Grogan PM, Gronseth GS.

Practice parameter: steroids, acyclovir,

and surgery for Bell's palsy (an evidence-based review): report of the Quality Standards Subcommittee of the
American Academy of Neurology. Neurology. 2001;56:8306. Accessed April 17, 2007, at:
http://www.aan.com/professionals/practice/pdfs

Treatment of Bells Palsy by

Liangui Balance Therapy: A Case
Report
Case Report Liangui Sun1,*

1 Beijing Yijiyuan Facial Neuroscience Academy, Beijing, China

* Corresponding author E-mail: chuzhenyun@126.com

Received 11 Apr 2013; Accepted 10 June 2013

2013 Sun; licensee InTech. This is an open access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,
distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract Background Liangui balance therapy combines Chinese traditional medicine and modern biophysical
treatment. It has achieved positive therapeutic effects in the treatment of Bells palsy. Method Facial images of the
patient are collected and digitally analysed with a Facial Image Data Pairing Diagnosis System. The specially
made medical ultrasonic coupling agent is applied to the confirmed lesion location. Result A 62yearold female
patient was taken as the subject, who was suffering from Bells palsy caused by surgical injury during
parotidectomy. The patient completely recovered from Bells palsy after being treated for eight months.
Conclusion Liangui balance therapy achieved improvement in a short time. The patient underwent longterm
treatment and showed significant improvement.

Keywords Bells Palsy, Liangui Balance Therapy, Facial Nerve Function

1. Introduction

Idiopathic facial paralysis is also called facial neuritis or Bells palsy. It is a peripheral facial paralysis caused

by unspecific injury to facial nerves located in the stylomastoid foramen. Facial distortion is the main symptom of
this disease. The causes, such as angiospasm, ischemia, or hydroncuscan, induce facial nerve compression and
denutrition, and finally result in facial paralysis. Without prompt and appropriate treatment, the condition will
leave severe sequelae. This disease affects patients regardless of age, although males are slightly more susceptible
than females. Generally, the onset of Bells palsy is acute. The most severe symptoms appear several hours or
several days after onset[1, 2]. Because of the sophisticated aetiology of facial nerve diseases, it is very difficult to
treat these diseases. Besides invasive therapies, such as surgery, injection, acupuncture and so on, noninvasive
treatments medication, swabbing, sticking, massage, etc. are also very common[3,4]. Since 1999 to 2012,
Beijing Yijiyuan Facial Neuroscience Academy developed a new treatment of facial nerve diseases Liangui
balance therapy. This therapy combines Chinese traditional medicine with modern biophysical treatments. The
treatment focuses on nerve endings and lesion points. A significant curative effect has been observed in a large
number of clinical cases. One classic case is reported in the following.

www.intechopen.com Liangui Sun: Treatment of Bells Palsy bIynLt.iaj.nignutei gBra.lamnecde.T,

h2e0r1a3p,y:VAol.C1a,se28R:e2p0o1r3t
1

2. Materials and Method

2.1 Diagnosis standard

The onset is acute. The patent generally has the experience of getting cold. Some patients develop symptoms such
as ear pain or feeling of discomfort. Hemifacial mimic muscles suddenly suffer palsy, forehead wrinkles
disappear, inability to close the eye on the affected side of the face is experienced, nasolabial grooves disappear,
there is deviation in the angle of the mouth, food catches in the cheek on the paralyzed side, there is a loss of
taste on the first 2/3 of the tongue, and the patient experiences sensitivity to sound and watering eyes. The
patient experiences no disturbance of consciousness or paralysis of limbs. The laboratory tests are normal.

2.2 Facial nerve function grading

This work uses the HouseBrackman facial nerve grading system 2.0[5].

2.3 Treatment

2.3.1 Instruments and materials

This work uses the Facial Image Data Pairing Diagnosis System, the Facial Nerve Energy Resonance Therapy
Machine, and specially made medical ultrasonic coupling agent (Tianjin Jiushengyuan Biotech Inc., Tianjin,
China).

2.3.2 Liangui Balance Therapy

Facial images of the patient were collected and digitally analysed with the Facial Image Data Pairing Diagnosis
System. A sketch of lesion locations was drawn, based on the facial nerve features, distribution of acupoints and
the medical record of the patient.

The specially made medical ultrasonic coupling agent, made from the natural ingredients containing neuron
activating substances, was applied at the lesion locations confirmed by the Facial Image Data Pairing Diagnosis
System. The lesions were then treated with Facial Nerve Energy Resonance Therapy Machine.

The therapeutic effect was traced and evaluated by image criteria and functional analysis. The therapy plan and
course of treatment were adjusted according to the change in the illness. (Click the following link to view video.)

Link to the video

Therapeutic regimen: At the beginning stage, the patient underwent the therapy once a day until the basic

functions of raising eyebrows and wrinkling forehead were restored. The course of therapy then switched to once
every two days. After the function of wrinkling nose returned to normal, the treatment interval was prolonged to
twice a week. The interval was extended to once a week when the performance of the mouth corner was normal.
The treatment will be applied once with a focus on rehabilitation after the face has regained the normal state.

2.3.3 Evaluation of the effect[6]

Recovery: Bilateral forehead wrinkles and nasolabial grooves are symmetrical; eyebrows can be raised and eyes
opened normally; lips close firmly when cheeks are blown out, no food is left between teeth when eating; no
distortion of commissure when talking and laughing; normal facial expression. Improved: Bilateral forehead
wrinkles and nasolabial grooves are basically symmetrical; eye cannot close firmly when cheeks blown out; no
food is left between the teeth when eating; the corner of the mouth is slightly asymmetrical. Ineffective: The
above effects are not achieved after two courses of treatment.

3. Result

3.1 Case description

The 62yearold
parotidectomy for parotid neoplasm in May 2011. The facial nerve of the patient was injured during the
operation. After the operation, the patient showed deviation of the angle of mouth to the right side. She went to
the Yijiyuan Facial Neuroscience Academy clinic in June 2011 with the chief complaint of discomfort in the left
facial area. She also complained of inability to close her left eye completely, watering eyes, and numbness in the
left ear.

female patient

underwent a

State of Rest

Raised Eyebrows

Closed Eyes

Displayed Teeth Figure 1. Images of presented case before treatment

Physical examination: leftside forehead wrinkle had disappeared; left eyebrow could not be raised; leftside
nasolabial groove had disappeared; leftside mimic

2 Int. j. integr. med., 2013, Vol. 1, 28:2013

www.intechopen.com

Wrinkled

Blownout

Nose

Cheeks

muscular atrophy and palsy (Figure 1). Based on the symptoms and the examination results, the patient was
diagnosed as House and Brackmann grade 5.

3.2 Treatment

The patient underwent the Liangui balance therapy with a Facial Nerve Energy Resonance Therapy Machine
based on the analysis results of the Facial Image Data Pairing Diagnosis System. After three months of treatment,
the symptom significantly improved (see Figure 2).

The face on the affected side is stretched by the uninjured side. After the oedema is eliminated, facial nerve
diseases of the dysfunction type can heal without specific treatment. The injury type can be caused when facial
nerves are damaged by trauma, birth injury, surgical injury or viral infection. These causes can induce nerve
dysfunction and peripheral nerves can suffer from denutrition. The contraction of facial muscles is thus induced.
Touchpoint adhesion between capillary vessels and nerve endings is formed because of facial muscle
contraction. The adhesion pulls the facial muscles and puts pressure on the trigeminal. The patient then suffers
from facial muscle spasms and trigeminal pain. There are the obvious muscular atrophy areas on the face of the
patient[7,8]. The patient in this study suffered from Bells palsy because of surgical injury; her condition
therefore belonged to the injury type.

Liangui balance therapy combines the Chinese traditional medicine principle of treating internal diseases by
external treatment with modern biophysics theory. The mechanism of Liangui balance therapy is based on the
anatomical position of facial nerves and the distribution of acupuncture points. The physiological properties of
facial nerves and Chinese traditional medical theory regarding meridiancollateral form the basis for the therapy.
Bells palsy patients generally show muscular atrophy on the face. The practice of confirming the lesion point and
applying treatment at the point of muscular atrophy is unique to Liangui balance therapy. For example, if the
patient cannot raise an eyebrow, it is essential to identify whether the patient can raise the geisoma, or inner
eyebrow. Based on anatomical position, a curve should be drawn from the hairline to the muscular atrophy point
at the nervus temporalis branch or parietal nerve branch ending.

