Special Senses
Special Senses
• The human body has two basic types of senses, called special senses and
general senses.
• Special senses have specialized sense organs that gather sensory information and
change it into nerve impulses.
• Special senses include vision, hearing, taste, and smell.
• Special senses are processed via cranial nerves and differ from the pathway
utilized in processing general senses.
Lacrimal
Apparatus:
Consists of
Lacrimal Gland (Tear Gland):
Located in the orbit above the eye.
- Secretes dilute saline (Lacrimal secretion/tears)
Lacrimal Canaliculi:
2 openings on medial margin of each eyelid.
- Drains tears into the Lacrimal Sac → Nasolacrimal Duct
→ Nose
VISUAL RECEPTORS
Rods
Very sensitive to light and have a low threshold
So, the rods are responsible for dim light vision or night vision or scotopic
vision
But, rods do not take part in resolving the details and boundaries of objects
(visual acuity) or the color of the objects (color vision)
Vision by rod is black, white or in the combination of black and white namely,
grey
Therefore, the colored objects appear faded or greyish in twilight
Rhodopsin or visual purple is the photosensitive pigment of rod cells
Rhodopsin
Conjugated protein with a molecular weight of 40,000
Made up of a protein called opsin and a chromophore
Opsin present in rhodopsin is known as scotopsin
Chromophore is a chemical substance that develops color in the cell
Chromophore present in the rod cells is called retinal
o Light Adaptation:
Occurs when we move from Darkness into Bright Light. We
are momentarily dazzled – as the retina is still “set” for dim
light. At this point, both Rods & Cones are strongly
stimulated, causing large amounts of Photopigment to be
broken down → Floods the brain with signals
→ Glare.
To Compensate, the Rod system quickly desensitises and
essentially turns off. The Cone system rapidly adapts, and
takes over. Hence, overall the retina Desensitises.
Can take up to 60sec.
o Dark Adaptation:
Occurs when we move from Brightness to Darkness.
Initially we see nothing but black because:
1. Cones stop functioning in low light. &
2. Because Rods have been ‘bleached’ out by the bright
light & are still turned off.
Once rhodopsin accumulates in the Rods, their function slowly
increases.
Can take more than 30mins.
Nervous pathway that transmits impulses from retina visual center in cerebral
cortex
In binocular vision, the light rays from temporal (outer) half of visual field fall
upon the nasal part of corresponding retina
The rays from nasal (inner) half of visual field fall upon the temporal part of
retina
Rods and cones which are present in the retina of eye form the visual receptors
Fibers from the visual receptors synapse with dendrites of bipolar cells of inner
nuclear layer of the retina
[Link] visual area (area 17), which is concerned with the perception of
visual impulses
[Link] visual area or visual association area (area 18), which is concerned
with the interpretation of visual impulses
[Link] eye field (area 19), which is concerned with the movement of eyes
Visual pathway consists of six components:
1. Optic nerve
2. Optic chiasma
3. Optic tract
4. Lateral geniculate body
5. Optic radiation
6. Visual cortex
Refractive errors of eye
[Link]
The eye with normal refractive power is called emmetropic eye and the
condition is called emmetropia
2. Hypermetropia
Myopia is the eye defect characterized by the inability to see the distant object
It is otherwise called short sightedness because the person can see near objects
clearly but not the distant objects
In myopia, the near vision is normal but the far point is not infinite, i.e. it is at
a definite distance
In extreme conditions, it may be only a few centimeter away from the eye
Light rays, after coming to a focus, disperse again so, a blurred image is
formed upon retina
Correction
By using concave lens
HYPERMETROPIA OR LONG SIGHTEDNESS
It is otherwise known as long sightedness because the person can see the
distant objects clearly but not the near objects
So, even though the refractive power of lens is normal, the light rays are not
converged enough to form a clear image on retina, i.e. the light rays are
brought to a focus behind retina
[Link]
Condition in which the two eyes have unequal refractive power
