SPECIAL SENSES

SENSE OF VISION

(ANATOMY OF EYEBALL REFER TO ANATOMY NOTES)

LAYERS OF RETINA

1. Layer of pigmented epithelium:

 Absorbs stray light and thereby reduces light scatter
 Phagocytize the ends of the outer segments of rods which are continuously shed
 Recycle the metabolized photopigments for reuse
2. Layers of rods and cones
 End organs of vision which transform light energy into visual (nerve) impulse
 RODS contains visual purple and used for peripheral vision /low light intensity (scotopic)
 CONES for highly discriminatory central vision (photopic vision) and color vision
3. External limiting membrane
 numerous connections made between Muller cells and inner segments of photoreceptors
 formed by glial cells
4. Outer nuclear layer
 Formed by nuclei of rods and cones
5. Outer plexiform layer
 Contains pre-synaptic and post-synaptic elements of synapses that exist between the
photoreceptors, bipolar cells and horizontal cells
6. Inner nuclear layer
 Bipolar cells small, oval and flattened cells. Its dendrites synapse with dendrites of
ganglion cell present in inner plexiform layer. Dendrites of B.C synapse with rods and cones
present in outer plexiform layer
 Horizontal cells transmits signals horizontally in the outer plexiform layer from rods and
cones to the bipolar cells and to enhance the visual contrast by causing lateral inhibition
 Amacrine cells make synaptic contact dendrites of both ganglion and bipolar cells and
connects to ganglion cells to one another and receive information at the synapse of bipolar cell
axon with ganglion cell dendrite and use this information for temporal processing
7. Inner plexiform layer
 Layer of synapse between bipolar cells, ganglion cells and amacrine cells
8. Ganglion cell layer
 Consists of ganglion cells, which are the output cells of the retina. They transmit visual
information to the brain.
9. Nerve fiber layer
 Consists of the axons of ganglion cells which pass through lamina cribrosa to form the optic
nerve
10. Inner limiting membrane
 Formed by projections of the Muller’s cells and separates the retina from vitreous
STRUCTURE OF PHOTORECEPTORS

RODS

 40-60 µm

Outer segments (Modified cilia)

 Cylindrical, highly refractile , transversely striated

 Photopigment Visual purple (RHODOPSIN)
 Composed of numerous lipid protein lamellar discs stacked one on top of the other and
surrounded by a cell membrane.

Inner segment

 thicker than the outer segment

 two regions: ellipsoid and myoid

CONES

 40-80 µm

Outer segment

 conical in shape, much shorter than that of rod

 longest at the fovea (80 μm)
 shortest at the periphery (40 μm)
 photopigment Iodopsin
 The lamellar discs infoldings of plasma membrane (1000-1200 discs/cone)

Inner segment

 cone ellipsoid is very plump

 Rich in mitochondria
 Nucleus is continuous with inner segment of cone
 lateral processes called cone foot or cone pedicle
VISUAL PIGMENTS

RHODOPSIN

 Opsin + Retinal = RHODOPSIN

 MW: 40,000
 Coupled with G protein
 Peak sensitivity to light: 493–505 nm
 Absorbs primarily yellow wavelength of light
 Transmits violet and red to appear purple by transmitted light

CONE PIGMENT

 Responsible for color vision

 Opsin protein is different, however retinal is not changed
 3 types of cones:
1. Blue = 430 nm
2. Green= 535 nm
3. Red= 565 nm

LIGHT INDUCED CHANGES

Light falls on visual pigments and initiates photochemical changes cascade of events initiated
causes PHOTOTRANSDUCTION

Events occurring

 Rhodopsin bleaching
 Rhodopsin regeneration
 Visual cycle

RHODOPSIN BLEACHING
RHODOPSIN REGENERATION

 All-trans retinal enters chromophore pool in the outer segment of photoreceptor and pigment
epithelial cells
 All trans retinal to all trans retinol by alcohol dehydrogenase then re esterified enter circulation
again
 REFER TO DIAGRAM ABOVE

VISUAL CYCLE

 rate at which the photochemicals are bleached is equal to the rate at which they are
regenerated
 EQUILIBRIUM is known as visual cycle

