3Cranial Nerves

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Neurologic examinationCRANIAL NERVES



Cranial Nerve (CN) Examination

1st CN Olfactory2nd CN Optic nerve

3rd, 4th, 6th CN Occulomotor, Trochlear

and Abducens

5th CN Trigeminal7th CN Facial

8th CN Vestibulolocochlear

9th CN Glossopharygeal

10th CN Vagus

11th CN Spinal accessory

12th CN Hypoglossal



The olfactory nerve is a special afferent cranial nerve composedof sensory fibers only.

Its sole function is to discern smells.

Olfaction depends on the integrity of the olfactory neurons in the

roof of the nasal cavity and their connections through the

olfactory bulb, tract, and stria to the olfactory cortex of themedial frontal and temporal lobes.

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 (OLFACTORY NERVE)



Cranial Nerve I



The optic nerve contains special sensory afferent fibers

that convey visual information from the retina to the

occipital lobe via the visual pathway.

Evaluation gives important information about the

nerves, optic chiasm, tracts, thalamus, optic radiations,and visual cortex.

CN 2 is also the afferent limb of the pupillary light reflex.

The optic nerve is tested in the office by visual acuity

measurement, color vision testing, pupil evaluation, visual field

testing, and optic nerve evaluation via ophthalmoscopy and/or stereo biomicroscopy.

Cranial Nerves Exam

CRANIAL NERVE 2 (OPTIC NERVE)



II - Optic

yExamine the Optic Fundi



Test Visual Acuity

1. Allow the patient to use their glasses if available. You are

interested in the patient's best corrected vision.

2. Position the patient 20 feet in front of the Snellen eye

chart (or hold a Rosenbaum pocket card at a 14 inch"reading" distance).

3. Have the patient cover one eye at a time with a card.

4. Ask the patient to read progressively smaller letters until

they can go no further.

5. Record the smallest line the patient read successfully

(20/20, 20/30, etc.) Repeat with the other eye.





There are hand held cards that look like Snellen Charts but are positioned

14 inches from the patient. These are used simply for convenience. Testing

and interpretation are as described for the Snellen.

Hand held visual acuity card



Screen Visual Fields by Confrontation

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 oppositeeye with a card.





Test Pupillary Reactions to Light

1. Dim the room lights as necessary.

2. Ask the patient to look into the distance.

3. Shine a bright light obliquely into each pupil in turn.

4. Look for both the direct (same eye) and consensual

(other eye) reactions.

5. Record pupil size in mm and any asymmetry or

irregularity.

o If abnormal, proceed with the test for accommodation.



y Test Pupillary Reactions to

Accommodation

1

. Hold your finger about1

0cm from the patient's nose.2.

y Ask them to alternate looking into the distance and at

your finger.

o Observe the pupillary response in each eye.



The pneumonic:

³S 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

CRANIAL NERVE 3 (OCULOMOTOR NERVE)

CRANIAL NERVE 4 (TROCHLEAR NERVE)

CRANIAL NERVE 3 (ABDUCENS NERVE)



Observe for PtosisyTest 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 across 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.

yTest Pupillary Reactions to Light





Testing CN III, IV, and VI:

To test the extraocular muscles, have the patientfollow 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) ismore 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 ³down 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 parasympatheticpreganglionic 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)



F ourth (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 thepresence 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)



S ixth (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 corneallight 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.

( FR OM ADAM S NEU R O)



This nerve has both motor and sensory components.

The sensory limb has 3 major branches, each

covering roughly 1/3 of the face.1. Ophthalmic

2. Maxillary

3. Mandibular

CRANIAL NERVE 5 (TRIGEMINAL)



Assessment of CN 5 Sensory Function: Use a sharp implement (e.g. broken wooden handle of

a cotton tipped applicator).

Ask the patient to close their eyes so that they receiveno visual cues.

Touch the sharp tip of the stick to the right and left sideof the forehead, assessing the Ophthalmic branch.

Touch the tip to the right and left side of the cheekarea, assessing the Maxillary branch.

