Bell’s Palsy 155
Bell’s Palsy
J J Halperin, Overlook Hospital – Atlantic Health,
Summit, NJ, USA
ã 2009 Elsevier Ltd. All rights reserved.
Introduction
Each cranial nerve has its own idiosyncratic propen-
sity to damage, dictated at least in part by its anatomy.
The fine filamentous nature of the trochlear (4th)
nerve makes it susceptible in minor head injury.
The long intracranial course of the abducens (6th)
puts it at risk with any increase in intracranial pres-
sure. The facial nerve (7th) has a particularly lengthy
and complex course, crossing the subarachnoid space,
winding through a long, narrow bony canal, exiting to
cross through the parotid gland; it should not be
surprising that it can be affected in a variety of circum-
stances. That the detailed pathophysiology of facial
nerve palsy remains unclear – over 185 years after
its initial description – is remarkable. However the
facial nerve’s peculiar anatomy must contribute to its
particular susceptibility to damage.
In recent years the number of disorders clearly
associated with the facial nerve has increased to
include sarcoidosis, Lyme disease, HIV, and herpes
(zoster and simplex) infections, yet pathophysiologic
insights remain frustratingly limited. The therapeutic
approach similarly has expanded, but each approach
remains controversial. The following overview will
attempt to summarize what is known, and elucidate
these controversies.
Background
Sir Charles Bell (1774–1842), a gifted Scottish-born
surgeon, anatomist, and illustrator, described the
course of the facial nerve, and the peculiar ‘blight’
that befalls it, in 1821. Interestingly, this arguably was
one of his lesser accomplishments. The first Professor
of Anatomy and Surgery of the College of Surgeons in
London, and the first Professor of Physiology at King’s
College, University of London, among his noteworthy
neurologic accomplishments was introducing the con-
cept that motor and sensory functions were segregated
in the spinal roots! Also responsible for describing
‘Bell’s phenomenon,’ he is, however, best memoria-
lized in the eponym for a ‘palsy’ (perhaps a somewhat
dubious honor). Over the years, many have described
the clinical concomitants of Bell’s palsy. Proposed
therapeutic interventions have ranged from surgical
decompression of all or part of the nerve, to psycho-
logical counseling, to numerous points in between.
The facial nerve’s anatomy is complex (schematically
shown in Figure 1) both functionally and anatomically.
Originating in a nucleus in the pontine tegmen-
tum, the motor fibers take a looping dorsal, then
ventral, course around the 6th nerve nucleus, joining
fibers connecting to the nucleus solitarius and lacrimal
and superior salivary parasympathetic nuclei as they
travel. Fibers exit the brain stem and travel adjacent to
the 8th nerve in the cerebellopontine angle, cross the
subarachnoid space, enter the internal auditory mea-
tus, and then traverse the longest, most complex
intraosseous course of any nerve in the body. Through-
out its course, components come and go. At the level
of the geniculate ganglion, parasympathetic fibers
(which exit the brain stem in the anatomically distinct
nervus intermedius) form the greater petrosal nerve
and project to the pterygopalatine ganglion, from
which postganglionic fibers pass to the lacrimal gland
and to the blood vessels of the Circle of Willis. Damage
to this branch results in disorders of lacrimation –
either increases or decreases. Clinical interpretation
of these changes is often confounded in facial nerve
palsy by the equally important contribution of mech-
anical exposure of the eye, which in and of itself can
lead either to increased tearing from irritation or to
exposure-related drying.
Other parasympathetic fibers continue with the
main trunk of the facial nerve, to emerge slightly
more peripherally and contribute to the chorda
tympani, through which fibers project to the sub-
mandibular ganglion, with postganglionic projec-
tions to the salivary nuclei. Neurons of the geniculate
ganglion convey sensory input from the nasopharynx,
tympanic membrane, and the ear canal. Although these
fibers travel with the facial nerve, they ultimately proj-
ect to the primary sensory nucleus of V and the nucleus
of the spinal tract of the trigeminal nerve.
