SLEEP, Vol. 33, No. 7, 2010
Sensory Function in Children—Tapia et al
CHILDREN WITH THE OBSTRUCTIVE SLEEP APNEA
SYNDROME (OSAS) HAVE UPPER AIRWAY COLLAPSE
AND RESULTANT OBSTRUCTIVE APNEA DURING
sleep. This is the consequence of an imbalance between the upper
airway structural load due to factors such as adenotonsillar hy-
pertrophy, and upper airway neuromotor tone.1-3 The pharyngeal
subatmospheric pressure, hypoxemia, and hypercapnia generated
during these apneic episodes4 may activate the dilatory muscles
of the upper airway, resulting in the reopening of the airway and
termination of the obstructive apnea.3,5,6
Upper airway mucosal sensory receptors may have a role in
the termination of an apnea by mediating upper airway tone.7-10
Previous studies in adults have demonstrated that attenuation of
upper airway mucosal sensation by topical anesthesia increases
the tendency to airway collapse.9,11 Furthermore, upper airway
anesthesia also induces apneas and hypopneas during sleep in
normal subjects8 and increases the frequency of obstructive
events in snorers.7,10 The findings of these studies suggest that
impairment of upper airway mucosal sensory function could
contribute to upper airway collapse during sleep. In addition,
previous studies performed in adult subjects have demonstrated
impaired mucosal sensory function in subjects with OSAS.12-16
However, it is unknown whether children with OSAS have im-
paired upper airway sensory function.
Huang et al. recently analyzed cortical processing of afferent
respiratory information by measuring respiratory-related evoked
potentials during sleep in children with OSAS and controls.17
They found blunted respiratory-related evoked potentials re-
sponses in children with OSAS, indicative of impaired afferent
processing. This may be due to impaired upper airway sensation.
Hence, we hypothesized that children with OSAS had dimin-
ished airway mucosal sensation during wakefulness compared
to controls. We therefore studied sensory function in the upper
airway of children with OSAS compared to normal age-, gen-
der-, and BMI-matched controls. Specifically, two-point dis-
crimination during wakefulness was determined in the upper
airway of subjects with OSAS compared to controls.
MATERIAL AND METHODS
Children between 6-16 years of age were included. The
younger age limit was selected to exclude children who could
not understand and cooperate with testing. The older age limit
was chosen to avoid overlap with adult OSAS. Patients with
OSAS were recruited from the Sleep Center at The Children’s
Hospital of Philadelphia following a recent clinical polysom-
nogram. Normal controls were recruited from the general com-
munity by means of advertisements. For screening purposes,
controls completed the validated Pediatric Sleep Questionnaire18
to exclude those with suspected sleep disordered breathing.
Those who passed the screening underwent a polysomnogram
to ensure normalcy. Other exclusion criteria for OSAS and con-
UPPER AIRWAY SENSORY FUNCTION IN CHILDREN WITH OSAS
Upper Airway Sensory Function in Children with Obstructive Sleep Apnea
Ignacio E. Tapia, MD; Preetam Bandla, MD; Joel Traylor, RPSGT; Laurie Karamessinis, CCRC; Jingtao Huang, PhD; Carole L. Marcus, MBBCh
Sleep Center, The Children’s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA
Study Objectives: Children with the obstructive sleep apnea syndrome (OSAS) have impaired responses to hypercapnia, subatmospheric pres-
sure, and inspiratory resistive loading during sleep. This may be due, in part, to an impairment in the afferent limb of the upper airway sensory
pathway. Therefore, we hypothesized that children with OSAS had diminished upper airway sensation compared to controls.
Setting: Academic hospital
Participants: Subjects with OSAS aged 6-16 years, and age- and BMI-matched controls.
Interventions: Two-point discrimination (TPD) was measured during wakefulness with modified calipers in the anterior tongue, right interior cheek,
and hard palate.
