CLINICAL STUDY
Peripheral Facial Nerve Paralysis After Upper Third Molar Extraction Sirmahan Cakarer, DDS, PhD,* Taylan Can, DDS,* Burak Cankaya, DDS, PhD,* Mehmet Ali Erdem, DDS, PhD,* Sinem Yazici, MD,Þ Emre Ayintap, MD, PhD,þ Ali Veysel O¨zden, MD,§ and Cengizhan Keskin, DDS, PhD* Abstract: Peripheral facial nerve paralysis (PFNP) after mandibular interventions has been reported in the literature. In most cases, paralysis begins immediately after the injection of the mandibular anesthesia, and duration of facial weakness is less than 12 hours. However, there are few documented cases of PFNP after maxillary dental or surgical procedures. A variety of mechanisms have been associated to PFNP, including viral reactivation, demyelination, edema, vasospasm, and trauma. The purpose of this presentation was to report a rare case of facial paralysis that occurred after an upper third molar extraction. The cause of the PFNP and the importance of the multidisciplinary approach in the management are emphasized. Key Words: Peripheral facial nerve paralysis, Bell palsy, local anesthesia, third molar (J Craniofac Surg 2010;21: 1825Y1827)
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acial nerve paralysis may be central or peripheral in origin. Peripheral facial nerve paralysis (PFNP) is the most frequent cranial nerve motor neuropathy. It may be due to traumatic, compressive, infective, inflammatory, and metabolic abnormalities.1,2 The occurrence of PFNP after a local dental block for maxillofacial or dental procedures is a rare but known complication.3 The spread of dental anesthetic fluid to the branches of facial nerve does cause facial paralysis immediately after injection into the alveolar nerve. Recovery takes a few hours, usually as long as the anesthesia lasts; however, acute PFNP can also develop several days after a dental procedure as reported in the present case. The cause of such delayed facial paralysis after dental treatment has not yet been clarified.1,4 On the other hand, only 6 cases of PFNP that occurred after upper dental or oral surgical procedures including tooth extraction, bimaxillary osteotomy, and apicectomy have been reported to date in the literature.3,5Y7 The authors report another case of a PFNP after an
From the *Department of Oral and Maxillofacial Surgery, Dentistry Faculty and †Department of Neurology, Cerrahpasa Medical Faculty, Istanbul University; ‡Department of Ophthalmology, Medicine Faculty, Mustafa Kemal University; and §Department of Physical Therapy and Rehabilitation, Medicine Faculty, Istanbul University, Istanbul, Turkey. Received April 12, 2010. Accepted for publication June 19, 2010. Address correspondence and reprint requests to Sirmahan Cakarer, DDS, PhD, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Istanbul University, Istanbul, Turkey; E-mail:
[email protected] The authors report no conflicts of interest. Copyright * 2010 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0b013e3181f43dcf
The Journal of Craniofacial Surgery
upper third molar extraction. The possible cause and management are discussed.
CLINICAL REPORT A 25-year-old man was referred to the Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Istanbul University, by his general dentist for the management of an unilateral facial paralysis that occurred after a left upper third molar extraction. The patient noticed a mild pain in the retroauricular area and severe weakness of the muscles of the left side of his face. He also informed that he was not able to close his left eye. His dentist was consulted, and the latter informed that he performed the tooth extraction without any radiological evaluation and also reported that the patient was given a periapical block with 2 mL of Jetocain (20 mg/ml lidocain HCl and 0.0125 mg/ml epinephrine HCl; ADEKA, Tokyo, Japan). The injection of the anesthetic solution was uneventful. The carious tooth was removed without difficulty. There was no sign of facial paralysis at the end of the extraction. At 24 hours after the upper third molar extraction, the patient returned to his dentist with complaints of weakness of the muscles of the left side of his face. The patient was referred to our department without any medical therapy. The patient’s previous medical history was unremarkable. On extraoral examination, he was found to have a lower motor neuron weakness of his left facial nerve. Bell sign of the left side and unilateral expressionless were observed (Figs. 1 and 2). Taste and hearing were normal. There was no pathologic sign in the wound area clinically and radiologically. No herpetic lesions were found. There was no past history of facial paralysis after a dental procedure. The patient was referred for the neurological and otorhinolaryngological evaluation. Magnetic resonance imaging findings confirmed the diagnosis and also showed that there was no problem in the function of the stapedius muscle. No sign of otitis was reported. The treatment was based on the prescription of corticosteroid therapy, with subsequent tapering (Table 1). The patient was referred to the Department of Ophthalmology for eye protection and to the Department of Physical Therapy and Rehabilitation for peripheral nerve stimulation. Eye care was focused on the protection of the cornea from dehydration and drying due to insufficient tearing. Lubricant eye drop (4 1), tobramycin ophthalmic solution (4 1), and lanolin eye ointment (during night) supported by eye patch were proposed. For 4 weeks, galvanic stimulation of the affected side of the facial nerve was performed, and mime therapy was recommended by the physiotherapist. Two weeks since the start of physiotherapy, the patient informed that the retroauricular pain was absent. Three months after management, the patient showed a marked improvement with almost normal facial expression muscle movements (Figs. 3 and 4).