Touch the tip to the right and left side of the jaw area,

assessing the Mandibular branch. The patient should be able to clearly identify when thesharp end touches their face. Of course, make surethat you do not push too hard as the face is normallyquite sensitive.




To assess this component:

1. Pull out a wisp of cotton.

2. While the patient is lookingstraight ahead, gently brushthe wisp against the lateralaspect of the sclera (outer white area of the eye ball).

3. This should cause the patient toblink.

Blinking also requires that CN 7 function normally, as it controls eye lid closure.


The Ophthalmic branch of CN 5 also receives sensory inputfrom the surface of the eye.



Assessment of CN 5 Motor Function:

Place your hand on both Temporalis muscles, locatedon the lateral aspects of the forehead.

Ask the patient to tightly close their jaw, causing themuscles beneath your fingers to become taught.

Then place your hands on both Masseter muscles,located just in front of the Temporo-Mandibular joints(point where lower jaw articulates with skull).

Ask the patient to tightly close their jaw, which shouldagain cause the muscles beneath your fingers tobecome taught. Then ask them to move their jaw fromside to side, another function of the Masseter.


The motor limb of CN 5 innervates the Temporalis and

Masseter muscles, both important for closing the jaw.






This nerve innervates many of the muscles of facial expression.

Assessment is performed as follows: First look at the patient¶s face. It should appear symmetric.

± There should be the same amount of wrinkles apparent oneither side of the forehead

± The nasolabial folds should be equal

± The corners of the mouth should be at the same height

If there is any question as to whether an apparent asymmetry if new or old, ask the patient for a picture for comparison.

Ask the patient to wrinkle their eyebrows and then close their eyestightly. You should not be able to open the patient¶s eyelids withthe application of gentle upwards pressure. CN 7 controls themuscles that close the eye lids (as opposed to CN 3, which

controls the muscles which open the lid). Ask the patient to smile. The corners of the mouth should rise to

the same height and equal amounts of teeth should be visible oneither side.

Ask the patient to puff out their cheeks. Both sides should puff equally and air should not leak from the mouth.

CRANIAL NERVE 7 (FACIAL)



Testing the facial nerve.

The patient wrinkles her forehead while

the two sides are compared. Patient

tightly shuts eyelids while examiner attempts to pry open. The two sides are

compared. Patient smiles and shows

her teeth while the examiner compares

the nasolabial folds on either side.



I nterpretation:

CN 7 has a precise pattern of innervation, whichhas 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 tomove up and down.

However, the LMNs that control the muscles of the

lower face are only innervated by the UMN fromthe opposite side of the face.







I nterpretation:

Thus, in the setting of CN 7 dysfunction, the pattern of weakness or paralysis observed will differ dependingon whether the UMN or LMN is affected.

UMN dysfunction: This might occur with a central nervoussystem event, such as a stroke. In the setting of RUMN CN 7 dysfunction, the patient would be able towrinkle their forehead on both sides of their face, asthe left CN 7 UMN cross innervates the R CN 7 LMN

that controls this movement. However, the patientwould 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.



I nterpretation: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.













CN 7 is also responsible for carrying taste

sensations from the anterior 2/3 of the tongue.

To test the sensory fibers of the facial nerve,

apply sugar, salt, or lemon juice on a cottonswab to the lateral aspect of each side of the

tongue and have the patient identify the taste.

Taste is often tested only when specific

pathology of the facial nerve is suspected.




CN 8 carries sound impulses from the cochlea to the brain.Prior to reaching the cochlea, the sound must firsttraverse the external canal and middle ear.

Assessment is performed as follows:

Stand behind the patient and ask them to close their eyes.

Whisper a few words from just behind one ear. Thepatient should be able to repeat these back accurately.Then perform the same test for the other ear.

Alternatively, place your fingers approximately 5 cmfrom one ear and rub them together. The patientshould be able to hear the sound generated. Repeatfor the other ear.

CRANIAL NERVE 8 (ACOUSTIC)



These tests are rather crude. Precise quantification,generally necessary whenever there is a subjectivedecline in acuity, requires special equipment andtraining.

