Online newspaper of professor Yasser Metwally

The author: Professor Yasser Metwally

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INTRODUCTION

Background: Facial paralysis is a disfiguring disorder that has a great impact on the patient. Facial nerve paralysis may be congenital, neoplastic, or result from infection, trauma, toxic, or iatrogenic causes. The most common cause of unilateral facial paralysis is Bell palsy, also known as idiopathic facial paralysis. Bell palsy is thought to account for approximately 60-75% of acute unilateral facial paralysis.

In 1550, Fallopius noted the narrow lumen in the temporal bone through which a part of the seventh cranial nerve passes. In 1828, Charles Bell made the distinction between the fifth and seventh cranial nerves, he noted that the seventh nerve was mainly involved in the motor function of the face and the fifth nerve was mainly concerned with the sensory perception of the face.

Even today, controversy still surrounds the etiology and treatment of Bell palsy. Clinical features of Bell palsy that may help distinguish this from other causes of facial paralysis include sudden onset of unilateral facial paralysis (less than 48 hours), absence of signs and symptoms of CNS disease, and absence of signs and symptoms of ear or posterior fossa disease.

Pathophysiology: The course of the facial nerve is tortuous, both centrally and peripherally.

The facial nerve nucleus lies within the reticular formation of the pons, adjacent to the fourth ventricle. The facial nerve roots include fibers from the motor, solitary and salivatory nuclei. The nervus intermedius comprises fibers from salivatory and solitary nuclei (it contains sensory fibers from the tongue, mucosa, and postauricular skin as well as parasympathetic fibers to the salivary and lacrimal glands). The fibers of the facial nerve then course around the sixth cranial nerve nucleus and exit the pons at the cerebellopontine angle. The fibers go through the internal auditory canal along with the vestibular portion of the eighth cranial nerve. The narrowest portion of the internal auditory canal is the labyrinthine segment. This is the location that is thought to be the most common site of compression of the facial nerve in Bell palsy.

The seventh cranial nerve contains parasympathetic fibers to the nose, palate and lacrimal glands. The preganglionic parasympathetic fibers that originate in the salivatory nucleus join the fibers from nucleus solitarius to form the nervus intermedius. These fibers then synapse with the submandibular ganglion, which has fibers that supply the sublingual and submandibular glands. The fibers from the nervus intermedius also supply the pterygopalatine ganglion, which has parasympathetic fibers that supply the nose, palate, and lacrimal glands.

The facial nerve passes through the stylomastoid foreman in the skull and terminates into the zygomatic, buccal, mandibular, and cervical branches. These nerves serve the muscles of facial expression, which include frontalis, orbicularis oculi, orbicularis oris, buccinator, and platysma. Other muscles innervated by the facial nerve include stapedius, stylohyoid, posterior belly of the digastric, occipitalis, and the anterior and posterior auricular muscles. All muscles of the facial nerve are derived from the second brachial arch.

The location of injury of the facial nerve in Bell palsy is peripheral to the seventh nerve nucleus. It is thought to occur near or at the geniculate ganglion. If the lesion is proximal to the geniculate ganglion, the motor paralysis is accompanied by gustatory and autonomic abnormalities. Lesions between the geniculate ganglion and the origin of the chorda tympani produce the same effect except that it spares lacrimation. If the lesion is at the stylomastoid foramen, it may result in facial paralysis only.

Bell palsy is thought to be caused by edema and ischemia resulting in compression of the facial nerve in its course through the bony canal. The cause of the edema and ischemia is still being debated. In the past, cold exposure, (eg chilly wind, cold air conditioning, or driving with the car window down) were considered the only triggers to Bell palsy. However, most authors believe that the herpes simplex virus (HSV) is the most likely cause. It is difficult to actually study the causal relationship between HSV and Bell palsy because of the ubiquitous nature of HSV.

In 1972, McCormick first suggested that HSV is responsible for idiopathic facial paralysis. This was based on the analogy that HSV was found in cold sores, and he hypothesized that HSV may remain latent in the geniculate ganglion. Since then, autopsy studies have shown HSV in geniculate ganglion of patients with Bell palsy. Murakami performed PCR for HSV in the endoneural fluid of the seventh nerve of patients who underwent surgery for Bell palsy. 11 of the 14 patients were found to have HSV in the endoneural fluid.

