olfaction.pptx

OLFACTION
Dr Grace vandana
MS ENT PG
NMCH

� The olfactory system contributes significantly to
a person’s quality of life.
� Odors are part of our everyday life, from the
pleasures of perfume, to the satisfactions of toast
and coffee, to the warnings of fire.
� The quality and intensity of that perception
depend on the anatomic state of the nasal
epithelium and the status of the peripheral and
central nervous system

EMBRYOLOGY
� Complete differentiation of olfactory cells occur by 11 weeks
of gestation.
� Olfactory receptors derive from neuroblasts. These
neuroblasts differentiates to form olfactory placodes.
� The central part of each placode invagiantes giving rise to
olfactory sac.
� Olfactory organ is the only part of the body in which the cell
bodies of neurons lie at the surface, directly in contact with
the external environment.
� In fetus a well developed vomeronasal organ is seen with
cellular configuration similar to olfactory epithelium on
either side of septum.
� It regresses in late fetal life and only remanant is seen in
adults.
� Human olfactory system operative at birth and neonates
respond preferentially to maternal odour.

ANATOMY
� Two independent nasal passages that are
dynamic conduits that subserve both respiration
and olfaction.

OLFACTORY EPITHELIUM
� 7 cm inside the nasal cavity
� 1cm2 on each side in the upper recesses of the
nasal chambers lining the cribriform plate and
sectors of the superior turbinate, middle
turbinate, and septum.
� The epithelium is pseudostratified columnar, and
it rests on a vascular lamina propria with no
submucosa
� This portion of mucosa can be readily identified
from the rest of the nasal mucosa by its unique
yellowish color.

� Throughout life, islands of respiratory-
like epithelial metaplasia appear within
the epithelium, presumably as a result
of cumulative viral, bacterial, and other
insults.
� The number of these clumps of
respiratory epithelium, which are found
in the olfactory area, increases with age,
suggesting that a loss of primary
olfactory neurons at least partially
explains the decreased olfactory ability
associated with aging

• THERE ARE ABOUT SIX TYPES OF CELLS IN
OLFACTORY EPITHELIUM
OLFACTORY RECEPTOR NEURONS:
� Bipolar cells
� Club shaped peripheral knob bearing cilia, central
nucleus and other end tapers as long thin non
myelinated axons
� Bundles of these axons in lamina propria surrounded
by group of schwann type of ensheathing cells to form
olfactory nerve.
� Allison et al estimate the rabbit to have approximately
50 million olfactory axons, whereas Jafek estimates
humans to have only 6 million bilaterally.

SUPPORTING
CELLS/SUSTENTACULAR CELLS
� Tall cells have an apical membrane that joins
tightly with the surface of the receptor cells and
the microvillar cells.
� Do not generate action potentials, nor are they
electrically coupled to each other
� Insulates the bipolar receptor cells from one
another, regulates mucus production, transports
molecules across the epithelium, and detoxifies
and degrades odourants.

MICROVILLAR CELLS
� flask-shaped, is located
near the epithelial surface,
and has an apical
membrane containing
microvilli that project into
the mucus overlying the
epithelium

BASAL CELLS
� Seen along the basal lamina.
� Two groups of replicating cells
� Horizontal basal cells
� Globose basal cells
� Positioned between the basal lamina the
horizontal basal cells & immature neurons.
� The globose basal cells multipotent basal cell
that can give rise to neurons and non-neuronal
cells, including the horizontal basal cells

DUCT CELL OF BOWMAN’S GLANDS
� The secretes most of the mucus within the olfactory
receptor region.

OLFACTORY MUCUS
� After the odorant molecules reach the olfactory region, they
must interact with the mucus overlying the receptor cells.
� The mucus apparently comes from both Bowman’s glands
deep in the lamina propria (only of serous type in humans)
and the adjacent respiratory mucosa (goblet cells)
� To reach the olfactory receptors, the odorant molecules must
be soluble in the mucus.
� Changes in the thickness or composition of the mucus can
influence the diffusion time required for odorant molecules to
reach the receptor sites
� Once in the olfactory mucus-epithelial system, the rate at
which the odorant is cleared also is important.

OLFACTORY BULB
� Located directly over the cribriform plate.
� First relay station in the olfactory pathway where the
primary olfactory neurons synapse with secondary
neurons.
� Neural components are arranged in six concentric layers:
� olfactory nerve
� Glomerular
� External plexiform
� Mitral cell and tuft cells
� Internal plexiform
� Granule cell

� The receptor cell axons of the olfactory nerve layer
→the glomeruli → synapse with the dendrites of the
mitral and tufted cells within the spherical glomeruli.
� These second order cells, in turn, send collaterals that
synapse within the periglomerular and external
plexiform layers, resulting in “reverberating” circuits in
which negative and positive feedback occur. mitral cells
modulate their own output by activating granule cells
(which are inhibitory to them).

