Facial palsy in the dental surgery. Case report and review Peter G. Miles, BDSc (Qld)*
Key words: Bell’s palsy, case reports, idiopathic facial palsy, loss of sensation. Abstract Facial palsy is a relatively uncommon condition with a variety of causes including dental intervention. A brief history of two cases of facial palsy with dental implications is presented. The aetiology of facial palsy is reviewed and the management of such cases is discussed. The option of immediate treatment of Bell’s palsy with prednisone is stressed. (Received for publication May 1991. Accepted August 1991.)
Introduction Facial palsy in the dental surgery is a rare occurrence and a diagnostic problem when it does present. Possible causes are numerous and include Bell’s palsy (idiopathic facial palsy), viral and other infections, trauma, diabetes, pregnancy, neoplastic infiltration and ischaemia of the facial nerve and its ComDression in the stvlomastoid Bell’s palsy is the most common type of lower motor neurone facial palsy. Involvement of the seventh cranial nerve to varying degrees results in a loss of tone to the muscles of facial expression. This can be very disfiguring and a cause of great distress to the patient. Other symptoms may also appear depending on where along the path of the facial nerve a disorder exists. The facial nerve is predominantly a motor nerve to the muscles of facial expression with sensation being supplied to the overlying regions by branches of the trigeminal (fifth cranial) nerve.
*Graduate Student, Orthodontic Department, University of Pittsburgh. 262
Anatomy The facial nerve emerges from the brain stem between the pons and medulla oblongata and then passes into the internal acoustic meatus with the vestibulocochlear (eighth cranial) nerve. It then enters the facial canal, expands into the geniculate ganglion and turns sharply backwards. Sweeping down behind the middle ear, it emerges from the skull at the stylomastoid foramen. Before the facial nerve exits at the stylomastoid foramen, three important branches leave the main trunk. The greater superficial petrosal nerve branches from the geniculate ganglion, the nerve to the stapedius muscle then leaves the facial nerve trunk followed by the chorda tympani nerve. These supply secretomotor fibres to the lacrimal gland, motor fibres to the stapedius muscle and taste fibres to the anterior two-thirds of the tongue respectively. In theory, a facial nerve lesion may therefore be localized by determining if any dis~rbancesin addition to facial Paralysis are Present- If a disorder occurs between the brain stem and the geniculate ganglion, signs of facial paralysis, loss Of lacrimation and loss of taste would be expected. In addition, there may be hyperacusis (sounds appearing louder) due to stapedius muscle paralysis. If the disorder occurs in the middle ear, lacrimation will be unaffected. A disorder occurring distal to the chorda tympani will exhibit facial paralysis only. Two cases of patients seeking a dental cause for their facial palsy are presented, one involving a concurrent loss of sensation to an ipselateral region of the face. Case 1 A twenty-six-year-old man had routine restorative work carried out on the lower right first molar under inferior alveolar block anaesthesia and on the maxillary right central incisor under labial infiltration anaesthesia. A total dose of 4.4 mL of two Australian Dental Journal 1992;37(4):262-5.
per cent lignocaine with 1:80 000 adrenaline was injected. Four days later the patient returned to the surgery concerned over his inability to close his right eye or to smile normally. The onset of symptoms was gradual over a period of two days. He also complained of toothache in the upper right first bicuspid which had been previously dressed. The necrotic pulp was extirpated at this appointment and a Ledermix paste? dressing was placed. Further questioning revealed a reduction of sensation to the lips and side of the tongue when compared with the contralateral side. This was most evident in the upper lip (supplied by the terminal branches of the second division of the trigeminal nerve). He was due to see a neurologist concerning headaches and, with the onset of these new symptoms, an immediate consultation was urged. No cause was elucidated or treatment offered by the neurologist and the symptoms resolved within a period of four weeks.
