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Central sleep apnea and partial obstruction of the upper airway.

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Central Sleep Apnea and Partial
Obstruction of the Upper Airway
Christian Guilleminault, MD, Maria Antonia Quera-Salvi, MD, German Nino-Murcia, MD,
and Markku Partinen, MD
~
~~
Seven men with central sleep apnea underwent polygraphic monitoring during sleep for at least 3 nights, in combination with other tests. Five patients had complaints of disturbed sleep; the other 2 were selected because they had
central sleep apnea caused by bilateral brainstem lesions. The first 5 had a small upper airway, documented by
cephalometric roentgenograms. Nasal continuous positive airway pressure, administered to improve the suspected
respiratory load during sleep, eliminated the central sleep apnea in the first 5 patients but had, as expected, no positive
effect on the central apnea of the 2 patients with brainstem lesions.
Guilleminault C , Quera-Salvh MA, Nino-Murcia G, Partinen M: Central sleep apnea and partial obstruction
of the upper airway. Ann Neurol 21:465-469, 1987
A cessation of breathing during sleep, or apnea, can be
of two major types: central, during which both diaphragmatic and upper respiratory activities cease; and
obstructive, during which air flow stops but diaphragmatic activity continues. A third type, called mixed, is a
combination of the other two apneas. Central apneas
occur in normal humans during rapid eye movement
(REM) sleep. O n the basis of a study of diaphragmatic
apnea during phasic REM sleep in normal humans and
mammals, Orem [9] has hypothesized that this phenomenon in normal individuals is the result of a predominance of phasic inhibition over phasic excitation
of segmental motoneurons.
Central apneas, however, may often signal a pathological condition. Probably related to a temporary failure of the central respiratory pattern generator, they
have been noted in association with specific lesions of
the central nervous system, with cardiovascular disease, with hypoxia of altitude, and with metabolic disorders. Dissociating them from mixed and obstructive
apneas can be accomplished using noninvasive techniques, except in cases of obesity when an endoesophageal pressure transducer or balloon may be
needed.
Here we report the occurrence of central apneas
related to partial upper airway obstruction. The presence of this phenomenon complicates the interpretation of nocturnal polygraphic recordings and makes it
difficult to choose the appropriate treatment for patients with sleep apnea The development of central
sleep apnea secondary to a partial upper airway ob-
From the Sleep Disorders Clinic and Research Center, Stanford
University School of Medicine, Stanford, CA 74305.
Received May 7, 1986, and in revised form July 14 and Aug 15.
Accepted for publication Sept 13, 1986.
struction probably involves several mechanisms, but
using nasal continuous positive airway pressure (nasal
CPAP) [9} as a diagnostic test can help identify this
group of subjects.
Patient Population
Five men, ranging in age from 18 to 7 3 years, were seen over
several years for complaints of a chronic decrease in daytime
alertness (Group A) (Table 1). Patients 1 and 4 had varied
medical histories, but both were intermittent snorers. Patient
1 had retrognathia and was considered a candidate for maxillofacial surgery. Patient 4 was obese (body mass index, 29.2
kg/m2),weighing 110 kg with a height of 194 cm, and had a
mild restrictive lung disease secondary to his obesity. Patients 2 , 3 , and 5 , all of whom were thin and elderly, reported disturbed nocturnal sleep with frequent awakenings
in the early morning (see Table 1).The initial clinical impression was that Patients 1 and 4 fit the diagnostic criteria for
obstructive sleep apnea syndrome, while Patients 2 , 3 , and 5
had insomnia-sleep apnea syndrome of the elderly, probably
associated with central apnea IS}.
Patients 6 and 7 (Group B) were 67 and 71 years of age,
respectively, and had similar medical histories. Both had had
repeated infarctions in the vertebrobasilar vascular region
and multiple brainstem lesions involving oculomotor function and swallowing difficulties.These were manifested in
Patient 6 by tetraparesis and in Patient 7 by bilateral pyramidal signs and predominant left hemiplegia. Both had disturbed nocturnal sleep with very frequent awakenings and
very poor daytime alertness; apnea had been observed during sleep by family members and was noted during clinical
electroencephalographic (EEG) recordings.
Address correspondence to Dr Gwlleminault, Sleep Disorders
Clinic and Research Center, TD 114, Stanford University School of
Medicine, Stanford, CA 74305.
465
Table 1 . Male Subjects witb Predominantly Central Sleep Apnea
No.
Patient
No.
Age
(vr)
Weight
(k)
Height
(cm)
REM
TRT
TST
Sleep
495
480
502
491
480
480
486
480
489
485
480
500
482
478
485
495
480
494
489
480
480
409
369
439
347
298
401
301
269
392
362
331
437
381
322
317
448
404
449
374
324
351
16
14
24
14
12
25
10
8
21
19
15
24
14
12
17
7
9
6
11
No.
