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Lecture 9. Cranial Nerves

The document outlines the twelve pairs of cranial nerves, detailing their functions, locations, and clinical implications of impairments. It categorizes the cranial nerves into sensory, motor, and mixed types, explaining their roles in bodily functions such as sensation, muscle movement, and autonomic control. Specific nerves like the Olfactory, Optic, and Vagus are discussed in terms of their anatomy and potential pathologies.

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Sameer Narula
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0% found this document useful (0 votes)
13 views

Lecture 9. Cranial Nerves

The document outlines the twelve pairs of cranial nerves, detailing their functions, locations, and clinical implications of impairments. It categorizes the cranial nerves into sensory, motor, and mixed types, explaining their roles in bodily functions such as sensation, muscle movement, and autonomic control. Specific nerves like the Olfactory, Optic, and Vagus are discussed in terms of their anatomy and potential pathologies.

Uploaded by

Sameer Narula
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Cranial Nerves

Lecture 9
Objectives

1. List twelve pairs of cranial nerves.


2. Explain functions and types of the twelve pairs of
cranial nerves.
3. Identify location and function of each cranial nerve
and discuss clinical applications of cranial nerve
impairments.
1. List twelve pairs of cranial nerves.

I – Olfactory IX – Glossopharyngeal
II – Optic X – Vagus
III –Oculomotor XI – Accessory (Spinal Accessory)
IV – Trochlear XII – Hypoglossal
V – Trigeminal
VI – Abducens
VII – Facial
VIII – Vestibulocochlear
2. Explain functions and types of twelve pairs of cranial nerves.
Cranial nerves, like spinal nerves, contain sensory or motor fibers, or a combination of these fibers. Cranial nerves innervate
muscles or glands or carry impulses from sensory receptors. They are called cranial nerves because they emerge from foramina
or fissures in the cranium and are covered by tubular sheaths derived from the cranial meninges. Cranial nerves carry one or
more of the following five main functional components:
Motor (efferent) fibers
1. Motor fibers innervating voluntary (striated) muscle: Somatic motor (general somatic efferent) axons innervate the striated
muscles in the orbit, tongue, and external muscles of the neck (sternocleidomastoid and trapezius) as well as striated muscles
of the face, palate, pharynx, and larynx. The muscles of the face, palate, pharynx, and larynx are derived from the pharyngea l
arches and their somatic motor innervation is CN III, IV, VI, VII, IX, XI, & XII.
2. Motor fibers involved in innervating glands and involuntary (smooth) muscle (e.g., in viscera and blood vessels). These
include visceral motor (general visceral efferent) axons that constitute the cranial outflow of the parasympathetic division of
the autonomic nervous system. The presynaptic (preganglionic) fibers that emerge from the brain synapse outside the central
nervous system in a parasympathetic ganglion. The postsynaptic (postganglionic) fibers innervate glands and smooth muscle
throughout the body: CN III, VII, IX, & X.
Sensory (afferent) fibers
3. Fibers conveying sensation from the viscera. These include visceral sensory (general visceral afferent) fibers conveying
information from the carotid body and sinus, pharynx, larynx, trachea, bronchi, lungs, heart, and gastrointestinal tract: CN X.
4. Fibers transmitting general sensation (e.g., touch, pressure, heat, cold) from the skin and mucous membranes. These inclu de
somatic (general) sensory fibers: mainly CN V, but also CN VII, IX, & X).
5. Fibers transmitting unique (special) sensation. These include special sensory fibers conveying taste and smell and those
serving the special senses of smell (I), vision (II), hearing, and balance (VIII), taste (VII, IX and X).
Olfactory Nerve: (CN I)

Anosmia – loss of smell .


Causes and risk factors:
aging, trauma,
inflammation of mucosa
due to infection or allergy,
neurogenic disorders (MS,
schizophrenia, epilepsy),
smoking, sniffing cocaine.

Rhinorrhea, a leakage of
the fluid through the nose
from the subarachnoid
space. Rhinorrhea may
result from skull base
fracture.
Optic nerve (CN II)
The optic nerve passes through the optic
canal (optic foramen) to enter the middle
cranial fossa, where it forms the optic
chiasm. Here, fibers from the nasal
(medial) half of each retina decussate in the
chiasm and join uncrossed fibers from the
temporal (lateral) half of the retina to form
the optic tract. Thus, fibers from the right
halves of both retinas form the right optic
tract, and those from the left halves form
the left optic tract. The decussation of
nerve fibers in the chiasm results in the
right optic tract conveying impulses from
the left visual field and vice versa.
Most fibers in the optic tracts terminate in the lateral
geniculate bodies (nuclei) of the thalamus. From these
nuclei, axons are relayed to the visual cortices of the
occipital lobes of the brain.
Demyelinating Diseases and the Optic Nerve
Because the optic nerves are actually CNS tracts, the myelin
sheath that surrounds the fibers from the point at which
they penetrate the sclera is formed by oligodendrocytes
rather than by Schwann cells. Consequently, the optic
nerves are susceptible to the effects of demyelinating
diseases of the CNS, such as multiple sclerosis (MS).
The visual field (VF) is what is seen by a person with both
eyes wide open and looking straight ahead.
VF seen by right eye only (with left closed) is different from
VF seen by left eye only
Visual field defects may result from a large number of
neurologic diseases. It is clinically important to be able to
link the defect to a likely location of the lesion.
Occulomotor Nerve (CN III)