The organism generates very week energy in an electromagnetic field and an electronic cloud over the facial
surface. The Facial Nerve Energy Resonance Therapy Machine utilizes the slight energy from the electromagnetic
field and the electronic cloud released by the facial surface to enable the nutritional ingredient in the specially
made medical ultrasonic coupling agent to permeate the surface of the face and generate the long term nutritive
layer surrounding the damaged nerve endings. This treatment improves the blood circulation and metabolism
around the lesion, and the injured nerve endings are allowed to progressively rehabilitate. As a result, nerve
conduction improves and nerve function recovers[9].

After reviewing over 50,000 cases of Bells palsy, we can state that the treatment of facial nerve diseases must
focus on the rehabilitation of nerve endings. Location targeting treatment should be adopted and the treatment
site should be adjusted according to alterations in the

Closed Eyes

Wrinkled Nose
Figure 2. Images of presented case after treatment for three months

3.3 Prognosis

The patient recovered completely after being treated for eight months. The symptom disappeared and the facial
nerve achieved functional restoration (see Figure 3).

State of Rest

Raised

Blownout

Displayed Teeth

State of Rest

Blownout Cheek
Figure 3. Images of presented case after treatment for 8 months

4. Discussion

Except spaceoccupying lesions (After search numberous references, this term is correct), there are two types of
facial nerve disease. One type is dysfunction;, the other is injury. Dysfunction is caused when facial nerves are
pressured by the hydroncus, which can happen for a range of reasons. This induces weakness or loss of nerve
conduction and results in dysfunction of facial nerves.

Raised Eyebrows

Closed Eyes

Wrinkled Nose

Displayed Teeth

www.intechopen.com

Liangui Sun: Treatment of Bells Palsy by Liangui Balance Therapy: A Case Report 3

patients condition. The Facial Image Data Pairing Diagnosis System and the Facial Nerve Energy Resonance
Therapy Machine systematize and digitalize the therapy. Diagnosis and treatment are therefore more objective
and standardized. Regardless of the severity and duration of the disease, Liangui balance therapy achieves
improvements in a short time and patients who undergo longterm treatment also show significant improvement.

6. Acknowledgements

Thanks to Ms Zhenyun Chu for her excellent video editing.

7. References

1. [1] Bateman DE (1992) Facial palsy. Br J Hosp Med. 47:430431.

2. [2] Peitersen E (1982) The natural history of Bells palsy. Am J Otol. 4:107111.

3. [3] Berg T, Bylund N, Marsk E, Jonsson L, Kanerva M, Hultcrantz M, Engstrom M (2012) The effect of
prednisolone on sequelae in Bells palsy. Arch Otolaryngol Head Neck Surg. 138(5):445449.

4. [4] Shoja MM, Tubbs RS, Loukas M, Shokkouhi G, Ardalan MR (2009) Facial palsy and its management
in the Kitab alHawi of Rhazes. Neurosurgery. 64:11881190.

[5] Vrabec JT, Backous DD, Djalilian HR, Gidley PW, Leonetti JP, Marzo SJ, Morrison D, Ng M, Ramsey MJ,
Schaitkin BM, Smouha E, Toh EH, Wax MK, Williamson RA, Smith EO; Facial Nerve Disorders Committee (2009)
Facial nerve grading system 2.0. Otolaryngol Head Neck Surg. 140:445450.

[6] Tao T, Jia S, Xu X, Tian S (1993) The diagnosis guideline for common clinical diseases. Beijing Medical
University and China Union Medical University Joint Publishing House, Beijing China..

[7] Grosheva M, Wittekindt C, GuntinasLichius O (2008) Prognostic value of electroneurography and

electromyography in facial palsy. Laryngoscope. 118(3):394397.

[8] Sajadi MM, Sajadi MR, Tabatabaie SM (2011) The history of facial palsy and spasm: Hippocrates to Razi.
Neurology. 77(2):174178.

[9] Zhang W Chen M, Yang C, Zhang W (2012) Prognostic value of facial nerve antidromic evoked potentials in
bell palsy: a preliminary study. Int J Otolaryngol. 2012; 2012:960469. doi: 10.1155/2012/960469. Epub 2011 Nov
23.. This is an ePub article, this number is article ID, Pubmed and original fulltext PDF all display the source like
this.
Bells Palsy: Diagnosis and
Management
JEFFREY D. TIEMSTRA, MD, and NANDINI KHATKHATE, MD

University of Illinois at Chicago College of Medicine, Chicago, Illinois

Bells palsy is a peripheral palsy of the facial nerve that results in muscle
weakness on one side of the face. Affected patients develop unilateral facial
paralysis over one to three days with forehead involvement and no other
neurologic abnormalities. Symptoms typically peak in the first week and then
gradually resolve over three weeks to three months. Bells palsy is more
common in patients with diabetes, and although it can affect persons of any
age, incidence peaks in the 40s. Bells palsy has been traditionally defined as
idiopathic; however, one possible etiology is infection with herpes simplex
virus type 1. Laboratory evaluation, when indicated by history or risk factors,
may include testing for diabetes mellitus and Lyme disease. A common short-
term complication of Bells palsy is incomplete eyelid closure with resultant
dry eye. A less common long-term complication is permanent facial weakness
with muscle contractures. Approximately 70 to 80 percent of patients will
recover spontaneously; however, treatment with a seven-day course of
acyclovir or valacyclovir and a tapering course of prednisone, initiated within
three days of the onset of symptoms, is recommended to reduce the time to
full recovery and increase the likelihood of complete recuperation. (Am Fam
Physi- cian 2007;76:997-1002, 1004. Copyright 2007 American Academy of
Family Physicians.)

Patient information:

A handout on Bells palsy, written by the authors of this article, is provided on page 1004.

Bells palsy is an idiopathic, acute constant exposure. Tear production decreases;

peripheral-nerve palsy involving the facial nerve, which supplies all the muscles of facial
expression.

The facial nerve also contains parasympathetic fibers to the lacrimal and salivary glands,
as well as limited sensory fibers supplying taste to the anterior two thirds of the tongue
(Figure 1). Bells palsy is named after Sir Charles Bell (1774-1842), who first described
the syn- drome along with the anatomy and function of the facial nerve. The annual
incidence of Bells palsy is 15 to 30 per 100,000 persons, with equal numbers of men and
women affected. There is no predilection for either side of the face. Bells palsy has been
described in patients of all ages, with peak incidence noted in the 40s. It occurs more
commonly in patients with diabetes and in pregnant women. Patients who have had one
episode of Bells palsy have an 8 percent risk of recurrence. 1,2

Clinical Presentation

Patients with Bells palsy typically complain of weakness or complete paralysis of all the
muscles on one side of the face. The facial creases and nasolabial fold disappear, the
fore- head unfurrows, and the corner of the mouth droops. The eyelids will not close and
the lower lid sags; on attempted closure, the eye rolls upward (Bells phenomenon). Eye
irrita- tion often results from lack of lubrication and
however, the eye may appear to tear excessively because of loss of lid control, which
allows tears to spill freely from the eye. Food and saliva can pool in the affected side of
the mouth and may spill out from the corner. Patients often complain of a feeling of
numbness from the paralysis, but facial sensation is preserved.

Patients with Bells palsy usually progress from onset of symptoms to maximal weak-
ness within three days and almost always within one week. A more insidious onset or
progression over more than two weeks should prompt reconsideration of the diag- nosis.
Left untreated, 85 percent of patients will show at least partial recovery within three
weeks of onset.3

Etiology and Differential Diagnosis

Bells palsy is believed to be caused by inflam- mation of the facial nerve at the
geniculate ganglion, which leads to compression and possible ischemia and
demyelination. This ganglion lies in the facial canal at the junction of the labyrinthine and
tympanic segments, where the nerve curves sharply toward the stylomastoid foramen.
Classically, Bells palsy has been defined as idiopathic, and the cause of the
inflammatory process in the facial nerve remains uncertain. Recently, attention has
focused on infection with herpes simplex virus type 1 (HSV-1) as a possible cause
because

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private, noncommercial use of one individual user of the Web site. All other rights reserved. Contact copyrights@aafp.org for copyright questions
and/or permission requests.

