Historic red flags casting doubt on the diagnosis of Bell’s palsy as the cause of a peripheral facial palsy include gradual onset over weeks to months, concomitant vertigo or hearing loss, constitutional symptoms, cancer, human immunodeficiency virus (HIV)45,46 or risk factors for HIV, and features suggesting Lyme disease (eg, endemic area, known tick bite, skin rash).47–49 Since the majority of patients with Bell’s palsy improve within several months, the lack of any improvement or a gradual progression from facial paresis to facial palsy should both raise a red flag. About 7% of patients with Bell’s palsy will have a recurrence,37–39 but when this occurs, it should be considered a red flag, prompting an evaluation (to include imaging and a lumbar puncture) for another cause.
Some of the red flags from the neurologic examination include bilateral facial palsy,50 involvement of other cranial nerves (as mentioned previously, the physician may see subtle signs of other cranial nerve involvement in Bell’s palsy), hemiparesis, hearing loss or nystagmus, ataxia, horizontal gaze palsy, or systemic weakness. Important findings on the head and neck examination to look for include vesicles in the external canal, tympanic membrane or palate, cervical adenopathy, otitis media, parotid mass, skin cancer, fissured tongue, and facial swelling.41,42 It is important to recognize that a peripheral facial palsy may be the first sign of an evolving disorder such as neurosarcoidosis, meningeal carcinomatosis, or Guillain-Barré syndrome.51
Several specific causes of peripheral facial palsy deserve highlighting. It is the most common neurologic manifestation of Lyme disease,47–49 and this should always be considered in patients who live in an endemic area, especially if the facial palsy is bilateral or in a child. Halperin and Golightly49 determined that 25% of facial palsies during the summer months in an endemic area were due to Lyme disease, based on serology. Because no other clinical features may suggest Lyme disease before or at the time of facial palsy (eg, erythema migrans), and serologic evidence may lag behind the earliest clinical manifestations,47 the decision to treat rests largely on the physician’s index of suspicion for Lyme disease. If no symptoms or signs occur other than facial palsy, such as cranial polyneuropathy or evidence of parenchymal involvement, then a lumbar puncture is probably not indicated.48 Even without antibiotics, the prognosis of Lyme disease facial palsy is favorable,52 and therefore treatment is aimed at preventing sequelae. As pointed out by the American Academy of Neurology (AAN) Practice parameter, “no definitive data exist to establish the superiority, or lack thereof, of either oral or parenteral treatment.”53 For facial palsy presumed to be from Lyme disease, it is reasonable to use an oral agent. If no clinical or serologic evidence confirms the diagnosis of Lyme disease at presentation, then steroids may be considered in case the diagnosis is actually Bell’s palsy; according to the AAN practice parameter, although evidence is limited, a short course of steroids is not likely to be harmful when treating Lyme disease.53
Ramsay Hunt syndrome (Case 5-3) is manifested by a peripheral facial palsy with erythema and vesicles in the external auditory canal, the tympanic membrane, or the oropharynx. It is due to reactivation of varicella-zoster virus in the geniculate ganglion.54 Accompanying symptoms reflect neighborhood involvement of the vestibulocochlear nerve including vertigo, hearing loss, and tinnitus.
About 5% of patients with sarcoidosis will have neurologic involvement, and in one-half of those cases, it is the presenting sign, with a peripheral facial palsy being the most common manifestation. Neurosarcoidosis is particularly important to consider with bilateral peripheral facial palsy. The diagnosis may be challenging and requires a careful search for evidence of systemic involvement and, ideally, pathologic confirmation.39,40 Another important consideration, particularly when bilateral facial palsy occurs, is Guillain-Barré syndrome, which may evolve rapidly from facial palsy into a more classic picture with bulbar and limb weakness with areflexia, but a subtype of Guillain-Barré syndrome manifests by only bifacial weakness and distal paresthesia.51
A 76-year-old man noticed ear pain followed by weakness of the right face. He did not experience hearing loss or vertigo. On examination, he had a right peripheral facial palsy and erythema and vesicles in the right ear (Figure 5-6). He was diagnosed as having geniculate zoster, Ramsay Hunt syndrome, and was treated with corticosteroids and acyclovir.
Comment. Although the involvement of the ear by zoster was readily apparent in this patient, in others it is subtle, necessitating careful inspection of the external auditory canal and tympanic membrane as well as the oropharynx. The presence of vertigo, hearing loss, and tinnitus may accompany Ramsay Hunt syndrome and are important red flags pointing away from Bell’s palsy.
