Facial nerve palsy BY DR. CHANDRA PRAKASH ARYA (B.Sc. B.D.S.; M.D.S.; P.M.S.; R.N.T.C.P.)

1. DR. CHANDRA PRAKASH ARYA
B.Sc.; B.D.S.; M.D.S.; P.M.S.;
R.N.T.C.P.
District Hospital, Mau

2. • INTRODUCTION
• FACIAL NERVE
• STRUCTURE
• EMBRYOLOGY
• FUNCTIONAL COMPONENTS
• SIGN AND SYMPTOMS
• CAUSES
• FUNCTIONS
• DIAGNOSIS
• CLASSIFICATION
• PROGNOSIS
• TREATMENT

3. INTRODUCTI
ON

4. • Facial nerve paralysis is a common problem that
involves the paralysis of any structures innervated
by the facial nerve. The pathway of the facial nerve is
long and relatively convoluted, and so there are a
number of causes that may result in facial nerve
paralysis. The most common is Bell's palsy, a
disease of unknown cause that may only be
diagnosed by exclusion.

6. FACIAL
NERVE

7. • The facial nerve is the
seventh cranial nerve,
or simply cranial nerve
VII. It emerges from the
brainstem between the
pons and the medulla,
controls the muscles of
facial expression, and
functions in the
conveyance of taste
sensations from the

8. STRUCTURE

9. Nucleus
• The cell bodies for the
facial nerve are grouped in
anatomical areas called
nuclei or ganglia. The cell
bodies for the afferent
nerves are found in the
geniculate ganglion for
taste sensation. The cell
bodies for muscular
efferent nerves are found in
the facial motor nucleus
whereas the cell bodies for
the parasympathetic

10. EMBRYOLOG
Y

11. • The facial nerve is developmentally derived from the
second pharyngeal arch, or branchial arch. The second
arch is called the hyoid arch because it contributes to
the formation of the lesser horn and upper body of the
hyoid bone (the rest of the hyoid is formed by the third
arch). The facial nerve supplies motor and sensory
innervation to the muscles formed by the second
pharyngeal arch, including the muscles of facial
expression, the posterior belly of the digastric,
stylohyoid and stapedius. The motor division of the
facial nerve is derived from the basal plate of the

12. • Although the anterior two
thirds of the tongue are
derived from the first
pharyngeal arch, which
gives rise to cranial nerve
V, not all innervation of the
tongue is supplied by CN V.
The lingual branch of the
mandibular division (V3) of
CN V supplies non-taste
sensation (pressure, heat,
texture) from the anterior
part of the tongue via
general visceral afferent
fibers. Nerve fibers for taste
are supplied by the chorda
tympani branch of cranial

13. FUNCTIONAL
COMPONENTS

14. • The facial nerve carries
axons of type GSA,
general somatic
afferent, to skin of the
posterior ear.
• The facial nerve also
carries axons of type
GVE, general visceral
efferent, which
innervate the
sublingual,
submandibular, and

15. • Axons of type SVE,
special visceral
efferent, innervate
muscles of facial
expression,
stapedius, the
posterior belly of
digastric, and the
stylohyoid.
• The axons of type
SVA, special visceral
afferent, provide taste

16. SIGN AND
SYMPTOMS

17. • Facial nerve paralysis is characterized by unilateral
facial weakness, with other symptoms including loss
of taste, hyperacusis, and decreased salivation and
tear secretion. Other signs may be linked to the
cause of the paralysis, such as vesicles in the ear,
which may occur if the facial palsy is due to shingles.
Symptoms may develop over several hours. Acute
facial pain radiating from the ear may precede the
onset of other symptoms.

18. • Bell’s palsy
While facial paralysis is often alarming, it does not always
mean that you are having a stroke. The most common
diagnosis is in fact Bell’s palsy. Symptoms of Bell’s palsy
can include a combination of:
• facial paralysis on one side (rarely are both sides of
the face affected)
• loss of blinking control on the affected side
• decreased tearing

20. • drooping of the mouth to
the affected side
• altered sense of taste
• slurred speech
• drooling
• pain in or behind the ear
• sound hypersensitivity on
the affected side
• difficulty eating or
drinking

21. • Stroke
People experiencing a stroke often experience the
same symptoms associated with Bell’s palsy. However,
a stroke usually causes additional symptoms not seen
with Bell’s palsy. The following symptoms in addition
to the symptoms of Bell’s palsy could indicate a
stroke:
• changes in level of consciousness
• confusion

22. • dizziness
• loss of
coordination
• seizure
• changes in
vision
• weakness in
arms or legs
on one side of

23. • Often times people experiencing a stroke will still have
the ability to blink and move their foreheads on the
affected side. This is not the case with Bell’s palsy.
• Since it is sometimes hard to distinguish between a
stroke and other causes of facial paralysis, it is a good
idea to get your loved one to a doctor quickly if you
notice facial paralysis.

24. CAUSES

25. Bell's palsy
• Bell's palsy is the most common cause of acute facial
nerve paralysis. There is no known cause of Bell's palsy,
although it has been associated with herpes simplex
infection. Bell's palsy may develop over several days, and
may last several months, in the majority of cases
recovering spontaneously. It is typically diagnosed
clinically, in patients with no risk factors for other causes,
without vesicles in the ear, and with no other neurological
signs. Recovery may be delayed in the elderly, or those
with a complete paralysis. Bell's palsy is often treated

26. • Although the most commonly known cause of facial
paralysis is Bell’s palsy, there are actually many
different causes of facial palsy, and treatment and
prognosis vary greatly depending on the cause.
Some of the main causes of facial palsy are listed
below:
• Viral infections such as Bell’s palsy and Ramsay Hunt
syndrome.
• Surgical causes: for example during removal of acoustic
neuroma or facial nerve tumor, or when operating on the
parotid gland.

