Bell’s palsy: clinicians usually recommend steroids, sometimes antivirals

Issue: October 2003

Steroids and antivirals

Leonid Skorin Jr., OD, DO, FAAO, FAOCO: Traditionally, Bell’s palsy is defined as an idiopathic, unilateral, lower motor-neuron facial paresis or paralysis of acute onset. No other etiology, such as infection, tumor, intracranial stroke or trauma should be present. Yet, recent work points increasingly to a viral etiology for many of these “idiopathic” palsies.

Researchers from Ehime University in Japan collected nerve and muscle specimens from patients with Bell’s palsy (Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell’s palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med. 1996;124:27-30.). Genome analysis for herpes simplex virus type 1 (HSV-1) was performed by using polymerase chain reaction (PCR). The PCR analysis, which is exquisitely sensitive in detecting minute amounts of viral DNA, revealed HSV-1 DNA in the majority of patients tested who had Bell’s palsy, but in none of the samples taken from control patients.

Further evidence of HSV-1 involvement includes the fact that numerous triggers known to reactivate latent HSV-1 also seem to cause Bell’s palsy. These include fever, upper respiratory tract infection, dental extraction, menstruation, stress and exposure to cold.

Because of this new evidence implicating HSV-1, researchers have studied the therapeutic effects of treating “idiopathic” Bell’s palsy with oral antiviral therapy in addition to oral prednisone (Adour KK, Ruboyianes JM, von Doersten PG, et al. Bell’s palsy treatment with acyclovir and prednisone compared with prednisone alone: a double-blinded, randomized, controlled trial. Ann Otol Rhinol Laryngol. 1996;105:371-378.). Treatment with acyclovir-prednisone resulted in improved prognosis for return of voluntary muscle motion and in preventing partial nerve degeneration. There was also less contracture with synkinesis.

Prior to this study, most patients were treated with oral prednisone alone. Prednisone helps decrease the inflammation and edema that causes a conduction block as the nerve passes through the narrow meatal foramen in the skull.

A recent evidence-based review regarding treatment recommendation for Bell’s palsy by the American Academy of Neurology found that steroids probably benefit these patients and that, possibly, antiviral agents should also be used (Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell’s palsy [an evidence-based review]: report of the quarterly Standards Subcommittee of the American Academy of Neurology. Neurology. 2001;56:830-836.).

Based on these data, my treatment regimen includes both prednisone and antiviral agents. I use prednisone 1 mg/kg of body weight daily (60 mg/day maximum) for 7 days, split into twice-daily dosing and then tapered off over the subsequent 3 days. For the antiviral component of the treatment regimen, I use either Zovirax (acyclovir, GlaxoSmithKline) 400 mg five times daily for 7 days or Valtrex (valacyclovir HCl, the hydrochloride salt of L-valyl ester of the antiviral drug acyclovir, Zovirax, GlaxoSmithKline) 500 mg three times daily for 7 days.

Leonid Skorin Jr., OD, DO, FAAO, FAOCO, writes the “Neuro Connection” column for Primary Care Optometry News. He practices in Albert Lea, Minn., and writes and lectures on ocular disease and neuro-ophthalmic disorders. He underwent fellowship training in neuro-ophthalmology. He may be contacted at the Albert Lea Eye Clinic, Mayo Health System, 1206 W. Front St., Albert Lea, MN 56007; (507) 373-8214; fax: (507) 373-2819; e-mail: skorin.leonid@mayo.edu. Dr. Skorin has no direct financial interest in any products he mentions, nor is he a paid consultant for any companies he mentions.