Bells Palsy

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendation

Patients with Bells palsy should be treated within three days of the onset of symptoms with a seven-day
course of oral acyclovir (Zovirax) or valacyclovir (Valtrex), plus a tapering course of oral prednisone.

Patients with complete paralysis who do not improve in two weeks on medication should be referred to an
otolaryngologist for evaluation for other causes of facial nerve palsy.

Patients should be monitored for eye irritation and be prescribed eye lubrication. Patients with corneal
abrasions should be referred to an ophthalmologist.

Evidence
rating References

B 15-17 C 19, 20 C 1, 23

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evi- dence; C =

consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence
rating system, see page 922 or http://www.aafp.org/afpsort.xml.

Visceral efferent fibers (facial expression muscles, stapedius muscle) Visceral motor fibers (lacrimal, salivary glands)
Special sensory fibers (supplies taste to anterior two thirds of the tongue)

Greater petrosal nerve

Geniculate ganglion

Superior salivatory nucleus

Motor nucleus of facial nerve

Chorda tympani nerve

Internal acoustic meatus

Figure 1. Anatomy of the facial nerve.

research has found elevated HSV-1 titers in affected patients. However, studies have
failed to isolate viral DNA in biopsy specimens, leav- ing the causative role of HSV-1 in
question.4,5

Many conditions can produce isolated facial nerve palsy identical to Bells palsy.
Structural lesions in the ear or parotid gland (e.g., cholesteatoma, salivary tumors) can
produce facial nerve compression and paral- ysis. Other causes of peripheral nerve
palsies include Guillain-Barre syndrome, Lyme dis- ease, otitis media, Ramsay Hunt
syndrome (an outbreak of herpes zoster in the facial nerve distribution), sarcoidosis, and
some influenza vaccines. Although these condi-

tions can present as isolated facial nerve palsies, they usually have additional features
that distinguish them from Bells palsy.

Patients with Lyme disease often have a history of tick exposure, rash, or arthralgias.
Facial nerve palsies from acute and chronic otitis media have a more gradual onset, with
accompanying ear pain and fever. Patients with Ramsay Hunt syndrome have a
pronounced prodrome of pain and often develop a vesicular eruption in the ear canal and
pharynx, although cases without the vesicular eruption (i.e., zoster sine herpete) have
been reported. Polyneuropathies (e.g., Guillain-Barre syndrome, sarcoidosis) will

998 American Family Physician www.aafp.org/afp

Volume 76, Number 7 October 1, 2007

ILLUSTRATION BY RENEE CANNON

A. Facial nerve lesion B. Supranuclear lesion (Bells palsy)

Nucleus of facial nerve (cranial nerve VII)

Lesion in facial nerve

Facial nerve

Supranuclear lesion

Figure 2. Patients with (A) a facial nerve lesion and (B) a supranuclear lesion with forehead
sparing.
more often affect both facial nerves. Tumors will present with a more insidious onset of
symptoms over weeks or months.

Central nervous system lesions (e.g., mul- tiple sclerosis, stroke, tumor) can also cause
facial nerve palsy. However, some motor neu- rons to the forehead cross sides at the
level of the brainstem, so the fibers in the facial nerve going to the forehead come from
both cere- bral hemispheres (Figure 2). Supranuclear (central) lesions affecting the facial
nerve will not paralyze the forehead on the affected side, resulting in a unilateral facial
paralysis with forehead sparing. Often, there will be at least some weakness of
extremities on the affected side as well. Table 11,6-8 summarizes the dif- ferential
diagnosis of Bells palsy.

Influenza vaccines in the past have been associated with peripheral neuropathies.
Although influenza vaccines currently avail- able in the United States have not been
associ- ated with Bells palsy,9-11 a recently developed Swiss intranasal vaccine was
found to have a very high risk of postvaccine facial nerve palsy and has been withdrawn
from use.12 Because influenza vaccines change annually,

public health officials should be notified of any cases of Bells palsy occurring in the six
weeks following vaccine administration.

Evaluation

A patient with an acute onset of unilateral facial weakness most likely has Bells palsy. A
careful history of the onset and progress of paralysis is important because gradual onset
of more than two weeks duration is strongly suggestive of a mass lesion. Medical history
should include recent rashes, arthralgias, or fevers; history of peripheral nerve palsy;
expo- sure to influenza vaccine or new medications; and exposure to ticks or areas
where Lyme disease is endemic. The physical examination should include careful
inspection of the ear canal, tympanic membrane, and oropharynx, as well as evaluation
of peripheral nerve func- tion in the extremities and palpation of the parotid gland. In
order to assess forehead involvement, physical examination should also include
evaluation of cranial nerve func- tion, including all facial muscles.

Laboratory testing is not usually indicated. However, because diabetes mellitus is pres-

October 1, 2007 Volume 76, Number 7 www.aafp.org/afp American Family Physician 999

ILLUSTRATION BY RENEE CANNON

Table 1. Differential Diagnosis for Facial Nerve Palsy

Disease

Nuclear (peripheral)

Lyme disease

Otitis media

Ramsay Hunt syndrome

Sarcoidosis or Guillain- Barre syndrome

Tumor

Supranuclear (central)

Multiple sclerosis Stroke

Tumor

Cause

Spirochete Borrelia burgdorferi

Bacterial pathogens

Herpes zoster virus

Autoimmune response

Cholesteatoma, parotid gland

Demyelination Ischemia, hemorrhage Metastases, primary

brain

Distinguishing factors

History of tick exposure, rash, or arthralgias; exposure to areas where Lyme disease is endemic

Gradual onset; ear pain, fever, and conductive hearing loss

Pronounced prodrome of pain; vesicular eruption in ear canal or pharynx

More often bilateral Gradual onset

Forehead spared
Additional neurologic symptoms Extremities on affected side often involved

Gradual onset; mental status changes; history of cancer

Information from references 1 and 6 through 8.

ent in more than 10 percent of patients with Bells palsy, fasting glucose or A1C testing
may be performed in patients with additional risk factors (e.g., family history, obesity,
older than 30 years).13 Antibiotic therapy may be of benefit; therefore, Lyme antibody
titers should be performed if the patients history suggests possible exposure. Signs and
symp- toms atypical for Bells palsy should prompt further evaluation. Patients with
insidious onset or forehead sparing should undergo imaging of the head. Those with
bilateral pal- sies or those who do not improve within the first two or three weeks after
onset of symp- toms should be referred to a neurologist

Treatment CORTICOSTEROIDS

Oral corticosteroids have traditionally been pre- scribed to reduce facial nerve
inflammation in patients with Bells palsy. Prednisone is typically prescribed in a 10-day
tapering course starting at 60 mg per day. A 2004 Cochrane review and meta-analysis of
three randomized controlled trials comparing corticosteroids with placebo found small
and statistically nonsignificant reductions in the percentage of patients with incomplete
recovery after six months (relative risk [RR] = 0.86; 95% confidence interval [CI], 0.47 to
1.59) and the percentage of patients with cosmetic complications (RR = 0.86; 95% CI,
0.38 to 1.98).14 However, these trials included only

117 patients; larger prospective trials are needed to establish the benefit of
corticosteroids.

