Bell Palsy: Clinical Examination and Management: Review
Bell Palsy: Clinical Examination and Management: Review
Bell Palsy: Clinical Examination and Management: Review
CME
CREDIT
EDUCATIONAL OBJECTIVE: Readers will distinguish Bell palsy from other causes of facial weakness
and apply current management guidelines
DONIKA K. PATEL, DO
KERRY H. LEVIN, MD
Bell palsy:
Clinical examination and management
ABSTRACT
Bell palsy is a common neurologic disorder characterized
by acute facial mononeuropathy of unclear cause presenting with unilateral facial weakness. Careful examination and a detailed history are important in making
an accurate diagnosis. Early recognition is essential, as
treatment with corticosteroids within 72 hours of onset
has been shown to hasten recovery. Fortunately, most
patients recover spontaneously within 3 weeks, even if
untreated.
KEY POINTS
Bell palsy is an acute disorder of the facial nerve causing unilateral facial weakness, pain, abnormal taste, and
reduced tearing.
Although herpes simplex virus reactivation is suspected
in the pathogenesis, the exact cause is unknown.
An additional workup is warranted for abnormalities
beyond isolated facial nerve palsy.
Guidelines recommend starting corticosteroids for
patients who present within 3 days of symptom onset.
There is no compelling evidence to support antiviral
therapy, physical therapy, acupuncture, or surgical
decompression.
doi:10.3949/ccjm.82a.14101
419
BELL PALSY
TABLE 1
Although
Bell palsy
is clinically
benign, its
disfigurement
can be
devastating
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INFLAMMATION IS BELIEVED
TO BE RESPONSIBLE
CCF
FIGURE 1
the patient attempts to close the eyes, the affected side shows incomplete closure and the
eye may remain partly open.
Assess the strength of the orbicularis oculi
by trying to open the eyes. The patient who
is attempting to close the eyelids tightly but
cannot will demonstrate the Bell phenomenon, ie, the examiner is able to force open
the eyelids, and the eyes are deviated upward
and laterally.
Closely observe the blink pattern, as the
involved side in Bell palsy may slightly lag behind the normal eye, and the patient may be
unable to close the eye completely.
Is the smile symmetric?
Note flattening of the nasolabial fold on one
side, which indicates facial weakness.
Can the patient puff out the cheeks?
Ask the patient to hold air in the mouth
against resistance. This assesses the strength
421
BELL PALSY
Facial palsy
that does not
improve after
3 weeks
should prompt
a referral to
a neurologist
422
TABLE 2
Cause
Distinguishing characteristics
Autoimmune diseases
Guillain-Barr syndrome
Multiple sclerosis
Diabetes
Meningitis, encephalitis
Herpes simplex
Lyme disease
Borrelia burgdorferi
Varicella zoster
Metabolic diseases
Infectious diseases
Neoplasm
ple ipsilateral cranial nerve palsies and contralateral limb weakness. Sarcoidosis and leptomeningeal carcinomatosis tend to involve the
skull base and present with multiple cranial
neuropathies.
Tumors of the brain or parotid gland have
an insidious onset and may cause systemic
signs such as fevers, chills, and weight loss.
Headache, seizures, and hearing loss indicate
an intracranial lesion. A palpable mass near
the ear, neck, or parotid gland requires imaging of the face to look for a parotid gland tumor.
Infection
A number of infections can cause acute facial
paralysis. The most common is herpes simplex
virus, and the next most common is varicella
zoster.14 Herpes simplex virus, Ramsay Hunt
syndrome, and Lyme disease may have associated pain and skin changes. Erythema of the
tympanic membrane suggests otitis media, especially in the setting of ear pain and hearing
loss.
Ramsay Hunt syndrome is caused by reactivation of the herpes zoster virus from the
geniculate ganglion, affecting the facial nerve.
Careful examination of the ear canal and the
oropharynx may show vesicles.
In Lyme disease, facial palsy is the most
common cranial neuropathy, seen in 50% to
63% of patients with Borrelia burgdorferi meningitis.16,17 In people with a history of rash,
arthralgia, tick bite, or travel to an endemic
region, Lyme titers should be checked before
starting the patient on corticosteroids.
Bilateral facial palsy is rare and occurs in
fewer than 1% of patients. It has been reported
in patients with Lyme disease, Guillain-Barr
syndrome, sarcoidosis, diabetes mellitus, viral
infection, and pontine glioma.18
Serologic testing,
electrodiagnostic
studies, and
imaging are not
routinely
necessary
to diagnose
Bell palsy
423
BELL PALSY
DIAGNOSTIC EVALUATION
Serologic testing, electrodiagnostic studies,
and imaging are not routinely necessary to
diagnose Bell palsy. However, referral to the
appropriate specialist (neurologist, otolaryngologist, optometrist, ophthalmologist) is advised if the patient has sparing of the forehead
muscle, multiple cranial neuropathies, signs of
infection, or persistent weakness without significant improvement at 3 weeks.
Most patients
with Bell palsy
recover
spontaneously
without
treatment
especially those
with mild
symptoms
Laboratory testing
A complete blood cell count with differential
may point to infection or a lymphoproliferative disorder. When indicated, screening for
diabetes mellitus with fasting blood glucose
or hemoglobin A1c may be helpful. In Lymeendemic regions, patients should undergo an
enzyme-linked immunosorbent assay or an indirect fluorescent antibody test to screen for
the disease. If positive, the diagnosis of Lyme
disease should be confirmed by Western blot.
