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Contemporary Management of Bell Palsy Tessa A. Hadlock, MD1
1 Department of Otolaryngology, Massachusetts Eye and Ear Infirmary
and Harvard Medical School, Boston, Massachusetts Facial Plast Surg 2015;31:93–102.
Abstract Keywords
► ► ► ► ►
Bell palsy facial reanimation synkinesis facial paralysis facial palsy
Address for correspondence Nate Jowett, MD, Department of Otolaryngology, Massachusetts Eye and Ear Infirmary and Harvard Medical School, Boston, Massachusetts (e-mail: [email protected]).
Bell palsy (BP) is the most common diagnosis in acute and chronic facial palsy. Although most patients fully recover, more than one-quarter will have residual dysfunction. Of these, nearly half will demonstrate severe limitations in facial expression. Though significant attention has been paid to acute management and prognosis, a paucity of literature exists addressing management of the long-term sequelae of BP. This article describes contemporary use of physical therapy, injectables, and static and dynamic surgical procedures in facial reanimation of acute and chronic BP.
In 1821, Sir Charles Bell first described idiopathic facial paralysis.1 Bell palsy (BP) remains the leading cause of facial palsy, accounting for approximately 70% of acute and 40% of chronic cases.2 It is believed to be the result of viral reactivation of latent herpes simplex virus (HSV), varicella-zoster virus (VZV), or human herpesvirus 6 (HHV-6), causing inflammation and ischemic entrapment of the facial nerve at the meatal foramen; however, conclusive evidence remains elusive.3,4 Without treatment, 70% of patients will fully recover, whereas an additional 15% will recover with only minor deficits.5 The remaining 15% develop variable patterns of predominantly synkinetic facial palsy (i.e., nonflaccid facial palsy [NFFP]6), resulting in profound negative impact on quality of life and well-being.7 Persistence of flaccid palsy in BP does not occur. Though the management of acute BP is relatively straightforward, the management of long-term sequelae differs across providers. This article aims to summarize one approach to the contemporary management of facial dysfunction following BP.
History BP is a diagnosis of exclusion. Risk factors include diabetes and pregnancy.8,9 The most common alternative causes of facial palsy include postsurgical insult, benign or malignant tumors, infection, and temporal bone trauma.2 Elucidation of the time course of symptoms is critical for proper diagnosis. Whereas the full extent of facial weakness in BP develops within 72 hours, malignancies demonstrate insidious onset
Issue Theme Current Concepts, State of the Art Treatment of Facial Paralysis; Guest Editor, Patrick J. Byrne, MD, FACS
with symptom progression, with rare exception.10 Schwannomas of the facial nerve and geniculate ganglion hemangiomas may present with flaccidity comixed with facial twitching and synkinesis; symptoms wax and wane and generally worsen over years to decades. Bilateral weakness should raise suspicion for an underlying infectious or inflammatory etiology. Recurrent BP is uncommon and should prompt further workup. Careful history will uncover additional signs and symptoms associated with disturbances in facial nerve components other than branchial motor. These may include decreased or increased tearing (parasympathetic), taste disturbances (special visceral afferent), otalgia, and postauricular pain (general somatic afferent). Additionally, patients will often report hyperacusis secondary to impaired stapedius function, and facial hypoesthesia of unclear etiology.11 Involvement of other cranial nerves should prompt immediate further workup, although controversy exists whether BP can in fact exist as a cranial polyneuropathy.12 In the acute setting of BP, flaccid paresis often results in ocular irritation and lack of facial symmetry, particularly with smile. When recovery is delayed, patients may progress to develop varying degrees of facial hyperactivity, whose exact pattern determines their chronic symptoms. Discomfort at the origin of the platysma is a common complaint, in addition to facial fatigue. Ocular symptoms are also prevalent, including periocular synkinesis resulting in a narrowed palpebral fissure width and excessive tearing (Bogorad syndrome). Inability to produce a meaningful smile occurs with severe
Copyright © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI http://dx.doi.org/ 10.1055/s-0035-1549040. ISSN 0736-6825.
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Nate Jowett, MD1
Contemporary Management of Bell Palsy
Jowett, Hadlock
synkinesis and is often a primary complaint. A facial nervespecific quality-of-life (QOL) survey—the Facial Clinimetric Evaluation (FaCE)—is given to all patients on initial presentation and following interventions to gauge intervention effectiveness.6,7,13–16
Physical Examination A thorough zonal assessment of facial function at rest and with volitional movement is essential (►Fig. 1). In the acute phase, the degree of paralytic lagophthalmos together with the presence or absence of Bell’s phenomenon is noted. In the chronic setting, it is important to document the brow position and its effect on the periocular complex; the palpebral fissure width; the presence of epiphora; the depth and orientation of the nasolabial fold (NLF); the position of the oral commissure; and the presence and degree of ocular, midfacial, mentalis, and platysmal synkinesis. Close attention should be paid to the contralateral healthy side with regard to whether weakening of the uninvolved hemi-brow or lip depressors would be likely to result in improved symmetry and facial aesthetics. The status of the masseteric and deep temporal branches of the mandibular division of the trigeminal nerve is assessed by palpation of the bulk and tone of the masseter and temporalis muscles, respectively, in case nerve transfer procedures are contemplated.
Documentation Photography and videography to document appearance at rest and with seven volitional facial movements (brow elevation, gentle and full-effort eye closure and smile, lip pucker, lower lip depression) is essential. Spontaneous smile may be
assessed through the use of a series of short humorous video clips to elicit laughter; a standardized video assay has recently been validated at our center for this purpose. Photo and videographic documentation should be repeated following spontaneous recovery and after each intervention as a means to reliably gauge progress. A protocol for documentation of outcomes data has been described.17
Investigations Where the history and physical examination is consistent with BP, no further investigations are generally required. One exception is in Lyme endemic areas; serology is prudent in these cases even in the absence of other symptoms.18,19 Electroneuronography (ENoG) at 3 to 14 days following symptom onset is indicated in patients who present with complete flaccid paralysis. Imaging studies are indicated where no recovery is demonstrated at 3 months.
