From the Sleep Research Center, Division of Pulmonary and Critical Care
Medicine, Case Western Reserve University, Cleveland, Ohio (N.N., K.P.S.);
Division of Sports Medicine, Department of Medicine, University Hospital, Ulm,
Germany (N.N., M.L.); and Division of Pulmonary Medicine, Department of
Medicine, University Hospital, Freiburg, Germany (P.W., I.J.).
Methods—Doppler sonography of the MCA was performed in
conjunction with nightly polysomnography in 11 men and one woman.
Results—A significant decline in blood flow occurred in 76%
(169/223) of obstructive hypopneas and in 80% (98/123) of obstructive
apneas, compared with only 14% (13/96) of central apneas
(P
Conclusions—With obstructive hypopneas and obstructive apneas,
MCA blood flow is more often decreased in comparison to central apneas.
MCA blood flow reductions occur with longer obstructive hypopneas and
with those hypopneas with greater falls in oxygen saturation. These
observations indicate pathophysiology relevant to an increased risk for
stroke in heavy snorers and patients with obstructive hypopneas and
apneas.
The earlier observations by Partinen and Palomaki8 and
Koskenvuo et al9 have been proved lately by a study of
Dyken et al10 (1996), who showed a significantly higher
incidence of sleep apnea in patients with stroke than in subjects
without stroke.
A study reported in 1993 by Somers et al11 described the
influence of rapid sympathetic nerve activity changes linked to muscle
tone changes in REM sleep and drew the conclusion that this phenomenon
could play a part in triggering ischemic events in patients
with vascular disease.
An intermediate factor for stroke might be alterations in cerebral
blood flow, but for this variable there are limited observations.
Rehan et al12 showed that blood flow velocity either was
unchanged or increased during central apneas in healthy term infants.
He showed, however, in another observation that blood flow and blood
flow velocity were influenced by respiratory patterns but not by sleep
stages in these infants.13 Hajak et al14 found
that average blood flow showed slight reduction in patients with sleep
apnea in wakefulness and stage I NREM sleep compared with healthy
control subjects. In REM sleep and NREM stages II through IV, however,
they found higher cerebral blood flow in sleep apnea patients than in
control subjects. In an earlier report by the same group,
Klingelhöfer et al15 reported increased blood flow
during apneic episodes in sleep apnea patients and blood flow decrease
during episodes with many arousals. Neither study reported the
consequences of an individual apnea or hypopnea on blood flow because
they were focusing on average blood flow during sleep stages and apneic
episodes as well as episodes with many arousals.
In a study of simulated obstructed breaths with Müller maneuvers
(high negative intrathoracic pressures against an obstruction), Andreas
et al16 demonstrated that during the obstructed effort a
significant reduction in blood flow to the MCA occurred, an event that
correlated with a fall in blood flow across the mitral and aortic
valves. This study in awake humans predicts that blood flow might fall
during an obstructive apnea or hypopnea during sleep. According to the
observations of Podszus et al,17 systemic blood pressure
decreases during obstructive apneas in elderly men.
The present study was planned to observe sleeping subjects for
changes in cerebral blood flow resulting from a single apneic or
hypopneic event. We postulated that central and obstructive events
would differ in regard to changes in cerebral blood flow as a result of
the absence or presence, respectively, of negative intrathoracic
pressures. Using continuous Doppler sonography, we examined
patients with sleep apnea to correlate MCA blood flow with apneas and
hypopneas.
All patients were self-reported heavy snorers, with a mean age of 54
years. Patient characteristics are shown in Table 1
Sleep and breathing parameters were assessed with the use
of 12-channel polysomnography (CNS Sleep Laboratory): C3 and C4 EEG,
two-channel electro-oculogram, chin electromyogram, leg electromyogram,
nasal and oral airflow assessed by thermistor, ECG, snoring sounds
assessed by a microphone placed over the extrathoracic trachea,
abdominal and chest wall movement assessed by a respiratory belt, and
arterial oxygen saturation assessed by pulse oximeter
(Nellcor Monitor).
