PHYSIOLOGY PRACTICLES FOR 4TH SEMESTER

1
OBJECTIVE:
Examination of olfactory nerve and studying the sense of smell.
ABSTRACT:
Smell is the sense of perceiving odors. The receptors of olfaction (smell) are located in roof of nasal cavity in
olfactory epithelium. Olfactory epithelium has bipolar olfactory sensory neurons, supporting cells and stem
cells. There are Bowmans glands also present which secrete mucous. Odorants are the substances which
produce smell. They are always volatile and must be water soluble so that may cross the mucous layer over
olfactory epithelium. Smell though not essential for life, is involved in enhancing the test of food, feeding,
identification of toxins, changing the mood and hunger etc. The nerve signals of olfaction are carried through
1st cranial nerve i.e. olfactory nerve but some somatosensory signal (irritants e.g. Ammonia) are mainly carried
by trigeminal nerve i.e. 5th cranial nerve. The olfactory centers present in brain are, anterior olfactory nucleus,
olfactory tubercle, piriform cortex, amygdala, and entorhinal cortex. Olfaction may vary with age, sex and
period of sexual cycle (in females only). Sensitivity of females is more than males. Similarly that of girls is
more than boys. While the olfactory sensitivity decreases with age. During pregnancy the sensitivity of smell is
increased. Nasal infections, poor hygiene of mouth, head injuries and tumors of brain may lead to olfactory
disturbances. The practical was performed on 10 girls and 10 boys. The substance used was clove oil. Test was
performed separately on each nostril. All were found having their olfactory nerves intact.
INTRODUCTION:
Smell is the sense that enables one to perceive odors.[1] Primary sensations of smell are; Camphoraceous,
Musky, Floral, Pepperminty, Ethereal, Pungent and Putrid.[2] The substances that produce an odor are termed
odorants. Smell helps in feeding and suckling behavior, hunting, mating, navigation and warning of
environmental toxins. It improves the taste of food, affects appetite and evokes memories. Human mothers and
infants can recognize each other by scent alone within a few hours after birth.[3]Smell and taste are generally
classified as visceral senses because of their close association with gastrointestinal function. The human sense
of smell depends on the functioning of cranial nerve I or olfactory nerve (mediates qualitative odor sensations
e.g., the smell of a rose, lemon or grass) and portions of cranial nerve V or trigeminal nerve (mediates
somatosensory overtones of odorants like warmth, coolness and irritation). It is important to remember because
some odorants (ammonia) are sensed largely by the trigeminal nerve.[3] Olfactory pathway starts from
olfactory epithelium (ciliated Pseudostraitified columnar, covers an area of 5 cm2) in the roof of the nasal
cavity near the septum. The olfactory epithelium is the place in the body where the nervous system is closest to
the external world. Epithelium is covered by a layer of mucus secreted by the supporting cells and Bowman
glands which dissolves the odorants and helps in sensation. The olfactory sensory neurons are bipolar.
Epithelium also contains supporting (sustentacular) cells and basal stem cells. All the three types of cell
collectively form olfactory apparatus. The stem cells generate new receptor cells to replace the damaged
neurons. In nasal cavity the dendrite of each neuron terminates in a knob containing unmyelinated cilia which
have receptors for odorants (odorant receptors) while the axons enter the olfactory bulbs passing through
cribriform plate and contact the dendrites of the mitral cells and tufted cells to form anatomically discrete
units called olfactory glomeruli. The axons of the mitral and tufted cells form olfactory tract and pass to five
regions of the olfactory cortex: anterior olfactory nucleus, olfactory tubercle, piriform cortex, amygdala,
and entorhinal cortex. From these regions, information travels directly to the frontal cortex or via the
thalamus to the orbitofrontal cortex. The pathway to the amygdala is involved with the emotional responses,
and the pathway to the entorhinal cortex is concerned with olfactory memories.[4]The olfactory receptors are Gprotein-coupled and involve cAMP 2nd messenger system. Unlike other sensory modalities that are first sent to

the thalamus and from there relayed to the cerebral cortex, the sense of smell is transmitted directly to the
cerebral cortex. [3] The olfactory threshold is the minimum amount of substance that can elicit olfaction. Due to
very minute threshold required, the sensitivity of smell is remarkable. Olfactory discrimination (identification
of different odorants) is remarkable while determination of differences in the intensity of any given odor is
poor.[4]The examination of sense of smell becomes important in some accidents of head injury. The most
widely available olfactory test is the Test Smell Identification. Clove oil is most commonly used substance for
test. While the menthol and choline is not used because they stimulate trigeminal nerve endings and may give
false result about 1st cranial. Other commercially available olfactory tests include the three-item forced-choice
microencapsulated Pocket Smell Test, the Brief Smell Identification Test and a squeeze-bottle odor threshold
test kit. [5] Older people are less sensitive than younger (due to olfactory mucosa damage and degenerative
changes in brain). Women have better sense of smell than men and girls have better than boys due to difference
of circulating hormones and their levels.[6] Anosmia is the inability to smell and hyposmia or hypesthesia is
the diminished olfactory sensitivity. Hyperosmia is enhanced olfactory sensitivity (hunger, nausea, obesity,
occupational, environmental) is less common than loss of smell. Physiological Hyperosmia occur in pregnant
women due to hormonal changes. Dysosmia (distorted sense of smell) can be caused by sinus infections,
partial damage to the olfactory nerves, and poor dental hygiene. Parosmia is the perception of odors that are
not present. The progressive decrease in sense of smell until the smell is completely undetectable is called
adaptation or desensitization, it is normal physiological response.[3] The most common causes of smell
disturbance are nasal and sinus disease, upper respiratory infection and head trauma. Other causes include;
Medications (antibiotics, Anticonvulsants, Antidepressants), Cocaine abuse (intranasal), Toxic chemical
exposure (e.g., benzene, carbon disulfide), Industrial agent exposure (e.g., ashes, chalk, lead, nickel),
Nutritional factors (e.g., vitamin deficiency [A, B6, B12], trace metal deficiency [zinc, copper], Congenital
conditions (e.g., congenital anosmia, Kallmann's syndrome).[3] Deficits in the sense of smell may precede
clinical motor symptoms by years and can be used to assess risk for developing Parkinson disease.[7] Patients
with smell dysfunction frequently report increased use of sugar and salt to compensate for diminished senses of
smell and taste, a practice that is harmful to those with diabetes mellitus or hypertension. Individuals with
Bardet-Biedl syndrome (BBS) have partial or complete anosmia. In this disease BBS proteins are absent in
olfactory neurons.
Material and Method:
To fulfill the objective, Students of A1 were divided into three groups each of ten. All the twenty students did
not eat anything 15 minutes before the test to avoid error. The test was performed separately on 10 boys and 10
girls. Before proceeding to test, hands were washed and gloves were worn. The nasal cavity was examined for
any obstruction etc. One nasal cavity was closed and clove oil was sniffed in other. Then he/she was asked to
identify the fragrance. Fragrance of clove oil was identified by student. Same procedure was repeated in 2nd
nasal cavity closing the other. Each student identified the clove oil fragrance.
Result:
All students identified the fragrance of clove oil indicating that the olfactory nerve was intact.
Discussion
Olfaction is not usually tested during the neurological examination unless the patient has mentioned a problem
with sense of smell. Testing is done by bringing the aromatic substance. Impaired smell most commonly occurs
from mucosal swelling and inflammation during sinusitis or an upper respiratory infection. A permanent loss
smell may occurs after severe head trauma, where the olfactory nerve branches are sheared where they pass
through cribriform plate. Condition in which permanent loss of smell occur called Ansomia.
References:

1. Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition.
2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.
2. Aurther C. Guyton, Jhon Hall, Textbook of medical physiology, The Chemical Senses-Taste and Smell,
Saunders, 12th, 2011, 648-652
3. STEVEN M. BROMLEY, Smell and Taste Disorders: A Primary Care Approach, Am Fam Physician
journal, 2000, 61(2), 427-436
4. Kim E. Barrett, Susan M. barman, Scott Boitano, Heddwen L. Brooks, Ganongs Review of Medical
Physiology, Smell and Test, Tata McGraw-HILL, 23rd, 2010, 219-223
5. Stuart Ira Fox, Human Physiology, Sensory Physiology, McGraw-HILL, 12th, 2011, 273-275
6. Richard L. Doly, Paul Shaman, Steven L. Applebaum, Smell identification ability: changes with age,
Doty et al, 1984, 226( 4681), 1441-1443
7. Haehner A, Hummel T, Olfactory dysfunction as a diagnostic marker for Parkinson's disease, Expert
Review of Neurotherapeutics journal. 2009, 9 (12), 1773-1779
8. Heather M Kulaga1, Carmen C Leitch, Erica R Eichers, Loss of BBS proteins causes anosmia in
humans and defects in olfactory cilia structure and function in the mouse, Nature Genetics journal,
2004, 36(9):994-998
2
OBJECTIVE
Examination of optic nerve and studying the sense of Vision
ABSTRACT:
Human eye is responsible for our one of the special senses sight. The signal for the chemical changes in the
eye is carried from optic nerve which is the 2nd cranial nerve. It detect any change in the rods and cones
present in retina and carry signal to visual cortex where it is integrated and then motor response is carried. The
visual centers are present in cortical and sub-cortical areas of brain. Accommodation is the ability of eye to
focus on near objects so that they may be seen clearly. Visual acuity determines the ability of eye for sharpness.
Visual field is the area seen by eye at any instant. Binocular field vision is the field of vision overlapped by two
eyes. Visual acuity is greatest at fovea centralist. With increasing age the accommodation of an eye decreases
due to increased elasticity of lens of eye and other factors. Males have greater ability to differentiate and to see
moving objects. Any defect in eye is examined through multiple tests such as confrontation test and perimetry
for visual field, reading snellens chart for visual acquity, ishihara chart for colour examination. Optic nerve
glioma, Ganglioglioma and loss of vision are some of the diseases caused from damage to optic nerve. Colour
blindness is a genetic disorder in which the victim is colour blind for one or two colours. For the sake of study,
group A2 students made sub-groups and performed test i.e. confrontation test, acuity test, near vision test and
colour test in physiology lab. Optic nerve was found to be intact in all students.
INTRODUCTION:
The sense of vision enables one to see. The eye is the organ which gives us the sense of vision (sight), allowing
us to observe and learn more about the surrounding world. The eye allows us to see and interpret the shapes,
colors, and dimensions of objects by processing the light they reflect or emit.[1] Retina is responsible for
detection of light through photoreceptors (rods and cons). It has four types of neurons in addition to receptor
cells i.e. bipolar cells, ganglion cells, horizontal cells and amacrine cells. The receptor cells synapse with
bipolar cells which in turn synapse with ganglion cells. The axons of ganglion cells converge and leave the eye
as optic nerve. Horizontal cells connect bipolar cells to one another while amacrine cells connect ganglion cells
to other ganglion cells.[2] As a result of light refraction by the cornea and lens, the right half of the visual field
is projected to the left half of the retina of both eyes (the temporal half of the left retina and the nasal half of
the right retina). The left half of the visual field is projected to the right half of the retina of both eyes. The

temporal half of the left retina and the nasal half of the right retina therefore see the same image. Axons from
left (temporal) half of the left retina pass to the left lateral geniculate nucleus of the thalamus. Axons from
nasal half of the right retina cross over (decussate) in the X-shaped optic chiasma and synapse in the left lateral
geniculate body. The left lateral geniculate thus receives input from both eyes that relates to the right half of the
visual field. The right lateral geniculate body, similarly, receives input from both eyes relating to the left half of
the visual field. Neurons in both lateral geniculate bodies of the thalamus in turn project to the striate cortex
of the occipital lobe in the cerebral cortex. This area is also called area 17 or Brodmann area (located on the
sides of calcarine fissure).[3] Brain areas activated by visual stimuli are cortical (occipital lobe, inferior
temporal cortex, posteroinferior parietal cortex, portions of frontal lobe and amygdala) and sub-cortical
(lateral geniculate bodies, superior colliculus, pulvinar, caudate nucleus, putamen and claustrum).[2] The
beginning of the optic nerve in the retina is called the optic nerve head or optic disc. Since there are no
photoreceptors (cones and rods) in the optic nerve head, this area of the retina cannot respond to light
stimulation and is known as the blind spot.[1] A little behind the bulb of the eye the central artery of the retina
with its accompanying vein perforates the optic nerve, and runs within it to the retina.[4] Rods are more
sensitive to light but do not distinguish colours. Cones require more light to be stimulated, so they contribute
very little to night vision. Cones can distinguish colours in daylight. Males have significantly greater
sensitivity for fine detail and for rapidly moving stimuli than females.[5] The ability of the eyes to keep the
image focused on the retina as the distance between the eyes and object varies is called accommodation [3] OR
It is the process by which the curvature of lens is increased to focus the light rays, on retina, emitted or
reflected from near object(s). It is done by the help of ciliary muscles of eye. The nearest point to the eye at
which object can be brought into clear focus by accommodation is called near point of vision. With
advancing age the hardness of lens increases thus limiting (decreasing) the ability of accommodation. In
addition to accommodation, the visual axes converge and pupil constricts when an individual looks at near
object. This three part response is called the near response.[2] Visual acuity refers to the sharpness of vision
(Shortest distance by which two lines can be separated and still be perceived as two lines). It depends on the
resolving power of the visual system.[3] Clinically the visual acuity is determined by the use of the Snellen
letter charts viewed at a distance of 20 ft (6 m). The results are expressed as a fraction. The numerator of the
fraction is 20 or 6, the distance at which the subject reads the chart. The denominator is the greatest distance
from the chart at which a normal individual can read the smallest line. Normal visual acuity is 20/20 (6/6). The
fovea centralist is the point where visual acuity is greatest.[2] Visual field or field of vision is the visual are
seen by an eye at a given instant. The area seen to nasal side is called nasal field of vision and area seen to
lateral side is called the temporal field of vision.[6] The overlapping area seen by both eyes at the same time is
known as the binocular (two-eyed) field of vision. Arteries, arterioles, and veins in the retina near its
vitreous surface can be seen through the ophthalmoscope. Vessels here being readily visible are of great value
in ophthalmoscopic examination for diagnosis of diabetes mellitus and hypertension.[2] Presbyopia is agerelated loss of the ability to alter the refractive power of the lens (and thus accommodation) to focus objects at
varying distances.[7] In Myopia (shortsightness, common in children) the distant objects are imaged in front of
retina, because the eye is too long for the focal length of its optics.[8] nerve gliomas comprise about 1% of all
intracranial tumours. They are almost always unilateral and occur more frequently in females. The symptoms
and signs include decreased visual function, proptosis (Exophthalmoses), optic disc swelling or pallor.[9] Colour
blindness is condition in which color-blind individuals are unable to distinguish certain colors (e.g. red-green
colour blindness), or have only a color weakness (e.g. blue weakness). The prefixes "prot-," "deuter-," and
"trit-" refer to defects of the red, green, and blue cone systems, respectively. Individuals with normal color
vision are called trichromats. Dichromats are individuals with only two cone systems; they may have
protanopia, deuteranopia, or tritanopia. Monochromats have only one cone system.[2] The visual field defects
include scotomata (blind spots found in portions of visual field other than optic disc area, caused by damage to
optic nerve) and retinitis pigmentosa (blindness in the peripheral field of vision caused by degeneration of
retina and deposition of melanin) [5]. Lebers Hereditary Optic Neuropathy (a rare form of inherited optic