OLFACTORY TRACT
� The mitral and tufted
cell axons project
ipsilaterally to the
primary olfactory cortex
via the olfactory tract
� Olfactory tract enters
brain 2 pathways
� Lateral Olfactory stria
� Medial Olfactory stria

�Medial olfactory stria:
� consists of a group of nuclei, located in the mid basal
portions of the brain
� Contain septal nuclei- feed into the hypothalamus and
other primitive portions of the brain’s limbic system
�Lateral olfactory stria:
� Composed of prepyriform pyriform cortex cortical portion
of amygdaloid nuclei. signal pathways almost all portions
of limbic system especially hippocampus- important for
learning like or dislike for food stuffs.

OLFACTORY CORTEX
� Primary olfactory cortex is comprised
� Anterior Olfactory Nucleus
� Pyriform Cortex
� Olfactory tubercle
� Entorhinal area
� Amygdaloid Cortex
� Corticomedial nuclear group of amygdala.

� Anterior Olfactory Nucleus--- Coordination of
inputs from contalateral olfactory cortex
� Transfer of Olfactory memories from one side to
other
� Pyriform Cortex---Olfactory discrimination
� Amygdala---Emotional response to olfactory
stimuli
� Entorhinal Cortex--- Olfactory Memories

OLFACTORY PATHWAY
� First order neuron : olfactory Epithelium to
glomerulus
� Second order neuron :It is formed of the cells of
the olfactory bulb (mitral cells & Tufted cells
passes centrally as the olfactory tract.
� Third order neuron: Pyriform Cortex(Area 28)
contain primary olfactory cortex, which contain
3rd order neuron

VOMERONASAL ORGAN
� Many mammals have an identifiable pit or groove in the
anteroinferior part of the nasal septum that contains
chemosensitive cells.
� In most of these animals, a nerve can be identified
connecting these cells to the central nervous system, to an
accessory olfactory bulb.
� Biopsy studies of the nasal mucosa in the small pit often seen
along the anteroinferior nasal septum (Jacobson’s organ)
show olfactory-like histology but no central connection.

VOMERONASAL ORGAN
� Electrical activity elicited by
certain compounds directly
delivered to the vomeronasal area
has been shown to cause changes
in blood pressure, heart rate, and
hormonal levels.
� It is believed to detect external
chemical signals called
pheromones.
� These signals, which are not
detected consciously as odors by
the olfactory system, mediate
human autonomic, psychological,
and endocrine responses.

PHYSIOLOGY
� Experiencing an odour is an input from
� Olfactory
� Trigeminal
� Glossopharyngeal
� Vagus nerves
� Olfactory nerve stimulation depends on odourant
molecules reaching the olfactory mucosa

� 2 types of air flow
� 1. orthonasal—usually
as a part of
inhalation.
� 2. retronasal – during
eating generated by
mouth and
pharyngeal motion.

� At physiologic airflow rates, approximately
� 50% of the total airflow passes through the middle
meatus,
� 35% flowing through the inferior meatus
� 15% flows through the olfactory region.
� Sniffing is a rapid change in flow velocity which
momentarily increases the olfactory molecules in
olfactory cleft.

� Four major specialized neural systems within the Left and
right sides of the nose:
� The main olfactory system (cranial nerve I or CN I).
� The accessory olfactory system(i.e.vomeronasal system).
� The trigeminal somatosensory system (cn v)
� The nervus terminalis or terminal nerve (CN 0).

� CN I mediates common odour sensations (e.g. vanilla,
rose, chocolate)
� CN V mediates both chemical and non-chemical
stimuli in the form of somatosensory sensations (e.g.,
irritation, burning, cooling, tickling, touch).
� CN V is also responsible for inducing reflexive
responses, such as secretions of mucus and halting of
inhalation, that help to prevent or minimize
chemicallyinduced or thermally-induced damage to
the linings of the nose and lungs.

� The vomeronasal system is non-functional in humans; while a
rudimentary vomeronasal tube is present on each side of the
septum with an opening into the human nose, it has no centrally-
projecting nerve and humans do not possess an accessory
olfactory bulb, the target of such a nerve.
� CN 0 was discovered after the other cranial nerves had been
named, and consists of a loose plexus of ganglionated nerves
that, in most mammals, is in close proximity to the vomeronasal
organ and nerve.
� Its neurons are immunoreactive to the peptide hormone
gonadotropin-releasing hormone (GnRH), implying an
association with endocrine processes.