Blood flow in the MCA was recorded with sonographic equipment (EME
type TC2–64) over one of the three sonographic windows of the left or
right temporal bone. The device was held in a special head
harness,18 modified for use during sleep with a snug
headband and straps to hold the position of the sonographic probe. The
Doppler signal, representative of velocity and flow
in the MCA, was recorded by the CNS Sleep Laboratory computer so
that a real-time comparison and analysis of the data could be
obtained (Fig 1
At completion of the polysomnography, EEG data together with the
Doppler signals were analyzed by inspection of the
record.19 Determination of obstructive and central
apneas as well as obstructive hypopneas in all 12 patients was
accomplished according to the following criteria. Apnea was defined as
an absence of inspiratory flow for at least 10 seconds.20
Central apneas were defined as total absence of nasal and oral
inspiratory flow and chest/abdominal movement during the period of
absence of inspiratory flow. Obstructive apneas were defined by a
decrease of greater than 80% in airflow in the presence of paradoxical
movements of the ribcage and abdomen. Obstructive hypopneas were
defined as a 50% to 80% reduction in airflow accompanied by lack of
synchrony of ribcage and abdominal motion.
A reduction in the blood flow was defined as a 50% or more reduction
in amplitude of the signal. Results of this decision were matched
separately with the type and duration of apnea and with the decrease in
arterial oxygen saturation from baseline value with each
abnormal breathing event. A representative sample of
the record is shown in Fig 1
Results are expressed as mean and SD. Differences between groups and
correlation with variables such as duration of apnea, desaturation
from baseline, and incidence of decreased blood flow of the MCA were
analyzed with the use of the Wilcoxon signed rank test
and, when indicated, Friedman two-way ANOVA (logistic regression
analysis). Differences with values of P
In regard to event type, all data combined showed a significant
(>50%) reduction in MCA blood flow (P<.0001); however,
the frequency of this varied by event type. A reduction of MCA blood
flow was observed in 98 of 123 obstructive apneas (80%) and 169 of 223
obstructive hypopneas (76%) (Fig 2
In regard to the duration of events, reduced MCA blood flow correlated
with all apneas (P<.01). Examined separately, a correlation
was significant with the duration of the hypopneas (P<.01)
but not with the duration of the obstructive apneas (P=.07)
or with the duration of central apneas (P=.17) (Fig 3
In regard to the change in oxygen saturation with events, there was a
statistically significant correlation (P<.05) between the
fall in arterial oxygen saturation and the occurrence of
reduced MCA blood flow in obstructive hypopnea (Fig 4
Both Partinen and Palomaki8 and later Koskenvuo et
al9 showed a strong epidemiological correlation between
loud snoring and the risk of stroke development. For instance, in one
study the unadjusted risk for stroke was 40 times higher in heavy
snorers than in nonsnorers.8 Causality could not be clearly
elucidated from these studies; however, it seemed reasonable to the
authors to assume a relation to effects of sleep-disordered breathing.
Subsequent studies examining nocturnal blood pressure in sleep apnea
patients,2 3 4 as well as the study by Fischer et
al21 measuring intracranial hemodynamics in
sleep apnea, suggest a direct effect of each sleep-related respiratory
event on blood pressure and cerebral perfusion, respectively. Other
pathophysiological pathways potentially operative
include hypoxia-induced vasodilatation22 or
reflex-mediated cerebral vasoconstriction in the MCA from acute
systemic hypertension,23 mechanisms identified as causes of
acute stroke.