DISCUSSION Peripheral facial nerve paralysis is a common diagnostic problem to physicians in many branches of medicine.8 Secondary
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TABLE 1. Medication Schedule During 14 Days
FIGURE 1. Inability to smile at the left side. facial nerve paralysis occur due to various causes such as metabolic diseases, stroke, infection, surgery, trauma, immune system disorders, some drugs, and syndromes.9 For cases without a readily identifiable cause, the term Bell palsy (BP) is used to denote the idiopathic origin. Despite the cause of BP remaining unknown, viral infection and vascular ischemia have been reported as possible causes.1,4,7 The present case is consistent with BP because of the lack of a specific cause. The immediate and delayed type of facial paralysis has been reported in the literature.3 This case is consistent with the delayed type because the paralysis developed 24 hours after the upper local dental anesthesia. On the other hand, the dentist of the patient informed that the procedure was performed easily; therefore, prolonged instrumental opening of the mouth resulting in the stretch of the facial nerve could not be a possible cause of facial paralysis in the present case. The mechanism to explain the facial weakness occurs after dental procedures remains uncertain.8 The literature reports 3 mechanisms, in which a dental procedure could damage a nervous structure: direct trauma to the nerve from a needle, intraneural hematoma formation or compression, and local anesthetic toxicity.2 The authors’ believe that direct trauma of the facial nerve could be very difficult via the upper posterior local anesthesia performed in the present case. Furthermore, such local mechanisms cannot explain the involvement of the upper divisions of the facial nerve and
FIGURE 2. Compromised eyebrow movement at the left side.
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Days
Medication
1Y5 6Y10 11Y14
8 mg of dexamethasone 1 1 intramuscularly 4 mg of dexamethasone 1 1 intramuscularly 2 mg of dexamethasone 1 1 tablet
chorda tympani or development of the facial weakness when an upper tooth was extracted.2 The use of several different local anesthetics including articaine, lidocaine, and bupivacaine, frequently with or without epinephrine, has been reported to be associated with facial paralysis developed after dental or oral surgical procedures.1Y3,7 Despite that lidocaine, which was also used in the present case, cause less nerve damage than procain and tetracain, it can also be neurotoxic. In fact, most local anesthetics are neurotoxic, but neurotoxicity normally occurs only when the local anesthetic is injected intrathecally.2 Another proposal was explained by Genthon et al.5 They reported the possibility of a retrograde injection in the posterior superior alveolar artery transporting the anesthetic solution into the medial meningeal artery and, from there, through petrosal branches to the facial nerve.5 The authors believe that the possible cause in the present case could be associated with the proposal of Genthon et al regarding the location of the dental block. This proposal is also consistent with the second mechanism that explains the facial weakness that occurs after dental procedures. Another possible mechanism is that dental surgery may have precipitated the latent viral infection and subsequent facial paralysis. Among viral infections, herpes simplex type 1 has received the most attention.8 On intraoral examination, any sign of herpes simplex virus was observed in the present case. Facial paralysis, as a complication of dental extraction, may result from direct tissue damage from a blast of air into the tissue with dissection through the facial spaces. Therefore, it is recommended not to use forced air while cleaning an extraction site. Careful water irrigation may accomplish the same task and minimize the risk of nerve injury.2 To clinically assess the severity of PFNP, various scoring systems are available. The most frequently applied is the HouseBrackmann facial nerve grading system.9 In the present case, the House-Brackmann system was chosen because it is a simple and robust method for assessing facial function.2 Regarding the clinical
FIGURE 3. Almost symmetrical smile. * 2010 Mutaz B. Habal, MD
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PFNP After Upper Third Molar Extraction
occur in up to 12% of cases.8 Three months after management, the patient showed a marked improvement, and no sign of recurrence was observed.
CONCLUSIONS Dental practitioners and oral and maxillofacial surgeons should be aware that the PFNP may also occur after maxillary procedures. The management of the PFNP certainly requires a multidisciplinary team that includes a neurologist, a otorhinolaryngologist, an ophthalmologist, and a physiotherapist. There is lack of randomized controlled studies that evaluate the effect of the steroids and antivirals in the management of PFNP. Nevertheless, it is believed that early management with the steroids is effective as reported in the present case. It should also be kept in mind that a close follow-up is required regarding the possibility of recurrence.