27. • Birth trauma: for example caused by forceps or facial
presentation delivery.
• Congenital conditions such as an abnormal development of
the facial nerve or muscle in the womb.
• Rare genetic syndromes such as Mobius syndrome or
CHARGE syndrome.
• Mobius syndrome is a bilateral facial paralysis resulting from
the underdevelopment of the VII cranial nerve (facial nerve),
which is present at birth. The VI cranial nerve, which controls
lateral eye movement, is also affected, so people with Mobius
syndrome cannot form facial expression or move their eyes
from side to side. Mobius syndrome is extremely rare, and its

28. Other causes of facial
paralysis or weakness
include:
• skull fracture or injury to the
face
• head or neck tumor
• middle ear infection or other
ear damage
• Lyme disease, a bacterial
disease transmitted to
humans by a tick bite
• autoimmune diseases such
as multiple sclerosis, which
affects the brain and spinal

29. • Diabetes mellitus
• Facial nerve paralysis, sometimes bilateral, is a
common manifestation of sarcoidosis of the nervous
system, neurosarcoidosis.
• Stroke: although a stroke can cause facial palsy it is
slightly different in that the problems are not caused
by direct damage to the facial nerve. The paralysis in
this case is caused by brain damage and the
messages not being transferred properly to the facial
nerve

30. FUNCTION

31. What functions do the facial
muscles perform?
• Raising the eyebrows
• Closing the eye
• Frowning
• Open mouth smiling
• Closed mouth smiling
• Pouting
• Lifting top lip.
• Pulling lower lip down
• Sticking bottom lip out
• Pulling jaw and corners of
mouth gently down
• Wrinkling nose

32. DIAGNOSIS

33. • A thorough medical history and physical examination,
including a neurological examination, are the first steps
in making a diagnosis. This alone may be sufficient to
diagnose Bell's Palsy, in the absence of other findings.
Additional investigations may be pursued, including
blood tests such as ESR for inflammation, and blood
sugar levels for diabetes. If other specific causes, such
as sarcoidosis or Lyme disease are suspected, specific
tests such as angiotensin converting enzyme levels,
chest x-ray or Lyme titer may be pursued. If there is a

34. • In addition, acute and convalescent serologic tests
for Lyme disease are done if patients have been in a
geographic area where ticks and Lyme disease are
endemic.
• For all patients, a chest x-ray is taken or CT is done
and serum ACE is measured to check for
sarcoidosis. Serum glucose is measured. Viral titers
are not helpful.

35. Clinical evaluation
• Chest x-ray or CT and serum ACE levels to check for
sarcoidosis
• MRI if onset was gradual or other neurologic deficits are
present
• Other testing if indicated by clinical findings
• Facial nerve palsy is diagnosed based on clinical
evaluation. There are no specific diagnostic tests.
• Facial nerve palsy can be distinguished from a central
facial nerve lesion (eg, due to hemispheric stroke or
tumor), which causes weakness primarily of the lower face,
sparing the forehead muscle and allowing patients to

36. CLASSIFICATI
ON

37. • Facial nerve paralysis may be divided into
supranuclear and infranuclear lesions.
Supranuclear and nuclear lesions
• Central facial palsy can be caused by a lacunar
infarct affecting fibers in the internal capsule going
to the nucleus. The facial nucleus itself can be
affected by infarcts of the pontine arteries. These are
corticobulbar fibers travelling in internal capsule.
Infranuclear lesions
• Infranuclear lesions refer to the majority of causes of
facial palsy.

39. PROGNOSIS

40. • In idiopathic facial nerve palsy, the extent of nerve
damage determines outcome. If some function
remains, full recovery typically occurs within several
months. Nerve conduction studies and
electromyography are done to help predict outcome.
The likelihood of complete recovery after total
paralysis is 90% if nerve branches in the face retain
normal excitability to supramaximal electrical
stimulation and is only about 20% if electrical
excitability is absent.

41. • Regrowth of nerve fibers may be misdirected,
innervating lower facial muscles with periocular
fibers and vice versa. The result is contraction of
unexpected muscles during voluntary facial
movements (synkinesia) or crocodile tears during
salivation. Chronic disuse of the facial muscles may
lead to contractures.

42. TREATMENT

43. • Primary neuropathy of facial nerve at the time of injury.
Interpositional graft by using sural or greater auricular
nerve grafts. Cranial nerve crossover, this is most
commonly seen following nerve sacrifice. Regional muscle
transposition using temporalis muscle masseter muscle.
Free muscle transfer like gracilis muscle.
• Protection for the cornea
• Corticosteroids for idiopathic facial nerve palsy
• Corneal drying must be prevented by frequent use of
natural tears, isotonic saline, or methylcellulose drops and
by intermittent use of tape or a patch to help close the eye,
particularly during sleep. Tarsorrhaphy is occasionally

44. • In idiopathic facial nerve palsy, corticosteroids, if
begun within 48 h after onset, result in faster and more
complete recovery. Prednisone 60 to 80 mg po
once/day is given for 1 wk, then decreased gradually
over the 2nd wk.
• Antiviral drugs effective against herpes simplex virus
(eg, valacyclovir 1 g po tid for 7 to 10 days, famciclovir
500 mg po tid for 5 to 10 days, acyclovir 400 mg po 5
times/day for 10 days) have been prescribed, but recent
data suggest that antiviral drugs provide no benefit.

45. THANK YOU