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(Stroke. 1997;28:1765-1772.)
© 1997 American Heart Association, Inc.
Articles |
Sleep-Disordered Breathing in Patients With Acute Supra- and Infratentorial Strokes
A Prospective Study of 39 Patients
From the Departments of Neurology (C.B., M.S.A.) and Neuroradiology (D.Q.), University of Michigan Hospitals, Ann Arbor, Mich.
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose Although recent studies suggest a high prevalence of obstructive sleep apnea (OSA) in patients with acute stroke, a systematic characterization of sleep-disordered breathing based on the severity and topography of stroke has not been performed.
Methods We prospectively studied 39 noncomatose adult subjects (15 women, 24 men; mean age, 57 years) with a first acute stroke. Sleep history, cardiovascular risk factors, stroke severity as estimated by the Scandinavian Stroke Scale, and extent of stroke demonstrated on a computed tomographic or magnetic resonance imaging scan of the brain were assessed. Polysomnography was performed a mean of 10 days (range, 1 to 49 days) after stroke onset. Monitoring of breathing during wakefulness, non–rapid eye movement sleep, and rapid eye movement sleep included measurements of nasal/oral airflow, respiratory effort, and oxygen saturation.
Results Breathing was abnormal during wakefulness in 7 (18%) subjects and during sleep in 26 (67%). Obstructive sleep apnea (apnea-hypopnea index >10) was found in 14 subjects, Cheyne-Stokes–like breathing was observed in 4, and a combination of obstructive sleep apnea and Cheyne-Stokes–like breathing was observed in 7. Sustained tachypnea and ataxic breathing were rare. No significant differences were found in age, body mass index, history of snoring or hypersomnia, or stroke topography or severity between subjects with and without sleep-disordered breathing. Prevalence and severity of breathing disturbances were also similar between patients with supratentorial stroke (n=28) and those with infratentorial (n=11) stroke.
Conclusions Sleep-disordered breathing is frequent in patients with acute stroke, rarely has localizing value, and can also be found in patients with mild neurological deficits. Respiratory disturbances in stroke victims can be explained only in part by topography and extension of acute brain damage.
Key Words: sleep apnea • Cheyne-Stokes breathing • stroke • respiration control
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Breathing is controlled by voluntary (behavioral) and automatic (metabolic) mechanisms that are governed by different although integrated neuronal systems. Voluntary respiration is assured by the cortex and the corticospinal system, whereas automatic respiration depends on hierarchically organized structures in the brainstem that are modulated by supratentorial influences.1 2 During wakefulness, breathing results from an interaction of voluntary and metabolic influences. During the transition from wakefulness to NREM sleep, voluntary control mechanisms abate, and breathing can become unstable with periodic oscillations in breathing amplitude. In NREM sleep, breathing becomes more regular because it is driven only by metabolic demands. During REM sleep, breathing again becomes irregular as an expression of a control system that is activated by the "dysrhythmic" nature of REM sleep.3
Considering the complexity of anatomy and physiology of breathing control, focal brain lesions, including strokes, impair breathing in different ways according to the extension and topography of the lesion. The effects of corticobulbar and corticospinal lesions that selectively affect volitional breathing are evident during wakefulness, as observed in patients with bifrontal, subcortical (capsular), ventral pontine (locked-in syndrome), or ventral medullary strokes.4 5 On the other hand, effects on automatic breathing differ with supra- and infratentorial strokes and may become evident only during sleep. Supratentorial strokes, particularly when bilateral, have been associated with Cheyne-Stokes respiration.6 Infratentorial strokes have been linked with central hyperventilation,4 7 irregular (ataxic or Biot's) breathing,8 apneustic breathing (inspiratory breath holding),9 OSA,10 central sleep apnea, and failure of automatic breathing ("Ondine's curse").11 12
Most studies that have assessed respiratory disturbances in stroke have raised doubts about the localizing value of breathing disturbances.8 13 14 In most investigations, however, breathing was assessed only by impedance pneumography, and recordings during sleep were not systematically performed. More recently, results of a few polysomnographic studies, one of which was performed in our laboratory, have suggested a high prevalence of sleep-disordered breathing in stroke patients.15 16 17 18 However, in these reports, breathing patterns during wakefulness, type of sleep-disordered breathing, clinical stroke severity, and the exact topography of stroke were not specified.