OLFACTORY TRANSDUCTION AND CODING
� Once the odorant molecule is dissolved in the olfactory mucus the
soluble binding proteins, like odorant-binding protein,enhance the
access of odorants to the olfactory receptors.
� Same odorant-binding protein molecules act to remove odorant
molecules from the region of the receptor cell after transduction.
� The actual transformation of odorant chemical information into an
electrical action potential occurs as a result of specific interactions
between odorant molecules and receptor proteins on the surface of
olfactory cilia.

� With the binding of the receptor to an odorant, adenylate
cyclase is activated by G protein– coupled receptors and
converts adenosine triphosphate (ATP) into cyclic adenosine
monophosphate( cAMP).
� The cAMP then binds to a Na, Ca ion channel to allow influx
of these ions. As more channels open, the cell depolarizes,
and an action potential is produced

� Once the peripheral olfactory receptor cells are
depolarized, there begins a convergence of
electrical information toward the olfactory bulb
→ glomeruli and mitral / tufted cells of the
olfactory bulb → Olfactory cortex

THEORIES OF OLFACTION
� Theories of odour quality
▪ Vibration theory of olfaction
▪ Shape theory/ specific site theory
▪ Penetration and puncture theory
� Theories of stimulation
▪ Vibration theory
▪ Olfactory pigment theory
▪ Enzyme theory
▪ Penetration and puncturing theory

VIBRATION THEORY OF OLFACTION
� The Vibration theory of smell proposes that a
molecule's smell character is due to its vibrational
frequency in the infrared range.
� RANDEBROCK(1968) suggested that olfactory
perceptors are peptide chains vibrating in alpha
helix. An odourant molecule forms a bond with the
peptide thus modulating the vibration. At the
other end of helix vibration is transmitted to
nerve.
� WRIGHT et al (1967) have claimed that
particular vibration frequencies allow the firing of
certain receptors and these correspond to
electrophysiological measurements in bulb.
�

PENETRATION AND
PUNCTURE THEORY
� Dave’s theory states that odorant molecules is able to
penetrate the olfactory receptor cell and diffuse
through it leaving a hole through which leakage of
ions occur initiating a nerve impulse.
� Different shapes of molecules may leave different size
holes. Depending upon the time taken by odorant
molecule to diffuse and the time taken by membrane
to heal (HOLE SHARPNESS FACTOR) the quality of
odour varies.

� OLFACTORY PIGMENT THEORY
� Rosenberg proposed that odorant molecules form complex
with certain olfactory pigments giving them an increased
electrical conductivity.
� Carotenes cis and trans forms- similar as rodopsins
� ENZYME THEORY
� Activity of certain enzymes can be altered by adsorption of
odorant molecules.

� PENETRATION AND PUNCTURING THEORY
� During excitation of nerve axon, K moves out and Na
moves in the cell. During resting phase pumping back
of ions occurs.
� It is the exchange of ions or Puncturing of the
membrane that sets off electrical discharge along the
nerve.
� Dave’s theory states that odorant molecules is able to
penetrate the olfactory receptor cell and diffuse
through it leaving a hole through which leakage of
ions occur initiating a nerve impulse

SHAPE THEORY
� The Shape theory of smell states that a molecule's
particular smell is due to a 'lock and key' mechanism
by which a scent molecule fits into olfactory receptors
in the nasal epithelium.
� More widely accepted than vibration theory

OLFACTORY DYSFUNCTION
� TYPESOF OLFACTORY DYSFUNCTION:
� Anosmia-absenceof smell
� Hyposmia/microsmia- diminished olfactorysensitivity
� Dysosmia-distorted senseof smell
� Phantosmia- perception of anodorant when none is presentl /
Olfactory hallucination.
� Agnosmia-inability to classify,contrast, or identify odor
sensationsverbally, eventhough the ability to distinguish
between odorants may be normal
� Hyperosmia-Abnormally acute smell function (Rare
condition )

CLASSIFICATION& ETIOLOGY
� TRANSPORT OLFACTORY LOSS
� Olfactory dysfunctions canbe causedby conditions that interfere
with the accessof the odorant to the olfactory neuro-epithelium
due to either swollen nasalmucous membrane, structural
changesand/or mucus secretion.
� Causes-Allergy rhinitis, Bacterial rhinitis and sinusitis,
� Congenital abnormality like encephalocele,
� Deviated NasalSeptum, Nasal neoplasms, Nasalpolyps, Nasal
surgery,Old age, Viral infections.

� SENSORY OLFACTORY LOSS Olfactory dysfunctions
can be caused by conditions that damage to the
neuroepithelium.
� Causes-Drugs that affect cell turn over and inhalations
of toxic chemicals, viral infections, neoplasms, radiation
therapy.

