We thank Wessendorf et al. for their comments. We agree that
performing polysomnography shortly after stroke onset is a difficult
task. [1] Both neurologists and sleep laboratory technicians had to be on
call 24 hours per day during more than one year to recount patients that
met inclusion and exclusion criteria .
Wessendorf et al. are correct concerning our error in table 2 of our
paper. A typographical mistake: patients with snoring and AHI<10 were
16 out of 19 instead of 9 out of 19. The statistical analyses in the
table, however, were performed based on the correct figures and, patients
with or without sleep apnea did not differ in history of snoring before
stroke onset (p=0.62 using Fisher’s exact test, two-tail, minimum expected
frequency was 1.5) and vascular risk factors. The amended table with the p
values using Pearson test when the minimum expected frequency was greater
than 5 and two-tail Fisher’s exact test when it was lower than 5. The p-
values for the categorical variables remain higher than 0.45; therefore,
the results and conlusions of our study are unchanged.
The discrepancy between our results and Wessendorf et al. [2]
regarding the association between snoring before stroke and sleep apnea is
difficult to explain. A type II error can not be excluded. However, two
other studies performed in acute care centers evaluating 128 [3] and 161
[4] patients with acute or recent stroke (mean delay of polysomnography
less than 10 days) found on multiple logistic regression analysis that
sleep apnea could not be predicted by a history of snoring prior to
stroke. Other possible explanations for this discrepancy is that
Wessendorf et al. [2] evaluated patients after 46 ± 20 days after stroke
onset and not during the acute phase of the disease (the AHI index
decreases in the stable phase of the stroke when compared to the acute
phase5), and that they studied patients from a rehabilitation center where
the most severe stroke patients are usually admitted (altough scales of
stroke severity are not provided in their article). The most important
points in our study which are that sleep apnea is frequent during the
first night after cerebral infaction and, associated with early neurologic
worsening and stroke onset while sleeping.
References:
1. Iranzo A, Santamaria J, Berenguer J, Sanchez M, Chamorro A.
Prevalence and clinical importance of sleep apnea in the first night
after cerebral infarction. Neurology 2002;58:911-916.
2. Wessendorf TE, Teschler H, Wang YM, Konietzko N, Thilmann AF.
Sleep-Disordered breathing among patients with first-ever stroke . J
Neurol 2000;247:41-47.
3. Bassetti C, Aldrich MS. Sleep apnea in acute cerebrovascular
diseases: final report on 128 patients. Sleep 1999;22:217-223.
4. Parra O, Arboix A, Bechich S, et al. Time course of sleep-related
breathing disorders in fist-ever stroke or transient ischemic attack. Am J
Respir Crit Care Med 2000;161:375-380.
Table 2. Clinical differences between patients with and without AHI
³10 on admission.
AHI <10(n=19) AHI ³10(n=31) P value
Hypertension (n) 13/ 21/ 0.96 *
Smoking (n) 7/ 11/ 0.92 *
Hyperlipidemia (n) 5/ 5/ 0.47 **
Habitual snoring (n) 16/ 28/ 0.62 **
Respiratory pauses(n)9/ 13/ 0.72 *
Somnolence (n) 1/ 4/ 0.63 **
* Pearson test when the minimum expected frequency was greater than
5
** Two-tail Fisher’s exact test when it was lower than 5
First number is AHI <10(n=19)
Second number is AHI 10³(n=31)
Third number is P value