Cranial Nerves
- I - Smell
- II - Visual acuity, visual fields and ocular fundi
- II,III - Pupillary reactions
- III,IV,VI - Extra-ocular movements, including opening of the eyes
- V - Facial sensation, movements of the jaw, and corneal reflexes
- VII - Facial movements and gustation
- VIII - Hearing and balance
- IX,X - Swallowing, elevation of the palate, gag reflex and gustation
- V,VII,X,XII - Voice and speech
- XI - Shrugging the shoulders and turning the head
- XII - Movement and protrusion of tongue
Cranial Nerve I
Evaluate
the patency of the nasal passages bilaterally by asking the patient to
breath in through their nose while the examiner occludes one nostril at a
time. Once patency is established, ask the patient to close their
eyes. Occlude one nostril, and place a small bar of soap near the
patent nostril and ask the patient to smell the object and report what
it is. Making certain the patient's eyes remain closed. Switch
nostrils and repeat. Furthermore, ask the patient to compare the
strength of the smell in each nostril.Very little localizing information can be obtained from testing the sense of smell. This part of the exam is often omitted, unless their is a reported history suggesting head trauma or toxic inhalation.
Cranial Nerve II
First
test visual acuity by using a pocket visual acuity chart. Perform this
part of the examination in a well lit room and make certain that if the
patient wears glasses, they are wearing them during the exam. Hold the
chart 14 inches from the patient's face, and ask the patient to cover
one of their eyes completely with their hand and read the lowest line on
the chart possible. Have them repeat the test covering the opposite
eye. If the patient has difficulty reading a selected line, ask them to
read the one above. Note the visual acuity for each eye.
Next
evaluate the visual fields via confrontation. Face the patient one
foot away, at eye level. Tell the patient to cover their right eye with
their right hand and look the examiner in the eyes. Instruct the
patient to remain looking you in the eyes and say "now" when the
examiner's fingers enter from out of sight, into their peripheral
vision. Once this is understood, cover your left eye with your left
hand (the opposite eye of the patient) and extend your arm and first 2
fingers out to the side as far as possible. Beginning with your hand
and arm fully extended, slowly bring your outstretched fingers
centrally, and notice when your fingers enter your field of vision. The
patient should say now at the same time you see your own fingers.
Repeat this maneuver a total of eight times per eye, once for every 45
degrees out of the 360 degrees of peripheral vision. Repeat the same
maneuver with the other eye.
Using
an ophthalmoscope, observe the optic disc, physiological cup, retinal
vessels and fovea. Note the pulsations of the optic vessels, check for a
blurring of the optic disc margin and a change in the optic disc's
color form its normal yellowish orangeThe initial change in the ophthalmoscopic examination in a patient with increased intracranial pressure is the loss of pulsations of the retinal vessels. This is followed by blurring of the optic disc margin and possibly retinal hemorrhages.