ANTIvIRAlS

Because of the possible role of HSV-1 in the etiology of Bells palsy, the antiviral drugs
acy- clovir (Zovirax) and valacyclovir (Valtrex) have been studied to determine if they
have any benefit in treatment. Either acyclovir 400 mg can be given five times per day
for seven days or valacyclovir 1 g can be given three times per day for seven days.
Although a 2004 Cochrane review found insufficient evidence to support the use of these
antivirals alone,15 two recent placebo-controlled trials demonstrated full recovery in a
higher percentage of patients treated with an antiviral drug in combination with
prednisolone than with prednisolone alone (100 percent versus 91 percent and 95
percent versus 90 percent).16,17 However, no benefit was seen when treatment was
delayed more than four days after the onset of symptoms (86 percent versus 87
percent).17

SPONTANEOuS RECOvERY

It is difficult to establish a statistically signifi- cant benefit of treatment in placebo-

controlled trials because Bells palsy has a high rate of spontaneous recovery. The
Copenhagen Facial Nerve Study evaluated 2,570 persons with untreated facial nerve
palsy, including 1,701 with idiopathic (Bells) palsy and 869 with

1000 American Family Physician www.aafp.org/afp Volume 76, Number 7 October 1, 2007

Table 2. Medications for Treatment of Bells Palsy

Medication

Acyclovir (Zovirax)

Valacyclovir (Valtrex)

Prednisone or prednisolone

Dosing

Adults: 400 mg five times daily for seven days

Children older than two years: 80 mg per kg daily divided every six hours for five days, with a maximal dose of
3,200 mg daily

Adults and children older than 12 years: 1 g three times daily for seven days

Adults: 60 mg daily for five days, then 40 mg daily for five days

Children: 2 mg per kg daily for seven to

10 days
Renal adjustment

Creatinine clearance:

Less than 10 mL per minute (0.17 mL per second): give half dose once daily

10 to 50 mL per minute (0.17 to 0.83 mL per second): give same dose every 12 to 24 hours

Creatinine clearance:

Less than 10 mL per minute: 500 mg daily

10 to 29 mL per minute (0.17 to 0.48 mL per second): 1 g daily

30 to 49 mL per minute (0.50 to 0.82 mL per second): 1 g twice daily

None

Hepatic adjustment

Undefined

None

Undefined

Adverse reactions

Gastrointestinal upset, headache, dizziness, elevated liver enzymes, aplastic anemia (rare)

Gastrointestinal upset, headache, dizziness, elevated liver enzymes, aplastic anemia (rare)

Headache, nervousness, edema, elevated blood pressure, elevated glucose

Cost*

$66 to $76 (generic)

$132 (brand)

$208 (brand)

$3 (generic) $6 (brand)

* Estimated cost to the pharmacist based on average wholesale prices (rounded to the nearest dollar) in Red Book. Montvale,
N.J.: Medical Economics Data, 2006. Cost to the patient will be higher, depending on prescription filling fee.

palsy from other causes; 70 percent had com- plete paralysis. Function returned within
three weeks in 85 percent of patients, with 71 per- cent of these patients recovering full
function. Of the 29 percent of patients with sequelae, 12 percent rated it slight, 13
percent rated it mild, and 4 percent rated it severe.3 Because of these findings, some
persons have questioned whether treatment for Bells palsy should be routinely
indicated; however, patients who have incomplete recovery will have obvious cosmetic
sequelae and will often be dissatisfied with their outcome. 18

Given the safety profile of acyclovir, vala- cyclovir, and short-course oral corticoste- roids,
patients who present within three days of the onset of symptoms and who do not have
specific contraindications to these medications should be offered combination therapy.
Patients who present with complete facial nerve paralysis have a lower rate of
spontaneous recovery and may be more likely to benefit from treatment. 1-3,19

OThER TREATMENTS

In the past, surgical decompression within three weeks of onset has been recommended
for patients who have persistent loss of function (greater than 90 percent loss on
electroneurography) at two weeks. How- ever, the most widely cited study supporting
this approach only reported results for a total of 34 treated patients at three differ- ent
sites, included a nonrandomized control group, and lacked a blinded evaluation of
outcome.20

The most common complication of sur- gery is postoperative hearing loss, which affects 3
to 15 percent of patients. Based on the significant potential for harms and the paucity of
data supporting benefit, the American Academy of Neurology does not currently
recommend surgical decompres- sion for Bells palsy. 19

Some published studies have reported benefit with acupuncture versus steroids and
placebo, but all had serious flaws in study design and reporting. 21 Table 2 sum- marizes
the available treatments.

October 1, 2007 Volume 76, Number 7 www.aafp.org/afp American Family Physician 1001

Bells Palsy

Complications

Patients with Bells palsy may be unable to close the eye on the affected side, which can
lead to irritation and corneal ulceration. The eye should be lubricated with artificial tears
until the facial paralysis resolves. Permanent eyelid weakness may require tarsorrhaphy
or implantation of gold weights in the upper lid. Facial asymmetry and muscular
contractures may require cosmetic surgical procedures or botulinum toxin (Botox)
injections. In these cases, consultation with an ophthalmologist or cosmetic surgeon is
needed.22,23

The Authors

Jeffrey D. TiemsTrA, mD, is an associate professor of clini- cal family medicine at the University of illinois at
Chicago College of medicine. He received his medical degree from rush University in Chicago, and completed a
family medicine residency at st. Paul University Hospital in Dallas, Tex.

NANDiNi KHATKHATe, mD, is the medical director of the family medicine Center and an assistant professor of
clini- cal family medicine at the University of illinois at Chicago College of medicine. she received her medical
degree from seth G.s. medical College in Bombay, india. Dr. Khatkhate completed general practice and
neurosurgery residencies in Ayrshire county, scotland, and a family medicine resi- dency at Cook County
Hospital in Chicago.

Address correspondence to Jeffrey D. Tiemstra, MD, Dept. of Family Medicine (M/C 663), University of Illinois at Chicago, 1919
W. Taylor St., Chicago, IL 60612 (e-mail: jtiemstr@uic.edu). Reprints are not available from the authors.

Author disclosure: Nothing to disclose.

REFERENCES

1. Gilden DH. Clinical practice. Bells palsy. N Engl J Med 2004;351:1323-31.

2. Morris AM, Deeks SL, Hill MD, Midroni G, Goldstein WC, Mazzulli T, et al. Annualized incidence and spec- trum of
illness from an outbreak investigation of Bells palsy. Neuroepidemiology 2002;21:255-61.
 3. Peitersen E. Bells palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiolo- gies. Acta
Otolaryngol Suppl 2002:4-30.

4. Linder T, Bossart W, Bodmer D. Bells palsy and herpes simplex virus: fact or mystery? Otol Neurotol 2005; 26:109-
13.

5. Stjernquist-Desatnik A, Skoog E, Aurelius E. Detection of herpes simplex and varicella-zoster viruses in patients with
Bells palsy by the polymerase chain reaction tech- nique. Ann Otol Rhinol Laryngol 2006;115:306-11.

6. Makeham TP, Croxson GR, Coulson S. Infective causes of facial nerve paralysis. Otol Neurotol 2007;28:100-3.

7. Redaelli de Zinis LO, Gamba P, Balzanelli C. Acute otitis

media and facial nerve paralysis in adults. Otol Neurotol 2003;24:113-7.

8. Keane JR. Bilateral seventh nerve palsy: analysis of 43 cases and review of the literature. Neurology 1994; 44:1198-202.

9. Zhou W, Pool V, DeStefano F, Iskander JK, Haber P, Chen RT, for the VAERS Working Group. A potential signal of Bells palsy
after parenteral inactivated influ- enza vaccines: reports to the Vaccine Adverse Event Reporting System (VAERS)United
States, 1991-2001. Pharmacoepidemiol Drug Saf 2004;13:505-10.

10. Izurieta HS, Haber P, Wise RP, Iskander J, Pratt D, Mink C, et al. Adverse events reported following live, cold-adapted,
intranasal influenza vaccine [Published correction appears in JAMA 2005;294:3092]. JAMA 2005;294:2720-5.

11. Zhou W, Pool V, Iskander JK, English-Bullard R, Ball R, Wise RP, et al. Surveillance for safety after immu- nization: Vaccine
Adverse Event Reporting System (VAERS)United States, 1991-2001 [Published cor- rection appears in MMWR Morb Mortal
Wkly Rep 2003;52:113]. MMWR Surveill Summ 2003;52:1-24.

12. Mutsch M, Zhou W, Rhodes P, Bopp M, Chen RT, Linder T, et al. Use of the inactivated intranasal influenza vac- cine and the
risk of Bells palsy in Switzerland. N Engl J Med 2004;350:896-903.

13. Adour K, Wingerd J, Doty HE. Prevalence of concurrent diabetes mellitus and idiopathic facial paralysis (Bells palsy).
Diabetes 1975;24:449-51.

14. Salinas RA, Alvarez G, Ferreira J. Corticosteroids for Bells palsy (idiopathic facial paralysis). Cochrane Data- base Syst Rev
2004;(4):CD001942.

15. Allen D, Dunn L. Aciclovir or valaciclovir for Bells palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2004;
(3):CD001869.

16. Hato N, Yamada H, Kohno H, Matsumoto S, Honda N, Gyo K, et al. Valacyclovir and prednisolone treatment for Bells palsy: a
multicenter, randomized, placebo- controlled study. Otol Neurotol 2007;28:408-13.