Most patients with Bell’s palsy are worried they have had a stroke, so reassurance and education are important parts of treatment along with counseling that the prognosis is favorable for most patients, particularly those with mild or moderate facial weakness at presentation. Because of weakness of eyelid closure and the risk of corneal exposure, particularly in those with complete palsy, patients should use lubricating drops frequently during waking hours and a lubricating ointment at night. The lid can be taped closed at night or a cellophane patch can be applied with care so that no direct contact with the cornea occurs.
The use of steroids and antivirals to improve the recovery of Bell’s palsy is based on the previously mentioned observations about the possible roles of edema and HSV type 1 in the pathophysiology and etiology, respectively, in Bell’s palsy. Here the author relies primarily on the AAN evidence-based guidelines. The first guideline published in 2001 found only five published studies of sufficient rigor upon which to determine the effectiveness of corticosteroids (two Class I, two Class II, and one Class III), and none were sufficiently powered to allow for a definitive recommendation.55 By pooling the results of the Class I and II studies, coupled with the safety of a short course of steroids, the authors of this guideline concluded that: “steroids are safe and probably effective in improving facial functional outcomes in patients with Bell’s palsy” (level B recommendation).55 Even less evidence, and no Class I studies, existed upon which to base a recommendation for acyclovir, which received a level C recommendation of being safe and possibly effective. The lack of unbiased studies and a high complication rate precluded any evidence-based recommendations on surgical decompression.55
The AAN evidence-based guideline on steroids and antivirals for the treatment of Bell’s palsy was updated in 2012,56 and the revised recommendations were based largely on two Class I studies published since the original review. The first study by Sullivan and colleagues57 compared four treatment arms: prednisolone alone (25 mg twice per day for 10 days), acyclovir alone (400 mg twice per day for 10 days), a combination of prednisolone and acyclovir, and placebo in patients age 16 or older who presented within 72 hours of onset of Bell’s palsy (Figure 5-7). The primary outcome was the degree of facial weakness observed in digital photographs by three blinded reviewers, using the House-Brackmann facial nerve grading system, at 3 and 9 months. Of 551 patients who underwent randomization, outcome data were available for 496 (90%).
The other Class I study by Engström and colleagues58 was similar, but instead of acyclovir, valacyclovir (1000 mg 3 times per day for 7 days) was used. More than 800 patients between ages 18 and 75, presenting within 72 hours, were randomly assigned to prednisolone (60 mg/d for 5 days then reduced by 10 mg/d) and placebo, valacyclovir and placebo, placebo and placebo, and prednisolone and valacyclovir. The primary outcome measure was time to complete recovery (score of 100) on the Sunnybrook facial nerve grading system. Similar to the study by Sullivan and colleagues,57 those patients who received prednisolone had a significantly higher rate of recovery at all time points, including the final assessment at 1 year compared to placebo and to the combination of valacyclovir and prednisolone (Figure 5-8). The lower rates of recovery, even for the placebo-placebo group in the study by Engström and colleagues,58 were attributed to the higher sensitivity of the Sunnybrook scale for residual weakness. No significant adverse effects occurred in either study.
An editorial following the publication of these two trials by Tyler32 concluded that “antiviral therapy should not be routinely used in patients with [Bell’s palsy].” Tyler did, however, point out the potential benefit of antivirals for treatment of Ramsay Hunt syndrome.32 The AAN evidence-based review gave a level A recommendation to the use of corticosteroids for treatment of Bell’s palsy within 72 hours of onset. Continuing, they reiterated that adding an antiviral to a corticosteroid offers no significant benefit regarding facial recovery. However, they pointed out that the 95% confidence interval of the two Class I studies could not rule out a modest effect of adding an antiviral and gave a Class C rating to the combination.56 When discussing the combination with patients, despite counseling that adding an antiviral to a steroid does not offer significant benefit (when also told that a benefit, even modest at best, cannot be “ruled out”), most patients, in the author’s experience, opt to take an antiviral.