Results: Thirteen children with OSAS and 9 controls were tested. The age (mean ± SD) for OSAS and controls was 11 ± 4 vs. 13 ± 2 years (NS);
OSAS BMI Z score 2.4 ± 0.5, controls 2.2 ± 0.5 (NS); OSAS apnea hypopnea index 31 ± 48, controls 0.4 ± 0.5 events/hour (P < 0.001). Children
with OSAS had impaired TPD in the anterior tongue (median [range]) = 9 [3–14] mm, controls 3 [1–7], P = 0.002) and hard palate (OSAS 6 [3–9]
mm, controls 3 [1–4], P < 0.001). TPD in the cheek was similar between the groups (P = 0.12).
Conclusion: TPD in the anterior tongue and hard palate was impaired in children with OSAS during wakefulness. We speculate that this impair-
ment might be due to a primary sensory function abnormality or secondary to nerve damage and/or hypoxemia caused by OSAS. Further studies
after treatment of OSAS are needed.
Keywords: Two-point, discrimination, palate
Citation: Tapia IE; Bandla P; Traylor J; Karamessinis L; Huang J; Marcus CL. Upper airway sensory function in children with obstructive sleep
apnea syndrome. SLEEP 2010;33(7):968-972.
Submitted for publication August, 2009
Submitted in final revised form December, 2009
Accepted for publication January, 2010
Address correspondence to: Carole L. Marcus, MBBCh, The Children’s
Hospital of Philadelphia, Pulmonary Division, 5th floor Wood, 34th & Civic
Center Blvd, Philadelphia, PA 19104; Tel: (267) 426-5842; Fax: (215) 590-
3500; E-mail: firstname.lastname@example.org
SLEEP, Vol. 33, No. 7, 2010
Sensory Function in Children—Tapia et al
trols included significant medical conditions other than OSAS,
medications that could interfere with sensory perception (such
as benzodiazepines and opiates), and a history of upper airway
surgery. The control and OSAS groups were matched for age,
gender, and BMI z-scores. The Institutional Review Board of
The Children’s Hospital of Philadelphia approved the study.
Informed consent was obtained from the parents/guardians of
subjects, and assent from the children.
Subjects were studied in the sleep laboratory at The Children’s
Hospital of Philadelphia as previously described.19 Polysomnog-
raphy data were digitally recorded using Rembrandt (Medcare,
Buffalo, NY). The electroencephalogram was recorded using
scalp electrodes (C3/A2, C4/A1, O1/A2, and O2/A1), and right
and left electroculograms were recorded. Muscle tone of the chin
was measured by submental electromyography. Oxyhemoglobin
saturation (SpO2) was measured by pulse oximetry (Masimo Rad-
9, Irvine, CA) that was set at 2-second averaging. Nasal pressure
was measured by cannula (Pro-Tech, Mukilteo, WA). As a back-
up, oronasal airflow was measured by an oronasal thermistor
(Pro-Tech, Mukilteo, WA). End-tidal CO2 was measured by side-
stream sample (Novametrix Medical Systems, Wallingford, CT).
Movements of the chest and abdomen were measured by respi-
ratory inductive plethysmography (SensorMedics, Yorba Linda,
CA). The electrocardiograph was recorded by a modified lead 1.
