Sleep disorders are a common complication in stroke patients and include daytime sleepiness, insomnia, allergic sleep, episodic sleepiness, circadian rhythm disorders, sleep-related movement disorders, and sleep apnea. The occurrence of post-stroke sleep disorders is associated with a variety of factors, including neurobiological and psychosocial factors. This article reviews the structural changes in sleep after stroke, the manifestations of sleep disorders, their epidemiology and their pathophysiological mechanisms. Sleep disorders can occur at all ages and affect the quality of life of patients. The third edition of the International Classification of Sleep Disorders (ICSD-3) classifies sleep disorders into eight categories, including insomnia disorders, sleep-related breathing disorders, central hypersomnia disorders, sleep-wake circadian rhythm disorders, heteronormative sleep, sleep-related movement disorders, and other sleep disorders. The interrelationship between sleep disorders and cerebrovascular disease has become a hot research topic in recent years. Sleep-disordered breathing in the acute phase of stroke is common and affects the prognosis of stroke. Post-stroke non-respiratory related sleep disorders daytime sleepiness, insomnia, heterogeneous sleep, episodic sleeping sickness, circadian rhythm disturbances, and sleep-related movement disorders have not received much attention from clinicians. A growing number of studies have shown that non-respiratory-related sleep disorders, especially daytime sleepiness and insomnia, also affect neurological recovery from stroke and reduce the quality of life of patients. Sleep structure in stroke patients 1. Sleep structure in the acute phase of stroke A meta-analysis of sleep structure characteristics in stroke patients showed decreased sleep efficiency, decreased total sleep time, increased wake time after sleep, increased N1 sleep, decreased N2 and slow wave sleep, and no changes in rapid eye movement (REM) sleep were found. Another study showed that REM latency was positively correlated with functional outcome 3 months after stroke, with a significantly lower REM latency in those with a poorer prognosis compared to those with a better prognosis. Patients in the acute phase of thalamic stroke have disturbed sleep architecture, as evidenced by decreased sleep efficiency, increased sleep latency, and decreased N2 and slow wave sleep. Altered sleep structure in patients with acute stroke is influenced by several factors: first, damage to neural tissue (direct damage to structures associated with the generation and maintenance of the sleep-wake cycle) and edema; second, post-stroke limitation of limb movement and pain; and third, environmental factors in the hospital such as constant light and noise. The production and maintenance of normal sleep structures play an important role in maintaining homeostasis in the body and consolidating learning and memory (including motor skill learning), which play a key role in the recovery of motor skills after the acute phase of stroke. Experimental animal studies have confirmed sleep as an effective treatment for neurological preservation and recovery. 2. Sleep structure after the acute phase of stroke Most studies have shown that patients’ sleep structure disorders improve after the acute phase of stroke. A polysomnographic study of 96 patients in a stroke rehabilitation unit showed no significant differences in total bedtime, total sleep time, sleep efficiency, REM and non-rapid eye movement (NREM) sleep proportions compared to controls without stroke history, but patients had a longer sleep latency. Another study investigating 20 stroke patients showed that 45% of patients had increased sleep latency despite normal total sleep time and sleep efficiency. Polysomnographic parameters in patients 5 to 24 months after stroke in the cerebral hemisphere were not significantly different from normal controls. However, 34% of patients with subarachnoid hemorrhage had severe sleep problems. A polysomnographic study of 20 of these patients with severe sleep disorders showed that 75% had fragmented sleep, 35% had increased sleep latency, and 55% had decreased sleep efficiency, which affected the patients’ quality of life. Post-stroke sleep disorders 1. Daytime sleepiness Sleepiness refers to an increased need for sleep or excessive sleepiness during the day. A study of 200 acute stroke patients showed that 49.5% of stroke patients had at least moderate daytime sleepiness. The prognosis of patients with post-stroke somnolence is worse. There are two mechanisms for the pathogenesis of post-stroke somnolence: one is related to the stroke site, where the reticular superior activating system maintains the waking state of the person, and because reticular superior fibers are concentrated