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16 Physiology ofLacrimal Drainage
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189
nation, because the system functions quite well
with the lacrimal sac completely open, as is the
case after dacryocystorhinostomy (DCR). This
shows that the canalicular pump is more important than the sac pump [1].
16.2.5 Flow fromtheSac totheNose
The ow of tears from the sac down through the
duct has been postulated to be a siphoning effect
and a gravitational effect. The fact that tears will
ow through the lacrimal system even when one
is standing on his head, means that it does not
only depend on the gravitational effect but some
other active mechanisms as well. The lling of
the sac and the increasing pressure in the sac
force the tears down through the duct. Each blink
expels the uid through the canaliculi to the sac
and the sac expels the uid to the duct [1].
16.3 Other Factors onTear Flow
16.3.1 Eect ofRespiration
It was postulated that respiration also plays a role
in drainage of tears from the duct into the nose
and that Bernoulli’s principle has some effect on
this function. However, since the duct narrows as
it approaches to the Hasner valve, Bernoulli’s
effect is minimal. On the other hand, after DCR
operation, common canaliculus opens directly
into the nose, and respiration and Bernoulli’s
principle plays a much more important role in
these operated cases [16].
16.3.2 Valves
sac into the canaliculi. This valve is not a real
valve but it functions like a valve because of the
anatomic angulation of the canaliculi and common canaliculus. This valve is especially important after DCR operation to prevent backow of
the tears from the nose into the canaliculi [17].
Although other valves at the punctum, the
ampulla, and at the junction of the nasolacrimal
sac and duct have been described in the literature,
these are mainly mucosal folds and do not have
much function.
16.3.3 Clinical Principles Derived
fromthePhysiologic
Information
The palpebral-canalicular pump mechanism in
lacrimal elimination is the major mechanism.
The canalicular pump is probably more important than the sac pump because following DCR
tears are still drained through the canaliculi to the
nose. In facial nerve paralysis, tears will not drain
into the nose because orbicularis muscle is not
functioning and cannot operate the canalicular
pump although there is a patent opening.
Therefore, the lacrimal canaliculi should be preserved and should not be damaged. Repeated
instrumentation of the lacrimal system or nasolacrimal duct probings may injure the canaliculi
and thus permanently impair lacrimal elimination. It is very difcult to restore scarred brosed
canaliculi. On the other hand, the pressure gradient between the canaliculi and the sac cannot be
produced if the canaliculus is slit open. This
information should caution clinicians against
performing overly aggressive procedures on the
lacrimal outow system [18].
The function of the valves is to prevent or
decrease the retrograde ow of tears and/or air
currents. The most important valve is Hasner
valve which is located at the lower end of the
nasolacrimal duct. Hasner valve prevents air currents from within the nose being drawn up into
the lacrimal duct [1].
Rosenmüller valve is located at the common
internal punctum and prevents backow from the
16.3.4 Role ofAnatomic Vascular
Organization
andtheImportance
ofCavernous Body
The blood vessels residing in nasolacrimal system includes specialized arteries (barrier arteries), venous lacunae (capacitance veins), veins
(throttle veins), and arteriovenous anastomoses.
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A. R. C. Çelebi and Ö. Ö. Celebi
In the physiology of tear outow control, the
cavernous body of the efferent tear ducts is also
signicant. By expanding and decreasing the
size of the cavernous body, the vessels aid in the
closing and opening of the lacrimal passage
lumen [19].
When the barrier arteries (arteries with an
anatomically additional muscular layer) are
opened and the throttle veins (veins with a muscle layer of helically arranged smooth muscle
cells in the tunica media) are closed, expanding
of the cavernous body occurs. However, if the
barrier arteries are closed and the throttle veins
are opened, blood ow to the convoluted venous
lacunae is diminished, allowing blood to ow
out of these veins, resulting in cavernous body
shrinkage and dilation of the lacrimal passage
lumen. When the shunts of the arteriovenous
anastomoses are open, direct blood ow between
arteries and venous lacunae is possible, avoiding
the subepithelially located capillary network and
allowing for rapid lling of venous lacunae. The
specialized blood vessels allow opening and
closing of the lumen of the lacrimal passage,
which is effected by the bulging and subsiding of
the cavernous body, while also controlling tear
outow. Furthermore, it was proposed that the
valves in the lacrimal sac and nasolacrimal duct
mentioned by Rosenmüller, Hanske, Aubaret,
Béraud, Krause, and Taillefer in the past may be
caused by different swelling states of the cavernous body [20].