It is reasonable to assume that HSV is the etiologic agent in Bell palsy. If this is true, then the virus is most likely to travel up the axons of the sensory nerves and reside in the ganglion cells. At times of stress the virus will reactivate, causing local damage to the myelin. Thus, Bell palsy may be secondary to viral and/or autoimmune reactions causing the facial nerve to demyelinate, resulting in unilateral facial paralysis.

Frequency:

• In the US: The annual incidence of Bell palsy is approximately 23/100,000.

  The right side is affected 63% of the time.

  Diabetics have up to a 29% higher risk of being affected by Bell palsy than non-diabetics. Thus, blood glucose levels at time of diagnosis of Bell palsy may detect undiagnosed diabetics.

• Internationally: The highest incidence was found in a study in Seckori, Japan, in 1986 and the lowest incidence was found in Sweden in 1971. Most population studies generally show an annual incidence of 15-30/100,000.

Mortality/Morbidity: The majority of patients who suffer from Bell palsy have neurapraxia or local nerve conduction block. These patients are likely to have a prompt and complete recovery of the nerve. Patients with axonotmesis, with disruption of the axons, have a fairly good recovery but it is usually not complete. The risk factors thought to be associated with a poor outcome in patient’s with Bell palsy include (1) age greater than 60 years, (2) complete paralysis, and (3) decreased taste or salivary flow on the side of paralysis (usually 10-25% compared to the patient’s normal side). Other factors thought to be associated with poor outcome include pain in the posterior auricular area and decreased lacrimation.

Patients generally have a good prognosis; approximately 80-90% of the patients will recover without noticeable disfigurement within one and a half to three months. Patients aged 60 years or older have approximately a 40% chance of complete recovery and have a higher rate of sequelae. Patients younger than 30 years have a 10-15% chance of partial recovery and sequelae. If no recovery occurs by 4 months, then the patient is more likely to have sequelae from the disease, which include synkinesis, crocodile tears, and rarely hemifacial spasm.

Synkinesis is an abnormal contracture of the facial muscles while smiling or closing the eyes. It may be mild and result in slight movement of the chin when the patient blinks, eye closure with smiling, or contracture around the mouth while blinking. Crocodile tears are observed; patients shed tears while they eat.

Video 1. Motor synkinesis following bell’ palsy

• Facial spasm is a very rare complication of Bell palsy. It occurs as tonic contraction of one side of the face. Spasms are more likely to occur during times of stress or fatigue and may occur during sleep. This condition may occur secondary to compression of the root of the seventh nerve by an aberrant blood vessel, tumor, or demyelination of the nerve root. It occurs most commonly in the fifth and sixth decades, and sometimes the etiology is not found. The presence of progressive facial hemispasm with other cranial nerve findings indicates a possibility of a brainstem lesion.

• Diabetics are 30% more likely to have only partial recovery; recurrence of Bell palsy is also more common among diabetics. Bell palsy accounts for only 23% of bilateral facial paralysis. The majority of patients with bilateral facial palsy have Guillain-Barré syndrome (GBS), sarcoidosis, Lyme disease, meningitis (neoplastic or infectious) or bilateral neurofibromas in patient’s with Neurofibromatosis 2. Recurrent Bell palsy occurs in 10-15% of patients. It may occur on the ipsilateral or contralateral side of the initial palsy. It is usually associated with a family history of recurrent Bell palsy. Approximately 30% of patients with recurrent ipsilateral facial palsy were found to have tumors of the seventh nerve or parotid gland. Patients with recurrent ipsilateral facial palsy should undergo MRI or high-resolution CT to rule out neoplastic or inflammatory (multiple sclerosis or sarcoidosis) cause of recurrence.

Sex:

• Bell palsy appears to affect the sexes equally. However, women aged 10-19 years are more likely to be affected than men.

• Pregnant women have a 3.3 times higher risk of being affected by Bell palsy than nonpregnant women, it occurs most frequently in the third trimester.

Age: The lowest incidence was found in persons younger than 10 years and the highest incidence was found in persons aged 60 years or older.