Fischer et al21 documented a mean reduction of blood flow
to the MCA during REM sleep, NREM sleep, and on awakening in patients
suffering from sleep apnea syndrome; however, no temporal relationship
between the presence or type of apnea was reported. The results of the
present study establish a direct relationship between individual
apneas and reduction in MCA blood flow (Fig 2
Duration of the event plays a role in the development of reduced
perfusion of the MCA, ie, the longer the event, the greater the
likelihood for a reduction in blood flow. This was particularly
observed for obstructive hypopneas, the
physiological marker of self-reported heavy
snoring. A weak association exists between the degree of desaturation
and the frequency of decreased blood flow of the MCA, and again this is
true only for obstructive hypopneas. These observations are unlikely to
be explained by differences in patient physiology, since each patient
demonstrated all event types. However, it must be noted that within all
analyzed events a duration longer than 22 seconds as well as an
oxygen desaturation greater than 15% was present in obstructive
hypopneas more than in obstructive apneas. This might be explained by
recruiting a patient group that presents all types of apneas, so
that obstructive hypopneas may be present in this patient group
more than in a more typical patient group with obstructive sleep apnea
and mainly obstructive apneas only. Because the majority of obstructive
hypopneas are in the group of events with a duration longer than 22
seconds and this possibly interferes with the fall in
arterial oxygen saturation in this group of events, it
gives the impression that oxygen desaturation is less likely to be
present in obstructive apneas.
An explanation for the relationship between partial airway obstruction
and decreased perfusion of the MCA might be provided by the observation
of Andreas et al,16 who were able to demonstrate reduced
blood flow during Müller maneuvers. Our study did not measure
pleural pressures or cardiac output and used the patterns of change in
air flow and chest wall motion as indicators of central or obstructive
events.
Our observation that a reduction in blood flow of the MCA occurred more
often with a longer duration of hypopnea suggests that there is an
interaction between respiratory efforts and the duration of the event
in regard to their impact on cerebral blood flow and on systemic blood
pressure.17 24 25 26 Increased time of partial obstructions
might lead to a greater likelihood for development of a high cardiac
preload, a lower cardiac afterload, activation of carotid body
baroreceptors, and vasodilatation by both increasing
arterial carbon dioxide and decreasing
oxygenation, all of which can contribute to a reduction
in cerebral blood flow. Termination of the hypopnea with an
unobstructed breath, however, rapidly results in a return to pre-event
levels of blood flow, suggesting that not all of these mechanisms are
operative. Termination may protect from decreasing blood flow resulting
from reflex or the direct effects of asphyxia. Thus, increased blood
flow velocity could be related to arousals or to arousal threshold;
however, in contrast to the previous conclusions of Klingelhöfer
et al,15 arousals are not the reason for blood flow
reductions.
We focused in our study on single events rather than on episodes or
sleep stages, and this may also explain the difference between our
findings and those of Klingelhöfer et al,15 ie, our
results do not suggest an increase in cerebral blood flow during apneic
events.
If negative intrathoracic pressures are indeed a major cause of the
decrease in MCA blood flow, one would not expect a decrease in MCA
perfusion during central apneas. This conclusion, namely that central
apneas are not associated with changes in cerebral blood flow, was
reached by Rehan et al12 in a study of infants. We observed
that reductions in MCA flow occurred much less frequently in central
than in obstructive events: 14% compared with 70% to 80%. By strict
definition, no inspiratory efforts and thus no negative inspiratory
pressure developments occur during central apneas. However,
misclassification of apnea type can occur in the absence of direct
measures of intrathoracic pressure.27 While such a
misclassification is less likely when both ribcage and abdominal
motions are measured, we acknowledge that upper airway obstructions may
have occurred and could be responsible for reduced MCA blood flow found
in the minority of central events. An alternative explanation is that
the decreased blood flow in a central apnea possibly reflects
hypoxic/hypercapnic cerebral vasodilatation; however, we found only a
weak significant correlation with MCA blood flow and the fall in
arterial oxygen saturation in obstructive hypopneas. This
observation may be influenced by the greater number of hypopneas
analyzed with longer duration and greater fall in
arterial oxygen saturation; in addition, a greater number
of analyzed obstructive apneas with oxygen desaturation would
have led to a stronger correlation between the fall in oxygen
saturation and decreased MCA blood flow.
We were unable to capture enough events to analyze differences
between sleep states. Perhaps with more advanced technology there will
be an opportunity to observe the effect of event type on cerebral blood
flow in regard to REM as well as NREM sleep. There may well be
differences between the two states, given the specific and different
influences of REM sleep on cardiovascular and
neurophysiological function.
