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Cerebral perfusion during sleep‐disordered breathing
Author(s) -
HAJAK GÖRAN,
ELHÖFER JÜRGEN KLING,
SCHULZVARSZEGI MARIA,
SANDER DIRK,
STAEDT JÜRGEN,
CONRAD BASTIAN,
RÜTHER ECKART
Publication year - 1995
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/j.1365-2869.1995.tb00203.x
Subject(s) - sleep disordered breathing , breathing , sleep and breathing , medicine , cerebral perfusion pressure , sleep (system call) , cardiology , anesthesia , perfusion , obstructive sleep apnea , computer science , operating system
SUMMARY Snoring, a leading symptom of the sleep apnoea syndrome (SAS), has been reported to be one of the risk factors for sleep‐related cerebral strokes. Episodes of apnoea are accompanied by hypoxaemia as well as hypercapnia. As CO 2 constitute a major regulatory factor controlling cerebral blood flow, it is likely that changes in cerebral perfusion are to be found in patients with SAS, which may be related to nocturnal stroke. A computer‐assisted pulsed (2 mHz) Doppler ultrasonography system has been modified for continuous long‐term and on‐line recording of cerebral haemodynamics together with simultaneous polysomnography, continuous blood pressure recordings, and measurement of the end‐expiratory CO 2 . The dynamics of cerebral blood flow velocity (CBFV) during sleep were measured in the right middle cerebral artery in 10 SAS patients. CBFV showed a characteristic nocturnal pattern with decreases during non‐rapid eye movement (NREM) sleep and increases during REM sleep. Changes in sleep stage patterns as well as awakenings from NREM sleep were not regularly accompanied by corresponding changes in CBFV. Dramatic increases in CBFV could be observed during apnoeic episodes, with maximum increases during REM sleep. CO 2 reactivity and changes in CBFV related to apnoea duration were markedly increased during sleep compared with the waking state in SAS patients. The dynamic feature of CBFV in relation to sleep patterns reflects quantitative uncoupling between cerebral electrical activity and cerebral perfusion during sleep in SAS patients as has been previously reported for normal subjects (Hajak et al . 1994). It supports a dissociation in the activity of central regulatory mechanisms during human sleep which might cause abnormal cerebral perfusion under certain circumstances. The increased CO 2 reactivity during sleep in SAS suggests a ‘hypersensitivity’ of intracranial vasoactive receptors and/or disturbances in the central autonomic control of cerebrovascular functions. It may be concluded that, under certain conditions, the interaction of decreased cerebral perfusion in SAS patients with sleep‐related cerebral perfusion patterns and haemodynamic changes during apnoeic episodes might lead to a critical reduction in cerebral perfusion.