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M. J. Aw and S. J. Kilty
86. Au J, Rudmik L.Cost of outpatient endoscopic sinus
surgery from the perspective of the Canadian government: a time-driven activity-based costing approach.
Int Forum Allergy Rhinol. 2013;3(9):748–54. https://
doi.org/10.1002/alr.21181.
87. Anderson WC, Szeer SJ. Cost-effectiveness and
comparative effectiveness of biologic therapy for
asthma: to biologic or not to biologic? Ann Allergy
Asthma Immunol. 2019;122(4):367–72. https://doi.
org/10.1016/j.anai.2019.01.018.
88. Scangas GA, Wu AW, Ting JY, et al. Cost utility
analysis of dupilumab versus endoscopic sinus surgery for chronic rhinosinusitis with nasal polyps.
Laryngoscope. 2021;131(1):E26–33. https://doi.
org/10.1002/lary.28648.
89. Patel GB, Peters AT. The role of biologics in
chronic rhinosinusitis with nasal polyps. Ear
Nose Throat J. 2021;100(1):44–7. https://doi.
org/10.1177/0145561320964653.
Nasal NO andIts Role
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inthePhysiology oftheNose
andDiagnosis
PeterW.Hellings andGlenisK.Scadding
11
Core Messages
• NO is a gas primarily produced within the
paranasal sinus cavities, playing a role in airway homeostasis.
• Nasal NO levels may be normal, increased, or
decreased in upper airway diseases.
• Nasal NO represents a screening test for primary ciliary dyskinesia.
11.1 Introduction
Since the last decade, growing attention has been
paid to nitric oxide (NO) as a noninvasive marker
of inammation of the airways. Exhaled NO
(eNO) measurement has become a routine diagnostic tool in monitoring lower airway inammation since it had been shown to be a noninvasive
parameter for monitoring lower airway inammation [1]. However, most of the NO is being
produced in the sinonasal cavities, without clear
insight into its precise role in upper airway
homeostasis. Nasal NO (nNO) may be involved
in the innate antibacterial effects of the airway
P. W. Hellings (*)
Department of Otorhinolaryngology, Head and Neck
Surgery, University Hospitals Leuven,
Leuven, Belgium
e-mail: peter.hellings@uz.kuleuven.ac.be
G. K. Scadding
Department of Allergy and Rhinology, Royal
National Throat, Nose and Ear Hospital, London, UK
mucosa, regulation of ciliary beat frequency, and/
or local regulation of blood ow. In addition,
nNO is believed to contribute to lower airway
homeostasis. The measurement of nNO is nowadays a good screening test for primary ciliary
dyskinesia and, therefore, has diagnostic value.
11.2 Nitric Oxide (NO)
Nitric oxide (NO) is a colorless and odorless gas
that is present in the air exhaled through the
mouth or nose. NO is produced from arginine and
oxygen by nitric oxide synthase (NOS) [2].
Constitutively expressed neuronal and endothelial forms exist as well as an induced form, iNOS,
which appears to be upregulated within the respiratory tract in response to pro-inammatory signals. NO came to prominence for its role in
vasodilatation and subsequently as a neurotransmitter and inammatory mediator. The role of
NO in the airways is complex [3], possibly
including antibacterial effects, pro-inammatory
effects, and regulation of blood ow and ciliary
beat frequency. Exhaled NO (eNO) levels are
raised in eosinophilic asthma, and measurement
of this has become a standardized, but not yet
widespread, tool in the diagnosis and management of asthma. It can potentially provide a rapid,
low-cost, objective measure of lower airway
inammation.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
Ö. Ö. Celebi, T. M. Önerci (eds.), Nasal Physiology and Pathophysiology of Nasal Disorders,
https://doi.org/10.1007/978-3-031-12386-3_11
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P. W. Hellings and G. K. Scadding
Far greater levels of NO are produced in the
upper than in the lower respiratory tract, with
major contributions from the sinuses and to a
lesser extent from the nasal mucosa.