Prognostic Factors Prognosis is excellent for those with less than full flaccid paralysis on presentation, for those whose facial function begins to recover within 4 weeks of symptom onset, and for those whose ENoG demonstrates less than 85% degeneration in the CMAP amplitude.20–23 Poor prognostic factors include advanced age,24 hypertension,25 marked taste disturbances,26 diabetes mellitus,27 and pregnancy-associated BP.28
Acute Management In the acute setting of BP, strong evidence exists that administration of high-dose corticosteroids within 72 hours of
Fig. 1 Acute flaccid (top) and chronic nonflaccid (bottom) facial palsy in Bell palsy. Complete flaccid paralysis on the affected side ( ) is demonstrated at rest (A), and with brow elevation (B), gentle eye closure (C), full-effort eye closure (D), gentle smile (E), full-effort smile (F), lip pucker (G), and lower lip depression (H). At 1 year following symptom onset, the face is symmetric at rest (I). There is periocular, midfacial, and mentalis synkinesis triggered by brow elevation (J) and by gentle (K) and full-effort (L) eye closure. Gentle (M) and full-effort (N) smile triggers synkinesis along the lateral border of the platysma without periocular synkinesis; in addition, commissure excursion is restricted on the affected side. Lip pucker (O) and attempts at lip depression (P) trigger mentalis and platysmal synkinesis. Lip depressor function remains weak on the affected side (P). Facial Plastic Surgery
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Facial Reanimation Interventions Interventions for facial movement impairment in BP consist of physical therapy, injectables, and static and dynamic surgical reanimation procedures. The interventions are targeted to the degree of dysfunction specific to the facial zone (►Table 1).
Physical Therapy The four pillars of a comprehensive therapy program consist of patient education, soft-tissue mobilization, biofeedback, and neuromuscular retraining.34,35 In the acute phase of BP,
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patient education and eyelid stretching are beneficial. Comprehensive physical therapy is offered to all patients with synkinesis, and to those who have undergone dynamic reanimation surgery. The primary goals of physical therapy for the patient with facial synkinesis include reduction in mass movement on the affected side and reduction in compensatory hyperactivity of the contralateral healthy side to achieve improved balance and reduce symptoms of facial fatigue. Following nerve and/or muscle transfer reanimation procedures, tailored physical therapy protocols are applied to optimize the surgical result.
Injectables Chemodenervation agents and facial fillers have become adjunctive mainstays of treatment in NFFP.7 Botulinum toxin (BTX) is used to reduce synkinesis through targeted injection, most commonly of the orbicularis oculi, mentalis, and platysma muscles. In cases where the ipsilateral zone is weak, BTX may be used to camouflage facial asymmetry through weakening of the contralateral paired-muscle, most commonly the frontalis or depressor labii inferioris (DLI) (►Fig. 2). A typical starting dose for weakening of the contralateral brow is 9 units of BTX distributed into three zones of the frontalis muscle in a triangular fashion, staying 1.5 cm above the browline to avoid ptosis. A typical starting dose for management of platysmal synkinesis is 20 units of BTX, distributed into four zones of the platysma muscle in a rectangular fashion, staying at least 2 cm below the jawline.
Table 1 Interventions in Bell palsy Setting
Physical therapy
Medical therapy and injectables
Static reanimation
Dynamic reanimation
Acute flaccid paralysisa
• Patient education • Eyelid stretching
• High-dose steroids þ/ antivirals within 72 h • Eyelid lubrication and night taping
• Eyelid weight (reversible)
• Not indicated
Chronic mild NFFP
• • • •
Patient education Eyelid stretching Biofeedback Neuromuscular retraining
• Botulinum toxin: – Contra- or bilateral brow – Ipsilateral periocular complex – Contralateral DLI – Mentalis – Ipsilateral platysma • Volumizing fillers: – Ipsi- or contralateral NLF – Ipsilateral upper lip
• Platysmectomy • DLI resection
• Not indicated
Chronic moderatesevere NFFP
• • • • •
Patient education Eyelid stretching Biofeedback Neuromuscular retraining Targeted physical therapy following dynamic reanimation
• Botulinum toxin: – Contra- or bilateral brow – Ipsilateral periocular complex – Contralateral DLI – Mentalis – Ipsilateral platysma • Volumizing fillers: – Ipsi- or contralateral NLF – Ipsilateral upper lip
• • • •
• Smile reanimation: – Temporalis transfer – Nerve transfer to free muscle or native facial musculature
Platysmectomy DLI resection HSN NLF adjustments
Abbreviations: DLI, depressor labii inferioris; HSN, highly selective neurectomy; NFFP, nonflaccid facial palsy; NLF, nasolabial fold. a Acute decompression of the labyrinthine segment of the facial nerve is considered when ENoG demonstrates >90% degeneration within 14 days of symptom onset for those with complete flaccid paralysis within 72 hours of symptom onset. Facial Plastic Surgery
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symptom onset shortens the time to complete recovery in adults.29 Antiviral monotherapy is contraindicated.30 There is no good evidence to support or reject the use of combination antiviral therapy.31 Many otolaryngologists routinely prescribe prednisone (60 mg p.o. 5 days followed by a 10mg/day taper over 5 days) in combination with valacyclovir (1 g p.o. BID 7 days) to all patients with BP up to 2 weeks from symptom onset. Patients who present with complete flaccid paralysis with an ENoG response demonstrating greater than 90% degeneration are referred to neurotology for consideration of surgical decompression within 14 days of symptom onset.31,32 The American Academy of Otolaryngology—Head and Neck Surgery recently published a clinical practice guideline summary on the acute management of BP.33
Jowett, Hadlock
Contemporary Management of Bell Palsy
Jowett, Hadlock
Fig. 2 Botulinum toxin use in Bell palsy–associated nonflaccid facial palsy (NFFP). Depressor labii inferioris (DLI) weakness with restricted commissure excursion is present on the affected () side (A). Chemodenervation of the contralateral DLI results in improved facial balance with smile (B).
