SURVEY OF OPHTHALMOLOGY
VOLUME 52 NUMBER 2 MARCH–APRIL 2007
MAJOR REVIEW
Ophthalmic Management of Facial Nerve Palsy:
A Review
Imran Rahman, MB BS, MRCOphth, and S. Ahmed Sadiq, MB BS, FRCS, MRCOphth, DO
Manchester Royal Eye Hospital, Manchester, United Kingdom
Abstract. Facial nerve palsy affects individuals of all ages, races, and sexes. Psychological and
functional implications of the paralysis present a devastating management problem to those afflicted,
as well as the carriers. Since Sir Charles Bell’s original description of facial palsy in 1821, our
understanding and treatment options have expanded. It is essential that a multidisciplinary approach,
encompassing ophthalmologists; Ear, Nose, and Throat surgeons; plastic surgeons; and psychologists
work closely to optimize patient management in a staged approach. Although the etiology remains
unknown, strong histological, cerebral spinal fluid, and radiological evidence suggests a possible
association with herpes simplex virus in idiopathic facial nerve palsy (Bell’s palsy). The use of steroids
has been suggested as a means of limiting facial nerve damage in the acute phase. Unfortunately, no
single randomized control trial has achieved an unquestionable benefit with the use of oral steroid
therapy and thus remains controversial. In the acute phase, ophthalmologists play a pivotal role in
preventing irreversible blindness from corneal exposure. This may be successfully achieved by using
intensive lubrication, medical therapy (botulinum toxin), or surgery (upper lid weighting or
tarsorraphy). Once the cornea is adequately protected and recovery deemed unlikely, longer term
planning for eyelid and facial reanimation may take place in an individualized manner. Onset is
sudden and management potentially lengthy. Physician empathy, knowledge, and experience are
essential in averting long-term lifestyle and psychological discomfort for patients. (Surv Ophthalmol
52:121--144, 2007. Ó 2007 Elsevier Inc. All rights reserved.)
Key words.
bell palsy
facial nerve palsy
management
I. Introduction
review
ated on movement. Nasal alar collapse, nasolabial
flattening, and drooling further add to social
stigma associated with an induced nasal muffled
speech.65 The absent lower lid nasal twist in facial
paralysis further exaggerates epiphora.20 Visual
problems as a consequence of palpebral fissure
widening, loss of the blink response, and orbicularis
function are exacerbated by gravitational effects,
culminating in the potential for corneal exposure.
This lagophthalmos is further aggravated by paralytic ectropion coupled with upper and lower eyelid
retraction.
Bell’s palsy (or idiopathic facial nerve palsy, IFNP)
represents a disfiguring condition. Individuals afflicted deal with physical and psychosocial disabilities that accompany the loss of facial nerve
function. Increased sensitivity to heat, cold, and
wind adds to the reduced quality of daily living.
The dysfunctional element of IFNP results from
an unnatural loss of movement on the side of the
face affected. The upper and lower eyelids, cheek,
and the corner of the mouth show abnormal
relaxation. This disfigurement is grossly exagger121
Ó 2007 by Elsevier Inc.
All rights reserved.
0039-6257/07/$--see front matter
doi:10.1016/j.survophthal.2006.12.009
122
Surv Ophthalmol 52 (2) March--April 2007
Each of these factors contributes to limited
corneal protection. Ultimately, corneal dryness,
ulceration, and blindness are imminent if intervention is delayed. Secondary visual problems may
ensue (for example, the paralytic eyebrow ptosis
generated may cause masking of the superior visual
field), and are generally treatable.
The oculoplastic surgeon, as part of a multidisciplinary team, has the primary aim of maintaining
good visual function and protecting the cornea
from sight-threatening complications induced by
the consequent lagophthalmos. Subsequent cosmetic aims include facial rehabilitation whereby
facial symmetry is restored in the periorbital and
mid facial regions.
Throughout this extended review, the main
emphasis will be placed on the most common cause
of facial paralysis, namely, Bell palsy and, to a lesser
extent, Ramsay--Hunt syndrome. However, although
we aim to discuss the acute management of these
causes, we will endeavor to provide a review of
longer-term management options of long-standing
facial nerve palsy of any cause.
Facial nerve paralysis has been known and
documented since ancient times.196 In 1797, a German professor, N.A. Freidreich, documented success
in the treatment of three patients with facial
paralysis.33 However, 23 years later the work by
Charles Bell on facial nerve innervation credited
Bell with the syndrome of idiopathic facial
palsy.126,181,182 Over the years the syndrome has
come to bear his name, Bell palsy.
Sir Charles Bell (1774--1842) was a Scottish
surgeon and anatomist. He graduated from the
University of Edinburgh in 1799. In 1814, Charles
Bell accepted a position as a surgeon at the
Middlesex Medical School, London. His dynamic
and well-respected opinions as a surgeon were
further consolidated when he was appointed Professor of Physiology in the newly established
University College London Medical School.
After his involvement in the Battle of Waterloo as
a surgeon of the British army, in 1815, Sir Charles
Bell continued his academic and surgical career. He
authored many texts on anatomy, some as a student,
and in 1821, his depiction of facial nerve palsy was
first described. Sir Charles Bell died in Worcestershire, England on April 28, 1842, aged 68. Reports
say he passed away a contented and pleased member
of the surgical profession.121,178,245
II. Anatomy
The facial nerve (seventh cranial nerve) is
branchial in origin. It contains gustatory and para-
RAHMAN AND SADIQ
sympathetic fibers often in a sensory root referred to
as the intermediate nerve. Emerging from the lower
border of the pons, between the olive and inferior
cerebellar peduncle and joined by the intermediate
nerve, the nerve trunks travel anterolaterally for 24
mm to the internal acoustic meatus. The labyrinthine artery, followed by continuation of the nerve
into the facial canal, accompanies entry into the
meatus. After a further 4 mm, the nerve turns
posteriorly in the direction of the internal auditory
meatus. At this bend lies the geniculate ganglion,
which receives fibers from the nervus intermedius.
Turning 40--80 and traversing posterlaterally along
the medial wall of the middle ear, adjacent to the
tympanic membrane, the nerve exits the cranium
via the stylomastoid foramen. Once the nerve exits
the foramen two branches are given off and the
main trunk of the facial nerve divides into upper
and lower divisions. These turn anteriorly in the
parotid gland. At this point, the nerve lies superficial to the retromandibular vein and external
carotid artery. It then divides into four branches
and one ramus: the temporal, zygomatic, buccal,
mandibular branches, and cervical ramus. These
branches go on to supply the facial musculature. Of
note, the temporal branch supplies part of the
frontalis muscle and superior parts of the orbicularis. The zygomatic branch innervates frontalis and
orbicularis oculi.43,100,134
The lacrimal gland requires a specific mention.
The lacrimal gland is responsible for the secretion
of tears. It has a larger orbital portion positioned in
the upper lateral border of the orbit. A smaller
palpebral portion lies behind the upper lid. The
nervus intermedius arising from the brainstem
continues from the lacrimal nucleus and becomes
continuous with the facial nerve. The greater
petrosal nerve leaves the facial leave within the
petrous temporal bone at the genu, synapsing in the
pterygopalatine ganglion. Pre-ganglionic parasympathetic fibers synapse with the cell bodies of
postganglionic fibers at the ganglion. These fibers
continue with the zygomatico-facial nerve via the
maxillary nerve, which terminate as the lacrimal
nerve in the lacrimal gland, providing the secretomotor function of the gland.
III. Epidemiology
A. PREVALENCE
The vast etiologies of facial nerve palsy prevent
accurate estimation of the incidence of facial nerve
palsy from all causes. Idiopathic causes are synonymous with Bell’s palsy, that is, facial paralysis or
paresis secondary to unknown cause(s). Estimates
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
vary between 17 and 35 cases per 100,000 for all
causes.69,90,103,124,183 A UK population study, and
a similar Canadian study, estimated the incidence of
idiopathic facial nerve palsy as between 13.1/
100,000 and 20.2/100,000.166,201 In cases of familial
facial nerve palsy a reported incidence of between
2.4% and 28.6% of all facial palsies is suggested.8,15,21,62,183,184,229,242
Reports of the incidence in neonates are well
documented. Perlow et al reported an incidence of
0.6--0.7 per 1,000 live births as a result of birth
trauma.186 Falco and Eriksson documented a rate of
1.8 per 1,000 as acquired cases of facial nerve palsy
in neonates secondary to birth trauma, 91% due to
forceps delivery.79 However, 89% recovered with
adequate follow-up.
In pregnancy, the incidence of IFNP is 45 per
100,000, compared to 17 per 100,000 in the nonpregnant state.105 This incidence increases drastically to 118 cases per 100,000 during the third
trimester.
B. SEX DISTRIBUTION
There is no universal agreement of sexual preponderance in facial nerve palsy,8,183 although
Devriese et al69 reported more males than females
in their cohort. Conversely, Park and Watkins177
found a greater proportion in women than men.