Leg movements were recorded by electromyography leads placed
over the anterior tibialis muscles of both legs. Sleep stages were
determined by the criteria of Rechtschaffen and Kales.20 Arous-
als were scored according to standards set by the American Sleep
Disorders Association.21 Scoring of respiratory variables was per-
formed on the basis of standards set by the American Thoracic
Society and previously published data on children.22,23 In order to
avoid overlap between groups, subjects with OSAS were included
if they had an apnea hypopnea index (defined as the sum of ob-
structive and mixed apneas and hypopneas, divided by total sleep
time) ≥ 5/hr, and controls were included if their apnea hypopnea
index was ≤ 1.5/hour.24,25
Sensory Function Testing
OSAS and controls underwent two-point discrimination testing
during wakefulness with the child seated comfortably. Two-point
discrimination was tested using the method of limits26 in the pos-
terior hard palate, the buccal mucosa of the right cheek, and the
anterior tongue, using a caliper with smooth, rounded wire tips
(Figure 1). The soft palate was not tested to avoid eliciting a gag
reflex in these young children.27 The cheek was selected as a con-
trol site because it is innervated by the buccal nerve, which is the
only sensory branch of the anterior division of the trigeminal man-
dibular nerve,28 and has not been described as an afferent of the
upper airway negative pressure reflex.29 Testing was performed
under direct visualization with the child opening the mouth and
protruding the tongue without tensing it. Either one or both ends
of the compass were placed in contact with the mucosa for 2 sec-
onds, with sufficient pressure to slightly indent the mucosa with-
out causing bleeding or discomfort. The stimulus was randomly
alternated between 1 and 2 points while establishing the thresh-
old to keep the subject focused. A 10-second rest between each
measurement was provided to prevent extinction. The subject was
instructed to indicate 1 versus 2 points by holding up the appropri-
ate number of fingers. Testing began using the largest inter-prong
distance that spatial constraints allowed, which was decreased by
2-mm increments to the smallest inter-prong distance that the sub-
ject/control could perceive as 2 points. Eighty-two percent of the
children were tested by one observer (I.T.). The testers were not
blinded to the OSAS status of the children.
Statistical analysis was performed with SigmaStat 3.0 (Systat
Software Inc., San Jose, CA). The Kolmogorov-Smirnov test was
used to test for normalcy. Normally distributed data are presented
as mean ± standard deviation (SD). Differences in demographics
and two-point discrimination in the tongue and hard palate be-
tween groups were compared with the unpaired t-test. Differences
in two-point discrimination in the cheek between groups were ex-
amined using the Mann-Whitney rank sum test. A P value < 0.05
was required for significance.
Study Group Characteristics
The subjects’ characteristics are shown in Table 1. Subjects had
moderate to severe OSAS by pediatric standards. As the OSAS
group tended to be obese, equally obese controls were recruited.
Children with OSAS had impaired two-point discrimination in
the anterior tongue (Figure 2). This impairment was even greater
in the palate (Figure 3). However, the degree of two-point dis-
crimination impairment was not influenced by age or severity of
OSAS at either site (Table 2). No difference was found between
OSAS subjects and controls when testing two-point discrimina-
tion in the cheek (P = 0.12). There was no significant difference in
the results based on who tested the subjects.
This study analyzed the sensory function in the upper airway
of children with OSAS and controls. We found that subjects
with OSAS had impaired detection of two-point discrimination
in the tongue and palate compared to age-, gender, and BMI-
matched controls. These findings prove that subjects with OSAS
have impairment in upper airway sensation during wakefulness
at an early age.
The upper airway is a complex neuromuscular area with more
than 30 pairs of muscles responsible for coordinated activities
such as breathing, swallowing, and coughing.30 The role of the
upper airway neuromotor tone in OSAS has been studied during
Figure 1—Two-point discrimination was tested with this modified caliper
with blunted points.
SLEEP, Vol. 33, No. 7, 2010
Sensory Function in Children—Tapia et al
natural sleep by measuring the change in maximal inspiratory air-
flow in response to increasing levels of subatmospheric pressure
applied via a nasal mask.2,7 Normal controls show reflex neuromo-
tor activation, manifested by upper airway dilation in response to
nasal subatmospheric pressure. This helps maintain upper airway
patency in the presence of subatmospheric pressure. In addition,
investigations in adults have shown reduced upper airway muscle
activation, measured by genioglossus electromyography, during
wakefulness13,31 and sleep31 after applying topical anesthesia to
the upper airway. Specifically, the nasal branch of the trigeminal,
facial, vagus, and glossopharyngeal nerves have been described
as the afferent innervation of the upper airway negative pressure
reflex.29 The hypoglossal and glossopharyngeal nerves have been
described as the efferent loop.29 Impairments in both afferent and/
or efferent loops can result in increased upper airway collapsibil-
ity. In the present study the hard palate, tongue, and cheek were
tested. The palate is innervated by the nasopalatine nerve (branch
of the trigeminal) and the anterior palatine nerve (branch of the
facial nerve). The tongue is innervated by the lingual nerve.32,33
The cheek was selected as a control site because it is innervated by
the buccal nerve, which is the only sensory branch of the anterior
division of the trigeminal mandibular nerve,28,34 and has not been
described as an afferent of the upper airway negative pressure re-
flex29 in contrast to the palate and tongue.
