BELL’S PALSY I. DEFINITION

Bell’s palsy is a form of facial paralysis of acute onset with an unknown etiology. It is presume to be due to a non-suppurative inflammation of the facial nerve inside its canal above the stylomastoid foramen. It was named after Sir Charles Bell who stated that the facial nerve is the mother of the face.

Bell’s palsy occurs when a nerve transmits faulty signals to muscles in the face. It happens with little or no warning symptoms may even suggest of stroke.

The functional components of the facial and intermediate nerve include: 1.) Special visceral efferent (SVE, branchiomotor) fibers, 2.) General visceral efferent (GVE, parasympathetic) fibers, 3.) Special visceral efferent (SVE, taste) and 4.) A few general somatic efferent (GSA, sensory) fibers. Special visceral efferent fibers of the motor component innervate the muscles of facial expression, the platysma, the buccinator and the stapedius muscles. Synapses with the postganglionic neurons occur in the pterygopalatine and submandibular ganglia. Postganglionic fibers from the pterygopalatine ganglion give rise to secretory and vasomotor fibers that innervate the lacrimal gland and the mucous membrane of the nose and mouth.

II. EPIDEMIOLOGY

Lifetime Prevalence: 6.4 per 100 Incidence: Increases with age Overall: 0.5 per year per 1000 Age 20: 0.1 per year per 1000 Age 80: 0.6 per year per 1000 Season: Occurs at all times of the year Equal prevalence between males and females Recurrence: 7% Side affected: Right side in 63%

III. ETIOLOGY

The exact cause of Bell’s Palsy is unknown. It commonly happens after:

Trauma to the facial nerve or

Pressure upon the facial nerve due to a tumor. It also has been associated with:

A viral infection, like viral meningitis

Flue-like illness

Headaches and colds

Chronic middle ear infection

High blood pressure and diabetes

Temporal bone fractures

Hemorrhages

Infectious diseases Three categories regarding the cause

Hereditary – due to the diameter of the axons

Vascular ischemic theory – exposure to cold

Viral theory IV. PATHOGENESIS

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

Within a day or two from exposure, there might be a slight fever and pain and stiffness in the neck region. The onset is sudden and acute. The patient often finds the face paralyzed upon waking in the morning. He may notice that the mouth is drawn to one side. The onset is accompanied by a dull ache behind the ear, mastoid region, around the angle of the jaw and spreading into the face. A few hours after, the patient may describe the weakness as being woody, stiff or

56

numb on one side of the face, but sensory testing is always normal. The mouth is dry and excessive tearing (crocodile tears) is usually present during the first few days of the palsy. Impairment is always present to some degree in almost all patients, but rarely beyond the second week of paralysis. About one-half of the cases attain maximum paralysis in 2 days and practically all cases, within 5 days.

V. CLINICAL MANIFESTATIONS

Signs and symptoms depend upon the location of the lesions: A. Lesion 1: outside the stylomastoid foramen. Since it is a LMN, the muscles of

both the upper and lower parts of the ipsilateral face are flaccid. – The forehead cannot be wrinkled – The upper eyelids closes slowly because of the pull of gravity – When an attempt to shut the eye is made, closure is incomplete and the

eyeball rolls up and outward (Bell’s Phenomenon) – Blinking or corneal reflex is lost on the affected side – Rolling of tears down the cheek – Saliva may dribble from the mouth – Due to paralysis of the Orbicularis Palpebrum, the palpebral fissure is

widened – The nasolabial fold is obliterated, the brow is wrinkled, the angle of the

mouth sags and the affected side is expressionless – The mouth is drawn to the actively contracting muscles on the opposite

side of the face B. Lesion 2: Facial canal (involving chorda tympani). All the signs of Lesion 1 are

present with the addition of the following: – Loss of tastes in the anterior two thirds of the tongue. This is because the

Chorda Tympani, a peripheral sensory fiber of the facial nerve, carries taste impressions form the anterior two thirds of the tongue.

– Reduced salivation on the activated side. This is because of the preganglionic parasympathetic secreto-motor innervation of the submaxillary and the sublingual glands enter the Chorda Tympani before finally ending in the submaxillary ganglion.

C. Lesion 3: Higher than the facial canal and involving the stapedius muscle. All the signs of Lesion 1 are present in addition with the following: – Hyperacusis – painful sensitivity to loud sound

D. Lesion 4: Involving the Geniculate Ganglion – Acute with pain behind and within the ear – Ramsey-hunt Syndrome associated with Herpes Zoster of the geniculate

ganglion E. Lesion 5: In internal auditory meatus

Since the internal auditory meatus transmits the acoustic nerve and the motor and sensory roots of the facial nerve, therefore, lesions at the site would naturally present with:

– Signs of Bell’s Palsy – Deafness from CN 8 involvement – Tinnitus or ringing in one or both ear – Defective vestibular responses

F. Lesion 6: At the emergence of the facial nerve from the pons (meningitis) this presents with Bell’s palsy with involvement of the CN V, VI and VIII probably because the nuclei of these nerves are located in the pons.