Cranial Nerves II and III
Ask
the patient to focus on an object in the distance. Observe the diameter
of the pupils in a dimly lit room. Note the symmetry between the
pupils. Next, shine the penlight or opthalmoscope light into one eye at
a time and check both the direct and consensual light responses in each
pupil. Note the rate of these reflexes. If they are sluggish or
absent, test for pupillary constriction via accommodation by asking the
patient to focus on the light pen itself while the examiner moves it
closer and closer to their nose. Normally, as the eyes accommodate to
the near object the pupils will constrict. The test for accomodation
should also be completed in a dimly lit room. End the evaluation of
cranial nerves II and III by observing the pupils in a well lit room and
note their size and possible asymmetry.Anisocoria is a neurological term indicating that one pupil is larger than another. Yet which pupil is abnormal? For example, if the right pupil is of a greater diameter than the left pupil in room light, is their a sympathetic lesion in the left eye or a parasympathetic lesion in the right eye? To determine this, observe and compare the asymmetry of the pupils in both bright and dim light. If the asymmetry is greatest in dim light than the sympathetic system is disrupted in the left eye, not allowing it to dilate in dim light, while the functioning right eye dilates even further in the dim light causing an increase in asymmetry. Conversely, if the asymmetry is greatest in bright light, then there is a parasympathetic lesion in the right eye. If the asymmetry remains the same in dim and bright light, then the anisocoria is physiologic. Ptosis is the lagging of an eyelid. It has 2 distinct etiologies. Sympathetics going to the eye innervate Muller's muscle, a small muscle that elevates the eyelid. The III cranial nerve also innervates a much larger muscle that elevates the eye lid: the levator palpebrae. Thus, disruption of either will cause ptosis. The ptosis from a III nerve palsy is of greater severity than the ptosis due to a lesion of the sympathetic pathway, due to the size of the muscles innervated. As an aside, the parasympathetics run with the III cranial nerve and are usually affected with an abnormal III cranial nerve. Anisocoria can only be produced if the efferent pathway of the pupillary light reflex is disrupted. A lesion of the afferent pathway along the II cranial does not yield anisocoria. To test for a lesion of the afferent pathway one must perform a "swinging light test". To interpret this test one must understand that the level of pupillary constriction is directly related to the total "perceived" illumination the brain appreciates from both eyes. If, for example, their is a 90% decrease in the afferent pathway in the left eye, shining a bright light in this eye will produce less constriction in both eyes (remember, the efferent pathways are functioning), compared to a bright light shining in the normal eye. Therefore with an afferent lesion, "swinging" the light back and forth between the eyes rapidly will cause the pupils to change diameter when the light goes from the normal eye (brain perceiving increased illumination) to the abnormal eye (brain perceiving less illumination). If both eyes are normal, no change would occur, because the total perceived illumination remains constant. This is called an afferent pupillary defect (APD) or Marcus-Gunn pupil.
Cranial Nerves III, IV and VI
Instruct
the patient to follow the penlight or opthalmoscope with their eyes
without moving their head. Move the penlight slowly at eye level, first
to the left and then to the right. Then repeat this horizontal sweep
with the penlight at the level of the patient's forehead and then chin.
Note extra-ocular muscle palsies and horizontal or vertical nystagmus.The limitation of movement of both eyes in one direction is called a conjugate lesion or gaze palsy, and is indicative of a central lesion. A gaze palsy can be either supranuclear (in cortical gaze centers) or nuclear (in brain stem gaze centers). If the gaze palsy is a nuclear gaze palsy, then the eyes can't be moved in the restricted direction voluntarily or by reflex, e.g. oculocephalic reflex. If the lesion is cortical, then only voluntary movement is absent and reflex movements are intact. Disconjugate lesions, where the eyes are not restricted in the same direction or if only one eye is restricted, are due to more peripheral disruptions: cranial nerve nuclei, cranial nerves or neuromuscular junctions. One exception to this rule is an isolated impairment of adduction of one eye, which is commonly due to an ipsilateral median longitudinal fasciculus (MLF) lesion. This lesion is also called an internuclear ophthalmoplegia (INO). In INO, nystagmus is often present when the opposite eye is abducted.
Gaze-evoked nystagmus (nystagmus that is apparent only when the patient looks to the side or down) may be caused by many drugs, including ethanol, barbiturates, and phenytoin (Dilantin). Ethanol and barbiturates (recreational or therapuetic) are the most common cause of nystagmus. Dilantin may evoke nystagmus at slight overdoses, and opthalmoplegia at massive overdoses.
Abnormal patterns of eye movements may help localize lesions in the central nervous system. Ocular bobbing is the rhythmical conjugate deviation of the eyes downward. Ocular bobbing is without the characteristic rapid component of nystagmus. This movement is characteristic of damage to the pons.
Downbeat nystagmus (including a rapid component) may indicate a lesion compressing on the cervicomedullary junction such as a meningioma or chordoma. An electronystagmogram (ENG) may be ordered to characterize abnormal eye movements. The basis of this test is that the there is an intrinsic dipole in each eyeball (the retina is negatively charged compared to the cornea. During an ENG, recording electrodes are placed on the skin around the eyes and the dipole movement is measured and eye movement is accurately characterized.