Table 1. Dental aetiologies of facial palsy ~~
Group Aetiology 1
2
3
4 5
6
Onset
Viral reactivation Few days due to any dental procedure Anaesthetic injection a) Direct Immediate b) Indirect via Several hours sympathetic to several plexus days Surgical a) Direct-severed nerve Immediate b) Indirect-swelling, Few hours to trauma, infection few days Dental infection Hours to few days External trauma Immediate to few days Others Neoplasms Gradual Autoimmune/ Sudden Syndromes Sudden DiabeteslPregnancy
Duration Weeks to months
30 min to 2h 30m Days to weeks
Indefinite Few days to weeks Few days to weeks Few days to indefinite Indefinite Short to long term Short to long term
Case 2
A woman in her late twenties expressed concern that her fractured lower right molar may have been the cause of her facial palsy. Three months previously, in her final week of pregnancy, she demonstrated the classic sudden onset of Bell's palsy in the right side of her face. An alteration in her perception of taste was also noted, suggesting involvement of the chorda tympani nerve. She was investigated by a neurologist and offered the option of steroidal therapy which she rehsed due to her pregnancy. Her symptoms had diminished at our examination three months afler onset. The fractured molar responded positively to pulpal vitality tests, no pathosis was evident on periapical radiographs and the tooth was subsequently restored with amalgam. One month later her symptoms were only slightly improved compared with the marked improvement shown in the first three months. Discussion A etiology Facial palsy potentially has many differing aetiologies, some of which are dentally related (Table 1). The term Bell's palsy was once commonly used to refer to all facial palsies but is now redefined as a viral polyneuritis of the facial nerve, probably from herpes simplex rea~tivation.'.~*~-* This is in contrast to, for example, Ramsay Hunt syndrome, which is due to varicella zoster virus (shingles) affecting the geniculate ganglion, although some symptoms may ?Ledennix paste. Lederle Pharmaceuticals, Wolfratshausen, Germany. Australian Dental Journal 1992;37:4.
appear to be the same.2 Ramsay Hunt syndrome is clinically differentiated from Bell's palsy by the e r u p tion of small vesicles which may appear on the tragus of the ear. Lesions may also occur on the tympanic membrane, soft palate, anterior two-thirds of the tongue and rarely as facial eruptions. This viral aetiology means topographic localization cannot definitively identify the site of Bell's palsy due to the patchy areas of longitudinal involvement of the facial nerve from the brain stem to the periphery.' A viral origin helps explain the appearance of symptoms in other cranial and peripheral nerves as in Case 1. Abdel Baki and co-workers9 found that 35 per cent of their cases with Bell's palsy had a motor conduction delay in one or more segments of the ulnar nerve, suggesting a more systemic condition. Hypoaesthesia of the trigeminal nerve, the glossopharyngeal nerve and the second cervical nerve, vagal motor weakness and trigeminal motor weakness with associated acute temporomandibular joint pain dysfunction syndrome may all be associated with Bell's p a l ~ y . ' ~ In ~ ~an' ~analysis ~ ' ~ of '~ it trigeminal neuropathy, Sawamura et ~ 1 . found may also share symptoms of impairment of taste, occasional facial palsy, vestibular insufficiency, hearing disturbance or hypoglossal palsy or signs of a cerebellar lesion. This led them to strongly suspect a viral origin. Several studies in patients with Bell's palsy have demonstrated elevated antibody titres to herpes simplex and other viruses belonging to the herpes virus group when compared with the general p~pulation.'~*'~ This supports the hypothesis that Bell's palsy is an auto-immune demyelination related 263
to viral infection. Virtually any dental manipulation may be a factor in triggering a viral reactivation resulting in facial palsy. A small number of cases have been reported where this was cited as the mechanism inv01ved.~~'~ This is a possible mechanism involved in Case 1 due to the involvement of the trigeminal nerve. Facial palsy may also be one of many possible cranial and peripheral nerve complications in AIDS patients.1s.16Some 60 per cent of all HIV infected patients develop neurological deficiencies during the course of the disease. Chilla, Booken and RascheI6 reported a case where Bell's palsy was the first symptom of HIV infection, although this would be a rare occurrence. Cases have been reported where the dental anaesthetic injection was believed to be the cause of the palsy.".'' This could be due to an anatomical variation in the facial nerve or parotid gland and injection of the anaesthetic into this region. This would have a local, direct and immediate action but would only be expected to last a few hours. This is an unlikely mechanism due to the particular anatomical features and tissue planes involved.18 The injection may also act indirectly via a sympathetic vascular reflex leading to an ischaemic paralysis. This may be due to the vasoconstrictor in the anaesthetic or the mechanical action of the needle itself, stimulating the sympathetic plexus associated with the external carotid artery.I4.l7 Oral surgery can be a factor in eliciting facial palsy. Any surgery in the region of the stylomastoid foramen and parotid gland may result in direct damage to the facial nerve and subsequent paralysis. Postoperative infections and oedema have been reported to induce facial paralysis subsequent to third molar removal, coronoidectomy and osteotomies of the mandible.14.'9.20-22 This has been variously attributed to the placement of retractors behind the ascending ramus, fracture of the styloid process, retropositioning of the prognathic mandible, postoperative oedema or haematoma, and coincidental Bell's palsy.21.22Other dental infections may also elicit a facial palsy due to an inflammatory response with or without compression of the facial nerve, as can acute middle ear infection^.'.'^ External trauma to the temporal or parotid regions containing the facial nerve may result in facial palsy similar to surgical trauma.I4 Many other conditions, syndromes and pathoses are associated with facial palsy. Conditions affecting the parotid gland such as neoplasms and sarcoidosis may elicit ~ymptoms.~ A high correlation between both diabetes and hypertension and Bell's palsy has been found when compared with the general popul a t i ~ nThe . ~ ~diabetic has been shown to be 4.5 times 264