The aim of this study was to perform a detailed analysis of breathing during both wakefulness and sleep and to assess its relation to the severity and topography of stroke in patients with a first acute stroke.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Over a period of 40 weeks conventional polysomnography was performed on 80 adult patients between the ages of 18 and 80 years who were admitted to the University of Michigan Hospitals with acute TIA or ischemic stroke. Patients in stupor or coma and those who were intubated or had critical cardiopulmonary conditions (including unstable heart function, respiratory insufficiency, and pneumonia) were excluded. For this study, we assessed 39 consecutive patients with a first acute ischemic stroke documented by CT or MRI of the brain. Forty-one patients were excluded because they presented with TIA (n=32) or had a previous stroke (n=9). Preliminary data on patients with TIA (n=13) and those with a first stroke or multiple strokes (n=23) are available elsewhere.15
Stroke Assessment
Patients were assessed clinically by one of the authors (C.B.)
within the first 2 days of hospitalization.
Cardiovascular risk factors that were recorded
included family history of stroke, hypertension (defined as a blood
pressure >160/90 mm Hg on at least two occasions before the
stroke), diabetes (fasting glucose level >6.0 mmol/L
before the stroke), hypercholesterolemia
(fasting blood cholesterol >6.5 mmol/L), and
smoking status (yes=current smoking or previous smoking for >10
pack-years). Any history of congestive heart failure and
coronary heart disease was also noted. The maximum stroke
severity was assessed by the SSS.19 A score of <30
indicates severe stroke.20 BMI was calculated as follows:
W/H2, where W=weight (in
kilograms) and H=height (in meters).
Clinical Sleep Assessment
Sleep and wake habits and symptoms preceding stroke were
assessed with a previously validated sleep disorders questionnaire that
includes questions about snoring and daytime sleepiness.21
Snoring was considered to be habitual when it was reported to occur
often or always. Daytime sleepiness was estimated by the
ESS22 and considered excessive when the score was >10.
When a reliable history could not be obtained from a patient because of
aphasia or confusion, information was obtained from relatives.
Stroke Studies
The stroke workup included standard blood tests, 12-lead
electrocardiography, chest x-ray, precranial
and transcranial Doppler ultrasonography, and CT and/or
MRI of the brain. Cerebral angiography was performed in 13 patients,
and echocardiography was performed in 32. Brain
images were reviewed with a standard protocol of evaluation by a
neuroradiologist (D.Q.) blinded to the clinical context. The etiology
of stroke was determined according to the criteria of the Trial of
Acute Stroke Treatment.23
Polysomnography
Polysomnography, performed 10±11 days after stroke (mean±SD;
range, 1 to 49 days), was performed overnight at the patient's bedside
using an 18-channel paper recording system with a paper speed
of 10 mm/s. We recorded eight electroencephalograms, two
electro-oculograms, one chin electromyogram, nasal/oral airflow
(thermistor), chest and abdominal wall excursion, heart rate,
hemoglobin saturation (SaO2), and two tibialis
anterior electromyograms. Sleep stage was scored visually according to
standard criteria.24 Amounts of NREM sleep stages 2
through 4, REM sleep, and total sleep time (NREM sleep stages 1 through
4 plus REM sleep) were calculated and expressed as percentages of
TRT.
Respiratory Analysis
The mean respiratory rate over 5 to 10 epochs of 30 seconds
duration each was calculated from the polygraphic recording
during relaxed wakefulness and during periods of NREM sleep and REM
sleep that were free of respiratory events or arousals. Respiratory
rate in NREM sleep was calculated during the deepest stage reached
during the recording. Apnea was defined as >80% reduction in
nasal/oral airflow lasting 
10 seconds. Hypopnea was scored
when an obvious reduction (usually >20%) in airflow, effort, or both
lasting 10 seconds was accompanied by an arousal or a decrease in
SaO2 of at least 4%. We chose more sensitive
criteria for the recognition of hypop-neas so that we could also
detect subtle breathing disturbances such as upper airway
resistance syndrome. Central apneas were identified by the absence of
respiratory effort during cessation of airflow. The number of apneas
plus hypopneas per hour of sleep was expressed as the AHI, and similar
indexes were calculated for total NREM and total REM sleep (when REM
sleep was >15 minutes) across the night. We also noted the maximum and
average durations of respiratory events, the minimum
SaO2, and the number of oxygen desaturations to
<85%.