C. AGE
Several studies have described the highest incidence of facial nerve palsy in the 15--45 year
group.69,155,177,183,190 Children under the age of 15
account for up to 14% of all causes of facial palsy.183
D. SEASONAL VARIATION
Seasonal variation in the incidence of facial palsy
remains uncertain. Peitersen,183 Park and Watkins,177 and Adour et al8 found no significant
seasonal variation. However, Devriese et al69 described more cases in winter months. Parry and
King245 observed only minor variations, with slightly
more cases in the winter, implicating a viral cause.
E. PROGNOSIS
Outlining the prognostic outcome of IFNP provides an estimation of the risk of nerve degeneration. It further enables guidance on timing of
therapies and offers advice to patients. Currently,
prognosis and prognostic indicators are obtained by
clinical evaluation of the initial presentation of signs
and symptoms, function testing, specific nerve
excitability, and response to medical therapy,
namely steroids and acyclovir.
123
The onset of idiopathic facial nerve palsy is
typically sudden, followed by progression over the
following 7--10 days. Spontaneous, complete recovery occurs in up to 70% of cases.155 In most
cases remission begins within 3--4 weeks, with
complete spontaneous recovery within 6 months.
In 1982, Peitersen184 described the natural history
of 1,109 cases over a 15-year period. He found that
70% recovered without sequelae. A further 13% had
barely detectable deficits of function and a significant 16% of patients experienced incomplete recovery of the paralysis. In a more recent review,
Peitersen in 2002183 noted 85% of the original 70%
who had spontaneous complete recovery recovered
within 3 weeks of onset of facial nerve paralysis and
the remaining 15% recovered over the subsequent
3--5 months. Interestingly, he found recovery to be
limited and halted between 3 weeks to 3 months.
During this period the facial nerve seems to be nonfunctioning, but in fact, is hypothesized to be in
a recovery mode. In total, 6.8% of patients in the
cohort suffered recurrence either on the ipsilateral
or contralateral side.
In an attempt to offer a valid prognosis, various
tests and clinical signs have aimed to evaluate factors
that may offer insight into recovery.
Patients presenting with incomplete paresis
recover well. Estimates vary between 93--98%
for spontaneous complete recovery in this
group.183,217,221,245 The presence of pain or altered
taste appears to have no prognostic value.155
Further, the older the patient, the less likely
complete recovery is to follow.69,109,124,190 In a large
study of approximately 2,500 IFNP patients, Peitersen183 found those aged less than 14 years old
recovered in 90% of cases. In the 15--29 age
groups, recovery lowered to 84%, further reducing
to 75% in the 30--44 age groups. In the over 60 age
group, complete spontaneous recovery was markedly limited to only 33% of cases, confirming the
presence of advancing age as a poor prognostic
indicator.
Associated physiological or pathological co-morbidity may alter prognosis (Table 1). Onset of facial
nerve palsy in pregnancy is generally considered to
have an unfavorable outcome.80,184,199,207 Gillman
et al93 found a significantly greater proportion of
pregnant patients progressed from incomplete to
complete facial palsy, of which only 52% went on to
almost complete recovery.
The presence of herpes zoster (Ramsay--Hunt
syndrome) generally provides evidence for poor
outcome. This more severe and painful cause of
facial palsy is known to cause late neural denervation, and to have a less favorable recovery profile
than Bell palsy.69
124
Surv Ophthalmol 52 (2) March--April 2007
TABLE 1
Factors Influencing Prognostic Outcome in Idiopathic
Facial Paralysis
Complete paralysis of facial muscles
Age above 60 years
Herpes zoster infection (Ramsay--Hunt syndrome)
Minimal recovery by 3 weeks
Pregnancy
Degeneration of the facial nerve as demonstrated by
electrophysiological testing (salivary flow test, possibly
electromyography)
Possible factors affecting prognosis: diabetes and
hypertension
Smith et al221 found hypertension, malaise, and
vertigo to be non-significant risk factors in the
prognosis of Bell’s palsy. Other studies have found
a correlation with poor prognosis when hypertension is coupled with IFNP.2,12 Similarly, Smith et
al221 found no prognostic value of diabetes, contrasting other observations of possible poor outcome associated with diabetes.116,143,183
A multitude of tests may confer variable prognostic value. The maximal stimulation test,157 that is,
a subjective evaluation of neuromuscular function
evoked by voluntary contractions, is useful as
a prognostic indicator, although not 100% reliable.
However, it is not good in determining whether
treatment is indicated or not.155
A salivary flow test is a useful prognostic indicator.
As a tool, the salivary flow test predicts denervation
before it begins, and may help in predicting patients
who could benefit from medical therapy.155
Taste, stapedius reflex, and nasolacrimal reflex
provide reliable prognostic data.76,183 However, Ralli
et al193 found no prognostic value of the stapedial
reflex in recurrent cases. In early reports, Buchthal47 demonstrated no prognostic significance of
electromyography. However, more recently114,218
electromyography has been shown to have a possible
role in predicting those patients who may have
eventual poor outcome.
In summary, 83% of all patients have good
recovery and 17% have unfavorable recovery without any treatment modality.183 A variable recurrence
rate of 3--15% is worth mentioning when counseling
patients.8,29,69,148,177,189
IV. Etiology
The myriad of etiologies may be broadly grouped
conveniently into infectious, neoplastic, traumatic,
and idiopathic. The most common causes of facial
nerve paralysis include idiopathic (Bell) palsy
(51%), facial nerve trauma (22%), and Ramsay--
RAHMAN AND SADIQ
Hunt syndrome (7%),114 but these estimated figures
vary.
A. PATHOPHYSIOLOGY AND THE ROLE
OF THE HERPES VIRUS IN BELL’S PALSY
The hypothesis that Bell’s palsy is derived from
herpes simplex virus (HSV) reactivation has gained
popularity since McCormick published his theory in
1972.162 HSV reactivation is now commonly thought
of as the cause for the majority of idiopathic cases of
facial nerve paralysis. In 1975, Adour et al7 found
significantly higher HSV antibody titers in 40 Bell’s
palsy patients compared to matched normals. They
further deduced HSV reactivation was associated or
even causative of Bell’s palsy. Data has since added
strength to this hypothesis. In the laboratory,
Murakami et al170 observed a 79% detection of the
HSV genome in facial nerve fluid of patients
afflicted with idiopathic facial paresis. Horda and
Takahashi110 observed a high frequency of HSV
antibodies in CSF suggestive that HSV results in
facial nerve demyelination in Bell’s palsy. Further
pathology data141 and radiological imaging233 have
been documented to support this etiopathogenic
model.
Histopathologically, it has been shown that the
entire facial nerve is infiltrated by inflammatory
cells, with edema, axonal changes, and myelin
breakdown suggesting a viral neuritis.141 In 2002,
Wakisaka et al239 reported a model of inoculating
HSV-1 into the auricle of mice and inducing facial
nerve paralysis. HSV-1 antibody was detected tracking along the facial nerve in various stages using
immunofluorescence.
Pathophysiologically, compressive forces have been
theorized to account for Bell’s palsy. Retention of
fluid resulting in perineural edema may result in
mechanical compression within the bony course of
the facial nerve. Observing an increased incidence
among pregnant women enhances support for this
theory.32,131,240 T2-weighted magnetic resonance
imaging (MRI) allows good visualization of the
meatal part of the facial nerve. Increased enhancement and thickening of the facial nerve have thus
been demonstrated in patients with idiopathic facial
nerve palsy,134 showing the bottleneck of the nerve
caused by inflammation. Studies should use gadolinium-DTPA contrast material as this increases
MRI intensity by shortening T1 and T2 relaxation
times. As it does not cross the blood--nerve barrier,
enhancements of inflamed and edematous tissue
are seen. Imaging may be of value in diagnosis
and management of facial palsy (i.e., although
facial nerve enhancement in both idiopathic facial
paresis and Ramsay--Hunt syndrome are identical,
125
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
Ramsay--Hunt syndrome demonstrates enhancement of 70% of structures other than the facial
nerve), but are prognostically unreliable.42
B. HERPES ZOSTER VIRUS INFECTION:
RAMSAY--HUNT SYNDROME
The herpes zoster virus is the most common
confirmed infective cause for facial nerve paralysis
resulting in the Ramsay--Hunt syndrome,229 although first described by Miehlke in 1904.164
Geniculate ganglionitis results in zoster vesicles in
the ear, external auditory canal, tongue, and hard
palate resulting from the closeness of the ganglion
to the vestibulcoclear nerve. In effect, Ramsay--Hunt
syndrome represents generalized inflammation of
surrounding nerve, muscle and skin. Zoster patients
portray a high incidence of complete paralysis
(88%).183 In comparison to Bell palsy, patients with
Ramsay--Hunt syndrome are less likely to recover
completely and have a more severe painful paralysis
associated with vestibulocochlear symptoms at onset. 21% achieve return to normal function and the
remaining 79% develop sequelae. Fifty-four percent
have a poor recovery.183
Ramsay--Hunt syndrome zoster sine herpete is
traditionally associated with Ramsay--Hunt syndrome. It is a condition in which localized radicular
pain is associated with virological evidence of
varicella-zoster virus (VZV). A proportion of patients
with Ramsay--Hunt syndrome develop facial paralysis
without vesicles in the mouth or ear, but present
a fourfold increase in VZV antibody titer.198 This
indicates that some patients with Bell’s palsy may in
fact suffer from Ramsay--Hunt syndrome. Murakami
et al169 observed a 38% incidence of vesicles in
patients with Ramsay--Hunt syndrome, 24% occurring on presentation of facial palsy and the remainder 14% over a 1-week period. Fututa90
described a 29% reactivation of VZV in patients
with idiopathic facial paralysis.