in the bilateral thalamus, midbrain, upper pons, and central pons medullar region, damage to these regions may cause somnolence. Cortical or subcortical infarcts (except thalamic) rarely involve the reticular superior activating system, but cerebral edema from large cerebral infarcts can affect the superior brainstem and cause somnolence. Hypersomnia due to infarction in the paramedian thalamus is more severe and is accompanied by impaired attention and memory, and hypersomnia may improve 12 months after infarction, while cognitive impairment persists. In a follow-up study using diffusion tensor fiber bundle imaging in a patient with a posterior communicating aneurysm rupture with subarachnoid hemorrhage combined with ventricular hemorrhage ventricular drainage surgery, the patient’s symptoms of somnolence improved while the impaired reticular superior activating system recovered. The other is secondary to sleep apnea, where patients with nocturnal hypoventilation experience increased daytime sleepiness due to frequent awakenings or being in a hypoxic state during sleep and still feeling spontaneous weakness and unconsciousness upon awakening in the morning. 2, Episodic sleep disorder Episodic sleep disorder may occur after stroke with localized lesions or diffuse injury. The brain regions damaged in patients with post-stroke episodic sleepiness are the hypothalamus and midbrain, and these damaged locations explain the patients’ clinical symptoms and decreased cerebrospinal fluid appetitive peptide levels. Injury to the ventral part of the pons can also cause the same clinical symptoms as in episodic sleeping sickness, but the patient’s appetite peptide level is not reduced. 3. Insomnia Insomnia refers to difficulty falling asleep, difficulty maintaining sleep, or early awakening, which can lead to daytime fatigue, impaired concentration, and irritability. The incidence of insomnia at 3-4 months after stroke was reported to be 57.9% in China, 55.6% had insomnia before stroke and 44.4% had new onset insomnia after stroke; in foreign countries, 56.7% of patients reported to have complaints of insomnia at 3-4 months after stroke, 37.5% met the diagnostic criteria of Diagnostic and Statistical Manual of Mental Disorders (DSM)-4, 38.6% had insomnia before stroke Symptoms or insomnia were secondary to stroke in 18.1%, and the incidence of insomnia was higher the more severe the disability after stroke. Post-stroke insomnia is often associated with stroke comorbidities. Stroke comorbidities such as sleep apnea, heart failure, anxiety, depression, pain and environmental factors (sound, light, monitoring equipment) play a role in the development of insomnia. The use of psychotropic drugs, dementia, and severity of stroke are also risk factors for insomnia after stroke; frontal lobe infarction and geriatric depression are independent risk factors for insomnia at 3 months of stroke, and diabetes mellitus and geriatric depression are independent risk factors for insomnia with daytime symptoms. A stroke patient with subcortical area, thalamus, thalamus-midbrain, and pontine periaqueductal area may have nocturnal agitation and excessive daytime sleepiness due to disturbance of the sleep-wake cycle; one stroke patient with atresia syndrome had polysomnography that confirmed insomnia lasting more than 1 month; patients with bilateral parthalamic median stroke are prone to drowsiness or even coma, and their sleep architecture is severely disrupted, with an increase in NREM stage I and a varying decrease in stage III. The patient’s sleep structure is severely damaged, with an increase in NREM stage I and varying degrees of decrease in stage III, and a significant decrease in REM, probably due to damage to the paracentral nucleus, a component of the inner nucleus of the bilateral thalamic plate, which causes transient disruption of the thalamo-cortical activation system, leading to impaired consciousness. 4. Altered sleep Altered sleep refers to abnormal behavior during sleep. Altered sleep includes nightmares, sleep terrors, sleep walking disorder, sleep talking disorder, confused awakenings, teeth grinding, sleep paralysis, and rapid eye movement sleep behavior disorder (RBD). With the exception of RBD, heteronormative sleep due to stroke has not been reported in the literature. Studies have reported one patient with RBD secondary to pontine injury with sudden collapse without other symptoms of episodic sleepiness and two other patients with RBD due to median infarction of the pontine side of the brain. This is associated with damage to the pathways associated with reduced muscle tone in the REM phase including structures near the nucleus accumbens. The third edition of the International Classification of Sleep Disorders lists eight categories of sleep-related movement