Based on our data, one could speculate that patients with central sleep
apneas should have the least risk for the development of stroke, and
those with a predominance of partial upper airway obstruction during
sleep (heavy snoring) would have the greatest risk. Epidemiological
studies like those of Partinen and Palomaki8 and Koskenvuo
et al9 documented a significantly increased risk for stroke
in those with self-reported heavy snoring, but further distinctions in
regard to respiratory events were not available. Others have jumped to
the conclusion that apneas rather than snoring per se are responsible
for the observed associations, but our data suggest that obstructive
hypopneas, the physiological correlate for heavy
snoring, have at least as great or an even greater significance than
either central or obstructive apneas. Individuals with predominantly
central events would be predicted to exhibit less risk for stroke;
however, such individuals are rarely found, except when central apneas
occur in the setting of heart failure. A prospective study would be one
way to determine the relative risk for the development of stroke in
regard to the type of sleep-disordered breathing.
Received July 15, 1997;
revision received October 10, 1997;
accepted October 10, 1997.
© 1998 American Heart Association, Inc.
Original Contributions
Blood Flow of the Middle Cerebral Artery With Sleep-Disordered Breathing
Correlation With Obstructive Hypopneas
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and
Purpose—Epidemiological data link heavy snoring to an increased
risk for stroke, an association often ascribed to hypertension and/or
sleep apnea. The aim of this study was to determine whether obstructive
hypopneas, central apneas, or obstructive apneas during sleep alter
blood flow of the middle cerebral artery (MCA). 
.0001). While duration of events was not
significantly different, MCA blood flow reductions were associated only
with the duration of the obstructive hypopneas (P.01)
and not with the duration of central (P=.17) or
obstructive (P=.07) apneas. The magnitude of fall in
arterial oxygen saturation from baseline correlated with a
reduced blood flow with obstructive hypopneas but not with obstructive
or central apneas.
Key Words: cerebral blood flow • oxygen • sleep apnea syndromes
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The medical
consequences of snoring and sleep apnea syndrome are gaining clinical
recognition for a possible association with systemic
hypertension1 2 3 4 5 and for risk of stroke.6 7 8 9
The theory is that the recurrent periods of asphyxia are the link to
these adverse health events.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Studies were performed in 11 men and 1 woman referred to one
sleep center for evaluation of snoring, disturbed sleep, and daytime
hypersomnolence. Patients were selected with the use of the following
criteria: (1) no disabling cardiopulmonary illnesses, such as
chronic obstructive lung disease, congestive heart failure, or asthma;
(2) presence of central apneas, obstructive apneas, and obstructive
hypopneas on a previous polysomnographic diagnostic study;
and (3) willingness to participate. This study was approved by the
ethics committee of the University of Freiburg, Germany. Consent was
obtained from all patients before the study, as approved by the ethics
committee of the University of Freiburg. 
. As a group, the patients were obese,
with a mean Broca index of 128.5%. Hypertension, defined as a blood
pressure above 140/90 mm Hg, was present in 5 of 12 patients.
There was a range of sleep-disordered breathing; on the average, this
group of patients had a moderately severe sleep apnea syndrome, defined
as an average apnea index above 30/h.
View this table:
[in a new window]
Table 1. Characteristics of 12 Patients With Sleep Apnea
Syndrome ). A significant reduction
in the signal was predetermined to be a 50% reduction in velocity. The
criterion for unacceptable measurements was lack of a flow signal,
usually the result of movement of the harness relative to the head
caused by a change in body position. If this occurred, the probe was
either reset to another one of the sonographic windows or repositioned
to the other temple. Sleep efficiency was predictably disturbed, and
few patients exhibited REM sleep.
View larger version (45K):
[in a new window]
Figure 1. Example of blood flow reduction during and at the
termination of obstructive apnea. EOG indicates electro-oculogram; EMG,
electromyogram; SaO2, oxygen saturation (arterial blood);
chest, motion of the chest wall; abdomen, abdominal motion; and BF,
blood flow velocity. Blood flow velocity is shown as a percentage of
maximum (100%). 