APPLIED ASPECT

Night blindness: (2mk)

 CAUSE: DEFICIENCY OF VITAMIN A

 Reduced amount of rhodopsin and retinal
 Decreased or no vision in dim light and night time
 In daylight , person can see

PHOTOTRANSDUCTION (Describe the steps of phototransduction. Add a note on dark current (5mk))

STEPS

1. ACTIVATION OF RHODOPSIN
 Formation of metarhodopsin II
2. ACTIVATION OF TRANSDUCIN
 The activated rhodopsin acts as an enzyme to activate many molecules of transducin (G-
protein)
 transducin gets replaced by GTP and the α subunit separates
3. CONVERSION of cGMP TO GMP
 α subunit activates phophosdiesterase enzyme
 Enzyme converts cGMP to GMP
 Reduction of cGMP in photoreceptor occurs
4. PRODUCTION OF RECEPTOR POTENTIAL
 In dark: Na+ channels are opened (these channels are cGMP ligand gated channel)
 In light: Na+ channels are closed (reduction of cGMP)
 Therefore, there will be hyperpolarization
FLOWCHART FOR PHOTRANDUCTION
DARK CURRENT

In the presence of light, instead of depolarization there is hyperpolarization. It is due to closure of cGMP
channels which allow influx of Na+. The Sodium-Potassium pump continues to remove Na+ and allows
entry of Potassium. Therefore, the electronegativity increases.

In the dark, Na+ channels are opened by action of cGMP Influx of Na+ in photoreceptors
Receptor potential = -40 mV

This phenomenon is known as dark current. It occurs only eyes.

VISUAL PATHWAY (Describe visual pathway and effects of its lesions (5mk))

 Axons of ganglion cells form the optic nerve and leaves the eye a little in the medial side of
posterior pole
 At the optic chiasma, all the fibres coming from nasal halves of retina cross to the opposite side
and join with fibres from the opposite temporal retina to form optic tracts
 Each optic tract relays at the dorsolateral geniculate nucleus.
 From the LGN, fibres run in geniculocalcarine tracts
 Fibres then pass by way of optic radiation to primary visual cortex present in calcarine area of
occipital lobe

SUMMARY OF VISUAL PATHWAY

Retina → optic nerve → optic chiasm → optic tract → lateral geniculate body → optic
radiation to primary visual cortex

LATERAL GENICULATE BODY

 Each LGB contains six well-defined layers

 Layers 1,4 and 6 receive input from the nasal half of the contralateral eye
 Layers 2, 3 and 5 receive input from the temporal half of the ipsilateral eye
 POINT TO POINT REPRESNETATION OF RETINA in each in layer of retina
 Layers 1 and 2 MAGNOCELLULAR LAYERS(M CELL)
 Layers 3-6 PARVOCELLULAR LAYERS(P CELL)
 FUNCTIONS OF LGB :
1. RELAY STATION: From the ganglion cells to the visual cortex via parvocellular and
magnocellular pathways
2. Visual perception and to ‘gate’ the transmission of signals:
 Control how much of the signals be allowed to pass to the cortex
 10-20 % RETINA
 80-90% Primary visual cortex (corticofugal fibres) fibres are involved in
visual processing related to the perception of orientation and motion
OTHER PATHWAYS

 To suprachiasmatic nucleus of hypothalamus for controlling circadian rhythm which changes

with day and night.
 To pretectal nucleus for activation of pupillary light reflex.
 To superior colliculus for controlling rapid directional movements of the eyes.
 To ventral lateral geniculate nucleus of thalamus to control behavioral functions.

