BELL’S PALSY PATHOPHYSIOLOGY

The pathophysiology of Bell's Palsy is not entirely clear, but is most likely related
to compression of the facial nerve due to demyelination, inflammation, or ischemia
(inadequate blood supply).

The facial nerve that is damaged is called the seventh cranial nerve (CN VII).
This nerve primarily moves the facial muscles, controls the salivary and tears glands,
and enables the front part of the tongue to detect tastes. The paired seventh cranial
nerve is located in the Fallopian canal in the skull, inferior to the ear and is connected to
the muscles on the face bilaterally. As well as controlling facial muscles and some
glands, it is also responsible for letting one open and close their eyes.
Predisposing
factors
Age: risk increases with age
(56 y/o) equal in men and
Gender:
women.

Race: higher if in Japanese

descent.
Genetics: approximately 4 %
of cases.

It is thought that viral infections or damage to the myelin sheath of the seventh
cranial nerve can bring on the disorder. Viral infections may lead to inflammation, which
in turn places pressure on the Fallopian canal leading to an infarction. Damage to the
myelin sheath of the nerve can cause the disruption or slowing of signals from the brain
to the facial muscles. It is also believed that the disorder can be brought on by patients
with Lyme disease, diabetes, high blood pressure, tumors, HIV, chickenpox, or even
trauma to the face or skull near the nerve.

Bell’s Palsy, but those primarily susceptible include pregnant women and those
with diabetes or upper respiratory ailments such as the cold or flu. Anecdotally,
exposure to cold is a frequently cited cause – for example, driving with a car window
open in frigid weather, or sleeping with the window open on a chilly night. Also, young
and middle aged adults are more likely to be affected. It is quite uncommon to see a
case in an individual ten or younger and sixty or older.

Short Description of Pathologic Process

From the course of the illness, it is presumed that the acute non-supportive
inflammation of unknown etiology causes swelling and/ or edema and hyperemia of
the nerve sheath, with compression of the axons in the narrow facial canal, thus
strangulating them and inhibits appropriate neural stimulation.

Pathophysiological Process

1. Inflammation - facial nerve becomes inflamed in reaction to the infection.

• (Rubor (redness), Calor (heat), Dolor (pain), Tumor

(swelling) and Function laesa (loss of function)
• Inflammatory reaction may hinder or block nerve
conductions.
• Usually at the internal auditory meatus,
 2. Compression - facial nerve is compressed against the skull’s hard bony surface
(because it passes through a narrow, bony canal called the Fallopian canal)

• 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
the narrowest; the meatal foramen in this segment has a diameter
of only about 0.66 mm.
• This is the only segment of the facial nerve that lacks anastomosing
arterial cascades, making the area vulnerable to embolic
phenomena, low-flow states, or vascular compression.
• Given the tight confines of the facial canal, it seems logical that
inflammatory, demyelinating, ischemic, or compressive processes
may impair the function of the facial nerve.

3. Infarction - the death of nerve cells due to insufficient blood oxygen and supply

• In some mild cases, there is damage only to the myelin sheath.

4. Interruption - damage to the myelin sheath of the nerve can cause the
disruption or slowing of signals or messages from the brain to the facial muscles.

• The block inhibits appropriate neural stimulation to the muscle by

the motor fibers of the facial nerve.
• As a result of its convoluted path through the temporal bone which is
only slightly larger in diameter than itself, the 10,000 neurons that
exist in the facial nerve are prone to impairment due to vascular
congestion with secondary ischemia.

5. Facial weakness or paralysis

• Damage to one of two facial nerves can possibly result in temporary

paralysis of the facial muscles, most often to only one side of the
face and in rare cases, both sides.

Onset and Symptoms

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.

Motor Sensory Parasympathetic

• movement of facial
expression muscles
except jaw,
• close eyes,
• labial speech sounds.
• taste- anterior two third of • secretion of saliva and
tongue tears.
• sensation to Pharynx
Motor

• The classic presentation of Bell's palsy is weakness on one side of the face. The
potential range of weakness is wide – it may range from difficulty blinking all the
way to a complete paralysis on one side of the face with an inability to close the
eye. Onset usually occurs acutely, but the weakness may worsen for 24 to 48
hours before stabilizing.
• Poor eyelid closure
• Brow droop
• Paralytic ectropion of the lower lid
• Mild, generalized mass contracture of the facial muscles, rendering the affected
palpebral fissure narrower than the opposite one (after several months)
• Aberrant regeneration of the facial nerve with motor synkinesis
 Reversed jaw winking (ie, contracture of the facial muscles with
twitching of the corner of the mouth or dimpling of the chin
occurring simultaneously with each blink)
 Autonomic synkinesis (ie, crocodile tears-tearing with chewing)

Sensory

• Alteration of taste (57%) or hearing is occasionally a symptom.

• People with Bell's palsy may describe the sensation of unilateral loss of facial
movement as deadness, loss of feeling, or numbness, although the affected part
of the face is neither asleep nor tingling.
• Aching of the ear or mastoid (60%)

Parasympathetic

• Decreased tear output/poor tear distribution

• Excessive tearing
• Hypersalivation

Medical Management

The objectives of management are to maintain facial muscle tone and to prevent or
minimize denervation. Steroidal therapy may be initiated to reduce inflammation and
edema, which reduces vascular compression and permits restoration of blood
circulation to the nerve. Early administration of corticosteroids appears to diminish
severity, relieve pain, and minimize denervation. Facial pain is controlled with analgesic
agents or heat applied to the involved side of the face. Additional modalities may
include electrical stimulation applied to the face to prevent muscle atrophy, or surgical
exploration of the facial nerve. Surgery may be performed if a tumor is suspected, for
surgical decompression of the facial nerve, and for surgical rehabilitation of a paralyzed
face.

• Analgesics- to relieve pain

• Steroids- to reduce facial nerve edema & improve edema & improve nerve
conduction & blood flow
• Possible electrotherapy
• Surgery for persistent paralysis
Nursing Considerations
• Watch for adverse effects of steroids use
• Apply moist heat to the affected side of the face-to reduce pain
• Help the pt maintain muscle tone:
• massaging the face with a gentle upward motion 2-3xdaily x 5-10mins
• exercise by grimacing in front of a mirror
• Protect eyes, have pt cover eye w/ an eye patch
• Prevent excessive wt loss:
• have him chew on unaffected side of his mouth
• provide a soft, nutritionally balanced diet, eliminating hot foods & fluids
• apply a facial sling to improve lip alignment
• Provide frequent & complete mouth care
• Offer psychological support

Gatera, Jad Paulo C.