more likely to develop Bell's palsy than the nondiabetic A higher incidence of Bell's palsy has been reported during pregnancy, in particular the last trimester and the first few weeks postp a r t ~ m . Bell's ~ ~ . ~palsy ~ occurs 3.3 times more frequently during ~regnancy.'.'~This has obvious direct relevance to Case 2. Management Due to the varied pathogenesis of idiopathic facial palsy, a number of treatments have been advocated. These include adrenocorticotrophic hormone the rap^,^"^ prednisone therapy,'.'4,28~29dimexide and nicotinic acid compresses,3O and surgical decompression of the facial nerve.'-3 Prednisone therapy is the most widely advocated and successful treatment but must be initiated as soon as possible to prevent prolonged symptoms due to demyelination. 1.28.31 Any delay in commencing steroids seems to be a major factor responsible for the failure of treatment.29Falco and ErikssonZ6found that steroids did not appear to influence recovery in the pregnancy-related cases. This we would expect as the condition is probably not due to a viral demyelination in such cases. Surgical decompression of the facial nerve has fallen into disfavour as it seldom appears to aid recovery of function.' If the facial nerve has been severed, end-to-end anastomosis of the proximal and distal segments of the facial nerve, grafting of a segment of sensory nerve into the defect in the facial nerve, and anastomosis of the proximal hypoglossal segment to the distal facial nerve segment are highly regarded methods of repair to the extratemporal facial nerve.' Management of facial palsy has been limited in the past to protection and lubrication of the eye. The role of the dentist in facial palsy is limited to the maintenance of oral hygiene which may suffer because of lost muscle tone. Occasionally the provision of aesthetic improvements such as lipsupporting prostheses is required in long-term cases. Although the majority of cases recover spontaneously, the possibility of prolonged or incomplete recovery must be considered when constructing a treatment regimen. The appearance of symptoms in other cranial nerves, in particular the trigeminal nerve, along with facial palsy need not necessarily be alarming. However, facial palsy does require immediate referral to the patient's medical practitioner for investigation and possible steroidal treatment.
Conclusion Although such occurrences are rare, dentists should be aware that certain dental procedures can Australian Dental Journal 1992;37:4.
initiate a facial palsy. Patients may also present to a dental surgery seeking a dental cause for their facial palsy as in the two cases presented. Those presenting in the dental surgery should be immediately referred to their medical practitioner for the option of steroidal therapy. For this to be a viable option, it must be initiated early in the condition or any benefits may be negated. Adjunctive treatment in the dental surgery is limited to oral hygiene maintenance and occasional provision of aesthetic improvements. With the increasing incidence of AIDS in the community and its high correlation with neurological defects, a test for HIV antigens or other serological markers may also be indicated. References 1. Adour KK. Diagnosis and management of facial paralysis. N Engl J Med 1982;307:348-51. 2. Gayford JJ, Haskell R. Clinical oral medicine. 2nd edn. Bristol: John Wright, 1979:234-44. 3. Shafer WG, Hine MK, Levy BM. A textbook of oral pathology. 3rd edn. Philadelphia: WB Saunders, 1974:800-01. 4. Adour KK, Hilsinger RL Jr, Callan EJ. Facial paralysis and Bell’s palsy: a protocol for differential diagnosis. Am J Otol 1985;N0~:S~ppl:68-73. 5. Shuaib A, Lee MA. Recurrent peripheral facial nerve palsy after dental procedures. Oral Surg Oral Med Oral Pathol 1990;70:738-40. 6. Adour KK, By1 FM, Hilsinger RL Jr, Kahn ZM, Sheldon MI. The true nature of Bell’s palsy: analysis of lo00 consecutive patients. Laryngoscope 1978;88:787-801. 7. Djupesland G, Berdal P, Johannsen TA, Degre M, Stein R, Skrede S. The role ofviral infection in acute peripheral facial palsy. Acta Otolaryngol Stockh 1975; 79:221-7. 8. Adour KK, Bell DN, Hilsinger RL Jr. Herpes simplex virus in idiopathic facial paralysis (Bell’s palsy). JAMA 1975;233:527-30. 9. Abdel Baki F, Maghazi H, Eassa A, Talaat F. Peripheral nerve involvement in acute Bell’s palsy. J Laryngol Otol 1988; 102:447-8. 10. Sawamura Y, Tashiro K, Shima K, Moriwaka F, Abe H. Clinical analysis of trigeminal neuropathy as initial manifestations - an aetiological study. No T o Shinkei 1988;40:863-8. 11. Hanner P, Badr G, Rosenhall U, Edstrom S. Trigeminal dysfunction in patients with Bell’s palsy. Acta Otolaryngol S t d h 1986; 101:224-30. 12. Mang WL, Bonkowsky VM. Acute viral infections in association with idiopathic peripheral facial paralysis. HNO 1987;35:310-3. 13. Nakamura K, Yanagihara N. Neutralization antibody to herpes simplex virus type 1 in Bell’s palsy. Ann Otol Rhinol Laryngol Suppl 1988;137:18-21. 14. Gray RLM. Peripheral facial nerve paralysis ofdental origin. Br J Oral Surg 1978;16:143-50.
