Impact of Sleep Disorders and Disturbed Sleep on Brain Health: A Scientific Statement From the American Heart Association
Accumulating evidence supports a link between sleep disorders, disturbed sleep, and adverse brain health, ranging from stroke to subclinical cerebrovascular disease to cognitive outcomes, including the development of Alzheimer disease and Alzheimer disease–related dementias. Sleep disorders such as sleep-disordered breathing (eg, obstructive sleep apnea), and other sleep disturbances, as well, some of which are also considered sleep disorders (eg, insomnia, sleep fragmentation, circadian rhythm disorders, and extreme sleep duration), have been associated with adverse brain health.
Understanding the causal role of sleep disorders and disturbances in the development of adverse brain health is complicated by the common development of sleep disorders among individuals with neurodegenerative disease. In addition to the role of sleep disorders in stroke and cerebrovascular injury, mechanistic hypotheses linking sleep with brain health and biomarker data (blood-based, cerebrospinal fluid-based, and imaging) suggest direct links to Alzheimer disease–specific pathology. These potential mechanisms and the increasing understanding of the “glymphatic system,” and the recognition of the importance of sleep in poststroke recovery, as well, support a biological basis for the indirect (through the worsening of vascular disease) and direct (through specific effects on neuropathology) connections between sleep disorders and brain health. Given promising evidence for the benefits of treatment and prevention, sleep disorders and disturbances represent potential targets for early treatment that may improve brain health more broadly. In this scientific statement, we discuss the evidence supporting an association between sleep disorders and disturbances and poor brain health ranging from stroke to dementia and opportunities for prevention and early treatment.
As the population ages, more adults will experience stroke, cognitive impairment, and dementia. Thus, identifying potential modifiable risk factors for poor brain health is increasingly critical. Sleep disturbances and disorders are common in aging adults and are linked to poor brain health through epidemiological data and supported by plausible biological mechanisms As a result, sleep disorders and disturbances represent an opportunity for potential prevention or treatment to reduce the burden of poor brain health in the population. This scientific statement will address these disturbances of sleep, including sleep disorders such as sleep-disordered breathing (SDB) and other sleep disturbances and disorders, as well, where sleep patterns may be abnormal, and will summarize known relationships with distinct brain health outcomes and identify priorities for future research.
Sleep is a biobehavioral state characterized by changes in brain electrical activity that manifest as altered consciousness, reduced sensory responsiveness, and decreased muscle tone. Key metrics used to quantify sleep architecture and duration are described in The 2 main sleep states are non–rapid eye movement sleep and rapid eye movement (REM). Non–rapid eye movement sleep includes 3 sleep stages (N1, N2, and N3) defined by distinct patterns of neurophysiological activity. Sleep stages occur across cycles that are ≈120 minutes in duration, resulting in 4 to 6 cycles per night. The Centers for Disease Control and Prevention recommends 7 to 9 hours of sleep per night for adults 18 to 64 years of age and 7 to 8 hours per night for older adults. Intrinsic and external stimuli that cause arousals can disturb the underlying structure of sleep, referred to as sleep architecture. Sleep architecture varies across the life span, with reduced sleep quality, including greater fragmentation and light sleep and significant reductions in N3 (slow-wave) and REM sleep, and quantity at older ages and among people with morbidities.
Multiple sleep disturbances affect brain health. These include disorders such as SDB and unhealthy patterns of sleep duration, continuity, timing, and circadian rhythms that disturb sleep but may not result from specific sleep disorders. This scientific statement focuses on those disturbances that are most pertinent to brain health, which are summarized and defined. We note that there are other forms of sleep disorders and disturbances that we do not discuss because they are not clearly linked to brain health (eg, restless leg syndrome). Obstructive sleep apnea (OSA) is the most common form of SDB and results in intermittent hypoxia and sleep fragmentation. OSA is diagnosed on the basis of the presence of symptoms and measures of respiratory events and oxygen saturation from overnight polysomnography (PSG), which yields the apnea-hypopnea index (AHI), a rate of apneic or hypopneic events per hour of sleep, along with other important indicators of SDB. Central sleep apnea is identified when the predominant respiratory event type is “central” (ie, lacking significant airflow limitation and showing reduced or absent respiratory effort).
Alterations in brain health encompass the spectrum of subclinical to clinical disease, including cerebrovascular imaging changes, clinically apparent stroke, cognitive decline, and dementia. Long-standing vascular disease can adversely affect brain health in multiple ways, of which stroke or cerebral hemorrhage are the most clinically apparent. Subclinical cerebrovascular disease, including silent infarcts, white matter hyperintensities (leukoaraiosis), cerebral microbleeds, enlarged perivascular spaces, and cerebral atrophy, is associated with long-term sequelae, including cognitive decline and dementia, impaired gait, and increased stroke risk. Alzheimer disease (AD) and AD-related dementias (ADRDs) encompass many pathophysiological conditions that can be comorbid. AD and the vascular contributions to cognitive impairment and dementia are the most common dementia subtypes.
Brain health can be assessed by clinical signs (for stroke), cognitive measures, and psychiatric evaluation, but also by imaging, blood, and, in some cases, cerebrospinal fluid (CSF) biomarkers that can help evaluate underlying pathology. Amyloid-β (Aβ) or tau positron emission tomography, or blood or CSF phosphorylated tau or Aβ levels may be indicators of underlying AD neuropathology. Neurofilament light chain, a marker of axonal injury, may indicate nonspecific underlying neurodegeneration. Of note, many other factors contribute to or may result from adverse brain health (eg, depression, substance abuse, and other aspects of mental health) but are beyond the scope of this scientific statement.
Sleep plays a central role in the optimization of cognitive performance. Experimental sleep deprivation studies show adverse effects of sleep loss on performance in numerous cognitive domains, including attention, executive function, and short-term memory, with cognitive processes that rely heavily on the prefrontal cortex particularly affected. Memory is among the most studied cognitive domains in relation to sleep, and accumulating literature details how sleep strengthens and promotes preserved recent learning, including episodic and procedural memory. Features of non–rapid eye movement sleep (especially slow oscillations and sleep spindles) and REM sleep play overlapping and complementary roles in the underlying process of memory consolidation in which new, unstable memories are relocated from the hippocampus to the neocortex, where they are more durable. Compared with younger adults, older adults may exhibit deficits in the consolidation of episodic memories, likely due to aging-related deterioration of brain structure and sleep quality and concomitant comorbidity.
Website: cognitivescientist.org
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