The clinical practice guidelines by the American Academy of Otolaryngology—Head and Neck Surgery Foundation, developed by specialists in a variety of related fields including neurology, made similar recommendations about the use of corticosteroids and antivirals for Bell’s palsy. They went on to address some of the other popularly touted treatments for Bell’s palsy, finding insufficient or poor-quality evidence to make any recommendations about the use of surgical decompression, acupuncture, and physical therapy to treat Bell’s palsy.43
LONG-TERM MANIFESTATIONS AND COMPLICATIONS
As the placebo arms of the previously mentioned studies demonstrate, up to 85% of patients with Bell’s palsy make a complete recovery within 1 year.57,58 Those left with facial weakness may be candidates for surgical procedures aimed at improving facial function, particularly when significant eyelid weakness occurs, with risk of exposure keratitis (this complication requires prompt ophthalmologic referral). These include implantation of a gold weight in the eyelid and other nerve or muscle transfer procedures that will not be reviewed here; patients should be referred to a surgeon experienced in these options.13,59
When residual weakness occurs in patients with Bell’s palsy, the apparent side of the weakness can be paradoxical. With an acute peripheral facial palsy, the nasolabial fold is flattened, and the palpebral fissure is widened. But with chronic weakness, a contracture may develop such that at rest, the nasolabial fold on the weak side is deeper and the palpebral fissure narrower (Case 5-4).60 The actual side of the weakness is readily apparent with movement, and synkinesia almost always occurs, confirming an old facial palsy. The author has been involved in a few cases where an old case of Bell’s palsy with contracture has been misinterpreted as new weakness on the patient’s good side of the face, leading to an erroneous diagnosis (usually stroke) and unnecessary testing before the findings are interpreted correctly and the history clarified. Patients are often unaware of residual weakness and synkinesia and may forget about having had Bell’s palsy many years earlier.
There are two types of synkinesias that develop after Bell’s palsy due to misdirection of regenerating fibers. The first is motor: with blinking, particularly if forceful, simultaneous contracture of the ipsilateral mouth or platysma occurs, and similarly, when smiling or showing teeth, contracture of the orbicular oculi and narrowing of the palpebral fissure occurs (Case 5-5). This is often asymptomatic but if patients are bothered, then botulinum toxin is the most effective treatment. Some patients go on to develop hemifacial spasm.61
Nonmotor fibers in the facial nerve may also misdirect, producing two types of synkinesias. The first is gustatory tearing in which salivation may be associated with lacrimation (so-called crocodile tears named for the myth that the crocodile either sheds a tear to attract its victim or sheds a tear as the victim is being eaten—in either case, the implication is that crocodile tears are insincere tears).
When salivation causes facial sweating, this is known as Frey syndrome or gustatory sweating, named for Lucja Frey, one of the first female Polish neurologists, whose productive career was cut tragically short by the Nazis.62 Although Frey was not the first to recognize this phenomenon, she is credited with discerning its physiology and pharmacology. Frey syndrome is encountered much more commonly after parotid surgery than Bell’s palsy (see the video from Reich and Grill62 for an example of Frey syndrome).
A 73-year-old man was seen for Parkinson disease and related a history of remote Bell’s palsy, from which he reported a good recovery. On examination, at rest (Figure 5-9A) the right nasolabial fold was flatter, and the palpebral fissure was wider, suggesting that was the side of the facial weakness. However, as Figures 5-9B and 5-9C demonstrate, he had a contracture on the left, which is the side of the weakness.
Comment. This case demonstrates that it can be easy to mistake the side of weakness from a previous case of Bell’s palsy, but the synkinesia is a sure giveaway.
Bell’s palsy is characterized by the spontaneous, acute (over 24 to 72 hours) onset of unilateral peripheral facial palsy in isolation—that is, no features from the history, neurologic examination, or general examination suggest an alternative diagnosis. Red flags casting doubt on the diagnosis of Bell’s palsy include gradual onset, concurrent vertigo or hearing loss, vesicles in the external auditory canal, living in an area endemic for Lyme disease, risk factors for HIV, and systemic cancer, among others. When no red flags exist, and the diagnostic criteria for Bell’s palsy are used, additional testing is usually not necessary. Even without treatment, most patients, especially those with facial paresis rather than palsy, will have a complete recovery. A 10-day course of corticosteroids has been shown to significantly increase the likelihood of recovery; adding an antiviral does not significantly improve the likelihood of recovery, but the possibility that doing so may have a modest benefit, at most, cannot be ruled out. Residual effects of Bell’s palsy include permanent weakness and motor and nonmotor synkinesia, the latter including gustatory tearing and gustatory sweating (Frey syndrome).
Supplemental Digital Content 5-1
Synkinesia after right facial nerve palsy. The 55-year-old woman in Case 5-5 developed a moderate right facial nerve palsy 20 years earlier as a consequence of the removal of a large acoustic neuroma, which gradually improved. When she blinks, co-contraction of the right orbicularis oris occurs, and when she smiles, co-contraction of the right orbicularis oculi occurs, causing the palpebral fissure to narrow; these are signs of aberrant regeneration of the facial nerve with synkinesia.
links.lww.com/CONT/A214 © 2017 American Academy of Neurology.
A 55-year-old woman had undergone surgery for a large right acoustic neuroma 20 years earlier and was followed by her neurologist for headaches. Postoperatively, she had had moderate facial weakness that gradually improved, and she eventually developed an asymptomatic synkinesia. When she blinked, simultaneous movement of the right lips and mentalis occurred, and when she smiled, contraction of the orbicularis oculi occurred (Supplemental Digital Content 5-1, links.lww.com/CONT/A214).