Cranial Nerve V
First,
palpate the masseter muscles while you instruct the patient to bite
down hard. Also note masseter wasting on observation. Next, ask the
patient to open their mouth against resistance applied by the instructor
at the base of the patient's chin. 
Next,
test gross sensation of the trigeminal nerve. Tell the patient to
close their eyes and say "sharp" or "dull" when they feel an object
touch their face. Allowing them to see the needle before this
examination may alleviate any fear of being hurt. Using the needle and
brush from your reflex hammer or the pin from a safety pin, randomly
touch the patient's face with either the needle or the brush. Touch the
patient above each temple, next to the nose and on each side of the
chin, all bilaterally. Ask the patient to also compare the strength of
the sensation of both sides. If the patient has difficulty
distinguishing pinprick and light touch, then proceed to check
temperature and vibration sensation using the vibration fork. One may
warm it or cool it under a running faucet.
Finally,
test the corneal reflex using a large Q-tip with the cotton extended
into a wisp. Ask the patient to look at a distant object and then
approaching laterally, touch the cornea (not the sclera) and look for
the eye to blink. Repeat this on the other eye. Some clinicians omit the corneal reflex unless there is sensory loss on the face as per history or examination, or if cranial nerve palsies are present at the pontine level.
Cranial Nerve VII
Initially, inspect the face during conversation and rest noting any
facial asymmetry including drooping, sagging or smoothing of normal
facial creases. Next, ask the patient to raise their eyebrows, smile
showing their teeth, frown and puff out both cheeks. Note asymmetry and
difficulty performing these maneuvers. Ask the patient to close their
eyes strongly and not let the examiner pull them open. When the patient
closes their eyes, simultaneously attempt to pull them open with your
fingertips. Normally the patient's eyes cannot be opened by the
examiner. Once again, note asymmetry and weakness.
When the whole side of the face is paralyzed the lesion is peripheral. When the forehead is spared on the side of the paralysis, the lesion is central (e.g., stroke). This is because a portion of the VII cranial nerve nucleus innervating the forehead receives input from both cerebral hemispheres. The portion of the VII cranial nerve nucleus innervating the mid and lower face does not have this dual cortical input. Hyperacusis (increased auditory volume in an affected ear) may be produced by damage to the seventh cranial nerve. This is because the seventh cranial nerve innervates the stapedius muscle in the middle ear which damps ossicle movements which decreases volume. With seventh cranial nerve damage this muscle is paralyzed and hyperacusis occurs. Furthermore, since the branch of the seventh cranial nerve to the stapedius begins very proximally, hyperacusis secondary to seventh cranial nerve dysfunction indicates a lesion close to seventh cranial nerve's origin at the brainstem.
Cranial Nerve VIII
Assess
hearing by instructing the patient to close their eyes and to say
"left" or "right" when a sound is heard in the respective ear.
Vigorously rub your fingers together very near to, yet not touching,
each ear and wait for the patient to respond. After this test, ask the
patient if the sound was the same in both ears, or louder in a specific
ear. If there is lateralization or hearing abnormalities perform the
Rinne and Weber tests using the 256 Hz tuning fork.
The
Weber test is a test for lateralization. Wrap the tuning fork strongly
on your palm and then press the butt of the instrument on the top of
the patient's head in the midline and ask the patient where they hear
the sound. Normally, the sound is heard in the center of the head or
equally in both ears. If their is a conductive hearing loss present,
the vibration will be louder on the side with the conductive hearing
loss. If the patient doesn't hear the vibration at all, attempt again,
but press the butt harder on the patient's head.
The
Rinne test compares air conduction to bone conduction. Wrap the tuning
fork firmly on your palm and place the butt on the mastoid eminence
firmly. Tell the patient to say "now" when they can no longer hear the
vibration. When the patient says "now", remove the butt from the
mastoid process and place the U of the tuning fork near the ear without
touching it.