Tachypnea was defined as a sustained respiratory rate of >25
breaths/min.13 Breathing was considered irregular or
ataxic when there was an erratic variation in respiratory frequency and
breathing effort with a >50% change in amplitude or
frequency.13 Sleep apnea was diagnosed when the AHI was
10. OSA was diagnosed when >50% of respiratory events were of the
obstructive or mixed type. Central sleep apnea was diagnosed when
50% of respiratory events were of the central type. CSB was defined
as periodic breathing with central apneas or hypopneas alternating with
hyperpnea in a crescendo-decrescendo pattern over at least 10% of the
total sleep time.25
Outcome
Short-term outcome, determined at the time of discharge from the
initial hospitalization, was defined as poor when the patient was still
dependent in terms of activities of daily living.
Statistical Analysis
We used the 
2 test for nominal
variables, the Mann-Whitney U test for ordinal
variables, and the unpaired t test for continuous
variables. All values are expressed as mean±SD. Statistical
significance was set at P<.05.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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There were 15 women and 24 men, with a mean age of 57±15 years (range, 24 to 78 years). Stroke was supratentorial in 28 patients and infratentorial in 11. Habitual snoring was reported in 56% of patients, and 26% of patients experienced excessive daytime sleepiness (ESS score >10) preceding the onset of stroke. Hypertension was present in 59% of patients; diabetes mellitus, in 26%; smoking, in 62%; hypercholesterolemia, in 57%; and increased BMI (>29), in 38%. Three subjects had bilateral strokes. The first patient's stroke was distributed in both anterior cerebral arteries. The second patient had a bilateral stroke at the midbrain level, and the third patient, at the ventrotegmental junction of the upper pons. According to SSS scores, stroke was severe (SSS score <30) in 26% of patients. A presumed stroke etiology was determined in 62% of patients (macroangiopathy, 42%; microangiopathy, 17%; cardioembolism, 12%; and others, 29%). At discharge, 32% of the patients were dependent (poor outcome).
Respiratory Findings
During quiet wakefulness, SaO2 was normal
in all but one patient with a mean value of 94.2±2.4 (range, 88% to
99%), and the respiratory rate was 19±3 breaths/min (range, 11 to 27
breaths/min). Respiratory abnormalities during wakefulness were found
in 7 subjects (18%) and included Cheyne-Stokes–like breathing (n=4),
sustained tachypnea (n=2), and irregular breathing with hiccup in 1
patient with Wallenberg's syndrome (Table 1
).
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During sleep, 26 subjects (67%) had disordered breathing, most
commonly OSA (36%), CSB (10%), or a combination of the two (18%)
(Table 1
). When subjects with and without sleep-disordered breathing
were compared, there were no statistically significant differences in
age (59 versus 52 years, respectively), history of habitual snoring
(62% versus 46%), history of hypersomnia (35% versus 17%), or SSS
score (37 versus 39). A trend (P=.05) toward a higher BMI
was found in patients with sleep breathing disturbances (30.2
versus 25.5). Conversely, the prevalence of sleep-disordered breathing
was similar in patients with and without hypertension. Compared with
patients with a good outcome, those with a poor outcome had a higher
prevalence of breathing disturbances (80% versus 58%,
respectively) and CSB (47% versus 17%), but these differences did not
reach statistical significance. Six of 7 subjects with breathing
abnormalities during wakefulness had a poor outcome. The prevalence and
type of breathing disturbance did not differ significantly
between patients evaluated within 48 hours of stroke onset (n=7) and
those evaluated between the third and seventh day (n=17) or later
(n=15).
OSA
OSA was present in 21 subjects (54%), of whom 7 were women
and 14 were men. Of these 21 subjects, 13 were habitual snorers, and 16
had significant OSA (AHI>20). All 7 subjects who reported both
habitual snoring and excessive daytime sleepiness had significant OSA.
OSA was present in 71% of subjects with bulbar or pseudobulbar
palsy (versus 54% with normal bulbar function) and in 59% of subjects
reporting habitual snoring (versus 47% without habitual snoring). The
SSS score of patients with or without significant OSA was similar (38
versus 40).
