Marked episodic elevation of cerebrospinal fluid pressure during nocturnal sleep in patients with sleep apnea hypersomnia syndrome

doi:10.1016/0013-4694(85)90033-1

Electroencephalography and Clinical Neurophysiology

Volume 60, Issue 3, March 1985, Pages 214-219

https://doi.org/10.1016/0013-4694(85)90033-1 Get rights and content

Abstract

The CSF pressure was measured continously at the lumbar level during nocturnal sleep in 3 patients with sleep apnea hypersomnia syndrome. Nocturnal sleep was very unstable with frequent episodes of obstructive sleep apnea. When the patients were awake and relaxed in the supine position, their CSF pressure was stable and within the normal range. Episodic marked elevations of CSF pressure occured frequently during sleep, and each elevation was preceded and accompanied by an episode of sleep apnea or hypopnea. Significant correlations were found between the duration of apneic episodes and increase of CSF pressure, and between decrease of SaO₂ or TcPO₂ and increase of CSF pressure. The duration of sleep apnea was longer, increase of CSF pressure was greater, and decreases of SaO₂ and TcPO₂ were more marked during REM sleep than during NREM sleep. It is suggested that the frequent marked episodic elevations of CSF pressure are caused by an increase in the intracranial vascular volume occuring mainly in response to transient hypercapnia and hypoxia, which are induced by pulmonary hypoventilation during the episodes of sleep apnea.

Résumé

La pression du liquide céphalo-rachidien (LCR) a été continuellement mesurée au niveau lombaire pendant le sommeil nocturne de 3 patients atteints d'un syndrome d'hypersomnie et d'apnée de sommeil. Le sommeil nocturne était trés instable avec de fréquents épisodes d'apnées obstructives de sommeil. Lorsque les patients étaient allongés sur le dos, éveillés et détendus, la pression de leur LCR était stable et dans la normale. De fortes élévations épisodiques de la pression du LCR apparaissaient fréquemment au cours du sommeil, chaque élévation étant précédéé d'une période d'apnée de sommeil ou d'hypopnée. Des corrélations significatives ont été trouvées entre l'augmentation de la presion du LCR et la durée de la période d'apnée, et entre cette augmentation et la diminution de SaO₂ ou de TcPO₂. Plus la durée de l'apnée de sommeil se prolongeait, plus l'augmentation de pression était marquée; les diminutions de SaO₂ et de TcPO₂ étaient plus importantes pendant le sommeil paradoxal que pendant le sommeil non paradoxal. Il est suggéré que les fréquentes et fortes augmentations de la pression du LCR sont causées par une augmentation du volume vasculaire intracrânien apparaissant en grande partie en réponse à une hypercapnie et à une hypoxie transitoires induites par l'hypoventilation pulmonaire des épisodes d'apnée de sommeil.

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Abstract

Résumé

Amer. J. Med.

Venous Return

Effects of arterial hypoxaemia, hypercapnea, and changes in cerebral perfusion pressure on mean cerebrospinal fluid and sagittal sinus pressure

Acta neurochir. (Wien)

Influence of systemic and cerebral vascular factors on the cerebrospinal fluid pulse waves

J. Neurosurg.

Arterial blood gas analysis during sleep in a patient with sleep apnea syndrome

Jap. J. EEG EMG

Sleep apnea and B wave of CSF pressure in patients with dementia

Jap. J. EEG EMG

The effects of altered arterial tensions of carbon dioxide and oxygen consumption of normal young men

J. clin. Invest.

Sleep and intracranial pressure change in patients with normal pressure hydrocephalus

Jap. J. EEG EMG