scholarly journals MRI evaluation of cerebrovascular reactivity in obstructive sleep apnea

2019 ◽  
Vol 40 (6) ◽  
pp. 1328-1337 ◽  
Author(s):  
Pei-Hsin Wu ◽  
Ana E Rodríguez-Soto ◽  
Zachary B Rodgers ◽  
Erin K Englund ◽  
Andrew Wiemken ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Rate Of Change ◽  
Cerebrovascular Reactivity ◽  
Breath Hold ◽  
High Temporal Resolution ◽  
Compensatory Mechanism ◽  
Whole Brain ◽  
Sagittal Sinus ◽  
Obstructive Sleep

Obstructive sleep apnea (OSA) is characterized by intermittent obstruction of the airways during sleep. Cerebrovascular reactivity (CVR) is an index of cerebral vessels' ability to respond to a vasoactive stimulus, such as increased CO2. We hypothesized that OSA alters CVR, expressed as a breath-hold index (BHI) defined as the rate of change in CBF or BOLD signal during a controlled breath-hold stimulus mimicking spontaneous apneas by being both hypercapnic and hypoxic. In 37 OSA and 23 matched non sleep apnea (NSA) subjects, we obtained high temporal resolution CBF and BOLD MRI data before, during, and between five consecutive BH stimuli of 24 s, each averaged to yield a single BHI value. Greater BHI was observed in OSA relative to NSA as derived from whole-brain CBF (78.6 ± 29.6 vs. 60.0 ± 20.0 mL/min2/100 g, P = 0.010) as well as from flow velocity in the superior sagittal sinus (0.48 ± 0.18 vs. 0.36 ± 0.10 cm/s2, P = 0.014). Similarly, BOLD-based BHI was greater in OSA in whole brain (0.19 ± 0.08 vs. 0.15 ± 0.03%/s, P = 0.009), gray matter (0.22 ± 0.09 vs. 0.17 ± 0.03%/s, P = 0.011), and white matter (0.14 ± 0.06 vs. 0.10 ± 0.02%/s, P = 0.010). The greater CVR is not currently understood but may represent a compensatory mechanism of the brain to maintain oxygen supply during intermittent apneas.

MRI evaluation of cerebral metabolic rate of oxygen (CMRO2) in obstructive sleep apnea

2022 ◽  
pp. 0271678X2110710
Author(s):  
Pei-Hsin Wu ◽  
Ana E Rodríguez-Soto ◽  
Andrew Wiemken ◽  
Erin K Englund ◽  
Zachary B Rodgers ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Blood Flow Rate ◽  
Oxygen Metabolism ◽  
Breath Hold ◽  
Sagittal Sinus ◽  
Obstructive Sleep ◽  
Significant Difference ◽  
Venous Oxygen Saturation ◽  
Brain Oxygen Metabolism

Patients with obstructive sleep apnea (OSA) are at elevated risk of developing systemic vascular disease and cognitive dysfunction. Here, cerebral oxygen metabolism was assessed in patients with OSA by means of a magnetic resonance-based method involving simultaneous measurements of cerebral blood flow rate and venous oxygen saturation in the superior sagittal sinus for a period of 10 minutes at an effective temporal resolution of 1.3 seconds before, during, and after repeated 24-second breath-holds mimicking spontaneous apneas, yielding, along with pulse oximetry-derived arterial saturation, whole-brain CMRO2 via Fick’s Principle. Enrolled subjects were classified based on their apnea-hypopnea indices into OSA (N = 31) and non-sleep apnea reference subjects (NSA = 21), and further compared with young healthy subjects (YH, N = 10). OSA and NSA subjects were matched for age and body mass index. CMRO2 was lower in OSA than in the YH group during normal breathing (105.6 ± 14.1 versus 123.7 ± 22.8 μmol O2/min/100g, P = 0.01). Further, the fractional change in CMRO2 in response to a breath-hold challenge was larger in OSA than in the YH group (15.2 ± 9.2 versus 8.5 ± 3.4%, P = 0.04). However, there was no significant difference in CMRO2 between OSA and NSA subjects. The data suggest altered brain oxygen metabolism in OSA and possibly in NSA as well.

scholarly journals Cerebral metabolic rate of oxygen in obstructive sleep apnea at rest and in response to breath-hold challenge

2015 ◽  
Vol 36 (4) ◽  
pp. 755-767 ◽  
Author(s):  
Zachary B Rodgers ◽  
Sarah E Leinwand ◽  
Brendan T Keenan ◽  
Lohith G Kini ◽  
Richard J Schwab ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Metabolic Rate ◽  
Small Sample Size ◽  
Small Sample ◽  
Cerebrovascular Reactivity ◽  
Apnea Hypopnea Index ◽  
Breath Hold ◽  
Cerebral Metabolic Rate ◽  
Obstructive Sleep