CSB
CSB was found during sleep in 11 subjects (Table 2),
and in 4 of these 11, CSB was also
present during wakefulness. In all 11 subjects with CSB, the
pattern was more marked during light NREM sleep, with longer duration
of hypopneas and apneas, and disappeared during REM sleep. Four of the
11 subjects with CSB had moderate to loud snoring during the
recording. In 7 of the 11, CSB was also associated with
obstructive respiratory events, which were often more evident during
REM sleep (Fig 1, a and b). Three of
these 7 were loud snorers. Seven of the 11 subjects had either a
history or the presence (on clinical examination or
echocardiography) of coronary heart disease
or heart failure, and an abnormal left ventricular ejection
fraction (<50%) was found in 5 of 9 subjects in whom
echocardiography was performed. A decreased level
of consciousness was present in the acute phase of stroke in 8 of
the 11 subjects, but only 6 were still somnolent at the time of
polysomnography. Only 2 subjects had a bilateral stroke.
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Sustained Tachypnea
Sustained tachypnea was found in four subjects. In two subjects,
one with a right frontal stroke and one with right pontocerebellar
stroke, tachypnea was present during both wakefulness and sleep. In
the other two, one with a left occipital stroke and one with a left
frontoparietal stroke, respiratory rate was 20 to 25 breaths/min during
wakefulness and >25 breaths/min during sleep. Aspiration pneumonia was
suspected in one subject, and compensated heart failure was present
in two others. One of the four had CSB before tachypnea.
Respiratory Findings According to Topography of Stroke
There were no significant differences between patients with
supratentorial stroke and those with infratentorial
stroke in terms of demographics, cardiovascular risk
factors, history of habitual snoring or hypersomnia, stroke severity,
sleep characteristics, or outcome (Tables 3 and 4).
Patients with infratentorial stroke had a shorter interval to
polysomnography and more severe sleep-disordered breathing in both NREM
and REM sleep than patients with infratentorial stroke. However, these
differences were not statistically significant.
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Supratentorial Stroke
Only 9 of 28 subjects (32%) with
supratentorial stroke had normal breathing. The
prevalence of breathing abnormalities, respiratory rates during
wakefulness and sleep, as well as type and severity of respiratory
disturbances were similar in patients with left-sided (n=15)
and right-sided (n=12) strokes.
Infratentorial Stroke
Three of six subjects with pontine stroke had abnormal breathing.
In a subject with right ventral pontine infarction and no known cardiac
disease, CSB was noted. A second subject with right pontocerebellar
stroke had only sustained tachypnea. A third subject with left
pontomedullary infarction had OSA. All three subjects with dorsolateral
medullary stroke had hiccups while awake and OSA while asleep. Two also
had prolonged desaturations suggestive of hypoventilation during sleep,
and one had irregular (ataxic) breathing during both wakefulness and
sleep. In all three patients, hiccups disappeared with sleep.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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In this prospective study, breathing abnormalities were found in 18% of 39 patients with acute stroke during wakefulness and in 67% during sleep. The higher prevalence of respiratory pattern disturbances (88%) found by Lee et al14 in a similar series of 49 stroke patients studied with impedance pneumography was probably a result of the inclusion of patients with stupor or coma. In both studies, breathing disturbances occurred more frequently during sleep, when potentially compensatory voluntary control mechanisms are inactive.
OSA
OSA was the most common form of sleep-disordered breathing and was
present in 54% of our patients. This confirms the results of
several recently published small studies with mostly selected series of
patients, which reported a 69% to 95% prevalence of OSA in patients
with acute stroke.15 16 17 18 Because the prevalence of OSA is
similar in patients with stroke and TIA,15 in most cases
OSA probably represents a predisposing condition rather than a
result of stroke. Stroke and OSA have several risk factors in common,
including obesity, age, alcohol consumption, and hypertension. In
individual patients, however, OSA may be aggravated or even occur de
novo after a stroke. This may occur as a consequence of bulbar or
pseudobulbar palsy leading to pharyngeal muscle dysfunction. Also,
periodic breathing related to brain damage can lead to a
disproportionate neural output to upper airway and chest wall muscles
and increase upper airway resistance.26 27 28 Finally, sleep
fragmentation related to acute stroke may perpetuate respiratory
instability and aggravate both central and obstructive sleep apnea (see
below).29 According to our results, the absence of
obesity, habitual snoring, hypersomnia, severe clinical deficits, and
pharyngeal dysfunction should not be considered sufficient to rule out
significant OSA (AHI>20) in patients with stroke. Furthermore, the
prevalence of OSA can be expected to be similar in men and
women16 and in supra- as well as infratentorial
strokes.
