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There are 12 paired cranial nerves in our brain.
The first two are purely sensory and located in the brain(cerebrum).
The 3rd and 4th are located in the midbrain for eye movement.
The remaining 8 nerves are divided equally between pons and medulla.
The nuclei of 5th,6th,7th,and 8th are located in the pons.
The nuclei of 9th,10th,11th and 12th are located in the medulla.
The cranial nerves can be involved by central and peripheral diseases.
It is mandatory to know the following about each nerve:
Name, Location , Function ,How to exam it and Causes of paralysis.
The causes can be infection , ischemia , inflammation , tumor , 2ry tumor ,
tuberculosis or degenerative in the form of multiple sclerosis.
The nerve weakness symptoms are the same for peripheral and central causes.
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Olfactory nerve - CN I
Nucleus - frontal lobe
Function - smell
The olfactory nerves consist of small unmyelinated axons that originate in the olfactory
epithelium in the roof of the nasal cavity; they pierce the cribriform plate of the ethmoid
and terminate in the olfactory bulb. Lesions of the nerve result in parosmia (altered sense
of smell) or anosmia (loss of smell).
The common cold is the most frequent cause of dysfunction. Dysfunction can be associated
with fractures of the cribriform plate of the ethmoid bone. Frontal lobe tumors may
compress the olfactory bulb and/or tracts and cause anosmia, but this is rare occurrence.
How to test?
Olfactory function is tested easily in each nostril separately by placing stimuli under one nostril
and occluding the opposing nostril while the patient is closing his eyes. The stimuli used should be
non-irritating and identifiable. Some example stimuli include cinnamon, coffee, cloves and
toothpaste. Commercially available scented scratch papers may also be used.
Bilateral loss can occur with rhinitis, smoking or aging. Unilateral loss indicates a possible nerve
lesion or deviated septum.
This test is usually skipped on a cranial nerve exam.
If you wish to test olfaction and don't have any "substance filled tubes" use an alcohol pad as a
screening test. Patients should be able to identify its distinctive odor from approximately 10 cm.
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Optic nerve - CN II
The optic nerve is a collection of axons that relay information from the rods and
cones of the retina. The temporal derivations reach the ipsilateral and the nasal
derivations the contralateral superior colliculi and the lateral geniculate bodies.
From there, axons extend to the calcarine cortex by means of the optic
radiation, traversing the temporal (Myer loop) and parietal lobes. Fibers
responsible for the pupillary light reflex bypass the geniculate body and reach
the pretectal area, from where they innervate the parasympathetic (midline)
portion of the third-nerve nucleus, enabling the consensual pupillary reflex.
Each optic tract contains ipsilateral temporal and contralateral nasal fibers
from the optic nerves.
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The following testing is appropriate:
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Acuity, by using the Snellen chart (near and distant vision)
Visual fields, by means of confrontation or perimetry if indicated
Color, with use of an Ishihara chart or by using common objects, such as a
multicolored tie or color accent markers
Funduscopy
Lesions of the visual pathways result in blindness and pupillary abnormalities, such
as the Marcus-Gunn pupil (retinal or optic nerve disease), scotomata, quadrant or
hemianopsias (optic tract and radiation), and hemianopsias with macular sparing
(calcarine cortex).
Lateral geniculate body
•
Fibers in the optic tracts:

Mainly terminate in the lateral geniculate bodies of the thalamus

A few fibers terminate in pretectal area and superior colliculus. These
fibers are related to light reflexes
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`Functions:
1. Visual acuity
2. Visual field
3. Visual colour
4. Fundoscopy
5. Light reflex
Visual acuity is tested in each eye separately. Ensure the patient's vision is
corrected with eyeglasses or a pinhole.
Bed site testing:
1.Stand
6 meter from the patients bed and ask him to close one eye while
opening the other .
2.Exame the acuity of every eye alone by asking the patient to count your fingers
3.Test the ability of the patient to count your fingers and come closer if he can’t
see you
4.Test his counting ability randomly (1-3-5) 0r (2-4)
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Visual fields are assess by asking the patient to cover one eye while the examiner
tests the opposite eye. The examiner wiggles the finger in each of the four
quadrants and asks the patient to state when the finger is seen in the periphery.
The examiner's visual fields should be normal, since it is used as the baseline.
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You should be half meter apart from the patient.
The heads should be on the same level.
Start from the periphery to the center with the finger midway
between the patient and the examiner .The patient is closing the
right eye and the examiner is closing the left eye and sitting facing
each other with the forearm extended and your finger mid way
from periphery , bring your finger to the field of vision.
The open eyes should then be staring directly at one another.
Once you have the ability to see your finger , the patient should also
see it.
This means the field of vision should be normal for examiner before
examining the paient.
a. The examiner should move their hand out towards the
periphery of his/her visual field on the side where the eyes
are open. The finger should be equidistant from both
persons.
b. The examiner should then move the wiggling finger in
towards them, along an imaginary line drawn between the
two persons.The patient and examiner should detect the
finger at more or less the same time.
c. The finger is then moved out to the diagonal corners of the
field and moved inwards from each of these directions.
Testing is then done starting at a point in front of the
closed eyes. The wiggling finger is moved towards the open
eyes.
d. The other eye is then tested.