FIGURE 4. Normal eyebrow movement.
observation, a diagnosis of a moderately severe dysfunction of the facial nerve or grade IVof the House-Brackmann grading system for facial paralysis was made. Management of patients with BP involves various fields including eye protection, therapeutic regimens, and physiotherapy. Patients with facial injury often experience corneal irritation and ulceration due to inadequate lubrication of the eyes and lid lag, which are potential causes for keratitis sicca. Therefore, it is very important to provide eye care including prophylaxis of corneal inflammation through local administration of antibiotic ointments (preferentially at night) and/or the use of artificial tear fluid during the day, as reported in the present case.10,11 Different therapeutic regimens including steroids and antivirals have been suggested for BP.11 According to a recent Cochrane review that evaluated 8 randomized controlled studies, corticosteroids were effective in the treatment of the BP.12 A recent randomized controlled study also showed that the early use of oral prednisolone in BP is effective.13 The discussion about the use of the antivirals in the treatment of BP continues.4,11,14Y16 In the present case, prescription of the dexamethasone during 2 weeks with subsequent tapering showed good result during treatment. The effect of physical therapy, including electrotherapy, exercises, biofeedback, manual therapy, and laser, for BP is reported by many authors. However, there is a lack of high-quality evidence to support the use of these strategies.17 Four weeks of galvanic stimulation of the nerve and mime therapy showed good results in the present case. Facial nerve paralysis can be categorized as complete, if there is inability in voluntary contraction of the facial muscles, hyperacusis, and loss of taste, or as incomplete. Facial nerve paralysis can improve up to 1 year. Patients with incomplete paralysis have a better prognosis than patients with complete paralysis. In patients with incomplete facial paralysis, up to 94% make a full recovery.9 In the present case, there was no sign of hyperacusis or loss of taste. Therefore, it was categorized as an incomplete facial nerve paralysis. Recurrence is not uncommon in BP, and this can
REFERENCES 1. Tazi M, Soichot P, Perrin D. Facial palsy following dental extraction: report of 2 cases. J Oral Maxillofac Surg 2003;61:840 2. Vasconcelos BC, Bessa-Nogueira RV, Maurette PE, et al. Facial nerve paralysis after impacted lower third molar surgery: a literature review and case report. Med Oral Patol Oral Cir Bucal 2006;11:175 3. Bernsen PLJA. Peripheral facial nerve paralysis after local upper dental anaesthesia. Peripheral Eur Neurol 1993;33:90 4. Furuta Y, Ohtani F, Fukuda S, et al. Reactivation of varicella-zoster virus in delayed facial palsy after dental treatment and oro-facial surgery. J Med Virol 2000;62:42 5. Genthon R, Mas JL, Bouche P, et al. Peripheral facial paralysis after dental anesthesia [in French]. Presse Med 1987; 6:1056 6. Rives JM, Flocard F, Ribot C, et al. Peripheral facial paralysis after dental local anesthesia. Presse Med 1989;8:729 7. Cousin GC. Facial nerve palsy following intra-oral surgery performed with local anaesthesia. J R Coll Surg Edinb 2000;45:330 8. Shuaib A, Lee MA. Recurrent peripheral facial nerve palsy after dental procedures. Oral Surg Oral Med Oral Pathol 1990; 70:738 9. Finsterer J. Management of peripheral facial nerve palsy. Eur Arch Otorhinolaryngol 2008;265:743 10. Li J, Goldberg G, Munin MC, et al. Post-traumatic bilateral facial palsy: a case report and literature review. Brain Inj 2004;18:315 11. Roob G, Fazekas F, Hartung HP. Peripheral facial palsy: etiology, diagnosis and treatment. Eur Neurol 1999;41:3 12. Salinas RA, Alvarez G, Daly F, et al. Corticosteroids for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2010;17: CD001942 13. Sullivan FM, Swan IR, Donnan PT, et al. A randomised controlled trial of the use of aciclovir and/or prednisolone for the early treatment of Bell’s palsy: the BELLS study. Health Technol Assess 2009;13:1 14. Sapiro SM. Bell’s palsy associated with acute herpetic gingivostomatitis. Oral Surg Oral Med Oral Pathol 1975;39:403 15. Lockhart P, Daly F, Pitkethly M, et al. Antiviral treatment for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2009;7: CD001869 16. Sipe J, Dunn L. Aciclovir for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2001;4:CD001869 17. Teixeira LJ, Soares BG, Vieira VP, et al. Physical therapy for Bell’s palsy (idiopathic facial paralysis). Cochrane Database Syst Rev 2008;16: CD006283
* 2010 Mutaz B. Habal, MD
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