3-Cranial Nerves

Examination of Nervous System
Hong Zhang, MD,PhD

Department of Neurology
Zhongnan Hospital of Wuhan University
When approching a patient with a
neurologic disorder always ask
youself
1. Where is the lesion? 2. What is the cause of the
• cerebrum lesion?
• cerebellum • vascular
• brainstem • infectious
• spinal cord • neuroplastic
• nerve root • degenerative
• peripheral nerve • inflammatory-immunologic
• neuromuscular junction • congenital-developmental
• muscle • traumatic
• not confined to one level • toxic
• metabolic
3. Is the lesion focal, multifocal or diffuse?
Neuroanatomy through Clinical Cases
• Hal Blumenfeld
Yale University School of Medicine
• Publishing Information: September 2001
• ISBN 0-87893-060-4
• INTRODUCTION
• MENTAL STATUS
• CRANIAL NERVES
• MOTOR EXAM
• REFLEXES
• COORDINATION AND GAIT
• SENSORY EXAM
CRANIAL NERVES
1. Olfaction (CN I)
2. Ophthalmoscopic Exam (CN II)
3. Vision (CN II)
4. Pupillary Responses (CN II, III)
5. Extraocular Movements (CN III, IV, VI)
6. Facial Sensation and Muscles of Mastication (CN V)
7. Muscles of Facial Expression and Taste (CN VII)
8. Hearing and Vestibular Sense (CN VIII)
9. Palate Elevation and Gag Reflex (CN IX, X)
10.Muscles of Articulation (CN V, VII, IX, X, XII)
11.Sternocleidomastoid and Trapezius Muscles (CN XI)
12.Tongue Muscles (CN XII)
Olfaction (CN I)
• Can the patient smell coffee or soap with
each nostril?
• Do not use noxious odors, since they may
stimulate pain fibers from CN V
• CN I is often not tested unless specific
pathology such as a subfrontal brain tumor
is suspected
Olfaction (CN I)
What is Being Tested?
• Impairment can be due to
1. nasal obstruction
2. damage to the olfactory nerves in the
nasal mucosa
3. damage to the nerves as they cross the
cribriform plate
4. intracranial lesions affecting the olfactory
bulbs
Opthalmoscopic Exam (CN II)
• Examine both retinas carefully

with an ophthalmoscope
• This exam allows direct visualization of
damage to
1. retina or retinal vessels
2. optic nerve atrophic changes
3. papilledema
4. other important abnormalities
Visual Acuity
• Test visual acuity for each
eye separately (by covering
one eye at a time) using an
eye chart
Color Vision
• Test each eye separately for ability to
distinguish colors
• Test for red desaturation, a sign of subtle
asymmetry in optic nerve function seen
• In optic neuritis, by asking the patient to
cover each eye alternately while looking at
a red object and report any relative
dullness of the color in one eye
Visual Fields
• Test visual fields for each eye by asking the
patient to fixate straight ahead and to report
when a finger can be seen moving in each
quadrant
• Alternatively, ask the patient to report how many
fingers are being shown in each quadrant
• More precise mapping of visual fields can be
done in the laboratory for patients who will be
followed over time
Visual Extinction
• Test for visual extinction on double
simultaneous stimulation by asking the patients
how many fingers they see when fingers are
presented to both sides at the same time
• In visual extinction, a form of hemineglect ,
patients do not report seeing the fingers on the
affected (usually left) side of the visual field,
although they can see fingers when they are
presented to that side alone
• In comatose or uncooperative patients,

visual fields can be tested roughly using
blink-to-threat, in which the examiner's
fingers are moved rapidly towards the
patient's eyes from each quadrant to see if
a blink occurs.