C. OTHER INFECTIVE CAUSES OF FACIAL PALSY
Borrelia Burgdorferi, the etiological organism in
Lyme disease, is a known cause of facial nerve palsy
in endemic regions.185 Tuberculous chronic middle
ear infections, although a rare entity, are important
and treatable, and as such must be considered in all
patients with chronic middle ear infections.137 Rare
infective causes include Dengue fever,180 leprosy,142
mumps,78 Epstein Barr virus/Cytomegalovirus,144
and polio.167
D. TRAUMATIC AND IATROGENIC CAUSES
Traumatic and iatrogenic facial nerve palsies most
commonly result from a multitude of blunt or
lacerating injuries to the cranio-facial region and
present with variable degrees of subsequent disabilities. Panosian176 described an unusual case of
molten metal entering the middle ear via the
external meatus resulting in facial paralysis from
possible heat injury to the nerve. However, more
commonly temporal bone fractures and surgical
incisions in close proximity to the facial nerve are
culprits. The facial nerve may be mobilized, manipulated, or even sacrificed in an attempt to remove
craniofacial tumors, such as acoustic neuromas. As
a result, a spectrum of dysfunction may result,
ranging from permanent complete paralysis to
a completely normal functioning nerve.130
E. INFILTRATION, COMPRESSION,
AND MALIGNANCY
In the absence of surgical intervention, facial
nerve paresis may result from tumors themselves,
either through direct compression, significant
stretching, or infiltration of the nerve. Cerebellopontine angle lesions may cause multiple cranial
nerve defects as well as affecting the seventh nerve
in isolation. Commonly, these may be due to
acoustic neuromas or meningiomas of the cranial
cavity. Matthies and Samii151 presented their experience of 1,000 acoustic neuromas. Of these, up to
17% of patients had signs of facial nerve dysfunction
prior to tumor resection. However, often these were
subclinical and not recognized by the patient. In
a follow up study,206 the authors described anatomical preservation of the facial nerve in 93% of
patients. If the nerve was sacrificed in order to
achieve complete tumor resection, either end-toend anastomosis or cable grafting was performed.
The overall figure of 1.7% of patients suffering
persistent paralysis postoperatively outlined their
initial careful preservation of the facial nerve if
possible, or aggressive initial and perioperative
treatment and restoration of facial nerve anatomy
if preservation was not possible.
Parotid tumors (benign or malignant), facial
nerve schwannomas, malignant tumors of the
external meatus, nasopharyngeal carcinomas, and
lymphomatous lesions may also result in facial nerve
paralysis/paresis.119,175 Infiltrations by sarcoid,214
leukemia,83,224 collagenosis, and amyloid41 may also
be causative.
F. CONGENITAL AND HEREDITARY CAUSES
There are several hereditary causes of facial nerve
paralysis. These include familial,230 Treacher-Collins syndrome,73 Moebius syndrome,150 Patau
syndrome, Edwards syndrome, and Goldenhar
syndrome.30
126
Surv Ophthalmol 52 (2) March--April 2007
G. OTHER CAUSES
Other causes of facial palsy include diabetes
mellitus,3,121 pregnancy,131,199 multiple sclerosis,64
Paget disease,89 and HIV.208
V. History
The sudden onset of facial paralysis is alarming
for patients. Palsy with sudden onset and rapid
evolution suggests Bell’s palsy. This is most often
unilateral and produces a maximal effect after 2
days, and resolution in 3 to 4 weeks. Associations
with hyperacusis, decreased lacrimation, and altered
taste add support to an idiopathic cause. However,
as Bell’s palsy is an isolated mononeuropathy,
association with other cranial nerves should alert
the examiner to other causes for the facial paralysis.
The multitude of etiologies requires careful history
taking and examination. Those with iatrogenic and
traumatic causes can be elicited by history alone.
Otalgia or facial/postauricular pain preceding the
paralysis may suggest Ramsay--Hunt syndrome. Postauricular pain has been demonstrated to occur 2--3
days prior to paresis or on the same day as the onset
of pareses.183 Severe pain and a vesicular rash may
then follow facial paralysis. Patients with a more
gradual onset and associated with multiple cranial
nerve abnormalities may indicate a neurological or
otological cause for the paresis and require thorough examination and imaging where appropriate.
Tuning fork and otoscope assessment of the ear is
an essential part of the examination. Head and neck
masses should be ruled out and rashes observed,
implicating possible infectious etiology.
Further examination should include full cranial
nerve assessment, including baseline visual acuity,
pupillary reactions, tear production, and optic disc
evaluation.
A typical history suggestive of Bell’s palsy may be
observed without investigation. Kumar et al134
suggest imaging with CT and MRI scanning is
indicated in selective cases, and should always
include the parotid gland. Furthermore, gadolinium-DTPA contrast pulse sequence was the most
beneficial method of evaluating the facial nerve for
pathology using MRI scans. Berrittini et al31 earlier
confirmed the importance of contrast enhanced
MRI scanning in Ramsay--Hunt syndrome, where
limitation of inflammation to the geniculate ganglion correlated with a good prognosis.
VI. Classification
In 1985, The American Academy of Otolaryngology endorsed the subjective House--Brackmann112
RAHMAN AND SADIQ
grading system as a standard for monitoring
peripheral facial nerve paralysis (Table 2). However,
limitations and subjectivity of the scale prevent
consistent reliability (Table 3).
The facial nerve is complex, encompassing both
motor functions (lacrimation and salivation) and
sensory functions (taste); regeneration may result in
aberration or synkinesis. Both factors are not adequately addressed with the House--Brackmann scale,
which does not measure actual facial movements.
To accommodate the shortcomings of the House-Brackmann scale, newer scales have developed. In
1985, Burres51 assessed seven standard facial expressions in a linear measurement technique. Points of
interest in facial movement were marked and
differences calculated. Burres and Fisch further
refined this method in 1986.50 This relied on
objective measurements, limiting observer error.
Although reliable, the system is complex, necessitating the need for lengthy, often time-consuming
calculations not suited to the clinical setting.
Modifications to this system were developed in the
Nottingham scale.171 This system is described as
incorporating synkinetic defects and provides
a more rapid clinical measure than the Burres and
Fisch method.
Recently, digitalized images have aided in developing newer grading systems. Subtraction techniques are used to compare the facial movements at
rest and on movement. Kang et al,122 Barrs et al,29
and Dulguerov et al74 provide excellent reviews of
the grading systems. Although inexpensive, it requires prolonged patient cooperation with difficult
interpretation of results. To date, no computerized
method allows easy, quick evaluation of facial nerve
function. However, it is hoped that in the future
a combination of the House--Brackmann scale and
a computerized digital technique may allow for
a standardized, easy-to-use, clinically useful objective
scale to be established.
The maximal static response of facial movement
allows actual measurement of facial movement by
tracking the positions of specific facial points
throughout a variety of facial movements. In 1997,
Bajaj-Luthra et al24 presented their findings on the
TABLE 2
House--Brackmann
112
Grading System for Facial Palsy
Grade 1 Normal function
Grade 2 Mild dysfunction
Grade 3 Reduced forehead movement, noticeable
synkinesis and contracture
Grade 4 No forehead movement, incomplete eye closure,
asymmetric mouth, disfiguring asymmetry
Grade 5 Minimal movement
Grade 6 No movement
127
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
TABLE 3
Studies Showing Treatment and Outcomes with the Use of Steroids in Bell’s Palsy
Study
Duration Before
Onset of
Treatment
Number
(days)
Year of Patients
Taverner231 1954
26
9
Adour
1972
304
14
May160
Brown45
Austin22
1976
1982
1993
51
82
76
2
3
5
Shafshak213 1994
160
6
Wolf244
239
5
1978
Method of
Treatment Allocation
Follow-up
(months)
Outcome of
Steroid Benefit
RCTb
Not
No significant benefit
specified
Uncontrolled, comparative
1
Possible benefit in
study. No randomization
recovery
RCTb
6
No significant benefit
Quasi randomized studya
12
No significant benefit
RCTb
6
Not statistically significant,
although a significant
improvement in facial
recovery documented
Prospective nonrandomized,
12
Statistically significant
unmatched, concurrent
treatment effect
controls
Prospective randomized
12
Steroids reduce synkinesis,
but do not alter long
term recovery
a
b
Randomized alternate patients.
