Sleep-disordered breathing (SDB) is an umbrella term for several chronic conditions in which partial or complete cessation of breathing occurs. The disorder is of increasing importance and is frequent in stroke patients. It comprises Obstructive Sleep Apnea (OSA), Central Sleep Apnoea (CSA), Hypoventilation syndromes, and other rarer forms of disturbed breathing. Obstructive sleep Apnea syndrome occurs more frequently, affecting 4-9% of the adult population.
OSA is characterized by repetitive episodes of partial or complete obstruction of the upper airway with elevated airway resistance defined as apneas and hypopneas which during sleep causes hypoxemia (decrease in blood oxygen saturation). In simple words, it occurs when throat muscles relax and lock the airway during sleep and is typically associated with snoring, apneas, and excessive daytime sleepiness because of a disruption of sleep architecture.
Studies have shown that there is an association between OSA and increased cardiovascular morbidity. People with habitual snoring and OSA have an increased risk of hypertension, Coronary Artery Disease (CAD), Congestive Heart Failure (CHF), and vascular mortality. The above findings indicate that OSA appears to be a cardiovascular risk factor. Moreover, some studies focused on Sleep Apnea and its frequency in patients with Transient Ischemic Attacks (TIA) and stroke (Portela, Campdelacreu, García, & Borrego, 2009). Thus, the increasing findings on the same suggest that sleep apnea is associated with cerebrovascular diseases.
SDB is more probably the cause rather than the consequence of the stroke. It is because apneas are essentially obstructive rather than central. Moreover, the frequency of SDB is not different between transient ischemic attacks and cerebral infarction. These findings indicate that the link between SDB and cerebrovascular disease might be explained, at least in part, by an increase in the progression of the atherosclerosis process involving cerebral vessels.
In another research on Sleep Apnea in Acute Cerebrovascular Diseases, several findings of general validity were stated.
The characteristics of Transient ischemic attack and stroke patients, including age and gender distribution; cardiovascular risk factors profile; time of onset, topography, severity, etiology, and outcome of stroke are similar to those reported in larger series of patients with acute cerebrovascular disease (Bassetti & Aldrich, 1999).
There is a 51% prevalence of habitual snoring in patients with sleep apnea, which is similar to the 48% to 58% snoring in patients with stroke (Bassetti & Aldrich, 1999).
Thus, Sleep Apnea may affect the course of cerebrovascular diseases in different ways. For instance, the neurohumoral consequences of recurrent respiratory events and hypoxemia may lead to hypertension, heart disease, decreased fibrinolysis, increased atherogenesis, and increased platelet aggregation.
Furthermore, hypopneas and apneas may cause Brady and tachyarrhythmias, decreased cardiac output, hypotension, decreased cerebral blood flow, increased intracranial pressure, and eventually brain ischemia. Research findings on habitual snoring as a risk factor for a stroke occurring at night are rare and contradictory (Palomäki, Partinen, Erkinjuntti, & Kaste, 1992).
The onset of a stroke may rarely be precipitated acutely by respiratory events in patients with and without sleep-disordered breathing
The significant role played by OSA in cerebrovascular diseases has potential implications for the prognosis.
First, among TIA patients, treatment of OSA may reduce vascular morbidity and stroke.
Second, in patients with acute stroke, recurrent hypoxemia and hemodynamic instability associated with OSA may limit the chances of recovery of ischemic but not yet irreversibly damaged neurons (ischemic penumbra).
Third, in patients recovering from acute stroke, hypersomnia and recurrent nocturnal hypoxemias secondary to OSA may hurt the neuropsychologic recovery and more generally stroke rehabilitation.
To conclude, we can say that OSA appears to be an independent risk factor for cerebrovascular diseases. Therefore, it should be systematically screened at the time it is suspected to treat it. However, there are several other implications from the demonstrated significant role OSA in increasing the predisposition to developing stroke. The treatment of SDB may reduce the possibility of further cerebrovascular disturbances.