Australian Dental Journal 1992;37:4
15. Levy RM, Bredesen DE, Rosenblum ML. Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): experience at UCSF and review ofthe literature. J Neurosurg 1985;62:475-95. 16. Chilla R, Booken G, Rasche H. Bell’s palsy as the initial symptom of HIV infection. Laryngol Rhinol Otol Stuttg 1987;66:629-30. 17. Tiwari IB, Keane T. Hemifacial palsy after inferior dental block. Br Med J 1970;1:798. 18. Stoy PJ, Gregg G. Bell’s palsy following local anaesthesia. Br Dent J 1951;91:292-3. 19. Chuong R. Contralateral facial palsy following coronoidectomy. Oral Surg Oral Med Oral Pathol 1984;57:23-5. 20. Rubin MM, Cozzi G. Unilateral facial palsy following intraoral coronoidectomies. Oral Surg Oral Med Oral Pathol 1987;64: 156-8. 21. Dendy RA. Facial nerve paralysis following sagittal split mandibular osteotomy: a case report. Br J Oral Surg 1973;11:101-5. 22. Guralnick W, Kelly JP. Palsy ofthe facial nerve after intraoral oblique osteotomies ofthe mandible. J Oral Surg 1979;37743. 23. Yanagihara N, Hyodo M. Association of diabetes mellitus and hypertension with Bell’s palsy and Ramsay Hunt syndrome. Ann Otol Rhinol Laryngol Suppl 1988;137:5-7. 24. Adour KK, Wingerd J, Doty HE. Prevalence ofconcurrent diabetes mellitus and idiopathic facial paralysis (Bell’s Palsy). Diabetes 1975;24:449-51. 25. McGregor JA, Guberman A, Amer J, Gwdlin R. Idiopathic facial nerve paralysis (Bell’s palsy) in late pregnancy and the early puerperium. Obstet Gynecol 1987;69:435-8. 26. Falco NA, Eriksson E. Idiopathic facial palsy in pregnancy and the puerperium. Surg Gynecol Obstet 1989;169:337-40. 27. Hilsinger RL Jr, Adour KK, Doty HE. Idiopathic facial paralysis, pregnancy, and the menstrual cycle. Ann Otol Rhinol Laryngol 1975;84:433-42. 28. Devriese PP, Schumacher T, Scheide A, de Jongh RH, Houtkooper JM. Incidence, prognosis and recovery of Bell’s palsy. A survey of about 1000 patients (1974-1983). Clin Otolaryngol 1990;15: 15-27. 29. A1 Husaini A, Jamal GA, Hilmi AM, Mathur VS. Steroid therapy in Bell’s palsy. Int J Clin Pharmacol Ther Toxicol 1986;24:430-2. 30. Farber FM. Treatment of primary neuritis ofthe facial nerve with compresses of dimexide and nicotinic acid. Zh Nevropatol Psikhiatr 1984;84:1161-3. 31. Katusic SK, Beard CM, Wiederholt WC, Bergstralh EJ, Kurland LT. Incidence, clinical features, and prognosis in Bell’s palsy, Rochester, Minnesota, 1968-1982. Ann Neurol 1986;20:622-7.
Address for correspon&nce/reprints: University of Pittsburgh, Dental Medicine Ortho., 3501 Terrace Street, Pittsburgh, PA, 15261, USA.