Obstructive sleep apnea (OSA) is associated with extensive neurologic comorbidities. It is hypothesized that the repeated nocturnal apneas experienced in patients with OSA may inhibit the normal apneic response, resulting in hypoxic brain injury and subsequent neurologic dysfunction. In this study, we applied the recently developed OxFlow MRI method for rapid quantification of cerebral metabolic rate of oxygen (CMRO2) during a volitional apnea paradigm. MRI data were analyzed in 11 OSA subjects and 10 controls (mean ± SD apnea-hypopnea index (AHI): 43.9 ± 18.1 vs. 2.9 ± 1.6 events/hour, P < 0.0001; age: 53.8 ± 8.2 vs. 45.3 ± 8.5 years, P = 0.027; BMI: 36.6 ± 4.4 vs. 31.9 ± 2.2 kg/m2, P = 0.0064). Although total cerebral blood flow and arteriovenous oxygen difference were not significantly different between apneics and controls ( P > 0.05), apneics displayed reduced baseline CMRO2 (117.4 ± 37.5 vs. 151.6 ± 29.4 µmol/100 g/min, P = 0.013). In response to apnea, CMRO2 decreased more in apneics than controls (−10.9 ± 8.8 % vs. −4.0 ± 6.7 %, P = 0.036). In contrast, group differences in flow-based cerebrovascular reactivity were not significant. Results should be interpreted with caution given the small sample size, and future studies with larger independent samples should examine the observed associations, including potential independent effects of age or BMI. Overall, these data suggest that dysregulation of the apneic response may be a mechanism for OSA-associated neuropathology.

393 Comparison of Oxygenation Abnormalities Between Obstructive Sleep Apnea and Central Sleep Apnea

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A156-A157
Author(s):  
Sikawat Thanaviratananich ◽  
Hao Cheng ◽  
Maria Pino ◽  
Krishna Sundar
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Demographic Data ◽  
Central Sleep Apnea ◽  
Nrem Sleep ◽  
Rate Of Change ◽  
Apnea Hypopnea Index ◽  
P Value ◽  
Obstructive Sleep ◽  
Cheyne Stokes Breathing

Abstract Introduction The apnea-hypopnea index (AHI) is used as a generic index to quantify both central sleep apnea (CSA) and obstructive sleep apnea (OSA) syndromes. Patterns of oxygenation abnormalities seen in CSA and OSA may be key to understanding differing clinical impacts of these disorders. Oxygen desaturation and resaturation slopes and durations in OSA and CSA were compared between OSA and CSA patients. Methods Polysomnographic data of patients aged 18 years or older with diagnosis of OSA and CSA, at University of Iowa Hospitals and Clinics, were analyzed and demographic data were collected. Oximetric changes during hypopneas and apneas were studied for desaturation/resaturation durations and desaturation/resaturation slopes. Desaturation and resaturation slopes were calculated as rate of change in oxygen saturation (ΔSpO2/Δtime). Comparison of hypoxemia-based parameters between patients with OSA and CSA was performed using unpaired t-test. Results 32 patients with OSA with median AHI of 15.4 (IQR 5.1 to 30.55) and median ODI of 15.47 (IQR 9.50 to 29.33) were compared to 15 patients with CSA with a median AHI of 20.4 (IQR 12.6 to 47.8) and median ODI of 27.56 (IQR 17.99 to 29.57). The mean number of desaturation and resaturation events was not significantly different between patients with OSA and CSA (OSA - 106.81±87.93; CSA - 130.67±76.88 with a p-value 0.1472). 4/15 CSA patients had Cheyne-Stokes breathing, 2/15 had treatment emergent central sleep apnea, 1/15 had methadone-associated CSA and for 8/15, no etiologies for CSA were found. Mean desaturation durations was significantly longer in OSA (20.84 s ± 5.67) compared to CSA (15.94 s ± 4.54) (p=0.0053) and consequently the desaturation slopes were steeper in CSA than OSA (-0.35%/sec ±0.180 vs. -0.243 ± 0.073; p=0.0064). The resaturation duration was not significantly longer in OSA (9.76 s ± 2.02) than CSA (9.057 s ± 2.17) (p=0.2857). Differences between desaturation duration and slopes between CSA and OSA persisted during REM and NREM sleep, and in supine sleep. Conclusion As compared to OSA, patients with CSA have different patterns of desaturations and resaturations with lesser hypoxic burden with CSA. This may have implications on the clinical outcomes seen between these two disorders. Support (if any):

An fMRI study of cerebrovascular reactivity and perfusion in obstructive sleep apnea patients before and after CPAP treatment

2014 ◽  
Vol 15 (8) ◽  
pp. 892-898 ◽  
Author(s):  
Olga Prilipko ◽  
Nelly Huynh ◽  
Moriah E. Thomason ◽  
Clete A. Kushida ◽  
Christian Guilleminault
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cerebrovascular Reactivity ◽  
Cpap Treatment ◽  
Fmri Study ◽  
Obstructive Sleep ◽  
Before And After