Gustatory tearing (Bogorad syndrome) is managed with lacrimal gland BTX injection. Following nerve-muscle transfer procedures, the toxin may be used to treat undesired hyperactivity, such as mastication-induced twitching following trigeminal-facial (V–VII) nerve transfers. Volumizing fillers, such as hyaluronic acid and fat grafts, are often beneficial in the midface and lips. In the patient with effacement of the NLF on the affected side, adding volume to the contralateral NLF may achieve a more symmetric resting appearance. Conversely, a trial of filler to the affected side should be considered when NFFP results in a deepened NLF.
Static and Dynamic Surgical Procedures Brow Acutely, the brow is ptotic and weak. In Bell palsy–associated NFFP, the brow is typically balanced or ptotic at rest, and may be immobile in severe cases. When ptotic, correction improves ocular hygiene and aesthetic symmetry (►Fig. 3). Brow ptosis correction may be performed under local anesthesia by means of a subgaleal temporal or endoscopic approach using a titanium bone anchor or a biodegradable polymeric device (Endotine, MicroAire Surgical Instruments, Charlottesville, Virginia). Direct brow lifting, midforehead brow lifting, and suture elevation using a titanium plate are also reasonable options.
Upper Lid Avoidance of exposure keratopathy is the goal of management in the acute flaccid phase of BP. In addition to lubricating eyedrops, eyelid massage, and overnight taping, eyelid weighting is offered to those with poor prognostic factors or who lack Bell’s phenomenon, and to patients who show no sign of recovery at 3 months. Platinum is preferred over gold, due to its decreased allergenicity and higher density, which permits for thinner profile weights.36 The procedure is performed under local anesthesia. An incision is made in the supratarsal crease, and a plane developed deep to the orbicularis oculi, exposing the anterior surface of the tarsal plate. The implant is centered between the pupil and the medial limbus, and secured to the tarsal plate with three 6–0 clear nylon sutures. The weight is removed without aesthetic consequence once recovery ensues (►Fig. 4).
Periocular Synkinesis Physical therapy, together with chemodenervation using BTX, is the primary means of management of periocular synkinesis. When this fails, permanent orbicularis oculi denervation by means of a two-step highly selective neurectomy (HSN) may be performed (►Fig. 5).37 The first step involves a preauricular incision with sub-superficial musculoaponeurotic system (SMAS) dissection under general anesthesia to
Fig. 3 Brow ptosis correction in Bell palsy–associated nonflaccid facial palsy (NFFP). Brow ptosis is demonstrated (white dotted line) at rest on the affected side () with associated upper eyelid ptosis (A). Following temporal brow lift using a bioabsorbable implant, brow position is corrected at rest (white dotted line) with improvement in palpebral fissure symmetry (B). Facial Plastic Surgery
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identify four or more facial nerve branches to the orbicularis oculi using a nerve stimulator. Branches are isolated using vessel loops, whose ends are then delivered through stab incisions in the overlying skin. After recovery from general anesthesia later in the day, the awake patient is asked to trigger the ocular synkinesis by smiling; branches are then divided in succession until a suitable decrease in synkinetic eye closure with smiling occurs without induction of lagoph-
thalmos. The remaining branches are then released in continuity back through the stab incisions.
Nasolabial Fold In the acute flaccid phase, the NLF is usually effaced. In the synkinetic setting, the fold may be effaced or deepened, its orientation either more vertical or more horizontal in comparison to the contralateral side. Injectables are first-line
Fig. 5 Periocular highly selective neurectomy (HSN) in Bell palsy–associated nonflaccid facial palsy (NFFP). Prior to the intervention, the palpebral fissure width on the affected side () is balanced at rest (A) and near-complete eye closure is present with gentle effort (B). The palpebral fissure width is markedly narrowed secondary to synkinesis triggered by gentle smile (C). Following HSN, the palpebral fissure width at rest (D) and with gentle eye closure is unchanged (E), while a significant reduction in synkinetic eye closure with smile is demonstrated (F). Facial Plastic Surgery
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Fig. 4 Platinum eyelid weighting in Bell palsy. At 3 months, the patient demonstrated persistent complete flaccid paralysis. The contour of the weight (arrowheads) is not readily discernible with the eyes open (A). With the eyes closed (B), a thin protrusion is seen (arrowheads) over the medial half of the upper lid. At 1 year the patient progressed to develop nonflaccid facial palsy (NFFP) and the eyelid weight was removed. No aesthetic consequence of the procedure is seen with eyes open (C) or closed (D). As is typical, unaided eye closure is adequate in NFFP.