This is the confrontation test.
It is important to move to the center of the field to look for the blind
spot which is the first finding to be seen in a patient with papilledema.
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Visual Field Deficits
Cut at level :1
A lesion of the right optic nerve causes a total loss of vision (blindness) in the
right eye DUE TO PERMENANT INCREASED INTRACRANIAL PRESSURE
Cut at level :2
A lesion of the optic chiasma causes a loss of vision in the temporal half of both
visual fields:
bitemporal hemianopsia DUE TO PITUITARY ADENOMA.
Cut at level: 3 & 4
A lesion of the right optic tract & right optic radiation just after the LGN causes
a loss of vision in the left hemifield: contralateral homonymous hemianopsia.
A lesion of both visual cortices causes a complete blindness.
'Fundoscopy
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Pupillary light reflex
The response of pupils to light is controlled by afferent (sensory) nerves CN 2
and efferent (motor) nerves CN 3. These innervate the ciliary muscle, which
controls the size of the pupil. Testing is performed as follows:
1. It helps if the room is a bit dim, the pupil become more dilated.
2. Using any light source (flashlight ), shine the light into one eye. This will
cause that pupil to constrict ((the direct response)).
3. Remove the light and then re-expose it to the same eye, though this time
observe the other pupil. It should also constrict, (consensual response).
4. If the patient's pupils are small at baseline or you are otherwise having
difficulty seeing the changes, take your free hand and place it above the
eyes so as to provide some shade . If you are still unable to appreciate a
response, ask the patient to close their eye, generating maximum darkness
and thus dilatation. Then ask the patient to open the eye and immediately
expose it to the light. This will (hopefully) make the change from dilated to
constricted very apparent.
5. Under normal conditions, both pupils will appear symmetric. Direct and
consensual response should be equal for both.
6. Asymmetry of the pupils is referred to as aniosocoria.
7. A number of conditions can also affect the size of the pupils.
Medications/intoxications which cause generalized sympathetic activation
will result in dilatation of both pupils. Other drugs(e.g. narcotics) cause
symmetric constrictionof the pupils. Eye drops known as mydriatic agents
are used to paralyze the muscles, resulting marked dilatation of the pupils.
Addiitonally, any process which causes increased intracranial pressure
can result in a dilated pupil that does not respond to light.
8. If the afferent nerve is not working, neither pupil will respond when light is
shined in the affected eye. Light shined in the normal eye, however, will
cause the affected pupil to constrict. That's because the efferent (signal to
constrict) response in this case is generated by the afferent impulse
received by the normally functioning eye. This is referred to as an afferent
pupil defect.
9. If the efferent nerve is not working, the pupil will appear dilated at baseline
and will have neither direct nor consensual pupillary responses.
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Oculomotor nerve - CN III
Function-purely motor supply all muscles of the eye except SO4LR6.
Normally, the eyes move in concert (ie when left eye moves left, right eye
moves in same direction to a similar degree). The brain takes the input from
each eye and puts it together to form a single image because the images are
projected over the two maculas as two inverted images and the brain is
reducing them into one image due to intact eye movements . This
coordinated movement depends on 6 extra ocular muscles that insert around
the eye balls and allow them to move in all directions.
Each muscle is innervated by one of 3 Cranial Nerves (CNs): CNs 3, 4 and 6.
Movements are described as:
elevation (pupil directed upwards),
depression (pupil directed downwards),
adbduction (pupil directed laterally),
adduction (pupil directed medially),
extorsion (top of eye rotating away from the nose),
and intorsion (top of eye rotating towards the nose).
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The 3 CNs responsible for eye movement and the muscles that they control are
as follows:
CN 4 (Trochlear): Controls the Superior Oblique muscle.
CN 6 (Abducens): Controls the Lateral Rectus muscle.
CN 3 (Oculomotor): Controls the remaining 4 muscles (inferior oblique, inferior
rectus, superior rectus, and medial rectus). CN3 also raises the eyelid and
mediates constriction of the pupil .( S O 4, L R 6 )
EOMs and their function:
The medial and lateral rectus muscles - their functions are very straight forward:
Lateral rectus: Abduction (ie lateral movement along the horizontal plane)
Medial rectus: Adduction (ie. Medial movement along the horizontal plane)
The remaining muscles each causes movement in more than one direction.
This is due to the fact that they insert on the eyeball at various angles.
The action which the muscle primarily performs is listed first, followed by
secondary and then tertiary actions.
Inferior rectus: depression, extorsion and adduction.
Superior rectus: elevation, intorsion and adduction
Superior oblique: intorsion, depression and abduction
Inferior oblique: extorsion, elevation and abduction
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The oculomotor nucleus of the nerve is located in the midbrain and innervates
the pupillary constrictors; the levator palpebrae superioris; the superior,
inferior, and medial recti; and the inferior oblique muscles.
 Motor for most of extraocular muscles.
 Also carries preganglionic parasympathetic fibers for pupillary constrictor
and ciliary muscle.
 Has two nuclei:
1- Main occulomotor nucleus;
 Lies in the mid brain, at the level of superior colliculus
2- Accessory nucleus (Edinger-Westphal nucleus);
 Lies dorsal to the main motor nucleus,
 Its cells are Preganglionic Parasympathetic Neurons.