Central
Apnea
No. Obstmctive Apnea
Highest
CPAP
Pressure
(cmH20)
1
0
10
10
0
0
0
0
0
0
No.
Mixed
Apnea
No. Desaturations
BeIow8556
No. Desaturations
Below 70%
hwest
O2 Saturation(%)
Type of
Recording
80
78
92
76
79
93
71
75
92
66
69
90
79
80
90
68
70
69
67
71
69
St
EP
CPAP 2
St
EP
CPAP 2
St
EP
CPAP 2
St
EP
CPAP 2
St
EP
CPAP 2
St
EP
CPAP 2
St
EP
CPAI’ 2
~
1
18
79
180
2
73
71
182
3
69
83
184
4
59
110
194
5
66
69
180
6
67
66
179
7
71
68
182
8
10
201
118
2
179
148
4
141
102
33
20
0
29
26
0
0
0
0
209
147
7
193
167
3
319
335
322
297
250
274
48
44
0
3
2
0
6
2
1
2
0
1
0
0
0
0
0
0
2
4
4
0
0
0
0
12
24
0
7.5
47
39
0
10
56
40
12.5
75
49
3
1
0
0
71
72
90
310
301
297
276
227
217
1
0
10
15
15
-
TRT = total recording time in minutes; TST = total sleep time in minutes; REM = rapid eye movement; CPAP = conttnuous positive airway pressure; St = standard
polygraphic recording with noninvasive technique; EP = polygraphic recording with esophageal balloon or pressure transducer.
Methods
Nasal CPAP Monitoring
All 7 subjects underwent a standard polygraphic evaluation
during sleep with noninvasive techniques and a nocturnal
evaluation using nasal CPAP as an investigative tool. The 5
subjects in Group A also underwent a nocturnal evaluation
using an esophageal balloon (4 patients) or a catheter-tip
pressure transducer (Bio-Tec BT5F) (1 patient). Each evaluation consisted of a minimum of 8 nocturnal hours of polygraphic monitoring. Patients in Group A also had a rhinolaryngological examination during which cephalometric
roentgenograms were taken to determine the width of the
upper airway above apd behind the base of the tongue.
The same noninvasive polygraphic variables as those selected
for night 1 of the study were monitored during nocturnal
sleep. Nasal CPAP was applied using the Sleep Easy apparatus (Respironics, Inc, Ivlonroeville, PA) for two consecutive nights. During night I of CPAP testing, positive airway
pressure was progressively increased and the effects on oxygen saturation, the duration and frequency of sleep apnea,
and sleep variables were monitored 1127. On night 2, nasal
CPAP was kept at the optimum pressure determined the
previous night. Patients 2 and 5 had a third night of recording wearing the Sleep Easy nasal CPAP mask but without air
pressure, that is, normal nasal breathing.
Polysomnograpby
The following variables were systematically recorded on a
Grass polygraph at 10 mm/sec paper speed: EEG, C3/A1C4IA2 of the 10-20 international electrode placement system, electrooculogram, chin electromyogram, and electrocardiogram (modified Vz lead). These variables were tabulated
to identify states of alertness and sleep stages. Air flow was
monitored using thermistors at the nostrils and mouth. Respiration was monitored by respiratory inductance plethysmography (RIP), calibrated to a spirometer (Patients 1
through 5, standing up or supine awake) or to thoracic and
abdominal strain gauges (Patients 6 and 7 ) . Oxygen saturation was recorded continuously during sleep using a Biox ear
oximeter (Biox, Inc, Denver, CO).
Polygraphic Recording with Esophageal Balloon
The same polysomnographic testing as described above was
performed; in addition, esophageal pressure changes were
continuously monitored using an endoesophageal balloon (or
a catheter-tip pressure transducer) and a Statham transducer.
466 Annals of Neurology Vol 21 No 5 May 1987
Cephalometric Roentgenogams
These specialized roentge nograms were performed and analyzed following the techniques reviewed by Riley and associates 111) for investigating maxillofacial anomalies as well
as the diameter of the upper airway at the base of the tongue.
Analysis of the Polygraphic Recordings
Sleep and wakefulness were scored by 30-second epochs
{lo), and apneas were scored following commonly used criteria [4). Duration, type, and the lowest oxygen saturation
reached at the end of eitch apneic event were determined.
Central apnea was scored when an absence of air flow of at
least 10 seconds’ duration was associated with an absence of
thoracoabdominal movements in patients monitored with
strain gauges, or decreased tidal volume of less than 100 ml,
in the absence of esophageal pressure changes, in those monitored by RIP. In Patients 1 through 5 (who were monitored
with RIP), 20 apneas ( I 0 in established stage 2 non-REM
[NREM) sleep and 10 in REM sleep) and the four breaths
following each apnea were selected for analysis.
