Holland NJ, Weiner GM. Recent developments in Bell's Palsy. Br Med J. 2004; 329:553-557
Peitersen E. Bell's palsy: the spontaneous course of 2,500 peripheral facial nerve palsies of different etiologies. Acta Otolaryngol Suppl. 2002; 549:4-30
Robertson D, Smith AJ. The microbiology of the acute dental abscess. J Med Microbiol. 2009; 58:155-162
Finsterer J. Management of peripheral facial nerve palsy. Eur Archiv Oto-rhino-laryngol. 2008; 265:743-752
Ramsey MJ, DerSimonian R, Holtel MR, Burgess LP. Corticosteroid treatment for idiopathic facial nerve paralysis: a meta-analysis. Laryngoscope. 2000; 110:335-341
Dresner SC.San Francisco: American Academy of Ophthalmology; 2000
Moore K, Agur A, Dalley A., 4th edn. Philadelphia: Lippincott Williams & Wilkins; 2011
Clark JR, Carlson RD, Sasaki CT, Pachies AR, Steere AC. Facial paralysis in Lyme disease. Laryngoscope. 1985; 95:1341-1345
Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2006; 43:1089-1134
Sreenivas V, Chaturvedi J, Pai C, Singh P, Sachadeva R, Balasubramanya A. Childhood facial palsy – a case report. J Otorhinolaryngol. 2012; 14:1-5
Murakami S, Mizobuchi M, Nakashiro Y, Doi T, Hato N, Yanagihara N. Bell's palsy and herpes simplex virus: identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med. 1996; 124:27-30
Salina RA, Alvarez G, Daly F, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2008;
Sullivan FM, Swan IRC, Donnan PT, Morrison JM, Smith BH, KcKinstry B Early treatment with prednisolone or acycylovir in Bell's Palsy. New Engl J Med. 2007; 357:1598-1607
Grogan PM, Gronseth GS. Practice parameter: steroids, acyclovir, and surgery for Bell's palsy (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2001; 56:830-836
Ramsey MJ, DerSimonian R, Holtel MR, Burgess LP. Corticosteroid treatment for idiopathic facial nerve paralysis: a meta-analysis. Laryngoscope. 2000; 110:335-341
Facial nerve palsy has specific symptomology, but varied aetiology. Prompt and thorough assessment is required to ascertain if upper or lower motor neurone damage has occurred. This report discusses a 6-year-old female, presenting in the Emergency Department with unilateral facial weakness. Initially thought to be facial swelling relating to her carious dentition, clinical assessment from the maxillofacial team identified that the patient had a unilateral facial palsy, later diagnosed as Bell's palsy. Her delayed presentation was due to initial misdiagnoses in primary care. This case report aims to highlight its aetiology, clinical features and appropriate management.
CPD/Clinical Relevance: To make the general dental practitioner aware of different causes of facial paralysis, and to provide GDPs with an algorithm to follow in the presentation of a facial palsy in the primary care setting.
Article
The most common cause of facial nerve paralysis is Bell's palsy, often thought to be the result of herpes simplex or herpes zoster virus activation.1,2 Statistically, it is most prevalent in patients aged between 15 and 45, and is often diagnosed after the exclusion of more serious causes of facial paralysis.2 Dental abscesses are relatively common causes of facial swellings. When dental pulp is breached, as a result of carious processes, or trauma to the dentition,3 it becomes infected and necrotic. Anaerobic bacterial organisms begin to colonize these tissues. Eventually, polymicrobial biofilms, and their harmful metabolic waste products, escape into the periapical tissues, causing dental abscess formation, which can track within the soft tissue spaces of the neck, resulting in facial swellings.
Presentation
A 6-year-old female presented in the Emergency Department at Nottingham Queen's Medical Centre (QMC). Her mother reported a 2-week history of a persistent left facial swelling, which started as toothache from the upper left quadrant. During this time frame, initial management was provided through her GP, who prescribed a course of amoxicillin, and her GDP, who advised tooth extractions of the carious deciduous dentition. Upon completion of the antibiotics, the facial swelling remained unchanged. It was this presentation that prompted their attendance at the QMC.