Distal to the geniculate ganglion and the greater
petrosal nerve, a small motor branch exits to inner-
vate the stapedius muscle. Damage to this results in
hyperacusis. Shortly thereafter, the chorda tympani
joins the nerve. This bundle, which, as mentioned,
carries efferent preganglionic parasympathetic fibers
destined to control salivary glands, also contains
fibers of the lingual nerve, conveying taste sensation
from the anterior two-thirds of the tongue. Cell bodies
of these neurons also reside in the geniculate ganglion;
fibers project centrally via the nervus intermedius to
the nucleus solitarius. The fibers that remain distal
156 Bell’s Palsy
Motor nucleus VII
Sup salivatory nucleus
Nucleus solitarius
Superficial petrosal nerve
Geniculate ganglion Pterygopalatine ganglion
(lacrimal glands)
Chorda tympani Nerve to stapedius
Lingual nerve
(anterior 2/3 tongue−taste)
(submandibular glands)
Motor trunk
(sensory branch to ear canal)
Figure 1 Schematic diagram of facial nerve.
to the chorda tympani are primarily motor, projecting
to the muscles of facial expression (forehead, periorbi-
tal, and perioral muscles) and a small group of sensory
fibers destined for the skin of the anterior wall of the
external auditory canal.
The nerve’s long course puts it at risk in multiple
locations. Meningeal processes (microbial or neoplas-
tic meningitis) can affect it in the subarachnoid space;
skull base tumors can compress it within the long bony
canal; inflammatory or neoplastic disease can involve it
as it traverses the parotid gland (e.g., in sarcoid). As a
fairly long peripheral nerve, it is at risk in peripheral
neuropathies, ranging from diffuse demyelinating
processes such as Guillain–Barré syndrome, to a mono-
neuropathy multiplex, as occurs in Lyme disease.
Clinical
Facial weakness can result not only from damage to
the facial nerve, but also from damage to descending
cortical projections. The clinical observation is that
damage to the central descending motor pathways
tends to affect movements of the mouth and cheek
far more than eye closure and forehead wrinkling.
This differentiation, which is generally obvious in the
postacute setting, may be less apparent immediately
following an acute central event (e.g., lacunar stroke),
particularly if it involves deep hemispheral white mat-
ter; in such individuals some eye closure and forehead
weakness may be evident acutely, improving over the
first few postevent days.
The disparity in involvement between the upper
and lower face is usually attributed to cortical input
to the forehead being bilateral, with that to the lower
face being more lateralized. An alternative hypothesis
suggested more recently is that the upper face actually
receives little cortical motor input from either
hemisphere; this would explain clinical observations
equally well.
Lesions of the facial nerve can occur anywhere along
its course. Damage in the pons is often accompanied by
abducens weakness, due to the close proximity of the
motor fibers of 7th to the 6th nerve nucleus. As with all
brain stem processes, the high density of eloquent struc-
tures tends to lead to multiple other associated findings,
leading to little uncertainty as to the location of the
lesion.
Damage to the nerve outside the brain stem can lead
to a number of symptom combinations, depending on
the location of the lesion along the nerve’s long course,
and also on whether damage is to all fascicles of
the nerve at that level, or just some. In theory, a proxi-
mal lesion would affect all functions, resulting in
abnormal lacrimation, hyperacusis, abnormal taste and
salivation, weakness, and a small area of hypesthesia
on the external ear. As lesions occur more and more
peripherally, fewer and fewer of these elements would
be evident. Curiously, when this has been studied,
in at least some cohorts of patients with facial
palsy, no such systematic segregation of syndromes
is evident, suggesting that lesions are selective at a
fascicular level within the nerve, as well as along its
longitudinal course.
The other common clinical concomitant of facial
nerve palsy is significant retroauricular pain ipsilateral
to the palsy. This often precedes facial weakness by
1 or even 2 days, and can be quite severe. Occurring
in the region of the stylomastoid foramen, where the
nerve exits the skull, this is often attributed to the nerve
swelling in its narrow canal. Given the small sensory
component of the nerve, it could also be neuropathic
referred pain, from damage to this small group of
periauricular afferents. This pain typically resolves in
the first few days; corticosteroids may speed this.
