You are on page 1of 36

Bell’s

Palsy
Also known as/

– Idiopathic facial paralysis


b. Peripheral Facial Paralysis
c. Refrigeration Palsy
d. Prosoplegia
Bell’s Palsy
paralysis of cranial
nerve VII (the
facial nerve)
resulting in
inability to
control facial
muscles on the
affected side.
Named after
Scottish anatomist Sir Charles Bell
(1774-1842), who first described the
syndrome along with the anatomy
and function of the facial nerve in
1821.
Anatomy
The facial nerve (seventh cranial
nerve) has 2 components. The larger
portion comprises efferent fibers that
stimulate the muscles of facial
expression. The smaller afferent
portion contains taste fibers to the
anterior two thirds of the tongue,
secretomotor fibers to the lacrimal
and salivary glands, and some pain
fibers.
Definition of bell’s palsy

 Most common acute mononeuropathy (disease


involving only one nerve), and is the most
common cause of acute facial nerve paralysis.

 LMN lesion of CN VII which occurs at or beyond


the stylomastoid foramen is commonly referred
to as a Bell's Palsy.

 Unilateral, peripheral facial paresis or paralysis


that has an abrupt onset and no detectable
cause.

 Facial paralysis of acute onset presumed to be


due to a non-suppurative inflammation of
unknown etiology of the facial nerve within its
canal above the stylomastoid foramen.
incidence

 75% of lesions of facial nerve fall into category of Bell’s


Palsy
 The problem can occur at any age, but rarely affects people
under the age of 15 or over the age of 60.
 Annual incidence of Bell's palsy is 15 to 30 per 100,000
persons.
 Equal numbers of men and women affected. There is no
predilection for either side of the face.
 Bell's palsy has been described in patients of all ages, with
peak incidence noted in the 40s.
 Occurs more commonly in patients with diabetes and in
pregnant women.
 Patients who have had one episode of Bell's palsy have an 8
percent risk of recurrence.1,2
 Each year, about 40,000 Americans develop Bell's palsy
 Between 8 percent and 10 percent will experience a
recurrence of the signs and symptoms, sometimes on the
opposite side of the face.
 And a small number of people never recover and continue to
etiology
It is due to an acute inflammation edema
involving the nerve within its canal. It may be
caused by any of the following:

1) exposure to cold and chill


2) secondary to viral (herpes simplex type1 and
2, herpes zoster) human herpesvirus (HHV);
varicella-zoster virus (VZV);influenza B; adenovirus
; coxsackievirus; Ebstein-Barr virus; hepatitis A, B,
and C viruses; cytomegalovirus (CMV);
3) Rubella infection
4) Diabetes
5) acute respirator tract infection
6) tumor which invade the temporal bone
7) fractures of the temporal bone
etiology
8) lymphocytes- mediated hypersensitivity
phenomenon
9) middle ear infection
10)meningitis
11) hemorrhage
12)infectious dse:
13)middle ear surgery
14) Genetics: A family history of Bell's
palsy has been reported in approximately
4% of cases. Inheritance in such cases may
be autosomal dominant with low
penetration. Which predisposing factors are
Theories regarding the cause
1) hereditary- due to the size of the
diameter of the facial canal
2) vascular ischemic theory
3) viral theory

Pathogenic process
From the course of the illness, it is
presumed that the acute non-suppurative
inflammation of unknown etiology cause
swelling and/ or edema and hyperemia of
the nerve sheath, with compression of the
axons in the narrow facial canal, thus
strangulating them.
Pathophysiology

A popular theory proposes that inflammation


and swelling of the facial nerve results in
compression of the nerve within the temporal
bone.
The facial nerve courses through a portion of the
temporal bone commonly referred to as the
facial canal. The first portion of the facial canal,
the labyrinthine segment, is narrowest;
the meatal foramen in this segment has a
diameter of only about 0.66 mm. Given the
tight confines of the facial canal, it seems
logical that inflammatory, demyelinating,
ischemic, or compressive processes may impair
Pathway
The path of the facial nerve is complex; this
may be the reason the nerve is vulnerable
to injury. Two portions of the facial nerve
leave the brain at the cerebellopontine
angle, traverse the posterior cranial fossa,
dive into the internal acoustic meatus,
pass through the facial canal in the
temporal bone, then angle sharply
backwards, where they pass behind the
middle ear and exit the cranium at the
stylomastoid foramen. From here, the
facial nerve bisects the parotid gland, and
then terminal branches extend from the
parotid plexus to innervate the muscles of
facial expression.
Component
anatomy
Primary cell body Course
Peripheral
termination
• Brachial MotorFacial Nucleus Temporal bone facial
ms of expression
side
Hyoid elevators
• Visceral MotorSuperior salivary d. Glands of nose,
Gland d. Greater palate,lacrimal
superficialpetrosal
b.
to sphenopalatine
Submaxillary,an
ganglion
d sublingual
e. Chorda typani to glands
submaxillary Anterior taste
• Visceral Sensory ganglion
Geniculate buds
Internal Acoustic
• Point’s of ganglion
Comparison Bell’s Palsy Meatus CVA, tumors,vascular
Central facial
• Etiology lesion
Paralysis
• UMNL/LMNL Unknown UMNL
• Types of Lesion
LMNL central, or supernuclear
• Distribution Peripheral or One side or
• Paralysis Nuclear
contralateral
One side,ipsilateral
Upper & lower Lower quadrant
• Nerve Affected
• Skin Condition quadrant
No specific nerve
VII dry
dry
• Marked facial asymmetry