 It receives; Corticonuclear fibers for the accommodation reflex, and from
the pretectal nucleus for the direct and consensual pupillary light reflexes.
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Lesions of CN III result in
1. DROPPING OF THE UPPER EYE LID( COMPLETE PTOSIS)
2. DILATED PUPIL
3. DIVERGENT SQUUINT
4. DIPLOPIA
5. DIFFICULY TO ADDUCT THE EYE( EYE LOOK OUT AND DOWN)
The eye is frequently turned out (divergent squint). In subtle cases,
patients complain of only diplopia if the eye lid elvated by the examiner or
blurred vision with acuity reduction if the optic nerve involved. The
exotropia seen in CN III paralysis can be distinguished from that in
internuclear ophthalmoplegia because in the latter convergence is
preserved.
Paralysis of CN III is the only ocular motor nerve lesion that results in diplopia in
more than 1 direction, distinguishing itself from CN IV paralysis (which also can
result in exotropia). Pupillary involvement is an additional clue to involvement of
CN III which divides the 3rd palsy in two types. Pupil-sparing CN III paralysis
occurs in diabetes mellitus, vasculitides , multiple sclerosis, hypertension,
atherosclerosis and hyperlipedemia.
2 types of lesion:
Medical 3rd N.palsey- pupil non dilated -nervosum within the nerve
Surgical 3rd N.palsey- dilated pupil –pressure over parasympathetic N.
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Any focally destructive lesion along the course of the third cranial nerve can cause
oculomotor nerve palsy or dysfunction. Some of the most frequent causes include
the following:
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Nuclear portion
o Infarction
o Hemorrhage
o Neoplasm
o Abscess
Fascicular midbrain portion
o Infarction
o Hemorrhage
o Neoplasm
o Abscess
Fascicular subarachnoid portion
o Aneurysm
o Infectious meningitis - Bacterial, fungal/parasitic, viral
o Meningeal infiltrative
o Carcinomatous/lymphomatous/leukemic infiltration, granulomatous
inflammation (sarcoidosis, lymphomatoid granulomatosis, Wegener
granulomatosis)
o Ophthalmoplegic migraine
Fascicular cavernous sinus portion
o Tumor - Pituitary adenoma, meningioma, craniopharyngioma,
metastatic carcinoma
[7]
o Pituitary apoplexy (infarction within existing pituitary adenoma)
o Vascular
o Giant intracavernous aneurysm
o Carotid artery-cavernous sinus fistula
o Carotid dural branch-cavernous sinus fistula
o Cavernous sinus thrombosis
o Ischemia from microvascular disease in vasa nervosa
o Inflammatory - Tolosa-Hunt syndrome (idiopathic or granulomatous
inflammation)
Fascicular orbital portion
o Inflammatory - Orbital inflammatory pseudotumor, orbital myositis
o Endocrine (thyroid orbitopathy)
o Tumor (eg, hemangioma, lymphangioma, meningioma)
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Trochlear nerve - CN IV

Type: motor
The nucleus of the nerve is located in the midbrain. It innervates the superior
oblique muscle, which function;

Primarily rotates the tip of the eye towards the nose (Intorsion)

Secondarily moves the eye downwards (depression)

Tertiarily moves the eye outwards ( abduction)

Rotates the eye ball downwards and laterally
Trochlear nerve typically allows a person to view the tip of his or her nose.
An isolated right superior oblique paralysis results in exotropia to the right (R),
double vision that increases on looking to the (L), and head tilt to the right (R).
The mnemonic is R, L, R (ie, the marching rule). The rule is L, R, L for left superior
oblique paralysis. This rule and the lack of ptosis and/or pupillary involvement
allow easy distinction of the exotropia of CN IV paralysis from that seen in CN III
paralysis.
It passes forward through middle cranial fossa in the lateral wall of the
cavernous sinus.
The nerve then enters the orbit through the superior orbital fissure.
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 Lesion results in vertical diplopia &
 Inability to rotate the eye infero-laterally.
 So, the eye deviates; upward and slightly inward.
This person has difficulty in walking downstairs.
Etiology
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Head trauma (most common) severe with loss of consciousness.
Consider the possibility of underlying structural abnormalities IN TRAUMA
Microvasculopathy secondary to diabetes, atherosclerosis, or hypertension
also may cause isolated fourth nerve palsy.
There are rare reports of thyroid ophthalmopathy and myasthenia gravis
presenting as isolated fourth nerve palsy.
Tumor, aneurysm, multiple sclerosis, or iatrogenic injury may present with
isolated fourth nerve palsy that may evolve over time to include other
cranial nerve palsies or neurologic symptoms.
Fourth nerve palsy may become manifest after cataract surgery. Patients
with underlying, well-controlled, and asymptomatic fourth nerve palsy may
decompensate gradually as they lose binocular function resulting from
cataract. Following restoration of good vision, these patients become
aware of diplopia.
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Abducens nerve - CN VI
 The nucleus of the nerve is located in the paramedian pontine region in
the floor of the fourth ventricle. It passes through cavernous sinus, lying
below and lateral to the internal carotid artery
 Then it enters the orbit through the superior orbital fissure.
