UNIVERSITY OF TECHNOLOG, JAMAICA

DEPARTMENT OF SCIENCE AND MATHEMATICS

UNIT 3 General Sense Organs

Sensory Receptors
Sensory receptors are the interface between your nervous system and your internal and external
environments. The General Senses of pain, temperature, touch, pressure, vibration and
proprioception (position sense) are distributed throughout the body.

The Special Senses are olfaction, vision, gustation (taste) equilibrium (balance) and hearing. These
sensations are provided by receptors that are structurally more complex than those of the general
senses. Special sensory receptors are located in sense organs such as the eye or ear, where they are
protected by surrounding tissues. The information provided by these receptors is distributed to
specific areas of the cerebral cortex and to centres throughout the brain stem.

Each receptor has a characteristic sensitivity. For example a touch receptor is very sensitive to
pressure but relatively insensitive to chemical stimuli, whereas a taste receptor is sensitive to
dissolved chemicals but insensitive to pressure. This concept is called receptor specificity.

The simplest receptors are the dendrites of sensory neurons. The dendrite processes, called free
nerve endings, are not protected by accessory structures. They can be stimulated by many different
stimuli. For example free nerve endings that respond to tissue damage by providing pain sensations
may be stimulated by chemical stimulation, pressure, temperature changes or trauma.

The area monitored by a single receptor cell is its receptive field. Whenever a sufficiently strong
stimulus arrives in the receptive field, the CNS receives the information “stimulus arriving at
receptor X”. The larger the receptive field the poorer your ability to localize a stimulus. For
example a touch receptor on the body surface may have a receptive field of 7 cm (2.5 inches) in
diameter. As a result you can describe a light touch there as affecting only a general area, not an
exact spot. On the tongue or fingertips, where the receptor fields are less than 4 millimeter in
diameter you can be very precise about the location of a stimulus.

General Senses
Receptors for the general senses are scattered throughout the body and are relatively simple in
structure. They are classified as exteroceptors, proprioceptors and interoceptors. Exteroceptors
provide information about the external environment.
Proprioceptors report the positions of the skeletal muscles and joints.
Interoceptors monitor visceral organs and functions.
Another classification system divides the receptors according to the nature of the stimulus that
excites them.
1. Nociceptors – pain
2. Thermoceptors – temperature
3. Mechano-receptors – touch, pressure, proprioception
4. Chemoreceptors – chemical sense

Each class of receptors has distinct structural and functional characteristics.

1. Nociceptors or Pain receptors are especially common in the superficial portions of the
skin, in joint capsules, and around the walls of blood vessels. There are few pain
receptors in other deep tissues or in most visceral organs. Pain receptors are free nerve

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 endings with large receptor fields. As a consequence it is often difficult to determine the
exact source of painful sensation.

There are three groups of nociceptors:

A) Those sensitive to temperature extremes
B) Those sensitive to mechanical damage
C) Those sensitive to dissolved chemicals such as those released by damaged cells.

A very strong stimulus, however, will excite all three receptor types. For that reason, people
describing very painful sensations whether caused by acids, heat or a deep cut – use similar
descriptive terms such as “burning”. Stimulation of the dendrites of nociceptors causes
depolarization. When the initial segment of the axon reaches threshold an action potential heads
towards the CNS. The sensory neurons use the amino acid glutamate and the neuropeptide
Substance P as neurotransmitters. The axon synapses on an interneuron whose axon crosses the
optical cord to ascend the lateral spinothalamic tract. After a synapse in the thalamus, the
information is relayed to the primary sensory cortex.
Two types of axons exist for nociceptors – Type A and type C carry painful sensations.

Myelinated Type A fibres carry sensations of fast pain example an injection or deep cut. These
sensations quickly reach the CNS where they often trigger somatic reflexes. In most cases the
arriving information permits localization of the stimulus to an area several inches in diameter.

Slower Type C fibres carry sensation of slow pain, or burning and aching pain. The individual
becomes aware of the pain but only has a general idea of the affected area.
Painful sensation ceases only after tissue damage has ended (i.e. healed).

2. Thermoreceptors- are free nerve endings located in the dermis of the skin, in skeletal
muscles, in the liver and in the hypothalamus. Cold receptors are three to four times more
numerous than warm receptors.
Temperature sensations are conducted along the same pathways that carry pain sensations. They
are sent to the reticular formation, the thalamus and the primary sensory cortex.
Thermoreceptors are phasic receptors. They are very active when the temperature is changing
but they quickly adapt to a stable temperature, example when you enter an air conditioned room
it may be unpleasant at first but with time the discomforts fades.

3. Mechano-receptors – are sensitive to stimuli that distort their cell membranes.

These membranes contain mechanically regulated ion channels whose gates open or close in
response to stretching, compression, twisting or other distortions of the membrane. There are
three classes of mechanoreceptors:
a) Tactile receptors – which provide sensations to touch, pressure and
vibrations.
b) Baroreceptors – which detect pressure changes in the walls of blood
vessels and in portions of the digestive, reproductive and urinary tracts.
c) Proprioreceptors – which monitor the position of joints and muscles.

4. Chemoreceptors – detect small changes in the concentration of specific chemicals or

compounds. These receptors respond only to water and lipid soluble substances that are dissolved in
the surrounding fluid. The chemoreceptors included in the general senses do not send information to
the primary sensory cortex, and we are not consciously aware of the sensations they provide. The
arriving sensory information is routed to the brain stem centers that deal with the autonomic control
of respiratory and cardiovascular function. Neurons in the respiratory centers of the brain respond
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to the H+ and carbon dioxide in the cerebrospinal fluid. Chemoreceptive neurons located within the
carotid and aortic bodies monitor carbon dioxide and oxygen concentrations in the arterial blood.

3.3 Special Sense Organs

Sensory receptors are specialized cells that provide your central nervous system with information
about conditions inside or outside your body. Sensory receptor detects an arriving stimulus and
translates it into an action potential that can be conducted to the CNS. Sensory receptors are the
interface between your nervous system and your internal and external environments. The general
senses of pain, temperature, touch, pressure, vibration and proprioception (the ability to sense the
position and location and orientation and movement of the body and its parts or simply the position
sense) are distributed throughout the body.

The special senses are Olfaction (smell), vision (sight), gustation (taste), equilibrium (balance) and
hearing. These sensations are provided by receptors that are structurally more complex than those
of the general senses. Special sensory receptors are located in sense organs such as the eye or ear,
where they are protected by surrounding tissues. The information provided by theses receptors is
distributed to specific areas of the cerebral cortex (the auditory cortex, the visual cortex and so
forth) and to centers throughout the brain stem.