The cause of subjective hearing loss can be assessedwith bedside testing. Hearing is broken into 2 phases:conductive and sensorineural. The conductive phaserefers to the passage of sound from the outside to thelevel of CN 8. This includes the transmission of soundthrough the external canal and middle ear. Sensorineural

refers to the transmission of sound via CN 8 to the brain.Identification of conductive (a much more commonproblem in the general population) defects is determinedas follows:




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 imaginaryline 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).




Weber Test




1. Grasp the 512 Hz tuning fork by the stem and strike it against thebony edge of your palm, generating a continuous tone.

2. Place the stem of the tuning fork on the mastoid bone, the bonyprominence located immediately behind the lower part of the ear.

The vibrations travel via the bones of the skull to CN 8, allowingthe patient to hear the sound.

3. Ask the patient to inform you when they can no longer appreciatethe sound. When this occurs, move the tuning fork such that thetines are placed right next to (but not touching) the opening of theear. At this point, the patient should be able to again hear thesound. This is because air is a better conducting medium thenbone.


Rinne Test:




Rinne Test:



Rinne Test:




I nterpretation:

The above testing is reserved for those instances when a patientcomplains of a deficit in hearing. Thus, on the basis of history, thereshould be a complaint of hearing decline in one or both ears.

In the setting of a conductive hearing loss (e.g. wax in the externalcanal), the Webber test will lateralize (i.e. sound will be heard better) inthe ear that has the subjective decline in hearing. This is because whenthere is a problem with conduction, competing sounds from the outside

cannot reach CN 8 via the external canal. Thus, sound generated by thevibrating tuning fork and traveling to CN 8 by means of bony conductionis better heard as it has no outside ³competition.´ You can transientlycreate a conductive hearing loss by putting the tip of your index finger inthe 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), theWebber test will lateralize to the ear which does not have the subjective

decline in hearing. This is because CN 8 is the final pathway throughwhich sound is carried to the brain. Thus, even though the bones of theskull will successfully transmit the sound to CN 8, it cannot then becarried to the brain due to the underlying nerve dysfunction.




I nterpretation:

In the setting of conductive hearing loss, bone conduction (BC)will be better then air conduction (AC) when assessed by theRinne Test. If there is a blockage in the passageway (e.g. wax)that carries sound from the outside to CN 8, then sound will bebetter heard when it travels via the bones of the skull. Thus, thepatient 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 beretained). This is because the problem is at the level of CN 8.Thus, regardless of the means (bone or air) by which the impulsegets to CN 8, there will still be a marked hearing decrement in theaffected ear. As AC is normally better then BC, this will still be the

case.




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 theaffected ear. If there is a sensorineural deficit, theWebber will lateralize to the normal ear.

Perform the Rinne test. If there is a conductive hearingdeficit, BC will be greater then or equal to AC in theaffected ear. If there is a sensorineural hearing deficit,

AC will be greater then BC in the affected ear.




These nerves are responsible for raising the soft palate of the mouth and the gag reflex, a protective mechanismwhich prevents food or liquid from traveling into thelungs. As both CNs contribute to these functions, theyare tested together.

Testing Elevation of the soft palate:

Ask the patient to open their mouth and say, ³ahhhh,´causing the soft palate to rise upward.

Look at the uvula, a midline structure hanging down

from the palate. If the tongue obscures your view, takea tongue depressor and gently push it down and out of the way.

The Uvula should rise up straight and in the midline.

CRANIAL NERVE 9 (GLOSSOPHARYNGEAL)

CRANIAL NERVE 10 (VAGUS)



Normal Oropharynx





I nterpretation:

If CN 9 on the right is not functioning, the uvula will be pulled to the left.





Left peritonsillar abscess: infection within left tonsil has

pushed uvula towards the right.





Testing the Gag Reflex:

Ask the patient to widely open their mouth. If you areunable to see the posterior pharynx (i.e. the back of their throat), gently push down with a tonguedepressor.

In some patients, the tongue depressor alone will elicita gag. In most others, additional stimulation isrequired. Take a cotton tipped applicator and gentlybrush it against the posterior pharynx or uvula. Thisshould generate a gag in most patients.