It innervates the lateral rectus, which abducts the eye. Isolated paralysis results
in convergent squint and inability to abduct the eye to the side of the lesion.
Patients complain of double vision on horizontal gaze only.
Symptom- diplopia on far vision as intracranial pressure increases
This finding is referred to as horizontal homonymous diplopia, which is the sine
qua non of isolated CN VI paralysis. Paralysis of CN VI may result from increased
intra cranial pressure without any lesion in the neuraxis, and it may result in
false localization if one is not aware of it.
Lesion results in:
 Inability to direct the affected eye laterally. (convergent squint).
 A nuclear lesion may also involve the nearby facial nucleus or axons of
the facial nerve, causing paralysis of all the ipsilateral facial muscles.
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Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in
which the affected eye shows impairment of adduction. If the patient looks to
right horizontally, he uses the right lateral rectus (6th) and left medial rectus (3rd)
by medial longitudinal fasiculus. The contralateral eye abducts, however with
nystagmus(right) . The left eye medial rectus is paralysed and cant follow the
right eye. Additionally, the divergence of the eyes leads to horizontal diplopia.
That is, if the right eye is affected the patient will "see double" when looking to
the left, seeing two images side-by-side. Convergence is generally preserved.
The disorder is caused by injury or dysfunction in the medial longitudinal
fasciculus (MLF), a heavily-myelinated tract that allows conjugate eye movement
by connecting the paramedian pontine reticular formation (PPRF)-abducens
nucleus complex of the contralateral side to the oculomotor nucleus of the
ipsilateral side.
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How to exam 3rd ,4th and 6th?
Cranial nerve testing is done such that the examiner can observe eye movements
in all directions. The movements should be smooth and coordinated. To assess,
proceed as follows:
1. Stand in front of the patient.
2. Ask them to follow your finger with their eyes and to locate the site of
diplopia while keeping their head in one position central and fixed .
3. You have to compare pupil sizes , nystagmus if present and weakness.
4. Using your finger , ask the patient to follow it tracing an imaginary( plus)
in front of them, making sure that your finger moves far enough out and
up so that you're able to see all appropriate eye movements
5. Horizontal on both sides , up and down
6. For oblique muscles, down in and out , up out and in( Z IMAGINARY LINE)
7. At the end, bring your finger directly in towards the patient's nose. This
will cause the patient to look cross-eyed and the pupils should constrict, a
response referred to as accommodation.
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Trigeminal nerve - CN V
•
Largest & one of most complex cranial nerve
•
Large sensory part & much smaller motor part
•
Sensory component has 3 divisions : ophthalmic, maxillary, mandibular.
•
Motor & prinicipal sensory nuclei – midpons
Spinal tract & nucleus (pain, temp) – pons to upper cervical
 Type: Mixed (sensory & motor).
 Fibers:
1. General somatic afferent:
Carrying general sensations from face.
2. Special visceral efferent:
Supplying muscles developed from the
(8 muscles).
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The nucleus of the nerve stretches from the midbrain (ie, mesencephalic nerve)
through the pons (ie, main sensory nucleus and motor nucleus) to the cervical
region (ie, spinal tract of the trigeminal nerve). It provides sensory innervation for
the face and supplies the muscles of mastication.
 Four nuclei: (3 sensory + 1 Motor).
 General somatic afferent:
1. Mesencephalic (midbrain & pons): receives proprioceptive fibers from face.
2. Principal (main) sensory (pons): receives touch fibers from face.
3. Spinal (pons, medulla & upper 2-3 cervical segments of spinal cord):
receives pain & temperature sensations from face.
 Special visceral efferent:
4.
Motor nucleus (pons): supplies:
 Four Muscles of mastication (temporalis, masseter, medial & lateral
pterygoid).
 Other four muscles (Anterior belly of digastric, mylohyoid, tensor tympani
& tensor palati).
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 Emerge from middle of the ventral surface of the pons by 2 roots (large
lateral sensory root & small medial motor root).
 Divides into 3 divisions (dendrites of trigeminal ganglion):
1. Ophthalmic.
2. Maxillary.
3. Mandibular.
 Axons of cells of motor nucleus join only the mandibular division.
Paralysis of the first division (ophthalmic; V1) is usually seen in the superior
orbital fissure syndrome and results in sensory loss over the forehead along with
paralysis of CN III and CN IV.
Paralysis of the second division (maxillary; V2) results in loss of sensation over
the cheek and is due to lesions of the cavernous sinus; it also results in
additional paralysis of V1, CN III and CN IV. Isolated V2 lesions result from
fractures of the maxilla.
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Complete paralysis of CN V results in sensory loss over the ipsilateral face and
weakness of the muscles of mastication. Attempted opening of the mouth results
in deviation of the jaw to the paralyzed side.
Assessment of CN 5 Sensory Function:
The sensory limb has 3 major branches, each covering roughly 1/3 of the face. They are:
the Ophthlamic, Maxillary, and Mandibular. Assessment is performed as follows:
1. Use a sharp object (e.g. broken wooden handle of a cotton tipped applicator).
2. Ask the patient to close their eyes so that they receive no visual cues.
3. Touch the sharp tip of the stick to the right and left side of the forehead, assessing
the Ophthalmic branch medially and laterally same areas.