Receptors and processors involved in smell or olfaction

The sense of smell depends on chemoreceptors provided by paired olfactory organs located in the
nasal cavity on either side of the nasal septum. These neurons project their axons to the olfactory
bulb of the brain, while their dendrites end in olfactory hairs on the surface of the nasal epithelium.
Molecules from the environment must diffuse through this mucus to reach the receptor proteins on
the olfactory hairs. The olfactory organs contain the following layers:
1. Olfactory epithelium which contains olfactory receptors, supporting cells and basal cells.
2. Lamina propria which is an underlying layer of loose connective tissue. This layer contains
olfactory glands also called Bowman’s Glands, whose secretions absorb water and form a
thick pigmented mucous. When air is
drawn through the nose the air swirls
and eddies within the nasal cavity. This
turbulence brings airborne compounds
to the olfactory organs. Sniffing
repeatedly increases the flow of air
across the olfactory epithelium,
intensifying the stimulation of the
receptors. Once compounds reach the
olfactory organs, water-soluble and
lipid-soluble materials diffuse into the
mucous before they can stimulate the
olfactory receptors.
The olfactory receptors are highly
modified neurons where the tip forms
a prominent knob that projects beyond
the epithelial surface. This projection

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 provides a base for up to 20 cilia and extends into the surrounding mucus. These cilia lie
parallel to the epithelium, exposing their surface area to the dissolved chemical compounds.
Olfactory reception occurs on the surface of the cilia as they interact with the dissolved
chemicals, called odorant binding proteins, on the membrane surface.
Odorants are chemicals that stimulate olfactory receptors; they are small organic molecules.
The stronger a smell the more soluble its molecules are in lipid or water. Binding of the
odorant to the binding protein leads to activation of adenylate cyclase, a G protein, the
enzyme that converts ATP to cyclic AMP (cAMP). The cAMP causes opening of sodium
channels in the membrane which results in depolarization. If sufficient depolarization occurs
an action potential is triggered in the axon and the information relayed to the CNS. The
more odorant molecules bind to receptors the greater the frequency of action potentials and
the greater the intensity of the perceived smell.
Although 10 to 20 million olfactory receptors are packed into an area of 5cm2, this cannot
compare with those of other vertebrates such as dogs, cats or fishes. A dog has 72 times
more receptor surface than a human. As we age the number of olfactory receptors decrease
resulting in diminished sense of smell. This explains grandma and grandpa’s excessive use
of perfumes or cologne.

Vermonasal Organ Senses Pheromones

The vermonasal organ (VNO) is a small paired tubular structure embedded in the nasal epithelium
of amphibians, reptiles and many mammals. In mammals the VNO is located on the septum
dividing the two nostrils. The VNO has a pore that opens into the nasal cavity. When the animal
sniffs, the VNO pulsates a draws a sample of nasal fluid over the chemoreceptors embedded in its
walls. The information from theses chemoreceptors goes to an accessory olfactory bulb in the brain,
and information from there goes tpo brain regions involved in sexual and other instinctive
behaviours.

In snakes the VNO opens into the roof of the mouth cavity. Each time the snake’s forked tongue
darts in and out, the fork fits into the VNO openings and present to the chemoreceptors a sample of
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molecules from the surrounding air. The snake uses its tongue to smell the environment, not to taste
it. In reptiles air flows to and from the lungs slowly (and can even stop entirely for long periods of
time) but the tongue can dart in and out many times in a second making the tongue a better organ of
smell than the lungs.

Gustation/The Sense of Taste

The sense of taste or gustation in humans and other vertebrates depends on clusters of
chemoreceptor cells called taste buds. The taste buds of terrestrial vertebrates are confined
to the mouth cavity but some fishes have taste buds in the skin that enhance their ability to
sense their environment. Some fishes living in turbid (muddy) waters are very sensitive to
small amounts of amino acids in the water around them and can find food without the use of
vision.
In humans gustation or taste provides information about the foods and liquids we consume.
The gustatory receptors are distributed over the superior surface of the tongue and adjacent
portions of the pharynx and larynx. By the time adulthood is reached, taste receptors on the
pharynx and larynx decrease in abundance and importance.
The most important taste receptors are on the tongue, though few remain on the epiglottis
and adjacent areas of the pharynx (after taste). Taste receptors and specialized epithelial cells
form sensory structures called taste buds. Humans have about ten thousand (10,000) taste
buds. The superior surface of the tongue bears epithelial projections called lingual papillae
of which there are three types:
(i) Filiform papillae (thread)
(ii) Fungiform papillae (mushroom)
(iii) Circumvallate papillae (around wall)

Filiform papillae provide friction against objects in the mouth. They do not contain taste
buds. Each fungiform papilla contains about five taste buds; each large circumvallate papilla
contains as many as 100 taste buds. The circumvallate papillae form a V near the posterior
regions of the tongue.

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 Each taste bud contains about 40 slender receptors called gustatory cells and many
supporting cells. Taste buds are recessed into the surrounding epithelium isolated from the
relatively unprocessed oral contents. Each gustatory cell extends slender microvillus,
sometimes called taste hairs, into the surrounding fluid through a narrow opening called the
taste pore. A typical gustatory cell lasts only ten days before it is replace by the division of
nearby epithelial cells.

Taste buds are monitored by cranial nerves VII (facial), IX (glossopharyngeal), and X
(vagus). The facial nerve monitors all taste buds located at the anterior two-thirds of the
tongue, from the tip to the line of circumvallate papillae. The circumvallate papillae and the
posterior one-third of the tongue are innervated by the glossopharyngeal nerve. The vagus
nerve innervates the taste buds scattered on the surface of the epiglottis. The sensory
afferents carried by these nerves synapse within the nucleus solitarius or solitary nucleus of
the medulla oblongata and the axons of the postsynaptic neurons enter the medial lemniscus.
There the neurons join axons that carry somatic sensory information on touch, pressure and
proprioception. After another synapse in the thalamus, the information is projected to the
appropriate portions of the primary sensory cortex. A conscious perception of taste is
produced as the information received from the taste buds is correlated with other sensory
data such as texture of food, taste sensations (peppery or hot). The level of stimulation from
olfactory receptors may increase taste perception by several thousand times. When you have
a cold airborne molecules cannot reach the olfactory receptors causing meals to taste bland.
This occurs though the taste buds are responding normally.

Vision
We rely on vision more than any other special sense. Our visual receptors are contained in
the eyes, elaborate structures that enable us not only to detect light but also to create detailed
visual images.

Accessory Structures of the Eye.

These include the eyelids, the superficial epithelium of the eye and the structure associated
with the production, secretions and removal of tears.
Eyelids or palpebrae are a continuation of the skin. The eyelids act like windshield wipers.
Their continual blinking movements keep the surface lubricated and free from dust and
debris. They can also close firmly to protect the delicate surface of the eye. The free
margins of the upper and lower eyelids are separated by the palpebral fissure but the two are
connected at the medial canthus. The eyelashes along the palpebral margins are very robust
hairs that prevent foreign matter and insects from reaching the surface of the eye.

The eyelashes are associated with the glands of Zeis, large sebaceous glands along the inner
margin of the lid that secrete a lipid-rich product that keeps the eyelids from sticking
together. At the medial canthus, the lacrimal caruncle, a soft tissue mass, contains glands
producing the thick secretions that contribute to the gritty deposits found after a good night’s
sleep. These glands are subject to occasional invasion of bacteria. A cyst or chalazion
generally results from the infection of a Meibomian gland. An infection in the sebaceous
gland of one of the eyelashes, a Meibomian gland or one of the sweat glands that open to the
surface between the follicles produces a painful localized swelling known as a sty.

The skin covering the visible surface of the eyelid is very thin. Beneath the skin lie the
muscle fibres responsible for closing and opening the eyelids. The epithelium covering the
inner surface of the eye is called the conjunctiva. It is a mucous membrane covered by a
specialized stratified squamous epithelium. The palpebral conjunctiva covers the inner
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 surface of the eyelids, and the ocular conjunctiva or bulbar conjunctiva covers the anterior
surface of the eye extending to the edges of the cornea, a transparent fibrous layer. The
cornea is covered by a very delicate squamous corneal epithelium, 5-7 cells thick, that is
continous with the ocular conjunctiva. A constant supply of fluid washes over the surface of
the eyeball, keeping the ocular conjunctiva and cornea moist and clean. Goblet cells within
the epithelium assist the various accessory glands in providing a superficial lubricant that
prevents friction and drying of the opposing conjunctival surfaces.

Conjunctivitis or pink eye results from damage to irritation of the conjunctival surface. The
most obvious symptom, reddening, is due to dilation of the blood vessels beneath the
conjunctival epithelium.

