The Laryngoscope C 2013 The American Laryngological, V

Rhinological and Otological Society, Inc.

Etiology, Diagnosis, and Management of Facial Palsy: 2000 Patients at a Facial Nerve Center Marc H. Hohman, MD; Tessa A. Hadlock, MD Objectives/Hypothesis: To evaluate the range and incidence of facial palsy etiologies in cases presenting to a tertiary facial nerve center, and to review the broad and evolving spectrum of diagnostic and management approaches to the condition. Study Design: Retrospective chart review. Methods: Records of patients referred for facial weakness between 2003 and 2013 were reviewed for cases of facial palsy. Cases of muscle dysfunction and primary hemifacial spasm were excluded. The remainder were analyzed by age, sex, and diagnosis. Diagnostic and treatment strategies were reviewed. Results: There were 1,989 records that met inclusion criteria. Bell’s palsy accounted for 38% of cases, acoustic neuroma resections 10%, cancer 7%, iatrogenic injuries 7%, varicella zoster 7%, benign lesions 5%, congenital palsy 5%, Lyme disease 4%, and other causes 17%. Sixty-one percent of patients were female. Mean age at presentation was 44.5 years (618.6 years). Diagnoses were revealed primarily by history, though serial physical examinations, radiography, and hematologic testing also contributed. Management strategies included observation, physical therapy, pharmacological therapy, chemodenervation, facial nerve exploration, decompression, repair, and the full array of static and dynamic surgical interventions. Conclusions: Bell’s palsy remains the most common facial palsy; females present more often for evaluation. Comprehensive diagnostic investigation is mandatory in atypical cases, and thorough management must be multidisciplinary. The algorithms presented herein outline a single center’s approach to the facial palsy patient, providing a framework that clinicians caring for these patients may adapt to their specific settings. Key Words: Facial nerve, facial paralysis, facial palsy. Level of Evidence: 2b Laryngoscope, 124:E283–E293, 2014

INTRODUCTION There are numerous causes of facial palsy (FP), though hemifacial weakness is often generally termed Bell’s palsy, named after the Scottish neurologist Charles Bell, who described sudden onset unilateral facial paralysis in 1821. Virally triggered, acute FP, to which the term Bell’s palsy (BP) refers, is one of the most common, and fortunately the most likely condition to result in eventual return to premorbid status; 70% to 90% of patients recover spontaneously.1,2 Other causes of FP routinely result in poorer recovery, and the clinician must discern among these to formulate a treatment plan. There are few analyses of large FP patient series, and the current 2,000 patient series marks the largest since Peitersen’s 2,570 patient series in 2002.2 Adour

From the Department of Otology and Laryngology (M.H.H., T.A.H.); Harvard Medical School, and the Facial Nerve Center (M.H.H., T.A.H.), Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A. Editor’s Note: This Manuscript was accepted for publication November 25, 2013. Presented at the 12th International Facial Nerve Symposium, Boston, Massachusetts, U.S.A., June 28, 2013–July 1, 2013 The authors have no funding, financial relationships, or conflicts of interest to disclose. Send correspondence to Tessa A. Hadlock, MD, Department of Otolaryngology, Division of Facial Plastic and Reconstructive Surgery, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114. E-mail: [email protected] DOI: 10.1002/lary.24542

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et al.3 and Devriese et al.4 both published 1,000-patient series, though they concentrated on the natural history of BP rather than the etiologies of FP. At our institution, a tertiary referral center for facial nerve disorders, we evaluate and treat a large number of patients with a broad range of conditions, and comparatively few cases of acute, uncomplicated BP. Although our patients are not necessarily representative of the general population, this referral pattern does result in a high throughput, allowing data accrual on 2,000 patients in a single decade. Based on this clinical experience and the state of the literature, our management strategies for FP continue to evolve. Herein, we describe our current approach to diagnosis and treatment of FP, examine the condition’s myriad etiologies, and present their relative frequencies in patients we have managed in the last 10 years.