Table 2. Polygraphic Respiratory Data During Sleep
Awake
Arterial Blood Gases
Patient
No.
Po,
PCO,
(mm Hg)
(mm Hg)
pH
Mean
Duration
Apnea, NREM
Sleep (sec)
1
2
89
78
82
74
82
39
36
7.38
7.41
7.40
7.40
7.39
20
22
19
25
21
Mean
Duration
Apnea, REM
Sleep (sec)
~
3
4
5
NREM
=
35
39
37
Mean Minute
Ventilation,
Quiet Awake
Supine (L/min)
~
31
33
29
38
36
~
10.0
8.7
9.0
10.0
11.0
Mean Minute
Ventilation
Following Apnea,
NREM Sleep
(Lirnin)
~
15.0
12.0
13.8
25.0
16.5
Mean Minute
Ventilation
Followidg Apnea,
REM Sleep
(Wmin)
~
14.3
11.7
14.5
26.0
17.0
non-rapid eye movement; REM = rapid eye movement.
Results
As shown in Table 1, all patients had a large number of
central apneas, independent of their initial complaint
and the technique used to monitor respiration. Patients in both groups had few mixed apneas. Mixed
apneas were better detected using the esophageal balloon, as expected, but the difference between the
number of mixed apneas on night 1 (noninvasive monitoring) and night 2 (esophageal balloon monitoring)
was not statistically significant.
Total sleep time on the night with the esophageal
balloon recording procedure was reduced in all patients, but was most severely reduced in Patient 7. This
patient had mild chronic swallowing problems while
awake that were related to the brainstem lesion. A
further swallowing disruption, more frequent coughing, and arousal due to the esophageal balloon occurred at night.
Cephalometric Roentgenogram Results
Patients 1 through 5 had a posterior airway space
(PAS) (defined as space behind the base of the tongue)
smaller than or equal to 7 mm. In Patient 4, soft tissue
had infiltrated markedly into the PAS. Patients 1, 2, 3,
and 5 had abnormal sella-nasion-point A (SNA), sellanasion-point B (SNB), and gnation-goniodsella-nasion
(Gn-Go/SN) angles [l 11, indicating a retropositioned
mandible in conjunction with a malocclusion. Patients
6 and 7 had a normal PAS.
AnaLysis of Sleep Apneic Episodes
In Patients 1 through 5, randomly selected apneic episodes were of similar duration during well-established
stage 2 NREM sleep. The duration of those selected
during REM sleep varied moderately, but the variation
was never longer than 13 seconds (Table 2). Minute
ventilation was calculated from the tidal volume determined by RIP for each of the first four breaths following the apnea. Patient 4 had a significant increase in
minute ventilation following apnea in both NREM and
REM sleep, 26 and 28 L/min, respectively. Since Patient 4 was overweight, the risk of error in measuring
tidal volume with RIP increased, but as this is usually
related to an underestihation of postapneic tidal volume, we do not believe it is an important problem.
The hyperventilation following apnea was absent or
moderate in Patients 1, 2, 3 , and 5 , who had minute
ventilations between 11.7 and 17 L/min.
Nasal CPAP Testing
Nasal CPAP administration in Patients 6 and 7, who
had bilateral brainstem lesions, did not reduce the central sleep apnea syndrome or the sleep apnea-related
oxygen saturation drops. In Patients 1 through 5, on
the other hand, central and mixed sleep apneas and
drops in oxygen saturation , disappeared with nasal
CPAP. In Patients 3 and 5, who slept with the mask on
their face but without applied positive airway pressure
(that is, with skin stimulation but normal atmospheric
breathing), there was no significant difference in the
number of apneas compared to baseline values.
Discussion
The terms periodic breathing and repetitive central apnea
are used to describe sleep-related respiratory phenomena in populations as diverse as premature infants with
breathing problems and adults sleeping at high altitudes [14}. Little consideration is given, however, to
the underlying mechanisms leading to the pauses.
The mechanisms responsible for central sleep apnea
are diverse and can be associated with various physiological conditions. The central apneas seen at sleep
onset have been linked to the shift from wakefulness
to sleep [lo). In some adults, breathing becomes more
periodic during stage 1 and stage 2 NREM and REM
sleep. Elderly subjects are more prone to apneas of all
types [13]. An instability within the respiratory control
system can be linked to most central sleep apneas. A
very different mechanism is responsible for the repetitive central apneas associated with bilateral or high
ventrolateral segmental lesions of the cervical spinal
cord and with lateral tegmental lesions of the pons and
m e d d a C3, 7). It involves destruction of the control
system or impairment of its drive. It has even been
Guilleminault et al: Apnea and Upper Airway Obstruction
467
postulated that obstructive sleep apnea may develop
secondary to periodic breathing or repetitive central
apnea during sleep C1, 2, 8, 141.