A small but measurable percent of the normalpopulation has either a minimal or non-existent gagreflex. Presumably, they make use of other mechanisms to prevent aspiration.





Gag testing is rather noxious. Some people are particularly sensitive to evenminimal stimulation. Perform this test when there is reasonable suspicionthat pathology exists.

This would include two major clinical situations:

If you suspect that the patient has suffered acute dysfunction, most

commonly in the setting of a stroke. These patients may complain of cough when they swallow. Or, they may suffer from recurrentpneumonia. Both of these events are signs of aspiration of food contentsinto the passageways of the lungs. These patients may also have other cranial nerve abnormalities as lesions affecting CN 9 and 10 often affectCNs 11 and 12, which are anatomically nearby.

Patient¶s suffering from sudden decreased level of consciousness. In this

setting, the absence of a gag might indicate that the patient is no longer able to reflexively protect their airway from aspiration. Strongconsideration should be given to intubating the patient, providing themwith a secure mechanical airway until their general condition improves.





CN 9 is also responsible for taste originating on the

posterior 1/3 of the tongue.

CN 10 also provides parasympathetic innervation to theheart, though this cannot be easily tested on physical

examination.





CN 11 innervates the muscles which permit shrugging of the shoulders (Trapezius) and turning the headlaterally (Sternocleidomastoid).

Assessment is performed as follows:

Place your hands on top of either shoulder and ask thepatient to shrug while you provide resistance.Dysfunction will cause weakness/absence of movement on the affected side.

Place your open left hand against the patient¶s right

cheek and ask them to turn into your hand while youprovide resistance. Then repeat on the other side. Theright Sternocleidomastoid muscle causes the head toturn to the left, and vice versa.

CRANIAL NERVE 11 (SPINAL ACCESSORY)









CN 12 is responsible for tongue movement.

Each CN 12 innervates one-half of the tongue.

Assessment is performed as follows: Ask the patient to stick their tongue straight out of their

mouth.

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.

CRANIAL NERVE 12 (HYPOGLOSSAL)






I nterpretation:

If the right CN 12 is dysfunctional, the tongue will deviateto the right. This is because the normally functioning lefthalf will dominate as it no longer has opposition from the

right. Similarly, the tongue would have limited or absentability to resist against pressure applied from outside theleft cheek.




Left CN 12 Dysfunction: Stroke has resulted in L CN 12 Palsy.

Tongue therefore deviates to the left.




Testing the hypoglossal nerve.

Patient is instructed to stick out the tongue and then

move it laterally against resistance.



Cranial Nerve Number Innervation(s) Primary Function(s) Test(s)

Olfactory I Sensory Smell Identify odors

Optic II Sensory Vision

Visual acuity,

fields, color,

nerve head

Oculomotor III Motor

Upper lid elevation,

extraocular eye

movement, pupil

constriction,

accommodation

Physiologic "H"

and near point

response

Trochlear IV Motor Superior oblique

musclePhysiologic "H"

Trigeminal V Motor Muscles of mastication Corneal reflex

Trigeminal V SensoryScalp, conjunctiva,

teeth

Clench jaw/palpate,

light touch

comparison

Abducens VI Motor Lateral rectus muscle Abduction,

physiologic "H"



Facial VII Motor Muscles of facial expression

Smile, puff

cheeks, wrinkle

forehead, pry

open closed lids

Facial VII SensoryTaste-anterior two thirds of

tongue

Vestibulocochlear VIII Sensory Hearing and balance

Rinne test for

hearing, Weber

test for balance

Glossopharyngeal IX Motor Tongue and pharynx Gag reflex

Glossopharyngeal IX SensoryTaste-posterior one third of

tongue

Vagus X Motor Pharynx, tongue, larynx,

thoracic and abdominal visceraGag reflex

Vagus X Sensory Larynx, trachea, esophagus

Accessory XI Motor Sternomastoid and trapezius

muscles

Shrug, head turn

against

resistance

Hypoglossal XII Motor Muscles of tongue Tongue deviation



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