MARCUS-GUNN or JAW WINKING PHENOMENON – seen in congenital ptosis, is the elevation of the optic eyelid on movement of the jaw to the contralateral side.

MARIN-AMAT SYNDROME – observed after peripheral facial paralysis, is referred to as an inverted Marcus-Gunn phenomenon. Closing of the eyes occurs when the patient opens the mouth forcefully or maximally.

57

VI. COMPLICATIONS The most serious complication that may happen with Bell’s palsy is the inability to

close the eyelids, exposing the eye to irritation and drying. Complications that may appear after apparent recovery.

A. Crocodile tears – there is lacrimation while chewing – The eye tears on the side of paralysis while taking strongly flavored food

into the mouth because of the saliva secretory fibers to the lacrimal nerve to innervate the lacrimal gland

– When marked contractures develops, the nasolabial furrow becomes deeper on the paralyzed side

B. Facial spasms – develops and persists indefinitely and initiated by facial movements – Usually begins in the orbicularis oculi muscles and gradually spread to

other muscles on that side of the face C. Associated movement synkinesis – attempts to move one group of facial

muscles results in contraction of all of them D. Nasal obstruction which could cause difficulty breathing through

VII. DIAGNOSIS

Criteria for diagnosis: A. Sudden onset of complete or partial paralysis of the muscles supplied by the

seventh cranial nerve B. Absence of other signs CNS diseases C. Absence of diseases of the middle ear or posterior fossa D. Absence of Herpes Zoster

The 4 electrodiagnostic test in the assessment of Bell’s Palsy are: A. Measurement of nerve excitability, this is done in the first 10 days following

onset of the lesion. B. Measurement of the NCV, this is done in the first 10 days following onset of

lesion also. C. The SDC, this is the graph of the excitability of the nerve, muscle or both; this

is done 10-14 days after onset when the motor endplate excitability is lost if the lesion is marked.

D. EMG, this will detect action potentials elicited by nerve stimulation when the muscle contraction is too weak to be observed by the unaided eye, with denervation, fibrillation potentials will appear.

Though it is not essential, some literature recommends formal audiometry to rule out associated nerve involvement and to evaluate the stapes reflex. Studies have demonstrated that if the paralysis is incomplete and the stapedial reflex is intact that full recovery is commonly seen in 3-6 weeks.

VIII. DIFFERENTIAL DIAGNOSIS

COMPARISON BELL’S PALSY AND FACIAL PARALYSIS POINTS OF COMPARISON BELL’SPALSY FACIAL PARALYSIS

1. Etiology Unknown CVA, tumors, vascular lesion

2. UMNL/LMNL LMNL UMNL

3. Type of lesion Peripheral or nuclear Central or supranuclear

4. Distribution ½ of the face, ipsilateral Lower ¼ of the face, contra.

5. Muscle tone Flaccid Spastic

6. Nerve affected Facial nerve No specific nerve (affect all)

7. Skin condition Dry Dry

It is important to test the facial nerve by having the patient first lift his/her eyebrows and then lower them. Mild weakness can be seen when the eyebrows do not lift symmetrically. Ask the patient to close his/her eyelids tightly. When the weakness is severe the eyelids do not close completely. Bell’s phenomena is seen when this occurs. Ask the patient to then smile or show his/her teeth.

When paralysis results from an upper rather than a lower motor lesion, involuntary contraction of the muscles of facial expression can occur in response to an emotional stimulus (but not for voluntary facial movement.) It is unclear what the anatomic pathways are for involuntary facial movement.

58

Physical findings may also include hyperesthesia or dysesthesia of cranial nerve 5 & 9 along with the 2nd cervical nerve. Abnormalities in hearing are not seen with Bell’s Palsy and should prompt the consideration of other diagnoses.

Acute facial muscle weakness: – Polyneuritis – Bell’s Palsy – 75% of cases – Herpes Zoster – Ramsey Hunt syndrome – Guillain-Barre syndrome – Myasthenia gravis – Idiopathic autoimmune disease – Trauma – Skull fracture or concussion – basilar or facial – Surgery – Penetrating facial injury – Birth trauma – Infectious – Otitis media – bacterial – Cholerteatoma – Lyme disease – Mumps – Tuberculosis – HIV related – Sarcoidosis – Cerebrovascular accidents – Neurologic disorders – Toxic – Thalidomide – INH – Melkersson-Rosenthal syndrome (recurrent alternating facial palsy,

furrowed tongue, faciolabial edema). Progressive or Chronic facial muscle weakness

– Tumors – Paratoid (any cell type) – Metastatic – Benign tumors

IX. PROGNOSIS

The amount of paralysis varies in each case, depending on the severity of the lesion. The total actual deficit may be determined for about 7 to 10 days because damage nerve fibers may conduct in the process of degeneration, swollen but undestroyed fibers temporarily may not function.

Spontaneous recovery may take places in mild cases within a few days at 85% of untreated patients who improve, the initial change appears within 3 weeks. The other 15% show signs of improvement within 3-6 months.

Some authors claim that more than a5 months, while some claim that most patients recover within a few weeks or in a month or two.