MATERIALS AND METHODS A chart review was performed for all patients seen at the Massachusetts Eye and Ear Infirmary Facial Nerve Center between June 2003 and June 2013; records of patients with FP were examined for diagnosis, sex, and age. House-Brackmann scores were not included, as this scale was designed for evaluation of recovering unilateral palsy, making it inapplicable to many of our patients.5 Patients with facial movement disorders due to primary muscular dysfunction or hemifacial spasm in the absence of synkinesis were excluded, as were those with complaints of FP but no evidence of weakness on physical

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examination. Cases of iatrogenic injury were classified conservatively; palsies due to excision of malignancies or intracranial masses were excluded from the iatrogenic category, as these cases are managed differently from cases of unexpected iatrogenic injury. In cases of malignancy in close proximity to the facial nerve, preoperative planning often includes a contingency for neural reconstruction, which mitigates additional uncertainty encountered in a return to the operating room to identify the site of injury and repair the nerve, which frequently occurs in cases of iatrogenic injury. Cases of FP following intracranial facial nerve manipulation were excluded from the iatrogenic injury category because reconstructive options proximal to the geniculate ganglion are limited in the absence of epineurium, and because the facial nerve, even though it may be nonfunctional, often remains anatomically intact after resection of the lesion. Review of the treatment plans, including physical therapy, chemodenervation, and surgical intervention, was undertaken, and our current treatment algorithms codified based upon trends developed in our center over the past decade. Data were compiled into an Excel spreadsheet (Microsoft Corp., Redmond, WA), which was used to tabulate demographic and etiological information. This study was approved by the institutional review board at the Massachusetts Eye and Ear Infirmary.

RESULTS Two thousand forty-seven records were reviewed; 1,989 were identified that met the inclusion criteria. The mean age at presentation was 44.5 years (618.6 years). There were 1,207 female patients and 782 males. BP accounted for the greatest number of cases (n 5 761), 38% of the series. Of these, 58 patients presented with recurrent FP. There were 82 cases of pregnancy-associated BP, occurring within 3 months preor postpartum (Table I). Acoustic neuroma was the second most common cause of FP in our series (n 5 203). The majority of these patients developed FP after resection; however, 12 cases developed FP after radiotherapy alone, and 13 patients presented with FP prior to treatment. Within the latter group, four reported sudden onset of palsy. Head and neck cancer accounted for 147 cases; the majority of cases resulted from resection, though 46 resulted from preoperative nerve involvement by the tumor. In eight of these cases, there was a history of rapid onset FP. The most common tumor location was the parotid gland itself (n 5 106), followed by intraparotid lymph node metastasis, and direct neural invasion of the facial nerve within the temporal bone. Iatrogenic facial nerve injuries, excluding cases due to resection of malignant or intracranial lesions, accounted for 143 cases. The most common associated procedure was temporomandibular joint surgery (n 5 31), with parotidectomy second (n 5 22), and tympanomastoidectomy third (n 5 12). Indications for parotidectomy included pleomorphic adenoma (n 5 19), vascular malformation (n 5 2), and recurrent sialadenitis (n 5 1). Indications for tympanomastoidectomy included chronic otitis media (n 5 8), cochlear implantation (n 5 2), endolymphatic decompression (n 5 1), and exostosis (n 5 1). Varicella zoster virus (VZV)-associated FP was separated into cases with a history of vesicular outbreak (Ramsay Hunt syndrome, n 5 122), and those without Laryngoscope 124: July 2014

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(zoster sine herpete, n 5 12). Two Ramsay Hunt syndrome patients presented with concomitant vocal fold paralysis. Trauma accounted for 113 cases, including temporal bone fractures and soft tissue injuries. Fractures were associated with motor vehicle accidents, falls, assaults, construction site accidents, and pedestrians struck by automobiles. There were also individual cases of birth trauma, manifested by the development of synkinesis in the child’s first 2 years of life, a soccer-related blow to the head, a pedestrian struck by a train, and a crush injury when the patient’s skull was caught between a boat and its dock. Two patients’ etiologies could not be determined from records. Benign tumors, such as geniculate ganglion hemangiomas and facial nerve schwannomas, were responsible for FP in 103 patients. There were 99 cases of congenital FP, the majority of which lacked a recognizable syndromic association; M€obius was the most common named syndrome. Lyme disease accounted for FP in 81 patients; seven cases demonstrated bilateral involvement. Lesions of the central nervous system, including medulloblastomas, vascular malformations, hemangiomas, and gliomas, were associated with 76 cases of FP. Autoimmune disease (n 5 32) occurred in twice as many females as males. Two patients experienced recurrent palsy, and 13 had bilateral involvement. GuillainBarre syndrome was the most common; all cases were bilateral, though not necessarily symmetrical. Seven cases did not fit the pattern of any well-characterized autoimmune disease, but did have positive hematologic testing (C-reactive protein, erythrocyte sedimentation rate, antinuclear antibodies, or rheumatoid factor), as well as a personal or family history of recurrent/bilateral FP or autoimmune disease. Infectious causes of FP accounted for 29 cases, with poliomyelitis suspected in 10. In these cases, patients from developing nations suffered childhood febrile illnesses with segmental paresis on examination, but no accompanying medical documentation. In nine cases, there were childhood febrile illnesses, but no characteristic pattern of poliomyelitis-associated FP. Otologic disease, including acute otitis media, cholesteatoma, and any other nonmalignant process that resulted in FP in the absence of surgical intervention occurred in 21 patients. Stroke affected 13 patients. In 34 cases, the diagnosis remained unclear.