The EYE.
The eyes are extremely sophisticated instruments, with each eyeball shaped like a slightly irregular
spheroid with an average diameter of 24mm; and weighing about 8 g. With the orbit, the eyeball
shares space with the extrinsic eye muscles, the lacrimal gland, the cranial nerves and blood vessels
that supply the eye and adjacent portions of the orbit and face.

The wall of the eye contains 3 distinct layers or tunics:

1. An outer fibrous tunic
2. An intermediate vascular tunic
3. An inner neural tunic
The visual receptor or photoreceptors are located within the neural tunic. The eyeball is hollow with
the interior divided into two cavities. The large posterior cavity is called the vitreous chamber
containing the gelatinous vitreous body. The smaller anterior cavity is subdivided into two
chambers, anterior and posterior. The shape of the eye is stabilized in part by the vitreous body and
the clear aqueous humor that fills the anterior cavity.

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The Fibrous Tunic
The fibrous tunic, the outermost layer of the eye consists of the sclera and the cornea. The fibrous
tunic provides:
1. Mechanical support and some degree of physical protection.
2. Serves as an attachment site for the extrinsic eye muscles and
3. Contains structures that assist in the focusing process

Most of the ocular surface is covered by the sclera or “white of the eye” which consists of dense
fibrous connective tissue containing both collagen and elastic fibres. This layer is thickest over the
posterior surface of the eye, near the exit of the optic nerve, and thinnest over the anterior surface.
The six extrinsic muscles insert on the sclera, blending their collagen fibres with those of the outer
tunic. The surface of the sclera contains small blood vessels and nerves that penetrate the sclera to
reach internal structures. The network of small vessels interior to the ocular conjunctiva generally
does not carry enough blood to lend an obvious colour to the sclera, but on close inspection the
vessels are visible as red lines against a white background of collagen fibres.

The transparent cornea is structurally continuous with the sclera; the limbus is the border between
the two. There are no blood vessels in the cornea. The superficial epithelial cells must obtain
oxygen and nutrients from the tears that flow across their free surfaces. There are also numerous
free nerve endings in the cornea, and it is the most sensitive part of the eye.

There are six muscles attached to the sclera that control the movements of the eye.
They are shown here:

Muscle Primary Function

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 Medial rectus moves eye towards nose
Lateral rectus moves eye away from nose
Superior rectus raises eye
Inferior rectus lowers eye
Superior oblique rotates eye
Inferior oblique rotates eye

The Vascular tunic (Uvea)

The vascular tunic or uvea contains numerous blood vessels, lymphatics and the intrinsic eye
muscles. The functions of the middle layer include:
1. providing a route for blood vessels and lymphatics that supply tissues of the eye.
2. regulating the amount of light that enters the eye.
3. secreting and absorbing the aqueous humor that circulates within the eye and
4. controlling the shape of the lens an essential part of the focusing process.

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The vascular tunic includes the iris, the ciliary body and the choroid.

The iris may be seen through the transparent corneal surface and contains blood vessels, pigmented
cells and two layers of smooth muscle fibres. When these muscles contract they change the diameter
of the central opening or the pupil of the iris. One group of muscles, the papillary constrictor
muscles, forms a series of concentric circles around the pupil. When these sphincter muscles
contract, the diameter of the pupil decreases. A second group of muscles, the papillary dilator
muscles, extends radically way from the edge of the pupil. Contraction of these muscles enlarges
the pupil. Both muscle groups are controlled by the autonomic nervous system. Parasympathetic
activation occurs in response to bright light which causes the pupil to dilate (the papillary reflex).

The body of the iris consists of highly vascular, pigmented, loose connective tissue. The anterior
surface has no epithelial covering, although there is an incomplete layer of fibroblasts and
melanocytes. Melanocytes are also scattered within the body of the iris. The posterior surface is
covered by a pigmented epithelium that contains melanin granules. This pigmented epithelium is
part of the neural tunic. Your eye colour is determined by the density of the pigmented epithelium.
When there are few melanocytes in the connective tissue of the iris, light passes through it and
bounces off the pigmented epithelium. The eye then appears blue. Individuals with gray, brown or
black eyes have increasing numbers of melanocytes in the body and surface of the iris. The eyes of
human albinos appear a very pale gray or blue-gray.

The Ciliary Body

At its periphery, the iris attaches to the anterior portion of the ciliary body. The ciliary body begins
at the junction between the cornea and the sclera. It extends posteriorly to the ora serrata, the
serrated anterior edge of the neural retina, which contains the visual receptors. The bulk of the
ciliary body consists of the ciliary muscle, a smooth muscular ring that projects into the interior of
the eye. Its epithelium is thrown into numerous folds called ciliary processes. The suspensory
ligaments of the lens attach to these processes. These connective tissue fibres hold the lens posterior

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to the iris and centered on the pupil. As a result any light passing through the pupil and headed for
the photoreceptors will pass through the lens.

The Choroid
The choroid is a vascular layer that separates the fibrous and neural tunic’s posterior the ora serrata.
It is covered by a sclera and attached to the outermost layer of the retina. The choroids contain an
extensive capillary network that delivers oxygen and nutrients to the retina. It also contains
melanocytes which are especially numerous near the sclera.

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The Neural Tunic
The neural tunic or retina is the innermost layer of the eye. It consists of a thin outer pigmented
layer and a thick inner layer, the neural retina, which contains the visual receptors and associated
neurons. The pigmented layer absorbs light that pass through the neural retina and the pigmented
cells have important biochemical interactions with the retinal photoreceptors. The neural retina
contains:
1. The photoreceptor that respond to light
2. supporting cells and neurons that perform preliminary processing and integration of
visual information
3. Blood vessels supplying tissues that line the posterior cavity.

The two retinal layers are normally very close together but not tightly interconnected. The
pigmented layer of the retina continues over the ciliary body and iris, although the neural retina
extends anteriorly only as far as the ora serrata. The neural retina thus forms a cup that establishes
the posterior and lateral boundaries of the posterior cavity.

The retina contains several layers of cells. The outermost layer, closest to the pigmented layer
contains the photoreceptors or cells that detect light. The photoreceptors are entirely dependent on
the diffusion of oxygen and nutrients from blood vessels in the choroids. In a detached retina the
neural retina becomes separated from the pigmented layer. This condition can result from a sudden
impact to the eye or from a variety of other factors. Unless the two layers of the neural tunic are
reattached the photoreceptors will degenerate and vision will be lost. Reattachment may be
achieved by “welding” the two layers together by means of laser beams focused through the cornea.

Two types of photoreceptors, rods and cones, are present in the retina. Rods do not discriminate
among different colours of light. They are very light sensitive and enable us to see in dimly or
poorly lit rooms, at twilight and in pale moonlight. Cones provide us with colour vision. There are
three types of cones, and their stimulation in various combinations provides the perception of
different colours. Cones give us sharper, clearer images than rods but require more intense light.

Cones and rods are not evenly distributed across the outer surface of the retina. Approximately 125
million rods form a broad band around the periphery of the retina. Roughly 6 million cones span the
posterior retinal surface. Most of these are concentrated in the area where a visual image arrives
after it passes through the cornea and lens. There are no rods in this region, which is known as the
yellow spot or macula lutea. The highest concentration of cones occurs in the central portion of the
macula lutea, an area called the fovea (shallow depression) or fovea centralis. The fovea is the site
of sharpest vision. When you look directly at an object, its image falls on this portion of the retina.
When you look directly at an object you are focusing its image on your fovea, the center of colour
vision. You see a very good image provided there is enough light to stimulate the cones. In very dim
light cones cannot function.