CSB
CSB was found in 28% of our patients. Because various definitions
of CSB are used in the literature, its frequency differs from one study
to another. Nevertheless, the approximately 50% prevalence reported in
studies monitoring chest and abdominal motions but not
nasal/oral airflow may represent an overestimation of
CSB in patients with periodic obstructive apneas.14 25 In
our experience, OSA and CSB frequently coexist in patients with acute
stroke. These patients often snore loudly, OSA is more pronounced in
REM sleep, and CSB is mostly confined to sleep onset and (light) NREM
sleep stages.30 Since the reports of Cheyne in 1818 and
Jackson in 1895 (see Brown and Plum31 ), CSB has been
linked to both heart failure and bilateral hemispheric strokes. Several
articles in the 1950s and early 1960s emphasized the "neural
theory" of CSB, confirming its association with bilateral
supratentorial strokes and decreased levels of
consciousness.6 31 32 Considering the invariable
presence of respiratory alkalosis, it was suggested that CSB
represents a disinhibited brainstem breathing pattern related
to neurogenic Paco2 hypersensitivity. In our study,
however, only 2 of 11 subjects with CSB had bilateral
supratentorial strokes, and only 6 were somnolent.
Other studies have similarly shown that CSB is frequent in patients
with unilateral and infratentorial acute brain
damage.13 14 Several factors in addition to acute brain
dysfunction may contribute to the high prevalence of CSB in stroke
patients. First, the prevalence of CSB increases with age in healthy
subjects.28 Second, heart failure with prolonged
circulation time can lead to a delayed information transfer from the
lungs to chemoreceptors in the brain and under- and overshooting of
ventilatory responses.33 Although cardiac disease was
present in most of our subjects with CSB, severe heart failure
(left ventricular ejection fraction 
30%) was present
in only 1, confirming the lack of correlation between degree of heart
failure and extent of CSB.34 Third, reduction of lung
volume secondary to obesity or lung disease, both of which are common
in stroke patients, decreases oxygen reserves. Minor variations in
ventilation can then lead to hypoxia, which by means of a
hyperbolic ventilatory response can contribute to breathing
instability. Fourth, frequent sleep stage shifts related to such
factors as pain, coughing, and urinary retention can further add to
ventilatory instability in stroke patients.33 Finally,
cardiopulmonary and sleep abnormalities associated with OSA may
predispose a patient to CSB. This may explain the positive effect of
CPAP on CSB observed in individual patients with CSB.
Sustained Tachypnea
This form of disordered breathing, also called "central
neurogenic hyperventilation," is defined as a metronomically
regular, rapid (>25 to 30 breaths/min) breathing pattern that cannot
be explained by hypoxemia. It was first described in six comatose
patients with bilateral paramedian ventrotegmental pontine
stroke.7 Subsequent studies have suggested that
pulmonary congestion secondary to neurogenic pulmonary
edema may be required to develop central
hyperventilation.35 Sustained tachypnea was rarely
observed in this study, possibly because of the exclusion of comatose
patients. Furthermore, three of our four subjects with increased
respiratory rate had cardiopulmonary abnormalities, and only
one of them had a pontine stroke. Based on the results of our study and
previous studies, central hyperventilation appears to be rare in stroke
patients, particularly in the absence of a decreased level of
consciousness or cardiorespiratory abnormalities. Hence, its localizing
value remains questionable,13 35 36 and, at least in an
awake patient, central hyperventilation is more suggestive of a pontine
neoplasm than a stroke.35 37
Other Classic Brainstem Breathing Abnormalities
Other classic brainstem breathing abnormalities include (1)
apneustic breathing, which was first reported in two patients with
bilateral ventrotegmental stroke in the upper pons9 ; (2)
irregular (ataxic) breathing; and (3) failure of automatic breathing
(Ondine's curse). The latter two breathing patterns have been
described in unilateral or bilateral lateral medullary lesions of
different origin, including stroke.2 11 12 These
respiratory patterns are rare. Only 1 of our 11 subjects with
infratentorial stroke had irregular breathing, and none had apneustic
breathing. Similarly, ataxic breathing and Ondine's curse were not
observed in a previous series of 23 patients with brainstem
infarction.8
Topography of Stroke and Sleep-Disordered Breathing
This study confirms the lack of topographic specificity of most
disturbances of automatic breathing in patients with acute
brain damage. In 49 patients with acute stroke, Lee et
al14 found abnormalities of respiratory patterns in 83%
of patients with unilateral hemispheric stroke, in 89% of those with
bilateral hemispheric stroke, and in all patients with brainstem
stroke. Other reports have confirmed that specific breathing
disturbances can be seen with variable stroke
topography.8 13 25 36 38 Considering the high prevalence
of respiratory abnormalities found in patients with minor neurological
deficits, it appears likely that "neurogenic" mechanisms related
to acute brain damage only partially explain respiratory findings in
acute stroke. An exception to this rule may be medullary strokes, which
appear to be characterized by the association of hiccups with irregular
(ataxic) breathing,13 OSA,10 39 40 and
reduced respiratory drive ranging from central hypoventilation and
central apneas to failure of automatic
breathing.11 12 41 42 The convergence of automatic and
voluntary respiratory control mechanisms in the lower brainstem makes
medullary damage more likely to give rise to primary neurogenic
breathing disturbances.