Originates from the


mesencephalon, and supplies
somatic motor innervation to four
extra-ocular muscles (superior,
medial, and inferior rectus and
inferior oblique) and to the levator
palpebrae superioris. It also
supplies proprioceptive
innervation to the previous
muscles, and visceral
(parasympathetic) innervation to
the smooth muscle of the
sphincter pupillae. The visceral
innervation causes constriction of
the pupil and ciliary muscle to
produce accommodation
(allowing the lens to become
more rounded) for near vision.
Characteristic signs of a complete
lesion of CN III are: Ptosis (drooping)
of the superior eyelid caused by
paralysis of the levator palpebrae
superioris. Eyeball (pupil) abducted
and directed slightly inferiorly (down
and out) because of unopposed
actions of the lateral rectus and
superior oblique.
No pupillary (light) reflex
(constriction of the pupil in response
to bright light) in the affected eye.
Dilation of the pupil resulting from
the interruption of the
parasympathetic fibers to the
sphincter pupillae leaves the dilator
pupillae unopposed.
No accommodation of the lens
(adjustment to increase convexity for
near vision) because of paralysis of
the ciliary muscle.
Trochlear Nerve (CN IV)
Originates between mesencephalon and pons. The trochlear nerve (CN IV) provides somatic motor and
proprioceptive innervation to the superior oblique. CN IV is rarely paralyzed alone. The characteristic
sign of trochlear nerve injury is diplopia (double vision) when looking down (e.g., when going down
stairs). Diplopia occurs because the superior oblique normally assists the inferior rectus in depressing the
pupil (directing the gaze downward) and is the only muscle to do so when the pupil is adducted.
Abducens Nerve (CN VI)

The abducent nerve (CN VI) provides


somatic motor to and proprioceptive
information from one extra-ocular
muscle, the lateral rectus.
Originates between pons and medulla.

CN VI has a long intracranial course. So, it


is often stretched when intracranial
pressure rises. A space-occupying brain
tumor may compress CN VI causing
paralysis of the lateral rectus muscle.
Complete paralysis of CN VI causes medial
deviation of the affected eye due to the
unopposed action of the medial rectus.
Trigeminal Nerve (CN V)
Originates from the pons and is the
largest of the cranial nerves, (except
Vagus) fibers extend from pons to face
and forms three divisions (trigeminal—
threefold) ophthalmic, maxillary, and
mandibular divisions.
The trigeminal nerve is major general
sensory nerve of the face transmitting
afferent impulses from touch,
temperature, and pain receptors. Cell
bodies of sensory neurons of all three
divisions are located in large trigeminal
(also called semilunar or gasserian)
ganglion. The mandibular division also
contains some motor fibers that
innervate chewing muscles.
Ophthalmic division (V1) fibers run from face to pons via
superior orbital fissure along with CN III, IV and VI. Bring
senses from the superior eye lid and nose (corneal and
sneezing reflexes). Carries out sympathetic fibers to
dilator pupillae and some other smooth muscles.

Maxillary division (V2) fibers run from face to pons via


foramen rotundum. Bring senses from the inferior eye lid
and maxillary face.

Mandibular division (V3) fibers pass via foramen ovale.


Mixed! (Sensory to mandible and motor for mastication).
CN V may be injured by trauma, tumors, aneurysms, or meningeal
infections causing: paralysis of the muscles of mastication with
deviation of the mandible toward the side of the lesion, loss of the
ability to appreciate soft tactile, thermal, or painful sensations in the
face, loss of the corneal reflex (blinking in response to the cornea
being touched) and the sneezing reflex.
Trigeminal Neuralgia. Trigeminal neuralgia (tic douloureux) is the
principal disease affecting the sensory root of CN V. It produces
excruciating, episodic pain that is usually restricted to the areas
supplied by the maxillary and/or mandibular divisions of CN V.
Facial Nerve (CN VII)

Originates between pons and medulla.