Contemporary Management of Bell Palsy
Jowett, Hadlock
management in achieving NLF balance. When these fail, static suspension may be used.38 Suspension using sutures may be used to better define the effaced NLF by placement of a heavy nylon or polypropylene suture immediately medial to the desired position of the fold with securement to the true temporalis fascia (TTF). Alternatively, suture placement immediately lateral to a hyperprominent NLF may help soften it, achieving an improvement in facial balance. In the case of effacement of the NLF in older patients, a further option involves the placement of a 3-cm strip of fascia lata secured medially to the dermal edge of a crescentic de-epithelized zone oriented along the desired plane of the NLF and laterally to the TTF.39
Smile Reanimation of smile in patients with NFFP requires the reestablishment of volitionally contractile muscle. Options include temporalis muscle transfer and nerve transfers to free muscle flaps or native facial musculature. The temporalis flap is performed through an incision extending from the temporal region inferiorly along the preauricular crease to the attachment point of the lobule and the retroauricular region. The temporoparietal fascia is elevated as a flap (TPFF) based on the superficial temporal vessels and rotated posterolaterally to expose the underlying muscle and true temporal fascia.40,41 A 1.5-cm strip of temporalis muscle is then elevated with its fascia, reflected over the zygomatic arch, and secured to the modiolus. Sequelae may include muscular prominence overlying the zygomatic arch, excess midfacial bulk, hollowing and/or alopecia in the temporalis fossa, and inadequate excursion of the transferred muscle. Meticulous surgical technique with inset of the TPFF to obliterate the donor site deficit is important in reducing the magnitude of the sequelae. Temporalis tendon transfer, also known as orthodromic temporalis transfer, involves exposing the temporalis tendon as it attaches to the coronoid process, removing it from the bone, and securing it to the modiolus using adynamic strips of fascia lata.42 This procedure has been described using a lateral, nasolabial, or intraoral incision. A third approach, known as lengthening temporalis myoplasty, involves mobilization and repositioning of the temporalis muscle to a more inferior position together with direct transfer of the tendon to the modiolus without intervening fascia.43 Relative contraindications to temporalis muscle transfer include disuse atrophy secondary to an edentulous state, preoperative wasting, or trigeminal dysfunction. Other dynamic smile reanimation options include nerve transfer to free muscle, such as gracilis transfer, or to the native facial musculature, the latter of which is autopreserved in the synkinetic face. Neuronal innervation is achieved via nerve transfer, sources of which may include split hypoglossal (XII–VII), masseteric or deep temporal branches of the trigeminal (V-VII), or cross-facial nerve grafting (CFNG). The tongue morbidity and synkinesis of the hypoglossal-facial transfer has led to a decline in its popularity. Five to seven transfers using either the masseteric44 or deep temporal branches are increasing in popularity secondary to minimal Facial Plastic Surgery
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donor site morbidity, minimal functional impairment (due to the redundancy of muscles driving jaw closure), ease of volitional triggering, and superior commissure excursion in comparison to CFNG due to higher motor neuron counts within the branch.45 Advantages of CFNG for smile over other nerve transfer techniques include reanimation of spontaneous (emotive) smile in addition to volitional smile, improved resting firing tone, and absence of facial twitching with mastication that is commonly seen with V-VII transfers. Disadvantages include a smile with less commissure excursion than that obtained using other nerve transfer techniques (due to fewer available motor axons), and a risk of causing noticeable weakness in the healthy hemiface. The procedure involves elevation of a sub-SMAS flap using a preauricular incision on the nonparalyzed side of the face. Facial nerve branches yielding isolated smile are identified using monopolar nerve stimulation; one or two branches are then sharply transected, depending on redundancy of innervation to the muscle. Next, a long sural nerve graft is harvested and inset in antidromic fashion in a subcutaneous tunnel across the upper lip. The proximal end of the graft is secured to the gingivobuccal sulcus on the paralyzed side with a 4–0 nylon suture for later retrieval. The distal end is coapted to the transected smile branches using 10–0 nylon sutures and fibrin glue. Axon growth across the graft is followed clinically using Tinel’s sign; tingling in the zygomaticus muscle groups on the donor side indicates the presence of regenerating axons. Second-stage free muscle transfer ensues 6 to 9 months later. a. Free Muscle Transfer Patients with reasonable life expectancy without significant comorbidities are candidates for free muscle transfer. Although the rectus,46 pectoralis minor,47 and latissimus dorsi48 are sometimes used, the gracilis, first described by Harii,49 remains the most popular choice of free muscle transfer for smile reanimation. Innervation is provided via CFNG or other nerve transfer, most commonly the ipsilateral masseter branch of the trigeminal (V-VII). The gracilis muscle is harvested from the medial aspect of the thigh, through an incision 1.5 cm posterior and parallel to a line connecting the pubic tubercle to the medial tibial condyle. The belly of the muscle is identified, followed by the neurovascular pedicle, which enters its deep surface 8 to 10 cm caudal to the pubic tubercle. The flap is harvested by removing approximately one third of the width of the muscle along a length of 15 cm. For inset, a subcutaneous flap is elevated using a preauricular incision extended below the mandible. The gracilis is secured to the modiolus, stretched to its resting length, and sutured to the TTF, taking into account the patient’s smile vector. Microvascular anastomoses ensue. In the two-stage procedure, the branch of the obturator nerve to gracilis is coapted to the banked CFNG stump deep to the gingivobuccal sulcus. In the single-stage procedure, coaptation is to the masseteric nerve, which is transected on the deep surface of the masseter within the mandibular notch. Movement is
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Fig. 6 Cross-facial nerve graft (CFNG) transfer to a free gracilis muscle in nonflaccid facial palsy (NFFP) for dynamic reanimation of smile. The patient developed NFFP subsequent to Ramsay Hunt syndrome zoster sine herpete. The affected side ( ) demonstrates a slightly deepened nasolabial fold (NLF) at rest (A), with impaired commissure excursion with gentle (B) and full-effort smile (C). Following CFNG transfer to free gracilis muscle, the NLF remains deepened at rest with a slightly more horizontal position (D) and significant improvement in commissure excursion is seen with gentle (E) and full-effort (F) smile.
expected after 3 to 6 months for V-VII transfer, whereas 8 to 10 months is required before movement is seen for CFNG transfer (►Fig. 6). Complications of free gracilis transfer for smile reanimation include failure to achieve dynamic smile (8%–30%), excessive facial bulk, incorrect vector of pull, and coactivation of the transferred muscle with mastication (V-VII) or blink (CFNG). When flap loss secondary to microvascular occlusion (
Contemporary Management of Bell Palsy Tessa A. Hadlock, MD1
1 Department of Otolaryngology, Massachusetts Eye and Ear Infirmary
and Harvard Medical School, Boston, Massachusetts Facial Plast Surg 2015;31:93–102.