Previous studies in children with OSAS have shown impair-
ment of the upper airway dilation reflex response to negative
pressure,2,7 manifested as increased upper airway collapsibility
compared to normal controls during wakefulness35 and sleep.2,7 In
addition, children with OSAS have diminished arousal responses
to hypercapnia,4,36 and inspiratory resistive loading37 but normal
acoustic arousal responses38 during sleep. The hypercapneic re-
sponse and two-point discrimination from the head and face have
different afferent pathways. The ventral trigeminothalamic tract
is the pathway for two-point discrimination from the tested sites.
The main site of CO2 chemoreception is the ventrolateral medulla
oblongata.39 Specifically, the cholinergic muscarinic receptors
found in this brainstem area appear to have an important modula-
tory role on the ventilatory response to hypercapnia.40 CO2-sensi-
tive neurons have been found in other areas of the brain but their
role in hypercapneic response is still unclear.39,41 Therefore, it is
Figure 2—Two-point discrimination in the tongue for children with
obstructive sleep apnea syndrome (OSAS) compared to controls. The Y
axis represents the inter-prong distance in mm. The box represents the
interquantile range; the central line represents the median; the whiskers
represent the 5th and 95th percentiles; and the dots represent the outliers.
Subjects with OSAS had decreased two-point discrimination compared to
controls (P = 0.002).
Two point discrimination (mm)
P = 0.002
Table 1—Study group characteristics
11 ± 4
2.4 ± 0.5
80 ± 12
23 ± 16
10 ± 5
50 ± 12
23 ± 12
17 ± 6
31 ± 48
82 ± 9
13 ± 2
2.2 ± 0.5
86 ± 6
15 ± 10
7 ± 4
50 ± 5
23 ± 9
20 ± 4
0.4 ± 0.5
94 ± 2
Males (N (%))
Sleep efficiency (%TST)
Arousal index (N/hour)
Stage 1 (% TST)
Stage 2 (% TST)
SWS (% TST)
REM (% TST)
SpO2 nadir (%)
Values are displayed as mean ± SD. BMI, body mass index; AHI,
apnea hypopnea index; TST, total sleep time; SWS, slow wave sleep;
SpO2, oxyhemoglobin saturation
Figure 3—Two-point discrimination in anterior palate for children with
the obstructive sleep apnea syndrome (OSAS) compared to controls.
The Y axis represents the inter-prong distance in mm. The box is the
interquantile range; the central line is the median; the whiskers are the
5th and 95th percentiles; and the dots are the outliers. The two-point
discrimination in the palate was impaired in OSAS subjects compared to
controls with a P value lower than 0.001.
Two-point discrimination (mm)
P < 0.001
Table 2—Pearson correlation coefficient results between two-point
discrimination in the tongue and hard palate vs. age and AHI
TPD, two-point discrimination; AHI, apnea hypopnea index
SLEEP, Vol. 33, No. 7, 2010
Sensory Function in Children—Tapia et al
possible gagging, all of our subjects could be tested without is-
sues following standard and reproducible methods.26,56,57 Stimuli
were presented in a random order to ensure that results were not
affected by potential observer’s bias, the child’s behavior, or at-
tention span. Children tolerated the testing well. Specifically, no
gag reflex was elicited in any subject. Similarly, the difference in
TPD in tongue and palate between the groups cannot be explained
by cognitive impairment in OSAS subjects,58-60 because otherwise
we would have found differences in the control site as well.