Retina → optic nerve → optic chiasm → optic tract → pretectal area and superior colliculus

LESIONS OF VISUAL PATHWAY

VISUAL ACUITY

 It is the degree to which the details and contours of objects are perceived
 It is expressed in terms of visual angle
 Visual acuity or acuteness of vision is defined as power of the eye to resolve two stimuli
separated in space.
 It is defined as minimum separable, i.e. minimum distance between two stimuli at which they
are just resolvable (can be perceived as two separate stimuli).
 It is expressed as reciprocal of the angle subtended by two stimuli at the nodal point of the eye
at which they are recognized as separate stimuli.
 In a normal person when angle subtended is ‘1 minute’, stimuli are just resolvable
 Factors affecting visual acuity:
1. Type of stimulus.
2. Illumination of the surface.
3. Time exposure.
4. Brightness contrast.
5. Normal and abnormal errors of refraction
 Chromatic aberration tends to reduce visual acuity and therefore use
of monochromatic light increases the visual acuity.
 Errors of refraction such as myopia, hypermetropia and astigmatism
reduce visual acuity.
6. Visual acuity also depends on the site of the retina where the image is formed. Visual
acuity is highest at fovea centralis where only cones are present and it tends to reduce
towards the periphery of retina.

VISUAL ADAPTATION

DARK ADAPTATION

When person remains in darkness for a long time, there is increased sensitivity of retina to light which is
known as dark adaptation

Dark adaptation occurs due to:

1. Increased sensitivity of retina to light.

Sensitivity to light is directly proportional to the antilogarithm of concentration of
photosensitive chemicals in rods and cones, i.e. small change in concentration of chemicals
brings about a very great change in sensitivity of retina to light.
In darkness there is synthesis of photosensitive chemicals in rods and cones from retinal as well
as from vitamin A.
Thus concentration of photosensitive chemicals in both the receptors increases which causes
increased sensitivity of retina to light. This is the main mechanism of dark adaptation.
2. Dilatation of pupil.
In darkness, pupil dilates and increases the amount of light entering into the eye.
3. Neural mechanism.
 It involves adaptation in the retinal neurons, the degree of adaptation is much less as compared
to adaptation of photochemical system; however, this adaptation occurs in seconds, i.e. more
quickly as compared to adaptation in the receptors.

Dark adaptation and vitamin A deficiency

Severe deficiency of vitamin A elevates the threshold for dark adaptation curve due to depletion of the
photosensitive pigment

LIGHT ADAPTATION

When a person is exposed to light, there is decreased sensitivity of retina to light. This is called light
adaptation. The process of light adaptation is very quick and occurs over a period of 5 min

Light adaptation occurs due to reduction in the concentration of photosensitive chemicals in rods and
cones due to their splitting into retinal and opsin. Therefore, in light adaptation, slow reaction
(interconversion between retinal and vitamin A) does not play any role and thus it occurs quickly.

THEORY OF COLOUR VISION

Young-Helmholtz theory

 There are 3 types of cone receptors with different pigments

 They are:
1. ERYTHROLABE(Porphyropsin) 565 nm
2. CHLOROLABE(Iodopsin) 535 nm
3. CYANOLABE (Cyanopsin) 440 nm
 By mixing these primary colours, any type of colour sensation can be produced
 Equal stimulation of these receptors results in white sensation
 Sensation of any colour is determined by relative frequency of impulses reaching the brain from
each of the three cone systems

COLOUR BLINDNESS

Insensitive to colours i.e. inability to recognize colours.

Inherited disorder (sex linked) affecting mostly males

Dyschromatopsia colour confusion due to deficiency of mechanism to perceive colours.

 Anomalous trichromatism(one or two colour mechanism is defect )

1. Protanomalousdefective red colour appreciation,
2. Deuteranomalous defective green colour appreciation.
3. Tritanomalous defective blue colour appreciation
 Dichromatism (one of the three primary colours is completely absent)
1. Protanopiacomplete red colour defect.
2. Deuteranopia complete defect for green colour.
3. Tritanopia absence of blue colour appreciation.
  Achromatopsia
1. Cone monochromatism the presence of only one primary colour and thus the persons
are truly colour blind.
2. Rod monochromatism complete or incomplete. It is inherited as an autosomal
recessive trait. It is characterized by:
 Total colour blindness
 Day blindness (visual acuity is about 6/60)

Astigmatism

Astigmatism is a type of refractive error wherein the refraction varies in the different meridia.
Consequently, the rays of light entering the eye cannot converge to a point focus but form focal lines.
Broadly, there are two types of astigmatism: regular and irregular.