Comment. This case demonstrates one of the complications of facial nerve palsy: the aberrant regeneration of motor fibers. The patient exhibits synkinesia between the orbicularis oculi and orbicularis oris, so that moving the mouth causes a contraction, which narrows the palpebral fissure, and eye closure causes retraction of the mouth. This symptom is often asymptomatic but, if bothersome, it can be treated with botulinum toxin.
* Bell’s palsy is characterized by the spontaneous acute (72 hours or fewer) onset of a unilateral peripheral facial nerve palsy without any accompanying signs, with neither the history nor examination suggesting an alternative diagnosis.
* Sir Charles Bell determined that the seventh cranial nerve controlled the muscles of facial expression.
* A peripheral (lower motor neuron) facial palsy weakens all the ipsilateral facial muscles, including the frontalis and orbicularis oculi. A central (upper motor neuron) facial palsy weakens only the contralateral two-thirds of the face, sparing the frontalis.
* In addition to innervating the muscles of facial expression, the facial nerve also conveys sensation from the external auditory canal, pinna, mastoid, and mucosa of the palate; innervates the stapedius muscle and the lacrimal and minor salivary glands; and carries taste from the anterior two-thirds of the tongue.
* Factors suggesting a worse prognosis for recovery of Bell’s palsy include diabetes mellitus, hypertension, older age, complete paralysis, lack of improvement by 1 month, non-ear pain, and decreased tearing.
* The cause of Bell’s palsy is not known but may be due to reactivation of herpes simplex virus type 1.
* The return of the ability to whistle can be a useful way to document improvement in Bell’s palsy (assuming the patient could whistle before its onset).
* Although typically no objective sensory loss occurs with Bell’s palsy, pain around the ear and face may occur, which at times can be severe. Prolonged pain outside of these areas may be a sign that the patient has an alternative cause of facial palsy.
* Some have suggested that Bell’s palsy is actually a cranial polyneuropathy. But, anything more than subtle signs implicating other cranial nerves should be viewed as a potential red flag, casting doubt on the diagnosis of Bell’s palsy.
* About 7% of patients with Bell’s palsy will have a recurrence.
* For typical cases of Bell’s palsy, with no red flags from the history or examination, no further workup, including imaging, is necessary.
* If a patient with Bell’s palsy is imaged with MRI (typically not necessary), enhancement of the intracanalicular and labyrinthine segments of the facial nerve may be seen.
* Red flags casting doubt on the diagnosis of Bell’s palsy include gradual onset, involvement of other cranial nerves, concurrent vertigo or hearing loss, bilaterality, risk for Lyme disease or human immunodeficiency virus, and systemic cancer.
* Lyme disease is a common cause of peripheral facial palsy in endemic areas during the summer months, but in the absence of potential exposure and without other characteristic signs, routine testing is not recommended.
* A careful head and neck examination is important in patients with a peripheral facial palsy with particular attention for vesicles on the tympanic membrane, external auditory canal, or soft palate, indicating herpes zoster (Ramsay Hunt syndrome).
* A peripheral facial palsy is the most common neurologic manifestation of neurosarcoidosis and is particularly important to consider if bilateral.
* A peripheral facial palsy may the first sign of Guillain-Barré syndrome, progressing to limb weakness, but a variant of Guillain-Barré syndrome occurs with only bifacial palsy.
* To protect the cornea in patients with Bell’s palsy, lubricating drops should be used frequently during the day, and a lubricating gel should be used at night along with taping the lid closed or using a patch that does not rest on the cornea.
* The American Academy of Neurology evidence-based review gave a level A recommendation to the use of corticosteroids within the first 72 hours of onset to increase the likelihood of improvement for Bell’s palsy. Combining an antiviral with a corticosteroid does not significantly improve the outcome of Bell’s palsy, and their use was given a level C recommendation for a possible modest benefit, at best.
* Residual facial weakness after Bell’s palsy can cause a contracture, making it appear at rest that the normal side is weak with a flatter nasolabial fold and widened palpebral fissure. When facial function is tested, the weak side is readily apparent.
* A motor synkinesia is a complication of Bell’s palsy. This is usually asymptomatic but, if bothersome, can be treated with botulinum toxin.
* Two nonmotor synkinesias after Bell’s palsy include gustatory lacrimation (crocodile tears) and gustatory sweating, known as Frey syndrome.
This article is dedicated to Donald H. Gilden, MD, FAAN (1937 to 2016), in recognition of his many contributions to Bell’s palsy and with appreciation of his friendship.
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