Somatic Motor: the facial nerve supplies the
striated muscles, mainly the muscles of facial
expression.
The motor part and sensory part of the facial
nerve enters the temporal bone via the
internal auditory meatus close to the inner ear
and CN VIII. Then it emerges from the
stylomastoid foramen and passes through the
parotid gland where it divides into five major
branches.
Facial Nerve (CN VII)

Visceral (Parasympathetic) Motor: the


parasympathetic fibers of CN VII provide
innervation of the lacrimal, nasal, pharyngeal,
and palatine glands and to the submandibular
ganglion for innervation of the sublingual and
submandibular salivary glands.

Somatic (General) Sensory: some fibers from


the geniculate ganglion supply a small area of
skin close to the external acoustic meatus.

Special Sensory (Taste): fibers carried by the


lingual nerve convey taste sensation from the
anterior two thirds of the tongue and soft
palate.
Injury to Facial Nerve
A lesion of CN VII is accompanied by a loss of
motor, gustatory (taste), and autonomic
functions. The motor paralysis of the facial
muscles involves upper and lower parts of
the face on the ipsilateral (same) side (Bell
palsy). Dry eyes and lower eye lead droop.
Because it passes through the facial canal,
CN VII is vulnerable to compression when a
viral infection produces inflammation of the
nerve (viral neuritis).
Corneal Reflex
Loss of the corneal reflex may occur if either
the ophthalmic nerve (CN V1) or the facial
nerve (CN VII) has lesion. The corneal reflex
is tested by touching the cornea with a
http://www.tabletsmanual.com/wiki/read/bells_palsy
cotton wisp. A bilateral blinking response
should result.
Vestibulocochlear nerve (CN VIII) The vestibulocochlear nerve (CN VIII) is a
special sensory nerve of hearing and
Originates between pons and medulla. equilibrium. Enters the internal acoustic
meatus. It separates into the vestibular and
cochlear nerves. The vestibular nerve is
concerned with equilibrium. The cochlear
nerve is concerned with hearing.
Injuries of the Vestibulocochlear Nerve
Although the vestibular and cochlear nerves
are essentially independent, peripheral lesions
often produce concurrent clinical effects
because of their close relationship. Hence
lesions of CN VIII may cause tinnitus (ringing or
buzzing of the ears), vertigo (dizziness, loss of
balance - ataxia), and impairment or loss of
hearing. Central lesions may involve either the
cochlear or vestibular divisions of CN VIII.
Glossopharyngeal Nerve (CN IX) Somatic (Branchial) Motor: motor fibers
The glossopharyngeal nerve (CN IX) emerges from the lateral aspect
pass to one muscle, the stylopharyngeus.
of the medulla and passes anterolaterally to leave the cranium Visceral (Parasympathetic) Motor:
through the jugular foramen. parasympathetic fibers provide for
innervation of the parotid gland.
Somatic (General) Sensory: The
pharyngeal, tonsillar, and lingual
branches supply the mucosa of the
oropharynx, soft palate, and posterior
third of the tongue. Stimuli determined
to be unusual or unpleasant here may
evoke the gag reflex or even vomiting.
Via the tympanic plexus CN IX supplies
the mucosa of the tympanic cavity,
pharyngotympanic tube, and the internal
surface of the tympanic membrane.
Glossopharyngeal Nerve (CN IX)
Special Sensory (Taste): taste fibers are conveyed from the posterior third of the tongue to
the sensory ganglia. Visceral Sensory: the carotid sinus nerve supplies the carotid sinus, a
baro-(presso-) receptor sensitive to changes in blood pressure, and the carotid body, a
chemoreceptor sensitive to blood gas (oxygen and carbon dioxide) levels. If a person is
hyperventilating the blood is alkaline. If a person is hypoventilating the blood is acidic.

Lesions of Glossopharyngeal Nerve


Isolated lesions of CN IX or its nuclei are uncommon. Injuries of CN IX result from infection or
tumors are usually accompanied by signs of involvement of adjacent nerves. Because CN IX,
CN X, and CN XI pass through the jugular foramen, tumors in this region produce multiple
cranial nerve palsies—the jugular foramen syndrome.
An isolated lesion would result in absence of taste on the posterior third of the tongue,
difficulty in swallowing, absent gag reflex on the side of the lesion, and palatal deviation
toward the unaffected side. The afferent (sensory) limb of the gag reflex is via the
glossopharyngeal nerve (CN IX) and the efferent (motor) limb is via the vagus nerve (CN X).
The gag reflex is absent in about 37% of normal individuals (Davies, 1995).
Vagus nerve (CN X) arises by a series of
rootlets from the lateral aspect of the medulla
that merge and leave the cranium through the
jugular foramen positioned between CN IX and
CN XI.
Visceral (Parasympathetic) Motor fibers from
the posterior (dorsal) nucleus of the vagus nerve
supply the thoracic and abdominal viscera to
the left colic (splenic) flexure.