-
265
Key words: Bell’s palsy, case reports, idiopathic facial palsy, loss of sensation. Abstract Facial palsy is a relatively uncommon condition with a variety of causes including dental intervention. A brief history of two cases of facial palsy with dental implications is presented. The aetiology of facial palsy is reviewed and the management of such cases is discussed. The option of immediate treatment of Bell’s palsy with prednisone is stressed. (Received for publication May 1991. Accepted August 1991.)
Introduction Facial palsy in the dental surgery is a rare occurrence and a diagnostic problem when it does present. Possible causes are numerous and include Bell’s palsy (idiopathic facial palsy), viral and other infections, trauma, diabetes, pregnancy, neoplastic infiltration and ischaemia of the facial nerve and its ComDression in the stvlomastoid Bell’s palsy is the most common type of lower motor neurone facial palsy. Involvement of the seventh cranial nerve to varying degrees results in a loss of tone to the muscles of facial expression. This can be very disfiguring and a cause of great distress to the patient. Other symptoms may also appear depending on where along the path of the facial nerve a disorder exists. The facial nerve is predominantly a motor nerve to the muscles of facial expression with sensation being supplied to the overlying regions by branches of the trigeminal (fifth cranial) nerve.
*Graduate Student, Orthodontic Department, University of Pittsburgh. 262
Anatomy The facial nerve emerges from the brain stem between the pons and medulla oblongata and then passes into the internal acoustic meatus with the vestibulocochlear (eighth cranial) nerve. It then enters the facial canal, expands into the geniculate ganglion and turns sharply backwards. Sweeping down behind the middle ear, it emerges from the skull at the stylomastoid foramen. Before the facial nerve exits at the stylomastoid foramen, three important branches leave the main trunk. The greater superficial petrosal nerve branches from the geniculate ganglion, the nerve to the stapedius muscle then leaves the facial nerve trunk followed by the chorda tympani nerve. These supply secretomotor fibres to the lacrimal gland, motor fibres to the stapedius muscle and taste fibres to the anterior two-thirds of the tongue respectively. In theory, a facial nerve lesion may therefore be localized by determining if any dis~rbancesin addition to facial Paralysis are Present- If a disorder occurs between the brain stem and the geniculate ganglion, signs of facial paralysis, loss Of lacrimation and loss of taste would be expected. In addition, there may be hyperacusis (sounds appearing louder) due to stapedius muscle paralysis. If the disorder occurs in the middle ear, lacrimation will be unaffected. A disorder occurring distal to the chorda tympani will exhibit facial paralysis only. Two cases of patients seeking a dental cause for their facial palsy are presented, one involving a concurrent loss of sensation to an ipselateral region of the face. Case 1 A twenty-six-year-old man had routine restorative work carried out on the lower right first molar under inferior alveolar block anaesthesia and on the maxillary right central incisor under labial infiltration anaesthesia. A total dose of 4.4 mL of two Australian Dental Journal 1992;37(4):262-5.
per cent lignocaine with 1:80 000 adrenaline was injected. Four days later the patient returned to the surgery concerned over his inability to close his right eye or to smile normally. The onset of symptoms was gradual over a period of two days. He also complained of toothache in the upper right first bicuspid which had been previously dressed. The necrotic pulp was extirpated at this appointment and a Ledermix paste? dressing was placed. Further questioning revealed a reduction of sensation to the lips and side of the tongue when compared with the contralateral side. This was most evident in the upper lip (supplied by the terminal branches of the second division of the trigeminal nerve). He was due to see a neurologist concerning headaches and, with the onset of these new symptoms, an immediate consultation was urged. No cause was elucidated or treatment offered by the neurologist and the symptoms resolved within a period of four weeks.
