ANATOMY AND PHYSIOLOGY
The facial nerve consists of a
motor and a sensory part, the
latter being frequently described
under the name of the nervus
intermedius (pars intermedii of
The two parts emerge at the
lower border of the pons in the
recess between the olive and the
inferior peduncle, the motor part
being the more medial,
immediately to the lateral side of
the sensory part is the acoustic
Plan of the facial and intermediate nerves and their
communication with other nerves.
THE MOTOR PORTION
The motor root arises from a nucleus which
lies deeply in the reticular formation of the
lower part of the pons. This nucleus is situated
above the nucleus ambiguus, behind the
superior olivary nucleus, and medial to the
spinal tract of the trigeminal nerve.
From this origin the fibers pursue a curved
course in the substance of the pons. They first
pass backward and medialward toward the
rhomboid fossa, and, reaching the posterior
end of the nucleus of the abducent nerve, run
upward close to the middle line beneath the
At the anterior end of the nucleus of the
abducent nerve they make a second bend, and
run downward and forward through the pons
to their point of emergence between the olive
and the inferior peduncle.
THE MOTOR PORTION
The facial nerve is a predominantly
motor nerve that innervates the
muscles of facial expression and the
muscles of the scalp and ear, as well
as the buccinator, platysma,
stapedius, stylohyoid, and posterior
belly of the digastric.
It contains parasympathetic
secretory fibers to the
submandibular and sublingual
salivary glands, the lacrimal gland
and to the mucous membranes of
the oral and nasal cavities which are
conveyed through the chorda
THE SENSORY PORTION
The sensory root arises from the genicular
ganglion, which is situated on the geniculum of
the facial nerve in the facial canal, behind the
hiatus of the canal. The cells of this ganglion are
unipolar, and the single process divides in a T-
shaped manner into central and peripheral
The central branches leave the trunk of the
facial nerve in the internal acoustic meatus, and
form the sensory root; the peripheral branches
are continued into the chorda tympani and
greater superficial petrosal nerves.
Entering the brain at the lower border of the
pons between the motor root and the acoustic
nerve, the fibers of the sensory root pass into
the substance of the medulla oblongata and
end in the upper part of the terminal nucleus of
the glossopharyngeal nerve and in the
It mediates taste from the anterior two-thirds of the
It also conveys exteroceptive sensation from the
eardrum and external auditory canal, proprioceptive
sensation from the muscles it supplies, and general
visceral sensation from the salivary glands and
mucosa of the nose and pharynx.
Branches of Communication
In the internal acoustic
At the genicular
In the facial canal……..
At its exit from the
Behind the ear…………
On the face……….
In the neck…………
With the acoustic nerve.
With the sphenopalatine ganglion by the greater
superficial petrosal nerve.
With the otic ganglion by a branch which joins the
lesser superficial petrosal nerve.
With the sympathetic on the middle meningeal
With the auricular branch of the vagus.
With the glossopharyngeal.
With the vagus.
With the great auricular.
With the auriculotemporal.
With the lesser occipital.
With the trigeminal.
With the cutaneous cervical.
Branches of Distribution
With the facial canal………
At its exit from the
On the face…
Nerve to the Stapedius
Muscles of the Face, Their Actions, and Innervations
NERVE BRANCH MUSCLE INNERVATIONS MUSCLE ACTION
Temporal branch FRONTALIS Raises eyebrows and skin over the
root of the nose; draws scalp
forward, throwing forehead into
Draws eyebrow down and
medially, produces vertical
wrinkles in the forehead (the
UPPER PART OF THE ORBICULARIS
Eyelid sphincter; palpebral portion
narrows palpebral fissure and
gently closes eyelids; orbital
portion draws skin of forehead,
temple, and cheek toward medial
orbit, pulls eyebrow down, draws
skin of cheek up; closes eye firmly
OCCIPITALIS Draws scalp backwards
PROCERUS (PYRAMIDALIS NASI) Draws medial eyebrow downward,
produces transverse wrinkles over
bridge of nose
NERVE BRANCH MUSCLE INNERVATIONS MUSCLE ACTION
Zygomatic Lower and lateral orbicularis
Buccal Orbicularis oculi
Levator anguli oris
Levator labii superioris
(quadratus labii superioris)
Compresses cheeks, , keeps
food under pressure of cheeks
Draws mouth backward and
portion of nose, draws the ala
Raises angle of mouth.