4. Touch the tip to the right and left side of the cheek area, assessing the Maxillary
branch.
5. Touch the tip to the right and left side of the jaw area, assessing the Mandibular
branch.
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Corneal reflex
The patient should be able to clearly identify when the sharp end touches their
face. Of course, make sure that you do not push too hard as the face is normally
quite sensitive. The Ophthalmic branch of CN 5 also receives sensory input from
the surface of the eye. To assess this component:
1. Pull out a wisp of cotton.
2. While the patient is looking straight ahead, come from behind and gently
brush the wisp against the cornea.
3. This should cause the patient to blink. Blinking also requires that CN 7
function normally, as it controls eye lid closure.
Muscles of Mastication
•
•
•
•
•
Masseter : close the jaw , protrude it slightly
Temporalis : close the jaw , retract it slightly
Medial pterygoids : close the jaw & protrude it
Lateral pterygoids : open the jaw & protrude it
Unilateral pterygoid weakness – jaw deviates towards the weak site.
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Assessment of CN 5 Motor Function: The motor limb of CN 5 innervates the
Temporalis and Masseter muscles, both important for closing the jaw.
Assessment is performed as follows:
1. Place your hand on both Temporalis ( lateral aspects of the forehead).
2. Ask the patient to tightly to clench his teeth, causing the muscles beneath
your fingers to become taught.
3. Then place your hands on both Masseter muscles, located just in from of
the Tempero-Mandibular joints .
4. Ask the patient to tightly close their jaw, which should again cause the
muscles beneath your fingers to become taught. Then ask them to move
their jaw from side to side, another function of the Massester
HERPES ZOSTER
OPTHALMIC HAEMANGIOMA
TRIGEMINAL GANGLION
 Occupies a depression in the middle cranial fossa.
 Importance: Contains cell bodies:
1. Whose dendrites carry sensations from the face.
2. Whose axons form the sensory root of trigeminal nerve
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Facial nerve - CN VII
• Type: Mixed ( Motor, special sensory, parasympathetic)
 Fibers:
1. Special visceral afferent: carrying taste sensation from anterior 2/3 of the
tongue.
2. Special visceral efferent: supplying muscles of fascial expression.
3. General visceral efferent: sends parasympathetic secretory fibers to
submandibular, sublingual, lacrimal, nasal & palatine glands.
The nucleus of the nerve lies ventral, lateral, and caudal to the CN VI nucleus; its
fibers elevate the floor of the fourth ventricle (facial colliculus) as they wind
around the CN VI nucleus. The nerve leaves the cranial cavity through the
stylomastoid foramen and innervates the muscles of facial expression and the
stapedius.
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 3 Nuclei in Pons :
1-Special visceral afferent: (nucleus solitarius) taste of the anterior 2/3 of tongue.
2-Special visceral efferent : (motor facial nucleus) : supplies: Muscles of face :
Buccinator, Posterior belly of digastric, Stylohyoid, Platysma, Stapedius, and
Occipitofrontalis.
3-General visceral efferent: (superior salivatory nucleus): sends preganglionic
parasympathetic secretory fibers to sublingual, submandibular, lacrimal, nasal &
palatine glands.
Although it is considered a pure motor nerve, it also innervates a small strip of
skin of the posteromedial aspect of the pinna and around the external auditory
canal. The nervus intermedius of Wrisberg((corda tympani)) conducts taste
sensation from the anterior two thirds of the tongue and supplies autonomic
fibers to the submaxillary and sphenopalatine ganglia, which innervate the
salivary and lacrimal glands.
COURSE OF FACIAL NERVE
 Emerges from the cerebellopontine angle by 2 roots:
1. Medial motor root: contains motor fibers.
2. Lateral root (Nervus intermedius): contains parasympathetic & taste fibers.
aaA212
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Has five intracranial segments:
1. Nucleus facialis and pontine segment.
2. Intracanalicular segment (Meatal)
3. Labyrinthine segment
4. Tympanic segment (horizontal)
5. Mastoid segment (vertical)
Then its emerges from the stylomasotid foramen and gives the extra-cranial
segment
-Passes through the internal auditory meatus to the inner ear where it runs in the
facial canal and gives abranch to stapedius muscle to control tympanic tone.
-Passes through the stylomastoid foramen & enters the parotid gland where it
ends.
Assessment is performed as follows:
1. First look at the patient's face. It should appear symmetric. That is:
a. There should be the same amount of wrinkles apparent on either
side of the forehead... barring asymmetric Bo-Tox injection!
b. The nasolabial folds (lines coming down from either side of the nose
towards the corners of the mouth) should be equal
c. The corners of the mouth should be at the same height
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A lower-motor-neuron lesion of the nerve, also known as peripheral facial paralysis, results in
complete ipsilateral facial paralysis; the face draws to the opposite side as the patient smiles.
Eye closure is impaired, and the ipsilateral palpebral fissure is wider.