Abstract Keywords
► ► ► ► ►
Bell palsy facial reanimation synkinesis facial paralysis facial palsy
Address for correspondence Nate Jowett, MD, Department of Otolaryngology, Massachusetts Eye and Ear Infirmary and Harvard Medical School, Boston, Massachusetts (e-mail: [email protected]).
Bell palsy (BP) is the most common diagnosis in acute and chronic facial palsy. Although most patients fully recover, more than one-quarter will have residual dysfunction. Of these, nearly half will demonstrate severe limitations in facial expression. Though significant attention has been paid to acute management and prognosis, a paucity of literature exists addressing management of the long-term sequelae of BP. This article describes contemporary use of physical therapy, injectables, and static and dynamic surgical procedures in facial reanimation of acute and chronic BP.
In 1821, Sir Charles Bell first described idiopathic facial paralysis.1 Bell palsy (BP) remains the leading cause of facial palsy, accounting for approximately 70% of acute and 40% of chronic cases.2 It is believed to be the result of viral reactivation of latent herpes simplex virus (HSV), varicella-zoster virus (VZV), or human herpesvirus 6 (HHV-6), causing inflammation and ischemic entrapment of the facial nerve at the meatal foramen; however, conclusive evidence remains elusive.3,4 Without treatment, 70% of patients will fully recover, whereas an additional 15% will recover with only minor deficits.5 The remaining 15% develop variable patterns of predominantly synkinetic facial palsy (i.e., nonflaccid facial palsy [NFFP]6), resulting in profound negative impact on quality of life and well-being.7 Persistence of flaccid palsy in BP does not occur. Though the management of acute BP is relatively straightforward, the management of long-term sequelae differs across providers. This article aims to summarize one approach to the contemporary management of facial dysfunction following BP.
History BP is a diagnosis of exclusion. Risk factors include diabetes and pregnancy.8,9 The most common alternative causes of facial palsy include postsurgical insult, benign or malignant tumors, infection, and temporal bone trauma.2 Elucidation of the time course of symptoms is critical for proper diagnosis. Whereas the full extent of facial weakness in BP develops within 72 hours, malignancies demonstrate insidious onset
Issue Theme Current Concepts, State of the Art Treatment of Facial Paralysis; Guest Editor, Patrick J. Byrne, MD, FACS
with symptom progression, with rare exception.10 Schwannomas of the facial nerve and geniculate ganglion hemangiomas may present with flaccidity comixed with facial twitching and synkinesis; symptoms wax and wane and generally worsen over years to decades. Bilateral weakness should raise suspicion for an underlying infectious or inflammatory etiology. Recurrent BP is uncommon and should prompt further workup. Careful history will uncover additional signs and symptoms associated with disturbances in facial nerve components other than branchial motor. These may include decreased or increased tearing (parasympathetic), taste disturbances (special visceral afferent), otalgia, and postauricular pain (general somatic afferent). Additionally, patients will often report hyperacusis secondary to impaired stapedius function, and facial hypoesthesia of unclear etiology.11 Involvement of other cranial nerves should prompt immediate further workup, although controversy exists whether BP can in fact exist as a cranial polyneuropathy.12 In the acute setting of BP, flaccid paresis often results in ocular irritation and lack of facial symmetry, particularly with smile. When recovery is delayed, patients may progress to develop varying degrees of facial hyperactivity, whose exact pattern determines their chronic symptoms. Discomfort at the origin of the platysma is a common complaint, in addition to facial fatigue. Ocular symptoms are also prevalent, including periocular synkinesis resulting in a narrowed palpebral fissure width and excessive tearing (Bogorad syndrome). Inability to produce a meaningful smile occurs with severe
Copyright © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI http://dx.doi.org/ 10.1055/s-0035-1549040. ISSN 0736-6825.
Downloaded by: Rutgers University. Copyrighted material.
Nate Jowett, MD1
Contemporary Management of Bell Palsy
Jowett, Hadlock
synkinesis and is often a primary complaint. A facial nervespecific quality-of-life (QOL) survey—the Facial Clinimetric Evaluation (FaCE)—is given to all patients on initial presentation and following interventions to gauge intervention effectiveness.6,7,13–16
Physical Examination A thorough zonal assessment of facial function at rest and with volitional movement is essential (►Fig. 1). In the acute phase, the degree of paralytic lagophthalmos together with the presence or absence of Bell’s phenomenon is noted. In the chronic setting, it is important to document the brow position and its effect on the periocular complex; the palpebral fissure width; the presence of epiphora; the depth and orientation of the nasolabial fold (NLF); the position of the oral commissure; and the presence and degree of ocular, midfacial, mentalis, and platysmal synkinesis. Close attention should be paid to the contralateral healthy side with regard to whether weakening of the uninvolved hemi-brow or lip depressors would be likely to result in improved symmetry and facial aesthetics. The status of the masseteric and deep temporal branches of the mandibular division of the trigeminal nerve is assessed by palpation of the bulk and tone of the masseter and temporalis muscles, respectively, in case nerve transfer procedures are contemplated.
Documentation Photography and videography to document appearance at rest and with seven volitional facial movements (brow elevation, gentle and full-effort eye closure and smile, lip pucker, lower lip depression) is essential. Spontaneous smile may be
assessed through the use of a series of short humorous video clips to elicit laughter; a standardized video assay has recently been validated at our center for this purpose. Photo and videographic documentation should be repeated following spontaneous recovery and after each intervention as a means to reliably gauge progress. A protocol for documentation of outcomes data has been described.17
Investigations Where the history and physical examination is consistent with BP, no further investigations are generally required. One exception is in Lyme endemic areas; serology is prudent in these cases even in the absence of other symptoms.18,19 Electroneuronography (ENoG) at 3 to 14 days following symptom onset is indicated in patients who present with complete flaccid paralysis. Imaging studies are indicated where no recovery is demonstrated at 3 months.