11.3 Nasal NO
Measurement of nNO represents a useful tool for
research purposes as well as for screening for
PCD [4]. Nasal nitric oxide may be normal,
raised, or lowered in disease states. However, its
measurement may be a useful tool in the diagnosis and management of patients with chronic rhinosinusitis, nasal polyps, and CF, as well as in the
diagnosis of PCD [4]. Levels of nNO may follow
the clinical changes after medical as well as surgical treatment in patients with CRS with/without nasal polyps [4].
Measuring both bronchial and nasal nitric
oxide may assist the combined management of
upper and lower airways, but is not routinely performed in clinical practice so far.
High levels of NO are produced constitutively
in normal individuals within the paranasal sinuses
by calcium-independent nitric oxide synthase,
with levels measured at 20–25ppb. Additionally,
nitric oxide is also formed in the nasal mucosa by
inducible NOS (iNOS) in response to inammation. NO and its metabolites are toxic to microorganisms and likely form part of the innate defense
mechanism of the respiratory tract. NO may also
stimulate cilia beat frequency within the epithelium and regulate nasal vascular tone.
11.4 Technique
forMeasuringnNO
As for exhaled NO (eNO), nNO can also be measured by chemiluminescence, using noninvasive
techniques, providing immediate results. A number of different techniques have been used to
ensure sampling from the upper airways only
including breath holding and breathing against
resistance.
In contrast to measuring eNO, high baseline
levels in nNO make background environmental
NO levels less of a problem. Conversely, there is a
high degree of interindividual variability among
healthy controls. Moreover, there is also a signicant degree of intraindividual variation over time,
meaning that changes of 20–25% or less may be
accounted for by normal variation rather than a
change in disease status or response to medication
[5]. Additionally, the lack of universal standardization of testing procedures means that levels
recorded by different study groups vary considerably even among equivalent patient populations.
The factors affecting eNO levels such as recent
exercise or time of day may similarly affect nNO
measurements. Local factors such as nasal volume
and patency may also be important.
11.5 Value ofnNO Measurement
inClinical Practice
Despite the above limitations, nNO has a number
of potentially useful clinical applications. With
regard to diagnosis, nNO is useful as a screening
tool for patients with possible PCD; levels less
than 100ppb, particularly if these persist following decongestion, should stimulate investigation
of mucociliary structure and function. The test is
objective and may be easier to perform than a
saccharine clearance test in younger children.
Similarly, nNO may provide a useful tool in the
diagnosis of CF in the context of upper respiratory tract symptoms; levels signicantly lower
than in controls have been reported in some studies, but not others. nNO has a potential role in the
diagnosis and assessment of CRS, especially
when associated with NP. Interestingly, despite
the increased expression of iNOS in polyp epithelium, low nNO levels have been found in two
large studies. Moreover, nNO inversely correlated with endoscopic NP size, CT scores, and
clinical severity of the disease. Conversely, in a
study involving chronic rhinosinusitis patients
with and without polyps, no correlation between
nNO and CT scores was found, although patients
were again found to have lower baseline nNO
than controls.
Low nNO levels in chronic rhinosinusitis are
thought to reect obstruction at the sinus ostium
11 Nasal NO andIts Role inthePhysiology oftheNose andDiagnosis
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129
and impairment of gas transfer out from the
sinuses. This is supported by the nding of raised
nNO following medical and surgical treatment of
rhinosinusitis with or without polyps [5].
A number of recent studies have focused on
the possible use of humming to improve the sensitivity of nNO measurements. Weitzberg and
Lundberg found that humming induced a large
increase in nNO [6] and that these increases
were not detected in patients with nasal polyps
and sinus ostium obstruction. Furthermore, they
suggested that the absence of a normal response
to humming during nNO measurement could be
used to identify allergic rhinitis with sinus
ostium obstruction. Whether this adds signicant value to standard testing has yet to be fully
appreciated.
