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Neurologic Examination: Cranial Nerves
Neurologic Examination: Cranial Nerves
CRANIAL NERVES
Cranial Nerve (CN) Examination
1st CN Olfactory
2nd CN Optic nerve
3rd, 4th, 6th CN Occulomotor, Trochlear
and Abducens
5th CN Trigeminal
7th CN Facial
8th CN Vestibulolocochlear
9th CN Glossopharygeal
10th CN Vagus
11th CN Spinal accessory
12th CN Hypoglossal
Cranial Nerves Exam
To test olfaction:
1. An odorant, such as concentrated vanilla, perfume or
coffee, is presented to each nostril in turn.
2. The patient is asked to sniff (with eyes closed) and
identify each smell.
Olfaction is frequently not tested because of unreliable
patient responses and lack of objective signs.
Cranial Nerve I
Cranial Nerves Exam
1. Stand two feet in front of the patient and have them look
into your eyes.
2. Hold your hands about one foot away from the patient's
ears, and wiggle a finger on one hand.
3. Ask the patient to indicate which side they see the finger
move.
4. Repeat two or three times to test both temporal fields.
5. If an abnormality is suspected, test the four quadrants of
each eye while asking the patient to cover the opposite
eye with a card.
Test Pupillary Reactions to Light
The pneumonic:
“S O 4 – L R 6 – All The Rest 3”
may help remind you which CN does what
Superior Oblique CN 4 –
Lateral Rectus CN 6 –
All The Rest of the muscles innervated by CN 3
Observe for Ptosis
Test Extraocular Movements
1.Stand or sit 3 to 6 feet in front of the patient.
2.Ask the patient to follow your finger with their eyes
without moving their head.
3.Check gaze in the six cardinal directions using a
cross or "H" pattern.
4.Pause during upward and lateral gaze to check for
nystagmus.
5.Check convergence by moving your finger toward
the bridge of the patient's nose.
Test Pupillary Reactions to Light
Testing CN III, IV, and VI:
To test the extraocular muscles, have the patient follow a
target through the six principal positions of gaze ("H"
pattern).
Right CN3 Lesion: Note patient's right eye is deviated
laterally and there is ptosis of the lid.
Right CN3 Lesion: The right pupil (upper left picture) is
more dilated than the left pupil.
It’s also worth noting that disorders of the extra ocular muscles
themselves (and not the CN which innervate them) can also lead to
impaired eye movement.
An example is a patient who has suffered a traumatic left orbital injury. The
inferior rectus muscle has become entrapped within the resulting fracture,
preventing the left eye from being able to look downward.
Clinical Effectsof Lesionsof the Third,
Fourth, and Sixth Ocular Nerves
Third (Oculomotor) Nerve A complete third nerve lesion causes
ptosis, or drooping of the upper eyelid (since the levator palpebrae
is supplied mainly by the third nerve), and an inability to rotate the
eye upward, downward, or inward. This corresponds to a combined
weakness of the medial, superior, and inferior recti and the inferior
oblique muscles. The remaining actions of the fourth and sixth
nerves give rise to the mnemonic “down and out” to describe the
position of the eye in third nerve palsy (Fig. 14-5B). When the lid
is passively elevated, the eye is found to be deviated outward and
slightly downward because of the unopposed actions of the intact
lateral rectus and superior oblique muscles. In addition, one finds
a dilated nonreactive pupil (iridoplegia) and paralysis of accommodation
(cycloplegia) due to interruption of the parasympathetic
fibers in the third nerve. However, the extrinsic and intrinsic eye
muscles may be affected separately. For example, infarction of the
central portion of the oculomotor nerve, as occurs in diabetic
ophthalmoplegia, typically spares the pupil, since the parasympathetic
preganglionic pupilloconstrictor fibers lie near the surface.
Conversely, compressive lesions of the nerve usually dilate the
pupil as an early manifestation. After injury, regeneration of the
third nerve fibers may be aberrant, in which case some of the fibers
that originally moved the eye in a particular direction now reach
another muscle or the iris; in the latter instance the pupil, which is
unreactive to light, may constrict when the eye is turned up and in.