The rods and cones synapse with approximately 6 million bipolar cells. These bipolar cells in turn
synapse within the layer of ganglion cells adjacent to the posterior cavity. A network of horizontal
cells extends across the outer portion of the retina at the level of the synapse between
photoreceptors and bipolar cells. A comparable layer of amacrine cells occurs where bipolar cells
synapse with ganglion cells. Horizontal and amacrine cells can facilitate or inhibit communication
between photoreceptors and ganglion cells, adjusting the sensitivity of the retina. The effect could
be compared with adjusting the contrast on your television. These activities play an important role
in the eye’s adjustment to dim or brightly lit environments.

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 Parts of the Eye and their Function.

The Optic Disc

Axons from about one million ganglion-cells converge on the optic disc, a circular region just
medial (situated in, or extending toward the middle) to the fovea. The optic disc is the origin of the
optic nerve. From this point, axons turn, penetrate the wall of the eye and proceed towards the
diencephalons (thalamus). There are no photoreceptors or other retinal structures at the optic disc.
Because light striking this area goes unnoticed, the optic disc is commonly called the blind spot.

Diagram of section through the

eye.

The Chambers of the Eye

The ciliary body and lens divide the interior of the eye into a large posterior cavity, the vitreous
chamber, and a smaller anterior cavity. The anterior cavity is subdivided into the anterior chamber,
which extends from the cornea to the iris, and a posterior chamber between the iris and the ciliary
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body and lens. Both chambers are filled with aqueous humor, which circulates within the anterior
cavity. The posterior cavity is filled with a gelatinous substance known as the vitreous humor.

Aqueous humor is formed by the active secretion of epithelial cells of the ciliary’s body ciliary
processes. The epithelial cells regulate its composition, which resembles that of cerebrospinal fluid.
The aqueous humor provides protection as a shock absorber and is an important route for nutrient
and waste transport. The pressure of the aqueous humor also helps to maintain the shape of the eye
and stabilizes the position of the retina, pressing the photoreceptor layer against the pigmented
layer. The pressure exerted by the fluid in the eye is referred to as intra-ocular pressure and may be
measured in the anterior chamber by bouncing a tiny blast of air off the surface of the eye, then
measuring the deflection produced. Normal intraocular pressure ranges from 12-21 mm Hg.

The vitreous humor helps stabilize the shape of the eye and gives additional physical support to the
retina. Unlike the aqueous humor, the vitreous humor is not replaced. Aqueous humor produced in
the posterior chamber, freely diffuses through the vitreous humor and across the surface of the
retina.

The Lens
The lens lies posterior to the cornea, held in place by the suspensory ligaments that originate on the
ciliary body of the choroids. The primary function of the lens is to focus the visual image on the
retinal photoreceptors, by changing its shape.
The lens consists of concentric layers of cells that are precisely organized. A dense fibrous capsule
covers the entire lens. The rounder the lens the more refraction occurs, so a very round lens has a
shorter focal distance (the distance between the center of the lens and its focal point) than a flatter
one. We focus images on the retina by changing the shape of the lens so as to keep the focal lens
constant. This process is called Accommodation. During accommodation the lens becomes rounder
to focus the image of a near by object on the retina, and it flattens when we focus on a distant
object.
The lens is held in place by the suspensory ligaments that originate at the ciliary body. Smooth
muscle fibres in the ciliary body act like sphincter muscles. When the ciliary muscle contracts, the
ciliary body moves toward the lens. This movement reduces the tension in the suspensory ligaments
and the elastic capsule pulls the lens into a more spherical shape. The rounder shape increases the
refractive powers of the lens, enabling it to bring light from nearby objects into focus on the retina.
When the ciliary muscles relax, the suspensory ligaments pull at the circumference of the lens,
making it relatively flat.

Colour Vision
An ordinary light bulb or the sun emits photons of all wavelengths. These photons stimulate both
rods and cones. When al types of cones or when rods are stimulated you see a “white” light. Your
eyes also detect photons that reach your retina after the photons bounce off objects around you. If
photons of all colour bounce off the objects, it will appear white to you; if all the photons are
absorbed by the object (so that none reach the retina) it will appear black. The object will appear to
have a particular colour if it reflects (transmits) photons from one portion of the visible spectrum
and absorbs the rest.

There are three types of cones: blue cones, green cones and red cones. Each type has a different
form of opsin (receptor protein, activated by light) and sensitivity to a different range of
wavelengths. Their stimulation in various combinations is the basis for colour vision. In a normal
individual the cone population consists of 16% blue cones, 10% green cones and 74% red cones.
Although their sensitivities overlap, each type is most sensitive to a specific portion of the visual
spectrum. Colour discrimination occurs through the integration of information arriving from all
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three types of cones. The perception of yellow, results from a combination of inputs from green
cones (highly stimulated), red cones (stimulated) and blue cones (relatively unaffected).

Colour blindness occurs when a person is unable to distinguish certain colours. The condition
occurs when one or more class of cones is nonfunctional. The cones may be entirely absent or
unable to manufacture the necessary visual pigments. The most common form of colour blindness is
re-green colour blindness, where the red cones are missing and the individual is unable to
distinguish red from green light.
Inherited colour blindness involving one or two cone pigments is not unusual. The genes for red and
green cone pigments are located on the X chromosome. Because women have two such
chromosomes (XX) they tend not to show the trait or rarely do; whereas men only have one X
chromosome paired wit a Y causing them to be more likely to display the colour blindness trait.

Light and Dark Adaptation

The sensitivity of your visual system varies with the intensity of illumination. After 30 minutes or
more in the dark almost all visual pigments will be fully receptive to stimulation. This is the dark-
adapted state. When dark-adapted, the visual system is extremely sensitive. For example a single
rod will hyperpolarize in response to a single photon of light. If as few as seven rods absorb photons
at one time, you will see a flash of light.

When the light comes on, at first it seems almost unbearably bright, but over the next few minutes
your sensitivity deceases as bleaching occurs. Eventually the rate of visual pigment breakdown is
balanced by the rate of reformation. This condition is the light adapted state.
A variety of central responses further adjust light sensitivity. Constriction of the pupil, via the
papillary constrictor reflex, reduces the amount of light entering your eye to 1/30 the maximum
dark-adapted levels. Dilating the pupil fully can produce a 30-fold increase in the amount of light
entering the eye and facilitating some of the synapses along the visual pathway can perhaps triple its
sensitivity. Hence the entire system may increase its efficiency by a factor of more than one million.

The Neural pathway of vision leads to the occipital lobe.

Generator potentials formed in the dendrites of the rods and cones pass through the cell bodies and
into their axons. At the synapse with the bipolar neurons, neurotransmitters cause an excitation of
the bipolar neurons. The bipolar neurons carry excitatory signals to the ganglion of neurons.

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Diagram of retinal layers

The nervous layer of the retina contains two types of cells that help to transmit information laterally,
the horizontal cells and the amacrine cells. The horizontal cells provide a lateral inhibition to
adjacent areas that are not as strongly activated. If the bipolar neurons are hyperpolarized or not
conveying signals, the horizontal cells serve to excite bipolar cells of adjacent peripheral fields.
Therefore, the input from the peripheral areas is antagonistic to the central area and serves to
increase the perceptual contrast of visual fields. These cells also help in colour differentiation.
Amacrine cells synapse with ganglion cells and provide input on changes in the intensity of
illumination on the retina.