11.6 Diagnosis ofPrimary Ciliary
Dyskinesia (PCD)
In children with rhinosinusitis presenting with
longstanding and persistent anterior rhinorrhea,
one may be interested in the evaluation of the
function of the mucociliary clearance system for
the exclusion of PCD.Normal mucociliary transport is essential for the maintenance of healthy
sinuses. In case of infection with secondary ciliary dysfunction and/or congenital dysfunction of
the cilia like in PCD, the mucociliary transport is
inadequate or has not taken place. In PCD, lack
of mucociliary transport may lead to chronic rhinosinusitis and bronchiectasis. In chronic inammation, mucostasis, hypoxia, microbial products,
and toxic inammatory mediators may induce
secondary ciliary changes like in secondary ciliary dyskinesia (SCD), with inadequate mucociliary transport. The mucociliary transport (MCT)
mechanism ensures the clearance of entrapped
particles in the mucus lining the nasal mucosa
toward the hypopharynx. Several nonabsorbable
substances have been used for the evaluation of
MCT in patients, like saccharin or dyes like
methylene blue. As the MCT can only be measured in cooperative patients with patent nasal
cavities and in the absence of severe mucosal disease, this test has limited diagnostic value due to
its low sensitivity and specicity.
No ideal test is available for the diagnosis of
PCD. In case of suspicion of PCD in a patient
with rhinosinusitis since birth, familial history of
PCD, and associated features of Kartagener syndrome, i.e., situs inversus and infertility, one
should consider diagnostic tests of ciliary function by evaluation of CBF, electron microscopic
evaluation of the dynein arms of the cilia, and/or
evaluation of the cilia after ciliogenesis invitro.
As these techniques are not available in routine
ENT practice, one may rely on measuring nasal
NO levels as low NO levels have been associated
with PCD and therefore represent a good screening tool for PCD.
11.7 Concluding Remarks
Nasal NO measurement represents a useful diagnostic tool in PCD. However, variable baseline
levels of nNO and interindividual variability
make nNO measurement of little value in the
diagnosis and management of uncomplicated
rhinitis.
References
1. Alving K, Weitzberg E, Lundberg JM. Increased
amount of nitric oxide in exhaled air of asthmatics.
Eur Respir J. 1993;6(9):1368–70.
2. Scadding G, Scadding GK.Update on the use of nitric
oxide as a non-invasive measure of airways inamma-
tion. Rhinology. 2009;47:115–20.
3. Scadding G. Nitric oxide in the airways. Curr Opin
Otolaryngol Head Neck Surg. 2007;15(4):258–63.
4. Scadding G, Hellings P, Alobid I, Bachert C, Fokkens
W, van Wijk RG, et al. Diagnostic tools in rhinol-
ogy EAACI position paper. Clin Transl Allergy.
2011;1(1):2.
5. Ragab SM, Lund VJ, Saleh HA, Scadding G.Nasal
nitric oxide in objective evaluation of chronic rhinosi-
nusitis therapy. Allergy. 2006;61(6):717–24.
6. Weitzberg E, Lundberg JO. Humming greatly
increases nasal nitric oxide. Am J Respir Crit Care
Med. 2002;166(2):144–5.
Physiology andPathophysiology
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ofSneezing andItching:
Mechanisms oftheSymptoms
MuratSongu andT.MetinOnerci
12
Core Messages
• Despite its being such a commonplace phenomenon suffered the world over, little is
known about the sneeze reex action, which
sometimes becomes a sign associated with a
series of different medical conditions.
• The sneezing reex may be divided into two
phases. The rst is a nasal or sensitive phase,
following stimulation of the nasal mucosa by
chemical or physical irritants. The efferent or
respiratory phase consists of eye closing, deep
inspiration, and then a forced expiration with
the initial closing of the glottis and increasing
intrapulmonary pressure. The sudden dilatation of the glottis gives rise to an explosive
exit of air through the mouth and nose, washing out mucosal debris and irritants.
• Clinical studies using positron emission
tomography indicate that there is no isolated
itching center in the brain but that there are
different cortical centers which are involved in
the processing of the itch.
• The factors that play role in the etiology of
sneeze reex are rhinitis, photic sneeze reex,
physical stimulants of the trigeminal nerve,
central nervous system pathologies, psychogenic sneezing, snatiation reex, and sexual
ideation.
