How Should I Manage This Man's Left Facial Paralysis

Family Practice Recertification, October 2014, Volume 32, Issue 10

A 45-year-old male accountant is seen by you complaining that when he awoke this morning, his wife noted a drooping of the right side of his face. Examination reveals a moderate right facial paralysis.

A 45-year-old male accountant is seen by you complaining that when he awoke this morning, his wife noted a drooping of the right side of his face. Examination reveals a moderate right facial paralysis.

What are the possible causes of this patient’s facial paralysis?

Idiopathic, peripheral facial paralysis or Bell’s palsy is the most likely cause of this patient’s facial paralysis. Other possible causes include tumors involving the parotid salivary gland, whether primary or metastatic, especially metastatic from previously treated skin cancers on the ipsilateral side of the face, strokes and brain tumors.

Infectious causes should not be overlooked and include herpes zoster oticus, also known as Ramsay Hunt syndrome, which typically impacts the geniculate ganglion of the facial nerve. Another possibility is “malignant” otitis externa which is essentially an osteomyelitis of the skull base and temporal bone caused by Pseudomonas aeruginosa in poorly controlled diabetics or other immunocompromised patients, or Lyme disease, especially in endemic regions where it may account for as many as 25% of cases of facial paralysis. Infectious mononucleosis, mumps and even leprosy should also be considered.

The patient relates that he has been feeling “under the weather” for the past 2 to 3 days with mild myalgias and a runny nose. He also notes that since this morning sounds seem distorted in the left ear.

What findings on history and physical examination would support the diagnosis of Bell’s palsy?

Bell’s palsy is typically rapid in onset with maximal paralysis occurring with 72 hours of initial onset. It is unilateral in presentation and impacts both the upper and lower branches of the mimetic facial musculature to an equal extent. In addition, other facial nerve branches such as those to the lacrimal gland, stapedius muscle and anterior two-thirds of the tongue are also affected resulting in varying degrees of associated symptoms such as dry eyes, hyperacusis and dysgeusia.

What findings would make the possibility of Bell’s palsy unlikely?

A careful history coupled with a thorough physical examination, including neurologic examination with a primary focus on cranial nerve function, should be conducted in all patients with findings which would support alternative diagnoses routinely sought. Such findings would include bilateral and/or slowly evolving facial paralysis, a paralysis that spares the musculature of the forehead, and significant asymmetry in the degree of paralysis amongst the various muscles supplied by the facial nerve’s branches.

In addition, the presence of a mass in the ipsilateral parotid gland, particularly in the case of a patient with a concurrent or prior cutaneous malignancy on the ipsilateral side of the face or scalp, the presence of otorrhea with or without associated mastoid tenderness involving the adjacent ear or the presence of vesicular lesions on the ipsilateral pinna would all call into question the presumptive diagnosis of Bell’s palsy.

Examination is notable only for the partial paralysis of the entire left side of the face, including forehead, eye area, and mouth. You make the presumptive diagnosis of Bell’s palsy.

What is the current thinking regarding the pathogenesis of Bell’s palsy?

Inflammation and edema of the facial nerve with resultant nerve compression is felt to be the basis of the facial paralysis characterizing Bell’s palsy. A presumptive viral etiology has been theorized for many patients with Bell’s palsy in the past based primarily on the findings of laboratory studies which have identified genomic sequences of the herpes simplex virus (HSV), varicella zoster virus and Epstein-Barr virus in a large percentage (79% versus normal controls) of the endoneurial fluid and muscle of patients with Bell’s palsy.

However, the role that viral infection or reactivation plays in the facial paralysis of Bell’s palsy has recently been called into question based primarily on the failure of randomized controlled studies using antiviral medications, both alone and in combination with the use of glucocorticoids, to show benefit in patients felt to have this diagnosis.

What advice should be given to patients regarding eye care?