CLINICAL PICTURE

History: Bell palsy is a diagnosis of exclusion. The diagnosis must be made on the basis of a thorough history and physical examination and use of diagnostic testing when necessary.

• Symptoms of Bell palsy include (1) acute onset of unilateral upper and lower facial paralysis (over a 48-hour period), (2) posterior auricular pain, (3) decreased tearing, (4) hyperacusis, and (5) taste disturbances.

• The paralysis must include the forehead and lower aspect of the face. The patient may complain of inability to close the eye or to smile on the affected side. He may also complain of increased saliva on the side of the paralysis. If the paralysis involves only the lower portion of the face, a central cause should be suspected (supranuclear). If the patient complains of contralateral weakness or diplopia in conjunction with the supranuclear facial palsy, a stroke or intracerebral lesion should be strongly suspected.

  • Half of the patient’s affected with Bell palsy may complain of posterior auricular pain. It is important to ask the patient if they have experienced trauma, which may account for the pain and facial paralysis.

  • One-third of the patients may experience hyperacusis in the ear ipsilateral to the paralysis, which is secondary to weakness of the stapedius muscle.

  • One-sixth of the patients experience decreased lacrimation.

  • Many patients complain of numbness on the side of the paralysis. Some authors believe that this is secondary to involvement of the trigeminal nerve whereas other authors argue that this symptom is probably due to lack of mobility of the facial muscles and not lack of sensation.

• If a patient has gradual onset of facial paralysis, weakness of the contralateral side, or history of trauma and infection, other causes of facial paralysis must be strongly considered. Patients who have bilateral facial palsy must be evaluated for GBS, Lyme disease, and meningitis.

• Recurrent ipsilateral facial paralysis must raise the suspicion of a tumor of the seventh nerve or parotid gland. If the patient complains of sudden onset of hearing loss and severe pain with the onset of facial paralysis, Ramsey-Hunt syndrome must be considered.

• Symptoms associated with seventh nerve neoplasm include slowly progressive paralysis, facial hyperkinesis, severe pain, recurrent palsy, and other cranial nerve involvement. Cerebellopontine tumors may affect the seventh, eighth, and fifth cranial nerves simultaneously. Patients with a progressive paralysis of the facial nerve beyond 3 weeks should be evaluated for neoplasm.

Physical:

• Initial inspection of the patient will demonstrate flattening of the forehead and nasolabial fold on the side affected with the palsy.

• On exam, when the patient is asked to raise his eyebrows, the side of the forehead with the palsy will remain flat.

• When the patient is asked to smile, his face becomes distorted and lateralizes to the side opposite the palsy.

• The patient is not able to completely close the eye on the affected side. On attempted eye closure, the eye rolls upward and inward on the affected side. This is known as Bell phenomenon and is considered a normal response to eye closure.

• A careful head, ears, eyes, nose, and throat (HEENT) exam must be carried out in all patients with facial paralysis.

  • Inspection of the external auditory canal (EAC) for vesicles, injection, infection, or trauma must be done.

  • The patient may have decreased sensation to pinprick in the posterior auricular area.

  • The patient who has paralysis of the stapedius muscle will complain of hyperacusis.

  • While examining the eyes, Bell phenomenon is observed on attempted eye closure.

  • With weakness/paralysis of the orbicularis oculi muscle (facial Nerve innervation) and normal function of the levator muscle (oculomotor nerve innervation) and Mueller muscle (sympathetic innervation) eye closure may be partial or absent. The tear reflex may also be absent in many cases of Bell palsy. Thus for these reasons the patient may have decreased tearing and susceptibility to corneal abrasion and dryness of the eye. It may appear that the patient has loss of corneal reflex on the affected side; however, the contralateral eye blinks when testing the corneal reflex on the affected side.

• A careful oral examination must also be preformed.

  • Taste and salivation are affected in many patients with Bell palsy. Taste may be assessed by holding the tongue with gauze and testing each side of the tongue independently with salt, sugar, and vinegar. The mouth must be washed after testing with different substances. The affected side has decreased taste as compared to the normal side.

• Careful neurologic examination is necessary in patients with facial paralysis.