This study has shown that children with OSAS have impaired
two-point discrimination perception in the tongue and palate com-
pared to age-, gender-, and BMI-matched normal controls despite
a relatively short duration of OSAS. However, it is unknown
whether the findings are secondary to a congenital abnormality
of sensory perception or secondary to selective nerve damage due
to chronic snoring and possibly mouth breathing. Further studies
post-treatment are needed to clarify the pathophysiology of the
upper sensory function in children with OSAS.
OSAS, obstructive sleep apnea syndrome
TPD, two-point discrimination
AHI, apnea hypopnea index
The authors thank the children participating in this study
and their families, and the sleep laboratory technicians for their
invaluable help. This research was supported by the National
Institutes of Health R01 HL58585.
This was not an industry supported study. Dr. Marcus has re-
ceived research support from Respironics. The other authors have
indicated no financial conflicts of interest.
1. Brooks LJ, Stephens BM, Bacevice AM. Adenoid size is related to sever-
ity but not the number of episodes of obstructive apnea in children. J
2. Marcus CL, McColley SA, Carroll JL, Loughlin GM, Smith PL, Schwartz
AR. Upper airway collapsibility in children with obstructive sleep apnea
syndrome. J Appl Physiol 1994;77:918-24.
3. Katz ES, Marcus CL, White DP. Influence of airway pressure on genio-
glossus activity during sleep in normal children. Am J Respir Crit Care
4. Marcus CL, Lutz J, Carroll JL, Bamford O. Arousal and ventilatory re-
sponses during sleep in children with obstructive sleep apnea. J Appl
5. Marcus CL, Katz ES, Lutz J, Black CA, Galster P, Carson KA. Upper
airway dynamic responses in children with the obstructive sleep apnea
syndrome. Pediatr Res 2005;57:99-107.
6. Marcus CL, Fernandes Do Prado LB, Lutz J, et al. Developmental chang-
es in upper airway dynamics. J Appl Physiol 2004;97:98-108.
7. Chadwick GA, Crowley P, Fitzgerald MX, O’Regan RG, McNicholas
WT. Obstructive sleep apnea following topical oropharyngeal anesthesia
in loud snorers. Am Rev Respir Dis 1991;143:810-3.
8. McNicholas WT, Coffey M, McDonnell T, O’Regan R, Fitzgerald MX.
Upper airway obstruction during sleep in normal subjects after selective
topical oropharyngeal anesthesia. Am Rev Respir Dis 1987;135:1316-9.
9. DeWeese EL, Sullivan TY. Effects of upper airway anesthesia on pharyn-
geal patency during sleep. J Appl Physiol 1988;64:1346-53.
reasonable to infer that the central integration of different respi-
ratory afferent inputs may be defective in subjects with OSAS,
rather than the afferent receptors themselves. Furthermore, Huang
et al. recently demonstrated blunted respiratory-related evoked
potentials response during sleep in OSAS indicative of impaired
afferent processing.19 Further research is warranted.
Obesity and overweight were not inclusion criteria of the
present study; however, it was not surprising that the mean BMI
Z-score in our OSAS group was 2.4 because the prevalence and
severity of pediatric obesity has increased significantly over the
past decades, all over the world.42 In the United States, the preva-
lence of overweight children aged 6 to 11 years doubled between
1980 and 2000. During the same period of time, the prevalence
of overweight children aged 12 to 17 years tripled.43,44 Further-
more, recent publications have stressed the role of obesity as a
risk factor for OSAS in children.45-47 Specifically, Redline et al.
found that obese children were 4-5 times most likely to have
sleep disordered breathing.48
To our knowledge, there are no publications analyzing the
effects of obesity on the sensory function in the upper airway.