Sometimes steroids, occasionally antivirals

Nicky R. Holdeman, OD, MD: Before considering treatment, clinicians must recall that not all facial palsies are idiopathic (Bell’s palsy). The idiopathic etiology, therefore, should be considered a diagnosis of exclusion, as up to 10% of cases are found to be due to a treatable condition. Other etiologies include infection (i.e., Lyme’s disease, otitis media, meningitis); inflammation (i.e., sarcoid); neoplasms (i.e., tumors of the parotid gland, tumors of the base of the skull, acoustic neuroma); head injury with fracture of the temporal bone; brain stem stroke; multiple sclerosis; and herpes zoster virus (HZV) infections (Ramsay-Hunt syndrome). Properly excluding other causes may occasionally require laboratory testing, imaging and various other diagnostic procedures.

Once it has been confirmed that the facial nerve palsy is indeed an isolated neurologic finding, treatment may be considered. It is important to remember that complete recovery occurs in 75% of patients within 60 days and that the primary goal of management should be to maintain an intact cornea. To ensure corneal integrity, treatment often involves taping, artificial tears, lubricating ointment, patching, moisture chambers, therapeutic contact lenses and humidification.

In regard to systemic therapy, Bell’s palsy has been attributed to an inflammatory reaction involving the facial nerve; however, the few autopsied cases of this disease have shown only nondescript changes in the facial nerve and not the inflammatory changes as is commonly presumed.

There has also been a suggested relationship of Bell’s palsy to reactivation of herpes simplex virus (HSV), but there is little evidence to support this hypothesis. Consequently, it is my view that oral treatment is often unnecessary, but may be appropriate for patients in whom an unsatisfactory outcome may be expected. I have found that the best clinical guide to prognosis is the severity of the palsy during the first few days after presentation. Patients with a clinically complete palsy when first seen are less likely to make a full recovery than those with an incomplete paralysis.

When confronted with a patient with a clinically complete palsy (i.e., total ipsilateral facial weakness, decreased tearing, hyperacusis and decreased taste to the anterior two-thirds of the tongue), or if there is severe pain, I will consider oral steroids assuming there are no contraindications. I use particular discretion in patients who might be pregnant, who have pre-existing peptic ulcer disease or who are diabetic. Thus, if a patient with a complete palsy presents within 4 days of onset and has no contraindications, I often prescribe prednisone 80 mg orally per day for 3 days, then 60 mg orally per day for 3 days, then 40 mg orally per day for 3 days, then 20 mg orally per day for 3 days and then discontinue use.

Oral antiviral agents are safe and efficacious for HSV or HZV and are well tolerated by most patients. Certainly, antiviral agents are appropriate for patients with Ramsay-Hunt syndrome, but if patients have a history of previous simplex infections or a strong history of a viral prodrome, I will often add oral antiviral agents to the steroid regimen.

Nicky R. Holdeman, OD, MD, is executive director of the University Eye Institute and chief of Medical Services at the University of Houston College of Optometry. He can be reached at the University of Houston College of Optometry, 505 J Davis Armistead Bldg., Houston, TX 77204-2020; (713) 743-1886; fax: (713) 743-0965; e-mail: NRHoldeman@uh.edu. Dr. Holdeman has no direct financial interest in any products he mentions, nor is he a paid consultant for any companies he mentions.

Neither — I refer

Andrew S. Gurwood, OD, FAAO: The answer to the question is easy. The explanation is complicated. I do not recommend oral steroids or oral antiviral medications for patients who present with facial nerve palsy because if and when these patients are ultimately started on any systemic management, it is by the neuro-specialist to whom I referred them. Bell’s palsy or idiopathic facial nerve palsy is a diagnosis of exclusion. In fact, I feel that the term idiopathic cranial nerve seven palsy (ICN VII P) is far more appropriate nomenclature. ICN VII P cannot be diagnosed without complete evaluation.

When patients have cranial nerve VII palsies, the role of the optometrist is to act as a gatekeeper, identifying the malady (cranial nerve VII palsy — central or peripheral), informing the internal medicine specialist of the potential etiologies, suggesting a course of testing to uncover the underlying cause and referring the patient to a neurologic specialist (neurologist or neuro-ophthalmologist) for confirmation of the diagnosis and definitive management (testing and treatment).