Sneeze is a coordinated protective respiratory
reex which occurs due to stimulation of the upper
respiratory tract, particularly the nasal cavity [1].
Apparently, activation of the central and peripheral
nervous system plays a major role in the pathophysiology of this process. Sensory nerves of the
afferent trigeminal system including myelinated
Aδ-bers and thin, nonmyelinated C-bers of the
nasal mucosa transmit signals generating sensations, including itching and motor reexes, such as
sneezing. These nerves can be stimulated for various reasons. Sneeze reex frequently accompanies
rhinitis of allergic or nonallergic origin. A sneeze
can also arise due to bright light or sun (ACHOO
syndrome), physical stimulants of the trigeminal
nerve, psychogenic or central nervous system
pathologies, and even due to a full stomach (snatiation reex) or sexual ideation. In this chapter,
we aimed to review the physiology, pathophysiology, etiology, diagnosis, treatment, and complications of sneezing and itching.
M. Songu (*)
Department of Otorhinolaryngology, Biruni
University Faculty of Medicine, İstanbul, Turkey
T. M. Onerci
Department of Otorhinolaryngology, Faculty of
Medicine, Hacettepe University, Ankara, Turkey
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
Ö. Ö. Celebi, T. M. Önerci (eds.), Nasal Physiology and Pathophysiology of Nasal Disorders,
https://doi.org/10.1007/978-3-031-12386-3_12
12.1 Historical Perspective
Sneezing has always been a remarkable sign and
a noteworthy occurrence throughout the history.
In Asia and Europe, the sneezing superstition
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M. Songu and T. M. Onerci
extends through a wide range of race, age, and
country. Homer tells in his epic literary work,
Odysseia, that Penelope rejoiced greatly when
her son Telemachus sneezed when she expressed
a wish. In another part, in Odysseia, the Athenian
General Xenophon gave a dramatic speech
exhorting his fellow soldiers to follow him to
liberty or to death against the Persians. He spoke
for an hour motivating his army and assuring
them a safe return to Athens until a soldier underscored his conclusion with a sneeze. Thinking
that this sneeze was a heavenly favorable sign
from the gods, the whole army sprang to an
attack. Xenophon’s death after the destruction of
his army by the Persians can be considered the
rst complication of sneezing in history.
Hippocrates has mentioned that sneezing is dangerous only prior to or following a pulmonary
disease. Otherwise, it is benecial, even in
patients with fatal illnesses. Celsus of Rome has
suggested that sneezing is evidence of convalescence from illness. Aristotle has proposed that
sneezing is a holy sign since it arises from lungs
which are the principle and most divine parts of
the body [2–4]. The Greeks and the Romans took
sneezing as a sign of wellness and expressed their
good wishes to the person who sneezed using the
phrase “live long” or “May Jupiter bless you.” In
pagan culture, a person who sneezed was believed
to get rid of the devil in his body and was congratulated passionately in every medium. It was
also believed that sneezing made a person’s body
open to invasion by Satan and evil spirits or even
caused part of one’s soul being “thrown out of the
body.” The remnant of this pagan tradition still
exists today in the expression “live a long life” or
“God bless you.” After the pandemics of the
plague in Europe, the view of sneezing changed
and it began to be assumed as a sign of a great
danger. In the fourteenth century, during the great
pandemic of plague, the so-called black death,
Pope Gregory VII declared the sentence “May
God bless you” as a short prayer to be said following every sneeze to protect against the plague
[5]. However, the plague eliminated one third of
the European population since the Pope, or the
powers that be, failed to think of taking measures
in order to protect the public against the disease-
causing rats or the eas, which were the real vectors. This short prayer used in the past by the
Christian population as a protection against disease is now a common everyday expression
which has been passed on to the modern Christian
society as an inheritance [6].
In the Talmud, which consists of religious
texts including the Jewish law and history, it is
considered to be a favorable omen if someone
sneezes while praying. It is a sign that just as God
looks favorably toward him on earth so too will
he look favorably toward him in heaven.