Regular astigmatism

The astigmatism is regular when the refractive power changes uniformly from one meridian to another
(i.e. there are two principal meridia)

Irregular astigmatism

It is characterized by an irregular change of refractive power in different meridia. There are multiple
meridia which admit no geometrical analysis.

Nystagmus

It is defined as regular and rhythmic to and fro involuntary oscillatory movements of the eyes.

Cause: occurs due to disturbance of the factors responsible for maintaining normal ocular posture.
These include disorders of sensory visual pathway, vestibular apparatus, semicircular canals, mid brain
and cerebellum.
ACCOMODATION REFLEX

During accommodation, when eyes are focused from distant to near object to achieve clear vision, three
reactions occur

Changes in the radius of curvature of the lens (more convex) by contraction of ciliary muscles
Pupillary constriction (meiosis) by contraction of sphincter pupillae
Convergence of eyes due to contraction of medial recti of eye balls.

ARGYLL ROBERTSON PUPIL (ARP)

Pupil is slightly small in size and reaction to near reflex is present ARP accommodation reflex
present
Both pupils are involved and dilate poorly with mydriatics
Cause: lesion in the region of tectum.
SENSE OF HEARING

1. FUNCTIONS OF MIDDLE EAR

IMPEDANCE MATCHING

Impedance is any obstacle in pathway of sound and is expressed as amount of energy lost when sound
passes in a medium.

In the ear, sound is to be conducted from air filled middle ear into fluid filled internal ear.

The amplitude of movement of stapes footplate with each sound vibration is 3/4 of amplitude of handle
of malleus

The ossicular lever system does not increase distance movement. Instead it reduces the distance
movement but increases the force by 1.3 times

Surface area of tympanic membrane is 55 mm 2 and that of oval window is 3.2 mm2.

The 17 fold difference times the 1.3 fold ratio of lever system causes about 22 times as much as total
force on fluid of cochlea

Fluid has more inertia than ar. Therefore, more force is required. Impedance matching is 50% to75% for
sound frequency between 300 to 3000 cycles per seconds.

ATTENUATION

When loud sounds are transmitted through the ossicular system and from there into CNS, a reflex is
initiated with a latent period of 40-80ms

Contraction of the tensor tympani pulls the malleus inwards

Contraction of the stapedius muscle pulls the stapes outwards

These two opposing forces cause entire ossicular system to become rigid

This increased rigidity reduces the low frequency sound wave below 1000 cycles per second

Reduction is by 30-40 decibels

2. Draw and label the organ of corti: Functions and structure

FUNCTIONS OF ORGAN OF CORTI

 Generate nerve impulses in response to vibration of basilar membrane

 Consists of 1 single row of inner hair cells and 3 or 4 rows of outer hair cells
 Movement of basilar membrane and reticular lamina cause the shearing movement of the inner
cells and when the shortest stereocilium moves towards the Kinocilium, depolarization occurs.
 Inner hairs transduce sound energy into electrical energy (90-95% of nerve endings)
 Outer hair cells are responsible for detection of sound and control the sensitivity of the inner hair
cells at different sound pitches, a phenomenon called “tuning” of the receptor system.

3. BASILAR MEMBRANE

 Fibrous membrane projecting from base of cochlea (modiolus)

 Consists of 20,000 to 30,000 basal fibers
 Basal fibers are stiff, elastic and reed like structures
 Basal fibers are fixed at basal end but not fixed at the distal end
 The lengths of the basilar fibers increase progressively beginning at the oval window and going
from the base of the cochlea to the apex. (0.04 mm to 0.5 mm)
 The diameters of the fibers decrease from the oval window to the helicotrema
 Short fibers near the oval window of the cochlea vibrate best at a very high frequency, whereas
the long, limber fibers near the tip of the cochlea vibrate best at a low frequency.
TRANSMISSION OF SOUND WAVE IN COCHLEA

 When the footplate of stapes moves inwards against the oval window, the round window must
bulge outward
 The effect of a sound is to cause the basilar membrane at base of cochlea to bend in direction of
round window
 Elastic tension that is built up in the basilar fibers as they bend towards the round window
initiates a fluid wave that travels along the basilar membrane towards the helicotrema
 Each wave is relatively weak at the outset but becomes strong when it reaches the portion of
the basilar membrane that has a resonant frequency equal to respective sound frequency
 At this point, the basilar membrane can vibrate back and forth with such ease that the energy in
wave is dissipated
 High frequency wave short distance
 Medium frequency wave Midway
 Low frequency wave long distance