(ADAMS NEURO)
Fourth (Trochlear) Nerve A lesion of the fourth nerve, which
innervates the superior oblique muscle, is the most common cause
of isolated symptomatic vertical diplopia. Although oculomotor
palsy was a more common cause of vertical diplopia in Keane’s
series, as stated earlier, in instances where this is the sole complaint,
trochlear palsy (and brainstem lesions) predominate. Paralysis
of the superior oblique muscle results in weakness of
downward movement of the affected eye, most marked when the
eye is turned inward, so that the patient complains of special
difficulty in reading or going down stairs. The affected eye tends
to deviate slightly upward. This defect may be overlooked in the
presence of a third nerve palsy if the examiner fails to note the
absence of an expected intorsion as the patient tries to move the
paretic eye downward. Head tilting to the opposite shoulder (Bielschowsky
sign) is especially characteristic of fourth nerve lesions;
this maneuver causes a compensatory intorsion of the unaffected
eye and ameliorates the double vision. Bilateral trochlear palsies,
as may occur rarely after head trauma, give a characteristic alternating
hyperdeviation depending on the direction of gaze (unilateral
traumatic trochlear paresis is more common). A detailed
review of the clinical approach to vertical diplopia is given by
Palla and Straumann.
(ADAMS NEURO)
Sixth (Abducens) Nerve Lesions of the sixth nerve result in a paralysis
of the abducens muscle and a resultant weakness of lateral or
outward movement as well as a crossing of the visual axes. The
affected eye deviates medially, i.e., in the direction of the opposing
muscle. With incomplete sixth nerve palsies, turning the head toward
the side of the paretic muscle overcomes the diplopia. The main
causes of individual oculomotor palsies and of combined palsies are
listed in Table 14-3 and are illustrated in Fig. 14-6 and below.
The Analysis of Diplopia Almost all instances of diplopia (i.e.,
seeing a single object as double) are the result of an acquired paralysis
or paresis of one or more extraocular muscles. The signs of
the oculomotor palsies, as described above, are manifest in various
degrees of completeness. Noting the relative positions of the corneal
light reflections and having the patient perform common versional
movements will usually disclose the faulty muscle(s) as the
eyes are turned into the field of action of the paretic muscle.
(FROM ADAMS NEURO)
CRANIAL NERVE 5 (TRIGEMINAL)
Interpretation:
CN 7 has a precise pattern of innervation, which
has important clinical implications.
The right and left upper motor neurons (UMNs)
each innervate both the right and left lower
motor neurons (LMNs) that allow the forehead to
move up and down.
However, the LMNs that control the muscles of the
lower face are only innervated by the UMN from
the opposite side of the face.
CRANIAL NERVE 7 (FACIAL)
CRANIAL NERVE 7 (FACIAL)
Interpretation:
Thus, in the setting of CN 7 dysfunction, the pattern of
weakness or paralysis observed will differ depending
on whether the UMN or LMN is affected.
UMN dysfunction: This might occur with a central nervous
system event, such as a stroke. In the setting of R
UMN CN 7 dysfunction, the patient would be able to
wrinkle their forehead on both sides of their face, as
the left CN 7 UMN cross innervates the R CN 7 LMN
that controls this movement. However, the patient
would be unable to effectively close their left eye or
raise the left corner of their mouth.
Right central CN7 dysfunction:
Note preserved ability to wrinkle forehead.
Left corner of mouth, however, is slightly lower than right.
Left nasolabial fold is slightly less pronounced compared with right.
Right central CN7 dysfunction:
Note preserved ability to wrinkle forehead.
Left corner of mouth, however, is slightly lower than right.
Left nasolabial fold is slightly less pronounced compared with right.
CRANIAL NERVE 7 (FACIAL)
Interpretation:
LMN dysfunction: This occurs most commonly in the setting
of Bell’s Palsy, an idiopathic, acute CN 7 peripheral
nerve palsy. In the setting of R CN 7 peripheral (LMN)
dysfunction, the patient would not be able to wrinkle
their forehead, close their eye or raise the corner of
their mouth on the right side. Left sided function would
be normal.
Left peripheral CN7 dysfunction:
Note loss of forehead wrinkle, ability to close eye, ability to raise corner of
mouth, and decreased nasolabial fold prominence on left.
Left peripheral CN7 dysfunction:
Note loss of forehead wrinkle, ability to close eye, ability to raise corner of
mouth, and decreased nasolabial fold prominence on left.
Left peripheral CN7 dysfunction:
Note loss of forehead wrinkle, ability to close eye, ability to raise corner of
mouth, and decreased nasolabial fold prominence on left.