neuropathy which mainly affects young men, causing them to lose central vision).[1] Several tests are performed
to examine visual field (Confrontation test or Donder's test, Tangent screen test or Goldmann field test and
perimetry), visual acuity (Snellen chart test), vision (Amsler grid, distance vision, and near vision testing) and
colour vision (Ishihara chart).[10]
MATERIAL AND METHOD:
To perform different tests of vision, A1-group students were divided into two groups of boys and girls each
comprising ten students. The tests were performed separately. For near-vision test, everybody was given books
to read and all students were able to read book easily at distance of about 14 inches. Results were noted for
separate aye and then both eyes. For far-vision (acuity test) Snellen chart was used; students their glasses
wearing corrective glasses wore. Then all were asked to cover one eye with his/her hand (or with a plain
occluder), and to start reading from the top of the chart at a distance of 6 meter or 20 ft. Then other eye was
examined in the same way. Finally both eyes were examined together. The smallest line he/she could read (the
VA) each time was expressed as a fraction, (e.g. 6/18 or 6/24) which was written on the chart. The Snellen
fraction was obtained by dividing the distance the at which chart was from the student (6 meters) with the
distance in meters at which each could see the smallest line on the chart. Some students were found to have
myopia. Colour examination test was performed by using ishihara chart. Students were asked to read the
ishihara chart. All read it easily showing absence of colourbliness. Confrontation test was used to check visual
field. To perform this test Student was asked to sit with 1or 2 meter distance from examiner and close one eye
and fixing his gaze on the examiner's eyes. The level of eyes of examiner and student were maintained on same
level. The examiner conducted finger movements, bringing his hands into his visual field from the sides.
Because vision is divided into four quadrants in brain, the examiner brought his finger in each quadrant
separately and each student was asked to tell whether the finger was visible or not. Another test for visual field
examination was done through perimetry. In this test each student sat in front of a concave dome of machine
and stared at an object in the middle. He was asked to press button every time he see a bright spot of light. All
students were found having normal visual field.
RESULT: The optic nerve of all the students was found intact.
REFERENCES:1. Ted M. Montgomery, the Optic Nerve. Anatomy, Physiology and Pathology of the Human Eye , 2013
2. Kim E. Barrett, Susan M. barman, Scott Boitano, Heddwen L. Brooks,
Ganongs Review of Medical Physiology, vision, Tata McGraw-HILL, 23rd, 2010, 181-190
3. Fox: Stuart Ira Fox, Human Physiology, Sensory Physiology, McGraw-HILL, 12th, 2011, 286-302
4. Henry Gray, Anatomy of the Human Body.20th edition, IX. Neurology 1918,5b, the Optic Nerve.
5. Israel Abramov, James Gordon, Olga Feldman, Sex & vision I: Spatio-temporal resolution, Biol Sex
Differ journal, 2012, 3, 1-2
6. Aurther C. Guyton, Jhon Hall, Textbook of medical physiology, The Eye III. Central Neurophysiology
of vision, Saunders, 12th, 2011, 648-652
7. C.T. Scialfa, D.W. Kline, Encyclopedia of Gerontology, Vision, 2nd, 2007, 653660
8. J. Wallma, Myopia, Encyclopedia of Neuroscience, illustrated edition, 2009, 11811186
9. N R Miller1, Primary tumours of the optic nerve and its sheath, Eye journal, 2004, 18 (11), 10261037
10. Franklin W. Lusby, A service of the U.S. National Library of Medicine, National Institutes of Health,
3
OBJECTIVE:
EXAMINATION OF OCCULOMOTOR, TROCHLEAR AND ABDUCENT NERVE

ABSTRACT:
The oculomotor ,trochlear and abducent is the 3rd , 4th and 6th cranial nerves . They are connected with each
other and are co-ordinated by medial longitudinal bundle ( MLB ) . The oculomotor nerves nucleus lies in
midbrain . If oculomotor nerve is paralysed there is ptosis due to paralysis of levator palpabrae so the eye ball
cannot move medially and upward and is deviated laterally and slightly downward due to paralysis of
superior , inferior and medial recti and inferior oblique muscle .Pupil remains dilated and light and
accommodation reflex become absent. It's causes are diabetes mellitus , mid brain lesion, cavernous sinus
thrombosis . The trochlear nerve is the 4th cranial nerve and it's nucleus lies in mid brain . Its the only cranial
nerve that emerges on dorsal surface and supplies superior oblique muscle . The trochlear nerve assists in
turning the eye downward and laterally . The abducent nerve is 6th cranial nerve. Its nucleus lies in Pons and
supplies rectus muscle. It is responsible for turning the eye laterally. To examine the nerve we do pupillary
light reflex. When light is poured into the eye , pupil constricts a reaction called pupillary light reflex . This
examination can be done by giving shine bright light into eyes from side and hand is placed over nose to
prevent the light entering the opposite eye . When light impinges on retina , a few of resulting impulses pass
from optic nerve to protactile nuclei , from here secondary impulse pass to the Edinger- Westphal nucleus and
finally back through parasympathetic nerve to constrict the sphincter of iris . Conversely in darkness the
reflection is inhibited which results in dilatation of pupil. It was found during light reflex that the nerves of all
individuals are intact.
INTRODUCTION:
The oculomotor ,trochlear and abducent is the 3rd , 4th and 5th cranial nerve .They are connected with each
other and coordinated by medial longitudinal bundle [1]. The oculomotor nerve is responsible for innervating
the muscles of eye i.e. superior , medial , inferior recti , inferior oblique and superior eyelid .( levator palpabrae
superiors ) . The nerve originated from ventral midbrain and is a motor nerve . It is composed of general
somatic efferent fibres and general visceral efferent fibers . The general somatic efferent fibres of the
oculomotor nerve are responsible for the motor function of six external muscles of the eye ball except superior
oblique and lateral rectus . The general visceral efferent fibres of the oculomotor nerve contain
parasympathetic fibers which relay in cilliary ganglion. The post ganglionic fibres supply cilliary muscle and
sphincter pupillae which causes construction of pupil and cilliary muscle to accommodate for near vision. The
oculomotor nerve has a pre-ganglionic nucleus in the mid brain and the nerve passes through the orbital fissure
along with trochlear , abducent and ophthalmic branch of trigeminal nerve . It synapse in the cilliary ganglion
of eye . During a clinical examination horizontal eye movement ( strabismus ) or an absent pupillary light
reflect may indicate a problem [2]. The trochlear nerve is smallest in no: of axons but possess greater
intracranial length . Its nucleus lies in the mid brain . It supplies superior oblique the only extra ocular muscle
that uses a pulley or trochlear to redirect its line of action . Trochlear nerve supply somatic motor fibre of
superior oblique muscle and send proprioceptive fibre to this muscle, which abducts, depresses and medially
rotates the eye ball . Abducent nerve originates from the brain stem between pons and medulla and is a motor
nerve. It is composed of general somatic efferent fibres which are responsible for controlling the lateral rectus
muscle that abduct the eye . A 3rd component is present in the oculomotor nerve only , this consist of general
visceral efferent ( or pre-ganglion parasympathetic ) fibres originating in the Edinger -Westphal nucleus which
is situated dorsal and rostral to oculomotor nucleus.They synapse in cilliary muscle ( involving the
accommodation ) and the sphincter pupillae [3]. Paralysis of 3rd cranial nerve results in ptosis that causes
dropping of upper eye lid due to paralysis of voluntary part of levator palpable superiors muscle and dilation of
the pupil will occur due to paralysis of parasympathetic fibres of splinter pupillae muscle; eye ball gets turned
downward and laterally due to unopposed action of lateral rectus and superior oblique muscle . There will be
also loss of accommodation due to paralysis of cilliary muscle . Compression of 3rd cranial nerve due to
extramural hematoma causes dilation of pupil . Parasympathetic fibres lying superficially are affected. First
pupil dilates on affected side and there is little response to light [4]. When 4th cranial nerve is damaged ,