  • A neurologic abnormality warrants neurologic referral and further testing such as MRI of the brain, lumbar puncture, and EMG where appropriate.

WORK-UP

Lab Studies:

• Serum titers for herpes simplex virus may be obtained, but this is usually not helpful due to the ubiquitous nature of this virus.

• Blood glucose or hemoglobin A1c may be obtained to determine if the patient has undiagnosed diabetes.

Imaging Studies:

• If the history and physical examination lead to a diagnosis of Bell palsy, then immediate imaging is not necessary.

• Imaging is also not required because most patients with Bell palsy improve within 8-10 weeks. If the paralysis does not improve or worsens, imaging may be useful.

• The MRI of patients with Bell palsy may show enhancement of the seventh nerve at, or near the geniculate ganglion. However, if the paralysis progresses over weeks, there is a high possibility of a neoplasm compressing the seventh cranial nerve. Tumors that compress or involve the seventh cranial nerve include schwannoma (most common), hemangioma, meningioma, and sclerosing hemangioma.

• MRI is preferred for imaging the cerebellopontine angle (CPA).

• If there is history of trauma, CT scan of the temporal bone may be required.

• If the patient has a palpable parotid mass, imaging may be necessary.

Other Tests:

• The following tests may be preformed in the office setting. However, they require both the patient and physician’s time. They may be helpful in assessing the extent of the damage to the seventh nerve.

  • The stethoscope loudness test may be used to assess the functioning of the stapedius muscle. The patient wears the stethoscope, and the activated tuning fork is placed at the bell of the stethoscope. The loud sound will lateralize to the side of the paralyzed stapedius muscle

  • The Schirmer blotting test may be used to assess tearing function. The use of benzene will stimulate the nasolacrimal reflex and the degree of tearing can be compared between the paralyzed and normal sides.

  • The salivary flow may also be tested. The physician places a small catheter into both the paralyzed and normal submandibular glands. The patient is then asked to suck on a lemon, and the salivary flow is compared between the two sides. The normal side is the control.

Procedures:

• Useful tests for evaluation of the function of the facial nerve include nerve conduction testing and electromyography (EMG).

  • These tests may aid in assessing the outcome of a patient who has persistent and severe Bell palsy. This test is most useful when performed 3-10 days after the onset of paralysis.

  • Nerve conduction responses are abnormal if there is a 50% difference in amplitude between the paralyzed and normal side, a difference of 90% between the 2 sides suggests a poorer prognosis.

  • May demonstrated that prognosis may be favorable if the motor amplitude of the affected side was greater than 25% of the normal side. An incomplete recovery was observed in patients whose results demonstrated less than 25% amplitude on the paralyzed side.

  • Blink reflexes can be used to measure conduction across the involved segment but they are commonly absent in Bell palsy.

• Brainstem auditory-evoked response (BAER) may be obtained in patients with peripheral seventh nerve lesions and other neurologic involvement.

  • BAER measures the transmission of response through the brainstem –notably a retrocochlear lesion.

  • Hendrix evaluated BAER of 17 patients with Bell palsy. He found no evidence of retrocochlear lesions of the auditory system in any of his patients with Bell palsy.

  • In another study by Shannon, BAER was recorded in 27 patients with Bell palsy; only 6 patients had prolonged brainstem transmission but normal auditory function.

  • These studies are small and do not support routine use of BAER in patients with Bell palsy. However, when a patient presents with multiple cranial neuropathies, i.e. VII and VIII nerves, BEAR may be useful.

Histologic Findings: A review of 12 autopsy cases of Bell palsy was summarized in Peter Dyck’s Peripheral Neuropathy. This stated that the majority of of cases showed inflammatory changes around the mastoid cells and walls of the arteries. The most common site of involvement was the geniculate ganglion.

Surgical findings described constriction of the nerve at the stylomastoid foramen with swelling of the nerve itself. Microscopic findings showed an inflammatory reaction with infiltration of macrophages on the nerve itself.

MANAGEMENT

Medical Care: In general, persons with true Bell palsy have an excellent prognosis. The goal of treatment is to improve function of the facial nerve and reduce neuronal damage. Many issues must be addressed in treating the patients with Bell palsy. The most important consideration is the onset of symptoms. Treatment may be considered for patients who have the onset of paralysis within 1-4 days of the initial office visit.