4. ENDOCOCHLEAR POTENTIAL

 Perilymph is a fluid in which the potassium ions concentration is very low. It is found
in the scala vestibule and scala tympani. It is similar to the CSF. (communicate
directly with the subarachnoid space around the brain)
 Endolymph that fills the scala media is an entirely different fluid secreted by the stria
vascularis. Endolymph contains a high concentration of potassium and a low
concentration of sodium.
 An electrical potential of about +80 millivolts exists all the time between endolymph
and perilymph, with positivity inside the scala media and negativity outside. This is
called the endocochlear potential
 Generated by continual secretion of positive potassium ions into the scala media by
the stria vascularis.
 Tops of the hair cells project through the reticular lamina and are bathed by the
endolymph
 Perilymph bathes the lower bodies of the hair cells
  The hair cells have a negative intracellular potential of −70 millivolts with respect to
the perilymph but −150 millivolts with respect to the endolymph at their upper
surfaces

5. AUDITORY PATHWAY

1st order neuron

 bipolar cells of the spiral ganglion
2nd order neuron
 1st group cross midline and run opposite to form trapezoid body. Fibers from
trapezoid body go to superior olivary nucleus
 2nd group terminate at the sup olivary nucleus nut via trapezoid body of the
same side
 3rd group terminates in nucleus of lateral lemniscus of same side
 4th group run into reticular formation, cross the midline as intermediate
trapezoid fibers and finally join the lateral lemniscus of opposite side
rd
3 order neuron
 They are in superior olivary nuclei and nucleus of lateral lemniscus
 Fibers terminate into medial geniculate body which forms the subcortical auditory
center
 From MGB , fibers go to temporal cortex via internal capsule via auditory radiations
 Some fibers from MGB go to inferior colliculus
CORTICAL AUDITORY CENTERS

1. PRIMARY AUDITORY CORTEX(41 AND 42 + WERNICKE AREA)

2. SECONDARY AUDITORY AREA (22)

Cortical auditory centers are concerned with the perception of auditory impulses, analysis of pitch and
intensity of sound and determination of source of sound

Areas 41 and 42 are concerned with perception of auditory impulses only

Rest by 22

6. DEAFNESS

CONDUCTIVE DEAFNESS- Any disease process which interferes with the conduction of sound from the
external ear to cochlea causes conductive hearing loss

CAUSES: (EXTERNAL EAR or MIDDLE EAR)

 External ear: any obstruction in the ear canal, e.g. by wax, tumours, atresia etc.
 Tympanic membrane, e.g. perforation.
 Middle ear cavity, e.g. fluid in the middle ear (as in otitis media).
 Ear ossicles, e.g. disruption of ear ossicles and fixation of ear ossicles (otosclerosis).
 Eustachian tube obstruction as in retracted tympanic membrane.

NERVE (SENSORINEURAL) DEAFNESS-loss results from lesions of cochlea (sensory type) or eighth cranial
nerve and its central connections (neural type)

CAUSES: (INTERNAL EAR)

 Infection of labyrinth (viral, bacterial or spirochaetal)

 Acoustic trauma-injury to labyrinth or eighth nerve.
 Noise trauma or noise-induced hearing loss occurs due to prolonged exposure to industrial
noise. Ototoxicity. Certain drugs cause damage to inner ear(streptomycin, neomycin, quinine,
chloroquine)
 Neoplasms (acoustic neuroma)
 Systemic disorders(diabetes mellitus, hypertension)
TINITUS-ringing sensation in the ear. It is caused by irritative stimulation of either the inner ear or the
vestibulocochlear nerve.

7. HEARING TESTS

1. RINNES TEST

 Air conduction (AC) of the ear is compared with bone conduction (BC)
 Base of a vibrating tuning fork is placed on the mastoid bone and when he stops hearing, it is
brought besides the meatus
 If he still hears, AC is more than BC and Rinne test is positive.