� NEURAL OLFACTORY LOSS •
� Olfactory dysfunctions canalso be causedby conditions that
damage the central olfactory pathways.
� Causes-AIDS,Alzheimer’s disease,Alcoholism, Chemical
Toxins,Cigarette smoke,Diabetes Mellitus, Depression, Drugs,
Huntington’s chorea, Hypothyroidism, Kallmann syndrome,
Korsakoff psychosis,Malnutrition, Neoplasm, Neurosurgery,
Parkinsons disease,Trauma,Vitamin B12def., Zinc deficiency

� Lesions of the olfactory system anterior to the
olfactory trigone (including the neuroepithelium, fila,
bulb, and tract) can result in total lack of smell on the
affected side.
� However, lesions within olfactory structures more
posterior to the olfactory trigone do not typically
cause complete loss.

� At present, no psychophysical methods to differentiate sensory
from neural hearingloss.
� History of olfactory loss gives an important clues to the cause.
� Leading causes of olfactory dysfunctions are head trauma and
viral infections.
� Head trauma are more common causeof anosmia in children
and young adults whereas viral infectionsare more common
cause in older adults.
� Congenital anosmia occurs in Kallmann syndrome and also in
albinism.
� Meningioma of inferior frontal region is the most common
neoplastic causeof anosmia.
� Dysomiais associated with depression.

APPROACHTO OLFACTORY
DYSFUNCTION
� DETAILEDMEDICALHISTORY
� Onset, course, nature of impairment, their previous illness and
then medications taken.
� PHYSICALEXAMINATION
� Thorough ENT, head and neck examinations including nasal
endoscopy.
� A neurological examination emphasizing the cranial nerves,
cerebellar and sensorimotor function is essential.
� Psychological examination like general mood and check for signsof
depression should be done.

❑LABORATORYFINDINGS
� Biopsy of olfactory neuroepithelium can be done
in rare cases
� IMAGING • Coronal Ct scan and MRI Brain are
useful.

� sudden olfactory loss suggests the possibility of head trauma,
infection, ischemia, or a psychogenic condition.
� Gradual loss the development of degenerative processes,
progressive obstructive lesions or tumors within the olfactory
receptor region or more central neural structures.
� Intermittent loss can be indicative of an intranasal inflammatory
process.
� A family history of smell dysfunction may suggest a genetic basis
Kallmann’s syndrome : Delayed puberty in association with
anosmia (with or without midline craniofacial abnormalities,
deafness, and renal anomalies

QUANTITATIVE OLFACTORY TESTING
� verify the validity of the patient’s complaint
� characterize the exact nature and degree of the
problem
� accurately monitor changes in function over time
� detect malingering
� obtain an objective basis for determining
compensation for disability.

� To assess olfaction unilaterally, the
naris contralateral to the tested side
should be occluded without
distorting the nasal valve region.
This can be easily accomplished by
sealing the contralateral naris using
a piece of MicrofoamTM.
� The patient is instructed to sniff the
stimulus normally and to exhale
through the mouth. Such occlusion
not only prevents air from entering
the olfactory cleft from the
contralateral naris

� UNIVERSITYOFPENNSYLVANIA
SMELLIDENTIFICATIONTEST (UPSIT)
� Most commonly used & most superior and reliable test.
� Self-administered in 10-15minutes
� Scored in <1 minute by non-med person
� Available in variouslanguages
� 40 “scratch & sniff “ patches
� Pt. chooses from 4 answers& must choose1 Dysfunction
classified as Normosmia, anosmia, mild, moderate or
severe microsmia,

OLFACTORY EVENT-RELATED POTENTIALS
(OERPS)
� synchronized brain electroencephalographic (EEG)
activity induced by repeated pulsatile presentations of
an odorant is isolated from overall EEG activity
� sensitive and useful in detecting malingering

ELECTRO-OLFACTOGRAM (EOG)
� Detected via an electrode placed on the surface of
the olfactory neuroepithelium
� Monophasic negative potential evoked by odors in
oflactory mucosa.

� Latent period – time taken by the stimulant particles to cross layer
of mucus onto epithelial surface.
� Slow negative monophsic potential
� Rises steeply and falls back exponentially towards base line.
� Rising phase rises faster with increasing strength of stimulus.
� Normal minimal identifiable odour is determained by delivering
smaller and smaller volumes of odourised air until patients
response becomes negative.

TREATMENT
� Transport olfactory loss
• Allergy management
• Antibiotic therapy
• Topicaland systemic glucocorticoid therapy
• Operations for nasalobstruction.
� Sensori neural Olfactory loss.
• No treatment with demonstrated efficacyf or Sensori neural
Olfactory loss. Fortunately, spontaneous recovery occurs.

olfaction.pptx

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