The authors report the case of a 35-year-old Arab man who presented with unilateral facial nerve palsy in the presence of an infected lower third molar. The paralysis occurred within hours of the development of a left-sided facial swelling. Surgical removal of the tooth and drainage of the abscess produced significant improvement in facial nerve function, and total resolution occurred prior to clinical follow-up 10 days later. The authors discuss the aetiology of this hemifacial paralysis and its significance as a clinical sign of third molar odontogenic infection.
Peripheral facial nerve paralysis is the commonest cranial nerve motor neuropathy . The causes range from cerebrovascular accident to iatrogenic damage, but there are few reports of facial nerve weakness or paralysis attributable to odontogenic infection . This case report describes a patient who presented with infection and swelling relating to the lower left third molar, and rapidly developed left-sided facial nerve paralysis. The authors discuss the aetiology of this palsy, and the significance of peripheral facial nerve paralysis as an important, albeit rare, sign of an infected lower third molar.
An otherwise healthy 35-year-old Arab male was referred to the authors’ maxillofacial surgery clinic from the hospital’s neurologist for evaluation of a left-sided submandibular facial swelling that had been gradually enlarging over the previous 48 h. The patient complained of severe pain from his decayed lower left third molar, which preceded the development of a left sided ‘droopy’ face ( Fig. 1 ). This started within hours of the left-sided submandibular swelling and progressed for the next 2 days. He had developed a complete left-sided lower motor neuron palsy of the facial nerve. The patient denied any history of trauma, surgery or other recent infections (viral infections, middle ear infections). Clinical examination also revealed a swelling involving the lower left buccal space with limited mouth opening (34 mm). On closer inspection of his palsy, there was loss of action of all muscles of facial expression on the left side, but no loss of taste of the anterior two-thirds of his tongue (chorda tympani), no hyperacusis (CNVII to stapedius) and no xerophthalmia (greater petrosal nerve). The neurologist and the authors’ team performed a full neurological examination which was unremarkable except for the left-sided lower motor neuron palsy of the facial nerve. The patient was admitted for further investigations, monitoring and incision and drainage of the abscess in the operating theatre.
Blood samples were sent to the hospital laboratory, and other than an elevated white blood cell count (16 × 10 3 cells/mm 3 ) with a ‘left shift’ in his polymorphonuclear neutrophils, his full blood count, urea and electrolytes and fasting glucose were all within the normal range. His C-reactive protein was slightly elevated at 8 mg/l. Blood samples were sent for Gram staining, culture and sensitivity, viral serology and an anti-nuclear antibody screen. His physiological parameters were all within normal on admission, and he was empirically started on intravenous antibiotics (cefuroxime 750 mg, three times daily), oral paracetamol and a non-steroidal anti-inflammatory drug (NSAID).
An orthopantomogram (OPG) showed a decayed medially impacted, partially erupted lower left third molar with an obvious apical radiolucency. The patient also had a contrast computerized tomography (CT) scan of his brain, cerebello-pontine angle, internal auditory meatus, and facial skeleton to rule out possible tumours, fractures and a stroke. The CT confirmed the presence of a 2 cm × 2.5 cm submandibular fascial space pus accumulation between skin and the mylohyoid muscle extending medially to the anterior belly of the digastric muscle.
He was taken to theatre where his lower left third molar was elevated and a 2 cm submandibular incision parallel to the inferior border of the mandible was made. The region was dissected bluntly under general anaesthesia. Exploration continued to the lateral and medial aspects of the angle of the mandible, where a large area of purulence was encountered and evacuated. About 2–3 ml of purulent, smelly blood speckled yellow exudate was drained from the incision site, which was sent for culture and sensitivity. A corrugated drain was inserted and left in situ for 24 h. The following morning the facial palsy was significantly improved. He was discharged the following day with a 5-day course of the same antibiotic and NSAIDs. After discussion with the neurologists, the patient was also started on a reducing dose of dexamethasone. All other blood tests were negative, including his blood cultures. The final cultures from the incision and drainage showed a few α-hemolytic streptococci, staphylococci, and a few anaerobic Gram-positive cocci. When he was reviewed 10 days later, there was complete resolution of his palsy ( Fig. 2 ).
Table 1 illustrates the different causes of facial nerve palsy and the clinical signs. In this patient’s case, trauma, malignancy and cerebrovascular accident were excluded. Bell’s palsy is the most common cause of unilateral facial paralysis. It is possibly due to reactivation of herpes simplex or herpes zoster within the geniculate ganglion but this is still being researched. It is conceivable that the facial weakness in this case was a coincident episode of Bell’s palsy. The dental infection was present before the swelling and paralysis. Dental manipulation has been implicated as a precipitating factor in recurrent Bell’s palsy, but the patient denied any previous episodes of facial nerve weakness .
|Common causes of the lesion||Facial palsy||Clinical features of the lesion||Comments|
|Idiopathic (Bell’s palsy)||↑||↓ or ↔||↑ or A||↑ or ↔||Clinical features are dependent on the location of the lesion|
|Iatrogenic trauma (local anaesthetic blocks and infiltrations and direct or indirect surgical trauma to CNVII e.g., parotidectomy)||↑||↔||A||↔||Trauma due to surgery in the anterior fossa and/or the temporal bone could have an effect on taste, hearing and lacrimation|
|Non-iatrogenic trauma (barotraumas, temporal bone and/or base of skull fractures)||↑||↓ or ↔||↑ or A||↑ or ↔||Other features could be present e.g., CNVIII damage|
|Viral: human immunodeficiency (HIV) infection, herpes simplex virus (HSV), Varicella zoster virus (VZV), Cytomegalovirus (CMV), Epstein-Barr virus (EBV)||↑||↓ or ↔||↑ or A||↑ or ↔||VZV infection of the geniculate ganglion is known as Ramsay–Hunt syndrome|
|Other infections: middle ear infections, Botulinus intoxication ( Clostridium botulinum ), Lyme disease ( Borrelia burgdorferi ), tetanus ( Clostridium tetani ), syphilis ( Treponema palladium )||↑||↓ or ↔||↑ or A||↔|
|Posterior cranial fossa tumours||↑||↓||↑||↑|
|Acoustic neuroma, Cholesteatoma||↑||↓ or ↔||↑ or A||↔||Lesion is usually between the geniculate ganglion and stylomastoid foramen|
|Acute or chronic leukaemia (granulocytic sarcoma or chloroma)||↑||↔||A||↔|
|Cerebrovascular accident (CVA), space occupying lesions (intracranial brain tumours)||↑||↓ or ↔||↑ or A||↑ or ↔||Ipsilateral Upper Motor Neuron facial nerve (CNVII) palsy (contralateral cortical control of CNVII remains intact)|
|Multiple sclerosis (MS)||↑||↓||↑||↑|
|Autoimmune: sarcoidosis (Heerfordt syndrome), scleroderma, Melkersson–Rosenthal syndrome||↑||↓||↑||↑|
|Metabolic: acute porphyria, diabetes mellitus (DM)||↑||↔||A||↔|