17. Hato N, Matsumoto S, Kisaki H, Takahasi H, Wakisaka H, Honda N, et al. Efficacy of early treatment of Bells palsy with oral
acyclovir and prednisolone. Otol Neu- rotol 2003;24:948-51.

18. Gillman GS, Schaitkin BM, May M, Klein SR. Bells palsy in pregnancy: a study of recovery outcomes. Otolaryn- gol Head
Neck Surg 2002;126:26-30.

19. Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bells palsy (an evidence-based review):
report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2001;56:830-6. Accessed April
17, 2007, at: http:// www.aan.com/professionals/practice/pdfs/gl0064.pdf.

20. Gantz BJ, Rubinstein JT, Gidley P, Woodworth GG. Surgical management of Bells palsy. Laryngoscope 1999;109:1177-88.

21. He L, Zhou D, Wu B, Li N, Zhou MK. Acupuncture for Bells palsy. Cochrane Database Syst Rev 2004;(1):CD002914.

22. Bulstrode NW, Harrison DH. The phenomenon of the late recovered Bells palsy: treatment options to improve facial
symmetry. Plast Reconstr Surg 2005;115:1466-71.

23. Holland NJ, Weiner GM. Recent developments in Bells palsy. BMJ 2004;329:553-7.
TITLE:BellsPalsy
SOURCE:GrandRoundsPresentation,DepartmentofOtolaryngology

TheUniversityofTexasMedicalBranch(UTMBHealth)DATE:October29,2012
RESIDENTPHYSICIAN:VietPham,MD
FACULTYPHYSICIAN:DaytonYoung,MD

FACULTYPHYSICIAN:TomokoMakishima,MD,PhDSERIESEDITOR:FrancisB.
Quinn,Jr.,MDARCHIVIST:MelindaStonerQuinn,MSICS

INTRODUCTION

First reported by Sir Charles Bell in 1818, Bells palsy describes a facial paralysis with few
associated symptoms that is rapid in onset and generally followed by spontaneous resolution.
Despite being the most common diagnosis of facial nerve paralysis, Bells palsy is actually a
diagnosis of exclusion and can induce a great deal of patient anxiety with its socially
devastating sequelae. Historically thought to be an idiopathic process, mounting evidence
conveys a significant role of the herpes simplex virus (HSV) in the pathogenesis of this
condition, and consequently, has imparted an importance influence on the direction of viable
treatment options.
FACIAL NERVE ANATOMY

The facial nerve is a large structure containing between 7,000-10,000 fibers. In addition to its
primary role in controlling somatic facial musculature movement, the facial nerve also
generates contributions to the sensation of taste with fibers from the nucleus tractus solitarius
and to parasympathetic secretomotor function with fibers from the superior salivatory
nucleus. The nerve can be divided into specific segments as it emerges from its origin in the
brainstem and courses through the temporal bone and out the stylomastoid foramen.

Sometimes referred to as the cisternal segment, the intracranial portion of the facial nerve
refers to the fibers as it leaves the motor nucleus in the brainstem, wraps around the abducens
nucleus, and exits out the ventral pons just medial to the spinal trigeminal nucleus. Axons
responsible for the parasympathetic and sensory functions of the facial nerve comprise the
nervus intermedius. Of note, the dorsal portion of the motor nucleus receives bilateral cortical
input while the ventral aspect of the nucleus only receives unilateral input from the
contralateral cortex. Consequently, control of the upper facial muscles is regulated by both
brain cortices, allowing a patient to demonstrate some upper movement despite a central
lesion. Conversely, a peripheral lesion will involve all of the facial muscle groups on the
ipsilateral side.

"This material was prepared by resident physicians in partial fulfillment of educational requirements established
for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery
and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group
discussion in a conference setting. No warranties, either express or implied, are made with respect to its
accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of
members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting
appropriate literature sources and informed professional opinion."

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Bell's Palsy October 2012

After exiting the brainstem, the facial nerve enters the internal auditory canal (IAC) and
represents the meatal segment. At an average length of 8mm and without releasing any
peripheral branches, the facial nerve and the nervus intermedius are separated from the
vestibulocochlear nerve by the falciform crest transversely and Bills Bar vertically to
traverse in the anterosuperior aspect of the IAC more distally. The labyrinthine segment
denotes where the facial nerve runs 3-4mm from the IAC to the geniculate ganglion and gives
off branches to the greater superficial petrosal, lesser petrosal, and external petrosal nerves.
The greater superficial petrosal nerve arises from the nervus intermedius and receives a
branch from the tympanic plexus as it carries parasympathetic fibers toward the
pterygopalatine ganglion along with taste fibers from the palate. It is joined by the deep
petrosal nerve from the internal carotid sympathetic plexus along the way to comprise the
Vidian nerve and regulate lacrimation. The lesser petrosal nerve serves a similar role as it
traverses past the tympanic plexus and synapses in the otic ganglion to deliver
parasympathetic fibers to the parotid gland via the auriculotemporal nerve.

As the facial nerve crosses between the cochlea and vestibule from the geniculate ganglion, it
takes a more horizontal orientation for 8-11mm as it goes posteriorly toward the pyramidal
eminence as the tympanic segment, sometimes aptly designated as the horizontal segment.
The mastoid segment signifies where the nerve travels 8-14mm vertically from the pyramidal
eminence toward the stylomastoid foramen in the temporal bone, and hence, it is occasionally
referred to as the vertical segment. Here, the facial nerve provides branches to the stapedius
muscle, and it sends parasympathetic innervations to the submandibular and sublingual
glands via the submandibular ganglion by way of the chorda tympani. The chorda tympani
also delivers taste fibers to the anterior two-thirds of the tongue. The posterior auricular nerve
arises from the facial nerve close to the stylomastoid foramen to join the auricular branch of
the vagus nerve to eventually innervate the intrinsic auricular muscles and the occipitalis.
After leaving the stylomastoid foramen, the facial nerve travels approximately 15-20mm
before dividing into the upper and lower major divisions at the pes anserinus, where it will
then be distributed among the temporal, zygomatic, buccal, marginal, and cervical branches.

HOUSE-BRACKMANN SCALE

The most commonly utilized classification schema to describe the severity of any facial palsy
is the House-Brackmann (HB) scale first introduced in 1985 and has served to help convey
among physicians the degree of facial paralysis using a universal system. Table 1 below
presents a visual adaptation of this system.

2
DEMOGRAPHICS

Bell's Palsy October 2012

Table1.HouseBrackmannScale

Bells palsy is felt to carry an incidence of approximately 30 out of 100,000 individuals,

although many have noted a higher rate in pregnant females (3.3. times greater) and diabetic
patients (4-5 times greater). Both genders tend to be affected equally around middle age, but
young females between 10-19 years of age and males older than 40 years of age have been
noted to be affected more often (2 times and 1.5 times greater, respectively). The right and
left facial nerves are equally involved, but simultaneous bilateral involvement is a rare event
with a 1% occurrence. Recurrence occurs 10% of the time, and only 10% of affected
individuals report a positive family history of similar symptoms.

NATURAL HISTORY

Peiterson provided an insightful investigation into the natural course and spontaneous
recovery rate of Bells palsy while monitoring the outcomes of more than 1,000 patients over
a fifteen-year period who did not receive treatment for their facial paresis (Peiterson 1985).
The mean age of onset was between 40-44 years, but it was less common in those younger
than 15 years and those older than 60 years of age. There was no gender predilection, and a
recurrence rate between 6-9% was observed in this population. Some associated symptoms
included a reduced stapedial reflex, phonophobia, postauricular pain, dysgeusia, and
decreased lacrimation.

Approximately 31% experienced a facial paresis with complete recovery occurring in 95% of
these patients. The remaining 69% presented with a complete facial paralysis, but some
recovery by three weeks after onset was noted in 85% of these patients. A satisfactory
outcome, referring to a recovery of facial function to a HB scale 1 or 2, was observed in 84%
of these individuals (HB 1 in 71% and HB 2 in 13%). Complete recovery was observed by
one month in 85%, but the other 15% progressed to complete degeneration with some signs
of recovery manifesting between 3-6 months afterward. These patients were noted to have a
higher incidence of sequelae such as diminished facial function, contractures, synkinesis, or
tearing.

