The Laryngoscope

C 2013 The American Laryngological,

V
Rhinological and Otological Society, Inc.

Etiology, Diagnosis, and Management of Facial Palsy: 2000 Patients

at a Facial Nerve Center

Marc H. Hohman, MD; Tessa A. Hadlock, MD

Objectives/Hypothesis: To evaluate the range and incidence of facial palsy etiologies in cases presenting to a tertiary
facial nerve center, and to review the broad and evolving spectrum of diagnostic and management approaches to the
condition.
Study Design: Retrospective chart review.
Methods: Records of patients referred for facial weakness between 2003 and 2013 were reviewed for cases of facial
palsy. Cases of muscle dysfunction and primary hemifacial spasm were excluded. The remainder were analyzed by age, sex,
and diagnosis. Diagnostic and treatment strategies were reviewed.
Results: There were 1,989 records that met inclusion criteria. Bell’s palsy accounted for 38% of cases, acoustic neuroma
resections 10%, cancer 7%, iatrogenic injuries 7%, varicella zoster 7%, benign lesions 5%, congenital palsy 5%, Lyme disease
4%, and other causes 17%. Sixty-one percent of patients were female. Mean age at presentation was 44.5 years (618.6
years). Diagnoses were revealed primarily by history, though serial physical examinations, radiography, and hematologic test-
ing also contributed. Management strategies included observation, physical therapy, pharmacological therapy, chemodenerva-
tion, facial nerve exploration, decompression, repair, and the full array of static and dynamic surgical interventions.
Conclusions: Bell’s palsy remains the most common facial palsy; females present more often for evaluation. Comprehen-
sive diagnostic investigation is mandatory in atypical cases, and thorough management must be multidisciplinary. The algo-
rithms presented herein outline a single center’s approach to the facial palsy patient, providing a framework that clinicians
caring for these patients may adapt to their specific settings.
Key Words: Facial nerve, facial paralysis, facial palsy.
Level of Evidence: 2b
Laryngoscope, 124:E283–E293, 2014

INTRODUCTION et al.3 and Devriese et al.4 both published 1,000-patient

There are numerous causes of facial palsy (FP),
though hemifacial weakness is often generally termed
Bell’s palsy, named after the Scottish neurologist Charles
Bell, who described sudden onset unilateral facial paraly-
sis in 1821. Virally triggered, acute FP, to which the term
Bell’s palsy (BP) refers, is one of the most common, and
fortunately the most likely condition to result in eventual
return to premorbid status; 70% to 90% of patients
recover spontaneously.1,2 Other causes of FP routinely
result in poorer recovery, and the clinician must discern
among these to formulate a treatment plan.
There are few analyses of large FP patient series,
and the current 2,000 patient series marks the largest
since Peitersen’s 2,570 patient series in 2002.2 Adour
From the Department of Otology and Laryngology (M.H.H., T.A.H.);
Harvard Medical School, and the Facial Nerve Center (M.H.H., T.A.H.),
Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A.
Editor’s Note: This Manuscript was accepted for publication
November 25, 2013.
Presented at the 12th International Facial Nerve Symposium,
Boston, Massachusetts, U.S.A., June 28, 2013–July 1, 2013
The authors have no funding, financial relationships, or conflicts
of interest to disclose.
Send correspondence to Tessa A. Hadlock, MD, Department of
Otolaryngology, Division of Facial Plastic and Reconstructive Surgery,
Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston,
MA 02114. E-mail: tessa_hadlock@meei.harvard.edu
DOI: 10.1002/lary.24542
series, though they concentrated on the natural history
of BP rather than the etiologies of FP. At our institution,
a tertiary referral center for facial nerve disorders, we
evaluate and treat a large number of patients with a
broad range of conditions, and comparatively few cases
of acute, uncomplicated BP. Although our patients are
not necessarily representative of the general population,
this referral pattern does result in a high throughput,
allowing data accrual on 2,000 patients in a single dec-
ade. Based on this clinical experience and the state of
the literature, our management strategies for FP con-
tinue to evolve. Herein, we describe our current
approach to diagnosis and treatment of FP, examine the
condition’s myriad etiologies, and present their relative
frequencies in patients we have managed in the last
10 years.
MATERIALS AND METHODS
A chart review was performed for all patients seen at the
Massachusetts Eye and Ear Infirmary Facial Nerve Center
between June 2003 and June 2013; records of patients with FP
were examined for diagnosis, sex, and age. House-Brackmann
scores were not included, as this scale was designed for evalua-
tion of recovering unilateral palsy, making it inapplicable to
many of our patients.5 Patients with facial movement disorders
due to primary muscular dysfunction or hemifacial spasm in
the absence of synkinesis were excluded, as were those with
complaints of FP but no evidence of weakness on physical

Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E283
examination. Cases of iatrogenic injury were classified conser-
vatively; palsies due to excision of malignancies or intracranial
masses were excluded from the iatrogenic category, as these
cases are managed differently from cases of unexpected iatro-
genic injury. In cases of malignancy in close proximity to the
facial nerve, preoperative planning often includes a contingency
for neural reconstruction, which mitigates additional uncer-
tainty encountered in a return to the operating room to identify
the site of injury and repair the nerve, which frequently occurs
in cases of iatrogenic injury. Cases of FP following intracranial
facial nerve manipulation were excluded from the iatrogenic
injury category because reconstructive options proximal to the
geniculate ganglion are limited in the absence of epineurium,
and because the facial nerve, even though it may be nonfunc-
tional, often remains anatomically intact after resection of the
lesion. Review of the treatment plans, including physical ther-
apy, chemodenervation, and surgical intervention, was under-
taken, and our current treatment algorithms codified based
upon trends developed in our center over the past decade.
Data were compiled into an Excel spreadsheet (Microsoft
Corp., Redmond, WA), which was used to tabulate demographic
and etiological information. This study was approved by the
institutional review board at the Massachusetts Eye and Ear
Infirmary.
RESULTS
Two thousand forty-seven records were reviewed;
1,989 were identified that met the inclusion criteria. The
mean age at presentation was 44.5 years (618.6 years).
There were 1,207 female patients and 782 males.
BP accounted for the greatest number of cases
(n 5 761), 38% of the series. Of these, 58 patients pre-
sented with recurrent FP. There were 82 cases of
pregnancy-associated BP, occurring within 3 months pre-
or postpartum (Table I).
Acoustic neuroma was the second most common
cause of FP in our series (n 5 203). The majority of these
patients developed FP after resection; however, 12 cases
developed FP after radiotherapy alone, and 13 patients
presented with FP prior to treatment. Within the latter
group, four reported sudden onset of palsy.
Head and neck cancer accounted for 147 cases; the
majority of cases resulted from resection, though 46
resulted from preoperative nerve involvement by the
tumor. In eight of these cases, there was a history of
rapid onset FP. The most common tumor location was
the parotid gland itself (n 5 106), followed by intraparo-
tid lymph node metastasis, and direct neural invasion of
the facial nerve within the temporal bone.
Iatrogenic facial nerve injuries, excluding cases due
to resection of malignant or intracranial lesions,
accounted for 143 cases. The most common associated
procedure was temporomandibular joint surgery (n 5 31),
with parotidectomy second (n 5 22), and tympanomastoi-
dectomy third (n 5 12). Indications for parotidectomy
included pleomorphic adenoma (n 5 19), vascular malfor-
mation (n 5 2), and recurrent sialadenitis (n 5 1). Indica-
tions for tympanomastoidectomy included chronic otitis
media (n 5 8), cochlear implantation (n 5 2), endolym-
phatic decompression (n 5 1), and exostosis (n 5 1).
Varicella zoster virus (VZV)-associated FP was sep-
arated into cases with a history of vesicular outbreak
(Ramsay Hunt syndrome, n 5 122), and those without
Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E284
(zoster sine herpete, n 5 12). Two Ramsay Hunt syn-
drome patients presented with concomitant vocal fold
paralysis.
Trauma accounted for 113 cases, including temporal
bone fractures and soft tissue injuries. Fractures were
associated with motor vehicle accidents, falls, assaults,
construction site accidents, and pedestrians struck by
automobiles. There were also individual cases of birth
trauma, manifested by the development of synkinesis in
the child’s first 2 years of life, a soccer-related blow to
the head, a pedestrian struck by a train, and a crush
injury when the patient’s skull was caught between a
boat and its dock. Two patients’ etiologies could not be
determined from records.
Benign tumors, such as geniculate ganglion heman-
giomas and facial nerve schwannomas, were responsible
for FP in 103 patients. There were 99 cases of congenital
FP, the majority of which lacked a recognizable syn-
dromic association; M€obius was the most common named
syndrome. Lyme disease accounted for FP in 81 patients;
seven cases demonstrated bilateral involvement. Lesions
of the central nervous system, including medulloblasto-
mas, vascular malformations, hemangiomas, and glio-
mas, were associated with 76 cases of FP.
Autoimmune disease (n 5 32) occurred in twice as
many females as males. Two patients experienced recur-
rent palsy, and 13 had bilateral involvement. Guillain-
Barre syndrome was the most common; all cases were
bilateral, though not necessarily symmetrical. Seven
cases did not fit the pattern of any well-characterized
autoimmune disease, but did have positive hematologic
testing (C-reactive protein, erythrocyte sedimentation
rate, antinuclear antibodies, or rheumatoid factor), as
well as a personal or family history of recurrent/bilateral
FP or autoimmune disease.
Infectious causes of FP accounted for 29 cases, with
poliomyelitis suspected in 10. In these cases, patients
from developing nations suffered childhood febrile ill-
nesses with segmental paresis on examination, but no
accompanying medical documentation. In nine cases,
there were childhood febrile illnesses, but no character-
istic pattern of poliomyelitis-associated FP.
Otologic disease, including acute otitis media, cho-
lesteatoma, and any other nonmalignant process that
resulted in FP in the absence of surgical intervention
occurred in 21 patients. Stroke affected 13 patients. In
34 cases, the diagnosis remained unclear.
DISCUSSION
The causes of FP are myriad, but in this series, as
in those cited above, BP was the dominant pathology.2,3
Interestingly, Peitersen’s ranking of etiologies then pro-
ceeded to congenital cases, VZV-associated FP, and trau-
matic palsy, which are all far less common in our series,
reflecting a difference in referral patterns between his
institution and ours, which is also a referral center for
acoustic neuromas and other complex head and neck
tumors.
Historically, BP has been a diagnosis of exclusion,
though several studies have demonstrated a link to
 TABLE I. TABLE I.
Distribution of Patients by Diagnosis and Sex. (Continued)
No. of No. of
Etiology Patients Males Females Etiology Patients Males Females