Upon clinical examination, the child had a generalized, carious primary dentition, but this was in the absence of abscesses, sinus tracts, tooth mobility and tenderness. More strikingly, the patient demonstrated signs of left-sided facial paralysis; she was unable to raise her left eyebrow to the same degree as her right, her left eye blink reflex was not present, and she had reduced emotional movements of the face. A normal neurological assessment followed: no numbness, weakness or abnormal sensation to any of the limbs, and no history of any memory loss, or alteration in behaviour or personality was identified.
Causes of her facial paralysis were systematically considered and excluded. Full blood count, urea and electrolytes and clotting were all normal. Furthermore, blood cultures were negative for any microbial insults. A meningococcal polymerase chain reaction test ruled out meningitis and blood samples were negative for Borrelia (Lyme disease) antibodies.
Eventually the diagnosis of Bell's palsy was confirmed. Due to the prolonged symptomology experienced by this child, steroid treatment was not indicated,4,5 and conservative management without medical intervention ensued.
Anatomy of the facial nerve
The presynaptic neurone of the facial nerve travels from the precentral gyrus in the frontal lobe, along the corticobulbar tract, to the facial motor nucleus. The neurone(s) synapses with the post-synaptic neurones, with presynaptic neurones from the left cortex synapsing with neurones innervating the right motor neurones and vice versa. However, the upper part of both facial nuclei receive innervation from both left and right central gyri, the result being that there is a bicortical representation of the frontalis muscle (Figure 1).1,6,7 The lower motor neurone of the facial nerve exits the nucleus, and then transverses the internal acoustic meatus, exiting via the stylomastoid foramen, before branching into its five separate peripheral branches in the parotid gland (Figure 2).
Figure 1. The bicortical representation of the frontalis muscle. Note how, if the lesion occurs in the right precentral gyrus, weakness only occurs to the lower left side of the face, due to efferent fibres from the left precentral gyrus innervating the superior left facial nucleus, thus resulting in forehead sparing (shown in blue). With lower motor neurone damage, the entire affected side of the face becomes paralysed (shown in red). Taken from Holland and Weiner.1Figure 2. The course of the facial nerve after it leaves the stylomastoid foramen. Any tumours, cysts, or other space-occupying lesions, as well as traumatic injuries in this area may affect the function of this nerve, and thus result in paraesthesia. Taken with kind permission from teachmeanatomy.info/head/cranial-nerves/facial-nerve/13
Aetiology of facial paralysis
Possible causes of facial paralysis include:
Upper motor neurone damage, eg cerebral infarct or brain tumours;
Acute suppurative ear disease and other otological conditions can cause damage to the facial nerve due to the close proximity to the nerve;
Trauma, causing abrasions or lacerations to the branches of the facial nerve, or fractures to the temporal bone, can disrupt facial nerve function;
Tumours and/or swellings of the parotid gland can lead to paralysis of the nerve fibres by compressing the facial nerve;10
Local anaesthetic affecting the facial nerve (can be a consequence during inferior dental blocks);
Bell's palsy.
In reference to the case report, Bell's palsy is the most common cause of facial paralysis within the literature. It is typically idiopathic but, in some cases, herpes simplex virus has been isolated from the facial nerve of Bell's palsy patients.11 Herpes zoster virus has also been linked to facial palsy symptomology, although it is typically associated with vesicles in the conchal bowl, soft palate or tongue, as well as tinnitus and loss of balance.1 Less common causes of Bell's palsy include Lyme disease, a spirochetal infection often caused from tick bites.8 Manifestations of these bites can lead to more serious conditions, such as Lyme meningitis and Lyme carditis, where hospitalization and IV antibiotics may be required.9
Bell's palsy generally occurs in an older age group, as compared to the patient discussed in this case report. Childhood Bell's palsy is a rare clinical entity, however, in patients of this age group, a rapid onset facial weakness is most likely to be a Bell's palsy. However, it is vital that this is confirmed with a good patient history, as a facial weakness that has occurred more gradually is more likely to be as a result of a compressive lesion which will require further investigation.10
Clinical features
Identifying the clinical features of unilateral facial paralysis should enable its origin to be narrowed down to either upper motor neurone or lower motor neurone damage to the facial nerve.