DISCUSSION The causes of FP are myriad, but in this series, as in those cited above, BP was the dominant pathology.2,3 Interestingly, Peitersen’s ranking of etiologies then proceeded to congenital cases, VZV-associated FP, and traumatic palsy, which are all far less common in our series, reflecting a difference in referral patterns between his institution and ours, which is also a referral center for acoustic neuromas and other complex head and neck tumors. Historically, BP has been a diagnosis of exclusion, though several studies have demonstrated a link to

Hohman and Hadlock: Diagnosis and Management of Facial Palsy

TABLE I. Distribution of Patients by Diagnosis and Sex. Etiology

Bell’s palsy Recurrent >2 episodes Pregnancy associated

No. of Patients

Males

Females

Lyme disease

81

40

41

58 24

Bilateral Central nervous system lesions

7 76

33

43

82

Autoimmune disease

32

11

21

11

18

7

14

6

7

11

23

No. of Patients

Males

Females

761

265

496

13 2

178

 Guillain-Barre

12

12 13

Melkersson-Rosenthal Sarcoidosis

7 2

4

Multiple sclerosis

2

Amyloidosis Antiphospholipid antibody

1 1

203 34

Postresection

Rapid onset Head and neck cancer Postresection Postradiation Postchemotherapy Onset of FP prior to diagnosis

Etiology

Bilateral Recurrent

Acoustic neuroma NF2 associated Postradiation Onset of FP prior to diagnosis

TABLE I. (Continued)

147 91

70

90

133

57

Other

7

Infectious Poliomyelitis

2 47

7 29 10

Meningitis/encephalitis

5

Human immunodeficiency virus Epstein-Barr virus

2 1

43

Mumps

1

Otologic surgery Cosmetic surgery

30 12

Cellulitis Other febrile illness

1 9

Neurosurgery

9

Rapid onset Iatrogenic injury Oral surgery Head and neck surgery

Temporal artery biopsy Other Varicella zoster Ramsay Hunt Zoster sine herpete Trauma Soft tissue trauma Temporal bone fracture

8 143 43

134

113

9 4

Pedestrian vs. car

4

Construction accident Other

3 6 103

Facial nerve tumor NF2-associated facial neuroma

80 6

Parotid tumor

17 6 99 75

Congenital unilateral lower lip paresis

8 6

Hemifacial microsomia

5

Branchio-oto-renal VACTERL

2 1

CHARGE

1

Chapple syndrome

1

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56

78

63

50

17 2

Barotrauma

1

Brainstem Cortical Unknown

45

31

58

68

21

Acute otitis media/mastoiditis Cholesteatoma Inflammatory pseudotumor Stroke

50 63 37

Nonsyndromic € bius syndrome Mo

Otologic

122 12

Fall Assault

Meningioma Congenital

100

3 3

Motor vehicle accident

Benign tumor

43

1 13 9 4 34

Cases listed in the otologic category represent facial weakness prior to any surgical instrumentation. FP 5 facial palsy. VACTERL 5 association of vertebral anomalies, anal atresia, cardiac defects, tracheoesophageal fistula, esophageal atresia, renal anomalies, and limb defects. CHARGE 5 syndrome of colobomata of the eyes, heart defects, atresia of the choanae, retardation of growth/development, genital/urinary anomalies, and ear anomalies. NF-2 5 neurofibromatosis type 2.

herpes simplex virus (HSV).3,6,7 Viral reactivation in the geniculate ganglion likely leads to the typical appearance of enhancement on magnetic resonance imaging,8 as well as the classic history of rapid onset hemifacial palsy, peaking within 72 hours, preceded by postauricular pain and accompanied by dysgeusia and/or hyperacusis.9 Because serological testing for HSV in the setting of FP is not commonly performed, the diagnosis is made clinically. Distinguishing HSV-associated FP from other virally mediated facial palsies can therefore be difficult, but for the purposes of this study, we refer to HSVassociated FP as BP. VZV may present with the classic Ramsay Hunt symptomatology of hemifacial palsy, sensorineural hearing loss and/or vestibulopathy, severe Hohman and Hadlock: Diagnosis and Management of Facial Palsy