disorders, two of which are associated with stroke: restless legs syndrome (RLS) and periodic limb movements (PLMs). rLS manifests as indescribable sensory abnormalities and discomfort in the resting state, especially at night in both lower extremities, with a strong desire to move the legs; PLMs refer to polysomnograph-monitored sleep during PLMs cause nocturnal awakening and daytime fatigue. PLMs coexist with RLS in 80% to 90% of patients. The only prospective study showed that the prevalence of RLS at 1 month after stroke was 12.4%. The region of cerebral infarction in patients with post-stroke RLS involved the pons, thalamus, internal capsule, basal ganglia region, and radial crown, and in 75% of patients the symptoms were bilateral, and in patients with unilateral symptoms, the limb contralateral to the lesion was affected. A study investigating 30 patients with brainstem stroke showed that in 2 patients the stroke aggravated previous RLS symptoms and in 1 patient new RLS symptoms appeared but were transient.Schuiling et al. showed that 25% of patients with subarachnoid hemorrhage had RLS or PLMs.Ruppert et al. first reported a patient with right ventral medial infarction of the cerebral bridge with RLS as the first manifestation. One case of unilateral PLMs, diagnosed by polysomnography, had worsened symptoms after radiographic coronary infarction. The current study found the presence of stroke-related PLMs or RLS in patients with damage to subcortical structures such as the basal ganglia, brainstem, and lateral thalamus, which are closely related to motor and sleep-wake cycles, and the absence of cortical inhibition of the basal ganglia pathway explains the mechanism of PLMs or RLS after stroke. 6. Sleep breathing disorders Sleep breathing disorders include obstructive sleep apnea syndrome (OSAS), central sleep apnea syndrome, and sleep hypoventilation syndrome. Abnormal breathing in the acute phase of stroke is common and may exist before stroke or may be induced by the site of stroke, and abnormal breathing is more common in patients with impaired consciousness. The prevalence of sleep breathing disorders in stroke patients is 62%. Sleep breathing disorders are a risk factor for cardiovascular and cerebrovascular disease, increasing its complications and mortality. The occurrence of cerebrovascular disease affects the severity of sleep apnea, making it worse over 5 years. Patients with ischemic stroke combined with OSAS have significantly increased mortality, and treatment with continuous positive pressure ventilation (CPAP) reduces the risk of death in these patients. 2014 U.S. guidelines for secondary prevention of stroke and transient ischemic attack state that sleep testing is recommended for patients with ischemic stroke/transient ischemic attack (TIA), and for patients with a history of ischemic stroke/TIA with sleep CPAP may be given to patients with a history of ischemic stroke/TIA with sleep apnea to improve clinical prognosis (Class IIb recommendation, Class B evidence). Either cerebral hemisphere infarction or brainstem infarction may lead to altered breathing as long as the infarct site involves breathing-related muscles (upper airway, intercostal muscles, diaphragm). Frontal lobe, basal ganglia, and internal capsule strokes may result in respiratory failure, and brainstem strokes may result in multiple forms of respiration, such as neurogenic hyperventilation (midbrain or pontine), deep inspiratory breathing, Beale’s breathing, central sleep apnea, and hypoventilation (medulla oblongata and superior medulla). Stroke exacerbates sleep apnea through involvement of the brainstem respiratory center and oropharyngeal muscles, but in most patients, sleep apnea occurs prior to stroke. A follow-up study of 161 stroke patients found that more than 2/3 of patients had an apnea hypoventilation index (AHI) of more than 10 breaths/h in the acute phase, and that both AHI and central apnea index (CAI) decreased significantly after 3 months compared with the acute phase, whereas the obstructive apnea index did not change. Summary: In conclusion, post-stroke sleep disorders are common. Sleep disturbances may exist before stroke, worsen after stroke, or may occur for the first time after stroke. Post-stroke sleep disturbances may be caused by the site of brain injury or may be related to post-stroke emotional state, environment, and other psychosocial factors. There is extensive research evidence that daytime sleepiness, insomnia, and sleep apnea affect the recovery of neurological function and quality of life in stroke patients. Clinicians should identify the types of post-stroke sleep disorders early, actively search for the causes of post-stroke sleep disorders, and make reasonable interventions to improve stroke prognosis and improve patients’ quality of life.