Bell’s Palsy

AKA:

- Peripheral Facial Palsy

- Idiopathic Facial Palsy
- Idiopathic Facial Nerve Palsy
- Acute peripheral Nerve Palsy
- Acute Peripheral Facial Palsy
- Facial Nerve Compression Palsy

NEUROANATOMICAL CONSIDERATION

Facial Nerve (CN VII)

- The seventh cranial nerve supplies all the muscles concerned with
facial expression
- The sensory component is small (the nervus intermedius); it conveys
taste sensation from the anterior 2/3 of the tongue and probably
cutaneous impulses from the anterior wall of the external auditory
canal.
- The motor nucleus of the seventh nerve lies anterior and lateral to
the abducens nucleus.
- After leaving the pons, the seventh nerve enters the internal
auditory meatus with the acoustic nerve.
- The nerve continues its course in its own bony channel, the facial
canal, and exits from the skull via the stylomastoid foramen.
- It then passes through the parotid gland and subdivides to supply
the facial muscles.

Clinical Notes

1. Complete Interruption of Facial Nerve at the Stylomastoid Foramen

- All Facial muscles of expression are paralyzed
- The corner of the mouth droops, the creases and skinfolds are effaced
- The forehead is unfurrowed, and the eyelids will not close.
- Upon attempted closure of the lids, the eye on the paralyzed side rolls upward (Bell’s phenomenon)
- The lower lid sags and falls away from the conjunctiva, permitting tears to spill over the cheek. Food
collects between the teeth and lips, and saliva may dribble from the corner of the mouth.
- The patient complains of a heaviness or numbness in the face, but sensory loss is rarely demonstrable
and taste is intact
2. If the Lesion is in the middle-ear portion
- taste is lost over the anterior two-thirds of the tongue on the same side.
- If the nerve to the stapedius is interrupted, there is hyperacusis (sensitivity to loud sounds).
- Lesions in the internal auditory meatus may affect the adjacent auditory and vestibular nerves, causing
deafness, tinnitus, or dizziness.
- Intrapontine lesions that paralyze the face usually affect the abducens nucleus as well, and often the
corticospinal and sensory tracts.
3. If the Facial Palsy has existed before for some time and Incomplete Recovery of Function
- (+) Diffused contraction of facial muscles
- (+) Narrowing of palpebral fissure
- (+) Deepening of nasolabial fold
- Attempts to move one group of facial muscles may result in contraction of all (associated movements,
or synkinesis).
 - Facial spasms, initiated by movements of the face, may develop (hemifacial spasm).
- Anomalous regeneration of seventh nerve fibers may result in other troublesome phenomena.
- If fibers originally connected with the orbicularis oculi come to innervate the orbicularis oris, closure of
the lids may cause a retraction of the mouth, or if fibers originally connected with muscles of the face
later innervate the lacrimal gland, anomalous tearing (“crocodile tears”) may occur with any activity of
the facial muscles, such as eating.
- Another facial synkinesia is triggered by jaw opening, causing closure of the eyelids on the side of the
facial palsy (jaw-winking

Epidemiology & Demographics

- Incidence: 20-30 cases per 100,000 people worldwide

- Peak Incidence: Patient less than 70 y/o and pregnant females, especially during the 3rd trimester and
1st post-partum week
- Predominant Sex: Both Gender are affected
- Predominant Age: The median age is 40 y/o
- Risk Factors
a. Diabetes Mellitus
b. Pregnancy
- Increases the incidence of Bell’s Palsy to 45 per 100,000 people worldwide
c. Herpes Simplex Virus (HSV Type 1

