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Facial nerve palsy following intra-oral surgery performed with local anaesthesia

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East Lancashire Maxillofacial Service, Blackburn Royal Infirmary, Blackburn BB2 3LR, U.K.


Case reports



The precise cause of Bell's palsy remains unclear. A variety of mechanisms have been linked to this palsy, including viral re-activation, demyelination, oedema, vasospasm and trauma. A link with dental treatment has been suggested previously, and a series of seven cases of facial nerve palsy following intra-oral surgery are reported. All of the patients had local anaesthetic solution containing adrenaline as the vasoconstrictor administered. There may be under-reporting of this association, as patients with facial nerve palsy are treated by specialists from several disciplines, not only maxillofacial surgeons. An association with local anaesthesia administered to permit dental treatment would have important medicolegal consequences, and perhaps go some way to explaining the pathophysiology of Bell's palsy.

Keywords: adrenaline, facial nerve palsy, local anaesthetic

J.R.Coll.Surg.Edinb., 45,October 2000, 330-333


The term facial nerve palsy is used when the paralysis is thought to be the result of a specific disease process. Facial nerve palsy has numerous associations, including strokes, acoustic nerve tumours, diabetes mellitus, multiple sclerosis, Lyme Disease, pregnancy, trauma, and viral infections including Herpes-Zoster. There are also reports of dental causes of facial paralysis,1-3 and it may complicate oro-facial granulomatosis, maxillo-facial surgical procedures (both intra- and extra-oral) and even fracture of the mandibular condylar neck.4-7 Facial nerve palsy has also been reported in patients infected with Human Immunodeficiency Virus, and may be the presenting symptom.8, 9

The term Bell's palsy is used to denote those cases of lower motor neurone facial nerve paralysis for which no specific cause is identified.

Seven cases of facial nerve palsy following dental or maxillofacial procedures are described. They can be easily distinguished from unintentional infiltration of the facial nerve in the parotid region with local anaesthetic because of the delay in onset of the facial weakness, and because the weakness persists for some considerable time after the effect of the local anaesthetic would have been expected to have worn off.


Case 1

A 38-year-old man had a right inferior dental nerve block to allow the replacement of an amalgam restoration in his lower second molar tooth. Over 6 hours he developed a progressive ipselateral facial weakness and hyperaccusis was noted. He was referred for specialist opinion after returning to the dental practice the following day.

On examination, he was found to have a lower motor neurone weakness of his right facial nerve, graded as II according to the House and Brackmann system (Table 1), and loss of taste on the anterior two-thirds of the tongue on the affected side. Full neurological and otological examinations were otherwise normal, and prednisolone and physiotherapy were commenced. Routine haematological and biochemical tests, ESR and CT scan were all normal. The weakness resolved after approximately 3 months.

Table 1: Grading of lower motor neurone weakness (after House and Brackmann)

Grade Description
I Normal
II Slight
III Moderate
IV Moderately severe
V Severe

Case 2

A 29-year-old man had local anaesthetic infiltration prior to the forceps extraction of the carious upper right third molar tooth. The following day he was referred with a right-sided facial weakness, which had gradually developed over 8 hours after the start of treatment. Thorough examination confirmed a Grade IV lower motor neurone paralyses of the right facial nerve, but no other findings were noted. Routine blood tests were all within normal ranges. The patient received prednisolone and physiotherapy, and the weakness improved over several months.

Case 3

A 45-year-old female patient had her lower left first premolar tooth extracted by a general dental practitioner, who had achieved anaesthesia by means of injecting close to the tooth. Within 24 hours of this apparently uncomplicated procedure she had developed a left facial weakness. Her dental treatment had been carried out by a dentist whilst she had been on holiday, and when she returned she had sought the advice of her general medical practitioner who had prescribed prednisolone, and referred her for specialist opinion.

Examination confirmed the Grade II lower motor neurone palsy, and a subsequent computerised tomography (CT) scan of brain, base of skull and parotid region was entirely normal. Despite early treatment with prednisolone, her palsy persisted for nine months without significant improvement.

Case 4

A 45-year-old man attended his general dental practitioner, and had a left sided inferior dental nerve block injection to allow a dental filling to be placed in his lower left first molar tooth. Approximately four hours later he noticed excess lacrimation affecting his right eye, and over the next 14 hours he developed a gradually progressive lower motor neurone palsy of his right facial nerve, assessed as Grade II.

Examination revealed no other neurological abnormalities. He received prednisolone, and the facial weakness resolved over several months.

Case 5

A 49-year-old man was referred via the Accident and Emergency Department with a left-sided facial palsy, initially noted some eighteen hours after he received an infiltration of local anaesthetic to allow dental fillings to be placed.

Examination confirmed a Grade I lower motor neurone lesion affecting the left facial nerve and treatment with prednisolone was initiated.

As he was only temporarily resident in the area, he was referred to a hospital nearer his home for further investigation and treatment.

Case 6

A 37-year-old woman underwent apicectomy of her left maxillary central and lateral incisor and canine teeth under day-case general anaesthesia, and the operative sites were infiltrated with 0.25% bupivacaine with adrenaline 1:200,000. Her past medical history included an occipital skull fracture as a child, from which she had made a full recovery with no neurological sequelae. At her post-operative review appointment 2 weeks after the apicectomies were performed Grade II weakness of the buccal branch of the facial nerve on the ipselateral side was noted. The patient stated that she had been aware of the weakness from the immediate postoperative period, but that she had not sought advice sooner as she had believed that post-operative swelling was the cause. It was difficult to explain the weakness as a result of direct damage to the nerve concerned, as it was out of the surgical field. A magnetic resonance image scan demonstrated areas of gliosis in her frontal lobes, consistent with a contre-coup injury sustained at the time of her childhood skull fracture, but no lesions were identified which could have caused the facial weakness. She was prescribed prednisolone, and the weakness improved, but had to discontinue the steroids because of side effects after 2 weeks.