If vesicles are present on examination, check
serum antibodies for herpes zoster. In the appropriate clinical setting, angiotensin-converting enzyme, human immunodeficiency
virus, and inflammatory markers can be tested.
Cerebrospinal fluid analysis is generally
not helpful in diagnosing Bell palsy but can
differentiate it from Guillain-Barr syndrome,
leptomeningeal carcinomatosis, and infection
involving the central nervous system.
Imaging
Imaging is not recommended in the initial
evaluation of Bell palsy unless symptoms and
the examination are atypical. From 5% to 7%
of cases of facial palsy are caused by a tumor
(eg, facial neuroma, cholesteatoma, hemangioma, meningioma), whether benign or malignant.14,15 Therefore, in patients with insidious onset of symptoms that do not improve in
about 3 weeks, contrast-enhanced computed
tomography or gadolinium-enhanced magnetic resonance imaging of the internal auditory
canal and face is warranted.
Electrodiagnostic studies
Electrodiagnostic testing is typically not part
of the evaluation of acute Bell palsy, but in
patients with complete paralysis, it may help
assess the degree of nerve injury and the
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TABLE 3
Examples
Corticosteroids
A (established as effective)
C (possibly effective)
a
b
Instruct
patients to call
at 2 weeks
to report
progress
Acupuncture: No recommendation
Currently, there is no recommendation for of symptoms
425
BELL PALSY
evaluated within or at 1 month, with close attention to facial weakness and eye irritation.
Further evaluation is needed if there has been
no improvement, if symptoms have worsened,
or if new symptoms have appeared.
The psychosocial impact of Bell palsy cannot be discounted, as the disfigurement can
have negative implications for self-esteem and
social relationships. Appropriate referral to an
ophthalmologist, neurologist, otolaryngologist, social worker, or a plastic surgeon may be
necessary.
COMPLICATIONS AND PROGNOSIS
Most patients with Bell palsy recover completely, but up to 30% have residual symptoms
at 6 months.14,20 Furthermore, although Bell
REFERENCES
1. Grzybowski A, Kaufman MH. Sir Charles Bell (1774-1842): contributions to neuro-ophthalmology. Acta Ophthalmol Scand 2007;
85:897901.
2. De Diego-Sastre JI, Prim-Espada MP, Fernndez-Garca F. The epidemiology of Bells palsy. Rev Neurol 2005; 41:287290. In Spanish.
3. Morris AM, Deeks SL, Hill MD, et al. Annualized incidence and
spectrum of illness from an outbreak investigation of Bells palsy.
Neuroepidemiology 2002; 21:255261.
4. Bosco D, Plastino M, Bosco F, et al. Bells palsy: a manifestation of
prediabetes? Acta Neurol Scand 2011; 123:6872.
5. Riga M, Kefalidis G, Danielides V. The role of diabetes mellitus in
the clinical presentation and prognosis of Bell palsy. J Am Board
Fam Med 2012; 25:819826.
6. Hilsinger RL Jr, Adour KK, Doty HE. Idiopathic facial paralysis,
pregnancy, and the menstrual cycle. Ann Otol Rhinol Laryngol 1975;
84:433442.
7. Savadi-Oskouei D, Abedi A, Sadeghi-Bazargani H. Independent role
of hypertension in Bells palsy: a case-control study. Eur Neurol 2008;
60:253257.
8. Murai A, Kariya S, Tamura K, et al. The facial nerve canal in patients
with Bells palsy: an investigation by high-resolution computed
tomography with multiplanar reconstruction. Eur Arch Otorhinolaryngol 2013; 270:20352038.
9. Blumenfeld H. Neuroanatomy Through Clinical Cases. 1st ed. Sunderland, MA: Sinauer; 2002:479484.
10. Murakami S, Mizobuchi M, Nakashiro Y, Doi T, Hato N, Yanagihara
N. Bell palsy and herpes simplex virus: identification of viral DNA in
endoneurial fluid and muscle. Ann Intern Med 1996; 124:2730.
11. Boahene DO, Olsen KD, Driscoll C, Lewis JE, McDonald TJ. Facial
nerve paralysis secondary to occult malignant neoplasms. Otolaryngol Head Neck Surg 2004; 130:459465.
12. DeJong RN. The Neurologic Examination: Incorporating the fundamentals of neuroanatomy and neurophysiology. 4th ed. New York,
NY: Harper & Row; 1979:178198.
13. House JW, Brackmann DE. Facial nerve grading system. Otolaryngol
Head Neck Surg 1985; 93:146147.
14. Peitersen E. Bells palsy: the spontaneous course of 2,500 peripheral
facial nerve palsies of different etiologies. Acta Otolaryngol Suppl
2002; 549:430.
15. Hohman MH, Hadlock TA. Etiology, diagnosis, and management
of facial palsy: 2000 patients at a facial nerve center. Laryngoscope
2014; 124:E283E293.
16. Ackermann R, Hrstrup P, Schmidt R. Tick-borne meningopolyneuri-
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