b recommendation with moderate evidence for considering OSAS screening after stroke or transient ischemic attack (TIA).

The diagnosis is primarily made through overnight respiratory monitoring, with polysomnography being the gold standard, although it is time- and resource-intensive and may be cumbersome for the patient. Limited polygraphic examinations can also be conducted both in hospitals and at home.

Research Questions:

1. What is the 1-year prevalence of post-stroke fatigue in a hospital-based cohort in Blekinge?
2. How many individuals with stroke have significant sleep-disordered breathing according to non-invasive measurement?
3. What proportion of individuals with post-stroke fatigue had significant sleep-disordered breathing during hospitalization?
4. Can early, non-invasive, and simple measurement of sleep-disordered breathing in hospitals predict a subgroup of stroke patients who will develop significant fatigue?
5. Is there evidence that treatment goals after stroke are achieved to a lesser extent in those with significant fatigue?