diplopia occurs on looking downward ; diplopia occur due to paralysis of right lateral rectus muscle on shifting
head towards right side diplopia decreases [5]. Paralysis of sixth nerve will lead to failure of abduction of the
affected eye.
METHODS AND MATERIAL:
The following practical was performed at the physiology lab lumhs. We selected 10 students for examination
of the light reflex. The material required for the reflex is torch. We asked the volunteer to look forward at a
distant object to avoid accommodation response. We then poured bright light into one eye from the side. A
hand should be placed over the nose to prevent the light from entering the opposite eye . Normally the response
is brisk constriction of pupil followed by slight relaxation. The response occurs on same side through direct
light reflex as well as on opposite side by consensual light reflex.
RESULT:
All boys and girls have normal light reflex.
DISCUSSION:
We examined the oculomotor nerve. It was concluded that that nerve is intact. Oculomotor nerve lesion
involves the dilatation of affected eyes pupil The efferent eye is dilated and fixed when light is shown into the
affected eye ,there is no response on that side [1]. In Argyll Robertson pupil(ARP) affected pupil is small and
irregular accommodative reflex is present and light reflex is absent [2]. Horner's syndrome occurs due to
damage to postganglionic sympathetic fibre of eye that supply muscles which hold the eye ball forward. Ptosis
(dropping of eyelid), mitosis (small pupil) are the signs of Horner's Syndrome.
REFRENCES:
1. J.Neurophysio .2011 jun:105(6):2863-73 pub.med.
2. Villiam M, Segnarbionx F, Bonnel f, Aubrey 1,arnaud B, the trochlear nerve anatomy . 1993: 15:169173
3. Salmons' NB, Solomon's dj, devilries jc. direct traumatic 3rd nerve palsy , pub.med 1980:58:109-11
4. Kwartz. Leather barrow b, Davis H. Diplopia 1990:21:3512
5. Rucker cw. the causes of paralysis of third, fourth and sixth nerve amj opthalmol 1966;61:1293-8
pub.med
6.Ravin JG; Argyll Robertson: ophthalmology 1998;105:867- 870.
7.pilley S, Thompson HS(1975) pupillary redilatation in horners syndrome . Br j ophthal 59:731-735.
4
Objective:
The Examination of Trigeminal Nerve
Abstract:
Trigeminal nerve is the fifth cranial nerve. It is the largest cranial nerve as it has sensory as well motor
branches. It divides into opthalmic, maxillary and mandibular divisions distal to the trigeminal
ganglion.Opthalmic neve is purely sensory which supplies the eyeball, lacrimal glands, conjunctiva, part of the
nasal mucosa, skin of the nose, eyelid and forehead. The maxillary nerve is also a purely sensory nerve that
supplies the middle third of the face and upper teeth. Mandibular nerve is a mixed nerve. It supplies sensation
to the lower third of the face, the tongue, floor of the mouth and the lower jaw. The motor root of the
mandibular nerve innervates the muscles of mastication, anterior belly of digastric, tensor muscles of the
tympanic membrane and mylohyoid. The practical was performed at Physiology Lab LUMHS to examine the
trigeminal nerve .It was concluded that fifth cranial nerve is intact in all the individuals.

Introduction
Trigeminal nerve is the fifth cranial nerve. It is the largest and the most complex of the twelve cranial nerves.
Trigeminal nerve is divided into ophthalmic, maxillary and mandibular nerves. It has both sensory and motor
fibers. Ophthalmic and maxillary are purely sensory nerves while mandibular is of mixed type.[1]Opthalmic
nerve is composed of general somatic afferent fibers. It arises from the trigeminal ganglion and passes forward
on the lateral wall of cavernous sinus. It gains access into the orbit via superior orbital fissure. It is. In the orbit
it divides into lacrimal nerve, frontal nerve, nasociliary nerve and infratrochlear nerve. It supplies sensation to
the cornea, ciliary body, lacrimal glands, conjunctiva, nasal mucosa and the skin of the nose, eyelids and
forehead. Maxillary nerve is composed of general somatic afferent fibers and leaves the cranial cavity through
foramen rotundum infereolateral to the cavernous sinus. It then enters the pterygopalatine fossa where it gives
off several branches. Its main trunk originates on the face through infraorbital foramen. It divides into
zygomatic and pterygopalatine nerves. It supplies sensation to the lower eyelid, cheek, nares, upper lip, upper
teeth and gums, nasal mucosa, roof of pharynx, air sinuses and part of meninges. Mandibular nerve is a mixed
nerve containing sensory general somatic afferent fibers. It leaves the cranial cavity through foramen ovale to
enter the masticatory space.here it divides into sensory and motor branvhes. It divides into masticatory nerve,
masseteric nerve, and temporal nerve. sensory fibers are present in the buccal and auriculotemporal nerve.
They supply lower lip, lower teeth and gums,chin and the lower jaw except at the angle of the jaw.[2]Its motor
fibers innervate the muscles of mastication, anterior belly of digastric, mylohyoid and tensor muscles of
tympanic membrane of the ear.[3]All the three divisions then travel backward from the sensory receptor sites of
the face to the trigeminal sensory ganglion. Trigeminal sensory ganglion is present in the brainstem extending
from the midbrain to the medulla. The nucleus is divided anatomically into three parts. They are spinal
trigeminal nucleus, main sensory nucleus and mesencephalic trigeminal nucleus.[4]The ascending pathways
from the main sensory nucleus and the nucleus of the spinal tract form an important secondary ascending
system.The fascicles of this tract, transmit impulses of pain and temperature.this system then terminates in the
nucleus of thalamus.While mesencephalic nucleus contains neurons that are proprioceptive in function which
terminates in the muscles of mastication. The sensory system projects from the brainstem to the thalamus.
thalamocortical sensory system mediates sensation from the periphery through the thalamus to the primary
sensory area of the cerebral cortex.With the exception of smell all the sensory information is sent to the
thalamus before sent to the cerebral cortex.[5]
Methods and Material
This practical was performed at the Department of Physiology Lab LUMHS, with 10 students both males and
females. The procedure was explained to the volunteers. To test the sensory portion volunteer was asked to
close his eyes. The sharp and blunt ends of the pin were touched on forehead, oral mucosa or cheek alternately
and he was asked to locate the area sensed. Next, two separate test tubes filled with hot and cold water were
placed on the cheek. To test the corneal conjunctival reflex the eye was touched with a wisp of cotton.
Volunteer blinked the tested eye with consensual reflex. To test the motor division, ask the volunteer to clench
his jaws and palpate the temporalis and masseter. Ask him to move the jaw from side to side against the force
of palm. Apply force on the chin using your index finger and tap it gently with a reflex hammer. Normally
mandible should be in the midline.
Result
Trigeminal nerve is intact in all the 10 students.
Discussion
Trigeminal nerve was examined in all the individuals. It was found that the nerve is intact . The most frequent
disorder of sensory division of the fifth cranial nerve is trigeminal neuralgia. It may be idiopathic, or caused by

compression, demyelination, injury to the nerve or by compression from an artery oa a vein along its pathway.
[6]
Pain is usually unilateral, tends to involve the second and third divisions of the sensory portion of trigeminal
nerve. It may be associated with minimal facial numbness or none and there are no other neurological
disorders.[7] The motor fibers in the mandibular division may also be damaged by leison of the nerve. Clinically
it is characterized by flaccid and paralysed muscles of mastication.In unilateral paralysis,as the mandible opens
it will swing to the paralyzed side due to action of pterygoids of the opposite side. Bilateral paralysis is
rare,associated with drooping of the lower jaw due to spasm of all the masticatory muscles.[8]
References
(1)Paulette Marrie Gillig (2010) The Trigeminal nerve and Facial nerve.Psychiatry(Edgmant) 7(1):13-16.
(2)Felizardo R,Boucher Y.Braud. (2009) Trigeminal projections on gustatory neurons of the nucleus of
solitatory tract..Brain Research;1288:60-68.
(3)Ted L Tewfik,Arien D.Meyers (2013) Trigeminal nerve anatomy.Medscape journal
(4)Kaufman DM. (2007) Clinical Neurology for psychiatrics.
(5)Liu,Grant (2005) Anatomy and Physiology of the trigeminal nerve and its clinical
connections.Neuroopthalmology Virtual Education Library.
(6)Helbig GM,Callahan JD,Conhen Gadol (2009) Varient intra neural vein,trigeminal nerve
relationships;an observation during microvascular decompression surgery for trigeminal
neuralgia.Neurosurgery.65:958-961.
(7)Emad Eskander and Fred G.Barker (2006) Case:A 61 year-old Man with Left sided Facial Pain.The
New England Journal of Medicine.355;183-188.
(8)Steven J.Scivani,David A.Keith and Leonard B.Kaban (2008). Temporomandibular joint disorders.
The New England Journal of Medicine; 359:2693-2705
5
OBJECTIVE:
TO EXAMINE THE FACIAL NERVE
INTRODUCTION:
The facial nerve is the seventh (VII) of twelve paired cranial nerves. It emerges from the brainstem between
the pons and the medulla, and controls the muscles of facial expression, and functions in the conveyance of
taste sensations from the anterior two-thirds of the tongue and oral cavity. It also supplies preganglionic
parasympathetic fibers to several head and neck ganglia [1]. The motor part of the facial nerve arises from the
facial nerve nucleus in the pons while the sensory and parasympathetic parts of the facial nerve arise from the
nervus intermedius.The motor part and sensory part of the facial nerve enters the petrous temporal bone via the
internal auditory meatus (intimately close to the inner ear) then runs a tortuous course (including two tight
turns) through the facial canal, emerges from the stylomastoid foramen and passes through the parotid gland,
where it divides into five major branches. Though it passes through the parotid gland, it does not innervate the
gland (This is the responsibility of cranial nerve IX, the glossopharyngeal nerve) [2]. The facial nerve forms the
geniculate ganglion prior to entering the facial canal. The branches of facial nerve is explained, Intra cranial:
(1) Greater petrosal nerve - provides parasympathetic innervation to several glands, including the nasal gland,
palatine gland, lacrimal gland, and pharyngeal gland. It also provides parasympathetic innervation to the
sphenoid sinus, frontal sinus, maxillary sinus, ethmoid sinus and nasal cavity. (2)Nerve to stapedius - provides
motor innervation for stapedius muscle in middle ear.(3) Chorda tympani supplies Submandibular gland,
Sublingual gland, Special sensory taste fibers for the anterior 2/3 of the tongue. Extra Cranial: Distal to
stylomastoid foramen, the following nerves branch off the facial nerve:(1)Posterior auricular nerve - controls
movements of some of the scalp muscles around the ear. (2)Branch to Posterior belly of Digastric muscle as
well as the Stylohyoid muscle. Five major facial branches (in parotid gland) - from top to bottom:

(1)Temporal branch of the facial nerve, (2)Zygomatic branch of the facial nerve, (3)Buccal branch of the facial
nerve, (4)Marginal mandibular branch of the facial nerve, (5)Cervical branch of the facial nerve.(4) Intra
operatively the facial nerve is recognized at 3 constant land marks:(I)At the tip of tragal cartilage where the
nerve is 1cm deep and inferior. (II)At the posterior belly of digastric by tracing this backwards to the tympanic
plate the nerve can be found between these two structures. (III)By locating the posterior facial vein at the
inferior aspect of the gland where the marginal branch would be seen crossing it[5]. Embryology the facial
nerve is the facial nerve is developmentally derived from the hyoid arch (second pharyngeal branchial arch).
The motor division of the facial nerve is derived from the basal plate of the embryonic pons, while the sensory
division originates from the cranial neural crest. People may suffer from acute facial nerve paralysis, which is
usually manifested by facial paralysis. Bell's palsy is one type of idiopathic acute facial nerve paralysis, which
is more accurately described as a multiple cranial nerve ganglionitis that involves the facial nerve, and most
likely results from viral infection and also sometimes as a result of Lyme disease.Iatrogenic Bell's Palsy may
also be as a result of an incorrectly placed dental local-anesthetic (Inferior alveolar nerve block). Although
giving the appearance of a hemi-plegic stroke, effects dissipate with the drug[6].
MATERIAL AND METHOD:
Testing the facial nerve: To test the motor supply, ask the patient to clench their teeth together, observing and
feeling the bulk of the masseter and temporalis muscles. Ask the patient to then open their mouth against
resistance.Finally perform the jaw jerk on the patient by placing your left index finger on their chin and
striking it with a tendon hammer. This should cause slight protrusion of the jaw.
-Muscles of the head and neck. - Feeling the masseter muscles. -Feeling the temporalis muscles. -The jaw jerk.
Voluntary facial movements, such as wrinkling the brow, showing teeth frowning, closing the eyes tightly
(inability to do so is called lagophthalmos)[1] , pursing the lips and puffing out the cheeks, all test the facial
nerve. There should be no noticeable asymmetry.
RESULT: All the student have normal facial nerve functioning.
DISCUSSION: In an UMN lesion, called central seven, only the lower part of the face on the contralateral
side will be affected, due to the bilateral control to the upper facial muscles (frontalis and orbicularis oculi)[7].
Lower motor neuron lesions can result in a CNVII palsy (Bell's palsy is the idiopathic form of facial nerve
palsy), manifested as both upper and lower facial weakness on the same side of the lesion. Taste can be tested
on the anterior 2/3 of the tongue. This can be tested with a swab dipped in a flavored solution, or with
electronic stimulation (similar to putting your tongue on a battery).Corneal reflex. The afferent arc is mediated
by the General Sensory afferents of the Trigeminal Nerve. The efferent arc occurs via the Facial Nerve. The
reflex involves consensual blinking of both eyes in response to stimulation of one eye. This is due to the Facial
Nerve's innervation of the muscles of facial expression, namely Orbicularis oculi, responsible for blinking.
Thus, the corneal reflex effectively tests the proper functioning of both Cranial Nerves V and VII [8].
REFERENCES:
1. J.Stroke and G.Chen.Emergency medicine journal (2012 ) ju0ly 23(7):554-557.
2. Hum.reprod(2009);7(5):701-710
3. Rolando Valer Zuela and Kemeth.Pan African Medical Journal (2011) :8:41
4. Baunstein, G.D., Rasor, J., Adler D., Danzer, H., Wade, M.E. Am. J. Obstet. Gynecol., 2010, Vol.
126:678.
5. Uotila, M., Ruoslahti, E., and Engvall, E.J., Immunol. Methods, 2011, Vol. 42, 11
6. Sollars, S. I. (2005). Chorda tympani nerve transection at different developmental ages produces
differential effects of taste bud volume and papillae morphology in the rat. The Journal of Neurobiology,
64, 310-320.

7. May M, Schaitkin B. May M, Schaitkin B, eds. The Facial Nerve, 2nd Edition. New York,
NY: Thieme; 2008.
8. Larrabee WF Jr, Makielski KH. Surgical Anatomy of the Face. New York: Raven Press; 1993
6
OBJECTIVE:
THE EXAMINATION OF VESTIBULOCOCHLEAR NERVE
ABSTRACT: The vestibulocochlear nerve is the eighth cranial nerve which emerges from brain between the
pons and medulla oblongata , behind the facial nerve . Its the sensory nerve that constitute of vestibular and
cochlear system. The vestibular system serves the vestibule of ear and semicircular canals, carrying the
impulses for the sense of equillibrium. The cochlear system serves the cochlea and carries impulses for the
sesnse of hearing. We performed the practical in the physiology department of LUMHS and we examined the
vestibulocochlear nerve individually of five boys and five girls. For vestibular system we did Rombergs test
and for cochlear system we performed Rinnes Test and Webers by using tunning fork and the result was
found that this nerve is intact. Whenever there is any condition that damage the eighth cranial nerve like
trauma , infection , or tumors that occurs either vestibular division or cochlear division it will affect both
system and hearing and balance are lost at same time and causes Hearing loss that include Conductive
hearing loss means loss of ability to transmits the sound waves and sensorineural hearing loss means is the
hearing loss due to damage of hair cells in organ of corti , Tinnitus and Vertigo.
INTRODUCTION;
The vestibulocochlear nerve also known as Auditory nerve or Acoustic
nerve is the eighth cranial nerve that is responsible for transmitting the sound and equillibrium information
from the inner ear to the brain. It is the sensory nerve that conducts two special senses ; hearing and balance. It
emerges from the junction of pons and medulla oblongata and enters to the internal acoustis meatus , along
with facial nerve and labryinth vessels, here it splits into two nerves; Vestibular nerve and Cochlear nerve [1].
The vestibular apparatus is the organ that sense the head position changes relative to gravity and it composed
of central process of bipolar neuron in the vestibular ganglion. The peripheral process extends in the macullae
of utricle, saccule and ampulae of semicircular ducts that is sensitive to rotational acceleration. The cochlear
nerve fibre travels away from cochlea of inner ear where it starts as a spiral ganglia. The auditory nerve fibre
provides a direct synaptic connection between hair cells of cochlea and cochlear nucleus and causes sensation
of hearing [2]. Any conditions that damage the vetibulocochlear nerve by diseases, trauma or any other
disruptive events that targeting this nerve there will be Deafness means hearing impairement or hearing loss is
a partial or total inability to hear and it inclide conductive deaness and sensorineural hearing loss.Conductive
deafness that results from process that occlude the conduction pathway, is caused by the failure of three tiny
bones inside the middle ear to pass along soundwaves to inner ear. Sensorineural hearing loss is the hearing
loss that occur due to damage of delicate hair cells of organ of corti . Tinnitus means ringing in the ears when
no other sound waves is present and its sounds like roaring, pulsing, whooshing, chirping, hissing, whistling or
clicking. It can occur in one ear or both ear due to damages of cochlear hair cells and its causes are head injury,
anemia, hypertension , loud noise exposure, hearing loss, too much wax in ear etc [3]. Vertigo is a subtype of
dizziness in which patient inappropriately experience the perception of motion, it also associated with nausea
vomitting as well as balance disorder that causing difficulties in standing and walking and it occurs due to
perpheral cause and centrall cause. Pripheral cause include the condition that damaging the inner ear and
vestibulocochlear nerve while central cause affect the brainstem, vestibulocerebellum or in rare case the
cortex[4].
Methods and Material:

The following practical was performed at physiology lab LUMHS, we selected 10 individuals five males and
five females for examining the nerve. We performed Rinne s Test and Webers Test by using a tunning fork
for examination of cochlear part and Romberg s Test for vestibular part. Tunning fork test: This test can be
used to differentiate conductive hearing and sensorineural hearing using the Rinne s Test and Webers test. In
Rinnes test we placed a vibrating tunning fork on the mastoid process if he can hear asked him to indicate
when it stops hearing, and then bring it to the external auditory meatus if he can hear it means air conduction is
better than bone conduction. This means that Rinnes test is positive. In Webers test we placed a vibrating
tunning fork on middle of forehead or vertex and asked him in which ear hearing is louder. Normally it heard
equally in both ears. If he heared equally then sound is symmetrical with no lateralization. In Romberg s Test
we asked him to stand with their feet together that touching eachother and the hand by sides, then asked him to
closed his eyes. If he sways or falls in close eyes and maintaining the balance by open eyes the test is positive.
RESULT:
On data analysis it was concluded that this nerve is intact.
DISCUSSION:
We examined the vestibulocochlear nerve and in conclusion it was that this nerve is intact. If there is any
damage to this nerve due to some disesases like paget s disease, drugs like aspirin, neurofibroma or damage to
brain that can not translate the message , there will be Deafness means impairement hearing , Tinnitus means
a sensation of ringing in ears , false sense of motion , Vertigo means loss of equilibrium , nystagmus and
Motion sickness means disagreement exists between visually perceived movement and the vestibular system
s sense of movement[5].
REFERENCES:
1. Wilson-Pauwek, L., Akesson, E. J., Stewart, P. A., & Spacey, S.(2002). Cranial nerves in health and
Brodal disease. Hamilton, ON: B.C. Decker, Inc.
2. Neurological Anatomy in Relation to Clinical Medicine, ed. 2. New York, Oxford University Press, , A.
1969.
3. Monrad-Krohn, G.H., Refsum, S.: The Clinical Examination of the Nervous System, ed. 12. London,
H.K. Lewis & Co., 1964.
4. Spillane, J.D.: The Atlas of Clinical Neurology, ed. 2. New York, Oxford University Press, 1975.
5. Walsh, F.B, Hoyt, W.F.: Clinical Neuro-ophthalmology, ed. 3. Baltimore, Williams & Wilkins Co.,
1969.
6
OBJECTIVE:
Examination of the Glossopharyngeal and the Vagus nerve.
INTRODUCTION:
The glossopharyngeal nerve is the ninth cranial nerve. The motor division of the glossopharyngeal nerve is
derived from the basal plate of the embryonic medulla oblongata, while the sensory division originates from
the cranial neural crest. The functions of the glossopharyngeal nerve are: It receives general sensory fibers
(ventral trigeminothalamic tract) from the tonsils, the pharynx, the middle ear and the posterior 1/3 of the
tongue, it receives special sensory fibers (taste) from the posterior one-third of the tongue, it receives visceral
sensory fibers from the carotid bodies, carotid sinus, it supplies parasympathetic fibers to the parotid gland via
the otic ganglion and it supplies motor fibers to stylopharyngeus muscle, the only motor component of this
cranial nerve. Another important aspect in the study of the glossopharyngeal nerve is the Glossopharyngeal
neuralgia. Glossopharyngeal neuralgia is a condition in which there are repeated episodes of severe pain in the

tongue, throat, ear, and tonsils, which can last from a few seconds to a few minutes. Glossopharyngeal
neuralgia is believed to be caused by irritation of the ninth cranial nerve, called the glossopharyngeal nerve.
Symptoms usually begin in people over age 40. In most cases, the source of irritation is never found. Some
possible causes for this type of nerve pain (neuralgia) are: Blood vessels pressing on the glossopharyngeal
nerve, growths at the base of the skull pressing on the glossopharyngeal nerve, tumors or infections of the
throat and mouth pressing on the glossopharyngeal nerve. Symptoms include severe pain in areas connected to
the ninth cranial nerve: Back of the nose and throat (nasopharynx), back of the tongue, Ear, Throat, Tonsil area
and Voice box (larynx).The vagus nerve is the longest of the cranial nerve. The vagus nerve wanders from the
brain stem through organs in the neck, thorax and abdomen. The nerve exits the brain stem through rootlets in
the medulla that are caudal to the rootlets for the ninth cranial nerve. The rootlets form the tenth cranial nerve
and exit the cranium via the jugular foramen. Similar to the ninth cranial nerve there are two sensory ganglia
associated with the vagus nerve. They are the superior and inferior vagal ganglia. The branchial motor
component of the vagus nerve originates in the medulla in the nucleus ambiguus. The nucleus ambiguus
contributes to the vagus nerve as three major branches which leave the nerve distal to the jugular foramen. The
pharyngeal branch travels between the internal and external carotid arteries and enters the pharynx at the upper
border of the middle constrictor muscle. It supplies the all the muscles of the pharynx and soft palate except the
stylopharyngeas and tensor palati. These include the three constrictor muscles, levator veli palatini,
salpingopharyngeus, palatopharyngeus and palatoglossal muscles. The superior laryngeal nerve branches distal
to the pharyngeal branch and descends lateral to the pharynx. It divides into an internal and external branch.
The internal branch is purely sensory and will be discussed later. The external branch travel to the cricothyroid
muscle which it supplies. The third branch is the recurrent branch of the vagus nerve and it travels a different
path on the left and right sides of the body. On the right side the recurrent branch leave the vagus anterior to the
subclavian artery and wraps back around the artery to ascend posterior to it. The right recurrent branch ascends
to a groove between the trachea and esophagus. The left recurrent branch leaves the vagus nerve on the aortic
arch and loops posterior to the arch to ascend through the superior mediastinum. The left recurrent branch
ascends along a groove between the esophagus and trachea. Both recurrent branches enter the larynx below the
inferior constrictor and supply intrinsic muscles of larynx excluding the cricothyroid. The visceromotor or
parasympathetic component of the vagus nerve originates from the dorsal motor nucleus of the vagus in the
dorsal medulla. These cells give rise to axons that travel in the vagus nerve. The visceromotor part of the vagus
innervates ganglionic neurons which are located in or adjacent to each target organ. The target organs in the
head-neck include glands of the pharynx and larynx (via the pharyngeal and internal branches). In the thorax
branches go to the lungs for bronchoconstriction, the esophagus for peristalsis and the heart for slowing of
heart rate. In the abdomen branches enter the stomach, pancreas, small intestine, large intestine and colon for
secretion and constriction of smooth muscle. The viscerosensory component of the vagus is derived from
nerves that have receptors in the abdominal viscera, esophagus, heart and aortic arch, lungs, bronchia and
trachea. Nerves in the abdomen and thorax join the left and right vagus nerves to ascend beside the left and
right common carotid arteries. Sensation from the mucous membranes of the epiglottis, base of the tongue,
aryepiglottic folds and the upper larynx travel via the internal laryngeal nerve. Sensation below the vocal folds
of the larynx is carried by the recurrent laryngeal nerves. The cell bodies that give rise to the peripheral
processes of the visceral sensory nerves of the vagus are located in the inferior vagal ganglion. The central
process exits the ganglion and enters the brain stem to terminate in the nucleus solitarius. The general sensory
components of the tenth cranial nerve conduct sensation from the larynx, pharynx, skin the external ear and
external auditory canal, external surface of the tympanic membrane, and the meninges of the posterior cranial
fossa. Sensation from the larynx travels via the recurrent laryngeal and internal branches of the vagus to reach
the inferior vagal ganglion. Sensory nerve fibers from the skin and tympanic membrane travel with auricular
branch of the vagus to reach the superior vagal ganglion. The central processes from both ganglia enter the
medulla and terminate in the nucleus of the spinal trigeminal tract.