Table 1. Dental aetiologies of facial palsy ~~
Group Aetiology 1
2
3
4 5
6
Onset
Viral reactivation Few days due to any dental procedure Anaesthetic injection a) Direct Immediate b) Indirect via Several hours sympathetic to several plexus days Surgical a) Direct-severed nerve Immediate b) Indirect-swelling, Few hours to trauma, infection few days Dental infection Hours to few days External trauma Immediate to few days Others Neoplasms Gradual Autoimmune/ Sudden Syndromes Sudden DiabeteslPregnancy
Duration Weeks to months
30 min to 2h 30m Days to weeks
Indefinite Few days to weeks Few days to weeks Few days to indefinite Indefinite Short to long term Short to long term
Case 2
A woman in her late twenties expressed concern that her fractured lower right molar may have been the cause of her facial palsy. Three months previously, in her final week of pregnancy, she demonstrated the classic sudden onset of Bell's palsy in the right side of her face. An alteration in her perception of taste was also noted, suggesting involvement of the chorda tympani nerve. She was investigated by a neurologist and offered the option of steroidal therapy which she rehsed due to her pregnancy. Her symptoms had diminished at our examination three months afler onset. The fractured molar responded positively to pulpal vitality tests, no pathosis was evident on periapical radiographs and the tooth was subsequently restored with amalgam. One month later her symptoms were only slightly improved compared with the marked improvement shown in the first three months. Discussion A etiology Facial palsy potentially has many differing aetiologies, some of which are dentally related (Table 1). The term Bell's palsy was once commonly used to refer to all facial palsies but is now redefined as a viral polyneuritis of the facial nerve, probably from herpes simplex rea~tivation.'.~*~-* This is in contrast to, for example, Ramsay Hunt syndrome, which is due to varicella zoster virus (shingles) affecting the geniculate ganglion, although some symptoms may ?Ledennix paste. Lederle Pharmaceuticals, Wolfratshausen, Germany. Australian Dental Journal 1992;37:4.
appear to be the same.2 Ramsay Hunt syndrome is clinically differentiated from Bell's palsy by the e r u p tion of small vesicles which may appear on the tragus of the ear. Lesions may also occur on the tympanic membrane, soft palate, anterior two-thirds of the tongue and rarely as facial eruptions. This viral aetiology means topographic localization cannot definitively identify the site of Bell's palsy due to the patchy areas of longitudinal involvement of the facial nerve from the brain stem to the periphery.' A viral origin helps explain the appearance of symptoms in other cranial and peripheral nerves as in Case 1. Abdel Baki and co-workers9 found that 35 per cent of their cases with Bell's palsy had a motor conduction delay in one or more segments of the ulnar nerve, suggesting a more systemic condition. Hypoaesthesia of the trigeminal nerve, the glossopharyngeal nerve and the second cervical nerve, vagal motor weakness and trigeminal motor weakness with associated acute temporomandibular joint pain dysfunction syndrome may all be associated with Bell's p a l ~ y . ' ~ In ~ ~an' ~analysis ~ ' ~ of '~ it trigeminal neuropathy, Sawamura et ~ 1 . found may also share symptoms of impairment of taste, occasional facial palsy, vestibular insufficiency, hearing disturbance or hypoglossal palsy or signs of a cerebellar lesion. This led them to strongly suspect a viral origin. Several studies in patients with Bell's palsy have demonstrated elevated antibody titres to herpes simplex and other viruses belonging to the herpes virus group when compared with the general p~pulation.'~*'~ This supports the hypothesis that Bell's palsy is an auto-immune demyelination related 263
to viral infection. Virtually any dental manipulation may be a factor in triggering a viral reactivation resulting in facial palsy. A small number of cases have been reported where this was cited as the mechanism inv01ved.~~'~ This is a possible mechanism involved in Case 1 due to the involvement of the trigeminal nerve. Facial palsy may also be one of many possible cranial and peripheral nerve complications in AIDS patients.1s.16Some 60 per cent of all HIV infected patients develop neurological deficiencies during the course of the disease. Chilla, Booken and RascheI6 reported a case where Bell's palsy was the first symptom of HIV infection, although this would be a rare occurrence. Cases have been reported where the dental anaesthetic injection was believed to be the cause of the palsy.".'' This could be due to an anatomical variation in the facial nerve or parotid gland and injection of the anaesthetic into this region. This would have a local, direct and immediate action but would only be expected to last a few hours. This is an unlikely mechanism due to the particular anatomical features and tissue planes involved.18 The injection may also act indirectly via a sympathetic vascular reflex leading to an ischaemic paralysis. This may be due to the vasoconstrictor in the anaesthetic or the mechanical action of the needle itself, stimulating the sympathetic plexus associated with the external carotid artery.I4.l7 Oral surgery can be a factor in eliciting facial palsy. Any surgery in the region of the stylomastoid foramen and parotid gland may result in direct damage to the facial nerve and subsequent paralysis. Postoperative infections and oedema have been reported to induce facial paralysis subsequent to third molar removal, coronoidectomy and osteotomies of the mandible.14.'9.20-22 This has been variously attributed to the placement of retractors behind the ascending ramus, fracture of the styloid process, retropositioning of the prognathic mandible, postoperative oedema or haematoma, and coincidental Bell's palsy.21.22Other dental infections may also elicit a facial palsy due to an inflammatory response with or without compression of the facial nerve, as can acute middle ear infection^.'.'^ External trauma to the temporal or parotid regions containing the facial nerve may result in facial palsy similar to surgical trauma.I4 Many other conditions, syndromes and pathoses are associated with facial palsy. Conditions affecting the parotid gland such as neoplasms and sarcoidosis may elicit ~ymptoms.~ A high correlation between both diabetes and hypertension and Bell's palsy has been found when compared with the general popul a t i ~ nThe . ~ ~diabetic has been shown to be 4.5 times 264