The weakness typically occurs fairly rapidly, evol-
ving over about 24 h, usually maximal within 48 h,
rarely progressing over as much as a week. Weakness
involves all parts of the affected side of the face –
forehead wrinkles are lost and the affected side of the
forehead cannot be elevated. Eye closure becomes
weak, often with sagging of the lower lid. The resulting
exposure of the cornea can be one of the most danger-
ous complications of this disorder. The corner of the
mouth cannot be lifted in a smile; lips cannot be sealed
or the cheek puffed on the affected side. Drooling out of
the affected corner of the mouth is often the patient’s
first hint of a significant problem. Many patients will
notice hyperacusis – although they rarely volunteer this
information. Similarly, they often note a change in taste

perception – in some this may be due to decreased
salivation but more often it is a true dysgeusia. Prov-
ing this requires testing taste on the two sides of the
anterior tongue, without allowing the patient to
retract the tongue back into the mouth between
tests, since diffusion of the test substance will immedi-
ately invalidate the test. Patients often describe numb-
ness on the affected side of the face, but objective
testing rarely confirms this. Most likely this represents
misperception of proprioceptive input with attempted
motion of the paralyzed facial muscles.
Epidemiology
The terms ‘facial palsy’ and ‘Bell’s palsy’ are not
synonymous – the latter term is usually restricted to
patients with idiopathic acute deficits of the facial
nerve.This definition is selected to exclude slowly evol-
ving facial nerve lesions such as those due to posterior
fossa or skull base tumors, as well as brain stem strokes,
skull base fractures, meningitis-associated multiple
cranial neuropathies, Ramsay Hunt syndrome, etc.
However, this definition now becomes problematic,
since there are quite suggestive data that in many
instances Bell’s palsy is caused by herpes simplex
virus. Since these cases are no longer idiopathic, must
they be removed from those considered to be Bell’s
palsy? What about patients with facial nerve palsies
associated with diabetes or with Lyme disease? Clearly,
at some point this more than semantic issue will require
resolution; for now, cases associated with herpes sim-
plex, Lyme disease, and diabetes are generally included
as Bell’s palsy.
The reported incidence of Bell’s palsy varies some-
what, but is generally felt to be about 20–25 cases per
100 000 population per year, affecting about 1 in
60–70 individuals in their lifetime. The disorder is
quite infrequent under the age of 10 years, increases
by decade from ages 10 to 39 years, is fairly constant
at about 35 cases per 100 000 from ages 40 to 69 years,
then increases to over 50 per 100 000 (10 times the
childhood incidence) in those over 70 years. There is
no significant male: female or side-to-side difference.
Involvement is bilateral occasionally; in about 6%
of cases it can be recurrent (the recurrence occurring
on either the previously affected or unaffected side).
The paralysis is complete in a significant proportion
of patients, estimates ranging from 45% to 70% in
different series. (The former number, from a popula-
tion-based study in Rochester, MN, probably reflects a
number as free of selection bias as possible.) No
seasonal or geographic clustering has been evident.
Bell’s palsy probably occurs with increased fre-
quency in diabetics. Hypertension has also been
considered a risk factor. Although it does appear
Bell’s Palsy 157
to increase the likelihood of incomplete recovery,
whether the incidence is increased among hyperten-
sives is unclear. Pregnancy has been reported as a risk
factor, but results have been conflicting; the most sys-
tematic studies have failed to support this association.
Incidence is increased in patients with sarcoidosis, in
whom involvement can be meningeal, within the
parotid, or at points in between. Similarly, incidence
is increased in HIV and Lyme infection. When bilateral
facial palsy occurs it may be indicative of the Guillain–
Barré syndrome, sarcoidosis, or Lyme disease.
Recovery is complete in the vast majority
(80–85%) of patients with Bell’s palsy. The degree of
improvement is commonly graded with the House and
Brackmann Grading Scale (Table 1). More extensive
lesions tend to predispose to incomplete recovery –
presence of pain in addition to the retroauricular
pain, complete facial paralysis, tearing changes, and
sensory changes are all associated with incomplete
recovery. Incomplete recovery is somewhat more
common among those over 55 years of age. In the
most extensive study of this, complete recovery
occurred in 90% of those under 55 years and 79% of
those 55 years and older. Although several comorbid-
ities are linked to Bell’s palsy, only hypertension is
associated with a somewhat worse prognosis.
Interestingly, when all of these factors were consid-
ered in a multivariate analysis, only complete para-
lysis, non-ear pain, and hypertension were found to
predict a somewhat worse prognosis. Other factors,
such as age, and other neurologic changes apparently
merely reflected the impact of these three factors.