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Bell's Palsy October 2012

PATHOPHYSIOLOGY

While originally felt to be an idiopathic process, two theories arose in an attempt to explain
the underlying process leading to Bells palsy.

McGovern postulated autonomic vascular instability, possibly triggered by cold temperature

or psychosomatically, resulted in spasm of arterioles nourishing the facial nerve (McGovern
1955). The suffocation of nutrients would induce a secondary ischemia and incite edema of
the nerve, and consequently, lead to compression against the fallopian canal and engender a
facial palsy.

Antoni coined the term acute infectious polyneuritis cerebralis acusticofacialis in 1919 to
suggest an infectious etiology to Bells palsy (Friedman 2000). Edema of the facial nerve was
also fundamental to the pathophysiologic process, but it was believed that this was related to
an inflammatory response to a viral presence. HSV was first proposed as the responsible
agent by McCormick in 1972, but it would be over twenty years later for other investigations
to lend credence to this line of thinking.

Burgess reported the presence of HSV type 1 (HSV-1) DNA in the temporal bone of a patient
who passed away six days after developing Bells palsy (Burgess 1994). Mice inoculated with
HSV-1 DNA in either the tongue or auricle exhibited a transient facial paresis approximately
6-9 days after inoculation with spontaneous recovery 3-7 days afterward. Neural edema was
noted on histological analysis with vacuolar degeneration and infiltration of inflammatory
cells. HSV antigens were encountered in the facial nerve, geniculate ganglion, and facial
nerve nucleus 6-20 days after inoculation (Surgita 1995). Murakami evaluated the endoneural
fluid of patients undergoing transmastoid decompression during the active phase of facial
palsy secondary to a myriad of etiologies and found HSV-1 in 11 out of 14 patients with
Bells palsy, but no signs of varicella-zoster virus (VZV) or Epstein Barr virus were
appreciated. Conversely, VZV but not HSV-1 was noted in those with Ramsay Hunt
syndrome while both viruses were not present in those with a facial palsy from trauma or
neoplasm (Murakami 1996). Furuta employed polymerase chain reaction to detect HSV-1 in
the saliva of patients with either Bells palsy or Ramsay Hunt and compared it to a control
group of people seropositive for HSV but without a facial paresis. HSV-1 was found in 50%
of individuals with Bells palsy compared to 19% of the control group. Furthermore, the
timing of testing appeared to play a significant role as 40% of those with Bells palsy and 7%
of those with Ramsay Hunt expressed HSV-1 when tested within 7 days of facial palsy before
it became essentially undetectable by the second week (Furuta 1998).

Lymphocytic infiltrate, myelin degeneration (McKeever 1987), and perineural edema

(Donoghue 1983, Podvinec 1984) have been histologically noted in Bells palsy, which is
especially prominent in the labyrinthine segment of the facial nerve. This is accompanied by
reports of a conduction block at this site (Gantz 1982) to suggest that the nerve gets entrapped
at the meatal foramen (Fisch 1983), the narrowest portion of the fallopian canal. Increased or
prolonged constriction results in ischemia and subsequent Wallerian degeneration of the
nerve.

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Bell's Palsy October 2012

PHYSICAL EXAMINATION

A thorough medical history and comprehensive physical examination is paramount to

approaching a patient with suspected Bells palsy. While it may not necessarily add a
significant amount of additional information if the abnormality is indeed related to Bells
palsy, it can exclude other conditions that may masquerade with a similar presentation.
Typically, Bells palsy occurs over a 24-48 hour span that can progress to complete paralysis
over 1-7 days. A neoplasm, such as a vestibular schwannoma, should be ruled out if evolution
progresses past three weeks. Aside from an absent ipsilateral acoustic reflex, patient should
present with a symmetrical audiological function, and a diagnosis of Bells palsy should be
questioned if there are vertiginous complaints.

Keeping cognizant of the contralateral upper motor neuron contribution to upper facial
muscle movement, there should be a high suspicion for a cerebrovascular accident or central
neurological lesion if the facial palsy does not encompass all of the facial nerve branches.
Chronic otitis media or cholesteatoma should be considered if there is concurrent ear disease,
while a vesicular eruption will warrant concern for Ramsay Hunt syndrome. Although a small
proportion of Bells palsy patients may present with bilateral weakness, systemic neurological
disorders with associated facial paralysis should be assessed such as Guillain-Barre syndrome
or Lyme disease. Individuals with type II neurofibromatosis may demonstrate bilateral facial
paralysis secondary to bilateral vestibular schwannomas. While regarded as a rare situation
that can occur with Bells palsy, facial palsy recurrence often argues against the diagnosis and
more to other conditions such as Melkersson-Rosenthal syndrome.

RADIOLOGY

Generally, the rationale behind radiographical imaging in the midst of Bells palsy is the
aspiration that it might help localize a lesion to attribute the facial palsy. Computed
tomography is better utilized to rule out other causes of facial paralysis including temporal
bone fractures, mastoiditis, or cholesteatoma. On the other hand, magnetic resonance
imagings (MRI) superiority in soft tissue delineation may identify an area of enhancement
along the course of the facial nerve, but there has been no significant correlation between the
site or degree of nerve enhancement and the clinical outcome. Ultimately, MRI is more
commonly utilized to exclude neoplasm such as vestibular schwannoma.

TOPOGRAPHY

Some have advocated topographical testing on the premise that a lesion can be localized
based on abnormalities that may affect the function of certain branches of the facial nerve.
For example, decreased lacrimation would manifest with an abnormal Schirmer test to
suggest a lesion near or involving the greater superficial petrosal nerve. Similarly, an absent
stapedial reflex would imply involvement of the stapedial branch of the facial nerve while
electrogustometry and salivary flow studies would evaluate the chorda tympani. However,
these endeavors have been unable to consistently predict the location of a lesion nor the
resulting clinical outcome.

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Bell's Palsy October 2012

AUDIOLOGY

As alluded above, individuals with Bells palsy typically exhibit symmetrical audiometric
function with the one exception that there may be an absence to the acoustic reflex ipsilateral
to the side of the paralysis. Similar to the reasoning with radiographical imaging, audiological
evaluation is employed more to exclude retrocochlear pathology which typically manifest
more with asymmetrical thresholds and decay, but not necessarily absence, to the acoustic
reflex.

ELECTROPHYSIOLOGY

Sunderlands classification describes five degrees of nerve injury. Neuropraxia is the first
degree and designates a localized conduction block but with structural continuity of the axon
so that Wallerian degeneration does not occur. Axonotmesis is the second degree of injury
and describes axoplasmic disruption but with endoneural sheath preservation. Unlike
neuropraxia, Wallerian degeneration does arise from this interrupted axonic integrity.
Neurotmesis groups together the third, fourth, and fifth degrees of nerve injury with
subdivisions depending on the status of the perineurium and epineurium. This disruption of
the axonal and supportive cells incites a more rapid Wallerian degeneration compared to
axonotmesis and is associated with a poorer and less predictable outcome.

Electrophysiologic tests draw upon these concepts and perhaps provide the most important
diagnostic tools in evaluating patients with Bells palsy from the prognostic information they
engender. These tests are not initiated in those who present with only a paresis; rather, they
are best employed three days after progression to a complete paralysis as Wallerian
degeneration may not occur early in the clinical course. Furthermore, assessing for objective
prognostic information in those with a partial facial paralysis may be superfluous in light of
the favorable prognosis for spontaneous recovery as outlined by Peiterson (Peiterson 1985).

Nerve excitability testing (NET) was first described by Hilger in 1964 and compares the
electrical thresholds required to elicit minimal voluntary muscle contraction between the
normal side and the paralyzed side of the face. A difference of 3.5mA is considered indicative
of severe degeneration and predictive of an unfavorable outcome. Inaccurate within the first
three days of the onset of complete paralysis, NET is dependent on subjective comparison
and potentially susceptible to inter-observer variability. Maximum stimulation testing (MST)
is similar to NET with the distinction that it compares muscle contraction with maximum
stimulation which can be uncomfortable for patients. A greater degree of muscle weakness is
concordant with worsening degeneration, and like NET, MST is also not useful within the
first three days of paralysis and subject to observer assessment.
Electroneuronography (ENoG) is another comparative electrophysiologic assessment but has
the advantage of being observer independent as a quantitative analysis. The evaluation entails
stimulating the facial nerve at the stylomastoid foramen and measuring the muscular response
near the nasolabial groove. The resulting action potential for both sides are tested and
presented as a percentage of degeneration comparing the affected side with the normal side of
the face. As with NET and MST, ENoG is inaccurate within the first three days of complete
paralysis.