. .05 were
considered statistically significant.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The tables present the number of apneas examined for each
patient in regard to the duration of events (Table 2) and the change in oxygen saturation
with an event (Table 3) in which there
was a technically acceptable blood flow signal recorded along with
all other polysomnographic variables. The tables demonstrate that a
range of event duration and desaturation with events was observed in
each patient but that the number of observations per patient was
limited. There was a difference in regard to the technical ability to
record MCA flow among patients that depended on the Apnea/Hypopnea
Index. With more affected individuals, movements and arousals occurred
more frequently than in those with less sleep disturbances.
Given the selection criteria (see "Subjects and Methods"),
observations were made of all types of events in all patients; however,
given the circumstances of the study, the number of observations per
patient was limited and too small to perform correlations for each
subject or in regard to sleep stage. Very little REM sleep was
observed, and as a result analyses were confined to events in
NREM sleep. There were no differences between patients with or without
hypertension. Thus, results were pooled across all patients according
to event type (obstructive apnea, obstructive hypopnea, or central
apnea).
View this table:
[in a new window]
Table 2. Number of Single Events Analyzed in Each
Patient According to Event Type (Obstructive Apnea, Obstructive
Hypopnea, and Central Apnea) and Duration in Seconds
View this table:
[in a new window]
Table 3. Number of Single Events in Each Single Patient
According to Event Type (Obstructive Apnea, Obstructive Hypopnea and
Central Apnea) and Associated Degree of Oxygen Desaturation (Change in
% SaO2) Occurring With the Event Number , Table 4), but only 13 of 96 central
apneas (14%) showed a reduction in MCA blood flow (Fig 2, Table 4).
This difference in the frequency of a reduced blood flow of the MCA
between central and obstructive apneas and hypopneas was significant.
The level of reduced blood flow during obstructive apneas was not
significantly different from that seen during obstructive
hypopneas.
View larger version (64K):
[in a new window]
Figure 2. Frequency with which decreased blood flow of the
MCA was observed during obstructive (Obstr.) apneas, obstructive
hypopneas, and central apneas. *Significantly different
(P<.0001) from central apneas.
View this table:
[in a new window]
Table 4. Duration of Apneas and Decrease in Oxygen Saturation
From Baseline in 12 Patients With Sleep Apnea Syndrome ). This was not the result of event
length, since the mean duration of events, either associated or not
associated with a reduction in MCA flow, was similar for the hypopneic
events (18.1±6.5 seconds), the central apnea group (17.2±5.9
seconds), and the obstructive apnea group (14.8±5.0 seconds)
(P=.3).
View larger version (11K):
[in a new window]
Figure 3. Frequency of reduced blood flow of the MCA during
123 obstructive apneas (OA), 223 obstructive hypopneas (OH), and 96
central apneas (CA) in relation to the duration (in seconds) of apneas.
*P<.0001 (Friedman two-way ANOVA) in OH;
P<.07 in OA; and P<.17 in CA. ). No such correlation existed for all
events (P=.1) or for obstructive apneas (P=.92)
or central apneas (P=.22) (Fig 4). The mean decline in
oxygen saturation was similar for central apneas (10.3±11.7%),
obstructive hypopneas (8.9±9.7%), and obstructive apneas (7.3±6.8%)
(Table 4). Similar conclusions were reached when we considered only the
events leading to a decreased perfusion of the MCA.
View larger version (12K):
[in a new window]
Figure 4. Frequency of reduced blood flow of the MCA during
123 obstructive apneas (OA), 223 obstructive hypopneas (OH), and 96
central apneas (CA) in relation to the decrease of arterial
oxygen saturation from baseline. *Significant (P<.05)
correlation between frequency of reduced blood flow of MCA and degree
of desaturation.
