Increased Flow Limitation During Sleep Is Associated With Increased Psychomotor Vigilance Task Lapses in...Suspected OSA, 2024, Staykov et al.

nataliezzz

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Increased Flow Limitation During Sleep Is Associated With Increased Psychomotor Vigilance Task Lapses in Individuals With Suspected OSA
Eric Staykov, Dwayne L Mann, Brett Duce, Samu Kainulainen, Timo Leppänen, Juha Töyräs, Ali Azarbarzin, Thomas Georgeson, Scott A Sands, Philip I Terrill
https://www.sciencedirect.com/science/article/abs/pii/S0012369223058233 (no full text link available)

Background
Impaired daytime vigilance is an important consequence of OSA, but several studies have reported no association between objective measurements of vigilance and the apnea-hypopnea index (AHI). Notably, the AHI does not quantify the degree of flow limitation, that is, the extent to which ventilation fails to meet intended ventilation (ventilatory drive).

Research Question
Is flow limitation during sleep associated with daytime vigilance in OSA?

Study Design and Methods
Nine hundred ninety-eight participants with suspected OSA completed a 10-min psychomotor vigilance task (PVT) before same-night in-laboratory polysomnography. Flow limitation frequency (percent of flow-limited breaths) during sleep was quantified using airflow shapes (eg, fluttering and scooping) from nasal pressure airflow. Multivariable regression assessed the association between flow limitation frequency and the number of lapses (response times > 500 ms, primary outcome), adjusting for age, sex, BMI, total sleep time, depression, and smoking status.

Results
Increased flow limitation frequency was associated with decreased vigilance: a 1-SD (35.3%) increase was associated with 2.1 additional PVT lapses (95% CI, 0.7-3.7; P = .003). This magnitude was similar to that for age, where a 1-SD increase (13.5 years) was associated with 1.9 additional lapses. Results were similar after adjusting for AHI, hypoxemia severity, and arousal severity. The AHI was not associated with PVT lapses (P = .20). In secondary exploratory analysis, flow limitation frequency was associated with mean response speed (P = .012), median response time (P = .029), fastest 10% response time (P = .041), slowest 10% response time (P = .018), and slowest 10% response speed (P = .005).

Interpretation
Increased flow limitation during sleep was associated with decreased daytime vigilance in individuals with suspected OSA, independent of the AHI. Flow limitation may complement standard clinical metrics in identifying individuals whose vigilance impairment most likely is explained by OSA.
 
There is no full-text link available and it's not on Sci-Hub.

Regarding flow limitation driving symptoms like decreased psychomotor vigilance and self-reported sleepiness (as shown in the study below - S4ME link), there needs to be some additional factor accounting for how flow limitation is driving these symptoms beyond flow limitation itself, since many asymptomatic people have significant flow limitation (for ex, see: A comparison of inspiratory airflow dynamics during sleep between upper airway resistance syndrome patients and healthy controls, Gold et al. 2013 - multiple controls [who were rigorously screened to be free of any medical conditions, fatigue/pain/etc.] had >90% of their breaths flow limited during stage 2 non-REM sleep).

Flow Limitation Is Associated with Excessive Daytime Sleepiness in Individuals without Moderate or Severe Obstructive Sleep Apnea, 2024, Mann et al.

This is where Dr. Gold's theory of UARS/OSAS being driven by a stress response in the brain to inspiratory flow limitation comes in (S4ME link - AI Summary)
 
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EDS = excessive daytime sleepiness (Epworth Sleepiness Scale [ESS] ≥11 here); the ESS isn't a great measure of true objective sleepiness (i.e. how quickly one falls asleep, as measured by mean sleep latency on multiple sleep latency testing - MSLT) and measures an uninterpretable mix of objective sleepiness and fatigue (I will share the data on that when it is published).
In regards to psychomotor vigilance test (PVT) performance specifically, the study below supports the notion that objective sleepiness (also "physiological sleepiness" - i.e. how quickly one falls asleep based on objective testing - MSLT) and self-reported excessive daytime sleepiness (measured by Epworth Sleepiness Scale - ESS) do not reflect the same underlying pathophysiology.