Elevates upper lip, dilates
NERVE BRANCH MUSCLE INNERVATIONS MUSCLE ACTION
Mandibular LOWER PART OF THE
Sphincter of the mouth;
closes lips; superficial fibers
protrude lips; deep fibers
draw lips in and press them
MENTALIS Protrudes lower lip, wrinkles
skin of chin.
RISORIUS Retracts angle of mouth
Depresses angle of mouth
Draws lower lip downward
Cervical PLATYSMA Pulls lower lip and angle of
mouth down; depresses
lower jaw; raises and wrinkles
skin of neck
Examination of the Motor Functions
Examination of facial nerve motor functions centers on assessment of
the actions of the muscles of facial expression.
Note the tone of the muscles of facial expression, and look for atrophy
Note the resting position of the face and whether there are any
abnormal muscle contractions.
Note the pattern of spontaneous blinking for frequency and symmetry.
A patient with parkinsonism may have infrequent blinking and an
immobile, expressionless, “masked” face. Facial dystonia causes an
abnormal fixed contraction of a part of the face, often imparting a
curious facial expression. Progressive supranuclear palsy may cause a
characteristic facial dystonia with knitting of the brows and widening of
the palpebral fissures.
Synkinesias are abnormal contractions of the face, often subtle,
synchronous with blinking or mouth movements; they suggest remote
facial nerve palsy with aberrant regeneration. Spontaneous contraction
of the face may be due to hemifacial spasm (HFS). Other types of
abnormal involuntary movements that may affect the facial muscles
include tremors, tics, myoclonic jerks, chorea, and athetosis.
Observe the nasolabial folds for depth and symmetry and note whether
there is any asymmetry in forehead wrinkling or in the width of the
palpebral fissures with the face at rest. A flattened nasolabial fold with
symmetric forehead wrinkles suggests a central (upper motor neuron)
facial palsy; a flattened nasolabial fold with smoothing of the forehead
wrinkles on the same side suggests a peripheral (lower motor neuron)
facial nerve palsy. Eyelid position and the width of the palpebral fissures
often provide subtle but important clinical clues. A unilaterally widened
palpebral fissure suggests a facial nerve lesion causing loss of tone in
the orbicularis oculi muscle, the eye closing sphincter; this is sometimes
confused with ptosis of the opposite eye. It is a common misconception
that facial nerve palsy causes ptosis.
Examples of primarily neurologic conditions include parkinsonism and related
extrapyramidal disorders (masked facies), progressive supranuclear palsy (facial
dystonia, omega sign), Möbius' syndrome, myotonic dystrophy (hatchet face,
myopathic face), facioscapulohumeral muscular dystrophy (myopathic face,
transverse smile), general paresis (facies paralytica), myasthenia gravis
(myasthenic snarl), facial nerve palsy (unilateral or bilateral), and Wilson's
disease (risus sardonicus). These are discussed in the sections dealing with
these particular diseases. There are of course numerous congenital syndromes
that cause distinctively dysmorphic facies.
Observe the movements during spontaneous facial expression as the patient
talks, smiles, or frowns. Certain upper motor neuron facial palsies are more
apparent during spontaneous smiling than when the patient is asked to smile or
show the teeth. In infants, facial movements are observed during crying.
Have the patient grin, vigorously drawing back the angles of the mouth and
baring the teeth. Note the symmetry of the expression, how many teeth are
seen on each side and the relative amplitude and velocity of the lower facial
contraction. Have the patient close eyes tightly and note the symmetry of the
upper facial contraction. How completely the patient buries the eyelashes on
the two sides is a sensitive indicator of orbicularis oculi strength.
Other useful movements include having the patient raise the eyebrows, singly or in
unison, and noting the excursion of the brow and the degree of forehead
wrinkling; close each eye in turn; corrugate the brow; puff out the cheeks; frown;
pucker; whistle; alternately smile and pucker; contract the chin muscles; and pull
the corners of the mouth down in an exaggerated frown to activate the platysma.