Randomized controlled trial.
use of anatomic and non-anatomic indices. The
anatomic index was defined as motion of the
specific points studied by the maximal static response assay that can be attributed solely to the pull
of the regional muscles governing the movement of
those points. The non-anatomic index was characteristic of a paralyzed hemiface in which the motions
imparted to specific ipsilateral facial points are
transmitted primarily by the pull of unaffected
contralateral muscles. By monitoring these points,
recovery and accurate documentation of changes in
facial nerve function could be measured over time
in cases of complete facial paralysis.
Electromyography (EMG) allows the blink reflex
to be evaluated in patients with facial nerve
paralysis. The method allows needle electromyographic detection of pathological spontaneous
fibrillation activity, suggesting nerve degeneration.
Although, not a grading system, EMG may allow
outcome prediction in acute facial nerve palsy, and
provide a measure of recovery.114 Sittel and Stennert218 found 80% accuracy for predicting unfavorable outcome when spontaneous fibrillation is
present in patients with acute facial nerve paresis/
paralysis. They suggested that this method might be
useful in providing patients with a prognostic indicator for poor recovery.
VII. Management
Therapy for facial nerve palsy begins by taking
a thorough clinical history, followed by a compre-
hensive examination. This should ascertain whether
the paralysis is acute or chronic in onset, unilateral
or bilateral, exclude secondary causes of facial palsy,
and differentiate between proximal and distal
lesions.
The aim of management of seventh nerve palsy is
oculoplastic rehabilitation by protecting globe integrity using minimal intervention and maximizing
convenience for the patient, thereby maintaining
good visual acuity. Ultimately, treatment is undertaken in stages. Initially, early stages of management
aim to speed recovery and limit corneal exposure
and restore the blink response. Seiff and
Chang211,212 describe a staged management approach to eyelid paralysis following facial nerve
paralysis (Table 4). This provides a good framework
for management planning of this very complex
condition. However, correction of complex synkinetic movements is not incorporated, and as such
the staged approach is slightly altered in this review.
A. SUPPORTIVE
1. Conservative
Protecting the cornea is the primary goal of
therapy. This may be achieved by promoting recovery of the facial paralysis or by meticulous
monitoring and treatment of corneal complications.
Often the lower third of the cornea is affected, but
this is dependent on the degree of lagophthalmos.
In the absence of Bell’s phenomenon and corneal
sensation, the entire cornea remains unprotected
even during forced eyelid closure. Complicating the
128
Surv Ophthalmol 52 (2) March--April 2007
TABLE 4
211,212
Seiff and Chang
Classification
of Facial Palsy Management
Stage
Stage
Stage
Stage
Stage
Stage
1
2
3
4
5
6
Supportive
General facial reanimation
Lower lid support
Passive upper lid animation
Dynamic lid reanimation
Soft tissue repositioning
decision of when to instigate appropriate treatment
is the likelihood of recovery. If recovery is expected,
less-invasive techniques may be deployed with careful monitoring.
Intensive lubrication with methycellulose preparations is the mainstay of treatment in the early
phases. Lubrication may be used in the form of
preservative-free tear drops during the day and
a more viscous ointment overnight. Taping of the
eyelids at night prevents exposure and trauma while
sleeping. However, patching and padding of the
affected eye maybe less useful and result in abrasive
trauma to the cornea.209 Moisture chambers have
been used to produce an orbital greenhouse with
good effect. Patients are asked to lubricate the eye
overnight and then apply a Cartella shield with an
overlying layer of cellophane dressing over the
orbital region, allowing moisture to be retained
within the formed pocket. Various moisture chambers are used and are dependent on patient
suitability, surgeon preference, and availability of
components.
In patients in whom tear production is reduced
and the previously described measures fail to
address exposure, punctal occlusion with the use
of punctal plugs maybe beneficial. Howcroft proposed a more novel idea.113 He used photoelectric
cells mounted on a spectacle frame to provide
a stimulus for closure of the paretic eyelid and
prevent exposure. However, this development never
gained favor.
2. Medical
a. Botulinum Toxin
Until relatively recently, failure of intensive
lubrication to protect the cornea would necessitate
a temporary or permanent tarsorrhaphy to close the
eyelids. However, botulinum toxin injection provides a good means of inducing a protective ptosis
by temporarily paralyzing the levator palpebrae
superioris, and thus protecting the cornea (Fig. 1).
Ellis and Daniell77 describe a series of 21 patients
who underwent botulinum toxin injection through
RAHMAN AND SADIQ
the levator palpebrae superioris. They found the
effect of the induced ptosis was sustained for a mean
of 46 days following an onset after 4 days. In 16 of
these patients, botulinum toxin induced ptosis
prevented further surgical intervention and afforded corneal healing. Sadiq and Downes205 used
a skin crease entry site to induce a ptosis. They
reported a 45% rate of temporary diplopia, but
advocated the use of botulinum toxin, as eyelid
scarring is avoided, topical therapy may be continued, and examination of the cornea remains
possible. If an orbital route for toxin injection is
used, persistent squints may develop, necessitating
squint corrective surgery.104
b. The Use of Steroids and Oral Acyclovir
It is clear from the literature that patients with
incomplete paralysis do well without treatment. The
majority will recover spontaneously.6,183,217,221,245
With initial complete paralysis, recovery is less
predictable. In a series of 1,701 patients, Peitersen183 described a 94% recovery rate in those with
incomplete palsy. In those with complete paralysis
approximately 60% spontaneously recover.
The use of medical therapy in the form of steroids
and oral acyclovir remains controversial. Studies of
immune complexes,4 lymphocyte populations,23
and CSF75,115 suggest a cell-mediated immune
response occurs in response to a viral insult to the
facial nerve in Bell’s palsy. It is therefore reasonable
and widely accepted that treatment with oral
steroids for idiopathic facial palsy may be beneficial.
Since Taverner presented the first randomized
controlled trial of oral prednisolone treatment in
1954,231 similar double-blind studies have differed
in the treatment benefit of steroids in idiopathic
facial palsy.
It must be understood, however, that nerve
conduction does not appear to become abnormal
until 3 days after the onset of paresis when nerve
degeneration develops.155,156 The goal of medical
therapy should therefore aim to treat those patients
whose symptoms and treatment commence within
this 3-day window. To date, seven adult-based
prospective studies have compared concurrent
patients treated with oral steroid therapy against
placebo controls in idiopathic facial paralysis.13,22,45,160,213,231,244 Commonly, 1 mg/kg of oral
prednisolone is given for 6 days and reduced
thereafter, over 4 consecutive days. However, 7 days
has been used by many of these studies as the
absolute upper limit for treatment from symptom
onset to the instigation of steroid therapy. Table 3
lists the seven studies and outcomes. Of the
seven trials, four showed no significant benefit of
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
129
Fig. 1. A series of photographs demonstrating exposure keratitis and a left brow ptosis (A) in a patient with Bell’s palsy.
There is significant lagophthalmos (B) and slight left lid retraction (C) once the eyebrow ptosis has been manually
neutralized. The patient underwent a supratarsal botulinum toxin injection (D) to induce a ptosis (E). The slight
lagophthalmos present with the right eye fully open disappears with relaxation of the lids (F), thus protecting the cornea
(G).
steroids,22,45,160,231 one showed a possible significant
benefit,13 and a further study demonstrated a decreased incidence of synkinesis through steroid
therapy, but no alteration in recovery.244 Only one
showed a statistically beneficial outcome with
systemic steroids.213 Much of the presented data in
the studies is inconsistent in the timing of treatment, length of treatment, and dosage of steroids.
As such, no definite conclusions and consensus has
been reached to convince the treating community
of the undisputed benefit of steroid therapy.
Grogan and Grosneth98 preformed an evidencebased review of steroid therapy in patients with Bell’s
palsy. They concluded that evidence remains insufficient to make recommendations on the benefit
of steroid therapy. This confirmed Stankiewicz’s
comprehensive literature review in 1987.226 However, from pooled data, they further established that
130
Surv Ophthalmol 52 (2) March--April 2007
steroid use in this setting was safe and ‘‘probably
effective in improving functional outcomes in
patients with Bell’s palsy (p. 830).’’
A meta-analysis of current literature by Ramsey et
al195 pooled three studies using inclusion criteria to
identify and assemble literature with least bias and
subjectivity in patients treated with steroids with
complete facial paralysis. In this setting they found
that steroid therapy provided clinically and statistically significant improvement in functionality and
recovery in those patients with complete facial
paralysis. Although 60% recovered spontaneously,
a further 17% improved with the use of steroids.