Disordered Breathing and Stroke Outcome
From a prognostic point of view, we found a trend toward a poorer
short-term functional outcome in patients with disordered breathing. In
particular, the presence of abnormal breathing during wakefulness and
sustained tachypnea13 38 may indicate a more severe
neurological deficit and herald a poor outcome. In patients with OSA
and stroke, Dyken et al16 found an increased 4-year
mortality rate of 20.8%. Similarly, Good et al17 reported
an association between 1-year mortality rate, poor long-term functional
outcome, and number of desaturations during overnight oximetry.
Impaired cerebral blood autoregulation and recurrent hypoxemia may
underlie the negative effect of OSA on cerebral
recovery.43 Also, sudden death secondary to respiratory
arrest has been considered one of the major contributors to the
elevated short-term mortality rate of patients with dorsolateral
medullary stroke.44 45
Study Limitations
First and most importantly, this study lacks an age- and
gender-matched control group with similar risk factors. Nevertheless,
the prevalence of sleep-disordered breathing found in our patients is
much higher than those reported previously by our center and other
centers for normal subjects in a similar age range.15 46
Second, patients with respiratory insufficiency or decreased levels of
consciousness were not included. Hence, the prevalence of
sleep-disordered breathing and particularly central sleep apnea found
in this population may differ somewhat from that of a nonselected
stroke population. Third, sleep studies were usually performed only
once, and the time from stroke onset varied. Although prevalence and
type of breathing disturbance did not differ significantly
between patients evaluated within 48 hours of stroke onset and those
evaluated later, results of repeated testing in individual patients
suggest the possibility of spontaneous improvement of CSB and OSA with
recovery from stroke. How timing of sleep studies may affect the
prevalence and severity of sleep-disordered breathing in stroke
patients therefore remains poorly understood. Fourth, endoesophageal
pressure monitoring, tidal volume measurements, gasometric
analyses, continuous CO2 recordings, and
assessment of ventilatory responses to O2 or
CO2 were not performed. Therefore, the prevalence of
certain respiratory abnormalities may have been underestimated.
Conclusions
Breathing disturbances are frequent in patients with acute
stroke. Assessment of breathing in stroke victims should include
recordings made while the patients is sleeping and monitoring
of both breathing effort and nasal/oral airflow. The lack of
correlation between most forms of sleep-disordered breathing and stroke
topography and severity suggests that neurogenic mechanisms related to
acute brain damage only partially account for the observed respiratory
abnormalities. Further studies are needed to assess the clinical
significance of disordered breathing with respect to treatment and
long-term prognosis of patients with acute stroke.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This research was supported in part by the Schweizerische Stiftung für medinisch-biologische Stipendien, the Roche Research Foundation, and the National Institute of Alcohol Abuse and Alcoholism (grant AA07378).
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Footnotes |
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Reprint requests to C. Bassetti, MD, Department of Neurology, University Hospital, Inselspital, 3010 Bern, Switzerland.
Received February 5, 1997; revision received May 8, 1997; accepted May 9, 1997.
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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