16.4 Conclusions
There are many factors which are important in
lacrimal drainage system. The palpebralcanalicular pump mechanism in lacrimal elimination is the major mechanism. The canalicular
pump is probably more important than the sac
pump because following DCR tears are still
drained through the canaliculi to the nose.
Damage to the canaliculi should be avoided since
the damage of the canaliculi impairs the lacrimal
elimination. After DCR operation, the physiology changes and some physiologic mechanisms
may play a more important role. Tear elimination
is equivalent through the upper and lower canalicular systems. Therefore, attention should be
given not to damage both the upper and lower
canaliculus (Figs.16.1, 16.2, 16.3, 16.4).
Fig. 16.1 Normal
anatomy of the
nasolacrimal system
(Courtesy of TESAV)
16 Physiology ofLacrimal Drainage
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Fig. 16.2 Schematic
representation of the
nasolacrimal system
(Courtesy of TESAV)
191
Fig. 16.3 The palpebral-canalicular pump mechanism in lacrimal elimination (Courtesy of TESAV)
Fig. 16.4 Sump
syndrome. If the
rhinostomy opening is
made too high during
DCR operation, the
drainage system will not
function properly
(Courtesy of TESAV)
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A. R. C. Çelebi and Ö. Ö. Celebi
References
1. Hurwitz JJ. Physiology of the lacrimal drainage
system. In: Hurwitz JJ, editor. The lacrimal system.
Philadelphia: Lippincott-Raven Publishers; 1996.
p.23–8.
2. Ahl NC, Hill JC.Horner’s muscle and the lacrimal
system. Arch Ophthalmol. 1982;100:488–93.
3. Paulsen F, Thale A, Kohla G, et al. Functional
anatomy of human lacrimal duct epithelium. Anat
Embryol. 1998;198:1–12.
4. Sisler HA. One-way ow in the lacrimal drainage
system: determinants from the basic sciences. Ann
Ophthalmol. 1982;14:76–7.
5. Daubert J, Nik N, Chandeyssoun PA, et al. Tear
ow analysis through the upper and lower systems.
Ophthal Plast Reconstr Surg. 1990;6:193–6.
6. Linberg JV, Moore CA. Symptoms of canalicular
obstruction. Ophthalmology. 1988;95:1077–9.
7. Meyer DR, Antonello A, Linberg JY. Assessment
of tear drainage after canalicular obstruction using
uorescein dye disappearance. Ophthalmology.
1990;97:1370–4.
8. White WL, Glover AT, Buckner AB, et al. Relative
canalicular tear ow as assessed by dacryoscintigraphy. Ophthalmology. 1989;96:167–9.
9. Jones LT.Anatomy of the tear system. Int Ophthalmol
Clin. 1973;13:3–22.
10. Doane MG.Blinking and the mechanics of the lacrimal
drainage system. Ophthalmology. 1981;88:844–51.
11. Becker BB. Tricompartment model of the lacrimal
pump mechanism. Ophthalmology. 1992;99:1139–45.
12. Jones LT. Epiphora. II. Its relation to the anatomic
structures and surgery of the medial canthal region.
Am J Ophthalmol. 1957;43:203–12.
13. Jones LT.Epiphora: its relation to the anatomic structures and surgery of the medial canthal region. Trans
Pac Coast Oto-Ophthalmol Soc. 1956;37:31–46.
14. Jordan DR, Mawn L, Anderson RL.Surgical anatomy
of the ocular Adnexa: a clinical approach. 1st ed. San
Francisco: American Academy of Ophthalmology;
2012. p.30–8.
15. Burkat CN, Hodges RR, Lucarelli MJ, et al.
Physiology of the lacrimal system. In: Tasman W,
Jaeger EA, editors. Duane’s foundations of clinical ophthalmology, vol. 2. Philadelphia: Lippincott
Williams&Wilkins; 2006. Chapter 2a.
16. Nik NA, Hurwitz JJ, Ching SH.The mechanism of
tear ow after DCR and Jones’ tube surgery. Arch
Ophthalmol. 1984;102:1643–6.
17. Corin S, Hurwitz JJ, Jaffer N, Botta EP.The true canalicular angle: a mathematical analysis. Ophthal Plast
Reconstr Surg. 1990;6:42–5.
18. Myron T, Clinton DM.Lacrimal drainage system. In:
Tasman W, Jaeger EA, editors. Duane’s clinical ophthalmology, vol. 4. Philadelphia: Lippincott Williams
& Wilkins; 2006. Chapter 13.