Bell’s palsy 761 265 496 Lyme disease 81 40 41

Recurrent 58 Bilateral 7
>2 episodes 24 Central nervous system lesions 76 33 43
Pregnancy associated 82 Autoimmune disease 32 11 21
Acoustic neuroma 203 70 133 Bilateral 13
NF2 associated 34 Recurrent 2
Postresection 178 
Guillain-Barre 12
Postradiation 12 Melkersson-Rosenthal 7
Onset of FP prior to diagnosis 13 Sarcoidosis 2
Rapid onset 4 Multiple sclerosis 2
Head and neck cancer 147 90 57 Amyloidosis 1
Postresection 91 Antiphospholipid antibody 1
Postradiation 7 Other 7
Postchemotherapy 2 Infectious 29 11 18
Onset of FP prior to diagnosis 47 Poliomyelitis 10
Rapid onset 8 Meningitis/encephalitis 5
Iatrogenic injury 143 43 100 Human immunodeficiency virus 2
Oral surgery 43 Epstein-Barr virus 1
Head and neck surgery 43 Mumps 1
Otologic surgery 30 Cellulitis 1
Cosmetic surgery 12 Other febrile illness 9
Neurosurgery 9 Otologic 21 7 14
Temporal artery biopsy 3 Acute otitis media/mastoiditis 17
Other 3 Cholesteatoma 2
Varicella zoster 134 56 78 Barotrauma 1
Ramsay Hunt 122 Inflammatory pseudotumor 1
Zoster sine herpete 12 Stroke 13 6 7
Trauma 113 63 50 Brainstem 9
Soft tissue trauma 50 Cortical 4
Temporal bone fracture 63 Unknown 34 11 23
Motor vehicle accident 37 Cases listed in the otologic category represent facial weakness prior
Fall 9 to any surgical instrumentation.
FP 5 facial palsy.
Assault 4 VACTERL 5 association of vertebral anomalies, anal atresia, cardiac
Pedestrian vs. car 4 defects, tracheoesophageal fistula, esophageal atresia, renal anomalies,
and limb defects.
Construction accident 3 CHARGE 5 syndrome of colobomata of the eyes, heart defects,
Other 6 atresia of the choanae, retardation of growth/development, genital/urinary
anomalies, and ear anomalies.
Benign tumor 103 45 58 NF-2 5 neurofibromatosis type 2.
Facial nerve tumor 80
NF2-associated facial neuroma 6
herpes simplex virus (HSV).3,6,7 Viral reactivation in the
Parotid tumor 17
geniculate ganglion likely leads to the typical appear-
Meningioma 6
ance of enhancement on magnetic resonance imaging,8
Congenital 99 31 68
as well as the classic history of rapid onset hemifacial
Nonsyndromic 75 palsy, peaking within 72 hours, preceded by postauricu-
€ bius syndrome
Mo 8 lar pain and accompanied by dysgeusia and/or hyperacu-
Congenital unilateral lower lip paresis 6 sis.9 Because serological testing for HSV in the setting of
Hemifacial microsomia 5 FP is not commonly performed, the diagnosis is made
Branchio-oto-renal 2 clinically. Distinguishing HSV-associated FP from other
VACTERL 1 virally mediated facial palsies can therefore be difficult,
CHARGE 1 but for the purposes of this study, we refer to HSV-
Chapple syndrome 1 associated FP as BP. VZV may present with the classic
Ramsay Hunt symptomatology of hemifacial palsy, sen-
sorineural hearing loss and/or vestibulopathy, severe

Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E285
pain, and vesicular outbreak on the pinna, tongue, or oral
mucosa. It may also present as zoster sine herpete, whose
symptoms mirror those encountered in Ramsay Hunt syn-
drome, but without skin or mucosal involvement.9 Lack of
rash in zoster sine herpete may produce diagnostic confu-
sion, as many patients with uncomplicated BP also com-
plain of disequilibrium and pain. One important
difference between FP of HSV origin and that of VZV ori-
gin is that BP may recur (7.6% of BP patients in our
series), whereas recurrence of zoster is very rare in immu-
nocompetent individuals.10 Regardless of which virus is
the culprit, our acute treatment regimen includes steroids,
antivirals, and eye protection, with audiometry if subjec-
tive hearing loss is noted (Fig. 1). Though studies have
not established acyclovir as an effective therapy for BP,
valacyclovir does appear to provide a benefit when admin-
istered in combination with steroids.1,11 Additionally,
patients who present acutely are offered electrodiagnostic
testing and facial nerve decompression, if appropriate,
based on the work of Gantz et al. and others.12–15 In our
experience, patients with VZV-associated FP tend to
recover more slowly than those with BP, although certain
patients (e.g., diabetics, elderly patients, and women with
pregnancy-associated BP) may also experience a pro-
longed recovery. We have not seen any patients with viral
FP fail to recover muscle tone within 12 months, though
patients who take longer than 10 weeks to demonstrate
the first signs of recovery often suffer a greater degree of
synkinesis, as do patients who suffer complete flaccid
paralysis within 24 hours of symptom onset.15

Fig. 1. Management of the patient with acute facial palsy (FP).12 Prednisone is administered as 60 mg PO daily for 5 days, followed by a
taper of 50 mg on day 6, then 40 mg, 30 mg, 20 mg, and 10 mg on day 10. A complete history and physical examination are paramount
when attempting to differentiate Bell’s palsy from malignant causes of FP. Patients with poor Bell’s phenomenon, corneal sensation deficit,
or persistent ocular discomfort should be considered for early platinum eyelid weight placement (e.g., post skull base tumor resection). The
eye care algorithm is highlighted at left and the electrodiagnostic testing algorithm at right. BID 5 twice daily; CN VII 5 cranial nerve VII;
EMG 5 electromyography; ENoG 5 electroneuronography; PO 5 orally. [Color figure can be viewed in the online issue, which is available at
www.laryngoscope.com.]

Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E286
 Viral FP accounted for over 60% of the rapid onset
(evolution of palsy complete within 72 hours of onset)
cases of FP in our series, but there are other clinical
entities that can mimic this presentation, making a thor-
ough history and physical exam imperative. Lyme dis-
ease, which was comparatively uncommon despite our
institution’s location in New England, may also present
with rapid onset FP. There is not always a history of
known tick bite or rash, and serological testing can be
equivocal; a high index of suspicion is therefore
required, particularly in patients who are active out-
doors.16,17 Lyme disease may also present with bilateral
FP, though this was not frequently seen in our series.
Treatment of Lyme disease involves a long course of dox-
ycycline, but because inflammation along the facial
nerve confers the risk of additional insult from HSV
reactivation, we prescribe valacyclovir along with antibi-
otics (Fig. 1). Debate remains regarding the role of ste-
roids in Lyme disease, as they decrease inflammation
while potentially depressing the immune system,
thereby increasing spirochete load.18
Other causes of rapid onset FP include autoimmune
disease, which may present a diagnostic challenge.19–21
Family history is important, as is a personal history of
not only other autoimmune disease, but also unex-
plained and seemingly unconnected symptoms: rashes,

Fig. 2. Diagnostic evaluation of the patient

with recurrent facial palsy (FP). When per-
forming magnetic resonance imaging (MRI)
for recurrent, segmental FP, it is important to
evaluate not only the white matter of the
brain, but also the entire length of the facial
nerve. Imaging and hematologic testing
should only be used to supplement a
thorough history and physical examination.
CN VII 5 cranial nerve VII. MS 5 multiple
sclerosis. CRP 5 C-reactive protein.
ESR 5 erythrocyte sedimentation rate.
ANCA 5 antineutrophil cytoplasmic antibod-
ies. ACE 5 angiotensin converting enzyme.
RF 5 rheumatoid factor. ANA 5 antinuclear
antibodies. SSA, SSB 5 skin-sensitizing anti-
bodies. FTA-ABS 5 fluorescent treponemal
antibody-absorption. VDRL 5 venereal dis-
ease research laboratory test for syphilis.
TSH 5 thyroid stimulating hormone.
CBC 5 complete blood count. [Color figure
can be viewed in the online issue, which is
available at www.laryngoscope.com.]

Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E287
orofacial edema, nasal septal perforation, multiple mis-
carriages, and others. When there is nothing in the his-
tory to differentiate autoimmune disease from BP, the
diagnosis may be missed; however, autoimmune disease
must be high on the differential diagnosis for the recur-
rent, bilateral, or alternating FP patient (Fig. 2).
A further consideration in rapid onset FP is neopla-
sia. The majority of tumors that present with facial
palsy do so insidiously, but malignancy may present
acutely as well.22–24 There were eight patients with
malignant tumors in our series who were erroneously
diagnosed with BP before referral to our center. Because
it is relatively rare for masses to present with acute FP,
we do not recommend imaging as part of the initial evalua-
tion for patients whose history is otherwise consistent with
BP. A thorough history and physical examination that
evaluates the cranial nerves, lymph nodes, parotid glands,
ears, and facial skin will often elucidate the presence of a
malignancy; however, if no sign of recovery is apparent
within 4 months of onset, the presence of a tumor should
Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E288
be considered even in the context of an otherwise unre-
markable history and physical examination.22,25
Insidious, progressive FP most likely represents
tumor, and patients with this presentation uniformly
require aggressive imaging. Our series describes malig-
nant tumors including primary parotid tumors, squa-
mous cell carcinoma in the parotid gland and/or facial
nerve, sarcomas, and benign tumors affecting the facial
nerve including facial nerve schwannomas and genicu-
late ganglion hemangiomas. Adjuvant treatments for
disease adjacent to or involving the facial nerve can also
contribute to additional facial weakness, for example,
radiation and chemotherapy. In the current series, we
are unable to discern the nature of the relationship
between change in facial function and adjuvant treat-
ments beyond a temporal association.
A thorough history may differentiate among causes
of FP, but many patients present with a known diagno-
sis, such as temporal bone fracture or iatrogenic injury.
In these cases, the diagnostic segment of the encounter
Fig. 3. Management of the patient
with facial palsy of traumatic or iat-
rogenic etiology. We administer
valacyclovir to patients with delayed
or incomplete facial paralysis
because of the potential for genicu-
late ganglion herpes simplex virus
reactivation in the setting of trau-
matic facial nerve insult. Timing of
repair or decompression remains
controversial, but earlier intervention
appears to result in improved out-
comes, and after 4 to 6 months,
outcomes may be poor due to mus-
cle atrophy before reneurotization is
complete. When considering elec-
trodiagnostic testing, if the index of
suspicion for nerve transection is
low, testing after 72 hours have
passed may be appropriate to rule
out severe injury. However, if the
index of suspicion is high, operating
before 72 hours have passed allows
use of a nerve stimulator intraopera-
tively, which may facilitate location
of the distal nerve stump. BID 5 t-
wice daily; FN 5 facial nerve;
PO 5 orally. [Color figure can be
viewed in the online issue, which is
available at www.laryngoscope.
com.]
may be brief, and more time may be allocated to discus-
sion of treatment. Iatrogenic injuries and trauma were
the fourth and sixth most common etiologies of FP in
this series, respectively; when these patients present
acutely, the likelihood of satisfactory recovery may be
increased through early operative intervention with
facial nerve exploration and decompression or repair
(Fig. 3).12–15,26,27
Care of the FP patient may be divided into three
parts: assessment, diagnosis (Fig. 4), and management,
which are often initiated simultaneously. In the majority
of cases, treatment may proceed along well-defined path-
ways; these algorithms help the physician to avoid over-
looking any aspect of the FP patient’s situation
(Fig. 5).28 Facial palsy >4 months in duration merits
special consideration, as most viral neuritis resolve spon-
taneously within this timeframe, and after 4 to 8 months,
muscle reactivity declines.29 Assessment involves a codi-
fied intake process, which includes a meticulous history
and physical examination, and photography in repose
and during specific facial expressions.25 A video clip of
these expressions is also recorded for review and com-
parison, and quality-of-life data are obtained. From a
clinical perspective, the first priority for the flaccid FP
patient is eye protection, following which, treatment will
be determined by the likelihood of spontaneous recovery
of facial function.28 Patients with flaccid FP for more
than 12 months, a history of facial nerve sacrifice, or
facial nerve malignancy are likely to remain flaccid, and
will proceed to reanimation once the underlying pathol-
ogy is addressed. Patients with synkinesis present a dif-
ferent set of challenges. For them, surgery is second-line
therapy, after conservative measures: facial nerve physi-
cal therapy (PT) and chemodenervation (Fig. 6).28,30–33
For patients unsatisfied after conservative management,
adjunctive procedures, such as platysmectomy and