Overall, 90% of patients are expected to recover from Bell’s palsy. However, for some patients, the symptoms may last longer. In a few cases, the symptoms may never completely disappear.

Good prognostic signs: – Incomplete paralysis in the first 5 to 7 days – Return of the voluntary power of the face at the end of 3 weeks from

onset – Slow progression – Younger age – Recovery of taste occurs in the first week – Electrodiagnostic tests normal

59

– If within a few days after onset electromyography shows that there is motor voluntary control in the facial muscles and facial nerve conduction remains normal or slightly slowed, recovery is likely to be rapid and complete.

Factors associated with poorer prognosis: – Age greater than 60 years old – Hypertension – Diabetes Mellitus – Hyperacusis – Diminished lacrimation – If the lesion of paralysis is complete – If no motor units can be detected by needle electrode exploration of the

facial musculature – If within a few days, the facial nerve is totally unexcitable. Spontaneous

fibrillation potentials recorded from the muscles within 2 to 3 weeks indicate that at least has undergone Wallerian degeneration

– Evidence of denervation after 10 days indicates a long delay in recovery and sometimes is incomplete

– Complete facial weakness – Pain other than ear pain – Changes in tearing

Usual Order of Recovery 1) Buccinator 2) Zygomatic muscles 3) Inferior levator 4) Orbicularis oculi 5) Frontalis

X. MEDICAL AND SURGICAL MANAGEMENT

Medical management – Eye patch or sunglasses are used to protect the eye and prevent

scratching of the cornea form dust and fingers. – Artificial tears are used in the daytime – Moisture chamber is used at nighttime – Bland ointment is applied during bedtime – A plastic wrap over the eye, fixated with a hairnet tape is used to keep the

eye moist – Consult an ophthalmologist if the patient complains of eye discomfort or if

the eye looks irritated even with usual care. Pharmacological management

– Oral steroids are used to reduce the inflammation and swelling of the facial nerve

– Analgesics are taken to relieve pain – Antiviral agents (acyclovir, famiclovir) may also be used to limit or reduce

damage to the nerve from possible viral causes. – Prednisone to the eye is used to prevent denervation, autonomic

synkinesia and progression of the palsy to paralysis and shortens the course of the weakness. A standard prednisone dose of 1 mg/kg/day for 10-14 days is used for patients seen within 21 days after the onset. It is followed by a tapering dose.

Surgical management – Surgery is rare in Bell’s palsy but may be used in long-standing cases for

aesthetic purposes. The eyelids may be stitched together for protection. – Surgery is indicated if:

o Paralysis is slowly progressing o No recovery after 6 months o If there is a mass in the parotid or between the mandible and the

mastoid.

60

o There are progressions of other cranial deficits. o Branches of the facial nerve is spared o There is previous history of malignancy o There is trauma with support for a traumatic resection

XI. PHYSICAL THERAPY ASSESSMENT Talk with the patient. Observe facial movements bilaterally. A total facial

weakness suggests a nuclear nerve lesion while partial paralysis suggests a supracondylar lesion.

Observe patient’s face at rest. This test will help differentiate a supracondylar from nuclear involvement with the same principle as No. 1

Let the patient close the eyes and lips and then forcefully open them. The amount of mouth and eyeball movement or opening visible is tested with resistance.

Let the patient show teeth or grimace voluntarily. A positive test would mean impaired mouth movements.

Let the patient whistle or blow. Patient may exhibit difficulty in holding in air. Tapping the cheek makes this test harder.

Taste test. Apply sugarcoated gauze to the anterior parts of the tongue and on the sides id difficulty is present. This will assess the sweet taste sensations bilaterally.

Test the frontalis muscle. Upon looking up, the eyebrows elevate and the forehead frowns.

Test for hyperacusis. Patient will usually cover the involved ear in the presence of a loud stimulus.

Electrical tests are conducted. XII. PHYSICAL THERAPY MANAGEMENT

During the acute and subacute stage. – Splinting for the paralyzed muscle to relieve the strain and preserve tone

for cosmesis. – Facial massage for 5 minutes twice a day in a chin-to-forehead direction to

maintain the tone. – Use eye patches, goggle or sunglasses to protect cornea from damage

and irritation. – IR to increase the blood supply and decrease skin resistance before ES

application. – ES application to the nerve and muscle. – HMP to hasten recovery and for relief of pain.

During paralysis – US over the nerve trunk, in front of the tragus of the ear to reduce

inflammation. – Massage is taught to the patient. The motion is upward and outward

applied to the paralyzed muscle to maintain skin suppleness, muscle elasticity and maintenance of blood and lymphatic flow.

– Patient education and advice. Patient should lie down at intervals to reduce the effects of gravity upon the paralyzed muscle. The eye should be blinked regularly because the blink reflex is lost.

Recovery stage – Mild IR to improve function and warmth to the muscle. – PNF for reeducation – Quick stretch technique to regain raising of eyebrows and corners of the

mouth. – Brushing, tapping or stroking along the length of the muscle. – Exercises for the muscles of the face performed in supine first then

progresses to sitting. Practiced for twice a day.