19. Paulsen F, Garreis F, Schicht M, etal. Anatomie und
Physiologie der ableitendenTränenwege [anatomy
and physiology of the nasolacrimal ducts]. HNO.
2016;64:354–66.
20. Paulsen F, Thale A, Hallmann U, etal. The cavernous body of the human efferent tear ducts: function in
tear outow mechanism. Invest Ophthalmol Vis Sci.
2000;41:965–70.
Intranasal Trigeminal Perception
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PhilippeRombaux, CarolineHuart, BasileLandis,
andThomasHummel
17
Core Messages
• Intranasal trigeminal system mediates the sensation of temperature, pressure, perception of
nasal airow during breathing, nociception,
and participates in the chemosensory perception of odorant stimuli.
• Chemosensory perception is not only mediated by free nerve endings in the nasal mucosa
but also by some trigeminal bers in close
contact with solitary chemosensory cells.
• Besides the sensory nerves, the parasympathetic and the orthosympathetic systems play
P. Rombaux (*) · C. Huart
Department of Otorhinolaryngology, Clinique
Universitaires Saint-Luc, Brussels, Belgium
Institute of Neuroscience, Université catholique de
Louvain, Brussels, Belgium
e-mail: philippe.rombaux@saintluc.uclouvain.be
B. Landis
Rhinology-Olfactology Unit, Department of
Otorhinolaryngology- Head and Neck Surgery,
Geneva University Hospitals, Geneva, Switzerland
The Inner Ear and Olfaction Lab, University of
Geneva Faculty of Medicine, Geneva, Switzerland
T. Hummel
Department of Otorhinolaryngology, Smell and Taste
Clinic, University of Dresden Medical School,
Dresden, Germany
e-mail: t.hummel@mail.zih.tu-dresden.de
an important role in the normal physiology of
the nose.
• Testing the intranasal trigeminal function,
both psychophysically and electrophysiologically, is possible and may be used in the
assessment of a patient with a chemosensory
dysfunction.
• Healthy subjects need to have intact trigeminal and olfactory systems to have a full complete picture of the chemosensory stimulus.
• Olfactory and trigeminal systems interact both
at a central and peripheral level.
• In patients with olfactory loss, a compensatory mechanism probably exists between the
olfactory and the trigeminal systems.
17.1 Introduction
The intranasal trigeminal system interacts with
the olfactory system to provide a complete chemosensory perception of the odorant stimuli. The
perception of nasal patency and nasal airow is
also mediated by trigeminal afferents. The trigeminal system is therefore mandatory for both
the chemosensory and the somatosensory perception and nasal mucosa with trigeminal nerve endings needs to be preserved in order to assume
these two functions.
© 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_17
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P. Rombaux et al.
Besides this protective somatosensory function, the intranasal trigeminal system also helps
the global chemosensory perception of the olfactory system. Indeed, most of the odorants stimulate the neural olfactory and intranasal trigeminal
systems [1].
Finally, the intranasal trigeminal system is
also capable of inducing neurogenic inammation
mainly through an axon reex located in the subepithelial level of the nasal mucosa.
The olfactory (cranial nerve I) and the trigeminal (cranial nerve V) systems interact at different
levels and this interaction is essential for the odor
sensation [2]. The olfactory system is more dedicated to identication tasks for hedonicity and
alimentary behavioral, recognition and memory,
behavioral and social comportments than the trigeminal system probably more oriented to protective function and reexes.
17.2 The Nerves oftheNose
Sensory nerve endings from branches of the trigeminal nerve are located in the epithelia of the
nose and sinuses, the eyelids and the cornea, the
oral cavity, and the skin. Fibers from the intranasal trigeminal nerve mediate the tactile sensation
of temperature, pressure, and perception of nasal
airow during breathing and participate in the
chemosensory perception of odorant stimuli.
Trigeminal receptors are located throughout the
epithelia of the nasal mucosa and contribute to
the global perception of odorous stimuli reaching
the nasal fossa and the upper airway.
The nasal cavity is innervated by two
branches of the trigeminal nerves, i.e., the ophthalmic and the maxillary branches. The ethmoid nerve innervating the anterior nasal
mucosa and the external surface of the nasal
fossa is part of the ophthalmic division, while
the nasopalatine nerve which innervates the
posterior part of the nasal cavity is part of the
maxillary division. The trigeminal nerve has
chemosensory and mechanosensory bers.