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Bell's Palsy October 2012

The prognostic value of ENoG was elucidated by Esslen when full recovery was noted in
88% of patients who demonstrated less than 90% degeneration on ENoG. This percentage
decreased significantly to 30% if there was between 90-95% degeneration, and full recovery
was not observed in those with complete degeneration (Esslen 1977). Fisch expanded on this
with the assertion that satisfactory spontaneous recovery was highly likely if there was less
than 90% degeneration on ENoG obtained within three weeks of paralysis onset. Patients
who exhibited 90% degeneration had a higher likelihood of progressing to 95% degeneration,
which is important in light of the conclusion that a permanent unsatisfactory result, denoted
as a residual facial palsy of a HB scale of 3 or worse, was present in 50% of individuals with
95-100% degeneration by two weeks of paralysis onset (Fisch 1981).

Electromyography (EMG) is a quantitative test that measures action potentials produced with
volitional muscle movement. Normal contraction is signaled by diphasic or triphasic
waveforms, fibrillation connotes degeneration, and polyphasic potentials indicate
reinnervation. EMG is most valuable as a complementary test to accompany ENoG as it can
better ascertain if a facial palsy is likely undergoing degeneration or regeneration. Because
regenerating nerve fibers do not complete a summation potential on ENoG, the presence of
defibrillation and motor unit potentials on EMG would suggest regeneration. Degeneration
would be favored if there was only fibrillation potentials and no voluntary motor units. An
important caveat to EMG in the setting of degeneration is that fibrillation will not be
encountered until approximately 10-14 days after onset of paralysis.

MEDICAL MANAGEMENT

Regardless of the degree of facial palsy present, the eye needs to be evaluated and managed
to avoid disastrous ocular-related consequences that will manifest if incomplete eye closure is
present such as a corneal abrasion or exposure keratitis. Especially in paretic cases, expectant
management may be an acceptable treatment modality if the patient is closely followed for
spontaneous recovery.

Numerous studies have investigated the role of steroids in addressing Bells palsy, typically
with regimens such as prednisone 1mg/kg/d up to 70-80mg. This is commonly tapered after
5-7 days, although treatment may be extended if no improvement is appreciated. Many
investigations have cited benefit to steroids (Adour 1972, Katusic 1986), especially if they
are implemented early in the course of the disease (Brown 1982, Williamson 1996). Shafshak
echoed the importance of prompt intervention, recommending beginning prednisolone within
24 hours of paralysis (Shafshak 1994).
Austin evaluated prednisone in a randomized, double-blinded, placebo-controlled trial and
concluded that there was improved recovery with the medication. A statistically insignificant
trend for denervation prevention was also observed (Austin 1993). This study and two others
were included in a meta-analysis of 27 prospective and 20 retrospective trials investigating
the benefit of steroids. These three studies qualified for the meta-analysis inclusion criteria
seeking prospective, controlled trials utilizing at least 400mg of prednisone started within
seven days of paralysis and concluded that steroids improved complete recovery by 17%.
There was a generally positive benefit observed in the excluded trials with an acquisition of
complete recovery ranging between 49-97% using steroids and 23-64% without (Ramsey
2000). The

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Bell's Palsy October 2012

latest Cochrane Review at the time of this manuscript concurs with this sentiment that
steroids increase the frequency of complete recovery (Salinas 2010).

There are reports that contradict these findings (May 1976, Stankiewitz 1987), and a
literature review of nine studies over a 45 year-span comparing steroids to placebo did not
note a difference in rate of recovery or synkinesis. Although acknowledging that most of
these investigations were underpowered and that there was a beneficial trend observed in
some of the studies, the mild side effect profile and potentially positive therapeutic effect to
steroids led to the conclusion that there was probable benefit with steroids (Grogan 2001).

Controversy arises with the use of steroids in the pediatric population with Bells palsy as no
benefit was observed in children (Prescott 1987). A literature review of nine reports over a
thirty year-period could not definitively support the role of steroids in this demographic. Only
one of the studies specifically targeted children, and no statistical sub-analysis was conducted
on this population in the other trials. Although some benefit was observed in four of the
investigations, heterogeneity among them all precluded a meta-analysis or establishing a
formal recommendation (Salman 2001).

Antivirals were evaluated as an adjuvant therapy to steroids in a double-blind trial combining

prednisone with either acyclovir or placebo initiated within three days of paralysis onset. The
combination of prednisone and acyclovir resulted in less facial weakness on MST and a lower
rate of unsatisfactory recovery (Adour 1996). As individual treatment modalities, however,
prednisone was felt to be more beneficial than acyclovir (De Diego 1998), and a subsequent
literature review cited a paucity of studies to assert a definite therapeutic benefit but
supported the notion of a possible benefit with adding acyclovir to prednisone given the
generally well-tolerated side effect profile to antiviral medications (Grogan 2001). Similar
positive observations were encountered with valacyclovir (Axelsson 2003, Hato 2007), and
the latest Cochrane Review at the time of this manuscript concluded that antivirals were
beneficial when added to steroids but not as a single treatment endeavor apart from steroids
(Lockhart 2009).

SURGICAL MANAGEMENT

Balance and Duel first postulated the utility of decompressing the facial nerve in 1932 for
surgical treatment in Bells palsy. The focus of intervention localized initially to the
stylomastoid foramen in the 1930s before transitioning more toward the tympanic segment in
the 1960s. Decompression was felt to yield benefit in some accounts (Giancarlo 1970), but
this was refuted in others, with the description of no improvement with decompression from
the geniculate ganglion down toward the stylomastoid foramen (McNeill 1974).

May had originally championed a transmastoid approach to decompress the facial nerve from
the geniculate ganglion to the labyrinthine segment but without involving the meatal foramen
(May 1979). This ideology was later recanted as no palpable benefit was observed even when
decompression was undertaken within 14 days (May 1984) nor with decompressing the
mastoid segment alone (May 1985).

A conduction block proximal to the geniculate ganglion was encountered during total nerve
decompression via a middle cranial fossa and transmastoid approach described by Fisch

8
Bell's Palsy October 2012

(Fisch 1972). This was further elaborated upon with the report of benefit to surgery if the
meatal foramen was decompressed within three weeks of paralysis onset when 90%
degeneration was noted on ENoG (Fisch 1981). Gantz supported this philosophy but
shortened the timeframe by which to intervene down to two weeks (Gantz 1999).

In this multicenter study, Gantz compared clinical outcomes between surgery and steroids
dependent on the amount of degeneration measured on ENoG. High-dose steroids without
antivirals were administered if there was less than 90% degeneration, but decompression
from the IAC through the tympanic segment via a middle cranial fossa approach was offered
if degeneration exceeded 90% with no EMG activity by two weeks. Patients who underwent
decompression past two weeks constituted a surgical control, while those who deferred
surgery were addressed with steroids. Similar to past trials, a favorable outcome, designated
as recovery to a HB I or II, was observed in patients with less than 90% degeneration on
ENoG. Furthermore, patients who were decompressed within two weeks experienced a
higher rate of HB I or II recovery compared to those who received steroids (91% vs. 42%)
and a lower rate of unfavorable outcomes to HB III or IV recovery (9% vs. 58%). There were
similar results between the surgical control and steroid management groups to insinuate the
importance of intervening within two weeks of paralysis (Gantz 1999).

Although the exact protocol may vary among institutions, most physicians have adopted a
similar treatment scheme as outlined by Brackmann in Figure 1 below.

Figure1.BellsPalsyTreatmentAlgorithm(Brackmann2010)

9
Bell's Palsy October 2012

CONCLUSION

Bells palsy is a diagnosis of exclusion but remains the most common diagnosis of facial
paralysis. Electrophysiological testing affords important prognostic information which may
significantly impact the treatment plan and promote appropriate patient counseling. HSV is
regarded as a significant factor in the pathogenesis of this condition and drives the rationale
behind treatment options employed to manage affected individuals. While there is general
consensus to the utility of steroid therapy, with or without antiviral treatment, spirited debate
and controversy continues to shroud the role of surgical decompression. Given the current
evidence, a multimodality approach may ultimately be warranted in select patients.