I do inform patients in whom I suspect ICN VII P that oral steroids and oral antiviral medications are in the armamentarium of treatment. It has been postulated for decades that idiopathic cranial nerve VII palsy is caused by inflammation. Hence, treatment with oral corticosteroids has been cited in the literature as being controversially beneficial for expediting its resolution. More recently, herpes simplex virus (HSV) has been postulated to be present and involved in inciting some cases of ICN VII P; however, even that is under disagreement.

Oral steroids are not casual agents. In some circumstances, they can produce exacerbation of existing systemic disease and allow dormant systemic diseases to blossom. Their mechanism of action gives them the capability of weakening the host, creating vulnerability. Further, they possess numerous other deleterious side effects.

Oral antiviral medications are unproven in this arena and, at best, remain a subject of debate. Despite the lack of clear indication, anecdotal evidence obtained through conversations that I have shared with neurologists and neuro-ophthalmologists indicates only a mild hesitation to proceed with dual therapy, employing the rationale that it may help and probably, in the absence of obvious contraindications, will not hurt. In any case, while I provide my confirmed ICN VII P patients with this information so they possess some awareness, given the complexities and diversity of opinions on the efficacy of treatment, I leave the suggesting and prescribing to the experts.

Andrew S. Gurwood, OD, FAAO, writes the “Pharmacology and the Eye” column for Primary Care Optometry News. He is an associate professor of clinical sciences and an attending optometric physician at the Eye Institute of the Pennsylvania College of Optometry. He is also a member of the clinical staff in the Department of Ophthalmology at Albert Einstein Medical Center in Philadelphia. Dr. Gurwood can be reached at the Pennsylvania College of Optometry, 1200 West Godfrey Ave., Philadelphia, PA 19141; (215) 276-6134; fax: (215) 276-1329; e-mail: Agurwood@pco.edu. Dr. Gurwood has no direct financial interest in any products he mentions, nor is he a paid consultant for any companies he mentions.

Steroids and antivirals

Michael J. Trad, OD: Bell’s palsy, or acute idiopathic facial palsy, represents about 90% of all cranial nerve VII palsies. Because most patients afflicted display improvement within 3 months, any treatment regimen may be considered controversial.

However, about 10% of cases result in some degree of permanent asymmetry of facial musculature, and 5% of patients exhibit severe deformity. The poor outcomes in the latter 10% to 20% of individuals inevitably fostered research into treatment regimens more effective than observation alone.

Oral steroids were initially used in an attempt to decrease swelling and improve microcirculation of the peripheral facial nerve. Later, oral antivirals (acyclovir or famciclovir) were prescribed – alone or in addition to steroids – due to their success in treating Ramsay Hunt syndrome and the discovery that herpes simplex virus type 1 was the most likely cause of Bell’s palsy (Burgess et al. Polymerase chain reaction amplification of herpes simplex viral DNA from the geniculate ganglion of a patient with Bell’s palsy. Ann Otol Rhinol Laryngol. 1994;103(10):775-779 and Murakami et al. Bell’s palsy and herpes simplex virus: identification of viral DNA and endoneural fluid and muscle. Ann Intern Med. 1996;124:27-30).

Although controversy still exists concerning the efficacy of medical therapy, Grogan and Gronseth’s 2001 review of the literature suggested that steroids were probably effective, and that acyclovir, when combined with prednisone, is possibly effective in improving facial outcomes or facial function.

By acknowledging the findings of these three studies and the demographic subset of untreated patients with permanent facial dysfunction, I prefer to treat properly screened patients during the first 3- to 7-day window of opportunity with both oral prednisone and oral acyclovir over a 10-day period.

Michael J. Trad, OD, writes the “Pharmacology and the Eye” column for Primary Care Optometry News. He can be reached at Medical Arts Center, 1620 Sauk Rd., Dixon, IL 61021; (815) 288-7711; fax: (815) 288-5077; e-mail: mjtrad4u@hotmail.com. He has no direct financial interest in any products he mentions, nor is he a paid consultant for any companies he mentions.