It is corrected by using different appropriate lens for each eye
[Link]
Astigmatism is the condition in which light rays are not brought to a sharp
point upon retina
For example, the stars appear as small dots of light to a person with normal eye
CAUSE OF ASTIGMATISM
Normally, the cornea and lens are smooth and curved equally in all directions,
helping to focus light rays sharply onto the retina at the back of your eye
However, if your cornea or lens isn't smooth and evenly curved, light rays
aren't refracted properly
When the shape of the lens is distorted, you have lenticular astigmatism
TYPES OF ASTIGMATISM
1. Regular Astigmatism
Loss of elasticity in lens and weakness of ocular muscles due to old age
In presbyopia, the anterior curvature of lens does not increase during near
vision
So, the light rays from near objects are not brought to focus on retina
CAUSES OF PRESBYOPIA
[Link] elasticity of lens is because of the physical changes in lens and its
capsule during old age. So, the anterior curvature is not increased during near vision
CORRECTION OF PRESBYOPIA
Presbyopia is corrected by using biconvex lens
GLAUCOMA
Group of diseases characterized by increased intraocular pressure, which
causes damage of optic nerve, resulting in blindness
In glaucoma, the drainage of aqueous humor through trabeculae is
blocked, resulting in increased intraocular pressure
When the intraocular pressure rises above 60 mm Hg, theoptic nerve fibers at
the optic disk are compressed
Initially it decreases the visual field (loss of peripheral vision),
which eventually leads to total blindness
However, with early treatment, often the eyes may be protected against
serious vision loss
Untreated glaucoma leads to permanent damage of the optic nerve and results
in blindness
In old age, glaucoma occurs due to the obstruction of
trabeculae by fibrous structures
Types of Glaucoma
● Elevation of intraocular pressure causing glaucoma can occur at any stage of
life
● Congenital glaucoma develops in babies born with increased intraocular
pressure
● Glaucoma in infants is called infantile glaucoma
● When it occurs in childhood, it is known as juvenile glaucoma
Causes of Glaucoma
Major cause of glaucoma is the blockage in drainage
system of aqueous humor in trabeculae, resulting in
increased intraocular pressure
Glaucoma also develops secondary to other disorders, which affect the eyes
Common causes of secondary glaucoma are Diabetes, inflammation
or injury to eye and excess use of drugs such as
corticosteroid
Symptoms of Glaucoma
CATARACT
Cataract is the opacity or cloudiness in the natural lens of the eye
It is the major cause of blindness worldwide
When lens becomes cloudy, light rays cannot pass through it easily and vision
is blurred
Cataract develops in old age after 55 to 60 years
Lens is situated within the sealed capsule
Old cells die and accumulate withinthe capsule
Over years, the accumulation of cells is associated with accumulation of
fluid and denaturation of proteins in lens fibers, causing
cloudiness of lens and blurred image
Causes of Cataract
In addition to age, cataract develops due to many other causes such as:
Eye injuries
Previous eye surgery
Diseases such as diabetes, Wilson disease and hypocalcemia
Long-term use of drugs such as steroids, diuretics and
tranquilizers
Long-term unprotected exposure to sunlight
Alcoholism
Family history
Diet containing large quantity of salt
Symptoms of Cataract
Ear Anatomy:
Outer Ear ( Air Filled)
o Pinna (Auricle):
The Outermost part of the ear
The bit that funnels sound waves into the External Auditory
Canal
Collects sound
Helps in sound localization
Most efficient in directing high frequency sounds to the
eardrum
Protection
Localization
Collect sound
Resonator
- Middle Ear:
(Air-Filled Cavity within the Temporal Bone)
o Tympanic Membrane (Eardrum):
Thin, translucent, connective Tissue Membrane (Skin on
outside, mucosa on inside)
Connect to the 3 Auditory Ossicles
Soundwaves cause it to vibrate → Causes the Auditory Ossicles
to Vibrate.
o The 3 Auditory Ossicles:
Malleus(“Hammer”/“Mallet”)
Incus (“Anvil”)
Stapes (“Stirrup”)
Note: 2 Skeletal Muscles (Tensor Tympani & Stapedius)
Reflexively contract when ears are assaulted by loud
sounds – Reduces Sound Conduction.
o Oval Window of the Cochlea:
Transfers Vibration of the Stapes → Into the Cochlea.