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pain, and vesicular outbreak on the pinna, tongue, or oral mucosa. It may also present as zoster sine herpete, whose symptoms mirror those encountered in Ramsay Hunt syndrome, but without skin or mucosal involvement.9 Lack of rash in zoster sine herpete may produce diagnostic confusion, as many patients with uncomplicated BP also complain of disequilibrium and pain. One important difference between FP of HSV origin and that of VZV origin is that BP may recur (7.6% of BP patients in our series), whereas recurrence of zoster is very rare in immunocompetent individuals.10 Regardless of which virus is the culprit, our acute treatment regimen includes steroids, antivirals, and eye protection, with audiometry if subjective hearing loss is noted (Fig. 1). Though studies have not established acyclovir as an effective therapy for BP,

valacyclovir does appear to provide a benefit when administered in combination with steroids.1,11 Additionally, patients who present acutely are offered electrodiagnostic testing and facial nerve decompression, if appropriate, based on the work of Gantz et al. and others.12–15 In our experience, patients with VZV-associated FP tend to recover more slowly than those with BP, although certain patients (e.g., diabetics, elderly patients, and women with pregnancy-associated BP) may also experience a prolonged recovery. We have not seen any patients with viral FP fail to recover muscle tone within 12 months, though patients who take longer than 10 weeks to demonstrate the first signs of recovery often suffer a greater degree of synkinesis, as do patients who suffer complete flaccid paralysis within 24 hours of symptom onset.15

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

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Viral FP accounted for over 60% of the rapid onset (evolution of palsy complete within 72 hours of onset) cases of FP in our series, but there are other clinical entities that can mimic this presentation, making a thorough history and physical exam imperative. Lyme disease, which was comparatively uncommon despite our institution’s location in New England, may also present with rapid onset FP. There is not always a history of known tick bite or rash, and serological testing can be equivocal; a high index of suspicion is therefore required, particularly in patients who are active outdoors.16,17 Lyme disease may also present with bilateral FP, though this was not frequently seen in our series.

Treatment of Lyme disease involves a long course of doxycycline, but because inflammation along the facial nerve confers the risk of additional insult from HSV reactivation, we prescribe valacyclovir along with antibiotics (Fig. 1). Debate remains regarding the role of steroids in Lyme disease, as they decrease inflammation while potentially depressing the immune system, thereby increasing spirochete load.18 Other causes of rapid onset FP include autoimmune disease, which may present a diagnostic challenge.19–21 Family history is important, as is a personal history of not only other autoimmune disease, but also unexplained and seemingly unconnected symptoms: rashes,

Fig. 2. Diagnostic evaluation of the patient with recurrent facial palsy (FP). When performing magnetic resonance imaging (MRI) for recurrent, segmental FP, it is important to evaluate not only the white matter of the brain, but also the entire length of the facial nerve. Imaging and hematologic testing should only be used to supplement a thorough history and physical examination. CN VII 5 cranial nerve VII. MS 5 multiple sclerosis. CRP 5 C-reactive protein. ESR 5 erythrocyte sedimentation rate. ANCA 5 antineutrophil cytoplasmic antibodies. ACE 5 angiotensin converting enzyme. RF 5 rheumatoid factor. ANA 5 antinuclear antibodies. SSA, SSB 5 skin-sensitizing antibodies. FTA-ABS 5 fluorescent treponemal antibody-absorption. VDRL 5 venereal disease research laboratory test for syphilis. TSH 5 thyroid stimulating hormone. CBC 5 complete blood count. [Color figure can be viewed in the online issue, which is available at www.laryngoscope.com.]