However, Horner et al. demonstrated that obese adults have large
deposits of fat in the soft palate and fat streaks in the tongue.49
Nevertheless, the impaired sensation noted in the children with
OSAS in the current study was not due to obesity alone, as the
controls were equally obese. Furthermore, in the current study,
children with OSAS had decreased sensation in the hard palate
as well as the tongue, although fat is not usually deposited in the
The palate TPD results are in agreement with those reported
in adults by Kimoff,12 Guilleminault,13 and Jobin,14 which could
suggest that a selective deficit in upper airway sensory perception
can be present even after the relatively shorter duration of OSAS
in children. A sensory neuropathy in the upper airway of adult
patients with OSAS has been described by Friberg et al.50-52 They
reported signs of neurogenic damage in palatopharyngeal muscle
biopsies of adults with OSAS that were more severe in those with
more severe OSAS. However it is still unknown whether this find-
ing is secondary to vibrational nerve damage or to a more general-
ized neurologic disorder or is a combination of both. Moreover,
the sole publication analyzing palatopharyngeal muscle biopsies
in children with OSAS compared to normal controls and snor-
ers failed to find histopathological differences between the three
groups, although the techniques used cannot eliminate the pres-
ence of a neuropathy.53 Hence, the etiology of the sensory function
deficit in OSAS has yet to be clarified.
The limitations of the present study include the unknown
duration of OSAS because families could not describe an accu-
rate time of onset of symptoms. In addition, the clinical history
has proved to be of limited value in the diagnosis of childhood
OSAS.54 Another limitation to be considered is that psychophysi-
cal methods, such as two-point discrimination testing, require the
active participation of the subject. Therefore, results can be affect-
ed by psychological confounding factors. However, when carried
out accurately and in a standardized manner, these methods can
be as valid as the more invasive neurophysiological techniques.55
Hence, we do not think that subjective issues affected the chil-
dren’s response to upper airway testing. Despite the challenges of
testing two-point discrimination with a caliper in the upper airway
in children, such as spatial constraints, short attention span, and
SLEEP, Vol. 33, No. 7, 2010
Sensory Function in Children—Tapia et al
36. Marcus CL, Gozal D, Arens R, et al. Ventilatory responses during wake-
fulness in children with obstructive sleep apnea. Am J Respir Crit Care
37. Marcus CL, Moreira GA, Bamford O, Lutz J. Response to inspiratory
resistive loading during sleep in normal children and children with ob-
structive apnea. J Appl Physiol 1999;87:1448-54.
38. Moreira GA, Tufik S, Nery LE, et al. Acoustic arousal responses in chil-
dren with obstructive sleep apnea. Pediatr Pulmonol 2005;40:300-5.
39. Mitchell RA, Loeschke HH, Massion WH, Severinghaus JW. Respira-
tory responses mediated through superficial chemosensitive areas on the
medulla. J Appl Physiol 1963;18:523-33.
40. Nattie EE, Wood J, Mega A, Goritski W. Rostral ventrolateral medulla
muscarinic receptor involvement in central ventilatory chemosensitivity.
J Appl Physiol 1989;66:1462-70.
41. Coates EL, Li A, Nattie EE. Widespread sites of brain stem ventilatory
chemoreceptors. J Appl Physiol 1993;75:5-14.
42. Lobstein T, Baur L, Uauy R, TaskForce IIO. Obesity in children and
young people: a crisis in public health. [see comment]. Obes Rev 2004;5
43. Ogden CL, Kuczmarski RJ, Flegal KM, et al. Centers for Disease Control
and Prevention 2000 growth charts for the United States: improvements
to the 1977 National Center for Health Statistics version. [see comment].
44. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends
in overweight among US children and adolescents, 1999-2000.[see com-
ment]. Jama 2002;288:1728-32.
45. Bixler EO, Vgontzas AN, Lin H-M, et al. Sleep disordered breathing in
children in a general population sample: prevalence and risk factors. [see
comment]. Sleep 2009;32:731-6.