MATERIALS AND METHODS:

Examination of the glossopharyngeal nerve is done by testing the general sensation and that of taste on the
posterior third of the tongue, but mostly it is done by checking the gag reflex. Gag reflex is a normal reflex in
humans that prevents the passage of anything from the throat, except during normal swallowing. Touching the
soft palate results in a very strong gag reflex in most healthy people. The gag reflex can also be used to make
someone vomit. Vagus nerve is tested by asking the person to speak. This gives a good indication to the
efficacy of the muscles. The uvula should be observed before and during the patient saying aah. Check that it
lies centrally and does not deviate on movement. Lesions:-Glossopharyngeal nerve if damaged can have
several effects on the human body. These effects include loss of bitter and sour taste, and impaired swallowing.
The clinical tests used to determine if the glossopharyngeal nerve has been damaged include testing the gag
reflex of the mouth, asking the patient to swallow or cough, and evaluating for speech impediments. The
clinician may also test the posterior one-third of the tongue with bitter and sour substances to evaluate for
impairment of taste.Vagus nerve.The patient complains of hoarse voice, difficulty in swallowing (dysphagia),
and choking when drinking fluid. There is also loss of gag reflex. Uvula deviates away from the side of lesion,
and there is failure of palate elevation.
RESULT:
All the students have normal glossopharyngeal and vagus reflex.
REFRENCES:
1. MedEd at Loyola GrossAnatomy/h_n/cn/cn1/cn9.htm
2. cranialnerves at The Anatomy Lesson by Wesley Norman (Georgetown University) (IX
3.www.nlm.nih.gov/medlineplus/ency/article/001636.htm
4.www.emedicine.medscape.com/article/1875813-overview
5. ^ a b Vibhuti N, Singh; Monika Gugneja (2005-08-22). "Supraventricular
Tachycardia".eMedicineHealth.com. Retrieved 2008-11-28.
6. "Exploring the Mind-Body Orgasm". Wired. 2007-01-10.
7. ^ Komisaruk, B.R, Whipple, B., Crawford, A., Grimes, S., Liu, W-C., Kalin, A., & Mosier, K. (2004).
Brain activation during vaginocervical self-stimulation and orgasm in women with complete spinal cord
injury: MRI evidence of mediation by the Vagus nerves.
7
OBJECTIVE:
Examination of the Accessory and the Hypoglossal nerve.
INTRODUCTION:
The accessory nerve (is the eleventh cranial nerve. It is composed of two parts, the cranial part and the spinal
part. The Cranial part (accessory portion) is the smaller of the two. Its fibers arise from the cells of the nucleus
and emerge as four or five delicate rootlets from the side of the medulla oblongata, below the roots of the
vagus. It runs laterally to the jugular foramen, where it interchanges fibers with the spinal portion or becomes
united to it for a short distance; here it is also connected by one or two filaments with the jugular ganglion of
the vagus. It then passes through the jugular foramen, separates from the spinal portion and is continued over

the surface of the ganglion nodosum of the vagus, to the surface of which it is adherent, and it is distributed
principally to the pharyngeal and superior laryngeal branches of the vagus. Through the pharyngeal branch it
probably supplies the muscles uvulae and levator veli palatine. Some few filaments from it are continued into
the trunk of the vagus below the ganglion, to be distributed with the recurrent nerve and probably also with the
cardiac nerves. The Spinal part (spinal portion) is firm in texture, and its fibers arise from the ventral horn cells
in the cord between C1 and C5. The fibers emerge from the cord laterally between the anterior and posterior
spinal nerve roots to form a single trunk, which ascends into the skull through the foramen magnum. It then
exits the skull through the jugular foramen, through which it passes, lying in the same sheath of dura mater as
the vagus, but separated from it by a fold of the arachnoids. In the jugular foramen, it receives one or two
filaments from the cranial part of the nerve, or else joins it for a short distance and then separates from it again.
As it exits from the jugular foramen, it runs backwards then descends obliquely behind the digastric and
stylohyoid muscles to the upper part of the sternocleidomastoid; it pierces this muscle, and courses obliquely
across the posterior triangle of the neck, to end in the deep surface of the trapezius muscle. As it traverses the
sternocleidomastoid it gives several filaments to the muscle, and joins with branches from the second cervical
nerve. In the posterior triangle it unites with the second and third cervical nerves, while beneath the trapezius it
forms a plexus with the third and fourth cervical nerves, and from this plexus fibers are distributed to the
muscle. Most consider the cranial part of the eleventh cranial nerve to be functionally part of the vagus nerve.
The accessory nerve is responsible for the motor innervation of the sternocleidomastoid and trapezius muscles.
The sternocleidomastoid acts in elevation of the thoracic cage and shoulder girdle, or, with fixation of the limb,
will act in lateral flexion of the head to the shoulder on the same side and rotate the head to direct the chin
upward to the opposite side. The trapezius muscle is one of several muscles that elevate the shoulder girdle and
retract the girdle dorsally. The hypoglossal nerve (cranial nerve 12) is the motor nerve of the tongue. Its fibers
arise from the cells of the hypoglossal nucleus, which is an upward prolongation of the base of the anterior
column of gray substance of the medulla spinalis. This nucleus is about 2 cm. in length, and its upper part
corresponds with the trigonum hypoglossi, or lower portion of the medial eminence of the rhomboid fossa .
The lower part of the nucleus extends downward into the closed part of the medulla oblongata, and there lies in
relation to the ventro-lateral aspect of the central canal. The fibers run forward through the medulla oblongata,
and emerge in the antero-lateral sulcus between the pyramid and the olive. The rootlets of this nerve are
collected into two bundles, which perforate the dura mater separately, opposite the hypoglossal canal in the
occipital bone, and unite together after their passage through it; in some cases the canal is divided into two by a
small bony spicule. The nerve descends almost vertically to a point corresponding with the angle of the
mandible. It is at first deeply seated beneath the internal carotid artery and internal jugular vein, and intimately
connected with the vagus nerve; it then passes forward between the vein and artery, and lower down in the
neck becomes superficial below the Digastricus. The nerve then loops around the occipital artery, and crosses
the external carotid and lingual arteries below the tendon of the Digastricus. It passes beneath the tendon of the
Digastricus, the Stylohyoideus, and the Mylohyoideus, lying between the last-named muscle and the
Hyoglossus, and communicates at the anterior border of the Hyoglossus with the lingual nerve; it is then
continued forward in the fibers of the Genioglossus as far as the tip of the tongue, distributing branches to its
muscular substance. Swallowing to clear mouth of saliva and other involuntary activities completed by the
tongue are controlled by the hypoglossal nerve; however, most functions are voluntary. Voluntary control
requires conscious thought and nerve pathways occur in the corticobulbar region in the spinal cord.

MATERILAS AND METHODS:

To test the integrity of the accessory nerve ,we simply asked our subject to rotate his head to one side against
resistance, causing the sternocleidomastoid of the opposite side to come into action. Then, we asked him to
shrug his shoulders, causing the trapezius muscles to come into action.To test the hypoglossal nerve is even
easier. We simply asked our subject to put out his tongue ( if a lesion is present, it should be noted that the
tongue will be deviated towards the paralyzed side). Pathology:- Injury to the spinal accessory nerve can cause
an accessory nerve disorder or spinal accessory nerve palsy, which results in diminished or absent function of
the sternocleidomastoid muscle and upper portion of the trapezius muscle.The distal part of the spinal
accessory nerve is most susceptible to injury. Throughout much of its course, the nerve is protected from injury
by the muscles it innervates. It is in the interval between protection from these muscles, which corresponds to
the distal part of the nerve, that the spinal accessory nerve is most vulnerable to injury.
RESULT:
All the students have intact nerve.
REFRENCES:
1. . ^ "The Accessory Nerve". Gray's Anatomy of the Human Body.
2. ^ "Spinal Accessory Nerve". Structure of the Human body, Loyola University Medical Education
Network. Archived from the original on 16 June 2007. Retrieved 2007-06-17.
3. ^ Duane E. Haines (2004). Neuroanatomy: an atlas of structures, sections, and systems. Hagerstown,
MD: Lippincott Williams & Wilkins. ISBN 0-7817-4677
4. 9http://education.yahoo.com/reference/gray/subjects/subject/207MedEd at Loyola
GrossAnatomy/h_n/cn/cn1/cn12.htm
5. cranialnerves at The Anatomy Lesson by Wesley Norman (Georgetown University)
8
OBJECTIVE:
Introduction to Reflexes and Reflex arc
ABSTRACT:
Reflex activity is the response to a peripheral nervous stimulation that occurs without our consciousness. It is a
protective type of mechanism and protects body from irreparable damages. and reflex arc is the anatomical
nervous pathway for a reflex action. Main properties of reflexes are one way conduction (Bell-Magendie Law),
reaction time, summation which may be spatial and temporal summation, occlusion, subliminal fringe,
recruitment, after discharge, rebound phenomenon and fatigue. In a normal person, when a muscle tendon is
tapped briskly, the muscle immediately contracts due to a two-neuron reflex arc involving the spinal or
brainstem segment that innervates the muscle. Hyporeflexia is an absent or diminished response to tapping. It
usually indicates a disease that involves one or more of the components of the two-neuron reflex arc
itself.Hyperreflexia refers to hyperactive or repeating (clonic) reflexes. These usually indicate an interruption
of corticospinal and other descending pathways that influence the reflex arc due to a suprasegmental lesion,
that is, a lesion above the level of the spinal reflex pathways. The main function of reflex is Protection. While
all sensory info eventually gets sent to the brain, a reflex can process a rapid, protective response in the spinal
cord without analysis and instruction from the brain. It is elicited even before pain/danger is perceived at a
conscious level. For the sake of study, group A1 students made sub-groups and performed test in physiology

lab and found that all students had normal reflexes.