According to a common belief that still exists in
the Republic of China and Japan, if a person
sneezes without a reason, this means that somebody else is talking about him. It is believed that
good things are told about him if he sneezes once
and bad things if twice. In Naples, the person
who sneezes thinks that he is remembered by
another person. In the Indian folkloric culture,
sneezing before starting work is believed to bring
bad luck; therefore, the work is started after a
glass of water is drunk to avoid bad luck [6].
12.2 Physiology
andPathophysiology
The largest part of the nasal cavity and the paranasal sinuses are covered by a multilayered ciliated epithelium in the respiratory region.
Olfactory cells, sustentacular cells, and submucosal adenoids are located on the roof of the
nose including areas of the medial and upper
nasal concha and upper septum in the olfactory
region [7]. The nasal mucosa is covered by a
bilayered secretion lm which is produced by
submucosal adenoidal and goblet cells. This
secretion lm includes a low viscous sol lm in
which cilia move and an apical, highly viscous
gel lm. This specic assembly serves the physiological cleaning of respiratory air through the
mucociliary apparatus. Cholinergic input causes
an increased secretion of the submucosal cells.
However, goblet cell stimulation has also been
shown by substance P (SP) releasing sensory
nerves in a rat model [8]. The cavernous tissue
of the nasal concha consists of venous sinusoids
12 Physiology andPathophysiology ofSneezing andItching: Mechanisms oftheSymptoms
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133
and regulates the respiratory resistance. Filling
of these sinusoids is regulated by sympathetic
stimulation as adrenergic bers are distributed
around arteries, arterioles, and veins of the
human nasal mucosa [7].
The sneezing reex may be divided into two
phases. The rst is a nasal or sensitive phase, following stimulation of the nasal mucosa by chemical or physical irritants. Many distal branches of
trigeminal nerve terminate in the facial skin
transmitting tactile, pain, and temperature sensations, while some branches distribute in the nasal
mucosal epithelium [9]. These branches are
myelinated sensory bers of small diameter
which terminate with receptor endings. Some of
these receptors are triggered by chemical stimuli,
while others are sensitive to tactile and mechanical stimuli [9]. Afferent neural stimuli are transmitted to the trigeminal ganglion via anterior
ethmoidal, posterior nasal, infraorbital, and ophthalmic branches of trigeminal nerve [10]. The
trigeminal nerve is important for the nociceptive
sensory supply of the nasal mucosa in addition to
the face, oral mucosa, cornea, and conjunctiva.
Itching and sneezing are generated by the activation of trigeminal afferent nerve terminals in the
nasal mucosa [11]. These nociceptive nerve bers
consist mainly of two types of bers: the thin
Aδ-bers that mediate acute perceptions with a
quick adaption and activation only during the
actual irritation and the nonmyelinated C-bers
which adapt slowly and communicate dull burning, difcult to locate perceptions, which outlast
acute pain [12]. In allergic rhinitis, immunologically triggered inammation results in the recruitment and activation of both types of bers that
result clinically in itching and sneezing [13].
Clinical studies using positron emission
tomography indicate that there is no isolated itching center in the brain but that there are different
cortical centers which are involved in the processing of the itch [14, 15]. Activation of the
anterior gyrus cinguli, the supplementary motor
cortex, and the inferior parietal lobe partly
explains the connection between itching and the
related reex of scratching [16, 17]. Using functional MRI, the activation of corresponding corti-
cal units following painful trigeminal stimulation
has been shown [18]. In this regard, neuropeptides produced in the cell body of C-ber neurons
can also be transported in granule structures
within the cytoplasm to nerve terminals in the
central nervous system. This leads to “central
sensitization,” a phenomenon associated with the
activation of nociceptive C-bers [19].
Upon reaching a threshold, the second
phase—the efferent or respiratory phase—begins
once a critical number of inspiratory and expiratory neurons have been recruited [20]. This consists of eye closing, deep inspiration, and then a
forced expiration with initial closing of the glottis
and increasing intrapulmonary pressure. The
sudden dilatation of the glottis gives rise to an
explosive exit of air through the mouth and nose,
washing out mucosal debris and irritants. A variety of injuries can occur during a sneeze, especially when a closed-airway sneeze is attempted,
and high Valsalva pressure is transmitted to the
other systems [21]. Setzen and Platt reported 52
unique sneeze-related injuries in the literature
that were categorized into six areas of injury:
intrathoracic, laryngeal/pharyngeal, ocular/
orbital, intracranial/neurological, otologic, and
other.