46. O’Brien LM, Sitha S, Baur LA, Waters KA. Obesity increases the risk for
persisting obstructive sleep apnea after treatment in children. Int J Pediatr
47. Lam Y-y, Chan EYT, Ng DK, et al. The correlation among obesity, apnea-
hypopnea index, and tonsil size in children. Chest 2006;130:1751-6.
48. Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk
factors for sleep-disordered breathing in children. Associations with
obesity, race, and respiratory problems. Am J Respir Crit Care Med
49. Horner RL, Mohiaddin RH, Lowell DG, et al. Sites and sizes of fat depos-
its around the pharynx in obese patients with obstructive sleep apnoea and
weight matched controls. Eur Respir J 1989;2:613-22.
50. Friberg D. Heavy snorer’s disease: a progressive local neuropathy. Acta
Otolaryngol (Stockh) 1999;119:925-33.
51. Friberg D, Ansved T, Borg K, Carlsson-Nordlander B, Larsson H, Svan-
borg E. Histological indications of a progressive snorers disease in an
upper airway muscle. Am J Respir Crit Care Med 1998;157:586-93.
52. Friberg D, Gazelius B, Hokfelt T, Nordlander B. Abnormal afferent nerve
endings in the soft palatal mucosa of sleep apnoics and habitual snorers.
Regul Pept 1997;71:29-36.
53. Vuono IMD, Zanoteli E, de Oliveira ASB, et al. Histological analysis
of palatopharyngeal muscle from children with snoring and obstructive
sleep apnea syndrome. Int J Pediatr Otorhinolaryngol 2007;71:283-90.
54. Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability
of clinical history to distinguish primary snoring from obstructive sleep
apnea syndrome in children. Chest 1995;108:610-8.
55. Vallbo AB, Johansson RS. Properties of cutaneous mechanoreceptors in
the human hand related to touch sensation. Hum Neurobiol 1984;3:3-14.
56. Shy ME, Frohman EM, So YT, et al. Quantitative sensory testing: re-
port of the Therapeutics and Technology Assessment Subcommittee
of the American Academy of Neurology.[see comment]. Neurology
57. Jacobs R, Wu CH, Goossens K, Van Loven K, Van Hees J, Van Steenber-
ghe D. Oral mucosal versus cutaneous sensory testing: a review of the
literature. J Oral Rehabil 2002;29:923-50.
58. Friedman B-C, Hendeles-Amitai A, Kozminsky E, et al. Adenotonsillec-
tomy improves neurocognitive function in children with obstructive sleep
apnea syndrome. Sleep 2003;26:999-1005.
59. Chervin RD, Ruzicka DL, Giordani BJ, et al. Sleep-disordered breathing,
behavior, and cognition in children before and after adenotonsillectomy.
60. Blunden S, Lushington K, Kennedy D, Martin J, Dawson D. Behavior
and neurocognitive performance in children aged 5-10 years who snore
compared to controls. J Clin Exp Neuropsychol 2000;22:554-68.
10. Litman RS, McDonough JM, Marcus CL, Schwartz AR, Ward DS.
Upper airway collapsibility in anesthetized children. Anesth Analg
11. Fogel RB, Malhotra A, Shea SA, Edwards JK, White DP. Reduced genio-
glossal activity with upper airway anesthesia in awake patients with OSA.
J Appl Physiol 2000;88:1346-54.
12. Kimoff RJ, Sforza E, Champagne V, Ofiara L, Gendron D. Upper airway
sensation in snoring and obstructive sleep apnea.[see comment]. Am J
Respir Crit Care Med 2001;164:250-5.
13. Guilleminault C, Li K, Chen N-H, Poyares D. Two-point palatal discrimi-
nation in patients with upper airway resistance syndrome, obstructive sleep
apnea syndrome, and normal control subjects. Chest 2002;122:866-70.
14. Jobin V, Champagne V, Beauregard J, Charbonneau I, McFarland DH,
Kimoff RJ. Swallowing function and upper airway sensation in obstruc-
tive sleep apnea. J Appl Physiol 2007;102:1587-94.