INTRODUCTION:
The mechanism by which sensory impulses is automatically converted into a rapidly, predictable, involuntary
motor impulses through involvement of CNS is called reflexes and the neural pathway for any reflex action is
allied reflex arc.(1) A reflex action is a autonomic (involuntary) neuromuscular action or instinctive unlearned
reaction elicited by known stimulus. All reflex arcs have a minimum of five functional elements: 1. Receptor 2.
Afferent Nerve 3. Centre 4. Efferent nerve 5. The effector organ. (2)Reflexes can be classified into five
categories depending upon various factors as follows. 1. Inborn and Acquired reflexes: - (a. Un conditioned
Reflexes. b. Conditioned Reflexes) 2.Depending upon Situation of Centre: -(a. Cortical Reflexes b. Cerebellar
Reflexes c. Midbrain Reflexes 4. Medullary Reflexes 5.Spinal Reflexes which further divided as (i. Segmental
Reflexes ii. Inter segmental Reflexes. iii. Supra segmental Reflexes) 3. Physiological reflexes: - a. (Flexor or
Protective Reflexes b. Extensor or Antigravity Reflexes) 4. Number of synapses (a. monosynaptic b.
polysynaptic 5.Clinically Classified Reflexes: - a. Superficial Reflexes are usually multi synaptic reflexes
which are elicited from surface of body. They are of two types i. skin reflexes like those cutaneous reflexes
which arises from skin by stimulation of cutaneous receptors. E.g:- Corneal Reflexes, Conjunctival Reflex,
Sneezing Reflex, Uvular Reflex ii. mucous membrane reflexes arises from mucous membrane. E.g:- Scapular
Reflex(C5-T1), Upper Abdominal Reflex(T6-T9), Lower Abdominal Reflex (T10-T12), Cremastric Reflex
(L1-L2), Gluteal Reflex(L4-S2), Plantar Reflex(L5-S2), Bulbocavernous Reflex(S3-S4),Anal Reflex(S4-S5)b.
Deep Reflexes are actually stretch reflexes which are elicited on stroking the tendons. e.g. Jaw Jerk, Biceps
Jerk(C5,C6), Triceps Jerk(C6-C8), Supinator Jerk (C7-C8), Finger Flexion Reflex(C8,T1), Knee Jerk(L2-L4),
Ankle Jerk(L5-S2). Note: - . The patellar (L2-L4) and ankle jerk reflex (L5-S2) processed at these level and
does not progress to the brain. And they are monosynaptic, two-neuron, reflex arc. And Biceps jerk (C5-C6)
reflex is a more complex, three neuron reflex (polysynaptic).c. Visceral Reflexes are those reflexes where at
least one part of reflex arc is autonomic nerve. e.g. Pupillary Reflex(Light Reflex, Accomodation Reflex,
Ciliospinal Reflex), Oculocardiac Reflex, Carotid Sinus Reflex etc. d. Pathological Reflexes are not normal
reflexes and their presence indicates pathological conditions within the body. E.g. Babinski s sign, Pendullar
movements, Clonus (ankle clonus, patellar clonus)[2]. Reflexes can also be classified on the basis of their
controlled in the body as autonomic or somatic reflexes. Somatic reflexes include spinal cord as well as
superficial reflexes. Spinal Reflexes (Stretch reflexes) are important postural reflexes that act to maintain
posture, balance, and locomotion[4]. The superficial cord reflexes (abdominal and plantar reflexes) are initiated
by stimulation of receptors in the skin and mucosa and depend both on brain participation and on the cord-level
reflex arc[5]. Cranial Nerve Reflexes mediated by cranial nerves are the Corneal reflex which is by trigeminal
nerve. The absence of this reflex is an ominous sign because it often indicates damage to the brain stem and
Gag reflexes which tests the motor responses of cranial nerves IX and X[6] . The autonomic reflexes include the
pupillary reflexes, the papillary light reflex and the consensual reflex. The consensual response, or any reflex
observed on one side of the body when the other side has been stimulated, is called a contra lateral response.
Any reflex occurring on the same side stimulated is referred to as an ipsi lateral response [7] .
Methods and Materials:
This practical was performed at the Department of Physiology Lab LUMHS, To perform examination of
superficial reflexes. A2-group students were divided into two groups of boys and girls each comprising ten
students. The tests were performed separately.and materials required in this is Reflex [knee] hammer,
examination couch, wisp of cotton, tongue depressor, torch etc. To examining Conjunctival reflex: Stand on
one side of the volunteer and ask him to look at a far object on the opposite side.A sterile piece of cotton is
twisted into a wisp and bring it from the back of the subject avoiding his visual attention.Touch the conjunctiva
and see the response. Both eyes are separately tested.Observation: Bilateral closure of the eyes.Receptors:
Touch receptors of the conjunctivaAfferent limb: Ophthalmic division of trigeminal nerve. Efferent limb:

Facial nerve. Effector muscle: Orbicularis oculi. Centre - Pons (Nucleus of Trigeminal Nerve) (2) Corneal
reflex: Tested in the same manner as above, but the stimulus is applied to the cornea (limbus) and observe the
bilateral closure of eyes. Here the receptors are touch receptors in cornea. Afferents limb, Efferent limb, centre
and effector muscle are same as above.(3) Pupillary reflex: which includes Light reflex: Direct and indirect
[consensual] light reflex and Accommodation reflex for examining Direct light reflex: Make the volunteers sit
comfortably and ask them to look at a distant object. Allow sufficient time for them to get adapted to the light
of the room as well as the distant object, so that a moderately dilated state of the pupil results. The subject
should be instructed not to look on to the light or to the movements of the examiners hands. One eye is
covered with the palm of the hand so that the light shown into the tested eye is prevented from falling into it.
Bring the source of light (torch) from the lower lateral field of the eye so that light directly falls into the eye.
Observe the pupil. It will constrict. Each eye should be tested separately.
Result:
All boys and girls have normal superficial reflexes.
Discussion:
After examining it has found that all volunteers have normal reflexes. but there are upper and lower motor
neuron lesions. Due to which there is an interruption in reflex pathway which may cause abnormal results of
many reflexes.UMN sends fibers to LMN, and exerts direct or indirect supra nuclear control over LMN of
cranial and spinal nerves. In UMN lesion there is loss of voluntary skilful movements, loss of superficial
reflexes, weakness but not atrophy, spasticity, hyperreflexia, muscles of lower part of face paralyzed, tongue
deviate to side opposite to lesion, psuedobulbar palsy(which results from UMNs bilateral lesion to muscles of
tongue(XII), face(VII) speech and swallowing( IX,X) due to pyramidal tract lesion also that individual
demonstrate inappropriate emotional outbursts). and babinskis (that is extension upward of the toes when the
sole of the foot is stroked firmly on the outer side from the heel to the front; normal in infants under the age of
two years but a sign of brain or spinal cord injury in older persons) sign.[8] In LMN lesion Flaccid Paralysis,
muscle atrophy, all face affected muscles paralyzed, tongue deviate to the lesion side, bulbar palsy(same as
psuedobulbar palsy but due to LMN lesion and that lesion signs found in innervated (CN VII,IX,X,XII))
muscle hyporeflexia, muscle hypotonicity and fasciculations[9] .
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