When the bipolar neurons stimulate the ganglion neurons, the ganglion neurons propagate action
potentials down their axons. The axons of the ganglion cells converge to form the optic nerve,
which leaves the posterior part of the eye at the optic disc. These axons pass through the optic
chiasma, which is the point at which some of the axons cross over to the opposite side. Axons from
the medial aspect of each eye cross over; axons from the lateral aspect of each eye do not cross
over. Upon passing through the optic chiasma, the axons enter into the optic tracts. Each optic tract
contains axons from the lateral aspect of the ipsilateral eye (Located on or affecting the same side of
the body) and axons from the medial aspect of the contra-lateral eye. Therefore each optic tract
contains information from the same half of the visual field. The right optic tract conveys
information on the left half of the visual field and vice versa.

16
 Diagram showing the visual
pathway.

The optic tracts end at the lateral geniculate nuclei of the thalamus. Here the ganglion neuron axons
synapse with thalamic neurons whose axons pass to the visual areas of the occipital lobes of the
cerebrum. The visual area of the right occipital lobe interprets information from the left half of an
object and the visual area of the left occipital lobe interprets information from the right half of an
object.

Photoreceptor bipolar neuron ganglion neuron optic

nerve

Optic chiasma optic tract lateral geniculate nucleus visual

cortex of
occipital
lobe

Equilibrium
The inner ear, a receptor complex located in the petrous portion of the temporal bone of the skull,
provides two senses- hearing and balance.
Equilibrium sensations inform us of the position of the head in space by monitoring gravity, linear
acceleration and rotation. Hearing enables us to detect and interpret sound waves. The basic
17
receptor mechanism for both senses is the same. The receptors or hair cells are simple mechano-
receptors. The complex structure of the inner ear and the different arrangement of accessory
structures account for the ability of the hair cells to respond to different stimuli and thus provide the
input for the two different senses.

Anatomy of the Ear

The ear is divided into three anatomical regions: the external ear, middle ear and inner ear.
The external ear is the visible portion that collects and directs sound waves to the ear drum or
tympanum.
The middle ear is an air-filled chamber located within the petrous portion of the temporal bone. The
structures within the middle ear collect sound waves and transmit them to the appropriate portion of
the inner ear. The inner ear contains the sensory organs for hearing and equilibrium.
The external ear includes the fleshy flap and cartilaginous pinna or auricle. Leading from the pinna
is the auditory canal or ear canal, where sound waves travel towards the tympanum. Sounds coming
from the sides or front are collected and channeled towards the ear canal.
The tympanic membrane is a very thin, transparent sheet separating the external and middle ear. The
tympanum is very delicate and is protected to some extent by the ear canal. Ceruminous glands,
integumentary glands along the ear canal secrete waxy materials that help deny access to foreign
objects or insects. The waxy secretion is called creumen, which also slows the growth of
microorganisms in the external auditory canal thereby reducing the chances of infection.

18
The Middle Ear
The Middle Ear or tympanic cavity is filled with air. It is separated from the ear canal by the
tympanum but communicates with the nasopharynx (superior portion of pharynx) through the
auditory tube or Eustachian tube and with the mastoid hair cells through a number of small and
variable connections. This tube is about 4 cm long and consists of two portions. The portion near
the inner ear is relatively narrow and is supported by cartilage. The portion near the opening into the
pharynx is relatively broad and funnel shaped. The auditory tube or Eustachian tube serves to
equalize pressure inside the eardrum with that outside the era drum. Unfortunately it may also
permit microorganisms to travel from the nasopharynx into the middle ear, which can lead to an
infection in the middle ear called otitis media.
The middle ear contains three tiny ear bones collectively called the auditory ossicles. These bones
connect the tympanic membrane with the receptor complex of the inner ear. The three auditor
ossicles are the malleus (hammer), incus (anvil) and stapes (stirrup). The malleus is attached to the
tympanic membrane and the incus. The incus attaches the malleus bone to the stapes. The base of
the stapes is bound to a ligamentous sheet that spans the oval window, an opening in the bone
surrounding the inner ear.
Vibrations from the tympanum convert arriving sound waves into mechanical movements. The
auditory ossicles act as levers that conduct these vibrations to the fluid-filled chamber of the inner
19
ear. The tympanic membrane produces a rocking motion of the stapes. The eardrum is 22 times
larger and heavier than the oval window so a 1 m movement of the tympanum produces 22 m
deflection of the base of the stapes. This little movement may increase from tympanum to oval
window. Because of this amplification we are able to hear faint sounds; however the degree of
amplification can be a problem when we are exposed to loud noises. Within the tympanic cavity,
two small muscles serve to protect the eardrum and ossicles from violent movements under very
noisy conditions.

The Inner Ear

The sense of equilibrium and hearing are provided by the receptors of the inner ear. The receptors
lie within a collection of fluid-filled tubes and chambers known as the membranous labyrinth,
which contains endolymph. Endolymph is a fluid with electrolyte concentrations different from
those of typical body fluids.
The bony labyrinth is a shell of dense bone that surrounds and protects the membranous labyrinth.
Its inner contours closely follow the contours of the membranous labyrinth and its outer walls are
fused with the surrounding temporal bone. Between the bony and membranous labyrinth flows the
perilymph, a liquid whose properties closely resemble those of cerebrospinal fluid. The bony
labyrinth can be subdivided into the vestibule, the semicircular canals and the cochlea.
The vestibule includes a pair of membranous sacs. The receptors in the sacs provide sensations of
gravity and linear acceleration.
The semicircular canals enclose slender semicircular ducts. Receptors in the semicircular ducts are
stimulated by rotation of the head. The combination of vestibular and semicircular canals is called
the vestibular complex; the fluid-filled chamber within the vestibule is broadly continuous with
those of the semicircular canals.

The cochlea is a spiral shaped, bony chamber that contains the cochlear duct of the membranous
labyrinth. Receptors within the cochlear duct provide the sense of hearing. The cochlear duct it
located between a pair of perilymph-filled chambers. The entire complex makes two and a half turns
around a central bony hub.
The walls of the bony labyrinth consist of dense bone everywhere except at two small areas near the
base of the cochlear spiral. The round window is a thin, membranous partition that separates the
perilymph of the cochlear chambers from the air spaces of the middle ear. Collagen fibres connect
the bony margins of the oval window to the base of the stapes. When a sound vibrates the tympanic
membrane, the movements are conducted by the auditory ossicles to the stapes. Movement of the
stapes ultimately leads to the stimulation of the receptors within the cochlear duct and we hear the
sound.

Receptor function in the Inner Ear

20
The sensory receptors in the inner ear are called hair cells. These hair cells are surrounded by
supporting cells and are monitored by sensory afferent fibres. The free surface of each hair cell
supports 80-100 long stereocilia, which resemble very long microvillus. Each hair cell in the
vestibule also contains a kinocilium, a single large cilium. Hair cells do not actively move their
kinocilia and stereocilia. However when an external force pushes against theses processes, the
distortion of the cell membrane alters the rate of chemical transmitter release by the hair cell.
Hair cells provide information about the direction and strength of mechanical stimuli. The stimuli
involved however are quite varied; gravity or acceleration in the vestibule, rotation in the
semicircular canals and sound in the cochlea. The sensitivities of the hair cells differ; because each
these regions have different accessory structures that determine which stimulus will provide the
force to deflect the kinocilia and stereocilia.

Equilibrium
Equlilibrium sensations are provided by receptors of the vestibular complex. The semicircular ducts
provide information about rotational movements of the head. For example when you turn your head
to the left stimulated receptors in the semicircular ducts tell you how raid the movement is and in
which direction. The saccule and the utricle provide information about your position with respect to
gravity. If you stand with your head tilted to one side, these receptors will report the angle involved
and whether your head tilts forwards or backwards. These receptors are also stimulated by receptors
are also stimulated by sudden acceleration. When your car accelerates from a stop, the saccular and
utricular receptors give you the impression of increasing speed.