2. Ask the patient to wrinkle their eyebrows and then close their eyes tightly.
CN 7 controls the muscles that close the eye lids (as opposed to CN 3,
which controls the muscles which open the lid). You should not be able to
open the patient's eyelids with the application of gentle upwards pressure.
3. Ask the patient to smile. The corners of the mouth should rise to the same
height and equal amounts of teeth should be visible on either side.
4. Ask the patient to puff out their cheeks. Both sides should puff equally
and air should not leak from the mouth.
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In summary , the facial N. start from pons , passes through cerebellopontine
angle , to facial canal where it gives stapedius muscle branch and then rotate
around the mastoid to give chorda tympani after emerging from stylomastoid
foramen to reach the parotid gland by dividing it into superficial and deep parts
to reach the face to divide into 5 branches.
The lesion here in its course is lowermotorneuron&involves half of face.
Where is the site of lesion in this long course?
loss of forehead wrinkle, inability to close eye, inability to raise corner of mouth
A. Exam the hearing on the same site of 7th palsy
1. Deafness
CPA lesion, pontine pathology.
2. Hyperacusis “hearing with loud frequencies” facial canal .
B. Exam the taste of anterior 2/3 of the tongue –mastoid bone.
C. Exam the external ear for vesicles.
D. Exam the mandible , parotid gland for swelling.
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In peripheral facial paralysis, different types of clinical presentations are
seen with nerve lesions at 4 levels, as described below.
Lesions of the meatal or canalicular segment
1.Facial paralysis with hearing loss .
2. loss of taste in the anterior two thirds of the tongue. This imply lesions in the
internal auditory canal from fracture of the temporal bone or at the
cerebellopontine angle from compression by a tumor.
Lesions of the labyrinthine or fallopian segment
Lesions that spare hearing (with hyperacusis) indicate lesions further down the
course of the nerve.
Loss of taste in the anterior two thirds of the tongue and loss of tearing imply
lesions that involve the chorda tympani and the secretomotor fibers to the
sphenopalatine ganglion in the labyrinthine segment, proximal to the greater
superficial petrosal nerve.
With lesions distal to the greater superficial petrosal nerve, lacrimation is normal
but hyperacusis is still present. Geniculate lesions in this segment cause pain in
the face.
Lesions of the horizontal or tympanic segment
The lesion is proximal to the departure of the nerve to the stapedius and results
in hyperacusis, loss of taste in the anterior two thirds of the tongue, and facial
motor weakness.
Lesions of the mastoid or vertical segment
loss of taste and facial paralysis occur. If the lesion is beyond the chorda
tympani in the vertical segment (as in lesions of the stylomastoid foramen), taste
is spared and only facial motor paralysis is seen.
UMN dysfunction: ( central)
This might occur with a central nervous system event, such as a stroke. In the
setting of RUMN CN 7 dysfunction, the patient would be able to wrinkle their
forehead on both sides of their face and closes his eyes as upper half has
bilateral supply from cerebrum, as the left CN 7 UMN cross innervates the R CN 7
LMN that controls this movement.
Involves the lower half of the face.
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Right central CN7 dysfunction:
Note preserved abiltiy to wrinkle forehead. Left corner of mouth, however,
is slightly lower than right. Left naso-labial fold is slightly less pronounced
compared with right.
Vestibulocochlear nerve - CN VIII
The vestibulocochlear nerve enters the brainstem at the pontomedullary junction
and contains the incoming fibers from the cochlea and the vestibular apparatus,
forming the eighth CN. It serves hearing and vestibular functions. Prior to
reaching the cochlea, the sound must first traverse the external canal and middle
ear. Hearing loss may be conductive or sensorineural.
Three tests help in evaluating the auditory component of the nerve.
Auditory acuity can be assessed very crudely on physical exam as follows:
1. Stand behind the patient and ask them to close their eyes.
2. Whisper a few words from just behind one ear. The patient should be able
to repeat these back accurately. Then do the same test for the other ear.
3. Alternatively, place your fingers approximately 5 cm from one ear and rub
them together. The patient should be able to hear the sound generated.
Repeat for the other ear.
Hearing is broken into 2 phases: conductive and sensorineural. The conductive
phase refers to the passage of sound from the outside to the level of CN 8. This
includes the transmission of sound through the external canal and middle ear.
Sensorineural refers to the transmission of sound via CN 8 to the brain.
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Weber Test:
1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony
edge of your palm, generating a continuous tone. Alternatively you can get
the fork to vibrate by "snapping" the ends between your thumb and index
finger.
2. Hold the stem against the patient's skull, along an imaginary line that is
equidistant from either ear.
3. The bones of the skull will carry the sound equally to both the right and
left CN 8. Both CN 8s, in turn, will transmit the impulse to the brain.
4. The patient should report whether the sound was heard equally in both
ears or better on one side than other (referred to as lateralizing to a side).
The vibrations are normally perceived equally in both ears because bone
conduction is equal. In conductive hearing loss, the sound is louder in the
abnormal ear than in the normal ear. In sensorineural hearing loss, lateralization
occurs to the normal ear.
Rinne Test:
1. Grasp the 512 Hz tuning fork by the stem and strike it against the bony edge
of your palm, generating a continuous tone.
2. Place the stem of the tuning fork on the mastoid bone.
3. The vibrations travel via the bones of the skull to CN 8, allowing the patient
to hear the sound.