Fig. 4. Diagnostic evaluation of the facial palsy patient without a history of facial nerve or temporal bone trauma. Note the role for positron-
emission tomography/computed tomography (PET/CT) imaging and possible facial nerve biopsy, to identify occult malignancy in cases
where the index of suspicion is high despite negative imaging studies.22 CN VII 5 cranial nerve VII; CT 5computed tomography;
CVA 5 cardiovascular accident; HIV 5 human immunodeficiency virus; HSV 5 herpes simplex virus; VZV 5 varicella zoster virus.
MRI 5 magnetic resonance imaging. IgG 5 immunoglobulin G. IgM 5 immunoglobulin M. CRP 5 C-reactive protein. ESR 5 erythrocyte sedi-
mentation rate. ANCA 5 antineutrophil cytoplasmic antibodies. ACE 5 angiotensin converting enzyme. RF 5 rheumatoid factor.
ANA 5 antinuclear antibodies. SSA, SSB 5 skin-sensitizing antibodies. FTA-ABS 5 fluorescent treponemal antibody-absorption. VDRL 5 ve-
nereal disease research laboratory test for syphilis. TSH 5 thyroid stimulating hormone. CBC 5 complete blood count. EBV 5 Epstein-Barr
virus. IAC 5 internal auditory canal. [Color figure can be viewed in the online issue, which is available at www.laryngoscope.com.]

Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E289

selective neurectomy may provide long-term sympto-
matic relief.34,35
Surgical facial reanimation, which many patients
and physicians view as the final step in the management
of FP, is not a single procedure, but rather a process.
Numerous surgical interventions have been employed,
from static and dynamic reanimation to neural reconstruc-
tion. Epineurial repair of a transected nerve is considered
the gold standard, whether through primary neurorrha-
phy or interposition grafting.36 We typically employ two or
three 10-0 nylon sutures (Ethilon; Ethicon Inc., Somer-
ville, NJ) and apply fibrin glue (Evicel; Ethicon Inc.)
around the repair site. Nerve transpositions may also be
useful, although exchanging the morbidity of one cranial
nerve deficit for another is hazardous; a substitute may
be cross-face nerve grafting. Another consideration when
contemplating nerve transposition is time course; because
nerves regenerate at about 1 mm/day,37 and muscles
undergo irreversible atrophy 12 to 18 months after dener-
vation,38 the interval during which neural reconstruction
techniques are applicable is often short, and frequently
the window of opportunity has closed before the patient
presents for evaluation. Nevertheless, there are cases in
which reinnervation may be effected after prolonged facial
dysfunction; patients who have preserved facial muscula-
ture as a result of synkinesis may be candidates for graft-
ing to specific distal nerve branches (e.g., those for
orbicularis oculi and zygomaticus major).
Static reanimation procedures, including brow lift,
eyelid weight placement, tarsal strip, and facial suspen-
Laryngoscope 124: July 2014 Hohman and Hadlock: Diagnosis and Management of Facial Palsy
E290
Fig. 5. Systematic zonal assessment
of the paralyzed face promotes a
comprehensive evaluation of
affected facial subunits and may
help to prevent overlooking any
problematic areas. NLF 5 nasola-
bial fold. [Color figure can be
viewed in the online issue, which is
available at www.laryngoscope.
com.]
sion techniques provide options for rehabilitation of upper,
middle, and lower facial zones, and may frequently be per-
formed under local anesthesia (Fig. 7).28,39–43 A low
threshold for periocular reanimation may spare patients
long-term corneal complications due to lagophthalmos
from upper eyelid retraction or lower lid laxity. Eyelid
weight placement is typically the first step; platinum is
the preferred material, as its density affords a slim profile
and fewer patients experience tissue reactions when com-
pared to gold.40 Minimally invasive asymmetric brow lift-
ing and tarsal strip procedures also improve eye comfort,
safety, and cosmesis.28,39,41,42 Last, reanimation of the mid
and lower face (i.e., nasolabial fold and oral commissure)
may also be achieved through static techniques.28,43,44
Some authors report the use of alloplastic materials for
static slings, but autologous fascia lata possesses the
advantage of reduced risk of extrusion and infection.45
Good surgical candidates may elect to undergo
dynamic smile rehabilitation. Two commonly employed
techniques are temporalis and gracilis muscle trans-
fers.45,46 At our institution, gracilis free muscle transfer is
the more frequent procedure, resulting in 8 mm of smile
excursion, on average.47 We perform gracilis transfer as a
one- or two-stage operation, innervating the flap with the
masseteric nerve or a cross-face nerve graft, respec-
tively.48 We offer temporalis flap reanimation to patients
who are poor free tissue transfer candidates, although
many surgeons employ this technique as a first-line option
with great success.49,50 At the time of muscle transfer, the
alar base is suspended with fascia lata, if the patient
Fig. 6. Management of the patient with facial palsy present for >4 months. Patients with palsy of >12 months duration, a history of facial
nerve sacrifice, or a history of malignancy involving the facial nerve are considered to have no potential for spontaneous recovery. [Color
figure can be viewed in the online issue, which is available at www.laryngoscope.com.]

Fig. 7. The algorithm enumerates indications and contraindications for various smile reanimation modalities. CN VII 5 cranial nerve VII.
[Color figure can be viewed in the online issue, which is available at www.laryngoscope.com.]
suffers from external nasal valve collapse.51 Although PT
has proven invaluable for improving quality of life in
patients with spontaneous facial function recovery, it is
also vital to the success of any dynamic reanimation pro-
cedure. Improvement of facial balance with contralateral
chemodenervation and lower lip weakening may also
improve quality of life, as will long-term follow-up with
reevaluation for adjunctive procedures to refine
results.28,52
CONCLUSION
We have described the etiology of FP in the last
2,000 patients seen at the Massachusetts Eye and Ear
Infirmary Facial Nerve Center, and provided an
algorithm-driven approach to diagnosis and manage-
ment, which has arisen and evolved with deepening
experience and careful longitudinal clinical follow-
up.22,25–29,32,34,35,39–41,47,48,51–53 Clinicians treating this
condition must possess an awareness of the wide variety
of FP etiologies; codifying the decision-making process is
likely to result in fewer missed diagnoses and better out-
comes. Although the data presented in this series are
informative, they do not quantify the overall incidence
or etiologic breakdown of FP. Because our institution is
a tertiary referral center, we treat a wide variety of
patients with a wide range of pathologies, significantly
biasing our data acquisition. However, the algorithmic
approach to diagnosis and management outlined herein,
based upon substantial clinical experience, may repre-
sent a starting point for the generation of clinical path-
ways, consensus statements, and prospective outcomes
studies going forward.
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