more likely to develop Bell's palsy than the nondiabetic A higher incidence of Bell's palsy has been reported during pregnancy, in particular the last trimester and the first few weeks postp a r t ~ m . Bell's ~ ~ . ~palsy ~ occurs 3.3 times more frequently during ~regnancy.'.'~This has obvious direct relevance to Case 2. Management Due to the varied pathogenesis of idiopathic facial palsy, a number of treatments have been advocated. These include adrenocorticotrophic hormone the rap^,^"^ prednisone therapy,'.'4,28~29dimexide and nicotinic acid compresses,3O and surgical decompression of the facial nerve.'-3 Prednisone therapy is the most widely advocated and successful treatment but must be initiated as soon as possible to prevent prolonged symptoms due to demyelination. 1.28.31 Any delay in commencing steroids seems to be a major factor responsible for the failure of treatment.29Falco and ErikssonZ6found that steroids did not appear to influence recovery in the pregnancy-related cases. This we would expect as the condition is probably not due to a viral demyelination in such cases. Surgical decompression of the facial nerve has fallen into disfavour as it seldom appears to aid recovery of function.' If the facial nerve has been severed, end-to-end anastomosis of the proximal and distal segments of the facial nerve, grafting of a segment of sensory nerve into the defect in the facial nerve, and anastomosis of the proximal hypoglossal segment to the distal facial nerve segment are highly regarded methods of repair to the extratemporal facial nerve.' Management of facial palsy has been limited in the past to protection and lubrication of the eye. The role of the dentist in facial palsy is limited to the maintenance of oral hygiene which may suffer because of lost muscle tone. Occasionally the provision of aesthetic improvements such as lipsupporting prostheses is required in long-term cases. Although the majority of cases recover spontaneously, the possibility of prolonged or incomplete recovery must be considered when constructing a treatment regimen. The appearance of symptoms in other cranial nerves, in particular the trigeminal nerve, along with facial palsy need not necessarily be alarming. However, facial palsy does require immediate referral to the patient's medical practitioner for investigation and possible steroidal treatment.
Conclusion Although such occurrences are rare, dentists should be aware that certain dental procedures can Australian Dental Journal 1992;37:4.
initiate a facial palsy. Patients may also present to a dental surgery seeking a dental cause for their facial palsy as in the two cases presented. Those presenting in the dental surgery should be immediately referred to their medical practitioner for the option of steroidal therapy. For this to be a viable option, it must be initiated early in the condition or any benefits may be negated. Adjunctive treatment in the dental surgery is limited to oral hygiene maintenance and occasional provision of aesthetic improvements. With the increasing incidence of AIDS in the community and its high correlation with neurological defects, a test for HIV antigens or other serological markers may also be indicated. References 1. Adour KK. Diagnosis and management of facial paralysis. N Engl J Med 1982;307:348-51. 2. Gayford JJ, Haskell R. Clinical oral medicine. 2nd edn. Bristol: John Wright, 1979:234-44. 3. Shafer WG, Hine MK, Levy BM. A textbook of oral pathology. 3rd edn. Philadelphia: WB Saunders, 1974:800-01. 4. Adour KK, Hilsinger RL Jr, Callan EJ. Facial paralysis and Bell’s palsy: a protocol for differential diagnosis. Am J Otol 1985;N0~:S~ppl:68-73. 5. Shuaib A, Lee MA. Recurrent peripheral facial nerve palsy after dental procedures. Oral Surg Oral Med Oral Pathol 1990;70:738-40. 6. Adour KK, By1 FM, Hilsinger RL Jr, Kahn ZM, Sheldon MI. The true nature of Bell’s palsy: analysis of lo00 consecutive patients. Laryngoscope 1978;88:787-801. 7. Djupesland G, Berdal P, Johannsen TA, Degre M, Stein R, Skrede S. The role ofviral infection in acute peripheral facial palsy. Acta Otolaryngol Stockh 1975; 79:221-7. 8. Adour KK, Bell DN, Hilsinger RL Jr. Herpes simplex virus in idiopathic facial paralysis (Bell’s palsy). JAMA 1975;233:527-30. 9. Abdel Baki F, Maghazi H, Eassa A, Talaat F. Peripheral nerve involvement in acute Bell’s palsy. J Laryngol Otol 1988; 102:447-8. 10. Sawamura Y, Tashiro K, Shima K, Moriwaka F, Abe H. Clinical analysis of trigeminal neuropathy as initial manifestations - an aetiological study. No T o Shinkei 1988;40:863-8. 11. Hanner P, Badr G, Rosenhall U, Edstrom S. Trigeminal dysfunction in patients with Bell’s palsy. Acta Otolaryngol S t d h 1986; 101:224-30. 12. Mang WL, Bonkowsky VM. Acute viral infections in association with idiopathic peripheral facial paralysis. HNO 1987;35:310-3. 13. Nakamura K, Yanagihara N. Neutralization antibody to herpes simplex virus type 1 in Bell’s palsy. Ann Otol Rhinol Laryngol Suppl 1988;137:18-21. 14. Gray RLM. Peripheral facial nerve paralysis ofdental origin. Br J Oral Surg 1978;16:143-50.
