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October 2013; 3 (5) The Nerve! Readers Speak

Early diagnosis and treatment of obstructive sleep apnea after stroke: Are we neglecting a modifiable stroke risk factor?Authors Respond:

Nitin K. Sethi, Maria Luisa Sacchetti, Arielle P. Davis, Martha E. Billings, W.T. Longstreth, Sandeep P. Khot
First published January 31, 2014, DOI: https://doi.org/10.1212/01.CPJ.0000444197.98857.83
Nitin K. Sethi
New York-Presbyterian Hospital:
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Maria Luisa Sacchetti
New York-Presbyterian Hospital:
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Arielle P. Davis
New York-Presbyterian Hospital:
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Martha E. Billings
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W.T. Longstreth Jr
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Sandeep P. Khot
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Early diagnosis and treatment of obstructive sleep apnea after stroke: Are we neglecting a modifiable stroke risk factor?Authors Respond:
Nitin K. Sethi, Maria Luisa Sacchetti, Arielle P. Davis, Martha E. Billings, W.T. Longstreth, Sandeep P. Khot
Neurol Clin Pract Oct 2013, 3 (5) 369-371; DOI: 10.1212/01.CPJ.0000444197.98857.83

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Davis et al.1 highlight the importance of timely identification of sleep-disordered breathing in patients who have had an acute stroke. In the immediate aftermath of a stroke, patients are frequently obtunded and so it is not unusual for symptoms of sleep-disordered breathing such as snoring, gasping, and choking sensation while asleep and excessive daytime sleepiness to be erroneously attributed to the stroke itself. While obstructive sleep apnea is the most common, central and mixed sleep apnea should be kept in mind especially in patients who have a bulbar stroke. Another unresolved issue is the appropriate time after a stroke when sleep apnea should be diagnosed and treated; the grade of sleep-disordered breathing may spontaneously improve and continuous positive airway pressure (CPAP) requirements decrease as the stroke becomes subacute and finally chronic. Repeating the sleep study and, if warranted, retitrating the CPAP a few months after the stroke is prudent.

Disclosures

N. Sethi serves as Associate Editor for The Eastern Journal of Medicine.

  • © 2013 American Academy of Neurology

I read with interest the article by Davis et al.1 on early diagnosis and treatment of obstructive sleep apnea (OSA) after stroke. In the article, the authors exhaustively argue the negative prognostic role of OSA on stroke clinical outcome and on its recurrence, as well as evidence of the positive effect of CPAP on patients' outcome. The reasons for patients' adherence to CPAP treatment were oversimplified. The authors neglected that some pathophysiologic mechanisms responsible for sleep-disordered breathing, such as a high loop gain, can be responsible for patients' unresponsiveness to CPAP.2 In fact, a central sleep apnea–hypopnea can be detected in cases with OSA-hypopnea when treated with CPAP.3 This phenomenon has been reported to occur in stroke patients, and can verify spontaneously in patients with congestive heart failure.4 Since CPAP treatment of stroke cases has given inconclusive results, the question arises whether clinical or diagnostic parameters, or both, are able to predict unresponsive cases; a high loop gain has been proposed as one of those parameters. A schematic representation of proposed responsible mechanisms is reported in the figure.Embedded Image

Disclosures

The author reports no disclosures.

Authors Respond:

We appreciate the responses and agree that sleep-disordered breathing is common after stroke and often not just simple OSA. In one series of 147 patients admitted to rehabilitation after a first-time stroke, 44% had a respiratory disturbance index ≥10, with problems mainly due to obstructive or predominately obstructive events vs predominately central in only 6.1%.5 Another study of patients with a first-ever stroke (73%) or transient ischemic attack (24%) found that in the first 48 to 72 hours after admission, 72% of patients had an apnea-hypopnea index >10, with 52.2% having predominantly obstructive events and 38.5% with predominantly central.6 As Dr. Sethi notes, the best time after stroke to diagnose and treat sleep apnea remains uncertain. Patient adherence to CPAP is highest when patients are treated early and while still on inpatient rehabilitation.7 While sleep-disordered breathing may improve spontaneously poststroke, OSA usually persists. In the study noted above, sleep studies repeated after 3 months showed substantial reductions in the central apnea index (6.2 to 3.3) when compared to the acute phase, but the obstructive apnea index was unchanged.6 Thus, repeating sleep studies and retitrating CPAP in the chronic phases poststroke may be justified. Dr. Sacchetti's letter accurately highlights that CPAP adherence in some cases can be related to pathophysiologic mechanisms such as high loop gain, which effectively leads to excessive ventilatory response to changes in Pco2.8 High loop gain may result in development of significant central apneas with the application of CPAP in 3% to 20% of patients with OSA, termed complex sleep apnea or CPAP-emergent central sleep apnea.9,10 While the majority of these central apneas resolve after months of continued therapy, in a minority of patients, 1.5% in one of the largest studies,9 they persist and contribute to intolerance and ineffectiveness of CPAP therapy. It remains difficult to predict which patients have a high loop gain phenotype and are at the highest risk for developing complex sleep apnea refractory to CPAP. While stroke is a known risk factor for central sleep apnea, whether stroke is also a risk factor for high loop gain is unknown. Thus, although complex sleep apnea may limit adherence, whether stroke is associated with an increased risk of this phenomena requires further study.

Disclosures

A. Davis was involved with a commercially sponsored clinical trial: PARTNER II Trial (“Placement of Aortic Transcatheter Valves Trial”) sponsored by Edwards Lifesciences. M. Billings has received a post-MD HSRD Fellowship from the Department of Veterans Affairs, Office of Research and Development, Health Services Research & Development. W.T. Longstreth, Jr., is a coinvestigator on several NIH-funded studies. S. Khot serves on the editorial board of Neurohospitalist and as a Section Editor of Clinical Pathological Conferences and Clinical Problem Solving.

References

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