REFERENCES

Adour KK, Ruboyianes JM, Von Doersten PG, et al. Bells palsy treatment with acyclovir and
prednisone compared with prednisone alone: a double blind, randomized controlled trial. Ann
Otol Rhinol Laryngol 1996; 105:371-378.

Adour KK, Wingerd J, Bell DN, et al. Prednisone treatment for idiopathic facial paralysis
(Bells palsy). N Engl J Med 1972; 287:1268-1272.

Austin JR, Peskind SP, Austin SG, et al. Idiopathic facial nerve paralysis: a randomized
double blind controlled study of placebo versus prednisone. Laryngoscope 1993; 103:1326-
1333. Axelsson S, Lindberg S, Stjernquist-Desatnik A. Outcome of treatment with
valacyclovir and

prednisone in patients with Bells palsy. Ann Otol Rhinol Laryngol 2003; 112:197-201.
Brackmann DE, Shelton C, Arriaga MA. Otologic Surgery, 3rd Ed. Philadelphia: Saunders,

2010. pp 336-338.
Briggs RD. Evaluation and Management of Bells Palsy. UTMB Department of
Otolaryngology

Grand Rounds 2002. Accessed 17 Sep 2012 <http://www.utmb.edu/otoref/grnds/Bells-Palsy-

2002-01/Bells-Palsy-2002-01.htm>.
Brown JS. Bells palsy: A 5 year review of 174 consecutive cases: An attempted double blind

study. Laryngoscope 1982; 92:1369-1373.

Burgess RC, Michaels L, Bale JF. Polymerase chain reaction amplification of herpes simplex

viral DNA from the geniculate ganglion of a patient with Bells palsy. Ann Otol Rhinol

Laryngol 1994; 103:775-779.

De Diego J I, Prim MP, De Sarria MJ, et al. Idiopathic facial paralysis: A randomized,

prospective, and controlled study using single-dose prednisone versus acyclovir three times

daily. Laryngoscope 1998; 108(4 Pt 1):573-575.

Dixon A, Gaillard F, et al. Facial Nerve (CN VII). Radiopaedia.org. Accessed 17 Sep 2012

<http://radiopaedia.org/articles/facial_nerve_(cn_vii)>.
Donoghue O. Histopathologic aspects of Bells palsy. Presented at American Academy of

OtolaryngologyHead and Neck Surgery. Anaheim, CA, Association for Research in

Otolaryngology, 1983.
Esslen E. The Acute Facial Palsies. New York: Springer, 1977.
Fisch U. Prognostic value of electrical tests in acute facial paralysis. Am J Otol 1984; 5:494-
498. Fisch U. Surgery for Bells palsy. Arch Otolarygol 1981; 107:1-11.
Fisch U, Esslen E. Total intratemproal exposure of the facial nerve. Arch Otolarygol 1972;

95:335-341.
Fisch U, Felix H. On the pathogenesis of Bells palsy. Acta Otolaryngol 1983; 95(5-6):532-
538.

10
Bell's Palsy October 2012

Furuta Y, Fukuda S, Chida E, et al. Reactivation of herpes simplex virus type 1 in patients
with Bells palsy. J Med Virol 1998; 54:162-166.

Freidman RA. The surgical management of Bells palsy: a review. Am J Otol 2000; 21:139-
144. Gantz BJ, Gmur A, Fisch U. Intraoperative evoked electromyography in Bells palsy.
Am J

Otolaryngol 1982; 3:273-278.

Gantz BJ, Rubinstein JT, Gidley P, et al: Surgical management of Bells palsy. Laryngoscope

1999; 109:1177-1188.
Grogan PM, Gronseth GS. Practice parameter: Steroids, acyclovir, and surgery for Bells
palsy

(an evidence-based review): Report of the Quality Standards Subcommittee of the American

Academy of Neurology. Neurology 2001; 56:830-836.

Hato N, Yamada H, Kohno H, et al. Valacyclovir and prednisolone treatment for Bells palsy:
a

multicenter, randomized, placebo-controlled study. Otol Neurotol 2007; 28(3): 408-413. Ho

K. Bell's Palsy: To Treat or Not to Treat. UTMB Department of Otolaryngology Grand

Rounds 2007. Accessed 17 Sep 2012 <http://www.utmb.edu/otoref/grnds/Bells-palsy-

070214/Bells-palsy-070214.mht>.
House JW, Brackmann DE. Facial nerve grading system. Otolaryngol Head Neck Surg 1985;

93:146-147.
Katusic SK, Beard CM, Wiederholt WC, et al. Incidence, clinical features, and prognosis in

Bells palsy, Rochester, Minnesota, 1968-1982. Ann Neurol 1986; 20:622-627. Lockhart P,
Daly F, Pitkethly M, et al. Antiviral treatment for Bells palsy (idiopathic facial

paralysis). Cochrane Database Syst Rev 2009; 7(4):CD001869.

Mancall EL, Brock DG, eds. Gray's Clinical Neuroanatomy: The Anatomic Basis for Clinical
Neuroscience, 1st Ed. Philadelphia: Elsevier Saunders 2011. pp 194-198.
May M. Total facial nerve in exploration. Laryngoscope 1979; 89:906-917.
May M, Klein SR, Taylor FH. Idiopathic (Bells) facial palsy: Natural history defies steroid
or

surgical treatment. Laryngoscope 1985; 95:406-499.

May M, Klein SR, Taylor FH. Indications for surgery for Bells palsy. Am J Otol 1984;
5:503-

512.
May M, Wette R, Hardin WB Jr, et al. The use of steroids in Bells palsy: A prospective

controlled study. Laryngoscope 1976; 86:1111-1122.

McCormick DP. Herpes-simplex virus as a cause of bells palsy. Lancet 1972; 1:937-939.
McGovern FH, Hansel JS. Decompression of the facial nerve in experimental Bells palsy.

Laryngoscope 1955; 71:1090.

McKeever P, Proctor B, Proud G. Cranial nerve lesions in Bells palsy. Otolaryngol Head
Neck

Surg 1987; 97:326-327.

Murakami S, Mizobuchi M, Nakashiro Y, et al. Bell palsy and herpes simplex virus:

identification of viral DNA in endoneural fluid and muscle. Ann Int Med 1996; 124:27-30.
Peiterson E. The natural history of bells palsy. Am J Otol 1982; 4:107-111.
Podvinec M. Facial nerve disorders: Anatomical, histological and clinical aspects. Adv

Otorhinolaryngol 1984; 32:124-193.

Prescott CA. Idiopathic facial nerve palsy in children and the effect of treatment with
steroids.

Int J Pediatr Otorhinolaryngol 1987; 13:257-264.

Ramsey MJ, DerSimonian R, Holter MR, et al. Corticosteroid treatment for idiopathic facial

nerve paralysis: A meta-analysis. Laryngoscope 2000; 110(3 Pt 1):335-341.

Salinas RA, Alvarez G, Daly F, Ferreira J. Corticosteroids for Bells palsy (idiopathic facial

paralysis). Cochrane Database Syst Rev 2010; 17(3):CD001942.

11
Bell's Palsy October 2012

Salman MS, MacGregor DL. Should children with Bells palsy be treated with
corticosteroids? A systematic review. J Child Neurol 2001; 16:565-568.

Shafshak TS, Essa AY, Bakey FA. The possible contributing factors for the success of steroid
therapy in Bells palsy: A clinical and electrophysiological study. J Laryngol Otol 1994;
108:940-943.
Stankiewicz JA. A review of the published data on steroids and idiopathic facial paralysis.
Otolaryngol Head Neck Surg 1987; 97:481-486.

Sugita T, Murakami S, Yanagihara N, et al. Facial nerve paralysis induced by herpes simplex
virus in mice: an animal model of acute and transient facial paralysis. Ann Otol Rhinol
Laryngol 1995; 104:574-581.

Williamson IG, Whelan TR. The clinical problem of Bells palsy: Is treatment with steroids
effective? Br J Gen Pract 1996; 46:743-747.

Wolf SM, Wagner JH, Davidson S, et al. Treatment of Bell palsy with prednisone: A
prospective, randomized study. Neurology 1978; 28:158-161.