Upper motor neurone damage will retain the classical presentations of emotional movements of the face, the blink reflex, and the ability to wrinkle the forehead (Figure 1). With lower motor neurone lesions of the facial nerve, none of these actions is present. In addition, drooling from the commissure is common, whilst lacrimation, taste and hearing may be affected. Ipsilateral taste lost from the tongue may also occur.12
Management of Bell's palsy
Patients who are otherwise fit and well will find their Bell's palsy spontaneously resolves within a couple of weeks. Nonetheless, literature supports medical intervention for acute management.14,15,16
It is typically treated with oral corticosteroid therapy.5,14 A randomized, double blind trial found that prednisolone gave the best chance of recovery, using the House-Brackmann grading scale.15 It is generally accepted that steroids are beneficial within the first 3 days of onset, however, using them up to a week after is generally regarded as good practice.4,5 A short course of prednisolone may result in 80–90% complete recovery; in the absence of such treatment, recovery may only be successful in 50–60% patients within the same timeframe.16 Acyclovir has been used to treat Bell's palsy in the past, but it is now considered substandard to steroids, although the literature highlights its logic due to Bell's palsy having potential viral aetiology.4,5,14,15,16,17,18 A Cochrane review found that antivirals used in conjunction with steroids may improve patient outcomes.14
During the acute phase of facial paralysis, patients may lose their blink reflex, due to the reduced function of the orbicularis oculi muscles.1,7 The application of an eyepatch, plus the prescription of an eye lubricant, such as methylcellulose-free eye ointment6 is recommended to avoid corneal drying and abrasion.10 Patients should also be informed about potential symptomology of corneal damage, including visual disturbances, pain and redness to the eyes, and be advised to seek urgent medical assessment should they develop. On occasion, permanent eyelid weakness may result from Bell's palsy, and in such incidences, surgical correction may be required.10 Generally, the facial palsy should disappear and muscle function will gradually return.
Management for general dental practitioners
In order to aid the general dental practitioner, during the course of this case report we have formed the following algorithm (Figure 3) on appropriate management for GDPs to follow in cases of facial weakness.
Figure 3. A suggested algorithm for the management of facial weakness in a general dental practice setting.
Figure 3 highlights the case of an acute facial palsy with eyebrow sparing. In an adult patient, this is highly indicative of a stroke, and may be either haemorrhagic or ischaemic in origin.19 The FAST algorithm pneumonic aids the practitioner in the assessment for stroke victim. As well as facial weakness, patients may have arm weakness, speech impairment and slurring. In these situations, the time taken to receive urgent medical attention is an important factor in order to minimize the long-lasting effects of the stroke.19
General dental practitioners can also direct patients currently suffering with Bell's palsy to a patient information website, entitled ‘Facing up to uncertainty’ available at www.evidentlycochrane.net/bells-palsy-facing-up-to-uncertainty/ This gives a patient perspective of the condition, and outlines various treatment modalities.20
Discussion
The literature highlights how the clinical presentation of Bell's palsy in patients under 15 years of age is uncommon.1,2 For this 6-year-old child, her diagnosis was extremely rare. The main symptom which guided the diagnosis to a lower motor neurone paralysis, like Bell's palsy, was her inability to wrinkle her forehead. In addition, her symptoms also pointed to a resolving facial palsy, because she could partially raise the left eyebrow upon examination.
Before attending the Emergency Department, the patient's general medical and dental practitioners failed to recognize the symptoms of Bell's palsy. This ultimately led to the delay in her diagnosis and subsequent treatment.
Conclusions
Timely diagnosis of Bell's palsy is required to enable patients to receive appropriate management with antivirals and steroids.10 Reasons for this include a known history of toothache in the associated area, and the facial asymmetry masquerading as a facial swelling. Furthermore, in this case, there were language barriers associated with taking a detailed history. Fortunately, no long-term harm resulted, because Bell's palsy tends to be a self-limiting disease and, in this instance, all other known causes of facial nerve paralysis were systematically excluded.