Australian Dental Journal 1992;37:4
15. Levy RM, Bredesen DE, Rosenblum ML. Neurological manifestations of the acquired immunodeficiency syndrome (AIDS): experience at UCSF and review ofthe literature. J Neurosurg 1985;62:475-95. 16. Chilla R, Booken G, Rasche H. Bell’s palsy as the initial symptom of HIV infection. Laryngol Rhinol Otol Stuttg 1987;66:629-30. 17. Tiwari IB, Keane T. Hemifacial palsy after inferior dental block. Br Med J 1970;1:798. 18. Stoy PJ, Gregg G. Bell’s palsy following local anaesthesia. Br Dent J 1951;91:292-3. 19. Chuong R. Contralateral facial palsy following coronoidectomy. Oral Surg Oral Med Oral Pathol 1984;57:23-5. 20. Rubin MM, Cozzi G. Unilateral facial palsy following intraoral coronoidectomies. Oral Surg Oral Med Oral Pathol 1987;64: 156-8. 21. Dendy RA. Facial nerve paralysis following sagittal split mandibular osteotomy: a case report. Br J Oral Surg 1973;11:101-5. 22. Guralnick W, Kelly JP. Palsy ofthe facial nerve after intraoral oblique osteotomies ofthe mandible. J Oral Surg 1979;37743. 23. Yanagihara N, Hyodo M. Association of diabetes mellitus and hypertension with Bell’s palsy and Ramsay Hunt syndrome. Ann Otol Rhinol Laryngol Suppl 1988;137:5-7. 24. Adour KK, Wingerd J, Doty HE. Prevalence ofconcurrent diabetes mellitus and idiopathic facial paralysis (Bell’s Palsy). Diabetes 1975;24:449-51. 25. McGregor JA, Guberman A, Amer J, Gwdlin R. Idiopathic facial nerve paralysis (Bell’s palsy) in late pregnancy and the early puerperium. Obstet Gynecol 1987;69:435-8. 26. Falco NA, Eriksson E. Idiopathic facial palsy in pregnancy and the puerperium. Surg Gynecol Obstet 1989;169:337-40. 27. Hilsinger RL Jr, Adour KK, Doty HE. Idiopathic facial paralysis, pregnancy, and the menstrual cycle. Ann Otol Rhinol Laryngol 1975;84:433-42. 28. Devriese PP, Schumacher T, Scheide A, de Jongh RH, Houtkooper JM. Incidence, prognosis and recovery of Bell’s palsy. A survey of about 1000 patients (1974-1983). Clin Otolaryngol 1990;15: 15-27. 29. A1 Husaini A, Jamal GA, Hilmi AM, Mathur VS. Steroid therapy in Bell’s palsy. Int J Clin Pharmacol Ther Toxicol 1986;24:430-2. 30. Farber FM. Treatment of primary neuritis ofthe facial nerve with compresses of dimexide and nicotinic acid. Zh Nevropatol Psikhiatr 1984;84:1161-3. 31. Katusic SK, Beard CM, Wiederholt WC, Bergstralh EJ, Kurland LT. Incidence, clinical features, and prognosis in Bell’s palsy, Rochester, Minnesota, 1968-1982. Ann Neurol 1986;20:622-7.
Address for correspon&nce/reprints: University of Pittsburgh, Dental Medicine Ortho., 3501 Terrace Street, Pittsburgh, PA, 15261, USA.
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