Abstract 208: Altered Cerebrovascular Reactivity Following One Month of Obstructive Sleep Apnea

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
David J Durgan ◽  
Randy F Crossland ◽  
Eric E Lloyd ◽  
Sharon C Phillips ◽  
Robert Bryan
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cerebral Arteries ◽  
Significant Risk ◽  
Fold Increase ◽  
Cerebrovascular Reactivity ◽  
No Production ◽  
No Donor ◽  
Obstructive Sleep ◽  
Increased Sensitivity

Obstructive sleep apnea (OSA) has been identified as a significant risk factor for stroke. However, little is known regarding the effects of OSA on the cerebrovascular wall. Using a novel rodent model of OSA we assessed the hypothesis that (1) OSA augments endothelin (ET-1) induced constrictions of cerebral arteries and (2) OSA attenuates dilations of cerebral arteries by agonist-induced nitric oxide (NO) release from the cerebrovascular endothelium. The repetitive airway closures associated with OSA lead to intermittent hypoxia/hypercapnia and reoxygenation, increased negative intrathoracic pressures, and arousals. In order to model the physiological consequences of OSA, we have chronically instrumented rats with inflatable endotracheal obstruction devices. Unanesthetized freely-ranging rats underwent 30 apneas/ hour for 8 hours/ day (sleep phase) for 1 month. During apnea pO 2 decreased from 122±3 to 67±3 mm Hg; pCO 2 increased from 43±1 to 51±1 mm Hg; pH decreased from 7.46±0.00 to 7.38±0.01; and hemoglobin O 2 saturation decreased from 94±1 to 82±1 % (n=5 and p<0.05 for each). Following 1 month of OSA blood pressure, plasma ET-1 and NO levels were similar in sham and OSA rats. Using the pressurized cerebral artery preparation, we observed a 17.5-fold increase in sensitivity to ET-1 (n=5-6, p<0.05) after 1 month of OSA. The increased sensitivity of OSA cerebral arteries to ET-1 was abolished by the ET-B receptor antagonist BQ-788 (n=6, NS). Additionally, constrictions to the ET-B specific agonist IRL-1620 were significantly greater in OSA, versus sham, cerebral arteries (n=6, p<0.05). Dilations to ATP (a P2Y 2 agonist which stimulates NO production in the endothelium) were attenuated in cerebral arteries from OSA rats by 40% (n=5-8, p<0.05). However dilations to the NO-donor MAHMA-NOnoate were similar between groups. In conclusion, 1 month of OSA results in (1) increased sensitivity of cerebral arteries to ET-1, likely through upregulation of ET-B receptors on the vascular smooth muscle and (2) decreased endothelial-derived NO production. These data suggest that OSA results in significant alterations to the cerebrovascular wall in the absence of hypertension.

scholarly journals Obstructive Sleep Apnea is Associated with Longitudinal Increases in Amyloid Burden in Elderly Mild Cognitive Impairment Individuals

2019 ◽  
Vol 15 (4) ◽  
pp. 71-77 ◽  
Author(s):  
Megan Hogan ◽  
Amanda Shim ◽  
Ogie Queen Umasabor-Bubu ◽  
Mukhtar Fahad ◽  
Omonigho Michael Bubu
Keyword(s):  
Obstructive Sleep Apnea ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Sleep Apnea ◽  
Rate Of Change ◽  
Amyloid Pet ◽  
Amyloid Burden ◽  
Obstructive Sleep ◽  
History Of ◽  
Over Time

Cross sectional analysis has shown an association between Obstructive Sleep Apnea (OSA) severity and Aβ burden using amyloid-PET among Mild Cognitive Impairment (MCI) patients. However, whether OSA accelerates longitudinal increases in amyloid beta (Aβ) burden in MCI patients is presently unclear. Study participants included a total of 798 subjects with a diagnosis of MCI and were a subset of the ADNI cohort (adni.loni.usc.edu). OSA was self-reported and participants were labeled either as OSA+ or OSA−. Aβ burden was determined by florbetapir SUVRs. To test whether OSA is associated with the rate of change in Aβ data longitudinally, multilevel mixed effects linear regression was used to fit the models with randomly varying intercepts and slopes allowing dependence on OSA status. The final model was adjusted for age, sex, body mass index, education, CPAP use status, history of respiratory disease, hypertension, diabetes, and history of cardiovascular disease. A significant variation in the change (slope) in Aβ volumes over time was seen (p<.0001). The covariance between the baseline Aβ level and Aβ volume change over time indicated that OSA subjects experienced greater mean change differences in brain Aβ volumes over time (p < .0001). The rate of change in Aβ deposition also varied significantly across OSA groups over the follow-up period. Obstructive Sleep Apnea possibly facilitates longitudinal increases in amyloid burden in elderly Mild Cognitive Impairment individuals. Further research examining mechanisms underlying effects of OSA on the longitudinal increases in Aβ burden is needed.

Sign in / Sign up

Export Citation Format

Share Document