Prognostic Factors Prognosis is excellent for those with less than full flaccid paralysis on presentation, for those whose facial function begins to recover within 4 weeks of symptom onset, and for those whose ENoG demonstrates less than 85% degeneration in the CMAP amplitude.20–23 Poor prognostic factors include advanced age,24 hypertension,25 marked taste disturbances,26 diabetes mellitus,27 and pregnancy-associated BP.28
Acute Management In the acute setting of BP, strong evidence exists that administration of high-dose corticosteroids within 72 hours of
Fig. 1 Acute flaccid (top) and chronic nonflaccid (bottom) facial palsy in Bell palsy. Complete flaccid paralysis on the affected side ( ) is demonstrated at rest (A), and with brow elevation (B), gentle eye closure (C), full-effort eye closure (D), gentle smile (E), full-effort smile (F), lip pucker (G), and lower lip depression (H). At 1 year following symptom onset, the face is symmetric at rest (I). There is periocular, midfacial, and mentalis synkinesis triggered by brow elevation (J) and by gentle (K) and full-effort (L) eye closure. Gentle (M) and full-effort (N) smile triggers synkinesis along the lateral border of the platysma without periocular synkinesis; in addition, commissure excursion is restricted on the affected side. Lip pucker (O) and attempts at lip depression (P) trigger mentalis and platysmal synkinesis. Lip depressor function remains weak on the affected side (P). Facial Plastic Surgery
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Downloaded by: Rutgers University. Copyrighted material.
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Contemporary Management of Bell Palsy
Facial Reanimation Interventions Interventions for facial movement impairment in BP consist of physical therapy, injectables, and static and dynamic surgical reanimation procedures. The interventions are targeted to the degree of dysfunction specific to the facial zone (►Table 1).
Physical Therapy The four pillars of a comprehensive therapy program consist of patient education, soft-tissue mobilization, biofeedback, and neuromuscular retraining.34,35 In the acute phase of BP,
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patient education and eyelid stretching are beneficial. Comprehensive physical therapy is offered to all patients with synkinesis, and to those who have undergone dynamic reanimation surgery. The primary goals of physical therapy for the patient with facial synkinesis include reduction in mass movement on the affected side and reduction in compensatory hyperactivity of the contralateral healthy side to achieve improved balance and reduce symptoms of facial fatigue. Following nerve and/or muscle transfer reanimation procedures, tailored physical therapy protocols are applied to optimize the surgical result.
Injectables Chemodenervation agents and facial fillers have become adjunctive mainstays of treatment in NFFP.7 Botulinum toxin (BTX) is used to reduce synkinesis through targeted injection, most commonly of the orbicularis oculi, mentalis, and platysma muscles. In cases where the ipsilateral zone is weak, BTX may be used to camouflage facial asymmetry through weakening of the contralateral paired-muscle, most commonly the frontalis or depressor labii inferioris (DLI) (►Fig. 2). A typical starting dose for weakening of the contralateral brow is 9 units of BTX distributed into three zones of the frontalis muscle in a triangular fashion, staying 1.5 cm above the browline to avoid ptosis. A typical starting dose for management of platysmal synkinesis is 20 units of BTX, distributed into four zones of the platysma muscle in a rectangular fashion, staying at least 2 cm below the jawline.
Table 1 Interventions in Bell palsy Setting
Physical therapy
Medical therapy and injectables
Static reanimation
Dynamic reanimation
Acute flaccid paralysisa
• Patient education • Eyelid stretching
• High-dose steroids þ/ antivirals within 72 h • Eyelid lubrication and night taping
• Eyelid weight (reversible)
• Not indicated
Chronic mild NFFP
• • • •
Patient education Eyelid stretching Biofeedback Neuromuscular retraining
• Botulinum toxin: – Contra- or bilateral brow – Ipsilateral periocular complex – Contralateral DLI – Mentalis – Ipsilateral platysma • Volumizing fillers: – Ipsi- or contralateral NLF – Ipsilateral upper lip
• Platysmectomy • DLI resection
• Not indicated
Chronic moderatesevere NFFP
• • • • •
Patient education Eyelid stretching Biofeedback Neuromuscular retraining Targeted physical therapy following dynamic reanimation
• Botulinum toxin: – Contra- or bilateral brow – Ipsilateral periocular complex – Contralateral DLI – Mentalis – Ipsilateral platysma • Volumizing fillers: – Ipsi- or contralateral NLF – Ipsilateral upper lip
• • • •
• Smile reanimation: – Temporalis transfer – Nerve transfer to free muscle or native facial musculature
Platysmectomy DLI resection HSN NLF adjustments
Abbreviations: DLI, depressor labii inferioris; HSN, highly selective neurectomy; NFFP, nonflaccid facial palsy; NLF, nasolabial fold. a Acute decompression of the labyrinthine segment of the facial nerve is considered when ENoG demonstrates >90% degeneration within 14 days of symptom onset for those with complete flaccid paralysis within 72 hours of symptom onset. Facial Plastic Surgery
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symptom onset shortens the time to complete recovery in adults.29 Antiviral monotherapy is contraindicated.30 There is no good evidence to support or reject the use of combination antiviral therapy.31 Many otolaryngologists routinely prescribe prednisone (60 mg p.o. 5 days followed by a 10mg/day taper over 5 days) in combination with valacyclovir (1 g p.o. BID 7 days) to all patients with BP up to 2 weeks from symptom onset. Patients who present with complete flaccid paralysis with an ENoG response demonstrating greater than 90% degeneration are referred to neurotology for consideration of surgical decompression within 14 days of symptom onset.31,32 The American Academy of Otolaryngology—Head and Neck Surgery recently published a clinical practice guideline summary on the acute management of BP.33
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Fig. 2 Botulinum toxin use in Bell palsy–associated nonflaccid facial palsy (NFFP). Depressor labii inferioris (DLI) weakness with restricted commissure excursion is present on the affected () side (A). Chemodenervation of the contralateral DLI results in improved facial balance with smile (B).