However, as up to 20% of facial palsy will progress
from incomplete to complete paralysis, the authors
recommend treatment with oral steroids in all cases
of Bell’s palsy.
If the overwhelming reports in the literature
believe HSV infection is pivotal in the etiology of
Bell’s palsy, it would then be reasonable to assume
a role for oral acyclovir in its treatment regimen.7,28,32,110,131,141,170,233,239,240 Acyclovir inhibits
DNA replication via its effect on HSV DNA polymerase. Because acyclovir affects only replicating
viruses, and if treatment is to be effective, it must be
instigated within the first 3 days following onset of
the palsy.
Although many entries in the literature comment
on the use of acyclovir in the treatment of Bell’s palsy,
only a handful stand out. A double-blind, placebocontrolled study comparing combined acyclovir/
prednisolone with placebo and prednisolone treatment alone was undertaken by Adour et al in
1996.10 They concluded that if seen within 3 days of
onset, acyclovir (400 mg five times daily) and
prednisolone (minimum of 30 mg twice daily)
treatment for 10 days was significantly better in
aiding recovery of facial paresis than steroids alone
(p ! 0.05), restoring normal function in 92% of
patients. This also held true for combination
therapy being more effective than prednisolone
alone in preventing nerve degeneration as measured by electrical testing (p50.05). Further,
contracture and synkinesis was found in 13% in
the acyclovir/prednisolone group compared to 28%
in the placebo. However, acyclovir alone has been
found to be less effective than prednisolone alone
and is therefore not recommended as monotherapy.67 These findings were confirmed by Hato
et al.102 In this study, combination therapy resulted
in 100% recovery if started within 3 days of
symptom onset, compared to 86% recovery if begun
between 4 and 7 days. Further, nerve degeneration
was also less if treated within 3 days with acyclovir
and prednisolone, compared to treatment after 3
days.
RAHMAN AND SADIQ
Although VZV reactivation usually has a poorer
prognosis than Bell’s palsy, administration of acyclovir within 3 days of onset of facial paralysis resulted in
a high rate of recovery of the facial nerve.168 With
zoster sine herpete, which may account for up to
29% of cases diagnosed as idiopathic, treatment
with acyclovir correlated with better outcomes. This
adds to the argument of treating all idiopathic cases
with acyclovir, as VZV may be causative but not
present with a vesicular rash.
3. Surgical
a. Surgical Decompression of the Facial Nerve
Surgical decompression of the facial nerve has
been postulated as a credible procedure to improve
recovery rates since 1932.27 The debate remains
spirited over the benefit of surgical decompression.
The difficulty remains that not all patients recover
spontaneously to House-Brackmann grade I or II. It
is these patients that require additional therapy.
Certainly, because evidence points to some benefit
with the use of steroid decompression with or
without acyclovir combination, surgical techniques
have all but lagged by the wayside. Adour and
Diamond9 concluded that surgical decompression
provided no additional benefit over the natural
history of idiopathic facial paralysis. In 1985, May et
al159 outlined their series of 38 patients with
complete facial paralysis. They commented on
surgical decompression offering no benefit in Bell’s
palsy, supporting the view of Adour and Diamond.9
Gantz et al91 presented a differing point of view in
1999. They believed patient selection and the site of
decompression limited the usefulness of surgical
decompression. In their multicenter prospective
study, they established the use of electroneurography (EnoG) and voluntary EMGs to identify patients
with facial paralysis with greater than 90% neural
degeneration and no voluntary EMG potentials
within 14 days of onset of weakness. These patients
underwent surgical decompression of the meatal
foramen, labyrinthine segment and geniculate
ganglion via the middle cranial fossa route within
14 days of weakness onset. Ninety-one percent of
patients achieved House--Brackmann grade I or II as
a result. They found this to be highly significant
compared to non-surgical controls. Postulating
further, it was commented that timing was of utmost
importance. Surgery should be performed urgently,
within 14 days of onset of symptoms, or decompression offered no benefit, confirming the earlier work
by Mechelse et al.163
Yanagihara et al248 reported on 101 cases of Bell’s
palsy undergoing surgical facial nerve decompression
131
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
following failure with steroid therapy. No benefit was
observed in this setting.
However, surgical intervention in the acute phase
of Bell’s palsy also remains controversial.
b. Tarsorrhaphy
Surgical measures are employed less frequently in
modern times to ensure adequate corneal protection
in the acute phase. There is less use of tarsorrhaphy
but there has been an increase in the use of other
rehabilitative procedures such as sub-obicularis oculi
fat lifts, load weights, and facial reanimation.
Tarsorraphy techniques to reduce the palpebral
aperture vary. Some employ central tarsorrhaphy,
whereas others advocate lateral tarsorrhaphy (Fig. 2)
with additional medial canthal procedures. Reduction of the palpebral aperture may also be achieved
using cyanoacrylate glue71 or a reversible suture
technique.95 Tarsorrhaphy is most suited to cases of
combined V and VII cranial nerve paresis as corneal
sensation may be impaired in such individuals.
However, tarsorrhaphy procedures have been
criticized for being cosmetically poor and often
ineffective. The loss of peripheral vision makes
tarsorrhaphy a last resort.
‘‘The adynamic lids often fail to protect even
a small area of cornea that is left exposed (p. 63).’’36
Although permanent tarsorrhaphy is now rarely
employed, the reversal of temporary tarsorrhaphy
may result in complications necessitating further
surgical intervention.187 However, in patients in
whom medical therapy is difficult and lacrimal
gland function is lost, tarsorrhaphy remains an
important treatment option. Repeat operations are
avoided and implant rejection is not an issue.
c. Lid Retraction (Passive Upper Lid Reanimation)
Lid retraction is a common phenomenon associated with facial nerve palsy. Lid retraction is
presumed to be secondary to unopposed action of
levator superioris. However, Aramideh et al16 suggested thixotrophy as a cause of lagophthalmos.
They described thixotrophy as ‘‘stiffness of a striated
muscle and formation of tight crossbridges between
the actin and myosin filaments within muscle fibers
causing stiffness of the muscle (p. 665).’’ They
hypothesized that this was the more likely cause of
lagophthalmos rather than paresis of orbicularis
oculi, and by simply manually stretching the levator,
lagophthalmos can be improved.16,17 More conventional methods for treating lid retraction are
dependent on the amount of lid retraction. Tyers
and Collin235 give a good account of the more
conventional methods of treating eyelid retraction,
which is graded towards the severity of lid retraction.
These include transconjunctival retractor recession,
levator recession (anterior or posterior approach
techniques), or Müllerectomy.
d. Lid Loading (Passive Upper Lid Reanimation)
Fig. 2. A patient with poor vision in the right eye
presenting a consecutive exotropia (A) and a left temporal
tarsorrhaphy preformed to limit corneal exposure in the
only eye with visual potential (B). The tarsorrhaphy was
reversed, resulting in an improvement in the patient’s
visual field and psychological state.
The concept of upper lid loading was first
introduced in the 1950s.215 Upper lid weighting
results in increased gravitational pull on the lid.
Aided by levator palpebrae relaxation, the paralyzed
eyelid may close passively, greatly reducing lagophthalmos (Fig. 3). Abell et al1 provided data confirming upper lid weights offer gravity-dependent
lid closure. In 1966, gold was first used as an
effective lid loading material,219 and the concept of
improving blink quality in paralyzed eyelids with
adequate lid closure gained favor (Fig. 4). This
allowed an alternative approach to tarsorrhaphy in
132
Surv Ophthalmol 52 (2) March--April 2007
RAHMAN AND SADIQ
Fig. 3. Lagophthalmos secondary to Bell’s palsy treated with temporary external eyelid weight. A: Demonstrating left
inferior conjunctival injection as a result of corneal exposure. B: Showing 3 mm of lagophthalmos. C: The application of
external upper lid weight. D: Lagophthalmos eliminated using the temporary external eyelid weight.
corneal protection, with better cosmesis and maintenance of visual function. Lid loading with 99.99%
pure gold (24 karats) is now the most common
surgical procedure preformed in facial nerve palsy
of any etiology. This is followed closely by combined
lateral tarsorrhaphy and an upper eyelid weight.234
Traditionally, weighting of the upper lid was not
preformed early in paralysis of the upper lid, but
instead, waited for spontaneous return to function.54 Snyder et al222 recently reported a series of
33 patients who underwent gold implantation
within 30 days of onset of facial paralysis. They
observed that gold implantation early in facial
paralysis was effective in 90% of cases in the
treatment of exposure keratitis due to paralytic
lagophthalmos; just as effective as late implantation
with no increase in the rate of complications. On
recovery, the weight is easily removed with no
residual side effects. This confirmed earlier reports
of potential benefits of early upper lid loading.123,223
Seiff and Boerner210 described the use of external
eyelid weights attached to upper lid pretarsal skin
with double-sided tape as an effective alternative to
surgical implantation in the short term.