The Semicircular Ducts

Receptors in the semicircular ducts respond to rotational movements of the head. These hair cells
are active during a movement but quiet when the body is motionless. The anterior, posterior and
lateral semicircular ducts are continuous with the utricle. Each semicircular duct contains an
ampulla, an expanded region that contains the sensory receptors. Hair cells attach to the walls of
the ampulla form a raised structure known as the crista. The kinocilia and stereocilia of the hair
cells are embedded in the cupula, a gelatinous structure. When your head rotates in the plane of the
duct, movement of the endolymph along the canal axis pushes the cupula and distorts the receptor
processes.

21
Fluid movement in one direction stimulate the hair cells and movement in the opposite direction
inhibits them. When the endolymph stops moving the elastic nature of the cupula makes it bounce
back to its normal position.
Even the most complex movements can be analysed in terms of motion in the three rotational
planes. Each semicircular duct responds to one of these rotational movements. A horizontal rotation
as in shaking your head “no” stimulates the hair cells of the lateral semicircular duct. Nodding “yes”
excites the anterior ducts and tilting your head from side to side activates the receptors in the
posterior duct.

22
23
Hearing
The receptors of the cochlear duct provide us with a sense of hearing that enables us to detect the
quietest whisper yet remain functional in a crowded, noisy room. The receptors responsible for
auditory sensations are hair cells similar to those of the vestibular complex. However their
replacement within the cochlear duct and the organization of the accessory structures shield them
from stimuli other than sound. In conveying vibrations from the tympanic membrane to the oval
window, the auditory ossicles convert pressure waves in the air to pressure pulses in the perilymph
of the cochlea. These pressure pulses stimulate hair cells along the cochlear spiral. The frequency of
the perceived sound is determined by how many of the hair cells at that location are stimulated.

The Cochlear Duct

The cochlear duct lies between a pair of perilymphatic chambers; the vestibular duct and the
tympanic duct. The vestibular and tympanic ducts are interconnected at the tip of the cochlear
spiral. The outer surfaces of these ducts are encased by the bony labyrinth everywhere except the
oval window and the round window. The hairs of the cochlear duct are located in a structure called
the Organ of Corti. This sensory structure sits above the basilar membrane, a membrane that
separates the cochlear duct from the tympanic duct. The hair cells are arranged in a series of
longitudinal rows. They lack kinocilia and their stereocilia are in contact with the overlying
tectorial membrane. This membrane is firmly attached to the inner wall of the cochlear duct. When
a portion of the basilar membrane bounces up and down, the stereocilia of the hair cells are
distorted. The basilar membrane moves in response to pressure waves within the perilymph. These
waves are produced when sounds arrive at the tympanic membrane.

24
The Hearing Process
The process of hearing can be divided into six basic steps:

1. Sound waves arrive at the tympanic membrane.

Sound waves enter the external auditory canal and travel toward the tympanic membrane. The
orientation of the canal provides some directional sensitivity. Sound waves approaching the side
of the head have direct access to the tympanic membrane on that side, whereas sound arriving
from another direction must bend around corners or pass through the pinna or other body
tissues.

2. Movement of the tympanic membrane causing displacement of the auditory ossicles.

The tympanic membrane provides the surface for sound collection, and it vibrates in resonance
to sound waves with frequencies between 20 – 20 000 Hz (in a young child). When the
tympanic membrane vibrates so do the malleus and, through their articulations, the incus and
stapes and the sound is amplified.

3. Movement of the stapes at the oval window establishes pressure waves in the
perilymph of the vestibular duct.
Liquids are incompressible; if you push down on one part of a water bed, the water bed bulges
somewhere else. Because the rest of the cochlea is sheathed in bone pressure applied at the oval
window can be relieved only at the round window. When the stapes moves inward the round
window bulges outward. As the stapes moves in and out, vibrating at the frequency of the sound
arriving at the tympanic membrane, it creates pulses or pressure waves within the perilymph.

4. The pressure waves distort the basilar membrane on their way to the round window of
the tympanic duct.

25
The pressure waves established by the movement of the stapes travel through the perilymph of
the vestibular and tympanic ducts to reach the round window. These pressure waves then distort
the basilar membrane. High-frequency sounds, with short wavelength, vibrate the basilar
membrane near the oval window. Low frequency sounds with longer wavelengths vibrate the
basilar membrane farther from the oval window. Thus frequency information is translated into
position information. The amount of force is a function of the intensity of the sound. The louder
the sound, the greater the movement of the basilar membrane.

5. Vibration of the basilar membrane causes vibration of hair cells against the tectorial
membrane.
Vibration of the affected region of the basilar membrane moves hair cells against the tectorial
membrane. This movement leads to the displacement of the stereocilia, which in turn opens ion
channels in their surfaces. A subsequent inrush of ions depolarizes the hair cells. Depolarization
leads to neurotransmitter release and thus to the stimulation of sensory neurons.
The hair cells of the organ of Corti are arranged in several rows. Very soft sound may stimulate
only a few hair cells in the portion of one row. As the intensity of a sound increases, not only do
these hair cells become more active, but additional hair cells are stimulated as well. The number
of hair cells responding in a given region of the organ of Corti thus provides information on the
intensity of the sound.

6. Information about the region and intensity of stimulation is relayed top the CNS over
the cochlear branch of the vestibulocochlear nerve (Nerve VIII).
The cell bodies of the bipolar sensory neurons that monitor the cochlear hair cells are located at
the center of the bony cochlea in the spiral ganglion. From there, the information is carried to
the cochlear nuclei of the medulla oblongata for subsequent distribution to other centres of the
brain.

26
Hearing in Fish

A very simple us e of hair cells to measure displacement can be seen in the lateral line sensory
system of fishes. The lateral line is a canal just under the surface of the skin that runs down
each side of the fish. Hair cells line he canal and their stereocilia, protected by capsules of
gelatinous material called cupulae, project into the stream of water that flows through the lateral
line canal when the fish moves through the water. Forward movement of the fish puts pressure
on the cupulae causing the stereocilia to bend in the direction that depolarizes the hair cells.
Since water is incompressible, disturbances in the water around the fish are translated into
pressure waves that can be picked up by the lateral line stereocilia. Thus the lateral line system
provides information about the fish’s movements as well as other moving objects such as
predators or prey. Sound in water also consists of pressure waves in water allowing fish to hear
through the lateral line system.

27
Accommodation Problems

In the healthy eye, when the ciliary muscles are relaxed and the lens is flattened, a distant image
will be focused on the retinal surface (Figure 17-15a). This condition is called emmetropia
(emmetro-, proper), or normal vision.
Figure 17-15b, c diagrams two common problems with the accommodation mechanism. If
the eyeball is too deep or the resting curvature of the lens too great, the image of a distant object
will form in front of the retina (Figure 17-15b). The individual will see distant objects as blurry and
out of focus. Vision at close range will be normal, because the lens will be able to round up as
needed to focus the image on the retina. As a result, such individuals are said to be nearsighted.
Their condition is more formally termed myopia (myein, to shut + ops, eye). Myopia can be treated
by placing a diverging less in front of the eye (Figure 17-15d). This lens shape, typical of the lens
used in prescription corrective glasses, spreads the light rays apart as if the object were closer to the
viewer.