Patients with Bell’s palsy are at significant risk for ipsilateral eye injury. This higher risk is multifactorial in origin, stemming from upper eyelid paralysis, with resultant lagophthalmos, lower lid paralysis, with resultant ectropion, as well as a reduction in lacrimal gland pump function.

Consequent corneal damage can be reduced by the consistent use of sunglasses, frequent use of lubricating eye drops and ophthalmic ointments, and patching or taping the affected eye, particularly when sleeping at night.

What is the role of glucocorticosteroid therapy and how should it be prescribed?

Oral steroid therapy, if commenced within 72 hours of the onset of facial paralysis in patients 16 years of age or older, has been shown to both reduce the time to recovery of facial function, as well as increase the likelihood of return of facial function. In terms of specific dosing and timing, a 10-day course of oral steroids with at least 5 days at a high dose (50 mg of prednisolone daily or 60 mg of prednisone daily) is felt to be effective.

What is the current thinking regarding antiviral therapy?

The use of antiviral medications as monotherapy for the treatment of Bell’s palsy does not appear to confer any treatment benefit. Results investigating its use in combination with oral corticosteroid therapy has been equivocal and therefore its role as an adjunct to glucocorticoid d therapy is unclear.

What is the natural course of Bell’s palsy?

The annual incidence of Bell’s palsy is approximately 23 per 100,000. Even without treatment, 70% of patients with a complete facial paralysis and nearly 95% with a partial paralysis due toBell’s palsy will regain full facial function within 6 months. Most patients demonstrate some recovery of facial function within 2-3 weeks after symptom presentation. Early and aggressive treatment would thus be expected to most likely benefit the 30% of Bell’s palsy patients whose initial recovery of facial function would otherwise be incomplete.

What role does neurodiagnostic and neuroimaging play in the management of Bell’s palsy?

Neurodiagnostic testing does not appear to provide any prognostic benefit in patients whose paralysis is incomplete. However, in patients who present with a Bell’s palsy in - whom complete unilateral facial paralysis is seen, neurodiagnostic tests are often helpful for both treating physicians and patients.

In particular, electroneuronography (ENoG) wherein skin surface electrodes are placed overlying various facial muscles to record their maximal response while the main trunk of the facial nerve (in front of the ear) is stimulated can help to quantify the extent of nerve damage.

Since the peripheral facial nerve branches are located distal to the likely site of facial nerve injury in Bell’s palsy, thought to be somewhere within the temporal bone, ENoG testing is best performed between 7-14 days after a facial nerve paralysis occurs. A paralyzed nerve whose response in mV amplitude exceeds 10% of that seen on the unaffected side suggests a likely full or near-full recovery of nerve function. Conversely, an EnoG response that is less than 10% of the normal side suggests a poorer nerve recovery potential in most circumstances.

With respect to neuroimaging options, an MRI scan with gadolinium contrast which traces the entire course of the facial nerve is the single most helpful radiographic study in a patient with facial nerve paralysis. This study should be obtained in Bell’s palsy patients whose presentation is felt to be clinically or historically inconsistent with Bell’s palsy as well as in any patient whose facial nerve paralysis does not demonstrate any improvement within three months after initial presentation.

Is there any role for neural stimulation and surgical decompression of the facial nerve?

The controversy surrounding the potential role for surgical decompression of the facial nerve in patients with Bell’s palsy stems from the uncertainty as to the site of greatest nerve compromise. As a result, surgical decompression for patients with complete facial paralysis must be directed at both the labyrinthine and mastoid segments of the facial nerve. To achieve this, a technically challenging middle cranial fossa surgical approach is required in an effort to maximize the possibility that the decompression procedure will be associated with an improvement in facial function.

Potential candidates for middle cranial fossa surgical decompression include those patients with persistent complete facial paralysis as well as those with poor ENoG scores, or less than 10% amplitude response, within the initial 14 days after the onset of their facial paralysis.

About the Author

Dr. Kedeshian is an Associate Clinical Professor of Head and Neck Surgery, David Geffen School of medicine at UCLA.