Gustatory tearing (Bogorad syndrome) is managed with lacrimal gland BTX injection. Following nerve-muscle transfer procedures, the toxin may be used to treat undesired hyperactivity, such as mastication-induced twitching following trigeminal-facial (V–VII) nerve transfers. Volumizing fillers, such as hyaluronic acid and fat grafts, are often beneficial in the midface and lips. In the patient with effacement of the NLF on the affected side, adding volume to the contralateral NLF may achieve a more symmetric resting appearance. Conversely, a trial of filler to the affected side should be considered when NFFP results in a deepened NLF.
Static and Dynamic Surgical Procedures Brow Acutely, the brow is ptotic and weak. In Bell palsy–associated NFFP, the brow is typically balanced or ptotic at rest, and may be immobile in severe cases. When ptotic, correction improves ocular hygiene and aesthetic symmetry (►Fig. 3). Brow ptosis correction may be performed under local anesthesia by means of a subgaleal temporal or endoscopic approach using a titanium bone anchor or a biodegradable polymeric device (Endotine, MicroAire Surgical Instruments, Charlottesville, Virginia). Direct brow lifting, midforehead brow lifting, and suture elevation using a titanium plate are also reasonable options.
Upper Lid Avoidance of exposure keratopathy is the goal of management in the acute flaccid phase of BP. In addition to lubricating eyedrops, eyelid massage, and overnight taping, eyelid weighting is offered to those with poor prognostic factors or who lack Bell’s phenomenon, and to patients who show no sign of recovery at 3 months. Platinum is preferred over gold, due to its decreased allergenicity and higher density, which permits for thinner profile weights.36 The procedure is performed under local anesthesia. An incision is made in the supratarsal crease, and a plane developed deep to the orbicularis oculi, exposing the anterior surface of the tarsal plate. The implant is centered between the pupil and the medial limbus, and secured to the tarsal plate with three 6–0 clear nylon sutures. The weight is removed without aesthetic consequence once recovery ensues (►Fig. 4).
Periocular Synkinesis Physical therapy, together with chemodenervation using BTX, is the primary means of management of periocular synkinesis. When this fails, permanent orbicularis oculi denervation by means of a two-step highly selective neurectomy (HSN) may be performed (►Fig. 5).37 The first step involves a preauricular incision with sub-superficial musculoaponeurotic system (SMAS) dissection under general anesthesia to
Fig. 3 Brow ptosis correction in Bell palsy–associated nonflaccid facial palsy (NFFP). Brow ptosis is demonstrated (white dotted line) at rest on the affected side () with associated upper eyelid ptosis (A). Following temporal brow lift using a bioabsorbable implant, brow position is corrected at rest (white dotted line) with improvement in palpebral fissure symmetry (B). Facial Plastic Surgery
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identify four or more facial nerve branches to the orbicularis oculi using a nerve stimulator. Branches are isolated using vessel loops, whose ends are then delivered through stab incisions in the overlying skin. After recovery from general anesthesia later in the day, the awake patient is asked to trigger the ocular synkinesis by smiling; branches are then divided in succession until a suitable decrease in synkinetic eye closure with smiling occurs without induction of lagoph-
thalmos. The remaining branches are then released in continuity back through the stab incisions.
Nasolabial Fold In the acute flaccid phase, the NLF is usually effaced. In the synkinetic setting, the fold may be effaced or deepened, its orientation either more vertical or more horizontal in comparison to the contralateral side. Injectables are first-line
Fig. 5 Periocular highly selective neurectomy (HSN) in Bell palsy–associated nonflaccid facial palsy (NFFP). Prior to the intervention, the palpebral fissure width on the affected side () is balanced at rest (A) and near-complete eye closure is present with gentle effort (B). The palpebral fissure width is markedly narrowed secondary to synkinesis triggered by gentle smile (C). Following HSN, the palpebral fissure width at rest (D) and with gentle eye closure is unchanged (E), while a significant reduction in synkinetic eye closure with smile is demonstrated (F). Facial Plastic Surgery
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Fig. 4 Platinum eyelid weighting in Bell palsy. At 3 months, the patient demonstrated persistent complete flaccid paralysis. The contour of the weight (arrowheads) is not readily discernible with the eyes open (A). With the eyes closed (B), a thin protrusion is seen (arrowheads) over the medial half of the upper lid. At 1 year the patient progressed to develop nonflaccid facial palsy (NFFP) and the eyelid weight was removed. No aesthetic consequence of the procedure is seen with eyes open (C) or closed (D). As is typical, unaided eye closure is adequate in NFFP.