o Eustachian (Pharyngotympanic) Tube:
Equalizes pressure between the Outer & Middle Ear
MIDDLE EAR
Middle ear or tympanic cavity is a small, narrow, irregular, laterally
compressed chamber
It is also known as tympanum
It is separated from external auditory meatus by tympanic membrane
Middle ear consists of the following structures:
1. Auditory ossicles
2. Auditory muscles
3. Eustachian tube
Tympanic Membrane:
Thin, semitransparent membrane
AUDITORY OSSICLES
Auditory ossicles are the three miniature bones, which are arranged in the form
of a chain, extending across the middle ear from the tympanic membrane to
oval window
Auditory ossicles are:
A: Malleus -hammer
B: Incus -anvil
C: Stapes- stirrup
i. Malleus
Malleus is otherwise called hammer
It has a handle, head and neck
Hand is called manubrium and it is attached to tympanic membrane
Neck extends from handle to the head
Head or capitulum articulates with the body of incus
Malleus Incus
ii. Incus
It looks like a premolar tooth
Incus has a body, one long process and one short process
Anterior surface of the body articulates with the head of malleus
The short process is attached to a ligament
The long process runs parallel to handle of malleus
Tip of the long process is like a knob called lenticular process and it
articulates with the next bone, stapes
iii. Stapes
Stapes is also called stirrup
AUDITORY MUSCLES
i. Tympanic reflex protects the tympanic membrane from being ruptured by loud
sound
ii. It also prevents fixation of footplate of stapes, against oval window, during
exposure to loud sound
iii. It helps to protect the cochlea from damaging effects of loud sounds
Contraction of tensor tympani and stapedius during exposure to loud sound
develops stiffness of the auditory ossicles so that, the transmission of sound
into cochlea is decreased
Eustachian Tube
The eustachian tube connects the front wall of the middle ear with the
nasopharynx
The eustachian tube also operates like a valve, which opens during swallowing
and yawning
This equalizes the pressure on either side of the eardrum, which is necessary
for optimal hearing
-
o Cochlea - HEARING:
The Spiral-Shaped Organ
Begins @ the Oval Window:
The Entry Point of the Cochlea.
The hole covered by membrane
Separates the air-filled middle ear from the fluid-filled
inner ear.
Ends @ the Round Window:
The Exit-Point of the Cochlea
Also covered by membrane
Also separates the air-filled middle ear from the fluid-
filled inner ear.
Consists of 3 Coiled Ducts – Separated by 2 Membranes:
Scala Vestibuli (Vestibular Duct):
o Begins @ the Oval Window
o Ends @ the apex of the Cochlea
o Filled with Perilymph.
o Separated from the Scala Media by the Vestibular
Membrane.
Scala Media (Cochlear Duct):
o Runs through the middle of the Cochlea.
o Separates the Vestibular Duct & Tympanic Duct.
o Filled with Endolymph.
o Separated from the Scala Tympani by the Basilar
Membrane.
o Contains the Spiral Organ of Corti: (See Next
Page)
Scala Tympani (Tympanic Duct):
o Begins @ the apex of the Cochlea
o Ends @ the Round Window
o Filled with Perilymph
.
The Spiral Organ of Corti:
Sits inside the Scala Media & runs along the Basilar
Membrane.
Composed of:
o The Tectorial Membrane (Overlying the Hair
Cells)
o Hair Cells (Receptors for hearing) – Associated
with cochlear nerve fibres:
1x Row of Inner Hair Cells – Has several
inputs to the Spiral Ganglion
- Sends most of the
auditory info.
3x Rows of Outer Hair Cells – Has Only 1
input to the Spiral Ganglion
- Plays a role in Signal
Amplification
o Supporting Cells
o The Basilar Membrane
Cochlear Branch of the Vestibulocochlear Nerve
Originates Here.
Audiotransduction:
- Soundwaves are funnelled by the Auricle of the ear into the External
Auditory Canal.
- → Soundwaves vibrate the Tympanic Membrane (Eardrum)
- → Eardrum vibration is passed through the Auditory Ossicles to the Oval
Window.
o Note: This transfer of vibration from the Eardrum→Oval
Window AMPLIFIES it by ≈20x (As the eardrum surface area
is ≈20x that of the Oval Window)
Receptor Type:
- Chemoreceptors (Respond to chemicals dissolved in solution)
TASTE BUDS
Sense organs for taste or gustatory sensation are the taste buds
Taste buds are ovoid bodies with a diameter of 50 μ to 70 μ
In adults, about 10,000 taste buds are present and the number is more in children
In old age, many taste buds degenerate and the taste sensitivity decreases
Filiform papillae
Fungiform papillae
Circumvallate papillae
1. Filiform Papillae
Filiform papillae are small and conical-shaped papillae, situated over the dorsum
of tongue These papillae contain less number of taste buds (only a few)
2. Fungiform Papillae
Fungiform papillae are round in shape and are situated over the anterior surface
of tongue near the tip
Numerous fungiform papillae are present
Each papilla contains moderate number of taste buds (up to 10)
[Link] papillae
Large structures present on the posterior part of tongue and are many in number
These papillae are arranged in the shape of ‘V’
Each papilla contains many taste buds (up to 100)
Taste bud
Bundle of taste receptor cells, with supporting cells embedded in the epithelial
covering of the papillae
Each taste bud contains about 40 cells, which are the modified epithelial cells
Cells of taste bud are divided into four groups:
Type of Cells in Taste Bud
Type I cells or sustentacular cells
Type II cells
Type III cells
Type IV cells or basal cells.