• Damage anywhere in the visual pathway
from the eye to the visual cortex can
cause specific deficits in the visual fields
of one or both eyes
• Importantly, some visual information from
each eye crosses to the opposite side at
the optic chiasm

• Lesions in front of the optic chiasm (eye,
optic nerve) cause visual deficits in one
eye
• Lesions behind the optic chiasm (optic
tract, thalamus, white matter, visual
cortex) cause visual field deficits that are
similar for both eyes
• Visual hemineglect or extinction is

usually caused by contralateral parietal
lesions, and less often by frontal or
thalamic lesions
• Neglect is usually more robust in lesions
of the right hemisphere
Pupillary Responses (CN II,
III)
• First, record the pupil size and shape at

rest
• Next, note the direct response, meaning
constriction of the illuminated pupil, as well
as the consensual response, meaning
constriction of the opposite pupil
III)
• In an afferent pupillary defect there is a
decreased direct response caused by
decreased visual function in one eye
• This can be demonstrated with the
swinging flashlight test, in which the
light is moved back and forth between the
eyes every two to three seconds
III)
• The afferent pupillary defect becomes
obvious when the flashlight is moved from
the normal to the affected eye, and the
affected pupil dilates in response to light
• Under normal conditions, the pupil
constricts in response to light
• Brief oscillations of pupillary size called
hippus occur normally in response to light
which should not be confused with an
afferent pupillary defect
III)
• Finally, test the pupillary response to

accommodation. Normally, the pupils
constrict while fixating on an object being
moved from far away to near the eyes
III)
• Direct response (pupil illuminated) is
impaired in lesions of
1. ipsilateral optic nerve
2. pretectal area
3. ipsilateral parasympathetics traveling in
CN III
4. pupillary constrictor muscle of the iris
III)
• Consensual response (contralateral
pupil illuminated) is impaired in lesions
of
1. contralateral optic nerve
2. pretectal area
3. ipsilateral parasympathetics traveling in
CN III
4. pupillary constrictor muscle
III)
• Accommodation (response to looking at
something moving toward the eye) is impaired
in lesions of
1. ipsilateral optic nerve
2. ipsilateral parasympathetics traveling in CN III
3. pupillary constrictor muscle
4. in bilateral lesions of the pathways from the
optic tracts to the visual cortex
5. Accommodation is spared in lesions of the
pretectal area
Extraocular Movements
(CN III, IV, VI)
• Check extraocular movements (eye
movements) by having the patient look in
all directions without moving their head
and ask them if they experiences any
double vision
• Test smooth pursuit by having the
patient follow an object moved across their
full range of horizontal and vertical eye
movements
Extraocular Movements
(CN III, IV, VI)
• Test convergence movements by having
the patient fixate on an object as it is
moved slowly towards a point right between
the patient's eyes
• Also, observe the eyes at rest to see if
there are any abnormalities such as
spontaneous nystagmus (see below)or
dysconjugate gaze (eyes not both fixated
on the same point) resulting in diplopia
(double vision)
III)
• Saccades are eye movements used to
rapidly refixate from one object to another
• The examiner can test saccades by
holding two widely spaced targets in front
of the patient (such as the examiner's
thumb on one hand and index finger on
the other) and asking the patient to look
back and forth between the targets
III)
• Test optokinetic nystagmus (OKN) by moving
a strip with parallel stripes on it in front of the
patient's eyes and asking them to watch the
stripes go by
• Normally, rhythmic eye movements called
nystagmus occur consisting of an alternating
slow phase with slow pursuit movements in the
direction of strip movement, and a rapid phase
with quick refixations back to midline
III)
• In comatose or severely lethargic patients,
the vestibulo-ocular reflex can be used to
test whether brainstem eye movement
pathways are intact
• The oculocephalic reflex, a form of the
vestibulo-ocular reflex, is tested by holding
the eyes open and rotating the head from
side to side or up and down
III)
• These maneuvers obviously should not be
performed in cases of head injury or other
cases of suspected cervical spine trauma
unless complete cervical spine films are
normal
• The reflex is present if the eyes move in
the opposite direction of the head
movements, and it is therefore sometimes
called doll's eyes
III)
• In awake patients, doll's eyes are usually
not present because voluntary eye
movements mask the reflex
• The absence of doll's eyes suggests
brainstem dysfunction in the comatose
patient but can be normal in the awake
patient
• More potent stimulus of the vestibulo-
ocular reflex used to evaluate comatose
patients is caloric stimulation
III)
• Careful testing can often identify abnormalities in
1. individual muscles
2. particular cranial nerves (oculomotor, trochlear,
or abducens) in their course from the brainstem
to the orbit
3. brainstem nuclei
4. higher-order centers and pathways in the cortex
and brainstem that control eye movements
III)