Mechanosensory bers are large fast- conducting
Aβ-bers. Thin and fast-conducting myelinated
Aδ-bers and thin and slow- conducting unmyelinated C-bers are responsible for thermoreception (cold and warm stimuli) and for
nociceptive perception (pain, painful mechanical, noxious chemical stimuli). The sensations
mediated by the trigeminal nerve are usually
described as burning, stinging, itching, tickling,
cooling, and warming feeling. Trigeminal-free
nerve endings have receptors which may be activated through several factors such as changes in
pressure, temperature, irritants, and humidity.
Substance P, calcitonin gene- related peptide
(CGRP), and other neuropeptides are found in
the trigeminal nerve bers [3]. Some trigeminal
bers are in close contact with solitary chemosensory cells located in the nasal epithelium and
are more responsible for chemosensory perception because they are responsive to both bitter
tastants and chemical irritants (Fig.17.1).
At the receptor level, one of the rst described
nociceptors was the ion channel receptor family,
and characterization of one of these receptors
was obtained with the nicotinic acetylcholine
receptor. Transient receptor potential (TRP)
channels are well expressed on sensory nerves
and may inuence cell function by mediating the
ux of cations across the plasma membrane into
the cytoplasm generating action potentials. Ion
channels in the TRP family can be opened by
many kinds of stimuli, i.e., chemical or physical.
The TRP family can be subdivided into six subfamilies and many of them are found at the free
nerve ending of the trigeminal nerve such as the
vanilloid receptor (TRPV1), the purinergic receptor (P2X), the acid-sensitive ion channels (ASIC/
DRASIC), the channel responsive to menthol
(TRPM8) (cooling), the channel responsive to
changes in heat and eugenol (TRPV3) (warming), and the channel responsive to isothiocyanate (TRPA1), the major compound of mustard
oil [4].
Mucus
Respirator
Tr igeminal nerve
ry
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Pericilliary fluid
Cilia
Ciliated cell
epithelium
Lamina
propria
Fig. 17.1 Trigeminal bers in close contact with solitary chemosensory cells and trigeminal nerve-free endings located
in the nasal epithelium and responsible for chemosensory and somatosensory perceptions
y
Non ciliated
cell
Goblet cell
Basal cell
Basal lamina
Tight junctions
Solitary chemosenso
cell
195
Like the skin sensory perception, the unmyelinated C-bers (slow conduction) are responsible for burning sensations, and the myelinated
Aδ-bers (fast conduction) are responsible for
stinging sensations.
The cell bodies of the trigeminal bers are
located in the Gasserian ganglion. Nerve bers
from the cell bodies thereafter participate in the
sensory afferent system and project to the trigeminal sensory nucleus that extends from the rostral
spinal cord to the midbrain. Interestingly, some
individual cells in the ganglion send axons to the
olfactory bulb indicating that some interaction
exists at this level. Neurons then project to the
amygdala and to the ventral posterior medial
nuclei of the thalamus. Most of the ascending
bers cross toward the contralateral side with
some bers ascending ipsilaterally (different for
the olfactory pathways [5]). The nerve projections terminate in the primary somatosensory
cortex (SI) and also in the secondary somatosensory cortex (SII) with a right hemispheric predominance [6–8]. Trigeminal activation also
leads to insular cortex activation and to ventral
orbitofrontal cortex mainly to the right side
explaining at the central level the interactions
with other chemosensory systems like taste and
olfaction [9].
Besides the sensory nerves, the parasympathetic and the orthosympathetic systems play an
important role in the normal physiology of the
nose [10]. Parasympathetic nerves have acetylcholine as the major neurotransmitter and act on
muscarinic receptors to induce increased glandular secretions and vasodilatation. Vasointestinal
peptide (VIP) is another neurotransmitter of the
parasympathetic system. The sympathetic system
with noradrenaline and neuropeptide Y (NPY) as
neurotransmitters acts on adrenergic receptors
and induces vasoconstriction and increases nasal
airway patency [11, 12].
Pathophysiological mechanisms and nasal
symptoms are explained by the interdigitation of
these neurologic systems, i.e., the trigeminal sensitive afferent (+ efferent axon reex), the efferent parasympathetic, and the efferent
orthosympathetic systems (autonomic systems)
(Fig.17.2).
