1993
DOI: 10.1378/chest.103.4.1118
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Cerebral Hemodynamics in Obstructive Sleep Apnea

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Cited by 51 publications
(48 citation statements)
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“…The latter might be secondary to (1) sympathetic surge-induced arterial hypertension and hypertensive arteriosclerosis, (2) vascular dysregulation due to imbalance between nitric oxide (vasodilator) and endothelin (vasoconstrictor), (3) abnormal platelet aggregation and activation leading to microinfarcts in the optic nerve, or (4) episodic-raised intracranial pressure. 6,15,17,18 The absence of statistically significant differences between the incidences of hightension glaucoma in the OSA arm (3.66%) and control arm (2.94%) in our study, speaks against the hypothesis of unrecognized, nocturnal high-tension glaucoma as a cause of the optic neuropathy, which was suggested by Marcus et al…”
Section: Discussioncontrasting
confidence: 46%
See 1 more Smart Citation
“…The latter might be secondary to (1) sympathetic surge-induced arterial hypertension and hypertensive arteriosclerosis, (2) vascular dysregulation due to imbalance between nitric oxide (vasodilator) and endothelin (vasoconstrictor), (3) abnormal platelet aggregation and activation leading to microinfarcts in the optic nerve, or (4) episodic-raised intracranial pressure. 6,15,17,18 The absence of statistically significant differences between the incidences of hightension glaucoma in the OSA arm (3.66%) and control arm (2.94%) in our study, speaks against the hypothesis of unrecognized, nocturnal high-tension glaucoma as a cause of the optic neuropathy, which was suggested by Marcus et al…”
Section: Discussioncontrasting
confidence: 46%
“…[1][2][3][4] OSA is well known to result in a number of health consequences: fragmentation of sleep leads to chronic sleep deprivation and daytime somnolence, hence affecting the patients' daily cognitive function and quality of life, increasing incidences of work-related and motor vehicle accidents; cardio-respiratory disturbances lead to elevated risks of complications such as hypertension, pulmonary hypertension, cardiac arrhythmia, myocardial infarction, congestive cardiac failure, and stroke. [1][2][3][4][5][6] Recently, possible ocular manifestations, including optic neuropathy in the form of visual field (VF) defect and disc oedema, normal-tension glaucoma (NTG), pseudotumour cerebri, nonarteritic anterior ischaemic optic neuropathy (NAAION); and anterior segment complications such as floppy eyelid syndrome, upper lid ptosis, lower lid ectropion, blepharochalasis, trichiasis, chronic conjunctivitis, keratoconus, exposure keratopathy, dry eyes, recurrent corneal erosion (RCE), keratitis, and progressive endotheliopathy have aroused ophthalmologists' concern. [7][8][9][10][11][12][13][14][15] However, there are limited evidences in published articles of causal relationship between OSA and the various ocular manifestations, especially in the Chinese locality.…”
Section: Introductionmentioning
confidence: 99%
“…Studies with transcranial Doppler, xenon inhalation or single-photon emission CT have shown a reduction in cerebral blood flow during non-REM sleep and an increase during REM sleep [49,50,51]. …”
Section: Confounding Risk Factors or Potential Mediators For Stroke Imentioning
confidence: 99%
“…TCD has been used to measure BF during sleep since 1990s. [23][24][25][26] However, TCD faces similar technical challenges of obtaining clean signals while patients were asleep, since the requirement to keep the Doppler probe in place in the medial cerebral artery during sleep was di±cult. 27 In addition TCD re°ects hemodynamics of the middle arteries but not of the arterioles, which are responsible for mediating cerebral autoregulation.…”
Section: Introductionmentioning
confidence: 99%