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management in achieving NLF balance. When these fail, static suspension may be used.38 Suspension using sutures may be used to better define the effaced NLF by placement of a heavy nylon or polypropylene suture immediately medial to the desired position of the fold with securement to the true temporalis fascia (TTF). Alternatively, suture placement immediately lateral to a hyperprominent NLF may help soften it, achieving an improvement in facial balance. In the case of effacement of the NLF in older patients, a further option involves the placement of a 3-cm strip of fascia lata secured medially to the dermal edge of a crescentic de-epithelized zone oriented along the desired plane of the NLF and laterally to the TTF.39
Smile Reanimation of smile in patients with NFFP requires the reestablishment of volitionally contractile muscle. Options include temporalis muscle transfer and nerve transfers to free muscle flaps or native facial musculature. The temporalis flap is performed through an incision extending from the temporal region inferiorly along the preauricular crease to the attachment point of the lobule and the retroauricular region. The temporoparietal fascia is elevated as a flap (TPFF) based on the superficial temporal vessels and rotated posterolaterally to expose the underlying muscle and true temporal fascia.40,41 A 1.5-cm strip of temporalis muscle is then elevated with its fascia, reflected over the zygomatic arch, and secured to the modiolus. Sequelae may include muscular prominence overlying the zygomatic arch, excess midfacial bulk, hollowing and/or alopecia in the temporalis fossa, and inadequate excursion of the transferred muscle. Meticulous surgical technique with inset of the TPFF to obliterate the donor site deficit is important in reducing the magnitude of the sequelae. Temporalis tendon transfer, also known as orthodromic temporalis transfer, involves exposing the temporalis tendon as it attaches to the coronoid process, removing it from the bone, and securing it to the modiolus using adynamic strips of fascia lata.42 This procedure has been described using a lateral, nasolabial, or intraoral incision. A third approach, known as lengthening temporalis myoplasty, involves mobilization and repositioning of the temporalis muscle to a more inferior position together with direct transfer of the tendon to the modiolus without intervening fascia.43 Relative contraindications to temporalis muscle transfer include disuse atrophy secondary to an edentulous state, preoperative wasting, or trigeminal dysfunction. Other dynamic smile reanimation options include nerve transfer to free muscle, such as gracilis transfer, or to the native facial musculature, the latter of which is autopreserved in the synkinetic face. Neuronal innervation is achieved via nerve transfer, sources of which may include split hypoglossal (XII–VII), masseteric or deep temporal branches of the trigeminal (V-VII), or cross-facial nerve grafting (CFNG). The tongue morbidity and synkinesis of the hypoglossal-facial transfer has led to a decline in its popularity. Five to seven transfers using either the masseteric44 or deep temporal branches are increasing in popularity secondary to minimal Facial Plastic Surgery
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donor site morbidity, minimal functional impairment (due to the redundancy of muscles driving jaw closure), ease of volitional triggering, and superior commissure excursion in comparison to CFNG due to higher motor neuron counts within the branch.45 Advantages of CFNG for smile over other nerve transfer techniques include reanimation of spontaneous (emotive) smile in addition to volitional smile, improved resting firing tone, and absence of facial twitching with mastication that is commonly seen with V-VII transfers. Disadvantages include a smile with less commissure excursion than that obtained using other nerve transfer techniques (due to fewer available motor axons), and a risk of causing noticeable weakness in the healthy hemiface. The procedure involves elevation of a sub-SMAS flap using a preauricular incision on the nonparalyzed side of the face. Facial nerve branches yielding isolated smile are identified using monopolar nerve stimulation; one or two branches are then sharply transected, depending on redundancy of innervation to the muscle. Next, a long sural nerve graft is harvested and inset in antidromic fashion in a subcutaneous tunnel across the upper lip. The proximal end of the graft is secured to the gingivobuccal sulcus on the paralyzed side with a 4–0 nylon suture for later retrieval. The distal end is coapted to the transected smile branches using 10–0 nylon sutures and fibrin glue. Axon growth across the graft is followed clinically using Tinel’s sign; tingling in the zygomaticus muscle groups on the donor side indicates the presence of regenerating axons. Second-stage free muscle transfer ensues 6 to 9 months later. a. Free Muscle Transfer Patients with reasonable life expectancy without significant comorbidities are candidates for free muscle transfer. Although the rectus,46 pectoralis minor,47 and latissimus dorsi48 are sometimes used, the gracilis, first described by Harii,49 remains the most popular choice of free muscle transfer for smile reanimation. Innervation is provided via CFNG or other nerve transfer, most commonly the ipsilateral masseter branch of the trigeminal (V-VII). The gracilis muscle is harvested from the medial aspect of the thigh, through an incision 1.5 cm posterior and parallel to a line connecting the pubic tubercle to the medial tibial condyle. The belly of the muscle is identified, followed by the neurovascular pedicle, which enters its deep surface 8 to 10 cm caudal to the pubic tubercle. The flap is harvested by removing approximately one third of the width of the muscle along a length of 15 cm. For inset, a subcutaneous flap is elevated using a preauricular incision extended below the mandible. The gracilis is secured to the modiolus, stretched to its resting length, and sutured to the TTF, taking into account the patient’s smile vector. Microvascular anastomoses ensue. In the two-stage procedure, the branch of the obturator nerve to gracilis is coapted to the banked CFNG stump deep to the gingivobuccal sulcus. In the single-stage procedure, coaptation is to the masseteric nerve, which is transected on the deep surface of the masseter within the mandibular notch. Movement is
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Fig. 6 Cross-facial nerve graft (CFNG) transfer to a free gracilis muscle in nonflaccid facial palsy (NFFP) for dynamic reanimation of smile. The patient developed NFFP subsequent to Ramsay Hunt syndrome zoster sine herpete. The affected side ( ) demonstrates a slightly deepened nasolabial fold (NLF) at rest (A), with impaired commissure excursion with gentle (B) and full-effort smile (C). Following CFNG transfer to free gracilis muscle, the NLF remains deepened at rest with a slightly more horizontal position (D) and significant improvement in commissure excursion is seen with gentle (E) and full-effort (F) smile.
expected after 3 to 6 months for V-VII transfer, whereas 8 to 10 months is required before movement is seen for CFNG transfer (►Fig. 6). Complications of free gracilis transfer for smile reanimation include failure to achieve dynamic smile (8%–30%), excessive facial bulk, incorrect vector of pull, and coactivation of the transferred muscle with mastication (V-VII) or blink (CFNG). When flap loss secondary to microvascular occlusion (