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
This observational study demonstrates a correlation between
obstructive apneas and hypopneas and the probability of an episodic
reduction in MCA blood flow in NREM sleep. The occurrence of blood flow
reduction increases with the duration of obstructive hypopnea and the
fall in oxygen saturation with obstructive hypopnea. In central apneas,
a reduction in MCA blood flow was less frequent. A reduction in blood
flow occurred during the event and returned to baseline at the
termination of the apnea. ). This real-time
correlation of blood flow with apneic events is not currently possible
to achieve with alternative methods of determining blood flow based on
metabolic tracers or spin resonance imaging. Based on the
data obtained, obstructive apneas and hypopneas compared with central
apneas lead much more frequently to a reduction in cerebral blood flow,
as assessed by the qualitative method of MCA Doppler
ultrasonography, during NREM sleep.
Selected Abbreviations and Acronyms
EEG
=
electroencephalogram, electroencephalography
MCA
=
middle cerebral artery
NREM
=
non–rapid eye movement
REM
=
rapid eye movement
Acknowledgments
We thank Prof Dr Schulte-Mönting, Institute for
Biomathematics, University of Freiburg, for statistical
analysis of our data, and Eugene C. Fletcher, MD, Professor of
Medicine, Louisville, Ky, for his advice and reading of the
manuscript.
Footnotes
Reprint requests to Nikolaus Netzer, MD, Case Western Reserve University, Department of Medicine, Division of Pulmonary and Critical Care Medicine, VA Medical Center 111 J (W), 10701 East Blvd, Cleveland, OH 44106.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  J. M. Golbin, V. K. Somers, and S. M. Caples Obstructive Sleep Apnea, Cardiovascular Disease, and Pulmonary Hypertension Proceedings of the ATS, February 15, 2008; 5(2): 200 - 206. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Ivancev, I. Palada, Z. Valic, A. Obad, D. Bakovic, N. M. Dietz, M. J. Joyner, and Z. Dujic Cerebrovascular reactivity to hypercapnia is unimpaired in breath-hold divers J. Physiol., July 15, 2007; 582(2): 723 - 730. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Munoz, J. Duran-Cantolla, E. Martinez-Vila, J. Gallego, R. Rubio, F. Aizpuru, and G. De La Torre Response to Letter by Lavie and Lavie Stroke, February 1, 2007; 38(2): 250 - 250. [Full Text] [PDF]
|
|
|
|
|
|
C. Selic, M. M. Siccoli, D. M. Hermann, and C. L. Bassetti Blood Pressure Evolution After Acute Ischemic Stroke in Patients With and Without Sleep Apnea Stroke, December 1, 2005; 36(12): 2614 - 2618. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. K. Yaggi, J. Concato, W. N. Kernan, J. H. Lichtman, L. M. Brass, and V. Mohsenin Obstructive Sleep Apnea as a Risk Factor for Stroke and Death. N. Engl. J. Med., November 10, 2005; 353(19): 2034 - 2041. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Parra, A. Arboix, J.M. Montserrat, L. Quinto, S. Bechich, and L. Garcia-Eroles Sleep-related breathing disorders: impact on mortality of cerebrovascular disease Eur. Respir. J., August 1, 2004; 24(2): 267 - 272. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P M Turkington, V Allgar, J Bamford, P Wanklyn, and M W Elliott Effect of upper airway obstruction in acute stroke on functional outcome at 6 months Thorax, May 1, 2004; 59(5): 367 - 371. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. S. M. Shamsuzzaman, B. J. Gersh, and V. K. Somers Obstructive Sleep Apnea: Implications for Cardiac and Vascular Disease JAMA, October 8, 2003; 290(14): 1906 - 1914. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. E. Meadows, H. M. A. Dunroy, M. J. Morrell, and D. R. Corfield Hypercapnic cerebral vascular reactivity is decreased, in humans, during sleep compared with wakefulness J Appl Physiol, June 1, 2003; 94(6): 2197 - 2202. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. o-D. L. Lattimore, D. S. Celermajer, and I. Wilcox Obstructive sleep apnea and cardiovascular disease J. Am. Coll. Cardiol., May 7, 2003; 41(9): 1429 - 1437. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Harbison, G.A. Ford, O.F.W. James, and G.J. Gibson Sleep-disordered breathing following acute stroke QJM, November 1, 2002; 95(11): 741 - 747. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. S.C. Hui, D. K.L. Choy, L. K.S. Wong, F. W.S. Ko, T. S.T. Li, J. Woo, and R. Kay Prevalence of Sleep-Disordered Breathing and Continuous Positive Airway Pressure Compliance* : Results in Chinese Patients With First-Ever Ischemic Stroke Chest, September 1, 2002; 122(3): 852 - 860. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Valipour, A.D. McGown, H. Makker, C. O'Sullivan, and S.G. Spiro Some factors affecting cerebral tissue saturation during obstructive sleep apnoea Eur. Respir. J., August 1, 2002; 20(2): 444 - 450. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P.M. Turkington, J. Bamford, P. Wanklyn, and M.W. Elliott Prevalence and Predictors of Upper Airway Obstruction in the First 24 Hours After Acute Stroke Stroke, August 1, 2002; 33(8): 2037 - 2042. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Iranzo, J. Santamaria, J. Berenguer, M. Sanchez, and A. Chamorro Prevalence and clinical importance of sleep apnea in the first night after cerebral infarction Neurology, March 26, 2002; 58(6): 911 - 916. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. S. T. LEUNG and T. DOUGLAS BRADLEY Sleep Apnea and Cardiovascular Disease Am. J. Respir. Crit. Care Med., December 15, 2001; 164(12): 2147 - 2165. [Full Text] [PDF]
|
|
|
|
|
|
T. MOOE, K. A. FRANKLIN, K. HOLMSTROM, T. RABBEN, and U. WIKLUND Sleep-disordered Breathing and Coronary Artery Disease . Long-term Prognosis Am. J. Respir. Crit. Care Med., November 15, 2001; 164(10): 1910 - 1913. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Parra Sleep-disordered breathing and stroke: is there a rationale for treatment? Eur. Respir. J., October 1, 2001; 18(4): 619 - 622. [Full Text] [PDF]
|
|
|
|
 |
|
 M Kamba, Y Inoue, S Higami, Y Suto, T Ogawa, and W Chen Cerebral metabolic impairment in patients with obstructive sleep apnoea: an independent association of obstructive sleep apnoea with white matter change J. Neurol. Neurosurg. Psychiatry, September 1, 2001; 71(3): 334 - 339. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Mohsenin and A. Culebras Sleep-Related Breathing Disorders and Risk of Stroke Editorial Comment : Balancing Sleep and Breathing Stroke, June 1, 2001; 32(6): 1271 - 1278. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.A. Harbison and G.J. Gibson Snoring, sleep apnoea and stroke: chicken or scrambled egg? QJM, October 1, 2000; 93(10): 647 - 654. [Full Text] [PDF]
|
|
|
|
|
|
O. PARRA, A. ARBOIX, S. BECHICH, L. GARCÍA-EROLES, J. M. MONTSERRAT, J. A. LÓPEZ, E. BALLESTER, J. M. GUERRA, and J. J. SOPEÑA Time Course of Sleep-related Breathing Disorders in First-Ever Stroke or Transient Ischemic Attack Am. J. Respir. Crit. Care Med., February 1, 2000; 161(2): 375 - 380. [Abstract] [Full Text]
|
|
|
|
|
|
C. Bassetti and M. Aldrich Night time versus daytime transient ischaemic attack and ischaemic stroke: a prospective study of 110 patients J. Neurol. Neurosurg. Psychiatry, October 1, 1999; 67(4): 463 - 467. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. I. QURESHI, W. CHRISTOPHER WINTER, and D. L. BLIWISE Sleep Fragmentation and Morning Cerebrovasomotor Reactivity to Hypercapnia Am. J. Respir. Crit. Care Med., October 1, 1999; 160(4): 1244 - 1247. [Abstract] [Full Text]
|
|
|
|
|
|
W. D. Leslie, S. Wali, M. Kryger, N. C. Netzer, and K. P. Strohl Blood Flow of the Middle Cerebral Artery With Sleep-Disordered Breathing: Correlation With Obstructive Hypopneas • Response Stroke, January 1, 1999; 30 (1): 188 - 190. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||