Somatic (Branchial) Motor fibers supply:


pharyngeal muscles via the pharyngeal plexus
with fibers of the glossopharyngeal nerve;
muscles of the soft palate and all muscles of the
larynx.
Somatic (General) Sensory: from dura mater of posterior cranial fossa; skin posterior to the ear;
external auditory canal; palate.

Special Sensory (Taste): carry sense of taste from the root of the tongue and the taste buds on
the epiglottis.

Visceral Sensory: convey sensory fibers: from mucosa of the inferior pharynx at the esophageal
junction, epiglottis, and epiglottic folds; mucosa of larynx; baroreceptors in the aortic arch;
chemoreceptors in the aortic bodies; thoracic and abdominal viscera.

Lesions of Vagus Nerve


Isolated lesions of CN X are uncommon. Injury to the pharyngeal branches of CN X results in
dysphagia (difficulty in swallowing). Lesions of the superior laryngeal nerve produce anesthesia
of the superior part of the larynx and paralysis of the cricothyroid muscle. The voice is weak and
tires easily. Proximal lesions of CN X also affect the pharyngeal and superior laryngeal nerves,
causing difficulty in swallowing and speaking. Tachycardia and cardiac arrhythmia may occur.
Severity of both Vagus nerves may result in death due to a large parasympathetic deficit.
Injury of a recurrent laryngeal
nerve (branch of CN X) may be
caused by aneurysms of the arch
of the aorta and may occur during
neck operations. Injury of the
recurrent laryngeal nerve causes
hoarseness and dysphonia
(difficulty in speaking) because of
paralysis of the vocal folds
(cords). Paralysis of both
recurrent laryngeal nerves causes
aphonia (loss of voice) and
inspiratory stridor (a harsh, high-
pitched respiratory sound).
Because of its longer course
Thyroidectomy lesions of the left recurrent
During a total thyroidectomy (excision of a thyroid gland with malignant tumors) the laryngeal nerve are more
parathyroid glands are in danger of being inadvertently damaged or removed. These common than those of the right.
glands are safe during subtotal thyroidectomy because the most posterior part of Proximal lesions of CN X also
the thyroid gland usually is preserved. Variability in the position of the parathyroid affect the pharyngeal and
glands, especially the inferior ones, puts them in danger of being removed during superior laryngeal nerves causing
surgery on the thyroid gland. If the parathyroid glands are inadvertently removed difficulty in swallowing and
during surgery, the patient suffers from tetany, a severe convulsive disorder. The speaking.
generalized convulsive muscle spasms result from a fall in blood calcium levels.
Accessory Nerve (CN XI)
Somatic motor innervation to the
sternocleidomastoid (SCM) and trapezius
muscles.
Injury to Spinal Accessory Nerve
Because of its nearly subcutaneous passage
through the posterior cervical region, CN XI is
susceptible to injury during surgical
procedures such as lymph node biopsy,
cannulation of the internal jugular vein, and
carotid endarterectomy.
Lesions of CN XI produce weakened ability to
shrug and atrophy of the upper part trapezius
and impairment of rotary movements of the
neck and chin to the opposite side as a result
of weakness of the SCM.
Clinical signs are dropped shoulder and
difficulty in rotating the neck.
Hypoglossal nerve (CN XII) is
somatic motor to intrinsic and
extrinsic muscles of the tongue
(styloglossus, hyoglossus,
genioglossus). The hypoglossal
nerve arises as a purely motor nerve
by several rootlets from the medulla
and leaves the cranium through the
hypoglossal canal.

Injury to Hypoglossal Nerve


Injury to CN XII paralyzes the ipsilateral half of the tongue. After some time, the tongue
atrophies, making it appear shrunken and wrinkled. When the tongue is protruded, its apex
deviates toward the paralyzed side because of the unopposed action of the genioglossus muscle
on the normal side of the tongue.
Blue Boxes in M&A pp. 524 Trigeminal Neuralgia, Lesions of
Trigeminal Nerve, Bell’s Palsy; pp. 548 Pupillary Light Reflex, Corneal
Reflex, Paralysis of Extra-ocular Muscles/Palsies of Orbital Nerves,
Oculomotor Nerve (CN III) Palsy, Abducent Nerve (CN VI) Palsy; pp.
569 Gag Reflex, Paralysis of Genioglossus, Injury to Hypoglossal Nerve

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