SLEEP-APNEA SYNDROME AND CEREBRAL HEMODYNAMICS

Citation
G. Hajak et al., SLEEP-APNEA SYNDROME AND CEREBRAL HEMODYNAMICS, Chest, 110(3), 1996, pp. 670-679
Citations number
48
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
110
Issue
3
Year of publication
1996
Pages
670 - 679
Database
ISI
SICI code
0012-3692(1996)110:3<670:SSACH>2.0.ZU;2-6
Abstract
The dynamics of cerebral blood flow velocity (CBFV) during sleep were investigated in the light middle cerebral artery of 10 patients with s leep apnea syndrome (SAS) (mean age, 37 years) and 10 healthy control subjects (mean age, 32 years) throughout the entire sleep period, A co mputer-assisted pulsed (2 MHz) transcranial Doppler ultrasonography sy stem was modified for continuous long-term and on-line recording of ce rebral hemodynamics. Concurrently, simultaneous polysomnography, conti nuous BP recordings, and measurement of the end-expiratory carbon diox ide were undertaken, CBFV showed comparable nocturnal profiles in both groups with decreases during non-rapid eye movement (NREM) sleep and increases during rapid eye movement (REM) sleep, indicating that the g eneral pattern of brain perfusion during normal sleep is maintained in SAS, Sleep stage changes were not regularly accompanied by correspond ing changes in CBFV, This reflected a quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep and i ndicated a dissociation in the activity of central regulatory mechanis ms, Sleep stage-related analysis showed slightly reduced CBFV in patie nts with SAS compared with healthy control subjects during wakefulness and the first NREM sleep period, suggesting depressed. brain activity in the patient group, The higher CBFV values observed in patients wit h SAS compared with control subjects during REM sleep and sleep stage 2, both preceding and following REM sleep, underline the influence of dynamically changing sleep patterns on cerebral perfusion in these pat ients, Reproducible rapid decreases in CBFV were related to EEG arousa ls. Since apneas are terminated by arousals, these results showed that direct neuronal influences on brain perfusion during apnea are eviden t.