S4ME link: Psychomotor Vigilance Test and Its Association With Daytime Sleepiness and Inflammation in Sleep Apnea: Clinical Implications, 2017, Li et al.
We studied 58 untreated patients with OSA...PVT variables included number of lapses, mean reciprocal of the fastest 10% and slowest 10% reaction times, and median of 1/reaction time [1/RT]. Higher ESS scores were significantly associated with greater number of lapses (β = .34, P = .02) and lower values of 1/RT (β = -.36, P = .01) and slowest 10% RTs (β = -.30, P = .04). No significant association was observed between PVT and MSLT.
 
how quickly one falls asleep based on objective testing - MSLT) and self-reported excessive daytime sleepiness (measured by Epworth Sleepiness Scale - ESS) do not reflect the same underlying pathophysiology.
What's the reason for pointing this out about MSLT and ESS in this thread, as I only see the abstract describing using the psychomotor vigilance test (PVT) but not those other two? Did you mean to say that objective sleepiness (MSLT) and objective vigilance (PVT) don't reflect the same pathology?
 
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What's the reason for pointing this out about MSLT and ESS in this thread, as I only see the abstract describing using the psychomotor vigilance test (PVT) but not those other two? Did you mean to say that objective sleepiness (MSLT) and objective vigilance (PVT) don't reflect the same pathology?
Good question...it made sense to me when I was posting it late last night lol. ESS (which we know is also associated with increased flow limitation, at least in AHI <15) was correlated with increased PVT lapses in the other study I linked, but MSLT was not. I think when this is tied together with some of the other evidence, it provides support for the notion that there are 2 phenotypes of OSAS: one that is characterized by fatigue (and often subjective daytime sleepiness - ESS) and decreased psychomotor vigilance (in which the stress response to inspiratory flow limitation may be the primary driver of symptoms?) and another characterized by objective sleepiness (and often inflammatory markers, cardiometabolic morbidity, etc.) in which the actual apneas/hypopneas/hypoxemias - perhaps in combination with some other factor/s - may be the primary driver of symptoms? - that's the subtype we're probably looking at in this study I shared where etanercept improved objective sleepiness on MSLT: Marked decrease in sleepiness in patients with sleep apnea by etanercept, a tumor necrosis factor-alpha antagonist, 2004, Vgontzas et al. However, we know it's also possible for mild sleep-disordered breathing patients with low AHIs/no significant hypoxemia to be objectively sleepy and for their sleepiness to be alleviated by CPAP on MSLT as that was shown in the first group of UARS patients identified: A cause of excessive daytime sleepiness. The upper airway resistance syndrome

So anyways...I was/am getting ahead of myself (I also have a new pair of glasses that are making me feel nauseous/dizzy and I am honestly having trouble following along with myself at this point lol). It probably makes much more sense to just make a whole thread about this once the data is actually published showing that the ESS is about equally correlated with fatigue severity scale (FSS) and mean sleep latency (MSL) on MSLT in OSA patients, but that FSS and MSL are not correlated with each other (it should [hopefully] be accepted soon...not sure how long it takes from that to actually being published online). Then bringing in some of these other studies that support the two different phenotypes of OSAS.

But it is interesting that objective sleepiness (MSLT) is not associated with decreased psychomotor vigilance, as it seems like it would be, right?
 
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Maybe you meant to post it in the other thread about ESS, and used the Insert Quote button on the wrong thread, since I see the quote in your post is from a different thread?
I'm pretty sure I meant to post it here, because in my mind all of these studies tie together (the increased flow limitation predicting ESS scores and PVT lapses, and the ESS - but not MSLT - predicting PVT lapses), but like I said, I'm getting ahead of myself, and I do think it makes sense to make a whole thread on this topic with some of the additional papers that provide evidence for these phenotypes once the paper by Dr. Gold et al. is published showing how FSS and MSLT are correlated with ESS - but not with each other - in OSA patients.
 
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