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4. Ask the patient to inform you when they can no longer appreciate the
sound. When this occurs, move the tuning fork such that the tines are
placed right next to (but not touching) the opening of the ear. At this point,
the patient should be able to again hear the sound. This is because air is a
better conducting medium then bone.
In conductive hearing loss, the patient does not continue to hear the sound,
since bone conduction in that case is better than air conduction. In sensorineural
hearing loss, both air conduction and bone conduction are decreased to a similar
extent.
The vestibular portion of the nerve enters the brainstem along with the cochlear
portion. It transmits information about linear and angular accelerations of the
head from the utricle, saccule, and semicircular canals of the membranous
labyrinth to the vestibular nucleus. These signals reach the superior (Bechterew),
lateral (Deiters), medial (Schwalbe), and inferior (Roller) nuclei and project to the
pontine gaze center through the medial longitudinal fasciculus; to the cervical and
upper thoracic levels of the spinal cord through the medial vestibulospinal tract;
to the cervical, thoracic, and lumbosacral regions of the ipsilateral spinal cord
through the lateral vestibulospinal tract; and to the ipsilateral flocculonodular
lobe, uvula, and fastigial nucleus of the cerebellum through the
vestibulocerebellar tract.
The Romberg test is performed to evaluate vestibular control of balance and
movement. When standing with feet placed together and eyes closed, the patient
tends to fall toward the side of vestibular hypofunction. When asked to take steps
forward and backward, the patient progressively deviates to the side of the lesion.
Results of the Romberg test may also be positive in patients with
polyneuropathies, and diseases of the dorsal columns, but these individuals do not
fall consistently to 1 side as do patients with vestibular dysfunction.
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Glossopharyngeal nerve - CN IX
The nucleus of the nerve lies in the medulla and is anatomically indistinguishable
from the CN X and CN XI nuclei (nucleus ambiguous). Its main function is sensory
innervation of the posterior third of the tongue and the pharynx. It also innervates
the pharyngeal musculature, particularly the stylopharyngeus, in concert with the
vagus nerve.
Vascular stretch afferents from the aortic arch and carotid sinus, as well as
chemoreceptor signals from the latter, travel in the nerve of Herring to join the
glossopharyngeal nerve; they reach the nucleus solitarius, which in turn is
connected to the dorsal motor nucleus of the vagus and plays a part in the neural
control of blood pressure.
Lesions affecting the glossopharyngeal nerve result in loss of taste in the posterior
third of the tongue and loss of pain and touch sensations in the same area, soft
palate, and pharyngeal walls. CN IX and CN X travel together, and their clinical
testing is not entirely separable.
Interpretation:
If CN 9 on the right is not functioning (e.g. in the setting of a stroke), the uvula will be
pulled to the left. The opposite occurs in the setting of left CN 9 dysfunction
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Starting in the nucleus ambiguous, the vagus nerve has a long and tortuous
course providing motor supply to the pharyngeal muscles (except the
stylopharyngeus and the tensor veli palati), palatoglossus, and larynx. Somatic
sensation is carried from the back of the ear, the external auditory canal, and
parts of the tympanic membrane, pharynx, larynx, and the dura of the posterior
fossa. It innervates the smooth muscles of the tracheobronchial tree, esophagus,
and GI tract up to the junction between the middle and distal third of the
transverse colon.
The vagus provides secretomotor fibers to the glands in the same region and
inhibits the sphincters of the upper GI tract. Along with visceral sensation from
the same region, the nerve participates in vasomotor regulation of blood pressure
by carrying the fibers of the stretch receptors and chemoreceptors (ie, aortic
bodies) of the aorta and providing parasympathetic innervation to the heart .
Testing Elevation of the soft palate:
1. Ask the patient to open their mouth and say, "ahhhh," causing the soft
palate to rise upward.
2. Look at the uvula, a midline structure hanging down from the palate. If the
tongue obscures your view, take a tongue depressor and gently push it down
and out of the way.
3. The Uvula should rise up straight and in the midline.
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Testing the Gag Reflex:
1. Ask the patient to widely open their mouth. If you are unable to see the
posterior pharynx (i.e. the back of their throat), gently push down with a
tongue depressor.
2. In some patients, the tongue depressor alone will elicit a gag. In most
others, additional stimulation is required. Take a cotton tipped applicator
and gently brush it against the posterior pharynx or uvula. This should
generate a gag in most patients.
3. A small but measurable percent of the normal population has either a
minimal or non-existent gag reflex.
The gag reflex (ie, tongue retraction and elevation and constriction of the
pharyngeal musculature in response to touching the posterior wall of the pharynx,
tonsillar area, or base of the tongue) and the palatal reflex (ie, elevation of the
soft palate and ipsilateral deviation of the uvula on stimulation of the soft palate)
are decreased in paralysis of CN IX and CN X. In unilateral CN IX and CN X
paralysis, touching these areas results in deviation of the uvula to the normal side.
Unilateral paralysis of the recurrent laryngeal branch of CN X results in hoarseness
of voice. Bilateral paralysis results in stridor and requires immediate attention to
prevent aspiration and its attendant complications.