The number of particles expelled during a
forceful sneeze, of which the sizes range from
0.5–5μm, is estimated to be 40,000. The estimations concerning the speed of a sneeze range
between 150 and 1045km/h (nearly 85% of the
sound velocity) [9]. In present days, scenario of
pandemic of Covid-19 the protective reexes
namely “Sneeze and Cough” have received
great importance but not in terms of protection
but in terms of spread of infection [22]. As the
ow of air during expiration is turbulent, it
causes damage to the Epithelial Lining Fluid
present in the respiratory conduit and also gets
admixed with the saliva in the oropharynx and
oral cavity and mucus in the nose to form droplets of various sizes. The spread of droplet cloud
in sneezing may range to 6m or more as compared to cough hence the concept of 1–2m of
social distancing does not hold good if the
patient is sneezing.
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M. Songu and T. M. Onerci
12.3 Etiology
The factors that play role in the etiology of sneeze
reex are listed in Table12.1.
12.3.1 Rhinitis
It is the inammation of the nasal mucosa causing nasal stufness, rhinorrhea, nasal pruritus,
and sneezing [23].
12.3.1.1 Allergic Rhinitis
Allergic rhinitis is the inammation of the
mucosa lining the nasal cavity in the form of IgEdependent type I hypersensitivity reaction [23].
Allergic rhinitis is a common disorder, which
represents a considerable burden both on individual patients and on society [24, 25]. Itching
and sneezing represent two of the main bothersome symptoms, apart from nasal obstruction
and rhinorrhea in allergic rhinitis [26]. In allergyrelated nasal inammation, it can be demonstrated that especially the neurotransmitter SP is
released by C-bers [13, 27]. SP is signicantly
increased in the nasal lavage of patients with
allergic rhinitis, in contrast to healthy subjects,
which is interpreted as a sustained stimulation of
the sensory system [28]. Exogenically administered SP results in a dose-dependent occurrence
of nasal symptoms in asymptomatic patients with
allergic rhinitis and controls, without elevation of
inammatory mediators. In addition to SP, other
neuropeptides, including calcitonin gene-related
peptide (CGRP) and vasoactive intestinal polypeptide (VIP), are increased in nasal lavage uids
after nasal provocation in allergic rhinitis [29].
An important feature of allergic rhinitis is hyperresponsiveness inuenced by products of the
Table 12.1 Etiology of the sneeze reex
(a) Rhinitis
(b) Photic sneeze reex (ACHOO syndrome)
(c) Physical stimulations of the trigeminal nerve
(d) Central nervous system pathologies
(e) Psychogenic (intractable) sneezing
(f) Snatiation* reex
(g) Sexual ideation or orgasm
allergic reaction including eicosanoids; cytokines
such as IL-6, Il-1β, and TNF-α; and, most importantly, neurotrophins including nerve growth factor (NGF) and brain-derived neurotrophic factor
(BDNF). NGF targets nociceptor bers, leading
to upregulated activity, increased SP content, and
dendrite sprouting [30]. The allergen-induced
increased BDNF expression in the nasal mucosa
signicantly correlated with the maximal increase
of total nasal symptom score in allergic rhinitis
[31] (Fig.12.1).
12.3.1.2 Infectious Rhinitis
In more than 50% of cases, rhinovirus is the
responsible agent for common cold (nasopharyngitis) which is the most common clinical form of
viral infections. Inhalation, close contact with the
infected person, contact with the objects contaminated with the virus such as door handles, school
desks, household goods or phones, are all ways of
contracting the virus. The most common prodromal manifestations include high fever, nasal irritation, and sneezing. Nasal symptoms are also
present in inuenza (u) caused by inuenza
virus; however, they are likely to be overshadowed
by malaise, fatigue, myalgia, and high fever.