In this study, a partial airway occlusion, related to
abnormal upper airway anatomy, was associated with
central apneas. Nasal CPAP, in this case, eliminated
the abnormal breathing pattern during sleep, but, as
expected, had no effect on central apneas secondary to
destruction of the control system 1121. Patient 1, who
responded to nasal CPAP during the acute treatment
trial, had maxillofacial surgery to correct his retrognathia. The subsequent increase in the size of the
upper airway was also associated with disappearance of
the central sleep apnea
To better understand the mechanisms involved in
the development and recurrence throughout nocturnal
sleep of the central apneas noted in Patients 1 through
5, one may consider what factors nasal CPAP and maxillofacial surgery both eliminate which might have an
impact on the sleep-related breathing problems. Maxillofacial surgery alters only the upper airway anatomy.
Nasal CPAP, which also maintains a patent upper airway during sleep, was also successful in eliminating
apnea in our patients, presumably through a similar
mechanism (improvement of upper airway patency
during sleep). This supports the role of an abnormal
upper airway anatomy in the genesis of central apneas.
Our 5 patients in Group A can be compared to children with Pierre Robin syndrome who have repetitive
central apneas during sleep and to 2 women we have
seen previously who developed central sleep apneas
after surgical retroplacement of the lower mandible
161. These cases also emphasize the association of central apneas to a narrow upper airway. In acute experiments, Dempsey and Skauud 121 have shown that
snorers, who often have upper airway narrowing during sleep, have an airway resistance ten times higher at
sleep onset than during wakefulness, compared to a
two- to four-fold increase in normal subjects. They
have also shown that hypoxia during sleep may lead to
respiratory instability with the development of posthyperventilation central apnea when a cluster of hyperpneic breaths is so large that it decreases Pco2 and
drives it below the "apneic threshold" during sleep E21.
Since we did not measure end-tidal C 0 2 in our patients, we can only speculate on the possible C 0 2 decrease that may have occurred during the postapneic
breaths. Patients 2, 3, and 5 were elderly and had low
normal Pco2values (between 35 and 37 mm Hg) during wakefulness. It could be argued that, even with a
mild to moderate increase in minute ventilation after
apnea, the combination of low body mass (with less
COZ storage capability) and the initial low arterial Pco2
with moderate postapnea hyperventilation may be sufficient to trigger the next central apnea. Patient 4
seems to be the most appropriate case to support this
468 Annals of Neurology Vol 21 No 5 May 1987
mechanism as an explanation for the repetitive central
apnea in the presence of a narrow upper airway 12,8].
We believe that, for patients who exhibit a chronic
sleep apnea syndrome, some factors are not emphasized enough in the current proposed models of the
genesis of central and obstructive sleep apneas, most
particularly the impact of upper airway anatomical abnormalities on breathing during sleep. We speculate
that the narrowed upper airway in our patients did
increase their vulnerability to develop sleep apnea.
The impact of chronic upper airway narrowing during
sleep on arousal responses, shifts in states of alertness,
and changes in breathing patterns at sleep onset have
never been appropriately assessed. Upper airway resistance increases with upper airway narrowing. This resistance increases further with the onset of sleep. Anatomical abnormalities are associated with many other
variables that may impair gas exchange. Stimulation of
stretch, mechano-, anld other receptors may be altered
by such factors as upper airway muscle tension, velocity of air flow, and diaphragmatic effects. Narrowing the airway may affect many of these anatomical
changes. We speculate that the anatomical abnormality
located in the upper airway may well be the first step
toward periodic breathing and respiratory instability at
the time of sleep onset. Further investigations of the
role of a narrow upper airway during sleep (that is, the
effect of a chronic respiratory load during sleep) on the
overall central control of ventilation are needed.
Finally, our report has direct clinical relevance: the
presence of a large nimber of central sleep apneas or
mixed sleep apneas with a long central component
does not eliminate the possibility that a partial upper
airway obstruction is responsible for the development
of diaphragmatic sleep apnea. As a correlate, in the
presence of central sleep apnea, one should investigate
the upper airway cliriically (history of bruxism; presence of dental malocclusion; appearance of uvula, soft
palate, palatopharyngeal and palatoglossal arches, tonsils, tongue) and confirm any abnormalities with imaging tests (cephalometric roentgenogram or computed
tomographic scan). Atlministering nasal CPAP may be
the best initial test because it may confirm the clinical
suspicion as well as provide effective long-term treatment.
Supported by General Clinical Research Center grant RR 00070,
funded by the National Inxitutes of Health.
We thank Meg Young for her editorial assistance.
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Guilleminault et al: Apnea and Upper Airway Obstruction 469
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