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orofacial edema, nasal septal perforation, multiple miscarriages, and others. When there is nothing in the history to differentiate autoimmune disease from BP, the diagnosis may be missed; however, autoimmune disease must be high on the differential diagnosis for the recurrent, bilateral, or alternating FP patient (Fig. 2). A further consideration in rapid onset FP is neoplasia. The majority of tumors that present with facial palsy do so insidiously, but malignancy may present acutely as well.22–24 There were eight patients with malignant tumors in our series who were erroneously diagnosed with BP before referral to our center. Because it is relatively rare for masses to present with acute FP, we do not recommend imaging as part of the initial evaluation for patients whose history is otherwise consistent with BP. A thorough history and physical examination that evaluates the cranial nerves, lymph nodes, parotid glands, ears, and facial skin will often elucidate the presence of a malignancy; however, if no sign of recovery is apparent within 4 months of onset, the presence of a tumor should

be considered even in the context of an otherwise unremarkable history and physical examination.22,25 Insidious, progressive FP most likely represents tumor, and patients with this presentation uniformly require aggressive imaging. Our series describes malignant tumors including primary parotid tumors, squamous cell carcinoma in the parotid gland and/or facial nerve, sarcomas, and benign tumors affecting the facial nerve including facial nerve schwannomas and geniculate ganglion hemangiomas. Adjuvant treatments for disease adjacent to or involving the facial nerve can also contribute to additional facial weakness, for example, radiation and chemotherapy. In the current series, we are unable to discern the nature of the relationship between change in facial function and adjuvant treatments beyond a temporal association. A thorough history may differentiate among causes of FP, but many patients present with a known diagnosis, such as temporal bone fracture or iatrogenic injury. In these cases, the diagnostic segment of the encounter

Fig. 3. Management of the patient with facial palsy of traumatic or iatrogenic etiology. We administer valacyclovir to patients with delayed or incomplete facial paralysis because of the potential for geniculate ganglion herpes simplex virus reactivation in the setting of traumatic facial nerve insult. Timing of repair or decompression remains controversial, but earlier intervention appears to result in improved outcomes, and after 4 to 6 months, outcomes may be poor due to muscle atrophy before reneurotization is complete. When considering electrodiagnostic testing, if the index of suspicion for nerve transection is low, testing after 72 hours have passed may be appropriate to rule out severe injury. However, if the index of suspicion is high, operating before 72 hours have passed allows use of a nerve stimulator intraoperatively, which may facilitate location of the distal nerve stump. BID 5 twice daily; FN 5 facial nerve; PO 5 orally. [Color figure can be viewed in the online issue, which is available at www.laryngoscope. com.]

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may be brief, and more time may be allocated to discussion of treatment. Iatrogenic injuries and trauma were the fourth and sixth most common etiologies of FP in this series, respectively; when these patients present acutely, the likelihood of satisfactory recovery may be increased through early operative intervention with facial nerve exploration and decompression or repair (Fig. 3).12–15,26,27 Care of the FP patient may be divided into three parts: assessment, diagnosis (Fig. 4), and management, which are often initiated simultaneously. In the majority of cases, treatment may proceed along well-defined pathways; these algorithms help the physician to avoid overlooking any aspect of the FP patient’s situation (Fig. 5).28 Facial palsy >4 months in duration merits special consideration, as most viral neuritis resolve spontaneously within this timeframe, and after 4 to 8 months, muscle reactivity declines.29 Assessment involves a codi-

fied intake process, which includes a meticulous history and physical examination, and photography in repose and during specific facial expressions.25 A video clip of these expressions is also recorded for review and comparison, and quality-of-life data are obtained. From a clinical perspective, the first priority for the flaccid FP patient is eye protection, following which, treatment will be determined by the likelihood of spontaneous recovery of facial function.28 Patients with flaccid FP for more than 12 months, a history of facial nerve sacrifice, or facial nerve malignancy are likely to remain flaccid, and will proceed to reanimation once the underlying pathology is addressed. Patients with synkinesis present a different set of challenges. For them, surgery is second-line therapy, after conservative measures: facial nerve physical therapy (PT) and chemodenervation (Fig. 6).28,30–33 For patients unsatisfied after conservative management, adjunctive procedures, such as platysmectomy and

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

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Fig. 5. Systematic zonal assessment of the paralyzed face promotes a comprehensive evaluation of affected facial subunits and may help to prevent overlooking any problematic areas. NLF 5 nasolabial fold. [Color figure can be viewed in the online issue, which is available at www.laryngoscope. com.]