Bacteria may inltrate the tissue and cause infections during the course of viral rhinitis due to
impairment of mucosal integrity and ciliary function. Clinical picture of rhinitis may occur during
the course of specic bacterial diseases such as
diphtheria, rhinoscleroma, lepra, tuberculosis,
syphilis, and glanders. Opportunistic fungal infections which develop in AIDS, chemotherapy, prolonged intensive care unit stay, and disorders of
neutrophil number and function such as neutropenia and diabetes may cause rhinitis.
12.3.1.3 Nonallergic Noninfectious
Rhinitis
Every sneezing paroxysm does not mean an allergic rhinitis or common cold. There are also many
rhinitis clinical pictures of unknown etiology that
may cause sneezing and are classied as “nonallergic noninfectious rhinitis.” The commonly
observed clinical pictures in this group are
NARES and vasomotor rhinitis and are usually
confused with allergic rhinitis.
Itching and sneezing
inflammatory cells
12 Physiology andPathophysiology ofSneezing andItching: Mechanisms oftheSymptoms
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Fig. 12.1 Schematic
presentation of the
processes involved in
“neurogenic
inammation” leading to
itching and sneezing.
Activation of afferent
trigeminal C-bers by
several stimuli including
allergen contact may
result in an efferent
liberation of substance P
(SP) and calcitonin
gene-related peptide
(CGRP) via axonal
reex. This further leads
to vasodilatation, edema,
and recruitment/
migration of
inammatory cells
Stimuli
Airway mucosa
Vasodilatation
C-fibers
SP, CGRP
Edema
135
Axonal reflex
Activation of
NARES (Nonallergic Rhinitis
withEosinophilia Syndrome)
It is a nasal hyperreactivity syndrome, manifested
by sneezing paroxysms and watery discharge
followed by nasal stufness and hyposmia in
which the increased eosinophil count exceeds
20% of total leukocyte number in the absence of
an IgE- dependent allergy [32]. The suspected etiology is the inltration of circulating eosinophils
into the site of inammation because of the
increased level of substance P as a result of alterations within the nasal mucosa due to irritation,
senility, or other factors.
Idiopathic (Vasomotor/Nonallergic
andNon-eosinophilic) Rhinitis
It is a short-course hyperreactive nasal mucosal
disease of sudden onset manifested by nasal
stufness, watery nasal discharge or postnasal
drip, and sneezing. Eosinophilia is not found in
nasal secretions and allergy tests are negative.
The most important clinical feature that differentiates vasomotor rhinitis from NARES is the sudden onset of the symptoms which relieve
immediately following the disappearance of triggering factors. Environmental factors including
cold and dry air, high amount of moisture, dyes,
chlorine water, perfume, tangs, cigarette smoke,
exhaust gas, and other inhaled irritants may initiate the symptoms of vasomotor rhinitis. A typical
example is a sudden onset of nasal stufness and
short-lasting though forceful sneezing paroxysm
in the morning time after being exposed to cold
and dry air. Individual factors such as fatigue,
stress, and sexual activity may develop the clinical picture as well [33].
12.3.1.4 Others Causes ofRhinitis
Many other clinical pictures classied as nonallergic and noninfectious rhinitis are also common
causes of sneezing. Occupational rhinitis is the
most commonly observed one among these clinical pictures and is triggered by dense cigarette
smoke, cold air, air fresheners, formaldehyde, and
other chemical irritants in the workplace [32, 34].