Among patients with none of these risk factors,
complete recovery occurred in 96%. With an overall
spontaneous recovery rate of about 85%, and 96%
among low-risk patients, it is not difficult to under-
stand why it has been so difficult to determine efficacy
of different treatment strategies, and why their use has
been controversial.
Pathophysiology
Understanding the mechanism underlying this mono-
neuropathy has been challenging. A few autopsy
cases, published many years ago, were felt to demon-
strate inflammatory changes in the affected nerve.
Subsequent review raised the possibility that the
observed changes were merely what one would expect
to see as part of Wallerian degeneration in a nerve
damaged more proximally. Surgical series reported
swollen-appearing nerves – since it is relatively uncom-
mon to explore normal facial nerves, subsequent
authors, including Sunderland, have suggested that
this was merely the nerve’s normal appearance.
158 Bell’s Palsy

Table 1 House and Brackmann facial nerve grading system

Grade Description Characteristics

I Normal Normal facial function in all areas

II Mild dysfunction Gross: slight weakness on close inspection; slight synkinesis
At rest: normal symmetry and tone
Motion
Forehead: moderate to good function
Eye: complete closure with minimal effort
Mouth: slight asymmetry
III Moderate dysfunction Gross: obvious but not disfiguring difference between two sides; noticeable but
not severe synkinesis, contracture, and/or hemifacial spasm
At rest: normal symmetry and tone
Motion
Forehead: slight to moderate movement
Eye: complete closure with effort
Mouth: slightly weak with maximum effort
IV Moderately severe Gross: obvious weakness and/or disfiguring asymmetry
At rest: normal symmetry and tone
Motion
Forehead: none
Eye: incomplete closure
Mouth: asymmetric with maximum effort
V Severe Gross: only barely perceptible motion
At rest: asymmetry
Motion
Forehead: none
Eye: incomplete closure
Mouth: slight movement
VI Total paralysis No movement

From House JW and Brackmann DE (1985) Facial nerve grading system. Otolaryngology – Head and Neck Surgery 93: 146–147.

Neurophysiologic observations have not been as
informative as one might wish. The standard method
used, electroneurography, consists of stimulating the
facial nerve at the stylomastoid foramen, recording
the compound muscle action potential on the face in a
way designed to span several muscles (a method that
can lead to unpredictable summation of the com-
pound muscle action potentials of different muscles),
and comparing the amplitude ratio of the affected
side to the unaffected side. In many series, only
patients with no elicitable response are sent to a
neurologist or electromyographer. More sophisticated
neurophysiologic studies suggest nerve demyelination
in milder cases, with significant axonal damage when
the paralysis is severe.
Anatomic studies have suggested that the meatal
foramen is the narrowest point along the facial
nerve’s bony canal; intraoperative neurophysiology
has suggested that this is the likely site of damage.
This has led to the hypothesis that the nerve swells as
a result of an inciting event and becomes entrapped at
the meatal foramen. Swelling at this confined point
could either produce focal demyelination and con-
duction block, block axoplasmic transport (resulting
in nerve damage), or lead to intranerve pressures
exceeding perfusion pressure (resulting in ischemic
damage). The highly redundant vascular supply of
the facial nerve generally makes widespread ischemia
seem unlikely, but such focal ischemia is somewhat
more plausible.
Recent work has implicated several specific in-
fections in the etiology of facial nerve palsy. Lyme
disease, infection with the tick-borne spirochete Borre-
lia burgdorferi, clearly is associated with facial nerve
lesions, which may be bilateral in as many as 25% of
such cases. The pathophysiology is unclear. This does
not appear to be due to a meningeal process, even
though Lyme disease can cause meningitis. Neurophy-
siologic studies suggest that this is due to a mononeur-
itis multiplex, although the precise mechanism
underlying this is unclear.
One of the most interesting sets of findings in the
past decade has focused on the possible association
between facial nerve palsy and herpes simplex-1 infec-
tion. In one of the best known studies, endoneurial
fluid was obtained – at least 15 days after onset of the
lesion – at the time of 7th nerve decompression in
14 patients with unrecovering Bell’s palsy. Eleven of
the 14 were polymerase chain reaction (PCR) positive
for HSV-1. Twelve of 13 tested patients had peripheral
blood serologic evidence of past HSV-1 infection.