• Atrophy of facial muscles

• Eyebrow droop

• Smoothing out of forehead


and nasolabial folds

• Drooping of the mouth corner

• Uncontrolled tearing

• Loss of efferent limb of


conjunctival reflex (cannot
close eye)

• Lips cannot be held tightly


together or pursed

• Diificulty keeping food in


Onset
Within a day or two after exposure, there
may be slight fever, pain behind the ear,
and pain and stiffness in the neck. The
onset is sudden or acute, and often, the
patient awakens to find the face
paralyzed. A feeling of stiffness and
numbness but sensory testing is normal.
About ½ of the cases attain maximum
paralysis in 48 hours and practically all
cases in 5 days.
Affected patients develop unilateral facial
paralysis over one to three days with
forehead involvement and no other
neurologic abnormalities. Symptoms
typically peak in the first week and then
Signs and symptoms

These depends upon the location of the lesion


 Lesion 1.
Outside the stylomastoid
foramen. As is it a lower motor
neuron lesion, the muscles of the
both lower and upper part of the
ipsilateral face are involved in a
flaccid paralysis forehead cannot be
wrinkled
lesion1
• Widened palpebral fissure is lost to paralysis of the
orbicularis palpebrum
• Upper eyelid closes slowly due to pull of gravity
• Bell’s Phenomenon – eyeball rotates upward and outward
when attempting to close the eye
• Blink or corneal reflex (-) in ipsilateral side
• Oculogyric auricular reflex (drawing back of ear on extreme
lat. Gaze
• Tears are apt to roll doen the cheek
• Obliterated nasolabial fold, unwrinkled brow, angle of the
mouth sags and the side of the face is expressionless
• Mouth is drawn to the opposite side
• Salivamay dribble from the mouth and food gathers
between cheek and gums
• Paralyzed lip may give an assymetric appearance and push
the tongue to the opposite side
• Atrophy is present, although rarely apparent because of
small ms bulk
• Electrical reaction of degeneration appears in 10-14 days,
depends upon the extent of damage
b. Lesion 2

In facial canal involving the chorda tympani


all signs of Lesion 1 is present as well as:

• Loss of taste in the anterior 2/3 of tongue


• Reduced salivation on affected side
c. Lesion 3
Higher than the facial canal involving the
stapedius muscle. + all signs of lesion 1
and 2

• Hyperacusis-pain sensitivity to loud


sounds
– Increased acuity of hearing
d. Lesion 4

Higher involving the geniculate + all signs of


Lesions 1,2&3
*Pain behind the ear
*Herpes of the typanum and concha may precede
the palsy
*Ramsay hunt syndrome

• Herpetic eruptions on the ipsilateral eardrum,


post. Part of auricle, tympanic membrane,
external auditory canal, pinna, or on the soft
palate
• Facial paralysis

e. Lesion 5

in the internal auditory meatus + all


the signs of Leisons 1-4

• Sign’s of Bell’s Palsy


• Deafness (CN8 involvement)
• Tinnitus
• Defective vestibular response
f. Lesion 6