selective neurectomy may provide long-term symptomatic relief.34,35 Surgical facial reanimation, which many patients and physicians view as the final step in the management of FP, is not a single procedure, but rather a process. Numerous surgical interventions have been employed, from static and dynamic reanimation to neural reconstruction. Epineurial repair of a transected nerve is considered the gold standard, whether through primary neurorrhaphy or interposition grafting.36 We typically employ two or three 10-0 nylon sutures (Ethilon; Ethicon Inc., Somerville, NJ) and apply fibrin glue (Evicel; Ethicon Inc.) around the repair site. Nerve transpositions may also be useful, although exchanging the morbidity of one cranial nerve deficit for another is hazardous; a substitute may be cross-face nerve grafting. Another consideration when contemplating nerve transposition is time course; because nerves regenerate at about 1 mm/day,37 and muscles undergo irreversible atrophy 12 to 18 months after denervation,38 the interval during which neural reconstruction techniques are applicable is often short, and frequently the window of opportunity has closed before the patient presents for evaluation. Nevertheless, there are cases in which reinnervation may be effected after prolonged facial dysfunction; patients who have preserved facial musculature as a result of synkinesis may be candidates for grafting to specific distal nerve branches (e.g., those for orbicularis oculi and zygomaticus major). Static reanimation procedures, including brow lift, eyelid weight placement, tarsal strip, and facial suspenLaryngoscope 124: July 2014

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sion techniques provide options for rehabilitation of upper, middle, and lower facial zones, and may frequently be performed under local anesthesia (Fig. 7).28,39–43 A low threshold for periocular reanimation may spare patients long-term corneal complications due to lagophthalmos from upper eyelid retraction or lower lid laxity. Eyelid weight placement is typically the first step; platinum is the preferred material, as its density affords a slim profile and fewer patients experience tissue reactions when compared to gold.40 Minimally invasive asymmetric brow lifting and tarsal strip procedures also improve eye comfort, safety, and cosmesis.28,39,41,42 Last, reanimation of the mid and lower face (i.e., nasolabial fold and oral commissure) may also be achieved through static techniques.28,43,44 Some authors report the use of alloplastic materials for static slings, but autologous fascia lata possesses the advantage of reduced risk of extrusion and infection.45 Good surgical candidates may elect to undergo dynamic smile rehabilitation. Two commonly employed techniques are temporalis and gracilis muscle transfers.45,46 At our institution, gracilis free muscle transfer is the more frequent procedure, resulting in 8 mm of smile excursion, on average.47 We perform gracilis transfer as a one- or two-stage operation, innervating the flap with the masseteric nerve or a cross-face nerve graft, respectively.48 We offer temporalis flap reanimation to patients who are poor free tissue transfer candidates, although many surgeons employ this technique as a first-line option with great success.49,50 At the time of muscle transfer, the alar base is suspended with fascia lata, if the patient

Hohman and Hadlock: Diagnosis and Management of Facial Palsy

Fig. 6. Management of the patient with facial palsy present for >4 months. Patients with palsy of >12 months duration, a history of facial nerve sacrifice, or a history of malignancy involving the facial nerve are considered to have no potential for spontaneous recovery. [Color figure can be viewed in the online issue, which is available at www.laryngoscope.com.]

Fig. 7. The algorithm enumerates indications and contraindications for various smile reanimation modalities. CN VII 5 cranial nerve VII. [Color figure can be viewed in the online issue, which is available at www.laryngoscope.com.]

suffers from external nasal valve collapse.51 Although PT has proven invaluable for improving quality of life in patients with spontaneous facial function recovery, it is also vital to the success of any dynamic reanimation procedure. Improvement of facial balance with contralateral chemodenervation and lower lip weakening may also improve quality of life, as will long-term follow-up with reevaluation for adjunctive procedures to refine results.28,52

CONCLUSION We have described the etiology of FP in the last 2,000 patients seen at the Massachusetts Eye and Ear Infirmary Facial Nerve Center, and provided an algorithm-driven approach to diagnosis and management, which has arisen and evolved with deepening experience and careful longitudinal clinical followup.22,25–29,32,34,35,39–41,47,48,51–53 Clinicians treating this condition must possess an awareness of the wide variety of FP etiologies; codifying the decision-making process is likely to result in fewer missed diagnoses and better outcomes. Although the data presented in this series are informative, they do not quantify the overall incidence or etiologic breakdown of FP. Because our institution is a tertiary referral center, we treat a wide variety of patients with a wide range of pathologies, significantly biasing our data acquisition. However, the algorithmic approach to diagnosis and management outlined herein, based upon substantial clinical experience, may represent a starting point for the generation of clinical pathways, consensus statements, and prospective outcomes studies going forward.

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Hohman and Hadlock: Diagnosis and Management of Facial Palsy

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Etiology, diagnosis, and management of facial palsy: 2000 patients at a facial nerve center.

To evaluate the range and incidence of facial palsy etiologies in cases presenting to a tertiary facial nerve center, and to review the broad and evol...
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