Case 7

A 35-year-old woman underwent a bimaxillary osteotomy under general anaesthesia for the correction of facial disproportion and malocclusion. Bupivacaine 0.25% with adrenaline 1:200,000 was injected at the operation sites to reduce per-operative haemorrhage and post-operative discomfort. On the first post-operative day weakness of the left lower eyelid was noted, but this was believed to be a transient post-operative complication. Her peri-operative drug regimen included dexamethasone 4mg TDS for 48 hours, before receiving depomedrone 20 mg as an intramuscular injection.

When reviewed in clinic two weeks after the operation she was noted to have a Grade IV lower motor neurone palsy affecting the left facial nerve (Figure 1). This had gradually worsened in the first few days after her peri-operative steroid regimen had been discontinued. Presumably, the high dose steroids she had received in the immediate post-operative period had suppressed the inflammatory process leading to post-operative facial weakness which had progressed when the steroid treatment was discontinued.

All haematological and biochemical tests were normal, as was a CT scan of brain and skull base. Treatment with prednisolone was started, and she also received physiotherapy. After 2 months partial recovery of the facial nerve was noted.

Figure 1: Weakness of the left cheek 2 weeks post-operatively



The facial nerve leaves the brainstem to run in the internal acoustic meatus with the eighth cranial nerve. It gives rise to various branches as it runs in the facial canal before it leaves the skull via the stylomastoid foramen. In addition to providing the motor innervation to the facial muscles, branches supply secretomotor fibres to the lacrimal gland and the submandibular ganglion, sensory fibres to the anterior two-thirds of the tongue via the chorda tympani, and motor fibres to the stapedius muscle in the middle ear. The site of a seventh cranial nerve lesion can be predicted by assessing which of the branches are involved. It is also possible to determine whether the lesion is of the upper or lower motor type, as in the latter case the forehead muscles are spared because of crossover innervation at a higher level.

Lower motor neurone lesions of the facial nerve can be the result of specific disease processes already mentioned. For those cases without a readily identifiable cause, the term Bell's Palsy is used to denote the idiopathic origin. There has been speculation that the pathogenesis of Bell's palsy is in fact a polyneuritis, following viral reactivation. Herpes Simplex Virus (HSV) has been implicated. HSV type 1 DNA had been isolated from facial nerve endoneurium.10 Ramsay-Hunt Syndrome classically consists of facial nerve palsy in association with vesicles on the tragus and soft palate, but other facial and oral sites can also be affected. Herpes Zoster Virus can be isolated from these vesicles. It has been suggested that other viruses could also cause facial palsy, and that dental treatment could lead to virus reactivation. Reflex sympathetic vasospasm in the vessels supplying the facial nerve following dental injections has also been suggested as the underlying mechanism for facial palsy following dental treatment.2,3 This would be mediated via the sympathetic nerve plexus which is distributed throughout the head and neck on vessels arising from the external carotid arteries. The stimulus for this vasospasm could be the adrenaline used as vasoconstrictor in the local anaesthetic, or direct damage from the needle itself. Ischaemia, swelling and nerve compression could follow. Case number four is important in this respect because the facial palsy developed on the side opposite the injection site, so direct trauma during the procedure to structures on the side of the facial weakness can be excluded.

There is evidence to support prednisolone therapy in the treatment of Bell's palsy, and it has been reported that delay in initiation of steroid treatment can adversely affect outcome.9,11,12,13 Combination treatment with aciclovir and corticosteroids may improve the outcome in idiopathic facial nerve paralysis. Physiotherapy, in the form of transcutaneous peripheral nerve stimulation, has an important role. If the facial nerve palsy results in weakness of the eyelids the eye must be protected. In the short term, patches are useful, as are chloramphenicol eye drops or ointment, and tarsorraphy is indicated when recovery is prolonged.


The author would like to thank the following Consultants for permission to report on their patients, and for their help with the article: Mr W. Simpson and Mr R.T. Tuffin, Maxillofacial Unit, Withington Hospital, Manchester M20 8LR; Mr S.G. Langton, Mr J.C. Lowry and Miss M.E. Morton, East Lancashire Maxillofacial Service, Blackburn Royal Infirmary, BB2 3LR. The assistance of Mrs Margaret Waddington at Blackburn Royal Infirmary, and the Department of Medical Illustration, The Royal Bolton Hospital with the clinical photographs is greatly appreciated.


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  11. Adour KK, Hilsinger LR JR, Callan EJ. Facial paralysis and Bell's palsy: a protocol for differential diagnosis. Am J Otol. 1985; Nov:suppl: 68-73
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  13. Al Husaini A, Jamal GA, Hilmi AM, Mathur VS. Steroid therapy in Bell's palsy. Int J Clin Pharmacol Ther Toxicol. 1986; 24: 430-2

Copyright date: 14th August 1999

Correspondence: G.C.S. Cousin, East Lancashire Maxillofacial Service, Blackburn Royal Infirmary, Blackburn BB2 3LR, U.K.

?000 The Royal College of Surgeons of Edinburgh, J.R.Coll.Surg.Edinb.

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