2. WEBERS TEST

 Base of the vibrating tuning fork is placed in the middle of the forehead or vertex and patient is
asked in which ear the sound is heard better.
 Normally, the sound is heard equally in both ears.
 In conductive hearing loss, the sound is lateralized (better heard) towards affected ear. This is
because the masking effect of environmental noise is absent in the affected ear.
 In sensorineural hearing loss, the sound is lateralized towards better ear because the sound is
reaching the normal cochlea through bone.

3. SCHWABACHS TEST

 In this test, patients’ bone conduction is compared with that of the examiner
 Normally, both the examiner and the subject hear the sound equally well.
 In conductive deafness, the patient hears the fork for longer period than the examiner (because
there is no masking effect of environmental noise).
 In sensorineural deafness, the examiner hears the tuning fork for a longer duration than the
patient.
SENSE OF TASTE

1. STRUCTURE OF TASTE BUDS

 Taste buds are stimulated by substances dissolved in oral fluids

 Taste buds are present in papillae but also on the epiglottis, pharynx and soft palate

 Taste buds are oval clusters of cell in epithelial layer with a small pore opening on the surface that
allows substances to reach the interior of taste buds
 Taste buds consist of:
 Gustatory receptor cells (ends in microvilli)
1. Supporting cells(sustentacular)
2. Taste cells are formed from epithelial cells surrounding the taste buds
 They migrate towards centre and mature before they degenerate in about 10 days
 Afferent cells have fibers which join to form 2-3 large fibers and each large fibers connects with one
or more taste cells
Papillae (REFER TO ANATOMY NOTES)

1. Fungiform rounded structures on tip of tongue

2. Filiform conical in shape and arranged in diverging rows to right and left
3. Circumvallate arranged in a V-shaped in front of sulcus terminalis
4. Foliate found on posterolateral surface

2. TASTE PATHWAY

 FIRST ORDER NEURONS

1. Anterior 2/3 of tongue – chorda tympani of facial nerve
2. Posterior 1/3 of tongue – glossopharyngeal nerve
3. Epiglottis and pharynx – Vagus nerve
 SECOND ORDER – NTS ------ > VPM (via medial leminiscus)
 THIRD ORDER NEURON – GUSTATORY CORTEX(parietal central cortex)
3. TASTE SENSATION

Receptor potential

Substances dissolved on tongue stimulates the taste receptors. These substances then act on microvilli
exposed in taste pores. This leads to generation of receptor potential in receptor cells and ultimately
leads to an action potential in the sensory nerves.

PRIMARY TASTE SENSATION

1. SWEET produced by a number of organic molecules including sugars, glycols, alcohols,

aldehydes, esters
Activation of receptor (GPCR)dissociation of G proteinactivates adenylyl cyclaseincreased
cAMPdepolarization
2. SOUR produced by acids
Increased extracellular H+ Increased cations permeability Depolarization of taste
receptors Generator potential in fibers  Action potential in sensory nerve
3. SALTY produced by the anions of ionizable salts especially the sodium chloride
SAME AS SOUR BUT IT IS CAUSED BY INCREASES SODIUM ECF
4. BITTER produced by alkaloids, such as quinine, caffeine, nicotine and strychnine
5. Activation of receptor (GPCR)dissociation of G proteinactivates phospholipase Cincreased
Ca+depolarization
6. UNAMI produced by glutamate particularly by monosodium glutamate used extensively in
Asian cooking. This taste is pleasant and sweet but differs from the standard sweet taste

4. APPLIED ASPECT

1. AGEUSIA Absence of taste sensation

CAUSES:

Lesions of the chorda tympani nerve cause loss of taste sensations in the anterior two-
thirds of tongue
 Lesions of glossopharyngeal nerve causes absence of taste sensations from the
posterior one-third of the tongue
 Drugs like captopril and penicillamine (sulphydryl groups) cause temporary loss of taste
sensation
2. HYPOGEUSIA diminished taste sensitivity
3. DYSGEUSIA disturbed sense of taste
SENSE OF SMELL

OLFACTORY PATHWAY
OLFACTORY TRANSDUCTION