Etiology

- Most cases of Bell palsy are thought to be secondary to either a viral inflammatory or immune injury.
Herpes simplex virus is thought to be the most common viral pathogen followed by herpes zoster.
- Other infectious causes include Epstein-Barr virus, cytomegalovirus, adenovirus, rubella, and mumps
- Bell’s palsy is a diagnosis of exclusion. However, the literature reports several possible causes of paralysis
of cranial nerve VII. These include but are not limited to an adverse event of immunization, reactivation
of herpes simplex virus type I, and upper respiratory tract infection.
- A virus-associated immune-mediated mechanism begins when a virus penetrates a cell of the
geniculate ganglion in the host organism.
- After penetration, the virus parasitizes the host cell’s replication proteins, producing a large number of
progeny.
- The immune system mounts an inflammatory reaction as the host cells are destroyed by viral replication.
Inflammation of the facial nerve alone can account for the symptoms of Bell’s palsy.
- These symptoms can be further exacerbated if the swollen facial nerve becomes entrapped in the
mental foramen and the labyrinthine segment of the temporal bone. In addition to immediate
replication, a virus can enter a latent state so it is present but inactive in the host cell.
- The virus can be activated at a later date following trauma or other stressful events

Mechanism of Injury

- Injury might be instigated by viral infection inducing the inflammatory process, resulting in facial nerve
demyelination/denervation.
- The reactivation of herpes simplex virus type I is thought to be the cause of most cases of Bell’s palsy
Pathophysiology
Clinical Signs & Symptoms

- Before onset of facial paralysis, patients often experience pain in or around the ear near the mastoid
process, cervical pain, and facial numbness with no sensory loss
- Within 24 hours of these symptoms, the following occur with varying extent, depending on the degree of
facial nerve involvement and lesion location:
✓ Progressive loss of motor control on one side of the face over 1 to 10 days
✓ Loss of facial asymmetry at rest and with facial expressions
✓ Nasal alar collapse, nasolabial flattening
✓ Loss of taste on the anterior 2/3 of the tongue
✓ Slowed or absent blink reflex
✓ Hyperacusis
✓ Excessive or reduced salivation
✓ Excessive or reduce tearing
✓ Facial muscle synkinesis
✓ Facial spasms
- There can be referred pain around the ear & neck

Physical Examination

- Asymmetrical resting facial posture

- No or diminished voluntary facial movement with eyebrow raise, eye closure, smile, snarl, pucker, and
frown
- Nasal, muffled speech
- Abnormal movement patterns (synkinesis)

Laboratory Evaluation

- Laboratory tests are not typically recommended. However, if the diagnosis of Bell palsy is in question
(e.g., bilateral facial nerve palsy, concern for a secondary etiology), then it is reasonable to pursue the
following tests:
✓ Lyme antibody followed by Western blot for positive cases for confirmation. Consider lumbar
puncture for CSF analysis for Lyme serologies
✓ ACE Level
✓ Glycosylated hemoglobin (HgA1C)
✓ HIV
✓ RPR and VDRL in CSF
✓ ESR

Imaging Studies

Imaging are not typically needed in this case

- Brain MRI is indicated in certain cases, such as an upper motor neuron pattern (able to wrinkle
forehead) where the temporalis branch of the facial nerve is spared
- Brain MRI with gadolinium is indicated either when other cranial nerve palsies are present or when a
meningeal process is suspected.
- CT temporal bone is indicated in cases of either trauma or complete facial paralysis in which the
surgeon is considering decompression
 - According to Harrison’s Internal Medicine 19th Edition, Magnetic resonance imaging (MRI) may reveal
swelling and uniform enhancement of the geniculate ganglion and facial nerve and, in some cases,
entrapment of the swollen nerve in the temporal bone.

