Idiopathic (Bell's) palsy is a benign weakness of the infratemporal portion of the facial nerve. It is typically a self-limiting process which is not life-threatening. It typically improves in 4-6 months and almost always by 12 (3).
A case study.
Incidence
This is a prevalent condition with an incidence ranging from 8 - 240/100,000 (6). There is no statistical difference between men and women though some studies show the highest incidence to be in 20-35 year olds. Both sides of the face are equally involved. Recurrent symptoms occur is < 10% of patients (4,6) It is bilateral in less than 1%. A positive family history is found in 2-14% (3, 6).
Anatomy
The seventh nerve is the cranial nerve with the longest interosseous course. It innervates the muscles of the face along with a branch (nervus intermedius) to the ear (stapes reflex), one to the salivary glands, lacrimal glands and for taste sensation onanterior 2/3 of the tongue. The facial nerve leaves the pons close to the abducen's (6th) cranial nerve. The facial nerve then enters the temporal bone through the internal auditory meatus. Here it lies in close proximity to the middle ear and as such pathological conditions of the middle ear can cause facial nerve problems. The facial nerve leaves the skull at the stylomastoid foramen and passes into the body of the parotid gland.
The innervation to the facial nerve from the cerebral cortex is both contralateral and ipsilateral on the upper portion of the face and only contralateral on the lower portion of the face. It is important to remember that central lesions only affect the lower half of the face of the contralateral side, while peripheral lesions affect both the upper and lower portions on the ipsilateral side (7).
Etiology
The cause of idiopathic Bell's Palsy is felt to be a sensory ganglionitis of the central nervous system with a secondary muscle palsy. The muscle paralysis is caused by inflammation and autoimmune demyelination instead of ischemic compression (1). The histology has also been well described.
Clinical Presentation
The patient typically presents with sudden onset of either a partial or total paralysis of all of the muscles on one side of the face. The onset of paralysis is often preceded by a viral prodrome.
In addition to weakness several other manifestations are common including:
Facial or Retroauricular Pain
Dysgeusia
Hyperacusis
Decreased Tearing
Important Points in the History
Presentation- was it sudden or slow?
Incomplete or complete?
Any recent accident or blow to the head?
Is there any associated pain or skin lesions?
Any associated symptoms such as hearing loss-acuity, dizziness, tinnitus?
Any problems with eye movement or abnormalities of taste?
Any associated medical problems or is the patient pregnant?
Any known prior medications, previous immunization history?
Does the patient have a history of any malignancies or are they HIV positive?
If the palsy is recurrent is it on the same or the opposite side?
It is important to test the facial nerve by having the patient first lift his eyebrows and then lower them. Mild weakness can be seen when the eyebrows do not lift symmetrically. Ask the patient to close his eye lids tightly. When the weakness is severe the eye does not close completely. Bell's phenomena is seen when this occurs. Ask the patient then to smile or show his teeth.
When paralysis results from an upper rather than a lower motor neuron 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 (7).
Physical findings may also include hypesthesia or dysesthesia of cranial nerves 5, 9 along with the second cervical nerve. Abnormalities in hearing are not seen with Bell's Palsy and should prompt the consideration of other diagnoses.
Causes of Facial Paralysis: Differential Diagnosis (taken from Ohye and Altenberger American Family Physician 1989; 40: 159-66)
Acute
Polyneuritis
Bell's Palsy
Herpes Zoster - Ramsay 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
Acute and Chronic
Cholesteatoma
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
Tumors
Parotid (any cell type)
Metastatic
Breast, lung, kidney, colon, skin
Congenital
Benign Tumors
How does one make the diagnosis?
The diagnosis can be made by a thorough history and clinical examination.
The diagnosis requires the exclusion of those lesions that can mimic Bell's Palsy such as tumor, trauma, infection and stroke.
All branches of the facial nerve should be involved diffusely - upper and lower parts of the face. Otoscopy should be performed to rule out middle ear pathology.
There should be no blebs or skin blisters.
There should be no ipsilateral parotid masses (2).
Though it is not essential, the ENT literature recommends formal audiometry to rule out associated 8 the 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 (6).
Treatment
Eye Care
All clinicians agree that good eye care is essential in these patients. Patients are given eyedrops during the day, ointment at bedtime and a moisture chamber at night. It is important not to scratch the cornea by patching or taping the eye. One easy way to keep the eye moist is by placing a small piece of plastic wrap over the eye and apply it to the face with hairnet tape. Ophthalmology consultation is only needed if the patient reports eye discomfort or if the eye looks irritated despite usual care (2).
The only uniformly recommended treatment for Bell's Palsy is serious eye care. The following therapies are used but remain controversial.
Steroids
Steroids have been used in this disorder for a long period of time. It is important to remember that this condition gets better spontaneously. Careful reviews of the world's literature have failed to definitely validate their usefulness despite widespread use by the ENT community. There is some evidence that steroids may prevent denervation, autonomic synkinesis (crocodile tears) and may prevent the progression of palsy to paralysis and shorten the course of the weakness. For those patients seen within 21 days of the onset of the weakness, a standard prednisone dose is 1 mg/kg/day for 10-14 days followed by a tapering dose (2,8).
Surgery
The need for surgical intervention remains controversial in the ENT literature. Over time there has been a decreasing trend towards surgery reflecting the natural history of this disorder and more stringent criteria in the literature (2). Some of the indications for surgical evaluation include (6):
When paralysis is sudden and complete and when EMG and NCV are dramatically reduced.
When paralysis is slowly progressive.
When no recovery is seen after 6 months ( though some authors say 12.)
When there is a mass in the parotid, or when noted between the mandible and the mastoid.
When progression of other cranial nerve deficits are seen.
When branches of the facial nerve are spared.
When there is a previous history of malignancy.
When there is trauma with support for a traumatic transection (5).
Hughes recommends that surgery be considered when there is persistent paralysis of the face and there is dramatically decreased EMG, NCV's at 3 weeks (2). The use of surgery is condition remains very limited.
Prognosis
The prognosis is typically good with 86% of patients having a complete recovery (6).
Risk factors for incomplete recovery:
Age over 55 years
Hypertension
Complete facial weakness
Pain other than ear pain
Changes in tearing