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Spinal accessory nerve - CN XI
From the nucleus ambiguous, the spinal accessory nerve joins the vagus nerve in
forming the recurrent laryngeal nerve to innervate the intrinsic muscles of the
larynx. The spinal portion of the nerve arises from the motor nuclei in the upper 5
or 6 cervical segments, enters the cranial cavity through the foramen magnum,
and exits through the jugular foramen .
CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius)
and turning the head laterally (Sternocleidomastoid).
1. Place your hands on top of either shoulder and ask the patient to shrug
while you provide resistance. Dysfunction will cause weakness/absence of
movement on the affected side.
2. Place your open left hand against the patient's right cheek and ask them to turn
into your hand while you provide resistance. Then repeat on the other side. The
right Sternocleidomasoid muscle (and thus right CN 11) causes the head to turn to
the left, and vice versa..
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Hypoglossal nerve - CN XII
The nucleus of this nerve lies in the lower medulla, and the nerve itself leaves the
cranial cavity through the hypoglossal canal (anterior condylar foramen). It
provides motor innervation for all the extrinsic and intrinsic muscles of the tongue
except the palatoglossus. To test the hypoglossal nerve, have the patient protrude
the tongue; when paralyzed on 1 side, the tongue deviates to the side of paralysis
on protrusion
Testing:
1. Ask the patient to stick their tongue straight out of their mouth.
2. If there is any suggestion of deviation to one side/weakness, direct them to
push the tip of their tongue into either cheek while you provide counter
pressure from the outside.
3. If the right CN 12 is dysfunctional, the tongue will deviate to the right. This
is because the normally functioning left half will dominate as it no longer
has opposition from the right. Similarly, the tongue would have limited or
absent ability to resist against pressure applied from outside the left cheek.
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Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and
XII, which occurs due to a lower motor neuron lesion either at nuclear or
fascicular level in the medulla oblongata or from lesions of the lower cranial
nerves outside the brainstem.
In contrast, pseudobulbar palsy describes impairment of function of cranial
nerves IX-XII due to upper motor neuron lesions of the corticobulbar tracts in the
mid-pons. For clinically evident dysfunction to occur, such lesions must be
bilateral as these cranial nerve nuclei receive bilateral innervation.
Symptoms
These include:








dysphagia (difficulty in swallowing)
Dysphonia (defective use of the voice)
Dysarthria (difficulty in articulating words due a CNS problem)
Dysphasia (difficulty in using or understanding words due to injury or
disease of the brain)
Difficulty in chewing
Nasal regurgitation
Slurring of speech
Shoking on liquids
Signs







Nasal speech lacking in modulation and difficulty with all consonants
Tongue is atrophic and shows fasciculations.
Dribbling of saliva.
Weakness of the soft palate, examined by asking the patient to say aah.
The jaw jerk is normal or absent.
The gag reflex is absent.
In addition, there may be lower motor neuron lesions of the limbs.
CAUSES







Genetic: acute intermittent porphyria
Vascular causes: medullary infarction
Degenerative diseases: motor neuron disease , syringobulbia
Inflammatory/infective: Guillain-Barré syndrome, poliomyelitis, Lyme
disease
Malignancy: brain-stem glioma
Toxic: botulism
Autoimmune: myasthenia gravis
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Pseudobulbar palsy results from an upper motor neuron lesion to the
corticobulbar pathways in the pyramidal tract. It is a result of bilateral
degeneration of the corticobulbar pathways. (Upper Motor Neuron tract to
cranial nerve motor nuclei).
Symptoms
These include:





Dysphagia (difficulty in swallowing)
Labile affect(inappropriate emotional outbursts).
Difficulty chewing
Dysarthria
Demonstrate slurred speech (often initial presentation).
signs
These include:





Speech is slow, thick and indistinct
Gag reflex is normal, exaggerated or absent
Tongue is small, stiff and spastic
Jaw jerk is brisk
There may be upper motor neuron lesion of the limbs
Causes
Pseudobulbar Palsy is caused by brain diseases that affect the motor fibers
traveling from the cerebral cortex to the lower Brain Stem . Mechanisms that can
explain Pseudobulbar Palsy are disinhibition of the motor neurons controlling
laughter and crying and that a reciprocal pathway exists between the cerebellum
and the brainstem that adjusts laughter and crying responses, making them
appropriate to context .
1.
2.
3.
4.
5.
6.
7.
Inflammatory
multiple sclerosis , behcets diseae
Vascular causes: Bilateral hemisphere infarction
Malignancy: High brain stem tumors
Metabolic causes: osmotic demyelination syndrome
Multiple System Atrophy (related to Parkinson's disease)
Degenerative disorders: motor neuron disease
Progressive Supranuclear Palsy
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Horner’s syndrome
“Disruption to the sympathetic supply to the head and neck”
• associated classically
with a ‘Pancoast’ tumour of
apex lung
also many other causes …. so
be able to trace the course of
the sympathetic fibres .
clinical features - Horner’s
on side of lesion:
• partial drooping upper eyelid
• constricted pupil
• ‘blood-shot’ eye
• warm, red skin
• dry face
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