Hormonal rhinitis may occur in cases of physiologically increased levels of estrogen such as
puberty, menstrual cycle, and pregnancy or in case
of receiving exogenous estrogen while on oral
contraceptives [32, 35]. Inhibiting acetylcholinesterase activity, estrogen leads to edema formation
in the nasal mucosa while progesterone causes
congestion through vasodilatation in capacitance
vessels and sneezing occurs [36]. As a result of
sympathetic hypoactivity in hypothyroidism, parasympathetic activity relatively increases leading to
vasodilatation in the nasal mucosa and an increase
in secretions. Drug- induced rhinitis may be manifested in two clinical patterns. In medicamentous
rhinitis, many drugs affect nasal mucosa through
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M. Songu and T. M. Onerci
different mechanisms of action and cause sneezing. It is usually observed in treatments with antihypertensive drugs (reserpine, guanethidine,
phentolamine, methyldopa, hydralazine, and prazosin), beta-blockers (propranolol, nadolol), aspirin, and other NSAIDs [37]. Rebound rhinitis, on
the other hand, develops as a result of prolonged
usage of vasoconstrictor drops or sprays [32, 33,
35]. In geriatric rhinitis, atrophy in submucosal
glands due to senility and severe irritation in sensitive nerve endings result in nasal stufness and
sticky and thick mucus which may cause sneezing.
Atrophic rhinitis is a rare pathological condition in
etiology of which bacterial infections, deciency
of vitamin A or D, and iron or estrogen deciencies are suspected. In contrast to clinical conditions concerned, many different factors may
develop irritant-induced rhinitis and cause sneezing [33]. Some of these include dust, smoke, perfume, powder, sharp odor, ammonia, inhalation of
corrosive gases or chemicals, mechanical obstruction of the nasal cavity, chymic irritation due to
cauterization or silver nitrate application, capsaicin, application of airow into superior nasal
meatus by a catheter, and repetitive nasal electrical stimulation [38–40]. Capsaicin, the active
ingredient obtained from hot chili peppers, stimulates the nasal small unmyelinated C-ber afferent nerves to release various tachykinins. These
nerves, with their somata in the trigeminal ganglion, transmit the information to the central nervous system through the trigeminal dorsal horn in
the medulla and lead to sneezing and a sense of
pain [41]. Although various peptides and tachykinins may be involved, it appears that the capsaicin-induced release of substance P is the most
potent trigger of the sneezing response [38, 40].
Capsaicin also precipitates sneezing through a
local axon reex [42].
12.3.2 Photic Sneeze Reex
It seems that some people really do sneeze when
they look at the sun or actually at any bright light
(there is nothing special about the sun). Photic
sneeze reex is also called ACHOO (autosomal
dominant compelling helio-ophthalmic outburst)
syndrome [43]. This reex was rst described in
the medical literature by Sedan in 1954 [44]. It
was shown to have an autosomal dominant inheritance pattern and is assumed to affect 17–35% of
the world population [45]. Photic sneeze reex
has been reported to be present in 23% of medical students [46]. According to a Swedish study,
24% of blood donors experienced sneezing on
visual exposure to strong light [47].
We do not know exactly why this happens, but
it might reect a “crossing” of pathways in the
brain, between pupillary light reex arc and
sneezing reex arc. The reex can be triggered
only after the rst exposure to light, never on
repetitive stimulation, and many reports cite a
refractory period before the reex can be elicited
suggesting that a polysynaptic pathway is
involved. The rst theory concerning the pathways mentioned belongs to Eckhardt etal. who
suggested that stimulation of the optic nerve triggers the trigeminal nerve [48]. The afferent
impulses of pupillary light reex are transmitted
via the optic nerve while the efferent impulses are
transmitted via the oculomotor nerve. According
to this theory, an indirect impulse is transmitted
to the ophthalmic division of the trigeminal
nerve. This impulse generates the nasal stimulation that causes sneezing by affecting the maxillary division of the trigeminal nerve as well. The
second theory of crossing pathways belongs to
Watson. Light falling on the retina stimulates
afferent bers to the pretectal nuclei, which then
send interneurons to the Edinger-Westphal
nuclei. The parasympathetic bers from the
Edinger-Westphal nuclei and the trigeminal afferent bers from the cornea both pass through the
ciliary ganglion, where they may participate in
transmission [49]. Parasympathetic generalization may also contribute to photic sneeze. Stimuli
which excite primarily one branch of the parasympathetic nervous system tend to activate other
branches. Thus, the parasympathetic branches of
the oculomotor nerve which are activated to generate pupillary constriction against the bright
light cause secretion and congestion in the nasal
mucosa by triggering the parasympathetic activation by the pterygopalatine ganglion. This process triggers sneezing [50].
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