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Prurit
sneezing
Sensory
Tr igeminal
ganglion
Parasympathetic
Sphenopalatine
ganglion
Sympathetic
Superior cervical ganglion
Orthodromic
Axon reflex
(antidromic)
Allergen
Ach
VIP
Nor
NPY
Chemosensory
stimulus
Neuropeptides
(SP, NKA,
CGRP)
Glands
Vessels
Rhinorrhea
Vasodilatation
Plasma exudation
Fig. 17.2 Interdigitation of the neurologic systems found in the nasal mucosa, i.e., the trigeminal sensitive afferent (+
efferent axon reex), the efferent parasympathetic, and the efferent orthosympathetic systems (autonomic systems)
17.3 Consequences ofActivation
ofTrigeminal Receptor
andNasal Reexes
The activation of the trigeminal system leads to
the perception of potentially noxious stimuli, to
a global chemosensory perception of odorant
stimuli, and to some nasal reexes. The nasal
fossa may be divided into two parts, the anterior
one most dedicated to the chemosensory perception and the posterior one most devoted to
mechanosensory functions. This has been demonstrated by Frasnelli etal. where it was clearly
stated that anterior nasal mucosa is more sensible to chemosensory stimuli than mechanical
stimuli, while the posterior nasal mucosa is
equally sensible to both chemosensory and
mechanical stimuli [13]. However, thresholds to
detect chemosensory stimuli such as CO2 are
lower when the stimulus is given in retronasally
compared to orthonasally [14].
Therefore, nasal mucosa should not be seen as
a homogenous tissue as it exhibits a varying
degree of sensitivity to trigeminal stimuli depending on the stimulus quality and location in the
nasal fossa [15].
Activation of trigeminal bers leads to protective reexes such as increasing secretions (saliva,
tears, nasal mucus), decreasing breathing, sweating initiation, and closure of the nasal passage by
augmentation of the turbinate volume.
Trigeminal nerve stimulation also induces
many reexes inducing different responses. The
nasal cycle is probably the best known neurologic mechanism leading to a uctuating congestion–decongestion of the nasal fossa secondary to
a changing tone in the vasculature controlled by
the autonomic system.
The naso-nasal reex is supposed to be mediated by the parasympathetic system and explains
many exacerbations of rhinorrhea and watery discharge [16].
The naso-ocular reex is bilateral and mostly
contralateral, secondary to chemosensory or tactile or physical stimuli. It induces watery eyes,
lacrimation, and redness of the conjunctiva.
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The “foot-cooling” reex is secondary to a cold
stimulation at the extremities of the inferior limb
inducing in the nose a reduced blood ow and subsequently a nasal decongestion. This is also very
similar to the reexes observed in the nose when
cooling of the face induces the same effect. Facial
cooling through trigeminal receptors may even
induce lower airway symptoms [17].
The naso-cardiovascular reex is secondary to
trigeminal activation in the nose and is responsible for bradycardia and hypotension, may be
present during nose surgery, and is of primary
importance for the anesthesiologist.
The naso-respiratory reex or naso-bronchial
reex is present when cold dry air is presented to
the subject’s nose inducing increased lower airway resistance.
Cold dry air stimulus may also be used to
induce both long-lasting painful sensations [18]
and secretory response in the nose [19]. This
mechanism is thought to be secondary to activation of capsaicin-sensitive bers; alternatively,
the change in the osmotic milieu of the respiratory epithelium may trigger the activation of the
nociceptive system. This may play a role in the
pathophysiology of nasal hyperactivity and in the
non-allergic noninfectious group of rhinitis [20]
and would lead to the development of capsaicinbased treatment for the patients suffering from
these diseases [21–26]. Capsaicin delivered intranasally has proven its effect in the treatment of
the nasal hyperreactivity found in idiopathic rhinitis patients [27].
These responses may be present after single
presentation of the stimulus or when repeated
application of the stimuli is delivered. C-bers
and Aδ-bers respond differently to repeated
chemical stimulus. If stimuli are repeated, the
burning painful sensation driven by C-bers is
increased, and this is the contrary for Aδ-bers
giving the stinging sensation. This is secondary
to central nervous summation more than increase
in the ring of the nerve bers at the periphery.
17.4 Neurogenic Inammation
The activation of sensory nerves and the release
of neuropeptides from neuroendocrine cells
found in the respiratory mucosa with a subsequent neurogenic inammation may explain at
least partially some diseases of the upper and
lower airways [28].
Stimulation of sensory trigeminal bers may
lead to the release of different neuropeptides such
as substance P, neurokinin A (NKA), neuropeptide K (NPK), and calcitonin gene-related peptide (CGRP). These neuropeptides are increased
in the upper and lower airways of these patients
with airway inammation in a similar way than
the inammatory components usually described
as eosinophils or some proinammatory cytokines [29].