• Spontaneous nystagmus can indicate
1. Toxic or metabolic conditions such as
drug overdose
2. alcohol intoxication
3. peripheral or central vestibular
dysfunction
Facial Sensation and Muscles of
Mastication (CN V)
• Test facial sensation using a cotton wisp

and a sharp object
• Also test for tactile extinction using double
simultaneous stimulation
Mastication (CN V)
• The corneal reflex, which involves both

CN V and CN VII
• It is tested by touching each cornea gently
with a cotton wisp and observing any
asymmetries in the blink response
Mastication (CN V)
• Feel the masseter muscles during jaw

clench
• Test for a jaw jerk reflex by gently tapping
on the jaw with the mouth slightly open
Mastication (CN V)

• Facial sensation can be impaired by
lesions of
1. trigeminal nerve (CN V)
2. trigeminal sensory nuclei in the
brainstem
3. ascending sensory pathways to the
thalamus and somatosensory cortex in
the postcentral gyrus
Mastication (CN V)

• The corneal blink reflex is mediated by
polysynaptic connections in the brainstem
between the trigeminal (CN V) and facial
(CN VII) nerves
• It can be impaired by lesions anywhere in
this circuit
Mastication (CN V)

• Extinction in the presence of intact
primary sensation is usually caused by
right parietal lesions
Mastication (CN V)

• Weakness of the muscles of mastication can
be due to lesions in
1. upper motor neuron (UMN) pathways
synapsing onto the trigeminal (CN V) motor
nucleus
2. lower motor neurons (LMNs) of the trigeminal
motor nucleus in the pons or as they exit the
brainstem to reach the muscles of mastication
3. neuromuscular junction
4. muscles themselves
Mastication (CN V)

• Presence of a jaw jerk reflex is abnormal,
especially if it is prominent
• It is a sign of hyperreflexia associated with
lesions of UMN pathways projecting to the
trigeminal motor nucleus
• Both the afferent and the efferent limbs of
the jaw jerk reflex are mediated by CN V
Muscles of Facial Expression
and Taste (CN VII)
• Look for asymmetry in facial shape or in

depth of furrows such as the nasolabial
fold
• Also look for asymmetries in spontaneous
facial expressions and blinking
and Taste (CN VII)
Ask patient to
1. Smile
2. puff out their cheeks
3. clench their eyes tight
4. wrinkle their brow
• Old photographs of the patient can often
aid your recognition of subtle changes.
and Taste (CN VII)
• Check taste with sugar, salt, or lemon
juice on cotton swabs applied to the lateral
aspect of each side of the tongue
• Like olfaction, taste is often tested only
when specific pathology is suspected,
such as in lesions of the facial nerve, or in
lesions of the gustatory nucleus (nucleus
solitarius)
and Taste (CN VII)

• Facial weakness can be caused by lesions of
1. upper motor neurons in the contralateral motor
cortex or descending central nervous system
pathways
2. lower motor neurons in the ipsilateral facial
nerve nucleus (CN VII) or exiting nerve fibers
3. the neuromuscular junction
4. face muscles
and Taste (CN VII)

• The upper motor neurons for the upper face (the
upper portions of the orbicularis oculi and the
frontalis muscles of the forehead) project to the
facial nuclei bilaterally
• Upper motor neuron lesions, such as a stroke,
cause contralateral face weakness sparing the
forehead
• Lower motor neuron lesions, such as a facial
nerve injury, typically cause weakness involving
the whole ipsilateral face
Hearing and Vestibular Sense
(CN VIII)
Hearing
• Can the patient hear fingers rubbed
together or words whispered just outside
of the auditory canal and identify which
ear hears the sound?
• A tuning fork can be used to distinguish
neural from mechanical conductive
hearing problems
(CN VIII)
Hearing
• In the Rinne test the sound heard when
holding a vibrating tuning fork just outside
each ear (air conduction), is compared to
the sound heard when placing the tuning
fork handle on each mastoid process
(bone conduction)
• Normal individuals will hear the tone better
by air conduction
(CN VIII)
Hearing
• In conductive hearing loss, bone conduction is
greater than air conduction, because bone
conduction bypasses problems in the external or
middle ear
• In sensorineural hearing loss, air conduction is
greater than bone conduction in both ears (as in
normal hearing), however, hearing is decreased
in the affected ear
(CN VIII)
Hearing
• In the Weber test, the tuning fork is
placed on the vertex of the skull in the
midline, and the patient is asked to report
the side where the tone sounds louder
• Normally, the tone sounds equal on both
sides
(CN VIII)
Hearing
• In sensorineural hearing loss, the tone
is louder on the normal side
• In conductive hearing loss, the tone is
louder on the affected side
• You can verify that the tone is louder on
the side of conductive hearing loss on
yourself by closing each ear alternately
while humming
(CN VIII)
Vestibular Sense
• Vestibular sense is generally not
specifically tested, except for in the
following important situations
1. Patients with vertigo
2. Patients with limitations of horizontal or
vertical gaze
3. Patients in coma
(CN VIII)
Patients with vertigo
• Barany or Hall-Pike positional testing can help
distinuish peripheral from central causes of
vertigo
• The patient sits on the bed or examining table,
and the examiner supports the patient's head as
the patient lays back with one ear down, and
with the head extending over the edge of the
table
• This maneuver does not need to be done
especially briskly
(CN VIII)