15. Nguyen ATD, Jobin V, Payne R, Beauregard J, Naor N, Kimoff RJ. Laryn-
geal and velopharyngeal sensory impairment in obstructive sleep apnea.
[see comment]. Sleep 2005;28:585-93.
16. Tun Y, Hida W, Okabe S, et al. Inspiratory effort sensation to added resistive
loading in patients with obstructive sleep apnea. Chest 2000;118:1332-8.
17. Huang J, Colrain IM, Melendres MC, et al. Cortical processing of respira-
tory afferent stimuli during sleep in children with the obstructive sleep
apnea syndrome. Sleep 2008;31:403-10.
18. Chervin RD, Dillon JE, Bassetti C, Ganoczy DA, Pituch KJ. Symp-
toms of sleep disorders, inattention, and hyperactivity in children. Sleep
19. Tapia IE, Karamessinis L, Bandla P, et al. Polysomnographic values in
children undergoing puberty: pediatric vs. adult respiratory rules in ado-
lescents. Sleep 2008;31:1737-44.
20. Rechtschaffen A, Kales. A manual of standardized terminology, tech-
niques and scoring systems for sleep stages on human subjects. Publica-
tion no. 204. Washington, DC: National Institutes of Health 1968.
21. EEG arousals: scoring rules and examples: a preliminary report from the
Sleep Disorders Atlas Task Force of the American Sleep Disorders As-
sociation. Sleep 1992;15:173-84.
22. Standards and indications for cardiopulmonary sleep studies in chil-
dren. American Thoracic Society. Am J Respir Crit Care Med 1996;153:
23. Marcus CL, Omlin KJ, Basinki DJ, et al. Normal polysomnographic
values for children and adolescents. [see comment]. Am Rev Respir Dis
24. Traeger N, Schultz B, Pollock AN, Mason T, Marcus CL, Arens R. Poly-
somnographic values in children 2-9 years old: additional data and review
of the literature. [see comment]. Pediatr Pulmonol 2005;40:22-30.
25. Uliel S, Tauman R, Greenfeld M, Sivan Y. Normal polysomnographic
respiratory values in children and adolescents. [see comment]. Chest
26. Ringel RL, Ewanowski SJ. Oral perception. I. Two-point discrimination.
J Speech Hear Res 1965;8:389-98.
27. Hughes TA, Wiles CM. Palatal and pharyngeal reflexes in health and in
motor neuron disease. J Neurol Neurosurg Psychiatry 1996;61:96-8.
28. Hendy CW, Robinson PP. The sensory distribution of the buccal nerve. Br
J Oral Maxillofac Surg 1994;32:384-6.
29. Horner RL, Innes JA, Holden HB, Guz A. Afferent pathway(s) for pha-
ryngeal dilator reflex to negative pressure in man: a study using upper
airway anaesthesia. J Physiol (Lond) 1991;436:31-44.
30. Arens R, Marcus CL. Pathophysiology of upper airway obstruction: a de-
velopmental perspective. Sleep 2004;27:997-1019.
31. Berry RB, McNellis MI, Kouchi K, Light RW. Upper airway anesthesia
reduces phasic genioglossus activity during sleep apnea. Am J Respir Crit
Care Med 1997;156:127-32.
32. Zur KB, Mu L, Sanders I. Distribution pattern of the human lingual nerve.
Clin Anat 2004;17:88-92.
33. Tamatsu Y, Gasser RF. Development of the sensory nerves to the dorsum
of the tongue in staged human embryos. Clin Anat 2004;17:99-106.
34. Tohma A, Mine K, Tamatsu Y, Shimada K. Communication between
the buccal nerve (V) and facial nerve (VII) in the human face. Ann Anat
35. Gozal D, Burnside MM. Increased upper airway collapsibility in children
with obstructive sleep apnea during wakefulness. [see comment]. Am J
Respir Crit Care Med 2004;169:163-7.