• The most widely accepted treatment for Bell palsy is corticosteroids. However, the use of steroids is still controversial because most patients recover without treatment.

  • The recommended dose of prednisone is 1 mg/kg or 60mg for 6 days, followed by a taper, for a total of 10 days. Many trials have been carried out to study the efficacy of prednisone in Bell palsy. Early studies had small numbers of patients and variable outcomes. In 1972, Adour conducted a large, controlled clinical trial, which found that 89% of patients treated with prednisone had full recovery as compared to 64% of patients treated with placebo. When using corticosteroids for the treatment of Bell palsy, caution should be used in patients with tuberculosis, peptic ulcer disease, diabetes mellitus, renal or hepatic dysfunction, or malignant hypertension.

• Since it is widely accepted that HSV is the likely etiologic agent of Bell palsy, trials using acyclovir have been conducted.

  • A prospective randomized trial with 101 patients comparing prednisone and acyclovir demonstrated that the prednisone group had a better clinical recovery. In another prospective randomized trial with 99 patients, prednisone monotherapy was compared to the combination of prednisone and acyclovir. This study demonstrated that combination therapy was more effective in preventing nerve degeneration as measured by electrodiagnostic tests.

  • Dose of acyclovir is 800 mg orally 5 times a day for a total of 10 days.

  • It is left to the discretion of the physician whether to use prednisone or combination therapy. For patients who have a contraindication to steroid therapy, acyclovir may be given as solitary treatment.

• It is universally accepted that eye care is imperative. The patient’s eye is at risk for drying, corneal abrasion, and corneal ulcers. Eye care includes artificial tears for use during the day as well as eyeglasses or shields. At night, eye lubricants may be used. If artificial tears are not effective during the daytime, then lubricants may be used; however, they may cause blurring of vision.

Surgical Care: Surgery for Bell palsy is controversial.

• In the past, surgical decompression of the facial nerve was considered for patients whose facial muscles demonstrated less than 90% of normal activity on electrophysiologic studies. Surgical decompression of the facial nerve involves a middle fossa craniotomy with an extradural approach. However, recent trials suggest this is not beneficial in patients with Bell palsy

Consultations: Based on the history and physical examination, if the initial impression is not Bell palsy, then a neurologic or otolaryngologic consultation is needed.

• If the paralysis persists for 6 months, neurology or otolaryngology consultation should be sought.

• Patients who complain of persistent dry eye or painful eye should be referred to an ophthalmologist.

MEDICATION

The goal of pharmacotherapy is to reduce morbidity and prevent complications.

FOLLOW-UP

Further Outpatient Care:

• If the paralysis is not resolved or is progressing to complete paralysis, a thorough neurologic and HEENT examination should be performed to rule out neoplastic causes of seventh nerve palsy.

• The patient should be followed up if the initial EMG shows less the 25% function of the involved facial muscles as compared to the normal side.

• If the residual paralysis is severe, referral for counseling should be made.

Complications:

• Approximately 30% of patients with Bell palsy experience sequelae of the paralysis, which include incomplete motor recovery, incomplete sensory regeneration, and parasympathetic impairment.

  • Incomplete motor recovery may manifest as oral incompetence or epiphora

  • Incomplete sensory recovery may result in dysgeusia (impairment of taste) or ageusia (loss of taste).

  • Parasympathetic impairment causes aberrant function of lacrimal glands, which manifests as crocodile tears; the patients complain of shedding tears while eating

Prognosis:

• The natural course of Bell palsy varies from early complete recovery to substantial nerve injury resulting in persistent paralysis and synkinesis.

• One-third of the patients regain complete recovery of facial motor function without sequelae.

• One-third of the patients have incomplete recovery of facial motor function. These patients do not have any noticeable abnormalities.

• The remainder of patients suffer from permanent neurologic and cosmetic abnormalities, which are apparent.

Patient Education:

• To prevent corneal abrasions, the patient should be educated concerning eye care.

• They should also be encouraged to do facial muscle exercises using passive range of motion as well as actively closing their eyes and smiling.

References

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