Cerebrovascular disease and the pathophysiology of obstructive sleep apnea

Abstract

Obstructive sleep apnea (OSA) is a common disorder and the major sleep-related risk factor for cerebrovascular disease. There is a dose-response relationship between the severity of OSA and the odds ratio for development of systemic hypertension. Observational studies have shown that patients with clinically significant OSA have increased incidence of cardiovascular and cerebrovascular disease, as well as increased incidence of sudden death in sleep. Following stroke, patients have a high prevalence of OSA, which diminishes the potential for rehabilitation, increases the risk of secondary stroke, and heightens mortality. Successful treatment of OSA with noninvasive positive airway pressure ventilation and with mandibular advancement devices lowers mean blood pressure. There is suggestive evidence that in patients with advanced OSA, permanent structural cerebral lesions may occur. Circadian changes during sleep contribute to an increase in the risk of cardiovascular and cerebrovascular accidents.

Safety and Tolerability of Early Noninvasive Ventilatory Correction Using Bilevel Positive Airway Pressure in Acute Ischemic Stroke

“…Expert opinion advocates that the proper steps that should be taken include unattended overnight polysomnography (within reach in hospital settings), followed by noninvasive ventilation when indicated. 10,23 Another potential alternative may be the use of an auto-bilevel unit that searches pressures and adapts pressure settings from breath to breath. Given the fact that ventilation functions in acute ischemic stroke patients are notoriously changeable as the stroke condition evolves, 9,10 this bilevel unit should be capable of modifying its pressures accordingly.…”

Metabolic syndrome and cerebral vasomotor reactivity in atherosclerotic disease

“…Indeed, there is mounting evidence underscoring impaired VMR as the intermediate link between stroke risk and various disease states including sleep apnoea syndrome [5,6]. Adding to the significance of VMR, our findings suggest that lower VMR or impaired cerebrovascular reserve might be the mediator of the higher rate of cerebrovascular ischaemic events in patients with MetS [2] and underscores the need for early identification of these patients.…”

Obstructive sleep apnoea-hypopnoea syndrome presenting in the neurology clinic: a prospective 5-year study

“…Of 4467 new patient referrals seen over the 5‐year period, a diagnosis of OSAHS was suspected on clinical grounds in 18 patients (=0.40%; M:F = 14 : 4; age range: 27–65 years, median 45.5 years; range: 2–10 cases/year). All were adjudged to have EDS, based on the history of the presenting complaint, and 11 had additional neurological symptoms: seizures or blackouts (6), headache (3) and report of poor memory (2).…”

“…Obstructive sleep apnoea–hypopnoea syndrome (OSAHS) is a cause of sleep deprivation as a consequence of repeated nocturnal arousals because of obstructed breathing when the upper airway collapses during inspiration (1). In addition to excessive daytime somnolence (EDS), various neurological problems have been reported in association with OSAHS, including stroke, blackouts, epileptic seizures, headaches, papilloedema, cognitive impairment and peripheral nerve dysfunction (2–7), such that the first clinical presentation of OSAHS may on the occasion be to a neurologist (7). As OSAHS is amenable to specific treatment, for example with nocturnal continuous positive airway pressure, which may lead to improvement not only of EDS but also other neurological features, identification of this condition is of importance.…”