The platysma can also be activated by having the patient open the mouth against
resistance or clinch the teeth. The patient may smile spontaneously after
attempting to whistle, or the examiner may make an amusing comment to assess
emotional facial movement. Because of their paucity of facial expression, patients
with Parkinson's disease may fail to smile after being asked to whistle: the whistle-
smile (Hanes) sign.
Trying to gently push down the uplifted eyebrow may detect mild weakness. It is
difficult to pry open the tightly shut orbicularis oculi in the absence of weakness.
Vigorously pulling with the thumbs may sometimes crack open a normal eye. If the
examiner can force the eye open with her small fingers, then the orbicularis oculi
is definitely weak. Likewise, it is difficult to force open the tightly pursed lips in a
normal individual. When the orbicularis oris sphincter is impaired, the examiner
may be able to force air out of the puffed cheek through the weakened lips.
Testing ear and scalp movements is seldom useful. The stylohyoid muscle and
posterior belly of the digastric cannot be adequately tested. With stapedius
weakness, the patient may complain of hyperacusis, especially for low tones.
DISORDERS OF FUNCTION
PERIPHERAL FACIAL PALSY
Lower motor neuron
Peripheral facial palsy
(PFP) may result from a
lesion anywhere from the
CN VII nucleus in the pons
to the terminal branches in
Results from an ipsilateral
CENTRAL FACIAL PALSY
Upper motor neuron
Central facial palsy (CFP) is
due to a lesion involving
the supranuclear pathways
before they synapse on the
Results from a
Peripheral Facial Palsy
There is flaccid weakness of all the muscles of facial
expression on the involved side, both upper and lower face,
and the paralysis is usually complete (prosopoplegia).
The affected side of the face is smooth; there are no wrinkles
on the forehead.
The eye is open; the inferior lid sags;.
The nasolabial fold is flattened; and the angle of the mouth
The patient cannot raise the eyebrow, wrinkle the forehead,
frown, close the eye, laugh, smile, bare the teeth, blow out
the cheeks, whistle, pucker, retract the angle of the mouth, or
contract the chin muscles or platysma on the involved side.
The cheek is flaccid and food accumulates between the teeth
and the paralyzed cheek.
The patient may bite the cheek or lip when chewing. Food,
liquids, and saliva may spill from the corner of the mouth. The
cheek may puff out on expiration because of buccinator
As shown in the picture she talks and smiles with one side of
the mouth, and the mouth is drawn to the sound side on
A patient with a peripheral facial
nerve palsy on the right
patient is attempting to retract
both angles of mouth.
Patient attempting to raise both
The facial asymmetry may cause an apparent deviation of
the tongue to the affected side.
A patient with an incomplete PFP may be able to close
the eye, but not with full power against resistance.
Inability to wink with the involved eye is common. The
palpebral fissure is open wider than normal, and there
may be inability to close the eye (lagophthalmos).
BELL’S PHENOMENON: During spontaneous blinking, the
involved eyelid tends to lag behind, sometimes
conspicuously. Attempting to close the involved eye
causes a reflex upturning of the eyeball. The iris may
completely disappear upwardly.
To elicit the levator sign of Dutemps and Céstan, have the
patient look down, then close the eyes slowly; because
the function of the levator palpebrae superioris is no
longer counteracted by the orbicularis oculi, the upper lid
on the paralyzed side moves upward slightly.
Akin to Bell's phenomenon is Negro's sign, where the
eyeball on the paralyzed side deviates outward and
elevates more than the normal one when the patient
raises the eyes.
Infranuclear paralysis of right
trigeminal, facial and hypoglossal
nerves in a patient with metastatic
Labials and vowels are produced by pursing the
lips; patients with peripheral facial weakness have
a great deal of difficulty in articulating these
Because of weakness of the lower lid sphincter,
tears may run over and down the cheek (epiphora),
especially if there is corneal irritation because of
inadequate eye protection. A lack of tearing may
signal very proximal involvement, above the origin
of the greater superficial petrosal nerve. With
severe weakness, the eye never closes, even in
The most common cause of PFP is Bell's palsy.