• The patient is asked to keep their eyes open and
report any sensations of vertigo, while the
examiner looks for nystagmus
• This change of position causes maximal
stimulation of the posterior semicircular canal of
the ear that is down, and of the anterior
semicircular canal of the ear that is up
• The maneuver is also done with the other ear
down
(CN VIII)

• With peripheral lesions
1. There is usually a delay of a few seconds
before the onset of nystagmus and vertigo
2. The nystagmus is horizontal or rotatory and
does not change directions
3. Nystagmus and vertigo then fade away within
about a minute
4. If the same maneuver is repeated, there is
often adaptation, so that the nystagmus and
vertigo are briefer and less intense each time
(CN VIII)

In contrast, with central lesions
1. Nystagmus and vertigo may begin
immediately, and there tends to be no
adaptation
2. Horizontal or rotatory nystagmus can also be
seen with central lesions
3. However, vertical nystagmus, nystagmus that
changes directions, or prominent nystagmus in
the absence of vertigo are seen only in central,
and not in peripheral lesions
(CN VIII)
Patients with limitations of horizontal or

vertical gaze
• Testing the vestibulo-ocular reflex can help
localize the lesion
• As we mentioned when discussing
Extraocular Muscles the vestibulo-ocular reflex
can be tested in two ways
• The first is using the oculocephalic maneuver, in
which the eyes are held open and the head is
turned rapidly either from side to side or up and
down
(CN VIII)
Patients with limitations of horizontal or

vertical gaze
• Testing the vestibulo-ocular reflex
• The second is using caloric testing, in
which cold or warm water is instilled into
one ear, producing asymmetric stimulation
of the semicircular canals
Caloric stimulation
Definition
• Caloric stimulation is a test which uses
differences in temperature to diagnose ear
nerve damage
• Caloric stimulation is done to check the
acoustic nerve, which provides hearing
and helps with balance
Caloric stimulation
How the Test is Performed
• This test stimulates the inner ear and nearby
nerves by delivering cold and warm water (air) to
the ear canal at different times
• One ear is tested at a time
• When cold water enters the ear, it should cause
rapid, side-to-side eye movements called
nystagmus. The eyes should move away from
the cold water and slowly back
• Next, warm water is placed into the ear. The
eyes should now move towards the warm water
then slowly away
Caloric stimulation
Why the Test is Performed

• This test may be recommended if you
have
1. Dizziness or vertigo
2. Hearing loss that may be due to certain
antibiotics
3. Certain types of anemia
4. Possible psychological causes of vertigo
(CN VIII)
Patients in coma
• The vestibulo-ocular reflex is often the
only way to test eye movements in these
patients
(CN VIII)
• Hearing loss can be caused by lesions in
1. acoustic and mechanical elements of the ear
2. neural elements of the cochlea
3. acoustic nerve (CN VIII)
• After the hearing pathways enter the brainstem,
they cross over at multiple levels and ascend
bilaterally to the thalamus and auditory cortex
• Clinically significant unilateral hearing loss is
invariably caused by peripheral neural or
mechanical lesions
(CN VIII)