28
If the eyeball is too shallow or the lens too flat, hyperopia results (Figure 17-15c). The ciliary
muscles must contract to focus even a distant object on the retina, and at close range the lens cannot
provide enough refraction to focus an image on the retina. Individuals with this problem are said to
be farsighted, because they can see distant objects most clearly. Older individuals become farsighted
as their lenses lose elasticity; this form of hyperopia is called presbyopia (presbys, old man).
Hyperopia can be corrected by placing a converging lens in front of the eye. This lens provides the
additional refraction needed to bring nearby objects into focus (Figure 17-15e).
Variable success at correcting myopia and hyperopia has been achieved by surgically
reshaping the cornea to alter its refractive powers. This procedure, called radial keratotomy,
remains controversial. Although roughly two-thirds of patients are satisfied with the results, corneal
healing takes several years. Many ophthalmological surgeons have expressed concerns that the
scarring that develops after radial keratotomy creates weak points in the cornea that may increase
the chances for a dangerous corneal rupture.
Another controversial procedure is photorefractive keratectomy (PRK), in which a
computer-guided laser shapes the cornea to exact specifications. Tissue is removed only to a depth
of 10-20 m – no more than about 10 percent of the cornea’s thickness. The entire procedure can be
done in less than a minute. Each year, an estimated 100,000 people undergo PRK therapy in the
United States. Advances in laser design and improvements in accuracy may make the procedure
more popular during the next decade.

29
Glaucoma
If aqueous humor cannot enter the canal of Schlemm (a circular channel in the eye that collects
aqueous humor from the anterior chamber and delivers it into the bloodstream), the condition of
glaucoma results.
Although drainage is impaired, the production of aqueous humor continues, and the intraocular
pressure begins to rise. The fibrous scleral coat cannot expand significantly, so the increasing
pressure begins to distort soft tissues within the eye. The tough sclera cannot enlarge like an
inflating balloon, but it does have one weak point, where the optic nerve penetrates the wall of the
eye. Because the optic nerve must penetrate all three tunics, it is not wrapped in connective tissue.
When intraocular pressures have risen to roughly twice normal levels, the distortion of the nerve
fibers begins to block action potential propagation, and vision begins to deteriorate. If this condition
is not corrected, blindness eventually results.
Glaucoma affects roughly 2 percent of the population over age 35. In most cases, the
primary factors responsible cannot be determined. Because glaucoma is a relatively common
condition – over 2 million cases in the United States alone – most eye exams include a test of
intraocular pressure. Glaucoma may be treated by the application of drugs that constrict the pupil
and tense the edge of the iris, making the surface more permeable to aqueous humor. Surgical
correction involves perforating the wall of the anterior chamber to encourage drainage. This
procedure is now performed by laser surgery on an outpatient basis.

Cataracts
This conditions results from the lens losing its clarity, that is, it becomes opaque. This prevents light
from effectively passing through the lens resulting in blurred vision. The condition worsens with
time and is most successfully treated by lens replacement surgery.

Hearing Deficits
There are probably more than 6 million people in the United States alone who have at least a partial
hearing deficit. Conductive deafness results from conditions in the outer or middle ear that blocks
the normal transfer of vibration from the tympanic membrane to the oval window. An external
auditory canal plugged with accumulated wax or trapped water may cause a temporary hearing loss.
Scarring or perforation of the tympanic membrane and immobilization of one or more of the
auditory ossicles are more serious causes of conductive deafness. In nerve deafness, the problem
lies within the cochlea or somewhere along the auditory pathway. The vibrations reach the oval
window and enter the perilymph, but the receptors either cannot respond or their response cannot
reach its central destinations.

For example:
Very loud (high-intensity) sounds can produce nerve deafness by breaking stereocilia off the
surfaces of the hair cells. Loud noises can cause damage to the hair cells in the inner ear and to the
hearing nerve, called sensorineural hearing loss or nerve deafness. (Sensorineural hearing loss also
can be caused by infection, head injury, aging, certain medications, birth defects, tumors, problems
with blood circulation or high blood pressure, and stroke.)

Damage can occur from a brief, intense noise such as an explosion, or from continuous loud noises
such as noises in a loud work environment. Hearing loss from loud noises may be immediate or
occur slowly over years of continuous exposure.

Immediate hearing loss is often accompanied by tinnitus, or ringing in the ears or head. Immediate
hearing loss can occur in one or both ears and often involves severe damage to the inner ear
structure.
30
Hearing loss from noise can be permanent or temporary. If the hearing loss is temporary, hearing
usually recovers within 16 hours of loud noise exposure.

Drugs such as the aminoglycoside antibiotics (neomycin or gentamicin) may diffuse into the
endolymph and kill the hair cells. Because hair cells and sensory nerves can also be
damaged by bacterial infection, the potential side effects must be balanced against the
severity of infection.

There are many treatment options for conductive deafness; treatment options for nerve are relatively
limited. Because many of these problems become progressively worse, early diagnosis improves the
chances of successful treatment.

Perforated Eardrum
A perforated eardrum is a hole or rupture in the eardrum, a thin membrane that separates the ear
canal and the middle ear. The medical term for eardrum is tympanic membrane. The middle ear is
connected to the nose by the eustachian tube, which equalizes pressure in the middle ear.

A perforated eardrum is often accompanied by decreased hearing and occasional discharge. Pain is
usually not persistent.

Causes Of Eardrum Perforation

The causes of perforated eardrum are usually from trauma or infection. A perforated eardrum can
occur:

If the ear is struck squarely with an open hand

With a skull fracture
After a sudden explosion
If an object (such as a bobby pin, Q-tip, or stick) is pushed too far into the ear canal.
As a result of hot slag (from welding) or acid entering the ear canal

Middle ear infections may cause pain, hearing loss, and spontaneous rupture (tear) of the ear-drum
resulting in a perforation. In this circumstance, there maybe infected or bloody drainage from the
ear. In medical terms, this is called otitis media with perforation. (Source:
http://www.entnet.org/healthinfo/ears/perforation.cfm)

In the short term, fatigue of the hair cells in the cochlea leads to short-term hearing loss, or
temporary threshold shift. It may last for a few minutes, hours or days after starting on a noisy job,
and is essentially a reversible adaption of the hair cells to an unwanted excess of sound energy.

In the longer term, permanent noise-induced hearing loss, or deafness, is produced if exposure
continues to noise of high intensity. The hair cells of the inner ear are eventually killed by such
high-intensity noise, which is why resulting hearing loss is permanent and irreversible.

Noise not only damages hearing sensitivity but can also give rise to tinnitus, a disturbing ringing in
the ear. This usually persists and is especially worrisome at night when it can prevent getting to
sleep. In people with normal hearing it is rarely heard, but as deafness sets in the echo becomes
tormenting.
31
With advancing years the auditory sensitivities diminish, particularly in the higher frequency end of
the spectrum (4000 to 6000 Hz). This occurs irrespective of whether a person has been exposed to
noise.

Very loud, impact noises from explosions cause a special form of damage termed acoustic trauma.
The burst of energy accompanying impulse noise can not kill the hair cells of the inner ear, but can
damage the eardrum and ossicles. The eardrum can generally repair itself over time, but the hair
cells can not. (Source: http://www.workcover.tas.gov.au/resource/noise.htm)

Motion Sickness
The exceedingly unpleasant symptoms of motion sickness include headache, sweating, flushing of
the face, nausea, vomiting, and various changes in mental perspective. (Sufferers may go from a
state of giddy excitement to almost suicidal despair in a matter of moments.) It has been suggested
that the condition results when central processing stations, such as the mesencephalic tectum,
receive conflicting sensory information. Why and how these conflicting reports result in nausea,
vomiting, and symptoms are not known. Sitting below the deck on a moving boat or reading in a car
or airplane tends to provide the necessary conditions. Your eyes (which are tracking lines on a page)
report that your position in space is not changing, but your labyrinthine receptors report that your
body is lurching and turning. As a result, seasick sailors watch the horizon rather than their
immediate surroundings so that their eyes will provide visual confirmation of the movements
detected by their inner ears. It is not known why some individuals are almost immune to motion
sickness, whereas others find travel by boat or plane almost impossible.
Drugs commonly administered prevent motion sickness include dimenhydrinate
(Dramamine), scopolamine, and promethazone. These compounds appear to depress activity at the
vestibular nuclei. Sedatives, such as prochlorperazine (Compazine), may also be effective.
Scopolamine can be administered across the skin surface by using an adhesive patch (Transderm-
Scop).