Seropositivity and PCR positivity were significantly

more common than among controls. This has led to a
number of therapeutic trials of antiviral therapy in
Bell’s palsy. Apparent response to this has led to a
general recommendation for antiviral treatment in
Bell’s palsy.
The herpes hypothesis is an intriguing one, although
gaps remain in our understanding. Methodologically,
PCR detection of viral DNA does not necessarily indi-
cate the virus is either viable or pathophysiologically
relevant. Herpes in particular is so ubiquitous that
the implications of finding it in anybody can only be
understood if comparable samples are obtained from
normal controls. The presence of virus so many days
after the onset of symptoms is curious. In other herpes
reactivation syndromes, the number of obtainable
virions – weeks after the onset – tends to be small.
Herpes viruses generally reside in sensory neurons.
Although the facial nerve is primarily motor, it does
contain sensory neurons (residing in the geniculate
ganglion). It is conceivable that reactivation from
the sensory neurons could result in sufficient swelling
to damage motor fibers. If this were the case, though,
one might expect more marked loss of sensation as
part of Bell’s palsy.
Diagnostic Approach
In addition to clinical assessment, electromyography
(EMG) can be informative. When the lesion is incom-
plete, blink reflexes can demonstrate slowing indicative
of demyelination. Since the lesion is typically intra-
cranial, the nerve portion peripheral to the stylomas-
toid foramen may remain excitable for several days
following onset, regardless of the severity of the dam-
age to the nerve. Inexcitability after day 5 suggests a
profound axonal lesion. Needle EMG can be useful in
differentiating between a truly complete lesion and one
sparing a few motor units, the latter having a signifi-
cantly better prognosis. Observation of widespread
changes of acute denervation obviously reflects a
more severe lesion with a worse prognosis. On the
other hand, evidence of reinnervation may be apparent
on needle EMG exam long before it is clinically
evident.
EMG can also be useful to demonstrate synkinesias –
regenerating nerves can be misdirected, resulting in eye
closure with attempted mouth movements, eye tearing
with attempted facial movements (‘crocodile tears’), or
other peculiar combinations.
Cerebrospinal fluid (CSF) examination is useful
primarily in assessing for inflammatory or neoplastic
processes in the subarachnoid space. Magnetic reso-
nance imaging (MRI) and computed tomography
(CT) imaging can be helpful in addressing structural
lesions of the brain stem, skull base, or nerve.
Bell’s Palsy 159
Treatment
The prognosis is generally excellent: 85% of all
patients will do well with no treatment whatever.
This, coupled with methodological concerns with
many of the treatment trials, has led to a rather conser-
vative approach to treatment on the part of many
physicians, particularly for nonhypertensive patients
with incomplete paralysis and no diffuse pain, for
whom rapid and complete recovery is almost assured.
Several aspects of care are mandatory. Eye damage
is one of the greatest threats to patients. They should
be instructed to patch the eye, particularly when
sleeping or when in a dusty environment. Lubricating
drops (methylcellulose) during the day, and ointment
at night, can be helpful. Weakness of the facial mus-
cles leads to a tendency for food to ‘pocket’ in the
cheek. Brushing the teeth after each meal can limit the
risk of dental caries. Patients with complete paralysis
can develop contracturing of the denervated muscles,
leading to additional facial distortion and potentially
limiting recovery when reinnervation occurs. Gentle
massage of the paralyzed muscles for at least
10–15 min daily is said to lessen the impact of this.
For patients in whom no recovery occurs, several
surgical options have been tried. Transplanting the
hypoglossal nerve to facial muscles can lead to some
facial muscle control on the paralyzed side (at the cost
of lingual hemiatrophy and paralysis). A weight in the
affected eyelid can facilitate eyelid closure and eye
protection. Occasionally the eyelid must be partially
sewn shut to protect the cornea.
The three areas of greatest therapeutic focus have
been corticosteroids, antivirals such as acyclovir, and
decompressive surgery. Unfortunately, the literature
on all three approaches has been highly variable in
scientific design, sample size adequacy, and interpre-
tation. Results for each have varied from negative to
compelling. The literature was recently explored in
depth by a task force of the American Academy of
Neurology, resulting in a practice parameter. In their
meta-analysis of the available, interpretable literature
regarding corticosteroids, the panel concluded that
corticosteroids were useful, improving outcomes by
16%. Usual regimens consisted of 1 mg kg 1 per day
(maximum dose 80 mg) divided into two doses per
day for 4 or 5 days, then tapering over 5 to 10 days.