Tell the patient to say "now" when they can no longer hear anything.
Normally, one will have greater air conduction than bone conduction and
therefore hear the vibration longer with the fork in the air. If the
bone conduction is the same or greater than the air conduction, there is
a conductive hearing impairment on that side. If there is a
sensineuronal hearing loss, then the vibration is heard substantially
longer than usual in the air. Make certain that you perform both the
Weber and Rinne tests on both ears. It would also be prudent to perform
an otoscopic examination of both eardrums to rule out a severe otitis
media, perforation of the tympanic membrane or even occlusion of the
external auditory meatus, which all may confuse the results of these
tests. Furthermore, if hearing loss is noted an audiogram is indicated
to provide a baseline of hearing for future reference.Because of the extensive bilateral connections of the auditory system, the only way to have an ipsilateral hearing loss is to have a peripheral lesion, i.e. at the cranial nerve nucleus or more peripherally. Bilateral hearing loss from a single lesion is invariably due to one located centrally.
Cranial Nerves IX and X
Ask
the patient to swallow and note any difficulty doing so. Ask the
patient if they have difficulty swallowing. Next, note the quality and
sound of the patient's voice. Is it hoarse or nasal? Ask the patient
to open their mouth wide, protrude their tongue, and say "AHH". While
the patient is performing this task, flash your penlight into the
patient's mouth and observe the soft palate, uvula and pharynx. The
soft palate should rise symmetrically, the uvula should remain midline
and the pharynx should constrict medially like a curtain. Often the
palate is not visualized well during this manuever. One may also try
telling the patient to yawn, which often provides a greater view of the
elevated palate. Also at this time, use a tongue depressor and the butt
of a long Q-tip to test the gag reflex. Perform this test by touching
the pharynx with the instrument on both the left and then on the right
side, observing the normal gag or cough. Some clinicians omit testing for the gag reflex unless there is dysarthria or dysphagia present by history or examination, or if cranial nerve palsies are present at the medullary level. Roughly 20% of normal individuals have a minimal or absent gag reflex. Dysarthria and dysphagia are due to incoordination and weakness of the muscles innervated by the nucleus ambiguus via the IX and X cranial nerves. The severity of the dysarthria or dysphagia is different for single versus bilateral central lesions. The deficiency is often minor if the lesion is centrally located and in only one cortical hemisphere, because each nucleus ambiguus receives input from both crerebral hemispheres. In contrast, bilateral central lesions, or "pseudobulbar palsies", often produce marked deficits in phonation and swallowing. Furthermore, on examination the quality of the dysarthria is distinct for central versus peripheral lesions. Central lesions produce a strained, strangled voice quality, while peripheral lesions produce a hoarse, breathy and nasal voice.
Cranial Nerve XI
This
cranial nerve is initially evaluated by looking for wasting of the
trapezius muscles by observing the patient from the rear. Once this is
done, ask the patient to shrug their shoulders as strong as they
possible can while the examiner resists this motion by pressing down on
the patient's shoulders with their hands. Next, ask the patient to turn
their head to the side as strongly as they possibly can while the
examiner once again resists with their hand.
Repeat this maneuver on the opposite side. The patient should
normally overcome the resistance applied by the examiner. Note
asymmetry.Peripheral lesions produce ipsilateral sternocleidomastoid (SCM) weakness and ipsilateral trapezius weakness. Central lesions produce ipsilateral SCM weakness and contralateral trapezius weakness, because of differing sources of cerebral innervation. This is a common clinical misunderstanding.
Cranial Nerve XII
The
hypoglossal nerve controls the intrinsic musculature of the tongue and
is evaluated by having the patient "stick out their tongue" and move it
side to side. Normally, the tongue will be protruded from the mouth and
remain midline. Note deviations of the tongue from midline, a complete
lack of ability to protrude the tongue, tongue atrophy and
fasciculations on the tongue.The tongue will deviate towards the side of a peripheral lesion, and to the opposite side of a central lesion.