Since its description in 1965 by Gastaut et al, OSA has been widely recognized as a clinical entity consisting of excessive daytime sleepiness, loud irregular snoring, obesity, dementia, and headache, especially morning headache. A central element in the pathogenesis of the condition is the upper-airway closure induced by sleep, giving rise to sleep apnea, increasing inspiratory efforts, hypoxic and hypercapnic episodes, and variations in intrathoracic and arterial pressures.
High blood pressure, complaints of headaches, and dementia are prevalent in patients with severe sleep apnea. Although the cerebrovascular hemodynamics are known to be of major importance in the regulation of the AP, very little is still known about the cerebrovascular hemodynamics and regulation during sleep apnea. other
Hypercapnia and hypoxia are known to influence cerebrovascular hemodynamics by increasing ICP because of cerebral vasodilation. It was therefore supposed that ICP might increase during apnea related to sleep. In order to test this hypothesis and to describe the relation between ICP, AP, and CVP, the present study was performed.
Materials and Methods
Six patients were selected by the following criteria: (1) mean number of apneas (apnea index) more than 40 apneas per hour; (2) mean duration of apnea longer than 20 seconds; (3) only OSA; (4) no medication taken; (5) normal findings on neurologic examination; and (6) a normal CT of the brain. Sleep was analyzed by use of central and occipital electrodes (C3, C4, Ol, and 02), EOG, and chin EMG. Sleep scoring was performed according to standard methods.
Respiration was measured by inductive plethysmography (Res-pitrace Corp) Obstructive apnea was determined by observations of paradoxic movements in the thoracic and abdominal band.
The tcPo2 and tcPco* were measured in the supraclavicular fossa (by use of Radiometer TCM 2 and 20, respectively).