Electrodiagnostic Studies

- Electrodiagnostic testing may be performed 2 wk after the onset of symptoms to assess the integrity of a
motor unit and the degree of nerve damage.
- Facial motor response remains normal for the first 3 days following an injury and then rapidly decreases
depending on the severity of the lesion.
- A facial motor study may be performed at 10 days and compared to the contralateral side.
- A motor response that is 10% the amplitude of the unaffected side on electrodiagnostic testing
corresponds with 90% motor axon degeneration.
- One study found that patient recovery was poor when this critical value was reached.
1. Electroneurography
- To determine presence/absence of compound muscle action potentials (CMAP). CMAPs are the
summed electrical activity of a population of muscle fibers.
- Absence of a CMAP, or a decrement relative to the unaffected side, are indicative of denervation
2. EMG
- Surface or needle electromyography (EMG) to record facial muscle activity
3. Nerve Conduction Velocity Test (NCV)
- To determine excitability of the facial nerve

Physical Therapy Assessment

1. Cranial Nerve Assessment for Facial Nerve

a. Sensory Part
- Taste may be tested by using sugar, tartaric acid or sodium
chloride. A small quantity of each substance is placed anteriorly
on the appropriate side of the protruded tongue.
b. Motor Part
- Observe patient as he talks and smiles, watching for:
✓ Eye closure
✓ Asymmetrical elevation of one corner of the mouth
✓ Flattening of nasolabial fold
- Patient is then instructed to
✓ Wrinkle forehead (frontalis)
✓ Close eyes with examiner attempts to open them (orbicularis
oculi)
✓ Purse lips while examiner presses cheeks (buccinator)
✓ Show teeth (orbicularis oris)
✓ Smile (Zygomaticus major)
Differential Diagnosis

1. Cortical Stroke
- forehead and periorbital muscles are spared in stroke patients because of bilateral innervation of the
upper face
2. Brainstem Stroke
- ipsilateral weakness in the upper and lower muscles of facial expression due to a stroke affecting the
nucleus or fascicle of the seventh nerve
3. Lyme Disease
- facial nerve palsy is the most common cranial neuropathy associated with Lyme disease. In Lyme
meningitis, facial nerve palsy may be unilateral or bilateral.
4. HIV
5. Ramsay Hunt Syndrome
- facial nerve paralysis associated with ipsilateral zoster oticus
6. Parotid Gland Tumors
7. Trauma/Temporal Bone Fracture
8. Meningeal Processes
a. Infectious
- Lyme disease, HIV, syphilis, leprosy, tuberculosis meningitis, fungal meningitis
b. Inflammation
- Sarcoidosis, Sjögren syndrome, and Guillain-Barré syndrome and its variants
c. Leptomeningeal carcinomatosis or lymphomatosis:
- breast cancer, lung cancer, and lymphoma are most common

Medical Outline Treatment for Bell’s Palsy

PT Management

(1) Protect cornea (artificial tears or temporary patching) until recovery allows for eyelid closure.

(2) Electrical stimulation to maintain tone, support function of facial muscles.

(3) Provide active facial muscle exercises.

(4) May require face sling to prevent overstretching of facial muscles.

(5) Provide functional retraining: foods that can be easily eaten, chewing with opposite side.

(6) Provide emotional support and reassurance.

Prognosis

- Complete recovery is experienced by 68% to 70% of patients; 13% to 27% of patients have nearly
complete recovery, experiencing minimal weakness with volitional movement and slight asymmetry
with eye closure and moving the corner of the mouth; and 5% to 16% of patients experience partial
recovery with incomplete activation of the forehead muscles, difficulty closing eye with maximal effort,
obvious asymmetry with movement of the corners of the mouth, synkinesis, contractures, and/or
hemifacial spasm.
- Within 3 weeks, 70% of patients begin recovering volitional control of facial muscles; 85% of these
patients have spontaneous complete recovery within 3 weeks; and the remaining 15% of patients
experience complete recovery within 3 to 5 months. For patients that do not recover within 3 to 5
months, their symptoms can linger for >1 year and complete recovery is improbable.
- Age may influence extent of recovery: 90% of patients <14 years old recover completely, 84% of
patients 15 to 19 years old recover completely, 75% of patients 30 to 44 years old recover completely,
and 33% of patients >60 years old recover completely.
- Pregnancy appears to reduce the likelihood of complete recovery because 52% of pregnant patients
experience complete recovery.
- A slow or absent blink reflex is associated with poor prognosis