Fig. 4. Gold weight with three bored holes for suture
attachment.
133
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
Complications of eyelid loading include skin
erosion, migration, extrusion, and cosmetic dissatisfaction. Jobe120 described 2,000 cases of gold
weight implantation and found only a 0.3% incidence of infection and 2.6% incidence of implant
extrusion (Fig. 5). However, Pickford et al188
described a much higher rate of extrusions (12%)
and migrations (7%). As the standard gold weights
range from 0.6 g to 1.6 g in 0.2-g increments,
modifications in width and size have attempted to
lower the rate of complication, prevent unsightly
cosmesis, and limit corneal astigmatism. Cies60
described weights with smaller widths, whereas
others have described further modifications to allow
suturing to the tarsus.179
In a further effort to decrease these complications,
synthetic and organic barrier materials, such as
human pericardium, have been used with good
results.85 Other less desirable but effective methods
of corneal protection in lagophthalmos include the
use of the Arion silicone slings18 and palpebral
springs.139 Arion silicone prosthesis, although technically more difficult than gold weight implantation,
aims to correct upper lid lagophthalmos and lower
lid ectropion in a single surgical procedure. However,
this is rarely preformed in modern practice. Wire
spring implants, however, offer greater potential for
lid closure independent of the gravitational effect.
Difficulties in exact placement, including bulging of
the spring through skin, infections, extrusions, and
consequent revisions has made wire springs a poor
alternative compared to gold weights.152
B. LOWER LID SUPPORT AND CANTHAL
TENDON SUSPENSION
In the longer term, surgical interventions remain
the mainstay in eyelid and facial reanimation once
Fig. 5. Prominent appearance of gold weight following
insertion. Note the poor cosmetic scar from the direct
brow lift.
the initial waiting period of 6--12 months for
recovery (in the absence of corneal exposure) is
over. Upper eyelid reanimation has been dealt with
earlier in this review. The role of an ophthalmologist
in facial reanimation should coincide with the
plastic surgeon’s role in correcting the ptotic
midfacial region. Lisman et al140 demonstrated
a superior success rate of lower lid reanimation
once the paralytic mid facial region had been
elevated.
Reanimation of the lower eyelid and lateral
canthal resuspension may assist in corneal protection. The extent of gravitational ectropion of the
lower lid is dependent on the level of laxity allowed
by the tarsal plate and medial and lateral canthal
tendons. The procedure of choice varies from
patient to patient and therefore requires an individualized approach. Leatherbarrow and Collin136
demonstrated, in a followup series of 65 patients
with facial paralysis, that several procedures are
needed, often in combination to achieve effective
functional and cosmetic results.
1. Medial and Lateral Canthal Support
In the modern setting, lateral tarsorrhaphy is
more commonly preformed in addition to a lateral
canthal sling, the enhanced sling. This horizontal
lid-shortening procedure allows the resuspension of
the lateral canthal tendon to the periosteum of the
lateral orbital rim, possibly at a higher level to
enhance the effect of the procedure.130 The use of
autogenous fascia lata has lost favor as a sling
support to the lateral canthus. Glat et al94 showed an
evolutionary change from lateral tarsal strip to
lateral canthoplasties in a series of 1,565 lateral
canthoplasties over a 13-year period. They emphasized the need for individualization of the procedure dependent on the preoperative anatomical
findings. In younger patients, or in cases of partial
impairment of orbicularis function, a lateral canthoplasty may be all that is required to bring the
atonic lower lid into a more favorable position.
To further augment the effects of lateral tarsal
slings, combined medial canthal procedures may be
used. Often, significant medial tendon laxity or
ectropion requires a corrective surgical procedure
to improve cosmesis and limit excessive watering
induced by facial nerve paralysis. Crawford et al66
described lid shortening with medial canthal tendon
tightening with excellent functional and cosmetic
results when coupled with McCord’s161 technique of
canalicular stump marsupialization. The long-term
benefit of such procedures has since been confirmed.228
134
Surv Ophthalmol 52 (2) March--April 2007
Similar to the lateral tarsal suspension, medial
ectropion may be corrected by a medial canthal
suspension as described by Castroviejo-Bolibar.53 The
lower lid medial tarsal suspension contributes to
lower lid stability by forming a tight adhesion between
an upper lid flap and the lower lid. After a 6-year
follow-up the procedure remained effective, and,
thus, is considered a permanent yet easily reversible
procedure. If medial canthal suspensions are required, it is better performed before any laterally
based procedures. This prevents lateral movement of
the punctum when there is medial canthal laxity.
2. Lower Lid Spacers
Often increased lower lid support is required to
counteract gravitational effects of the atonic facial
musculature contributing to lower eyelid retraction.
Lower lid spacers provide stiffer upward support
and aid in reconstruction. Hard palate mucosal
grafts63 and tarsus have been used successfully.
Jackson118 described his results of 41 patients treated
with conchal cartilage grafts to provide lower lid
support, with good short-term results. May et al158
reported further evidence for the use of auricular
cartilage implantation as an alternative. Matrix
derived from cadaveric human dermis, AlloDerm
(Lifecell Corporation, The Woodlands, TX) have
been successfully used as a lower lid spacer.203
3. Sub-orbicularis Oculi Fat (SOOF) Lift
Improving facial cosmesis should remain the final
stage in facial nerve palsy rehabilitation and should
only be considered if corneal integrity is maintained. Integral to this is the mid facial rehabilitation, which, although challenging, may improve
lower lid surgery success.140
Sub-orbicularis oculi fat (SOOF) is an important
anatomical structure, widely accepted in plastic
surgery practice as a reliable and aesthetic method
of mid-facial reanimation associated with normal
aging mid facial ptosis. Facial paralysis secondary to
atrophic and atonic facial musculature presents
a similar unilateral dilemma as aging mid-facial
ptosis, and as such requires correction to address
the facial asymmetry. Lifting the SOOF removes the
traction on the lower lid induced by the atonic mid
face.
When SOOF lifts are combined with subperiosteal
face lifting, facial asymmetry may be addressed and
vertical face lifting overcome while avoiding an
unnatural tension on the skin.111,191,194 Theoretically, suspension of the midfacial musculature may
elevate the sagged mouth angle and raise the upper
lip resulting in superior resting facial asymmetry.5
Further refinements of SOOF lifts, combined with
RAHMAN AND SADIQ
subperiosteal face lifting, have been described, some
using an endoscopic approach.49,68,147 In 2000,
Olver174 described the successful use of a transconjunctival SOOF lift, with minimal complications,
when combined with a standard lateral tarsal strip as
an effective rehabilitative procedure for lower lid
retraction secondary to facial paralysis.
C. STATIC AND DYNAMIC LID REANIMATION
Static reanimation by repositioning gravitational
induced drooping is traditionally performed using
fascia.225 Fascia lata slings may be used to raise the
atonic mid and lower facial musculature and
counteract the gravitational effect. However, it is
not a new concept.44 Through several specific skin
incisions, the fascia lata is passed and anchored to
periosteum toward one end, with the other end
passing through subcutaneous tissue, acting as
a sling to raise facial structures.225 A degree of
dynamic reanimation may be achieved by passing
the sling around the masseter muscle.145 Nonetheless, sling techniques are useful in providing some
benefit in form and function in the paralyzed
face.106
More recently synthetic materials have been
introduced.65 These materials have the benefit of
eliminating risk to the donor site. They are sterile,
thin, and do not induce foreign body reactions.
Expanded polytetrafluorethylene (Gore Tex; W.L.
Gore, Flagstaff, AZ) is the most commonly used,52
but complications of extrusion, loss of support, and
infection has limited its use. Fisher and Frodel84
reported on their use of a newer non-synthetic facial
sling, AlloDerm (Lifecell Corp., Branchburg, NJ),
with favorable results.
In cases of chronic lagophthalmos secondary to
irreversible or long-standing facial nerve paralysis,
dynamic reconstruction of eye closure may offer
some degree of symmetry and voluntary eyelid
movement. Introduced at the turn of the previous
century, the transfer of a muscle from one region to
another using its own nerve supply is one of the
most common procedures used in facial dynamic
reanimation.
Temporalis muscle transposition is the most
common of the muscle transfer procedures, popularized by Baker and Conley.25 Transfer of the
temporalis muscle to areas around the eyelid allows
eye closure when chewing, as the eyelids close on
contraction of the temporalis. Lagophthalmos remains a potential problem at night as the principle
relies on conscious effects on the patients’ behalf to
chew or clench the jaw to induce such eye closure.