Idiopathic facial paralysis (Bell's palsy) frequently
follows a viral infection or an immunization.
Symptoms often begin with pain behind the ear,
followed within a day or two by facial weakness.
There is peripheral facial weakness involving both
upper and lower face. The paralysis is complete in
approximately 70% of patients.
The most common symptoms accompanying
Bell's palsy are increased tearing, pain in or
around the ear, and taste abnormalities like
Dysgeusia and ageusia occurs.
There may be drooling and difficulty
speaking due to the slack facial muscles.
Patients are often unable to close the eye;
Liquids and saliva may drool from the
affected corner of the mouth and tears may
spill down the cheek.
Facial Weakness of Central Origin
In a supranuclear, upper motor neuron or central facial palsy (CFP), there is
weakness of the lower face, with relative sparing of the upper face. The
upper face has both contralateral and ipsilateral supranuclear innervation,
and cortical innervation of the facial nucleus may be more extensive for the
lower face than the upper. The paresis is rarely complete.
A lesion involving the corticobulbar fibers anywhere prior to their synapse
on the facial nerve nucleus will cause a CFP. Lesions are most often in the
cortex or internal capsule. Occasionally, a lesion as far caudal as the medulla
can cause a CFP because of involvement of the aberrant pyramidal tract.
The upper face is not necessarily completely spared, but it is always
involved to a lesser degree than the lower face.
There may be subtle weakness of the orbicularis oculi, the palpebral fissure
may be slightly wider on the involved side, and there may be a decrease in
palpable lid vibrations.
Involvement of the corrugator and frontalis is unusual, and the patient
should be able to elevate the eyebrow and wrinkle the forehead with no
more than minimal asymmetry.
Lesions are most often in the cortex or internal capsule. There is
considerable individual variation in facial innervation, and the
extent of weakness in a CFP may vary from the lower half to two-
thirds of the face.
The upper face is not necessarily completely spared, but it is
always involved to a lesser degree than the lower face.
There may be subtle weakness of the orbicularis oculi, the
palpebral fissure may be slightly wider on the involved side, and
there may be a decrease in palpable lid vibrations.
However, involvement of the corrugator and frontalis is unusual,
and the patient should be able to elevate the eyebrow and
wrinkle the forehead with minimal asymmetry.
Inability to independently wink the involved eye may be the only
Even if there is some degree of upper facial involvement in a CFP, the
patient is always able to close the eye, Bell's phenomenon is absent, the
corneal reflex is present, and the orbicularis oculi reflex may be
In CFP the lower face is weak, the nasolabial fold is shallow, and facial
mobility is decreased. However, the lower face weakness is never as severe
as with a PFP, which suggests that there may be some direct cortical
innervation to the lower face as well as the upper.
There are two variations of CFP: (a) volitional, or voluntary; and (b)
emotional, or mimetic. In most instances of CFP, the facial asymmetry is
present both when the patient is asked to smile or show the teeth, and
during spontaneous facial movements such as smiling and laughing.
However, spontaneous movements and deliberate, willful movements may
show different degrees of weakness (Figure 16.7). When asymmetry is
more apparent with one than the other, the facial weakness is said
to be dissociated. Facial asymmetry more apparent with spontaneous
expression, as when laughing, is called a mimetic, emotive or emotional
facial palsy (EFP), see Figure 16.7C; weakness more marked on voluntary
contraction, when the patient is asked to smile or bare her teeth, is called a
volitional facial palsy (VFP)
Panels A-C. Patient with left thalamic tumor with face at rest (A), on voluntarily baring the teeth
(B), and on reflex smiling (C); there is right facial paresis on smiling but not on voluntary
contraction, an emotional facial palsy. Panels D-F. Patient with a lesion of the corticobulbar
fibers in the genu of the left internal capsule with face at rest (D), on voluntarily baring the teeth
(E), and on reflex smiling (F); there is right facial paresis on voluntary contraction but not on
smiling, a volitional facial palsy.