Type I cells and type IV cells are supporting cells
Type III cells are the taste receptor cells
Function of type II cell is unknown
Type I, II and III cells have microvilli, which project into an
opening in epithelium covering the tongue
This opening is called taste pore
-
- Basic Taste Sensations:
o Sweet - Sugars, some Amino Acids, Lead Salts
o Sour - Acids
o Salt - Metal Ions (Particularly Sodium)
o Bitter - Alkaloids (Quinine, Caffeine, and Nicotine) – Note: Dislike for
bitter is Protective.
o Umami - “Delicious” - Glutamate (Steak, Cheese) & MSG.
o Note: Most ‘tastes’ are a mixture of these basic taste sensations.
- Physiology of Taste:
o Tasting requires a chemical to dissolve in the saliva, then diffuse
through a Taste Pore, and contact
Gustatory Hairs.
o Binding of chemical induces a depolarising potential → Release of
Neurotransmitter.
o Neurotransmitter → Triggers dendrites of sensory nerves → Action
Potentials.
o Note: Different receptor cells have different thresholds (Eg: Bitter cells
are very sensitive)
- Taste Transduction:
o Basic Overview:
Stimulation of Gustatory Cell → leads to an ↑in intracellular
[Ca+] → Causes NT Release → Stimulates sensory nerves.
o Each taste-quality has its own way of stimulating the receptor cells:
Salty – due to Na+ influx → directly depolarises the Gustatory
Cell.
Sour – due to H+ either: 1) Entering the cell, 2) Opening
Ion Channels, or 3) Blocking K+ Channels
Bitter, Sweet & Umami – G-Protein Linked Receptors that
produce depolarisation.
- Gustatory Pathway:
o Afferent fibres from taste buds run in 3 Cranial Nerves:
Facial (first 2/3 of tongue)
Glossopharyngeal (last 1/3 of tongue)
Vagus (Epiglottis & Lower Pharynx)
o Afferent Fibres synapse in the Solitary Nucleus of the Medulla →
Thalamus → Gustatory Cortex in Parietal Lobes.
OLFACTION (SMELL)
Olfaction (Smell):
* Olfaction is a chemoreception that forms the sense of smell.
* Olfaction has many purposes, such as the detection of hazards,
pheromones, and food.
* It integrates with other senses to form the sense of flavour.
* Olfaction occurs when odorants bind to specific sites
on olfactory receptors located in the nasal cavity.
OLFACTION
Olfactory receptors are situated in olfactory mucus membrane, which is the
modified mucus membrane that lines upper part of nostril
Olfactory mucus membrane consists of 10 to 20 millions of olfactory
receptor cells supported by the sustentacular cells
Mucosa also contains mucus-secreting Bowman glands
Olfactory receptor cell is a bipolar neuron
Dendrite of this neuron is short and it has an expanded end called olfactory
rod
From olfactory rod, about 10 to 12 cilia arise
Cilia are non-myelinated, with a length of 2 μ and a diameter of 0.1 μ
These cilia project to the surface of olfactory mucus membrane
Mucus secreted by Bowman glands continuously lines the olfactory mucosa
Mucus contains some proteins, which increase the actions of odoriferous
substances on receptor cells
Olfactory pathway
* Axons of the bipolar olfactory receptors pierce the cribriform plate of
ethmoid bone and reach the olfactory bulb.
* Here, the axons synapse with the dendrites of mitral cells.
* Different groups of these synapses form globular structures, called olfactory
glomeruli.
* The axons of mitral cells leave the olfactory bulb and form olfactory tract.
* The olfactory tract runs backwards and ends in olfactory cortex through the
intermediate and lateral olfactory stria.
* The olfactory cortex includes the structures, which form a part of limbic
system.
* The structures are anterior olfactory nucleus, prepyriform cortex, olfactory
tubercle and amygdala.
Abnormalities of olfactory sensation
ANOSMIA
* Anosmia refers to total loss of sensation of smell.
* It may be temporary or permanent.
* Temporary anosmia is due to obstruction of nose which occurs during
common cold, nasal sinus and allergic conditions.
* Permanent anosmia occurs during lesion in olfactory tract, meningitis and
degenerative conditions such as Parkinson’s disease and Alzheimer’s
disease.
HYPOSMIA
* It is the reduced ability to recognize and to detect any odour.
* The odour can be detected only at higher concentrations.
* It is the most common disorder of smell.
* It may be temporary or permanent.
* It occurs due to the same cause of anosmia.
HYPEROSMIA
* It is the increased or exaggerated olfactory sensation.
* It is also called olfactory hyperesthesia.
It occurs in brain injury, epilepsy and neurotic conditions.