Ueda et al238 compared the use of gold weights and
temporalis muscle transfer in the management of
135
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
lagophthalmos. They found lid loading to be far
superior to temporalis transfer in preventing
lagophthalmos, and therefore advocated its use as
first line. May and Drucker154 described a series of
224 cases of temporalis muscle transfer, with poor
outcome in reanimated eye closure. The effectiveness of improved mouth function and restoration of
the smile was much more marked in such cases.
However, with its reliable and immediate effect (3--6
weeks), coupled with no risk of synkinesis, Frey et
al88 described the use of temporalis muscle transfer
as the first step in facial reanimation.
Other authors have also described the early use of
temporalis transposition. Cheney et al56 reported
their use of temporalis muscle transfer in the early
management of lagophthalmos with 90% of patients
achieving improved symmetry and better movement
of the corner of the mouth. May153,154 described
procedure success as the patient’s ability to voluntarily smile and show teeth.
Complications are unusual, although a reported
12% risk of infection has been described.153,154
Ectopic bone formation has been described as a rare
complication of temporalis muscle transfer years
after surgery.26
Free muscle grafts with microneurovascular anastomosis are fast becoming a standardized procedure
in the rehabilitation of long-standing facial
palsies.101,236 Such cross-face nerve grafts—namely,
gracilis muscle transplants—use innervation from
the contralateral healthy side to allow dynamic
movements of the affected side.87,149,216 Dynamic
facial reanimation using such grafts will allow the
restoration of involuntary emotional facial expressions. Frey et al88 discussed the use of free gracilis
muscle transfer as a more efficient procedure in
terms of overall movement of eye closure when
compared to temporalis muscle transfer. Eyelid
excursions and symmetry is more pronounced with
free muscle grafting, with functional results remaining for longer compared to temporalis muscle
transfer. However, effects are not as immediate
compared to temporalis muscle transfer, with
lagophthalmos present for up to a year. Further
disadvantages of gracilis muscle transfer include the
ability of the procedure to produce synkinetic
movements, although often asymptomatic in nature.
Other microvascular free grafts used include
pectoralis minor,232 latissmus dorsi,106 trapezius
flap,204 and internus abdominus muscles.241
suitably protected and free from the risk of
ulceration. This is generally needed to improve
patient cosmesis and the superior visual field, which
is restricted by overhanging skin secondary to brow
ptosis.209 As such, the position of the brow in such
atonic musculature must be considered as a part of
blepharoplasty assessment. With this in mind, brow
lifts may well be effective in isolation. A direct brow
lift with fixation to the underlying periosteum is the
most common technique employed. Passot178 first
described the direct brow lift in the 1930s.
This method allows surgeons accurate control
into the amount of brow lifted. However, several
disadvantages, such as the presence of an unattractive postoperative scar or numbness and paraesthesiae as a consequence of trauma to sensory nerves,
have seen new developments, including endoscopic,
mid-forehead, and coronal brow lifting. Booth et
al37 reported their experience with direct brow lifts
over a 13-year period. In their 54 brow-lift procedures, parasthesia and numbness was the most
common complication, occurring in 74% of patients. Ueda et al,237 confirming a high rate of this
complication, reported a 27.5% incidence of forehead parasthesia. A prominent unsightly scar was
documented in two patients (three brows) in
Booth’s series. Wound infections were unusual.
Green et al97 suggested watchful skin closure could
prevent unsightly scars, but if formed maybe
disguised effectively with spectacles. Further, a modification of direct brow lifting using a forehead
crease may be used to camouflage scars within the
crease.192
Direct brow lifts have largely been superseded by
endoscopic brow lifts for cosmetic rehabilitation.
The advantages include rapid postoperative recovery, reduced risk of paraesthesia, and a small
hairline hidden scar. However, disadvantages should
be kept in mind, that is, high failure rates for an
expensive, often time-consuming procedure.135
Withey et al243 revealed a study of 100 cases
undergoing endoscopic brow lifting. They described
a high rate of complications; 71% altered sensation,
24% hair loss, and an 11% incidence of asymmetry.
However, other authors report much lower complication rates with this procedure.108,227
Following correction of the brow ptosis, excess
upper lid skin may be excised with a conservative
blepharoplasty to avoid aggravating corneal exposure and lagophthalmos.
D. REPOSITIONING OF SOFT TISSUE
1. Brow Ptosis and Blepharoplasty
Repositioning of soft tissue in the periocular
region can be considered when the cornea is
VIII. Sequelae/Synkinesis
Other than the risk of exposure keratitis and
corneal dryness, early complications of idiopathic
136
Surv Ophthalmol 52 (2) March--April 2007
RAHMAN AND SADIQ
facial palsy, such as pain, epiphora, and hyperacusis,
are often self-limiting and require no specific
treatments. Later complications are troublesome
and may present difficult management issues.
A. INCIDENCE
The incidence of sequelae (paresis, contracture,
crocodile tears, dry eye, and associated movements)
of idiopathic facial palsy varies. Yamamoto et al247
observed sequelae occurring in 30 of 330 cases of
Bell’s palsy (9.1%), over a mean follow-up of 39
months following onset of symptoms. Kawai125
described an incidence of 19% in a cohort of 351
patients with facial paralysis. Peitersen183 graded
sequelae as slight (just visible) in 12%, moderate
(clearly visible) in 13%, and severe (disfiguring) in
4% in a cohort of 1,701 cases of idiopathic facial
paralysis. In general, all three studies demonstrated
that the severest form of sequelae developed in the
presence of a causative pathology, for example,
herpes zoster, often resulting in complete facial
nerve paralysis.
Involuntary uncoordinated muscle movement
(undesired movement) associated with voluntary
movement (desired movement) of the muscle is
described as synkinesis secondary to aberrant regeneration. Aberrant regeneration of the facial
nerve following Bell’s palsy is an unusual phenomenon. The actual incidence is unknown, but is more
common with patients who suffer the more severe
nerve injuries, that is, complete or near complete
facial paralysis.194 In this group, an incidence of up
to 34% has been observed,11 most commonly after
24--39 weeks of facial palsy onset.241 Austin et al22
reported an incidence of sequelae of 13%. Peitersen183 described an overall incidence of sequelae in
29% of the 1,701 Bell palsy patients.
Fig. 6. A case of aberrant regeneration following Bell’s
palsy. A: The normal position of the right lids when
resting. B: The same eyelids on chewing (oral-ocular
synkinesis). Note the subtle lowering of the upper lid and
raising of the lower lid.
nerves, such as facial-trigeminal,202 and facialoculomotor synkinesis.138
B. SYNKINESIS
Many patterns of aberrant regeneration have
been observed secondary to partial recovery from
peripheral facial nerve palsy. Patterns of synkinesis
impart added psychosocial distress to patients. Some
patients feel these abnormal movements to be more
distressing than the onset of facial paralysis itself.173
Movement of the mouth with voluntary eye closure
(ocular-oral synkinesis),40 eyelid to massenteric
synkinesis,55 brow to oral synkinesis, gustolacrimal
reflex (nerve supply to salivary gland misdirected to
lacrimal gland),197 and contraction of stapedius with
eye closure (oculostapedial synkinesis)70 have been
reported. However, the incidence may be underestimated, as recognition of this phenomenon may
not be accurate (Fig. 6).55 Rarely, aberrant innervation may result between two adjacent cranial
1. Mechanisms
The etiology for synkinesis is unclear. Several
mechanisms have been proposed. Somatotopy is the
term used to describe the correct plan of nervous
innervation throughout the body. This map is
disrupted in patients who develop synkinesis.58
The regeneration of facial nerve fibers has been
shown to be reorganized in the facial nucleus
following attempts at spontaneous reinnervation
following peripheral nerve insults. Fernandez et al82
used horseradish peroxidase labeling techniques to
map the location of regenerated nerve fibers in the
facial nucleus. He found up to 80% of nerve fibers
revealed misguided axonal regeneration, and were
therefore located outside their normal region.
Further support for facial nucleus disorganization
137
OPHTHALMIC MANAGEMENT OF FACIAL NERVE PALSY
as an important association in synkinesis has been
shown in human and animal studies.129,146
During regeneration, excessive collateral branching of the axons occurs. These extra axons form the
basis of regeneration and may contribute to the
abnormal location of regenerated axon in the facial
nucleus and result in synkinesis.14 Unlike neonates,
this axon sprouting is not inhibited or regulated by
chemoattractants to the normal locations. This may
represent an associated mechanism in synkinetic
movements.128 Choi and Raisman57 found that
these collateral branches did not only occur at the
site of the lesion, but may be found along the entire
course of the facial nerve.
Hyperexcitability96,172 of the facial nucleus and
ephaptic phenomenon35,86,146 (electrical energy
transferred from one neuron to an adjacent neuron
in the absence of an anatomical connection between
them) has also been implicated in the formation of
aberrant nerve fibers. A combination of all these
factors is likely to contribute to facial nerve
synkinesis.