Treated patients did not recover more quickly, but
a greater percentage recovered fully. Some studies
have suggested the acute retroauricular pain improves
more rapidly with steroids. Patients faired best if
treated in the first week. Although it is often stated
that the earlier the treatment, the better the response,
beyond the observation that treatment is only useful
in the first week there are no compelling data that the
160 Bell’s Palsy
timing of treatment within this window affects the
likelihood of recovery – a somewhat surprising obser-
vation given that the major nerve damage is thought to
occur in the first 48 h. Notably, a Cochrane analysis
questioned the validity of the conclusion that steroids
are effective, because of methodological problems
with several of the largest included studies.
Even fewer studies are available concerning use
of acyclovir. Here, too, a meta-analysis led to the
conclusion that treating all patients with acyclovir
improved the proportion of patients recovering by
22%. Given the small number of studies available,
and their sometimes conflicting conclusions, this was
felt to be less compelling, but was recommended as
appropriate treatment. Again, the fact that this treat-
ment is usually given – and appears to be effective – at
a time that maximal nerve damage has already
occurred is theoretically puzzling.
Finally, with regard to decompressive surgery, the
task force found no scientifically compelling study.
While earlier studies were negative, one more recent
study of patients in whom recovery was thought to be
extremely unlikely by clinical and EMG criteria, who
underwent a far more extensive decompression extend-
ing to the meatal foramen, provided encouraging
results, with 91% of patients improving significantly
(but with no controls).
Overall, the likelihood of recovery is great, appar-
ently enhanced with early treatment with corticoster-
oids and/or acyclovir-like antivirals. In the appropriate
setting, potentially contributing disorders such as Lyme
disease, HIV, or sarcoidosis need to be considered,
and treated appropriately if found Surgical treat-
ment remains unproved, but is occasionally attempted
in situations in which the likelihood of recovery
seems very limited. In general, prevention of secondary
complications, such as exposure keratitis, dental decay,
and muscle contractures, is the most important aspect
of treatment.
See also: Axonal Injury: Neuronal Responses; Brainstem
and Cranial Nerves; Electromyography (EMG) and Nerve
Conduction Studies; Optic Nerve, Optic Chiasm and Optic
Tracts; Peripheral Nerve Regeneration: An Overview.
Further Reading
Adour KK, Ruboyianes JM, Von Doersten PG, et al. (1996) Bell’s
Palsy treatment with acyclovir and prednisone compared with
prednisone alone: A double blind, randomized, controlled trial.
Annals of Otology, Rhinology and Laryngology 105: 371–378.
Adour KK, Wingerd J, Bell DN, et al. (1972) Prednisone treatment
for idiopathic facial paralysis. New England Journal of
Medicine 287: 1268–1272.
Gantz BJ, Rubinstein JT, Gidley P, et al. (1999) Surgical manage-
ment of Bell’s palsy. Laryngoscope 109: 1177–1188.
Gilden DH (2004) Bell’s palsy. New England Journal of Medicine
351: 1323–1331.
Grogan PM and Gronseth GS (2001) Practice parameter: Steroids,
acyclovir, and surgery for Bell’s palsy (an evidence based
review). Neurology 56: 830–836.
Halperin JJ (2003) Facial nerve palsy associated with Lyme disease.
Muscle & Nerve 28: 516–517.
House JW and Brackmann DE (1985) Facial nerve grading system.
Otalaryngology – Head and Neck Surgery 93: 146–147.
Katusic SK, Beard CM, Widerholt WC, et al. (1986) Incidence,
clinical features and prognosis in Bell’s palsy, Rochester,
Minnesota 1968–1982. Annals of Neurology 20: 622–627.
Murakami S, Mizobuchi M, Nakashiro Y, et al. (1996) Bell palsy and
herpes simplex virus: Identification of viral DNA in endoneurial
fluid and muscle. Annals of Internal Medicine 124: 27–30.
Salinas R, Alvarez G, and Ferreira J (2004) Corticosteroids for
Bell’s palsy (idiopathic facial paralysis). Cochrane Database
of Systematic Reviews 4: CD001942.