Abnormalities in vestibular testing can be
associated with lesions in
1. vestibular apparatus of the inner ear
2. vestibular portion of CN VIII
3. vestibular nuclei in the brainstem, the
cerebellum
4. pathways in the brainstem (such as the medial
longitudinal fasciculus) that connect the
vestibular and oculomotor systems
Palate Elevation and Gag Reflex
(CN IX, X)
• Does the palate elevate symmetrically

when the patient says, "Aah"?
• Does the patient gag when the posterior
pharynx is brushed?
• The gag reflex needs to be tested only in
patients with suspected brainstem
pathology, impaired consciousness, or
impaired swallowing
Palate Elevation and Gag Reflex
(CN IX, X)

Palate elevation and the gag reflex are
impaired in lesions involving
1. CN IX
2. CN X
4. pharyngeal muscles
Muscles of Articulation
(CN V, VII, IX, X, XII)
Is the patient's speech
1. Hoarse ?
2. Slurred ?
3. Quiet ?
4. Breathy ?
5. Nasal ?
6. Low or high pitched?
• It is often important to ask if the patient's
speech has changed from baseline
• Note that dysarthria, abnormal

pronunciation of speech, is not the same
as aphasia
• Aphasia is an abnormality in language
production or comprehension

Abnormal articulation of speech can occur in
lesions involving
1. muscles of articulation
3. peripheral or central portions of CN V,
VII, IX, X, or XII

Speech production can be abnormal as a result of
lesions in
1. Motor cortex
2. Cerebellum
3. Basal ganglia
4. Descending pathways to the brainstem
Sternocleidomastoid and
Trapezius Muscles (CN XI)
Ask the patient to

1. Shrug their shoulders
2. Turn their head in both directions
3. Raise their head from the bed
4. Flexing forward against the force of your
hands

Weakness in the sternocleidomastoid or
trapezius muscles can be caused by
lesions in
1. muscles
3. lower motor neurons of the accessory
spinal nerve (CN XI)

• Unilateral upper motor neuron lesions in the
cortex or descending pathways cause
contralateral weakness of the trapezius, with
relative sparing of sternocleidomastoid strength
• This may be explained by bilateral upper motor
neuron projections controlling the
sternocleidomastoid, in analogy to the
bilateral projections controlling the upper face
Tongue Muscles (CN XII)
• Note any atrophy or fasciculations

(spontaneous quivering movements caused by
firing of muscle motor units) of the tongue while
it is resting on the floor of the mouth
• Ask the patient to stick their tongue straight out
and note whether it curves to one side or the
other
• Ask the patient to move their tongue from side to
side and push it forcefully against the inside of
each cheek
• Fasciculations and atrophy are signs of lower

motor neuron lesions
• Unilateral tongue weakness causes the
tongue to deviate toward the weak side
• Lesions of the motor cortex cause
contralateral tongue weakness
Tongue weakness can result from lesions of

1. tongue muscles
3. lower motor neurons of the hypoglossal nerve
(CN XII)
4. upper motor neurons originating in the motor
cortex
A summary of the cranial nerves
and their respective functioning
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
THANK
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3-Cranial Nerves

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Examination of Nervous System

Hong Zhang, MD,PhD

• Publishing Information: September 2001

• Examine both retinas carefully

• In comatose or uncooperative patients,

What is Being Tested?

What is Being Tested?

• Visual hemineglect or extinction is

• First, record the pupil size and shape at

• Finally, test the pupillary response to

What is Being Tested?

• Test facial sensation using a cotton wisp

• The corneal reflex, which involves both

• Feel the masseter muscles during jaw

What is Being Tested?

What is Being Tested?

What is Being Tested?

What is Being Tested?

What is Being Tested?

• Look for asymmetry in facial shape or in

What is Being Tested?

What is Being Tested?

Patients with vertigo

Patients with vertigo

Patients with vertigo

Patients with limitations of horizontal or

Patients with limitations of horizontal or

Why the Test is Performed

What is Being Tested?

• Does the palate elevate symmetrically

What is Being Tested?

• Note that dysarthria, abnormal

What is Being Tested?

What is Being Tested?

Ask the patient to

What is Being Tested?

What is Being Tested?

• Note any atrophy or fasciculations

• Fasciculations and atrophy are signs of lower

Tongue weakness can result from lesions of

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