CRANIAL NERVE 7 (FACIAL)
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 then the other (referred to as
lateralizing to a side).
CRANIAL NERVE 8 (ACOUSTIC)
Weber Test
CRANIAL NERVE 8 (ACOUSTIC)
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, the bony
prominence located immediately behind the lower part of the ear.
The vibrations travel via the bones of the skull to CN 8, allowing
the patient to hear the sound.
3. 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.
CRANIAL NERVE 8 (ACOUSTIC)
Rinne Test:
CRANIAL NERVE 8 (ACOUSTIC)
Rinne Test:
CRANIAL NERVE 8 (ACOUSTIC)
Interpretation:
• The above testing is reserved for those instances when a patient
complains of a deficit in hearing. Thus, on the basis of history, there
should be a complaint of hearing decline in one or both ears.
• In the setting of a conductive hearing loss (e.g. wax in the external canal),
the Webber test will lateralize (i.e. sound will be heard better) in the ear
that has the subjective decline in hearing. This is because when there is
a problem with conduction, competing sounds from the outside cannot
reach CN 8 via the external canal. Thus, sound generated by the
vibrating tuning fork and traveling to CN 8 by means of bony conduction
is better heard as it has no outside “competition.” You can transiently
create a conductive hearing loss by putting the tip of your index finger in
the external canal of one ear. If you do this while performing the Webber
test, the sound will be heard on that side.
• In the setting of a sensorineural hearing loss (e.g. a tumor of CN 8), the
Webber test will lateralize to the ear which does not have the subjective
decline in hearing. This is because CN 8 is the final pathway through
which sound is carried to the brain. Thus, even though the bones of the
skull will successfully transmit the sound to CN 8, it cannot then be
carried to the brain due to the underlying nerve dysfunction.
CRANIAL NERVE 8 (ACOUSTIC)
Interpretation:
• In the setting of conductive hearing loss, bone conduction (BC)
will be better then air conduction (AC) when assessed by the
Rinne Test. If there is a blockage in the passageway (e.g. wax)
that carries sound from the outside to CN 8, then sound will be
better heard when it travels via the bones of the skull. Thus, the
patient will note BC to be better then or equal to AC in the ear
with the subjective decline in hearing.
• In the setting of a sensorineural hearing loss, air conduction will
still be better then bone conduction (i.e. the normal pattern will be
retained). This is because the problem is at the level of CN 8.
Thus, regardless of the means (bone or air) by which the impulse
gets to CN 8, there will still be a marked hearing decrement in the
affected ear. As AC is normally better then BC, this will still be the
case.
CRANIAL NERVE 8 (ACOUSTIC)
Summary:
• Identifying conductive vs sensorineural hearing deficits
requires historical information as well as the results of
Webber and Rinne testing.
• First determine by history and crude acuity testing
which ear has the hearing problem.
• Perform the Webber test. If there is a conductive
hearing deficit, the Webber will lateralize to the
affected ear. If there is a sensorineural deficit, the
Webber will lateralize to the normal ear.
• Perform the Rinne test. If there is a conductive hearing
deficit, BC will be greater then or equal to AC in the
affected ear. If there is a sensorineural hearing deficit,
AC will be greater then BC in the affected ear.
CRANIAL NERVE 9 (GLOSSOPHARYNGEAL)
CRANIAL NERVE 10 (VAGUS)
Normal Oropharynx
CRANIAL NERVE 9 (GLOSSOPHARYNGEAL)
CRANIAL NERVE 10 (VAGUS)
Interpretation:
If CN 9 on the right is not functioning, the uvula will be pulled to the left.
CRANIAL NERVE 9 (GLOSSOPHARYNGEAL)
CRANIAL NERVE 10 (VAGUS)
Gag testing is rather noxious. Some people are particularly sensitive to even
minimal stimulation. Perform this test when there is reasonable suspicion
that pathology exists.
Interpretation:
• 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.
CRANIAL NERVE 12 (HYPOGLOSSAL)
Clench
Trigeminal V Sensory Scalp, conjunctiva, teeth jaw/palpate, light
touch comparison
Abduction,
Abducens VI Motor Lateral rectus muscle
physiologic "H"
Smile, puff
cheeks, wrinkle
Facial VII Motor Muscles of facial expression
forehead, pry open
closed lids