2. Management of Sequelae and Synkinetic
Movements
Voluntary eye closure with mouth synkinesis (i.e.,
co-contraction of the orbicularis oculi and oris
resulting in involuntary eye closure with pursing
lips) is the commonest pattern of synkinesis
following facial nerve paralysis.99,165
a. Botulinum Toxin
Botulinum toxin A, a neurotoxin produced by
clostridium botulinum, is used commonly to relieve
the symptoms of synkinesis. The neurotoxin acts by
inhibiting presynaptic release of acetylcholine,
thereby producing a functional denervation of
endplates. However, due to the temporary nature
of such a block, injections are repeated on a 3 to 5
monthly basis. Nevertheless, synkinetic movements
are markedly lessened by its use.38,59 Interestingly,
Chua et al59 noted that a similar effect maybe
produced with the use of lower doses of botulinum
toxin (40 U compared to 120 U), thus reducing the
incidence of botulinum toxin induced side effects.
Similarly, Armstrong et al19 noted a significant
benefit of lower doses in limiting side effects without
detriment to the therapeutic outcome.
b. Crocodile Tears
Crocodile tears deserve a special mention. The
formation of crocodile tears is a variation of
aberrant regeneration, similar to Frey Syndrome.72
The parasympathetic nerve fibers innervating the
lacrimal gland are misrouted. A synkinetic misrouting of postganglionic fibers induces excess lacrimation on chewing, resulting in excess watering.
Although a rare syndrome, risk factors for the
development of gustatory lacrimation include those
suffering incomplete facial paralysis246 and secondary to surgery for acoustic neuromas.117 The use of
botulinum toxin has been shown to be effective in
inhibiting crocodile tear formation by injection
directly into the lacrimal gland.39,70,107,127,197 The
effect is temporary and requires recurrent treatments, albeit at very low doses. Over-treatment may
inhibit complete lacrimation and result in ptosis,
strabismus, dry eye, and excessive lagophthalmos.70
Riemann et al197 successfully reported the use of
a transconjunctival intraglandular injection in the
treatment of crocodile tears. Compared to the more
usual transcutaneous injection, no side effects were
reported. Electromyography guided injection of
toxin may aid more accurate delivery.34 In some
specific forms of aberrant regeneration, such as
tinnitus on eye closure (oculostapedial synkinesis),
individualized treatment may be necessary.70
c. Physical Therapy
Patients practice certain pre-taught muscle contraction exercises on the affected side of the face in
similar amplitude and duration as the unaffected
normal side to reduce facial asymmetry while in the
resting state and when using facial expressions.
These should be performed twice daily.92,177 Using
electromyogenic (EMG) biofeedback strategies to
retrain facial neuromusculature in cases of ocular to
oral and brow to oral synkinetic movements,
combined with a home exercise program, may
further reduce facial asymmetry.46,200 In a series of
14 patients using surface EMG biofeedback physical
training, Brach et al40 reported a reduction of
synkinesis in 12 (of 13) patients with brow to oral
synkinesis, and 12 (of 14) patients with ocular to
oral synkinesis.
IX. Facial Asymmetry
Facial asymmetry with dynamic movements remains a major concern for patients with long-standing
facial paralysis. Several management options are
available to these individuals:
i) Explanation of the problem and physical
therapy (see above), coupled with EMG biofeedback.
ii) Surgical weakening of the facial nerve on the
normal side. This weakening can be graded
138
Surv Ophthalmol 52 (2) March--April 2007
RAHMAN AND SADIQ
according to the degree of recovery of the
facial paralysis. The procedure may be repeated
if greater weakening is required. The weakened
facial nerve can regenerate over time.
iii) Chemo-denervation of the normal side with
botulinum toxin.19,48,61,133,220
In this setting botulinum toxin reduces the
relative hyperkinesis of the contralateral side to
the paralysis, resulting in a more symmetrical
function of the face. This, like most other treatments with botulinum toxin, is an effective method
requiring repeat injections on a serial basis. The
dose can be altered to tailor the amount of weakness
required. Recently, Bulstrode and Harrison48 described their experience with this method in 23
followed-up patients. Patients underwent ipsilateral
orbicularis oculi botulinum toxin injections, followed by contralateral forehead rhytides and depressor anguli oris injections. They noted that facial
asymmetry and patient satisfaction was greater in
dynamic movements of the face rather than static
assessment.
visible, in idiopathic facial nerve paralysis the
etiology remains uncertain. It is becoming clearer
from the literature, past and present, that herpes
simplex virus has a role to play in worsening the
paralysis, if not instigating its onset. Unfortunately,
the use of steroids and/or acyclovir remains uncertain in this setting, as up to 70% of affected
individuals recover spontaneously.
Ophthalmologists have a central role in the
acute phase in protecting the cornea and maintaining vision. It must be remembered that facial
nerve paralysis has a multitude of causes and
requires a multidisciplinary approach with allied
specialties to ascertain the etiology, some of which
remain life-threatening. In the longer term, eyelid
reanimation in conjunction with facial reanimation
(especially that of the lower face) requires a multidisciplinary approach, and affords excellent results.
However, each case should be treated as individual
and the needs and concerns of the patient should
be addressed empathetically prior to surgical
intervention.
X. Other Therapies
XII. Method of Literature Search
A. SYMPATHETIC CERVICAL BLOCK
Vasodilation of the vasculature of the facial nerve
may contribute to the swelling and edema associated
with nerve inflammation. Targeting the sympathetic
pathway may lessen the dilation and consequent
inflammation. Fearnley et al reported no benefit
using procaine for this purpose.81
B. MASSAGE
Theoretically, massaging the facial muscles may
aid in maintaining tone of the facial muscles.
However, no significant studies have been performed.
We undertook MEDLINE (www.ncbi.nlm.nih.gov/entrez/medline.html) and PubMed (www.pubmed.nl/) searches using the following keywords:
Bell’s palsy, idiopathic facial paralysis, facial palsy and
added the keyword for each section while writing.
Citations from the reference lists of reviewed articles
were also obtained. Although many articles were
reviewed but not cited in the text, the exclusion or
inclusion of any article was based on relevance.
Often the search revealed vast quantities of articles
within the search field; articles were then selected
on the basis of originality and the value to the paper
on the whole. Non-English articles were translated
into English using library services and the help of
colleagues.
C. USE OF VASODILATORS
The use of drugs, such as histamine and nitrates,
to induce vasodilation has not been shown to
achieve any beneficial effect. Conversely, Korkis132
expressed concern and reservation in the use of
vasodilators as consequent increase in edema may
worsen outcome.
XI. Summary
Facial nerve paralysis spans across all races and
ages. It occurs most commonly in the 15- to 45-yearold age group and represents social and psychological stigma. However, although some etiologies are
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The authors reported no proprietary or commercial interest in
any product mentioned or concept discussed in this article. The
authors wish to to express their gratitude to the library staff at the
Manchester Royal Infirmary, Manchester, UK for their kind
assistance above and beyond the call of duty in obtaining
references, no matter how obscure. They also wish to thank the
library staff for aiding in translation of non-English articles.
Reprint address: S.A. Sadiq, MB BS, FRCS, MRCOphth, DO,
Manchester Royal Eye Hospital, Oxford Road, Manchester M13
9WH, United Kingdom.
144
Surv Ophthalmol 52 (2) March--April 2007
Outline
I. Introduction
II. Anatomy
III. Epidemiology
A.
B.
C.
D.
E.
Prevalence
Sex distribution
Age
Seasonal variation
Prognosis
IV. Etiology
A. Pathophysiology and the role of the Herpes
virus in Bell palsy
B. Herpes zoster virus infection: Ramsay--Hunt
syndrome
C. Other infective causes of facial palsy
D. Traumatic and iatrogenic causes
E. Infiltration, compression, and malignancy
F. Congenital and hereditary causes
G. Other causes
V. History
VI. Classification
VII. Management
A. Supportive
1. Conservative
2. Medical
a. Botulinum Toxin
b. The use of steroids and oral acyclovir
3. Surgical
a. Surgical decompression of the facial
nerve
b. Tarsorrhaphy
RAHMAN AND SADIQ
c. Lid retraction (passive upper lid reanimation)
d. Lid loading (passive upper lid reanimation)
B. Lower lid support and canthal tendon
suspension
1. Medial and lateral canthal support
2. Lower lid spacers
3. Sub-orbicularis oculi fat (SOOF) Lift
C. Static and dynamic lid reanimation
D. Repositioning of soft tissue
1. Brow ptosis and blepharoplasty
VIII. Sequelae/synkinesis
A. Incidence
B. Synkinesis
1. Mechanisms
2. Management of sequelae and synkinetic
movements
a. Botulinum Toxin
b. Crocodile tears
c. Physical therapy
IX. Facial asymmetry
X. Other therapies
A. Sympathetic cervical block
B. Massage
C. Use of vasodilators
XI. Summary
XII. Method of Literature Search