At the immergence of CNVII from pons


Involvement of CNV & CN8
May also invove CNVI,XI,XII

• Marcus-Gunn or jaw winking


phenomenon- seen in the congenital
ptosis,elevation of ptotic eyelid on the
mov’t of jaw to the contaralateral
• Marin Amat Syndrome- closure of the
eye occurs when patient open the
mouth forcefully and maximally
dx
• Electrodiagnostic testing with nerve conduction studies
and electromyography allow for the determination of the
presence or absence of a motor response within 1 week of
onset. A motor response upon stimulation of the facial
nerve is a good prognostic indicator. Electrodiagnostic
testing is also useful later in the course of Bell's palsy to
evaluate aberrant regeneration. In addition, the
preservation of taste perception and submandibular
salivary flow along with the presence of a motor response
on electrodiagnostic testing are all associated with a more
favorable recovery.
• MRI imaging
• CSF analysis
• Submandibular salivary flow rates are typically not
evaluated routinely in patients with Bell's palsy. However, it
has been shown that a flow rate greater than 50% of
normal correlates with complete recovery of facial
function.15
• Titers for Lyme disease and herpesviruses, primarily
varicella-zoster virus and herpes simplex virus type 1
herpes, should be obtained in patients presenting with new-
onset Bell's palsy, particularly when clinical symptoms
• No specific laboratory tests exist to confirm the diagnosis of
Bell's palsy. Clinical setting determines tests that may be of
value. Results of the following laboratory tests may confirm
or suggest other potential causes in the differential
diagnosis:
– Complete blood count
– Erythrocyte sedimentation rate
– Thyroid function studies
– Lyme titer
– Serum glucose level
– Rapid plasma reagin (RPR) or Venereal Disease
Research Laboratory (VDRL) test
– Human immunodeficiency virus (HIV) antibodies
– Cerebral spinal fluid analysis
– Immunoglobulin M (IgM), immunoglobulin G (IgG), and
immunoglobulin A (IgA) titers for CMV; rubella; HSV;
hepatitis A virus; hepatitis B virus; hepatitis C virus; VZV;
M pneumoniae; and Borrelia burgdorferi
prognosis

• Depends on severity of lesion


• Total actual deficit may not be
determined for about 7-10 days
because damaged fibers may
conduct during the process of
degeneration, and undestroyed fibers
may not function temporarily
• Spontaneous recovery may take
place in mild cases
tx
The evidence for many therapies is based on a study
released by the Quality Standards Subcommittee of the American
Academy of Neurology (AAN) in 2001 which established practice
parameters regarding the effectiveness of corticosteroids,
antivirals, and decompression surgery as treatment for Bell's
palsy.16 While the evidence for various therapies is not definitive,
several treatments offer some benefit.
• Prednisone
• The use of oral prednisone in the treatment of Bell's palsy has
been the subject of much debate.
• Acyclovir and prednisone –maximal effect on dx within
3days of onset

• In patients with facial nerve palsy secondary to Lyme disease, a 2-


to 4-week course of amoxicillin or doxycycline should be started.
In some patients with acute onset of Bell's palsy, a reactivation of
herpes viruses, primarily varicella-zoster virus and herpes simplex
virus type 1 may be involved. Antiviral medications can be used in
these patients.
• Eye patching and use of eye drops
These measures, which minimize the risk of corneal irritation
and abrasion, are recommended when the patient cannot fully
close the eye on the affected side.
• Facial retraining
Facial retraining exercises may help to facilitate facial
movement for some patients although this approach is still very
controversial. A recent small study of 24 patients with long-
standing paralysis who received neuromuscular facial retraining
demonstrated improved symmetry in dual-channel
electromyographic readings and increased facial movement.19
• Botulinum toxin
Botulinum toxin (Botox) can be used to treat the crocodile
tears associated with Bell's palsy. Hyperlacrimation can be very
problematic for patients and botulinum toxin may help these
patients. Injections are to the submandibular salivary gland or
periglandular area. The effect lasts 3 to 4 months and may require
reinjection. The most common side effect, which is probably due
to diffusion of the botulinum toxin, is increased weakness of the
eyelid (ptosis).
• Facial nerve decompression surgery
Facial nerve decompression has been evaluated and has
been performed in some patients with prolonged Bell's palsy.
Patients in whom less aggressive treatments have failed and have
not recovered satisfactory function may choose to have this
surgical procedure. However, there are no evidence-based
recommendations for its use.16 Permanent unilateral
PT management
• IR
• ES
• Facial massage
• Facial excercise
• Taping
Good prognosis
• Recovery of taste in 1st week
• Incomplete paralysis in the 1st 5-7
days
• EMG shows there are motor units
voluntary control in CNVII w/in few
days after onset
• Return to voluntary motor power at
the end of 3 weeks from onset
Poor prognosis

1. Age > than 60


2. Hypertension
3. DM
4. Hyperacusis
5. Diminished lacrimation
6. Complete paralysis
7. No motor detectable by needle electrode
exploration of facial musculature
8. Inexcitable CNVII,spontaneous fibrillation w/in 2-
3 weeks (+) wallerian degeneration
9. Evidence of denervation after 10 days