There is a strong evidence that neuroendocrine cells, sensory neurons, and proinammatory immune cells interact and promote
inammation and airway hyperreactivity.
Neurotrophins such as nerve growth factor (NGF)
or neurotrophins-3–4 are also linked to the development of a neurogenic inammation.
In animals, dendrites of intranasal trigeminal
nerve endings can be stimulated in an antidromic
way. This antidromic stimulation is called the
“axon reex” and leads to the release of inammatory neuropeptides from the varicosities of the
nerve, producing vasodilation, increased vascular
permeability, and glandular activation. This phenomenon has been clinically proven in humans
where specic activation of the intranasal trigeminal nerve ending produces nasal obstruction,
congestion, watery discharge, and sneezing. This
axon reex probably plays a major role in the
development of nasal hyperreactivity, nonallergic noninfectious rhinitis known as idiopathic rhinitis, and even allergic rhinitis via the
substance P which exacerbates the eosinophilic
recruitment after allergen challenge (for review,
see [30]).
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17.5 Psychophysical Testing
oftheIntranasal Trigeminal
Function
Testing of trigeminal function with psychophysics is based on threshold measurement, rating of
suprathreshold stimuli, discrimination tasks, and
lateralization tasks [31, 32].
Trigeminal function assessed with psychophysical testing revealed that sensitivity decreases
with age [33].
Psychophysical evidence exists for qualitative
specicity of the human intranasal trigeminal
system. The nasal trigeminal system is less sensitive than the olfactory system for the majority of
odorant stimuli. Recognition threshold of trigeminal stimulus such as CO2 was measured between
32 and 47% v/v for stimuli of 200ms duration at
an airow of 8l/min at body temperature. The
threshold for detection can be lowered if stimulation duration is increased [14].
Considering pain ratings, increase in per-
ceived or painful sensitivity occurs more rapidly for trigeminal stimulus than for olfactory
stimuli [34].
The trigeminal and the olfactory systems
also have a different contribution on the presentation of mixed compounds. In normosmic
subjects, trigeminal stimuli are perceived as
more intense when they are accompanied by an
olfactory stimulus while the olfactory stimulus
seems to have no effect when a mixed compound is presented. The trigeminal stimulus
may induce an additive or even a hyperadditive
effect on the perception after a mixed stimulus
presentation [35].
Qualitative discrimination task with trigeminal irritants demonstrates that human are capable
to discriminate among different trigeminal stimuli even in the absence of any olfactory stimuli
given concomitantly [36], even if this ability
seems to decrease with age [37]. In contrast to
odor stimulation, trigeminal stimuli can produce
increase in pain intensity when repeated stimuli
are given with a short interval demonstrating a
sensitization effect while on the contrary a desen-
sitization effect exists when repeated stimuli are
delivered with long interstimulus interval [38,
39]. Temporal integration of trigeminal informa-
tion is thus different than olfactory temporal integration. Psychophysical studies with capsaicin
have demonstrated a sensitization effect meaning
that the subjective pain rating was increased after
the second stimulation if the interstimulus interval was less than 1min. On the contrary with a
second stimulation delivered after 4min, a desensitization effect was observed. This leads to the
idea that repetitive delivery to the nasal mucosa
was perhaps a treatment for patients with hyperalgia in the nasal fossa or for patients with nonallergic noninfectious rhinitis [38]. However, this
mechanism is linked to the type of the stimulus,
and sensitization and desensitization in the nasal
cavity do not follow the same processes in relation to the molecules studied [40].
Lateralization task revealed that trigeminal
stimuli are perceived without error when the subjects blindfolded is asked to determine the side of
stimulation and that this ability is lost for olfactory stimuli or when the odor has a mixed property between trigeminal and pure olfactory
valence [41]. In others words, pure olfactory
stimuli cannot be localized to the nasal cavity
while on the contrary pure trigeminal stimuli can
be localized. The results are lower in patients
with an olfactory dysfunction independent of the
cause of the olfactory problem [42].
Subjective ratings of nasal patency are also
inuenced by the trigeminal system. For example, stimulation of the nasal fossa with menthol is
accompanied by an increase of perceived nasal
patency [43], while on the contrary, anesthesia of
the nasal mucosa leads to a perception of
decreased nasal patency even in both cases objective nasal patency did not change.
Many studies have been conducted on anosmic subject, and trigeminal thresholds were
found to be higher in anosmic subjects than in
control [44]. Age-related decline of intranasal
sensitivity was reported with not only psychophysical but also electrophysiological evidence [45].
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