32
Smelling disorders
Definition

Smelling disorders are disturbances of the olfactory sense, which is known as the sense of smell.
These nasal dysfunctions range from the total loss of smell (anosmia) to dysosmia, a distorted
sense of smell.

Description

An awareness of how the olfactory system works is helpful for understanding how smelling
disorders affect the sense of smell. People detect odours because sensory receptors located in the
nose carry smell sensations to the brain. The receptors, which are nerve cell endings, are found in
the mucous membrane in the roof of the nose. This section of the nose called the olfactory area is
located just below the brain's frontal lobes.

In the olfactory area are millions of tiny olfactory cells. Each cell contains about 12 cilia, tiny hairs
that extend into a mucus layer. The mucus moistens the cilia. Mucus also catches odour molecules,
while receptors in the cilia stimulate the molecules and send nerve impulses to the brain.

Olfactory nerve fibers carry the impulse to two olfactory bulbs located in the brain. Information is
processed in the bulbs and then sent to the cerebral cortex. Once the transmission is inside the smell
center of the brain, a person experiences the sense of smell.

A person with a normal sense of smell (normosmia) is able to distinguish 10,000 odours. The sense
of smell stimulates salivary glands. As a result, smelling disorders often affect the sense of taste.
The olfactory sense allows people to experience pleasurable odors like the scent of roses. And smell
is thought to contribute to sexual attraction.

A smelling disorder that affects the sense of smell is generally not life-threatening. However, it can
be dangerous. Without a sense of smell, a person might eat spoiled food. Lack of a sense of smell
could pose a health risk if a person has little appetite and fails to eat enough. Furthermore, without a
sense of smell, a person might not detect a gas leak or the smell of something burning. Loss of smell
and the resulting loss of taste may lead to depression.

Types of smelling disorders

Smelling disorders differ in the way that the sense of smell is affected and how long a person has
the disorder. For example, anosmia, the loss of the sense of smell, is often a temporary symptom of
a cold or flu. However, a head injury could cause permanent anosmia. In addition, a head injury
could produce dysosmia, the distorted sense of smell that could cause a person to hallucinate a foul
odour.

Smelling disorders are categorized as:

 Anosmia, the loss of the sense of smell. It is the most common smelling disorder. This
condition can be temporary or permanent.
 Dysosmia is a distorted sense of smell. A person senses non-existent unpleasant odours. It
can be caused by medical and mental conditions.

33
  Hyperosmia is an increased sensitivity to smell. It can be a characteristic of someone with a
neurotic or histrionic personality.
 Hyposmia is the diminished sense of smell. This is usually a temporary condition that a
person may experience after a case of acute influenza. Sometimes this condition is referred
to as partial anosmia.
 Presbyosmia refers to the lessening or loss of the olfactory sense that occurs when a person
ages.

Causes and symptoms

Anosmia is the most common type of smelling disorder. Loss of the olfactory sense is generally
caused by nasal congestion or obstruction. Temporary partial anosmia often occurs when a person
has a cold, the flu, or some types of rhinitis, especially hay fever (allergic rhinitis). During these
conditions, nasal mucus membranes become inflamed. Other causes for anosmia are:
 Nasal polyps and other disorders that prevent air from getting to the area in the nose where
the smell receptors are found. Hay fever or an allergy may cause one or more polyps to show
up.
 Viral upper respiratory infection.
 Atrophic rhinitis. This condition causes mucus membrane to waste away. The person may
experience some level of permanent anosmia. One symptom of this condition is that a
person expels a foul-smelling discharge.
 Hypertrophic rhinitis. Mucous membrane thickens, covering the olfactory nerve endings. If
not treated, hypertrophic rhinitis can lead to permanent anosmia. This discharge could
overpower other odors.
 Cigarettes. Smoking aggravates the nose's membrane and intensifies nasal polyp symptoms.
 A crooked nose or a deviated septum.
 When the olfactory bulbs, tracts, or central connections are destroyed. This can occur in
situations such as head trauma, infections or nasal or sinus surgery.
 Head injury. If both olfactory nerves are torn during a head injury, permanent anosmia
results.
 Medications such as antihistamines and decongestants, especially prolonged use of
decongestants.
 Drugs like amphetamines, estrogen, naphazoline, phenothiazines, and resperine.
 The aging process may cause the sense to lessen. In most cases, there is no other obvious
cause for the disorder.
 A tumor behind the nose or in the membranes surrounding the brain.
 Lead poisoning.
 Exposure to insecticides or other chemicals.
 Radiation therapy.
 Nervous disorders.
 Idiopathic loss, which means there is no diagnosable cause for the condition.

Anosmia symptoms

Most people with anosmia can distinguish salty, sweet, bitter, and sour tastes since the tongue
senses these tastes. However, people with anosmia cannot sense other tastes. Since taste is largely
based on the olfactory sense, people complain of losing the sense of taste.

Basic treatments for anosmia

The sense of smell should return after a condition like a cold or the flu ends. Decongestants such as
Sudafed help reduce congestion related to colds, allergies, and sinus conditions. Manufacturer's
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dosage recommendations should be followed. If anosmia is related to excessive use of nasal
decongestants, a person should discontinue use of those medications.

Saline sprays can be used to clean the interior of the nose.

If smoking causes anosmia, a person should quit smoking.

The sense of smell may return after treatment of allergic or bacterial rhinitis and sinusitis. An over-
the-counter antihistamine such as Actifed may provide relief.

If allergies cause anosmia, adjustments should be made to avoid allergens. If dust causes allergies,
care should be taken to clean areas such as the bedroom.

Antibiotics may be prescribed for infections.

Dysosmia

Infected nasal sinuses and damage to the olfactory bulbs can cause dysosmia, the distorted sense of
smell. Head trauma can cause this disorder. Poor oral hygiene can lead to dysosmia. In these cases,
a person may also find that disagreeable odours are accompanied by the sensing of unpleasant
tastes. In addition, brain-stem disease can cause smelling disorders. An epileptic seizure can include
olfactory hallucinations.

 Mental conditions such as depression and schizophrenia may be accompanied by dysosmia.

In addition, when persons are severely dependent on alcohol and quit drinking, they may
experience dysosmia.

Diagnosis

If a smelling disorder is a symptom of a mental condition such as schizophrenia, diagnosis should

be part of treatment for that condition.

When the condition is caused by a medical condition such as allergies or a viral infection, a person
may notice that the olfactory sense is impaired during that condition. If the smelling disorder
continues after the person is well, an appointment should be made with a primarily health care
provider.

Diagnosis of smelling disorders begins with a health assessment to determine the cause of the
olfactory impairment. The patient's primary care doctor will ask if the patient has a cold, allergies,
sinusitis, or an upper respiratory infection.

Treatment of a head injury or follow-up medical appointment should address smelling disorders. In
all cases, discussion of the symptoms covers issues such as when the smelling disorder started, if
this has been an ongoing problem, and whether the disorder is becoming more intense. The
assessment will include questions about whether the patient can taste food and if the disorder affects
all odours or specific smells. The patient will also be asked about medications taken.

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Source: http://www.healthatoz.com/healthatoz/Atoz/ency/smelling_disorders.jsp

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